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6d4df4629faf24e5847c1cc0b0ef897f6cc3549c | wikidoc | CCDC186 | CCDC186
CCDC186 is a protein that in humans is encoded by the CCDC186 gene The CCDC186 gene is also known as the CTCL-tumor associated antigen with accession number NM_018017.
# Gene
## Location
CCDC186 has the chromosome location of 10q25.3 and is 53,750 bases in size oriented on the minus strand. PSORTII Protein k-NN Prediction indicated that C10orf118 is 65.2% of the time nuclear, 17.4% cytosolic, 8.7% mitochondrial, 4.3% vesicles of secretory system, and 4.3% endoplasmic reticulum.
## Expression
Analysis of gene expression in humans and other species indicates C10orf118 is ubiquitously expressed in all tissue types at varying developmental stages. An EST profile from NCBI displayed the greatest expression in bone marrow, kidneys, and the prostate cell lines. Breakdown by health state indicates high expression of C10orf118 in bladder carcinoma and prostate cancer.
# Protein
## General Properties
The protein of CCDC186 (NP_060487) is 898 amino acids in length. The predicted molecular weight is 103.7kdal and the isoelectric point is predicted to be 5.92.
## Composition
A serine rich region is observed in amino acids 710-747. A compositional analysis revealed that C10orf118 is Proline (1.1%) poor and Glutamic acid (14.1%) and Lysine (12.0%) rich.
## Interactions
CCDC186 protein was found to interact with proteins PLEKAH5, Ezra, GAMMAHV.ORF23, and SMAD3.
## Homology
Orthologous sequences of CCDC186 were not found to be in bacteria, archea, protist, or plants. CCDC186 has no human paralogs. The date of divergence for the orthologous sequences highly correlates with the sequences similarity in that the percent identity decreases as you go back in time. Closely related orthologs include mammals and birds and moderately related orthologs include other vertebrates such as fish, reptiles, and amphibians. Distantly related orthologous sequences are primarily observed in invertebrates.
## Motifs
## Post Translational Modification
CCDC186 is predicted to undergo multiple posttranslational modifications including predicted O-beta-GlcNAc attachment, phosphorylation, a nuclear export signal, glycation of lysines, GlcNAc O-glycosylation, N-glycosylation, and NetCorona sites.
## Clinical significance
Prior research indicates that the open reading frame of C10orf118 is linked to cutaneous T-cell lymphoma by a tumor antigen L14-2. The protein CCDC186 is also found at higher than normal levels in the breast cancer cell line BC 8701. | CCDC186
CCDC186 is a protein that in humans is encoded by the CCDC186 gene [2] The CCDC186 gene is also known as the CTCL-tumor associated antigen with accession number NM_018017.[3]
# Gene
## Location
CCDC186 has the chromosome location of 10q25.3 and is 53,750 bases in size oriented on the minus strand. PSORTII Protein k-NN Prediction indicated that C10orf118 is 65.2% of the time nuclear, 17.4% cytosolic, 8.7% mitochondrial, 4.3% vesicles of secretory system, and 4.3% endoplasmic reticulum.[4]
## Expression
Analysis of gene expression in humans and other species indicates C10orf118 is ubiquitously expressed in all tissue types at varying developmental stages. An EST profile from NCBI displayed the greatest expression in bone marrow, kidneys, and the prostate cell lines. Breakdown by health state indicates high expression of C10orf118 in bladder carcinoma and prostate cancer.[7]
# Protein
## General Properties
The protein of CCDC186 (NP_060487) is 898 amino acids in length. The predicted molecular weight is 103.7kdal and the isoelectric point is predicted to be 5.92.[8]
## Composition
A serine rich region is observed in amino acids 710-747. A compositional analysis revealed that C10orf118 is Proline (1.1%) poor and Glutamic acid (14.1%) and Lysine (12.0%) rich.[8]
## Interactions
CCDC186 protein was found to interact with proteins PLEKAH5, Ezra, GAMMAHV.ORF23, and SMAD3.[9][10]
## Homology
Orthologous sequences of CCDC186 were not found to be in bacteria, archea, protist, or plants. CCDC186 has no human paralogs. The date of divergence for the orthologous sequences highly correlates with the sequences similarity in that the percent identity decreases as you go back in time. Closely related orthologs include mammals and birds and moderately related orthologs include other vertebrates such as fish, reptiles, and amphibians. Distantly related orthologous sequences are primarily observed in invertebrates.[8][12]
## Motifs
## Post Translational Modification
CCDC186 is predicted to undergo multiple posttranslational modifications including predicted O-beta-GlcNAc attachment, phosphorylation, a nuclear export signal, glycation of lysines, GlcNAc O-glycosylation, N-glycosylation, and NetCorona sites.[14]
## Clinical significance
Prior research indicates that the open reading frame of C10orf118 is linked to cutaneous T-cell lymphoma by a tumor antigen L14-2.[15] The protein CCDC186 is also found at higher than normal levels in the breast cancer cell line BC 8701.[16] | https://www.wikidoc.org/index.php/CCDC186 | |
a628476c49fc6a65f4e6ec3a28286ea237ce4db1 | wikidoc | CCDC90B | CCDC90B
Coiled coil domain containing 90B, also known as CCDC90B, is a protein encoded by the CCDC90B gene.
# Gene
CCDC90B is located on chromosome 11 in humans. It is neighbored by:
- PCF11, a mammalian pre-mRNA cleavage complex 2 protein
- ANKRD42, ankyrin repeat protein involved with calcium ion bonding
- BC070093
- DLG2, a member of the membrane-associated guanylate kinase (MAGUK) family
# Protein
## Structure
This protein is characterized by the presence of a domain of unknown function, DUF1640. This domain is a characteristic of the entire protein with the exception of the first twenty-three amino acid residues - MNSRQAWRLFLSQGRGDRWVSRP - which are a mitochondrial targeting site and cleaved.
The protein has seven predicted alpha helices, a characteristic of coiled-coil proteins.
## Predicted Properties
Molecular Weight: 26.72 kDa
Isoelectric point: 7.5
Transmembrane Helices: None
Post-translation modifications:
## Cellular Location
CCDC90B is presumably a mitochondrial protein. It is predicted to contain at least three specific phosphorylation sites: Protein Kinase C Phosphorylation sites, Casein Kinase II Phosphorylation sites, and cAMP/cGMP Dependant Phosphorylation sites. | CCDC90B
Coiled coil domain containing 90B, also known as CCDC90B, is a protein encoded by the CCDC90B gene.
# Gene
CCDC90B is located on chromosome 11 in humans. It is neighbored by:[1]
- PCF11, a mammalian pre-mRNA cleavage complex 2 protein
- ANKRD42, ankyrin repeat protein involved with calcium ion bonding
- BC070093
- DLG2, a member of the membrane-associated guanylate kinase (MAGUK) family
# Protein
## Structure
This protein is characterized by the presence of a domain of unknown function, DUF1640. This domain is a characteristic of the entire protein with the exception of the first twenty-three amino acid residues - MNSRQAWRLFLSQGRGDRWVSRP - which are a mitochondrial targeting site and cleaved.
The protein has seven predicted alpha helices, a characteristic of coiled-coil proteins.
## Predicted Properties
Molecular Weight: 26.72 kDa
Isoelectric point: 7.5
Transmembrane Helices: None
Post-translation modifications:[2]
## Cellular Location
CCDC90B is presumably a mitochondrial protein. It is predicted to contain at least three specific phosphorylation sites: Protein Kinase C Phosphorylation sites, Casein Kinase II Phosphorylation sites, and cAMP/cGMP Dependant Phosphorylation sites. | https://www.wikidoc.org/index.php/CCDC90B | |
9549f3d760738dd3f7a00e385dfaf38a32f44e76 | wikidoc | CCNDBP1 | CCNDBP1
Cyclin-D1-binding protein 1 is a protein that in humans is encoded by the CCNDBP1 gene.
This gene was identified by the interaction of its gene product with Grap2, a leukocyte-specific adaptor protein important for immune cell signaling. The protein encoded by this gene was shown to interact with cyclin D. Transfection of this gene in cells was reported to reduce the phosphorylation of Rb gene product by cyclin D-dependent protein kinase, and inhibit E2F1-mediated transcription activity. This protein was also found to interact with helix-loop-helix protein E12 and is thought to be a negative regulator of liver-specific gene expression. Two alternatively spliced variants, which encode distinct isoforms, have been reported.
# Interactions
CCNDBP1 has been shown to interact with GRAP2 and Cyclin D1. | CCNDBP1
Cyclin-D1-binding protein 1 is a protein that in humans is encoded by the CCNDBP1 gene.[1][2]
This gene was identified by the interaction of its gene product with Grap2, a leukocyte-specific adaptor protein important for immune cell signaling. The protein encoded by this gene was shown to interact with cyclin D. Transfection of this gene in cells was reported to reduce the phosphorylation of Rb gene product by cyclin D-dependent protein kinase, and inhibit E2F1-mediated transcription activity. This protein was also found to interact with helix-loop-helix protein E12 and is thought to be a negative regulator of liver-specific gene expression. Two alternatively spliced variants, which encode distinct isoforms, have been reported.[2]
# Interactions
CCNDBP1 has been shown to interact with GRAP2[3] and Cyclin D1.[1] | https://www.wikidoc.org/index.php/CCNDBP1 | |
b563af1930a8fe7c561d5e155c1e4a17b10627fa | wikidoc | CD200R1 | CD200R1
Cell surface transmembrane glycoprotein CD200 receptor 1 is a protein that in humans is encoded by the CD200R1 gene. CD200R1 is expressed on the surface of myeloid cells and CD4+ T cells. It interacts with CD200 transmembrane glycoprotein that can be expressed on variety of cells including neurons, epithelial cells, endothelial cells, fibroblasts, and lymphoid cells.
CD200R1 activation regulates the expression of pro-inflammatory molecules such as tumor necrosis factor (TNF-alpha), interferons, and inducible nitric oxide synthase (iNOS).
# Function
This gene encodes a receptor for the OX-2 membrane glycoprotein. Both the receptor and substrate are cell surface glycoproteins containing two immunoglobulin-like domains. This receptor is restricted to the surfaces of myeloid lineage cells and the receptor-substrate interaction may function as a myeloid downregulatory signal. Mouse studies of a related gene suggest that this interaction may control myeloid function in a tissue-specific manner. Alternative splicing of this gene results in multiple transcript variants. | CD200R1
Cell surface transmembrane glycoprotein CD200 receptor 1 is a protein that in humans is encoded by the CD200R1 gene.[1][2][3] CD200R1 is expressed on the surface of myeloid cells[4] and CD4+ T cells.[5] It interacts with CD200 transmembrane glycoprotein that can be expressed on variety of cells including neurons,[6] epithelial cells,[7] endothelial cells,[8] fibroblasts,[9] and lymphoid cells.[10]
CD200R1 activation regulates the expression of pro-inflammatory molecules such as tumor necrosis factor (TNF-alpha),[11] interferons, and inducible nitric oxide synthase (iNOS).[12]
# Function
This gene encodes a receptor for the OX-2 membrane glycoprotein. Both the receptor and substrate are cell surface glycoproteins containing two immunoglobulin-like domains. This receptor is restricted to the surfaces of myeloid lineage cells and the receptor-substrate interaction may function as a myeloid downregulatory signal. Mouse studies of a related gene suggest that this interaction may control myeloid function in a tissue-specific manner. Alternative splicing of this gene results in multiple transcript variants.[3] | https://www.wikidoc.org/index.php/CD200R1 | |
cbf69df954316790915873dbcbe1843d6d894445 | wikidoc | CDK2AP1 | CDK2AP1
Cyclin-dependent kinase 2-associated protein 1 is an enzyme that in humans is encoded by the CDK2AP1 gene.
# Function
The protein encoded by this gene is a specific CDK2-associated protein, which is thought to negatively regulate CDK2 activity by sequestering monomeric CDK2, and targeting CDK2 for proteolysis. This protein was found to also interact with DNA polymerase alpha/primase and mediate the phosphorylation of the large p180 subunit, which suggested the regulatory role in DNA replication during S phase of the cell cycle. A similar gene in hamster was isolated from, and functions as a growth suppressor of normal keratinocytes.
# Interactions
CDK2AP1 has been shown to interact with Cyclin-dependent kinase 2.
It interacts with unnamed protein product (BC006130) which may mediate inhibitory effect of CDK2AP1 on cell proliferation. | CDK2AP1
Cyclin-dependent kinase 2-associated protein 1 is an enzyme that in humans is encoded by the CDK2AP1 gene.[1][2][3]
# Function
The protein encoded by this gene is a specific CDK2-associated protein, which is thought to negatively regulate CDK2 activity by sequestering monomeric CDK2, and targeting CDK2 for proteolysis. This protein was found to also interact with DNA polymerase alpha/primase and mediate the phosphorylation of the large p180 subunit, which suggested the regulatory role in DNA replication during S phase of the cell cycle. A similar gene in hamster was isolated from, and functions as a growth suppressor of normal keratinocytes.[3]
# Interactions
CDK2AP1 has been shown to interact with Cyclin-dependent kinase 2.[4]
It interacts with unnamed protein product (BC006130) which may mediate inhibitory effect of CDK2AP1 on cell proliferation.[5] | https://www.wikidoc.org/index.php/CDK2AP1 | |
642302c94ff8fafbe193c627d569b093f3265b52 | wikidoc | CEACAM1 | CEACAM1
Carcinoembryonic antigen-related cell adhesion molecule 1 (biliary glycoprotein) (CEACAM1) also known as CD66a (Cluster of Differentiation 66a), is a human glycoprotein, and a member of the carcinoembryonic antigen (CEA) gene family.
# Function
This gene encodes a member of the carcinoembryonic antigen (CEA) gene family, which belongs to the immunoglobulin superfamily. Two subgroups of the CEA family, the CEA cell adhesion molecules and the pregnancy-specific glycoproteins, are located within a 1.2 Mb cluster on the long arm of chromosome 19. Eleven pseudogenes of the CEA cell adhesion molecule subgroup are also found in the cluster. The encoded protein was originally described in bile ducts of liver as biliary glycoprotein. Subsequently, it was found to be a cell–cell adhesion molecule detected on leukocytes, epithelia, and endothelia. The encoded protein mediates cell adhesion via homophilic as well as heterophilic binding to other proteins of the subgroup. Multiple cellular activities have been attributed to the encoded protein, including roles in the differentiation and arrangement of tissue three-dimensional structure, angiogenesis, apoptosis, tumor suppression, metastasis, and the modulation of innate and adaptive immune responses. Multiple transcript variants encoding different isoforms have been reported, but the full-length nature of only two has been determined.
In melanocytic cells CEACAM1 gene expression may be regulated by MITF.
# Interactions
CEACAM1 has been shown to interact with PTPN11 and Annexin A2. | CEACAM1
Carcinoembryonic antigen-related cell adhesion molecule 1 (biliary glycoprotein) (CEACAM1) also known as CD66a (Cluster of Differentiation 66a), is a human glycoprotein, and a member of the carcinoembryonic antigen (CEA) gene family.[1]
# Function
This gene encodes a member of the carcinoembryonic antigen (CEA) gene family, which belongs to the immunoglobulin superfamily. Two subgroups of the CEA family, the CEA cell adhesion molecules and the pregnancy-specific glycoproteins, are located within a 1.2 Mb cluster on the long arm of chromosome 19. Eleven pseudogenes of the CEA cell adhesion molecule subgroup are also found in the cluster. The encoded protein was originally described in bile ducts of liver as biliary glycoprotein. Subsequently, it was found to be a cell–cell adhesion molecule detected on leukocytes, epithelia, and endothelia. The encoded protein mediates cell adhesion via homophilic as well as heterophilic binding to other proteins of the subgroup. Multiple cellular activities have been attributed to the encoded protein, including roles in the differentiation and arrangement of tissue three-dimensional structure, angiogenesis, apoptosis, tumor suppression, metastasis, and the modulation of innate and adaptive immune responses. Multiple transcript variants encoding different isoforms have been reported, but the full-length nature of only two has been determined.[1]
In melanocytic cells CEACAM1 gene expression may be regulated by MITF.[2]
# Interactions
CEACAM1 has been shown to interact with PTPN11[3] and Annexin A2.[4] | https://www.wikidoc.org/index.php/CEACAM1 | |
73f2a794dd44a7cd252ee46d92634b05512f7807 | wikidoc | CEACAM3 | CEACAM3
Carcinoembryonic antigen-related cell adhesion molecule 3 (CEACAM3) also known as CD66d (Cluster of Differentiation 66d), is a member of the carcinoembryonic antigen (CEA) gene family..
This gene encodes a member of the family of carcinoembryonic antigen-related cell adhesion molecules (CEACAMs), which are used by several bacterial pathogens to bind and invade host cells. The encoded transmembrane protein directs phagocytosis of several bacterial species that is dependent on the small GTPase Rac. It is thought to serve an important role in controlling human-specific pathogens by the innate immune system. Alternatively spliced transcript variants have been described, but their biological validity has not been determined.
# Use
CEACAM3 is expressed exclusively on granulocytes and used as granulocyte marker. | CEACAM3
Carcinoembryonic antigen-related cell adhesion molecule 3 (CEACAM3) also known as CD66d (Cluster of Differentiation 66d), is a member of the carcinoembryonic antigen (CEA) gene family..[1]
This gene encodes a member of the family of carcinoembryonic antigen-related cell adhesion molecules (CEACAMs), which are used by several bacterial pathogens to bind and invade host cells. The encoded transmembrane protein directs phagocytosis of several bacterial species that is dependent on the small GTPase Rac. It is thought to serve an important role in controlling human-specific pathogens by the innate immune system. Alternatively spliced transcript variants have been described, but their biological validity has not been determined.[1]
# Use
CEACAM3 is expressed exclusively on granulocytes and used as granulocyte marker.[2] | https://www.wikidoc.org/index.php/CEACAM3 | |
8191ac289dd2f0108560bfd4f77f61781cbcf487 | wikidoc | CE mark | CE mark
The CE marking (also known as CE mark) is a mandatory conformity mark on many products placed on the single market in the European Economic Area (EEA).
# Significance
By affixing the CE marking, the manufacturer, its authorized representative, or person placing the product on the market or putting it into service asserts that the item meets all the essential requirements of the relevant European Directive(s). Examples of European Directives requiring CE marking include toy safety, machinery, low-voltage equipment, R&TTE, and EM compatibility. There are about 25 Directives requiring CE marking. .
Officially, CE has no meaning as an abbreviation, but may have originally stood for Communauté Européenne or Conformité Européenne, French for European Conformity.
# Declaration of conformity
The CE marking is a mandatory European marking for certain product groups to indicate conformity with the essential health and safety requirements set out in European Directives. To permit the use of a CE mark on a product, proof that the item meets the relevant requirements must be documented. Sometimes this is achieved using an external test house which evaluates the product and its documentation. Often it is achieved by a company-internal self-certification process. In any case the responsible organization (manufacturer, representative, importer) has to issue a EC-Declaration of Conformity (EC-DoC) indicating his identity (location, etc.), the list of European Directives he declares compliance with, a list of standards the product complies with, and a legally binding signature on behalf of the organization. The EC-DoC underlines the sole responsibility of the manufacturer. Parts of the certification process for the CE marking could be performed by 3rd party test houses or certification bodies; in case that this is mandatory the CE symbol also includes a number that identifies the so called Notified Body.
To be strictly accurate, there are two forms of Declaration, either a "Declaration of Conformity" or a "Declaration of Incorporation". Generally speaking this is only the case under the Machinery Directive, for example, a stand alone machine, which requires only a power source to operate would be issued with a Declaration of Conformity. Whereas, a machine which requires additional systems, attachments, feed conveyors etc, before it can provide its intended function, must be issued with a Declaration of Incorporation. In this latter case it is illegal to CE Mark such a machine. This can only be achieved once the machine has been finally installed and all other elements incorporated into the system, then a final Risk Assessment is performed to verify compliance of the system and a final Declaration of Conformity is then issued.
Furthermore, these directives are based upon what the European Commission calls a New Approach, whereby if any of the Article 100A Directives apply to your product, then you must apply them. More information on these and other directives can be found at or
Directives providing the requirements for the CE marking are created by the European Union (EU), but the markings are required throughout the European Economic Area (EEA). According to information provided by the Swiss Government for Swiss Exporters the CE Mark is not compulsory in Switzerland except for products for export to the European Union.)
# Origin of mark
The mark was designed by Arthur Eisenmenger according to an article in The Guardian 2001-12-23. The various components of the CE marking must have substantially the same vertical dimension, which may not be less than 5mm.
# Mutual recognition of conformity assessment
There are numerous Agreements on Mutual Recognition of Conformity Assessment between the European Union and other countries such as the USA, Japan, Canada, Australia, New Zealand and Israel. Consequently the CE mark is now found on many products from these countries.
Turkey (which is not a member of the EEA) also requires products to show CE marking as affirmations of conformity.
# The e mark
The similar "e mark", rather than the CE logo, is used on motor vehicles and components for motor vehicles
(The "e mark" for motor vehicles is not to be confused with the estimated sign on food labels ). | CE mark
The CE marking (also known as CE mark) is a mandatory conformity mark on many products placed on the single market in the European Economic Area (EEA).
# Significance
By affixing the CE marking, the manufacturer, its authorized representative, or person placing the product on the market or putting it into service asserts that the item meets all the essential requirements of the relevant European Directive(s). Examples of European Directives requiring CE marking include toy safety, machinery, low-voltage equipment, R&TTE, and EM compatibility. There are about 25 Directives requiring CE marking. [1].
Officially, CE has no meaning as an abbreviation, but may have originally stood for Communauté Européenne or Conformité Européenne, French for European Conformity.
# Declaration of conformity
The CE marking is a mandatory European marking for certain product groups to indicate conformity with the essential health and safety requirements set out in European Directives. To permit the use of a CE mark on a product, proof that the item meets the relevant requirements must be documented. Sometimes this is achieved using an external test house which evaluates the product and its documentation. Often it is achieved by a company-internal self-certification process. In any case the responsible organization (manufacturer, representative, importer) has to issue a EC-Declaration of Conformity (EC-DoC) indicating his identity (location, etc.), the list of European Directives he declares compliance with, a list of standards the product complies with, and a legally binding signature on behalf of the organization. The EC-DoC underlines the sole responsibility of the manufacturer. Parts of the certification process for the CE marking could be performed by 3rd party test houses or certification bodies; in case that this is mandatory the CE symbol also includes a number that identifies the so called Notified Body.
To be strictly accurate, there are two forms of Declaration, either a "Declaration of Conformity" or a "Declaration of Incorporation". Generally speaking this is only the case under the Machinery Directive, for example, a stand alone machine, which requires only a power source to operate would be issued with a Declaration of Conformity. Whereas, a machine which requires additional systems, attachments, feed conveyors etc, before it can provide its intended function, must be issued with a Declaration of Incorporation. In this latter case it is illegal to CE Mark such a machine. This can only be achieved once the machine has been finally installed and all other elements incorporated into the system, then a final Risk Assessment is performed to verify compliance of the system and a final Declaration of Conformity is then issued.
Furthermore, these directives are based upon what the European Commission calls a New Approach, whereby if any of the Article 100A Directives apply to your product, then you must apply them. More information on these and other directives can be found at [1] or [2]
Directives providing the requirements for the CE marking are created by the European Union (EU), but the markings are required throughout the European Economic Area (EEA). According to information provided by the Swiss Government for Swiss Exporters the CE Mark is not compulsory in Switzerland except for products for export to the European Union.)
# Origin of mark
The mark was designed by Arthur Eisenmenger according to an article in The Guardian 2001-12-23. The various components of the CE marking must have substantially the same vertical dimension, which may not be less than 5mm.[2]
# Mutual recognition of conformity assessment
There are numerous Agreements on Mutual Recognition of Conformity Assessment between the European Union and other countries such as the USA, Japan, Canada, Australia, New Zealand and Israel. Consequently the CE mark is now found on many products from these countries.
Turkey (which is not a member of the EEA) also requires products to show CE marking as affirmations of conformity.
# The e mark
The similar "e mark", rather than the CE logo, is used on motor vehicles and components for motor vehicles
[3] [4] [5].
(The "e mark" for motor vehicles is not to be confused with the estimated sign on food labels [6]). | https://www.wikidoc.org/index.php/CE_mark | |
c553623619b57bff179b2d19184f9d8e042fb100 | wikidoc | CFAP157 | CFAP157
Cilia and flagella associated protein 157 (CFAP157) also known as chromosome 9 open reading frame 117 (c9orf117) is a protein that in humans is encoded by the CFAP157 gene.
CFAP157 gene is "specifically required during spermatogenesis for flagellum morphogenesis and sperm motility and may be required to suppress the formation of supernumerary axonemes and ensure a correct ultrastructure," according to UniProt.
# Gene
## Location
CFAP157 is located on chromosome 9, 9q34.11 in human from base pair 127,706,989 to base pair 127,716,002.
## Features
The size of the gene is 9,013 bases, and the orientation is plus strand. The gene holds 9 exons.
# mRNA
The most common variant of mRNAs of CFAP157 contains 1,722 base pairs.
## Expression
CFAP157 is expressed in many human body tissues such as cervix, lung, testis, and uterus. People who have uterine tumor are likely to have an expression in CFAP157. This gene is expressed in both adults and fetuses.
# Protein
There are 520 amino acids in CFAP157 in human. The protein is glutamine extremely rich, and glycine poor. The protein is quite neutral with the isoelectric point at pH 7.4. The average mass of the protein is estimated to be 60,531.748 Da, and the absorption coefficient is estimated to be 25,440 M−1 cm−1.
CFAP157 is primarily composed of α-helices, and there is no transmembrane helix. The protein structure making program called Phyre is used to create the predicted structure of CFAP157.
# Homology
There is no known paralog for CFAP157 in human. CFAP157 has numerous orthologs. The following table contains some of orthologs including human, common chimpanzee, rhesus macaque, cattle, dog, mouse, rat, tropical clawed frog, and zebra fish.
# Interacting Proteins
P14335 (Kunjin virus strain MRM61C) is the virus that interacts with CFAP157 via two-hybrid screening. Kunjin virus is not as severe as other viruses, but this is a noticeable discovery because it is possible to exploit the interaction to develop new types of medicine. Researchers at the University of Queensland discovered a new medical use for the Kunjin virus in 2005, and the possible treatments include HIV/cancer vaccines. | CFAP157
Cilia and flagella associated protein 157 (CFAP157) also known as chromosome 9 open reading frame 117 (c9orf117) is a protein that in humans is encoded by the CFAP157 gene.
CFAP157 gene is "specifically required during spermatogenesis for flagellum morphogenesis and sperm motility and may be required to suppress the formation of supernumerary axonemes and ensure a correct ultrastructure,"[1] according to UniProt.
# Gene
## Location
CFAP157 is located on chromosome 9, 9q34.11 in human from base pair 127,706,989 to base pair 127,716,002.[2]
## Features
The size of the gene is 9,013 bases, and the orientation is plus strand.[2] The gene holds 9 exons.[3]
# mRNA
The most common variant of mRNAs of CFAP157 contains 1,722 base pairs.[3]
## Expression
CFAP157 is expressed in many human body tissues such as cervix, lung, testis, and uterus. People who have uterine tumor are likely to have an expression in CFAP157. This gene is expressed in both adults and fetuses.[4]
# Protein
There are 520 amino acids in CFAP157 in human.[5] The protein is glutamine extremely rich, and glycine poor. The protein is quite neutral with the isoelectric point at pH 7.4.[6] The average mass of the protein is estimated to be 60,531.748 Da, and the absorption coefficient is estimated to be 25,440 M−1 cm−1.
CFAP157 is primarily composed of α-helices, and there is no transmembrane helix. The protein structure making program called Phyre is used to create the predicted structure of CFAP157.
# Homology
There is no known paralog for CFAP157 in human. CFAP157 has numerous orthologs. The following table contains some of orthologs including human, common chimpanzee, rhesus macaque, cattle, dog, mouse, rat, tropical clawed frog, and zebra fish.[7]
# Interacting Proteins
P14335 (Kunjin virus strain MRM61C) is the virus that interacts with CFAP157 via two-hybrid screening. Kunjin virus is not as severe as other viruses, but this is a noticeable discovery because it is possible to exploit the interaction to develop new types of medicine. Researchers at the University of Queensland discovered a new medical use for the Kunjin virus in 2005, and the possible treatments include HIV/cancer vaccines.[8] | https://www.wikidoc.org/index.php/CFAP157 | |
7d2bdd1666e04109eac62c7f5352458a93fcb0b3 | wikidoc | CHCHD10 | CHCHD10
Coiled-coil-helix-coiled-coil-helix domain-containing protein 10, mitochondrial, also known as Protein N27C7-4 is a protein that in humans is encoded by the CHCHD10 gene.
# Structure
The CHCHD10 gene is located on the q arm of chromosome 22 at position 11.23 and it spans 2,138 base pairs. The CHCHD10 gene produces a 14.9 kDa protein composed of 149 amino acids. It is enriched at cristae junctions in the intermembrane space of the mitochondria. The structure of the protein contains a nonstructured N-terminal region, a hydrophobic helix and a C-terminal CHCH domain which contains a Cx(9)C motif and two additional cysteines. A total of four cysteines are predicted to form two disulfide bonds.
# Function
This gene encodes for a mitochondrial protein that is enriched at cristae junctions in the intermembrane space. It may play a role in cristae morphology maintenance or oxidative phosphorylation.
# Clinical significance
CHCHD10-related disorders include Myopathy, isolated mitochondrial, autosomal dominant (IMMD), Frontotemporal dementia and/or amyotrophic lateral sclerosis 2 (FTDALS2), Spinal muscular atrophy, Jokela type (SMAJ).
## Frontotemporal dementia and/or amyotrophic lateral sclerosis 2 (FTDALS2)
Frontotemporal dementia and/or amyotrophic lateral sclerosis 2 (FTDALS2) is a neurodegenerative disorder with high intrafamilial variation with phenotypes such as
frontotemporal dementia and/or amyotrophic lateral sclerosis. Frontotemporal dementia is characterized by frontal and temporal lobe atrophy associated with neuronal loss, gliosis, and dementia. Patients exhibit progressive changes in social, behavioral, and/or language function. Amyotrophic lateral sclerosis is characterized by the death of motor neurons in the brain, brainstem, and spinal cord, resulting in fatal paralysis.
## Spinal muscular atrophy, Jokela type (SMAJ)
Spinal muscular atrophy, Jokela type (SMAJ) is an autosomal dominant, slowly progressive, lower motor neuron disease. SMAJ is characterized by adult-onset of muscle cramps and fasciculations affecting the proximal and distal muscles of the upper and lower limbs. The disorder results in weakness and mild muscle atrophy later in life.
## Myopathy, isolated mitochondrial, autosomal dominant (IMMD)
Myopathy, isolated mitochondrial, autosomal dominant (IMMD) is a mitochondrial myopathy presenting with severe exercise intolerance, progressive proximal weakness, and lactic acidemia. The disorder is slowly progressive, with later involvement of facial muscles, muscles of the upper limbs, and distal muscles.
## Others
Mutations in CHCHD10 has also been found to be associated with cerebellar ataxia, frontotemporal dementia (FTD), and other mitochondrial diseases.
# Interactions
CHCHD10 has been known to interact with C1QBP, CLPX,FAF1,RNASEH1,ZNF444,KLF13, and other proteins. | CHCHD10
Coiled-coil-helix-coiled-coil-helix domain-containing protein 10, mitochondrial, also known as Protein N27C7-4 is a protein that in humans is encoded by the CHCHD10 gene.[1][2][3]
# Structure
The CHCHD10 gene is located on the q arm of chromosome 22 at position 11.23 and it spans 2,138 base pairs.[1] The CHCHD10 gene produces a 14.9 kDa protein composed of 149 amino acids.[4][5] It is enriched at cristae junctions in the intermembrane space of the mitochondria.[1] The structure of the protein contains a nonstructured N-terminal region, a hydrophobic helix and a C-terminal CHCH domain which contains a Cx(9)C motif and two additional cysteines. A total of four cysteines are predicted to form two disulfide bonds.[6]
# Function
This gene encodes for a mitochondrial protein that is enriched at cristae junctions in the intermembrane space. It may play a role in cristae morphology maintenance or oxidative phosphorylation.[1]
# Clinical significance
CHCHD10-related disorders include Myopathy, isolated mitochondrial, autosomal dominant (IMMD),[7] Frontotemporal dementia and/or amyotrophic lateral sclerosis 2 (FTDALS2),[8] Spinal muscular atrophy, Jokela type (SMAJ).[2][3]
## Frontotemporal dementia and/or amyotrophic lateral sclerosis 2 (FTDALS2)
Frontotemporal dementia and/or amyotrophic lateral sclerosis 2 (FTDALS2) is a neurodegenerative disorder with high intrafamilial variation with phenotypes such as
frontotemporal dementia and/or amyotrophic lateral sclerosis. Frontotemporal dementia is characterized by frontal and temporal lobe atrophy associated with neuronal loss, gliosis, and dementia. Patients exhibit progressive changes in social, behavioral, and/or language function. Amyotrophic lateral sclerosis is characterized by the death of motor neurons in the brain, brainstem, and spinal cord, resulting in fatal paralysis.[2][3]
## Spinal muscular atrophy, Jokela type (SMAJ)
Spinal muscular atrophy, Jokela type (SMAJ) is an autosomal dominant, slowly progressive, lower motor neuron disease. SMAJ is characterized by adult-onset of muscle cramps and fasciculations affecting the proximal and distal muscles of the upper and lower limbs. The disorder results in weakness and mild muscle atrophy later in life.[2][3]
## Myopathy, isolated mitochondrial, autosomal dominant (IMMD)
Myopathy, isolated mitochondrial, autosomal dominant (IMMD) is a mitochondrial myopathy presenting with severe exercise intolerance, progressive proximal weakness, and lactic acidemia. The disorder is slowly progressive, with later involvement of facial muscles, muscles of the upper limbs, and distal muscles.[2][3]
## Others
Mutations in CHCHD10 has also been found to be associated with cerebellar ataxia, frontotemporal dementia (FTD), and other mitochondrial diseases.[8][2][3]
# Interactions
CHCHD10 has been known to interact with C1QBP, CLPX,FAF1,RNASEH1,ZNF444,KLF13, and other proteins.[9][2][3] | https://www.wikidoc.org/index.php/CHCHD10 | |
d952e488c0111c1ca081ce28a7d9f30f362ce235 | wikidoc | CLC bio | CLC bio
CLC bio is a bioinformatics solution provider based in Aarhus, Denmark. CLC bio's software workbenches have more than 50,000 users in more than 100 countries around the globe.
# Software
The company started out making a free desktop workbench for basic bioinformatics, CLC Free Workbench, which was released in July 2005. Commercial workbenches for advanced bioinformatics have been added since. CLC bio's software is platform independent and can thus be used for both Mac OS X, Windows, and Linux.
# Hardware
The company has also developed high-performance computing solutions, focusing on accelerating scientifically proven algorithms such as HMMER, Smith-Waterman and ClustalW. CLC Bioinformatics Cube and CLC Bioinformatics Cell have garnered considerable positive attention in several independent industry publications such as GenomeWeb, BioInform, and Bio-IT World. | CLC bio
CLC bio is a bioinformatics solution provider based in Aarhus, Denmark. CLC bio's software workbenches have more than 50,000 users in more than 100 countries around the globe.
# Software
The company started out making a free desktop workbench for basic bioinformatics, CLC Free Workbench, which was released in July 2005. Commercial workbenches for advanced bioinformatics have been added since. CLC bio's software is platform independent and can thus be used for both Mac OS X, Windows, and Linux.
# Hardware
The company has also developed high-performance computing solutions, focusing on accelerating scientifically proven algorithms such as HMMER, Smith-Waterman and ClustalW. CLC Bioinformatics Cube [1] and CLC Bioinformatics Cell [2] have garnered considerable positive attention in several independent industry publications such as GenomeWeb[1], BioInform, and Bio-IT World[2].
# External links
- Official website | https://www.wikidoc.org/index.php/CLC_bio | |
58e7fa8c30bc392610fc8a915ba326cfa72e3761 | wikidoc | CLEC16A | CLEC16A
C-type lectin domain family 16, also known as CLEC16A, is a protein that in humans is encoded by the CLEC16A gene.
# Function
Little is known regarding the function of the CLEC16A protein, however it is shown to be highly expressed on B-lymphocytes, natural killer (NK) and dendritic cells. Despite its name CLEC16A may not function as a lectin because its C-type lectin domain is only 20 amino-acids long.
# Clinical significance
Polymorphisms in the CLEC16A gene are associated with an increased risk of multiple sclerosis as well as type I diabetes. | CLEC16A
C-type lectin domain family 16, also known as CLEC16A, is a protein that in humans is encoded by the CLEC16A gene.[1][2][3]
# Function
Little is known regarding the function of the CLEC16A protein, however it is shown to be highly expressed on B-lymphocytes, natural killer (NK) and dendritic cells. Despite its name CLEC16A may not function as a lectin because its C-type lectin domain is only 20 amino-acids long.[4]
# Clinical significance
Polymorphisms in the CLEC16A gene are associated with an increased risk of multiple sclerosis[5] as well as type I diabetes.[4] | https://www.wikidoc.org/index.php/CLEC16A | |
69d89d27d23cf3eee5b82093b4aeff59ac570172 | wikidoc | CNTNAP2 | CNTNAP2
Contactin-associated protein-like 2 is a protein that in humans is encoded by the CNTNAP2 gene.
Since the most recent reference human genome GRCh38, CNTNAP2 is the longest gene in the human genome
This gene encodes a member of the neurexin family which functions in the vertebrate nervous system as cell adhesion molecules and receptors. This protein, like other neurexin proteins, contains epidermal growth factor repeats and laminin G domains. In addition, it includes an F5/8 type C domain, discoidin/neuropilin- and fibrinogen-like domains, thrombospondin N-terminal-like domains and a putative PDZ binding site. This protein is localized at the juxtaparanodes of myelinated axons and associated with potassium channels. It may play a role in the local differentiation of the axon into distinct functional subdomains. This gene encompasses almost 1.6% of chromosome 7 and is one of the largest genes in the human genome. It may represent a positional candidate gene for the DFNB13 form of nonsyndromic deafness.
# Clinical significance
CNTNAP2 has been associated with autism spectrum disorder but accounts for very few cases.
CNTNAP2 may also be related to a disorder called specific language impairment.
# Interactions
CNTNAP2 has been shown to interact with CNTN2. | CNTNAP2
Contactin-associated protein-like 2 is a protein that in humans is encoded by the CNTNAP2 gene.[1][2][3]
Since the most recent reference human genome GRCh38, CNTNAP2 is the longest gene in the human genome [4]
This gene encodes a member of the neurexin family which functions in the vertebrate nervous system as cell adhesion molecules and receptors. This protein, like other neurexin proteins, contains epidermal growth factor repeats and laminin G domains. In addition, it includes an F5/8 type C domain, discoidin/neuropilin- and fibrinogen-like domains, thrombospondin N-terminal-like domains and a putative PDZ binding site. This protein is localized at the juxtaparanodes of myelinated axons and associated with potassium channels. It may play a role in the local differentiation of the axon into distinct functional subdomains. This gene encompasses almost 1.6% of chromosome 7 and is one of the largest genes in the human genome.[5] It may represent a positional candidate gene for the DFNB13 form of nonsyndromic deafness.[3]
# Clinical significance
CNTNAP2 has been associated with autism spectrum disorder but accounts for very few cases.[6][7][8]
CNTNAP2 may also be related to a disorder called specific language impairment.[9]
# Interactions
CNTNAP2 has been shown to interact with CNTN2.[10] | https://www.wikidoc.org/index.php/CNTNAP2 | |
1d489790ec47ae6c93e9d2d4ce70b89a22a8e9f8 | wikidoc | CSRP2BP | CSRP2BP
CSRP2 binding protein is a protein that in humans is encoded by the CSRP2BP gene.
CSRP2 is a protein containing two LIM domains, which are double zinc finger motifs found in proteins of diverse function. CSRP2 and some related proteins are thought to act as protein adapters, bridging two or more proteins to form a larger protein complex. The protein encoded by this gene binds to one of the LIM domains of CSRP2 and contains an acetyltransferase domain. Although the encoded protein has been detected in the cytoplasm, it is predominantly a nuclear protein. Alternatively spliced transcript variants have been described.
# Model organisms
Model organisms have been used in the study of CSRP2BP function. A conditional knockout mouse line, called Csrp2bptm1a(KOMP)Wtsi was generated as part of the International Knockout Mouse Consortium program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.
Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.
Twenty seven tests were carried out on mutant mice and eight significant abnormalities were observed. Fewer than expected homozygous mutant embryos were identified during gestation. Fewer also survived until weaning. Male homozygous mutant's eyelids fail to open, they had abnormal eye size, a decreased susceptibility to bacterial infection and a decreased body length. Female homozygous mutants had a decreased lean body mass. Animals of both sex also had corneal opacity and spinal abnormalities (including scoliosis and fusion of vertebral arches). | CSRP2BP
CSRP2 binding protein is a protein that in humans is encoded by the CSRP2BP gene.[1]
CSRP2 is a protein containing two LIM domains, which are double zinc finger motifs found in proteins of diverse function. CSRP2 and some related proteins are thought to act as protein adapters, bridging two or more proteins to form a larger protein complex. The protein encoded by this gene binds to one of the LIM domains of CSRP2 and contains an acetyltransferase domain. Although the encoded protein has been detected in the cytoplasm, it is predominantly a nuclear protein. Alternatively spliced transcript variants have been described.[1]
# Model organisms
Model organisms have been used in the study of CSRP2BP function. A conditional knockout mouse line, called Csrp2bptm1a(KOMP)Wtsi[12][13] was generated as part of the International Knockout Mouse Consortium program — a high-throughput mutagenesis project to generate and distribute animal models of disease to interested scientists.[14][15][16]
Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion.[10][17]
Twenty seven tests were carried out on mutant mice and eight significant abnormalities were observed.[10] Fewer than expected homozygous mutant embryos were identified during gestation. Fewer also survived until weaning. Male homozygous mutant's eyelids fail to open, they had abnormal eye size, a decreased susceptibility to bacterial infection and a decreased body length.[10] Female homozygous mutants had a decreased lean body mass. Animals of both sex also had corneal opacity and spinal abnormalities (including scoliosis and fusion of vertebral arches).[10] | https://www.wikidoc.org/index.php/CSRP2BP | |
ea838c07994bb2339946c5190e96ec991256f0dd | wikidoc | CTTNBP2 | CTTNBP2
Cortactin-binding protein 2 is a protein that in humans is encoded by the CTTNBP2 gene.
# Function
This gene encodes a protein with six ankyrin repeats and several proline-rich regions. A similar gene in rat interacts with a central regulator of the actin cytoskeleton.
# Interactions
CTTNBP2 has been shown to interact with:
- MOBKL3,
- PPP2CA,
- RP6-213H19.1,
- STRN3, and
- STRN.
# Model organisms
Model organisms have been used in the study of CTTNBP2 function. A conditional knockout mouse line called Cttnbp2tm1b(KOMP)Wtsi was generated at the Wellcome Trust Sanger Institute. Male and female animals underwent a standardized phenotypic screen to determine the effects of deletion. Additional screens performed: - In-depth immunological phenotyping | CTTNBP2
Cortactin-binding protein 2 is a protein that in humans is encoded by the CTTNBP2 gene.[1][2]
# Function
This gene encodes a protein with six ankyrin repeats and several proline-rich regions. A similar gene in rat interacts with a central regulator of the actin cytoskeleton.[2]
# Interactions
CTTNBP2 has been shown to interact with:
- MOBKL3,[3]
- PPP2CA,[3]
- RP6-213H19.1,[3]
- STRN3,[3] and
- STRN.[3]
# Model organisms
Model organisms have been used in the study of CTTNBP2 function. A conditional knockout mouse line called Cttnbp2tm1b(KOMP)Wtsi was generated at the Wellcome Trust Sanger Institute.[4] Male and female animals underwent a standardized phenotypic screen[5] to determine the effects of deletion.[6][7][8][9] Additional screens performed: - In-depth immunological phenotyping[10] | https://www.wikidoc.org/index.php/CTTNBP2 | |
4645d4fb2f96c4caba7c9f356e9c35e6689aa744 | wikidoc | CXorf36 | CXorf36
Chromosome X open reading frame 36 (CXorf36) is a gene that in humans encodes a protein “hypothetical protein LOC79742”. This protein has a function that is not currently very well understood. Other known aliases are “FLJ14103, DKFZp313K0825, FLJ55198, PRO3743, FLJ55198, hCG1981635, bA435K1.1,” and “4930578C19Rik.”
# Gene
The CXorf36 gene is located at Xp11.3.
It can be transcribed into 8 different transcript variants, which in turn can produce 6 different isoforms of the protein.
The genomic DNA is 52,529 base pairs long, while the longest mRNA that it produces is 4,735 bases long.
## Gene Neighborhood
CXorf36 is closely surrounded by the following genes on chromosome X:
- DUSP21
- KDM6A
- MIR222
- TBX20
CXorf36 is also surrounded by two other genes on chromosome X that have been implicated in X-linked mental retardation.
- Synaptophysin
- CASK
# Protein
The longest protein isoform that is produced by the CXorf36 gene is termed hypothetical protein LOC79742 isoform 1 and is 433 amino acids long. The protein has a predicated molecular weight of 48.6 kDa and isoelectric point of 8.11.
## Domains
The CXorf36 gene protein product contains a region of low complexity from position 16 to position 40.
## Post-translational Modification
The CXorf36 protein is predicted to undergo phosphorylation at several serines, threonines, and tyrosines throughout the structure. However, many of these sites are predicted at serines. There is also a predicted N-linked glycosylation site at position 100 on the protein product.
# Expression
CXorf36 is shown to be expressed ubiquitously at low levels in various tissues throughout the body. It is expressed highly in the ciliary ganglion, ovary, and uterus corpus. However, highest expression is seen in the trigeminal ganglion tissue.
# Conservation
CXorf36 has one paralog in humans known as C3orf58. Orthologs have been found in all mammals and through numerous eukaryotes. However, conservation of the full gene halts past this, most likely a result of duplication from the ancestral gene into CXorf36 and C3orf58. The full list of organisms in which orthologs have been found is given below.
- Pongo abelii
- Macaca mulatta
- Callithrix jacchus
- Canis familiaris
- Ailuropoda melanoleuca
- Equus caballus
- Oryctolagus cuniculus
- Mus musculus
- Rattus norvegicus
- Monodelphis domestica
- Ornithorhynchus anatinus
- Taeniopygia guttata
- Gallus gallus
- Danio rerio
- Bos taurus | CXorf36
Chromosome X open reading frame 36 (CXorf36) is a gene that in humans encodes a protein “hypothetical protein LOC79742”. This protein has a function that is not currently very well understood.[1][2] Other known aliases are “FLJ14103, DKFZp313K0825, FLJ55198, PRO3743, FLJ55198, hCG1981635, bA435K1.1,” and “4930578C19Rik.”[3]
# Gene
The CXorf36 gene is located at Xp11.3.
It can be transcribed into 8 different transcript variants, which in turn can produce 6 different isoforms of the protein.[4]
The genomic DNA is 52,529 base pairs long,[1] while the longest mRNA that it produces is 4,735 bases long.
## Gene Neighborhood
CXorf36 is closely surrounded by the following genes on chromosome X:[1]
- DUSP21
- KDM6A
- MIR222
- TBX20
CXorf36 is also surrounded by two other genes on chromosome X that have been implicated in X-linked mental retardation.[5]
- Synaptophysin
- CASK
# Protein
The longest protein isoform that is produced by the CXorf36 gene is termed hypothetical protein LOC79742 isoform 1 and is 433 amino acids long.[6] The protein has a predicated molecular weight of 48.6 kDa and isoelectric point of 8.11.[7]
## Domains
The CXorf36 gene protein product contains a region of low complexity from position 16 to position 40.[8]
## Post-translational Modification
The CXorf36 protein is predicted to undergo phosphorylation at several serines, threonines, and tyrosines throughout the structure.[9] However, many of these sites are predicted at serines. There is also a predicted N-linked glycosylation site at position 100 on the protein product.[10]
# Expression
CXorf36 is shown to be expressed ubiquitously at low levels in various tissues throughout the body. It is expressed highly in the ciliary ganglion, ovary, and uterus corpus. However, highest expression is seen in the trigeminal ganglion tissue.[11]
# Conservation
CXorf36 has one paralog in humans known as C3orf58.[12] Orthologs have been found in all mammals and through numerous eukaryotes.[13] However, conservation of the full gene halts past this, most likely a result of duplication from the ancestral gene into CXorf36 and C3orf58. The full list of organisms in which orthologs have been found is given below.
- Pongo abelii
- Macaca mulatta
- Callithrix jacchus
- Canis familiaris
- Ailuropoda melanoleuca
- Equus caballus
- Oryctolagus cuniculus
- Mus musculus
- Rattus norvegicus
- Monodelphis domestica
- Ornithorhynchus anatinus
- Taeniopygia guttata
- Gallus gallus
- Danio rerio
- Bos taurus | https://www.wikidoc.org/index.php/CXorf36 | |
2135688bd665248a1e76ac39560dca2199497d43 | wikidoc | CXorf66 | CXorf66
CXorf66 also known as Chromosome X Open Reading Frame 66, is a 361aa protein in humans that is encoded by the CXorf66 gene. The protein encoded is predicted to be a type 1 transmembrane protein; however, its exact function is currently unknown. CXorf66 has one alias: RP11-35F15.2.
There is a patent for CXorf66 under the file US 8586006 by the Institute for Systems Biology and Integrated Diagnostics, Inc.
CXorf66 protein is a potential novel cancer biomarker.
# Gene
CXorf66 is located on Chromosome X at Xq27.1 and is on the complement strand. The CXorf66 gene is located between ATP11C ATPase, MIR505, and HNRNPA3P3. In addition to this, according to OMIM, CXorf66 is positioned between SOX3, SPANXB1, and CDR1.
# mRNA
## Splice variants
CXorf66 only consists of one known splice variant with three exons (1-117, 118-271, and 272-1288bp) and two introns. Locations of junctions occur at 30aa and 81aa .
CXorf66 has only been found to have only one polyadenylation site.
# Protein
## Composition
With 57 serines and 42 lysines, the CXorf66 protein is both serine and lysine rich. CXorf66 has a molecular weight of 39.9kdal and an isoelectric point of 9.89.
## Domains
CXorf66 protein has a predicted signal peptide from 1-19aa, a topological domain from 20-47aa, a transmembrane domain from 48-68aa, and a second topological domain from 69-361aa. A signal peptide cleavage site is predicted to occur between the 17-18aa. Upon analyzing the protein's composition (serine and lysine rich) and post-translational modifications (high levels of phosphorylation), it is predicted that the first topological domain is extracellular, while the topological domain is cytoplasmic. A visual can be seen in Figure II.
Three repeat motifs of DKPV , SEAK , and PKRS have been found in the human CXorf66 protein. These repeats are conserved in other primates like Gorilla gorilla gorilla and Macaca mulatta, but are not present in other mammals.
## SNPs
There is one natural variant of the population (frequency 0.436) at 233aa from proline to leucine in the CXorf66 protein, with proline being the ancestral encoded amino acid. No effects have been observed with this missense mutation.
## Interacting proteins
- Figure III. STRING Predicted Protein Interactions for Human CXorf66
Figure III. STRING Predicted Protein Interactions for Human CXorf66
Based on STRING's predicted protein interaction, CXorf66 has medium level scoring for being tied to the proteins listed in Figure III. It is important to note that all proteins listed are not experimentally determined.
# Regulation
## Transcription
### Promoter
There is only one known promoter predicted by Genomatix for the CXorf66 protein on the negative strand from 139047554-139048298 that is 745bp in length. When BLAT Search Alignment was used for the CXorf66 promoter generated, numerous hits with high identity were retrieved for various genes on different chromosomes. The following are a few generated top scoring search results that share a high percent identity:
Uniquely, TESK2 is a testis-specific protein kinase, which correlates with predicted CXorf66 tissue expression.
### Transcription factors
Through the use of Genomatix, a table was generated of the top 20 transcription factors and their binding sites in the CXorf66 promoter (see Figure IV).
## Translation
CXorf66 has two miRNAs, hsa-mir-1290 and hsa-miR-4446-5p predicted to bind to the 3' UTR region of the mRNA.
### Post-translational modifications
An N-glycoslyation site has been predicted by Expasy's NetNGlyc at NGSS with a secondary site also possible at NGTN . Utilizing NetPhos, a total of 48 phosphorylation sites have been predicted (41 Serines, 2 Threonines, and 5 Tyrosines), all of which occur after the predicted transmembrane domain, suggesting cytoplasmic topology. Using YinOYang, many O-GlcNAc sites have been predicted. All that include high potential occur after the 48-68aa transmembrane region. A SUMOplot Analysis conducted of Homo sapiens CXorf66 protein, discovered a high probability of a sumolyation motif at position K241, alongside low probability motifs at K316 and K186. With sumoylation having a role in various cellular processes like nuclear-cytosolic transport and transcriptional regulation, it is expected CXorf66 is modified by a SUMO protein post-translation.
### Subcellular localization
Using PSORT II, there is a nuclear localization signal of PYKKKHL at 268aa. This signal can be seen to be conserved in fellow primate species; however, is not present in other mammals. In addition to this, following SDSC's Biology Workbench's SAPS kNN-Prediction, the CXorf66 protein for humans and the mouse homolog have a 47.8% likelihood to end up in the nuclear region of a cell. For more distant homologs, like Bos taurus, that do not have nuclear localization signals however, CXorf66 has a 34.8% likelihood to end up in the extracellular, including cell wall region, or plasma membrane regions. To view several homologs and their nuclear localization signals, see Figure V.
# Homology
CXorf66 has no known paralogs in humans; however CXorf66 has conserved homologs throughout the Mammalia kingdom. Highly conserved in primates, a noticeable rapid evolution has been spotted for CXorf66, see Figure VI, explaining the greater number of orthologs in mammals, rather than in invertebrates, birds, and reptiles.
# Expression
From Unigene's EST cDNA Tissue Abundance display and Protein Atlas, CXorf66 has a moderately high expression levels in testes, in addition to higher expression levels in fetus tissue in comparison to other developmental stages. CXorf66 protein also has a notable low presence in both the control endometrium total RNA and endometriosis total RNA. CXorf66 has been portrayed to have notable presence in the plasma and platelet. Based upon PaxDb data, CXorf66 has been found ranking in the top 5% for one study of human plasma and in the top 25% for another study conducted with human platelet. In addition to this, there has been a noticeable 60–100% CXorf66 protein presence in both non-failing and dilated cardiomyopathy septum tissue. Furthermore, CXorf66 has a ~75% protein presence in peripheral blood mononuclear cells.
- CXorf66 Protein Presence in Dilated Cardiomyopathy Septum Tissue
CXorf66 Protein Presence in Dilated Cardiomyopathy Septum Tissue
- CXorf66 Protein Presence in Peripheral Blood Mononuclear Cells
CXorf66 Protein Presence in Peripheral Blood Mononuclear Cells
- CXorf66 Protein Presence in Endometriosis Total RNA
CXorf66 Protein Presence in Endometriosis Total RNA | CXorf66
CXorf66 also known as Chromosome X Open Reading Frame 66, is a 361aa protein in humans that is encoded by the CXorf66 gene. The protein encoded is predicted to be a type 1 transmembrane protein; however, its exact function is currently unknown.[1] CXorf66 has one alias: RP11-35F15.2.[1]
There is a patent for CXorf66 under the file US 8586006 by the Institute for Systems Biology and Integrated Diagnostics, Inc.[2]
CXorf66 protein is a potential novel cancer biomarker.[3]
# Gene
CXorf66 is located on Chromosome X at Xq27.1 and is on the complement strand.[4] The CXorf66 gene is located between ATP11C ATPase, MIR505, and HNRNPA3P3.[4] In addition to this, according to OMIM, CXorf66 is positioned between SOX3, SPANXB1, and CDR1.[5]
# mRNA
## Splice variants
CXorf66 only consists of one known splice variant with three exons (1-117, 118-271, and 272-1288bp) and two introns.[6] Locations of junctions occur at 30aa [G] and 81aa [M].[6]
CXorf66 has only been found to have only one polyadenylation site.[7]
# Protein
## Composition
With 57 serines and 42 lysines, the CXorf66 protein is both serine and lysine rich.[8] CXorf66 has a molecular weight of 39.9kdal and an isoelectric point of 9.89.[8]
## Domains
CXorf66 protein has a predicted signal peptide from 1-19aa, a topological domain from 20-47aa, a transmembrane domain from 48-68aa, and a second topological domain from 69-361aa.[9] A signal peptide cleavage site is predicted to occur between the 17-18aa.[10] Upon analyzing the protein's composition (serine and lysine rich) and post-translational modifications (high levels of phosphorylation), it is predicted that the first topological domain [20-47aa] is extracellular, while the topological domain [69-361aa] is cytoplasmic. A visual can be seen in Figure II.[11]
Three repeat motifs of DKPV [31-34 and 204-207aa], SEAK [97-100 and 287-290aa], and PKRS [161-164 and 245-248aa] have been found in the human CXorf66 protein. These repeats are conserved in other primates like Gorilla gorilla gorilla and Macaca mulatta, but are not present in other mammals.[12]
## SNPs
There is one natural variant of the population (frequency 0.436) at 233aa from proline to leucine in the CXorf66 protein, with proline being the ancestral encoded amino acid. No effects have been observed with this missense mutation.[9][13]
## Interacting proteins
- Figure III. STRING Predicted Protein Interactions for Human CXorf66
Figure III. STRING Predicted Protein Interactions for Human CXorf66
Based on STRING's predicted protein interaction, CXorf66 has medium level scoring for being tied to the proteins listed in Figure III.[14] It is important to note that all proteins listed are not experimentally determined.
# Regulation
## Transcription
### Promoter
There is only one known promoter predicted by Genomatix for the CXorf66 protein on the negative strand from 139047554-139048298 that is 745bp in length.[15] When BLAT Search Alignment was used for the CXorf66 promoter generated, numerous hits with high identity were retrieved for various genes on different chromosomes. The following are a few generated top scoring search results that share a high percent identity:[16]
Uniquely, TESK2 is a testis-specific protein kinase, which correlates with predicted CXorf66 tissue expression.
### Transcription factors
Through the use of Genomatix, a table was generated of the top 20 transcription factors and their binding sites in the CXorf66 promoter (see Figure IV).[15]
## Translation
CXorf66 has two miRNAs, hsa-mir-1290 and hsa-miR-4446-5p predicted to bind to the 3' UTR region of the mRNA.[17]
### Post-translational modifications
An N-glycoslyation site has been predicted by Expasy's NetNGlyc at NGSS [24aa] with a secondary site also possible at NGTN [21aa].[18] Utilizing NetPhos, a total of 48 phosphorylation sites have been predicted (41 Serines, 2 Threonines, and 5 Tyrosines), all of which occur after the predicted transmembrane domain, suggesting cytoplasmic topology.[19] Using YinOYang, many O-GlcNAc sites have been predicted. All that include high potential occur after the 48-68aa transmembrane region.[20] A SUMOplot Analysis conducted of Homo sapiens CXorf66 protein, discovered a high probability of a sumolyation motif at position K241, alongside low probability motifs at K316 and K186. With sumoylation having a role in various cellular processes like nuclear-cytosolic transport and transcriptional regulation, it is expected CXorf66 is modified by a SUMO protein post-translation.[21]
### Subcellular localization
Using PSORT II, there is a nuclear localization signal of PYKKKHL at 268aa.[22] This signal can be seen to be conserved in fellow primate species; however, is not present in other mammals. In addition to this, following SDSC's Biology Workbench's SAPS kNN-Prediction, the CXorf66 protein for humans and the mouse homolog have a 47.8% likelihood to end up in the nuclear region of a cell. For more distant homologs, like Bos taurus, that do not have nuclear localization signals however, CXorf66 has a 34.8% likelihood to end up in the extracellular, including cell wall region, or plasma membrane regions.[8][22] To view several homologs and their nuclear localization signals, see Figure V.
# Homology
CXorf66 has no known paralogs in humans; however CXorf66 has conserved homologs throughout the Mammalia kingdom. Highly conserved in primates, a noticeable rapid evolution has been spotted for CXorf66, see Figure VI, explaining the greater number of orthologs in mammals, rather than in invertebrates, birds, and reptiles.[23]
# Expression
From Unigene's EST cDNA Tissue Abundance display and Protein Atlas, CXorf66 has a moderately high expression levels in testes, in addition to higher expression levels in fetus tissue in comparison to other developmental stages.[25][26] CXorf66 protein also has a notable low presence in both the control endometrium total RNA and endometriosis total RNA.[27] CXorf66 has been portrayed to have notable presence in the plasma and platelet.[1] Based upon PaxDb data, CXorf66 has been found ranking in the top 5% for one study of human plasma and in the top 25% for another study conducted with human platelet.[28] In addition to this, there has been a noticeable 60–100% CXorf66 protein presence in both non-failing and dilated cardiomyopathy septum tissue.[29] Furthermore, CXorf66 has a ~75% protein presence in peripheral blood mononuclear cells.[30]
- CXorf66 Protein Presence in Dilated Cardiomyopathy Septum Tissue
CXorf66 Protein Presence in Dilated Cardiomyopathy Septum Tissue
- CXorf66 Protein Presence in Peripheral Blood Mononuclear Cells
CXorf66 Protein Presence in Peripheral Blood Mononuclear Cells
- CXorf66 Protein Presence in Endometriosis Total RNA
CXorf66 Protein Presence in Endometriosis Total RNA | https://www.wikidoc.org/index.php/CXorf66 | |
d00805670fc4a64c4fc3278e939b26e1aaf3188b | wikidoc | CXorf67 | CXorf67
Uncharacterized protein CXorf67 is a protein that in humans is encoded by the CXorf67 gene. The Accession Number for the human gene is NM_203407. Aliases include MGC47837 and LOC340602. The gene is located on the positive strand of the X chromosome at Xp11.22. The mRNA is 1939 base pairs long and contains 1 exon and no introns.
# Expression
Expression of CXorf67 in humans is generally low in all tissues. Higher RNA expression has been reported in the testis and placenta and relatively higher nuclear protein expression has been observed in the placenta, testis and ovarian follicles.
# Protein
The translated human CXorf67 protein is 503 amino acids in length. The protein has a molecular weight of 51.9 kdal and an isoelectric point of 10.432
## Interactions
Protein interaction of CXorf67 with UBC (polyubiquitin-C) in humans was identified using a two-hybrid screening. Currently no other protein interactions have been identified in humans.
# Function
The function of CXorf67 is currently unknown, however the fusion of CXorf67 with the MBTD1 gene has been linked to low-grade endometrial stromal sarcoma in humans. Sequence variants of the chromosomal region Xp11.22 are also predicted to confer susceptibility to prostate cancer in humans. | CXorf67
Uncharacterized protein CXorf67 is a protein that in humans is encoded by the CXorf67 gene. The Accession Number for the human gene is NM_203407.[1] Aliases include MGC47837 and LOC340602.[2] The gene is located on the positive strand of the X chromosome at Xp11.22.[2] The mRNA is 1939 base pairs long and contains 1 exon and no introns.[3]
# Expression
Expression of CXorf67 in humans is generally low in all tissues. Higher RNA expression has been reported in the testis and placenta and relatively higher nuclear protein expression has been observed in the placenta, testis and ovarian follicles.[4]
# Protein
The translated human CXorf67 protein is 503 amino acids in length.[3] The protein has a molecular weight of 51.9 kdal and an isoelectric point of 10.432[5]
## Interactions
Protein interaction of CXorf67 with UBC (polyubiquitin-C) in humans was identified using a two-hybrid screening.[6] Currently no other protein interactions have been identified in humans.
# Function
The function of CXorf67 is currently unknown, however the fusion of CXorf67 with the MBTD1 gene has been linked to low-grade endometrial stromal sarcoma in humans.[7] Sequence variants of the chromosomal region Xp11.22 are also predicted to confer susceptibility to prostate cancer in humans.[8] | https://www.wikidoc.org/index.php/CXorf67 | |
6f1bea61fee278cf472198984bb5f16c1d70baf1 | wikidoc | CYP24A1 | CYP24A1
Cytochrome P450 family 24 subfamily A member 1 (abbreviated CYP24A1) is a member of the cytochrome P450 superfamily of enzymes encoded by the CYP24A1 gene. It is a mitochondrial monooxygenase which catalyzes reactions including 24-hydroxylation of calcitriol (1,25-dihydroxyvitamin D3). It has also been identified as vitamin D3 24-hydroxylase.(EC 1.14.15.16)
# Function
CYP24A1 is an enzyme expressed in the mitochondrion of humans and other species. It catalyzes hydroxylation reactions which lead to the degradation of 1,25-dihydroxyvitamin D3, the physiologically active form of vitamin D. Hydroxylation of the side chain produces calcitroic acid and other metabolites which are excreted in bile.
CYP24A1 was identified in the early 1970s and was first thought to be involved in vitamin D metabolism as the renal 25-hydroxyvitamin D3-24-hydroxylase, modifying calcifediol (25-hydroxyvitamin D) to produce 24,25-dihydroxycholecalciferol (24,25-dihydroxyvitamin D). Subsequent studies using recombinant CYP24A1 showed that it could also catalyze multiple other hydroxylation reactions at the side chain carbons known as C-24 and C-23 in both 25-OH-D3 and the active hormonal form, 1,25-(OH)2D3. It is now considered responsible for the entire five-step, 24-oxidation pathway from 1,25-(OH)2D3 producing calcitroic acid.
CYP24A1 also is able to catalyse another pathway which starts with 23-hydroxylation of 1,25-(OH)2D3 and culminates in 1,25-(OH)2D3-26,23-lactone.
The side chains of the ergocalciferol (vitamin D2) derivatives, 25-OH-D2 and 1,25-(OH)2D2, are also hydroxylated by CYP24A1.
The structure of CYP24A1 is highly conserved between different species although the balance of functions can differ. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
This enzyme plays an important role in calcium homeostasis and the vitamin D endocrine system through its regulation of the level of vitamin D3.
## Interactive pathway map
Click on genes, proteins and metabolites below to link to respective articles.
- ↑ The interactive pathway map can be edited at WikiPathways: "VitaminDSynthesis_WP1531"..mw-parser-output cite.citation{font-style:inherit}.mw-parser-output q{quotes:"\"""\"""'""'"}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-lock-free a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-limited a,.mw-parser-output .cs1-lock-registration a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-subscription a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{display:none;font-size:100%}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}
# Regulation
CYP24A1 is expressed in tissues which are considered targets for vitamin D, including kidney, intestine and bone. Transcription of the CYP24A1 gene is markedly inducible by 1,25-(OH)2D3 binding to the vitamin D receptor. The gene has a strong, positive vitamin D response element in the promoter. Through regulation of CYP24A1 expression, a negative feedback control system is created to limit the effects of 1,25-(OH)2D3.
PTH and FGF23 also regulate CYP24A1 gene expression. Additionally, it is translationally regulated via IRES within the 5'UTR, which is responsive to an inflammatory environment.
# Clinical relevance
Abnormal functioning CYP24A1 is thought to be one of the causes of severe infantile hypercalcemia. Patients with mutations of the CYP24A1 gene have elevated serum calcium concentrations, elevated serum 1,25-(OH)2D, suppressed PTH concentrations, hypercalciuria, nephrocalcinosis, nephrolithiasis, and sometimes reduced bone density. Variations in the gene may also be found in people with renal stones. | CYP24A1
Cytochrome P450 family 24 subfamily A member 1 (abbreviated CYP24A1) is a member of the cytochrome P450 superfamily of enzymes encoded by the CYP24A1 gene. It is a mitochondrial monooxygenase which catalyzes reactions including 24-hydroxylation of calcitriol (1,25-dihydroxyvitamin D3).[1] It has also been identified as vitamin D3 24-hydroxylase.(EC 1.14.15.16)
# Function
CYP24A1 is an enzyme expressed in the mitochondrion of humans and other species. It catalyzes hydroxylation reactions which lead to the degradation of 1,25-dihydroxyvitamin D3, the physiologically active form of vitamin D. Hydroxylation of the side chain produces calcitroic acid and other metabolites which are excreted in bile.[1][2]
CYP24A1 was identified in the early 1970s and was first thought to be involved in vitamin D metabolism as the renal 25-hydroxyvitamin D3-24-hydroxylase, modifying calcifediol (25-hydroxyvitamin D) to produce 24,25-dihydroxycholecalciferol (24,25-dihydroxyvitamin D). Subsequent studies using recombinant CYP24A1 showed that it could also catalyze multiple other hydroxylation reactions at the side chain carbons known as C-24 and C-23 in both 25-OH-D3 and the active hormonal form, 1,25-(OH)2D3. It is now considered responsible for the entire five-step, 24-oxidation pathway from 1,25-(OH)2D3 producing calcitroic acid.[2]
CYP24A1 also is able to catalyse another pathway which starts with 23-hydroxylation of 1,25-(OH)2D3 and culminates in 1,25-(OH)2D3-26,23-lactone.[2]
The side chains of the ergocalciferol (vitamin D2) derivatives, 25-OH-D2 and 1,25-(OH)2D2, are also hydroxylated by CYP24A1.[2]
The structure of CYP24A1 is highly conserved between different species although the balance of functions can differ.[2] Alternatively spliced transcript variants encoding different isoforms have been found for this gene.
This enzyme plays an important role in calcium homeostasis and the vitamin D endocrine system through its regulation of the level of vitamin D3.
## Interactive pathway map
Click on genes, proteins and metabolites below to link to respective articles. [§ 1]
- ↑ The interactive pathway map can be edited at WikiPathways: "VitaminDSynthesis_WP1531"..mw-parser-output cite.citation{font-style:inherit}.mw-parser-output q{quotes:"\"""\"""'""'"}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-lock-free a{background:url("https://upload.wikimedia.org/wikipedia/commons/thumb/6/65/Lock-green.svg/9px-Lock-green.svg.png")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-limited a,.mw-parser-output .cs1-lock-registration a{background:url("https://upload.wikimedia.org/wikipedia/commons/thumb/d/d6/Lock-gray-alt-2.svg/9px-Lock-gray-alt-2.svg.png")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-subscription a{background:url("https://upload.wikimedia.org/wikipedia/commons/thumb/a/aa/Lock-red-alt-2.svg/9px-Lock-red-alt-2.svg.png")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{display:none;font-size:100%}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}
# Regulation
CYP24A1 is expressed in tissues which are considered targets for vitamin D, including kidney, intestine and bone. Transcription of the CYP24A1 gene is markedly inducible by 1,25-(OH)2D3 binding to the vitamin D receptor.[2] The gene has a strong, positive vitamin D response element in the promoter. Through regulation of CYP24A1 expression, a negative feedback control system is created to limit the effects of 1,25-(OH)2D3.[2]
PTH and FGF23 also regulate CYP24A1 gene expression.[2] Additionally, it is translationally regulated via IRES within the 5'UTR, which is responsive to an inflammatory environment.[3]
# Clinical relevance
Abnormal functioning CYP24A1 is thought to be one of the causes of severe infantile hypercalcemia.[4] Patients with mutations of the CYP24A1 gene have elevated serum calcium concentrations, elevated serum 1,25-(OH)2D, suppressed PTH concentrations, hypercalciuria, nephrocalcinosis, nephrolithiasis, and sometimes reduced bone density. Variations in the gene may also be found in people with renal stones.[5] | https://www.wikidoc.org/index.php/CYP24A1 | |
b1e2b4ef8ad1ca7e5bbb1b2514c17b95b6da3045 | wikidoc | CYP26A1 | CYP26A1
Cytochrome P450 26A1 is a protein that in humans is encoded by the CYP26A1 gene.
# Function
This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This endoplasmic reticulum protein acts on retinoids, including all-trans-retinoic acid (RA), with both 4-hydroxylation and 18-hydroxylation activities. This enzyme regulates the cellular level of retinoic acid which is involved in regulation of gene expression in both embryonic and adult tissues. Two alternatively spliced transcript variants of this gene, which encode the distinct isoforms, have been reported.
CYP26A1 is over-expressed in colorectal cancer cells compared to normal colonic epithelium but is of no independent prognostic value in patients with colorectal cancer. | CYP26A1
Cytochrome P450 26A1 is a protein that in humans is encoded by the CYP26A1 gene.[1][2][3]
# Function
This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This endoplasmic reticulum protein acts on retinoids, including all-trans-retinoic acid (RA), with both 4-hydroxylation and 18-hydroxylation activities. This enzyme regulates the cellular level of retinoic acid which is involved in regulation of gene expression in both embryonic and adult tissues. Two alternatively spliced transcript variants of this gene, which encode the distinct isoforms, have been reported.[3]
CYP26A1 is over-expressed in colorectal cancer cells compared to normal colonic epithelium but is of no independent prognostic value in patients with colorectal cancer.[4] | https://www.wikidoc.org/index.php/CYP26A1 | |
11ff81051542fc2f1b1ef0b52c6a70af7f305278 | wikidoc | CYP26B1 | CYP26B1
Cytochrome P450 26B1 is a protein that in humans is encoded by the CYP26B1 gene.
This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases that catalyze many reactions involved in drug metabolism and the synthesis of cholesterol, steroids and other lipids. The enzyme encoded by this gene is involved in the specific inactivation of all-trans-retinoic acid to hydroxylated forms, such as 4-oxo-, 4-OH-, and 18-OH-all-trans-retinoic acid.
In a developing mouse embryo, CYP26B1 is expressed in the distal tip of the forming limb bud with an abundance in the apical ectodermal ridge. In a knockout mouse model, mice manifest with severe limb malformations and die after birth due to respiratory distress. However, if the expression of CYP26B1 is conditionally deleted only prior to E9.5, the limbs are not as severely truncated and more digits are visible. Research suggests that this differenece is attributable to the timing of chrondroblast differentiation.
CYP26B1 has been shown to be over-expressed in colorectal cancer cells compared to normal colonic epithelium. CYP26B1 expression was also independently prognostic in patients with colorectal cancer and strong expression was associated with a poorer outcome.
In a genome-wide study, CCHCR1, TCN2, TNXB, LTA, FASN, and CYP26B1 were identified as loci associated with a risk for developing esophageal squamous cell carcinoma. Of these loci, CYP26B1 exhibited the highest effect size. Moreover, the CYP26B1 locus was found to have two alleles with differing capacities to catabolize all-trans retinoic acid, a chemotherapeutic agent. When the allele with the higher catabolic capacity, rs138478634-GA, was overexpressed, cell proliferation was significantly enhanced in comparison to the other allele, rs138478634-GG. Additionally, research is suggestive of a lifestyle interaction where individuals with the risk allele who partake in smoking or drinking present with an odd-ratio over 2-fold higher than smokers or drinkers without the variant or individuals who refrain. | CYP26B1
Cytochrome P450 26B1 is a protein that in humans is encoded by the CYP26B1 gene.[1][2]
This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases that catalyze many reactions involved in drug metabolism and the synthesis of cholesterol, steroids and other lipids. The enzyme encoded by this gene is involved in the specific inactivation of all-trans-retinoic acid to hydroxylated forms, such as 4-oxo-, 4-OH-, and 18-OH-all-trans-retinoic acid.[2]
In a developing mouse embryo, CYP26B1 is expressed in the distal tip of the forming limb bud with an abundance in the apical ectodermal ridge. In a knockout mouse model, mice manifest with severe limb malformations and die after birth due to respiratory distress.[3] However, if the expression of CYP26B1 is conditionally deleted only prior to E9.5, the limbs are not as severely truncated and more digits are visible. Research suggests that this differenece is attributable to the timing of chrondroblast differentiation.[4]
CYP26B1 has been shown to be over-expressed in colorectal cancer cells compared to normal colonic epithelium. CYP26B1 expression was also independently prognostic in patients with colorectal cancer and strong expression was associated with a poorer outcome.[5]
In a genome-wide study, CCHCR1, TCN2, TNXB, LTA, FASN, and CYP26B1 were identified as loci associated with a risk for developing esophageal squamous cell carcinoma. Of these loci, CYP26B1 exhibited the highest effect size. Moreover, the CYP26B1 locus was found to have two alleles with differing capacities to catabolize all-trans retinoic acid, a chemotherapeutic agent. When the allele with the higher catabolic capacity, rs138478634-GA, was overexpressed, cell proliferation was significantly enhanced in comparison to the other allele, rs138478634-GG. Additionally, research is suggestive of a lifestyle interaction where individuals with the risk allele who partake in smoking or drinking present with an odd-ratio over 2-fold higher than smokers or drinkers without the variant or individuals who refrain.[6] | https://www.wikidoc.org/index.php/CYP26B1 | |
f29d6f41740cff7aa5ce473eead297f8d8866df1 | wikidoc | CYP26C1 | CYP26C1
CYP26C1 (cytochrome P450, family 26, subfamily c, polypeptide 1) is a protein which in humans is encoded by the CYP26C1 gene.
This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This enzyme is involved in the catabolism of all-trans- and 9-cis-retinoic acid, and thus contributes to the regulation of retinoic acid levels in cells and tissues.
CYP26C1 was found to show no expression in colorectal cancer cells or normal colonic epithelium. | CYP26C1
CYP26C1 (cytochrome P450, family 26, subfamily c, polypeptide 1) is a protein which in humans is encoded by the CYP26C1 gene.[1]
This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This enzyme is involved in the catabolism of all-trans- and 9-cis-retinoic acid, and thus contributes to the regulation of retinoic acid levels in cells and tissues.[2]
CYP26C1 was found to show no expression in colorectal cancer cells or normal colonic epithelium.[3] | https://www.wikidoc.org/index.php/CYP26C1 | |
350cd00ff0136b478efb90514cc501958331c694 | wikidoc | CYP27C1 | CYP27C1
CYP27C1 (cytochrome P450, family 27, subfamily C, polypeptide 1) is a protein that in humans is encoded by the CYP27C1 gene.
This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids.
# Popular culture
CYP27C1 is the topic of the comic Sherman's lagoon for May 26, 2016. In response to Hawthorne's inquiry about the chemical, Ernest explains that it is an enzyme that enhances ability to see infrared light, allowing fish to see better in murky waters. Ernest can see however that Hawthorne is more interested in how to synthesize it commercially. | CYP27C1
CYP27C1 (cytochrome P450, family 27, subfamily C, polypeptide 1) is a protein that in humans is encoded by the CYP27C1 gene.[1][2]
This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids.[3]
# Popular culture
CYP27C1 is the topic of the comic Sherman's lagoon for May 26, 2016.[4] In response to Hawthorne's inquiry about the chemical, Ernest explains that it is an enzyme that enhances ability to see infrared light, allowing fish to see better in murky waters. Ernest can see however that Hawthorne is more interested in how to synthesize it commercially. | https://www.wikidoc.org/index.php/CYP27C1 | |
8438f7cd313a1f8d43becd9c2469fdd128edbe0d | wikidoc | CYP2C18 | CYP2C18
Cytochrome P450 2C18 is a protein that in humans is encoded by the CYP2C18 gene.
# Function
This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This protein localizes to the endoplasmic reticulum but its specific substrate has not yet been determined. The gene is located within a cluster of cytochrome P450 genes on chromosome 10q24. An additional gene, CYP2C17, was once thought to exist; however, CYP4217 is now considered an artefact based on a chimera of CYP2C18 and CYP2C19.
CYP2C18 also possesses epoxygenase activitiy: it can attack various long-chain polyunsaturated fatty acids at their double (i.e. alkene) bonds to form epoxide products that act as signaling agents. It metabolizes: 1) arachidonic acid to various epoxyeicosatrienoic acids (also termed EETs); 2) linoleic acid to 9,10-epoxy octadecaenoic acids (also termed vernolic acid, linoleic acid 9:10-oxide, or leukotoxin) and 12,13-epoxy-octadecaenoic (also termed coronaric acid, linoleic acid 12,13-oxide, or isoleukotoxin); 3) docosohexaenoic acid to various epoxydocosapentaenoic acids (also termed EDPs); and 4) eicosapentaenoic acid to various epoxyeicosatetraenoic acids (also termed EEQs).
While CYP2C19, CYP2C8, CYP2C9, CYP2J2, and possibly CYP2S1 are the main producers of EETs and, very likely EEQs, EDPs, and the epoxides of linoleic acid, CYP2C18 may contribute to the production of these metabolites in certain tissues. | CYP2C18
Cytochrome P450 2C18 is a protein that in humans is encoded by the CYP2C18 gene.[1][2][3]
# Function
This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This protein localizes to the endoplasmic reticulum but its specific substrate has not yet been determined. The gene is located within a cluster of cytochrome P450 genes on chromosome 10q24. An additional gene, CYP2C17, was once thought to exist; however, CYP4217 is now considered an artefact based on a chimera of CYP2C18 and CYP2C19.[3]
CYP2C18 also possesses epoxygenase activitiy: it can attack various long-chain polyunsaturated fatty acids at their double (i.e. alkene) bonds to form epoxide products that act as signaling agents. It metabolizes: 1) arachidonic acid to various epoxyeicosatrienoic acids (also termed EETs); 2) linoleic acid to 9,10-epoxy octadecaenoic acids (also termed vernolic acid, linoleic acid 9:10-oxide, or leukotoxin) and 12,13-epoxy-octadecaenoic (also termed coronaric acid, linoleic acid 12,13-oxide, or isoleukotoxin); 3) docosohexaenoic acid to various epoxydocosapentaenoic acids (also termed EDPs); and 4) eicosapentaenoic acid to various epoxyeicosatetraenoic acids (also termed EEQs).[4][5][6]
While CYP2C19, CYP2C8, CYP2C9, CYP2J2, and possibly CYP2S1 are the main producers of EETs and, very likely EEQs, EDPs, and the epoxides of linoleic acid, CYP2C18 may contribute to the production of these metabolites in certain tissues.[5][7] | https://www.wikidoc.org/index.php/CYP2C18 | |
dd27b1afca757145ba2063bde3636c58613df66d | wikidoc | CYP2C19 | CYP2C19
Cytochrome P450 2C19 (abbreviated CYP2C19) is an enzyme. This protein, a member of the cytochrome P450 mixed-function oxidase system, is involved in the metabolism of xenobiotics, including many proton pump inhibitors and antiepileptics. In humans, the CYP2C19 protein is encoded by the CYP2C19 gene. CYP2C19 is a liver enzyme that acts on at least 10% of drugs in current clinical use, most notably the antiplatelet treatment clopidogrel (Plavix) also drugs that treat pain associated with ulcers, such as omeprazole, antiseizure drugs such as mephenytoin, the antimalarial proguanil, and the anxiolytic diazepam.
CYP2C19 has been annotated as (R)-limonene 6-monooxygenase and (S)-limonene 6-monooxygenase in UniProt.
# Function
The gene encodes a member of the cytochrome P450 superfamily of enzymes. These proteins are monooxygenases that catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This protein localizes to the endoplasmic reticulum and is known to metabolize many drugs. Polymorphism within this gene is associated with variable ability to metabolize mephenytoin, known as the poor metabolizer and extensive metabolizer phenotypes. The gene is located within a cluster of cytochrome P450 genes on chromosome no.10 arm q24.
CYP2C19 also possesses epoxygenase activitiy: it is one of the principal enzymes responsible for attacking various long-chain polyunsaturated fatty acids at their double (i.e. alkene) bonds to form epoxide products that act as signaling agents. It metabolizes:
- arachidonic acid to various epoxyeicosatrienoic acids (also termed EETs);
- linoleic acid to 9,10-epoxy octadecaenoic acids (also termed vernolic acid, linoleic acid 9:10-oxide, or leukotoxin) and 12,13-epoxy-octadecaenoic (also termed coronaric acid, linoleic acid 12,13-oxide, or isoleukotoxin);
- docosohexaenoic acid to various epoxydocosapentaenoic acids (also termed EDPs); and
- eicosapentaenoic acid to various epoxyeicosatetraenoic acids (also termed EEQs).
Along with CYP2C19, CYP2C8, CYP2C9, CYP2J2, and possibly CYP2S1 are the main producers of EETs and, very likely EEQs, EDPs, and the epoxides of linoleic acid.
# Genetic polymorphism and pharmacogenomics
Genetic polymorphism (mainly CYP2C19*2, CYP2C19*3 and CYP2C19*17) exists for CYP2C19 expression, with approximately 3–5% of European and 15–20% of Asian populations being poor metabolizers with no CYP2C19 function. This may reduce the efficacy of clopidogrel (Plavix). The basis for this reduced effect of clopidogrel in patients who have a gene of reduced activity may seem somewhat paradoxical, but can be understood as follows. Clopidogrel is administered as a “prodrug;” that is, a drug that is inactive when taken, and then depends on the action of an enzyme in the body in order to be activated. In patients who have a gene of reduced activity, clopidogrel may not be metabolized to its active form and therefore not achieve pharmacological effect in the body. In patients with an abnormal CYP2C19 variant certain benzodiazepines should be avoided, such as diazepam (Valium), lorazepam (Ativan), oxazepam (Serax), and temazepam (Restoril). On the basis of their ability to metabolize (S)-mephenytoin or other CYP2C19 substrates, individuals can be classified as extensive metabolizers (EM) or poor metabolizers (PM). Eight variant alleles (CYP2C19*2 to CYP2C19*8) that predict PMs have been identified.
# Ligands
The following is a table of selected substrates, inducers and inhibitors of CYP2C19. Where classes of agents are listed, there may be exceptions within the class.
Inhibitors of CYP2C19 can be classified by their potency, such as:
- Strong being one that causes at least a 5-fold increase in the plasma AUC values, or more than 80% decrease in clearance of substrates.
- Moderate being one that causes at least a 2-fold increase in the plasma AUC values, or 50-80% decrease in clearance of substrates.
- Weak being one that causes at least a 1.25-fold but less than 2-fold increase in the plasma AUC values, or 20-50% decrease in clearance of substrates. | CYP2C19
Cytochrome P450 2C19 (abbreviated CYP2C19) is an enzyme. This protein, a member of the cytochrome P450 mixed-function oxidase system, is involved in the metabolism of xenobiotics, including many proton pump inhibitors and antiepileptics. In humans, the CYP2C19 protein is encoded by the CYP2C19 gene.[1][2] CYP2C19 is a liver enzyme that acts on at least 10% of drugs in current clinical use,[3] most notably the antiplatelet treatment clopidogrel (Plavix) also drugs that treat pain associated with ulcers, such as omeprazole, antiseizure drugs such as mephenytoin, the antimalarial proguanil, and the anxiolytic diazepam.[4]
CYP2C19 has been annotated as (R)-limonene 6-monooxygenase and (S)-limonene 6-monooxygenase in UniProt.
# Function
The gene encodes a member of the cytochrome P450 superfamily of enzymes. These proteins are monooxygenases that catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This protein localizes to the endoplasmic reticulum and is known to metabolize many drugs. Polymorphism within this gene is associated with variable ability to metabolize mephenytoin, known as the poor metabolizer and extensive metabolizer phenotypes. The gene is located within a cluster of cytochrome P450 genes on chromosome no.10 arm q24.[5]
CYP2C19 also possesses epoxygenase activitiy: it is one of the principal enzymes responsible for attacking various long-chain polyunsaturated fatty acids at their double (i.e. alkene) bonds to form epoxide products that act as signaling agents. It metabolizes:
- arachidonic acid to various epoxyeicosatrienoic acids (also termed EETs);
- linoleic acid to 9,10-epoxy octadecaenoic acids (also termed vernolic acid, linoleic acid 9:10-oxide, or leukotoxin) and 12,13-epoxy-octadecaenoic (also termed coronaric acid, linoleic acid 12,13-oxide, or isoleukotoxin);
- docosohexaenoic acid to various epoxydocosapentaenoic acids (also termed EDPs); and
- eicosapentaenoic acid to various epoxyeicosatetraenoic acids (also termed EEQs).[6][7][8]
Along with CYP2C19, CYP2C8, CYP2C9, CYP2J2, and possibly CYP2S1 are the main producers of EETs and, very likely EEQs, EDPs, and the epoxides of linoleic acid.[7][9]
# Genetic polymorphism and pharmacogenomics
Genetic polymorphism (mainly CYP2C19*2, CYP2C19*3 and CYP2C19*17) exists for CYP2C19 expression, with approximately 3–5% of European and 15–20% of Asian populations being poor metabolizers with no CYP2C19 function.[10][11] This may reduce the efficacy of clopidogrel (Plavix). The basis for this reduced effect of clopidogrel in patients who have a gene of reduced activity may seem somewhat paradoxical, but can be understood as follows. Clopidogrel is administered as a “prodrug;” that is, a drug that is inactive when taken, and then depends on the action of an enzyme in the body in order to be activated. In patients who have a gene of reduced activity, clopidogrel may not be metabolized to its active form and therefore not achieve pharmacological effect in the body. In patients with an abnormal CYP2C19 variant certain benzodiazepines should be avoided, such as diazepam (Valium), lorazepam (Ativan), oxazepam (Serax), and temazepam (Restoril).[12] On the basis of their ability to metabolize (S)-mephenytoin or other CYP2C19 substrates, individuals can be classified as extensive metabolizers (EM) or poor metabolizers (PM).[11] Eight variant alleles (CYP2C19*2 to CYP2C19*8) that predict PMs have been identified.[11]
# Ligands
The following is a table of selected substrates, inducers and inhibitors of CYP2C19. Where classes of agents are listed, there may be exceptions within the class.
Inhibitors of CYP2C19 can be classified by their potency, such as:
- Strong being one that causes at least a 5-fold increase in the plasma AUC values, or more than 80% decrease in clearance of substrates.[13]
- Moderate being one that causes at least a 2-fold increase in the plasma AUC values, or 50-80% decrease in clearance of substrates.[13]
- Weak being one that causes at least a 1.25-fold but less than 2-fold increase in the plasma AUC values, or 20-50% decrease in clearance of substrates.[13] | https://www.wikidoc.org/index.php/CYP2C19 | |
d17e0df9ab02158c205f66ade02a3a65d6c24813 | wikidoc | CYP4A11 | CYP4A11
Cytochrome P450 4A11 is a protein that in humans is encoded by the CYP4A11 gene.
# Function
This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This protein localizes to the endoplasmic reticulum and hydroxylates medium-chain fatty acids such as laurate and myristate.
CYP4A11 is highly expressed in the liver and kidney.
CYP4A11 along with CYP4A22, CYP4F2, and CYP4F3 metabolize arachidonic acid to 20-Hydroxyeicosatetraenoic acid (20-HETE) by an Omega oxidation reaction with the predominant 20-HETE-synthesizing enzymes in humans being CYP4F2 followed by CYP4A11; 20-HETE regulates blood flow, vascularization, blood pressure, and kidney tubule absorption of ions in rodents and possibly humans.
Gene polymorphism variants of CYP4A11 are associated with the development of hypertension and cerebral infarction (i.e. ischemic stroke) in humans (see 20-Hydroxyeicosatetraenoic acid). In its capacity to form hydroxyl fatty acid, CYP4A11 is classified as a CYP monooxygease.
CYP4A11 also has epoxygenase activity in that it metablizes docosahexaenoic acid to epoxydocosapentaenoic acids (EDPs; primarily 19,20-epoxy-eicosapentaenoic acid isomers ) and eicosapentaenoic acid to epoxyeicosatetraenoic acids (EEQs, primarily 17,18-EEQ isomers). CYP4A11 does not convert arachidonic acid to epoxides. CYP4F8 and CYP4F12 likewise possess both monooxygenase activity for arachidonic acid and epoxygenase activity for docosahexaenoic and eicosapentenoic acids. In vitro studies on human and animal cells and tissues and in vivo animal model studies indicate that certain EDPs and EEQs (16,17-EDPs, 19,20-EDPs, 17,18-EEQs have been most often examined) have actions which often oppose those of 20-HETE, principally in the areas of blood pressure regulation, blood vessel thrombosis, and cancer growth (see 20-Hydroxyeicosatetraenoic acid, Epoxyeicosatetraenoic acid, and Epoxydocosapentaenoic acid sections on activities and clinical significance). These studies also indicate that the EPAs and EEQs are: 1) more potent than the CYP450 epoxygenase (e.g. CYP2C8, CYP2C9, CYP2C19, CYP2J2, and CYP2S1)-formed epoxides of arachidonic acid (termed EETs) in decreasing hypertension and pain perception; 2) more potent than or at least equal in potency to the EETs in suppressing inflammation; and 3) act oppositely from the EETs in that they inhibit angiogenesis, endothelial cell migration, endothelial cell proliferation, and the growth and metastasis of human breast and prostate cancer cell lines whereas EETs have stimulatory effects in each of these systems. Consumption of omega-3 fatty acid-rich diets dramatically raises the serum and tissue levels of EDPs and EEQs in animals as well as humans and in humans are by far the most prominent change in the profile of PUFA metabolites caused by dietary omega-3 fatty acids.
Members of the CYP4A and CYP4F sub-families and CYP2U1 may also ω-hydroxylate and thereby reduce the activity of various fatty acid metabolites of arachidonic acid including LTB4, 5-HETE, 5-oxo-eicosatetraenoic acid, 12-HETE, and several prostaglandins that are involved in regulating various inflammatory, vascular, and other responses in animals and humans. This hydroxylation-induced inactivation may underlie the proposed roles of the cytochromes in dampening inflammatory responses and the reported associations of certain CYP4F2 and CYP4F3 single nucleotide variants with human Krohn's disease and Coeliac disease, respectively.
T8590C single nucleotide polymorphism (SNP), rs1126742, in the CYPA411 gene produces a protein with significantly reduced catalytic activity due to a loss-of-function mechanism; this SNP has been associated with hypertension in some but not all population studies. This result could be due to a decline in the production of EEQs and EPDs, which as indicated above, have blood pressure lowering actions. | CYP4A11
Cytochrome P450 4A11 is a protein that in humans is encoded by the CYP4A11 gene.[1][2]
# Function
This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This protein localizes to the endoplasmic reticulum and hydroxylates medium-chain fatty acids such as laurate and myristate.[2]
CYP4A11 is highly expressed in the liver and kidney.[3]
CYP4A11 along with CYP4A22, CYP4F2, and CYP4F3 metabolize arachidonic acid to 20-Hydroxyeicosatetraenoic acid (20-HETE) by an Omega oxidation reaction with the predominant 20-HETE-synthesizing enzymes in humans being CYP4F2 followed by CYP4A11; 20-HETE regulates blood flow, vascularization, blood pressure, and kidney tubule absorption of ions in rodents and possibly humans.
[4] Gene polymorphism variants of CYP4A11 are associated with the development of hypertension and cerebral infarction (i.e. ischemic stroke) in humans (see 20-Hydroxyeicosatetraenoic acid).[5][6][7][8][9][10] In its capacity to form hydroxyl fatty acid, CYP4A11 is classified as a CYP monooxygease.
CYP4A11 also has epoxygenase activity in that it metablizes docosahexaenoic acid to epoxydocosapentaenoic acids (EDPs; primarily 19,20-epoxy-eicosapentaenoic acid isomers [i.e. 19,20-EDPs]) and eicosapentaenoic acid to epoxyeicosatetraenoic acids (EEQs, primarily 17,18-EEQ isomers).[11] CYP4A11 does not convert arachidonic acid to epoxides. CYP4F8 and CYP4F12 likewise possess both monooxygenase activity for arachidonic acid and epoxygenase activity for docosahexaenoic and eicosapentenoic acids. In vitro studies on human and animal cells and tissues and in vivo animal model studies indicate that certain EDPs and EEQs (16,17-EDPs, 19,20-EDPs, 17,18-EEQs have been most often examined) have actions which often oppose those of 20-HETE, principally in the areas of blood pressure regulation, blood vessel thrombosis, and cancer growth (see 20-Hydroxyeicosatetraenoic acid, Epoxyeicosatetraenoic acid, and Epoxydocosapentaenoic acid sections on activities and clinical significance). These studies also indicate that the EPAs and EEQs are: 1) more potent than the CYP450 epoxygenase (e.g. CYP2C8, CYP2C9, CYP2C19, CYP2J2, and CYP2S1)-formed epoxides of arachidonic acid (termed EETs) in decreasing hypertension and pain perception; 2) more potent than or at least equal in potency to the EETs in suppressing inflammation; and 3) act oppositely from the EETs in that they inhibit angiogenesis, endothelial cell migration, endothelial cell proliferation, and the growth and metastasis of human breast and prostate cancer cell lines whereas EETs have stimulatory effects in each of these systems.[12][13][14][15] Consumption of omega-3 fatty acid-rich diets dramatically raises the serum and tissue levels of EDPs and EEQs in animals as well as humans and in humans are by far the most prominent change in the profile of PUFA metabolites caused by dietary omega-3 fatty acids.[12][15][16]
Members of the CYP4A and CYP4F sub-families and CYP2U1 may also ω-hydroxylate and thereby reduce the activity of various fatty acid metabolites of arachidonic acid including LTB4, 5-HETE, 5-oxo-eicosatetraenoic acid, 12-HETE, and several prostaglandins that are involved in regulating various inflammatory, vascular, and other responses in animals and humans.[17][18] This hydroxylation-induced inactivation may underlie the proposed roles of the cytochromes in dampening inflammatory responses and the reported associations of certain CYP4F2 and CYP4F3 single nucleotide variants with human Krohn's disease and Coeliac disease, respectively.[19][20][21]
T8590C single nucleotide polymorphism (SNP), rs1126742,[22] in the CYPA411 gene produces a protein with significantly reduced catalytic activity due to a loss-of-function mechanism; this SNP has been associated with hypertension in some but not all population studies.[23] This result could be due to a decline in the production of EEQs and EPDs, which as indicated above, have blood pressure lowering actions. | https://www.wikidoc.org/index.php/CYP4A11 | |
896cd92ecf9988afc546b15dd35fae86335a069f | wikidoc | CYP4A22 | CYP4A22
CYP4A22 (cytochrome P450, family 4, subfamily A, polypeptide 22) also known as fatty acid omega-hydroxylase is a protein which in humans is encoded by the CYP4A22 gene.
This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This gene is part of a cluster of cytochrome P450 genes on chromosome 1p33.
CYP4A22 was once considered, along with CYP4A11, CYP4F2, and CYP4F3, as active in metabolizing arachidonic acid to 20-hydroxyeicosatetraenoic acid (20-HETE) by an omega oxidation reaction with the predominant 20-HETE-synthesizing enzymes in humans being CYP4F2 followed by CYP4A11; 20-HETE regulates blood flow, vascularization, blood pressure, and kidney tubule absorption of ions in rodents and possibly humans. However, human CYP4A22 is expressed at very low levels in few tissues and may not be a functional enzyme in regard to the metabolism of arachidnoic acid to 20-HETE. | CYP4A22
CYP4A22 (cytochrome P450, family 4, subfamily A, polypeptide 22) also known as fatty acid omega-hydroxylase is a protein which in humans is encoded by the CYP4A22 gene.[1]
This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This gene is part of a cluster of cytochrome P450 genes on chromosome 1p33.[2]
CYP4A22 was once considered, along with CYP4A11, CYP4F2, and CYP4F3, as active in metabolizing arachidonic acid to 20-hydroxyeicosatetraenoic acid (20-HETE) by an omega oxidation reaction with the predominant 20-HETE-synthesizing enzymes in humans being CYP4F2 followed by CYP4A11; 20-HETE regulates blood flow, vascularization, blood pressure, and kidney tubule absorption of ions in rodents and possibly humans.[3] However, human CYP4A22 is expressed at very low levels in few tissues and may not be a functional enzyme in regard to the metabolism of arachidnoic acid to 20-HETE.[4][5] | https://www.wikidoc.org/index.php/CYP4A22 | |
f36fdf75eec5f26e781d73d251e4a50f4f989cd3 | wikidoc | CYP4F11 | CYP4F11
CYP4F11 (cytochrome P450, family 4, subfamily F, polypeptide 11) is a protein that in humans is encoded by the CYP4F11 gene. This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This gene is part of a cluster of cytochrome P450 genes on chromosome 19. Another member of this family, CYP4F2, is approximately 16 kb away. Alternatively spliced transcript variants encoding the same protein have been found for this gene.
# Expression
CYP4F11 is expressed in liver, kidney, heart, brain, and skeletal muscle and is overexpressed in ovarian and colon cancers; perhaps relativant to its overexpression in ovarian cancer, its gene has an estrogen receptor α responsive site in its Promoter (genetics) site.
# Activities and possible functions
CYP4F11 is active in metabolism of many drugs including benzphetamine, ethylmorphine, chlorpromazine, imipramine, and erythromycin;.
The cytochrome is also able to hydroxylate short-chain and 3-hydroxylated medium chain fatty acidss by attaching a hydroxyl residue to their terminal carbon by omega oxidation in a reaction that may be critical to the processing of these fatty acids. It likewise omega-hydroxylates Vitamin Ks including menaquinone in a metabolic step which is essential for their further metabolism by beta oxidation and probably thereby their removal by catabolism to regulate their tissue levels.
CYP4F11 omega-hydroxylates leukotriene B4 (LTB4) to 20-hydroxy-LTB4, 5-Hydroxyicosatetraenoic acid (5-HETE) to 20-hydroxy-5-HETE (i.e. 5,20-diHETE), 12-hydroxyeicosatetraenoic acid (12-HETE) to 12,20-diHETE, lipoxins and possibly 5-oxo-eicosatetraenoic acid (5-oxo-ETE) to their 20-hydroxy metabolites; these reactions begin the inactivation of these pro- (LTB4, 5-HETE, 12-HETE, and 5-oxo-ETE) and anti- (lipoxins) cell signaling agents; however, it is relatively weak compared to, and therefore possibly not as physiologically relevant as, other CYP4Fs such as CYP4F2, CYP4F3a, CYP4F3b, CYP4A11 and CYP4F2 in doing so. The enzyme also hydroxylates arachidonic acid (i.e. eicosatetraenoic acid to 20-Hydroxyeicosatetraenoic acid) (20-HETE) although other cytochromes such as CYP4A11 and CYP4F2 appear more important in this metabolic conversion. 20-HETE is a short-lived potent signaling agent that functions to regulate blood flow, vascularization, blood pressure, and kidney tubule absorption of ions in rodents and possibly humans. Gene polymorphism variants of CYP4A11 are associated with the development of hypertension and cerebral infarction (i.e. ischemic stroke) in humans (see 20-Hydroxyeicosatetraenoic acid). In spite of its relative impotency and/or importance in accomplishing these omega-hydroxylations, CYP4F11 may contribute to them in certain tissues.
# Further reading
Johnson AL, Edson KZ, Totah RA, Rettie AE. Cytochrome P450 ω-Hydroxylases in Inflammation and Cancer. Adv. Pharmacol. 74:223-62, 2015. | CYP4F11
CYP4F11 (cytochrome P450, family 4, subfamily F, polypeptide 11) is a protein that in humans is encoded by the CYP4F11 gene.[1] This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This gene is part of a cluster of cytochrome P450 genes on chromosome 19. Another member of this family, CYP4F2, is approximately 16 kb away. Alternatively spliced transcript variants encoding the same protein have been found for this gene.[2]
# Expression
CYP4F11 is expressed in liver, kidney, heart, brain, and skeletal muscle and is overexpressed in ovarian and colon cancers; perhaps relativant to its overexpression in ovarian cancer, its gene has an estrogen receptor α responsive site in its Promoter (genetics) site.[3]
# Activities and possible functions
CYP4F11 is active in metabolism of many drugs including benzphetamine, ethylmorphine, chlorpromazine, imipramine, and erythromycin;.[3]
The cytochrome is also able to hydroxylate short-chain and 3-hydroxylated medium chain fatty acidss by attaching a hydroxyl residue to their terminal carbon by omega oxidation in a reaction that may be critical to the processing of these fatty acids.[4] It likewise omega-hydroxylates Vitamin Ks including menaquinone in a metabolic step which is essential for their further metabolism by beta oxidation and probably thereby their removal by catabolism to regulate their tissue levels.[4]
CYP4F11 omega-hydroxylates leukotriene B4 (LTB4) to 20-hydroxy-LTB4, 5-Hydroxyicosatetraenoic acid (5-HETE) to 20-hydroxy-5-HETE (i.e. 5,20-diHETE), 12-hydroxyeicosatetraenoic acid (12-HETE) to 12,20-diHETE, lipoxins and possibly 5-oxo-eicosatetraenoic acid (5-oxo-ETE) to their 20-hydroxy metabolites; these reactions begin the inactivation of these pro- (LTB4, 5-HETE, 12-HETE, and 5-oxo-ETE) and anti- (lipoxins) cell signaling agents; however, it is relatively weak compared to, and therefore possibly not as physiologically relevant as, other CYP4Fs such as CYP4F2, CYP4F3a, CYP4F3b, CYP4A11 and CYP4F2 in doing so.[3][4] The enzyme also hydroxylates arachidonic acid (i.e. eicosatetraenoic acid to 20-Hydroxyeicosatetraenoic acid) (20-HETE) although other cytochromes such as CYP4A11 and CYP4F2 appear more important in this metabolic conversion.[3] 20-HETE is a short-lived potent signaling agent that functions to regulate blood flow, vascularization, blood pressure, and kidney tubule absorption of ions in rodents and possibly humans.[5] Gene polymorphism variants of CYP4A11 are associated with the development of hypertension and cerebral infarction (i.e. ischemic stroke) in humans (see 20-Hydroxyeicosatetraenoic acid).[6][7][8][9][10][11] In spite of its relative impotency and/or importance in accomplishing these omega-hydroxylations, CYP4F11 may contribute to them in certain tissues.
# Further reading
Johnson AL, Edson KZ, Totah RA, Rettie AE. Cytochrome P450 ω-Hydroxylases in Inflammation and Cancer. Adv. Pharmacol. 74:223-62, 2015.[4] | https://www.wikidoc.org/index.php/CYP4F11 | |
e00a02b0f203f31eb7a6276f150f7aec00faf969 | wikidoc | CYP4F12 | CYP4F12
Cytochrome P450 4F12 is a protein that in humans is encoded by the CYP4F12 gene.
This gene encodes a member of the cytochrome P450 superfamily of enzymes and is part of a cluster of cytochrome P450 genes on chromosome 19. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This protein likely localizes to the endoplasmic reticulum. CYP4F12 is expressed in the liver and throughout the gastrointestinal track, is known to metabolize the anti-histamine drugs, ebastine and terfenadine, and therefore is suggested to be positioned for and possibly involved in the processing of these and perhaps other drugs.
When expressed in yeast the enzyme is capable of oxidizing arachidonic acid by adding a hydroxyl residue to carbons 18 or 19 to form 18-hydroxyeicosatetraenoic acid (18-HETE) or 19-HETE; however, its physiological function in doing so has not been determined. CYP4F12 also metabolizes prostaglandin H2 (PGH2) and PGH1 to their corresponding 19-hydroxyl analogs in a reaction that might serve to reduce their activities. In addition to these monooxygenase actions, CYP458 possesses epoxygenase activity: it metabolizes the omega-3 fatty acids, docosahexaenoic acid (DHA) and eicosapentaenoic acid, (EPA) to their corresponding epoxides, the epoxydocosapentaenoic acids (EDPs) and epoxyeicosatetraenoic acids (EEQs), respectively. The enzyme metabolizes DHA primarily to 19R,20S-epoxyeicosapentaenoic acid and 19S,20R-epoxyeicosapentaenoic acid isomers (termed 19,20-EDP) and EPA primarily to 17R,18S-eicosatetraenic acid and 17S,18R-eicosatetraenic acid isomers (termed 17,18-EEQ). 19-HETE is an inhibitor of 20-HETE, a broadly active signaling molecule which acts to onstrict arterioles, elevate blood pressure, promote inflammation responses, and stimulates the growth of various types of tumor cells; however the in vivo ability and significance of 19-HETE in inhibiting 20-HETE has not been demonstrated (see 20-Hydroxyeicosatetraenoic acid). The EDPs (see Epoxydocosapentaenoic acid) and EEQs (see epoxyeicosatetraenoic acid) have a broad range of activities. In various animal models and in vitro studies on animal and human tissues, they decrease hypertension and pain perception; suppress inflammation; inhibit angiogenesis, endothelial cell migration and endothelial cell proliferation; and inhibit the growth and metastasis of human breast and prostate cancer cell lines. It is suggested that the EDP and EEQ metabolites function in humans as they do in animal models and that, as products of the omega-3 fatty acids, DHA acid and EPA, the EDP and EEQ metabolites contribute to many of the beneficial effects attributed to dietary omega-3 fatty acids. EDP and EEQ metabolites are short-lived, being inactivated within seconds or minutes of formation by epoxide hydrolases, particularly soluble epoxide hydrolase, and therefore act locally.
The fatty acid metabolizing activity, including the ability to form epoxides, of CYP4F12 is very similar to that of CYP4F8. However, it and CYP4F8 are not regarded as being major contributors in forming the cited epoxides in humans although they might do so in tissues where they are highly expressed. | CYP4F12
Cytochrome P450 4F12 is a protein that in humans is encoded by the CYP4F12 gene.[1][2]
This gene encodes a member of the cytochrome P450 superfamily of enzymes and is part of a cluster of cytochrome P450 genes on chromosome 19.[2][3] The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This protein likely localizes to the endoplasmic reticulum. CYP4F12 is expressed in the liver and throughout the gastrointestinal track, is known to metabolize the anti-histamine drugs, ebastine and terfenadine, and therefore is suggested to be positioned for and possibly involved in the processing of these and perhaps other drugs.[3][4]
When expressed in yeast the enzyme is capable of oxidizing arachidonic acid by adding a hydroxyl residue to carbons 18 or 19 to form 18-hydroxyeicosatetraenoic acid (18-HETE) or 19-HETE; however, its physiological function in doing so has not been determined. CYP4F12 also metabolizes prostaglandin H2 (PGH2) and PGH1 to their corresponding 19-hydroxyl analogs in a reaction that might serve to reduce their activities.[5] In addition to these monooxygenase actions, CYP458 possesses epoxygenase activity: it metabolizes the omega-3 fatty acids, docosahexaenoic acid (DHA) and eicosapentaenoic acid, (EPA) to their corresponding epoxides, the epoxydocosapentaenoic acids (EDPs) and epoxyeicosatetraenoic acids (EEQs), respectively.[6] The enzyme metabolizes DHA primarily to 19R,20S-epoxyeicosapentaenoic acid and 19S,20R-epoxyeicosapentaenoic acid isomers (termed 19,20-EDP) and EPA primarily to 17R,18S-eicosatetraenic acid and 17S,18R-eicosatetraenic acid isomers (termed 17,18-EEQ).[6] 19-HETE is an inhibitor of 20-HETE, a broadly active signaling molecule which acts to onstrict arterioles, elevate blood pressure, promote inflammation responses, and stimulates the growth of various types of tumor cells; however the in vivo ability and significance of 19-HETE in inhibiting 20-HETE has not been demonstrated (see 20-Hydroxyeicosatetraenoic acid). The EDPs (see Epoxydocosapentaenoic acid) and EEQs (see epoxyeicosatetraenoic acid) have a broad range of activities. In various animal models and in vitro studies on animal and human tissues, they decrease hypertension and pain perception; suppress inflammation; inhibit angiogenesis, endothelial cell migration and endothelial cell proliferation; and inhibit the growth and metastasis of human breast and prostate cancer cell lines.[7][8][9][10] It is suggested that the EDP and EEQ metabolites function in humans as they do in animal models and that, as products of the omega-3 fatty acids, DHA acid and EPA, the EDP and EEQ metabolites contribute to many of the beneficial effects attributed to dietary omega-3 fatty acids.[7][10][11] EDP and EEQ metabolites are short-lived, being inactivated within seconds or minutes of formation by epoxide hydrolases, particularly soluble epoxide hydrolase, and therefore act locally.
The fatty acid metabolizing activity, including the ability to form epoxides, of CYP4F12 is very similar to that of CYP4F8. However, it and CYP4F8 are not regarded as being major contributors in forming the cited epoxides in humans although they might do so in tissues where they are highly expressed.[5] | https://www.wikidoc.org/index.php/CYP4F12 | |
af97b9c3f2a41c6bb701706249059a035e0293f3 | wikidoc | CYP4F22 | CYP4F22
CYP4F22 (cytochrome P450, family 4, subfamily F, polypeptide 22) is a protein that in humans is encoded by the CYP4F22 gene.
This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This gene is part of a cluster of cytochrome P450 genes on chromosome 19 and encodes an enzyme thought to play a role in the 12(R)-lipoxygenase pathway. Mutations in this gene are the cause of ichthyosis lamellar type 3.
# Activity
CYP4F22, like other CYP4F proteins, is a Cytochrome P450 omega hydroxylase, i.e. an enzyme that metabolizes fatty acids to their omega hydroxyl derivatives (see Omega oxidation). This hydroxylation may: a) produce a biologically important signaling molecule such as occurs in the metabolism of 20-carbon straight chain polyunsaturated fatty acid, arachidonic acid, to 20-Hydroxyeicosatetraenoic acid, b) inactivate a biologically important product such as the metabolism of the arachidonic acid metabolite, 5-oxo-eicosatetraenoic acid, to its ~100-fold less potent product, 5-oxo-20-hydroxy-eicosatetraenoic acid, or c) be the first step in the further metabolism of xenobiotics or natural compounds CYP4F22 serves the latter function. It is a type 1 Integral membrane protein located in the endoplasmic reticulum of cells in the stratum granulosum of mammalian, including human, skin where it functions to attach an omega hydroxyl residue to fatty acids that are exceptionally long, 28 or more carbons, i.e. the very long chain fatty acids (VLCFA). These VLCFA targets need not be free fatty acids but also can be acylated in an amide bond to sphingosine to form an acylceramide.
# Function
CYP4F22 omega hydroxylates the VLCFA in esterified omega-oxyacyl-sphingosine complex to form an esterified omega-hydroxyacyl-sphingosine complex. This step is critical for delivering the wax-like, extremely hydrophobic VLCFA to the stratum corneum near the skin surface. It is these skin surface VLCFA which create and maintain the skin's ability to function as a water barrier.
CYP4F22, like many of the CYP4F series of CYPs, may prove to serve other functions but its role in hydroxylating VLCFA in the skin's water barrier function, as defined in genetic studies (see below), has dominated research on it.
# Genetic studies
A small number of newborns with Congenital ichthyosiform erythroderma have been found to have autosomal recessive lose of function mutations in CYP4F22. Of the varies subtypes of congenital ichthyosiform erythroderma, these mutations have been associated almost exclusively with the Lamellar ichthyosis subtype. | CYP4F22
CYP4F22 (cytochrome P450, family 4, subfamily F, polypeptide 22) is a protein that in humans is encoded by the CYP4F22 gene.[1]
This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. This gene is part of a cluster of cytochrome P450 genes on chromosome 19 and encodes an enzyme thought to play a role in the 12(R)-lipoxygenase pathway. Mutations in this gene are the cause of ichthyosis lamellar type 3.[2]
# Activity
CYP4F22, like other CYP4F proteins, is a Cytochrome P450 omega hydroxylase, i.e. an enzyme that metabolizes fatty acids to their omega hydroxyl derivatives (see Omega oxidation). This hydroxylation may: a) produce a biologically important signaling molecule such as occurs in the metabolism of 20-carbon straight chain polyunsaturated fatty acid, arachidonic acid, to 20-Hydroxyeicosatetraenoic acid, b) inactivate a biologically important product such as the metabolism of the arachidonic acid metabolite, 5-oxo-eicosatetraenoic acid, to its ~100-fold less potent product, 5-oxo-20-hydroxy-eicosatetraenoic acid, or c) be the first step in the further metabolism of xenobiotics or natural compounds[3] CYP4F22 serves the latter function. It is a type 1 Integral membrane protein located in the endoplasmic reticulum of cells in the stratum granulosum of mammalian, including human, skin where it functions to attach an omega hydroxyl residue to fatty acids that are exceptionally long, 28 or more carbons, i.e. the very long chain fatty acids (VLCFA).[4][5] These VLCFA targets need not be free fatty acids but also can be acylated in an amide bond to sphingosine to form an acylceramide.
# Function
CYP4F22 omega hydroxylates the VLCFA in esterified omega-oxyacyl-sphingosine complex to form an esterified omega-hydroxyacyl-sphingosine complex. This step is critical for delivering the wax-like, extremely hydrophobic VLCFA to the stratum corneum near the skin surface. It is these skin surface VLCFA which create and maintain the skin's ability to function as a water barrier.[6][7][8][9]
CYP4F22, like many of the CYP4F series of CYPs, may prove to serve other functions but its role in hydroxylating VLCFA in the skin's water barrier function, as defined in genetic studies (see below), has dominated research on it.
# Genetic studies
A small number of newborns with Congenital ichthyosiform erythroderma have been found to have autosomal recessive lose of function mutations in CYP4F22.[10][11] Of the varies subtypes of congenital ichthyosiform erythroderma, these mutations have been associated almost exclusively with the Lamellar ichthyosis subtype.[11] | https://www.wikidoc.org/index.php/CYP4F22 | |
1001836d806b34aa852f3ac248f27e6131026851 | wikidoc | Cabbage | Cabbage
The cabbage (Brassica oleracea Capitata Group), is a plant of the Family Brassicaceae (or Cruciferae). It is a herbaceous, biennial, and dicotyledonous flowering plant with leaves forming a characteristic compact cluster. Cabbages grown late in autumn and in the beginning of winter are called coleworts.
The cabbage is derived from a leafy wild mustard plant, native to the Mediterranean region. It was known to the ancient Greeks and Romans; Cato the Elder praised this vegetable for its medicinal properties, declaring that "it is first of all the vegetables".. The English name derives from the Normanno-Picard caboche ("head"). Cabbage was developed by ongoing artificial selection for suppression of the internode length. The dense core of the cabbage is called the babchka. It is related to the turnip.
The sharp or bitter taste sometimes present in cabbage is due to glucosinolate(s).
# Uses
The only part of the plant that is normally eaten is the leafy head; more precisely, the spherical cluster of immature leaves, excluding the partially unfolded outer leaves.
The so-called 'cabbage head' is widely consumed raw, cooked, or preserved in a great variety of dishes. Cabbage is a leaf vegetable.
## Raw
Raw cabbage is usually sliced into thin strips or shredded for use in salads, such as coleslaw. It can also replace iceberg lettuce in sandwiches. Cabbage is an excellent source of Vitamin C.
## Cooked
Cabbage is often added to soups or stews. Cabbage soup is popular in central Europe and eastern Europe, and cabbage is an ingredient in some kinds of borscht. Cabbage is also used in many popular dishes in India. Boiling tenderizes the leaves and releases sugars, which leads to the characteristic "cabbage" aroma. Boiled cabbage has become stigmatized in North America because of its strong cooking odor and the belief that it causes flatulence. Boiled cabbage as an accompaniment to meats and other dishes can be an opportune source of vitamins and dietary fiber. Stuffed cabbage is an East European and Middle Eastern delicacy. The leaves are softened by parboiling or placing the whole head of cabbage in the freezer, and then filled with chopped meat and/or rice.
## Fermented and preserved
Cabbage is the basis for the German sauerkraut and Korean kimchi. To pickle cabbage it is placed in a jar, covered with water and salt, and left in a warm place for several days to ferment. Sauerkraut was historically prepared at home in large batches, as a way of storing food for the winter. Cabbage can also be pickled in vinegar with various spices, alone or in combination with other vegetables. Korean baechu kimchi is usually sliced thicker than its European counterpart, and the addition of onions, chilies, minced garlic and gingers is common.
## Medicinal properties
In European folk medicine, cabbage leaves are used to treat acute inflammation. A paste of raw cabbage may be placed in a cabbage leaf and wrapped around the affected area to reduce discomfort. Some claim it is effective in relieving painfully engorged breasts in breastfeeding women.
Cabbage contains significant amounts of glutamine, an amino acid, which has anti-inflammatory properties.
It is a source of indol-3-carbinol, or I3C, a compound used as an adjuvent therapy for recurrent respiratory papillomatosis, a disease of the head and neck caused by human papillomavirus (usually types 6 and 11) that causes growths in the airway that can lead to death.
# Varieties
There are many varieties of cabbage based on shape and time of maturity. Traditional varieties include "Late Flat Dutch", "Early Jersey Wakefield" (a conical variety), "Danish Ballhead" (late, round -headed). Savoy Cabbage has a round head with crinkled leaves. Red cabbage is a small, round headed type with dark red leaves. Krautman is the most common variety for commercial production of sauerkrauts.
# Cultivation
Broadly speaking, cabbage varieties come in two groups, early and late. The early varieties mature in about 45 days. They produce small heads which do not keep well and are intended for consumption while fresh. The late cabbage matures in about 87 days, and produces a larger head.
Cabbage can be started indoors or sowed directly. Like all brassicae, cabbage is a cool season crop, so early and late plantings do better than those maturing in the heat of the summer.
Control of insect pests is important, particularly in commercial production where appearance is a driver of success. The pesticides sevin and malathion are both listed for use on cabbage. The caterpillars of some butterflies in the family Pieridae (the "whites") feed on brassicas and can be serious pests; see also List of Lepidoptera that feed on Brassica.
Cabbages keep well and were thus a common winter vegetable before refrigeration and long-distance shipping of produce.
China is leader in production of cabbages followed by India and then Russian Federation.
# Related Brassica oleracea varieties
Besides cabbage proper, the species Brassica oleracea has many distinctive cultivars, which are commonly known by other names: broccoli (Italica Group), cauliflower (Botrytis Group), kale, collard greens, and spring greens (Acephala Group), kohlrabi (Gongylodes Group), brussels sprouts (Gemmifera Group), Chinese kale or Chinese broccoli (Alboglabra Group), broccolini (Italica × Alboglabra Group), and broccoflower (Italica × Botrytis Group).
# Linguistic associations
During World War II, "kraut" (cabbage) was a racial slur for Germans. In Hebrew, the term "rosh kruv" (cabbage head) implies stupidity.
In England in the late 1950s, French language teachers taught from a textbook the phrase "ma petite chou" -- my little cabbage -- as an endearment from a man to a woman. This is still used today as can be seen at:
“See there ma petite chou, now everything is worked out.” Patricia turned and walked back to the desk. “Gérard, why must you call me ma petite chou all the time?”
“Ma chérie, it is an endearment. If you understood that in French…”
She cut him off mid sentence. “I know what it means Gérard. Even with my limited French vocabulary I know that it means my small cabbage.”
“But that is not the endearment. You do not understand…”'
In England, cabbage is a slang synonym for "cash", especially paper money. | Cabbage
Template:Nofootnotes
Template:Infobox Cultivar
Template:Nutritionalvalue
The cabbage (Brassica oleracea Capitata Group), is a plant of the Family Brassicaceae (or Cruciferae). It is a herbaceous, biennial, and dicotyledonous flowering plant with leaves forming a characteristic compact cluster. Cabbages grown late in autumn and in the beginning of winter are called coleworts.
The cabbage is derived from a leafy wild mustard plant, native to the Mediterranean region. It was known to the ancient Greeks and Romans; Cato the Elder praised this vegetable for its medicinal properties, declaring that "it is first of all the vegetables".[1]. The English name derives from the Normanno-Picard caboche ("head"). Cabbage was developed by ongoing artificial selection for suppression of the internode length. The dense core of the cabbage is called the babchka[citation needed]. It is related to the turnip.
The sharp or bitter taste sometimes present in cabbage is due to glucosinolate(s).
# Uses
The only part of the plant that is normally eaten is the leafy head; more precisely, the spherical cluster of immature leaves, excluding the partially unfolded outer leaves.
The so-called 'cabbage head' is widely consumed raw, cooked, or preserved in a great variety of dishes. Cabbage is a leaf vegetable.
## Raw
Raw cabbage is usually sliced into thin strips or shredded for use in salads, such as coleslaw. It can also replace iceberg lettuce in sandwiches. Cabbage is an excellent source of Vitamin C.
## Cooked
Cabbage is often added to soups or stews. Cabbage soup is popular in central Europe and eastern Europe, and cabbage is an ingredient in some kinds of borscht. Cabbage is also used in many popular dishes in India. Boiling tenderizes the leaves and releases sugars, which leads to the characteristic "cabbage" aroma. Boiled cabbage has become stigmatized in North America because of its strong cooking odor and the belief that it causes flatulence. Boiled cabbage as an accompaniment to meats and other dishes can be an opportune source of vitamins and dietary fiber. Stuffed cabbage is an East European and Middle Eastern delicacy. The leaves are softened by parboiling or placing the whole head of cabbage in the freezer, and then filled with chopped meat and/or rice.
## Fermented and preserved
Cabbage is the basis for the German sauerkraut and Korean kimchi. To pickle cabbage it is placed in a jar, covered with water and salt, and left in a warm place for several days to ferment. Sauerkraut was historically prepared at home in large batches, as a way of storing food for the winter. Cabbage can also be pickled in vinegar with various spices, alone or in combination with other vegetables. Korean baechu kimchi is usually sliced thicker than its European counterpart, and the addition of onions, chilies, minced garlic and gingers is common.
## Medicinal properties
In European folk medicine, cabbage leaves are used to treat acute inflammation.[2] A paste of raw cabbage may be placed in a cabbage leaf and wrapped around the affected area to reduce discomfort. Some claim it is effective in relieving painfully engorged breasts in breastfeeding women.[3]
Cabbage contains significant amounts of glutamine, an amino acid, which has anti-inflammatory properties.
It is a source of indol-3-carbinol, or I3C, a compound used as an adjuvent therapy for recurrent respiratory papillomatosis, a disease of the head and neck caused by human papillomavirus (usually types 6 and 11) that causes growths in the airway that can lead to death.
# Varieties
There are many varieties of cabbage based on shape and time of maturity. Traditional varieties include "Late Flat Dutch", "Early Jersey Wakefield" (a conical variety), "Danish Ballhead" (late, round -headed). Savoy Cabbage has a round head with crinkled leaves. Red cabbage is a small, round headed type with dark red leaves. Krautman is the most common variety for commercial production of sauerkrauts.
# Cultivation
Broadly speaking, cabbage varieties come in two groups, early and late. The early varieties mature in about 45 days. They produce small heads which do not keep well and are intended for consumption while fresh. The late cabbage matures in about 87 days, and produces a larger head.
Cabbage can be started indoors or sowed directly. Like all brassicae, cabbage is a cool season crop, so early and late plantings do better than those maturing in the heat of the summer.
Control of insect pests is important, particularly in commercial production where appearance is a driver of success. The pesticides sevin and malathion are both listed for use on cabbage. The caterpillars of some butterflies in the family Pieridae (the "whites") feed on brassicas and can be serious pests; see also List of Lepidoptera that feed on Brassica.
Cabbages keep well and were thus a common winter vegetable before refrigeration and long-distance shipping of produce.
China is leader in production of cabbages followed by India and then Russian Federation.
# Related Brassica oleracea varieties
Besides cabbage proper, the species Brassica oleracea has many distinctive cultivars, which are commonly known by other names: broccoli (Italica Group), cauliflower (Botrytis Group), kale, collard greens, and spring greens (Acephala Group), kohlrabi (Gongylodes Group), brussels sprouts (Gemmifera Group), Chinese kale or Chinese broccoli (Alboglabra Group), broccolini (Italica × Alboglabra Group), and broccoflower (Italica × Botrytis Group).
# Linguistic associations
During World War II, "kraut" (cabbage) was a racial slur for Germans. In Hebrew, the term "rosh kruv" (cabbage head) implies stupidity.
In England in the late 1950s, French language teachers taught from a textbook the phrase "ma petite chou" -- my little cabbage -- as an endearment from a man to a woman. This is still used today as can be seen at: [4]
“See there ma petite chou, now everything is worked out.” Patricia turned and walked back to the desk. “Gérard, why must you call me ma petite chou all the time?”
“Ma chérie, it is an endearment. If you understood that in French…”
She cut him off mid sentence. “I know what it means Gérard. Even with my limited French vocabulary I know that it means my small cabbage.”
“But that is not the endearment. You do not understand…”'
In England, cabbage is a slang synonym for "cash", especially paper money.[5] | https://www.wikidoc.org/index.php/Cabbage | |
29b7737725192a5c28b5c8c023ae38b75ea4a259 | wikidoc | Cadaver | Cadaver
# Overview
A cadaver or corpse is a dead body. "Cadaver" is normally used as a more formal term for a body being used in medical training or research.
# Human decay
Different stages of decomposition can help determine how long a body has been dead.
The first stage is self digestion, also known as autolysis. This happens when the cells break down the body into elements the cells can eat; this creates a liquid that gets between the layers of skin and makes the skin peel off. During this stage, flies (when present) start to lay eggs in the openings of the body: eyes, nostrils, mouth, ears, open wounds, and other orifices. Hatched larvae (maggots) subsequently get under the skin and start to eat the body.
The second stage of decomposition is bloating; bacteria in the gut begin to break down the tissues of the body, releasing gas that accumulates in the intestines, which becomes trapped due to the early collapse of the small intestine. This bloating occurs largely in the abdomen, and sometimes in the mouth and genitals. The tongue may swell. This usually happens in about the second week of decomposition. Gas accumulation and bloating will continue until the body is decomposed sufficiently for the gas to escape.
The third stage is putrefaction. It is the last and longest stage. Putrefaction is where the larger structures of the body break down, and tissues liquefy. The digestive organs, the brain, and lungs are the first to disintegrate. Under normal conditions, the organs are unidentifiable after three weeks. The muscles can be eaten by bacteria or devoured by carnivorous animals. Eventually, sometimes after several years, all that remains is the skeleton.
# Embalming
When a corpse is buried the body will still eventually decompose by the actions of anaerobic bacteria. In many countries, corpses buried in coffins are embalmed. An embalmer may clean and shave the face, fill the eye sockets with cotton to make them appear full, and suture the jaw together to keep it from hanging open. Embalming fluid is then pumped into the body via an artery (commonly carotid). This rehydrates the tissues and severely reduces the pace of decomposition.
Embalming is used to preserve the corpse temporarily, but may last for years. In some societies, such as the United States, make-up is applied to the corpse to make the body presentable for public presentation.
# A brief history of cadavers
The methods of preserving cadavers, and their acquisition, have changed over the last 200 years. Criminals who were executed for their crimes were used as the first cadavers. The demand for cadavers increased when the number of criminals being executed decreased. Since corpses were in such high demand, some people decided to steal bodies from graves in order to keep the market supplied. From 1827 to 1828 in Scotland, murders were carried out, so that the bodies could be sold to medical schools for cash. These were known as the West Port murders. The Anatomy Act of 1832 was formed and passed because of the murders. Cadavers used to be used when they were fresh, but that did not always work out, and it was hard to keep them preserved. Preservation was needed in order to carry out classes and lessons about the human body. Glutaraldehyde was the first main chemical used for embalming and preserving the body. Glutaraldehyde leaves a yellow stain in the tissues, which can interfere with observation and research. Formaldehyde is the chemical that is used as the main embalming chemical now. It is a colorless solution that maintains the tissue in its life-like texture and can keep the body well preserved for up to six weeks.
# Abusive cadaver use
Human bodies and remains are being sold illegally all over the world without permission from deceased. At UCLA, Henry Reid and Ernest Nelson were found guilty of harvesting body parts and selling them to other companies from the Willed Body Program. In the case of Leigh Ajan, her mother’s body was sent to the Tulane University for research on kidney and heart diseases. Not long after arriving at Tulane University, she was sent to a brokerage for bodies. This brokerage usually sells the bodies to the U.S. Army to be used for land mine tests. Along with the U.S. Army, body parts have been sold to other companies and people instead of being cremated or buried. In Annie Cheney’s book she writes about bodies being sold from brokers to clients, such as scientists, pharmaceutical companies, and tissue banks. It is suspected that there are more cases of abuse gone undealt with or undiscovered, and more currently happening.
# Body snatching over the years
But cadavers have not always been treated with the same respect they are given today. Before modern science cadavers were stolen from graves, relatives, and criminals to provide for science.
Herophilus, the “father of anatomy”, lived in 300 BC in Alexandria, Egypt. He was the first physician to dissect bodies. According to rumor, he dissected live criminals.
The tradition of dissecting criminals was carried up into the eighteenth and nineteenth century when anatomy schools became popular in England and Scotland. At that time, Christians believed in the literal raising from the dead. Because the souls of dissected bodies could not go to heaven, people rarely offered their bodies to science. The only cadavers available were criminals', and anatomists were portrayed as no better than an executioner.
Anatomy schools began to steal bodies from graves. "Grave robbers" were technically people who stole jewelry from the deceased, but stealing the dead body was not a crime. Some anatomy instructors encouraged this "body snatching". Students sometimes paid tuition in corpses or dug up bodies as late night pranks.
Some respected anatomy instructors dug up bodies themselves. The anatomist Thomas Sewell, who later became the personal physician for three U.S. presidents, was convicted in 1818 of digging up a corpse for dissection.
Anatomists would even dissect members of their own family. William Harvey, the man famous for discovering the circulatory system, was so dedicated he dissected his father and sister.
By 1828 anatomists were paying others to do the digging. At that time, London anatomy schools employed ten full time body snatchers and about two hundred part timer workers during the dissection season. This period ran from October to May, when the winter cold slowed down the decomposition of the bodies. A crew of six or seven could dig up about 312 bodies. The average body snatcher made about 1,000 dollars a year, ten times more than the average unskilled laborer of that time period, with summers off.
The poor were most vulnerable, because they could not afford coffins to keep the body snatchers out.
Disposing of the dissected body was difficult, and rumors have appeared about how the anatomist might have managed. They could have buried the cadavers out behind the school. Perhaps they gave the bodies to zoo keepers or fed the bodies to vultures kept specifically for this purpose. One colorful story has the anatomists making soap and candles to give away as gifts.
Stories appeared of people murdering for the money they could make off cadaver sales. Two of the most famous are that of Burke and Hare, and that of Bishop, May, and Williams.
- Burke and Hare — Burke and Hare ran a boardinghouse. When one of their tenants died, they brought him to Alexander Monro’s anatomy rooms in Edinburgh where they were paid seven pounds for the body. Realizing the possible profit, they supposedly murdered sixteen people over the next nine months and sold their bodies to different anatomists. They were eventually caught. Burke was found guilty, hanged, and publicly dissected. Hare escaped England where he worked as a plasterer’s apprentice until they found out who he was and threw him in a lime pit. He was blinded and begged on the streets for the rest of his life.
- Bishop, May and Williams — These body snatchers also killed three boys, ages ten, eleven and fourteen years old. The anatomist that they sold the cadavers to was suspicious. To delay their departure the anatomist said he needed to break a fifty pound note. He sent for the police who arrested the men. In Bishop's confession he stated, “I have followed the course of obtaining a lively hood as a body snatcher for twelve years, and have obtained and sold, I think from 500 to 1,000 bodies”
By the 1890s body snatching was less common and by the 20th century it had all but disappeared. Embalming and preservation of cadavers became more advanced and education in medical schools improved. Students no longer had to quickly dissect bodies before they decomposed. These dissections were orderly and complete. Improvements in medical school, including a graded curriculum, meant doctors were better educated. The medical profession received new esteem by diagnosing and healing more people. With that respect came a larger supply of cadavers, making body snatching almost non-existent. | Cadaver
# Overview
A cadaver or corpse is a dead body. "Cadaver" is normally used as a more formal term for a body being used in medical training or research.
# Human decay
Different stages of decomposition can help determine how long a body has been dead.
The first stage is self digestion, also known as autolysis. This happens when the cells break down the body into elements the cells can eat; this creates a liquid that gets between the layers of skin and makes the skin peel off. During this stage, flies (when present) start to lay eggs in the openings of the body: eyes, nostrils, mouth, ears, open wounds, and other orifices. Hatched larvae (maggots) subsequently get under the skin and start to eat the body.
The second stage of decomposition is bloating; bacteria in the gut begin to break down the tissues of the body, releasing gas that accumulates in the intestines, which becomes trapped due to the early collapse of the small intestine. This bloating occurs largely in the abdomen, and sometimes in the mouth and genitals. The tongue may swell. This usually happens in about the second week of decomposition. Gas accumulation and bloating will continue until the body is decomposed sufficiently for the gas to escape.
The third stage is putrefaction. It is the last and longest stage. Putrefaction is where the larger structures of the body break down, and tissues liquefy. The digestive organs, the brain, and lungs are the first to disintegrate. Under normal conditions, the organs are unidentifiable after three weeks. The muscles can be eaten by bacteria or devoured by carnivorous animals. Eventually, sometimes after several years, all that remains is the skeleton.
# Embalming
When a corpse is buried the body will still eventually decompose by the actions of anaerobic bacteria. In many countries, corpses buried in coffins are embalmed. An embalmer may clean and shave the face, fill the eye sockets with cotton to make them appear full, and suture the jaw together to keep it from hanging open. Embalming fluid is then pumped into the body via an artery (commonly carotid). This rehydrates the tissues and severely reduces the pace of decomposition.
Embalming is used to preserve the corpse temporarily, but may last for years. In some societies, such as the United States, make-up is applied to the corpse to make the body presentable for public presentation.
# A brief history of cadavers
The methods of preserving cadavers, and their acquisition, have changed over the last 200 years. Criminals who were executed for their crimes were used as the first cadavers. The demand for cadavers increased when the number of criminals being executed decreased. Since corpses were in such high demand, some people decided to steal bodies from graves in order to keep the market supplied. From 1827 to 1828 in Scotland, murders were carried out, so that the bodies could be sold to medical schools for cash. These were known as the West Port murders. The Anatomy Act of 1832 was formed and passed because of the murders. Cadavers used to be used when they were fresh, but that did not always work out, and it was hard to keep them preserved. Preservation was needed in order to carry out classes and lessons about the human body. Glutaraldehyde was the first main chemical used for embalming and preserving the body. Glutaraldehyde leaves a yellow stain in the tissues, which can interfere with observation and research. Formaldehyde is the chemical that is used as the main embalming chemical now. It is a colorless solution that maintains the tissue in its life-like texture and can keep the body well preserved for up to six weeks.
# Abusive cadaver use
Human bodies and remains are being sold illegally all over the world without permission from deceased. At UCLA, Henry Reid and Ernest Nelson were found guilty of harvesting body parts and selling them to other companies from the Willed Body Program. In the case of Leigh Ajan, her mother’s body was sent to the Tulane University for research on kidney and heart diseases. Not long after arriving at Tulane University, she was sent to a brokerage for bodies. This brokerage usually sells the bodies to the U.S. Army to be used for land mine tests. Along with the U.S. Army, body parts have been sold to other companies and people instead of being cremated or buried. In Annie Cheney’s book she writes about bodies being sold from brokers to clients, such as scientists, pharmaceutical companies, and tissue banks. It is suspected that there are more cases of abuse gone undealt with or undiscovered, and more currently happening.
# Body snatching over the years
But cadavers have not always been treated with the same respect they are given today. Before modern science cadavers were stolen from graves, relatives, and criminals to provide for science.
Herophilus, the “father of anatomy”, lived in 300 BC in Alexandria, Egypt. He was the first physician to dissect bodies. According to rumor, he dissected live criminals.
The tradition of dissecting criminals was carried up into the eighteenth and nineteenth century when anatomy schools became popular in England and Scotland. At that time, Christians believed in the literal raising from the dead. Because the souls of dissected bodies could not go to heaven, people rarely offered their bodies to science. The only cadavers available were criminals', and anatomists were portrayed as no better than an executioner.
Anatomy schools began to steal bodies from graves. "Grave robbers" were technically people who stole jewelry from the deceased, but stealing the dead body was not a crime. Some anatomy instructors encouraged this "body snatching". Students sometimes paid tuition in corpses or dug up bodies as late night pranks.
Some respected anatomy instructors dug up bodies themselves. The anatomist Thomas Sewell, who later became the personal physician for three U.S. presidents, was convicted in 1818 of digging up a corpse for dissection.
Anatomists would even dissect members of their own family. William Harvey, the man famous for discovering the circulatory system, was so dedicated he dissected his father and sister.
By 1828 anatomists were paying others to do the digging. At that time, London anatomy schools employed ten full time body snatchers and about two hundred part timer workers during the dissection season. This period ran from October to May, when the winter cold slowed down the decomposition of the bodies. A crew of six or seven could dig up about 312 bodies. The average body snatcher made about 1,000 dollars a year, ten times more than the average unskilled laborer of that time period, with summers off.
The poor were most vulnerable, because they could not afford coffins to keep the body snatchers out.
Disposing of the dissected body was difficult, and rumors have appeared about how the anatomist might have managed. They could have buried the cadavers out behind the school. Perhaps they gave the bodies to zoo keepers or fed the bodies to vultures kept specifically for this purpose. One colorful story has the anatomists making soap and candles to give away as gifts.
Stories appeared of people murdering for the money they could make off cadaver sales. Two of the most famous are that of Burke and Hare, and that of Bishop, May, and Williams.
- Burke and Hare — Burke and Hare ran a boardinghouse. When one of their tenants died, they brought him to Alexander Monro’s anatomy rooms in Edinburgh where they were paid seven pounds for the body. Realizing the possible profit, they supposedly murdered sixteen people over the next nine months and sold their bodies to different anatomists. They were eventually caught. Burke was found guilty, hanged, and publicly dissected. Hare escaped England where he worked as a plasterer’s apprentice until they found out who he was and threw him in a lime pit. He was blinded and begged on the streets for the rest of his life.
- Bishop, May and Williams — These body snatchers also killed three boys, ages ten, eleven and fourteen years old. The anatomist that they sold the cadavers to was suspicious. To delay their departure the anatomist said he needed to break a fifty pound note. He sent for the police who arrested the men. In Bishop's confession he stated, “I have followed the course of obtaining a lively hood as a body snatcher for twelve years, and have obtained and sold, I think from 500 to 1,000 bodies”
By the 1890s body snatching was less common and by the 20th century it had all but disappeared. Embalming and preservation of cadavers became more advanced and education in medical schools improved. Students no longer had to quickly dissect bodies before they decomposed. These dissections were orderly and complete. Improvements in medical school, including a graded curriculum, meant doctors were better educated. The medical profession received new esteem by diagnosing and healing more people. With that respect came a larger supply of cadavers, making body snatching almost non-existent. | https://www.wikidoc.org/index.php/Cadaver | |
20b938ce9df4bdd7deeb8ce1bc5048de76a57f42 | wikidoc | Calcium | Calcium
Calcium (Template:PronEng) is the chemical element with the symbol Ca and atomic number 20. It has an atomic mass of 40.078. Calcium is a soft grey alkaline earth metal, and is the fifth most abundant element in the Earth's crust. It is essential for living organisms, particularly in cell physiology, and is the most common metal in many animals.
# Notable characteristics
The most abundant isotope, 40Ca, has a nucleus of 20 protons and 20 neutrons. This is the heaviest stable isotope of any element which has equal numbers of protons and neutrons. In supernova explosions, calcium is formed from the reaction of carbon with various numbers of alpha particles (helium nuclei), until the most common calcium isotope (containing 10 helium nuclei) has been synthesized. Calcium is the seventh most common element, by mass, in Earth's oceans.
Chemically calcium is reactive and moderately soft for a metal (though harder than lead, it can be cut with a knife with difficulty). It is a silvery metallic element that must be extracted by electrolysis from a fused salt like calcium chloride. Once produced, it rapidly forms a grey-white oxide and nitride coating when exposed to air. It is somewhat difficult to ignite, in character rather like magnesium, but when lit, the metal burns in air with a brilliant high-intensity red light. Calcium metal reacts with water, evolving hydrogen gas at a rate rapid enough to be noticeable (unlike its sister magnesium) but not fast enough at room temperature to generate much heat. Part of the slowness of the calcium-water reaction results from the metal being partly protected by insoluble white calcium hydroxide. In water solutions of acids where the salt is water soluble, calcium reacts vigorously.
Calcium salts are colorless from any contribution of the calcium, and ionic solutions of calcium (Ca2+) are colorless as well. Many calcium salts are not soluble in water. When in solution, the calcium ion to the human taste varies remarkably, being reported as mildly salty, sour, "mineral like" or even "soothing." It is apparent that many animals can taste, or develop a taste, for calcium, and use this sense to detect the mineral in salt licks or other sources. . In human nutrition, soluble calcium salts may be added to tart juices without much effect to the average palate.
Calcium is the fifth most abundant element by mass in the human body, where it is a common cellular ionic messenger with many functions, and serves also as a structural element in bone. It is the relatively high atomic-numbered calcium in the skeleton which causes bone to be radio-opaque. Of the human body's solid components after drying (as for example, after cremation), about a third of the total mass is the approximately one kilogram of calcium which composes the average skeleton (the remainder being mostly phosphorus and oxygen).
# Applications
## Calcium compounds
- Calcium cyclamate (Ca(C6H11NHSO4)2) was used as a sweetening agent but is no longer permitted for use because of suspected cancer-causing properties.
- Calcium gluconate (Ca(C6H11O7)2) is used as a food additive and in vitamin pills.
- Calcium permanganate (Ca(MnO4)2) is used in liquid rocket propellant, textile production, as a water sterilizing agent and in dental procedures.
- Calcium phosphate (Ca3(PO4)2) is used as a supplement for animal feed, fertilizer, in commercial production for dough and yeast products, in the manufacture of glass, and in dental products.
- Calcium tungstate (CaWO4) is used in luminous paints, fluorescent lights and in X-ray studies.
# Nutrition
Calcium is an important component of a healthy diet. Calcium is essential for the normal growth and maintenance of bones and teeth, and calcium requirements must be met throughout life. Long-term calcium deficiency can lead to osteoporosis, in which the bone deteriorates and there is an increased risk of fractures. While a lifelong deficit can affect bone and tooth formation, over-retention can cause hypercalcemia (elevated levels of calcium in the blood), impaired kidney function and decreased absorption of other minerals.
High calcium intakes or high calcium absorption were previously thought to contribute to the development of kidney stones. However, more recent studies show that high dietary calcium intakes actually decrease the risk for kidney stones. Vitamin D is needed to absorb calcium. Dairy products, such as milk and cheese, are a well-known source of calcium. However, some individuals are allergic to dairy products and even more people, particularly those of non Indo-European descent, are lactose-intolerant, leaving them unable to consume non-fermented dairy products in quantities larger than about half a liter per serving. Others, such as vegans, avoid dairy products for ethical and health reasons. Fortunately, many good sources of calcium exist. These include seaweeds such as kelp, wakame and hijiki; nuts and seeds (like almonds and sesame); blackstrap molasses; beans; oranges; amaranth; collard greens; okra; rutabaga; broccoli; dandelion leaves; kale; sardines; and fortified products such as orange juice and soy milk. An overlooked source of calcium is eggshell, which can be ground into a powder and mixed into food or a glass of water.
The calcium content of most foods can be found in the USDA National Nutrient Database.
# Dietary calcium supplements
Calcium supplements are used to prevent and to treat calcium deficiencies. There are conflicting recommendations about when to take calcium supplements. However, most experts agree that no more than 500 mg should be taken at a time because the percent of calcium absorbed decreases as the amount of calcium in the supplement increases. It is recommended to spread doses throughout the day, with the last dose near bedtime. Recommended daily calcium intake varies from 1000 to 1500 mg, depending upon the stage of life.
In July 2006, a report citing research from Fred Hutchinson Cancer Research Center in Seattle, Washington claimed that women in their 50s gained 5 pounds less in a period of 10 years by taking more than 500 mg of calcium supplements than those who did not. However, the doctor in charge of the study, Dr. Alejandro J. Gonzalez also noted it would be "going out on a limb" to suggest calcium supplements as a weight-limiting aid.
- Calcium carbonate is the most common and least expensive calcium supplement. It can be difficult to digest and causes gas in some people. Taking magnesium with it can help to prevent constipation. Calcium carbonate is 40% elemental calcium. 1000 mg will provide 400 mg of calcium. It is recommended to take this supplement with food to aid in absorption. In some calcium supplements based on calcium carbonate, vitamin D is added to aid in absorption. Vitamin D is needed for the absorption of calcium from the stomach and for the functioning of calcium in the body.
- Coral Calcium is a salt of calcium derived from fossilized coral reefs. Coral calcium is comprised of calcium carbonate and trace minerals.
- Calcium citrate is more easily absorbed (bioavailability is 2.5 times higher than calcium carbonate), easier to digest and less likely to cause constipation and gas than calcium carbonate. It also has a lower risk of contributing to the formation of kidney stones. Calcium citrate is about 21% elemental calcium. 1000 mg will provide 210 mg of calcium. It is more expensive than calcium carbonate and more of it must be taken to get the same amount of calcium.
- Calcium phosphate costs more than calcium carbonate, but less than calcium citrate. It is easily absorbed and is less likely to cause constipation and gas than either.
- Calcium lactate and calcium aspartate are both more difficult to digest and are more expensive than calcium carbonate
- Calcium chelates have been chemically bonded with an agent that the body recognizes as food. This form is generally known to be better absorbed by the human body than all other forms of calcium due to the bond.
The National Nutritional Food Association — NNFA (Newport Beach, Calif.) defines a chelate very specifically, and several criteria must be met in order for chelation to actually occur. Some of the claimed "chelates" on the market are the various Krebs (Citric Acid) Cycle chelates, such as citrate, malate, and aspartate. Dicalcium malate (chelated with malic acid) is a newer form of a true calcium chelate. It contains a high amount of elemental calcium (30%).
## Prevention of fractures due to osteoporosis
Such studies often do not test calcium alone, but rather combinations of calcium and vitamin D. Randomized controlled trials found both positive and negative benefit. The different results may be explained by doses of calcium and underlying rates of calcium supplementation in the control groups. However, it is clear that increasing the intake of calcium promotes deposition of calcium in the bones, where it is of more benefit in preventing the compression fractures resulting from the osteoporotic thinning of the dendritic web of the bodies of the vertebrae, than it is at preventing the more serious cortical bone fractures which happen at hip and wrist.
## Prevention cancer?
A meta-analysis by the international Cochrane Collaboration of two randomized controlled trialsfound that calcium "might contribute to a moderate degree to the prevention of adenomatous colonic polyps".
More recent studies were conflicting, and one which was positive for effect (Lappe, et al.) did control for a possible anti-carcinogenic effect of vitamin D, which was found to be an independent positive influence from calcium-alone on cancer risk (see second study below) .
- A randomized controlled trial found that 1000 mg of elemental calcium and 400 IU of vitamin D3 had no effect on colorectal cancer
- A randomized controlled trial found that 1400–1500 mg supplemental calcium and 1100 IU vitamin D3 reduced aggregated cancers with a relative risk of 0.402.
- An observational cohort study found that high calcium and vitamin D intake was associated with "lower risk of developing premenopausal breast cancer"
# Calcium categories
- Antacid
- Calcium carbonate
- Antihyperkalemic
- Calcium chloride;
- Calcium gluconate Injection
- Antihypermagnesemic
- Calcium chloride;
- Calcium gluceptate;
- Calcium gluconate Injection
- Antihyperphosphatemic
- Calcium carbonate;
- Calcium citrate
- Antihypocalcemic
- Calcium acetate;
- Calcium carbonate;
- Calcium chloride;
- Calcium citrate;
- Calcium glubionate;
- Calcium gluceptate;
- Calcium gluconate;
- Calcium glycerophosphate & Calcium lactate;
- Calcium lactate;
- Calcium lactate: Gluconate and Calcium carbonate;
- Calcium phosphate, Dibasic;
- Calcium phosphate, Tribasic
- Cardiotonic
- Calcium chloride;
- Calcium gluconate Injection
- Electrolyte replenisher
- Calcium acetate;
- Calcium chloride;
- Calcium gluceptate;
- Calcium gluconate Injection
- Nutritional supplement, mineral
- Calcium carbonate;
- Calcium citrate;
- Calcium glubionate, Oral;
- Calcium gluceptate and Calcium gluconate;
- Calcium gluconate, Oral;
- Calcium lactate;
- Calcium lactate: Gluconate and Calcium carbonate;
- Calcium phosphate, Dibasic;
- Calcium phosphate, Tribasic | Calcium
Template:Infobox calcium
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Calcium (Template:PronEng) is the chemical element with the symbol Ca and atomic number 20. It has an atomic mass of 40.078. Calcium is a soft grey alkaline earth metal, and is the fifth most abundant element in the Earth's crust. It is essential for living organisms, particularly in cell physiology, and is the most common metal in many animals.
# Notable characteristics
The most abundant isotope, 40Ca, has a nucleus of 20 protons and 20 neutrons. This is the heaviest stable isotope of any element which has equal numbers of protons and neutrons. In supernova explosions, calcium is formed from the reaction of carbon with various numbers of alpha particles (helium nuclei), until the most common calcium isotope (containing 10 helium nuclei) has been synthesized. Calcium is the seventh most common element, by mass, in Earth's oceans.
Chemically calcium is reactive and moderately soft for a metal (though harder than lead, it can be cut with a knife with difficulty). It is a silvery metallic element that must be extracted by electrolysis from a fused salt like calcium chloride.[1] Once produced, it rapidly forms a grey-white oxide and nitride coating when exposed to air. It is somewhat difficult to ignite, in character rather like magnesium, but when lit, the metal burns in air with a brilliant high-intensity red light. Calcium metal reacts with water, evolving hydrogen gas at a rate rapid enough to be noticeable (unlike its sister magnesium) but not fast enough at room temperature to generate much heat. Part of the slowness of the calcium-water reaction results from the metal being partly protected by insoluble white calcium hydroxide. In water solutions of acids where the salt is water soluble, calcium reacts vigorously.
Calcium salts are colorless from any contribution of the calcium, and ionic solutions of calcium (Ca2+) are colorless as well. Many calcium salts are not soluble in water. When in solution, the calcium ion to the human taste varies remarkably, being reported as mildly salty, sour, "mineral like" or even "soothing." It is apparent that many animals can taste, or develop a taste, for calcium, and use this sense to detect the mineral in salt licks or other sources. [2]. In human nutrition, soluble calcium salts may be added to tart juices without much effect to the average palate.
Calcium is the fifth most abundant element by mass in the human body, where it is a common cellular ionic messenger with many functions, and serves also as a structural element in bone. It is the relatively high atomic-numbered calcium in the skeleton which causes bone to be radio-opaque. Of the human body's solid components after drying (as for example, after cremation), about a third of the total mass is the approximately one kilogram of calcium which composes the average skeleton (the remainder being mostly phosphorus and oxygen).
# Applications
## Calcium compounds
- Calcium cyclamate (Ca(C6H11NHSO4)2) was used as a sweetening agent but is no longer permitted for use because of suspected cancer-causing properties.
- Calcium gluconate (Ca(C6H11O7)2) is used as a food additive and in vitamin pills.
- Calcium permanganate (Ca(MnO4)2) is used in liquid rocket propellant, textile production, as a water sterilizing agent and in dental procedures.
- Calcium phosphate (Ca3(PO4)2) is used as a supplement for animal feed, fertilizer, in commercial production for dough and yeast products, in the manufacture of glass, and in dental products.
- Calcium tungstate (CaWO4) is used in luminous paints, fluorescent lights and in X-ray studies.
# Nutrition
Calcium is an important component of a healthy diet. Calcium is essential for the normal growth and maintenance of bones and teeth, and calcium requirements must be met throughout life. Long-term calcium deficiency can lead to osteoporosis, in which the bone deteriorates and there is an increased risk of fractures. While a lifelong deficit can affect bone and tooth formation, over-retention can cause hypercalcemia (elevated levels of calcium in the blood), impaired kidney function and decreased absorption of other minerals.[4]
High calcium intakes or high calcium absorption were previously thought to contribute to the development of kidney stones. However, more recent studies show that high dietary calcium intakes actually decrease the risk for kidney stones.[5] Vitamin D is needed to absorb calcium. Dairy products, such as milk and cheese, are a well-known source of calcium. However, some individuals are allergic to dairy products and even more people, particularly those of non Indo-European descent, are lactose-intolerant, leaving them unable to consume non-fermented dairy products in quantities larger than about half a liter per serving. Others, such as vegans, avoid dairy products for ethical and health reasons. Fortunately, many good sources of calcium exist. These include seaweeds such as kelp, wakame and hijiki; nuts and seeds (like almonds and sesame); blackstrap molasses; beans; oranges; amaranth; collard greens; okra; rutabaga; broccoli; dandelion leaves; kale; sardines; and fortified products such as orange juice and soy milk. An overlooked source of calcium is eggshell, which can be ground into a powder and mixed into food or a glass of water.[6]
The calcium content of most foods can be found in the USDA National Nutrient Database.[7]
# Dietary calcium supplements
Calcium supplements are used to prevent and to treat calcium deficiencies. There are conflicting recommendations about when to take calcium supplements. However, most experts agree that no more than 500 mg should be taken at a time because the percent of calcium absorbed decreases as the amount of calcium in the supplement increases.[3] It is recommended to spread doses throughout the day, with the last dose near bedtime. Recommended daily calcium intake varies from 1000 to 1500 mg, depending upon the stage of life.
In July 2006, a report citing research from Fred Hutchinson Cancer Research Center in Seattle, Washington claimed that women in their 50s gained 5 pounds less in a period of 10 years by taking more than 500 mg of calcium supplements than those who did not. However, the doctor in charge of the study, Dr. Alejandro J. Gonzalez also noted it would be "going out on a limb" to suggest calcium supplements as a weight-limiting aid.[8]
- Calcium carbonate is the most common and least expensive calcium supplement. It can be difficult to digest and causes gas in some people. Taking magnesium with it can help to prevent constipation. Calcium carbonate is 40% elemental calcium. 1000 mg will provide 400 mg of calcium. It is recommended to take this supplement with food to aid in absorption. In some calcium supplements based on calcium carbonate, vitamin D is added to aid in absorption. Vitamin D is needed for the absorption of calcium from the stomach and for the functioning of calcium in the body.[9][10]
- Coral Calcium is a salt of calcium derived from fossilized coral reefs. Coral calcium is comprised of calcium carbonate and trace minerals.
- Calcium citrate is more easily absorbed (bioavailability is 2.5 times higher than calcium carbonate), easier to digest and less likely to cause constipation and gas than calcium carbonate. It also has a lower risk of contributing to the formation of kidney stones. Calcium citrate is about 21% elemental calcium. 1000 mg will provide 210 mg of calcium. It is more expensive than calcium carbonate and more of it must be taken to get the same amount of calcium.
- Calcium phosphate costs more than calcium carbonate, but less than calcium citrate. It is easily absorbed and is less likely to cause constipation and gas than either.
- Calcium lactate and calcium aspartate are both more difficult to digest and are more expensive than calcium carbonate
- Calcium chelates have been chemically bonded with an agent that the body recognizes as food. This form is generally known to be better absorbed by the human body than all other forms of calcium due to the bond.
The National Nutritional Food Association — NNFA (Newport Beach, Calif.) defines a chelate very specifically, and several criteria must be met in order for chelation to actually occur. Some of the claimed "chelates" on the market are the various Krebs (Citric Acid) Cycle chelates, such as citrate, malate, and aspartate. Dicalcium malate (chelated with malic acid) is a newer form of a true calcium chelate. It contains a high amount of elemental calcium (30%).
## Prevention of fractures due to osteoporosis
Such studies often do not test calcium alone, but rather combinations of calcium and vitamin D. Randomized controlled trials found both positive[11][12] and negative[13][14][15][16] benefit. The different results may be explained by doses of calcium and underlying rates of calcium supplementation in the control groups.[17] However, it is clear that increasing the intake of calcium promotes deposition of calcium in the bones, where it is of more benefit in preventing the compression fractures resulting from the osteoporotic thinning of the dendritic web of the bodies of the vertebrae, than it is at preventing the more serious cortical bone fractures which happen at hip and wrist.
## Prevention cancer?
A meta-analysis[12] by the international Cochrane Collaboration of two randomized controlled trials[18][19]found that calcium "might contribute to a moderate degree to the prevention of adenomatous colonic polyps".
More recent studies were conflicting, and one which was positive for effect (Lappe, et al.) did control for a possible anti-carcinogenic effect of vitamin D, which was found to be an independent positive influence from calcium-alone on cancer risk (see second study below) [20].
- A randomized controlled trial found that 1000 mg of elemental calcium and 400 IU of vitamin D3 had no effect on colorectal cancer[21]
- A randomized controlled trial found that 1400–1500 mg supplemental calcium and 1100 IU vitamin D3 reduced aggregated cancers with a relative risk of 0.402.[22]
- An observational cohort study found that high calcium and vitamin D intake was associated with "lower risk of developing premenopausal breast cancer"[23]
# Calcium categories
- Antacid
- Calcium carbonate
- Antihyperkalemic
- Calcium chloride;
- Calcium gluconate Injection
- Antihypermagnesemic
- Calcium chloride;
- Calcium gluceptate;
- Calcium gluconate Injection
- Antihyperphosphatemic
- Calcium carbonate;
- Calcium citrate
- Antihypocalcemic
- Calcium acetate;
- Calcium carbonate;
- Calcium chloride;
- Calcium citrate;
- Calcium glubionate;
- Calcium gluceptate;
- Calcium gluconate;
- Calcium glycerophosphate & Calcium lactate;
- Calcium lactate;
- Calcium lactate: Gluconate and Calcium carbonate;
- Calcium phosphate, Dibasic;
- Calcium phosphate, Tribasic
- Cardiotonic
- Calcium chloride;
- Calcium gluconate Injection
- Electrolyte replenisher
- Calcium acetate;
- Calcium chloride;
- Calcium gluceptate;
- Calcium gluconate Injection
- Nutritional supplement, mineral
- Calcium carbonate;
- Calcium citrate;
- Calcium glubionate, Oral;
- Calcium gluceptate and Calcium gluconate;
- Calcium gluconate, Oral;
- Calcium lactate;
- Calcium lactate: Gluconate and Calcium carbonate;
- Calcium phosphate, Dibasic;
- Calcium phosphate, Tribasic | https://www.wikidoc.org/index.php/Calcium | |
d47ceb9642613556d7d95a4e36b91962646529ba | wikidoc | Calorad | Calorad
Calorad is a liquid protein weight loss supplement which was first introduced to the US and Canadian marketplace in 1984. It has been advertised on both television and radio.
Calorad is a liquid dietary supplement composed primarily of 3,000 mg (3 grams) of Type II hydrolyzed collagen (hydrolysate) from either beef (bovine) or tuna (marine) sources and 8 mg of aloe vera, both of which are listed as active ingredients. The supplement label lists that it is fat-free and carbohydrate-free and that 1 serving (1/2 ounce) provides 3 grams of protein and 10 calories. It also comes in a Kosher formulation. The primary claim made for the product is that regular use causes weight loss without loss of lean muscle mass. While weight loss and body fat reduction can be achieved simply by following the labeled instruction to avoid eating within three hours prior to sleep, most individuals following this regimen alone are not successful in accomplishing long-term weight loss.
Although the manufacturer does not make claims for Calorad in the treatment or cure of disease, the manufacturer does cite published clinical trials conducted with Type II hydrolyzed collagen (collagen hydrolysate), the primary ingredient in Calorad:
Osteoarthritis and Osteoporosis:
Type II hydrolyzed collagen (collagen hydrolysate) in Osteoarthritis and Osteoporosis,
Rheumatoid arthritis: Type II hydrolyzed collagen in Rheumatoid Arthritis,
Autoimmune Disease and Rheumatoid Arthritis: Type II collagen in Oral desensitization in the treatment of human immune diseases including Rheumatoid Arthritis, and
Fibromyalgia: Type II collagen (collagen hydrolysat) and its effect on Symptoms of Chronic Fibromyalgia and Temporomandibular Joint Pain.
The manufacturer claims that 40% of subjects will lose weight within 1 month, 75% after 2 months and 87% after 3 months. The manufacturer offers a 30-day satisfaction guarantee which is posted on the manufacturer's website. In support of these claims, Essentially Yours Industries cites a clinical study of Calorad (also unpublished and non-peer reviewed) by Joel B. Lao, MD. Dr. Lao is a Doctor of Internal Medicine, and medical consultant in the Philippines who studied the effects of Calorad and its effect on overweight and/or obese individuals. The subjects included 50 overweight or obese individuals who were observed over a 90-day period. One bottle of Calorad was provided to each of the subjects every month for a 3-month period. In month 1, the average weight loss was 5.7 pounds. By month 3, subjects had an average reduction of 10 pounds, and an average inch loss at the waist of 3 inches.
The claim that Calorad builds or maintains lean muscle mass without any increasing demand on the user's musculature is based upon an unpublished and non-peer reviewed study by Davis et al in which 300 subjects between the ages of 17-77 years, were followed for 1 year and most of whom lost weight (an average of 3.75 pounds per month) but maintained lean muscle mass. Rena Davis holds a Master of Science (MSc) and is a practicing Clinical Nutritionist and former Biochemist. Davis states: "We also found that in the entire group, less than 0.6, or less than 1 per cent, had any loss of lean muscle mass. And 36 per cent of the group actually gained lean muscle mass during that time."
The manufacturer (Essentially Yours Industries) states that most subjects on a weight loss regimen lose lean muscle mass along with fat and water weight, so that maintaining lean muscle mass is a benefit seen with Calorad users.
Rationale for Collagen use for Weight Loss:
There is a precedent for liquid collagen use to elicit weight loss. The US Patent database lists a 30-year-old patent entitled:
Method of treating obesity by the oral administration of a predigested protein composition,
US Patent #4,042,687 which was filed in June of 1976 by Gans et al (who are not associated with Essentially Yours Industries, the manufacturer of Calorad). This patent describes much of the science around liquid collagen use for weight loss, and the scientific rationale behind the use of liquid collagen for weight loss. Results gleaned from this early study also underscored the importance of not using collagen as the sole source of nutrition (a caution listed on the bottle of Calorad today).
When first introduced, the manufacturer claimed that Calorad could cause the user to "lose weight while you sleep", repair joints, and prevent or reduce the symptoms of arthritis. The manufacturer has since dropped these claims because they are "medical treatment claims" and require a drug treatment classification approved by the FDA, and are usually only granted following submission of large clinical trials similar to those conducted by pharmaceutical companies in substantiation of these claims. Essentially Yours Industries has not conducted this type of rigorous trial on Calorad in support of such claims. The manufacurer has replaced these claims with the current claim that Calorad "promotes sleep and improves the health and appearance of hair, nails and skin" (all of which are not medical treatment claims).
Calorad has not been evaluated by the US Food and Drug Administration, and all marketing materials related to the product carry a disclaimer to the effect that it is nothing more than "a food supplement and is not intended to diagnose, treat, cure, or prevent any disease." | Calorad
Calorad is a liquid protein weight loss supplement which was first introduced to the US and Canadian marketplace in 1984. It has been advertised on both television and radio.
Calorad is a liquid dietary supplement composed primarily of 3,000 mg (3 grams) of Type II hydrolyzed collagen (hydrolysate) from either beef (bovine) or tuna (marine) sources and 8 mg of aloe vera, both of which are listed as active ingredients. The supplement label lists that it is fat-free and carbohydrate-free and that 1 serving (1/2 ounce) provides 3 grams of protein and 10 calories. It also comes in a Kosher formulation. The primary claim made for the product is that regular use causes weight loss without loss of lean muscle mass. While weight loss and body fat reduction can be achieved simply by following the labeled instruction to avoid eating within three hours prior to sleep, most individuals following this regimen alone are not successful in accomplishing long-term weight loss.
Although the manufacturer does not make claims for Calorad in the treatment or cure of disease, the manufacturer does cite published clinical trials conducted with Type II hydrolyzed collagen (collagen hydrolysate), the primary ingredient in Calorad:
Osteoarthritis and Osteoporosis:
Type II hydrolyzed collagen (collagen hydrolysate) in Osteoarthritis and Osteoporosis,
Rheumatoid arthritis: Type II hydrolyzed collagen in Rheumatoid Arthritis,
Autoimmune Disease and Rheumatoid Arthritis: Type II collagen in Oral desensitization in the treatment of human immune diseases including Rheumatoid Arthritis, and
Fibromyalgia: Type II collagen (collagen hydrolysat) and its effect on Symptoms of Chronic Fibromyalgia and Temporomandibular Joint Pain.
The manufacturer claims that 40% of subjects will lose weight within 1 month, 75% after 2 months and 87% after 3 months. The manufacturer offers a 30-day satisfaction guarantee which is posted on the manufacturer's website. In support of these claims, Essentially Yours Industries cites a clinical study of Calorad (also unpublished and non-peer reviewed) by Joel B. Lao, MD. Dr. Lao is a Doctor of Internal Medicine, and medical consultant in the Philippines who studied the effects of Calorad and its effect on overweight and/or obese individuals. The subjects included 50 overweight or obese individuals who were observed over a 90-day period. One bottle of Calorad was provided to each of the subjects every month for a 3-month period. In month 1, the average weight loss was 5.7 pounds. By month 3, subjects had an average reduction of 10 pounds, and an average inch loss at the waist of 3 inches.
The claim that Calorad builds or maintains lean muscle mass without any increasing demand on the user's musculature is based upon an unpublished and non-peer reviewed study by Davis et al in which 300 subjects between the ages of 17-77 years, were followed for 1 year and most of whom lost weight (an average of 3.75 pounds per month) but maintained lean muscle mass. Rena Davis holds a Master of Science (MSc) and is a practicing Clinical Nutritionist and former Biochemist. Davis states: "We also found that in the entire group, less than 0.6, or less than 1 per cent, had any loss of lean muscle mass. And 36 per cent of the group actually gained lean muscle mass during that time."
The manufacturer (Essentially Yours Industries) states that most subjects on a weight loss regimen lose lean muscle mass along with fat and water weight, so that maintaining lean muscle mass is a benefit seen with Calorad users.
Rationale for Collagen use for Weight Loss:
There is a precedent for liquid collagen use to elicit weight loss. The US Patent database lists a 30-year-old patent entitled:
Method of treating obesity by the oral administration of a predigested protein composition,
US Patent #4,042,687 which was filed in June of 1976 by Gans et al (who are not associated with Essentially Yours Industries, the manufacturer of Calorad). This patent describes much of the science around liquid collagen use for weight loss, and the scientific rationale behind the use of liquid collagen for weight loss. Results gleaned from this early study also underscored the importance of not using collagen as the sole source of nutrition (a caution listed on the bottle of Calorad today).
When first introduced, the manufacturer claimed that Calorad could cause the user to "lose weight while you sleep", repair joints, and prevent or reduce the symptoms of arthritis. The manufacturer has since dropped these claims because they are "medical treatment claims" and require a drug treatment classification approved by the FDA, and are usually only granted following submission of large clinical trials similar to those conducted by pharmaceutical companies in substantiation of these claims. Essentially Yours Industries has not conducted this type of rigorous trial on Calorad in support of such claims. The manufacurer has replaced these claims with the current claim that Calorad "promotes sleep and improves the health and appearance of hair, nails and skin" (all of which are not medical treatment claims).
Calorad has not been evaluated by the US Food and Drug Administration, and all marketing materials related to the product carry a disclaimer to the effect that it is nothing more than "a food supplement and is not intended to diagnose, treat, cure, or prevent any disease."
# External links
- Official site
- A positive assessment of Calorad
- A critical assessment of Calorad | https://www.wikidoc.org/index.php/Calorad | |
7678008ab055c029379ef8b354711759a276d9e1 | wikidoc | calorie | calorie
The calorie is a pre-SI unit of energy, in particular heat. In most fields, its use is archaic, and the SI unit of energy, the joule, has become accepted. However, it remains in common use as a unit of food energy. It was first defined by Professor Nicolas Clément in 1824 as a kilogram-calorie, and this definition entered French and English dictionaries between 1841 and 1867. Etymology: French calorie, from Latin calor (heat).
The unit calorie has historically been used in two major alternate definitions that differ by a factor of 1000:
- The small calorie, gram calorie, or calorie (symbol: cal) is the amount of heat (energy) required to raise the temperature of one gram of water by 1 °C.
- The large calorie, kilogram calorie, kilocalorie (symbol: kcal), or Calorie (capital C) is the amount of heat (energy) needed to increase the temperature of one kg of water by 1 °C, exactly 1000 small calories, or about 4.184 kJ.
The second form is the one commonly used to express food energy. Its most common name is calorie; kilocalorie is sometimes used, more often in the symbol "kcal" than in the spelled out word.
Apart from these two major alternate definitions, there exist also minor variants of the definition of this unit, which differ in the exact experimental conditions used, most notably the start temperature of the water (see section below).
The factors used to convert measurements in calories to their equivalents in joules are numerically equivalent to expressions of the specific heat capacity of water in SI units. See "Versions" below for an explanation of the units.
# Versions
The energy needed to increase the temperature of a gram of water by 1 degree Celsius depends on the starting temperature and is difficult to measure precisely. Accordingly, there have been several definitions of the calorie:
- Thermochemical calorie (calth): 4.184 J exactly.
- 15 °C calorie (cal15): the amount of energy required to warm 1 g of air-free water from 14.5 °C to 15.5 °C at a constant pressure of 101.325 kPa (1 atm). Experimental values of this calorie ranged from 4.1852 J to 4.1858 J. The CIPM in 1950 published a mean experimental value of 4.1855 J, noting an uncertainty of 0.0005 J.
- 20 °C calorie: the amount of energy required to warm 1 g of air-free water from 19.5 °C to 20.5 °C at a constant pressure of 101.325 kPa (1 atm). This is about 4.182 J.
- 4 °C calorie: the amount of energy required to warm 1 g of air-free water from 3.5 °C to 4.5 °C at a constant pressure of 101.325 kPa (1 atm).
- Mean calorie: 1/100 of the amount of energy required to warm 1 g of air-free water from 0 °C to 100 °C at a constant pressure of 101.325 kPa (1 atm). This is about 4.190 J
- International Steam Table Calorie (1929): (1/860) W h = (180/43) J exactly. This is approximately 4.1868 J.
- International Steam Table Calorie (1956) (calIT): 1.163 mW h = 4.1868 J exactly. This definition was adopted by the Fifth International Conference on Properties of Steam (London, July 1956).
- IUNS calorie: 4.182 J exactly. This is a ratio adopted by the Committee on Nomenclature of the International Union of Nutritional Sciences.
The two perhaps most popular definitions used in older literature are the "15 °C calorie" and the "thermochemical calorie". Since the many different definitions are a source of confusion and error, all calories are now deprecated in favour of the SI unit for heat and energy: the joule (J). | calorie
The calorie is a pre-SI unit of energy, in particular heat.[1] In most fields, its use is archaic, and the SI unit of energy, the joule, has become accepted. However, it remains in common use as a unit of food energy. It was first defined by Professor Nicolas Clément in 1824 as a kilogram-calorie, and this definition entered French and English dictionaries between 1841 and 1867. Etymology: French calorie, from Latin calor (heat).
The unit calorie has historically been used in two major alternate definitions that differ by a factor of 1000:
- The small calorie, gram calorie, or calorie (symbol: cal) is the amount of heat (energy) required to raise the temperature of one gram of water by 1 °C.
- The large calorie, kilogram calorie, kilocalorie (symbol: kcal), or Calorie (capital C) is the amount of heat (energy) needed to increase the temperature of one kg of water by 1 °C, exactly 1000 small calories, or about 4.184 kJ.
The second form is the one commonly used to express food energy. Its most common name is calorie; kilocalorie is sometimes used, more often in the symbol "kcal" than in the spelled out word.
Apart from these two major alternate definitions, there exist also minor variants of the definition of this unit, which differ in the exact experimental conditions used, most notably the start temperature of the water (see section below).
The factors used to convert measurements in calories to their equivalents in joules are numerically equivalent to expressions of the specific heat capacity of water in SI units. See "Versions" below for an explanation of the units.
# Versions
The energy needed to increase the temperature of a gram of water by 1 degree Celsius depends on the starting temperature and is difficult to measure precisely. Accordingly, there have been several definitions of the calorie:
- Thermochemical calorie (calth): 4.184 J exactly.[1]
- 15 °C calorie (cal15): the amount of energy required to warm 1 g of air-free water from 14.5 °C to 15.5 °C at a constant pressure of 101.325 kPa (1 atm). Experimental values of this calorie ranged from 4.1852 J to 4.1858 J. The CIPM in 1950 published a mean experimental value of 4.1855 J, noting an uncertainty of 0.0005 J.[1]
- 20 °C calorie: the amount of energy required to warm 1 g of air-free water from 19.5 °C to 20.5 °C at a constant pressure of 101.325 kPa (1 atm). This is about 4.182 J.
- 4 °C calorie: the amount of energy required to warm 1 g of air-free water from 3.5 °C to 4.5 °C at a constant pressure of 101.325 kPa (1 atm).
- Mean calorie: 1/100 of the amount of energy required to warm 1 g of air-free water from 0 °C to 100 °C at a constant pressure of 101.325 kPa (1 atm). This is about 4.190 J
- International Steam Table Calorie (1929): (1/860) W h = (180/43) J exactly. This is approximately 4.1868 J.
- International Steam Table Calorie (1956) (calIT): 1.163 mW h = 4.1868 J exactly. This definition was adopted by the Fifth International Conference on Properties of Steam (London, July 1956).[1]
- IUNS calorie: 4.182 J exactly. This is a ratio adopted by the Committee on Nomenclature of the International Union of Nutritional Sciences.[2]
The two perhaps most popular definitions used in older literature are the "15 °C calorie" and the "thermochemical calorie". Since the many different definitions are a source of confusion and error, all calories are now deprecated in favour of the SI unit for heat and energy: the joule (J). | https://www.wikidoc.org/index.php/Calorie | |
d0e6eabc94382e086a23f5c0c1eef309f7dc1f77 | wikidoc | Candirú | Candirú
Candirú (candiru without an accent in official Portuguese spelling; also canero, toothpick fish, or willy fish) refers to parasitic freshwater catfish of a number of genera in the family Trichomycteridae. They are found in the Amazon River and have a reputation among the natives as the most feared fish in its waters, even over the piranha. They are eel-shaped and translucent, making them almost impossible to see in the water. Some species have been known to grow to a size of 6 inches (~15 cm) in length.
The definition of candirú differs between authors. The word has been used to refer to only Vandellia cirrhosa, the entire genus Vandellia, the subfamily Vandelliinae, or even the two subfamilies Vandelliinae and Stegophilinae.
# Parasitism
While the members of the subfamily Vandelliinae feed on blood, members of Stegophilinae may feed on scales, mucus, or carrion.
This fish is feared to attack humans and swim into an orifice (the vagina, anus, or even the penis—and deep into the urethra). Because of spines protruding from the fish, it is almost impossible to remove except through surgery. The fish locates its host by following a water flow to its source and thus urinating while bathing increases the chance of a candirú homing in on a human urethra. Natives have also been known to bathe facing the current, as doing so would decrease the chances of the organism lodging itself in the rectum. Other orifices such as the penis or vagina are covered up with the use of hands.
Though there have been documented candirú attacks on humans, there is no evidence the fish can survive once inside a human. A traditional cure involves the use of two plants, the Jagua plant (Genipa americana) and the Buitach apple which are inserted (or their extract in the case of tight spaces) into the affected area. In theory, these two plants together will kill and then dissolve the fish. More often, infection causes shock and death in the victim before the candirú can be removed.
A well-circulated myth is that the candirú is capable of swimming up the stream of urine in mid-air to a victim standing on shore or a boat. This is physically impossible as the maximum swimming velocity of the fish is opposed by the downward velocity of the urine stream, and the further impossible act of the 5-14 mm wide fish maintaining position and thrust within a 2–7 mm wide column of fluid. They are also probably not attracted to urine as commonly thought.
# Popular culture
- The candirú has been featured on the television shows Grey's Anatomy (where it was called the "penis fish"), The Venture Bros., and Law & Order: Special Victims Unit. Dr. Oz discussed the candirú on The Oprah Winfrey Show on May 21, 2007. It was sought after in Nick Baker's Weird Creatures, a British TV series about the world's strangest animals.
- It has also been mentioned in the films Anaconda, The Rundown, Medicine Man, Sniper and the Rifftrax version of Predator
- It is also mentioned in the books Amazonia by James Rollins, The Codex by Douglas Preston, Born Survivor by Bear Grylls, Naked Lunch by William S. Burroughs, and is referred to in A History of the World in 10½ Chapters by Julian Barnes. It is mentioned in the afterword to Peeps by Scott Westerfeld, and is misrepresented in Ted Bell's novel Spy as swimming up the urine stream of someone standing knee-deep in water, then living inside the person.
- The Candirú was featured in a recent episode of Weird Nature, which runs on The Science Channel. | Candirú
Template:Wikify
Candirú (candiru without an accent in official Portuguese spelling; also canero, toothpick fish, or willy fish) refers to parasitic freshwater catfish of a number of genera in the family Trichomycteridae. They are found in the Amazon River and have a reputation among the natives as the most feared fish in its waters, even over the piranha.[1] They are eel-shaped and translucent, making them almost impossible to see in the water. Some species have been known to grow to a size of 6 inches (~15 cm) in length.
The definition of candirú differs between authors. The word has been used to refer to only Vandellia cirrhosa, the entire genus Vandellia, the subfamily Vandelliinae, or even the two subfamilies Vandelliinae and Stegophilinae.[2][3][4][5]
# Parasitism
While the members of the subfamily Vandelliinae feed on blood, members of Stegophilinae may feed on scales, mucus, or carrion.[6]
This fish is feared to attack humans and swim into an orifice (the vagina, anus, or even the penis—and deep into the urethra).[4] Because of spines protruding from the fish, it is almost impossible to remove except through surgery.[7] The fish locates its host by following a water flow to its source and thus urinating while bathing increases the chance of a candirú homing in on a human urethra. Natives have also been known to bathe facing the current, as doing so would decrease the chances of the organism lodging itself in the rectum.[citation needed] Other orifices such as the penis or vagina are covered up with the use of hands.
Though there have been documented candirú attacks on humans, there is no evidence the fish can survive once inside a human. A traditional cure involves the use of two plants, the Jagua plant (Genipa americana) and the Buitach apple which are inserted (or their extract in the case of tight spaces) into the affected area. In theory, these two plants together will kill and then dissolve the fish. More often, infection causes shock and death in the victim before the candirú can be removed.
A well-circulated myth is that the candirú is capable of swimming up the stream of urine in mid-air to a victim standing on shore or a boat. This is physically impossible as the maximum swimming velocity of the fish is opposed by the downward velocity of the urine stream, and the further impossible act of the 5-14 mm wide fish maintaining position and thrust within a 2–7 mm wide column of fluid. They are also probably not attracted to urine as commonly thought.[4]
# Popular culture
- The candirú has been featured on the television shows Grey's Anatomy (where it was called the "penis fish"),[8] The Venture Bros., and Law & Order: Special Victims Unit. Dr. Oz discussed the candirú on The Oprah Winfrey Show on May 21, 2007. It was sought after in Nick Baker's Weird Creatures, a British TV series about the world's strangest animals.
- It has also been mentioned in the films Anaconda, The Rundown, Medicine Man, Sniper and the Rifftrax version of Predator
- It is also mentioned in the books Amazonia by James Rollins, The Codex by Douglas Preston, Born Survivor by Bear Grylls, Naked Lunch by William S. Burroughs, and is referred to in A History of the World in 10½ Chapters by Julian Barnes. It is mentioned in the afterword to Peeps by Scott Westerfeld, and is misrepresented in Ted Bell's novel Spy as swimming up the urine stream of someone standing knee-deep in water, then living inside the person.
- The Candirú was featured in a recent episode of Weird Nature, which runs on The Science Channel. | https://www.wikidoc.org/index.php/Candir%C3%BA | |
11883a274fb9f830e083e37dcd3afa9d1ecf9c4d | wikidoc | Canning | Canning
# Overview
Canning is a method of preserving food where the food is sealed in an airtight container. It prevents microorganisms from entering and proliferating inside.
To prevent the food from being spoiled before and during containment, quite a number of methods are used: pasteurization, boiling, other means of high temperature applied over a period of time, refrigeration, outright freezing, drying, vacuum treatment, antimicrobial agents that are natural to the indegenous recipe of the foodstuff being preserved, or otherwise are applied to the contents of the can, a sufficient dose of ionizing radiation, submersion in a strongly saline, acid, base, osmotically extreme (e.g. very sugary) or otherwise microbially challenging environments.
No such countermeasure is perfectly dependable as a preservative. E.g. spore-forming thermo-resistant microorganisms, such as Clostridium botulinum (the causative agent of botulism) can still survive.
From a public safety point of view, foods with low acidity, i.e. pH more than 4.6 need sterilization under high temperature (116-130°C). Foods that must be pressure canned include most vegetables, meats, seafood, poultry, and dairy products. The only foods that may be safely canned in an ordinary boiling water bath are highly acidic ones with a pH below 4.6, such as fruits, pickled vegetables, or other foods to which acidic additives have been added.
# History
During the first years of the French Revolutionary Wars, the notable French newspaper Le Monde, prompted by the government, offered a hefty cash award of 12,000 Francs to any inventor who could come up with a cheap and effective method of preserving large amounts of food. The massive armies of the period required regular supplies of quality food, and so preservation became a necessity. In 1809, the French confectioner Nicolas François Appert observed that food cooked inside a jar did not spoil unless the seals leak, thus developed a method of sealing food inside glass jars. The reason why food did not spoil was unknown at the time, since it would be another 50 years before Louis Pasteur demonstrated the role of microbes in food spoilage. However, glass containers presented challenges for transportation.
Glass jars were largely replaced in commercial canneries with cylindrical tin or wrought-iron canisters (later shortened to "cans") following the work of Peter Durand (1810). Cans are both cheaper and quicker to make and much more resilient than fragile glass jars. Glass jars have, however, remained popular for some high-value products and in home canning. Tin-openers were not to be invented for another thirty years — at first, soldiers had to cut the cans open with bayonets or smash them open with rocks. The French Army began experimenting with issuing tinned foods to its soldiers, but the slow process of tinning foods and the even slower development and transport stages prevented the army from shipping large amounts around the French Empire, and the war ended before the process could be perfected. Unfortunately for Appert, the factory which he had built with his prize money was burned down in 1814 by Allied soldiers invading France.
Following the end of the Napoleonic Wars, the canning process was gradually put into practice in other European countries and in the United States. Based on Appert's methods of food preservation, Peter Durand patented a process in the United Kingdom in 1810, developing a process of packaging food in sealed airtight wrought-iron cans. Initially, the canning process was slow and labour-intensive, as each can had to be hand-made and took up to six hours to cook properly, making tinned food too expensive for ordinary people to buy. In 1824 meats and stews produced by the Appert method were carried by Sir William Edward Parry in his voyage to find a northwestern passage to India.
Throughout the mid-nineteenth century, tinned food became a status symbol amongst middle-class households in Europe, becoming something of a frivolous novelty. Early methods of manufacture employed poisonous lead solder for sealing the tins, which had disastrous consequences for the 1845 Franklin expedition to the Arctic Ocean.
Increasing mechanisation of the canning process, coupled with a huge increase in urban populations across Europe, resulted in a rising demand for tinned food. A number of inventions and improvements followed, and by the 1860s, the time to cook food in sealed cans had been reduced from around six hours to only thirty minutes. Canned food also began to spread beyond Europe — Robert Ayars established the first American canning factory in New York City in 1812, using improved tin-plated wrought-iron cans for preserving oysters, meats, fruits and vegetables. Demand for tinned food greatly increased during wars. Large-scale wars in the nineteenth century, such as the Crimean War, American Civil War, and Franco-Prussian War introduced increasing numbers of working-class men to tinned food, and allowed canning companies to expand their businesses to meet military demands for non-perishable food, allowing companies to manufacture in bulk and sell to wider civilian markets after wars ended. Urban populations in Victorian era Britain demanded ever-increasing quantities of cheap, varied, good-quality food that they could keep on the shelves at home without having to go to the shops every day for fresh produce. In response, companies such as Nestlé, Heinz, and others emerged to provide shops with good-quality tinned food for sale to ordinary working class city-dwellers. The late 19th century saw the range of tinned food available to urban populations greatly increase, as rival canning companies competed with each other using novel foodstuffs, highly decorated printed labels, and lower prices.
Demand for tinned food skyrocketed during World War I, as military commanders sought vast quantities of cheap, high-calorie food to feed their millions of soldiers; food which could be transported safely, would survive trench conditions, and which would not spoil in between the factory and the front lines. Throughout the war soldiers generally subsisted on very low-quality tinned foodstuffs, such as the British "Bully Beef" (cheap corned beef), pork and beans and Maconochies Irish Stew, but by 1916 widespread boredom with cheap tinned food amongst soldiers resulted in militaries purchasing better-quality food, in order to improve low morale, and the first complete meals in a tin began to appear. In 1917 the French Army began issuing tinned French cuisine, such as coq au vin, whilst the Italian Army experimented with tinned ravioli and spaghetti bolognese. Shortages of tinned food in the British Army in 1917 led to the government issuing cigarettes and even amphetamines to soldiers to suppress their appetites. After the war, companies that had supplied tinned food to national militaries improved the quality of their goods for sale on the civilian market.
Many early Texan citizens used canning as a source of food preservation.
Today, tin-coated steel is the material most commonly used. Laminate vacuum pouches are also now used for canning, such as those found in an MRE.
# Double seams
Modern double seams provide an airtight seal to the tin can. This airtight nature is crucial to keeping bacteria out of the can and keeping its contents sealed inside. Thus, double seamed cans are also known as Sanitary Cans. Developed in 1900 in Europe, this sort of can was made of the traditional cylindrical body made with tin plate; however, the two ends (lids) were attached using what is now called a double seam. A can thus sealed is impervious to the outside world by creating two tight continuous folds between the can’s cylindrical body and the lid at each end. This eliminated the need for solder and allowed improvements in the speed of manufacturing, thereby lowering the cost.
Double seams make extensive use of rollers in shaping the can, lid and the final double seam. To make a sanitary can and lid suitable for double seaming, manufacture begins with a sheet of coated tin plate. To create the can body rectangles are cut and curled around a die and welded together creating a cylinder with a side seam.
Rollers are then used to flare out one or both ends of the cylinder to create a quarter circle flange around the circumference. Great care and precision are required to ensure that the welded sides are perfectly aligned, as any misalignment will mean that the shape of the flange is inconsistent, compromising its integrity.
A circle is then cut from the sheet using a die cutter. The circle is shaped in a stamping press to create a downward countersink to fit snugly in to the can body. The result can be compared to an upside down and very flat top hat. The outer edge is then curled down and around approximately 140 degrees using rollers creating the end curl.
The final result is a steel tube with a flanged edge, and a countersunk steel disc with a curled edge. A rubber compound is put inside the curl.
## Seaming
The body and end are brought together in a seamer and held in place by the base plate and chuck, respectively. The base plate provides a sure footing for the can body during the seaming operation and the chuck fits snugly in to the end (lid). The result is the countersink of the end sits inside the top of the can body just below the flange. The end curl protrudes slightly beyond the flange.
See: Can Seamers
## First operation
Once brought together in the seamer, the seaming head presses a special first operation roller against the end curl. The end curl is pressed against the flange curling it in toward the body and under the flange. The flange is also bent downward and the end and body are now loosely joined together. The 1st operation roller is then retracted. At this point during manufacture five thicknesses of steel exist in the seam. From the outside in they are; a) End, b) Flange, c) End Curl, d) Body, e) Countersink. This is the first seam. All the parts of the seam are now aligned and ready for the final stage.
## Second operation
The seaming head then engages the second operation roller against the partly formed seam. The second operation presses all five steel components together tightly to form the final seal. The five layers in the final seam are then called; a) End, b) Body Hook, c) Cover Hook, d) Body, e) Countersink. All sanitary cans require a filling medium within the seam as metal to metal contact, otherwise such an arrangement would not maintain its hermetic seal for very long. In most cases a rubberized sealing compound is placed inside the end curl radius, forming the actual critical contact point between the end and the body.
Probably the most important innovation since the introduction of double seams is the welded side seam. Prior to the welded side seam the can body was folded and/or soldered together, leaving a relatively thick side seam. The thick side seam meant that at the side seam end juncture the end curl had more metal to curl around before closing in behind the Body Hook or flange, leaving a greater opportunity for error. | Canning
# Overview
Canning is a method of preserving food where the food is sealed in an airtight container. It prevents microorganisms from entering and proliferating inside.
To prevent the food from being spoiled before and during containment, quite a number of methods are used: pasteurization, boiling, other means of high temperature applied over a period of time, refrigeration, outright freezing, drying, vacuum treatment, antimicrobial agents that are natural to the indegenous recipe of the foodstuff being preserved, or otherwise are applied to the contents of the can, a sufficient dose of ionizing radiation, submersion in a strongly saline, acid, base, osmotically extreme (e.g. very sugary) or otherwise microbially challenging environments.
No such countermeasure is perfectly dependable as a preservative. E.g. spore-forming thermo-resistant microorganisms, such as Clostridium botulinum (the causative agent of botulism) can still survive.
From a public safety point of view, foods with low acidity, i.e. pH more than 4.6 need sterilization under high temperature (116-130°C). Foods that must be pressure canned include most vegetables, meats, seafood, poultry, and dairy products. The only foods that may be safely canned in an ordinary boiling water bath are highly acidic ones with a pH below 4.6[1], such as fruits, pickled vegetables, or other foods to which acidic additives have been added.
# History
During the first years of the French Revolutionary Wars, the notable French newspaper Le Monde, prompted by the government, offered a hefty cash award of 12,000 Francs to any inventor who could come up with a cheap and effective method of preserving large amounts of food. The massive armies of the period required regular supplies of quality food, and so preservation became a necessity. In 1809, the French confectioner Nicolas François Appert observed that food cooked inside a jar did not spoil unless the seals leak, thus developed a method of sealing food inside glass jars. The reason why food did not spoil was unknown at the time, since it would be another 50 years before Louis Pasteur demonstrated the role of microbes in food spoilage. However, glass containers presented challenges for transportation.
Glass jars were largely replaced in commercial canneries with cylindrical tin or wrought-iron canisters (later shortened to "cans") following the work of Peter Durand (1810). Cans are both cheaper and quicker to make and much more resilient than fragile glass jars. Glass jars have, however, remained popular for some high-value products and in home canning.[1] Tin-openers were not to be invented for another thirty years — at first, soldiers had to cut the cans open with bayonets or smash them open with rocks. The French Army began experimenting with issuing tinned foods to its soldiers, but the slow process of tinning foods and the even slower development and transport stages prevented the army from shipping large amounts around the French Empire, and the war ended before the process could be perfected. Unfortunately for Appert, the factory which he had built with his prize money was burned down in 1814 by Allied soldiers invading France.
Following the end of the Napoleonic Wars, the canning process was gradually put into practice in other European countries and in the United States. Based on Appert's methods of food preservation, Peter Durand patented a process in the United Kingdom in 1810, developing a process of packaging food in sealed airtight wrought-iron cans. Initially, the canning process was slow and labour-intensive, as each can had to be hand-made and took up to six hours to cook properly, making tinned food too expensive for ordinary people to buy. In 1824 meats and stews produced by the Appert method were carried by Sir William Edward Parry in his voyage to find a northwestern passage to India.
Throughout the mid-nineteenth century, tinned food became a status symbol amongst middle-class households in Europe, becoming something of a frivolous novelty. Early methods of manufacture employed poisonous lead solder for sealing the tins, which had disastrous consequences for the 1845 Franklin expedition to the Arctic Ocean.
Increasing mechanisation of the canning process, coupled with a huge increase in urban populations across Europe, resulted in a rising demand for tinned food. A number of inventions and improvements followed, and by the 1860s, the time to cook food in sealed cans had been reduced from around six hours to only thirty minutes. Canned food also began to spread beyond Europe — Robert Ayars established the first American canning factory in New York City in 1812, using improved tin-plated wrought-iron cans for preserving oysters, meats, fruits and vegetables. Demand for tinned food greatly increased during wars. Large-scale wars in the nineteenth century, such as the Crimean War, American Civil War, and Franco-Prussian War introduced increasing numbers of working-class men to tinned food, and allowed canning companies to expand their businesses to meet military demands for non-perishable food, allowing companies to manufacture in bulk and sell to wider civilian markets after wars ended. Urban populations in Victorian era Britain demanded ever-increasing quantities of cheap, varied, good-quality food that they could keep on the shelves at home without having to go to the shops every day for fresh produce. In response, companies such as Nestlé, Heinz, and others emerged to provide shops with good-quality tinned food for sale to ordinary working class city-dwellers. The late 19th century saw the range of tinned food available to urban populations greatly increase, as rival canning companies competed with each other using novel foodstuffs, highly decorated printed labels, and lower prices.
Demand for tinned food skyrocketed during World War I, as military commanders sought vast quantities of cheap, high-calorie food to feed their millions of soldiers; food which could be transported safely, would survive trench conditions, and which would not spoil in between the factory and the front lines. Throughout the war soldiers generally subsisted on very low-quality tinned foodstuffs, such as the British "Bully Beef" (cheap corned beef), pork and beans and Maconochies Irish Stew, but by 1916 widespread boredom with cheap tinned food amongst soldiers resulted in militaries purchasing better-quality food, in order to improve low morale, and the first complete meals in a tin began to appear. In 1917 the French Army began issuing tinned French cuisine, such as coq au vin, whilst the Italian Army experimented with tinned ravioli and spaghetti bolognese. Shortages of tinned food in the British Army in 1917 led to the government issuing cigarettes and even amphetamines to soldiers to suppress their appetites. After the war, companies that had supplied tinned food to national militaries improved the quality of their goods for sale on the civilian market.
Many early Texan citizens used canning as a source of food preservation.
Today, tin-coated steel is the material most commonly used. Laminate vacuum pouches are also now used for canning, such as those found in an MRE.
# Double seams
Modern double seams provide an airtight seal to the tin can. This airtight nature is crucial to keeping bacteria out of the can and keeping its contents sealed inside. Thus, double seamed cans are also known as Sanitary Cans. Developed in 1900 in Europe, this sort of can was made of the traditional cylindrical body made with tin plate; however, the two ends (lids) were attached using what is now called a double seam. A can thus sealed is impervious to the outside world by creating two tight continuous folds between the can’s cylindrical body and the lid at each end. This eliminated the need for solder and allowed improvements in the speed of manufacturing, thereby lowering the cost.
Double seams make extensive use of rollers in shaping the can, lid and the final double seam. To make a sanitary can and lid suitable for double seaming, manufacture begins with a sheet of coated tin plate. To create the can body rectangles are cut and curled around a die and welded together creating a cylinder with a side seam.
Rollers are then used to flare out one or both ends of the cylinder to create a quarter circle flange around the circumference. Great care and precision are required to ensure that the welded sides are perfectly aligned, as any misalignment will mean that the shape of the flange is inconsistent, compromising its integrity.
A circle is then cut from the sheet using a die cutter. The circle is shaped in a stamping press to create a downward countersink to fit snugly in to the can body. The result can be compared to an upside down and very flat top hat. The outer edge is then curled down and around approximately 140 degrees using rollers creating the end curl.
The final result is a steel tube with a flanged edge, and a countersunk steel disc with a curled edge. A rubber compound is put inside the curl.
## Seaming
The body and end are brought together in a seamer and held in place by the base plate and chuck, respectively. The base plate provides a sure footing for the can body during the seaming operation and the chuck fits snugly in to the end (lid). The result is the countersink of the end sits inside the top of the can body just below the flange. The end curl protrudes slightly beyond the flange.
See: Can Seamers
## First operation
Once brought together in the seamer, the seaming head presses a special first operation roller against the end curl. The end curl is pressed against the flange curling it in toward the body and under the flange. The flange is also bent downward and the end and body are now loosely joined together. The 1st operation roller is then retracted. At this point during manufacture five thicknesses of steel exist in the seam. From the outside in they are; a) End, b) Flange, c) End Curl, d) Body, e) Countersink. This is the first seam. All the parts of the seam are now aligned and ready for the final stage.
## Second operation
The seaming head then engages the second operation roller against the partly formed seam. The second operation presses all five steel components together tightly to form the final seal. The five layers in the final seam are then called; a) End, b) Body Hook, c) Cover Hook, d) Body, e) Countersink. All sanitary cans require a filling medium within the seam as metal to metal contact, otherwise such an arrangement would not maintain its hermetic seal for very long. In most cases a rubberized sealing compound is placed inside the end curl radius, forming the actual critical contact point between the end and the body.
Probably the most important innovation since the introduction of double seams is the welded side seam. Prior to the welded side seam the can body was folded and/or soldered together, leaving a relatively thick side seam. The thick side seam meant that at the side seam end juncture the end curl had more metal to curl around before closing in behind the Body Hook or flange, leaving a greater opportunity for error. | https://www.wikidoc.org/index.php/Canning | |
8a83282423daf79fb8b7d4c6eb9f905fe3388cc8 | wikidoc | Cannula | Cannula
A cannula (from Latin "little reed"; plural cannulae) is a flexible tube which when inserted into the body is used either to withdraw fluid or insert medication.
Decannulation is the permanent removal of a cannula (extubation), especially of a tracheostomy cannula.
# Medicine
Cannulae normally come with a trocar attached which allows puncturing of the body to get into the intended space. Intravenous cannulae are the most common in hospital use. A variety of cannulae are used to establish cardiopulmonary bypass in cardiac surgery. Nasal cannula is a piece of plastic tubing which runs under the nose and is used to administer oxygen.
## IV cannulation
A venous cannula is inserted into a vein, primarily for the administration of intravenous fluids and medicines. An arterial cannula is inserted into an artery, commonly the radial artery, and is used during major operations and in critical care areas to measure beat-to-beat blood pressure and to draw repeated blood samples.
Complications may arise in the vein as a result of the cannulation procedure, the 4 main groups of complication are:
- hematoma: a collection of blood. Can result from failure to puncture the vein when the cannula is inserted or when the cannula is removed. Selection of an appropriate vein and gently applying pressure slightly above the insertion point as you remove the cannula may prevent this.
- infiltration: when infusate enters the subcutaneous tissue instead of the vein. To prevent this a cannula with accurate trim distances may be used. It is essential to fix the cannula in place firmly.
- embolism: this can be caused by air, a thrombus, or fragment of a catheter breaking off and entering the venous system. Such things can go on to lodge in an artery, blocking circulation to the corresponding area. To avoid air embolus, make sure that there is no air in the system. To avoid a thromboembolism use a smaller cannula. Avoid the catheter breaking by never reinserting the needle.
- phlebitis: an inflammation of the vein resulting from mechanical or chemical irritation or from an infection. Phlebitis can be avoided by carefully choosing the site for cannulation and by checking the type of infusate you use.
# Veterinary use
A cannula is also used in an emergency procedure to relieve pressure and bloating in cattle due most commonly to their accidentally grazing wilted legume or legume-dominant pastures, particularly alfalfa, ladino, and red and white clover.
They are also a component used in the insertion of the Verichip.
# Body piercing
Cannulae are used in body piercing when using a standard IV needle (usually between 18GA and 12GA, although may be as large as 0GA, in which case the procedure is known as dermal punching and uses a biopsy punch without a cannula), and for inserting hooks for suspensions.
During piercing, the fistula is created by inserting the needle. The needle is then removed, leaving the cannula in place, which is sometimes trimmed down. The cannula is then removed and sterile jewellery is inserted into the fistula simultaneously, in order to minimise trauma to the fresh fistula caused by insertion of blunt-ended jewellery.
# Non-medical use
Cannulae are used in laboratory chemistry to transfer a liquid between flasks without exposing it to the atmosphere. In this case, the cannula can be thought of as a double-ended needle, made of stainless steel or plastic. Larger bores (16-22 gauge) are usually used to avoid clogging. The sharp ends allow them to penetrate septa easily.
In biological research, a push-pull cannula, which both withdraws and injects fluid, can be used to determine the effect of a certain chemical on a specific cell. The push part of the cannula is fiilled with a physiological solution plus the chemical of interest and is then injected slowly into the local cellular environment of a cell. The pull cannula then draws liquid from the extracellular medium, thus measuring the cellular response to the chemical of interest. This technique is especially used for neuroscience.
In general aviation, a cannula refers to a piece of plastic tubing which runs under the nose and is used to administer oxygen in non-pressurized aircraft flying above 10,000 feet above sea level in Canada and above 12,500 feet above sea level in the United States. | Cannula
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
A cannula (from Latin "little reed"; plural cannulae) is a flexible tube which when inserted into the body is used either to withdraw fluid or insert medication.
Decannulation is the permanent removal of a cannula (extubation)[1], especially of a tracheostomy cannula.[2]
# Medicine
Cannulae normally come with a trocar attached which allows puncturing of the body to get into the intended space. Intravenous cannulae are the most common in hospital use. A variety of cannulae are used to establish cardiopulmonary bypass in cardiac surgery. Nasal cannula is a piece of plastic tubing which runs under the nose and is used to administer oxygen.
## IV cannulation
A venous cannula is inserted into a vein, primarily for the administration of intravenous fluids and medicines. An arterial cannula is inserted into an artery, commonly the radial artery, and is used during major operations and in critical care areas to measure beat-to-beat blood pressure and to draw repeated blood samples.
Complications may arise in the vein as a result of the cannulation procedure, the 4 main groups of complication are:
- hematoma: a collection of blood. Can result from failure to puncture the vein when the cannula is inserted or when the cannula is removed. Selection of an appropriate vein and gently applying pressure slightly above the insertion point as you remove the cannula may prevent this.
- infiltration: when infusate enters the subcutaneous tissue instead of the vein. To prevent this a cannula with accurate trim distances may be used. It is essential to fix the cannula in place firmly.
- embolism: this can be caused by air, a thrombus, or fragment of a catheter breaking off and entering the venous system. Such things can go on to lodge in an artery, blocking circulation to the corresponding area. To avoid air embolus, make sure that there is no air in the system. To avoid a thromboembolism use a smaller cannula. Avoid the catheter breaking by never reinserting the needle.
- phlebitis: an inflammation of the vein resulting from mechanical or chemical irritation or from an infection. Phlebitis can be avoided by carefully choosing the site for cannulation and by checking the type of infusate you use.
# Veterinary use
A cannula is also used in an emergency procedure to relieve pressure and bloating in cattle due most commonly to their accidentally grazing wilted legume or legume-dominant pastures, particularly alfalfa, ladino, and red and white clover[3].
They are also a component used in the insertion of the Verichip.
# Body piercing
Cannulae are used in body piercing when using a standard IV needle (usually between 18GA and 12GA, although may be as large as 0GA, in which case the procedure is known as dermal punching and uses a biopsy punch without a cannula), and for inserting hooks for suspensions.
During piercing, the fistula is created by inserting the needle. The needle is then removed, leaving the cannula in place, which is sometimes trimmed down. The cannula is then removed and sterile jewellery is inserted into the fistula simultaneously, in order to minimise trauma to the fresh fistula caused by insertion of blunt-ended jewellery.
# Non-medical use
Cannulae are used in laboratory chemistry to transfer a liquid between flasks without exposing it to the atmosphere. In this case, the cannula can be thought of as a double-ended needle, made of stainless steel or plastic. Larger bores (16-22 gauge) are usually used[4] to avoid clogging. The sharp ends allow them to penetrate septa easily.
In biological research, a push-pull cannula, which both withdraws and injects fluid, can be used to determine the effect of a certain chemical on a specific cell. The push part of the cannula is fiilled with a physiological solution plus the chemical of interest and is then injected slowly into the local cellular environment of a cell. The pull cannula then draws liquid from the extracellular medium, thus measuring the cellular response to the chemical of interest. This technique is especially used for neuroscience.
In general aviation, a cannula refers to a piece of plastic tubing which runs under the nose and is used to administer oxygen in non-pressurized aircraft flying above 10,000 feet above sea level in Canada and above 12,500 feet above sea level in the United States. | https://www.wikidoc.org/index.php/Cannula | |
d51397d5241210b4d2e477ce754a2401801dfbe2 | wikidoc | Capsule | Capsule
The word capsule, or encapsulation, may refer to:
- Capsule (anatomy), a cover or envelope partly or wholly surrounding a structure.
- Capsule (microbiology), a layer that lies outside the cell wall of bacteria.
- Capsule (pharmacy), a small gelatinous case enclosing a dose of medication.
- Another name for the sporangium of mosses and hornworts.
- Capsular contracture, the scar tissue naturally forming around breast implants.
de:Kapsel
eo:Kapsulo
id:Kapsul
lt:Kapsulė
nl:Kapsel | Capsule
The word capsule, or encapsulation, may refer to:
- Capsule (anatomy), a cover or envelope partly or wholly surrounding a structure.
- Capsule (microbiology), a layer that lies outside the cell wall of bacteria.
- Capsule (pharmacy), a small gelatinous case enclosing a dose of medication.
- Another name for the sporangium of mosses and hornworts.
- Capsular contracture, the scar tissue naturally forming around breast implants.
Template:Disambig
de:Kapsel
eo:Kapsulo
id:Kapsul
lt:Kapsulė
nl:Kapsel
Template:WH
Template:WS | https://www.wikidoc.org/index.php/Capsule | |
f2a721809d6fda3bd41af064a2d8f135f2533751 | wikidoc | Charaka | Charaka
# Overview
Charaka, sometimes spelled Caraka, born c. 300 BC in a Maga Brahmin family was one of the principal contributors to the ancient art and science of Ayurveda, a system of medicine and lifestyle thought to be developed about 5000 years ago in Ancient India.
# Acharya Charaka & Ayurveda
The term Caraka is a label said to apply to ‘wandering scholars’ or ‘wandering physicians.’ see Charaka Samhita.
According to Charaka's translations health and disease are not predetermined and life may be prolonged by human effort and attention to lifestyle.
The following statements are attributed to Charaka:
These remarks appear obvious today, though they are often not heeded, and were made by Charaka, in his famous Ayurvedic treatise Charaka Samhita. The treatise contains many such remarks which are held in reverence even today. Some of them are in the fields of physiology, etiology and embryology.
Charaka was the first physician to present the concept of digestion, metabolism and immunity. According to his translations of the Vedas, a body functions because it contains three dosha or principles, namely movement (vata), transformation (pitta) and lubrication and stability (kapha). The doshas are also sometimes called humours, namely, bile, phlegm and wind. These dosha are produced when dhatus (blood, flesh and marrow) act upon the food eaten.
For the same quantity of food eaten, one body, however, produces dosha in an amount different from another body. That is why one body is different from another. For instance, it is more weighty, stronger, more energetic.
Further, illness is caused when the balance among the three dosha in a human body is disturbed. To restore the balance he prescribed medicinal drugs. Although he was aware of germs in the body, he did not give them any importance.
Charaka knew the fundamentals of genetics. For instance, he knew the factors determining the sex of a child. A genetic defect in a child, like lameness or blindness, he said, was not due to any defect in the mother or the father, but in the ovum or sperm of the parents (an accepted fact today).
Charaka studied the anatomy of the human body and various organs. He gave 360 as the total number of bones, including teeth, present in the body. He wrongly believed that the heart had one cavity, but he was right when he considered it to be a controlling centre. He claimed that the heart was connected to the entire body through 13 main channels. Apart from these channels, there were countless other ones of varying sizes which supplied not only nutrients to various tissues but also provided passage to waste products. He also claimed that any obstruction in the main channels led to a disease or deformity in the body.
Under the guidance of the ancient physician Atreya, Agnivesa had written an encyclopedic treatise in the eighth century B.C. However, it was only when Charaka revised this treatise that it gained popularity and came to be known as Charakasamhita. For two millennia it remained a standard work on the subject and was translated into many foreign languages, including Arabic and Latin.
# Contributions
According to the Charaka tradition, there existed six schools of medicine, founded by the disciples of the sage Punarvasu Ātreya. Each of his disciples, Agnivesha, Bhela, Jatūkarna, Parāshara, Hārīta, and Kshārapāni, composed a Samhitā. Of these, the one composed by Agnivesha was considered the best. The Agnivesha Samhitā was later revised by Charaka and it came to be known as Charaka Samhitā. The Charaka Samhitā was revised by Dridhbala.
Āyurveda is traditionally divided into eight branches which, in Charaka's scheme, are:
- Sūtra-Sthāna, general principles
- Nidāna-Sthāna, pathology
- Vimāna-Sthāna, diagnostics
- Sharīra-Sthāna, physiology and anatomy
- Indriya-Sthāna, prognosis
- Chikitsā-Sthāna, therapeutics
- Kalpa-Sthāna, pharmacy
- Siddhi-Sthāna, successful treatment
# Charaka Samhita
The Charak Samhita contains 120 adhyayas (chapters), divided into 8 parts.
- Sutra Sthana
- Nidan Sthana
- Viman Sthana
- Sharir Sthana
- Indriya Sthana
- Chikitsa Sthana
- Kalpa Sthana
- Siddhi Sthana
de:Charaka
hi:चरक
ml:ചരകന്
sv:Charaka | Charaka
# Overview
Charaka, sometimes spelled Caraka, born c. 300 BC in a Maga Brahmin family was one of the principal contributors to the ancient art and science of Ayurveda, a system of medicine and lifestyle thought to be developed about 5000 years ago in Ancient India.
# Acharya Charaka & Ayurveda
The term Caraka is a label said to apply to ‘wandering scholars’ or ‘wandering physicians.’ see Charaka Samhita.
According to Charaka's translations health and disease are not predetermined and life may be prolonged by human effort and attention to lifestyle.
The following statements are attributed to Charaka:
These remarks appear obvious today, though they are often not heeded, and were made by Charaka, in his famous Ayurvedic treatise Charaka Samhita. The treatise contains many such remarks which are held in reverence even today. Some of them are in the fields of physiology, etiology and embryology.
Charaka was the first physician to present the concept of digestion, metabolism and immunity. According to his translations of the Vedas, a body functions because it contains three dosha or principles, namely movement (vata), transformation (pitta) and lubrication and stability (kapha). The doshas are also sometimes called humours, namely, bile, phlegm and wind. These dosha are produced when dhatus (blood, flesh and marrow) act upon the food eaten.
For the same quantity of food eaten, one body, however, produces dosha in an amount different from another body. That is why one body is different from another. For instance, it is more weighty, stronger, more energetic.
Further, illness is caused when the balance among the three dosha in a human body is disturbed. To restore the balance he prescribed medicinal drugs. Although he was aware of germs in the body, he did not give them any importance.
Charaka knew the fundamentals of genetics. For instance, he knew the factors determining the sex of a child. A genetic defect in a child, like lameness or blindness, he said, was not due to any defect in the mother or the father, but in the ovum or sperm of the parents (an accepted fact today).
Charaka studied the anatomy of the human body and various organs. He gave 360 as the total number of bones, including teeth, present in the body. He wrongly believed that the heart had one cavity, but he was right when he considered it to be a controlling centre. He claimed that the heart was connected to the entire body through 13 main channels. Apart from these channels, there were countless other ones of varying sizes which supplied not only nutrients to various tissues but also provided passage to waste products. He also claimed that any obstruction in the main channels led to a disease or deformity in the body.
Under the guidance of the ancient physician Atreya, Agnivesa had written an encyclopedic treatise in the eighth century B.C. However, it was only when Charaka revised this treatise that it gained popularity and came to be known as Charakasamhita. For two millennia it remained a standard work on the subject and was translated into many foreign languages, including Arabic and Latin.
# Contributions
According to the Charaka tradition, there existed six schools of medicine, founded by the disciples of the sage Punarvasu Ātreya. Each of his disciples, Agnivesha, Bhela, Jatūkarna, Parāshara, Hārīta, and Kshārapāni, composed a Samhitā. Of these, the one composed by Agnivesha was considered the best. The Agnivesha Samhitā was later revised by Charaka and it came to be known as Charaka Samhitā. The Charaka Samhitā was revised by Dridhbala.
Āyurveda is traditionally divided into eight branches which, in Charaka's scheme, are:
- Sūtra-Sthāna, general principles
- Nidāna-Sthāna, pathology
- Vimāna-Sthāna, diagnostics
- Sharīra-Sthāna, physiology and anatomy
- Indriya-Sthāna, prognosis
- Chikitsā-Sthāna, therapeutics
- Kalpa-Sthāna, pharmacy
- Siddhi-Sthāna, successful treatment
# Charaka Samhita
The Charak Samhita contains 120 adhyayas (chapters), divided into 8 parts.
- Sutra Sthana
- Nidan Sthana
- Viman Sthana
- Sharir Sthana
- Indriya Sthana
- Chikitsa Sthana
- Kalpa Sthana
- Siddhi Sthana
de:Charaka
hi:चरक
ml:ചരകന്
sv:Charaka
Template:WH
Template:WS | https://www.wikidoc.org/index.php/Caraka | |
73405fd4adfbbb7f78d105a0d0539db1f9f7258b | wikidoc | Carbide | Carbide
# Overview
In chemistry, a carbide is a compound of carbon with a more electronegative element. Carbides are important industrially: for example, calcium carbide is a feedstock for the chemical industry and iron carbide, Fe3C (cementite), is formed in steels to improve their properties.
Many carbides can be generally classified by chemical bonding type as follows:
- salt-like ionic compounds
- covalent compounds
- interstitial compounds
- "intermediate" transition metal carbides (a group of carbides that in bonding terms sit between the salt-like and interstitial carbides).
In addition to the carbides there are other groups of binary carbon compounds, i.e.
- graphite intercalation compounds
- alkali metal fullerides
- endohedral fullerenes, where the metal atom is encapsulated inside a fullerene molecule
- metallacarbohedrenes(met-cars) which are cluster compounds containing C2 units.
# Examples
Some examples are:-
- Calcium carbide (CaC2) important industrially and an ionic salt
- Silicon carbide (SiC), carborundum, a covalent compound
- Tungsten carbide (often called simply carbide) widely used for cutting tools and an interstitial compound
- Cementite (iron carbide; Fe3C) an important constituent of steel
- Boron carbide
- Tantalum carbide
- Titanium carbide
See Category:Carbides for a bigger list.
# Types of carbides
## Ionic salts
Salt like carbides are formed by the metals of
- group 1 (the alkali metals )
- group 2 (the alkaline earths )
- group 3 (scandium, yttrium and lanthanum)
- group 11(copper, silver and gold)
- group 12 (zinc ,cadmium and mercury)
- only aluminium from group 13, (gallium, indium and thallium do not appear to form carbides).
- lanthanides when forming MC2 and M2C3 carbides
- actinides when forming MC2 and M2C3 carbides
Most commonly they are salts of C22− and are called acetylides, ethynides, acetylenediides or very rarely, percarbides.
Some compounds contain other anionic species:
- C4−, sometimes called methanides (or methides) because they hydrolyse to give methane gas.
- C34− ion, sometimes called sesquicarbides, they hydrolyse to give methylacetylene.
The naming of ionic carbides is not consistent and can be quite confusing.
### Acetylides
The polyatomic ion C22− contains a triple bond between the two carbon atoms. Examples are the carbides of the alkali metals e.g. Na2C2, some alkaline earths, e.g. CaC2 and lanthanoids e.g. LaC2. The C-C bond distance ranges from 109.2pm in CaC2 (similar to ethyne), to 130.3 pm in LaC2 and 134pm in UC2. The bonding in LaC2 has been described in terms of LaIII with the extra electron delocalised into the antibonding orbital on C22−, explaining the metallic conduction.
### Methanides
The monatomic ion C4− is a very strong base, and will combine with four protons to form methane. Methanides commonly react with water to form methane, however reactions with other substances are common.
C4− + 4H+ → CH4
Examples of compounds that contain C4− are Be2C and Al4C3.
### Sesquicarbides
The polyatomic ion C34− is found in e.g. Li4C3, Mg2C3. The ion is linear and is isoelectronic with CO2. The C-C distance in Mg2C3 is 133.2 pm. Mg2C3 yields methylacetylene, CH3CCH, on hydrolysis which was the first indication that it may contain C34−.
## Covalent carbides
Silicon and boron form covalent carbides. Silicon carbide has two similar crystalline forms, which are both related to the diamond structure. Boron carbide, B4C, on the other hand has an unusual structure which includes icosahedral boron units linked by carbon atoms. In this respect boron carbide is similar to the boron rich borides. Both silicon carbide, SiC, (carborundum) and boron carbide, B4C are very hard materials and refractory. Both materials are important industrally. Boron also forms other covalent carbides, e.g. B25C.
## Interstitial carbides
## Properties
The carbides of the group 4, 5 and 6 transition metals (with the exception of chromium) are often described as interstitial compounds. These carbides are chemically quite inert, have metallic properties and are refractory. Some exhibit a range of stoichiometries, e.g. titanium carbide, TiC. Titanium carbide and tungsten carbide are important industrially and are used to coat metals in cutting tools.
## Structure
The longheld view is that the carbon atoms fit into octahedral interstices in a close packed metal lattice when the metal atom radius is greater than approximately 135 pm:
- When the metal atoms are cubic close packed, (ccp), then filling all of the octahedral interstices with carbon achieves 1:1 stoichiometry with the rock salt structure, (note that in rock salt, NaCl, it is the chloride anions that are cubic close packed).
- When the metal atoms are hexagonal close packed, (hcp), as the octahedral interstices lie directly opposite each other on either side of the layer of metal atoms, filling only only one of these with carbon achieves 2:1 stoichiometry with the CdI2 structure.
The following table shows actual structures of the metals and their carbides. (N.B. the body centred cubic structure adopted by vanadium, niobium, tantalum, chromium, molybdenum and tungsten is not a close packed lattice.) The notation "h/2" refers to the M2C type structure described above, which is only an approximate description of the actual structures. The simple view that the lattice of the pure metal "absorbs" carbon atoms can be seen to be untrue as the packing of the metal atom lattice in the carbides is different from the packing in the pure metal.
For a long time the non stoichiometric phases were believed to be disordered with a random filling of the interstices, however short and longer range ordering has been detected.
## Intermediate transition metal carbides
In these the transition metal ion is smaller than the critical 135 pm and the structures are not interstitial but are more complex. Multiple stoichiometries are common, for example iron forms a number of carbides, Fe3C, Fe7C3 and Fe2C. The best known is cementite, Fe3C, which is present in steels.
These carbides are more reactive than the interstitial carbides, for example the carbides of Cr, Mn, Fe, Co and Ni all are hydrolysed by dilute acids and sometimes by water, to give a mixture of hydrogen and hydrocarbons. These compounds share features with both the inert interstitals and the more reactive salt-like carbides. | Carbide
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
# Overview
In chemistry, a carbide is a compound of carbon with a more electronegative element. Carbides are important industrially: for example, calcium carbide is a feedstock for the chemical industry and iron carbide, Fe3C (cementite), is formed in steels to improve their properties.
Many carbides can be generally classified by chemical bonding type as follows[1]:
- salt-like ionic compounds
- covalent compounds
- interstitial compounds
- "intermediate" transition metal carbides (a group of carbides that in bonding terms sit between the salt-like and interstitial carbides).
In addition to the carbides there are other groups of binary carbon compounds, i.e.[1]
- graphite intercalation compounds
- alkali metal fullerides
- endohedral fullerenes, where the metal atom is encapsulated inside a fullerene molecule
- metallacarbohedrenes(met-cars) which are cluster compounds containing C2 units.
# Examples
Some examples are[1]:-
- Calcium carbide (CaC2) important industrially and an ionic salt
- Silicon carbide (SiC), carborundum, a covalent compound
- Tungsten carbide (often called simply carbide) widely used for cutting tools and an interstitial compound
- Cementite (iron carbide; Fe3C) an important constituent of steel
- Boron carbide
- Tantalum carbide
- Titanium carbide
See Category:Carbides for a bigger list.
# Types of carbides
## Ionic salts
Salt like carbides are formed by the metals of[1]
- group 1 (the alkali metals )
- group 2 (the alkaline earths )
- group 3 (scandium, yttrium and lanthanum)
- group 11(copper, silver and gold)
- group 12 (zinc ,cadmium and mercury)
- only aluminium from group 13, (gallium, indium and thallium do not appear to form carbides).
- lanthanides when forming MC2 and M2C3 carbides
- actinides when forming MC2 and M2C3 carbides
Most commonly they are salts of C22− and are called acetylides, ethynides, acetylenediides or very rarely, percarbides.
Some compounds contain other anionic species:[1]
- C4−, sometimes called methanides (or methides) because they hydrolyse to give methane gas.
- C34− ion, sometimes called sesquicarbides, they hydrolyse to give methylacetylene.
The naming of ionic carbides is not consistent and can be quite confusing.
### Acetylides
The polyatomic ion C22− contains a triple bond between the two carbon atoms. Examples are the carbides of the alkali metals e.g. Na2C2, some alkaline earths, e.g. CaC2 and lanthanoids e.g. LaC2.[1] The C-C bond distance ranges from 109.2pm in CaC2 (similar to ethyne), to 130.3 pm in LaC2 and 134pm in UC2.[1] The bonding in LaC2 has been described in terms of LaIII with the extra electron delocalised into the antibonding orbital on C22−, explaining the metallic conduction.[1]
### Methanides
The monatomic ion C4− is a very strong base, and will combine with four protons to form methane. Methanides commonly react with water to form methane, however reactions with other substances are common.
C4− + 4H+ → CH4
Examples of compounds that contain C4− are Be2C and Al4C3.[1]
### Sesquicarbides
The polyatomic ion C34− is found in e.g. Li4C3, Mg2C3.[1] The ion is linear and is isoelectronic with CO2.[1] The C-C distance in Mg2C3 is 133.2 pm.[2] Mg2C3 yields methylacetylene, CH3CCH, on hydrolysis which was the first indication that it may contain C34−.
## Covalent carbides
Silicon and boron form covalent carbides.[1] Silicon carbide has two similar crystalline forms, which are both related to the diamond structure.[1] Boron carbide, B4C, on the other hand has an unusual structure which includes icosahedral boron units linked by carbon atoms. In this respect boron carbide is similar to the boron rich borides. Both silicon carbide, SiC, (carborundum) and boron carbide, B4C are very hard materials and refractory. Both materials are important industrally. Boron also forms other covalent carbides, e.g. B25C.
## Interstitial carbides
## Properties
The carbides of the group 4, 5 and 6 transition metals (with the exception of chromium) are often described as interstitial compounds.[1] These carbides are chemically quite inert, have metallic properties and are refractory. Some exhibit a range of stoichiometries, e.g. titanium carbide, TiC. Titanium carbide and tungsten carbide are important industrially and are used to coat metals in cutting tools.[3]
## Structure
The longheld view is that the carbon atoms fit into octahedral interstices in a close packed metal lattice when the metal atom radius is greater than approximately 135 pm:[1]
- When the metal atoms are cubic close packed, (ccp), then filling all of the octahedral interstices with carbon achieves 1:1 stoichiometry with the rock salt structure, (note that in rock salt, NaCl, it is the chloride anions that are cubic close packed).
- When the metal atoms are hexagonal close packed, (hcp), as the octahedral interstices lie directly opposite each other on either side of the layer of metal atoms, filling only only one of these with carbon achieves 2:1 stoichiometry with the CdI2 structure.
The following table [1][3]shows actual structures of the metals and their carbides. (N.B. the body centred cubic structure adopted by vanadium, niobium, tantalum, chromium, molybdenum and tungsten is not a close packed lattice.) The notation "h/2" refers to the M2C type structure described above, which is only an approximate description of the actual structures. The simple view that the lattice of the pure metal "absorbs" carbon atoms can be seen to be untrue as the packing of the metal atom lattice in the carbides is different from the packing in the pure metal.
For a long time the non stoichiometric phases were believed to be disordered with a random filling of the interstices, however short and longer range ordering has been detected[4].
## Intermediate transition metal carbides
In these the transition metal ion is smaller than the critical 135 pm and the structures are not interstitial but are more complex. [1] Multiple stoichiometries are common, for example iron forms a number of carbides, Fe3C, Fe7C3 and Fe2C.[1] The best known is cementite, Fe3C, which is present in steels.[1]
These carbides are more reactive than the interstitial carbides, for example the carbides of Cr, Mn, Fe, Co and Ni all are hydrolysed by dilute acids and sometimes by water, to give a mixture of hydrogen and hydrocarbons.[1] These compounds share features with both the inert interstitals and the more reactive salt-like carbides.[1] | https://www.wikidoc.org/index.php/Carbide | |
676a7a658924f0fcb9d95e3543bec7bf85cd5e9b | wikidoc | Symptom | Symptom
# Overview
A symptom is a medical sign indicating the nature of the disease. It is usually subjective, observed by the patient, and not measured.
# Loose definition
A symptom may loosely be said to be a physical condition which indicates a particular illness or disorder.
An example of a symptom in this sense of the word would be a rash. However this is also known as a sign as explained in below.
# Possible causes of a symptom
Some symptoms, such as nausea, occur in a wide range of disease processes, whereas other symptoms are fairly specific for a narrow range of illnesses. For example, a sudden loss of sight in one eye has a significantly smaller number of possible causes.
# Misleading symptoms
Some symptoms can be misleading to the patient or the medical practitioner caring for them. For example, inflammation of the gallbladder often gives rise to pain in the right shoulder, which may understandably lead the patient to attribute the pain to a non-abdominal cause such as muscle strain, rather than the real cause.
# Symptoms and diagnosis
The terms chief complaint, presenting symptom, or presenting complaint is used to describe the initial concern which brings a patient to a doctor. The symptom that leads to a diagnosis is called a cardinal symptom.
# Symptom vs sign
A symptom can more simply be defined as any feature which is noticed by the patient. A sign is noticed by the doctor or others. It is not necessarily the nature of the sign or symptom which defines it, but who observes it.
The same feature may be noticed by both doctor and patient, and so is at once both a sign and a symptom. A sign or a symptom may be one, the other, or both, depending on the observer(s).
Some features, such as pain, can only be symptoms. A doctor cannot feel a patient's pain. Others can only be signs, such as a blood cell count measured by a doctor or a laboratory.
# Engineering definition
In engineering, symptom may be used to refer to an undesired effect occurring in a system. To eliminate the effect, a root cause analysis is performed which traces the symptom to its cause and again through the cause's cause and so on until the subsystem is identified that can be changed to eliminate the symptom. | Symptom
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
# Overview
A symptom is a medical sign indicating the nature of the disease. It is usually subjective,[1] observed by the patient,[2] and not measured.[3]
# Loose definition
A symptom may loosely be said to be a physical condition which indicates a particular illness or disorder.[4]
An example of a symptom in this sense of the word would be a rash. However this is also known as a sign as explained in below.
# Possible causes of a symptom
Some symptoms, such as nausea, occur in a wide range of disease processes, whereas other symptoms are fairly specific for a narrow range of illnesses. For example, a sudden loss of sight in one eye has a significantly smaller number of possible causes.
# Misleading symptoms
Some symptoms can be misleading to the patient or the medical practitioner caring for them. For example, inflammation of the gallbladder often gives rise to pain in the right shoulder, which may understandably lead the patient to attribute the pain to a non-abdominal cause such as muscle strain, rather than the real cause.
# Symptoms and diagnosis
The terms chief complaint, presenting symptom, or presenting complaint is used to describe the initial concern which brings a patient to a doctor. The symptom that leads to a diagnosis is called a cardinal symptom.
# Symptom vs sign
A symptom can more simply be defined as any feature which is noticed by the patient. A sign is noticed by the doctor or others. It is not necessarily the nature of the sign or symptom which defines it, but who observes it.
The same feature may be noticed by both doctor and patient, and so is at once both a sign and a symptom. A sign or a symptom may be one, the other, or both, depending on the observer(s).
Some features, such as pain, can only be symptoms. A doctor cannot feel a patient's pain. Others can only be signs, such as a blood cell count measured by a doctor or a laboratory.
# Engineering definition
In engineering, symptom may be used to refer to an undesired effect occurring in a system. To eliminate the effect, a root cause analysis is performed which traces the symptom to its cause and again through the cause's cause and so on until the subsystem is identified that can be changed to eliminate the symptom. | https://www.wikidoc.org/index.php/Cardinal_symptom | |
1674911ce7d7b400023e1ca903592545594a59ac | wikidoc | Digoxin | Digoxin
# Disclaimer
WikiDoc MAKES NO GUARANTEE OF VALIDITY. WikiDoc is not a professional health care provider, nor is it a suitable replacement for a licensed healthcare provider. WikiDoc is intended to be an educational tool, not a tool for any form of healthcare delivery. The educational content on WikiDoc drug pages is based upon the FDA package insert, National Library of Medicine content and practice guidelines / consensus statements. WikiDoc does not promote the administration of any medication or device that is not consistent with its labeling. Please read our full disclaimer here.
# Overview
Digoxin is a cardiac glycoside that is FDA approved for the treatment of atrial fibrillation, atrial flutter, and heart failure. Common adverse reactions include dizziness, headache, mental disorder, nausea, and vomiting.
# Adult Indications and Dosage
## FDA-Labeled Indications and Dosage (Adult)
- Dosing Information
- Loading dose: 10-15 mcg/kg PO administer half the total loading dose initially, then ¼ the loading dose every 6 to 8 hours twice.
- Maintenance dose: 3.4-5.1 mcg/kg/day PO once daily.
- Dosing Information
- Loading dose: 10-15 mcg/kg PO administer half the total loading dose initially, then ¼ the loading dose every 6 to 8 hours twice.
- Maintenance dose: 3.4-5.1 mcg/kg/day PO once daily.
## Off-Label Use and Dosage (Adult)
### Guideline-Supported Use
There is limited information regarding Off-Label Guideline-Supported Use of SandboxAlonso in adult patients.
### Non–Guideline-Supported Use
There is limited information regarding Off-Label Non–Guideline-Supported Use of SandboxAlonso in adult patients.
# Pediatric Indications and Dosage
## FDA-Labeled Indications and Dosage (Pediatric)
- Dosing Information
- Loading dose
- 5-10 years old: 20-45 mcg/kg PO administer half the total loading dose initially, then ¼ the loading dose every 6 to 8 hours twice.
- >10 year old: 10-15 mcg/kg PO administer half the total loading dose initially, then ¼ the loading dose every 6 to 8 hours twice.
- Maintenence dose:
- 5-10 years: 6.4 – 12.9 mcg/kg/day PO or 3.2 – 6.4 mcg/kg/day Twice daily.
- More than 10 years: 3.4 – 5.1 mcg/kg/day PO.
## Off-Label Use and Dosage (Pediatric)
### Guideline-Supported Use
There is limited information regarding Off-Label Guideline-Supported Use of SandboxAlonso in pediatric patients.
### Non–Guideline-Supported Use
- Dosage information
- 0.01 mg/kg orally 3 times daily for the first 2 doses, then 0.0035 mg/kg 3 times daily
- Dosage information
- Maternal 0.25 to 0.375 mg PO daily alone or with verapamil.
# Contraindications
- Ventricular fibrillation
- Known hypersensitivity to digoxin (reactions seen include unexplained rash, swelling of the mouth, lips or throat or a difficulty in breathing). A hypersensitivity reaction to other digitalis preparations usually constitutes a contraindication to digoxin.
# Warnings
Patients with Wolff-Parkinson-White syndrome who develop atrial fibrillation are at high risk of ventricular fibrillation. Treatment of these patients with digoxin leads to greater slowing of conduction in the atrioventricular node than in accessory pathways, and the risks of rapid ventricular response leading toventricular fibrillation are thereby increased.
Digoxin may cause severe sinus bradycardia or sino-atrial block particularly in patients with pre-existing sinus node disease and may cause advanced or complete heart block in patients with pre-existing incomplete AV block. Consider insertion of a pacemaker before treatment with digoxin.
Signs and symptoms of digoxin toxicity include anorexia, nausea, vomiting, visual changes and cardiac arrhythmias . Toxicity is usually associated with digoxin levels greater than 2 ng/mL although symptoms may also occur at lower levels. Low body weight, advanced age or impaired renal function, hypokalemia, hypercalcemia, or hypomagnesemia may predispose to digoxin toxicity. Obtain serum digoxin levels in patients with signs or symptoms of digoxin therapy and interrupt or adjust dose if necessary. Assess serum electrolytes and renal function periodically.
The earliest and most frequent manifestation of digoxin toxicity in infants and children is the appearance of cardiac arrhythmias, including sinus bradycardia. In children, the use of digoxin may produce any arrhythmia The most common are conduction disturbances or supraventricular tachyarrhythmias, such as atrial tachycardia (with or without block) and junctional (nodal) tachycardia. Ventricular arrhythmias are less common. Sinus bradycardia may be a sign of impending digoxin intoxication, especially in infants, even in the absence of first-degree heart block. Any arrhythmias or alteration in cardiac conduction that develops in a child taking digoxin should initially be assumed to be a consequence of digoxin intoxication.
Given that adult patients with heart failure have some symptoms in common with digoxin toxicity, it may be difficult to distinguish digoxin toxicity from heart failure. Misidentification of their etiology might lead the clinician to continue or increase digoxin dosing, when dosing should actually be suspended. When the etiology of these signs and symptoms is not clear, measure serum digoxin levels.
It may be desirable to reduce the dose of or discontinue digoxin for 1-2 days prior to electrical cardioversion of atrial fibrillation to avoid the induction of ventricular arrhythmias, but physicians must consider the consequences of increasing the ventricular response if digoxin is decreased or withdrawn. If digitalis toxicity is suspected, elective cardioversion should be delayed. If it is not prudent to delay cardioversion, the lowest possible energy level should be selected to avoid provoking ventricular arrhythmias.
Digoxin is not recommended in patients with acute myocardial infarction because digoxin may increase myocardial oxygen demand and lead to ischemia.
Digoxin can precipitate vasoconstriction and may promote production of pro-inflammatory cytokines; therefore, avoid use in patients with myocarditis.
Patients with heart failure associated with preserved left ventricular ejection fraction may experience decreased cardiac output with use of digoxin. Such disorders include restrictive cardiomyopathy, constrictive pericarditis, amyloid heart disease, and acutecor pulmonale. Patients with idiopathic hypertrophic subaortic stenosis may have worsening of the outflow obstruction due to the inotropic effects of digoxin. Patients with amyloid heart disease may be more susceptible to digoxin toxicity at therapeutic levels because of an increased binding of digoxin to extracellular amyloid fibrils.
Digoxin should generally be avoided in these patients, although it has been used for ventricular rate control in the subgroup of patients with atrial fibrillation.
Hypocalcemia can nullify the effects of digoxin in humans; thus, digoxin may be ineffective until serum calcium is restored to normal. These interactions are related to the fact that digoxin affects contractility and excitability of the heart in a manner similar to that of calcium.
Hypothyroidism may reduce the requirements for digoxin.
Heart failure and/or atrial arrhythmias resulting from hypermetabolic or hyperdynamic states (e.g., hyperthyroidism, hypoxia, or arteriovenous shunt) are best treated by addressing the underlying condition. Atrial arrhythmias associated with hypermetabolic states are particularly resistant to digoxin treatment. Patients with beri beri heart disease may fail to respond adequately to digoxin if the underlying thiamine deficiency is not treated concomitantly.
# Adverse Reactions
## Clinical Trials Experience
### Infant and Children
The side effects of digoxin in infants and children differ from those seen in adults in several respects. Although digoxin may produce anorexia, nausea, vomiting, diarrhea, and CNS disturbances in young patients, these are rarely the initial symptoms of overdosage. Rather, the earliest and most frequent manifestation of excessive dosing with digoxin in infants and children is the appearance of cardiac arrhythmias, including sinus bradycardia. In children, the use of digoxin may produce any arrhythmia. The most common are conduction disturbances or supraventricular tachyarrhythmias, such as atrial tachycardia (with or without block) and junctional (nodal) tachycardia. Ventricular arrhythmias are less common. Sinus bradycardia may be a sign of impending digoxin intoxication, especially in infants, even in the absence of first-degree heart block. Any arrhythmia or alteration in cardiac conduction that develops in a child taking digoxin should be assumed to be caused by digoxin, until further evaluation proves otherwise.
## Postmarketing Experience
There is limited information regarding Digoxin Postmarketing Experience in the drug label.
# Drug Interactions
Caution should be exercised when combining digoxin with any drug that may cause significant deterioration in renal function (e.g., ACE inhibitors, angiotensin receptor blockers,nonsteroidal anti-inflammatory drugs , COX-2 inhibitors) since a decline in glomerular filtration or tubular secretion may impair the excretion of digoxin.
- Dofetilid : Concomitant administration with digoxin was associated with a higher rate of torsades de pointes
- Sotalol: Proarrhythmic events were more common in patients receiving sotalol and digoxin than on either alone; it is not clear whether this represents an interaction or is related to the presence of CHF, a known risk factor for proarrhythmia, in patients receiving digoxin.
- Dronedarone: Sudden death was more common in patients receiving digoxin with dronedarone than on either alone; it is not clear whether this represents an interaction or is related to the presence of advanced heart disease, a known risk factor for sudden death in patients receiving digoxin.
- Teriparatide: Sporadic case reports have suggested that hypercalcemia may predispose patients to digitalis toxicity. Teriparatide transiently increases serum calcium.
Potassium-depleting diuretics are a major contributing factor to digitalis toxicity.
Calcium, particularly if administered rapidly by the intravenous route, may produce serious arrhythmias in digitalized patients.
Quinidine, verapamil, amiodarone, propafenone, indomethacin, itraconazole, alprazolam, and spironolactone raise the serum digoxin concentration due to a reduction in clearance and/or in volume of distribution of the drug, with the implication that digitalis intoxication may result.
Erythromycin and clarithromycin (and possibly othermacrolide antibiotics) and tetracycline may increase digoxin absorption in patients who inactivate digoxin by bacterial metabolism in the lower intestine, so that digitalis intoxication may result (see Pharmacology).
Decrease gut motility, which may increase digoxin absorption.
May interfere with intestinal digoxin absorption, resulting in unexpectedly low serum concentrations.
May decrease serum digoxin concentration, especially in patients with renal dysfunction, by increasing the non-renal clearance of digoxin.
Thyroid administration to a digitalized, hypothyroid patient may increase the dose requirement of digoxin.
Concomitant use of digoxin and sympathomimetics increases the risk of cardiac arrhythmias.
Succinylcholine may cause a sudden extrusion of potassium from muscle cells, and may thereby cause arrhythmias in digitalized patients.
Use with digoxin may be useful in combination to control atrial fibrillation, their additive effects on AV node conduction can result in advanced or complete heart block.
Both digitalis glycosides and beta-blockers slow atrioventricular conduction and decrease heart rate. Concomitant use can increase the risk of bradycardia. Digoxin concentrations are increased by about 15% when digoxin and carvedilol are administered concomitantly. Therefore, increased monitoring of digoxin is recommended when initiating, adjusting, or discontinuing carvedilol.
### Drug/Laboratory Test Interactions
- Endogenous substances of unknown composition (digoxin-like immunoreactive substances ) can interfere with standard radioimmunoassays for digoxin. The interference most often causes results to be falsely positive or falsely elevated, but sometimes it causes results to be falsely reduced. Some assays are more subject to these failings than others. Several LC/MS/MS methods are available that may provide less susceptibility to DLIS interference.
- DLIS are present in up to half of all neonates and in varying percentages of pregnant women, patients with hypertrophic cardiomyopathy, patients with renal or hepatic dysfunction, and other patients who are volume-expanded for any reason. The measured levels of DLIS (as digoxin equivalents) are usually low (0.2-0.4 ng/mL), but sometimes they reach levels that would be considered therapeutic or even toxic.
- In some assays, spironolactone, canrenone, and potassium canrenoate may be falsely detected as digoxin, at levels up to 0.5 ng/mL. Some traditional Chinese and Ayurvedic medicine substances like Chan Su, Siberian Ginseng, Asian Ginseng, Ashwagandha, or Dashen can cause similar interference.
Spironolactone and DLIS are much more extensively protein-bound than digoxin. As a result, assays of free digoxin levels in protein-free ultrafiltrate (which tend to be about 25% less than total levels, consistent with the usual extent of protein binding) are less affected by spironolactone or DLIS.
- It should be noted that ultrafiltration does not solve all interference problems with alternative medicines. The use of an LC/MS/MS method may be the better option according to the good results it provides, especially in terms of specificity and limit of quantization.
# Use in Specific Populations
### Pregnancy
Pregnancy Category (FDA): C
Animal reproduction studies have not been conducted with digoxin. It is also not known whether digoxin can cause fetal harm when administered to a pregnant woman or can affect reproductive capacity. Digoxin should be given to a pregnant woman only if clearly needed.
Pregnancy Category (AUS): A
There is no Australian Drug Evaluation Committee (ADEC) guidance on usage of Digoxin in women who are pregnant.
### Labor and Delivery
There is no FDA guidance on use of Digoxin during labor and delivery.
### Nursing Mothers
Studies have shown that digoxin concentrations in the mother’s serum and milk are similar. However, the estimated exposure of a nursing infant to digoxin via breastfeeding will be far below the usual infant maintenance dose. Therefore, this amount should have no pharmacologic effect upon the infant. Nevertheless, caution should be exercised when digoxin is administered to a nursing woman.
### Pediatric Use
Newborn infants display considerable variability in their tolerance to digoxin. Premature and immature infants are particularly sensitive to the effects of digoxin, and the dosage of the drug must not only be reduced but must be individualized according to their degree of maturity. Digitalis glycosides can cause poisoning in children due to accidental ingestion.
### Geriatic Use
The majority of clinical experience gained with digoxin has been in the elderly population. This experience has not identified differences in response or adverse effects between the elderly and younger patients. However, this drug is known to be substantially excreted by the kidney, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function. Because elderly patients are more likely to have decreased renal function, care should be taken in dose selection, which should be based on renal function, and it may be useful to monitor renal function
### Gender
In a study of 184 patients, the clearance of digoxin was 12% lower in female than in male patients. This difference is not likely to be clinically important.
### Race
The impact of race differences on digoxin pharmacokinetics have not been formally studied. Because digoxin is primarily eliminated as unchanged drug via the kidney and because there are no important differences in creatinine clearance among races, pharmacokinetic differences due to race are not expected.)
### Renal Impairment
Since the clearance of digoxin correlates withcreatinine clearance, patients with renal impairment generally demonstrate prolonged digoxin elimination half-lives and greater exposures to digoxin. Therefore, titrate carefully in these patients based on clinical response and based on monitoring of serum digoxin concentrations, as appropriate.
### Hepatic Impairment
Because only a small percentage (approximately 13%) of a dose of digoxin undergoes metabolism, hepatic impairment would not be expected to significantly alter the pharmacokinetics of digoxin. In a small study, plasma digoxin concentration profiles in patients with acute hepatitis generally fell within the range of profiles in a group of healthy subjects. No dosage adjustments are recommended for patients with hepatic impairment; however, serum digoxin concentrations should be used, as appropriate, to help guide dosing in these patients.
### Females of Reproductive Potential and Males
There is no FDA guidance on the use of Digoxin in women of reproductive potentials and males.
### Immunocompromised Patients
There is no FDA guidance one the use of Digoxin in patients who are immunocompromised.
# Administration and Monitoring
### Administration
- Oral
- In selecting a LANOXIN dosing regimen, it is important to consider factors that affect digoxin blood levels (e.g., body weight, age, renal function, concomitant drugs) since toxic levels of digoxin are only slightly higher than therapeutic levels. Dosing can be either initiated with a loading dose followed by maintenance dosing if rapid titration is desired or initiated with maintenance dosing without a loading dose.
- Consider interruption or reduction in digoxin dose prior to electrical cardioversion.
Use digoxin solution to obtain the appropriate dose in infants, young pediatric patients, or patients with very low body weight.
- Intravenous:
- In selecting a digoxin dosing regimen, it is important to consider factors that affect digoxin blood levels (e.g., body weight, age, renal function, concomitant drugs) since toxic levels of digoxin are only slightly higher than therapeutic levels. Dosing can be either initiated with a loading dose followed by maintenance dosing if rapid titration is desired or initiated with maintenance dosing without a loading dose.
- Parenteral administration of digoxin should be used only when the need for rapid digitalization is urgent or when the drug cannot be taken orally. Intramuscular injection can lead to severe pain at the injection site, thus intravenous administration is preferred. If the drug must be administered by the intramuscular route, it should be injected deep into the muscle followed by massage. For adults, no more than 500 mcg of Digoxin Injection should be injected into a single site. For pediatric patients, see the full prescribing information for pediatric digoxin injection (not available from West-Ward) for specific recommendations.
- Administer the dose over a period of 5 minutes or longer and avoid bolus administration to prevent systemic and coronary vasoconstriction. Mixing of Digoxin Injection with other drugs in the same container or simultaneous administration in the same intravenous line is not recommended.
- Digoxin Injection can be administered undiluted or diluted with a 4-fold or greater volume of Sterile Water for Injection, 0.9% Sodium Chloride Injection, or 5% Dextrose Injection. The use of less than a 4-fold volume of diluent could lead to precipitation of the digoxin. Immediate use of the diluted product is recommended.
- If tuberculin syringes are used to measure very small doses do not flush with the parenteral solution after its contents are expelled into an indwelling vascular catheter to avoid over administration of digoxin.
- Consider interruption or reduction in digoxin dose prior to electrical cardioversion
### Switching from Intravenous Digoxin to Oral Digoxin
When switching from intravenous to oral digoxin formulations, make allowances for differences in bioavailability when calculating maintenance dosages
### Monitoring
Monitor for signs and symptoms of digoxin toxicity and clinical response. Adjust dose based on toxicity, efficacy, and blood levels.
Serum digoxin levels less than 0.5 ng/mL have been associated with diminished efficacy, while levels above 2 ng/mL have been associated with increased toxicity without increased benefit.
Interpret the serum digoxin concentration in the overall clinical context, and do not use an isolated measurement of serum digoxin concentration as the basis for increasing or decreasing the digoxin dose. Serum digoxin concentrations may be falsely elevated by endogenous digoxin-like substances . If the assay is sensitive to these substances, consider obtaining a baseline digoxin level before starting digoxin and correct post-treatment values by the reported baseline level.
Obtain serum digoxin concentrations just before the next scheduled digoxin dose or at least 6 hours after the last dose. The digoxin concentration is likely to be 10-25% lower when sampled right before the next dose (24 hours after dosing) compared to sampling 8 hours after dosing (using once-daily dosing). However, there will be only minor differences in digoxin concentrations using twice daily dosing whether sampling is done at 8 or 12 hours after a dose.
# IV Compatibility
## Solution
### Compatible
- 0.9% Sodium Chloride
- 5% Dextrose
# Overdosage
## Acute Overdose
### Signs and Symptoms
- Adults: The most common signs and symptoms of digoxin toxicity are nausea, vomiting, anorexia, and fatigue that occur in 30 to 70% of patients who are overdosed. Extremely high serum concentrations produce hyperkalemia especially in patients with impaired renal function. Almost every type of cardiac arrhythmia has been associated with digoxin overdose and multiple rhythm disturbances in the same patient are common. Peak cardiac effects occur 3 to 6 hours following ingestion and may persist for 24 hours or longer. Arrhythmias that are considered more characteristic of digoxin toxicity are new-onset Mobitz type 1 A-V block, accelerated junctional rhythms, non-paroxysmal atrial tachycardia withA-V block, and bi-directional ventricular tachycardia. Cardiac arrest from asystole or ventricular fibrillation is usually fatal.
- Digoxin toxicity is related to serum concentration. As digoxin serum levels increase above 1.2 ng/mL, there is a potential for increase in adverse reactions. Furthermore, lower potassium levels increases the risk for adverse reactions. In adults with heart disease, clinical observations suggest that an overdose of digoxin of 10 to 15 mg results in death of half of patients. A dose above 25 mg ingested by an adult without heart disease appeared to be uniformly fatal if no Digoxin Immune Fab (DIGIBIND®, DIGIFAB®) was administered.
- Among the extra-cardiac manifestations, gastrointestinal symptoms (e.g., nausea, vomiting, anorexia) are very common (up to 80% incidence) and precede cardiac manifestations in approximately half of the patients in most literature reports. Neurologic manifestations (e.g., dizziness, various CNS disturbances), fatigue, and malaise are very common. Visual manifestations may also occur with aberration in color vision (predominance of yellow green) the most frequent. Neurological and visual symptoms may persist after other signs of toxicity have resolved. In chronic toxicity, nonspecific extra-cardiac symptoms, such as malaise and weakness, may predominate.
- Children: In pediatric patients, signs and symptoms of toxicity can occur during or shortly after the dose of digoxin. Frequent non-cardiac effects are similar to those observed in adults although nausea and vomiting are not seen frequently in infants and small pediatric patients. Other reported manifestations of overdose are weight loss in older age groups, failure to thrive in infants, abdominal pain caused by mesenteric artery ischemia, drowsiness, and behavioral disturbances including psychotic episodes. Arrhythmias and combinations of arrhythmias that occur in adult patients can also occur in pediatric patients although sinus tachycardia, supraventricular tachycardia, and rapid atrial fibrillation are seen less frequently in pediatric patients. Pediatric patients are more likely to develop A-V conduction disturbances, or sinus bradycardia. Any arrhythmia in a child treated with digoxin should be considered related to digoxin until otherwise ruled out. In pediatric patients aged 1 to 3 years without heart disease, clinical observations suggest that an overdose of digoxin of 6 to 10 mg would result in death of half of the patients. In the same population, a dose above 10 mg resulted in death if no Digoxin Immune Fab were administered.
### Management
- Patients who have intentionally or accidently ingested massive doses of digoxin should receive activated charcoal orally or by nasogastric tube regardless of the time since ingestion since digoxin recirculates to the intestine by enterohepatic circulation. In addition to cardiac monitoring, temporarily discontinue digoxin until the adverse reaction resolves. Correct factors that may be contributing to the adverse reactions .
- In particular, correct hypokalemia and hypomagnesemia.
- Digoxin is not effectively removed from the body by dialysisbecause of its large extravascular volume of distribution. Life threatening arrhythmias (ventricular tachycardia, ventricular fibrillation, high degree A-V block, bradyarrhythma, sinus arrest) or hyperkalemia requires administration of Digoxin Immune Fab.
- Digoxin Immune Fab has been shown to be 80 to 90% effective in reversing signs and symptoms of digoxin toxicity. Bradycardia and heart block caused by digoxin are parasympathetically mediated and respond to atropine.
- A temporary cardiac pacemaker may also be used. Ventricular arrhythmias may respond to lidocaine or phenytoin. When a large amount of digoxin has been ingested, especially in patients with impaired renal function, hyperkalemiamay be present due to release of potassium from skeletal muscle. In this case, treatment with Digoxin Immune Fab is indicated; an initial treatment with glucose and insulin may be needed if the hyperkalemia is life-threatening.
- Once the adverse reaction has resolved, therapy with digoxin may be reinstituted following a careful reassessment of dose.
## Chronic Overdose
### Signs and Symptoms
The most common signs and symptoms of digoxin toxicity are nausea, vomiting, anorexia, and fatigue that occur in 30 to 70% of patients who are overdosed.
### Management
- If there is suspicion of toxicity, discontinue digoxin and place the patient on a cardiac monitor. Correct factors such as electrolyte abnormalities, thyroid dysfunction, and concomitant medications .
- Correct hypokalemia by administering potassium so that serum potassium is maintained between 4.0 and 5.5 mmol/L. Potassium is usually administered orally, but when correction of the arrhythmia is urgent and serum potassium concentration is low, potassium may be administered by the intravenous route.
- Monitor electrocardiogram for any evidence of potassium toxicity (e.g., peaking of T waves) and to observe the effect on the arrhythmia. Avoid potassium salts in patients with bradycardia or heart block. Symptomatic arrhythmias may be treated with Digoxin Immune Fab.
# Pharmacology
## Mechanism of Action
All of digoxin’s actions are mediated through its effects on Na-K ATPase. This enzyme, the “sodium pump,” is responsible for maintaining the intracellular milieu throughout the body by moving sodium ions out of and potassium ions into cells. By inhibiting Na-K ATPase, digoxin
- causes increased availability of intracellular calcium in the myocardium and conduction system, with consequent increased inotropy, increased automaticity, and reduced conduction velocity
- indirectly causes parasympathetic stimulation of the autonomic nervous system, with consequent effects on the sino-atrial (SA) and atrioventricular (AV) nodes
- reduces catecholamine reuptake at nerve terminals, rendering blood vessels more sensitive to endogenous or exogenous catecholamines
- increases baroreceptor sensitization, with consequent increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increment in mean arterial pressure
- increases (at higher concentrations) sympathetic outflow from the central nervous system (CNS) to both cardiac and peripheral sympathetic nerves
allows (at higher concentrations) progressive efflux of intracellular potassium, with consequent increase in serum potassium levels.
The cardiologic consequences of these direct and indirect effects are an increase in the force and velocity of myocardial systolic contraction (positive inotropic action), a slowing of the heart rate (negative chronotropic effect), decreased conduction velocity through the AV node, and a decrease in the degree of activation of the sympathetic nervous system and renin-angiotensin system (neurohormonal deactivating effect).
## Structure
Digoxin is one of the cardiac (or digitalis) glycosides, a closely related group of drugs having in common specific effects on the myocardium. These drugs are found in a number of plants. Digoxin is extracted from the leaves of Digitalis lanata. The term “digitalis” is used to designate the whole group of glycosides. The glycosides are composed of 2 portions: a sugar and a cardenolide (hence “glycosides”).
Digoxin is described chemically as (3β,5β,12β)-3--12,14-dihydroxy-card-20(22)-enolide. Its molecular formula is C41H64O14, its molecular weight is 780.95.
Digoxin exists as clear to white odorless crystals or white, odorless crystalline powder that melts with decomposition above 230°C. The drug is practically insoluble in water and in ether; slightly soluble in diluted (50%) alcohol and in chloroform; and freely soluble in pyridine.
Digoxin injection USP is a sterile solution of digoxin for intravenous or intramuscular injection. Each mL contains: digoxin 0.25 mg, propylene glycol 40% (v/v), anhydrous ethanol 10% (v/v), dibasic sodium phosphate 0.3% (w/v) and anhydrous citric acid 0.08% (w/v) to adjust pH between 6.8 and 7.2, and water for injection. Dilution is not required.
## Pharmacodynamics
The times to onset of pharmacologic effect and to peak effect of preparations of digoxin are shown in the table below.
Hemodynamic Effects: Short- and long-term therapy with the drug increases cardiac output and lowers pulmonary artery pressure, pulmonary capillary wedge pressure, and systemic vascular resistance in patients with heart failure. These hemodynamic effects are accompanied by an increase in the left ventricular ejection fraction and a decrease in end-systolic and end-diastolic dimensions.
ECG Changes: The use of therapeutic doses of digoxin may cause prolongation of thePR interval and depression of theST segment on the electrocardiogram. Digoxin may produce false positive ST-T changes on the electrocardiogram during exercise testing. These electrophysiologic effects are not indicative of toxicity. Digoxin does not significantly reduce heart rate during exercise.
## Pharmacokinetics
Distribution: Following drug administration, a 6 to 8 hour tissue distribution phase is observed. This is followed by a much more gradual decline in the serum concentration of the drug, which is dependent on the elimination of digoxin from the body. The peak height and slope of the early portion (absorption/distribution phases) of the serum concentration-time curve are dependent upon the route of administration and the absorption characteristics of the formulation. Clinical evidence indicates that the early high serum concentrations do not reflect the concentration of digoxin at its site of action, but that with chronic use, the steady-state post-distribution serum concentrations are in equilibrium with tissue concentrations and correlate with pharmacologic effects. In individual patients, these post-distribution serum concentrations may be useful in evaluating therapeutic and toxic effects.
Digoxin is concentrated in tissues and therefore has a large apparent volume of distribution (approximately 475 to 500 L). Digoxin crosses both the blood-brain barrier and the placenta. At delivery, the serum digoxin concentration in the newborn is similar to the serum concentration in the mother. Approximately 25% of digoxin in the plasma is bound to protein. Serum digoxin concentrations are not significantly altered by large changes in fat tissue weight, so that its distribution space correlates best with lean (i.e., ideal) body weight, not total body weight.
Metabolism: Only a small percentage (13%) of a dose of digoxin is metabolized in healthy volunteers. The urinary metabolites, which include dihydrodigoxin, digoxigenin bisdigitoxoside, and their glucuronide and sulfate conjugates are polar in nature and are postulated to be formed via hydrolysis, oxidation, and conjugation. The metabolism of digoxin is not dependent upon the cytochrome P-450 system, and digoxin is not known to induce or inhibit thecytochrome P-450 system.
Excretion: Elimination of digoxin follows first-order kinetics (that is, the quantity of digoxin eliminated at any time is proportional to the total body content). Following intravenous administration to healthy volunteers, 50 to 70% of a digoxin dose is excreted unchanged in the urine. Renal excretion of digoxin is proportional to creatinine clearance and is largely independent of urine flow. In healthy volunteers with normal renal function, digoxin has a half-life of 1.5 to 2 days. The half-life in anuric patients is prolonged to 3.5 to 5 days. Digoxin is not effectively removed from the body by dialysis, exchange transfusion, or during cardiopulmonary bypass because most of the drug is bound to extravascular tissues.
## Nonclinical Toxicology
Digoxin showed no genotoxic potential in in vitro studies (Ames test and mouse lymphoma). No data are available on the carcinogenic potential of digoxin, nor have studies been conducted to assess its potential to affect fertility.
# Clinical Studies
Two 12-week, double-blind, placebo-controlled studies enrolled 178 (RADIANCE trial) and 88 (PROVED trial) patients with NYHA class II or III heart failure previously treated with digoxin, a diuretic, and an ACE inhibitor (RADIANCE only) and randomized them to placebo or treatment with LANOXIN. Both trials demonstrated better preservation of exercise capacity in patients randomized to LANOXIN. Continued treatment with LANOXIN reduced the risk of developing worsening heart failure, as evidenced by heart failure-related hospitalizations and emergency care and the need for concomitant heart failure therapy.
The Digitalis Investigation Group (DIG) main trial was a 37-week, multicenter, randomized, double-blind mortality study comparing digoxin to placebo in 6800 adult patients with heart failure and left ventricular ejection fraction ≤0.45. At randomization, 67% were NYHA class I or II, 71% had heart failure of ischemic etiology, 44% had been receiving digoxin, and most were receiving a concomitant ACE inhibitor (94%) and diuretics (82%). As in the smaller trials described above, patients who had been receiving open-label digoxin were withdrawn from this treatment before randomization. Randomization to digoxin was again associated with a significant reduction in the incidence of hospitalization, whether scored as number of hospitalizations for heart failure (relative risk 75%), risk of having at least one such hospitalization during the trial (RR 72%), or number of hospitalizations for any cause (RR 94%). On the other hand, randomization to digoxin had no apparent effect on mortality (RR 99%, with confidence limits of 91 to 107%).
Digoxin has also been studied as a means of controlling the ventricular response to chronic atrial fibrillation in adults. Digoxin reduced the resting heart rate, but not the heart rate during exercise.
In 3 different randomized, double-blind trials that included a total of 315 adult patients, digoxin was compared to placebo for the conversion of recent-onset atrial fibrillation to sinus rhythm. Conversion was equally likely, and equally rapid, in the digoxin and placebo groups. In a randomized 120-patient trial comparing digoxin, sotalol, and amiodarone, patients randomized to digoxin had the lowest incidence of conversion to sinus rhythm, and the least satisfactory rate control when conversion did not occur.
In at least one study, digoxin was studied as a means of delaying reversion to atrial fibrillation in adult patients with frequent recurrence of this arrhythmia. This was a randomized, double-blind, 43-patient crossover study. Digoxin increased the mean time between symptomatic recurrent episodes by 54%, but had no effect on the frequency of fibrillatory episodes seen during continuous electrocardiographic monitoring.
# How Supplied
LANOXIN (digoxin) Tablets, Scored 125 mcg (0.125 mg): Bottles of 100 with child-resistant cap (NDC 24987-242-55), (NDC 24987-242-57) and 1,000 (NDC 24987-242-75), (NDC 24987-242-76); unit dose pack of 100 (NDC 24987-242-56). Imprinted with LANOXIN and Y3B (yellow).
LANOXIN (digoxin) Tablets, Scored 250 mcg (0.25 mg): Bottles of 100 with child-resistant cap (NDC 24987-249-55), (NDC 24987-249-57), 1,000 (NDC -24987-249-75), (NDC-24987-249-76), and 5,000 (NDC 24987-249-80); unit dose pack of 100 (NDC 24987-249-56). Imprinted with LANOXIN and X3A (white).
- National Drug Code (NDC): see above
- Manufactured by: Manufactured by DSM Pharmaceuticals, Inc. Greenville, NC 27834
- Distributed by:Covis Pharmaceuticals, Inc. Cary, NC 27511
Digoxin Injection, USP is available as:
500 mcg/2 mL (250 mcg/mL) ampuls packaged in 25s
- National Drug Code (NDC):(NDC 0641-1410-35)
- Manufactured by: HIKMA FARMACÊUTICA (PORTUGAL), S.A. Estrada do Rio da Mό, 8, 8A e 8B – Fervença – 2705-906 Terrugem SNT, PORTUGAL
- Distributed by:WEST-WARD PHARMACEUTICALS Eatontown, NJ 07724 USA
Digoxin Solution:Each 1 mL of clear, colorless Digoxin Oral Solution contains 0.05 mg (50 mcg).
The Digoxin Oral Solution bottles are to be used with the graduated droppers provided in the carton. Starting at 0.2 mL, this 1 mL dropper is marked in divisions of 0.1 mL, corresponding to 5 mcg or 0.005 mg of digoxin.
The calibrated dropper supplied with the 60 mL bottle of Digoxin Oral Solution is not appropriate to measure doses below 0.2 mL. Doses less than 0.2 mL require appropriate methods or measuring devices designed to administer an accurate amount to the patient, such as a graduated syringe
- National Drug Code (NDC):NDC:17856-0057
- Manufactured by:Roxane Laboratories, Inc. Columbus, Ohio 43216
- Distributed by:Atlantic Biologicals Corps
## Storage
- Storage: Store at 25°C (77°F); excursions permitted to 15 to 30°C (59 to 86°F) in a dry place.
- Keep out of reach of children.
- Storage: Store at 20˚-25˚C (68˚-77˚F), excursions permitted to 15˚-30˚C (59˚-86˚F).
- Storage:Store at 25°C (77°F); excursions permitted to 15° to 30°C (59° to 86°F). - Protect from light.
# Images
## Drug Images
## Package and Label Display Panel
# Patient Counseling Information
- Advise patients that digoxin is a cardiac glycoside used to treat heart failure and heart arrhythmias.
- Instruct patients to take this medication as directed by their physician.
- Advise patients that many drugs can interact with digoxin. Instruct patients to inform their doctor and pharmacist if they are taking any over the counter medications, including herbal *medication, or are started on a new prescription.
- Advise patient that blood tests will be necessary to ensure that their digoxin dose is appropriate for them.
- Advise patients to contact their doctor or a health care professional if they experience nausea, vomiting, persistent diarrhea, confusion, weakness, or visual disturbances (including *blurred vision, green-yellow color disturbances, halo effect) as these could be signs that the dose of digoxin may be too high.
- Advise parents or caregivers that the symptoms of having too high digoxin doses may be difficult to recognize in infants and pediatric patients. Symptoms such as weight loss, failure to thrive in infants, abdominal pain, and behavioral disturbances may be indications of digoxin toxicity.
- Suggest to the patient to monitor and record their heart rate and blood pressure daily.
- Instruct women of childbearing potential who become or are planning to become pregnant to consult a physician prior to initiation or continuing therapy with digoxin.
# Precautions with Alcohol
Alcohol-SandboxAlonso interaction has not been established. Talk to your doctor about the effects of taking alcohol with this medication.
# Brand Names
- Digoxin
- Digox
- Lanoxin
# Look-Alike Drug Names
- Digoxin — Dioxin
- Digoxin — Digitoxin
# Drug Shortage Status
Drug Shortage
# Price | Digoxin
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Alonso Alvarado, M.D. [2]
# Disclaimer
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# Overview
Digoxin is a cardiac glycoside that is FDA approved for the treatment of atrial fibrillation, atrial flutter, and heart failure. Common adverse reactions include dizziness, headache, mental disorder, nausea, and vomiting.
# Adult Indications and Dosage
## FDA-Labeled Indications and Dosage (Adult)
- Dosing Information
- Loading dose: 10-15 mcg/kg PO administer half the total loading dose initially, then ¼ the loading dose every 6 to 8 hours twice.
- Maintenance dose: 3.4-5.1 mcg/kg/day PO once daily.
- Dosing Information
- Loading dose: 10-15 mcg/kg PO administer half the total loading dose initially, then ¼ the loading dose every 6 to 8 hours twice.
- Maintenance dose: 3.4-5.1 mcg/kg/day PO once daily.
## Off-Label Use and Dosage (Adult)
### Guideline-Supported Use
There is limited information regarding Off-Label Guideline-Supported Use of SandboxAlonso in adult patients.
### Non–Guideline-Supported Use
There is limited information regarding Off-Label Non–Guideline-Supported Use of SandboxAlonso in adult patients.
# Pediatric Indications and Dosage
## FDA-Labeled Indications and Dosage (Pediatric)
- Dosing Information
- Loading dose
- 5-10 years old: 20-45 mcg/kg PO administer half the total loading dose initially, then ¼ the loading dose every 6 to 8 hours twice.
- >10 year old: 10-15 mcg/kg PO administer half the total loading dose initially, then ¼ the loading dose every 6 to 8 hours twice.
- Maintenence dose:
- 5-10 years: 6.4 – 12.9 mcg/kg/day PO or 3.2 – 6.4 mcg/kg/day Twice daily.
- More than 10 years: 3.4 – 5.1 mcg/kg/day PO.
## Off-Label Use and Dosage (Pediatric)
### Guideline-Supported Use
There is limited information regarding Off-Label Guideline-Supported Use of SandboxAlonso in pediatric patients.
### Non–Guideline-Supported Use
- Dosage information
- 0.01 mg/kg orally 3 times daily for the first 2 doses, then 0.0035 mg/kg 3 times daily[1][2]
- Dosage information
- Maternal 0.25 to 0.375 mg PO daily alone or with verapamil.[3]
# Contraindications
- Ventricular fibrillation
- Known hypersensitivity to digoxin (reactions seen include unexplained rash, swelling of the mouth, lips or throat or a difficulty in breathing). A hypersensitivity reaction to other digitalis preparations usually constitutes a contraindication to digoxin.
# Warnings
Patients with Wolff-Parkinson-White syndrome who develop atrial fibrillation are at high risk of ventricular fibrillation. Treatment of these patients with digoxin leads to greater slowing of conduction in the atrioventricular node than in accessory pathways, and the risks of rapid ventricular response leading toventricular fibrillation are thereby increased.
Digoxin may cause severe sinus bradycardia or sino-atrial block particularly in patients with pre-existing sinus node disease and may cause advanced or complete heart block in patients with pre-existing incomplete AV block. Consider insertion of a pacemaker before treatment with digoxin.
Signs and symptoms of digoxin toxicity include anorexia, nausea, vomiting, visual changes and cardiac arrhythmias [first-degree, second-degree (Wenckebach), or third-degree heart block (including asystole); atrial tachycardia with block; AV dissociation; accelerated junctional (nodal) rhythm; unifocal or multiform ventricular premature contractions (especially bigeminy or trigeminy); ventricular tachycardia; and ventricular fibrillation]. Toxicity is usually associated with digoxin levels greater than 2 ng/mL although symptoms may also occur at lower levels. Low body weight, advanced age or impaired renal function, hypokalemia, hypercalcemia, or hypomagnesemia may predispose to digoxin toxicity. Obtain serum digoxin levels in patients with signs or symptoms of digoxin therapy and interrupt or adjust dose if necessary. Assess serum electrolytes and renal function periodically.
The earliest and most frequent manifestation of digoxin toxicity in infants and children is the appearance of cardiac arrhythmias, including sinus bradycardia. In children, the use of digoxin may produce any arrhythmia The most common are conduction disturbances or supraventricular tachyarrhythmias, such as atrial tachycardia (with or without block) and junctional (nodal) tachycardia. Ventricular arrhythmias are less common. Sinus bradycardia may be a sign of impending digoxin intoxication, especially in infants, even in the absence of first-degree heart block. Any arrhythmias or alteration in cardiac conduction that develops in a child taking digoxin should initially be assumed to be a consequence of digoxin intoxication.
Given that adult patients with heart failure have some symptoms in common with digoxin toxicity, it may be difficult to distinguish digoxin toxicity from heart failure. Misidentification of their etiology might lead the clinician to continue or increase digoxin dosing, when dosing should actually be suspended. When the etiology of these signs and symptoms is not clear, measure serum digoxin levels.
It may be desirable to reduce the dose of or discontinue digoxin for 1-2 days prior to electrical cardioversion of atrial fibrillation to avoid the induction of ventricular arrhythmias, but physicians must consider the consequences of increasing the ventricular response if digoxin is decreased or withdrawn. If digitalis toxicity is suspected, elective cardioversion should be delayed. If it is not prudent to delay cardioversion, the lowest possible energy level should be selected to avoid provoking ventricular arrhythmias.
Digoxin is not recommended in patients with acute myocardial infarction because digoxin may increase myocardial oxygen demand and lead to ischemia.
Digoxin can precipitate vasoconstriction and may promote production of pro-inflammatory cytokines; therefore, avoid use in patients with myocarditis.
Patients with heart failure associated with preserved left ventricular ejection fraction may experience decreased cardiac output with use of digoxin. Such disorders include restrictive cardiomyopathy, constrictive pericarditis, amyloid heart disease, and acutecor pulmonale. Patients with idiopathic hypertrophic subaortic stenosis may have worsening of the outflow obstruction due to the inotropic effects of digoxin. Patients with amyloid heart disease may be more susceptible to digoxin toxicity at therapeutic levels because of an increased binding of digoxin to extracellular amyloid fibrils.
Digoxin should generally be avoided in these patients, although it has been used for ventricular rate control in the subgroup of patients with atrial fibrillation.
Hypocalcemia can nullify the effects of digoxin in humans; thus, digoxin may be ineffective until serum calcium is restored to normal. These interactions are related to the fact that digoxin affects contractility and excitability of the heart in a manner similar to that of calcium.
Hypothyroidism may reduce the requirements for digoxin.
Heart failure and/or atrial arrhythmias resulting from hypermetabolic or hyperdynamic states (e.g., hyperthyroidism, hypoxia, or arteriovenous shunt) are best treated by addressing the underlying condition. Atrial arrhythmias associated with hypermetabolic states are particularly resistant to digoxin treatment. Patients with beri beri heart disease may fail to respond adequately to digoxin if the underlying thiamine deficiency is not treated concomitantly.
# Adverse Reactions
## Clinical Trials Experience
### Infant and Children
The side effects of digoxin in infants and children differ from those seen in adults in several respects. Although digoxin may produce anorexia, nausea, vomiting, diarrhea, and CNS disturbances in young patients, these are rarely the initial symptoms of overdosage. Rather, the earliest and most frequent manifestation of excessive dosing with digoxin in infants and children is the appearance of cardiac arrhythmias, including sinus bradycardia. In children, the use of digoxin may produce any arrhythmia. The most common are conduction disturbances or supraventricular tachyarrhythmias, such as atrial tachycardia (with or without block) and junctional (nodal) tachycardia. Ventricular arrhythmias are less common. Sinus bradycardia may be a sign of impending digoxin intoxication, especially in infants, even in the absence of first-degree heart block. Any arrhythmia or alteration in cardiac conduction that develops in a child taking digoxin should be assumed to be caused by digoxin, until further evaluation proves otherwise.
## Postmarketing Experience
There is limited information regarding Digoxin Postmarketing Experience in the drug label.
# Drug Interactions
Caution should be exercised when combining digoxin with any drug that may cause significant deterioration in renal function (e.g., ACE inhibitors, angiotensin receptor blockers,nonsteroidal anti-inflammatory drugs [NSAIDs], COX-2 inhibitors) since a decline in glomerular filtration or tubular secretion may impair the excretion of digoxin.
- Dofetilid : Concomitant administration with digoxin was associated with a higher rate of torsades de pointes
- Sotalol: Proarrhythmic events were more common in patients receiving sotalol and digoxin than on either alone; it is not clear whether this represents an interaction or is related to the presence of CHF, a known risk factor for proarrhythmia, in patients receiving digoxin.
- Dronedarone: Sudden death was more common in patients receiving digoxin with dronedarone than on either alone; it is not clear whether this represents an interaction or is related to the presence of advanced heart disease, a known risk factor for sudden death in patients receiving digoxin.
- Teriparatide: Sporadic case reports have suggested that hypercalcemia may predispose patients to digitalis toxicity. Teriparatide transiently increases serum calcium.
Potassium-depleting diuretics are a major contributing factor to digitalis toxicity.
Calcium, particularly if administered rapidly by the intravenous route, may produce serious arrhythmias in digitalized patients.
Quinidine, verapamil, amiodarone, propafenone, indomethacin, itraconazole, alprazolam, and spironolactone raise the serum digoxin concentration due to a reduction in clearance and/or in volume of distribution of the drug, with the implication that digitalis intoxication may result.
Erythromycin and clarithromycin (and possibly othermacrolide antibiotics) and tetracycline may increase digoxin absorption in patients who inactivate digoxin by bacterial metabolism in the lower intestine, so that digitalis intoxication may result (see Pharmacology).
Decrease gut motility, which may increase digoxin absorption.
May interfere with intestinal digoxin absorption, resulting in unexpectedly low serum concentrations.
May decrease serum digoxin concentration, especially in patients with renal dysfunction, by increasing the non-renal clearance of digoxin.
Thyroid administration to a digitalized, hypothyroid patient may increase the dose requirement of digoxin.
Concomitant use of digoxin and sympathomimetics increases the risk of cardiac arrhythmias.
Succinylcholine may cause a sudden extrusion of potassium from muscle cells, and may thereby cause arrhythmias in digitalized patients.
Use with digoxin may be useful in combination to control atrial fibrillation, their additive effects on AV node conduction can result in advanced or complete heart block.
Both digitalis glycosides and beta-blockers slow atrioventricular conduction and decrease heart rate. Concomitant use can increase the risk of bradycardia. Digoxin concentrations are increased by about 15% when digoxin and carvedilol are administered concomitantly. Therefore, increased monitoring of digoxin is recommended when initiating, adjusting, or discontinuing carvedilol.
### Drug/Laboratory Test Interactions
- Endogenous substances of unknown composition (digoxin-like immunoreactive substances [DLIS]) can interfere with standard radioimmunoassays for digoxin. The interference most often causes results to be falsely positive or falsely elevated, but sometimes it causes results to be falsely reduced. Some assays are more subject to these failings than others. Several LC/MS/MS methods are available that may provide less susceptibility to DLIS interference.
- DLIS are present in up to half of all neonates and in varying percentages of pregnant women, patients with hypertrophic cardiomyopathy, patients with renal or hepatic dysfunction, and other patients who are volume-expanded for any reason. The measured levels of DLIS (as digoxin equivalents) are usually low (0.2-0.4 ng/mL), but sometimes they reach levels that would be considered therapeutic or even toxic.
- In some assays, spironolactone, canrenone, and potassium canrenoate may be falsely detected as digoxin, at levels up to 0.5 ng/mL. Some traditional Chinese and Ayurvedic medicine substances like Chan Su, Siberian Ginseng, Asian Ginseng, Ashwagandha, or Dashen can cause similar interference.
Spironolactone and DLIS are much more extensively protein-bound than digoxin. As a result, assays of free digoxin levels in protein-free ultrafiltrate (which tend to be about 25% less than total levels, consistent with the usual extent of protein binding) are less affected by spironolactone or DLIS.
- It should be noted that ultrafiltration does not solve all interference problems with alternative medicines. The use of an LC/MS/MS method may be the better option according to the good results it provides, especially in terms of specificity and limit of quantization.
# Use in Specific Populations
### Pregnancy
Pregnancy Category (FDA): C
Animal reproduction studies have not been conducted with digoxin. It is also not known whether digoxin can cause fetal harm when administered to a pregnant woman or can affect reproductive capacity. Digoxin should be given to a pregnant woman only if clearly needed.
Pregnancy Category (AUS): A
There is no Australian Drug Evaluation Committee (ADEC) guidance on usage of Digoxin in women who are pregnant.
### Labor and Delivery
There is no FDA guidance on use of Digoxin during labor and delivery.
### Nursing Mothers
Studies have shown that digoxin concentrations in the mother’s serum and milk are similar. However, the estimated exposure of a nursing infant to digoxin via breastfeeding will be far below the usual infant maintenance dose. Therefore, this amount should have no pharmacologic effect upon the infant. Nevertheless, caution should be exercised when digoxin is administered to a nursing woman.
### Pediatric Use
Newborn infants display considerable variability in their tolerance to digoxin. Premature and immature infants are particularly sensitive to the effects of digoxin, and the dosage of the drug must not only be reduced but must be individualized according to their degree of maturity. Digitalis glycosides can cause poisoning in children due to accidental ingestion.
### Geriatic Use
The majority of clinical experience gained with digoxin has been in the elderly population. This experience has not identified differences in response or adverse effects between the elderly and younger patients. However, this drug is known to be substantially excreted by the kidney, and the risk of toxic reactions to this drug may be greater in patients with impaired renal function. Because elderly patients are more likely to have decreased renal function, care should be taken in dose selection, which should be based on renal function, and it may be useful to monitor renal function
### Gender
In a study of 184 patients, the clearance of digoxin was 12% lower in female than in male patients. This difference is not likely to be clinically important.
### Race
The impact of race differences on digoxin pharmacokinetics have not been formally studied. Because digoxin is primarily eliminated as unchanged drug via the kidney and because there are no important differences in creatinine clearance among races, pharmacokinetic differences due to race are not expected.)
### Renal Impairment
Since the clearance of digoxin correlates withcreatinine clearance, patients with renal impairment generally demonstrate prolonged digoxin elimination half-lives and greater exposures to digoxin. Therefore, titrate carefully in these patients based on clinical response and based on monitoring of serum digoxin concentrations, as appropriate.
### Hepatic Impairment
Because only a small percentage (approximately 13%) of a dose of digoxin undergoes metabolism, hepatic impairment would not be expected to significantly alter the pharmacokinetics of digoxin. In a small study, plasma digoxin concentration profiles in patients with acute hepatitis generally fell within the range of profiles in a group of healthy subjects. No dosage adjustments are recommended for patients with hepatic impairment; however, serum digoxin concentrations should be used, as appropriate, to help guide dosing in these patients.
### Females of Reproductive Potential and Males
There is no FDA guidance on the use of Digoxin in women of reproductive potentials and males.
### Immunocompromised Patients
There is no FDA guidance one the use of Digoxin in patients who are immunocompromised.
# Administration and Monitoring
### Administration
- Oral
- In selecting a LANOXIN dosing regimen, it is important to consider factors that affect digoxin blood levels (e.g., body weight, age, renal function, concomitant drugs) since toxic levels of digoxin are only slightly higher than therapeutic levels. Dosing can be either initiated with a loading dose followed by maintenance dosing if rapid titration is desired or initiated with maintenance dosing without a loading dose.
- Consider interruption or reduction in digoxin dose prior to electrical cardioversion.
Use digoxin solution to obtain the appropriate dose in infants, young pediatric patients, or patients with very low body weight.
- Intravenous:
- In selecting a digoxin dosing regimen, it is important to consider factors that affect digoxin blood levels (e.g., body weight, age, renal function, concomitant drugs) since toxic levels of digoxin are only slightly higher than therapeutic levels. Dosing can be either initiated with a loading dose followed by maintenance dosing if rapid titration is desired or initiated with maintenance dosing without a loading dose.
- Parenteral administration of digoxin should be used only when the need for rapid digitalization is urgent or when the drug cannot be taken orally. Intramuscular injection can lead to severe pain at the injection site, thus intravenous administration is preferred. If the drug must be administered by the intramuscular route, it should be injected deep into the muscle followed by massage. For adults, no more than 500 mcg of Digoxin Injection should be injected into a single site. For pediatric patients, see the full prescribing information for pediatric digoxin injection (not available from West-Ward) for specific recommendations.
- Administer the dose over a period of 5 minutes or longer and avoid bolus administration to prevent systemic and coronary vasoconstriction. Mixing of Digoxin Injection with other drugs in the same container or simultaneous administration in the same intravenous line is not recommended.
- Digoxin Injection can be administered undiluted or diluted with a 4-fold or greater volume of Sterile Water for Injection, 0.9% Sodium Chloride Injection, or 5% Dextrose Injection. The use of less than a 4-fold volume of diluent could lead to precipitation of the digoxin. Immediate use of the diluted product is recommended.
- If tuberculin syringes are used to measure very small doses do not flush with the parenteral solution after its contents are expelled into an indwelling vascular catheter to avoid over administration of digoxin.
- Consider interruption or reduction in digoxin dose prior to electrical cardioversion
### Switching from Intravenous Digoxin to Oral Digoxin
When switching from intravenous to oral digoxin formulations, make allowances for differences in bioavailability when calculating maintenance dosages
### Monitoring
Monitor for signs and symptoms of digoxin toxicity and clinical response. Adjust dose based on toxicity, efficacy, and blood levels.
Serum digoxin levels less than 0.5 ng/mL have been associated with diminished efficacy, while levels above 2 ng/mL have been associated with increased toxicity without increased benefit.
Interpret the serum digoxin concentration in the overall clinical context, and do not use an isolated measurement of serum digoxin concentration as the basis for increasing or decreasing the digoxin dose. Serum digoxin concentrations may be falsely elevated by endogenous digoxin-like substances [see Drug Interactions (7.4)]. If the assay is sensitive to these substances, consider obtaining a baseline digoxin level before starting digoxin and correct post-treatment values by the reported baseline level.
Obtain serum digoxin concentrations just before the next scheduled digoxin dose or at least 6 hours after the last dose. The digoxin concentration is likely to be 10-25% lower when sampled right before the next dose (24 hours after dosing) compared to sampling 8 hours after dosing (using once-daily dosing). However, there will be only minor differences in digoxin concentrations using twice daily dosing whether sampling is done at 8 or 12 hours after a dose.
# IV Compatibility
## Solution
### Compatible
- 0.9% Sodium Chloride
- 5% Dextrose
# Overdosage
## Acute Overdose
### Signs and Symptoms
- Adults: The most common signs and symptoms of digoxin toxicity are nausea, vomiting, anorexia, and fatigue that occur in 30 to 70% of patients who are overdosed. Extremely high serum concentrations produce hyperkalemia especially in patients with impaired renal function. Almost every type of cardiac arrhythmia has been associated with digoxin overdose and multiple rhythm disturbances in the same patient are common. Peak cardiac effects occur 3 to 6 hours following ingestion and may persist for 24 hours or longer. Arrhythmias that are considered more characteristic of digoxin toxicity are new-onset Mobitz type 1 A-V block, accelerated junctional rhythms, non-paroxysmal atrial tachycardia withA-V block, and bi-directional ventricular tachycardia. Cardiac arrest from asystole or ventricular fibrillation is usually fatal.
- Digoxin toxicity is related to serum concentration. As digoxin serum levels increase above 1.2 ng/mL, there is a potential for increase in adverse reactions. Furthermore, lower potassium levels increases the risk for adverse reactions. In adults with heart disease, clinical observations suggest that an overdose of digoxin of 10 to 15 mg results in death of half of patients. A dose above 25 mg ingested by an adult without heart disease appeared to be uniformly fatal if no Digoxin Immune Fab (DIGIBIND®, DIGIFAB®) was administered.
- Among the extra-cardiac manifestations, gastrointestinal symptoms (e.g., nausea, vomiting, anorexia) are very common (up to 80% incidence) and precede cardiac manifestations in approximately half of the patients in most literature reports. Neurologic manifestations (e.g., dizziness, various CNS disturbances), fatigue, and malaise are very common. Visual manifestations may also occur with aberration in color vision (predominance of yellow green) the most frequent. Neurological and visual symptoms may persist after other signs of toxicity have resolved. In chronic toxicity, nonspecific extra-cardiac symptoms, such as malaise and weakness, may predominate.
- Children: In pediatric patients, signs and symptoms of toxicity can occur during or shortly after the dose of digoxin. Frequent non-cardiac effects are similar to those observed in adults although nausea and vomiting are not seen frequently in infants and small pediatric patients. Other reported manifestations of overdose are weight loss in older age groups, failure to thrive in infants, abdominal pain caused by mesenteric artery ischemia, drowsiness, and behavioral disturbances including psychotic episodes. Arrhythmias and combinations of arrhythmias that occur in adult patients can also occur in pediatric patients although sinus tachycardia, supraventricular tachycardia, and rapid atrial fibrillation are seen less frequently in pediatric patients. Pediatric patients are more likely to develop A-V conduction disturbances, or sinus bradycardia. Any arrhythmia in a child treated with digoxin should be considered related to digoxin until otherwise ruled out. In pediatric patients aged 1 to 3 years without heart disease, clinical observations suggest that an overdose of digoxin of 6 to 10 mg would result in death of half of the patients. In the same population, a dose above 10 mg resulted in death if no Digoxin Immune Fab were administered.
### Management
- Patients who have intentionally or accidently ingested massive doses of digoxin should receive activated charcoal orally or by nasogastric tube regardless of the time since ingestion since digoxin recirculates to the intestine by enterohepatic circulation. In addition to cardiac monitoring, temporarily discontinue digoxin until the adverse reaction resolves. Correct factors that may be contributing to the adverse reactions [see Warnings and Precautions].
- In particular, correct hypokalemia and hypomagnesemia.
- Digoxin is not effectively removed from the body by dialysisbecause of its large extravascular volume of distribution. Life threatening arrhythmias (ventricular tachycardia, ventricular fibrillation, high degree A-V block, bradyarrhythma, sinus arrest) or hyperkalemia requires administration of Digoxin Immune Fab.
- Digoxin Immune Fab has been shown to be 80 to 90% effective in reversing signs and symptoms of digoxin toxicity. Bradycardia and heart block caused by digoxin are parasympathetically mediated and respond to atropine.
- A temporary cardiac pacemaker may also be used. Ventricular arrhythmias may respond to lidocaine or phenytoin. When a large amount of digoxin has been ingested, especially in patients with impaired renal function, hyperkalemiamay be present due to release of potassium from skeletal muscle. In this case, treatment with Digoxin Immune Fab is indicated; an initial treatment with glucose and insulin may be needed if the hyperkalemia is life-threatening.
- Once the adverse reaction has resolved, therapy with digoxin may be reinstituted following a careful reassessment of dose.
## Chronic Overdose
### Signs and Symptoms
The most common signs and symptoms of digoxin toxicity are nausea, vomiting, anorexia, and fatigue that occur in 30 to 70% of patients who are overdosed.
### Management
- If there is suspicion of toxicity, discontinue digoxin and place the patient on a cardiac monitor. Correct factors such as electrolyte abnormalities, thyroid dysfunction, and concomitant medications [see Dosage and Administration].
- Correct hypokalemia by administering potassium so that serum potassium is maintained between 4.0 and 5.5 mmol/L. Potassium is usually administered orally, but when correction of the arrhythmia is urgent and serum potassium concentration is low, potassium may be administered by the intravenous route.
- Monitor electrocardiogram for any evidence of potassium toxicity (e.g., peaking of T waves) and to observe the effect on the arrhythmia. Avoid potassium salts in patients with bradycardia or heart block. Symptomatic arrhythmias may be treated with Digoxin Immune Fab.
# Pharmacology
## Mechanism of Action
All of digoxin’s actions are mediated through its effects on Na-K ATPase. This enzyme, the “sodium pump,” is responsible for maintaining the intracellular milieu throughout the body by moving sodium ions out of and potassium ions into cells. By inhibiting Na-K ATPase, digoxin
- causes increased availability of intracellular calcium in the myocardium and conduction system, with consequent increased inotropy, increased automaticity, and reduced conduction velocity
- indirectly causes parasympathetic stimulation of the autonomic nervous system, with consequent effects on the sino-atrial (SA) and atrioventricular (AV) nodes
- reduces catecholamine reuptake at nerve terminals, rendering blood vessels more sensitive to endogenous or exogenous catecholamines
- increases baroreceptor sensitization, with consequent increased carotid sinus nerve activity and enhanced sympathetic withdrawal for any given increment in mean arterial pressure
- increases (at higher concentrations) sympathetic outflow from the central nervous system (CNS) to both cardiac and peripheral sympathetic nerves
allows (at higher concentrations) progressive efflux of intracellular potassium, with consequent increase in serum potassium levels.
The cardiologic consequences of these direct and indirect effects are an increase in the force and velocity of myocardial systolic contraction (positive inotropic action), a slowing of the heart rate (negative chronotropic effect), decreased conduction velocity through the AV node, and a decrease in the degree of activation of the sympathetic nervous system and renin-angiotensin system (neurohormonal deactivating effect).
## Structure
Digoxin is one of the cardiac (or digitalis) glycosides, a closely related group of drugs having in common specific effects on the myocardium. These drugs are found in a number of plants. Digoxin is extracted from the leaves of Digitalis lanata. The term “digitalis” is used to designate the whole group of glycosides. The glycosides are composed of 2 portions: a sugar and a cardenolide (hence “glycosides”).
Digoxin is described chemically as (3β,5β,12β)-3-[(O-2,6-dideoxy-β-D-ribo-hexopyranosyl-(1→4)-O-2,6-dideoxy-β-D-ribo-hexopyranosyl-(1→4)-2,6-dideoxy-β-D-ribo-hexopyranosyl)oxy]-12,14-dihydroxy-card-20(22)-enolide. Its molecular formula is C41H64O14, its molecular weight is 780.95.
Digoxin exists as clear to white odorless crystals or white, odorless crystalline powder that melts with decomposition above 230°C. The drug is practically insoluble in water and in ether; slightly soluble in diluted (50%) alcohol and in chloroform; and freely soluble in pyridine.
Digoxin injection USP is a sterile solution of digoxin for intravenous or intramuscular injection. Each mL contains: digoxin 0.25 mg, propylene glycol 40% (v/v), anhydrous ethanol 10% (v/v), dibasic sodium phosphate 0.3% (w/v) and anhydrous citric acid 0.08% (w/v) to adjust pH between 6.8 and 7.2, and water for injection. Dilution is not required.
## Pharmacodynamics
The times to onset of pharmacologic effect and to peak effect of preparations of digoxin are shown in the table below.
Hemodynamic Effects: Short- and long-term therapy with the drug increases cardiac output and lowers pulmonary artery pressure, pulmonary capillary wedge pressure, and systemic vascular resistance in patients with heart failure. These hemodynamic effects are accompanied by an increase in the left ventricular ejection fraction and a decrease in end-systolic and end-diastolic dimensions.
ECG Changes: The use of therapeutic doses of digoxin may cause prolongation of thePR interval and depression of theST segment on the electrocardiogram. Digoxin may produce false positive ST-T changes on the electrocardiogram during exercise testing. These electrophysiologic effects are not indicative of toxicity. Digoxin does not significantly reduce heart rate during exercise.
## Pharmacokinetics
Distribution: Following drug administration, a 6 to 8 hour tissue distribution phase is observed. This is followed by a much more gradual decline in the serum concentration of the drug, which is dependent on the elimination of digoxin from the body. The peak height and slope of the early portion (absorption/distribution phases) of the serum concentration-time curve are dependent upon the route of administration and the absorption characteristics of the formulation. Clinical evidence indicates that the early high serum concentrations do not reflect the concentration of digoxin at its site of action, but that with chronic use, the steady-state post-distribution serum concentrations are in equilibrium with tissue concentrations and correlate with pharmacologic effects. In individual patients, these post-distribution serum concentrations may be useful in evaluating therapeutic and toxic effects.
Digoxin is concentrated in tissues and therefore has a large apparent volume of distribution (approximately 475 to 500 L). Digoxin crosses both the blood-brain barrier and the placenta. At delivery, the serum digoxin concentration in the newborn is similar to the serum concentration in the mother. Approximately 25% of digoxin in the plasma is bound to protein. Serum digoxin concentrations are not significantly altered by large changes in fat tissue weight, so that its distribution space correlates best with lean (i.e., ideal) body weight, not total body weight.
Metabolism: Only a small percentage (13%) of a dose of digoxin is metabolized in healthy volunteers. The urinary metabolites, which include dihydrodigoxin, digoxigenin bisdigitoxoside, and their glucuronide and sulfate conjugates are polar in nature and are postulated to be formed via hydrolysis, oxidation, and conjugation. The metabolism of digoxin is not dependent upon the cytochrome P-450 system, and digoxin is not known to induce or inhibit thecytochrome P-450 system.
Excretion: Elimination of digoxin follows first-order kinetics (that is, the quantity of digoxin eliminated at any time is proportional to the total body content). Following intravenous administration to healthy volunteers, 50 to 70% of a digoxin dose is excreted unchanged in the urine. Renal excretion of digoxin is proportional to creatinine clearance and is largely independent of urine flow. In healthy volunteers with normal renal function, digoxin has a half-life of 1.5 to 2 days. The half-life in anuric patients is prolonged to 3.5 to 5 days. Digoxin is not effectively removed from the body by dialysis, exchange transfusion, or during cardiopulmonary bypass because most of the drug is bound to extravascular tissues.
## Nonclinical Toxicology
Digoxin showed no genotoxic potential in in vitro studies (Ames test and mouse lymphoma). No data are available on the carcinogenic potential of digoxin, nor have studies been conducted to assess its potential to affect fertility.
# Clinical Studies
Two 12-week, double-blind, placebo-controlled studies enrolled 178 (RADIANCE trial) and 88 (PROVED trial) patients with NYHA class II or III heart failure previously treated with digoxin, a diuretic, and an ACE inhibitor (RADIANCE only) and randomized them to placebo or treatment with LANOXIN. Both trials demonstrated better preservation of exercise capacity in patients randomized to LANOXIN. Continued treatment with LANOXIN reduced the risk of developing worsening heart failure, as evidenced by heart failure-related hospitalizations and emergency care and the need for concomitant heart failure therapy.
The Digitalis Investigation Group (DIG) main trial was a 37-week, multicenter, randomized, double-blind mortality study comparing digoxin to placebo in 6800 adult patients with heart failure and left ventricular ejection fraction ≤0.45. At randomization, 67% were NYHA class I or II, 71% had heart failure of ischemic etiology, 44% had been receiving digoxin, and most were receiving a concomitant ACE inhibitor (94%) and diuretics (82%). As in the smaller trials described above, patients who had been receiving open-label digoxin were withdrawn from this treatment before randomization. Randomization to digoxin was again associated with a significant reduction in the incidence of hospitalization, whether scored as number of hospitalizations for heart failure (relative risk 75%), risk of having at least one such hospitalization during the trial (RR 72%), or number of hospitalizations for any cause (RR 94%). On the other hand, randomization to digoxin had no apparent effect on mortality (RR 99%, with confidence limits of 91 to 107%).
Digoxin has also been studied as a means of controlling the ventricular response to chronic atrial fibrillation in adults. Digoxin reduced the resting heart rate, but not the heart rate during exercise.
In 3 different randomized, double-blind trials that included a total of 315 adult patients, digoxin was compared to placebo for the conversion of recent-onset atrial fibrillation to sinus rhythm. Conversion was equally likely, and equally rapid, in the digoxin and placebo groups. In a randomized 120-patient trial comparing digoxin, sotalol, and amiodarone, patients randomized to digoxin had the lowest incidence of conversion to sinus rhythm, and the least satisfactory rate control when conversion did not occur.
In at least one study, digoxin was studied as a means of delaying reversion to atrial fibrillation in adult patients with frequent recurrence of this arrhythmia. This was a randomized, double-blind, 43-patient crossover study. Digoxin increased the mean time between symptomatic recurrent episodes by 54%, but had no effect on the frequency of fibrillatory episodes seen during continuous electrocardiographic monitoring.
# How Supplied
LANOXIN (digoxin) Tablets, Scored 125 mcg (0.125 mg): Bottles of 100 with child-resistant cap (NDC 24987-242-55), (NDC 24987-242-57) and 1,000 (NDC 24987-242-75), (NDC 24987-242-76); unit dose pack of 100 (NDC 24987-242-56). Imprinted with LANOXIN and Y3B (yellow).
LANOXIN (digoxin) Tablets, Scored 250 mcg (0.25 mg): Bottles of 100 with child-resistant cap (NDC 24987-249-55), (NDC 24987-249-57), 1,000 (NDC -24987-249-75), (NDC-24987-249-76), and 5,000 (NDC 24987-249-80); unit dose pack of 100 (NDC 24987-249-56). Imprinted with LANOXIN and X3A (white).
- National Drug Code (NDC): see above
- Manufactured by: Manufactured by DSM Pharmaceuticals, Inc. Greenville, NC 27834
- Distributed by:Covis Pharmaceuticals, Inc. Cary, NC 27511
Digoxin Injection, USP is available as:
500 mcg/2 mL (250 mcg/mL) ampuls packaged in 25s
- National Drug Code (NDC):(NDC 0641-1410-35)
- Manufactured by: HIKMA FARMACÊUTICA (PORTUGAL), S.A. Estrada do Rio da Mό, 8, 8A e 8B – Fervença – 2705-906 Terrugem SNT, PORTUGAL
- Distributed by:WEST-WARD PHARMACEUTICALS Eatontown, NJ 07724 USA
Digoxin Solution:Each 1 mL of clear, colorless Digoxin Oral Solution contains 0.05 mg (50 mcg).
The Digoxin Oral Solution bottles are to be used with the graduated droppers provided in the carton. Starting at 0.2 mL, this 1 mL dropper is marked in divisions of 0.1 mL, corresponding to 5 mcg or 0.005 mg of digoxin.
The calibrated dropper supplied with the 60 mL bottle of Digoxin Oral Solution is not appropriate to measure doses below 0.2 mL. Doses less than 0.2 mL require appropriate methods or measuring devices designed to administer an accurate amount to the patient, such as a graduated syringe
- National Drug Code (NDC):NDC:17856-0057
- Manufactured by:Roxane Laboratories, Inc. Columbus, Ohio 43216
- Distributed by:Atlantic Biologicals Corps
## Storage
- Storage: Store at 25°C (77°F); excursions permitted to 15 to 30°C (59 to 86°F) in a dry place.
- Keep out of reach of children.
- Storage: Store at 20˚-25˚C (68˚-77˚F), excursions permitted to 15˚-30˚C (59˚-86˚F).
- Storage:Store at 25°C (77°F); excursions permitted to 15° to 30°C (59° to 86°F). * Protect from light.
# Images
## Drug Images
## Package and Label Display Panel
# Patient Counseling Information
- Advise patients that digoxin is a cardiac glycoside used to treat heart failure and heart arrhythmias.
- Instruct patients to take this medication as directed by their physician.
- Advise patients that many drugs can interact with digoxin. Instruct patients to inform their doctor and pharmacist if they are taking any over the counter medications, including herbal *medication, or are started on a new prescription.
- Advise patient that blood tests will be necessary to ensure that their digoxin dose is appropriate for them.
- Advise patients to contact their doctor or a health care professional if they experience nausea, vomiting, persistent diarrhea, confusion, weakness, or visual disturbances (including *blurred vision, green-yellow color disturbances, halo effect) as these could be signs that the dose of digoxin may be too high.
- Advise parents or caregivers that the symptoms of having too high digoxin doses may be difficult to recognize in infants and pediatric patients. Symptoms such as weight loss, failure to thrive in infants, abdominal pain, and behavioral disturbances may be indications of digoxin toxicity.
- Suggest to the patient to monitor and record their heart rate and blood pressure daily.
- Instruct women of childbearing potential who become or are planning to become pregnant to consult a physician prior to initiation or continuing therapy with digoxin.
# Precautions with Alcohol
Alcohol-SandboxAlonso interaction has not been established. Talk to your doctor about the effects of taking alcohol with this medication.
# Brand Names
- Digoxin
- Digox
- Lanoxin
# Look-Alike Drug Names
- Digoxin — Dioxin
- Digoxin — Digitoxin
# Drug Shortage Status
Drug Shortage
# Price | https://www.wikidoc.org/index.php/Cardoxin | |
4a905144aeece4756e13f9930791f240c1ccbd8a | wikidoc | Carmine | Carmine
Carmine
Carmine (IPA: ]]), also called Crimson Lake, Cochineal, Natural Red 4, C.I. 75470 or E120, is a pigment of a bright red color obtained from the carminic acid produced by some scale insects, such as the cochineal and the Polish cochineal, and is used as a general term for a particularly deep red color. Carmine is used in the manufacture of artificial flowers, paints, rouge, cosmetics, food additives, and crimson ink.
# Production
Carmine may be prepared from cochineal, by boiling dried insects in water to extract the carminic acid and then treating the clear solution with alum, cream of tartar, stannous chloride, or potassium hydrogen oxalate; the coloring and animal matters present in the liquid are thus precipitated. Other methods are in use; sometimes egg white, fish glue, or gelatine are added before the precipitation.
The quality of carmine is affected by the temperature and the degree of illumination during its preparation, sunlight being requisite for the production of a brilliant hue. It differs also according to the amount of alumina present in it. It is sometimes adulterated with cinnabar, starch and other materials; from these the carmine can be separated by dissolving it in ammonia. Good carmine should crumble readily between the fingers when dry.
Carmine lake is a pigment obtained by adding freshly precipitated alumina to decoction of cochineal.
Carmine can be used as a staining agent in microbiology, as a Best's carmine to stain glycogen, mucicarmine to stain acidic mucopolysaccharides, and carmalum to stain cell nuclei. In these applications, it is applied together with a mordant, usually an Al(III) salt.
# Allergic reactions to carmine
Carmine is used as a food dye in many different products such as juice, ice cream, yogurt, and candies, eyeshadow, lipstick, etc. Although principally a red dye, it is found in many foods that are shades of red, pink, and purple. As a food dye it has been known to cause severe allergic reactions and anaphylactic shock in some people.
Food products containing carmine-based food dye may prove to be a concern for people who are allergic to carmine, or people who choose not consume any or certain animals, such as vegetarians, vegans, and followers of religions with dietary law (e.g. kashrut in Judaism and halaal in Islam).
# Local regulations for use of Carmine in foodstuffs
## In the United States
In the United States, Carmine is approved as dye for foodstuffs.
Carmine is not required by the FDA to be explicitly named in all ingredient lists, and may sometimes be represented under "natural coloring" or "added coloring." As of the end of January 2006, the FDA is evaluating a proposal that would require food products containing carmine to list it by name on the ingredient label. It was also announced that the FDA will separately review the ingredient labels of prescription drugs which contain colorings derived from carmine. A request from the Center for Science in the Public Interest Article titled: "FDA Urged to Improve Labeling of or Ban Carmine Food Coloring"
" TITLE 21--FOOD AND DRUGS
Although concerns over hazards from allergic reactions have been asserted, the United States Food and Drug Administration agency (FDA) has not banned the use of carmine and states it found no evidence of a "significant hazard" to the general population.
## In the European Union
In the European Union the use of carmine in foodstuffs is regulated under the European Commission's directives governing food additives in general (, ) and food dyes in particular () and listed under the names Cochineal, Carminic acid, Carmines and Natural Red 4 as additive E 120 in the list of EU-approved food additives (). The directive governing food dyes approves the use of carmine for certain groups of foodstuffs only (a list of approved uses is included in Annexes I and III of EU-Directive 94/36 ) and specifies a maximum amount which is permitted or restricts it to the quantum satis.
The EU-Directive 2000/13/EC on food labeling mandates that carmines (like all food additives) must be included in the list of ingredients of a food product with its additive category and listed name or additive number, that is either as Food colour carmines or as Food colour E 120 in the local language(s) of the market(s) the product is sold in.
Although concerns of hazards from allergic reactions were raised, the use of carmine in foodstuffs is not banned in the EU. However, the use of carmine in foodstuffs has been discouraged by european food safety authorities, and although it is predominately used as colouring in alcoholic beverages, it can still be found in foods such as supermarket Indian curries. A re-evaluation process of the approval status of several food colors (including carmine) was started by the Panel on food additives, flavourings, processing aids and materials in contact with food of the European Food Safety Authority in early 2006 and is scheduled to be completed by 2008 ( Accessed on 2 January 2007, ) | Carmine
Carmine
Carmine (IPA: [[[:Template:IPA]]]), also called Crimson Lake, Cochineal, Natural Red 4, C.I. 75470 or E120, is a pigment of a bright red color obtained from the carminic acid produced by some scale insects, such as the cochineal and the Polish cochineal, and is used as a general term for a particularly deep red color. Carmine is used in the manufacture of artificial flowers, paints, rouge, cosmetics, food additives, and crimson ink.
# Production
Carmine may be prepared from cochineal, by boiling dried insects in water to extract the carminic acid and then treating the clear solution with alum, cream of tartar, stannous chloride, or potassium hydrogen oxalate; the coloring and animal matters present in the liquid are thus precipitated. Other methods are in use; sometimes egg white, fish glue, or gelatine are added before the precipitation.
The quality of carmine is affected by the temperature and the degree of illumination during its preparation, sunlight being requisite for the production of a brilliant hue. It differs also according to the amount of alumina present in it. It is sometimes adulterated with cinnabar, starch and other materials; from these the carmine can be separated by dissolving it in ammonia. Good carmine should crumble readily between the fingers when dry.
Carmine lake is a pigment obtained by adding freshly precipitated alumina to decoction of cochineal.
Carmine can be used as a staining agent in microbiology, as a Best's carmine to stain glycogen, mucicarmine to stain acidic mucopolysaccharides, and carmalum to stain cell nuclei. In these applications, it is applied together with a mordant, usually an Al(III) salt.
# Allergic reactions to carmine
Carmine is used as a food dye in many different products such as juice, ice cream, yogurt, and candies, eyeshadow, lipstick, etc. Although principally a red dye, it is found in many foods that are shades of red, pink, and purple. As a food dye it has been known to cause severe allergic reactions and anaphylactic shock in some people[1].
Food products containing carmine-based food dye may prove to be a concern for people who are allergic to carmine, or people who choose not consume any or certain animals, such as vegetarians, vegans, and followers of religions with dietary law (e.g. kashrut in Judaism and halaal in Islam).
# Local regulations for use of Carmine in foodstuffs
## In the United States
In the United States, Carmine is approved as dye for foodstuffs.
Carmine is not required by the FDA to be explicitly named in all ingredient lists, and may sometimes be represented under "natural coloring" or "added coloring." As of the end of January 2006, the FDA is evaluating a proposal[1] that would require food products containing carmine to list it by name on the ingredient label. It was also announced that the FDA will separately review the ingredient labels of prescription drugs which contain colorings derived from carmine. A request from the Center for Science in the Public Interest Article titled: "FDA Urged to Improve Labeling of or Ban Carmine Food Coloring" http://www.cspinet.org/new/carmine_8_24_98.htm
" TITLE 21--FOOD AND DRUGS
[[2]]
Although concerns over hazards from allergic reactions have been asserted, the United States Food and Drug Administration agency (FDA) has not banned the use of carmine and states it found no evidence of a "significant hazard" to the general population.[3]
## In the European Union
In the European Union the use of carmine in foodstuffs is regulated under the European Commission's directives governing food additives in general ([4], [5]) and food dyes in particular ([6]) and listed under the names Cochineal, Carminic acid, Carmines and Natural Red 4 as additive E 120 in the list of EU-approved food additives ([7]). The directive governing food dyes approves the use of carmine for certain groups of foodstuffs only (a list of approved uses is included in Annexes I and III of EU-Directive 94/36 [8]) and specifies a maximum amount which is permitted or restricts it to the quantum satis.
The EU-Directive 2000/13/EC [9] on food labeling mandates that carmines (like all food additives) must be included in the list of ingredients of a food product with its additive category and listed name or additive number, that is either as Food colour carmines or as Food colour E 120 in the local language(s) of the market(s) the product is sold in.
Although concerns of hazards from allergic reactions were raised, the use of carmine in foodstuffs is not banned in the EU. However, the use of carmine in foodstuffs has been discouraged by european food safety authorities, and although it is predominately used as colouring in alcoholic beverages, it can still be found in foods such as supermarket Indian curries. A re-evaluation process of the approval status of several food colors (including carmine) was started by the Panel on food additives, flavourings, processing aids and materials in contact with food of the European Food Safety Authority in early 2006 and is scheduled to be completed by 2008 ([10] Accessed on 2 January 2007, [11]) | https://www.wikidoc.org/index.php/Carmine | |
c3f22de838ae42224c7e62cccaabb454e8cce7b4 | wikidoc | Caspase | Caspase
# Overview
Caspases are a family of calcium-dependent cysteine proteases, which play essential roles in apoptosis (programmed cell death), necrosis and inflammation.
Caspases are essential in cells for apoptosis, one of the main types of programmed cell death in development and most other stages of adult life, and have been termed "executioner" proteins for their roles in the cell. Some caspases are also required in the immune system for the maturation of cytokines. Failure of apoptosis is one of the main contributions to tumour development and autoimmune diseases; this coupled with the unwanted apoptosis that occurs with ischaemia or Alzheimer's disease, has boomed the interest in caspases as potential therapeutic targets since they were discovered in the mid 1990s.
They are called cysteine proteases, because they use a cysteine residue to cut those proteins, and are called caspases because the cysteine residue cleaves their substrate proteins at specific asparagine residues.
# Types of caspase proteins
Eleven caspases have so far been identified in humans. There are two types of apoptotic caspases: initiator (apical) caspases and effector (executioner) caspases.
- Initiator caspases (e.g. CASP2, CASP8, CASP9 and CASP10) cleave inactive pro-forms of effector caspases, thereby activating them.
- Effector caspases (e.g. CASP3, CASP6, CASP7) in turn cleave other protein substrates within the cell resulting in the apoptotic process. The initiation of this cascade reaction is regulated by caspase inhibitors.
CASP4 and CASP5, which are overexpressed in some cases of vitiligo and associated autoimmune diseases caused by NALP1 variants, are not currently classified as initiator or effector in Mesh. This is because they are inflammatory caspases, which in concert with CASP1, are involved in cytokine maturation. CASP14, is not involved in apoptosis or inflammation, but instead is involved in skin cell development.
# The caspase cascade
Caspases are regulated at a post-translational level, ensuring that they can be rapidly activated. They are first synthesized as inactive pro-caspases, that consist of a prodomain, a small subunit and a large subunit. Initiator caspases possess a longer prodomain than the effector caspases, whose prodomain is very small. The prodomain of the initiator caspases contain domains such as a CARD domain (e.g. caspases-2 and -9) or a death effector domain (DED) (caspases-8 and -10) that enables the caspases to interact with other molecules that regulate their activation. These molecules respond to stimuli which cause the clustering of the initiator caspases. This allows them to autoactivate, so that they can then proceed to activate the effector caspases.
The caspase cascade can be activated by :
- Granzyme B (released by cytotoxic T lymphocytes and NK cells) which is known to activate caspase-3 and -7
- death receptors (like FAS, TRAIL receptors and TNF receptor) which can activate caspase-8 and -10
- the apoptosome (regulated by cytochrome c and the Bcl-2 family) which activates caspase-9.
Some of the final targets of caspases include:
- nuclear lamins
- ICAD/DFF45 (Inhibitor of Caspase Activated DNase or DNA Fragmentation Factor 45)
- PARP (Poly(ADP) Ribose Polymerase)
- PAK2 (P21-Activated Kinase 2).
The exact contribution that the cleavage of many caspase substrates makes to the biochemistry and morphology of apoptosis is unclear. However, the function of ICAD/DFF45 is to restrain the enzyme CAD (Caspase Activated DNase). The cleavage and inactivation of ICAD/DFF45 by a caspase allows CAD to enter the nucleus and fragment the DNA, causing the characteristic 'DNA ladder' seen in apoptotic cells.
# Discovery of caspases, their functions and roles
The importance of caspases to apoptosis and programmed cell death was originally established by Robert Horvitz and colleagues who found that the ced-3 gene was required for the cell death that took place during the development of the nematode C. elegans. Horvitz and his colleague Junying Yuan found in 1993 that the protein encoded by the ced-3 gene was a cysteine protease with similar properties to the mammalian interleukin-1-beta converting enzyme (ICE) (now known as caspase 1) which at the time was the only known caspase. Following this discovery, the other mammalian caspases, in addition to caspases in other organisms such as the fruit fly Drosophila melanogaster, were soon identified and characterised. A consortium of researchers in the field decided upon the caspase nomenclature early in 1996, as in many instances a particular caspase had been identified simultaneously by more than one lab, who would each give the protein a different name (e.g. caspase 3 was variously known as CPP32, apopain and Yama). The caspases are numbered in the order in which they were identified, hence the renaming of ICE to caspase 1. Ironically, although ICE was the first mammalian caspase to be characterised due to its similarity to the nematode death gene ced-3, it seems that the principal role for this enzyme is in mediating inflammation rather than in cell death. For overviews of the discovery of not just caspases but other aspects of apoptosis see articles by Danial and Korsmeyer, Yuan and Horvitz, and by Li et al. in the January 23rd 2004 edition of the journal 'Cell'. However, more recent studies have demonstrated that caspase proteases are also critical regulators of nondeath functions, most notably involving the maturation of a wide variaty of cell types such as red blood cells and skeletal muscle myoblasts, | Caspase
# Overview
Caspases are a family of calcium-dependent cysteine proteases, which play essential roles in apoptosis (programmed cell death), necrosis and inflammation.
Caspases are essential in cells for apoptosis, one of the main types of programmed cell death in development and most other stages of adult life, and have been termed "executioner" proteins for their roles in the cell. Some caspases are also required in the immune system for the maturation of cytokines. Failure of apoptosis is one of the main contributions to tumour development and autoimmune diseases; this coupled with the unwanted apoptosis that occurs with ischaemia or Alzheimer's disease, has boomed the interest in caspases as potential therapeutic targets since they were discovered in the mid 1990s.
They are called cysteine proteases, because they use a cysteine residue to cut those proteins, and are called caspases because the cysteine residue cleaves their substrate proteins at specific asparagine residues.
# Types of caspase proteins
Eleven caspases have so far been identified in humans. There are two types of apoptotic caspases: initiator (apical) caspases and effector (executioner) caspases.
- Initiator caspases (e.g. CASP2, CASP8, CASP9 and CASP10) cleave inactive pro-forms of effector caspases, thereby activating them.
- Effector caspases (e.g. CASP3, CASP6, CASP7) in turn cleave other protein substrates within the cell resulting in the apoptotic process. The initiation of this cascade reaction is regulated by caspase inhibitors.
CASP4 and CASP5, which are overexpressed in some cases of vitiligo and associated autoimmune diseases caused by NALP1 variants,[1] are not currently classified as initiator or effector in Mesh. This is because they are inflammatory caspases, which in concert with CASP1, are involved in cytokine maturation. CASP14, is not involved in apoptosis or inflammation, but instead is involved in skin cell development.
# The caspase cascade
Caspases are regulated at a post-translational level, ensuring that they can be rapidly activated. They are first synthesized as inactive pro-caspases, that consist of a prodomain, a small subunit and a large subunit. Initiator caspases possess a longer prodomain than the effector caspases, whose prodomain is very small. The prodomain of the initiator caspases contain domains such as a CARD domain (e.g. caspases-2 and -9) or a death effector domain (DED) (caspases-8 and -10) that enables the caspases to interact with other molecules that regulate their activation. These molecules respond to stimuli which cause the clustering of the initiator caspases. This allows them to autoactivate, so that they can then proceed to activate the effector caspases.
The caspase cascade can be activated by :
- Granzyme B (released by cytotoxic T lymphocytes and NK cells) which is known to activate caspase-3 and -7
- death receptors (like FAS, TRAIL receptors and TNF receptor) which can activate caspase-8 and -10
- the apoptosome (regulated by cytochrome c and the Bcl-2 family) which activates caspase-9.
Some of the final targets of caspases include:
- nuclear lamins
- ICAD/DFF45 (Inhibitor of Caspase Activated DNase or DNA Fragmentation Factor 45)
- PARP (Poly(ADP) Ribose Polymerase)
- PAK2 (P21-Activated Kinase 2).
The exact contribution that the cleavage of many caspase substrates makes to the biochemistry and morphology of apoptosis is unclear. However, the function of ICAD/DFF45 is to restrain the enzyme CAD (Caspase Activated DNase). The cleavage and inactivation of ICAD/DFF45 by a caspase allows CAD to enter the nucleus and fragment the DNA, causing the characteristic 'DNA ladder' seen in apoptotic cells.
# Discovery of caspases, their functions and roles
The importance of caspases to apoptosis and programmed cell death was originally established by Robert Horvitz and colleagues who found that the ced-3 gene was required for the cell death that took place during the development of the nematode C. elegans. Horvitz and his colleague Junying Yuan [2]found in 1993 that the protein encoded by the ced-3 gene was a cysteine protease with similar properties to the mammalian interleukin-1-beta converting enzyme (ICE) (now known as caspase 1) which at the time was the only known caspase. Following this discovery, the other mammalian caspases, in addition to caspases in other organisms such as the fruit fly Drosophila melanogaster, were soon identified and characterised. A consortium of researchers in the field decided upon the caspase nomenclature early in 1996, as in many instances a particular caspase had been identified simultaneously by more than one lab, who would each give the protein a different name (e.g. caspase 3 was variously known as CPP32, apopain and Yama). The caspases are numbered in the order in which they were identified, hence the renaming of ICE to caspase 1. Ironically, although ICE was the first mammalian caspase to be characterised due to its similarity to the nematode death gene ced-3, it seems that the principal role for this enzyme is in mediating inflammation rather than in cell death. For overviews of the discovery of not just caspases but other aspects of apoptosis see articles by Danial and Korsmeyer,[3] Yuan and Horvitz,[4] and by Li et al.[5] in the January 23rd 2004 edition of the journal 'Cell'. However, more recent studies have demonstrated that caspase proteases are also critical regulators of nondeath functions, most notably involving the maturation of a wide variaty of cell types such as red blood cells and skeletal muscle myoblasts, | https://www.wikidoc.org/index.php/Caspase | |
6fd166c95a05fccbe3bc97642feeb4a85b6e2ee3 | wikidoc | Casting | Casting
Casting is a manufacturing process by which a liquid material is (usually) poured into a mold, which contains a hollow cavity of the desired shape, and then allowed to solidify. The solid casting is then ejected or broken out to complete the process. Casting may be used to form hot liquid metals or various materials that cold set after mixing of components (such as epoxies, concrete, plaster and clay). Casting is most often used for making complex shapes that would be otherwise difficult or uneconomical to make by other methods.
Casting is a 6000 year old process. The oldest surviving casting is a copper frog from 3200 BC.
The casting process is subdivided into two distinct subgroups: expendable and non-expendable mold casting.
# Expendable mold casting
Expendable mold casting is a generic classification that includes sand, plastic, shell, plaster, and investment (lost-wax technique) moldings. This method of mold casting involves the use of temporary, non-reusable molds.
## Waste molding of plaster
A durable plaster intermediate is often used as a stage toward the production of a bronze sculpture or as a pointing guide for the creation of a carved stone. With the completion of a plaster, the work is more durable (if stored indoors) than a clay original which must be kept moist to avoid cracking. With the low cost plaster at hand, the expensive work of bronze casting or stone carving may be deferred until a prosperous patron is found, and as such work is considered to be a technical, rather than artistic process, it may even be deferred beyond the lifetime of the artist.
In waste molding a simple and thin plaster mold, reinforced by sisal or burlap, is cast over the original clay mixture. When cured, it is then removed from the damp clay, incidentally destroying the fine details in undercuts present in the clay, but which are now captured in the mold. The mold may then at any later time (but only once) be used to cast a plaster positive image, identical to the original clay. The surface of this "plaster" may be further refined and may be painted and waxed to resemble a finished bronze casting.
## Sand casting
Sand casting is one of the most popular and simplest types of casting that has been used for centuries. Sand casting allows for smaller batches to be made compared to permanent mold casting and at a very reasonable cost. Not only does this method allow manufacturers to create products at a low cost, but there are other benefits to sand casting, such as very small size operations. From castings that fit in the palm of your hand to train beds (one casting can create the entire bed for one rail car), it can all be done with sand casting. Sand casting also allows most metals to be cast depending on the type of sand used for the molds.
Sand casting requires a lead time of days for production at high output rates (1-20 pieces/hr-mold) and is unsurpassed for large-part production. Green (moist) sand has almost no part weight limit, whereas dry sand has a practical part mass limit of 2300-2700 kg. Minimum part weight ranges from 0.075-0.1 kg. The sand is bonded together using clays (as in green sand) or chemical binders, or polymerized oils (such as motor oil). Sand can be recycled many times in most operations and requires little additional input.
## Plaster casting (of metals)
Plaster casting is similar to sand molding except that plaster is substituted for sand. Plaster compound is actually composed of 70-80% gypsum and 20-30% strengthener and water. Generally, the form takes less than a week to prepare, after which a production rate of 1-10 units/hr-mold is achieved, with items as massive as 45 kg and as small as 30 g with very high surface resolution and fine tolerances. Parts that are typically made by plaster casting are lock components, gears, valves, fittings, tooling, and ornaments. Plaster casting is an inexpensive alternative to other molding processes due to the low cost of the plaster and the mold production. It may be disadvantageous, however, because the mold quality is dependent on several factors, "including consistency of the plaster molding composition, mold pouring procedures, and plaster curing techniques." If these factors are not closely monitored, the mold can result in distorted dimensions, shrinking upon drying and poor mold surfaces.
Once used and cracked away, normal plaster cannot easily be recast. Plaster casting is normally used for non-ferrous metals such as aluminium-, zinc-, or copper-based alloys. It cannot be used to cast ferrous material because sulfur in gypsum slowly reacts with iron. The plaster itself cannot stand temperatures above 1200oC, which also limits the materials to be cast in plaster. Prior to mold preparation the pattern is sprayed with a thin film of parting compound to prevent the mold from sticking to the pattern. The unit is shaken, so plaster fills the small cavities around the pattern. The plaster sets, usually in about 15 minutes, and the pattern is removed. The plaster is dried at temperatures between 120o and 260oC. The mold is preheated and the molten metal poured in.
Plaster casting represents a step up in sophistication and requires skill. The automatic functions are easily handed over to robots, yet the higher-precision pattern designs required demand even higher levels of direct human assistance.
## Casting of plaster, concrete, or plastic resin
Plaster itself may be cast, as can other chemical setting materials such as concrete or plastic resin - either using single-use waste molds as noted above or multiple-use piece molds, or molds made of small ridged pieces or of flexible material such as latex rubber (which is in turn supported by an exterior mold). When casting plaster or concrete, the finished product is, unlike marble, relatively unattractive, lacking in transparency, and so it is usually painted, often in ways that give the appearance of metal or stone. Alternatively, the first layers cast may contain colored sand so as to give an appearance of stone. By casting concrete, rather than plaster, it is possible to create sculptures, fountains, or seating for outdoor use. A simulation of high-quality marble may be made using certain chemically-set plastic resins (for example epoxy or polyester) with powdered stone added for coloration, often with multiple colors worked in. The latter is a common means of making attractive washstands, washstand tops and shower stalls, with the skilled working of multiple colors resulting in simulated staining patterns as is often found in natural marble or travertine.
## Shell molding
Shell molding is also similar to sand molding except that a mixture of sand and 3-6% resin holds the grains together. Shell molding also uses sand with a much smaller grain than green-sand. Set-up and production of shell mold patterns takes weeks, after which an output of 5-50 pieces/hr-mold is attainable. Aluminium and magnesium products average about 13.5 kg as a normal limit, but it is possible to cast items in the 45-90 kg range. Shell mold walling varies from 3-10 mm thick, depending on the forming time of the resin.
Shell molding is used for small parts that require high precision. Some examples include gear housings, cylinder heads and connecting rods. It is also used to make high-precision molding cores. This process makes it so complex parts can be cast with less labor.
There are a dozen different stages in shell mold processing that include:
- Initially preparing a metal-matched plate
- Mixing resin and sand
- Heating pattern, usually to between 505-550 K
- Inverting the pattern (the sand is at one end of a box and the pattern at the other, and the box is inverted for a time determined by the desired thickness of the mill)
- Curing shell and baking it
- Removing investment
- Inserting cores
- Repeating for other half
- Assembling mold
- Pouring mold
- Removing casting
- Cleaning and trimming.
The sand-resin mix can be recycled by burning off the resin at high temperatures.
## Investment casting
Investment casting (known as lost-wax casting in art) is a process that has been practised for thousands of years, with the lost-wax process being one of the oldest known metal forming techniques. From 5000 years ago, when bees wax formed the pattern, to today’s high technology waxes, refractory materials and specialist alloys, the castings, ensure high-quality components are produced with the key benefits of accuracy, repeatability, versatility and integrity.
Investment casting derives its name from the fact that the pattern is invested, or surrounded, with a refractory material. The wax patterns require extreme care for they are not strong enough to withstand forces encountered during the mold making. One advantage of investment casting it that the wax can be reused.
The process is suitable for repeatable production of net shape components, from a variety of different metals and high performance alloys. Although generally used for small castings, this process has been used to produce complete aircraft door frames, with steel castings of up to 300 kg and aluminium castings of up to 30 kg. Compared to other casting processes such as die casting or sand casting, it can be an expensive process, however the components that can be produced using investment casting can incorporate intricate contours, and in most cases the components are cast near net shape, so requiring little or no rework once cast.
# Non-expendable mold casting
Non-expendable mold casting differs from expendable processes in that the mold need not be reformed after each production cycle. This technique includes at least four different methods: permanent, die, centrifugal, and continuous casting.
## Permanent mold casting
Permanent mold casting (typically for non-ferrous metals) requires a set-up time on the order of weeks to prepare a steel tool, after which production rates of 5-50 pieces/hr-mold are achieved with an upper mass limit of 9 kg per iron alloy item (cf., up to 135 kg for many nonferrous metal parts) and a lower limit of about 0.1 kg. Steel cavities are coated with a refractory wash of acetylene soot before processing to allow easy removal of the workpiece and promote longer tool life. Permanent molds have a limited life before wearing out. Worn molds require either refinishing or replacement. Cast parts from a permanent mold generally show 20% increase in tensile strength and 30% increase in elongation as compared to the products of sand casting.
The only necessary input is the coating applied regularly. Typically, permanent mold casting is used in forming iron, aluminum, magnesium, and copper based alloys. The process is highly automated.
## Die casting
Die casting is the process of forcing molten metal under high pressure into mold cavities (which are machined into dies). Most die castings are made from nonferrous metals, specifically zinc, copper, and aluminum based alloys, but ferrous metal die castings are possible. The die casting method is especially suited for applications where many small to medium sized parts are needed with good detail, a fine surface quality and dimensional consistency.
## Centrifugal casting
Centrifugal casting is both gravity- and pressure-independent since it creates its own force feed using a temporary sand mold held in a spinning chamber at up to 900 N (90 g). Lead time varies with the application. Semi- and true-centrifugal processing permit 30-50 pieces/hr-mold to be produced, with a practical limit for batch processing of approximately 9000 kg total mass with a typical per-item limit of 2.3-4.5 kg.
Industrially, the centrifugal casting of railway wheels was an early application of the method developed by German industrial company Krupp and this capability enabled the rapid growth of the enterprise.
Small art pieces such as jewelry are often cast by this method using the lost wax process, as the forces enable the rather viscous liquid metals to flow through very small passages and into fine details such as leaves and petals. This effect is similar to the benefits from vacuum casting, also applied to jewelry casting.
## Continuous casting
Continuous casting is a refinement of the casting process for the continuous, high-volume production of metal sections with a constant cross-section. Molten metal is poured into an open-ended, water-cooled copper mold, which allows a 'skin' of solid metal to form over the still-liquid centre. The strand, as it is now called, is withdrawn from the mold and passed into a chamber of rollers and water sprays; the rollers support the thin skin of the strand while the sprays remove heat from the strand, gradually solidifying the strand from the outside in. After solidification, predetermined lengths of the strand are cut off by either mechanical shears or travelling oxyacetylene torches and transferred to further forming processes, or to a stockpile. Cast sizes can range from strip (a few millimetres thick by about five metres wide) to billets (90 to 160 mm square) to slabs (1.25 m wide by 230 mm thick). Sometimes, the strand may undergo an initial hot rolling process before being cut.
Continuous casting is used due to the lower costs associated with continuous production of a standard product, and also increases the quality of the final product. Metals such as steel, copper and aluminium are continuously cast, with steel being the metal with the greatest tonnages cast using this method.
# Cooling rate
The rate at which a casting cools affects its microstructure, quality, and properties.
The cooling rate is largely controlled by the molding media used for making the mold. When the molten metal is poured into the mold, the cooling down begins. This happens because the heat within the molten metal flows into the relatively cooler parts of the mold. Molding materials transfer heat from the casting into the mold at different rates. For example, some molds made of plaster may transfer heat very slowly, while a mold made entirely of steel would transfer the heat very fast. This cooling down ends with (solidification) where the liquid metal turns to solid metal.
At its basic level a foundry may pour a casting without regard to controlling how the casting cools down and the metal freezes within the mold. However, if proper planning is not done the result can be gas porosities and shrink porosities within the casting. To improve the quality of a casting and engineer how it is made, the foundry engineer studies the geometry of the part and plans how the heat removal should be controlled.
Where heat should be removed quickly, the engineer will plan the mold to include special heat sinks to the mold, called chills. Fins may also be designed on a casting to extract heat, which are later removed in the cleaning (also called fettling) procees. Both methods may be used at local spots in a mold where the heat will be extracted quickly.
Where heat should be removed slowly, a riser or some padding may be added to a casting. A riser is an additional larger cast piece which will cool more slowly than the place where is it attached to the casting.
Generally speaking, an area of the casting which is cooled quickly will have a fine grain structure and an area which cools slowly will have a coarse grain structure.
# Shrinkage
Castings shrink when they cool. Like nearly all materials, metals are less dense as a liquid than a solid. During solidification (freezing), the metal density dramatically increases. This results in a volume decrease for the metal in a mold. Solidification shrinkage is the term used for this contraction. Cooling from the freezing temperature to room temperature also involves a contraction. The easiest way to explain this contraction is that is the reverse of thermal expansion. Compensation for this natural phenomenon must be considered in two ways.
## Solidification shrinkage
The shrinkage caused by solidification can leave cavities in a casting, weakening it. Risers provide additional material to the casting as it solidifies. The riser (sometimes called a "feeder") is designed to solidify later than the part of the casting to which it is attached. Thus the liquid metal in the riser will flow into the solidifying casting and feed it until the casting is completely solid. In the riser itself there will be a cavity showing where the metal was fed. Risers add cost because some of their material must be removed, by cutting away from the casting which will be shipped to the customer. They are often necessary to produce parts which are free of internal shrinkage voids. One method that assists in keeping the metal molten in the riser longer is the utilisation of an exothermic sleeve.
Sometimes, to promote directional solidification, chills must be used in the mold. A chill is any material which will conduct heat away from the casting more rapidly that the material used for molding. Thus if silica sand is used for molding, a chill may be made of copper, iron, aluminum, graphite, zircon sand, chromite or any other material with the ability to remove heat faster locally from the casting. All castings solidify with progressive solidification but in some designs a chill is used to control the rate and sequence of solidification of the casting.
## Patternmaker's shrink (thermal contraction)
Shrinkage after solidification can be dealt with by using an oversized pattern designed for the relevant alloy. Pattern makers use special "contraction rulers" (also called "shrink rules") to make the patterns used by the foundry to make castings to the design size required. These rulers are 1 - 6% oversize, depending on the material to be cast. These rulers are mainly referred to by their actual changes to the size. For example a 1/100 ruler would add 1 mm to 100 mm if measured by a "standard ruler" (hence being called a 1/100 contraction ruler). Using such a ruler during pattern making will ensure an oversize pattern. Thus, the mold is larger also, and when the molten metal solidifies it will shrink and the casting will be the size required by the design, if measured by a standard ruler. A pattern made to match an existing part would be made as follows: First, the existing part would be measured using a standard ruler, then when constructing the pattern, the pattern maker would use a contraction ruler, ensuring that the casting would contract to the correct size. | Casting
Template:Otheruses1
Casting is a manufacturing process by which a liquid material is (usually) poured into a mold, which contains a hollow cavity of the desired shape, and then allowed to solidify. The solid casting is then ejected or broken out to complete the process. Casting may be used to form hot liquid metals or various materials that cold set after mixing of components (such as epoxies, concrete, plaster and clay). Casting is most often used for making complex shapes that would be otherwise difficult or uneconomical to make by other methods.
Casting is a 6000 year old process.[1] The oldest surviving casting is a copper frog from 3200 BC.[1]
The casting process is subdivided into two distinct subgroups: expendable and non-expendable mold casting.
# Expendable mold casting
Expendable mold casting is a generic classification that includes sand, plastic, shell, plaster, and investment (lost-wax technique) moldings. This method of mold casting involves the use of temporary, non-reusable molds.
## Waste molding of plaster
A durable plaster intermediate is often used as a stage toward the production of a bronze sculpture or as a pointing guide for the creation of a carved stone. With the completion of a plaster, the work is more durable (if stored indoors) than a clay original which must be kept moist to avoid cracking. With the low cost plaster at hand, the expensive work of bronze casting or stone carving may be deferred until a prosperous patron is found, and as such work is considered to be a technical, rather than artistic process, it may even be deferred beyond the lifetime of the artist.
In waste molding a simple and thin plaster mold, reinforced by sisal or burlap, is cast over the original clay mixture. When cured, it is then removed from the damp clay, incidentally destroying the fine details in undercuts present in the clay, but which are now captured in the mold. The mold may then at any later time (but only once) be used to cast a plaster positive image, identical to the original clay. The surface of this "plaster" may be further refined and may be painted and waxed to resemble a finished bronze casting.
## Sand casting
Sand casting is one of the most popular and simplest types of casting that has been used for centuries. Sand casting allows for smaller batches to be made compared to permanent mold casting and at a very reasonable cost. Not only does this method allow manufacturers to create products at a low cost, but there are other benefits to sand casting, such as very small size operations. From castings that fit in the palm of your hand to train beds (one casting can create the entire bed for one rail car), it can all be done with sand casting. Sand casting also allows most metals to be cast depending on the type of sand used for the molds.[2]
Sand casting requires a lead time of days for production at high output rates (1-20 pieces/hr-mold) and is unsurpassed for large-part production. Green (moist) sand has almost no part weight limit, whereas dry sand has a practical part mass limit of 2300-2700 kg. Minimum part weight ranges from 0.075-0.1 kg. The sand is bonded together using clays (as in green sand) or chemical binders, or polymerized oils (such as motor oil). Sand can be recycled many times in most operations and requires little additional input.
## Plaster casting (of metals)
Plaster casting is similar to sand molding except that plaster is substituted for sand. Plaster compound is actually composed of 70-80% gypsum and 20-30% strengthener and water. Generally, the form takes less than a week to prepare, after which a production rate of 1-10 units/hr-mold is achieved, with items as massive as 45 kg and as small as 30 g with very high surface resolution and fine tolerances. Parts that are typically made by plaster casting are lock components, gears, valves, fittings, tooling, and ornaments.[3] Plaster casting is an inexpensive alternative to other molding processes due to the low cost of the plaster and the mold production. It may be disadvantageous, however, because the mold quality is dependent on several factors, "including consistency of the plaster molding composition, mold pouring procedures, and plaster curing techniques."[4] If these factors are not closely monitored, the mold can result in distorted dimensions, shrinking upon drying and poor mold surfaces.
Once used and cracked away, normal plaster cannot easily be recast. Plaster casting is normally used for non-ferrous metals such as aluminium-, zinc-, or copper-based alloys. It cannot be used to cast ferrous material because sulfur in gypsum slowly reacts with iron. The plaster itself cannot stand temperatures above 1200oC, which also limits the materials to be cast in plaster. Prior to mold preparation the pattern is sprayed with a thin film of parting compound to prevent the mold from sticking to the pattern. The unit is shaken, so plaster fills the small cavities around the pattern. The plaster sets, usually in about 15 minutes, and the pattern is removed. The plaster is dried at temperatures between 120o and 260oC. The mold is preheated and the molten metal poured in. [3]
Plaster casting represents a step up in sophistication and requires skill. The automatic functions are easily handed over to robots, yet the higher-precision pattern designs required demand even higher levels of direct human assistance.
## Casting of plaster, concrete, or plastic resin
Plaster itself may be cast, as can other chemical setting materials such as concrete or plastic resin - either using single-use waste molds as noted above or multiple-use piece molds, or molds made of small ridged pieces or of flexible material such as latex rubber (which is in turn supported by an exterior mold). When casting plaster or concrete, the finished product is, unlike marble, relatively unattractive, lacking in transparency, and so it is usually painted, often in ways that give the appearance of metal or stone. Alternatively, the first layers cast may contain colored sand so as to give an appearance of stone. By casting concrete, rather than plaster, it is possible to create sculptures, fountains, or seating for outdoor use. A simulation of high-quality marble may be made using certain chemically-set plastic resins (for example epoxy or polyester) with powdered stone added for coloration, often with multiple colors worked in. The latter is a common means of making attractive washstands, washstand tops and shower stalls, with the skilled working of multiple colors resulting in simulated staining patterns as is often found in natural marble or travertine.
## Shell molding
Shell molding is also similar to sand molding except that a mixture of sand and 3-6% resin holds the grains together. Shell molding also uses sand with a much smaller grain than green-sand. Set-up and production of shell mold patterns takes weeks, after which an output of 5-50 pieces/hr-mold is attainable. Aluminium and magnesium products average about 13.5 kg as a normal limit, but it is possible to cast items in the 45-90 kg range. Shell mold walling varies from 3-10 mm thick, depending on the forming time of the resin.
Shell molding is used for small parts that require high precision. Some examples include gear housings, cylinder heads and connecting rods. It is also used to make high-precision molding cores. This process makes it so complex parts can be cast with less labor.
There are a dozen different stages in shell mold processing that include:
- Initially preparing a metal-matched plate
- Mixing resin and sand
- Heating pattern, usually to between 505-550 K
- Inverting the pattern (the sand is at one end of a box and the pattern at the other, and the box is inverted for a time determined by the desired thickness of the mill)
- Curing shell and baking it
- Removing investment
- Inserting cores
- Repeating for other half
- Assembling mold
- Pouring mold
- Removing casting
- Cleaning and trimming.
The sand-resin mix can be recycled by burning off the resin at high temperatures.
## Investment casting
Investment casting (known as lost-wax casting in art) is a process that has been practised for thousands of years, with the lost-wax process being one of the oldest known metal forming techniques. From 5000 years ago, when bees wax formed the pattern, to today’s high technology waxes, refractory materials and specialist alloys, the castings, ensure high-quality components are produced with the key benefits of accuracy, repeatability, versatility and integrity.
Investment casting derives its name from the fact that the pattern is invested, or surrounded, with a refractory material. The wax patterns require extreme care for they are not strong enough to withstand forces encountered during the mold making. One advantage of investment casting it that the wax can be reused.[5]
The process is suitable for repeatable production of net shape components, from a variety of different metals and high performance alloys. Although generally used for small castings, this process has been used to produce complete aircraft door frames, with steel castings of up to 300 kg and aluminium castings of up to 30 kg. Compared to other casting processes such as die casting or sand casting, it can be an expensive process, however the components that can be produced using investment casting can incorporate intricate contours, and in most cases the components are cast near net shape, so requiring little or no rework once cast.
# Non-expendable mold casting
Non-expendable mold casting differs from expendable processes in that the mold need not be reformed after each production cycle. This technique includes at least four different methods: permanent, die, centrifugal, and continuous casting.
## Permanent mold casting
Permanent mold casting (typically for non-ferrous metals) requires a set-up time on the order of weeks to prepare a steel tool, after which production rates of 5-50 pieces/hr-mold are achieved with an upper mass limit of 9 kg per iron alloy item (cf., up to 135 kg for many nonferrous metal parts) and a lower limit of about 0.1 kg. Steel cavities are coated with a refractory wash of acetylene soot before processing to allow easy removal of the workpiece and promote longer tool life. Permanent molds have a limited life before wearing out. Worn molds require either refinishing or replacement. Cast parts from a permanent mold generally show 20% increase in tensile strength and 30% increase in elongation as compared to the products of sand casting.
The only necessary input is the coating applied regularly. Typically, permanent mold casting is used in forming iron, aluminum, magnesium, and copper based alloys. The process is highly automated.
## Die casting
Die casting is the process of forcing molten metal under high pressure into mold cavities (which are machined into dies). Most die castings are made from nonferrous metals, specifically zinc, copper, and aluminum based alloys, but ferrous metal die castings are possible. The die casting method is especially suited for applications where many small to medium sized parts are needed with good detail, a fine surface quality and dimensional consistency.[6]
## Centrifugal casting
Centrifugal casting is both gravity- and pressure-independent since it creates its own force feed using a temporary sand mold held in a spinning chamber at up to 900 N (90 g). Lead time varies with the application. Semi- and true-centrifugal processing permit 30-50 pieces/hr-mold to be produced, with a practical limit for batch processing of approximately 9000 kg total mass with a typical per-item limit of 2.3-4.5 kg.
Industrially, the centrifugal casting of railway wheels was an early application of the method developed by German industrial company Krupp and this capability enabled the rapid growth of the enterprise.
Small art pieces such as jewelry are often cast by this method using the lost wax process, as the forces enable the rather viscous liquid metals to flow through very small passages and into fine details such as leaves and petals. This effect is similar to the benefits from vacuum casting, also applied to jewelry casting.
## Continuous casting
Continuous casting is a refinement of the casting process for the continuous, high-volume production of metal sections with a constant cross-section. Molten metal is poured into an open-ended, water-cooled copper mold, which allows a 'skin' of solid metal to form over the still-liquid centre. The strand, as it is now called, is withdrawn from the mold and passed into a chamber of rollers and water sprays; the rollers support the thin skin of the strand while the sprays remove heat from the strand, gradually solidifying the strand from the outside in. After solidification, predetermined lengths of the strand are cut off by either mechanical shears or travelling oxyacetylene torches and transferred to further forming processes, or to a stockpile. Cast sizes can range from strip (a few millimetres thick by about five metres wide) to billets (90 to 160 mm square) to slabs (1.25 m wide by 230 mm thick). Sometimes, the strand may undergo an initial hot rolling process before being cut.
Continuous casting is used due to the lower costs associated with continuous production of a standard product, and also increases the quality of the final product. Metals such as steel, copper and aluminium are continuously cast, with steel being the metal with the greatest tonnages cast using this method.
# Cooling rate
The rate at which a casting cools affects its microstructure, quality, and properties.
The cooling rate is largely controlled by the molding media used for making the mold. When the molten metal is poured into the mold, the cooling down begins. This happens because the heat within the molten metal flows into the relatively cooler parts of the mold. Molding materials transfer heat from the casting into the mold at different rates. For example, some molds made of plaster may transfer heat very slowly, while a mold made entirely of steel would transfer the heat very fast. This cooling down ends with (solidification) where the liquid metal turns to solid metal.
At its basic level a foundry may pour a casting without regard to controlling how the casting cools down and the metal freezes within the mold. However, if proper planning is not done the result can be gas porosities and shrink porosities within the casting. To improve the quality of a casting and engineer how it is made, the foundry engineer studies the geometry of the part and plans how the heat removal should be controlled.
Where heat should be removed quickly, the engineer will plan the mold to include special heat sinks to the mold, called chills. Fins may also be designed on a casting to extract heat, which are later removed in the cleaning (also called fettling) procees. Both methods may be used at local spots in a mold where the heat will be extracted quickly.
Where heat should be removed slowly, a riser or some padding may be added to a casting. A riser is an additional larger cast piece which will cool more slowly than the place where is it attached to the casting.
Generally speaking, an area of the casting which is cooled quickly will have a fine grain structure and an area which cools slowly will have a coarse grain structure.
# Shrinkage
Castings shrink when they cool. Like nearly all materials, metals are less dense as a liquid than a solid. During solidification (freezing), the metal density dramatically increases. This results in a volume decrease for the metal in a mold. Solidification shrinkage is the term used for this contraction. Cooling from the freezing temperature to room temperature also involves a contraction. The easiest way to explain this contraction is that is the reverse of thermal expansion. Compensation for this natural phenomenon must be considered in two ways.
## Solidification shrinkage
The shrinkage caused by solidification can leave cavities in a casting, weakening it. Risers provide additional material to the casting as it solidifies. The riser (sometimes called a "feeder") is designed to solidify later than the part of the casting to which it is attached. Thus the liquid metal in the riser will flow into the solidifying casting and feed it until the casting is completely solid. In the riser itself there will be a cavity showing where the metal was fed. Risers add cost because some of their material must be removed, by cutting away from the casting which will be shipped to the customer. They are often necessary to produce parts which are free of internal shrinkage voids. One method that assists in keeping the metal molten in the riser longer is the utilisation of an exothermic sleeve. http://www.gw-svr-a.org.uk/4566_castings.html
Sometimes, to promote directional solidification, chills must be used in the mold. A chill is any material which will conduct heat away from the casting more rapidly that the material used for molding. Thus if silica sand is used for molding, a chill may be made of copper, iron, aluminum, graphite, zircon sand, chromite or any other material with the ability to remove heat faster locally from the casting. All castings solidify with progressive solidification but in some designs a chill is used to control the rate and sequence of solidification of the casting.
## Patternmaker's shrink (thermal contraction)
Shrinkage after solidification can be dealt with by using an oversized pattern designed for the relevant alloy. Pattern makers use special "contraction rulers" (also called "shrink rules") to make the patterns used by the foundry to make castings to the design size required. These rulers are 1 - 6% oversize, depending on the material to be cast. These rulers are mainly referred to by their actual changes to the size. For example a 1/100 ruler would add 1 mm to 100 mm if measured by a "standard ruler" (hence being called a 1/100 contraction ruler). Using such a ruler during pattern making will ensure an oversize pattern. Thus, the mold is larger also, and when the molten metal solidifies it will shrink and the casting will be the size required by the design, if measured by a standard ruler. A pattern made to match an existing part would be made as follows: First, the existing part would be measured using a standard ruler, then when constructing the pattern, the pattern maker would use a contraction ruler, ensuring that the casting would contract to the correct size. | https://www.wikidoc.org/index.php/Casting | |
c597c5d8f376c4ebd16fe0dc3864235451cb4f0e | wikidoc | Cat flu | Cat flu
Cat flu is feline upper respiratory tract disease. It is generally a misnomer since it usually does not refer to an infection by an influenza virus. Instead it is a syndrome: a term meaning any flu-like respiratory disease in a cat. The signs of this disease may be caused by one or more of several different infectious agents (pathogens):
- Official name of causitive agent - (a related more common term)
- Feline viral rhinotracheitis - (cat common cold)
- Feline calicivirus - (cat respiratory disease)
- Bordetella bronchiseptica - (cat kennel cough)
- H5N1 (cat avian flu) (see Global spread of H5N1#Felidae (cats))
# Sources and notes
- Control Cat Flu (future-of-vaccination.co.uk)
- Feline upper respiratory tract disease - Cat Flu (fabcats.org)
# Further reading
- Cat Health (sniksnak.com)
- Cat Care Vaccination (cats.org.uk)
- Cat Flu (yorkcats.org.uk)
- Cat Flu (ae18.com)
de:Katzenschnupfen
nl:niesziekte | Cat flu
Cat flu is feline upper respiratory tract disease. It is generally a misnomer since it usually does not refer to an infection by an influenza virus. Instead it is a syndrome: a term meaning any flu-like respiratory disease in a cat. The signs of this disease may be caused by one or more of several different infectious agents (pathogens):
- Official name of causitive agent - (a related more common term)
- Feline viral rhinotracheitis - (cat common cold)
- Feline calicivirus - (cat respiratory disease)
- Bordetella bronchiseptica - (cat kennel cough)
- H5N1 (cat avian flu) (see Global spread of H5N1#Felidae (cats))
# Sources and notes
- Control Cat Flu (future-of-vaccination.co.uk)
- Feline upper respiratory tract disease - Cat Flu (fabcats.org)
# Further reading
- Cat Health (sniksnak.com)
- Cat Care Vaccination (cats.org.uk)
- Cat Flu (yorkcats.org.uk)
- Cat Flu (ae18.com)
Template:Veterinary-med-stub
de:Katzenschnupfen
nl:niesziekte | https://www.wikidoc.org/index.php/Cat_flu | |
d90506a609256fe75fc08ef883a242762b541a9d | wikidoc | Catador | Catador
A Catador (Plural: Catadores) is a Cigar taster/tester in Cuba.
As part of their quality control, cigar factories employ a team to test a random selection of each Torcedor's (Cigar roller) production, so every week the work of each torcedor will have been blind tested.
A Catador will only smoke a small portion of each cigar, and will score each cigar on a scale From Poor to Excellent on the following:
- Appearance and construction
- Aroma
- Burn
- Draw
- Consistency
- Strength
- Flavour
- Quality
In any single session, they will test between 3 and 5 cigars and only drink unsweetened black tea between each cigar tested. The majority of the tests take place in mornings only. | Catador
A Catador (Plural: Catadores) is a Cigar taster/tester in Cuba.
As part of their quality control, cigar factories employ a team to test a random selection of each Torcedor's (Cigar roller) production, so every week the work of each torcedor will have been blind tested.
A Catador will only smoke a small portion of each cigar, and will score each cigar on a scale From Poor to Excellent on the following:
- Appearance and construction
- Aroma
- Burn
- Draw
- Consistency
- Strength
- Flavour
- Quality
In any single session, they will test between 3 and 5 cigars and only drink unsweetened black tea between each cigar tested. The majority of the tests take place in mornings only. | https://www.wikidoc.org/index.php/Catador | |
5a1e962552671b7fb58d6ab8726a32b9c561f4bb | wikidoc | Catechu | Catechu
Catechu (also known as cutch, cashoo, or Japan earth) is an extract of any of several species of Acacia—but especially Acacia catechu—produced by boiling the wood in water and evaporating the resulting brew.
Catechu (called katha in Hindi) is an astringent and has been used since ancient times in Ayurvedic medicine as well as in breath-freshening spice mixtures. Black Catechu has recently also been utilized by Blavod Drinks Ltd. to dye their vodka black.
Also called cutch, it is a brown dye used for tanning and dyeing and for preserving fishing nets and sails.
White cutch, also known as gambier, gambeer, or gambir, has the same uses. | Catechu
Catechu (also known as cutch, cashoo, or Japan earth) is an extract of any of several species of Acacia—but especially Acacia catechu—produced by boiling the wood in water and evaporating the resulting brew.
Catechu (called katha in Hindi) is an astringent and has been used since ancient times in Ayurvedic medicine as well as in breath-freshening spice mixtures. Black Catechu has recently also been utilized by Blavod Drinks Ltd. to dye their vodka black. [1]
Also called cutch, it is a brown dye used for tanning and dyeing and for preserving fishing nets and sails.
White cutch, also known as gambier, gambeer, or gambir, has the same uses.
# External links
- An OCR'd version of the US Dispensatory by Remington and Wood, 1918.
br:Gwez-kachou
de:Gerber-Akazie
eo:Kateĉuo
ta:காசுக்கட்டி
Template:Alt-med-stub | https://www.wikidoc.org/index.php/Catechu | |
0bf3947d6a89f3f634e93b9251dba3deefe5e372 | wikidoc | Cathine | Cathine
# Overview
Cathine (β-hydroxyamphetamine) is a monoamine alkaloid found in the shrub Catha edulis (khat).
# Pharmacology
Closely related to ephedrine, cathinone and other amphetamines, it may contribute to the stimulant effect of Catha edulis, although another constituent, cathinone appears to show stronger activity. Cathine is one of the optical isomers of phenylpropanolamine, an appetite suppressant and decongestant which is possibly associated with an increased risk of hemorrhagic stroke.
# Regulation
The World Anti-Doping Agency's list of prohibited substances (used for the Olympic Games among other athletic events) bars cathine in concentrations of over 5 micrograms per milliliter in urine. Cathine is a Schedule III drug under the Convention on Psychotropic Substances. In the United States, it is classified as a Schedule IV controlled substance.
In Hong Kong, Cathine is regulated under Schedule 1 of Hong Kong's Chapter 134 Dangerous Drugs Ordinance. It can only be used legally by health professionals and for university research purporses. The substance can be given by pharmacists under a prescription. Anyone who supplies the substance without prescription can be fined $10000(HKD). The penalty for trafficking or manufacturing the substance is a $5,000,000 (HKD) fine and life imprisonment. Possession of the substance for consumption without license from the Department of Health is illegal with a $1,000,000 (HKD) fine and/or 7 years of jail time. | Cathine
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
# Overview
Cathine (β-hydroxyamphetamine) is a monoamine alkaloid found in the shrub Catha edulis (khat).
# Pharmacology
Closely related to ephedrine, cathinone and other amphetamines, it may contribute to the stimulant effect of Catha edulis, although another constituent, cathinone appears to show stronger activity. Cathine is one of the optical isomers of phenylpropanolamine, an appetite suppressant and decongestant which is possibly associated with an increased risk of hemorrhagic stroke.
# Regulation
The World Anti-Doping Agency's list of prohibited substances (used for the Olympic Games among other athletic events) bars cathine in concentrations of over 5 micrograms per milliliter in urine. Cathine is a Schedule III drug under the Convention on Psychotropic Substances.[1] In the United States, it is classified as a Schedule IV controlled substance.
In Hong Kong, Cathine is regulated under Schedule 1 of Hong Kong's Chapter 134 Dangerous Drugs Ordinance. It can only be used legally by health professionals and for university research purporses. The substance can be given by pharmacists under a prescription. Anyone who supplies the substance without prescription can be fined $10000(HKD). The penalty for trafficking or manufacturing the substance is a $5,000,000 (HKD) fine and life imprisonment. Possession of the substance for consumption without license from the Department of Health is illegal with a $1,000,000 (HKD) fine and/or 7 years of jail time. | https://www.wikidoc.org/index.php/Cathine | |
71bb646db81d9fb97629dda7a87012a9de5d45a1 | wikidoc | Cathode | Cathode
A cathode is an electrode through which (positive) electric current flows out of a polarized electrical device. Mnemonic: CCD (Cathode Current Departs).
To dispel a common misconception, often incorrectly inferred from the correct fact that in all electrochemical devices positively charged cations move towards the cathode and/or negatively charged anions move away from it, cathode polarity is not always negative but depends on the device type, and sometimes even in which mode it operates, as determined by the above current direction based universal definition. Examples:
- In a discharging battery or galvanic cell (drawing) the cathode is the positive terminal, where conventional current flows out. This outwards current is carried internally by positive ions moving from the electrolyte to the positive cathode (chemical energy is responsible for this "uphill" motion). It is continued externally by electrons moving inwards, negative charge moving one way amounting to positive current flowing the other way.
- In a recharging battery, or an electrolytic cell, the cathode is the negative terminal, which sends current back to the external generator.
- In a diode, it is the negative terminal at the pointed end of the arrow symbol, where current flows out of the device. Note electrode naming for diodes is always based on the direction of the forward current (that of the arrow, in which the current flows "most easily"), even for types such as zener diodes or solar cells where the current of interest is the reverse current.
- In a cathode ray tube, it is the negative terminal where electrons flow in, i.e., where current flows out of the device.
An electrode through which current flows the other way (into the device) is termed an anode.
# Etymology
The word was coined in 1834 from the Greek κάθοδος (kathodos), 'descent' or 'way down', by William Whewell, who had been consulted by Michael Faraday over some new names needed to complete a paper on the recently discovered process of electrolysis. In that paper Faraday explained that when an electrolytic cell is oriented so that electric current traverses the "decomposing body" (electrolyte) in a direction "from East to West, or, which will strengthen this help to the memory, that in which the sun appears to move", the cathode is where the current leaves the electrolyte, on the West side: "kata downwards, `odos a way ; the way which the sun sets" (, reprinted in ).
The use of 'West' to mean the 'out' direction (actually 'out' → 'West' → 'sunset' → 'down') may appear unnecessarily contrived. Previously, as related in the first reference cited above, Faraday had used the more straightforward term "exode" (the doorway where the current exits). His motivation for changing it to something meaning 'the West electrode' (other candidates had been "westode", "occiode" and "dysiode") was to make it immune to a possible later change in the direction convention for current, whose exact nature was not known at the time. The reference he used to this effect was the Earth's magnetic field direction, which at that time was believed to be invariant. He fundamentally defined his arbitrary orientation for the cell as being that in which the internal current would run parallel to and in the same direction as a hypothetical magnetizing current loop around the local line of latitude which would induce a magnetic dipole field oriented like the Earth's. This made the internal current East to West as previously mentioned, but in the event of a later convention change it would have become West to East, so that the West electrode would not have been the 'way out' any more. Therefore "exode" would have become inappropriate, whereas "cathode" meaning 'West electrode' would have remained correct with respect to the unchanged direction of the actual phenomenon underlying the current, then unknown but, he thought, unambiguously defined by the magnetic reference. In retrospect the name change was unfortunate, not only because the Greek roots alone do not reveal the cathode's function any more, but more importantly because, as we now know, the Earth's magnetic field direction on which the "cathode" term is based is subject to reversals whereas the current direction convention on which the "exode" term was based has no reason to change in the future.
Since the later discovery of the electron an easier to remember, and more durably correct technically although historically false etymology has been suggested: cathode, from the Greek kathodos, 'way down', 'the way (down) into the cell (or other device) for electrons'.
# Flow of electrons
The flow of electrons is always from anode to cathode outside of the cell or device, regardless of the cell or device type and operating mode, with the exception of diodes where electrode naming always assumes current flows in the forward direction (that of the arrow symbol), i.e., electrons flow in the opposite direction, even when the diode reverse-conducts either by accident (breakdown of a normal diode) or by design (breakdown of a Zener diode, photo-current of a photodiode or solar cell).
# Chemistry cathode
In chemistry, a cathode is the (negative or positive, depending on whether the cell is electrolytic or galvanic) electrode of an electrochemical cell at which reduction occurs (electrons are added to cations to complete the valence shell or bond). The cathode supplies electrons to the positively charged cations which flow to it from the electrolyte (even if the cell is galvanic, i.e., when the cathode is positive and therefore would be expected to repel the positively charged cations; this is due to electrode potential relative to the electrolyte solution being different for the anode and cathode metal/electrolyte systems in a galvanic cell).
## Electrolytic cell
In an electrolytic cell, the cathode is where the negative polarity is applied to drive the cell. Common results of reduction at the cathode are hydrogen gas or pure metal from metal ions.
## Galvanic cell
In a galvanic cell, the cathode is where the positive pole is connected to allow the circuit to be completed: as the anode of the galvanic cell gives off electrons, they return from the circuit into the cell through the cathode.
## Electroplating metal cathode
When metal ions are reduced from ionic solution onto the cathode, they form a pure metal surface on the cathode. Items to be plated with pure metal are attached to and become part of the cathode in the electrolytic solution.
# Electronics and physics cathode
In physics or electronics, a cathode is an electrode that emits electrons into the device.
## Vacuum tubes
In a vacuum tube or electronic vacuum system, the cathode emits free electrons. Electrons are extracted from metal electrodes either by heating the electrode, causing thermionic emission, or by applying a strong electric field and causing field emission. Electrons can also be emitted from the electrodes of certain metals when light of frequency greater than the threshold frequency falls on it. This effect is called photoelectric emission.
## Cold cathodes and hot cathodes
Cathodes used for field emission in vacuum tubes are called cold cathodes. Heated electrodes or hot cathodes, frequently called filaments, are much more common. Most radios and television sets prior to the 1970s used filament-heated-cathode electron tubes for signal selection and processing; to this day, a hot cathode forms the source of the electron beam(s) in cathode ray tubes in many television sets and computer monitors. Hot electron emitters are also used as the electrodes in fluorescent lamps and in the source tubes of X-ray machines.
## Diodes
In a semiconductor diode, the cathode is the N–doped layer of the PN junction. Initially, the N-doped layer supplies electrons to flow into the junction (N-doped for negative charge carriers). The electrons given by the N-doped layer combine with 'holes' supplied from the P-doped layer. The electrons and holes combining create a 'depleted' zone at the junction, leaving behind in the cathode a thin layer of positive ions which gives a base positive charge to the junction's cathode side of the device. (The anode side has a base negative charge at the junction, since it supplied 'holes' to the recombinant region and the doped ions have one electron more than their full valence shell of electrons). As a negative charge is applied to the cathode from the circuit external to the diode, more N-doped ions are able to supply electrons to the recombinant region and the diode becomes conductive, which allows electrons to flow though the diode from the cathode to the anode (electrons flow from the N-doped to the P-doped side when the bias is overcome). Like a typical diode, there is a fixed anode and cathode in a zener diode, but it will conduct current in the reverse direction (electrons from anode to cathode) if its breakdown or Zener voltage is exceeded. | Cathode
A cathode is an electrode through which (positive) electric current flows out of a polarized electrical device. Mnemonic: CCD (Cathode Current Departs).
To dispel a common misconception, often incorrectly inferred from the correct fact that in all electrochemical devices positively charged cations move towards the cathode and/or negatively charged anions move away from it, cathode polarity is not always negative but depends on the device type, and sometimes even in which mode it operates, as determined by the above current direction based universal definition. Examples:
- In a discharging battery or galvanic cell (drawing) the cathode is the positive terminal, where conventional current flows out. This outwards current is carried internally by positive ions moving from the electrolyte to the positive cathode (chemical energy is responsible for this "uphill" motion). It is continued externally by electrons moving inwards, negative charge moving one way amounting to positive current flowing the other way.
- In a recharging battery, or an electrolytic cell, the cathode is the negative terminal, which sends current back to the external generator.
- In a diode, it is the negative terminal at the pointed end of the arrow symbol, where current flows out of the device. Note electrode naming for diodes is always based on the direction of the forward current (that of the arrow, in which the current flows "most easily"), even for types such as zener diodes or solar cells where the current of interest is the reverse current.
- In a cathode ray tube, it is the negative terminal where electrons flow in, i.e., where current flows out of the device.
An electrode through which current flows the other way (into the device) is termed an anode.
# Etymology
The word was coined in 1834 from the Greek κάθοδος (kathodos), 'descent' or 'way down', by William Whewell, who had been consulted[1] by Michael Faraday over some new names needed to complete a paper on the recently discovered process of electrolysis. In that paper Faraday explained that when an electrolytic cell is oriented so that electric current traverses the "decomposing body" (electrolyte) in a direction "from East to West, or, which will strengthen this help to the memory, that in which the sun appears to move", the cathode is where the current leaves the electrolyte, on the West side: "kata downwards, `odos a way ; the way which the sun sets" ([2], reprinted in [3]).
The use of 'West' to mean the 'out' direction (actually 'out' → 'West' → 'sunset' → 'down') may appear unnecessarily contrived. Previously, as related in the first reference cited above, Faraday had used the more straightforward term "exode" (the doorway where the current exits). His motivation for changing it to something meaning 'the West electrode' (other candidates had been "westode", "occiode" and "dysiode") was to make it immune to a possible later change in the direction convention for current, whose exact nature was not known at the time. The reference he used to this effect was the Earth's magnetic field direction, which at that time was believed to be invariant. He fundamentally defined his arbitrary orientation for the cell as being that in which the internal current would run parallel to and in the same direction as a hypothetical magnetizing current loop around the local line of latitude which would induce a magnetic dipole field oriented like the Earth's. This made the internal current East to West as previously mentioned, but in the event of a later convention change it would have become West to East, so that the West electrode would not have been the 'way out' any more. Therefore "exode" would have become inappropriate, whereas "cathode" meaning 'West electrode' would have remained correct with respect to the unchanged direction of the actual phenomenon underlying the current, then unknown but, he thought, unambiguously defined by the magnetic reference. In retrospect the name change was unfortunate, not only because the Greek roots alone do not reveal the cathode's function any more, but more importantly because, as we now know, the Earth's magnetic field direction on which the "cathode" term is based is subject to reversals whereas the current direction convention on which the "exode" term was based has no reason to change in the future.
Since the later discovery of the electron an easier to remember, and more durably correct technically although historically false etymology has been suggested: cathode, from the Greek kathodos, 'way down', 'the way (down) into the cell (or other device) for electrons'.
# Flow of electrons
The flow of electrons is always from anode to cathode outside of the cell or device, regardless of the cell or device type and operating mode, with the exception of diodes where electrode naming always assumes current flows in the forward direction (that of the arrow symbol), i.e., electrons flow in the opposite direction, even when the diode reverse-conducts either by accident (breakdown of a normal diode) or by design (breakdown of a Zener diode, photo-current of a photodiode or solar cell).
# Chemistry cathode
In chemistry, a cathode is the (negative or positive, depending on whether the cell is electrolytic or galvanic) electrode of an electrochemical cell at which reduction occurs (electrons are added to cations to complete the valence shell or bond). The cathode supplies electrons to the positively charged cations which flow to it from the electrolyte (even if the cell is galvanic, i.e., when the cathode is positive and therefore would be expected to repel the positively charged cations; this is due to electrode potential relative to the electrolyte solution being different for the anode and cathode metal/electrolyte systems in a galvanic cell).
## Electrolytic cell
In an electrolytic cell, the cathode is where the negative polarity is applied to drive the cell. Common results of reduction at the cathode are hydrogen gas or pure metal from metal ions.
## Galvanic cell
In a galvanic cell, the cathode is where the positive pole is connected to allow the circuit to be completed: as the anode of the galvanic cell gives off electrons, they return from the circuit into the cell through the cathode.
## Electroplating metal cathode
When metal ions are reduced from ionic solution onto the cathode, they form a pure metal surface on the cathode. Items to be plated with pure metal are attached to and become part of the cathode in the electrolytic solution.
# Electronics and physics cathode
In physics or electronics, a cathode is an electrode that emits electrons into the device.
## Vacuum tubes
In a vacuum tube or electronic vacuum system, the cathode emits free electrons. Electrons are extracted from metal electrodes either by heating the electrode, causing thermionic emission, or by applying a strong electric field and causing field emission. Electrons can also be emitted from the electrodes of certain metals when light of frequency greater than the threshold frequency falls on it. This effect is called photoelectric emission.
## Cold cathodes and hot cathodes
Cathodes used for field emission in vacuum tubes are called cold cathodes. Heated electrodes or hot cathodes, frequently called filaments, are much more common. Most radios and television sets prior to the 1970s used filament-heated-cathode electron tubes for signal selection and processing; to this day, a hot cathode forms the source of the electron beam(s) in cathode ray tubes in many television sets and computer monitors. Hot electron emitters are also used as the electrodes in fluorescent lamps and in the source tubes of X-ray machines.
## Diodes
In a semiconductor diode, the cathode is the N–doped layer of the PN junction. Initially, the N-doped layer supplies electrons to flow into the junction (N-doped for negative charge carriers). The electrons given by the N-doped layer combine with 'holes' supplied from the P-doped layer. The electrons and holes combining create a 'depleted' zone at the junction, leaving behind in the cathode a thin layer of positive ions which gives a base positive charge to the junction's cathode side of the device. (The anode side has a base negative charge at the junction, since it supplied 'holes' to the recombinant region and the doped ions have one electron more than their full valence shell of electrons). As a negative charge is applied to the cathode from the circuit external to the diode, more N-doped ions are able to supply electrons to the recombinant region and the diode becomes conductive, which allows electrons to flow though the diode from the cathode to the anode (electrons flow from the N-doped to the P-doped side when the bias is overcome). Like a typical diode, there is a fixed anode and cathode in a zener diode, but it will conduct current in the reverse direction (electrons from anode to cathode) if its breakdown or Zener voltage is exceeded. | https://www.wikidoc.org/index.php/Cathode | |
802bd6f26e177bd0210bcc26e33a0b23f4f6634f | wikidoc | Catuaba | Catuaba
The name catuaba is used for the infusions of the bark of a number of trees native to Brazil. The most widely used barks are derived from the trees Trichilia catigua and Erythroxylum vacciniifolium. Other catuaba preparations use the bark of trees from the following genera or families : Anemopaegma, Ilex, Micropholis, Phyllanthus, Secondatia, Tetragastris and species from the Myrtaceae.
It is often claimed that catuaba is derived from the tree Erythroxylum catuaba, but this tree has been only described once, (in 1904), and it is not known today to what tree this name referred. The name E. catuaba is therefore not a recognised species (Kletter et al; 2004).
Local synonyms are Chuchuhuasha, Tatuaba, Pau de Reposta, Piratancara and Caramuru. A commercial liquid preparation, Catuama, contains multiple ingredients, one of these being catuaba from Trichilia catigua.
An infusion of the bark is used in traditional Brazilian medicine as an aphrodisiac and central nervous system stimulant. These claims have not been confirmed in scientific studies, but a journalist for the Discovery Channel claims that "reports in scientific journals and at conferences have supported use for sexual enhancement. In catuaba, a group of three alkaloids dubbed catuabine A, B and C are believed to enhance sexual function by stimulating the nervous system"
A study by Manabe et al. (1992) showed that catuaba extracts from Trichilia catigua were useful in preventing potentially lethal bacterial infections and HIV infection in mice.
Catuaba bark and preparations are sold as aphrodisiacs and remedies for erectile dysfunction in health food stores and through online retailers. | Catuaba
The name catuaba is used for the infusions of the bark of a number of trees native to Brazil. The most widely used barks are derived from the trees Trichilia catigua and Erythroxylum vacciniifolium. Other catuaba preparations use the bark of trees from the following genera or families : Anemopaegma, Ilex, Micropholis, Phyllanthus, Secondatia, Tetragastris and species from the Myrtaceae.
It is often claimed that catuaba is derived from the tree Erythroxylum catuaba, but this tree has been only described once, (in 1904), and it is not known today to what tree this name referred. The name E. catuaba is therefore not a recognised species (Kletter et al; 2004).
Local synonyms are Chuchuhuasha, Tatuaba, Pau de Reposta, Piratancara and Caramuru. A commercial liquid preparation, Catuama, contains multiple ingredients, one of these being catuaba from Trichilia catigua.
An infusion of the bark is used in traditional Brazilian medicine as an aphrodisiac and central nervous system stimulant. These claims have not been confirmed in scientific studies, but a journalist for the Discovery Channel claims that "reports in scientific journals and at conferences have supported [catuaba's] use for sexual enhancement. In catuaba, a group of three alkaloids dubbed catuabine A, B and C are believed to enhance sexual function by stimulating the nervous system"
A study by Manabe et al. (1992) showed that catuaba extracts from Trichilia catigua were useful in preventing potentially lethal bacterial infections and HIV infection in mice.
Catuaba bark and preparations are sold as aphrodisiacs and remedies for erectile dysfunction in health food stores and through online retailers. | https://www.wikidoc.org/index.php/Catuaba | |
a5c3787aded1c2da0648e807856b123464c41511 | wikidoc | Celgene | Celgene
Celgene Corporation Template:Nasdaq is a manufacturer of drug therapies for cancer and inflammatory disorders. It is incorporated in Delaware and headquartered in Summit, New Jersey. As of January 1, 2007, the company had 1,287 full-time employees, 725 of whom were engaged primarily in research and development activities. The company's major products are THALOMID® (thalidomide), which is approved for the acute treatment of the cutaneous manifestations of moderate to severe erythema nodosum leprosum ("ENL"), as well as in combination with dexamethasone for patients with newly diagnosed multiple myeloma, and REVLIMID® (lenalidomide), for which the company has received FDA and EMEA approval in combination with dexamethasone for the treatment of multiple myeloma patients who have received at least one prior therapy. REVLIMID® is also approved in the United States for the treatment of patients with transfusion-dependent anemia due to Low- or Intermediate-1-risk MDS associated with a deletion 5q cytogenetic abnormality with or without additional cytogenetic abnormalities. Both THALOMID® and REVLIMID® are sold through proprietary risk-management distribution programs to ensure safe and appropriate use of these pharmaceuticals. Celgene also receives royalties from Novartis Pharma AG on sales of the entire RITALIN® family of drugs, which are widely used to treat Attention Deficit Hyperactivity Disorder (ADHD).
Celgene Cellular Therapeutics, a subsidiary, is a public cord blood bank.
# History
In 1986, Celgene, originally a unit of the Celanese Corporation, was spun off as an independent company following the merger of Celanese Corporation with American Hoechst Corporation.
In July 1998, Celgene received approval from the FDA to market THALOMID® for the acute treatment of the cutaneous manifestations of moderate to severe ENL.
In April 2000, Celgene reached an agreement with Novartis Pharma AG to license d-MPH, Celgene's chirally pure version of RITALIN®. The FDA subsequently granted approval to market d-MPH, or FOCALIN®, in November 2001.
In August 2000, Celgene acquired Signal Pharmaceuticals, Inc., a privately held company that searches for and develops pharmaceuticals that regulate disease-related genes. Signal Pharmaceuticals, Inc. now operates as Celgene Research San Diego, a wholly owned subsidiary of Celgene Corporation.
In December 2002, Celgene acquired Anthrogenesis, a privately held New Jersey-based biotherapeutics company and cord blood banking business, which is developing technology for the recovery of stem cells from placental tissues following the completion of full-term successful pregnancies. Anthrogenesis now operates as Celgene Cellular Therapeutics, a wholly owned subsidiary of Celgene.
In December 2005, Celgene received approval from the FDA to market REVLIMID® for the treatment of patients with transfusion-dependent anemia due to Low- or Intermediate-1-risk MDS associated with a deletion 5q cytogenetic abnormality with or without additional cytogenetic abnormalities.
In May 2006, Celgene received approval for THALOMID® in combination with dexamethasone for the treatment of patients with newly diagnosed multiple myeloma.
In June 2007, Celgene received full marketing authorization for REVLIMID® in combination with dexamethasone as a treatment for patients with multiple myeloma who have received at least one prior therapy by the European Commission.
# Products | Celgene
Template:Infobox Company
Celgene Corporation Template:Nasdaq is a manufacturer of drug therapies for cancer and inflammatory disorders. It is incorporated in Delaware and headquartered in Summit, New Jersey. As of January 1, 2007, the company had 1,287 full-time employees, 725 of whom were engaged primarily in research and development activities.[1] The company's major products are THALOMID® (thalidomide), which is approved for the acute treatment of the cutaneous manifestations of moderate to severe erythema nodosum leprosum ("ENL"), as well as in combination with dexamethasone for patients with newly diagnosed multiple myeloma, and REVLIMID® (lenalidomide), for which the company has received FDA and EMEA approval in combination with dexamethasone for the treatment of multiple myeloma patients who have received at least one prior therapy. REVLIMID® is also approved in the United States for the treatment of patients with transfusion-dependent anemia due to Low- or Intermediate-1-risk MDS associated with a deletion 5q cytogenetic abnormality with or without additional cytogenetic abnormalities. Both THALOMID® and REVLIMID® are sold through proprietary risk-management distribution programs to ensure safe and appropriate use of these pharmaceuticals. Celgene also receives royalties from Novartis Pharma AG on sales of the entire RITALIN® family of drugs, which are widely used to treat Attention Deficit Hyperactivity Disorder (ADHD).
Celgene Cellular Therapeutics, a subsidiary, is a public cord blood bank.
# History
In 1986, Celgene, originally a unit of the Celanese Corporation, was spun off as an independent company following the merger of Celanese Corporation with American Hoechst Corporation.
In July 1998, Celgene received approval from the FDA to market THALOMID® for the acute treatment of the cutaneous manifestations of moderate to severe ENL.
In April 2000, Celgene reached an agreement with Novartis Pharma AG to license d-MPH, Celgene's chirally pure version of RITALIN®. The FDA subsequently granted approval to market d-MPH, or FOCALIN®, in November 2001.
In August 2000, Celgene acquired Signal Pharmaceuticals, Inc., a privately held company that searches for and develops pharmaceuticals that regulate disease-related genes. Signal Pharmaceuticals, Inc. now operates as Celgene Research San Diego, a wholly owned subsidiary of Celgene Corporation.
In December 2002, Celgene acquired Anthrogenesis, a privately held New Jersey-based biotherapeutics company and cord blood banking business, which is developing technology for the recovery of stem cells from placental tissues following the completion of full-term successful pregnancies. Anthrogenesis now operates as Celgene Cellular Therapeutics, a wholly owned subsidiary of Celgene.
In December 2005, Celgene received approval from the FDA to market REVLIMID® for the treatment of patients with transfusion-dependent anemia due to Low- or Intermediate-1-risk MDS associated with a deletion 5q cytogenetic abnormality with or without additional cytogenetic abnormalities.
In May 2006, Celgene received approval for THALOMID® in combination with dexamethasone for the treatment of patients with newly diagnosed multiple myeloma.
In June 2007, Celgene received full marketing authorization for REVLIMID® in combination with dexamethasone as a treatment for patients with multiple myeloma who have received at least one prior therapy by the European Commission.
# Products | https://www.wikidoc.org/index.php/Celgene | |
d2380ebb293ce8969847481ca2ac444bf0554e3e | wikidoc | Celsius | Celsius
# Overview
The Celsius temperature scale (previously known as the centigrade scale). The degree Celsius (symbol: °C) can refer to a specific temperature on the Celsius scale as well as serve as unit increment to indicate a temperature interval (a difference between two temperatures or an uncertainty). “Celsius” is named after the Swedish astronomer Anders Celsius (1701 – 1744), who developed a similar temperature scale two years before his death.
From 1744 until 1954, 0 °C on the Celsius scale was defined as the melting point of ice and 100 °C was defined as the boiling point of water under a pressure of one standard atmosphere; this close equivalency is taught in schools today. However, the unit “degree Celsius” and the Celsius scale are currently, by international agreement, defined by two different points: absolute zero, and the triple point of specially prepared water. This definition also precisely relates the Celsius scale to the Kelvin scale, which is the SI base unit of temperature (symbol: K). Absolute zero—the temperature at which no energy remains in a substance—is defined as being precisely 0 K and −273.15 °C. The triple point of water is defined as being precisely 273.16 K and 0.01 °C.
This definition fixes the magnitude of both the degree Celsius and the unit kelvin as being precisely 1 part in 273.16 parts the difference between absolute zero and the triple point of water. Thus, it sets the magnitude of one degree Celsius and the kelvin to be exactly equivalent. Additionally, it establishes the difference between the two scales’ null points as being precisely 273.15 degrees Celsius (−273.15 °C = 0 K and 0.01 °C = 273.16 K).
Some key temperatures relating the Celsius scale to other temperature scales are shown in the table below.
# History
In 1742, Anders Celsius (1701 – 1744) created a "reversed" version of the modern Celsius temperature scale whereby zero represented the boiling point of water and one hundred represented the freezing point of water. In his paper Observations of two persistent degrees on a thermometer, he recounted his experiments showing that ice’s melting point was effectively unaffected by pressure. He also determined with remarkable precision how water’s boiling point varied as a function of atmospheric pressure. He proposed that zero on his temperature scale (water’s boiling point) would be calibrated at the mean barometric pressure at mean sea level. This pressure is known as one standard atmosphere. In 1954, Resolution 4 of the 10th CGPM (the General Conference on Weights and Measures) established internationally that one standard atmosphere was a pressure equivalent to 1,013,250 dynes per cm2 (101.325 kPa).
In 1744, coincident with the death of Anders Celsius, the famous Swedish botanist Carolus Linnaeus (1707 – 1778) effectively reversed Celsius’s scale upon receipt of his first thermometer featuring a scale where zero represented the melting point of ice and 100 represented water’s boiling point. His custom-made “linnaeus-thermometer,” for use in his greenhouses, was made by Daniel Ekström, Sweden’s leading maker of scientific instruments at the time and whose workshop was located in the basement of the Stockholm observatory. As often happened in this age before modern communications, numerous physicists, scientists, and instrument makers are credited with having independently developed this same scale; among them were Pehr Elvius, the secretary of the Royal Swedish Academy of Sciences (which had an instrument workshop) and with whom Linnaeus had been corresponding; Christian of Lyons; Daniel Ekström, the instrument maker; and Mårten Strömer (1707 – 1770) who had studied astronomy under Anders Celsius.
The first known document reporting temperatures in this modern “forward” Celsius scale is the paper Hortus Upsaliensis dated 16 December 1745 that Linnaeus wrote to a student of his, Samuel Nauclér. In it, Linnaeus recounted the temperatures inside the orangery at the Botanical Garden of Uppsala University:
"... since the caldarium (the hot part of the greenhouse) by the angle of the windows, merely from the rays of the sun, obtains such heat that the thermometer often reaches 30 degrees, although the keen gardener usually takes care not to let it rise to more than 20 to 25 degrees, and in winter not under 15 degrees ..."
For the next 204 years, the scientific and thermometry communities world-wide referred to this scale as the “centigrade scale”. Temperatures on the centigrade scale were often reported simply as “degrees” or, when greater specificity was desired, “degrees centigrade”. The symbol for temperature values on this scale was °C (in several formats over the years). Because the term “centigrade” was also the Spanish and French language name for a unit of angular measurement (one-hundredth of a right angle) and had a similar connotation in other languages, the term “centesimal degree” was used when very precise, unambiguous language was required by international standards bodies such as the Bureau international des poids et mesures (BIPM). The 9th CGPM (Conférence générale des poids et mesures) and the CIPM (Comité international des poids et mesures) formally adopted “degree Celsius” (symbol: °C) in 1948. For lay-people worldwide — including school textbooks — the full transition from centigrade to Celsius is far from complete, with centigrade still the commonly used term in many communities.
In modern days the word "degrees" is often omitted: for example, on the BBC weather, the forecaster may read a temperature as "30 Celsius" instead of "30 degrees Celsius".
# Formatting
The “degree Celsius” is the only SI unit whose full unit name contains an uppercase letter.
The following are permissible ways to express degree Celsius: singular / (plural)
- degree Celsius / degrees Celsius
- °C
The general rule is that the numerical value always precedes the unit, and a space is always used to separate the unit from the number, e.g., “23 °C” (not “23°C” nor “23° C”). Thus the value of the quantity is the product of the number and the unit, the space being regarded as a multiplication sign (just as a space between units implies multiplication).
The only exceptions to this rule are for the unit symbols for degree, minute, and second for plane angle, °, ′, and ″, respectively, for which no space is left between the numerical value and the unit symbol.
# The special Unicode °C character
Unicode includes a special “°C” character at U+2103 (decimal value 8451) for compatibility with CJK encodings that provide such a character (as such, in most fonts the width is the same as for fullwidth characters). Its appearance is similar to the one synthesized by individually typing its two components (°) and (C). To better see the difference between the two, shown below is the degree Celsius character followed immediately by the two-component version:
℃ °C
When viewed on computers that properly support and map Unicode, the above line may be similar to the line below (size may vary):
Depending on the operating system, web browser, and the default font, the “C” in the Unicode character may be narrower and slightly taller than a plain uppercase C; precisely the opposite may be true on other platforms. However, there will usually be a discernible difference between the two.
# Temperatures and intervals
The degree Celsius is a special name for the kelvin for use in expressing Celsius temperatures. The degree Celsius is also subject to the same rules as the kelvin with regard to the use of its unit name and symbol. Thus, besides expressing specific temperatures along its scale (e.g. “Gallium melts at 29.7646 °C” and “The temperature outside is 23 degrees Celsius”), the degree Celsius is also suitable for expressing temperature intervals: differences between temperatures or their uncertainties (e.g. “The output of the heat exchanger is hotter by 40 degrees Celsius”, and “Our standard uncertainty is ±3 °C”). Because of this dual usage, one must not rely upon the unit name or its symbol to denote that a quantity is a temperature interval; it must be unambiguous through context or explicit statement that the quantity is an interval.
# Why technical articles use a mix of Kelvin and Celsius scales
In science (especially) and in engineering, the Celsius scale and the kelvin are often used simultaneously in the same article (e.g. “…its measured value was 0.01023 °C with an uncertainty of 70 µK…”). This practice is permissible because 1) the degree Celsius is a special name for the kelvin for use in expressing Celsius temperatures, and 2) the magnitude of the degree Celsius is precisely equal to that of the kelvin. Notwithstanding the official endorsement provided by decision #3 of Resolution 3 of the 13th CGPM, which stated “a temperature interval may also be expressed in degrees Celsius,” the practice of simultaneously using both “°C” and “K” remains widespread throughout the scientific world as the use of SI prefixed forms of the degree Celsius (such as “µ°C” or “microdegrees Celsius”) to express a temperature interval has not been well-adopted.
This practice should be avoided for literature directed to lower-level technical fields and in non-technical articles intended for the general public where both the kelvin and its symbol, K, are not well recognized and could be confusing.
# The melting and boiling points of water
One effect of defining the Celsius scale at the triple point of Vienna Standard Mean Ocean Water (273.16 kelvins and 0.01 °C), and at absolute zero (zero kelvins and −273.15 °C), is that neither the melting nor the boiling point of water under one standard atmosphere (101.325 kPa) remain defining points for the Celsius scale. In 1948 when the 9th General Conference on Weights and Measures (CGPM) in Resolution 3 first considered using the triple point of water as a defining point, the triple point was so close to being 0.01 °C greater than water’s known melting point, it was simply defined as precisely 0.01 °C. However, current measurements show that the triple and melting points of Vienna Standard Mean Ocean Water (VSMOW) are actually very slightly (\textstyle\frac{373.15}{273.15} (approximately 36.61% thermodynamically hotter). When adhering strictly to the two-point definition for calibration, the boiling point of VSMOW under one standard atmosphere of pressure is actually 373.1339 K (99.9839 °C). When calibrated to ITS-90 (a calibration standard comprising many definition points and commonly used for high-precision instrumentation), the boiling point of VSMOW is slightly less, about 99.974 °C.
This boiling–point difference of 16.1 millikelvins (thousandths of a degree Celsius) between the Celsius scale’s original definition and the current one (based on absolute zero and the triple point) has little practical meaning in real life because water’s boiling point is extremely sensitive to variations in barometric pressure. For example, an altitude change of only 28 cm (11 inches) causes water’s boiling point to change by one millikelvin.
# Worldwide adoption
Throughout the world, except in the U.S. and a few other countries (for example, Belize ), the Celsius temperature scale is used for practically all purposes. The only exceptions are some specialist fields (e.g., low-temperature physics, astrophysics, light temperature in photography) where the closely related Kelvin scale dominates instead. Even in the U.S., almost the entire scientific world and most engineering fields, especially high-tech ones, use the Celsius scale. The general U.S. population (not considering foreign immigrants), however, remains more accustomed to the Fahrenheit scale, which is therefore the scale that most U.S. broadcasters use in weather forecasts. The Fahrenheit scale is also commonly used in the U.S. for body temperatures. The United Kingdom has almost exclusively used the Celsius scale since the 1970s (but it is often called centigrade). A notable exception is that some broadcasters and publications still quote Fahrenheit air temperatures in weather forecasts (especially during summer), for the benefit of generations born before about 1950, and air-temperature thermometers sold still show both scales for the same reason. | Celsius
# Overview
Template:Temperature
The Celsius temperature scale (previously known as the centigrade scale). The degree Celsius (symbol: °C) can refer to a specific temperature on the Celsius scale as well as serve as unit increment to indicate a temperature interval (a difference between two temperatures or an uncertainty). “Celsius” is named after the Swedish astronomer Anders Celsius (1701 – 1744), who developed a similar temperature scale two years before his death.
From 1744 until 1954, 0 °C on the Celsius scale was defined as the melting point of ice and 100 °C was defined as the boiling point of water under a pressure of one standard atmosphere; this close equivalency is taught in schools today. However, the unit “degree Celsius” and the Celsius scale are currently, by international agreement, defined by two different points: absolute zero, and the triple point of specially prepared water. This definition also precisely relates the Celsius scale to the Kelvin scale, which is the SI base unit of temperature (symbol: K). Absolute zero—the temperature at which no energy remains in a substance—is defined as being precisely 0 K and −273.15 °C. The triple point of water is defined as being precisely 273.16 K and 0.01 °C.
This definition fixes the magnitude of both the degree Celsius and the unit kelvin as being precisely 1 part in 273.16 parts the difference between absolute zero and the triple point of water. Thus, it sets the magnitude of one degree Celsius and the kelvin to be exactly equivalent. Additionally, it establishes the difference between the two scales’ null points as being precisely 273.15 degrees Celsius (−273.15 °C = 0 K and 0.01 °C = 273.16 K).
Some key temperatures relating the Celsius scale to other temperature scales are shown in the table below.
# History
In 1742, Anders Celsius (1701 – 1744) created a "reversed" version of the modern Celsius temperature scale whereby zero represented the boiling point of water and one hundred represented the freezing point of water. In his paper Observations of two persistent degrees on a thermometer, he recounted his experiments showing that ice’s melting point was effectively unaffected by pressure. He also determined with remarkable precision how water’s boiling point varied as a function of atmospheric pressure. He proposed that zero on his temperature scale (water’s boiling point) would be calibrated at the mean barometric pressure at mean sea level. This pressure is known as one standard atmosphere. In 1954, Resolution 4 of the 10th CGPM (the General Conference on Weights and Measures) established internationally that one standard atmosphere was a pressure equivalent to 1,013,250 dynes per cm2 (101.325 kPa).
In 1744, coincident with the death of Anders Celsius, the famous Swedish botanist Carolus Linnaeus (1707 – 1778) effectively reversed [3] Celsius’s scale upon receipt of his first thermometer featuring a scale where zero represented the melting point of ice and 100 represented water’s boiling point. His custom-made “linnaeus-thermometer,” for use in his greenhouses, was made by Daniel Ekström, Sweden’s leading maker of scientific instruments at the time and whose workshop was located in the basement of the Stockholm observatory. As often happened in this age before modern communications, numerous physicists, scientists, and instrument makers are credited with having independently developed this same scale;[4] among them were Pehr Elvius, the secretary of the Royal Swedish Academy of Sciences (which had an instrument workshop) and with whom Linnaeus had been corresponding; Christian of Lyons; Daniel Ekström, the instrument maker; and Mårten Strömer (1707 – 1770) who had studied astronomy under Anders Celsius.
The first known document[5] reporting temperatures in this modern “forward” Celsius scale is the paper Hortus Upsaliensis dated 16 December 1745 that Linnaeus wrote to a student of his, Samuel Nauclér. In it, Linnaeus recounted the temperatures inside the orangery at the Botanical Garden of Uppsala University:
"... since the caldarium (the hot part of the greenhouse) by the angle of the windows, merely from the rays of the sun, obtains such heat that the thermometer often reaches 30 degrees, although the keen gardener usually takes care not to let it rise to more than 20 to 25 degrees, and in winter not under 15 degrees ..."
For the next 204 years, the scientific and thermometry communities world-wide referred to this scale as the “centigrade scale”. Temperatures on the centigrade scale were often reported simply as “degrees” or, when greater specificity was desired, “degrees centigrade”. The symbol for temperature values on this scale was °C (in several formats over the years). Because the term “centigrade” was also the Spanish and French language name for a unit of angular measurement (one-hundredth of a right angle) and had a similar connotation in other languages, the term “centesimal degree” was used when very precise, unambiguous language was required by international standards bodies such as the Bureau international des poids et mesures (BIPM). The 9th CGPM (Conférence générale des poids et mesures) and the CIPM (Comité international des poids et mesures) formally adopted “degree Celsius” (symbol: °C) in 1948.[6] For lay-people worldwide — including school textbooks — the full transition from centigrade to Celsius is far from complete, with centigrade still the commonly used term in many communities.
In modern days the word "degrees" is often omitted: for example, on the BBC weather, the forecaster may read a temperature as "30 Celsius" instead of "30 degrees Celsius".
# Formatting
The “degree Celsius” is the only SI unit whose full unit name contains an uppercase letter.
The following are permissible ways to express degree Celsius: singular / (plural)
- degree Celsius / degrees Celsius
- °C
- ℃
The general rule is that the numerical value always precedes the unit, and a space is always used to separate the unit from the number, e.g., “23 °C” (not “23°C” nor “23° C”). Thus the value of the quantity is the product of the number and the unit, the space being regarded as a multiplication sign (just as a space between units implies multiplication).
The only exceptions to this rule are for the unit symbols for degree, minute, and second for plane angle, °, ′, and ″, respectively, for which no space is left between the numerical value and the unit symbol.[7]
# The special Unicode °C character
Unicode includes a special “°C” character at U+2103 (decimal value 8451) for compatibility with CJK encodings that provide such a character (as such, in most fonts the width is the same as for fullwidth characters). Its appearance is similar to the one synthesized by individually typing its two components (°) and (C). To better see the difference between the two, shown below is the degree Celsius character followed immediately by the two-component version:
℃ °C
When viewed on computers that properly support and map Unicode, the above line may be similar to the line below (size may vary):
Depending on the operating system, web browser, and the default font, the “C” in the Unicode character may be narrower and slightly taller than a plain uppercase C; precisely the opposite may be true on other platforms. However, there will usually be a discernible difference between the two.
# Temperatures and intervals
The degree Celsius is a special name for the kelvin for use in expressing Celsius temperatures.[8] The degree Celsius is also subject to the same rules as the kelvin with regard to the use of its unit name and symbol. Thus, besides expressing specific temperatures along its scale (e.g. “Gallium melts at 29.7646 °C” and “The temperature outside is 23 degrees Celsius”), the degree Celsius is also suitable for expressing temperature intervals: differences between temperatures or their uncertainties (e.g. “The output of the heat exchanger is hotter by 40 degrees Celsius”, and “Our standard uncertainty is ±3 °C”).[9] Because of this dual usage, one must not rely upon the unit name or its symbol to denote that a quantity is a temperature interval; it must be unambiguous through context or explicit statement that the quantity is an interval.[10]
# Why technical articles use a mix of Kelvin and Celsius scales
In science (especially) and in engineering, the Celsius scale and the kelvin are often used simultaneously in the same article (e.g. “…its measured value was 0.01023 °C with an uncertainty of 70 µK…”). This practice is permissible because 1) the degree Celsius is a special name for the kelvin for use in expressing Celsius temperatures, and 2) the magnitude of the degree Celsius is precisely equal to that of the kelvin. Notwithstanding the official endorsement provided by decision #3 of Resolution 3 of the 13th CGPM, which stated “a temperature interval may also be expressed in degrees Celsius,” the practice of simultaneously using both “°C” and “K” remains widespread throughout the scientific world as the use of SI prefixed forms of the degree Celsius (such as “µ°C” or “microdegrees Celsius”) to express a temperature interval has not been well-adopted.
This practice should be avoided for literature directed to lower-level technical fields and in non-technical articles intended for the general public where both the kelvin and its symbol, K, are not well recognized and could be confusing.
# The melting and boiling points of water
One effect of defining the Celsius scale at the triple point of Vienna Standard Mean Ocean Water (273.16 kelvins and 0.01 °C), and at absolute zero (zero kelvins and −273.15 °C), is that neither the melting nor the boiling point of water under one standard atmosphere (101.325 kPa) remain defining points for the Celsius scale. In 1948 when the 9th General Conference on Weights and Measures (CGPM) in Resolution 3 first considered using the triple point of water as a defining point, the triple point was so close to being 0.01 °C greater than water’s known melting point, it was simply defined as precisely 0.01 °C. However, current measurements show that the triple and melting points of Vienna Standard Mean Ocean Water (VSMOW) are actually very slightly (<0.001 °C) greater than 0.01 °C apart. Thus, the actual melting point of ice is very slightly (less than a thousandth of a degree) below 0 °C. Also, defining water’s triple point at 273.16 K precisely defined the magnitude of each 1 °C increment in terms of the absolute thermodynamic temperature scale (referencing absolute zero). Now decoupled from the actual boiling point of water, the value “100 °C” is hotter than 0 °C — in absolute terms — by a factor of precisely <math>\textstyle\frac{373.15}{273.15}</math> (approximately 36.61% thermodynamically hotter). When adhering strictly to the two-point definition for calibration, the boiling point of VSMOW under one standard atmosphere of pressure is actually 373.1339 K (99.9839 °C). When calibrated to ITS-90 (a calibration standard comprising many definition points and commonly used for high-precision instrumentation), the boiling point of VSMOW is slightly less, about 99.974 °C.[11]
This boiling–point difference of 16.1 millikelvins (thousandths of a degree Celsius) between the Celsius scale’s original definition and the current one (based on absolute zero and the triple point) has little practical meaning in real life because water’s boiling point is extremely sensitive to variations in barometric pressure. For example, an altitude change of only 28 cm (11 inches) causes water’s boiling point to change by one millikelvin.
# Worldwide adoption
Throughout the world, except in the U.S. and a few other countries (for example, Belize [12]), the Celsius temperature scale is used for practically all purposes. The only exceptions are some specialist fields (e.g., low-temperature physics, astrophysics, light temperature in photography) where the closely related Kelvin scale dominates instead. Even in the U.S., almost the entire scientific world and most engineering fields, especially high-tech ones, use the Celsius scale. The general U.S. population (not considering foreign immigrants), however, remains more accustomed to the Fahrenheit scale, which is therefore the scale that most U.S. broadcasters use in weather forecasts. The Fahrenheit scale is also commonly used in the U.S. for body temperatures. The United Kingdom has almost exclusively used the Celsius scale since the 1970s (but it is often called centigrade). A notable exception is that some broadcasters and publications still quote Fahrenheit air temperatures in weather forecasts (especially during summer), for the benefit of generations born before about 1950, and air-temperature thermometers sold still show both scales for the same reason. | https://www.wikidoc.org/index.php/Celsius | |
bf757f6138f52ebe34f5755bea4f563e2d44b276 | wikidoc | Incisor | Incisor
# Overview
Incisors (from Latin incidere, "to cut") are the first kind of tooth in heterodont mammals. They are located in the premaxilla.
# Function
In many herbivorous or omnivorous mammals, such as the human and the horse, they are adapted for shearing sharply. In cats, the incisors are small and do not do much; biting off meat is done with the canines and the carnassials. In elephants, the upper incisors are modified into curved tusks, just as is the case with Narwhals, where normally one of them develops into a straight and twisted tusk. The incisors of rodents grow throughout life and are worn by gnawing.
# Number and types of incisors
## In humans
Humans normally have eight (8) incisors, two of each type. The types of incisors are:
- maxillary central incisor
- maxillary lateral incisor
- mandibular central incisor
- mandibular lateral incisor
## In animals
Among other animals, some other primates, cats and horses have twelve. The rodents have four. Rabbits and hares (lagomorphs) were once considered rodents, but are distinguished by having eight--1 small pair, called "peg teeth" is directly behind the most anterior pair.
### The Rodent incisor
The rodent incisor is one of the evolutionary adaptations that make rodents such a successful group. There are two incisors in the upper jaw and two in the lower jaw. The incisors are separated from the molars by a diastema region, an area without any teeth. The tissue of the incisor is regenerated from the apical end and constantly wears down at the distal tip. The ever-growing incisor can be subdivided into two areas, the crown analogue and the root analogue.
The crown analogue is the labial half of the incisor. It is characterized by an enlarged cervical loop at the apical end. The cervical loop is the epithelial stem cell niche. The epithelial progeny of the crown analogue's cervical loop differentiates into ameloblasts that produce enamel.
The root analogue is the lingual half of the incisor. It's cervical loop is much smaller and the epithelium does not differentiate into ameloblasts, but instead forms a root sheath and fragments into epithelial cell rests of Malassez typical of root epithelium. The root analogue is covered in dentin and cementum like a normal root.
# Additional images
- Mouth (oral cavity)
- Left maxilla. Outer surface.
- Base of skull. Inferior surface. | Incisor
Template:Infobox Anatomy
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
# Overview
Incisors (from Latin incidere, "to cut") are the first kind of tooth in heterodont mammals. They are located in the premaxilla.
# Function
In many herbivorous or omnivorous mammals, such as the human and the horse, they are adapted for shearing sharply. In cats, the incisors are small and do not do much; biting off meat is done with the canines and the carnassials. In elephants, the upper incisors are modified into curved tusks, just as is the case with Narwhals, where normally one of them develops into a straight and twisted tusk. The incisors of rodents grow throughout life and are worn by gnawing.
# Number and types of incisors
## In humans
Humans normally have eight (8) incisors, two of each type. The types of incisors are:
- maxillary central incisor
- maxillary lateral incisor
- mandibular central incisor
- mandibular lateral incisor
## In animals
Among other animals, some other primates, cats and horses have twelve. The rodents have four. Rabbits and hares (lagomorphs) were once considered rodents, but are distinguished by having eight--1 small pair, called "peg teeth" is directly behind the most anterior pair.
### The Rodent incisor
The rodent incisor is one of the evolutionary adaptations that make rodents such a successful group. There are two incisors in the upper jaw and two in the lower jaw. The incisors are separated from the molars by a diastema region, an area without any teeth. The tissue of the incisor is regenerated from the apical end and constantly wears down at the distal tip. The ever-growing incisor can be subdivided into two areas, the crown analogue and the root analogue.
The crown analogue is the labial half of the incisor. It is characterized by an enlarged cervical loop at the apical end. The cervical loop is the epithelial stem cell niche. The epithelial progeny of the crown analogue's cervical loop differentiates into ameloblasts that produce enamel.
The root analogue is the lingual half of the incisor. It's cervical loop is much smaller and the epithelium does not differentiate into ameloblasts, but instead forms a root sheath and fragments into epithelial cell rests of Malassez typical of root epithelium. The root analogue is covered in dentin and cementum like a normal root.
# Additional images
- Mouth (oral cavity)
- Left maxilla. Outer surface.
- Base of skull. Inferior surface. | https://www.wikidoc.org/index.php/Central_incisor | |
5dd63048c976107c3c1eb136b9ef915bac24856f | wikidoc | Vacuole | Vacuole
Vacuoles are found in the cytoplasm of most plant cells and some animal cells. Vacuoles are membrane-bound compartments within some eukaryotic cells that can serve a variety of secretory, excretory, and storage functions. Vacuoles and their contents are considered to be distinct from the cytoplasm, and are classified as ergastic according to some authors. Vacuoles are especially conspicuous in most plant cells.
# Functions
In general, vacuole functions include also
- Removing unwanted structural debris
- Isolating materials that might be harmful or a threat to the cell
- Containing waste products
- Maintaining internal hydrostatic pressure or turgor within the cell
- Maintaining an acidic internal pH
- Containing small molecules
- Exporting unwanted substances from the cell
- Enabling the cell to change shape
Vacuoles also play a major role in autophagy, maintaining a balance between biogenesis (production) and degradation (or turnover), of many substances and cell structures. They also aid in destruction of invading bacteria or of misfolded proteins that have begun to build up within the cell. The vacuole is a major part in the plant and animal cell.
# Protists
Some protists and macrophages use food vacuoles as a stage in phagocytosis—the intake of large molecules, particles, or even other cells, by the cell for digestion. They are also called "storage sacs."
A contractile vacuole is used to pump excess water out of the cell to reduce osmotic pressure and keep the cell from bursting, which is referred to as cytolysis or osmotic lysis.
# Budding yeast
In budding yeast cells, vacuoles act as storage compartments of amino acids and detoxification compartments. Under conditions of starvation, proteins are degraded in vacuoles; this is called autophagy. First, cytoplasms, mitochondrion, and small organelles are covered with multiplex plasma membranes called autophagosomes. Next, the autophagosomes fuse the vacuoles. Finally, the cytoplasms and the organelles are degraded.
In a vacuole of budding yeast, black particles sometimes appear, called a dancing body. The dancing body moves actively in the vacuole and appears and disappears within 10 minutes to several hours. In previous research, it was suggested but not proven that the main component of the dancing body is polyphosphate acid. But the main component has been determined to be crystallized sodium polyphosphate and its function has been studied. It is thought that its function is to supply and store phosphates in budding yeast cells.
# Plants
Most mature plant cells have one or several vacuoles that typically occupy more than 30% of the cell's volume, and that can occupy as much as 90% of the volume for certain cell types and conditions. A vacuole is surrounded by a membrane called the tonoplast.
This vacuole houses large amounts of a liquid called cell sap, composed of water, enzymes, inorganic ions (like K+ and Cl-), salts (such as calcium), and other substances, including toxic byproducts removed from the cytosol to avoid interference with metabolism. Toxins present in the vacuole may also help to protect some plants from predators. Transport of protons from cytosol to vacuole aids in keeping cytoplasmic pH stable, while making the vacuolar interior more acidic, allowing degradative enzymes to act. Although having a large central vacuole is the most common case, the size and number of vacuoles may vary in different tissues and stages of development. Cells of the vascular cambium, for example, have many small vacuoles in winter, and one large one in summer.
Aside from storage, the main role of the central vacuole is to maintain turgor pressure against the cell wall. Proteins found in the tonoplast control the flow of water into and out of the vacuole through active transport, pumping potassium (K+) ions into and out of the vacuolar interior. Due to osmosis, water will diffuse into the vacuole, placing pressure on the cell wall. If water loss leads to a significant decline in turgor pressure, the cell will plasmolyse. Turgor pressure exerted by vacuoles is also helpful for cellular elongation: as the cell wall is partially degraded by the action of auxins, the less rigid wall is expanded by the pressure coming from within the vacuole. Vacuoles can help some plant cells to reach considerable size. Another function of a central vacuole is that it pushes all contents of the cell's cytoplasm against the cellular membrane, and thus keeps the chloroplasts closer to light.
The vacuole also stores the pigments in flowers and fruits.
# Animals
Vacuoles in animals are a part of the processes of exocytosis and endocytosis.
Exocytosis is the extrusion process of proteins from the Golgi apparatus initially enter secretory granules, where processing of prohormones to the mature hormones occurs before exocytosis, and also allows the animal cell to rid waste products.
Endocytosis is the reverse of exocytosis. There are various types. Phagocytosis ("cell eating") is the process by which bacteria, dead tissue, or other bits of material visible under the microscope are engulfed by cells. The material makes contact with the cell membrane, which then invaginates. The invagination is pinched off, leaving the engulfed material in the membrane-enclosed vacuole and the cell membrane intact. Pinocytosis ("cell drinking") is essentially the same process, the difference being that the substances ingested are in solution and not visible under the microscope
Hydropic (vacuolar) changes are of importance of identifying various pathologies, such as the reversible cell swelling in renal tubules caused by hypoperfusion of the kidneys during open heart surgery. | Vacuole
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Vacuoles are found in the cytoplasm of most plant cells and some animal cells. Vacuoles are membrane-bound compartments within some eukaryotic cells that can serve a variety of secretory, excretory, and storage functions. Vacuoles and their contents are considered to be distinct from the cytoplasm, and are classified as ergastic according to some authors.[1] Vacuoles are especially conspicuous in most plant cells.
# Functions
In general, vacuole functions include also
- Removing unwanted structural debris
- Isolating materials that might be harmful or a threat to the cell
- Containing waste products
- Maintaining internal hydrostatic pressure or turgor within the cell
- Maintaining an acidic internal pH
- Containing small molecules
- Exporting unwanted substances from the cell
- Enabling the cell to change shape
Vacuoles also play a major role in autophagy, maintaining a balance between biogenesis (production) and degradation (or turnover), of many substances and cell structures. They also aid in destruction of invading bacteria or of misfolded proteins that have begun to build up within the cell. The vacuole is a major part in the plant and animal cell.
# Protists
Some protists and macrophages use food vacuoles as a stage in phagocytosis—the intake of large molecules, particles, or even other cells, by the cell for digestion. They are also called "storage sacs."
A contractile vacuole is used to pump excess water out of the cell to reduce osmotic pressure and keep the cell from bursting, which is referred to as cytolysis or osmotic lysis.
# Budding yeast
In budding yeast cells, vacuoles act as storage compartments of amino acids and detoxification compartments. Under conditions of starvation, proteins are degraded in vacuoles; this is called autophagy. First, cytoplasms, mitochondrion, and small organelles are covered with multiplex plasma membranes called autophagosomes. Next, the autophagosomes fuse the vacuoles. Finally, the cytoplasms and the organelles are degraded.
In a vacuole of budding yeast, black particles sometimes appear, called a dancing body. The dancing body moves actively in the vacuole and appears and disappears within 10 minutes to several hours. In previous research, it was suggested but not proven that the main component of the dancing body is polyphosphate acid. But the main component has been determined to be crystallized sodium polyphosphate and its function has been studied. It is thought that its function is to supply and store phosphates in budding yeast cells.
# Plants
Most mature plant cells have one or several vacuoles that typically occupy more than 30% of the cell's volume, and that can occupy as much as 90% of the volume for certain cell types and conditions.[2] A vacuole is surrounded by a membrane called the tonoplast.
This vacuole houses large amounts of a liquid called cell sap, composed of water, enzymes, inorganic ions (like K+ and Cl-), salts (such as calcium), and other substances, including toxic byproducts removed from the cytosol to avoid interference with metabolism. Toxins present in the vacuole may also help to protect some plants from predators. Transport of protons from cytosol to vacuole aids in keeping cytoplasmic pH stable, while making the vacuolar interior more acidic, allowing degradative enzymes to act. Although having a large central vacuole is the most common case, the size and number of vacuoles may vary in different tissues and stages of development. Cells of the vascular cambium, for example, have many small vacuoles in winter, and one large one in summer.
Aside from storage, the main role of the central vacuole is to maintain turgor pressure against the cell wall. Proteins found in the tonoplast control the flow of water into and out of the vacuole through active transport, pumping potassium (K+) ions into and out of the vacuolar interior. Due to osmosis, water will diffuse into the vacuole, placing pressure on the cell wall. If water loss leads to a significant decline in turgor pressure, the cell will plasmolyse. Turgor pressure exerted by vacuoles is also helpful for cellular elongation: as the cell wall is partially degraded by the action of auxins, the less rigid wall is expanded by the pressure coming from within the vacuole. Vacuoles can help some plant cells to reach considerable size. Another function of a central vacuole is that it pushes all contents of the cell's cytoplasm against the cellular membrane, and thus keeps the chloroplasts closer to light.
The vacuole also stores the pigments in flowers and fruits.
# Animals
Vacuoles in animals are a part of the processes of exocytosis and endocytosis.
Exocytosis is the extrusion process of proteins from the Golgi apparatus initially enter secretory granules, where processing of prohormones to the mature hormones occurs before exocytosis, and also allows the animal cell to rid waste products.
Endocytosis is the reverse of exocytosis. There are various types. Phagocytosis ("cell eating") is the process by which bacteria, dead tissue, or other bits of material visible under the microscope are engulfed by cells. The material makes contact with the cell membrane, which then invaginates. The invagination is pinched off, leaving the engulfed material in the membrane-enclosed vacuole and the cell membrane intact. Pinocytosis ("cell drinking") is essentially the same process, the difference being that the substances ingested are in solution and not visible under the microscope [3]
Hydropic (vacuolar) changes are of importance of identifying various pathologies, such as the reversible cell swelling in renal tubules caused by hypoperfusion of the kidneys during open heart surgery. | https://www.wikidoc.org/index.php/Central_vacuole | |
8197db6f7f3e84214eb72fe69a566223be206569 | wikidoc | Cetacea | Cetacea
The order Cetacea (Template:IPAEng, L. cetus, whale) includes whales, dolphins and porpoises.
Cetus is Latin and is used in biological names to mean "whale"; its original meaning, "large sea animal," was more general. It comes from Ancient Greek κῆτος (kētos), meaning "whale" or "any huge fish or sea monster". Cetology is the branch of marine science associated with the study of cetaceans.
Cetaceans are the mammals most fully adapted to aquatic life. Their body is fusiform (spindle-shaped). The forelimbs are modified into flippers. The tiny hindlimbs are vestigial; they do not attach to the backbone and are hidden within the body. The tail has horizontal flukes.
Cetaceans are nearly hairless, and are insulated by a thick layer of blubber. As a group, they are noted for their high intelligence.
The order Cetacea contains ninety species, all marine except for five species of freshwater dolphins. The order is divided into two suborders, Mysticeti (baleen whales) and Odontoceti (toothed whales, which includes dolphins and porpoises).
# Respiration, vision, hearing and echolocation
As mammals, cetaceans need to breathe air. Because of this, they need to come to the water's surface to exhale carbon dioxide and inhale a fresh supply of oxygen. During diving, a muscular action closes the blowholes (nostrils), which remain closed until the cetacean next breaks the surface; when it surfaces, the muscles open the blowholes and warm air is exhaled.
Cetaceans' blowholes have evolved to a position on top of the head, allowing more time to expel stale air and inhale fresh air. When the stale air, warmed from the lungs, is exhaled, it condenses as it meets the cold air outside. As with a terrestrial mammal breathing out on a cold day, a small cloud of 'steam' appears. This is called the 'blow' or 'spout' and is different in terms of shape, angle and height, for each cetacean species. Cetaceans can be identified at a distance, using this characteristic, by experienced whalers or whale-watchers.
Cetaceans can go underwater for much longer periods of time than other mammals. Their duration under water varies greatly between speicies due to large physiological differences between many members of this Order. There are two studied advantages of cetacean physiology that let this Order (and other marine mammals) forage underwater for extended periods of time without breathing at the water surface.
Myoglobin concentrations in skeletal muscle of mammals have much variation. A New Zealand white rabbit has 0.08+/-0.06 g (in a 100 g Wet muscle) of myoglobin, whereas a Northern bottlenose whale has 6.34 g (in a 100 g Wet muscle) of myoglobin. Myoglobin, by nature, has a higher affinity to oxygen than haemoglobin. That is, myoglobin retains oxygen molecules better than hemoglobin. Therefore, it is useful to have higher concentrations of myoglobin when needed and there is no oxygen available for re-uptake. The higher the myoglobin concentration in cetacean skeletal muscle, the longer they can stay underwater and forage.
Increased body size is another way of elongating dive duration of large cetaceans. This is true because of two considered aspects. An increase in body size means that there is increase in muscle mass, therefore, increase in muscle oxygen stores. Another aspect is the universal correlation of mass and metabolic rate (Kleiber's law). In layman’s terms Kleiber’s law states that the metabolic rate of a large animal is slower than a small animal per unit mass. From this we can conclude that larger animals will use up less oxygen than smaller animals (per mass unit).
The cetacean's eyes are set well back and to either side of its huge head. This means that cetaceans with pointed 'beaks' (such as dolphins) have good binocular vision forward and downward but others, with blunt heads (such as the Sperm Whale), can see either side but not directly ahead or directly behind. Tear glands secrete greasy tears, which protect the eyes from the salt in the water. Cetaceans also have an almost spherical lens in their eyes, which is most efficient at focusing what little light there is in the deep waters. Cetaceans make up for their generally quite poor vision (with the exception of the dolphin) with excellent hearing.
As with the eyes, the cetacean's ears are also small. Life in the sea accounts for the cetacean's loss of its external ears, whose function is to collect airborne sound waves and focus them in order for them to become strong enough to hear well. However, water is a better conductor of sound than air, so the external ear was no longer needed: It is no more than a tiny hole in the skin, just behind the eye. The inner ear, however, has become so well developed that the cetacean can not only hear sounds dozens of miles away, but it can also discern from which direction the sound comes.
Some cetaceans are capable of echolocation. Many toothed whales emit clicks similar to those in echolocation, but it has not been demonstrated that they echolocate. Mysticeti have little need of echolocation, as they prey upon small fish that would be impractical to locate with echolocation. Some members of Odontoceti, such as dolphins and porpoises, do perform echolocation. These cetaceans use sound in the same way as bats - they emit a sound (called a click), which then bounces off an object and returns to them. From this, cetaceans can discern the size, shape, surface characteristics and movement of the object, as well as how far away it is. With this ability cetaceans can search for, chase and catch fast-swimming prey in total darkness. Echolocation is so advanced in most Odontoceti that they can distinguish between prey and non-prey (such as humans or boats); captive cetaceans can be trained to distinguish between, for example, balls of different sizes or shapes.
Cetaceans also use sound to communicate, whether it be groans, moans, whistles, clicks or the complex 'singing' of the Humpback Whale.
# Feeding
When it comes to food and feeding, cetaceans can be separated into two distinct groups. The toothed whales, Odontoceti like sperm whales, beluga whales, dolphins and porpoises, usually have lots of teeth that they use for catching fish, squid or other marine life. They do not chew their food, but swallow it whole. In the rare cases that they catch large prey, as when Orca (Orcinus orca) catch a seal, they tear chunks off it that in turn are swallowed whole.
The baleen whales or Mysticeti do not have teeth. Instead they have plates made of keratin (the same substance as human fingernails) which hang down from the upper jaw. These plates act like a giant filter, straining small animals (such as krill and fish) from the seawater. Cetaceans included in this group include the Blue Whale, the Humpback Whale, the Bowhead Whale and the Minke Whale.
Not all Mysticeti feed on plankton: the larger whales tend to eat small shoaling fish, such as herrings and sardine, called micronecton. One species of Mysticeti, the Gray Whale (Eschrichtius robustus), is a benthic feeder, primarily eating sea floor crustaceans.
# Mammalian nature
Cetaceans are mammals, that is, members of the class Mammalia. The closest living relative of cetaceans is the hippopotamus.
As mammals, cetaceans have characteristics that are common to all mammals: They are warm-blooded, breathe in air through their lungs, bear their young alive and suckle them on their own milk, and have hair, although very little of it.
Another way of discerning a cetacean from a fish is by the shape of the tail. The tail of a fish is vertical and moves from side to side when the fish swims. The tail of a cetacean – called a fluke – is horizontal and moves up and down, as cetaceans' spines bend in the same manner as a human spine.
# Taxonomic listing
The classification here closely follows Dale W. Rice, Marine Mammals of the World: Systematics and Distribution (1998), which has become the standard taxonomy reference in the field. There is very close agreement between this classification and that of Mammal Species of the World: 3rd Edition (Wilson and Reeder eds., 2005). Any differences are noted using the abbreviations "Rice" and "MSW3" respectively. Further differences due to recent discoveries are also noted.
Discussion of synonyms and subspecies are relegated to the relevant genus and species articles.
- ORDER CETACEA
Suborder Mysticeti: Baleen whales
Family Balaenidae: Right whales and Bowhead Whale
Genus Balaena
Bowhead Whale, Balaena mysticetus
Genus Eubalaena
North Atlantic Right Whale, Eubalaena glacialis
North Pacific Right Whale, Eubalaena japonica
Southern Right Whale, Eubalaena australis
Family Balaenopteridae: Rorquals
Subfamily Balaenopterinae
Genus Balaenoptera
Common Minke Whale, Balaenoptera acutorostrata
Antarctic Minke Whale, Balaenoptera bonaerensis
Sei Whale, Balaenoptera borealis
Bryde's Whale, Balaenoptera brydei
Eden's Whale Balaenoptera edeni - Rice lists this as a separate species, MSW3 does not
Balaenoptera omurai - MSW3 lists this is a synonym of Bryde's Whale but suggests this may be temporary.
Blue Whale, Balaenoptera musculus
Fin Whale, Balaenoptera physalus
Subfamily Megapterinae
Genus Megaptera
Humpback Whale, Megaptera novaeangliae
† Genus Eobalaenoptera
† Harrison's Whale, Eobalaenoptera harrisoni
Family Eschrichtiidae
Genus Eschrichtius
Gray Whale, Eschrichtius robustus
Family Neobalaenidae: Pygmy Right Whale
Genus Caperea
Pygmy Right Whale, Caperea marginata
Suborder Odontoceti: toothed whales
Family Delphinidae: Dolphin
Genus Cephalorhynchus
Commerson's Dolphin, Cephalorhyncus commersonii
Chilean Dolphin, Cephalorhyncus eutropia
Heaviside's Dolphin, Cephalorhyncus heavisidii
Hector's Dolphin, Cephalorhyncus hectori
Genus Delphinus
Long-beaked Common Dolphin, Delphinus capensis
Short-beaked Common Dolphin, Delphinus delphis
Arabian Common Dolphin, Delphinus tropicalis. Rice recognises this as a separate species. MSW3 does not.
Genus Feresa
Pygmy Killer Whale, Feresa attenuata
Genus Globicephala
Short-finned Pilot Whale, Globicephala macrorhyncus
Long-finned Pilot Whale, Globicephala melas
Genus Grampus
Risso's Dolphin, Grampus griseus
Genus Lagenodelphis
Fraser's Dolphin, Lagenodelphis hosei
Genus Lagenorhynchus
Atlantic White-sided Dolphin, Lagenorhynchus acutus
White-beaked Dolphin, Lagenorhynchus albirostris
Peale's Dolphin, Lagenorhynchus australis
Hourglass Dolphin, Lagenorhynchus cruciger
Pacific White-sided Dolphin, Lagenorhynchus obliquidens
Dusky Dolphin, Lagenorhynchus obscurus
Genus Lissodelphis
Northern Right Whale Dolphin, Lissodelphis borealis
Southern Right Whale Dolphin, Lissodelphis peronii
Genus Orcaella
Irrawaddy Dolphin, Orcaella brevirostris
Australian Snubfin Dolphin, Orcaella heinsohni. 2005 discovery, thus not recognized by Rice or MSW3 and subject to revision.
Genus Orcinus
Killer Whale, Orcinus orca
Genus Peponocephala
Melon-headed Whale, Peponocephala electra
Genus Pseudorca
False Killer Whale, Pseudorca crassidens
Genus Sotalia
Tucuxi, Sotalia fluviatilis, but see the species article for a discussion
Genus Sousa
Pacific Humpback Dolphin, Sousa chinensis
Indian Humpback Dolphin, Sousa plumbea
Atlantic Humpback Dolphin, Sousa teuszii
Genus Stenella
Pantropical Spotted Dolphin, Stenella attenuata
Clymene Dolphin, Stenella clymene
Striped Dolphin, Stenella coeruleoalba
Atlantic Spotted Dolphin, Stenella frontalis
Spinner Dolphin, Stenella longirostris
Genus Steno
Rough-toothed Dolphin, Steno bredanensis
Genus Tursiops - Rice and MSW3 tentatively agree on this classification but see species article for more detail.
Indian Ocean Bottlenose Dolphin, Tursiops aduncus
Common Bottlenose Dolphin, Tursiops truncatus
Family Monodontidae
Genus Delphinapterus
Beluga, Delphinapterus leucas
Genus Monodon
Narwhal, Monodon monoceros
Family Phocoenidae: Porpoises
Genus Neophocaena
Finless Porpoise, Neophocaena phocaenoides
Genus Phocoena
Spectacled Porpoise, Phocoena dioptrica
Harbour Porpoise, Phocoena phocaena
Vaquita, Phocoena sinus
Burmeister's Porpoise, Phocoena spinipinnis
Genus Phocoenoides
Dall's Porpoise, Phocoenoides dalli
Family Physeteridae: Sperm Whale family
Genus Physeter
Sperm Whale, Physeter catodon (syn. P. macrocephalus)
Family Kogiidae - MSW3 treats Kogia as a member of Physeteridae
Genus Kogia
Pygmy Sperm Whale, Kogia breviceps
Dwarf Sperm Whale, Kogia sima
Superfamily Platanistoidea: River dolphins
Family Iniidae
Genus Inia
Amazon River Dolphin, Inia geoffrensis
Family Lipotidae - MSW3 treats Lipotes as a member of Iniidae
Genus Lipotes
† Baiji, Lipotes vexillifer
Family Pontoporiidae - MSW3 treats Pontoporia as a member of Iniidae
Genus Pontoporia
Franciscana, Pontoporia blainvillei
Family Platanistidae
Genus Platanista
Ganges and Indus River Dolphin, Platanista gangetica. MSW3 treats Platanista minor as a separate species, with common names Ganges River Dolphin and Indus River Dolphin, respectively.
Family Ziphidae, Beaked whales
Genus Berardius
Arnoux's Beaked Whale, Berardius arnuxii
Baird's Beaked Whale (North Pacific Bottlenose Whale), Berardius bairdii
Subfamily Hyperoodontidae
Genus Hyperoodon
Northern Bottlenose Whale, Hyperoodon ampullatus
Southern Bottlenose Whale, Hyperoodon planifrons
Genus Indopacetus
Indo-Pacific Beaked Whale (Longman's Beaked Whale), Indopacetus pacificus
Genus Mesoplodon, Mesoplodont Whale
Sowerby's Beaked Whale, Mesoplodon bidens
Andrews' Beaked Whale, Mesoplodon bowdoini
Hubbs' Beaked Whale, Mesoplodon carlhubbsi
Blainville's Beaked Whale, Mesoplodon densirostris
Gervais' Beaked Whale, Mesoplodon europaeus
Ginkgo-toothed Beaked Whale, Mesoplodon ginkgodens
Gray's Beaked Whale, Mesoplodon grayi
Hector's Beaked Whale, Mesoplodon hectori
Layard's Beaked Whale, Mesoplodon layardii
True's Beaked Whale, Mesoplodon mirus
Perrin's Beaked Whale, Mesoplodon perrini. This species was recognised in 2002 and as such is listed by MSW3 but not Rice.
Pygmy Beaked Whale, Mesoplodon peruvianus
Stejneger's Beaked Whale, Mesoplodon stejnegeri
Spade Toothed Whale, Mesoplodon traversii
Genus Tasmacetus
Tasman Beaked Whale (Shepherd's Beaked Whale), Tasmacetus shepherdi
Genus Ziphius
Cuvier's Beaked Whale, Ziphius cavirostris
- Suborder Mysticeti: Baleen whales
Family Balaenidae: Right whales and Bowhead Whale
Genus Balaena
Bowhead Whale, Balaena mysticetus
Genus Eubalaena
North Atlantic Right Whale, Eubalaena glacialis
North Pacific Right Whale, Eubalaena japonica
Southern Right Whale, Eubalaena australis
Family Balaenopteridae: Rorquals
Subfamily Balaenopterinae
Genus Balaenoptera
Common Minke Whale, Balaenoptera acutorostrata
Antarctic Minke Whale, Balaenoptera bonaerensis
Sei Whale, Balaenoptera borealis
Bryde's Whale, Balaenoptera brydei
Eden's Whale Balaenoptera edeni - Rice lists this as a separate species, MSW3 does not
Balaenoptera omurai - MSW3 lists this is a synonym of Bryde's Whale but suggests this may be temporary.
Blue Whale, Balaenoptera musculus
Fin Whale, Balaenoptera physalus
Subfamily Megapterinae
Genus Megaptera
Humpback Whale, Megaptera novaeangliae
† Genus Eobalaenoptera
† Harrison's Whale, Eobalaenoptera harrisoni
Family Eschrichtiidae
Genus Eschrichtius
Gray Whale, Eschrichtius robustus
Family Neobalaenidae: Pygmy Right Whale
Genus Caperea
Pygmy Right Whale, Caperea marginata
- Family Balaenidae: Right whales and Bowhead Whale
Genus Balaena
Bowhead Whale, Balaena mysticetus
Genus Eubalaena
North Atlantic Right Whale, Eubalaena glacialis
North Pacific Right Whale, Eubalaena japonica
Southern Right Whale, Eubalaena australis
- Genus Balaena
Bowhead Whale, Balaena mysticetus
- Bowhead Whale, Balaena mysticetus
- Genus Eubalaena
North Atlantic Right Whale, Eubalaena glacialis
North Pacific Right Whale, Eubalaena japonica
Southern Right Whale, Eubalaena australis
- North Atlantic Right Whale, Eubalaena glacialis
- North Pacific Right Whale, Eubalaena japonica
- Southern Right Whale, Eubalaena australis
- Family Balaenopteridae: Rorquals
Subfamily Balaenopterinae
Genus Balaenoptera
Common Minke Whale, Balaenoptera acutorostrata
Antarctic Minke Whale, Balaenoptera bonaerensis
Sei Whale, Balaenoptera borealis
Bryde's Whale, Balaenoptera brydei
Eden's Whale Balaenoptera edeni - Rice lists this as a separate species, MSW3 does not
Balaenoptera omurai - MSW3 lists this is a synonym of Bryde's Whale but suggests this may be temporary.
Blue Whale, Balaenoptera musculus
Fin Whale, Balaenoptera physalus
Subfamily Megapterinae
Genus Megaptera
Humpback Whale, Megaptera novaeangliae
- Subfamily Balaenopterinae
Genus Balaenoptera
Common Minke Whale, Balaenoptera acutorostrata
Antarctic Minke Whale, Balaenoptera bonaerensis
Sei Whale, Balaenoptera borealis
Bryde's Whale, Balaenoptera brydei
Eden's Whale Balaenoptera edeni - Rice lists this as a separate species, MSW3 does not
Balaenoptera omurai - MSW3 lists this is a synonym of Bryde's Whale but suggests this may be temporary.
Blue Whale, Balaenoptera musculus
Fin Whale, Balaenoptera physalus
- Genus Balaenoptera
Common Minke Whale, Balaenoptera acutorostrata
Antarctic Minke Whale, Balaenoptera bonaerensis
Sei Whale, Balaenoptera borealis
Bryde's Whale, Balaenoptera brydei
Eden's Whale Balaenoptera edeni - Rice lists this as a separate species, MSW3 does not
Balaenoptera omurai - MSW3 lists this is a synonym of Bryde's Whale but suggests this may be temporary.
Blue Whale, Balaenoptera musculus
Fin Whale, Balaenoptera physalus
- Common Minke Whale, Balaenoptera acutorostrata
- Antarctic Minke Whale, Balaenoptera bonaerensis
- Sei Whale, Balaenoptera borealis
- Bryde's Whale, Balaenoptera brydei
- Eden's Whale Balaenoptera edeni - Rice lists this as a separate species, MSW3 does not
- Balaenoptera omurai - MSW3 lists this is a synonym of Bryde's Whale but suggests this may be temporary.
- Blue Whale, Balaenoptera musculus
- Fin Whale, Balaenoptera physalus
- Subfamily Megapterinae
Genus Megaptera
Humpback Whale, Megaptera novaeangliae
- Genus Megaptera
Humpback Whale, Megaptera novaeangliae
- Humpback Whale, Megaptera novaeangliae
- † Genus Eobalaenoptera
† Harrison's Whale, Eobalaenoptera harrisoni
- † Harrison's Whale, Eobalaenoptera harrisoni
- Family Eschrichtiidae
Genus Eschrichtius
Gray Whale, Eschrichtius robustus
- Genus Eschrichtius
Gray Whale, Eschrichtius robustus
- Gray Whale, Eschrichtius robustus
- Family Neobalaenidae: Pygmy Right Whale
Genus Caperea
Pygmy Right Whale, Caperea marginata
- Genus Caperea
Pygmy Right Whale, Caperea marginata
- Pygmy Right Whale, Caperea marginata
- Suborder Odontoceti: toothed whales
Family Delphinidae: Dolphin
Genus Cephalorhynchus
Commerson's Dolphin, Cephalorhyncus commersonii
Chilean Dolphin, Cephalorhyncus eutropia
Heaviside's Dolphin, Cephalorhyncus heavisidii
Hector's Dolphin, Cephalorhyncus hectori
Genus Delphinus
Long-beaked Common Dolphin, Delphinus capensis
Short-beaked Common Dolphin, Delphinus delphis
Arabian Common Dolphin, Delphinus tropicalis. Rice recognises this as a separate species. MSW3 does not.
Genus Feresa
Pygmy Killer Whale, Feresa attenuata
Genus Globicephala
Short-finned Pilot Whale, Globicephala macrorhyncus
Long-finned Pilot Whale, Globicephala melas
Genus Grampus
Risso's Dolphin, Grampus griseus
Genus Lagenodelphis
Fraser's Dolphin, Lagenodelphis hosei
Genus Lagenorhynchus
Atlantic White-sided Dolphin, Lagenorhynchus acutus
White-beaked Dolphin, Lagenorhynchus albirostris
Peale's Dolphin, Lagenorhynchus australis
Hourglass Dolphin, Lagenorhynchus cruciger
Pacific White-sided Dolphin, Lagenorhynchus obliquidens
Dusky Dolphin, Lagenorhynchus obscurus
Genus Lissodelphis
Northern Right Whale Dolphin, Lissodelphis borealis
Southern Right Whale Dolphin, Lissodelphis peronii
Genus Orcaella
Irrawaddy Dolphin, Orcaella brevirostris
Australian Snubfin Dolphin, Orcaella heinsohni. 2005 discovery, thus not recognized by Rice or MSW3 and subject to revision.
Genus Orcinus
Killer Whale, Orcinus orca
Genus Peponocephala
Melon-headed Whale, Peponocephala electra
Genus Pseudorca
False Killer Whale, Pseudorca crassidens
Genus Sotalia
Tucuxi, Sotalia fluviatilis, but see the species article for a discussion
Genus Sousa
Pacific Humpback Dolphin, Sousa chinensis
Indian Humpback Dolphin, Sousa plumbea
Atlantic Humpback Dolphin, Sousa teuszii
Genus Stenella
Pantropical Spotted Dolphin, Stenella attenuata
Clymene Dolphin, Stenella clymene
Striped Dolphin, Stenella coeruleoalba
Atlantic Spotted Dolphin, Stenella frontalis
Spinner Dolphin, Stenella longirostris
Genus Steno
Rough-toothed Dolphin, Steno bredanensis
Genus Tursiops - Rice and MSW3 tentatively agree on this classification but see species article for more detail.
Indian Ocean Bottlenose Dolphin, Tursiops aduncus
Common Bottlenose Dolphin, Tursiops truncatus
Family Monodontidae
Genus Delphinapterus
Beluga, Delphinapterus leucas
Genus Monodon
Narwhal, Monodon monoceros
Family Phocoenidae: Porpoises
Genus Neophocaena
Finless Porpoise, Neophocaena phocaenoides
Genus Phocoena
Spectacled Porpoise, Phocoena dioptrica
Harbour Porpoise, Phocoena phocaena
Vaquita, Phocoena sinus
Burmeister's Porpoise, Phocoena spinipinnis
Genus Phocoenoides
Dall's Porpoise, Phocoenoides dalli
Family Physeteridae: Sperm Whale family
Genus Physeter
Sperm Whale, Physeter catodon (syn. P. macrocephalus)
Family Kogiidae - MSW3 treats Kogia as a member of Physeteridae
Genus Kogia
Pygmy Sperm Whale, Kogia breviceps
Dwarf Sperm Whale, Kogia sima
Superfamily Platanistoidea: River dolphins
Family Iniidae
Genus Inia
Amazon River Dolphin, Inia geoffrensis
Family Lipotidae - MSW3 treats Lipotes as a member of Iniidae
Genus Lipotes
† Baiji, Lipotes vexillifer
Family Pontoporiidae - MSW3 treats Pontoporia as a member of Iniidae
Genus Pontoporia
Franciscana, Pontoporia blainvillei
Family Platanistidae
Genus Platanista
Ganges and Indus River Dolphin, Platanista gangetica. MSW3 treats Platanista minor as a separate species, with common names Ganges River Dolphin and Indus River Dolphin, respectively.
Family Ziphidae, Beaked whales
Genus Berardius
Arnoux's Beaked Whale, Berardius arnuxii
Baird's Beaked Whale (North Pacific Bottlenose Whale), Berardius bairdii
Subfamily Hyperoodontidae
Genus Hyperoodon
Northern Bottlenose Whale, Hyperoodon ampullatus
Southern Bottlenose Whale, Hyperoodon planifrons
Genus Indopacetus
Indo-Pacific Beaked Whale (Longman's Beaked Whale), Indopacetus pacificus
Genus Mesoplodon, Mesoplodont Whale
Sowerby's Beaked Whale, Mesoplodon bidens
Andrews' Beaked Whale, Mesoplodon bowdoini
Hubbs' Beaked Whale, Mesoplodon carlhubbsi
Blainville's Beaked Whale, Mesoplodon densirostris
Gervais' Beaked Whale, Mesoplodon europaeus
Ginkgo-toothed Beaked Whale, Mesoplodon ginkgodens
Gray's Beaked Whale, Mesoplodon grayi
Hector's Beaked Whale, Mesoplodon hectori
Layard's Beaked Whale, Mesoplodon layardii
True's Beaked Whale, Mesoplodon mirus
Perrin's Beaked Whale, Mesoplodon perrini. This species was recognised in 2002 and as such is listed by MSW3 but not Rice.
Pygmy Beaked Whale, Mesoplodon peruvianus
Stejneger's Beaked Whale, Mesoplodon stejnegeri
Spade Toothed Whale, Mesoplodon traversii
Genus Tasmacetus
Tasman Beaked Whale (Shepherd's Beaked Whale), Tasmacetus shepherdi
Genus Ziphius
Cuvier's Beaked Whale, Ziphius cavirostris
- Family Delphinidae: Dolphin
Genus Cephalorhynchus
Commerson's Dolphin, Cephalorhyncus commersonii
Chilean Dolphin, Cephalorhyncus eutropia
Heaviside's Dolphin, Cephalorhyncus heavisidii
Hector's Dolphin, Cephalorhyncus hectori
Genus Delphinus
Long-beaked Common Dolphin, Delphinus capensis
Short-beaked Common Dolphin, Delphinus delphis
Arabian Common Dolphin, Delphinus tropicalis. Rice recognises this as a separate species. MSW3 does not.
Genus Feresa
Pygmy Killer Whale, Feresa attenuata
Genus Globicephala
Short-finned Pilot Whale, Globicephala macrorhyncus
Long-finned Pilot Whale, Globicephala melas
Genus Grampus
Risso's Dolphin, Grampus griseus
Genus Lagenodelphis
Fraser's Dolphin, Lagenodelphis hosei
Genus Lagenorhynchus
Atlantic White-sided Dolphin, Lagenorhynchus acutus
White-beaked Dolphin, Lagenorhynchus albirostris
Peale's Dolphin, Lagenorhynchus australis
Hourglass Dolphin, Lagenorhynchus cruciger
Pacific White-sided Dolphin, Lagenorhynchus obliquidens
Dusky Dolphin, Lagenorhynchus obscurus
Genus Lissodelphis
Northern Right Whale Dolphin, Lissodelphis borealis
Southern Right Whale Dolphin, Lissodelphis peronii
Genus Orcaella
Irrawaddy Dolphin, Orcaella brevirostris
Australian Snubfin Dolphin, Orcaella heinsohni. 2005 discovery, thus not recognized by Rice or MSW3 and subject to revision.
Genus Orcinus
Killer Whale, Orcinus orca
Genus Peponocephala
Melon-headed Whale, Peponocephala electra
Genus Pseudorca
False Killer Whale, Pseudorca crassidens
Genus Sotalia
Tucuxi, Sotalia fluviatilis, but see the species article for a discussion
Genus Sousa
Pacific Humpback Dolphin, Sousa chinensis
Indian Humpback Dolphin, Sousa plumbea
Atlantic Humpback Dolphin, Sousa teuszii
Genus Stenella
Pantropical Spotted Dolphin, Stenella attenuata
Clymene Dolphin, Stenella clymene
Striped Dolphin, Stenella coeruleoalba
Atlantic Spotted Dolphin, Stenella frontalis
Spinner Dolphin, Stenella longirostris
Genus Steno
Rough-toothed Dolphin, Steno bredanensis
Genus Tursiops - Rice and MSW3 tentatively agree on this classification but see species article for more detail.
Indian Ocean Bottlenose Dolphin, Tursiops aduncus
Common Bottlenose Dolphin, Tursiops truncatus
- Genus Cephalorhynchus
Commerson's Dolphin, Cephalorhyncus commersonii
Chilean Dolphin, Cephalorhyncus eutropia
Heaviside's Dolphin, Cephalorhyncus heavisidii
Hector's Dolphin, Cephalorhyncus hectori
- Commerson's Dolphin, Cephalorhyncus commersonii
- Chilean Dolphin, Cephalorhyncus eutropia
- Heaviside's Dolphin, Cephalorhyncus heavisidii
- Hector's Dolphin, Cephalorhyncus hectori
- Genus Delphinus
Long-beaked Common Dolphin, Delphinus capensis
Short-beaked Common Dolphin, Delphinus delphis
Arabian Common Dolphin, Delphinus tropicalis. Rice recognises this as a separate species. MSW3 does not.
- Long-beaked Common Dolphin, Delphinus capensis
- Short-beaked Common Dolphin, Delphinus delphis
- Arabian Common Dolphin, Delphinus tropicalis. Rice recognises this as a separate species. MSW3 does not.
- Genus Feresa
Pygmy Killer Whale, Feresa attenuata
- Pygmy Killer Whale, Feresa attenuata
- Genus Globicephala
Short-finned Pilot Whale, Globicephala macrorhyncus
Long-finned Pilot Whale, Globicephala melas
- Short-finned Pilot Whale, Globicephala macrorhyncus
- Long-finned Pilot Whale, Globicephala melas
- Genus Grampus
Risso's Dolphin, Grampus griseus
- Risso's Dolphin, Grampus griseus
- Genus Lagenodelphis
Fraser's Dolphin, Lagenodelphis hosei
- Fraser's Dolphin, Lagenodelphis hosei
- Genus Lagenorhynchus
Atlantic White-sided Dolphin, Lagenorhynchus acutus
White-beaked Dolphin, Lagenorhynchus albirostris
Peale's Dolphin, Lagenorhynchus australis
Hourglass Dolphin, Lagenorhynchus cruciger
Pacific White-sided Dolphin, Lagenorhynchus obliquidens
Dusky Dolphin, Lagenorhynchus obscurus
- Atlantic White-sided Dolphin, Lagenorhynchus acutus
- White-beaked Dolphin, Lagenorhynchus albirostris
- Peale's Dolphin, Lagenorhynchus australis
- Hourglass Dolphin, Lagenorhynchus cruciger
- Pacific White-sided Dolphin, Lagenorhynchus obliquidens
- Dusky Dolphin, Lagenorhynchus obscurus
- Genus Lissodelphis
Northern Right Whale Dolphin, Lissodelphis borealis
Southern Right Whale Dolphin, Lissodelphis peronii
- Northern Right Whale Dolphin, Lissodelphis borealis
- Southern Right Whale Dolphin, Lissodelphis peronii
- Genus Orcaella
Irrawaddy Dolphin, Orcaella brevirostris
Australian Snubfin Dolphin, Orcaella heinsohni. 2005 discovery, thus not recognized by Rice or MSW3 and subject to revision.
- Irrawaddy Dolphin, Orcaella brevirostris
- Australian Snubfin Dolphin, Orcaella heinsohni. 2005 discovery, thus not recognized by Rice or MSW3 and subject to revision.
- Genus Orcinus
Killer Whale, Orcinus orca
- Killer Whale, Orcinus orca
- Genus Peponocephala
Melon-headed Whale, Peponocephala electra
- Melon-headed Whale, Peponocephala electra
- Genus Pseudorca
False Killer Whale, Pseudorca crassidens
- False Killer Whale, Pseudorca crassidens
- Genus Sotalia
Tucuxi, Sotalia fluviatilis, but see the species article for a discussion
- Tucuxi, Sotalia fluviatilis, but see the species article for a discussion
- Genus Sousa
Pacific Humpback Dolphin, Sousa chinensis
Indian Humpback Dolphin, Sousa plumbea
Atlantic Humpback Dolphin, Sousa teuszii
- Pacific Humpback Dolphin, Sousa chinensis
- Indian Humpback Dolphin, Sousa plumbea
- Atlantic Humpback Dolphin, Sousa teuszii
- Genus Stenella
Pantropical Spotted Dolphin, Stenella attenuata
Clymene Dolphin, Stenella clymene
Striped Dolphin, Stenella coeruleoalba
Atlantic Spotted Dolphin, Stenella frontalis
Spinner Dolphin, Stenella longirostris
- Pantropical Spotted Dolphin, Stenella attenuata
- Clymene Dolphin, Stenella clymene
- Striped Dolphin, Stenella coeruleoalba
- Atlantic Spotted Dolphin, Stenella frontalis
- Spinner Dolphin, Stenella longirostris
- Genus Steno
Rough-toothed Dolphin, Steno bredanensis
- Rough-toothed Dolphin, Steno bredanensis
- Genus Tursiops - Rice and MSW3 tentatively agree on this classification but see species article for more detail.
Indian Ocean Bottlenose Dolphin, Tursiops aduncus
Common Bottlenose Dolphin, Tursiops truncatus
- Indian Ocean Bottlenose Dolphin, Tursiops aduncus
- Common Bottlenose Dolphin, Tursiops truncatus
- Family Monodontidae
Genus Delphinapterus
Beluga, Delphinapterus leucas
Genus Monodon
Narwhal, Monodon monoceros
- Genus Delphinapterus
Beluga, Delphinapterus leucas
- Beluga, Delphinapterus leucas
- Genus Monodon
Narwhal, Monodon monoceros
- Narwhal, Monodon monoceros
- Family Phocoenidae: Porpoises
Genus Neophocaena
Finless Porpoise, Neophocaena phocaenoides
Genus Phocoena
Spectacled Porpoise, Phocoena dioptrica
Harbour Porpoise, Phocoena phocaena
Vaquita, Phocoena sinus
Burmeister's Porpoise, Phocoena spinipinnis
Genus Phocoenoides
Dall's Porpoise, Phocoenoides dalli
- Genus Neophocaena
Finless Porpoise, Neophocaena phocaenoides
- Finless Porpoise, Neophocaena phocaenoides
- Genus Phocoena
Spectacled Porpoise, Phocoena dioptrica
Harbour Porpoise, Phocoena phocaena
Vaquita, Phocoena sinus
Burmeister's Porpoise, Phocoena spinipinnis
- Spectacled Porpoise, Phocoena dioptrica
- Harbour Porpoise, Phocoena phocaena
- Vaquita, Phocoena sinus
- Burmeister's Porpoise, Phocoena spinipinnis
- Genus Phocoenoides
Dall's Porpoise, Phocoenoides dalli
- Dall's Porpoise, Phocoenoides dalli
- Family Physeteridae: Sperm Whale family
Genus Physeter
Sperm Whale, Physeter catodon (syn. P. macrocephalus)
- Genus Physeter
Sperm Whale, Physeter catodon (syn. P. macrocephalus)
- Sperm Whale, Physeter catodon (syn. P. macrocephalus)
- Family Kogiidae - MSW3 treats Kogia as a member of Physeteridae
Genus Kogia
Pygmy Sperm Whale, Kogia breviceps
Dwarf Sperm Whale, Kogia sima
- Genus Kogia
Pygmy Sperm Whale, Kogia breviceps
Dwarf Sperm Whale, Kogia sima
- Pygmy Sperm Whale, Kogia breviceps
- Dwarf Sperm Whale, Kogia sima
- Superfamily Platanistoidea: River dolphins
Family Iniidae
Genus Inia
Amazon River Dolphin, Inia geoffrensis
Family Lipotidae - MSW3 treats Lipotes as a member of Iniidae
Genus Lipotes
† Baiji, Lipotes vexillifer
Family Pontoporiidae - MSW3 treats Pontoporia as a member of Iniidae
Genus Pontoporia
Franciscana, Pontoporia blainvillei
Family Platanistidae
Genus Platanista
Ganges and Indus River Dolphin, Platanista gangetica. MSW3 treats Platanista minor as a separate species, with common names Ganges River Dolphin and Indus River Dolphin, respectively.
- Family Iniidae
Genus Inia
Amazon River Dolphin, Inia geoffrensis
- Genus Inia
Amazon River Dolphin, Inia geoffrensis
- Amazon River Dolphin, Inia geoffrensis
- Family Lipotidae - MSW3 treats Lipotes as a member of Iniidae
Genus Lipotes
† Baiji, Lipotes vexillifer
- Genus Lipotes
† Baiji, Lipotes vexillifer
- † Baiji, Lipotes vexillifer
- Family Pontoporiidae - MSW3 treats Pontoporia as a member of Iniidae
Genus Pontoporia
Franciscana, Pontoporia blainvillei
- Genus Pontoporia
Franciscana, Pontoporia blainvillei
- Franciscana, Pontoporia blainvillei
- Family Platanistidae
Genus Platanista
Ganges and Indus River Dolphin, Platanista gangetica. MSW3 treats Platanista minor as a separate species, with common names Ganges River Dolphin and Indus River Dolphin, respectively.
- Genus Platanista
Ganges and Indus River Dolphin, Platanista gangetica. MSW3 treats Platanista minor as a separate species, with common names Ganges River Dolphin and Indus River Dolphin, respectively.
- Ganges and Indus River Dolphin, Platanista gangetica. MSW3 treats Platanista minor as a separate species, with common names Ganges River Dolphin and Indus River Dolphin, respectively.
- Family Ziphidae, Beaked whales
Genus Berardius
Arnoux's Beaked Whale, Berardius arnuxii
Baird's Beaked Whale (North Pacific Bottlenose Whale), Berardius bairdii
Subfamily Hyperoodontidae
Genus Hyperoodon
Northern Bottlenose Whale, Hyperoodon ampullatus
Southern Bottlenose Whale, Hyperoodon planifrons
Genus Indopacetus
Indo-Pacific Beaked Whale (Longman's Beaked Whale), Indopacetus pacificus
Genus Mesoplodon, Mesoplodont Whale
Sowerby's Beaked Whale, Mesoplodon bidens
Andrews' Beaked Whale, Mesoplodon bowdoini
Hubbs' Beaked Whale, Mesoplodon carlhubbsi
Blainville's Beaked Whale, Mesoplodon densirostris
Gervais' Beaked Whale, Mesoplodon europaeus
Ginkgo-toothed Beaked Whale, Mesoplodon ginkgodens
Gray's Beaked Whale, Mesoplodon grayi
Hector's Beaked Whale, Mesoplodon hectori
Layard's Beaked Whale, Mesoplodon layardii
True's Beaked Whale, Mesoplodon mirus
Perrin's Beaked Whale, Mesoplodon perrini. This species was recognised in 2002 and as such is listed by MSW3 but not Rice.
Pygmy Beaked Whale, Mesoplodon peruvianus
Stejneger's Beaked Whale, Mesoplodon stejnegeri
Spade Toothed Whale, Mesoplodon traversii
Genus Tasmacetus
Tasman Beaked Whale (Shepherd's Beaked Whale), Tasmacetus shepherdi
Genus Ziphius
Cuvier's Beaked Whale, Ziphius cavirostris
- Genus Berardius
Arnoux's Beaked Whale, Berardius arnuxii
Baird's Beaked Whale (North Pacific Bottlenose Whale), Berardius bairdii
- Arnoux's Beaked Whale, Berardius arnuxii
- Baird's Beaked Whale (North Pacific Bottlenose Whale), Berardius bairdii
- Subfamily Hyperoodontidae
Genus Hyperoodon
Northern Bottlenose Whale, Hyperoodon ampullatus
Southern Bottlenose Whale, Hyperoodon planifrons
Genus Indopacetus
Indo-Pacific Beaked Whale (Longman's Beaked Whale), Indopacetus pacificus
Genus Mesoplodon, Mesoplodont Whale
Sowerby's Beaked Whale, Mesoplodon bidens
Andrews' Beaked Whale, Mesoplodon bowdoini
Hubbs' Beaked Whale, Mesoplodon carlhubbsi
Blainville's Beaked Whale, Mesoplodon densirostris
Gervais' Beaked Whale, Mesoplodon europaeus
Ginkgo-toothed Beaked Whale, Mesoplodon ginkgodens
Gray's Beaked Whale, Mesoplodon grayi
Hector's Beaked Whale, Mesoplodon hectori
Layard's Beaked Whale, Mesoplodon layardii
True's Beaked Whale, Mesoplodon mirus
Perrin's Beaked Whale, Mesoplodon perrini. This species was recognised in 2002 and as such is listed by MSW3 but not Rice.
Pygmy Beaked Whale, Mesoplodon peruvianus
Stejneger's Beaked Whale, Mesoplodon stejnegeri
Spade Toothed Whale, Mesoplodon traversii
- Genus Hyperoodon
Northern Bottlenose Whale, Hyperoodon ampullatus
Southern Bottlenose Whale, Hyperoodon planifrons
- Northern Bottlenose Whale, Hyperoodon ampullatus
- Southern Bottlenose Whale, Hyperoodon planifrons
- Genus Indopacetus
Indo-Pacific Beaked Whale (Longman's Beaked Whale), Indopacetus pacificus
- Indo-Pacific Beaked Whale (Longman's Beaked Whale), Indopacetus pacificus
- Genus Mesoplodon, Mesoplodont Whale
Sowerby's Beaked Whale, Mesoplodon bidens
Andrews' Beaked Whale, Mesoplodon bowdoini
Hubbs' Beaked Whale, Mesoplodon carlhubbsi
Blainville's Beaked Whale, Mesoplodon densirostris
Gervais' Beaked Whale, Mesoplodon europaeus
Ginkgo-toothed Beaked Whale, Mesoplodon ginkgodens
Gray's Beaked Whale, Mesoplodon grayi
Hector's Beaked Whale, Mesoplodon hectori
Layard's Beaked Whale, Mesoplodon layardii
True's Beaked Whale, Mesoplodon mirus
Perrin's Beaked Whale, Mesoplodon perrini. This species was recognised in 2002 and as such is listed by MSW3 but not Rice.
Pygmy Beaked Whale, Mesoplodon peruvianus
Stejneger's Beaked Whale, Mesoplodon stejnegeri
Spade Toothed Whale, Mesoplodon traversii
- Sowerby's Beaked Whale, Mesoplodon bidens
- Andrews' Beaked Whale, Mesoplodon bowdoini
- Hubbs' Beaked Whale, Mesoplodon carlhubbsi
- Blainville's Beaked Whale, Mesoplodon densirostris
- Gervais' Beaked Whale, Mesoplodon europaeus
- Ginkgo-toothed Beaked Whale, Mesoplodon ginkgodens
- Gray's Beaked Whale, Mesoplodon grayi
- Hector's Beaked Whale, Mesoplodon hectori
- Layard's Beaked Whale, Mesoplodon layardii
- True's Beaked Whale, Mesoplodon mirus
- Perrin's Beaked Whale, Mesoplodon perrini. This species was recognised in 2002 and as such is listed by MSW3 but not Rice.
- Pygmy Beaked Whale, Mesoplodon peruvianus
- Stejneger's Beaked Whale, Mesoplodon stejnegeri
- Spade Toothed Whale, Mesoplodon traversii
- Genus Tasmacetus
Tasman Beaked Whale (Shepherd's Beaked Whale), Tasmacetus shepherdi
- Tasman Beaked Whale (Shepherd's Beaked Whale), Tasmacetus shepherdi
- Genus Ziphius
Cuvier's Beaked Whale, Ziphius cavirostris
- Cuvier's Beaked Whale, Ziphius cavirostris
†Extinct | Cetacea
The order Cetacea (Template:IPAEng, L. cetus, whale) includes whales, dolphins and porpoises.
Cetus is Latin and is used in biological names to mean "whale"; its original meaning, "large sea animal," was more general. It comes from Ancient Greek κῆτος (kētos), meaning "whale" or "any huge fish or sea monster". Cetology is the branch of marine science associated with the study of cetaceans.
Cetaceans are the mammals most fully adapted to aquatic life. Their body is fusiform (spindle-shaped). The forelimbs are modified into flippers. The tiny hindlimbs are vestigial; they do not attach to the backbone and are hidden within the body. The tail has horizontal flukes.
Cetaceans are nearly hairless, and are insulated by a thick layer of blubber. As a group, they are noted for their high intelligence.
The order Cetacea contains ninety species, all marine except for five species of freshwater dolphins. The order is divided into two suborders, Mysticeti (baleen whales) and Odontoceti (toothed whales, which includes dolphins and porpoises).
# Respiration, vision, hearing and echolocation
As mammals, cetaceans need to breathe air. Because of this, they need to come to the water's surface to exhale carbon dioxide and inhale a fresh supply of oxygen. During diving, a muscular action closes the blowholes (nostrils), which remain closed until the cetacean next breaks the surface; when it surfaces, the muscles open the blowholes and warm air is exhaled.
Cetaceans' blowholes have evolved to a position on top of the head, allowing more time to expel stale air and inhale fresh air. When the stale air, warmed from the lungs, is exhaled, it condenses as it meets the cold air outside. As with a terrestrial mammal breathing out on a cold day, a small cloud of 'steam' appears. This is called the 'blow' or 'spout' and is different in terms of shape, angle and height, for each cetacean species. Cetaceans can be identified at a distance, using this characteristic, by experienced whalers or whale-watchers.
Cetaceans can go underwater for much longer periods of time than other mammals. Their duration under water varies greatly between speicies due to large physiological differences between many members of this Order. There are two studied[citation needed] advantages of cetacean physiology that let this Order (and other marine mammals) forage underwater for extended periods of time without breathing at the water surface.
Myoglobin concentrations in skeletal muscle of mammals have much variation. A New Zealand white rabbit has 0.08+/-0.06 g (in a 100 g Wet muscle) of myoglobin[1], whereas a Northern bottlenose whale has 6.34 g (in a 100 g Wet muscle) of myoglobin[2]. Myoglobin, by nature, has a higher affinity to oxygen than haemoglobin. That is, myoglobin retains oxygen molecules better than hemoglobin. Therefore, it is useful to have higher concentrations of myoglobin when needed and there is no oxygen available for re-uptake. The higher the myoglobin concentration in cetacean skeletal muscle, the longer they can stay underwater and forage.
Increased body size is another way of elongating dive duration of large cetaceans. This is true because of two considered aspects. An increase in body size means that there is increase in muscle mass, therefore, increase in muscle oxygen stores. Another aspect is the universal correlation of mass and metabolic rate (Kleiber's law). In layman’s terms Kleiber’s law states that the metabolic rate of a large animal is slower than a small animal per unit mass. From this we can conclude that larger animals will use up less oxygen than smaller animals (per mass unit).
The cetacean's eyes are set well back and to either side of its huge head. This means that cetaceans with pointed 'beaks' (such as dolphins) have good binocular vision forward and downward but others, with blunt heads (such as the Sperm Whale), can see either side but not directly ahead or directly behind. Tear glands secrete greasy tears, which protect the eyes from the salt in the water. Cetaceans also have an almost spherical lens in their eyes, which is most efficient at focusing what little light there is in the deep waters. Cetaceans make up for their generally quite poor vision (with the exception of the dolphin) with excellent hearing.
As with the eyes, the cetacean's ears are also small. Life in the sea accounts for the cetacean's loss of its external ears, whose function is to collect airborne sound waves and focus them in order for them to become strong enough to hear well. However, water is a better conductor of sound than air, so the external ear was no longer needed: It is no more than a tiny hole in the skin, just behind the eye. The inner ear, however, has become so well developed that the cetacean can not only hear sounds dozens of miles away, but it can also discern from which direction the sound comes.
Some cetaceans are capable of echolocation. Many toothed whales emit clicks similar to those in echolocation, but it has not been demonstrated that they echolocate. Mysticeti have little need of echolocation, as they prey upon small fish that would be impractical to locate with echolocation. Some members of Odontoceti, such as dolphins and porpoises, do perform echolocation. These cetaceans use sound in the same way as bats - they emit a sound (called a click), which then bounces off an object and returns to them. From this, cetaceans can discern the size, shape, surface characteristics and movement of the object, as well as how far away it is. With this ability cetaceans can search for, chase and catch fast-swimming prey in total darkness. Echolocation is so advanced in most Odontoceti that they can distinguish between prey and non-prey (such as humans or boats); captive cetaceans can be trained to distinguish between, for example, balls of different sizes or shapes.
Cetaceans also use sound to communicate, whether it be groans, moans, whistles, clicks or the complex 'singing' of the Humpback Whale.
# Feeding
When it comes to food and feeding, cetaceans can be separated into two distinct groups. The toothed whales, Odontoceti like sperm whales, beluga whales, dolphins and porpoises, usually have lots of teeth that they use for catching fish, squid or other marine life. They do not chew their food, but swallow it whole. In the rare cases that they catch large prey, as when Orca (Orcinus orca) catch a seal, they tear chunks off it that in turn are swallowed whole.
The baleen whales or Mysticeti do not have teeth. Instead they have plates made of keratin (the same substance as human fingernails) which hang down from the upper jaw. These plates act like a giant filter, straining small animals (such as krill and fish) from the seawater. Cetaceans included in this group include the Blue Whale, the Humpback Whale, the Bowhead Whale and the Minke Whale.
Not all Mysticeti feed on plankton: the larger whales tend to eat small shoaling fish, such as herrings and sardine, called micronecton. One species of Mysticeti, the Gray Whale (Eschrichtius robustus), is a benthic feeder, primarily eating sea floor crustaceans.
# Mammalian nature
Cetaceans are mammals, that is, members of the class Mammalia. The closest living relative of cetaceans is the hippopotamus.[3][4]
As mammals, cetaceans have characteristics that are common to all mammals: They are warm-blooded, breathe in air through their lungs, bear their young alive and suckle them on their own milk, and have hair, although very little of it.
Another way of discerning a cetacean from a fish is by the shape of the tail. The tail of a fish is vertical and moves from side to side when the fish swims. The tail of a cetacean – called a fluke – is horizontal and moves up and down, as cetaceans' spines bend in the same manner as a human spine.
# Taxonomic listing
Template:Seealso
The classification here closely follows Dale W. Rice, Marine Mammals of the World: Systematics and Distribution (1998), which has become the standard taxonomy reference in the field. There is very close agreement between this classification and that of Mammal Species of the World: 3rd Edition (Wilson and Reeder eds., 2005). Any differences are noted using the abbreviations "Rice" and "MSW3" respectively. Further differences due to recent discoveries are also noted.
Discussion of synonyms and subspecies are relegated to the relevant genus and species articles.
- ORDER CETACEA
Suborder Mysticeti: Baleen whales
Family Balaenidae: Right whales and Bowhead Whale
Genus Balaena
Bowhead Whale, Balaena mysticetus
Genus Eubalaena
North Atlantic Right Whale, Eubalaena glacialis
North Pacific Right Whale, Eubalaena japonica
Southern Right Whale, Eubalaena australis
Family Balaenopteridae: Rorquals
Subfamily Balaenopterinae
Genus Balaenoptera
Common Minke Whale, Balaenoptera acutorostrata
Antarctic Minke Whale, Balaenoptera bonaerensis
Sei Whale, Balaenoptera borealis
Bryde's Whale, Balaenoptera brydei
Eden's Whale Balaenoptera edeni - Rice lists this as a separate species, MSW3 does not
Balaenoptera omurai - MSW3 lists this is a synonym of Bryde's Whale but suggests this may be temporary.
Blue Whale, Balaenoptera musculus
Fin Whale, Balaenoptera physalus
Subfamily Megapterinae
Genus Megaptera
Humpback Whale, Megaptera novaeangliae
† Genus Eobalaenoptera
† Harrison's Whale, Eobalaenoptera harrisoni
Family Eschrichtiidae
Genus Eschrichtius
Gray Whale, Eschrichtius robustus
Family Neobalaenidae: Pygmy Right Whale
Genus Caperea
Pygmy Right Whale, Caperea marginata
Suborder Odontoceti: toothed whales
Family Delphinidae: Dolphin
Genus Cephalorhynchus
Commerson's Dolphin, Cephalorhyncus commersonii
Chilean Dolphin, Cephalorhyncus eutropia
Heaviside's Dolphin, Cephalorhyncus heavisidii
Hector's Dolphin, Cephalorhyncus hectori
Genus Delphinus
Long-beaked Common Dolphin, Delphinus capensis
Short-beaked Common Dolphin, Delphinus delphis
Arabian Common Dolphin, Delphinus tropicalis. Rice recognises this as a separate species. MSW3 does not.
Genus Feresa
Pygmy Killer Whale, Feresa attenuata
Genus Globicephala
Short-finned Pilot Whale, Globicephala macrorhyncus
Long-finned Pilot Whale, Globicephala melas
Genus Grampus
Risso's Dolphin, Grampus griseus
Genus Lagenodelphis
Fraser's Dolphin, Lagenodelphis hosei
Genus Lagenorhynchus
Atlantic White-sided Dolphin, Lagenorhynchus acutus
White-beaked Dolphin, Lagenorhynchus albirostris
Peale's Dolphin, Lagenorhynchus australis
Hourglass Dolphin, Lagenorhynchus cruciger
Pacific White-sided Dolphin, Lagenorhynchus obliquidens
Dusky Dolphin, Lagenorhynchus obscurus
Genus Lissodelphis
Northern Right Whale Dolphin, Lissodelphis borealis
Southern Right Whale Dolphin, Lissodelphis peronii
Genus Orcaella
Irrawaddy Dolphin, Orcaella brevirostris
Australian Snubfin Dolphin, Orcaella heinsohni. 2005 discovery, thus not recognized by Rice or MSW3 and subject to revision.
Genus Orcinus
Killer Whale, Orcinus orca
Genus Peponocephala
Melon-headed Whale, Peponocephala electra
Genus Pseudorca
False Killer Whale, Pseudorca crassidens
Genus Sotalia
Tucuxi, Sotalia fluviatilis, but see the species article for a discussion
Genus Sousa
Pacific Humpback Dolphin, Sousa chinensis
Indian Humpback Dolphin, Sousa plumbea
Atlantic Humpback Dolphin, Sousa teuszii
Genus Stenella
Pantropical Spotted Dolphin, Stenella attenuata
Clymene Dolphin, Stenella clymene
Striped Dolphin, Stenella coeruleoalba
Atlantic Spotted Dolphin, Stenella frontalis
Spinner Dolphin, Stenella longirostris
Genus Steno
Rough-toothed Dolphin, Steno bredanensis
Genus Tursiops - Rice and MSW3 tentatively agree on this classification but see species article for more detail.
Indian Ocean Bottlenose Dolphin, Tursiops aduncus
Common Bottlenose Dolphin, Tursiops truncatus
Family Monodontidae
Genus Delphinapterus
Beluga, Delphinapterus leucas
Genus Monodon
Narwhal, Monodon monoceros
Family Phocoenidae: Porpoises
Genus Neophocaena
Finless Porpoise, Neophocaena phocaenoides
Genus Phocoena
Spectacled Porpoise, Phocoena dioptrica
Harbour Porpoise, Phocoena phocaena
Vaquita, Phocoena sinus
Burmeister's Porpoise, Phocoena spinipinnis
Genus Phocoenoides
Dall's Porpoise, Phocoenoides dalli
Family Physeteridae: Sperm Whale family
Genus Physeter
Sperm Whale, Physeter catodon (syn. P. macrocephalus)
Family Kogiidae - MSW3 treats Kogia as a member of Physeteridae
Genus Kogia
Pygmy Sperm Whale, Kogia breviceps
Dwarf Sperm Whale, Kogia sima
Superfamily Platanistoidea: River dolphins
Family Iniidae
Genus Inia
Amazon River Dolphin, Inia geoffrensis
Family Lipotidae - MSW3 treats Lipotes as a member of Iniidae
Genus Lipotes
† Baiji, Lipotes vexillifer
Family Pontoporiidae - MSW3 treats Pontoporia as a member of Iniidae
Genus Pontoporia
Franciscana, Pontoporia blainvillei
Family Platanistidae
Genus Platanista
Ganges and Indus River Dolphin, Platanista gangetica. MSW3 treats Platanista minor as a separate species, with common names Ganges River Dolphin and Indus River Dolphin, respectively.
Family Ziphidae, Beaked whales
Genus Berardius
Arnoux's Beaked Whale, Berardius arnuxii
Baird's Beaked Whale (North Pacific Bottlenose Whale), Berardius bairdii
Subfamily Hyperoodontidae
Genus Hyperoodon
Northern Bottlenose Whale, Hyperoodon ampullatus
Southern Bottlenose Whale, Hyperoodon planifrons
Genus Indopacetus
Indo-Pacific Beaked Whale (Longman's Beaked Whale), Indopacetus pacificus
Genus Mesoplodon, Mesoplodont Whale
Sowerby's Beaked Whale, Mesoplodon bidens
Andrews' Beaked Whale, Mesoplodon bowdoini
Hubbs' Beaked Whale, Mesoplodon carlhubbsi
Blainville's Beaked Whale, Mesoplodon densirostris
Gervais' Beaked Whale, Mesoplodon europaeus
Ginkgo-toothed Beaked Whale, Mesoplodon ginkgodens
Gray's Beaked Whale, Mesoplodon grayi
Hector's Beaked Whale, Mesoplodon hectori
Layard's Beaked Whale, Mesoplodon layardii
True's Beaked Whale, Mesoplodon mirus
Perrin's Beaked Whale, Mesoplodon perrini. This species was recognised in 2002 and as such is listed by MSW3 but not Rice.
Pygmy Beaked Whale, Mesoplodon peruvianus
Stejneger's Beaked Whale, Mesoplodon stejnegeri
Spade Toothed Whale, Mesoplodon traversii
Genus Tasmacetus
Tasman Beaked Whale (Shepherd's Beaked Whale), Tasmacetus shepherdi
Genus Ziphius
Cuvier's Beaked Whale, Ziphius cavirostris
- Suborder Mysticeti: Baleen whales
Family Balaenidae: Right whales and Bowhead Whale
Genus Balaena
Bowhead Whale, Balaena mysticetus
Genus Eubalaena
North Atlantic Right Whale, Eubalaena glacialis
North Pacific Right Whale, Eubalaena japonica
Southern Right Whale, Eubalaena australis
Family Balaenopteridae: Rorquals
Subfamily Balaenopterinae
Genus Balaenoptera
Common Minke Whale, Balaenoptera acutorostrata
Antarctic Minke Whale, Balaenoptera bonaerensis
Sei Whale, Balaenoptera borealis
Bryde's Whale, Balaenoptera brydei
Eden's Whale Balaenoptera edeni - Rice lists this as a separate species, MSW3 does not
Balaenoptera omurai - MSW3 lists this is a synonym of Bryde's Whale but suggests this may be temporary.
Blue Whale, Balaenoptera musculus
Fin Whale, Balaenoptera physalus
Subfamily Megapterinae
Genus Megaptera
Humpback Whale, Megaptera novaeangliae
† Genus Eobalaenoptera
† Harrison's Whale, Eobalaenoptera harrisoni
Family Eschrichtiidae
Genus Eschrichtius
Gray Whale, Eschrichtius robustus
Family Neobalaenidae: Pygmy Right Whale
Genus Caperea
Pygmy Right Whale, Caperea marginata
- Family Balaenidae: Right whales and Bowhead Whale
Genus Balaena
Bowhead Whale, Balaena mysticetus
Genus Eubalaena
North Atlantic Right Whale, Eubalaena glacialis
North Pacific Right Whale, Eubalaena japonica
Southern Right Whale, Eubalaena australis
- Genus Balaena
Bowhead Whale, Balaena mysticetus
- Bowhead Whale, Balaena mysticetus
- Genus Eubalaena
North Atlantic Right Whale, Eubalaena glacialis
North Pacific Right Whale, Eubalaena japonica
Southern Right Whale, Eubalaena australis
- North Atlantic Right Whale, Eubalaena glacialis
- North Pacific Right Whale, Eubalaena japonica
- Southern Right Whale, Eubalaena australis
- Family Balaenopteridae: Rorquals
Subfamily Balaenopterinae
Genus Balaenoptera
Common Minke Whale, Balaenoptera acutorostrata
Antarctic Minke Whale, Balaenoptera bonaerensis
Sei Whale, Balaenoptera borealis
Bryde's Whale, Balaenoptera brydei
Eden's Whale Balaenoptera edeni - Rice lists this as a separate species, MSW3 does not
Balaenoptera omurai - MSW3 lists this is a synonym of Bryde's Whale but suggests this may be temporary.
Blue Whale, Balaenoptera musculus
Fin Whale, Balaenoptera physalus
Subfamily Megapterinae
Genus Megaptera
Humpback Whale, Megaptera novaeangliae
- Subfamily Balaenopterinae
Genus Balaenoptera
Common Minke Whale, Balaenoptera acutorostrata
Antarctic Minke Whale, Balaenoptera bonaerensis
Sei Whale, Balaenoptera borealis
Bryde's Whale, Balaenoptera brydei
Eden's Whale Balaenoptera edeni - Rice lists this as a separate species, MSW3 does not
Balaenoptera omurai - MSW3 lists this is a synonym of Bryde's Whale but suggests this may be temporary.
Blue Whale, Balaenoptera musculus
Fin Whale, Balaenoptera physalus
- Genus Balaenoptera
Common Minke Whale, Balaenoptera acutorostrata
Antarctic Minke Whale, Balaenoptera bonaerensis
Sei Whale, Balaenoptera borealis
Bryde's Whale, Balaenoptera brydei
Eden's Whale Balaenoptera edeni - Rice lists this as a separate species, MSW3 does not
Balaenoptera omurai - MSW3 lists this is a synonym of Bryde's Whale but suggests this may be temporary.
Blue Whale, Balaenoptera musculus
Fin Whale, Balaenoptera physalus
- Common Minke Whale, Balaenoptera acutorostrata
- Antarctic Minke Whale, Balaenoptera bonaerensis
- Sei Whale, Balaenoptera borealis
- Bryde's Whale, Balaenoptera brydei
- Eden's Whale Balaenoptera edeni - Rice lists this as a separate species, MSW3 does not
- Balaenoptera omurai - MSW3 lists this is a synonym of Bryde's Whale but suggests this may be temporary.
- Blue Whale, Balaenoptera musculus
- Fin Whale, Balaenoptera physalus
- Subfamily Megapterinae
Genus Megaptera
Humpback Whale, Megaptera novaeangliae
- Genus Megaptera
Humpback Whale, Megaptera novaeangliae
- Humpback Whale, Megaptera novaeangliae
- † Genus Eobalaenoptera
† Harrison's Whale, Eobalaenoptera harrisoni
- † Harrison's Whale, Eobalaenoptera harrisoni
- Family Eschrichtiidae
Genus Eschrichtius
Gray Whale, Eschrichtius robustus
- Genus Eschrichtius
Gray Whale, Eschrichtius robustus
- Gray Whale, Eschrichtius robustus
- Family Neobalaenidae: Pygmy Right Whale
Genus Caperea
Pygmy Right Whale, Caperea marginata
- Genus Caperea
Pygmy Right Whale, Caperea marginata
- Pygmy Right Whale, Caperea marginata
- Suborder Odontoceti: toothed whales
Family Delphinidae: Dolphin
Genus Cephalorhynchus
Commerson's Dolphin, Cephalorhyncus commersonii
Chilean Dolphin, Cephalorhyncus eutropia
Heaviside's Dolphin, Cephalorhyncus heavisidii
Hector's Dolphin, Cephalorhyncus hectori
Genus Delphinus
Long-beaked Common Dolphin, Delphinus capensis
Short-beaked Common Dolphin, Delphinus delphis
Arabian Common Dolphin, Delphinus tropicalis. Rice recognises this as a separate species. MSW3 does not.
Genus Feresa
Pygmy Killer Whale, Feresa attenuata
Genus Globicephala
Short-finned Pilot Whale, Globicephala macrorhyncus
Long-finned Pilot Whale, Globicephala melas
Genus Grampus
Risso's Dolphin, Grampus griseus
Genus Lagenodelphis
Fraser's Dolphin, Lagenodelphis hosei
Genus Lagenorhynchus
Atlantic White-sided Dolphin, Lagenorhynchus acutus
White-beaked Dolphin, Lagenorhynchus albirostris
Peale's Dolphin, Lagenorhynchus australis
Hourglass Dolphin, Lagenorhynchus cruciger
Pacific White-sided Dolphin, Lagenorhynchus obliquidens
Dusky Dolphin, Lagenorhynchus obscurus
Genus Lissodelphis
Northern Right Whale Dolphin, Lissodelphis borealis
Southern Right Whale Dolphin, Lissodelphis peronii
Genus Orcaella
Irrawaddy Dolphin, Orcaella brevirostris
Australian Snubfin Dolphin, Orcaella heinsohni. 2005 discovery, thus not recognized by Rice or MSW3 and subject to revision.
Genus Orcinus
Killer Whale, Orcinus orca
Genus Peponocephala
Melon-headed Whale, Peponocephala electra
Genus Pseudorca
False Killer Whale, Pseudorca crassidens
Genus Sotalia
Tucuxi, Sotalia fluviatilis, but see the species article for a discussion
Genus Sousa
Pacific Humpback Dolphin, Sousa chinensis
Indian Humpback Dolphin, Sousa plumbea
Atlantic Humpback Dolphin, Sousa teuszii
Genus Stenella
Pantropical Spotted Dolphin, Stenella attenuata
Clymene Dolphin, Stenella clymene
Striped Dolphin, Stenella coeruleoalba
Atlantic Spotted Dolphin, Stenella frontalis
Spinner Dolphin, Stenella longirostris
Genus Steno
Rough-toothed Dolphin, Steno bredanensis
Genus Tursiops - Rice and MSW3 tentatively agree on this classification but see species article for more detail.
Indian Ocean Bottlenose Dolphin, Tursiops aduncus
Common Bottlenose Dolphin, Tursiops truncatus
Family Monodontidae
Genus Delphinapterus
Beluga, Delphinapterus leucas
Genus Monodon
Narwhal, Monodon monoceros
Family Phocoenidae: Porpoises
Genus Neophocaena
Finless Porpoise, Neophocaena phocaenoides
Genus Phocoena
Spectacled Porpoise, Phocoena dioptrica
Harbour Porpoise, Phocoena phocaena
Vaquita, Phocoena sinus
Burmeister's Porpoise, Phocoena spinipinnis
Genus Phocoenoides
Dall's Porpoise, Phocoenoides dalli
Family Physeteridae: Sperm Whale family
Genus Physeter
Sperm Whale, Physeter catodon (syn. P. macrocephalus)
Family Kogiidae - MSW3 treats Kogia as a member of Physeteridae
Genus Kogia
Pygmy Sperm Whale, Kogia breviceps
Dwarf Sperm Whale, Kogia sima
Superfamily Platanistoidea: River dolphins
Family Iniidae
Genus Inia
Amazon River Dolphin, Inia geoffrensis
Family Lipotidae - MSW3 treats Lipotes as a member of Iniidae
Genus Lipotes
† Baiji, Lipotes vexillifer
Family Pontoporiidae - MSW3 treats Pontoporia as a member of Iniidae
Genus Pontoporia
Franciscana, Pontoporia blainvillei
Family Platanistidae
Genus Platanista
Ganges and Indus River Dolphin, Platanista gangetica. MSW3 treats Platanista minor as a separate species, with common names Ganges River Dolphin and Indus River Dolphin, respectively.
Family Ziphidae, Beaked whales
Genus Berardius
Arnoux's Beaked Whale, Berardius arnuxii
Baird's Beaked Whale (North Pacific Bottlenose Whale), Berardius bairdii
Subfamily Hyperoodontidae
Genus Hyperoodon
Northern Bottlenose Whale, Hyperoodon ampullatus
Southern Bottlenose Whale, Hyperoodon planifrons
Genus Indopacetus
Indo-Pacific Beaked Whale (Longman's Beaked Whale), Indopacetus pacificus
Genus Mesoplodon, Mesoplodont Whale
Sowerby's Beaked Whale, Mesoplodon bidens
Andrews' Beaked Whale, Mesoplodon bowdoini
Hubbs' Beaked Whale, Mesoplodon carlhubbsi
Blainville's Beaked Whale, Mesoplodon densirostris
Gervais' Beaked Whale, Mesoplodon europaeus
Ginkgo-toothed Beaked Whale, Mesoplodon ginkgodens
Gray's Beaked Whale, Mesoplodon grayi
Hector's Beaked Whale, Mesoplodon hectori
Layard's Beaked Whale, Mesoplodon layardii
True's Beaked Whale, Mesoplodon mirus
Perrin's Beaked Whale, Mesoplodon perrini. This species was recognised in 2002 and as such is listed by MSW3 but not Rice.
Pygmy Beaked Whale, Mesoplodon peruvianus
Stejneger's Beaked Whale, Mesoplodon stejnegeri
Spade Toothed Whale, Mesoplodon traversii
Genus Tasmacetus
Tasman Beaked Whale (Shepherd's Beaked Whale), Tasmacetus shepherdi
Genus Ziphius
Cuvier's Beaked Whale, Ziphius cavirostris
- Family Delphinidae: Dolphin
Genus Cephalorhynchus
Commerson's Dolphin, Cephalorhyncus commersonii
Chilean Dolphin, Cephalorhyncus eutropia
Heaviside's Dolphin, Cephalorhyncus heavisidii
Hector's Dolphin, Cephalorhyncus hectori
Genus Delphinus
Long-beaked Common Dolphin, Delphinus capensis
Short-beaked Common Dolphin, Delphinus delphis
Arabian Common Dolphin, Delphinus tropicalis. Rice recognises this as a separate species. MSW3 does not.
Genus Feresa
Pygmy Killer Whale, Feresa attenuata
Genus Globicephala
Short-finned Pilot Whale, Globicephala macrorhyncus
Long-finned Pilot Whale, Globicephala melas
Genus Grampus
Risso's Dolphin, Grampus griseus
Genus Lagenodelphis
Fraser's Dolphin, Lagenodelphis hosei
Genus Lagenorhynchus
Atlantic White-sided Dolphin, Lagenorhynchus acutus
White-beaked Dolphin, Lagenorhynchus albirostris
Peale's Dolphin, Lagenorhynchus australis
Hourglass Dolphin, Lagenorhynchus cruciger
Pacific White-sided Dolphin, Lagenorhynchus obliquidens
Dusky Dolphin, Lagenorhynchus obscurus
Genus Lissodelphis
Northern Right Whale Dolphin, Lissodelphis borealis
Southern Right Whale Dolphin, Lissodelphis peronii
Genus Orcaella
Irrawaddy Dolphin, Orcaella brevirostris
Australian Snubfin Dolphin, Orcaella heinsohni. 2005 discovery, thus not recognized by Rice or MSW3 and subject to revision.
Genus Orcinus
Killer Whale, Orcinus orca
Genus Peponocephala
Melon-headed Whale, Peponocephala electra
Genus Pseudorca
False Killer Whale, Pseudorca crassidens
Genus Sotalia
Tucuxi, Sotalia fluviatilis, but see the species article for a discussion
Genus Sousa
Pacific Humpback Dolphin, Sousa chinensis
Indian Humpback Dolphin, Sousa plumbea
Atlantic Humpback Dolphin, Sousa teuszii
Genus Stenella
Pantropical Spotted Dolphin, Stenella attenuata
Clymene Dolphin, Stenella clymene
Striped Dolphin, Stenella coeruleoalba
Atlantic Spotted Dolphin, Stenella frontalis
Spinner Dolphin, Stenella longirostris
Genus Steno
Rough-toothed Dolphin, Steno bredanensis
Genus Tursiops - Rice and MSW3 tentatively agree on this classification but see species article for more detail.
Indian Ocean Bottlenose Dolphin, Tursiops aduncus
Common Bottlenose Dolphin, Tursiops truncatus
- Genus Cephalorhynchus
Commerson's Dolphin, Cephalorhyncus commersonii
Chilean Dolphin, Cephalorhyncus eutropia
Heaviside's Dolphin, Cephalorhyncus heavisidii
Hector's Dolphin, Cephalorhyncus hectori
- Commerson's Dolphin, Cephalorhyncus commersonii
- Chilean Dolphin, Cephalorhyncus eutropia
- Heaviside's Dolphin, Cephalorhyncus heavisidii
- Hector's Dolphin, Cephalorhyncus hectori
- Genus Delphinus
Long-beaked Common Dolphin, Delphinus capensis
Short-beaked Common Dolphin, Delphinus delphis
Arabian Common Dolphin, Delphinus tropicalis. Rice recognises this as a separate species. MSW3 does not.
- Long-beaked Common Dolphin, Delphinus capensis
- Short-beaked Common Dolphin, Delphinus delphis
- Arabian Common Dolphin, Delphinus tropicalis. Rice recognises this as a separate species. MSW3 does not.
- Genus Feresa
Pygmy Killer Whale, Feresa attenuata
- Pygmy Killer Whale, Feresa attenuata
- Genus Globicephala
Short-finned Pilot Whale, Globicephala macrorhyncus
Long-finned Pilot Whale, Globicephala melas
- Short-finned Pilot Whale, Globicephala macrorhyncus
- Long-finned Pilot Whale, Globicephala melas
- Genus Grampus
Risso's Dolphin, Grampus griseus
- Risso's Dolphin, Grampus griseus
- Genus Lagenodelphis
Fraser's Dolphin, Lagenodelphis hosei
- Fraser's Dolphin, Lagenodelphis hosei
- Genus Lagenorhynchus
Atlantic White-sided Dolphin, Lagenorhynchus acutus
White-beaked Dolphin, Lagenorhynchus albirostris
Peale's Dolphin, Lagenorhynchus australis
Hourglass Dolphin, Lagenorhynchus cruciger
Pacific White-sided Dolphin, Lagenorhynchus obliquidens
Dusky Dolphin, Lagenorhynchus obscurus
- Atlantic White-sided Dolphin, Lagenorhynchus acutus
- White-beaked Dolphin, Lagenorhynchus albirostris
- Peale's Dolphin, Lagenorhynchus australis
- Hourglass Dolphin, Lagenorhynchus cruciger
- Pacific White-sided Dolphin, Lagenorhynchus obliquidens
- Dusky Dolphin, Lagenorhynchus obscurus
- Genus Lissodelphis
Northern Right Whale Dolphin, Lissodelphis borealis
Southern Right Whale Dolphin, Lissodelphis peronii
- Northern Right Whale Dolphin, Lissodelphis borealis
- Southern Right Whale Dolphin, Lissodelphis peronii
- Genus Orcaella
Irrawaddy Dolphin, Orcaella brevirostris
Australian Snubfin Dolphin, Orcaella heinsohni. 2005 discovery, thus not recognized by Rice or MSW3 and subject to revision.
- Irrawaddy Dolphin, Orcaella brevirostris
- Australian Snubfin Dolphin, Orcaella heinsohni. 2005 discovery, thus not recognized by Rice or MSW3 and subject to revision.
- Genus Orcinus
Killer Whale, Orcinus orca
- Killer Whale, Orcinus orca
- Genus Peponocephala
Melon-headed Whale, Peponocephala electra
- Melon-headed Whale, Peponocephala electra
- Genus Pseudorca
False Killer Whale, Pseudorca crassidens
- False Killer Whale, Pseudorca crassidens
- Genus Sotalia
Tucuxi, Sotalia fluviatilis, but see the species article for a discussion
- Tucuxi, Sotalia fluviatilis, but see the species article for a discussion
- Genus Sousa
Pacific Humpback Dolphin, Sousa chinensis
Indian Humpback Dolphin, Sousa plumbea
Atlantic Humpback Dolphin, Sousa teuszii
- Pacific Humpback Dolphin, Sousa chinensis
- Indian Humpback Dolphin, Sousa plumbea
- Atlantic Humpback Dolphin, Sousa teuszii
- Genus Stenella
Pantropical Spotted Dolphin, Stenella attenuata
Clymene Dolphin, Stenella clymene
Striped Dolphin, Stenella coeruleoalba
Atlantic Spotted Dolphin, Stenella frontalis
Spinner Dolphin, Stenella longirostris
- Pantropical Spotted Dolphin, Stenella attenuata
- Clymene Dolphin, Stenella clymene
- Striped Dolphin, Stenella coeruleoalba
- Atlantic Spotted Dolphin, Stenella frontalis
- Spinner Dolphin, Stenella longirostris
- Genus Steno
Rough-toothed Dolphin, Steno bredanensis
- Rough-toothed Dolphin, Steno bredanensis
- Genus Tursiops - Rice and MSW3 tentatively agree on this classification but see species article for more detail.
Indian Ocean Bottlenose Dolphin, Tursiops aduncus
Common Bottlenose Dolphin, Tursiops truncatus
- Indian Ocean Bottlenose Dolphin, Tursiops aduncus
- Common Bottlenose Dolphin, Tursiops truncatus
- Family Monodontidae
Genus Delphinapterus
Beluga, Delphinapterus leucas
Genus Monodon
Narwhal, Monodon monoceros
- Genus Delphinapterus
Beluga, Delphinapterus leucas
- Beluga, Delphinapterus leucas
- Genus Monodon
Narwhal, Monodon monoceros
- Narwhal, Monodon monoceros
- Family Phocoenidae: Porpoises
Genus Neophocaena
Finless Porpoise, Neophocaena phocaenoides
Genus Phocoena
Spectacled Porpoise, Phocoena dioptrica
Harbour Porpoise, Phocoena phocaena
Vaquita, Phocoena sinus
Burmeister's Porpoise, Phocoena spinipinnis
Genus Phocoenoides
Dall's Porpoise, Phocoenoides dalli
- Genus Neophocaena
Finless Porpoise, Neophocaena phocaenoides
- Finless Porpoise, Neophocaena phocaenoides
- Genus Phocoena
Spectacled Porpoise, Phocoena dioptrica
Harbour Porpoise, Phocoena phocaena
Vaquita, Phocoena sinus
Burmeister's Porpoise, Phocoena spinipinnis
- Spectacled Porpoise, Phocoena dioptrica
- Harbour Porpoise, Phocoena phocaena
- Vaquita, Phocoena sinus
- Burmeister's Porpoise, Phocoena spinipinnis
- Genus Phocoenoides
Dall's Porpoise, Phocoenoides dalli
- Dall's Porpoise, Phocoenoides dalli
- Family Physeteridae: Sperm Whale family
Genus Physeter
Sperm Whale, Physeter catodon (syn. P. macrocephalus)
- Genus Physeter
Sperm Whale, Physeter catodon (syn. P. macrocephalus)
- Sperm Whale, Physeter catodon (syn. P. macrocephalus)
- Family Kogiidae - MSW3 treats Kogia as a member of Physeteridae
Genus Kogia
Pygmy Sperm Whale, Kogia breviceps
Dwarf Sperm Whale, Kogia sima
- Genus Kogia
Pygmy Sperm Whale, Kogia breviceps
Dwarf Sperm Whale, Kogia sima
- Pygmy Sperm Whale, Kogia breviceps
- Dwarf Sperm Whale, Kogia sima
- Superfamily Platanistoidea: River dolphins
Family Iniidae
Genus Inia
Amazon River Dolphin, Inia geoffrensis
Family Lipotidae - MSW3 treats Lipotes as a member of Iniidae
Genus Lipotes
† Baiji, Lipotes vexillifer
Family Pontoporiidae - MSW3 treats Pontoporia as a member of Iniidae
Genus Pontoporia
Franciscana, Pontoporia blainvillei
Family Platanistidae
Genus Platanista
Ganges and Indus River Dolphin, Platanista gangetica. MSW3 treats Platanista minor as a separate species, with common names Ganges River Dolphin and Indus River Dolphin, respectively.
- Family Iniidae
Genus Inia
Amazon River Dolphin, Inia geoffrensis
- Genus Inia
Amazon River Dolphin, Inia geoffrensis
- Amazon River Dolphin, Inia geoffrensis
- Family Lipotidae - MSW3 treats Lipotes as a member of Iniidae
Genus Lipotes
† Baiji, Lipotes vexillifer
- Genus Lipotes
† Baiji, Lipotes vexillifer
- † Baiji, Lipotes vexillifer
- Family Pontoporiidae - MSW3 treats Pontoporia as a member of Iniidae
Genus Pontoporia
Franciscana, Pontoporia blainvillei
- Genus Pontoporia
Franciscana, Pontoporia blainvillei
- Franciscana, Pontoporia blainvillei
- Family Platanistidae
Genus Platanista
Ganges and Indus River Dolphin, Platanista gangetica. MSW3 treats Platanista minor as a separate species, with common names Ganges River Dolphin and Indus River Dolphin, respectively.
- Genus Platanista
Ganges and Indus River Dolphin, Platanista gangetica. MSW3 treats Platanista minor as a separate species, with common names Ganges River Dolphin and Indus River Dolphin, respectively.
- Ganges and Indus River Dolphin, Platanista gangetica. MSW3 treats Platanista minor as a separate species, with common names Ganges River Dolphin and Indus River Dolphin, respectively.
- Family Ziphidae, Beaked whales
Genus Berardius
Arnoux's Beaked Whale, Berardius arnuxii
Baird's Beaked Whale (North Pacific Bottlenose Whale), Berardius bairdii
Subfamily Hyperoodontidae
Genus Hyperoodon
Northern Bottlenose Whale, Hyperoodon ampullatus
Southern Bottlenose Whale, Hyperoodon planifrons
Genus Indopacetus
Indo-Pacific Beaked Whale (Longman's Beaked Whale), Indopacetus pacificus
Genus Mesoplodon, Mesoplodont Whale
Sowerby's Beaked Whale, Mesoplodon bidens
Andrews' Beaked Whale, Mesoplodon bowdoini
Hubbs' Beaked Whale, Mesoplodon carlhubbsi
Blainville's Beaked Whale, Mesoplodon densirostris
Gervais' Beaked Whale, Mesoplodon europaeus
Ginkgo-toothed Beaked Whale, Mesoplodon ginkgodens
Gray's Beaked Whale, Mesoplodon grayi
Hector's Beaked Whale, Mesoplodon hectori
Layard's Beaked Whale, Mesoplodon layardii
True's Beaked Whale, Mesoplodon mirus
Perrin's Beaked Whale, Mesoplodon perrini. This species was recognised in 2002 and as such is listed by MSW3 but not Rice.
Pygmy Beaked Whale, Mesoplodon peruvianus
Stejneger's Beaked Whale, Mesoplodon stejnegeri
Spade Toothed Whale, Mesoplodon traversii
Genus Tasmacetus
Tasman Beaked Whale (Shepherd's Beaked Whale), Tasmacetus shepherdi
Genus Ziphius
Cuvier's Beaked Whale, Ziphius cavirostris
- Genus Berardius
Arnoux's Beaked Whale, Berardius arnuxii
Baird's Beaked Whale (North Pacific Bottlenose Whale), Berardius bairdii
- Arnoux's Beaked Whale, Berardius arnuxii
- Baird's Beaked Whale (North Pacific Bottlenose Whale), Berardius bairdii
- Subfamily Hyperoodontidae
Genus Hyperoodon
Northern Bottlenose Whale, Hyperoodon ampullatus
Southern Bottlenose Whale, Hyperoodon planifrons
Genus Indopacetus
Indo-Pacific Beaked Whale (Longman's Beaked Whale), Indopacetus pacificus
Genus Mesoplodon, Mesoplodont Whale
Sowerby's Beaked Whale, Mesoplodon bidens
Andrews' Beaked Whale, Mesoplodon bowdoini
Hubbs' Beaked Whale, Mesoplodon carlhubbsi
Blainville's Beaked Whale, Mesoplodon densirostris
Gervais' Beaked Whale, Mesoplodon europaeus
Ginkgo-toothed Beaked Whale, Mesoplodon ginkgodens
Gray's Beaked Whale, Mesoplodon grayi
Hector's Beaked Whale, Mesoplodon hectori
Layard's Beaked Whale, Mesoplodon layardii
True's Beaked Whale, Mesoplodon mirus
Perrin's Beaked Whale, Mesoplodon perrini. This species was recognised in 2002 and as such is listed by MSW3 but not Rice.
Pygmy Beaked Whale, Mesoplodon peruvianus
Stejneger's Beaked Whale, Mesoplodon stejnegeri
Spade Toothed Whale, Mesoplodon traversii
- Genus Hyperoodon
Northern Bottlenose Whale, Hyperoodon ampullatus
Southern Bottlenose Whale, Hyperoodon planifrons
- Northern Bottlenose Whale, Hyperoodon ampullatus
- Southern Bottlenose Whale, Hyperoodon planifrons
- Genus Indopacetus
Indo-Pacific Beaked Whale (Longman's Beaked Whale), Indopacetus pacificus
- Indo-Pacific Beaked Whale (Longman's Beaked Whale), Indopacetus pacificus
- Genus Mesoplodon, Mesoplodont Whale
Sowerby's Beaked Whale, Mesoplodon bidens
Andrews' Beaked Whale, Mesoplodon bowdoini
Hubbs' Beaked Whale, Mesoplodon carlhubbsi
Blainville's Beaked Whale, Mesoplodon densirostris
Gervais' Beaked Whale, Mesoplodon europaeus
Ginkgo-toothed Beaked Whale, Mesoplodon ginkgodens
Gray's Beaked Whale, Mesoplodon grayi
Hector's Beaked Whale, Mesoplodon hectori
Layard's Beaked Whale, Mesoplodon layardii
True's Beaked Whale, Mesoplodon mirus
Perrin's Beaked Whale, Mesoplodon perrini. This species was recognised in 2002 and as such is listed by MSW3 but not Rice.
Pygmy Beaked Whale, Mesoplodon peruvianus
Stejneger's Beaked Whale, Mesoplodon stejnegeri
Spade Toothed Whale, Mesoplodon traversii
- Sowerby's Beaked Whale, Mesoplodon bidens
- Andrews' Beaked Whale, Mesoplodon bowdoini
- Hubbs' Beaked Whale, Mesoplodon carlhubbsi
- Blainville's Beaked Whale, Mesoplodon densirostris
- Gervais' Beaked Whale, Mesoplodon europaeus
- Ginkgo-toothed Beaked Whale, Mesoplodon ginkgodens
- Gray's Beaked Whale, Mesoplodon grayi
- Hector's Beaked Whale, Mesoplodon hectori
- Layard's Beaked Whale, Mesoplodon layardii
- True's Beaked Whale, Mesoplodon mirus
- Perrin's Beaked Whale, Mesoplodon perrini. This species was recognised in 2002 and as such is listed by MSW3 but not Rice.
- Pygmy Beaked Whale, Mesoplodon peruvianus
- Stejneger's Beaked Whale, Mesoplodon stejnegeri
- Spade Toothed Whale, Mesoplodon traversii
- Genus Tasmacetus
Tasman Beaked Whale (Shepherd's Beaked Whale), Tasmacetus shepherdi
- Tasman Beaked Whale (Shepherd's Beaked Whale), Tasmacetus shepherdi
- Genus Ziphius
Cuvier's Beaked Whale, Ziphius cavirostris
- Cuvier's Beaked Whale, Ziphius cavirostris
†Extinct | https://www.wikidoc.org/index.php/Cetacea | |
0a9843746d364631683d8196ddf4a858f4d9ca2f | wikidoc | Chancre | Chancre
A chancre is a painless ulceration formed during the primary stage of syphilis. This infectious lesion forms approximately 21 days after the initial exposure to Treponema pallidum, the gram-negative spirochaete bacterium yielding syphilis. Chancres transmit the sexually transmissible disease of syphilis through direct physical contact. These ulcers usually form on or around the anus, mouth, penis, and vagina. Chancres may diminish between three to six weeks without the application of medication.
In addition, chancres are associated with the sleeping sickness, African trypanosomiasis, subsequent to the bite of a tsetse fly.
# Pathological Findings
- Chancres (shang-ker) on the penis due to a primary syphilitic infection.
- Chancre, Syphilis, painless | Chancre
Template:Search infobox
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
A chancre is a painless ulceration formed during the primary stage of syphilis. This infectious lesion forms approximately 21 days after the initial exposure to Treponema pallidum, the gram-negative spirochaete bacterium yielding syphilis. Chancres transmit the sexually transmissible disease of syphilis through direct physical contact. These ulcers usually form on or around the anus, mouth, penis, and vagina. Chancres may diminish between three to six weeks without the application of medication. [1] [2]
In addition, chancres are associated with the sleeping sickness, African trypanosomiasis, subsequent to the bite of a tsetse fly.
# Pathological Findings
- Chancres (shang-ker) on the penis due to a primary syphilitic infection.
- Chancre, Syphilis, painless | https://www.wikidoc.org/index.php/Chancre | |
c32f3809bbd973f63aa34635137e278246953e61 | wikidoc | Charges | Charges
Charge is usually thought of as a property of matter that is responsible for electrical phenomena, existing in a positive or negative form.
# Theoretical charges
Def. "the quantity of unbalanced positive or negative ions in or on an object; measured in coulombs" is called charge, or electric charge.
# Chargons
Def. "a quasiparticle produced as a result of electron spin-charge separation" is called a chargon.
A chargon possesses the charge of an electron without a spin.
A spinon, in turn, possesses the spin of an electron without charge. The suggestion is that an elementary particle such as a positron may consist of at least two parts: spin and charge.
In the figure at the top of the page "the 1D parabola tracks the spin excitation (spinon)."
Def. a "quasiparticle, corresponding to the orbital energy of an electron, which can result from an electron apparently ‘splitting’ under certain conditions" is called an orbiton.
Both an orbiton and a spinon are kinetic or kinematic concepts applied to an electron.
Def. "a discrete particle having zero rest mass, no electric charge, and an indefinitely long lifetime" is called a photon.
An electron may be thought of as a stable subatomic particle with a charge of negative one.
# Electrons
“The electron is a subatomic particle with a negative charge, equal to -1.60217646x10-19 C. Current, or the rate of flow of charge, is defined such that one coulomb, so 1/-1.60217646x10-19, or 6.24150974x1018 electrons flowing past a point per second give a current of one ampere. The charge on an electron is often given as -e. Note that charge is always considered positive, so the charge of an electron is always negative."
Def. the "quantity of matter which a body contains, irrespective of its bulk or volume" is called mass.
"The electron has a mass of 9.10938188x10-31 kg, or about 1/1840 that of a proton. The mass of an electron is often written as me."
"When working, these values can usually be safely approximated to:
It has no known components or substructure; in other words, it is generally thought to be an elementary particle. The intrinsic angular momentum (spin) of the electron is a half-integer value in units of ħ, which means that it is a fermion.
# Positrons
Def. "he antimatter equivalent of an electron, having the same mass but a positive charge" is called a positron.
# Muons
"TeV muons from γ ray primaries ... are rare because they are only produced by higher energy γ rays whose flux is suppressed by the decreasing flux at the source and by absorption on interstellar light."
The muon from the Greek letter mu (μ) used to represent it) is an elementary particle similar to the electron, with unitary negative electric charge (−1) and a spin of 1⁄2. Together with the electron, the tau, and the three neutrinos, it is classified as a lepton. As is the case with other leptons, the muon is not believed to have any sub-structure at all (i.e., is not thought to be composed of any simpler particles).
The muon is an unstable subatomic particle with a mean lifetime of 6994220000000000000♠2.2 μs. This comparatively long decay lifetime (the second longest known) is due to being mediated by the weak interaction. The only longer lifetime for an unstable subatomic particle is that for the free neutron, a baryon particle composed of quarks, which also decays via the weak force. Muon decay produces three particles, an electron plus two neutrinos of different types.
Like all elementary particles, the muon has a corresponding antiparticle of opposite charge (+1) but equal mass and spin: the antimuon (also called a positive muon). Muons are denoted by Template:SubatomicParticle and antimuons by Template:SubatomicParticle.
# Tauons
Because of their short lifetime, the range of the tau is mainly set by their decay length, which is too small for bremsstrahlung to be noticeable. Their penetrating power appears only at ultra-high velocity / ultra-high energy (above PeV energies), when time dilation extends their path-length.
The tau was anticipated in a 1971 paper by Yung-Su Tsai. Providing the theory for this discovery, the tau was detected in a series of experiments between 1974 and 1977 by Martin Lewis Perl with his and Tsai's colleagues at the SLAC-Lawrence Berkeley National Laboratory (LBL) group.
"We have discovered 64 events of the form
for which we have no conventional explanation."
The symbol τ was derived from the Greek τρίτον (triton, meaning "third" in English), since it was the third charged lepton discovered.
The tau is the only lepton that can decay into hadrons – the other leptons do not have the necessary mass. Like the other decay modes of the tau, the hadronic decay is through the weak nuclear force (weak interaction).
The branching ratio of the dominant hadronic tau decays are:
- 25.52% for decay into a charged pion, a neutral pion, and a tau neutrino;
- 10.83% for decay into a charged pion and a tau neutrino;
- 9.30% for decay into a charged pion, two neutral pions, and a tau neutrino;
- 8.99% for decay into three charged pions (of which two have the same electrical charge) and a tau neutrino;
- 2.70% for decay into three charged pions (of which two have the same electrical charge), a neutral pion, and a tau neutrino;
- 1.05% for decay into three neutral pions, a charged pion, and a tau neutrino.
The branching ratio of the common purely leptonic tau decays are:
- 17.82% for decay into a tau neutrino, electron and electron antineutrino;
- 17.39% for decay into a tau neutrino, muon and muon antineutrino.
The tau lepton is predicted to form exotic atoms like other charged subatomic particles. One of such, called tauonium by the analogy to muonium, consists of an antitauon and an electron: Template:SubatomicParticleTemplate:SubatomicParticle.
Another one is an onium atom Template:SubatomicParticleTemplate:SubatomicParticle called true tauonium and is difficult to detect due to tau's extremely short lifetime at low (non-relativistic) energies needed to form this atom. Its detection is important for quantum electrodynamics.
An "upward traveling, radio-detected cosmic-ray-like impulsive event characteristics closely matching an extensive air shower. This event, observed in the third flight of the Antarctic Impulsive Transient Antenna (ANITA), a NASA-sponsored long-duration balloon payload, is consistent with a similar event reported in a previous flight. These events may be produced by the atmospheric decay of an upward-propagating τ-lepton produced by a ντ interaction, although their relatively steep arrival angles create tension with the standard model (SM) neutrino cross section. Each of the two events have a posteriori background estimates of ≲10−2 events. If these are generated by τ-lepton decay, then either the charged-current ντ cross section is suppressed at EeV energies, or the events arise at moments when the peak flux of a transient neutrino source was much larger than the typical expected cosmogenic background neutrinos."
The upward traveling event is detected and described in the image and graph on the lower right. "Top: Interferometric map of the arrival direction of the anomalous CR event 15717147. Bottom: ANITA combined amplitude spectral density (ASD) for the event, from 50-800 MHz, including data from the ANITA Low Frequency Antenna (ALFA). A simulated upward-propagating extensive air shower spectral-density curve is overlain."
# Neutrinos
A neutrino is an electrically neutral, weakly interacting elementary subatomic particle with half-integer spin. Neutrinos do not carry electric charge, which means that they are not affected by the electromagnetic forces that act on charged particles such as electrons and protons. Neutrinos are affected only by the weak sub-atomic force, of much shorter range than electromagnetism, and gravity, which is relatively weak on the subatomic scale. They are therefore able to travel great distances through matter without being affected by it.
"If neutrinos have negligible rest mass, the present density expected for relic neutrinos from the big bang is nν = 110 (Tγ/2.7 K)3 cm–3 for each two-component species. This is of order the photon density nγ, differing just by a factor 3/11 (i.e. a factor 3/4 because neutrinos are fermions rather than bosons, multiplied by 4/11, the factor by which the neutrinos are diluted when e+–e– annihilation boosts the photon density). This conclusion holds for non-zero masses, provided that mvc2 is far below the thermal energy (~ 5 MeV) at which neutrinos decoupled from other species and that the neutrinos are stable for the Hubble time. Comparison with the baryon density, related to Ω via nb = 1.5 x 10–5 Ωb h2 cm–3, shows that neutrinos outnumber baryons by such a big factor that they can be dynamically dominant over baryons even if their masses are only a few electron volts. In fact, a single species of neutrino would yield a contribution to Ω of Ωv = 0.01 h–2 (mv)eV, so if h = 0.5, only 25 eV is sufficient to provide the critical density."
"Neutrinos of nonzero mass would be dynamically important not only for the expanding universe as a whole but also for large bound systems such as clusters of galaxies. This is because they would now be moving slowly: if the universe had cooled homogeneously, primordial neutrinos would now be moving at around 200 (mv)-1eV km s–1. They would be influenced even by the weak (~ 10–5 c2) gravitational potential fluctuations of galaxies and clusters. If the three (or more) types of neutrinos have different masses, then the heaviest will obviously be gravitationally dominant, since the numbers of each species should be the same."
# Photons
Def. "a discrete particle having zero rest mass, no electric charge, and an indefinitely long lifetime" is called a photon.
# Intermediate bosons
The Template:SubatomicParticle and Template:SubatomicParticle bosons are elementary particles with a spin of 1.
"The W field should exhibit a universal coupling strength for all the fundamental lepton doublets . This implies - apart from small phase-space corrections - equality of the branching ratios of the decay processes"
# Weak interactions
It "is the weak process
that controls the main burning reactions in the sun."
# Hypotheses
- Electron-positron annihilation is the reorientation of the spinons and chargons to generate two identical photons, or 0.511 MeV γ rays, that are out of phase with each other and have their own kinematics including the spinons and chargons.
- Nucleons are composed of electrons, positrons and neutrinos.
# Acknowledgements
The content on this page was first contributed by: Henry A. Hoff.
Initial content for this page in some instances came from Wikiversity. | Charges
Editor-In-Chief: Henry A. Hoff
Charge is usually thought of as a property of matter that is responsible for electrical phenomena, existing in a positive or negative form.
# Theoretical charges
Def. "the quantity of unbalanced positive or negative ions in or on an object; measured in coulombs"[1] is called charge, or electric charge.
# Chargons
Def. "a quasiparticle produced as a result of electron spin-charge separation"[2] is called a chargon.
A chargon possesses the charge of an electron without a spin.
A spinon, in turn, possesses the spin of an electron without charge. The suggestion is that an elementary particle such as a positron may consist of at least two parts: spin and charge.
In the figure at the top of the page "the 1D parabola tracks the spin excitation (spinon)."[3]
Def. a "quasiparticle, corresponding to the orbital energy of an electron, which can result from an electron apparently ‘splitting’ under certain conditions"[4] is called an orbiton.
Both an orbiton and a spinon are kinetic or kinematic concepts applied to an electron.
Def. "a discrete particle having zero rest mass, no electric charge, and an indefinitely long lifetime"[5] is called a photon.
An electron may be thought of as a stable subatomic particle with a charge of negative one.
# Electrons
“The electron is a subatomic particle with a negative charge, equal to -1.60217646x10-19 C. Current, or the rate of flow of charge, is defined such that one coulomb, so 1/-1.60217646x10-19, or 6.24150974x1018 electrons flowing past a point per second give a current of one ampere. The charge on an electron is often given as -e. Note that charge is always considered positive, so the charge of an electron is always negative."[6]
Def. the "quantity of matter which a body contains, irrespective of its bulk or volume"[7] is called mass.
"The electron has a mass of 9.10938188x10-31 kg, or about 1/1840 that of a proton. The mass of an electron is often written as me."[6]
"When working, these values can usually be safely approximated to:
It has no known components or substructure; in other words, it is generally thought to be an elementary particle.[8][9] The intrinsic angular momentum (spin) of the electron is a half-integer value in units of ħ, which means that it is a fermion.
# Positrons
Def. "[t]he antimatter equivalent of an electron, having the same mass but a positive charge"[10] is called a positron.
# Muons
"TeV muons from γ ray primaries ... are rare because they are only produced by higher energy γ rays whose flux is suppressed by the decreasing flux at the source and by absorption on interstellar light."[11]
The muon from the Greek letter mu (μ) used to represent it) is an elementary particle similar to the electron, with unitary negative electric charge (−1) and a spin of 1⁄2. Together with the electron, the tau, and the three neutrinos, it is classified as a lepton. As is the case with other leptons, the muon is not believed to have any sub-structure at all (i.e., is not thought to be composed of any simpler particles).
The muon is an unstable subatomic particle with a mean lifetime of 6994220000000000000♠2.2 μs. This comparatively long decay lifetime (the second longest known) is due to being mediated by the weak interaction. The only longer lifetime for an unstable subatomic particle is that for the free neutron, a baryon particle composed of quarks, which also decays via the weak force. Muon decay produces three particles, an electron plus two neutrinos of different types.
Like all elementary particles, the muon has a corresponding antiparticle of opposite charge (+1) but equal mass and spin: the antimuon (also called a positive muon). Muons are denoted by Template:SubatomicParticle and antimuons by Template:SubatomicParticle.
# Tauons
Because of their short lifetime, the range of the tau is mainly set by their decay length, which is too small for bremsstrahlung to be noticeable. Their penetrating power appears only at ultra-high velocity / ultra-high energy (above PeV energies), when time dilation extends their path-length.[12]
The tau was anticipated in a 1971 paper by Yung-Su Tsai.[13] Providing the theory for this discovery, the tau was detected in a series of experiments between 1974 and 1977 by Martin Lewis Perl with his and Tsai's colleagues at the SLAC-Lawrence Berkeley National Laboratory (LBL) group.[14]
"We have discovered 64 events of the form
for which we have no conventional explanation."[14]
The symbol τ was derived from the Greek τρίτον (triton, meaning "third" in English), since it was the third charged lepton discovered.[15]
The tau is the only lepton that can decay into hadrons – the other leptons do not have the necessary mass. Like the other decay modes of the tau, the hadronic decay is through the weak nuclear force (weak interaction).[16]
The branching ratio of the dominant hadronic tau decays are:[17]
- 25.52% for decay into a charged pion, a neutral pion, and a tau neutrino;
- 10.83% for decay into a charged pion and a tau neutrino;
- 9.30% for decay into a charged pion, two neutral pions, and a tau neutrino;
- 8.99% for decay into three charged pions (of which two have the same electrical charge) and a tau neutrino;
- 2.70% for decay into three charged pions (of which two have the same electrical charge), a neutral pion, and a tau neutrino;
- 1.05% for decay into three neutral pions, a charged pion, and a tau neutrino.
The branching ratio of the common purely leptonic tau decays are:[17]
- 17.82% for decay into a tau neutrino, electron and electron antineutrino;
- 17.39% for decay into a tau neutrino, muon and muon antineutrino.
The tau lepton is predicted to form exotic atoms like other charged subatomic particles. One of such, called tauonium by the analogy to muonium, consists of an antitauon and an electron: Template:SubatomicParticleTemplate:SubatomicParticle.[18]
Another one is an onium atom Template:SubatomicParticleTemplate:SubatomicParticle called true tauonium and is difficult to detect due to tau's extremely short lifetime at low (non-relativistic) energies needed to form this atom. Its detection is important for quantum electrodynamics.[18]
An "upward traveling, radio-detected cosmic-ray-like impulsive event [has] characteristics closely matching an extensive air shower. This event, observed in the third flight of the Antarctic Impulsive Transient Antenna (ANITA), a NASA-sponsored long-duration balloon payload, is consistent with a similar event reported in a previous flight. These events may be produced by the atmospheric decay of an upward-propagating τ-lepton produced by a ντ interaction, although their relatively steep arrival angles create tension with the standard model (SM) neutrino cross section. Each of the two events have a posteriori background estimates of ≲10−2 events. If these are generated by τ-lepton decay, then either the charged-current ντ cross section is suppressed at EeV energies, or the events arise at moments when the peak flux of a transient neutrino source was much larger than the typical expected cosmogenic background neutrinos."[19]
The upward traveling event is detected and described in the image and graph on the lower right. "Top: Interferometric map of the arrival direction of the anomalous CR event 15717147. Bottom: ANITA combined amplitude spectral density (ASD) for the event, from 50-800 MHz, including data from the ANITA Low Frequency Antenna (ALFA). A simulated upward-propagating extensive air shower spectral-density curve is overlain."[19]
# Neutrinos
A neutrino is an electrically neutral, weakly interacting elementary subatomic particle[20] with half-integer spin. Neutrinos do not carry electric charge, which means that they are not affected by the electromagnetic forces that act on charged particles such as electrons and protons. Neutrinos are affected only by the weak sub-atomic force, of much shorter range than electromagnetism, and gravity, which is relatively weak on the subatomic scale. They are therefore able to travel great distances through matter without being affected by it.
"If neutrinos have negligible rest mass, the present density expected for relic neutrinos from the big bang is nν = 110 (Tγ/2.7 K)3 cm–3 for each two-component species. This is of order the photon density nγ, differing just by a factor 3/11 (i.e. a factor 3/4 because neutrinos are fermions rather than bosons, multiplied by 4/11, the factor by which the neutrinos are diluted when e+–e– annihilation boosts the photon density). This conclusion holds for non-zero masses, provided that mvc2 is far below the thermal energy (~ 5 MeV) at which neutrinos decoupled from other species and that the neutrinos are stable for the Hubble time. Comparison with the baryon density, related to Ω via nb = 1.5 x 10–5 Ωb h2 cm–3, shows that neutrinos outnumber baryons by such a big factor that they can be dynamically dominant over baryons even if their masses are only a few electron volts. In fact, a single species of neutrino would yield a contribution to Ω of Ωv = 0.01 h–2 (mv)eV, so if h = 0.5, only 25 eV is sufficient to provide the critical density."[21]
"Neutrinos of nonzero mass would be dynamically important not only for the expanding universe as a whole but also for large bound systems such as clusters of galaxies. This is because they would now be moving slowly: if the universe had cooled homogeneously, primordial neutrinos would now be moving at around 200 (mv)-1eV km s–1. They would be influenced even by the weak (~ 10–5 c2) gravitational potential fluctuations of galaxies and clusters. If the three (or more) types of neutrinos have different masses, then the heaviest will obviously be gravitationally dominant, since the numbers of each species should be the same."[21]
# Photons
Def. "a discrete particle having zero rest mass, no electric charge, and an indefinitely long lifetime"[5] is called a photon.
# Intermediate bosons
The Template:SubatomicParticle and Template:SubatomicParticle bosons are elementary particles with a spin of 1.
"The W field should exhibit a universal coupling strength for all the fundamental lepton doublets [...]. This implies - apart from small phase-space corrections - equality of the branching ratios of the decay processes"
# Weak interactions
It "is the weak process
that controls the main burning reactions in the sun."[22]
# Hypotheses
- Electron-positron annihilation is the reorientation of the spinons and chargons to generate two identical photons, or 0.511 MeV γ rays, that are out of phase with each other and have their own kinematics including the spinons and chargons.
- Nucleons are composed of electrons, positrons and neutrinos.
# Acknowledgements
The content on this page was first contributed by: Henry A. Hoff.
Initial content for this page in some instances came from Wikiversity. | https://www.wikidoc.org/index.php/Charges | |
8d4a066043e49ae0dd594ba424a917a619640847 | wikidoc | Reagent | Reagent
A reactant or reagent is a substance consumed during a chemical reaction. Solvents and catalysts, although they are involved in the reaction, are usually not referred to as reactants.
Although the terms reactant and reagent are often used interchangeably, reagent is often used in a more specialized sense as "a test substance that is added to a system in order to bring about a reaction or to see whether a reaction occurs". Examples of such analytical reagents include Fehling's reagent and Tollens' reagent. In organic chemistry, reagents are compounds or mixtures, usually composed of inorganic or small organic molecules, that are used to effect a transformation on an organic substrate. Examples of organic reagents include the Collins reagent, Fenton's reagent, and Grignard reagent.
In another use of the term, when purchasing or preparing chemicals, "reagent-grade" describes chemical substances of sufficient purity for use in chemical analysis, chemical reactions or physical testing. Purity standards for reagents are set by organizations such as ASTM International. For instance, reagent-quality water must have very low levels of impurities like sodium and chloride ions, silica, and bacteria, as well as a very high electrical resistivity. | Reagent
A reactant or reagent is a substance consumed during a chemical reaction.[1] Solvents and catalysts, although they are involved in the reaction, are usually not referred to as reactants.
Although the terms reactant and reagent are often used interchangeably, reagent is often used in a more specialized sense as "a test substance that is added to a system in order to bring about a reaction or to see whether a reaction occurs".[1] Examples of such analytical reagents include Fehling's reagent and Tollens' reagent. In organic chemistry, reagents are compounds or mixtures, usually composed of inorganic or small organic molecules, that are used to effect a transformation on an organic substrate. Examples of organic reagents include the Collins reagent, Fenton's reagent, and Grignard reagent.
In another use of the term, when purchasing or preparing chemicals, "reagent-grade" describes chemical substances of sufficient purity for use in chemical analysis, chemical reactions or physical testing. Purity standards for reagents are set by organizations such as ASTM International. For instance, reagent-quality water must have very low levels of impurities like sodium and chloride ions, silica, and bacteria, as well as a very high electrical resistivity. | https://www.wikidoc.org/index.php/Chemical_reagent | |
5426a85d13e644abc783623535458082c4e16755 | wikidoc | Chemist | Chemist
A chemist is a scientist trained in the science of chemistry. Chemists study the composition of matter and its small-scale properties such as density and acidity instead of large-scale properties like size and shape. Chemists carefully describe the properties they study in terms of quantities, with detail on the level of molecules and their component atoms. Chemists carefully measure substance proportions, reaction rates, and other chemical properties.
Chemists use this knowledge to learn the composition, structure, chemical reactivity, and properties of unfamiliar substances, as well as to reproduce and synthesize large quantities of useful naturally occurring substances and create new artificial substances and useful processes. Chemists may specialize in any number of subdisciplines of chemistry. Materials scientists and metallurgists share much of the same education and skills with chemists. Chemical engineers are concerned with the physical processes necessary to carry out industrial reactions (heating, cooling, mixing, diffusion etc) and to separate and purify the products, and work with industrial chemists on the development of new processes.
# History
The roots of chemistry can be traced to the phenomenon of burning. Fire was a mystical force that transformed one substance into another and thus was of primary interest to mankind. It was fire that led to the discovery of iron and glass. After gold was discovered and became a precious metal, many people were interested to find a method that could convert other substances into gold. This led to the protoscience called Alchemy. The word chemist is derived from the New Latin noun chimista, an abbreviation of alchimista (alchemist). Alchemists discovered many chemical processes that led to the development of modern chemistry. Chemistry as we know it today, was invented by Antoine Lavoisier with his law of Conservation of mass in 1783. The discoveries of the chemical elements has a long history culminating in the creation of the periodic table by Dmitri Mendeleyev. The Nobel Prize in Chemistry created in 1901 gives an excellent overview of chemical discovery in the past 100 years.
# Education
Jobs for chemists usually require at least a bachelor's degree, but many positions, especially those in research, require a Ph.D. Most undergraduate programs emphasize mathematics and physics as well as chemistry, partly because chemistry is also known as "the central science", thus chemists ought to have an all-rounded knowledge about science. At the Master's level and higher, students tend to specialize in a particular field. Fields of specialization include biochemistry, organic chemistry, inorganic chemistry, analytical chemistry, theoretical chemistry, quantum chemistry and physical chemistry. Postdoctoral experience may be required for certain positions.
# Employment
The three major employers of chemists are academic institutions, industry, especially the chemical industry and the pharmaceutical industry, and government laboratories.
Chemistry typically is divided into several major sub-disciplines. There are also several main cross-disciplinary and more specialized fields of chemistry. There is a great deal of overlap between different branches of chemistry, as well as with other scientific fields such as biology, medicine, physics, and several engineering disciplines.
- Analytical chemistry is the analysis of material samples to gain an understanding of their chemical composition and structure. Analytical chemistry incorporates standardized experimental methods in chemistry. These methods may be used in all subdisciplines of chemistry, excluding purely theoretical chemistry.
- Biochemistry is the study of the chemicals, chemical reactions and chemical interactions that take place in living organisms. Biochemistry and organic chemistry are closely related, for example, in medicinal chemistry.
- Inorganic chemistry is the study of the properties and reactions of inorganic compounds. The distinction between organic and inorganic disciplines is not absolute and there is much overlap, most importantly in the sub-discipline of organometallic chemistry. Inorganic chemistry is also the study of atomic and molecular structure and bonding.
- Medicinal chemistry is the science involved with designing, synthesizing and developing pharmaceutical drugs. Medicinal chemistry involves the identification, synthesis and development of new chemical entities suitable for therapeutic use. It also includes the study of existing drugs, their biological properties, and their quantitative structure-activity relationships.
- Organic chemistry is the study of the structure, properties, composition, mechanisms, and chemical reaction of organic compounds.
- Physical chemistry is the study of the physical fundamental basis of chemical systems and processes. In particular, the energetics and dynamics of such systems and processes are of interest to physical chemists. Important areas of study include chemical thermodynamics, chemical kinetics, electrochemistry, quantum chemistry, statistical mechanics, and spectroscopy. Physical chemistry has large overlap with theoretical chemistry and molecular physics. Physical chemistry involves the use of calculus in deriving equations.
- Theoretical chemistry is the study of chemistry via theoretical reasoning (usually within mathematics or physics). In particular the application of quantum mechanics to chemistry is called quantum chemistry. Since the end of the second world war, the development of computers has allowed a systematic development of computational chemistry, which is the art of developing and applying computer programs for solving chemical problems. Theoretical chemistry has large overlap with condensed matter physics and molecular physics.See Reductionism.
All the above major areas of chemistry employ chemists. Other fields where chemical degrees are useful include Astrochemistry, Atmospheric chemistry, Chemical Engineering, Chemo-informatics, Electrochemistry, Environmental science, Forensic science, Geochemistry, Green chemistry, History of chemistry, Materials science, Medical science, Molecular Biology, Molecular genetics, Nanotechnology, Nuclear chemistry, Oenology, Organometallic chemistry, Petrochemistry, Pharmacology, Photochemistry, Phytochemistry, Polymer chemistry, Supramolecular chemistry and Surface chemistry. | Chemist
Template:This
A chemist is a scientist trained in the science of chemistry. Chemists study the composition of matter and its small-scale properties such as density and acidity instead of large-scale properties like size and shape. Chemists carefully describe the properties they study in terms of quantities, with detail on the level of molecules and their component atoms. Chemists carefully measure substance proportions, reaction rates, and other chemical properties.
Chemists use this knowledge to learn the composition, structure, chemical reactivity, and properties of unfamiliar substances, as well as to reproduce and synthesize large quantities of useful naturally occurring substances and create new artificial substances and useful processes. Chemists may specialize in any number of subdisciplines of chemistry. Materials scientists and metallurgists share much of the same education and skills with chemists. Chemical engineers are concerned with the physical processes necessary to carry out industrial reactions (heating, cooling, mixing, diffusion etc) and to separate and purify the products, and work with industrial chemists on the development of new processes.
# History
The roots of chemistry can be traced to the phenomenon of burning. Fire was a mystical force that transformed one substance into another and thus was of primary interest to mankind. It was fire that led to the discovery of iron and glass. After gold was discovered and became a precious metal, many people were interested to find a method that could convert other substances into gold. This led to the protoscience called Alchemy. The word chemist is derived from the New Latin noun chimista, an abbreviation of alchimista (alchemist). Alchemists discovered many chemical processes that led to the development of modern chemistry. Chemistry as we know it today, was invented by Antoine Lavoisier with his law of Conservation of mass in 1783. The discoveries of the chemical elements has a long history culminating in the creation of the periodic table by Dmitri Mendeleyev. The Nobel Prize in Chemistry created in 1901 gives an excellent overview of chemical discovery in the past 100 years.
# Education
Jobs for chemists usually require at least a bachelor's degree, but many positions, especially those in research, require a Ph.D. Most undergraduate programs emphasize mathematics and physics as well as chemistry, partly because chemistry is also known as "the central science", thus chemists ought to have an all-rounded knowledge about science. At the Master's level and higher, students tend to specialize in a particular field. Fields of specialization include biochemistry, organic chemistry, inorganic chemistry, analytical chemistry, theoretical chemistry, quantum chemistry and physical chemistry. Postdoctoral experience may be required for certain positions.
# Employment
The three major employers of chemists are academic institutions, industry, especially the chemical industry and the pharmaceutical industry, and government laboratories.
Chemistry typically is divided into several major sub-disciplines. There are also several main cross-disciplinary and more specialized fields of chemistry. There is a great deal of overlap between different branches of chemistry, as well as with other scientific fields such as biology, medicine, physics, and several engineering disciplines.
- Analytical chemistry is the analysis of material samples to gain an understanding of their chemical composition and structure. Analytical chemistry incorporates standardized experimental methods in chemistry. These methods may be used in all subdisciplines of chemistry, excluding purely theoretical chemistry.
- Biochemistry is the study of the chemicals, chemical reactions and chemical interactions that take place in living organisms. Biochemistry and organic chemistry are closely related, for example, in medicinal chemistry.
- Inorganic chemistry is the study of the properties and reactions of inorganic compounds. The distinction between organic and inorganic disciplines is not absolute and there is much overlap, most importantly in the sub-discipline of organometallic chemistry. Inorganic chemistry is also the study of atomic and molecular structure and bonding.
- Medicinal chemistry is the science involved with designing, synthesizing and developing pharmaceutical drugs. Medicinal chemistry involves the identification, synthesis and development of new chemical entities suitable for therapeutic use. It also includes the study of existing drugs, their biological properties, and their quantitative structure-activity relationships.
- Organic chemistry is the study of the structure, properties, composition, mechanisms, and chemical reaction of organic compounds.
- Physical chemistry is the study of the physical fundamental basis of chemical systems and processes. In particular, the energetics and dynamics of such systems and processes are of interest to physical chemists. Important areas of study include chemical thermodynamics, chemical kinetics, electrochemistry, quantum chemistry, statistical mechanics, and spectroscopy. Physical chemistry has large overlap with theoretical chemistry and molecular physics. Physical chemistry involves the use of calculus in deriving equations.
- Theoretical chemistry is the study of chemistry via theoretical reasoning (usually within mathematics or physics). In particular the application of quantum mechanics to chemistry is called quantum chemistry. Since the end of the second world war, the development of computers has allowed a systematic development of computational chemistry, which is the art of developing and applying computer programs for solving chemical problems. Theoretical chemistry has large overlap with condensed matter physics and molecular physics.See Reductionism.
All the above major areas of chemistry employ chemists. Other fields where chemical degrees are useful include Astrochemistry, Atmospheric chemistry, Chemical Engineering, Chemo-informatics, Electrochemistry, Environmental science, Forensic science, Geochemistry, Green chemistry, History of chemistry, Materials science, Medical science, Molecular Biology, Molecular genetics, Nanotechnology, Nuclear chemistry, Oenology, Organometallic chemistry, Petrochemistry, Pharmacology, Photochemistry, Phytochemistry, Polymer chemistry, Supramolecular chemistry and Surface chemistry.
Template:BranchesofChemistry | https://www.wikidoc.org/index.php/Chemist | |
fdb259667b460ba7c1229b8598f56d8dd3fa8ed0 | wikidoc | Cheroot | Cheroot
The Cheroot or Stogie is a cylindrical cigar with both ends clipped during manufacture. Since cheroots do not taper, they are inexpensive to roll mechanically, and their low cost makes them particularly popular. Typically, stogies have a length of 3.5 to 6.5 inches, and a ring gauge of 34 to 37. (Ring gauge is a measure of diameter, scaled in 64ths of an inch. A stogie is slightly over 1/2" in diameter.)
The term stogie is often misused to refer to any cigar with a foul stench. Many stogies are made of flavored tobaccos, and given that a stogie may last a half hour, as opposed to the 2-8 minutes that a cigarette typically lasts, there can be quite a stench produced.
The word stogie is short for Conestoga. The cigar was the smoke of choice for teamsters driving Conestoga wagons in the cigar-making Conestoga valley area around Lancaster, Pennsylvania. The word cheroot comes from French cheroute, from Tamil curuttu/churuttu/shuruttu - roll of tobacco. This word could have been absorbed into the French language from Tamil during the early 16th century, when the French were trying to stamp their presence in South India. The word could have then been absorbed into English from French.
# Mark Twain on cigars
Samuel "Mark Twain" Clemens is shown smoking a stogie in many of his photographs. His beloved did not approve of such a vile habit, and he made many jokes about this preference for inexpensive cigars. At one lecture, he indicated that he paid $5 a barrel for his cigars because he was incurably extravagant.
In the March 26, 1911 New York Times, Mark Twain was quoted posthumously from a 1905 letter to L. M. Powers in which he wrote, "I know a good cigar better than you do, for I have had sixty years' experience. No, that is not what I mean; I mean I know a bad cigar better than anybody else. I judge by the price only; if it costs above 5 cents, I know it to be either foreign or half foreign and unsmokable.
"By me I have many boxes of Havana cigars, of all prices, from 20 cents apiece up to $1.66 apiece; I bought none of them; they were all presents; they are an accumulation of several years. I have never smoked one of them, and never shall. I work them off on the visitor. You shall have a chance when you come."
Modern day stogie fans include Rush Limbaugh, and filmmaker Francis Ford Coppola, who offers his own private-label stogies for sale at his winery.
Singer Roger Miller, who was known for enjoying smoking in general, included this line in his song, "King of the Road": "I smoke old stogies I have found / Short, but not too big around."
# The Asian connection
Cheroots are traditional in Burma and India, consequently, popular among the British during the days of the British Empire. They are often associated with Burma in literature:
Apparently, Cheroot smoking was also associated with resistance against tropical disease in India. Verrier Elwin wrote in his 1957 forward to Leaves from the Jungle: Life in a Gond Village,
"A final thing strikes me as I re-read the pages of the Diary that follows is that I seem to have spent much of my time falling ill. I attribute this to the fact that in those days I was a non-smoker. Since I took to the cheroot, I have not had a single attack of malaria, and my health improved enormously in later years." (Leaves from the Jungle: Life in a Gond Village, OUP 1992, p.xxix)
A reader will note that malaria was most often contracted by mosquito bites and most likely the cheroot's aroma, by sticking to the skin and hiding the sweat's scent, which draws mosquitoes, contributed to make the smoker less of a target for their bites. | Cheroot
The Cheroot or Stogie is a cylindrical cigar with both ends clipped during manufacture. Since cheroots do not taper, they are inexpensive to roll mechanically, and their low cost makes them particularly popular. Typically, stogies have a length of 3.5 to 6.5 inches, and a ring gauge of 34 to 37. (Ring gauge is a measure of diameter, scaled in 64ths of an inch. A stogie is slightly over 1/2" in diameter.)
The term stogie is often misused to refer to any cigar with a foul stench. Many stogies are made of flavored tobaccos, and given that a stogie may last a half hour, as opposed to the 2-8 minutes that a cigarette typically lasts, there can be quite a stench produced.
The word stogie is short for Conestoga. The cigar was the smoke of choice for teamsters driving Conestoga wagons in the cigar-making Conestoga valley area around Lancaster, Pennsylvania. The word cheroot comes from French cheroute, from Tamil curuttu/churuttu/shuruttu - roll of tobacco. This word could have been absorbed into the French language from Tamil during the early 16th century, when the French were trying to stamp their presence in South India. The word could have then been absorbed into English from French.[1]
# Mark Twain on cigars
Samuel "Mark Twain" Clemens is shown smoking a stogie in many of his photographs. His beloved did not approve of such a vile habit, and he made many jokes about this preference for inexpensive cigars. At one lecture, he indicated that he paid $5 a barrel for his cigars because he was incurably extravagant.
In the March 26, 1911 New York Times, Mark Twain was quoted posthumously from a 1905 letter to L. M. Powers in which he wrote, "I know a good cigar better than you do, for I have had sixty years' experience. No, that is not what I mean; I mean I know a bad cigar better than anybody else. I judge by the price only; if it costs above 5 cents, I know it to be either foreign or half foreign and unsmokable.
"By me I have many boxes of Havana cigars, of all prices, from 20 cents apiece up to $1.66 apiece; I bought none of them; they were all presents; they are an accumulation of several years. I have never smoked one of them, and never shall. I work them off on the visitor. You shall have a chance when you come."
Modern day stogie fans include Rush Limbaugh, and filmmaker Francis Ford Coppola, who offers his own private-label stogies for sale at his winery.
Singer Roger Miller, who was known for enjoying smoking in general, included this line in his song, "King of the Road": "I smoke old stogies I have found / Short, but not too big around."
# The Asian connection
Cheroots are traditional in Burma and India, consequently, popular among the British during the days of the British Empire. They are often associated with Burma in literature:
Apparently, Cheroot smoking was also associated with resistance against tropical disease in India. Verrier Elwin wrote in his 1957 forward to Leaves from the Jungle: Life in a Gond Village,
"A final thing strikes me as I re-read the pages of the Diary that follows is that I seem to have spent much of my time falling ill. I attribute this to the fact that in those days I was a non-smoker. Since I took to the cheroot, I have not had a single attack of malaria, and my health improved enormously in later years." (Leaves from the Jungle: Life in a Gond Village, OUP 1992, p.xxix)
A reader will note that malaria was most often contracted by mosquito bites and most likely the cheroot's aroma, by sticking to the skin and hiding the sweat's scent, which draws mosquitoes, contributed to make the smoker less of a target for their bites. | https://www.wikidoc.org/index.php/Cheroot | |
c950f36e0193af8abe70b3d24e9672ceb6483378 | wikidoc | Chervil | Chervil
Chervil (Anthriscus cerefolium) is a delicate annual herb related to parsley. Sometimes called garden chervil, it is used to season mild-flavoured dishes and is a constituent of the French herb mixture fines herbes.
# Biology
A member of the Apiaceae, chervil is native to the Caucasus but was spread by the Romans through most of Europe, where it is now naturalised.
The plants grow to 40-70cm, with tripinnate leaves that may be curly. The small white flowers form small umbels, 2.5-5cm across. The fruit is about 1cm long, oblong-ovoid with a slender, ridged beak.
## Root Chervil
Another type of chervil is grown as a root vegetable, sometimes called turnip rooted chervil or tuberous-rooted chervil. This type of chervil produces much thicker roots than types cultivated for their leaves. It was once a popular vegetable in the 19th century. It is now virtually forgotten and is little known in Britain and the United States, root chervil is very common in French cuisine, where it is used in most soups or stews.
Though it looks similar to parsnip it tastes quite different. Parsnips are among the closest relatives of parsley in the umbellifer family of herbs, although the similarity of the names is a coincidence, parsnip meaning "forked turnip". It is not related to real turnips.
# Uses
## Culinary
Sometimes referred to as "gourmet's parsley", chervil is used to season poultry, seafood, and young vegetables. It is particularly popular in France, where it is added to omelettes, salads and soups. More delicate than parsley, it has a faint taste of liquorice.
## Horticulture
Chervil is sometimes used as a trap crop by gardeners to protect vegetable plants from slugs.
## Medical
Chervil had various traditional uses. Pregnant women bathed in an infusion of it; a lotion of it was used as a skin cleanser; and it was used medicinally as a blood purifier.
# Cultivation
Chervil grows to a height of 12 to 26 inches. Chervil prefers a cool and moist location, otherwise it rapidly goes to seed. | Chervil
Chervil (Anthriscus cerefolium) is a delicate annual herb related to parsley. Sometimes called garden chervil, it is used to season mild-flavoured dishes and is a constituent of the French herb mixture fines herbes.
# Biology
A member of the Apiaceae, chervil is native to the Caucasus but was spread by the Romans through most of Europe, where it is now naturalised.[1]
The plants grow to 40-70cm, with tripinnate leaves that may be curly. The small white flowers form small umbels, 2.5-5cm across. The fruit is about 1cm long, oblong-ovoid with a slender, ridged beak.[1]
## Root Chervil
Another type of chervil is grown as a root vegetable, sometimes called turnip rooted chervil or tuberous-rooted chervil. This type of chervil produces much thicker roots than types cultivated for their leaves. It was once a popular vegetable in the 19th century. It is now virtually forgotten and is little known in Britain and the United States, root chervil is very common in French cuisine, where it is used in most soups or stews.
Though it looks similar to parsnip it tastes quite different. Parsnips are among the closest relatives of parsley in the umbellifer family of herbs, although the similarity of the names is a coincidence, parsnip meaning "forked turnip". It is not related to real turnips.
# Uses
## Culinary
Sometimes referred to as "gourmet's parsley", chervil is used to season poultry, seafood, and young vegetables. It is particularly popular in France, where it is added to omelettes, salads and soups. More delicate than parsley, it has a faint taste of liquorice.
## Horticulture
Chervil is sometimes used as a trap crop by gardeners to protect vegetable plants from slugs.
## Medical
Chervil had various traditional uses. Pregnant women bathed in an infusion of it; a lotion of it was used as a skin cleanser; and it was used medicinally as a blood purifier.
# Cultivation
Chervil grows to a height of 12 to 26 inches.[citation needed] Chervil prefers a cool and moist location, otherwise it rapidly goes to seed. | https://www.wikidoc.org/index.php/Chervil | |
069674146a2d02ad8b3b035598e51ae2deba3466 | wikidoc | Chigger | Chigger
# Overview
Chigger or chigoe can refer to either of two parasitic arthropods with similar behaviors: the chigoe flea (Tunga penetrans), found in tropical climates and the larva of a harvest mite that, when carrying a tiny parasite called Orientia tsutsugamushi, causes scrub typhus. The larvae are also called scrub mite, red mite and several other names, and they are found throughout temperate and tropical zones; the name chigger originated as a corruption of chigoe, but the harvest mite is what is most commonly called a chigger in North America.
# Pathophysiology
- Chiggers do burrow into the skin but do not suck blood. It attaches to its host, injects digestive enzymes into the bite wound, and then sucks up the digested tissue.
- Warm, rainy days make these parasitic and predatory mites reproduce into large populations. Once the ground temperature is regularly above 60°F, the harvest mite lays eggs, and “chigger season” is underway. This season typically begins in April and ends in the early autumn/first “frost.”
- Chiggers do not like sunlight or humidity. During the wet season, chiggers are usually found in tall grass and other vegetation.
- During dry seasons, chiggers are most found underneath brush and shady areas.
# Treatment
## Medical Treatment
To reduce the itching, apply an anti-itch cream that contains hydrocortisone, calamine, or benzyl benzoate. If you are sensitive to these medications or have questions, be sure to ask your health-care professional or pharmacist
## Prevention
- Keep grass short.
- Remove brush and wood debris where potential mite hosts may live.
- Keep major host away from the area, such as - rodents and other small mammals. Secure trash cans to discourage wildlife from coming near your home.
- Sunlight that penetrates the grass will make the lawn drier and make it less favorable for chigger survival.
- Apply insect repellant to your feet, legs, and mid-section.
# Related Chapters
- Insect bite relief stick
- Schmidt Sting Pain Index | Chigger
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]
# Overview
Chigger or chigoe can refer to either of two parasitic arthropods with similar behaviors: the chigoe flea (Tunga penetrans), found in tropical climates and the larva of a harvest mite that, when carrying a tiny parasite called Orientia tsutsugamushi, causes scrub typhus. The larvae are also called scrub mite, red mite and several other names, and they are found throughout temperate and tropical zones; the name chigger originated as a corruption of chigoe, but the harvest mite is what is most commonly called a chigger in North America.
# Pathophysiology
- Chiggers do burrow into the skin but do not suck blood. It attaches to its host, injects digestive enzymes into the bite wound, and then sucks up the digested tissue.
- Warm, rainy days make these parasitic and predatory mites reproduce into large populations. Once the ground temperature is regularly above 60°F, the harvest mite lays eggs, and “chigger season” is underway. This season typically begins in April and ends in the early autumn/first “frost.”
- Chiggers do not like sunlight or humidity. During the wet season, chiggers are usually found in tall grass and other vegetation.
- During dry seasons, chiggers are most found underneath brush and shady areas.
# Treatment
## Medical Treatment
To reduce the itching, apply an anti-itch cream that contains hydrocortisone, calamine, or benzyl benzoate. If you are sensitive to these medications or have questions, be sure to ask your health-care professional or pharmacist
## Prevention
- Keep grass short.
- Remove brush and wood debris where potential mite hosts may live.
- Keep major host away from the area, such as - rodents and other small mammals. Secure trash cans to discourage wildlife from coming near your home.
- Sunlight that penetrates the grass will make the lawn drier and make it less favorable for chigger survival.
- Apply insect repellant to your feet, legs, and mid-section.
# Related Chapters
- Insect bite relief stick
- Schmidt Sting Pain Index | https://www.wikidoc.org/index.php/Chigger | |
728e17f84d22c4075f1ea71e787e5e0b94406281 | wikidoc | Chin-up | Chin-up
The chin-up (also known as a chin) is a strength training exercise designed to strengthen the latissimus dorsi muscle.
# Form
A chin-up has a specific form. The movement begins with the arms extended above the head, gripping a fixed chin-up bar (or bar attached to a pulley in the case of the similar pulldown exercise, with the palms facing away from the exerciser) with a supinated grip (palms facing the exerciser). The body is pulled up, or weight pulled down, until the bar approaches or touches the upper chest. The weight is lowered until the arms are straight, and the exercise is generally repeated.
Chin-ups can be performed with a kip, where the legs and back impart momentum to aid the exercise, or from a dead hang, where the body is kept still. Performing the chin-up correctly can be tricky because of the natural tendency to do most of the work with the biceps rather than the lats. Initiating the pull with the shoulder blades helps avoid this problem. The exercise is most effective when the body is lowered down to a full extension.
Chin-ups are often incorrectly referred to as pull-ups. The term pull-up is traditionally used when the exercise is performed with a pronated grip.
# Muscles targeted
Chin-ups target the latissimus dorsi muscle, assisted by the brachialis, brachioradialis, biceps brachii , teres major, posterior deltoid, infraspinatus, teres minor, rhomboids, levator scapulae, middle and lower trapezius and pectoralis muscles. Chin-ups are thought to build width and thickness to one's back, as well as to promote growth of the biceps, brachialis, brachioradialis and pronator teres.
# Variations
- Sternal chinups — this variant employs a full range of motion, raising the sternum to the bar. The elbows are nearly directly below the shoulders this way.
- Towel chin-ups — a towel is looped over the bar, and instead of the bar, the towel is gripped.
- Weighted chin-ups — weight is added with dangling from a dipping belt, or via weighted belt or vest, ankle weights, chains, medicine ball between the knees, dumbbell between the feet or kettlebells on top of the feet.
- One handed chin-ups — one hand grips the bar; the other hand holds the wrist/forearm of the gripping hand. It stresses the grip equally to a one-arm chin-up, but lessens the amount of work the biceps and lat of the gripping arm have to do compared to it.
- One forearmed chin-ups — one hand grips the bar; the other hand holds the upper arm of the gripping hand between the elbow and shoulder. It stresses the grip and bicep equally to a one-arm chin-up, but lessens the amount of work the lat of the gripping arm has to do compared to it.
- One arm chin-ups — one hand grips the bar; the other hand does not assist with the pull, it cannot touch the other arm.
- Drop chin-ups — the grip is released at the top of the movement, and the bar caught towards the bottom of the movement, to incorporate a slight drop. This variant is for advanced athletes only.
- Supine chin-ups — in the supine position (with the feet initially supported), the arms are held perpendicular to the body as the grip the bar; the chest is pulled towards the bar instead of the chin. This exercise is performed in the horizontal (transverse) plane, whereas other chin-up variations are performed in the vertical (coronal) plane. As a result, this variation recruits the trapezius and teres major muscles much more than a vertical chin-up would and is often considered a type of row.
# Exercises that help
A useful exercise for beginners is the negative chin-up, where one is assisted to the top position and executes a slow, controlled descent. This is useful for those not strong enough to perform a concentric chin-up, and can also be used to keep training at the same weight when one is too exhausted to continue performing the concentric portion of the exercise.
Beginners who are not strong enough to perform a chin-up may make use of an assisted chin-up machine, where one stands on a bar with a counterweight to reduce the weight that one pulls up. These machines frequently also include a dip bar, allowing for assisted dipping. This keeps the exercise a closed-chain movement.
Another machine, which is open-chain (the person remains stationary, the resistance moves) which mimics the movement and is also helpful to training is the lat pulldown. Unlike the counterweight machine, the lat pulldown can provide as much or more resistance as a normal chin-up or pull-up through use of a counterweight stack. The lifter locks a pad into place above their thighs (near to the hip) to prevent them from rising off the ground when the resistance provided by the counter-weight (lifted through a pulley mechanism) goes beyond their body's. | Chin-up
The chin-up (also known as a chin) is a strength training exercise designed to strengthen the latissimus dorsi muscle.
# Form
A chin-up has a specific form. The movement begins with the arms extended above the head, gripping a fixed chin-up bar (or bar attached to a pulley in the case of the similar pulldown exercise, with the palms facing away from the exerciser) with a supinated grip (palms facing the exerciser). The body is pulled up, or weight pulled down, until the bar approaches or touches the upper chest. The weight is lowered until the arms are straight, and the exercise is generally repeated.
Chin-ups can be performed with a kip, where the legs and back impart momentum to aid the exercise, or from a dead hang, where the body is kept still. Performing the chin-up correctly can be tricky because of the natural tendency to do most of the work with the biceps rather than the lats. Initiating the pull with the shoulder blades helps avoid this problem. The exercise is most effective when the body is lowered down to a full extension.
Chin-ups are often incorrectly referred to as pull-ups. The term pull-up is traditionally used when the exercise is performed with a pronated grip.
# Muscles targeted
Chin-ups target the latissimus dorsi muscle, assisted by the brachialis, brachioradialis, biceps brachii , teres major, posterior deltoid, infraspinatus, teres minor, rhomboids, levator scapulae, middle and lower trapezius and pectoralis muscles. Chin-ups are thought to build width and thickness to one's back, as well as to promote growth of the biceps, brachialis, brachioradialis and pronator teres.
# Variations
- Sternal chinups — this variant employs a full range of motion, raising the sternum to the bar. The elbows are nearly directly below the shoulders this way.
- Towel chin-ups — a towel is looped over the bar, and instead of the bar, the towel is gripped.
- Weighted chin-ups — weight is added with dangling from a dipping belt, or via weighted belt or vest, ankle weights, chains, medicine ball between the knees, dumbbell between the feet or kettlebells on top of the feet.
- One handed chin-ups — one hand grips the bar; the other hand holds the wrist/forearm of the gripping hand. It stresses the grip equally to a one-arm chin-up, but lessens the amount of work the biceps and lat of the gripping arm have to do compared to it.
- One forearmed chin-ups — one hand grips the bar; the other hand holds the upper arm of the gripping hand between the elbow and shoulder. It stresses the grip and bicep equally to a one-arm chin-up, but lessens the amount of work the lat of the gripping arm has to do compared to it.
- One arm chin-ups — one hand grips the bar; the other hand does not assist with the pull, it cannot touch the other arm.
- Drop chin-ups — the grip is released at the top of the movement, and the bar caught towards the bottom of the movement, to incorporate a slight drop. This variant is for advanced athletes only.
- Supine chin-ups — in the supine position (with the feet initially supported), the arms are held perpendicular to the body as the grip the bar; the chest is pulled towards the bar instead of the chin. This exercise is performed in the horizontal (transverse) plane, whereas other chin-up variations are performed in the vertical (coronal) plane. As a result, this variation recruits the trapezius and teres major muscles much more than a vertical chin-up would and is often considered a type of row.
# Exercises that help
A useful exercise for beginners is the negative chin-up, where one is assisted to the top position and executes a slow, controlled descent. This is useful for those not strong enough to perform a concentric chin-up, and can also be used to keep training at the same weight when one is too exhausted to continue performing the concentric portion of the exercise.
Beginners who are not strong enough to perform a chin-up may make use of an assisted chin-up machine, where one stands on a bar with a counterweight to reduce the weight that one pulls up. These machines frequently also include a dip bar, allowing for assisted dipping. This keeps the exercise a closed-chain movement.
Another machine, which is open-chain (the person remains stationary, the resistance moves) which mimics the movement and is also helpful to training is the lat pulldown. Unlike the counterweight machine, the lat pulldown can provide as much or more resistance as a normal chin-up or pull-up through use of a counterweight stack. The lifter locks a pad into place above their thighs (near to the hip) to prevent them from rising off the ground when the resistance provided by the counter-weight (lifted through a pulley mechanism) goes beyond their body's. | https://www.wikidoc.org/index.php/Chin-up | |
1c04d776b52ed982253ae27f7687ec74be8ca9d9 | wikidoc | Melasma | Melasma
Synonyms and keywords: Chloasma, mask of pregnancy.
# Overview
Melasma (also known as chloasma or the mask of pregnancy when present in pregnant women) is a tan or dark facial skin discoloration. Although it can affect anyone, melasma is particularly common in women, especially pregnant women and those who are taking oral contraceptives or hormone replacement therapy (HRT) medications.The ratio of female to male is 9:1 and is more common in yellow to brown skin color ( Fitzpatrick's skin photo type III to V) .The lesions usually develops in middle age and persists for many years. In post menopause women , the lesions usually fade spontaneously. Prolong exposure to sunlight is the most important etiologic factor. It is also prevalent in men and women of Native American descent (on the forearms) and in men and women of German/Russian Jewish descent (on the face).
# Symptoms
The symptoms of melasma are brown to dark brown , irregular patches commonly found on the mid-face, upper cheek, nose, lips, upperlip, and forehead. Early lesions have well defined irregular margin,while older lesions tend to be grayish brown color with irregular and ill-defined border. These patches often develop gradually over time. clinically melasma had been divided into two clinical types 1) centro-facial and 2) zygoma types. Melasma does not cause any other symptoms beyond the cosmetic discoloration.
# Cause
Melasma is thought to be the stimulation of melanocytes or pigment-producing cells by the female sex hormones estrogen and progesterone to produce more melanin pigments when the skin is exposed to sun. Women with a light brown skin type who are living in regions with intense sun exposure are particularly susceptible to developing this condition.
Genetic predisposition is also a major factor in determining whether someone will develop melasma.Recent study of pathology changes of melasma had revealed that majority of melasma also had increase in number of melanocytes. The average increase is about 30% together with proliferation of small blood vessels in the dermis . Melanin dropping into dermis together with presence of macrophages containing melanins (melanophages) are commonly found in long standing cases. These three findings may explain the chronicity of melasma. Proliferate and dilated blood vessels may contribute to chronicity by being the source of cytokines ,prostaglandins and leukotrienes that stimulate melanin synthesis.
The incidence of melasma also increases in patients with thyroid disease. It is thought that the overproduction of melanocyte-stimulating hormone (MSH) brought on by stress can cause outbreaks of this condition. Other rare causes of melasma include allergic reaction to medications and cosmetics. Drugs like conjugated estrogens causes melasma
Melasma Suprarenale (Latin - of the adrenals) is a symptom of Addison's disease, particularly when caused by pressure or minor injury to the skin, as discovered by Dr. FJJ Schmidt of Rotterdam in 1859.
## Medications
Estropipate
# Diagnosis
Melasma is usually diagnosed visually or with assistance of a Wood's lamp (340 - 400 nm wavelength). Under Wood's lamp, excess melanin in the epidermis can be distinguished from that of the dermis. By this technique melasma can be divided into two types 1) epidermal 2) mixed (epidermal+ dermal). This diffentiation is important for planning of management.
# Physical examination
## Gallery
### Head
- url = >
- url = >
# Treatment
The discoloration usually disappears spontaneously over a period of several months after giving birth or stopping the oral contraceptives or hormone replacement therapy. In cases without definite causes, the lesions may persist for many years. In cases that severity of lesions justify the treatment, the following are the common treatment methods available: 1) Avoiding of exposure to strong sunlight (ultraviolet range ) with UVA-blocker sunscreen (320-400 nm) prevention. Since UVA is the most important wavelength of sunlight that stimulate hyperpigmentation. The over the counter UVA-sunscreen with PA more than +++ and SPF more than 30 is recommended. 2)Reduction of melanin synthesis, the most commonly use drug is hydroquinone 2-4% . To enhance effectiveness ,4% hydroquinone is combined with tretinoin(0.05%) and steroids(fluocinolone acetonide 0.01%) and has been named Kligman's formula. This formula had been proved to be the most effective in clearing of epidermal melasma. More than 60% will have complete clearing by three months. The problem of this formula is its long term side effects.At present Tri-Luma TM (Galderma,USA) is the only one triple drugs approved by USA-FDA for treatment of melasma. Hydroquinone has been associated with many complictions in dark skin patients i.e. contact dermatitis, exogenous ochronosis, confetti-like hypopigmentation and rebound hyperpigmentation. Others topical treatments that had been used for treatments include arbutin, kojic acid, licorice extract, azelaic acid, vitamin C, soy, green tea , decapeptides, ,glove extract etc. The results were inferior to Kligman's formular but claimed to have lower incidence of complications. Many of these products are ingredients of over the counter whitening creams. In some countries hydroquinone has not been approved , because of concern of mutagenic and toxicity e.g. Japan. The second technique for treatment of melasma is by enhancing peeling of epithelial cells by chemicals e.g. retinoic acid, glycolic , salycylic acid. Facial peels with glycolic or alpha hydroxy acids are popular in many countries. For mixed type with dermal melanophages and dilated blood vessels, usually resisted to topical treatments. These types are justified for method with deeper effects to melanocytes and melanophages. Recently two laser systems have been shown to be effective for treatment of deep lesions of melasma 1) flat beam, high energy Q-switched NdYAG (1064 nm)(Medlite c6/Revlite, Hoya-Conbio,USA) 2) Fractional Erbium Glass (1550 nm) laser. The first technique originate from Asia where mixed melasma are more common. The technique has been called "Laser toning" which work by superficial vaporization of epidermis, fragmentation and dispersion of melanins in melanocytes and melanophages and reduction of melanocytes. Thesecond technique works by partial reduction of epidermal melanocytes and transepidermal elimination of dermal melanins. Both technique needs mutiple treatments until the lesions fade. Intense pulse light (IPL) or frequency-doubled Q-switched NdYAG laser ( 532 nm) which was effective for superficial hyperpigmentation often resulted in transient improvemnt with rapid recurrence or worsening of lesions.In Asia , many doctors are treating melasma with oral tranexamic acid 1-2 Gram/day. This medicine has not been approved for this condition. The most serious complication of this medicine is thromboembolism. Prolong use of this medicine should be discouraged. Recently intradermal injection of 4% tranexamic acid had been reported to be effective treatment of melasma. After multiple laser treatments and hyperpigmentation decrease to close to normal skin colour, topical maintainance with effective medication should be administered . Cure may be unlikely for melasma, life long sunlight protection and topical antioxidants with safe antimelanin synthesis has to be applied as long as possible. | Melasma
Editor-in-Chief: Niwat Polnikorn, M.D. Associate Editor(s)-in-Chief: Jesus Rosario Hernandez, M.D. [1].
Synonyms and keywords: Chloasma, mask of pregnancy.
# Overview
Melasma (also known as chloasma or the mask of pregnancy when present in pregnant women) is a tan or dark facial skin discoloration. Although it can affect anyone, melasma is particularly common in women, especially pregnant women and those who are taking oral contraceptives or hormone replacement therapy (HRT) medications.The ratio of female to male is 9:1 and is more common in yellow to brown skin color ( Fitzpatrick's skin photo type III to V) .The lesions usually develops in middle age and persists for many years. In post menopause women , the lesions usually fade spontaneously. Prolong exposure to sunlight is the most important etiologic factor. It is also prevalent in men and women of Native American descent (on the forearms) and in men and women of German/Russian Jewish descent (on the face).
# Symptoms
The symptoms of melasma are brown to dark brown , irregular patches commonly found on the mid-face, upper cheek, nose, lips, upperlip, and forehead. Early lesions have well defined irregular margin,while older lesions tend to be grayish brown color with irregular and ill-defined border. These patches often develop gradually over time. clinically melasma had been divided into two clinical types 1) centro-facial and 2) zygoma types. Melasma does not cause any other symptoms beyond the cosmetic discoloration.
# Cause
Melasma is thought to be the stimulation of melanocytes or pigment-producing cells by the female sex hormones estrogen and progesterone to produce more melanin pigments when the skin is exposed to sun. Women with a light brown skin type who are living in regions with intense sun exposure are particularly susceptible to developing this condition.
Genetic predisposition is also a major factor in determining whether someone will develop melasma.Recent study of pathology changes of melasma had revealed that majority of melasma also had increase in number of melanocytes. The average increase is about 30% together with proliferation of small blood vessels in the dermis . Melanin dropping into dermis together with presence of macrophages containing melanins (melanophages) are commonly found in long standing cases. These three findings may explain the chronicity of melasma. Proliferate and dilated blood vessels may contribute to chronicity by being the source of cytokines ,prostaglandins and leukotrienes that stimulate melanin synthesis.
The incidence of melasma also increases in patients with thyroid disease. It is thought that the overproduction of melanocyte-stimulating hormone (MSH) brought on by stress can cause outbreaks of this condition. Other rare causes of melasma include allergic reaction to medications and cosmetics. Drugs like conjugated estrogens causes melasma
Melasma Suprarenale (Latin - of the adrenals) is a symptom of Addison's disease, particularly when caused by pressure or minor injury to the skin, as discovered by Dr. FJJ Schmidt of Rotterdam in 1859.
## Medications
Estropipate
# Diagnosis
Melasma is usually diagnosed visually or with assistance of a Wood's lamp (340 - 400 nm wavelength). Under Wood's lamp, excess melanin in the epidermis can be distinguished from that of the dermis. By this technique melasma can be divided into two types 1) epidermal 2) mixed (epidermal+ dermal). This diffentiation is important for planning of management.
# Physical examination
## Gallery
### Head
- url = http://www.atlasdermatologico.com.br/disease.jsf?diseaseId=285>
- url = http://www.atlasdermatologico.com.br/disease.jsf?diseaseId=285>
# Treatment
The discoloration usually disappears spontaneously over a period of several months after giving birth or stopping the oral contraceptives or hormone replacement therapy. In cases without definite causes, the lesions may persist for many years. In cases that severity of lesions justify the treatment, the following are the common treatment methods available: 1) Avoiding of exposure to strong sunlight (ultraviolet range ) with UVA-blocker sunscreen (320-400 nm) prevention. Since UVA is the most important wavelength of sunlight that stimulate hyperpigmentation. The over the counter UVA-sunscreen with PA more than +++ and SPF more than 30 is recommended. 2)Reduction of melanin synthesis, the most commonly use drug is hydroquinone 2-4% . To enhance effectiveness ,4% hydroquinone is combined with tretinoin(0.05%) and steroids(fluocinolone acetonide 0.01%) and has been named Kligman's formula. This formula had been proved to be the most effective in clearing of epidermal melasma. More than 60% will have complete clearing by three months. The problem of this formula is its long term side effects.At present Tri-Luma TM (Galderma,USA) is the only one triple drugs approved by USA-FDA for treatment of melasma. Hydroquinone has been associated with many complictions in dark skin patients i.e. contact dermatitis, exogenous ochronosis, confetti-like hypopigmentation and rebound hyperpigmentation. Others topical treatments that had been used for treatments include arbutin, kojic acid, licorice extract, azelaic acid, vitamin C, soy, green tea , decapeptides, ,glove extract etc. The results were inferior to Kligman's formular but claimed to have lower incidence of complications. Many of these products are ingredients of over the counter whitening creams. In some countries hydroquinone has not been approved , because of concern of mutagenic and toxicity e.g. Japan. The second technique for treatment of melasma is by enhancing peeling of epithelial cells by chemicals e.g. retinoic acid, glycolic , salycylic acid. Facial peels with glycolic or alpha hydroxy acids are popular in many countries. For mixed type with dermal melanophages and dilated blood vessels, usually resisted to topical treatments. These types are justified for method with deeper effects to melanocytes and melanophages. Recently two laser systems have been shown to be effective for treatment of deep lesions of melasma 1) flat beam, high energy Q-switched NdYAG (1064 nm)(Medlite c6/Revlite, Hoya-Conbio,USA) 2) Fractional Erbium Glass (1550 nm) laser. The first technique originate from Asia where mixed melasma are more common. The technique has been called "Laser toning" which work by superficial vaporization of epidermis, fragmentation and dispersion of melanins in melanocytes and melanophages and reduction of melanocytes. Thesecond technique works by partial reduction of epidermal melanocytes and transepidermal elimination of dermal melanins. Both technique needs mutiple treatments until the lesions fade. Intense pulse light (IPL) or frequency-doubled Q-switched NdYAG laser ( 532 nm) which was effective for superficial hyperpigmentation often resulted in transient improvemnt with rapid recurrence or worsening of lesions.In Asia , many doctors are treating melasma with oral tranexamic acid 1-2 Gram/day. This medicine has not been approved for this condition. The most serious complication of this medicine is thromboembolism. Prolong use of this medicine should be discouraged. Recently intradermal injection of 4% tranexamic acid had been reported to be effective treatment of melasma. After multiple laser treatments and hyperpigmentation decrease to close to normal skin colour, topical maintainance with effective medication should be administered . Cure may be unlikely for melasma, life long sunlight protection and topical antioxidants with safe antimelanin synthesis has to be applied as long as possible. | https://www.wikidoc.org/index.php/Chloasma | |
8df948d8c291d17a998423ef0324a3ce4154b7fd | wikidoc | Chordee | Chordee
Steven C. Campbell, M.D., Ph.D.
# Overview
Chordee is a condition in which the penis curves downward (that is, in a ventral direction). The curvature is usually most obvious during erection, but resistance to straightening is often apparent in the flaccid state as well. In many cases but not all, chordee is associated with hypospadias.
# Presentation
It is usually considered a congenital malformation of unknown cause. Since at an early stage of fetal development the penis is curved downward, it has been proposed that chordee results from an arrest of penile development at that stage.
The curvature of a chordee can involve
- tethering of the skin with urethra and corpora of normal size;
- curvature induced by fibrosis and contracture of the fascial tissue (Buck's fascia or dartos) surrounding the urethra;
- disproportionately large corpora in relation to the urethral length without other demonstrable abnormality of either; or
- a short, fibrotic urethra that tethers the penis downward (the least common type).
Severe degrees of chordee are usually associated with hypospadias, but mild degrees of curvature may occur in many otherwise normal males. When the curved penis is small and accompanied by hypospadias, deficiency of prenatal androgen effect can be inferred.
# Treatment
The principal treatment of chordee is surgery in infancy, usually by a pediatric urologist.
The preferred time for surgery is between the ages of 6 and 18 months, before the child develops castration and body image anxiety.
Correction is usually successful. | Chordee
Template:Search infobox
Steven C. Campbell, M.D., Ph.D.
# Overview
Chordee is a condition in which the penis curves downward (that is, in a ventral direction). The curvature is usually most obvious during erection, but resistance to straightening is often apparent in the flaccid state as well. In many cases but not all, chordee is associated with hypospadias.
# Presentation
It is usually considered a congenital malformation of unknown cause. Since at an early stage of fetal development the penis is curved downward, it has been proposed that chordee results from an arrest of penile development at that stage.
The curvature of a chordee can involve
- tethering of the skin with urethra and corpora of normal size;
- curvature induced by fibrosis and contracture of the fascial tissue (Buck's fascia or dartos) surrounding the urethra;
- disproportionately large corpora in relation to the urethral length without other demonstrable abnormality of either; or
- a short, fibrotic urethra that tethers the penis downward (the least common type).
Severe degrees of chordee are usually associated with hypospadias, but mild degrees of curvature may occur in many otherwise normal males. When the curved penis is small and accompanied by hypospadias, deficiency of prenatal androgen effect can be inferred.
# Treatment
The principal treatment of chordee is surgery in infancy, usually by a pediatric urologist.
The preferred time for surgery is between the ages of 6 and 18 months, before the child develops castration and body image anxiety.
Correction is usually successful.
# External links
- Template:FPnotebook
Template:WS | https://www.wikidoc.org/index.php/Chordee | |
27197e9a3a6902a3c333f79a5bb7d0914f1730d3 | wikidoc | Chordin | Chordin
Chordin is a bone morphogenetic protein antagonist composed of four small cysteine-rich domains, whose function is not known. In humans, the chordin peptide is encoded by the CHRD gene.
# History
Chordin was originally identified in the African clawed frog (Xenopus laevis) in the laboratory of Edward M. De Robertis as a key developmental protein that dorsalizes early vertebrate embryonic tissues.
# Structure
The Chordin polypeptide is 941 amino acids long and 120 kDa large. There are five named isoforms of this protein that are produced by alternative splicing.
# Function
It dorsalizes the developing embryo by binding ventralizing TGFβ proteins such as bone morphogenetic proteins. It may also play a role in organogenesis.
In mice, Chordin is expressed in the node but not in the anterior visceral endoderm. It has been found to be required for forebrain development. In developing mice that are deficient in both chordin and noggin, the head is nearly absent. This is significant because when only noggin is deficient there are mild defects but the head still forms.
Chordin is also involved in avian gastrulation. It is expressed in the anterior cells of Koller's sickle, which form the anterior cells of the primitive streak, a key structure through which gastrulation occurs. | Chordin
Chordin is a bone morphogenetic protein antagonist composed of four small cysteine-rich domains, whose function is not known. In humans, the chordin peptide is encoded by the CHRD gene.[1]
# History
Chordin was originally identified in the African clawed frog (Xenopus laevis) in the laboratory of Edward M. De Robertis as a key developmental protein that dorsalizes early vertebrate embryonic tissues.[2]
# Structure
The Chordin polypeptide is 941 amino acids long and 120 kDa large[3]. There are five named isoforms of this protein that are produced by alternative splicing.[4]
# Function
It dorsalizes the developing embryo by binding ventralizing TGFβ proteins such as bone morphogenetic proteins.[5] It may also play a role in organogenesis.
In mice, Chordin is expressed in the node but not in the anterior visceral endoderm. It has been found to be required for forebrain development.[6] In developing mice that are deficient in both chordin and noggin, the head is nearly absent. This is significant because when only noggin is deficient there are mild defects but the head still forms.[7]
Chordin is also involved in avian gastrulation. It is expressed in the anterior cells of Koller's sickle, which form the anterior cells of the primitive streak, a key structure through which gastrulation occurs.[8] | https://www.wikidoc.org/index.php/Chordin | |
3e7004b3e1092adc3beb8fc81de5de07af9dd71d | wikidoc | Chorion | Chorion
The chorion surrounds the embryo and other membranes. It consists of two layers: an outer formed by the primitive ectoderm or trophoblast, and an inner by the somatic mesoderm; with this latter the amnion is in contact.
The trophoblast is made up of an internal layer of cubical or prismatic cells, the cytotrophoblast or layer of Langhans, and an external layer of richly nucleated protoplasm devoid of cell boundaries, the syncytiotrophoblast.
It undergoes rapid proliferation and forms numerous processes, the chorionic villi, which invade and destroy the uterine decidua and at the same time absorb from it nutritive materials for the growth of the embryo.
The chorionic villi are at first small and non-vascular, and consist of trophoblast only, but they increase in size and ramify, while the mesoderm, carrying branches of the umbilical vessels, grows into them, and in this way they are vascularized.
Blood is carried to the villi by the branches of the umbilical arteries, and after circulating through the capillaries of the villi, is returned to the embryo by the umbilical veins. Until about the end of the second month of pregnancy the villi cover the entire chorion, and are almost uniform in size, but after this they develop unequally.
The greater part of the chorion is in contact with the decidua capsularis, and over this portion the villi, with their contained vessels, undergo atrophy, so that by the fourth month scarcely a trace of them is left, and hence this part of the chorion becomes smooth, and is named the chorion læve; as it takes no share in the formation of the placenta, it is also named the non-placental part of the chorion.
On the other hand, the villi on that part of the chorion which is in contact with the decidua placentalis increase greatly in size and complexity, and hence this part is named the chorion frondosum.
# Additional images
- Section through the embryo.
- Diagram illustrating early formation of allantois and differentiation of body-stalk.
- Diagram showing later stage of allantoic development with commencing constriction of the yolk-sac.
- Scheme of placental circulation. | Chorion
Template:Infobox Anatomy
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
The chorion surrounds the embryo and other membranes. It consists of two layers: an outer formed by the primitive ectoderm or trophoblast, and an inner by the somatic mesoderm; with this latter the amnion is in contact.
The trophoblast is made up of an internal layer of cubical or prismatic cells, the cytotrophoblast or layer of Langhans, and an external layer of richly nucleated protoplasm devoid of cell boundaries, the syncytiotrophoblast.
It undergoes rapid proliferation and forms numerous processes, the chorionic villi, which invade and destroy the uterine decidua and at the same time absorb from it nutritive materials for the growth of the embryo.
The chorionic villi are at first small and non-vascular, and consist of trophoblast only, but they increase in size and ramify, while the mesoderm, carrying branches of the umbilical vessels, grows into them, and in this way they are vascularized.
Blood is carried to the villi by the branches of the umbilical arteries, and after circulating through the capillaries of the villi, is returned to the embryo by the umbilical veins. Until about the end of the second month of pregnancy the villi cover the entire chorion, and are almost uniform in size, but after this they develop unequally.
The greater part of the chorion is in contact with the decidua capsularis, and over this portion the villi, with their contained vessels, undergo atrophy, so that by the fourth month scarcely a trace of them is left, and hence this part of the chorion becomes smooth, and is named the chorion læve; as it takes no share in the formation of the placenta, it is also named the non-placental part of the chorion.
On the other hand, the villi on that part of the chorion which is in contact with the decidua placentalis increase greatly in size and complexity, and hence this part is named the chorion frondosum.
# Additional images
- Section through the embryo.
- Diagram illustrating early formation of allantois and differentiation of body-stalk.
- Diagram showing later stage of allantoic development with commencing constriction of the yolk-sac.
- Scheme of placental circulation. | https://www.wikidoc.org/index.php/Chorion | |
53cbc15092f437981ea3d06f6c506932054e37d5 | wikidoc | Choroid | Choroid
The choroid, also known as the choroidea or choroid coat, is the vascular layer of the eye lying between the retina and the sclera, with a thickness about 0.5 mm. The choroid provides oxygen and nourishment to the outer layers of the retina .
Along with the ciliary body and iris, the choroid forms the uveal tract. In humans and other primates, darkly colored melanin pigment in the choroid helps limit reflections within the eye that would potentially result in the perception of confusing images. Poor vision frequently results from lack of this pigmentation in human albinos. By contrast, the choroid of many other animals contains reflective materials that help to collect light in dim situations; this is one type of tapetum lucidum.
The red eye effect on photos is caused by the reflection of light from choroid. It appears red because of the choroid's blood vessels.
# Layers
The structure of the choroid is generally divided into four layers:
- Haller's layer - outermost layer of the choroid consisting of larger diameter blood vessels
- Sattler's layer - layer of medium diameter blood vessels
- Choriocapillaris - layer of capillaries
- Bruch's membrane - innermost layer of the choroid | Choroid
Template:Infobox Anatomy
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
The choroid, also known as the choroidea or choroid coat, is the vascular layer of the eye lying between the retina and the sclera, with a thickness about 0.5 mm. The choroid provides oxygen and nourishment to the outer layers of the retina [2].
Along with the ciliary body and iris, the choroid forms the uveal tract. In humans and other primates, darkly colored melanin pigment in the choroid helps limit reflections within the eye that would potentially result in the perception of confusing images. Poor vision frequently results from lack of this pigmentation in human albinos. By contrast, the choroid of many other animals contains reflective materials that help to collect light in dim situations; this is one type of tapetum lucidum.
The red eye effect on photos is caused by the reflection of light from choroid. It appears red because of the choroid's blood vessels.
# Layers
The structure of the choroid is generally divided into four layers:
- Haller's layer - outermost layer of the choroid consisting of larger diameter blood vessels
- Sattler's layer - layer of medium diameter blood vessels
- Choriocapillaris - layer of capillaries
- Bruch's membrane - innermost layer of the choroid | https://www.wikidoc.org/index.php/Choroid | |
853d93fe8b3233b6fdb2908dde0f1afa71659e2d | wikidoc | Cineole | Cineole
# Overview
Eucalyptol is a natural organic compound that is a colorless liquid. It is a cyclic ether and a monoterpenoid.
Eucalyptol is also known by a variety of synonyms: 1,8-cineol, 1,8-cineole, cajeputol, 1,8-epoxy-p-menthane, 1,8-oxido-p-menthane, eucalyptol, eucalyptole, 1,3,3-trimethyl-2-oxabicyclooctane, cineol, cineole.
In 1870, F.S. Cloez identified and ascribed the name eucalyptol to the dominant portion of Eucalyptus globulus oil. Eucalyptus oil, the generic collective name for oils from the Eucalyptus genus, should not be confused with the chemical compound eucalyptol.
# Composition
Eucalyptol comprises up to 90 percent of the essential oil of some species of the generic product Eucalyptus oil, hence the common name of the compound. It is also found in camphor laurel, bay leaves, tea tree, mugwort, sweet basil, wormwood, rosemary, common sage, cannabis sativa, and other aromatic plant foliage. Eucalyptol with a purity from 99.6 to 99.8 percent can be obtained in large quantities by fractional distillation of eucalyptus oil.
Although it can be used internally as a flavoring and medicine ingredient at very low doses, typical of many essential oils (volatile oils), eucalyptol is toxic if ingested at higher than normal doses.
# Properties
Eucalyptol has a fresh camphor-like smell and a spicy, cooling taste. It is insoluble in water, but miscible with ether, ethanol, and chloroform. The boiling point is 176 °C and the flash point is 49 °C. Eucalyptol forms crystalline adducts with halogen acids, o-cresol, resorcinol, and phosphoric acid. Formation of these adducts are useful for purification.
# Uses
## Flavoring and fragrance
Because of its pleasant spicy aroma and taste, eucalyptol is used in flavorings, fragrances, and cosmetics. Cineole-based eucalyptus oil is used as a flavouring at low levels (0.002%) in various products, including baked goods, confectionery, meat products and beverages. In a 1994, report released by five top cigarette companies, eucalyptol was listed as one of the 599 additives to cigarettes. It is claimed that it is added to improve the flavor.
## Medicinal
Eucalyptol is an ingredient in many brands of mouthwash and cough suppressant, as well as an inactive ingredient in body powder.
## Insecticide and repellent
Eucalyptol is used as an insecticide and insect repellent.
In contrast, eucalyptol is one of many compounds that are attractive to males of various species of orchid bees, which gather the chemical to synthesize pheromones; it is commonly used as bait to attract and collect these bees for study.
# Toxicology
In higher-than-normal doses, eucalyptol is hazardous via ingestion, skin contact, or inhalation. It can have acute health effects on behavior, respiratory tract, and nervous system. The acute oral Template:LD50 is 2480 mg/kg (rat). It is classified as a reproductive toxin for females and a suspect reproductive toxin for males.
# Scientific study
- In a 2003 study, eucalyptol was found to control airway mucus hypersecretion and asthma; after, in a previous study, the authors found eucalyptol to suppress arachidonic acid metabolism and cytokine production in human monocytes.
- In a 2004 study, it was found to inhibit cytokine production in cultured human lymphocytes and monocytes.
- In a 2004 study, eucalyptol was found to be an effective treatment for nonpurulent rhinosinusitis. Treated subjects experienced less headache on bending, frontal headache, sensitivity of pressure points of trigeminal nerve, impairment of general condition, nasal obstruction, and rhinological secretion. Side effects from treatment were minimal.
- A 2000 study found eucalyptol to reduce inflammation and pain when applied topically.
- In a 2002 study, it was found to kill leukaemia cells of two cultured human leukemia cell lines, but not cells of a human stomach cancer cell line in vitro.
# List of plants that contain the chemical
- Cannabis
- Cinnamomum camphora, Camphor laurel (50%)
- Eucalyptus cneorifolia
- Eucalyptus dives,
- Eucalyptus dumosa
- Eucalyptus globulus
- Eucalyptus goniocalyx
- Eucalyptus horistes
- Eucalyptus kochii
- Eucalyptus leucoxylon
- Eucalyptus oleosa
- Eucalyptus polybractea
- Eucalyptus radiata
- Eucalyptus sideroxylon
- Eucalyptus smithii
- Eucalyptus staigeriana
- Eucalyptus tereticornis
- Eucalyptus viridis
- Helichrysum gymnocephalum
- Kaempferia galanga, Galangal, (5.7%)
- Laurus nobilis, Bay Laurel, (45%)
- Melaleuca alternifolia, Tea-tree, (0–15%)
- Salvia lavandulifolia, Spanish sage (13%)
- Turnera diffusa, Damiana
- Umbellularia californica, Pepperwood (22.0%)
- Zingiber officinale, Ginger
# Compendial status
- British Pharmacopoeia
- Martindale: The Extra Pharmacopoeia 31
N.B. Listed as "cineole" in some pharmacopoeia. | Cineole
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
# Overview
Eucalyptol is a natural organic compound that is a colorless liquid. It is a cyclic ether and a monoterpenoid.
Eucalyptol is also known by a variety of synonyms: 1,8-cineol, 1,8-cineole, cajeputol, 1,8-epoxy-p-menthane, 1,8-oxido-p-menthane, eucalyptol, eucalyptole, 1,3,3-trimethyl-2-oxabicyclo[2,2,2]octane, cineol, cineole.
In 1870, F.S. Cloez identified and ascribed the name eucalyptol to the dominant portion of Eucalyptus globulus oil.[1] Eucalyptus oil, the generic collective name for oils from the Eucalyptus genus, should not be confused with the chemical compound eucalyptol.
# Composition
Eucalyptol comprises up to 90 percent of the essential oil of some species of the generic product Eucalyptus oil,[1] hence the common name of the compound. It is also found in camphor laurel, bay leaves, tea tree, mugwort, sweet basil, wormwood, rosemary, common sage, cannabis sativa, and other aromatic plant foliage. Eucalyptol with a purity from 99.6 to 99.8 percent can be obtained in large quantities by fractional distillation of eucalyptus oil.
Although it can be used internally as a flavoring and medicine ingredient at very low doses, typical of many essential oils (volatile oils), eucalyptol is toxic if ingested at higher than normal doses.[2]
# Properties
Eucalyptol has a fresh camphor-like smell and a spicy, cooling taste. It is insoluble in water, but miscible with ether, ethanol, and chloroform. The boiling point is 176 °C and the flash point is 49 °C. Eucalyptol forms crystalline adducts with halogen acids, o-cresol, resorcinol, and phosphoric acid. Formation of these adducts are useful for purification.
# Uses
## Flavoring and fragrance
Because of its pleasant spicy aroma and taste, eucalyptol is used in flavorings, fragrances, and cosmetics. Cineole-based eucalyptus oil is used as a flavouring at low levels (0.002%) in various products, including baked goods, confectionery, meat products and beverages.[3] In a 1994, report released by five top cigarette companies, eucalyptol was listed as one of the 599 additives to cigarettes.[4] It is claimed that it is added to improve the flavor.
## Medicinal
Eucalyptol is an ingredient in many brands of mouthwash and cough suppressant, as well as an inactive ingredient in body powder.
## Insecticide and repellent
Eucalyptol is used as an insecticide and insect repellent.[5][6]
In contrast, eucalyptol is one of many compounds that are attractive to males of various species of orchid bees, which gather the chemical to synthesize pheromones; it is commonly used as bait to attract and collect these bees for study.[7]
# Toxicology
In higher-than-normal doses, eucalyptol is hazardous via ingestion, skin contact, or inhalation. It can have acute health effects on behavior, respiratory tract, and nervous system. The acute oral Template:LD50 is 2480 mg/kg (rat). It is classified as a reproductive toxin for females and a suspect reproductive toxin for males.[2]
# Scientific study
- In a 2003 study, eucalyptol was found to control airway mucus hypersecretion and asthma; after, in a previous study, the authors found eucalyptol to suppress arachidonic acid metabolism and cytokine production in human monocytes.[8][9]
- In a 2004 study, it was found to inhibit cytokine production in cultured human lymphocytes and monocytes.[10]
- In a 2004 study, eucalyptol was found to be an effective treatment for nonpurulent rhinosinusitis. Treated subjects experienced less headache on bending, frontal headache, sensitivity of pressure points of trigeminal nerve, impairment of general condition, nasal obstruction, and rhinological secretion. Side effects from treatment were minimal.[11]
- A 2000 study found eucalyptol to reduce inflammation and pain when applied topically.[12]
- In a 2002 study, it was found to kill leukaemia cells of two cultured human leukemia cell lines, but not cells of a human stomach cancer cell line in vitro.[13]
# List of plants that contain the chemical
- Cannabis[14]
- Cinnamomum camphora, Camphor laurel (50%)[15]
- Eucalyptus cneorifolia[citation needed]
- Eucalyptus dives,[citation needed]
- Eucalyptus dumosa[citation needed]
- Eucalyptus globulus[16]
- Eucalyptus goniocalyx[citation needed]
- Eucalyptus horistes[citation needed]
- Eucalyptus kochii[citation needed]
- Eucalyptus leucoxylon[citation needed]
- Eucalyptus oleosa[citation needed]
- Eucalyptus polybractea[citation needed]
- Eucalyptus radiata[citation needed]
- Eucalyptus sideroxylon[citation needed]
- Eucalyptus smithii[citation needed]
- Eucalyptus staigeriana[17]
- Eucalyptus tereticornis[citation needed]
- Eucalyptus viridis[citation needed]
- Helichrysum gymnocephalum [18]
- Kaempferia galanga, Galangal, (5.7%)[19]
- Laurus nobilis, Bay Laurel, (45%)[citation needed]
- Melaleuca alternifolia, Tea-tree, (0–15%)[citation needed]
- Salvia lavandulifolia, Spanish sage (13%)[20]
- Turnera diffusa, Damiana[21]
- Umbellularia californica, Pepperwood (22.0%)[22]
- Zingiber officinale, Ginger[citation needed]
# Compendial status
- British Pharmacopoeia [23]
- Martindale: The Extra Pharmacopoeia 31 [24]
N.B. Listed as "cineole" in some pharmacopoeia. | https://www.wikidoc.org/index.php/Cineole | |
0e549a16f4bd7d0b7180cf3e2fe7aa3f48febb3b | wikidoc | Citrate | Citrate
A citrate is an ionic form of citric acid, such as C3H5O(COO)33−, that is, citric acid minus three hydrogen ions.
# Citrate family
Citrates are compounds containing this group, either ionic compounds, the salts, or analogous covalent compounds, esters. An example of a salt is sodium citrate and an ester is trimethyl citrate. See category for a bigger list.
# Other citric acid ions
Since citric acid is a multifunctional acid, intermediate ions exist, hydrogen citrate ion, HC6H5O72− and dihydrogen citrate ion, H2C6H5O7−. These may form salts as well, called acid salts.
# pH
Salts of the hydrogen citrate ions are weakly acidic, while salts of the citrate ion itself (with an inert cation such as sodium ion) are weakly basic.
# Buffering
Citrate is a key component in the commonly used SSC 20X hybridization buffer. There exists authoritative literature (Maniatis) that incorrectly instructs the preparation of this buffer to include 3M NaCl and 0.3M Sodium Citrate, to be titrated up with NaOH to a pH of 7. When the two components are actually mixed together, the pH is slightly basic. Therefore, the pH of the solution should instead be titrated down to 7 with HCl.
Citric acid can act as a mild chelating agent.
# Metabolism
## TCA cycle
Citrate is an intermediate in the TCA (Krebs) Cycle. After the pyruvate dehydrogenase complex forms acetyl CoA, from pyruvate and five cofactors (Thiamine pyrophosphate, lipoamide, FAD, NAD+, and CoA), citrate synthase catalyzes the condensation of oxaloacetate with Acetyl CoA to form citrate. Citrate continues in the TCA cycle via aconitase with the eventual regeneration of oxaloacetate, which can combine with another molecule of acetyl CoA and continue cycling.
See also TCA cycle
## Role in Glycolysis
High concentration of citrate can inhibit phosphofructokinase, the pace-maker of glycolysis. | Citrate
Template:Chembox new
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
# For patient information, click here
A citrate is an ionic form of citric acid, such as C3H5O(COO)33−, that is, citric acid minus three hydrogen ions.
# Citrate family
Citrates are compounds containing this group, either ionic compounds, the salts, or analogous covalent compounds, esters. An example of a salt is sodium citrate and an ester is trimethyl citrate. See category for a bigger list.
# Other citric acid ions
Since citric acid is a multifunctional acid, intermediate ions exist, hydrogen citrate ion, HC6H5O72− and dihydrogen citrate ion, H2C6H5O7−. These may form salts as well, called acid salts.
# pH
Salts of the hydrogen citrate ions are weakly acidic, while salts of the citrate ion itself (with an inert cation such as sodium ion) are weakly basic.
# Buffering
Citrate is a key component in the commonly used SSC 20X hybridization buffer. There exists authoritative literature (Maniatis) that incorrectly instructs the preparation of this buffer to include 3M NaCl and 0.3M Sodium Citrate, to be titrated up with NaOH to a pH of 7. When the two components are actually mixed together, the pH is slightly basic. Therefore, the pH of the solution should instead be titrated down to 7 with HCl.
Citric acid can act as a mild chelating agent.
# Metabolism
## TCA cycle
Citrate is an intermediate in the TCA (Krebs) Cycle. After the pyruvate dehydrogenase complex forms acetyl CoA, from pyruvate and five cofactors (Thiamine pyrophosphate, lipoamide, FAD, NAD+, and CoA), citrate synthase catalyzes the condensation of oxaloacetate with Acetyl CoA to form citrate. Citrate continues in the TCA cycle via aconitase with the eventual regeneration of oxaloacetate, which can combine with another molecule of acetyl CoA and continue cycling.
See also TCA cycle
## Role in Glycolysis
High concentration of citrate can inhibit phosphofructokinase, the pace-maker of glycolysis. | https://www.wikidoc.org/index.php/Citrate | |
d43c835831c0a7e8a317f203aec244430885069b | wikidoc | Cloning | Cloning
# Overview
Cloning is the process of creating an identical copy of something. In biology, it collectively refers to processes used to create copies of DNA fragments (molecular cloning), cells (cell cloning), or organisms. The term also encompasses situations whereby organisms reproduce asexually.
# Etymology
The term clone is derived from κλών, the Greek word for "twig, branch", referring to the process whereby a new plant can be created from a twig. In horticulture, the spelling clon was used until the twentieth century; the final e came into use to indicate the vowel is a "long o" instead of a "short o". Since the term entered the popular lexicon in a more general context, the spelling clone has been used exclusively.
# Molecular cloning
Molecular cloning refers to the procedure of isolating a defined DNA sequence and obtaining multiple copies of it in vivo. Cloning is frequently employed to amplify DNA fragments containing genes, but it can be used to amplify any DNA sequence such as promoters, non-coding sequences and randomly fragmented DNA. It is utilised in a wide array of biological experiments and practical applications such as large scale protein production. Occasionally, the term cloning is misleadingly used to refer to the identification of the chromosomal location of a gene associated with a particular phenotype of interest, such as in positional cloning. In practice, localization of the gene to a chromosome or genomic region does not necessarily enable one to isolate or amplify the relevant genomic sequence.
In essence, in order to amplify any DNA sequence in a living organism, that sequence must be linked to an origin of replication, a sequence element capable of directing the propagation of itself and any linked sequence. In practice, however, a number of other features are desired and a variety of specialised cloning vectors exist that allow protein expression, tagging, single stranded RNA and DNA production and a host of other manipulations.
Cloning of any DNA fragment essentially involves four steps: fragmentation, ligation, transfection, and screening/selection. Although these steps are invariable among cloning procedures a number of alternative routes can be selected, these are summarised as a ‘cloning strategy’.
Initially, the DNA of interest needs to be isolated to provide a relevant DNA segment of suitable size. Subsequently, a ligation procedure is employed whereby the amplified fragment is inserted into a vector. The vector (which is frequently circular) is linearised by means of restriction enzymes, and incubated with the fragment of interest under appropriate conditions with an enzyme called DNA ligase. Following ligation the vector with the insert of interest is transfected into cells. A number of alternative techniques are available, such as chemical sensitivation of cells, electroporation and biolistics. Finally, the transfected cells are cultured. As the aforementioned procedures are of particularly low efficiency, there is a need to identify the cells that have been successfully transfected with the vector construct containing the desired insertion sequence in the required orientation. Modern cloning vectors include selectable antibiotic resistance markers, which allow only cells in which the vector has been transfected, to grow. Additionally, the cloning vectors may contain colour selection markers which provide blue/white screening (α-factor complementation) on X-gal medium. Nevertheless, these selection steps do not absolutely guarantee that the DNA insert is present in the cells obtained. Further investigation of the resulting colonies is required to confirm that cloning was successful. This may be accomplished by means of PCR, restriction fragment analysis and/or DNA sequencing.Do not delete my edits or ill delete the deleters page!!!
# Cellular cloning
Cloning a cell means to derive a population of cells from a single cell. In the case of unicellular organisms such as bacteria and yeast, this process is remarkably simple and essentially only requires the inoculation of the appropriate medium. However, in the case of cell cultures from higher organisms, cell cloning is an arduous task as these cells will not readily grow in standard media.
A useful tissue culture technique used to clone distinct lineages of cell lines involves the use of cloning rings (cylinders). According to this technique, a single-cell suspension of cells which have been exposed to a mutagenic agent or drug used to drive selection is plated at high dilution to create isolated colonies; each arising from a single and potentially clonally distinct cell. At an early growth stage when colonies consist of only a few of cells, sterile polystyrene rings (cloning rings), which have been dipped in grease are placed over an individual colony and a small amount of trypsin is added. Cloned cells are collected from inside the ring and transferred to a new vessel for further growth.
# Organism
Organism cloning refers to the procedure of creating a new multicellular organism, genetically identical to another. In essence this form of cloning is an asexual method of reproduction, where fertilization or inter-gamete contact does not take place. Asexual reproduction is a naturally occurring phenomenon in many species, including most plants (see vegetative reproduction) and some insects.
## Horticultural
The term clone is used in horticulture to mean all descendants of a single plant, produced by vegetative reproduction or apomixis. Many horticultural plant cultivars are clones, having been derived from a single individual, multiplied by some process other than sexual reproduction. As an example, some European cultivars of grapes represent clones that have been propagated for over two millennia. Other examples are potato and banana. Grafting can be regarded as cloning, since all the shoots and branches coming from the graft are genetically a clone of a single individual, but this particular kind of cloning has not come under ethical scrutiny and is generally treated as an entirely different kind of operation.
Many trees, shrubs, vines, ferns and other herbaceous perennials form clonal colonies. Parts of a large clonal colony often become detached from the parent, termed fragmentation, to form separate individuals. Some plants also form seeds asexually, termed apomixis, e.g. dandelion.
## Animals
Clonal derivation exists in nature in some animal species and is referred to as parthenogenesis. An example is the "Little Fire Ant" (Wasmannia auropunctata), which is native to Central and South America but has spread throughout many tropical environments.
## First cloned buffalo
On September 15, 2007, the Philippines announced its development of Southeast Asia’s first cloned water buffalo. The Philippine Council for Agriculture, Forestry and Natural Resources Research and Development (PCARRD), under the Department of Science and Technology in Los Baños, Laguna appoved this project. The Department of Agriculture’s Philippine Carabao Center (PCC) will implement “Cloning through somatic cell nuclear transfer as a tool for genetic improvement in water buffaloes.” “Super buffalo calves” will be produced. There will be no modification or alteration of the genetic materials, as in GMOs (genetically modified organisms).
## Therapeutic cloning
Therapeutic cloning refers to a procedure which produces cells, specific body parts, and organs to be utilized for medical purposes. Although this has only been realized with parts of bladders, early cleavage-stage human embryos have been cloned and this is the subject of much active research. Currently, patients subjected to transplantation are administered immunosuppressive drugs to prevent recognition of the foreign transplant by their immune system and its subsequent rejection. The ability to clonally derive tissues and organs from the patients' own cells would abolish the need for immunosuppressive drugs and would allow the patients to live a life without the potentially serious side-effects of immunosuppressive drugs. More importantly, the ability to clonally derive organs would alleviate the current shortage of transplants and would possibly reduce waiting times for transplants to become available.
## Reproductive cloning
Reproductive cloning uses "somatic cell nuclear transfer" (SCNT) to create animals that are genetically identical. This process entails the transfer of a nucleus from a donor adult cell (somatic cell) to an egg which has no nucleus. If the egg begins to divide normally it is transferred into the uterus of the surrogate mother.
Such clones are not strictly identical since the somatic cells may contain mutations in their nuclear DNA. Additionally, the mitochondria in the cytoplasm also contains DNA and during SCNT this DNA is wholly from the donor egg, thus the mitochondrial genome is not the same as that of the nucleus donor cell from which it was produced. This may have important implications for cross-species nuclear transfer in which nuclear-mitochondrial incompatibilities may lead to death.
### Species cloned
The modern cloning techniques involving nuclear transfer have been successfully performed on several species. Landmark experiments in chronological order:
- Tadpole: (1952) Many scientists questioned whether cloning had actually occurred and unpublished experiments by other labs were not able to reproduce the reported results.
- Carp: (1963) In China, embryologist Tong Dizhou cloned a fish. He published the findings in an obscure Chinese science journal which was never translated into English.
- Sheep: (1996) From early embryonic cells by Steen Willadsen. Megan and Morag cloned from differentiated embryonic cells in June 1995 and Dolly the sheep in 1997.
- Rhesus Monkey: Tetra (female, January 2000) from embryo splitting
- Cattle: Alpha and Beta (males, 2001) and (2005) Brazil
- Cat: CopyCat "CC" (female, late 2001), Little Nicky, 2004, was the first cat cloned for commercial reasons
- Mule: Idaho Gem, a john mule born 2003-05-04, was the first horse-family clone.
- Horse: Prometea, a Haflinger female born 2003-05-28, was the first horse clone.
For a complete list see: List of animals that have been cloned.
### Health aspects
The success rate of cloning has been low: Dolly the sheep was born after 277 eggs were used to create 29 embryos, which only produced three lambs at birth, only one of which lived. Seventy calves have been created from 9,000 attempts and one third of them died young; Prometea took 328 attempts. Notably, although the first clones were frogs, no adult cloned frog has yet been produced from a somatic adult nucleus donor cell.
There were early claims that Dolly the Sheep had accelerated aging. Aging of this type is thought to be due to the shortening of telomeres, regions at the tips of chromosomes which prevent genetic threads from fraying every time a cell divides. Over time telomeres get worn down until cell-division is no longer possible — this is thought to be a cause of aging. Dolly died in the year 2003. Ian Wilmut said that Dolly's early death had nothing to do with cloning but with a respiratory infection common to lambs raised like Dolly.
Analysis of telomeres from cloned cows showed that they were longer than noncloned calves. This suggests clones could live longer life spans although many died young after excessive growth. Researchers think that this could eventually be developed to reverse aging in humans, provided that aging is based chiefly on the shortening of telomeres. Although some work has been performed on telomeres and aging in nuclear transfer clones, the evidence is at an early stage.
### Dolly the Sheep
Dolly (1996-07-05 – 2003-02-14), a Finn Dorsett ewe, was the first mammal to have been successfully cloned from an adult cell. She was cloned at the Roslin Institute in Scotland and lived there until her death when she was six. On 2003-04-09 her stuffed remains were placed at Edinburgh's Royal Museum, part of the National Museums of Scotland.
Dolly was publically significant because the effort showed that the genetic material from a specific adult cell, programmed to express only a distinct subset of its genes, could be reprogrammed to grow an entire new organism. Before this demonstration, there was no proof for the widely spread hypothesis that differentiated animal cells can give rise to entire new organisms.
### Human cloning
Human cloning is the creation of a genetically identical copy of an existing or previously existing human. The term is generally used to refer to artificial human cloning; human clones in the form of identical twins are commonplace, with their cloning occurring during the natural process of reproduction. There are two commonly discussed types of human cloning: therapeutic cloning and reproductive cloning. A third type of cloning called replacement cloning exists in theory, and is a combination of therapeutic and reproductive cloning. Replacement cloning entails the replacement of an extensively damaged, failed, or failing body through cloning followed by whole or partial brain transplant. It has been proposed as a way to greatly extend lifespan.
Human cloning is among the most controversial forms of the practice. There have been numerous demands for all progress in the human cloning field to be halted. Some people and groups oppose therapeutic cloning but many more oppose reproductive cloning. The American Association for the Advancement of Science (AAAS) and other scientific organizations have made public statements suggesting that human reproductive cloning be banned until safety issues are resolved . Serious ethical issues have arisen in discussions of harvesting of organs from clones. Some people have considered the idea of growing organs separately from a human organism - in doing this, a new organ supply could be established without the moral implications of harvesting them from human organisms. Research is also being done on the idea of growing organs that are biologically acceptable to the human body inside of other organisms, such as pigs or cows, then transplanting them to humans.
### Cloning extinct and endangered species
Cloning, or more precisely, the reconstruction of functional DNA from extinct species has, for decades, been a dream of some scientists. The possible implications of this were dramatized in the best-selling novel by Michael Crichton and high budget Hollywood thriller Jurassic Park. In real life, one of the most anticipated targets for cloning was once the Woolly Mammoth, but attempts to extract DNA from frozen mammoths have been unsuccessful, though a joint Russo-Japanese team is currently working toward this goal.
In 2001, a cow named Bessie gave birth to a cloned Asian gaur, an endangered species, but the calf died after two days. In 2003, a banteng was successfully cloned, followed by three African wildcats from a thawed frozen embryo. These successes provided hope that similar techniques (using surrogate mothers of another species) might be used to clone extinct species. Anticipating this possibility, tissue samples from the last bucardo (Pyrenean Ibex) were frozen immediately after it died. Researchers are also considering cloning endangered species such as the giant panda, ocelot, and cheetah. The "Frozen Zoo" at the San Diego Zoo now stores frozen tissue from the world's rarest and most endangered species.
In 2002, geneticists at the Australian Museum announced that they had replicated DNA of the Thylacine (Tasmanian Tiger), extinct about 65 years previous, using polymerase chain reaction. However, on 2005-02-15 the museum announced that it was stopping the project after tests showed the specimens' DNA had been too badly degraded by the (ethanol) preservative. Most recently, on 2005-05-15, it was announced that the Thylacine project would be revived, with new participation from researchers in New South Wales and Victoria.
One of the continuing obstacles in the attempt to clone extinct species is the need for nearly perfect DNA. Cloning from a single specimen could not create a viable breeding population in sexually reproducing animals. Furthermore, even if males and females were cloned, the question would remain open if they would be viable at all in the absence of parents that could teach or show them their natural behavior. Essentially, if cloning an extinct species succeeded — it must be considered that cloning still is an experimental technology that succeeds only by chance — it is far more likely than not that any resulting animals, even if they were healthy, would be little more than curios or museum pieces.
Cloning endangered species is a highly ideological issue. Many conservation biologists and environmentalists vehemently oppose cloning endangered species — not because they think it won't work but because they think it may deter donations to help preserve natural habitat and wild animal populations. The "rule-of-thumb" in animal conservation is that, if it is still feasible to conserve habitat and viable wild populations, breeding in captivity should not be undertaken in isolation.
In a 2006 review, David Ehrenfeld concludes that cloning in animal conservation is an experimental technology that, at its present state, cannot be expected to work except by pure chance and utterly fails a cost-benefit analysis. Furthermore, he says, it is likely to siphon funds from established and working projects and does not address any of the issues underlying animal extinction (such as habitat destruction, hunting or other overexploitation, and an impoverished gene pool). While cloning technologies are well-established and used on a regular basis in plant conservation, care must be taken to ensure genetic diversity. He concludes:
## Embryo
Somatic cell nuclear transfer can also be used to create a clonal embryo. The most likely scenario for this is to produce embryos for use in research, particularly stem cell research. This process is also called "research cloning" or "therapeutic cloning."
Therapeutic cloning, also called "embryo cloning," is the production of human embryos for use in research. The goal of this process is not to create cloned human beings, but rather to harvest stem cells that can be used to study human development and to treat disease. Stem cells are important to biomedical researchers because they can be used to generate virtually any type of specialized cell in the human body. Stem cells are extracted from the egg after it has divided for 5 days. The egg at this stage of development is called a blastocyst. Many researchers hope that one day stem cells can be used to serve as replacement cells to treat heart disease, Alzheimer's, cancer, and other diseases.
Scientists believe that cloning may be used to create stem cells genetically compatible with the somatic cell donor. Cloning in stem cell research, called research cloning or therapeutic cloning, has not yet been successful: no embryonic stem cell lines have been derived from clonal embryos. The process might provide a way to grow organs in host carriers, so that organs could be produced which would be completely compatible with the original tissue donor. Host carrier growing poses a risk of trans-species diseases if the host is of a different species (e.g., a pig).
In human beings, this is a highly controversial issue for several reasons. It involves creating human embryos in vitro and then destroying them during the process of attempting to obtain embryonic stem cells. But proposals to use cloning techniques in human stem cell research raise a set of concerns beyond the moral status of the embryo. These have led a number of individuals and organizations, who are not opposed in principle to human embryonic stem cell research, to be concerned about or opposed to, human research cloning. One concern is that cloning in human stem cell research will lead to the reproductive cloning of humans. A second concern relates to the appropriate sourcing of the eggs that are needed. Research cloning requires a large number of human eggs, which can only be obtained from women. A third concern is the feasibility of developing stem cell therapies from cloning. | Cloning
# Overview
Cloning is the process of creating an identical copy of something. In biology, it collectively refers to processes used to create copies of DNA fragments (molecular cloning), cells (cell cloning), or organisms. The term also encompasses situations whereby organisms reproduce asexually.
# Etymology
The term clone is derived from κλών, the Greek word for "twig, branch", referring to the process whereby a new plant can be created from a twig. In horticulture, the spelling clon was used until the twentieth century; the final e came into use to indicate the vowel is a "long o" instead of a "short o". Since the term entered the popular lexicon in a more general context, the spelling clone has been used exclusively.
# Molecular cloning
Molecular cloning refers to the procedure of isolating a defined DNA sequence and obtaining multiple copies of it in vivo. Cloning is frequently employed to amplify DNA fragments containing genes, but it can be used to amplify any DNA sequence such as promoters, non-coding sequences and randomly fragmented DNA. It is utilised in a wide array of biological experiments and practical applications such as large scale protein production. Occasionally, the term cloning is misleadingly used to refer to the identification of the chromosomal location of a gene associated with a particular phenotype of interest, such as in positional cloning. In practice, localization of the gene to a chromosome or genomic region does not necessarily enable one to isolate or amplify the relevant genomic sequence.
In essence, in order to amplify any DNA sequence in a living organism, that sequence must be linked to an origin of replication, a sequence element capable of directing the propagation of itself and any linked sequence. In practice, however, a number of other features are desired and a variety of specialised cloning vectors exist that allow protein expression, tagging, single stranded RNA and DNA production and a host of other manipulations.
Cloning of any DNA fragment essentially involves four steps: fragmentation, ligation, transfection, and screening/selection. Although these steps are invariable among cloning procedures a number of alternative routes can be selected, these are summarised as a ‘cloning strategy’.
Initially, the DNA of interest needs to be isolated to provide a relevant DNA segment of suitable size. Subsequently, a ligation procedure is employed whereby the amplified fragment is inserted into a vector. The vector (which is frequently circular) is linearised by means of restriction enzymes, and incubated with the fragment of interest under appropriate conditions with an enzyme called DNA ligase. Following ligation the vector with the insert of interest is transfected into cells. A number of alternative techniques are available, such as chemical sensitivation of cells, electroporation and biolistics. Finally, the transfected cells are cultured. As the aforementioned procedures are of particularly low efficiency, there is a need to identify the cells that have been successfully transfected with the vector construct containing the desired insertion sequence in the required orientation. Modern cloning vectors include selectable antibiotic resistance markers, which allow only cells in which the vector has been transfected, to grow. Additionally, the cloning vectors may contain colour selection markers which provide blue/white screening (α-factor complementation) on X-gal medium. Nevertheless, these selection steps do not absolutely guarantee that the DNA insert is present in the cells obtained. Further investigation of the resulting colonies is required to confirm that cloning was successful. This may be accomplished by means of PCR, restriction fragment analysis and/or DNA sequencing.Do not delete my edits or ill delete the deleters page!!!
# Cellular cloning
Cloning a cell means to derive a population of cells from a single cell. In the case of unicellular organisms such as bacteria and yeast, this process is remarkably simple and essentially only requires the inoculation of the appropriate medium. However, in the case of cell cultures from higher organisms, cell cloning is an arduous task as these cells will not readily grow in standard media.
A useful tissue culture technique used to clone distinct lineages of cell lines involves the use of cloning rings (cylinders). According to this technique, a single-cell suspension of cells which have been exposed to a mutagenic agent or drug used to drive selection is plated at high dilution to create isolated colonies; each arising from a single and potentially clonally distinct cell. At an early growth stage when colonies consist of only a few of cells, sterile polystyrene rings (cloning rings), which have been dipped in grease are placed over an individual colony and a small amount of trypsin is added. Cloned cells are collected from inside the ring and transferred to a new vessel for further growth.
# Organism
Organism cloning refers to the procedure of creating a new multicellular organism, genetically identical to another. In essence this form of cloning is an asexual method of reproduction, where fertilization or inter-gamete contact does not take place. Asexual reproduction is a naturally occurring phenomenon in many species, including most plants (see vegetative reproduction) and some insects.
## Horticultural
The term clone is used in horticulture to mean all descendants of a single plant, produced by vegetative reproduction or apomixis. Many horticultural plant cultivars are clones, having been derived from a single individual, multiplied by some process other than sexual reproduction. As an example, some European cultivars of grapes represent clones that have been propagated for over two millennia. Other examples are potato and banana. Grafting can be regarded as cloning, since all the shoots and branches coming from the graft are genetically a clone of a single individual, but this particular kind of cloning has not come under ethical scrutiny and is generally treated as an entirely different kind of operation.
Many trees, shrubs, vines, ferns and other herbaceous perennials form clonal colonies. Parts of a large clonal colony often become detached from the parent, termed fragmentation, to form separate individuals. Some plants also form seeds asexually, termed apomixis, e.g. dandelion.
## Animals
Clonal derivation exists in nature in some animal species and is referred to as parthenogenesis. An example is the "Little Fire Ant" (Wasmannia auropunctata), which is native to Central and South America but has spread throughout many tropical environments.
## First cloned buffalo
On September 15, 2007, the Philippines announced its development of Southeast Asia’s first cloned water buffalo. The Philippine Council for Agriculture, Forestry and Natural Resources Research and Development (PCARRD), under the Department of Science and Technology in Los Baños, Laguna appoved this project. The Department of Agriculture’s Philippine Carabao Center (PCC) will implement “Cloning through somatic cell nuclear transfer as a tool for genetic improvement in water buffaloes.” “Super buffalo calves” will be produced. There will be no modification or alteration of the genetic materials, as in GMOs (genetically modified organisms).[1]
## Therapeutic cloning
Therapeutic cloning refers to a procedure which produces cells, specific body parts, and organs to be utilized for medical purposes. Although this has only been realized with parts of bladders[2], early cleavage-stage human embryos have been cloned[3][4] and this is the subject of much active research. Currently, patients subjected to transplantation are administered immunosuppressive drugs to prevent recognition of the foreign transplant by their immune system and its subsequent rejection. The ability to clonally derive tissues and organs from the patients' own cells would abolish the need for immunosuppressive drugs and would allow the patients to live a life without the potentially serious side-effects of immunosuppressive drugs. More importantly, the ability to clonally derive organs would alleviate the current shortage of transplants and would possibly reduce waiting times for transplants to become available.
## Reproductive cloning
Reproductive cloning uses "somatic cell nuclear transfer" (SCNT) to create animals that are genetically identical. This process entails the transfer of a nucleus from a donor adult cell (somatic cell) to an egg which has no nucleus. If the egg begins to divide normally it is transferred into the uterus of the surrogate mother.
Such clones are not strictly identical since the somatic cells may contain mutations in their nuclear DNA. Additionally, the mitochondria in the cytoplasm also contains DNA and during SCNT this DNA is wholly from the donor egg, thus the mitochondrial genome is not the same as that of the nucleus donor cell from which it was produced. This may have important implications for cross-species nuclear transfer in which nuclear-mitochondrial incompatibilities may lead to death.
### Species cloned
The modern cloning techniques involving nuclear transfer have been successfully performed on several species. Landmark experiments in chronological order:
- Tadpole: (1952) Many scientists questioned whether cloning had actually occurred and unpublished experiments by other labs were not able to reproduce the reported results.
- Carp: (1963) In China, embryologist Tong Dizhou cloned a fish. He published the findings in an obscure Chinese science journal which was never translated into English.[5]
- Sheep: (1996) From early embryonic cells by Steen Willadsen. Megan and Morag cloned from differentiated embryonic cells in June 1995 and Dolly the sheep in 1997.
- Rhesus Monkey: Tetra (female, January 2000) from embryo splitting
- Cattle: Alpha and Beta (males, 2001) and (2005) Brazil[6]
- Cat: CopyCat "CC" (female, late 2001), Little Nicky, 2004, was the first cat cloned for commercial reasons
- Mule: Idaho Gem, a john mule born 2003-05-04, was the first horse-family clone.
- Horse: Prometea, a Haflinger female born 2003-05-28, was the first horse clone.
For a complete list see: List of animals that have been cloned.
### Health aspects
The success rate of cloning has been low: Dolly the sheep was born after 277 eggs were used to create 29 embryos, which only produced three lambs at birth, only one of which lived. Seventy calves have been created from 9,000 attempts and one third of them died young; Prometea took 328 attempts. Notably, although the first clones were frogs, no adult cloned frog has yet been produced from a somatic adult nucleus donor cell.
There were early claims that Dolly the Sheep had accelerated aging. Aging of this type is thought to be due to the shortening of telomeres, regions at the tips of chromosomes which prevent genetic threads from fraying every time a cell divides. Over time telomeres get worn down until cell-division is no longer possible — this is thought to be a cause of aging. Dolly died in the year 2003. Ian Wilmut said that Dolly's early death had nothing to do with cloning but with a respiratory infection common to lambs raised like Dolly.
Analysis of telomeres from cloned cows showed that they were longer than noncloned calves. This suggests clones could live longer life spans although many died young after excessive growth. Researchers think that this could eventually be developed to reverse aging in humans, provided that aging is based chiefly on the shortening of telomeres. Although some work has been performed on telomeres and aging in nuclear transfer clones, the evidence is at an early stage.[7]
### Dolly the Sheep
Dolly (1996-07-05 – 2003-02-14), a Finn Dorsett ewe, was the first mammal to have been successfully cloned from an adult cell. She was cloned at the Roslin Institute in Scotland and lived there until her death when she was six. On 2003-04-09 her stuffed remains were placed at Edinburgh's Royal Museum, part of the National Museums of Scotland.
Dolly was publically significant because the effort showed that the genetic material from a specific adult cell, programmed to express only a distinct subset of its genes, could be reprogrammed to grow an entire new organism. Before this demonstration, there was no proof for the widely spread hypothesis that differentiated animal cells can give rise to entire new organisms.
### Human cloning
Human cloning is the creation of a genetically identical copy of an existing or previously existing human. The term is generally used to refer to artificial human cloning; human clones in the form of identical twins are commonplace, with their cloning occurring during the natural process of reproduction. There are two commonly discussed types of human cloning: therapeutic cloning and reproductive cloning. A third type of cloning called replacement cloning exists in theory, and is a combination of therapeutic and reproductive cloning. Replacement cloning entails the replacement of an extensively damaged, failed, or failing body through cloning followed by whole or partial brain transplant. It has been proposed as a way to greatly extend lifespan.
Human cloning is among the most controversial forms of the practice.[8] There have been numerous demands for all progress in the human cloning field to be halted. Some people and groups oppose therapeutic cloning but many more oppose reproductive cloning. The American Association for the Advancement of Science (AAAS) and other scientific organizations have made public statements suggesting that human reproductive cloning be banned until safety issues are resolved [9]. Serious ethical issues have arisen in discussions of harvesting of organs from clones. Some people have considered the idea of growing organs separately from a human organism - in doing this, a new organ supply could be established without the moral implications of harvesting them from human organisms. Research is also being done on the idea of growing organs that are biologically acceptable to the human body inside of other organisms, such as pigs or cows, then transplanting them to humans.
### Cloning extinct and endangered species
Cloning, or more precisely, the reconstruction of functional DNA from extinct species has, for decades, been a dream of some scientists. The possible implications of this were dramatized in the best-selling novel by Michael Crichton and high budget Hollywood thriller Jurassic Park. In real life, one of the most anticipated targets for cloning was once the Woolly Mammoth, but attempts to extract DNA from frozen mammoths have been unsuccessful, though a joint Russo-Japanese team is currently working toward this goal.[10]
In 2001, a cow named Bessie gave birth to a cloned Asian gaur, an endangered species, but the calf died after two days. In 2003, a banteng was successfully cloned, followed by three African wildcats from a thawed frozen embryo. These successes provided hope that similar techniques (using surrogate mothers of another species) might be used to clone extinct species. Anticipating this possibility, tissue samples from the last bucardo (Pyrenean Ibex) were frozen immediately after it died. Researchers are also considering cloning endangered species such as the giant panda, ocelot, and cheetah. The "Frozen Zoo" at the San Diego Zoo now stores frozen tissue from the world's rarest and most endangered species.[11][12]
In 2002, geneticists at the Australian Museum announced that they had replicated DNA of the Thylacine (Tasmanian Tiger), extinct about 65 years previous, using polymerase chain reaction.[13] However, on 2005-02-15 the museum announced that it was stopping the project after tests showed the specimens' DNA had been too badly degraded by the (ethanol) preservative. Most recently, on 2005-05-15, it was announced that the Thylacine project would be revived, with new participation from researchers in New South Wales and Victoria.
One of the continuing obstacles in the attempt to clone extinct species is the need for nearly perfect DNA. Cloning from a single specimen could not create a viable breeding population in sexually reproducing animals. Furthermore, even if males and females were cloned, the question would remain open if they would be viable at all in the absence of parents that could teach or show them their natural behavior. Essentially, if cloning an extinct species succeeded — it must be considered that cloning still is an experimental technology that succeeds only by chance — it is far more likely than not that any resulting animals, even if they were healthy, would be little more than curios or museum pieces.
Cloning endangered species is a highly ideological issue. Many conservation biologists and environmentalists vehemently oppose cloning endangered species — not because they think it won't work but because they think it may deter donations to help preserve natural habitat and wild animal populations. The "rule-of-thumb" in animal conservation is that, if it is still feasible to conserve habitat and viable wild populations, breeding in captivity should not be undertaken in isolation.
In a 2006 review, David Ehrenfeld concludes that cloning in animal conservation is an experimental technology that, at its present state, cannot be expected to work except by pure chance and utterly fails a cost-benefit analysis.[14] Furthermore, he says, it is likely to siphon funds from established and working projects and does not address any of the issues underlying animal extinction (such as habitat destruction, hunting or other overexploitation, and an impoverished gene pool). While cloning technologies are well-established and used on a regular basis in plant conservation, care must be taken to ensure genetic diversity. He concludes:
## Embryo
Somatic cell nuclear transfer can also be used to create a clonal embryo. The most likely scenario for this is to produce embryos for use in research, particularly stem cell research. This process is also called "research cloning" or "therapeutic cloning."
Therapeutic cloning, also called "embryo cloning," is the production of human embryos for use in research. The goal of this process is not to create cloned human beings, but rather to harvest stem cells that can be used to study human development and to treat disease. Stem cells are important to biomedical researchers because they can be used to generate virtually any type of specialized cell in the human body. Stem cells are extracted from the egg after it has divided for 5 days. The egg at this stage of development is called a blastocyst. Many researchers hope that one day stem cells can be used to serve as replacement cells to treat heart disease, Alzheimer's, cancer, and other diseases.
Scientists believe that cloning may be used to create stem cells genetically compatible with the somatic cell donor. Cloning in stem cell research, called research cloning or therapeutic cloning, has not yet been successful: no embryonic stem cell lines have been derived from clonal embryos. The process might provide a way to grow organs in host carriers, so that organs could be produced which would be completely compatible with the original tissue donor. Host carrier growing poses a risk of trans-species diseases if the host is of a different species (e.g., a pig).
In human beings, this is a highly controversial issue for several reasons. It involves creating human embryos in vitro and then destroying them during the process of attempting to obtain embryonic stem cells. But proposals to use cloning techniques in human stem cell research raise a set of concerns beyond the moral status of the embryo. These have led a number of individuals and organizations, who are not opposed in principle to human embryonic stem cell research, to be concerned about or opposed to, human research cloning. One concern is that cloning in human stem cell research will lead to the reproductive cloning of humans. A second concern relates to the appropriate sourcing of the eggs that are needed. Research cloning requires a large number of human eggs, which can only be obtained from women. A third concern is the feasibility of developing stem cell therapies from cloning.
# External links and references
- Cloning Fact Sheet from Human Genome Project Information website.
- 'Cloning' Freeview video by the Vega Science Trust and the BBC/OU
- Clone Guide - Cloning News Website with a Resource to Cloning information in the World
- The Reproductive Cloning Network. Cloning articles, resources and links
- Cloning in Focus, an accessible and comprehensive look at cloning research from the University of Utah's Genetic Science Learning Center
- Click and Clone. Try it yourself in the virtual mouse cloning laboratory, from the University of Utah's Genetic Science Learning Center
- Cloning timeline: from CNN
- "Cloning Addendum: A statement on the cloning report issues by the President's Council on Bioethics," The National Review, July 15, 2002 8:45am
- The President's Council on Bioethics
- Cloning educational resources and news from LiveScience.com | https://www.wikidoc.org/index.php/Cloned | |
6c220f1dc5137d33a00c77678711be8f76b4210c | wikidoc | Cochlea | Cochlea
The cochlea is the auditory portion of the inner ear. Its core component is the Organ of Corti, the sensory organ of hearing, which is distributed along the partition separating fluid chambers in the coiled tapered tube of the cochlea.
The name is from the Latin for snail, which is from the Greek kokhlias "snail, screw," from kokhlos "spiral shell,"(etymology) in reference to its coiled shape; the cochlea is coiled in most mammals, monotremes being the exceptions.
# Anatomy
## Structures
The cochlea is a spiralled, hollow, conical chamber of bone. Its structures include:
- the scala vestibuli (containing perilymph), which lies superior to the cochlear duct and abuts the oval window.
- the scala tympani (containing perilymph), which lies inferior to the scala media and terminates at the round window.
- the scala media (containing endolymph), which is the membraneous cochlear duct containing the organ of Corti.
- the helicotrema is the location where the scala tympani and the scala vestibuli merge
- Reissner's membrane separates the scala vestibuli from the scala media.
- The basilar membrane, a main structural element that determines the mechanical wave propagation properties of the cochlear partition, separates the scala media from the scala tympani.
- The Organ of Corti is the sensory epithelium, a cellular layer on the basilar membrane, powered by the potential difference between the perilymph and the endolymph. It is lined with hair cells—sensory cells topped with hair-like structures called stereocilia.
## Function
In brief: the cochlea is filled with a watery liquid, which moves in response to the vibrations coming from the middle ear via the oval window. As the fluid moves, thousands of "hair cells" are set in motion, and convert that motion to electrical signals that are communicated via neurotransmitters to many thousands of nerve cells. These primary auditory neurons transform the signals into electrical impulses known as action potentials, which travel along the auditory nerve to structures in the brainstem for further processing.
The stapes of the middle ear transmits to the fenestra ovalis (oval window) on the outside of the cochlea, which vibrates the perilymph (fluid) in the scala vestibuli (upper chamber of the cochlea).
This motion of perilymph in turn vibrates the endolymph in the scala media, the perilymph in the scala tympani, the basilar membrane, and organ of Corti, thus causing movements of the hair bundles of the hair cells, acoustic sensor cells that convert vibration into electrical potentials. The hair cells in the organ of Corti are tuned to certain sound frequencies, being responsive to high frequencies near the oval window and to low frequencies near the apex of the cochlea.
The hair cells are arranged in four rows in the organ of Corti along the entire length of the cochlear coil. Three rows consist of outer hair cells (OHCs) and one row consists of inner hair cells (IHCs). The inner hair cells provide the main neural output of the cochlea. The outer hair cells, instead, mainly receive neural input from the brain, which influences their motility as part of the cochlea’s mechanical pre-amplifier. The input to the OHC is from the olivary body via the medial olivocochlear bundle.
For very low frequencies (below 20Hz), the pressure waves propagate along the complete route of the cochlea - up scala vestibuli, around helicotrema and down scala tympani to the round window. Frequencies this low do not activate the organ of Corti and are below the threshold for hearing. Higher frequencies do not propagate to the helicotrema but are transmitted through the endolymph in the cochlear duct to the perilymph in the scala tympani.
A very strong movement of the endolymph due to very loud noise may cause hair cells to die. This is a common cause of partial hearing loss and is the reason why users of firearms or heavy machinery should wear earmuffs or earplugs.
## Detailed anatomy
The walls of the hollow cochlea are made of bone, with a thin, delicate lining of epithelial tissue. This coiled tube is divided through most of its length by a membrane partition. Two fluid-filled spaces (scalae) are formed by this dividing membrane.
The fluid in both is called perilymph: a clear solution of electrolytes and proteins. The two scalae (fluid-filled chambers) communicate with each other through an opening at the top (apex) of the cochlea called the helicotrema, a common space that is the one part of the cochlea that lacks the lengthwise dividing membrane.
At the base of the cochlea each scala ends in a membrane that faces the middle ear cavity. The scala vestibuli ends at the oval window, where the footplate of the stapes sits. The footplate rocks when the ear drum moves the ossicular chain; sending the perilymph rippling with the motion, the waves moving away from footplate and towards helicotrema. Those fluid waves then continue in the perilymph of the scala tympani. The scala tympani ends at the round window, which bulges out when the waves reach it -providing pressure relief. This one-way movement of waves from oval window to round window occurs because the middle ear directs sound to the oval window, but shields the round window from being struck by sound waves from the external ear. It is important, because waves coming from both directions, from the round and oval window would cancel each other out. In fact, when the middle ear is damaged such that there is no tympanic membrane or ossicular chain, and the round window is oriented outward rather than set under a bit of a ledge in the round window niche, there is a maximal conductive hearing loss of about 60 dB.
The lengthwise partition that divides most of the cochlea is itself a fluid-filled tube, the third scalae. This central column is called the scala media or cochlear duct. Its fluid, endolymph, also contains electrolytes and proteins, but is chemically quite different from perilymph. Whereas the perilymph is rich in sodium salts, the endolymph is rich in potassium salts.
The cochlear duct is supported on three sides by a rich bed of capillaries and secretory cells (the stria vascularis), a layer of simple squamous epithelial cells (Reissner's membrane), and the basilar membrane, on which rests the receptor organ for hearing - the organ of Corti. The cochlear duct is almost as complex on its own as the ear itself.
The ear is a very active organ. Not only does the cochlea "receive" sound, it generates it! Some of the hair cells of the cochlear duct can change their shape enough to move the basilar membrane and produce sound. This process is important in fine tuning the ability of the cochlea to accurately detect differences in incoming acoustic information. The sound produced by the inner ear is called an otoacoustic emission (OAE), and can be recorded by a microphone in the ear canal. Otoacoustic emissions are important is some types of tests for hearing impairment.
# Comparative physiology
The coiled form of cochlea is unique to mammals. In birds and in other non-mammalian vertebrates the compartment containing the sensory cells for hearing is occasionally also called “cochlea”, although it is not coiled up. Instead it forms a blind-ended tube, also called the cochlear duct. This difference apparently evolved in parallel with the differences in frequency range of hearing and in frequency resolution between mammals and non-mammalian vertebrates. Most bird species do not hear above 4–5 kHz, the currently known maximum being ~ 11 kHz in the barn owl. Some marine mammals hear up to 200 kHz. The superior frequency resolution in mammals is due to their unique mechanism of pre-amplification of sound by active cell-body vibrations of outer hair cells. A long coiled compartment, rather than a short and straight one, provides more space for frequency dispersion and is therefore better adapted to the highly derived functions in mammalian hearing.
As the study of the cochlea should fundamentally be focused upon the level of hair cells, it is important to note the anatomical and physiological differences between the hair cells of various species. In birds, for instance, instead of outer and inner hair cells, there are tall and short hair cells. There are several similarities of note in regard to this comparative data. For one, the tall hair cell is very similar in function to that of the inner hair cell and the short hair cell is very similar in function to that of the outer hair cell. One unavoidable difference, however, is that while all hair cells are attached to a tectorial membrane in birds, only the outer hair cells are attached to the tectorial membrane in mammals. | Cochlea
Template:Infobox Anatomy
The cochlea is the auditory portion of the inner ear. Its core component is the Organ of Corti, the sensory organ of hearing, which is distributed along the partition separating fluid chambers in the coiled tapered tube of the cochlea.
The name is from the Latin for snail, which is from the Greek kokhlias "snail, screw," from kokhlos "spiral shell,"(etymology) in reference to its coiled shape; the cochlea is coiled in most mammals, monotremes being the exceptions.
# Anatomy
## Structures
The cochlea is a spiralled, hollow, conical chamber of bone. Its structures include:
- the scala vestibuli (containing perilymph), which lies superior to the cochlear duct and abuts the oval window.
- the scala tympani (containing perilymph), which lies inferior to the scala media and terminates at the round window.
- the scala media (containing endolymph), which is the membraneous cochlear duct containing the organ of Corti.
- the helicotrema is the location where the scala tympani and the scala vestibuli merge
- Reissner's membrane separates the scala vestibuli from the scala media.
- The basilar membrane, a main structural element that determines the mechanical wave propagation properties of the cochlear partition, separates the scala media from the scala tympani.
- The Organ of Corti is the sensory epithelium, a cellular layer on the basilar membrane, powered by the potential difference between the perilymph and the endolymph. It is lined with hair cells—sensory cells topped with hair-like structures called stereocilia.
## Function
In brief: the cochlea is filled with a watery liquid, which moves in response to the vibrations coming from the middle ear via the oval window. As the fluid moves, thousands of "hair cells" are set in motion, and convert that motion to electrical signals that are communicated via neurotransmitters to many thousands of nerve cells. These primary auditory neurons transform the signals into electrical impulses known as action potentials, which travel along the auditory nerve to structures in the brainstem for further processing.
The stapes of the middle ear transmits to the fenestra ovalis (oval window) on the outside of the cochlea, which vibrates the perilymph (fluid) in the scala vestibuli (upper chamber of the cochlea).
This motion of perilymph in turn vibrates the endolymph in the scala media, the perilymph in the scala tympani, the basilar membrane, and organ of Corti, thus causing movements of the hair bundles of the hair cells, acoustic sensor cells that convert vibration into electrical potentials. The hair cells in the organ of Corti are tuned to certain sound frequencies[1], being responsive to high frequencies near the oval window and to low frequencies near the apex of the cochlea.
The hair cells are arranged in four rows in the organ of Corti along the entire length of the cochlear coil. Three rows consist of outer hair cells (OHCs) and one row consists of inner hair cells (IHCs). The inner hair cells provide the main neural output of the cochlea. The outer hair cells, instead, mainly receive neural input from the brain, which influences their motility as part of the cochlea’s mechanical pre-amplifier. The input to the OHC is from the olivary body via the medial olivocochlear bundle.
For very low frequencies (below 20Hz), the pressure waves propagate along the complete route of the cochlea - up scala vestibuli, around helicotrema and down scala tympani to the round window. Frequencies this low do not activate the organ of Corti and are below the threshold for hearing. Higher frequencies do not propagate to the helicotrema but are transmitted through the endolymph in the cochlear duct to the perilymph in the scala tympani.
A very strong movement of the endolymph due to very loud noise may cause hair cells to die. This is a common cause of partial hearing loss and is the reason why users of firearms or heavy machinery should wear earmuffs or earplugs.
## Detailed anatomy
The walls of the hollow cochlea are made of bone, with a thin, delicate lining of epithelial tissue. This coiled tube is divided through most of its length by a membrane partition. Two fluid-filled spaces (scalae) are formed by this dividing membrane.
The fluid in both is called perilymph: a clear solution of electrolytes and proteins. The two scalae (fluid-filled chambers) communicate with each other through an opening at the top (apex) of the cochlea called the helicotrema, a common space that is the one part of the cochlea that lacks the lengthwise dividing membrane.
At the base of the cochlea each scala ends in a membrane that faces the middle ear cavity. The scala vestibuli ends at the oval window, where the footplate of the stapes sits. The footplate rocks when the ear drum moves the ossicular chain; sending the perilymph rippling with the motion, the waves moving away from footplate and towards helicotrema. Those fluid waves then continue in the perilymph of the scala tympani. The scala tympani ends at the round window, which bulges out when the waves reach it -providing pressure relief. This one-way movement of waves from oval window to round window occurs because the middle ear directs sound to the oval window, but shields the round window from being struck by sound waves from the external ear. It is important, because waves coming from both directions, from the round and oval window would cancel each other out. In fact, when the middle ear is damaged such that there is no tympanic membrane or ossicular chain, and the round window is oriented outward rather than set under a bit of a ledge in the round window niche, there is a maximal conductive hearing loss of about 60 dB.
The lengthwise partition that divides most of the cochlea is itself a fluid-filled tube, the third scalae. This central column is called the scala media or cochlear duct. Its fluid, endolymph, also contains electrolytes and proteins, but is chemically quite different from perilymph. Whereas the perilymph is rich in sodium salts, the endolymph is rich in potassium salts.
The cochlear duct is supported on three sides by a rich bed of capillaries and secretory cells (the stria vascularis), a layer of simple squamous epithelial cells (Reissner's membrane), and the basilar membrane, on which rests the receptor organ for hearing - the organ of Corti. The cochlear duct is almost as complex on its own as the ear itself.
The ear is a very active organ. Not only does the cochlea "receive" sound, it generates it! Some of the hair cells of the cochlear duct can change their shape enough to move the basilar membrane and produce sound. This process is important in fine tuning the ability of the cochlea to accurately detect differences in incoming acoustic information. The sound produced by the inner ear is called an otoacoustic emission (OAE), and can be recorded by a microphone in the ear canal. Otoacoustic emissions are important is some types of tests for hearing impairment.
# Comparative physiology
The coiled form of cochlea is unique to mammals. In birds and in other non-mammalian vertebrates the compartment containing the sensory cells for hearing is occasionally also called “cochlea”, although it is not coiled up. Instead it forms a blind-ended tube, also called the cochlear duct. This difference apparently evolved in parallel with the differences in frequency range of hearing and in frequency resolution between mammals and non-mammalian vertebrates. Most bird species do not hear above 4–5 kHz, the currently known maximum being ~ 11 kHz in the barn owl. Some marine mammals hear up to 200 kHz. The superior frequency resolution in mammals is due to their unique mechanism of pre-amplification of sound by active cell-body vibrations of outer hair cells. A long coiled compartment, rather than a short and straight one, provides more space for frequency dispersion and is therefore better adapted to the highly derived functions in mammalian hearing.[2]
As the study of the cochlea should fundamentally be focused upon the level of hair cells, it is important to note the anatomical and physiological differences between the hair cells of various species. In birds, for instance, instead of outer and inner hair cells, there are tall and short hair cells. There are several similarities of note in regard to this comparative data. For one, the tall hair cell is very similar in function to that of the inner hair cell and the short hair cell is very similar in function to that of the outer hair cell. One unavoidable difference, however, is that while all hair cells are attached to a tectorial membrane in birds, only the outer hair cells are attached to the tectorial membrane in mammals. | https://www.wikidoc.org/index.php/Cochlea | |
2fdb6419e0a60975bb1ab2d069558484013baabd | wikidoc | Codeine | Codeine
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# Black Box Warning
# Overview
Codeine is an analgesic opioid that is FDA approved for the treatment of mild to moderate pain. There is a Black Box Warning for this drug as shown here. Common adverse reactions include constipation, nausea, vomiting, dizziness, lightheadedness, sedation, somnolence, and dyspnea.
# Adult Indications and Dosage
## FDA-Labeled Indications and Dosage (Adult)
- Pain (mild to moderate): 15 to 60 mg orally up to every 4 hours as needed; MAX 360 mg/24 h
## Off-Label Use and Dosage (Adult)
### Guideline-Supported Use
There is limited information about Off-Label Guideline-Supported Use of Codeine in adult patients.
### Non–Guideline-Supported Use
There is limited information about Off-Label Non–Guideline-Supported Use of Codeine in adult patients.
# Pediatric Indications and Dosage
## FDA-Labeled Indications and Dosage (Pediatric)
- Safety and effectiveness in pediatric patients younger than 18 years have not been established.
- Contraindicated for postoperative pain control in pediatric patients undergoing tonsillectomy or adenoidectomy.
## Off-Label Use and Dosage (Pediatric)
### Guideline-Supported Use
There is limited information about Off-Label Guideline-Supported Use of Codeine in pediatric patients.
### Non–Guideline-Supported Use
There is limited information about Off-Label Non–Guideline-Supported Use of Codeine in pediatric patients.
# Contraindications
Codeine sulfate is contraindicated for postoperative pain management in children who have undergone tonsillectomy and/or adenoidectomy.
- Codeine sulfate is contraindicated in patients with known hypersensitivity to codeine or any components of the product. Persons known to be hypersensitive to certain other opioids may exhibit cross-sensitivity to codeine.
- Codeine sulfate is contraindicated in patients with respiratory depression in the absence of resuscitative equipment.
- Codeine sulfate is contraindicated in patients with acute or severe bronchial asthma or hypercarbia.
- Codeine sulfate is contraindicated in any patient who has or is suspected of having paralytic ileus.
# Warnings
- Death Related to Ultra-Rapid Metabolism of Codeine to Morphine
- Respiratory depression and death have occurred in children who received codeine in the post-operative period following tonsillectomy and/or adenoidectomy and had evidence of being ultra-rapid metabolizers of codeine (i.e., multiple copies of the gene for cytochrome P450 isoenzyme 2D6 or high morphine concentrations). Deaths have also occurred in nursing infants who were exposed to high levels of morphine in breast milk because their mothers were ultra-rapid metabolizers of codeine.
- Some individuals may be ultra-rapid metabolizers because of a specific CYP2D6 genotype (gene duplications denoted as *1/*1xN or *1/*2xN). The prevalence of this CYP2D6 phenotype varies widely and has been estimated at 0.5 to 1% in Chinese and Japanese, 0.5 to 1% in Hispanics, 1 to 10% in Caucasians, 3% in African Americans, and 16 to 28% in North Africans, Ethiopians, and Arabs. Data are not available for other ethnic groups. These individuals convert codeine into its active metabolite, morphine, more rapidly and completely than other people. This rapid conversion results in higher than expected serum morphine levels. Even at labeled dosage regimens, individuals who are ultra-rapid metabolizers may have life-threatening or fatal respiratory depression or experience signs of overdose (such as extreme sleepiness, confusion, or shallow breathing).
- Children with obstructive sleep apnea who are treated with codeine for post-tonsillectomy and/or adenoidectomy pain may be particularly sensitive to the respiratory depressant effects of codeine that has been rapidly metabolized to morphine. Codeine is contraindicated for post-operative pain management in all pediatric patients undergoing tonsillectomy and/or adenoidectomy.
- When prescribing codeine, healthcare providers should choose the lowest effective dose for the shortest period of time and inform patients and caregivers about these risks and the signs of morphine overdose.
- Respiratory Depression
- Respiratory depression is the primary risk of codeine sulfate. Respiratory depression occurs more frequently in elderly or debilitated patients and in those suffering from conditions accompanied by hypoxia, hypercapnia, or upper airway obstruction, in whom even moderate therapeutic doses may significantly decrease pulmonary ventilation. Codeine produces dose-related respiratory depression.
- Caution should be exercised when codeine sulfate is used postoperatively, in patients with pulmonary disease or shortness of breath, or whenever ventilatory function is depressed. Use opioids, including codeine sulfate, with extreme caution in patients with chronic obstructive pulmonary disease or cor pulmonale and in patients having a substantially decreased respiratory reserve (e.g., severe kyphoscoliosis), hypoxia, hypercapnia, or pre-existing respiratory depression. In such patients, even usual therapeutic doses of codeine sulfate may increase airway resistance and decrease respiratory drive to the point of apnea. Consider alternative non-opioid analgesics and use codeine sulfate only under careful medical supervision at the lowest effective dose in such patients.
- Misuse and Abuse of Opioids
- Codeine sulfate is an opioid agonist of the morphine-type and a Schedule II controlled substance. Such drugs are sought by drug abusers and people with addiction disorders. Diversion of Schedule II products is an act subject to criminal penalty.
- Patients should be assessed for their risk for opioid abuse or addiction prior to being prescribed opioids
- Codeine can be abused in a manner similar to other opioid agonists, legal or illicit. This should be considered when prescribing or dispensing codeine sulfate in situations where the physician or pharmacist is concerned about an increased risk of misuse, abuse, or diversion.
- Codeine may be abused by crushing, chewing, snorting or injecting the product. Misuse and abuse of codeine sulfate poses a significant risk to the abuser that could result in overdose and death.
- Concerns about abuse, addiction, and diversion should not prevent the proper management of pain. Healthcare professionals should contact their State Professional Licensing Board or State Controlled Substances Authority for information on how to prevent and detect abuse or diversion of this product.
- Interaction with Alcohol and Drugs of Abuse
- Codeine sulfate may be expected to have additive effects when used in conjunction with alcohol, other opioids, or illicit drugs that cause central nervous system depression, because respiratory depression, hypotension, profound sedation, coma or death may result.
- Head Injury and Increased Intracranial Pressure
- Respiratory depressant effects of opioids and their capacity to elevate cerebrospinal fluid pressure resulting from vasodilation following CO2 retention may be markedly exaggerated in the presence of head injury, other intracranial lesions or a pre-existing increase in intracranial pressure. Furthermore, opioids including codeine sulfate, can produce effects on pupillary response and consciousness, which may obscure neurologic signs of further increases in intracranial pressure in patients with head injuries.
- Hypotensive Effect
- Codeine sulfate may cause severe hypotension in an individual whose ability to maintain blood pressure has already been compromised by a depleted blood volume or concurrent administration of drugs such as phenothiazines or general anesthetics. Codeine sulfate may produce orthostatic hypotension and syncope in ambulatory patients.
- Administer codeine sulfate with caution to patients in circulatory shock, as vasodilation produced by the drug may further reduce cardiac output and blood pressure.
- Gastrointestinal Effects
- Do not administer codeine sulfate to patients with gastrointestinal obstruction, especially paralytic ileus because codeine sulfate diminishes propulsive peristaltic waves in the gastrointestinal tract and may prolong the obstruction.
- Chronic use of opioids, including codeine sulfate, may result in obstructive bowel disease especially in patients with underlying intestinal motility disorder. Codeine sulfate may cause or aggravate constipation.
- The administration of codeine sulfate may obscure the diagnosis or clinical course of patients with acute abdominal conditions.
- Use in Pancreatic/Biliary Tract Disease
- Use codeine sulfate with caution in patients with biliary tract disease, including acute pancreatitis, as codeine sulfate may cause spasm of the sphincter of Oddi and diminish biliary and pancreatic secretions.
- Special Risk Patients
- Use codeine sulfate with caution in patients with severe renal or hepatic impairment, hypothyrodism, Addison's disease, prostatic hypertrophy, or urethral stricture and in elderly or debilitated patients. The usual precautions should be observed and the possibility of respiratory depression should be kept in mind.
- Extreme caution should be exercised in the administration of codeine sulfate to patients with CNS depression, acute alcoholism, and delirium tremens.
- All opioids may aggravate convulsions in patients with convulsive disorders, and all opioids may induce or aggravate seizures in some clinical settings.
- Keep Codeine Sulfate Oral Solution out of the reach of children. In case of accidental ingestion, seek emergency medical help immediately.
- Driving and Operating Machinery
- Caution patients that codeine sulfate could impair the mental and/or physical abilities needed to perform potentially hazardous activities such as driving a car or operating machinery.
- Caution patients about the potential combined effects of codeine sulfate with other CNS depressants, including other opioids, phenothiazines, sedative/hypnotics, and alcohol.
# Adverse Reactions
## Clinical Trials Experience
- Serious adverse reactions associated with codeine are respiratory depression and, to a lesser degree, circulatory depression, respiratory arrest, shock, and cardiac arrest.
- The most frequently observed adverse reactions with codeine administration include drowsiness, lightheadedness, dizziness, sedation, shortness of breath, nausea, vomiting, sweating, and constipation.
- Other adverse reactions include allergic reactions, euphoria, dysphoria, abdominal pain, and pruritis.
- Other less frequently observed adverse reactions expected from opioid analgesics, including codeine sulfate, include:
- Cardiovascular system: faintness, flushing, hypotension, palpitations, syncope
- Digestive System: abdominal cramps, anorexia, diarrhea, dry mouth, gastrointestinal distress, pancreatitis
- Nervous system: anxiety, drowsiness, fatigue, headache, insomnia, nervousness, shakiness, somnolence, vertigo, visual disturbances, weakness
- Skin and Appendages: rash, sweating, urticaria
## Postmarketing Experience
There is limited information regarding Codeine Postmarketing Experience in the drug label.
# Drug Interactions
- Central Nervous System (CNS) Depressants
- Concurrent use of other opioids, antihistamines, antipsychotics, antianxiety agents, or other CNS depressants (including sedatives, hypnotics, general anesthetics, antiemetics, phenothiazines, or other tranquilizers or alcohol) concomitantly with codeine sulfate may result in additive CNS depression, respiratory depression, hypotension, profound sedation, or coma. Use codeine sulfate with caution and in reduced dosages in patients taking these agents.
- Mixed Agonist/Antagonist Opioid Analgesics
- Do not administer mixed agonist/antagonist analgesics (i.e., pentazocine, nalbuphine, and butorphanol) to patients who have received or are receiving a course of therapy with a pure opioid agonist analgesic such as codeine sulfate. In these patients, mixed agonist/ antagonist analgesics may reduce the analgesic effect and/or may precipitate withdrawal symptoms.
- Anticholinergics
- Anticholinergics or other medications with anticholinergic activity when used concurrently with opioid analgesics may result in increased risk of urinary retention and/or severe constipation, which may lead to paralytic ileus.
- Antidepressants
- Use of monoamine oxidase inhibitors (MAOIs) or tricyclic antidepressants with codeine sulfate may increase the effect of either the antidepressant or codeine. MAOIs markedly potentiate the action of morphine, the major metabolite of codeine. Codeine should not be used in patients taking MAOIs or within 14 days of stopping such treatment.
- CYP2D6 and CYP3A4 Inhibitors and Inducers
- Codeine is metabolized by the cytochrome P450 2D6 and 3A4 isoenzymes. Patients taking CYP2D6 inhibitors or CYP3A4 inhibitors or inducers may demonstrate an altered response to codeine, therefore analgesic activity should be monitored.
- Inhibitors of CYP2D6 or CYP3A4: Since the CYP2D6 and CYP3A4 isoenzymes play a major role in the metabolism of codeine, drugs that inhibit CYP3A4 (e.g., macrolide antibiotics (e.g., erythromycin), azole-antifungal agents (e.g., ketoconazole), protease inhibitors (e.g., ritonavir)), or CYP2D6 activity (e.g., certain cardiovascular drugs including amiodarone and quinidine as well as polycyclic antidepressants), may cause decreased clearance of codeine which could lead to an increase in codeine plasma concentrations. If coadministration with codeine sulfate oral solution is necessary, caution is advised when initiating therapy with, currently taking, or discontinuing CYP450 inhibitors. Evaluate these patients at frequent intervals and consider dose adjustments until stable drug effects are achieved.
- Inducers of CYP3A4: CYP450 inducers, such as rifampin, carbamazepine, and phenytoin, may induce the metabolism of codeine and, therefore, may cause increased clearance of the drug which could lead to a decrease in codeine plasma concentrations, lack of efficacy or, possibly, development of an abstinence syndrome in a patient who had developed physical dependence to codeine. If co-administration with codeine sulfate oral solution is necessary, caution is advised when initiating therapy with, currently taking, or discontinuing CYP3A4 inducers. Evaluate these patients at frequent intervals and consider dose adjustments until stable drug effects are achieved.
- Drug-Laboratory Test Interaction
- Codeine may cause an elevation of plasma amylase and lipase due to the potential of codeine to produce spasm of the sphincter of Oddi. Determination of these enzyme levels may be unreliable for some time after an opiate agonist has been given.
# Use in Specific Populations
### Pregnancy
Pregnancy Category (FDA): C
- There are no adequate and well-controlled studies in pregnant women. Codeine should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
- Codeine has been shown to have embryolethal and fetotoxic effects (reduced fetal body weights and delayed or incomplete ossification) in the hamster, rat and mouse models at approximately 2 to 4 times the maximum recommended human dose of 360 mg/day based on a body surface area comparison. Maternally toxic doses that were approximately 7 times the maximum recommended human dose of 360 mg/day, were associated with evidence of resorptions and incomplete ossification, including meningioencephalocele and cranioschisis. In contrast, codeine did not demonstrate evidence of embryotoxicity or fetotoxicity in the rabbit model at doses up to 2 times the maximum recommended human dose of 360 mg/day based on a body surface area comparison.
- Nonteratogenic Effects
- Neonatal codeine withdrawal has occurred in infants born to addicted and nonaddicted mothers who had been taking codeine-containing medications in the days prior to delivery. Typical symptoms of narcotic withdrawal include irritability, excessive crying, tremors, hyperreflexia, seizures, fever, vomiting, diarrhea, and poor feeding. These signs occur shortly after birth and may require specific treatment.
- Codeine (30 mg/kg) administered subcutaneously to pregnant rats during pregnancy and for 25 days after delivery increased neonatal mortality at birth. This dose is 0.8 times the maximum recommended human dose of 360 mg/day on a body surface area comparison.
Pregnancy Category (AUS):
There is no Australian Drug Evaluation Committee (ADEC) guidance on usage of Codeine in women who are pregnant.
### Labor and Delivery
- Opioid analgesics cross the placenta and may produce respiratory depression and psycho-physiologic effects in neonates. Codeine is not recommended for use in women during and immediately prior to labor. Occasionally, opioid analgesics may prolong labor through actions which temporarily reduce the strength, duration, and frequency of uterine contractions. However, this effect is not consistent and may be offset by an increased rate of cervical dilatation, which tends to shorten labor. Closely observe neonates whose mothers received opioid analgesics during labor for signs of respiratory depression. Have a specific opioid antagonist, such as naloxone, available for reversal of opioidinduced respiratory depression in the neonate.
### Nursing Mothers
- Codeine is secreted into human milk. In women with normal codeine metabolism (normal CYP2D6 activity), the amount of codeine secreted into human milk is low and dose-dependent. However, some women are ultra-rapid metabolizers of codeine. These women achieve higher-than-expected serum levels of codeine's active metabolite, morphine, leading to higher-than-expected levels of morphine in breast milk and potentially dangerously high serum morphine levels in their breastfed infants. Therefore, maternal use of codeine can potentially lead to serious adverse reactions, including death, in nursing infants.
- The risk of infant exposure to codeine and morphine through breast milk should be weighed against the benefits of breastfeeding for both the mother and the baby. Caution should be exercised when codeine is administered to a nursing woman. If a codeine containing product is selected, the lowest dose should be prescribed for the shortest period of time to achieve the desired clinical effect. Mothers using codeine should be informed about when to seek immediate medical care and how to identify the signs and symptoms of neonatal toxicity, such as drowsiness or sedation, difficulty breastfeeding, breathing difficulties, and decreased tone, in their baby. Nursing mothers who are ultrarapid metabolizers may also experience overdose symptoms such as extreme sleepiness, confusion, or shallow breathing. Prescribers should closely monitor mother-infant pairs and notify treating pediatricians about the use of codeine during breast-feeding.
### Pediatric Use
The safety, effectiveness and the pharmacokinetics of codeine sulfate in pediatric patients below the age of 18 have not been established.
- Respiratory depression and death have occurred in children with obstructive sleep apnea who received codeine in the post-operative period following tonsillectomy and/or adenoidectomy and had evidence of being ultra-rapid metabolizers of codeine (i.e., multiple copies of the gene for cytochrome P450 isoenzyme 2D6 or high morphine concentrations). These children may be particularly sensitive to the respiratory depressant effects of codeine that has been rapidly metabolized to morphine. Codeine is contraindicated for post-operative pain management in all pediatric patients undergoing tonsillectomy and/ or adenoidectomy.
### Geriatic Use
Codeine may cause confusion and over-sedation in the elderly (aged 65 and older). In general, use caution when selecting a dose for an elderly patient, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy.
### Gender
There is no FDA guidance on the use of Codeine with respect to specific gender populations.
### Race
There is no FDA guidance on the use of Codeine with respect to specific racial populations.
### Renal Impairment
Codeine pharmacokinetics may be altered in patients with renal failure. Clearance may be decreased and the metabolites may accumulate to much higher plasma levels in patients with renal failure as compared to patients with normal renal function. Start these patients cautiously with lower doses of codeine sulfate or with longer dosing intervals and titrate slowly while carefully monitoring for side effects.
### Hepatic Impairment
No formal studies have been conducted in patients with hepatic impairment so the pharmacokinetics of codeine in this patient population are unknown. Start these patients cautiously with lower doses of codeine sulfate or with longer dosing intervals and titrate slowly while carefully monitoring for side effects.
### Females of Reproductive Potential and Males
There is no FDA guidance on the use of Codeine in women of reproductive potentials and males.
### Immunocompromised Patients
There is no FDA guidance one the use of Codeine in patients who are immunocompromised.
# Administration and Monitoring
### Administration
There is limited information regarding Codeine Administration in the drug label.
### Monitoring
There is limited information regarding Codeine Monitoring in the drug label.
# IV Compatibility
There is limited information regarding the compatibility of Codeine and IV administrations.
# Overdosage
- Acute overdose with codeine is characterized by respiratory depression (a decrease in respiratory rate and/or tidal volume, Cheyne-Stokes respiration, cyanosis), extreme somnolence progressing to stupor or coma, skeletal muscle flaccidity, cold and clammy skin, constricted pupils, and sometimes bradycardia and hypotension. In severe overdosage, apnea, circulatory collapse, cardiac arrest, and death may occur.
- Codeine may cause miosis, even in total darkness. Pinpoint pupils are a sign of opioid overdose but are not pathognomonic (e.g., pontine lesions of hemorrhagic or ischemic origin may produce similar findings). Marked mydriasis rather than miosis may be seen with hypoxia in overdose situations.
- Treatment
- Give primary attention to re-establishment of a patent airway and institution of assisted or controlled ventilation. Employ supportive measures (including oxygen and vasopressors) in the management of circulatory shock and pulmonary edema accompanying overdose as indicated. Cardiac arrest or arrhythmias may require cardiac massage or defibrillation. Induction of emesis is not recommended because of the potential for CNS depression and seizures. Activated charcoal is recommended if the patient is awake and able to protect his/her airway. In persons who are at risk for abrupt onset of seizures or mental status depression, activated charcoal should be administered by medical or paramedical personnel capable of airway management to prevent aspiration in the event of spontaneous emesis. Severe agitation or seizures should be treated with an intravenous benzodiazepine.
- The pure opioid antagonist, naloxone, is a specific antidote to respiratory depression resulting from opioid overdose. Since the duration of reversal is expected to be less than the duration of action of codeine sulfate, carefully monitor the patient until spontaneous respiration is reliably re-established. If the response to opioid antagonists is suboptimal or only brief in nature, administer additional antagonist as directed by the label of the product.
- Do not administer opioid antagonists in the absence of clinically significant respiratory or circulatory depression secondary to codeine sulfate overdose. In an individual physically dependent on opioids, administration of the usual dose of the antagonist will precipitate an acute withdrawal syndrome. The severity of the withdrawal symptoms experienced will depend on the degree of physical dependence and the dose of the antagonist administered. Reserve use of an opioid antagonist for cases where such treatment is clearly needed. If it is necessary to treat serious respiratory depression in the physically dependent patient, initiate administration of the antagonist with care and titrate with smaller than usual doses.
# Pharmacology
## Mechanism of Action
- Codeine is an opioid agonist, related to morphine, but with less potent analgesic properties. Codeine is selective for the mu receptor, but with a much weaker affinity than morphine. The analgesic properties of codeine have been speculated to come from its conversion to morphine, although the exact mechanism of analgesic action remains unknown.
- Effects of the Central Nervous System (CNS): The principal therapeutic action of codeine is analgesia. Although the precise mechanism of the analgesic action is unknown, specific CNS opiate receptors and endogenous compounds with morphine-like activity have been identified throughout the brain and spinal cord and are likely to play a role in the expression and perception of analgesic effects. Other CNS effects of codeine include anxiolysis, euphoria, and feelings of relaxation. Codeine causes respiratory depression, in part by a direct effect on the brainstem respiratory centers. Codeine and other related opioids depress the cough reflex by direct effect on the cough center in the medulla. Codeine may also cause miosis.
- Effects on the Gastrointestinal Tract and on Other Smooth Muscle: Gastric, biliary and pancreatic secretions may be decreased by codeine. Codeine also causes a reduction in motility and is associated with an increase in tone in the antrum of the stomach and duodenum. Digestion of food in the small intestine is delayed and propulsive contractions are decreased. Propulsive peristaltic waves in the colon are decreased, while tone is increased to the point of spasm. The end result may be constipation. Codeine can cause a marked increase in biliary tract pressure as a result of the spasm of the sphincter of Oddi. Codeine may also cause spasms of the sphincter of the urinary bladder.
- Effects on the Cardiovascular System: In therapeutic doses, codeine does not usually exert major effects on the cardiovascular system. Codeine produces peripheral vasodilation which may result in orthostatic hypotension and fainting. Release of histamine can occur, which may play a role in opioid-induced hypotension. Manifestations of histamine release and/or peripheral vasodilation may include pruritus, flushing, red eyes, and sweating.
- Endocrine System: Opioid agonists have been shown to have a variety of effects on the secretion of hormones. Opioids inhibit the secretion of ACTH, cortisol, and luteinizing hormone (LH) in humans. They also stimulate prolactin, growth hormone (GH) secretion, and pancreatic secretion of insulin and glucagons in humans and other species, rats and dogs. Thyroid stimulating hormone (TSH) has been shown to be both inhibited and stimulated by opioids.
- Immune System: Opioids have been shown to have a variety of effects on components of the immune system in in vitro and animal models. The clinical significance of these findings is unknown.
## Structure
- Chemically, codeine sulfate is morphinan-6-ol,7,8-didehydro-4,5-epoxy-3-methoxy- 17-methyl-(5α,6α)-, sulfate (2:1) (salt), trihydrate. Codeine sulfate trihydrate is a fine, white, crystalline powder which is soluble in water and insoluble in chloroform and ether. Its empirical formula is (C18H21NO3)2 ∙ H2SO4 ∙ 3H2O and its molecular weight is 750.85 g/mol.
- Its structure is as follows:
- Each 5 mL of oral solution contains 30 mg of codeine sulfate, USP and the following inactive ingredients: ascorbic acid, citric acid, disodium edetate, FD&C Red No. 40, FD&C Yellow No. 6, glycerin, Orange Flavor XBF-7098189 (artificial flavors, propylene glycol), sodium benzoate, sorbitol, sucralose, and water. The pH of the oral solution is 3.3.
## Pharmacodynamics
- Codeine plasma concentrations do not correlate with codeine brain concentrations or relief of pain.
- The minimum effective concentration varies widely and is influenced by a variety of factors, including the extent of previous opioid use, age and general medical condition. Effective doses in tolerant patients may be significantly higher than in opioid-naïve patients.
## Pharmacokinetics
- Absorption: Codeine, when administered as codeine sulfate, is absorbed from the gastrointestinal tract with maximum plasma concentration occurring 60 minutes post administration.
- Food Effects: When 60 mg codeine sulfate was administered 30 minutes after ingesting a high fat/high calorie meal, there was no significant change in the rate and extent of absorption of codeine.
- Steady-state: Administration of 15 mg codeine sulfate every four hours for 5 days resulted in steady-state concentrations of codeine, morphine, morphine-3-glucuronide (M3G) and morphine-6-glucuronide (M6G) within 48 hours.
- Distribution: Codeine has been reported to have an apparent volume of distribution of approximately 3-6 L/kg, indicating extensive distribution of the drug into tissues. Codeine has low plasma protein binding with about 7-25% of codeine bound to plasma proteins.
- Metabolism: About 70-80% of the administered dose of codeine is metabolized by conjugation with glucuronic acid to codeine-6-glucuronide (C6G, about 60%) and via O-demethylation to morphine (about 5-10%) and N-demethylation to norcodeine (about 10%) respectively. UDP-glucuronosyltransferase (UGT) 2B7 and 2B4 are the major enzymes mediating glucurodination of codeine to C6G. Cytochrome P450 2D6 is the major enzyme responsible for conversion of codeine to morphine (about 5-10%) and P450 3A4 is the major enzyme mediating conversion of codeine to norcodeine. Morphine and norcodeine are further metabolized by conjugation with glucuronic acid. The glucuronide metabolites of morphine are morphine-3-glucuronide (M3G) and morphine-6- glucuronide (M6G). Morphine and M6G are known to have analgesic activity in humans. The analgesic activity of C6G in humans is unknown. Norcodeine and M3G are generally not considered to possess analgesic properties.
- Elimination: Approximately 90% of the total dose of codeine is excreted through the kidneys, of which approximately 10% is unchanged codeine. Plasma half-lives of codeine and its metabolites have been reported to be approximately 3 h
## Nonclinical Toxicology
- Carcinogenesis: Two year carcinogenicity studies have been conducted in F344/N rats and B6C3F1 mice. There was no evidence of carcinogenicity in male and female rats, respectively, at dietary doses up to 70 and 80 mg/kg/day of codeine (approximately 2 times the maximum recommended daily dose of 360 mg/day for adults on a mg/m2 basis) for two years. Similarly there was no evidence of carcinogenicity activity in male and female mice at dietary doses up to 400 mg/kg/day of codeine (approximately 5 times the maximum recommended daily dose of 360 mg/day for adults on a mg/m2 basis) for two years.
- Mutagenesis: Codeine was not mutagenic in the in vitro bacterial reverse mutation assay or clastogenic in the in vitro Chinese hamster ovary cell chromosome aberration assay.
- Impairment of Fertility: No animal studies were conducted to evaluate the effect of codeine on male or female fertility.
- Reproduction and Developmental Toxicology
- Studies on the reproductive and developmental effects of codeine have been reported in the published literature in hamsters, rats, mice and rabbits.
- A study in hamsters administered 150 mg/kg twice daily of codeine (oral; approximately 7 times the maximum recommended daily dose of 360 mg/day for adults on a mg/m2 basis) reported the development of cranial malformations (i.e., meningoencephalocele) in several fetuses examined; as well as the observation of increases in the percentage of resorptions per litter examined. Doses of 50 and 150 mg/kg, bid resulted in fetotoxicity as demonstrated by decreased fetal body weight. In an earlier study in hamsters, doses of 73-360 mg/kg level (oral; approximately 2-8 times the maximum recommended daily dose of 360 mg/day for adults on a mg/m2 basis), reportedly produced cranioschisis in all of the fetuses examined.
- In studies in rats, doses at the 120 mg/kg level (oral; approximately 3 times the maximum recommended daily dose of 360 mg/day for adults on a mg/m2 basis), in the toxic range for the adult animal, were associated with an increase in embryo resorption at the time of implantation.
- In pregnant mice, a single 100 mg/kg dose (subcutaneous; approximately 1.4 times the recommended daily dose of 360 mg/day for adults on a mg/mg2 basis) reportedly resulted in delayed ossification in the offspring.
- No teratogenic effects were observed in rabbits administered up to 30 mg/kg (approximately 2 times the maximum recommended daily dose of 360 mg/day for adults on a mg/m2 basis) of codeine during organogenesis.
# Clinical Studies
There is limited information regarding Codeine Clinical Studies in the drug label.
# How Supplied
- Codeine Sulfate Oral Solution
- Codeine Sulfate Oral Solution, 30 mg per 5 mL is a clear, reddish-orange to orange solution available in one strength as follows:
- 30 mg per 5 mL Oral Solution
- NDC 51224-300-10: Bottle of 500 mL, packed in a carton with five oral syringes (5 mL) and one measuring cup (5 mL)
## Storage
- Store at controlled room temperature, 20° to 25°C (68° to 77°F), excursions permitted between 15° and 30°C (between 59° and 86°F).
- Protect from light and moisture.
- Dispense in well-closed container as defined in the USP/NF.
- All opioids, including codeine sulfate, are liable to diversion and misuse both by the general public and healthcare workers and should be handled accordingly.
# Images
## Drug Images
## Package and Label Display Panel
# Patient Counseling Information
- Advise patients that codeine sulfate is a narcotic pain medication and should be taken only as directed.
- Advise patients that some people have a genetic variation that results in codeine changing into morphine more rapidly and completely than other people. Most people are unaware of whether they are an ultra-rapid codeine metabolizer or not. These higher-than-normal levels of morphine in the blood may lead to life-threatening or fatal respiratory depression or signs of overdose such as extreme sleepiness, confusion, or shallow breathing. Children with this genetic variation who were prescribed codeine after tonsillectomy and/or adenoidectomy for obstructive sleep apnea may be at greatest risk based on reports of several deaths in this population due to respiratory depression. Codeine is contraindicated in all children who undergo tonsillectomy and/or adenoidectomy. Advise caregivers of children receiving codeine for other reasons to monitor for signs of respiratory depression.
- Advise patients that nursing mothers taking codeine can have higher morphine levels in their breast milk if they are ultra-rapid metabolizers. These higher levels of morphine in breast milk may lead to life-threatening or fatal side effects in nursing babies. Advise nursing mothers to watch for signs of morphine toxicity in their infants which includes increased sleepiness (more than usual), difficulty breastfeeding, breathing difficulties, or limpness. Instruct nursing mothers to talk to the baby's doctor immediately if they notice these signs and, if they cannot reach the doctor right away, to take the baby to an emergency room or call 911 (or local emergency services).
- Advise patients not to adjust the dose of codeine sulfate without consulting a physician or other healthcare professional.
- Instruct patients on how to measure and take the correct dose of Codeine Sulfate Oral Solution.
- Advise patients that codeine may cause drowsiness, dizziness, or lightheadedness and may impair the mental and/or physical abilities required for the performance of potentially hazardous tasks (e.g., driving, operating machinery). Advise patients started on codeine sulfate or patients whose dose has been adjusted to refrain from any potentially dangerous activity until it is established that they are not adversely affected.
- Advise patients that codeine sulfate will add to the effects of alcohol and other CNS depressants (such as antihistamines, sedatives, hypnotics, tranquilizers, general anesthetics, phenothiazines, other opioids, and monoamine oxidase inhibitors).
- Advise patients not to combine codeine sulfate with central nervous system depressants (sleep aids, tranquilizers) except by the orders of the prescribing physician, and not to combine with alcohol because dangerous additive effects may occur, resulting in serious injury or death.
- Advise patients that codeine sulfate is a potential drug of abuse. They must protect it from theft. It should never be given to anyone other than the individual for whom it was prescribed.
- Advise patients to keep codeine sulfate in a secure place out of the reach of children.
- Advise patients of the potential for severe constipation when taking codeine sulfate; appropriate laxatives and/or stool softeners as well as other appropriate treatments should be initiated from the onset of therapy.
- Advise patients of the most common adverse events that may occur while taking codeine sulfate: drowsiness, lightheadedness, dizziness, sedation, shortness of breath, nausea, vomiting, constipation, and sweating.
- Advise patients that if they miss one dose of Codeine Sulfate Oral Solution they can take the dose when they remember it if they have pain, or they can wait for the next dose.
- If patients have been receiving treatment with codeine sulfate for more than a few weeks and cessation of therapy is indicated, counsel them on the importance of safely tapering the dose and that abruptly discontinuing the medication could precipitate withdrawal symptoms. Provide a dose schedule to accomplish a gradual discontinuation of the medication.
- Advise women of childbearing potential who become or are planning to become pregnant to consult a physician prior to initiating or continuing therapy with codeine sulfate.
- Advise patients that safe use in pregnancy has not been established and prolonged use of opioid analgesics during pregnancy may cause fetal-neonatal physical dependence, and neonatal withdrawal may occur.
- Read the Medication Guide that comes with Codeine Sulfate Oral Solution before you start taking it and each time you get a new prescription. There may be new information. This Medication Guide does not take the place of talking with your healthcare provider about your medical condition or your treatment.
### What is the most important information I should know about Codeine Sulfate Oral Solution?
- Codeine Sulfate Oral Solution can cause serious side effects, including death.
- Take Codeine Sulfate Oral Solution exactly as prescribed by your healthcare provider. If you take the wrong dose or strength of Codeine Sulfate Oral Solution, you could overdose and die.
- It is especially important when you take Codeine Sulfate Oral Solution that you know exactly what dose and strength to take, and the right way to measure your medicine. Your healthcare provider or pharmacist should show you the right way to measure your medicine.
- Always use the oral syringe provided with Codeine Sulfate Oral Solution, 30 mg per 5 mL (6 mg/mL) to help make sure you measure the right amount.
### What is Codeine Sulfate Oral Solution?
- Codeine Sulfate Oral Solution is in a group of drugs called narcotic pain relievers. Codeine Sulfate Oral Solution is only for people who have mild to moderately severe pain.
- Codeine Sulfate Oral Solution is a federally controlled substance (CII) because it is an opioid pain medicine that can be abused by people who abuse prescription medicines or street drugs.
- Prevent theft, misuse or abuse. Keep Codeine Sulfate Oral Solution in a safe place to keep it from being stolen. Codeine Sulfate can be a target for people who misuse or abuse prescription medicines or street drugs.
- Never give Codeine Sulfate Oral Solution to anyone else, even if they have the same symptoms you have. It may harm them or even cause death.
- Selling or giving away this medicine is against the law.
- It is not known if Codeine Sulfate Oral Solution is safe and effective in children under age 18 years of age.
### Who should not take Codeine Sulfate Oral Solution?
- Do not give Codeine Sulfate Oral Solution to a child to treat pain after tonsillectomy or adenoidectomy surgery.
- Do not take Codeine Sulfate Oral Solution if you:
- Are allergic to Codeine or any of the ingredients in Codeine Sulfate Oral Solution. See the end of this Medication guide for a complete list of ingredients in Codeine Sulfate Oral Solution.
- Are having an asthma attack or have severe asthma, trouble breathing, or lung problems.
- Have a bowel blockage, called paralytic ileus.
### What should I tell my healthcare provider before taking Codeine Sulfate?
- Before taking Codeine Sulfate Oral Solution, tell your healthcare provider if you:
- Have trouble breathing or lung problems
- Have had a head injury
- Have liver or kidney problems
- Have been told by your healthcare provider that you are a "rapid metabolizer" of certain medicines
- Have had adrenal gland problems, such as Addison's disease
- Have severe scoliosis that affects your breathing
- Have thyroid problems
- Have problems urinating or enlargement of your prostate
- Have had convulsions or seizures
- Have a past or present drinking problem or alcoholism
- Have severe mental problems
- Have constipation or other bowel problems
- Have problems with your pancreas or gallbladder
- Have past or present substance abuse or drug addiction
- Plan to have surgery
- Have any other medical conditions
- Are pregnant or plan to become pregnant. It is not known if Codeine Sulfate Oral Solution will harm your unborn baby. Talk to your healthcare provider if you are pregnant or plan to become pregnant. If you take Codeine Sulfate Oral Solution right before your baby is born, your newborn could have breathing problems. Your baby may also have withdrawal symptoms because his body has become used to the medicine.
- Symptoms of withdrawal in a newborn baby may include:
- Irritability
- Vomiting
- Weight loss
- Fever
- Diarrhea or more stools than normal
- Being very active
- Problems sleeping
- High pitched cry
- Shaking (tremors)
- Are breast-feeding or plan to breast-feed.
- See the box with Important information at the top of this Medication Guide.
- If you stop breast-feeding, your baby may have withdrawal symptoms. See the list of withdrawal symptoms above. If your baby has any of these symptoms you need to contact your healthcare provider right away. If you can not reach your healthcare provider, take your baby to your local hospital emergency room or call your local emergency medical service. You and your healthcare provider should decide if you will take Codeine Sulfate Oral Solution or breast-feed.
- Tell your healthcare provider about all the medicines you take, including prescription and non-prescription medicines, vitamins, and herbal supplements. Sometimes the doses of medicines that you take with Codeine Sulfate Oral Solution may need to be changed if used together. Codeine Sulfate Oral Solution and other medicines may affect each other causing serious side effects. Be especially careful about taking other medicines that make you sleepy such as:
- Sleeping pills
- Anti-depressants
- Other pain medicines
- Anticholinergic medicines
- Anti-nausea medicines
- Antibiotic or antifungal medicines
- Tranquilizers
- Heart medicines
- Antihistamines
- Anti-seizure medicines
- Anti-anxiety medicines
- Do not take Codeine Sulfate Oral Solution if you already take a monoamine oxidase inhibitor medicine (MAOI) or within 14 days after you stop taking an MAOI medicine.
- Do not take any new medicine while using Codeine Sulfate until you have talked with your healthcare provider or pharmacist. They will tell you if it is safe to take other medicines with Codeine Sulfate Oral Solution.
- Ask your healthcare provider if you are not sure if your medicine is one listed above.
- Know the medicines you take. Keep a list of them and show it to your healthcare provider and pharmacist when you get a new medicine.
### How should I take Codeine Sulfate Oral Solution?
- See "What is the most important information I should know about Codeine Sulfate Oral Solution?"
- Take Codeine Sulfate Oral Solution exactly as prescribed. Do not change your dose unless your healthcare provider tells you to. Your healthcare provider may change your dose after seeing how the medicine affects you. Call your healthcare provider if your pain is not well controlled with your prescribed dose of Codeine Sulfate Oral Solution. You can take Codeine Sulfate Oral Solution with or without food.
- Make sure you understand exactly how to measure your dose. Always use the oral syringe provided with your Codeine Sulfate Oral Solution, 30 mg per 5 mL (6 mg/mL) to help make sure you measure the right amount. Ask your healthcare provider or pharmacist if you are not sure what dose of Codeine Sulfate Oral Solution you should take or if you are not sure how to use the oral syringe.
- Do not stop taking Codeine Sulfate Oral Solution suddenly. If you have been taking Codeine Sulfate Oral Solution for more than a few weeks, stopping Codeine Sulfate Oral Solution suddenly can make you sick with withdrawal symptoms (for example, nausea, vomiting, diarrhea, anxiety, and shivering). If your healthcare provider decides you no longer need Codeine Sulfate Oral Solution, ask how to slowly reduce this medicine. Do not stop taking Codeine Sulfate Oral Solution without talking to your healthcare provider.
- If you take too much Codeine Sulfate Oral Solution, call your healthcare provider or go to the nearest hospital emergency room right away.
- If you miss one dose of Codeine Sulfate Oral Solution you can take the dose when you remember it if you have pain, or you can wait for the next dose.
- Talk with your healthcare provider regularly about your pain to see if you still need to take Codeine Sulfate.
### What should I avoid while taking Codeine Sulfate Oral Solution?
- You should not drink alcohol while using Codeine Sulfate Oral Solution. Drinking alcohol with Codeine Sulfate Oral Solution may increase your risk of having dangerous side effects or death.
- Do not drive, operate heavy machinery, or do other dangerous activities, especially when you start taking Codeine Sulfate Oral Solution and when your dose is changed, until you know how Codeine Sulfate Oral Solution affects you. Codeine Sulfate Oral Solution can make you sleepy. Ask your healthcare provider to tell you when it is okay to do these activities.
### What are the possible side effects of Codeine Sulfate Oral Solution?
- See "What is the most important information I should know about Codeine Sulfate Oral Solution?"
- Codeine Sulfate Oral Solution can cause serious breathing problems that can become life-threatening, especially if Codeine Sulfate is used the wrong way. Call your healthcare provider or get help right away if:
- Your breathing slows down
- You have shallow breathing (little chest movement with breathing)
- You feel faint, dizzy, confused, or
- You have any other unusual symptoms
- These can be symptoms that you have taken too much Codeine Sulfate Oral Solution (overdose) or the dose is too high for you. These symptoms may lead to serious problems or death if not treated right away.
- Codeine Sulfate Oral Solution can cause your blood pressure to drop. This can make you feel dizzy if you get up fast from sitting or lying down. Low blood pressure is also more likely to happen if you take other medicines that can also lower your blood pressure. Severe low blood pressure can happen if you lose blood or take certain other medicines.
- There is a risk of abuse or addiction with Codeine Sulfate Oral Solution. The risk is higher if you are or have been addicted to or abused other medicines, street drugs, or alcohol, or if you have a history of mental problems.
- Codeine Sulfate Oral Solution can cause physical dependence. Do not stop taking Codeine Sulfate Oral Solution or any other opioid without talking to your healthcare provider about how to slowly stop your medicine. You could become sick with uncomfortable withdrawal symptoms because your body has become used to these medicines. Physical dependence is not the same as drug addiction. Tell your healthcare provider if you have any of these symptoms of withdrawal while slowly stopping Codeine Sulfate Oral Solution:
- Feel restless
- Dilated pupils of your eyes
- Tearing eyes
- Feel irritable or anxious
- Runny nose
- Trouble sleeping
- Yawning
- Increase in your blood pressure
- Sweating
- Faster breathing, or faster heart beats
- Chills or hair on your arms "stand up"
- Nausea, loss of appetite, vomiting, diarrhea, stomach-area (abdominal) cramps
- Muscle aches, backache
- Common side effects of Codeine Sulfate Oral Solution include:
- Constipation
- Dizziness
- Nausea
- Drowsiness
- Sleepiness
- Vomiting
- Lightheadedness
- Sweating
- Constipation (not often enough or hard bowel movements) is a very common side effect of pain medicines from the opioid class. Talk to your healthcare provider about dietary changes, and the use of laxatives (medicines to treat constipation) and stool softeners to prevent or treat constipation while taking Codeine Sulfate Oral Solution.
- Tell your healthcare provider if you have any side effect that bothers you or that does not go away.
- These are not all the possible side effects of Codeine Sulfate Oral Solution. For more information, ask your healthcare provider or pharmacist.
- Call your healthcare provider for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088.
### How should I store Codeine Sulfate Oral Solution?
- Store Codeine Sulfate Oral Solution at room temperature, between 59°F to 86°F (15°C to 30°C), away from the light.
- Keep Codeine Sulfate Oral Solution out of the reach of children. Accidental overdose by a child is a medical emergency and can lead to death.
### General Information about Codeine Sulfate Oral Solution
- Medicines are sometimes prescribed for purposes other than those listed in a Medication Guide. Do not use Codeine Sulfate Oral Solution for a condition for which it was not prescribed. Do not give your Codeine Sulfate Oral Solution to other people, even if they have the same symptoms you have. Selling or giving away Codeine Sulfate Oral Solution may harm others, may cause death, and is against the law.
- This Medication Guide summarizes the most important information about Codeine Sulfate Oral Solution. If you would like more information, talk with your healthcare provider. You can ask your healthcare provider or pharmacist for information about Codeine Sulfate Oral Solution that is written for healthcare professionals.
- For more information about Codeine Sulfate Oral Solution, go to www.roxane.com, or call Roxane Laboratories, Inc. at 1-800-962-8364.
### What are the ingredients in Codeine Sulfate Oral Solution?
- Active ingredient: codeine sulfate
- Inactive ingredients: ascorbic acid, citric acid, disodium edetate, FD&C Red No. 40, FD&C Yellow No. 6, glycerin, Orange Flavor XBF-7098189 (artificial flavors, propylene glycol), sodium benzoate, sorbitol, sucralose, and water
- Instructions for Use
- Codeine Sulfate (koh-deen) (CII)
- Oral Solution
- Oral Syringe
- Important information about measuring Codeine Sulfate Oral Solution:
- Always use the oral syringe provided with your Codeine Sulfate Oral Solution to make sure you measure the right amount.
- Measure the dose of medicine from the widest part of the plunger. Do not measure from the narrow tip. See Figure 1.
- Remove the protective storage cap from the syringe.
- Insert the tip of the oral syringe into the medicine bottle.
- Pull back the plunger to the line that matches the dose prescribed by your healthcare provider.
- Remove the oral syringe from the medicine bottle.
- Take your medicine by slowly pushing the plunger until the oral syringe is empty.
- Replace the cap and oral syringe in a dry and clean place.
# Precautions with Alcohol
Alcohol-Codeine interaction has not been established. Talk to your doctor about the effects of taking alcohol with this medication.
# Brand Names
There is limited information regarding Codeine Brand Names in the drug label.
# Look-Alike Drug Names
There is limited information regarding Codeine Look-Alike Drug Names in the drug label.
# Drug Shortage Status
# Price | Codeine
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Chetan Lokhande, M.B.B.S [2]
# Disclaimer
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# Black Box Warning
# Overview
Codeine is an analgesic opioid that is FDA approved for the treatment of mild to moderate pain. There is a Black Box Warning for this drug as shown here. Common adverse reactions include constipation, nausea, vomiting, dizziness, lightheadedness, sedation, somnolence, and dyspnea.
# Adult Indications and Dosage
## FDA-Labeled Indications and Dosage (Adult)
- Pain (mild to moderate): 15 to 60 mg orally up to every 4 hours as needed; MAX 360 mg/24 h
## Off-Label Use and Dosage (Adult)
### Guideline-Supported Use
There is limited information about Off-Label Guideline-Supported Use of Codeine in adult patients.
### Non–Guideline-Supported Use
There is limited information about Off-Label Non–Guideline-Supported Use of Codeine in adult patients.
# Pediatric Indications and Dosage
## FDA-Labeled Indications and Dosage (Pediatric)
- Safety and effectiveness in pediatric patients younger than 18 years have not been established.
- Contraindicated for postoperative pain control in pediatric patients undergoing tonsillectomy or adenoidectomy.
## Off-Label Use and Dosage (Pediatric)
### Guideline-Supported Use
There is limited information about Off-Label Guideline-Supported Use of Codeine in pediatric patients.
### Non–Guideline-Supported Use
There is limited information about Off-Label Non–Guideline-Supported Use of Codeine in pediatric patients.
# Contraindications
Codeine sulfate is contraindicated for postoperative pain management in children who have undergone tonsillectomy and/or adenoidectomy.
- Codeine sulfate is contraindicated in patients with known hypersensitivity to codeine or any components of the product. Persons known to be hypersensitive to certain other opioids may exhibit cross-sensitivity to codeine.
- Codeine sulfate is contraindicated in patients with respiratory depression in the absence of resuscitative equipment.
- Codeine sulfate is contraindicated in patients with acute or severe bronchial asthma or hypercarbia.
- Codeine sulfate is contraindicated in any patient who has or is suspected of having paralytic ileus.
# Warnings
- Death Related to Ultra-Rapid Metabolism of Codeine to Morphine
- Respiratory depression and death have occurred in children who received codeine in the post-operative period following tonsillectomy and/or adenoidectomy and had evidence of being ultra-rapid metabolizers of codeine (i.e., multiple copies of the gene for cytochrome P450 isoenzyme 2D6 or high morphine concentrations). Deaths have also occurred in nursing infants who were exposed to high levels of morphine in breast milk because their mothers were ultra-rapid metabolizers of codeine.
- Some individuals may be ultra-rapid metabolizers because of a specific CYP2D6 genotype (gene duplications denoted as *1/*1xN or *1/*2xN). The prevalence of this CYP2D6 phenotype varies widely and has been estimated at 0.5 to 1% in Chinese and Japanese, 0.5 to 1% in Hispanics, 1 to 10% in Caucasians, 3% in African Americans, and 16 to 28% in North Africans, Ethiopians, and Arabs. Data are not available for other ethnic groups. These individuals convert codeine into its active metabolite, morphine, more rapidly and completely than other people. This rapid conversion results in higher than expected serum morphine levels. Even at labeled dosage regimens, individuals who are ultra-rapid metabolizers may have life-threatening or fatal respiratory depression or experience signs of overdose (such as extreme sleepiness, confusion, or shallow breathing).
- Children with obstructive sleep apnea who are treated with codeine for post-tonsillectomy and/or adenoidectomy pain may be particularly sensitive to the respiratory depressant effects of codeine that has been rapidly metabolized to morphine. Codeine is contraindicated for post-operative pain management in all pediatric patients undergoing tonsillectomy and/or adenoidectomy.
- When prescribing codeine, healthcare providers should choose the lowest effective dose for the shortest period of time and inform patients and caregivers about these risks and the signs of morphine overdose.
- Respiratory Depression
- Respiratory depression is the primary risk of codeine sulfate. Respiratory depression occurs more frequently in elderly or debilitated patients and in those suffering from conditions accompanied by hypoxia, hypercapnia, or upper airway obstruction, in whom even moderate therapeutic doses may significantly decrease pulmonary ventilation. Codeine produces dose-related respiratory depression.
- Caution should be exercised when codeine sulfate is used postoperatively, in patients with pulmonary disease or shortness of breath, or whenever ventilatory function is depressed. Use opioids, including codeine sulfate, with extreme caution in patients with chronic obstructive pulmonary disease or cor pulmonale and in patients having a substantially decreased respiratory reserve (e.g., severe kyphoscoliosis), hypoxia, hypercapnia, or pre-existing respiratory depression. In such patients, even usual therapeutic doses of codeine sulfate may increase airway resistance and decrease respiratory drive to the point of apnea. Consider alternative non-opioid analgesics and use codeine sulfate only under careful medical supervision at the lowest effective dose in such patients.
- Misuse and Abuse of Opioids
- Codeine sulfate is an opioid agonist of the morphine-type and a Schedule II controlled substance. Such drugs are sought by drug abusers and people with addiction disorders. Diversion of Schedule II products is an act subject to criminal penalty.
- Patients should be assessed for their risk for opioid abuse or addiction prior to being prescribed opioids
- Codeine can be abused in a manner similar to other opioid agonists, legal or illicit. This should be considered when prescribing or dispensing codeine sulfate in situations where the physician or pharmacist is concerned about an increased risk of misuse, abuse, or diversion.
- Codeine may be abused by crushing, chewing, snorting or injecting the product. Misuse and abuse of codeine sulfate poses a significant risk to the abuser that could result in overdose and death.
- Concerns about abuse, addiction, and diversion should not prevent the proper management of pain. Healthcare professionals should contact their State Professional Licensing Board or State Controlled Substances Authority for information on how to prevent and detect abuse or diversion of this product.
- Interaction with Alcohol and Drugs of Abuse
- Codeine sulfate may be expected to have additive effects when used in conjunction with alcohol, other opioids, or illicit drugs that cause central nervous system depression, because respiratory depression, hypotension, profound sedation, coma or death may result.
- Head Injury and Increased Intracranial Pressure
- Respiratory depressant effects of opioids and their capacity to elevate cerebrospinal fluid pressure resulting from vasodilation following CO2 retention may be markedly exaggerated in the presence of head injury, other intracranial lesions or a pre-existing increase in intracranial pressure. Furthermore, opioids including codeine sulfate, can produce effects on pupillary response and consciousness, which may obscure neurologic signs of further increases in intracranial pressure in patients with head injuries.
- Hypotensive Effect
- Codeine sulfate may cause severe hypotension in an individual whose ability to maintain blood pressure has already been compromised by a depleted blood volume or concurrent administration of drugs such as phenothiazines or general anesthetics. Codeine sulfate may produce orthostatic hypotension and syncope in ambulatory patients.
- Administer codeine sulfate with caution to patients in circulatory shock, as vasodilation produced by the drug may further reduce cardiac output and blood pressure.
- Gastrointestinal Effects
- Do not administer codeine sulfate to patients with gastrointestinal obstruction, especially paralytic ileus because codeine sulfate diminishes propulsive peristaltic waves in the gastrointestinal tract and may prolong the obstruction.
- Chronic use of opioids, including codeine sulfate, may result in obstructive bowel disease especially in patients with underlying intestinal motility disorder. Codeine sulfate may cause or aggravate constipation.
- The administration of codeine sulfate may obscure the diagnosis or clinical course of patients with acute abdominal conditions.
- Use in Pancreatic/Biliary Tract Disease
- Use codeine sulfate with caution in patients with biliary tract disease, including acute pancreatitis, as codeine sulfate may cause spasm of the sphincter of Oddi and diminish biliary and pancreatic secretions.
- Special Risk Patients
- Use codeine sulfate with caution in patients with severe renal or hepatic impairment, hypothyrodism, Addison's disease, prostatic hypertrophy, or urethral stricture and in elderly or debilitated patients. The usual precautions should be observed and the possibility of respiratory depression should be kept in mind.
- Extreme caution should be exercised in the administration of codeine sulfate to patients with CNS depression, acute alcoholism, and delirium tremens.
- All opioids may aggravate convulsions in patients with convulsive disorders, and all opioids may induce or aggravate seizures in some clinical settings.
- Keep Codeine Sulfate Oral Solution out of the reach of children. In case of accidental ingestion, seek emergency medical help immediately.
- Driving and Operating Machinery
- Caution patients that codeine sulfate could impair the mental and/or physical abilities needed to perform potentially hazardous activities such as driving a car or operating machinery.
- Caution patients about the potential combined effects of codeine sulfate with other CNS depressants, including other opioids, phenothiazines, sedative/hypnotics, and alcohol.
# Adverse Reactions
## Clinical Trials Experience
- Serious adverse reactions associated with codeine are respiratory depression and, to a lesser degree, circulatory depression, respiratory arrest, shock, and cardiac arrest.
- The most frequently observed adverse reactions with codeine administration include drowsiness, lightheadedness, dizziness, sedation, shortness of breath, nausea, vomiting, sweating, and constipation.
- Other adverse reactions include allergic reactions, euphoria, dysphoria, abdominal pain, and pruritis.
- Other less frequently observed adverse reactions expected from opioid analgesics, including codeine sulfate, include:
- Cardiovascular system: faintness, flushing, hypotension, palpitations, syncope
- Digestive System: abdominal cramps, anorexia, diarrhea, dry mouth, gastrointestinal distress, pancreatitis
- Nervous system: anxiety, drowsiness, fatigue, headache, insomnia, nervousness, shakiness, somnolence, vertigo, visual disturbances, weakness
- Skin and Appendages: rash, sweating, urticaria
## Postmarketing Experience
There is limited information regarding Codeine Postmarketing Experience in the drug label.
# Drug Interactions
- Central Nervous System (CNS) Depressants
- Concurrent use of other opioids, antihistamines, antipsychotics, antianxiety agents, or other CNS depressants (including sedatives, hypnotics, general anesthetics, antiemetics, phenothiazines, or other tranquilizers or alcohol) concomitantly with codeine sulfate may result in additive CNS depression, respiratory depression, hypotension, profound sedation, or coma. Use codeine sulfate with caution and in reduced dosages in patients taking these agents.
- Mixed Agonist/Antagonist Opioid Analgesics
- Do not administer mixed agonist/antagonist analgesics (i.e., pentazocine, nalbuphine, and butorphanol) to patients who have received or are receiving a course of therapy with a pure opioid agonist analgesic such as codeine sulfate. In these patients, mixed agonist/ antagonist analgesics may reduce the analgesic effect and/or may precipitate withdrawal symptoms.
- Anticholinergics
- Anticholinergics or other medications with anticholinergic activity when used concurrently with opioid analgesics may result in increased risk of urinary retention and/or severe constipation, which may lead to paralytic ileus.
- Antidepressants
- Use of monoamine oxidase inhibitors (MAOIs) or tricyclic antidepressants with codeine sulfate may increase the effect of either the antidepressant or codeine. MAOIs markedly potentiate the action of morphine, the major metabolite of codeine. Codeine should not be used in patients taking MAOIs or within 14 days of stopping such treatment.
- CYP2D6 and CYP3A4 Inhibitors and Inducers
- Codeine is metabolized by the cytochrome P450 2D6 and 3A4 isoenzymes. Patients taking CYP2D6 inhibitors or CYP3A4 inhibitors or inducers may demonstrate an altered response to codeine, therefore analgesic activity should be monitored.
- Inhibitors of CYP2D6 or CYP3A4: Since the CYP2D6 and CYP3A4 isoenzymes play a major role in the metabolism of codeine, drugs that inhibit CYP3A4 (e.g., macrolide antibiotics (e.g., erythromycin), azole-antifungal agents (e.g., ketoconazole), protease inhibitors (e.g., ritonavir)), or CYP2D6 activity (e.g., certain cardiovascular drugs including amiodarone and quinidine as well as polycyclic antidepressants), may cause decreased clearance of codeine which could lead to an increase in codeine plasma concentrations. If coadministration with codeine sulfate oral solution is necessary, caution is advised when initiating therapy with, currently taking, or discontinuing CYP450 inhibitors. Evaluate these patients at frequent intervals and consider dose adjustments until stable drug effects are achieved.
- Inducers of CYP3A4: CYP450 inducers, such as rifampin, carbamazepine, and phenytoin, may induce the metabolism of codeine and, therefore, may cause increased clearance of the drug which could lead to a decrease in codeine plasma concentrations, lack of efficacy or, possibly, development of an abstinence syndrome in a patient who had developed physical dependence to codeine. If co-administration with codeine sulfate oral solution is necessary, caution is advised when initiating therapy with, currently taking, or discontinuing CYP3A4 inducers. Evaluate these patients at frequent intervals and consider dose adjustments until stable drug effects are achieved.
- Drug-Laboratory Test Interaction
- Codeine may cause an elevation of plasma amylase and lipase due to the potential of codeine to produce spasm of the sphincter of Oddi. Determination of these enzyme levels may be unreliable for some time after an opiate agonist has been given.
# Use in Specific Populations
### Pregnancy
Pregnancy Category (FDA): C
- There are no adequate and well-controlled studies in pregnant women. Codeine should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus.
- Codeine has been shown to have embryolethal and fetotoxic effects (reduced fetal body weights and delayed or incomplete ossification) in the hamster, rat and mouse models at approximately 2 to 4 times the maximum recommended human dose of 360 mg/day based on a body surface area comparison. Maternally toxic doses that were approximately 7 times the maximum recommended human dose of 360 mg/day, were associated with evidence of resorptions and incomplete ossification, including meningioencephalocele and cranioschisis. In contrast, codeine did not demonstrate evidence of embryotoxicity or fetotoxicity in the rabbit model at doses up to 2 times the maximum recommended human dose of 360 mg/day based on a body surface area comparison.
- Nonteratogenic Effects
- Neonatal codeine withdrawal has occurred in infants born to addicted and nonaddicted mothers who had been taking codeine-containing medications in the days prior to delivery. Typical symptoms of narcotic withdrawal include irritability, excessive crying, tremors, hyperreflexia, seizures, fever, vomiting, diarrhea, and poor feeding. These signs occur shortly after birth and may require specific treatment.
- Codeine (30 mg/kg) administered subcutaneously to pregnant rats during pregnancy and for 25 days after delivery increased neonatal mortality at birth. This dose is 0.8 times the maximum recommended human dose of 360 mg/day on a body surface area comparison.
Pregnancy Category (AUS):
There is no Australian Drug Evaluation Committee (ADEC) guidance on usage of Codeine in women who are pregnant.
### Labor and Delivery
- Opioid analgesics cross the placenta and may produce respiratory depression and psycho-physiologic effects in neonates. Codeine is not recommended for use in women during and immediately prior to labor. Occasionally, opioid analgesics may prolong labor through actions which temporarily reduce the strength, duration, and frequency of uterine contractions. However, this effect is not consistent and may be offset by an increased rate of cervical dilatation, which tends to shorten labor. Closely observe neonates whose mothers received opioid analgesics during labor for signs of respiratory depression. Have a specific opioid antagonist, such as naloxone, available for reversal of opioidinduced respiratory depression in the neonate.
### Nursing Mothers
- Codeine is secreted into human milk. In women with normal codeine metabolism (normal CYP2D6 activity), the amount of codeine secreted into human milk is low and dose-dependent. However, some women are ultra-rapid metabolizers of codeine. These women achieve higher-than-expected serum levels of codeine's active metabolite, morphine, leading to higher-than-expected levels of morphine in breast milk and potentially dangerously high serum morphine levels in their breastfed infants. Therefore, maternal use of codeine can potentially lead to serious adverse reactions, including death, in nursing infants.
- The risk of infant exposure to codeine and morphine through breast milk should be weighed against the benefits of breastfeeding for both the mother and the baby. Caution should be exercised when codeine is administered to a nursing woman. If a codeine containing product is selected, the lowest dose should be prescribed for the shortest period of time to achieve the desired clinical effect. Mothers using codeine should be informed about when to seek immediate medical care and how to identify the signs and symptoms of neonatal toxicity, such as drowsiness or sedation, difficulty breastfeeding, breathing difficulties, and decreased tone, in their baby. Nursing mothers who are ultrarapid metabolizers may also experience overdose symptoms such as extreme sleepiness, confusion, or shallow breathing. Prescribers should closely monitor mother-infant pairs and notify treating pediatricians about the use of codeine during breast-feeding.
### Pediatric Use
The safety, effectiveness and the pharmacokinetics of codeine sulfate in pediatric patients below the age of 18 have not been established.
- Respiratory depression and death have occurred in children with obstructive sleep apnea who received codeine in the post-operative period following tonsillectomy and/or adenoidectomy and had evidence of being ultra-rapid metabolizers of codeine (i.e., multiple copies of the gene for cytochrome P450 isoenzyme 2D6 or high morphine concentrations). These children may be particularly sensitive to the respiratory depressant effects of codeine that has been rapidly metabolized to morphine. Codeine is contraindicated for post-operative pain management in all pediatric patients undergoing tonsillectomy and/ or adenoidectomy.
### Geriatic Use
Codeine may cause confusion and over-sedation in the elderly (aged 65 and older). In general, use caution when selecting a dose for an elderly patient, usually starting at the low end of the dosing range, reflecting the greater frequency of decreased hepatic, renal, or cardiac function, and of concomitant disease or other drug therapy.
### Gender
There is no FDA guidance on the use of Codeine with respect to specific gender populations.
### Race
There is no FDA guidance on the use of Codeine with respect to specific racial populations.
### Renal Impairment
Codeine pharmacokinetics may be altered in patients with renal failure. Clearance may be decreased and the metabolites may accumulate to much higher plasma levels in patients with renal failure as compared to patients with normal renal function. Start these patients cautiously with lower doses of codeine sulfate or with longer dosing intervals and titrate slowly while carefully monitoring for side effects.
### Hepatic Impairment
No formal studies have been conducted in patients with hepatic impairment so the pharmacokinetics of codeine in this patient population are unknown. Start these patients cautiously with lower doses of codeine sulfate or with longer dosing intervals and titrate slowly while carefully monitoring for side effects.
### Females of Reproductive Potential and Males
There is no FDA guidance on the use of Codeine in women of reproductive potentials and males.
### Immunocompromised Patients
There is no FDA guidance one the use of Codeine in patients who are immunocompromised.
# Administration and Monitoring
### Administration
There is limited information regarding Codeine Administration in the drug label.
### Monitoring
There is limited information regarding Codeine Monitoring in the drug label.
# IV Compatibility
There is limited information regarding the compatibility of Codeine and IV administrations.
# Overdosage
- Acute overdose with codeine is characterized by respiratory depression (a decrease in respiratory rate and/or tidal volume, Cheyne-Stokes respiration, cyanosis), extreme somnolence progressing to stupor or coma, skeletal muscle flaccidity, cold and clammy skin, constricted pupils, and sometimes bradycardia and hypotension. In severe overdosage, apnea, circulatory collapse, cardiac arrest, and death may occur.
- Codeine may cause miosis, even in total darkness. Pinpoint pupils are a sign of opioid overdose but are not pathognomonic (e.g., pontine lesions of hemorrhagic or ischemic origin may produce similar findings). Marked mydriasis rather than miosis may be seen with hypoxia in overdose situations.
- Treatment
- Give primary attention to re-establishment of a patent airway and institution of assisted or controlled ventilation. Employ supportive measures (including oxygen and vasopressors) in the management of circulatory shock and pulmonary edema accompanying overdose as indicated. Cardiac arrest or arrhythmias may require cardiac massage or defibrillation. Induction of emesis is not recommended because of the potential for CNS depression and seizures. Activated charcoal is recommended if the patient is awake and able to protect his/her airway. In persons who are at risk for abrupt onset of seizures or mental status depression, activated charcoal should be administered by medical or paramedical personnel capable of airway management to prevent aspiration in the event of spontaneous emesis. Severe agitation or seizures should be treated with an intravenous benzodiazepine.
- The pure opioid antagonist, naloxone, is a specific antidote to respiratory depression resulting from opioid overdose. Since the duration of reversal is expected to be less than the duration of action of codeine sulfate, carefully monitor the patient until spontaneous respiration is reliably re-established. If the response to opioid antagonists is suboptimal or only brief in nature, administer additional antagonist as directed by the label of the product.
- Do not administer opioid antagonists in the absence of clinically significant respiratory or circulatory depression secondary to codeine sulfate overdose. In an individual physically dependent on opioids, administration of the usual dose of the antagonist will precipitate an acute withdrawal syndrome. The severity of the withdrawal symptoms experienced will depend on the degree of physical dependence and the dose of the antagonist administered. Reserve use of an opioid antagonist for cases where such treatment is clearly needed. If it is necessary to treat serious respiratory depression in the physically dependent patient, initiate administration of the antagonist with care and titrate with smaller than usual doses.
# Pharmacology
## Mechanism of Action
- Codeine is an opioid agonist, related to morphine, but with less potent analgesic properties. Codeine is selective for the mu receptor, but with a much weaker affinity than morphine. The analgesic properties of codeine have been speculated to come from its conversion to morphine, although the exact mechanism of analgesic action remains unknown.
- Effects of the Central Nervous System (CNS): The principal therapeutic action of codeine is analgesia. Although the precise mechanism of the analgesic action is unknown, specific CNS opiate receptors and endogenous compounds with morphine-like activity have been identified throughout the brain and spinal cord and are likely to play a role in the expression and perception of analgesic effects. Other CNS effects of codeine include anxiolysis, euphoria, and feelings of relaxation. Codeine causes respiratory depression, in part by a direct effect on the brainstem respiratory centers. Codeine and other related opioids depress the cough reflex by direct effect on the cough center in the medulla. Codeine may also cause miosis.
- Effects on the Gastrointestinal Tract and on Other Smooth Muscle: Gastric, biliary and pancreatic secretions may be decreased by codeine. Codeine also causes a reduction in motility and is associated with an increase in tone in the antrum of the stomach and duodenum. Digestion of food in the small intestine is delayed and propulsive contractions are decreased. Propulsive peristaltic waves in the colon are decreased, while tone is increased to the point of spasm. The end result may be constipation. Codeine can cause a marked increase in biliary tract pressure as a result of the spasm of the sphincter of Oddi. Codeine may also cause spasms of the sphincter of the urinary bladder.
- Effects on the Cardiovascular System: In therapeutic doses, codeine does not usually exert major effects on the cardiovascular system. Codeine produces peripheral vasodilation which may result in orthostatic hypotension and fainting. Release of histamine can occur, which may play a role in opioid-induced hypotension. Manifestations of histamine release and/or peripheral vasodilation may include pruritus, flushing, red eyes, and sweating.
- Endocrine System: Opioid agonists have been shown to have a variety of effects on the secretion of hormones. Opioids inhibit the secretion of ACTH, cortisol, and luteinizing hormone (LH) in humans. They also stimulate prolactin, growth hormone (GH) secretion, and pancreatic secretion of insulin and glucagons in humans and other species, rats and dogs. Thyroid stimulating hormone (TSH) has been shown to be both inhibited and stimulated by opioids.
- Immune System: Opioids have been shown to have a variety of effects on components of the immune system in in vitro and animal models. The clinical significance of these findings is unknown.
## Structure
- Chemically, codeine sulfate is morphinan-6-ol,7,8-didehydro-4,5-epoxy-3-methoxy- 17-methyl-(5α,6α)-, sulfate (2:1) (salt), trihydrate. Codeine sulfate trihydrate is a fine, white, crystalline powder which is soluble in water and insoluble in chloroform and ether. Its empirical formula is (C18H21NO3)2 ∙ H2SO4 ∙ 3H2O and its molecular weight is 750.85 g/mol.
- Its structure is as follows:
- Each 5 mL of oral solution contains 30 mg of codeine sulfate, USP and the following inactive ingredients: ascorbic acid, citric acid, disodium edetate, FD&C Red No. 40, FD&C Yellow No. 6, glycerin, Orange Flavor XBF-7098189 (artificial flavors, propylene glycol), sodium benzoate, sorbitol, sucralose, and water. The pH of the oral solution is 3.3.
## Pharmacodynamics
- Codeine plasma concentrations do not correlate with codeine brain concentrations or relief of pain.
- The minimum effective concentration varies widely and is influenced by a variety of factors, including the extent of previous opioid use, age and general medical condition. Effective doses in tolerant patients may be significantly higher than in opioid-naïve patients.
## Pharmacokinetics
- Absorption: Codeine, when administered as codeine sulfate, is absorbed from the gastrointestinal tract with maximum plasma concentration occurring 60 minutes post administration.
- Food Effects: When 60 mg codeine sulfate was administered 30 minutes after ingesting a high fat/high calorie meal, there was no significant change in the rate and extent of absorption of codeine.
- Steady-state: Administration of 15 mg codeine sulfate every four hours for 5 days resulted in steady-state concentrations of codeine, morphine, morphine-3-glucuronide (M3G) and morphine-6-glucuronide (M6G) within 48 hours.
- Distribution: Codeine has been reported to have an apparent volume of distribution of approximately 3-6 L/kg, indicating extensive distribution of the drug into tissues. Codeine has low plasma protein binding with about 7-25% of codeine bound to plasma proteins.
- Metabolism: About 70-80% of the administered dose of codeine is metabolized by conjugation with glucuronic acid to codeine-6-glucuronide (C6G, about 60%) and via O-demethylation to morphine (about 5-10%) and N-demethylation to norcodeine (about 10%) respectively. UDP-glucuronosyltransferase (UGT) 2B7 and 2B4 are the major enzymes mediating glucurodination of codeine to C6G. Cytochrome P450 2D6 is the major enzyme responsible for conversion of codeine to morphine (about 5-10%) and P450 3A4 is the major enzyme mediating conversion of codeine to norcodeine. Morphine and norcodeine are further metabolized by conjugation with glucuronic acid. The glucuronide metabolites of morphine are morphine-3-glucuronide (M3G) and morphine-6- glucuronide (M6G). Morphine and M6G are known to have analgesic activity in humans. The analgesic activity of C6G in humans is unknown. Norcodeine and M3G are generally not considered to possess analgesic properties.
- Elimination: Approximately 90% of the total dose of codeine is excreted through the kidneys, of which approximately 10% is unchanged codeine. Plasma half-lives of codeine and its metabolites have been reported to be approximately 3 h
## Nonclinical Toxicology
- Carcinogenesis: Two year carcinogenicity studies have been conducted in F344/N rats and B6C3F1 mice. There was no evidence of carcinogenicity in male and female rats, respectively, at dietary doses up to 70 and 80 mg/kg/day of codeine (approximately 2 times the maximum recommended daily dose of 360 mg/day for adults on a mg/m2 basis) for two years. Similarly there was no evidence of carcinogenicity activity in male and female mice at dietary doses up to 400 mg/kg/day of codeine (approximately 5 times the maximum recommended daily dose of 360 mg/day for adults on a mg/m2 basis) for two years.
- Mutagenesis: Codeine was not mutagenic in the in vitro bacterial reverse mutation assay or clastogenic in the in vitro Chinese hamster ovary cell chromosome aberration assay.
- Impairment of Fertility: No animal studies were conducted to evaluate the effect of codeine on male or female fertility.
- Reproduction and Developmental Toxicology
- Studies on the reproductive and developmental effects of codeine have been reported in the published literature in hamsters, rats, mice and rabbits.
- A study in hamsters administered 150 mg/kg twice daily of codeine (oral; approximately 7 times the maximum recommended daily dose of 360 mg/day for adults on a mg/m2 basis) reported the development of cranial malformations (i.e., meningoencephalocele) in several fetuses examined; as well as the observation of increases in the percentage of resorptions per litter examined. Doses of 50 and 150 mg/kg, bid resulted in fetotoxicity as demonstrated by decreased fetal body weight. In an earlier study in hamsters, doses of 73-360 mg/kg level (oral; approximately 2-8 times the maximum recommended daily dose of 360 mg/day for adults on a mg/m2 basis), reportedly produced cranioschisis in all of the fetuses examined.
- In studies in rats, doses at the 120 mg/kg level (oral; approximately 3 times the maximum recommended daily dose of 360 mg/day for adults on a mg/m2 basis), in the toxic range for the adult animal, were associated with an increase in embryo resorption at the time of implantation.
- In pregnant mice, a single 100 mg/kg dose (subcutaneous; approximately 1.4 times the recommended daily dose of 360 mg/day for adults on a mg/mg2 basis) reportedly resulted in delayed ossification in the offspring.
- No teratogenic effects were observed in rabbits administered up to 30 mg/kg (approximately 2 times the maximum recommended daily dose of 360 mg/day for adults on a mg/m2 basis) of codeine during organogenesis.
# Clinical Studies
There is limited information regarding Codeine Clinical Studies in the drug label.
# How Supplied
- Codeine Sulfate Oral Solution
- Codeine Sulfate Oral Solution, 30 mg per 5 mL is a clear, reddish-orange to orange solution available in one strength as follows:
- 30 mg per 5 mL Oral Solution
- NDC 51224-300-10: Bottle of 500 mL, packed in a carton with five oral syringes (5 mL) and one measuring cup (5 mL)
## Storage
- Store at controlled room temperature, 20° to 25°C (68° to 77°F), excursions permitted between 15° and 30°C (between 59° and 86°F).
- Protect from light and moisture.
- Dispense in well-closed container as defined in the USP/NF.
- All opioids, including codeine sulfate, are liable to diversion and misuse both by the general public and healthcare workers and should be handled accordingly.
# Images
## Drug Images
## Package and Label Display Panel
# Patient Counseling Information
- Advise patients that codeine sulfate is a narcotic pain medication and should be taken only as directed.
- Advise patients that some people have a genetic variation that results in codeine changing into morphine more rapidly and completely than other people. Most people are unaware of whether they are an ultra-rapid codeine metabolizer or not. These higher-than-normal levels of morphine in the blood may lead to life-threatening or fatal respiratory depression or signs of overdose such as extreme sleepiness, confusion, or shallow breathing. Children with this genetic variation who were prescribed codeine after tonsillectomy and/or adenoidectomy for obstructive sleep apnea may be at greatest risk based on reports of several deaths in this population due to respiratory depression. Codeine is contraindicated in all children who undergo tonsillectomy and/or adenoidectomy. Advise caregivers of children receiving codeine for other reasons to monitor for signs of respiratory depression.
- Advise patients that nursing mothers taking codeine can have higher morphine levels in their breast milk if they are ultra-rapid metabolizers. These higher levels of morphine in breast milk may lead to life-threatening or fatal side effects in nursing babies. Advise nursing mothers to watch for signs of morphine toxicity in their infants which includes increased sleepiness (more than usual), difficulty breastfeeding, breathing difficulties, or limpness. Instruct nursing mothers to talk to the baby's doctor immediately if they notice these signs and, if they cannot reach the doctor right away, to take the baby to an emergency room or call 911 (or local emergency services).
- Advise patients not to adjust the dose of codeine sulfate without consulting a physician or other healthcare professional.
- Instruct patients on how to measure and take the correct dose of Codeine Sulfate Oral Solution.
- Advise patients that codeine may cause drowsiness, dizziness, or lightheadedness and may impair the mental and/or physical abilities required for the performance of potentially hazardous tasks (e.g., driving, operating machinery). Advise patients started on codeine sulfate or patients whose dose has been adjusted to refrain from any potentially dangerous activity until it is established that they are not adversely affected.
- Advise patients that codeine sulfate will add to the effects of alcohol and other CNS depressants (such as antihistamines, sedatives, hypnotics, tranquilizers, general anesthetics, phenothiazines, other opioids, and monoamine oxidase [MAO] inhibitors).
- Advise patients not to combine codeine sulfate with central nervous system depressants (sleep aids, tranquilizers) except by the orders of the prescribing physician, and not to combine with alcohol because dangerous additive effects may occur, resulting in serious injury or death.
- Advise patients that codeine sulfate is a potential drug of abuse. They must protect it from theft. It should never be given to anyone other than the individual for whom it was prescribed.
- Advise patients to keep codeine sulfate in a secure place out of the reach of children.
- Advise patients of the potential for severe constipation when taking codeine sulfate; appropriate laxatives and/or stool softeners as well as other appropriate treatments should be initiated from the onset of therapy.
- Advise patients of the most common adverse events that may occur while taking codeine sulfate: drowsiness, lightheadedness, dizziness, sedation, shortness of breath, nausea, vomiting, constipation, and sweating.
- Advise patients that if they miss one dose of Codeine Sulfate Oral Solution they can take the dose when they remember it if they have pain, or they can wait for the next dose.
- If patients have been receiving treatment with codeine sulfate for more than a few weeks and cessation of therapy is indicated, counsel them on the importance of safely tapering the dose and that abruptly discontinuing the medication could precipitate withdrawal symptoms. Provide a dose schedule to accomplish a gradual discontinuation of the medication.
- Advise women of childbearing potential who become or are planning to become pregnant to consult a physician prior to initiating or continuing therapy with codeine sulfate.
- Advise patients that safe use in pregnancy has not been established and prolonged use of opioid analgesics during pregnancy may cause fetal-neonatal physical dependence, and neonatal withdrawal may occur.
- Read the Medication Guide that comes with Codeine Sulfate Oral Solution before you start taking it and each time you get a new prescription. There may be new information. This Medication Guide does not take the place of talking with your healthcare provider about your medical condition or your treatment.
### What is the most important information I should know about Codeine Sulfate Oral Solution?
- Codeine Sulfate Oral Solution can cause serious side effects, including death.
- Take Codeine Sulfate Oral Solution exactly as prescribed by your healthcare provider. If you take the wrong dose or strength of Codeine Sulfate Oral Solution, you could overdose and die.
- It is especially important when you take Codeine Sulfate Oral Solution that you know exactly what dose and strength to take, and the right way to measure your medicine. Your healthcare provider or pharmacist should show you the right way to measure your medicine.
- Always use the oral syringe provided with Codeine Sulfate Oral Solution, 30 mg per 5 mL (6 mg/mL) to help make sure you measure the right amount.
### What is Codeine Sulfate Oral Solution?
- Codeine Sulfate Oral Solution is in a group of drugs called narcotic pain relievers. Codeine Sulfate Oral Solution is only for people who have mild to moderately severe pain.
- Codeine Sulfate Oral Solution is a federally controlled substance (CII) because it is an opioid pain medicine that can be abused by people who abuse prescription medicines or street drugs.
- Prevent theft, misuse or abuse. Keep Codeine Sulfate Oral Solution in a safe place to keep it from being stolen. Codeine Sulfate can be a target for people who misuse or abuse prescription medicines or street drugs.
- Never give Codeine Sulfate Oral Solution to anyone else, even if they have the same symptoms you have. It may harm them or even cause death.
- Selling or giving away this medicine is against the law.
- It is not known if Codeine Sulfate Oral Solution is safe and effective in children under age 18 years of age.
### Who should not take Codeine Sulfate Oral Solution?
- Do not give Codeine Sulfate Oral Solution to a child to treat pain after tonsillectomy or adenoidectomy surgery.
- Do not take Codeine Sulfate Oral Solution if you:
- Are allergic to Codeine or any of the ingredients in Codeine Sulfate Oral Solution. See the end of this Medication guide for a complete list of ingredients in Codeine Sulfate Oral Solution.
- Are having an asthma attack or have severe asthma, trouble breathing, or lung problems.
- Have a bowel blockage, called paralytic ileus.
### What should I tell my healthcare provider before taking Codeine Sulfate?
- Before taking Codeine Sulfate Oral Solution, tell your healthcare provider if you:
- Have trouble breathing or lung problems
- Have had a head injury
- Have liver or kidney problems
- Have been told by your healthcare provider that you are a "rapid metabolizer" of certain medicines
- Have had adrenal gland problems, such as Addison's disease
- Have severe scoliosis that affects your breathing
- Have thyroid problems
- Have problems urinating or enlargement of your prostate
- Have had convulsions or seizures
- Have a past or present drinking problem or alcoholism
- Have severe mental problems
- Have constipation or other bowel problems
- Have problems with your pancreas or gallbladder
- Have past or present substance abuse or drug addiction
- Plan to have surgery
- Have any other medical conditions
- Are pregnant or plan to become pregnant. It is not known if Codeine Sulfate Oral Solution will harm your unborn baby. Talk to your healthcare provider if you are pregnant or plan to become pregnant. If you take Codeine Sulfate Oral Solution right before your baby is born, your newborn could have breathing problems. Your baby may also have withdrawal symptoms because his body has become used to the medicine.
- Symptoms of withdrawal in a newborn baby may include:
- Irritability
- Vomiting
- Weight loss
- Fever
- Diarrhea or more stools than normal
- Being very active
- Problems sleeping
- High pitched cry
- Shaking (tremors)
- Are breast-feeding or plan to breast-feed.
- See the box with Important information at the top of this Medication Guide.
- If you stop breast-feeding, your baby may have withdrawal symptoms. See the list of withdrawal symptoms above. If your baby has any of these symptoms you need to contact your healthcare provider right away. If you can not reach your healthcare provider, take your baby to your local hospital emergency room or call your local emergency medical service. You and your healthcare provider should decide if you will take Codeine Sulfate Oral Solution or breast-feed.
- Tell your healthcare provider about all the medicines you take, including prescription and non-prescription medicines, vitamins, and herbal supplements. Sometimes the doses of medicines that you take with Codeine Sulfate Oral Solution may need to be changed if used together. Codeine Sulfate Oral Solution and other medicines may affect each other causing serious side effects. Be especially careful about taking other medicines that make you sleepy such as:
- Sleeping pills
- Anti-depressants
- Other pain medicines
- Anticholinergic medicines
- Anti-nausea medicines
- Antibiotic or antifungal medicines
- Tranquilizers
- Heart medicines
- Antihistamines
- Anti-seizure medicines
- Anti-anxiety medicines
- Do not take Codeine Sulfate Oral Solution if you already take a monoamine oxidase inhibitor medicine (MAOI) or within 14 days after you stop taking an MAOI medicine.
- Do not take any new medicine while using Codeine Sulfate until you have talked with your healthcare provider or pharmacist. They will tell you if it is safe to take other medicines with Codeine Sulfate Oral Solution.
- Ask your healthcare provider if you are not sure if your medicine is one listed above.
- Know the medicines you take. Keep a list of them and show it to your healthcare provider and pharmacist when you get a new medicine.
### How should I take Codeine Sulfate Oral Solution?
- See "What is the most important information I should know about Codeine Sulfate Oral Solution?"
- Take Codeine Sulfate Oral Solution exactly as prescribed. Do not change your dose unless your healthcare provider tells you to. Your healthcare provider may change your dose after seeing how the medicine affects you. Call your healthcare provider if your pain is not well controlled with your prescribed dose of Codeine Sulfate Oral Solution. You can take Codeine Sulfate Oral Solution with or without food.
- Make sure you understand exactly how to measure your dose. Always use the oral syringe provided with your Codeine Sulfate Oral Solution, 30 mg per 5 mL (6 mg/mL) to help make sure you measure the right amount. Ask your healthcare provider or pharmacist if you are not sure what dose of Codeine Sulfate Oral Solution you should take or if you are not sure how to use the oral syringe.
- Do not stop taking Codeine Sulfate Oral Solution suddenly. If you have been taking Codeine Sulfate Oral Solution for more than a few weeks, stopping Codeine Sulfate Oral Solution suddenly can make you sick with withdrawal symptoms (for example, nausea, vomiting, diarrhea, anxiety, and shivering). If your healthcare provider decides you no longer need Codeine Sulfate Oral Solution, ask how to slowly reduce this medicine. Do not stop taking Codeine Sulfate Oral Solution without talking to your healthcare provider.
- If you take too much Codeine Sulfate Oral Solution, call your healthcare provider or go to the nearest hospital emergency room right away.
- If you miss one dose of Codeine Sulfate Oral Solution you can take the dose when you remember it if you have pain, or you can wait for the next dose.
- Talk with your healthcare provider regularly about your pain to see if you still need to take Codeine Sulfate.
### What should I avoid while taking Codeine Sulfate Oral Solution?
- You should not drink alcohol while using Codeine Sulfate Oral Solution. Drinking alcohol with Codeine Sulfate Oral Solution may increase your risk of having dangerous side effects or death.
- Do not drive, operate heavy machinery, or do other dangerous activities, especially when you start taking Codeine Sulfate Oral Solution and when your dose is changed, until you know how Codeine Sulfate Oral Solution affects you. Codeine Sulfate Oral Solution can make you sleepy. Ask your healthcare provider to tell you when it is okay to do these activities.
### What are the possible side effects of Codeine Sulfate Oral Solution?
- See "What is the most important information I should know about Codeine Sulfate Oral Solution?"
- Codeine Sulfate Oral Solution can cause serious breathing problems that can become life-threatening, especially if Codeine Sulfate is used the wrong way. Call your healthcare provider or get help right away if:
- Your breathing slows down
- You have shallow breathing (little chest movement with breathing)
- You feel faint, dizzy, confused, or
- You have any other unusual symptoms
- These can be symptoms that you have taken too much Codeine Sulfate Oral Solution (overdose) or the dose is too high for you. These symptoms may lead to serious problems or death if not treated right away.
- Codeine Sulfate Oral Solution can cause your blood pressure to drop. This can make you feel dizzy if you get up fast from sitting or lying down. Low blood pressure is also more likely to happen if you take other medicines that can also lower your blood pressure. Severe low blood pressure can happen if you lose blood or take certain other medicines.
- There is a risk of abuse or addiction with Codeine Sulfate Oral Solution. The risk is higher if you are or have been addicted to or abused other medicines, street drugs, or alcohol, or if you have a history of mental problems.
- Codeine Sulfate Oral Solution can cause physical dependence. Do not stop taking Codeine Sulfate Oral Solution or any other opioid without talking to your healthcare provider about how to slowly stop your medicine. You could become sick with uncomfortable withdrawal symptoms because your body has become used to these medicines. Physical dependence is not the same as drug addiction. Tell your healthcare provider if you have any of these symptoms of withdrawal while slowly stopping Codeine Sulfate Oral Solution:
- Feel restless
- Dilated pupils of your eyes
- Tearing eyes
- Feel irritable or anxious
- Runny nose
- Trouble sleeping
- Yawning
- Increase in your blood pressure
- Sweating
- Faster breathing, or faster heart beats
- Chills or hair on your arms "stand up"
- Nausea, loss of appetite, vomiting, diarrhea, stomach-area (abdominal) cramps
- Muscle aches, backache
- Common side effects of Codeine Sulfate Oral Solution include:
- Constipation
- Dizziness
- Nausea
- Drowsiness
- Sleepiness
- Vomiting
- Lightheadedness
- Sweating
- Constipation (not often enough or hard bowel movements) is a very common side effect of pain medicines from the opioid class. Talk to your healthcare provider about dietary changes, and the use of laxatives (medicines to treat constipation) and stool softeners to prevent or treat constipation while taking Codeine Sulfate Oral Solution.
- Tell your healthcare provider if you have any side effect that bothers you or that does not go away.
- These are not all the possible side effects of Codeine Sulfate Oral Solution. For more information, ask your healthcare provider or pharmacist.
- Call your healthcare provider for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088.
### How should I store Codeine Sulfate Oral Solution?
- Store Codeine Sulfate Oral Solution at room temperature, between 59°F to 86°F (15°C to 30°C), away from the light.
- Keep Codeine Sulfate Oral Solution out of the reach of children. Accidental overdose by a child is a medical emergency and can lead to death.
### General Information about Codeine Sulfate Oral Solution
- Medicines are sometimes prescribed for purposes other than those listed in a Medication Guide. Do not use Codeine Sulfate Oral Solution for a condition for which it was not prescribed. Do not give your Codeine Sulfate Oral Solution to other people, even if they have the same symptoms you have. Selling or giving away Codeine Sulfate Oral Solution may harm others, may cause death, and is against the law.
- This Medication Guide summarizes the most important information about Codeine Sulfate Oral Solution. If you would like more information, talk with your healthcare provider. You can ask your healthcare provider or pharmacist for information about Codeine Sulfate Oral Solution that is written for healthcare professionals.
- For more information about Codeine Sulfate Oral Solution, go to www.roxane.com, or call Roxane Laboratories, Inc. at 1-800-962-8364.
### What are the ingredients in Codeine Sulfate Oral Solution?
- Active ingredient: codeine sulfate
- Inactive ingredients: ascorbic acid, citric acid, disodium edetate, FD&C Red No. 40, FD&C Yellow No. 6, glycerin, Orange Flavor XBF-7098189 (artificial flavors, propylene glycol), sodium benzoate, sorbitol, sucralose, and water
- Instructions for Use
- Codeine Sulfate (koh-deen) (CII)
- Oral Solution
- Oral Syringe
- Important information about measuring Codeine Sulfate Oral Solution:
- Always use the oral syringe provided with your Codeine Sulfate Oral Solution to make sure you measure the right amount.
- Measure the dose of medicine from the widest part of the plunger. Do not measure from the narrow tip. See Figure 1.
- Remove the protective storage cap from the syringe.
- Insert the tip of the oral syringe into the medicine bottle.
- Pull back the plunger to the line that matches the dose prescribed by your healthcare provider.
- Remove the oral syringe from the medicine bottle.
- Take your medicine by slowly pushing the plunger until the oral syringe is empty.
- Replace the cap and oral syringe in a dry and clean place.
# Precautions with Alcohol
Alcohol-Codeine interaction has not been established. Talk to your doctor about the effects of taking alcohol with this medication.
# Brand Names
There is limited information regarding Codeine Brand Names in the drug label.
# Look-Alike Drug Names
There is limited information regarding Codeine Look-Alike Drug Names in the drug label.
# Drug Shortage Status
# Price | https://www.wikidoc.org/index.php/Codeine | |
e2607f9d69ab66deffadd579f6aa7fe91c104b49 | wikidoc | Cofilin | Cofilin
ADF/cofilin is a family of actin-binding proteins which disassembles actin filaments.
Actin-binding proteins regulate assembly and disassembly of actin filaments. Cofilin, a member of the ADF/cofilin family is actually a protein with 70% sequence homology to ADF, making it part of the ADF/cofilin family of small ADP-binding proteins . The protein binds to actin monomers and filaments, G actin and F actin, respectively. Cofilin causes depolymerization at the minus end of filaments, thereby preventing their reassembly. The protein is known to sever actin filaments by creating more positive ends on filament fragments. Cofilin/ADF(destrin) is likely to sever F-actin without capping and prefers ADP-actin. These monomers can be recycled by profilin, activating monomers to go back into filament form again by an ADP-to-ATP exchange. ATP-actin is then available for assembly .
# Structure
Cofilin alters F-actin structure to make it twisted. The structure is a helix, proposed to bind G-actin. ADF/Destrin fits better with a twist in F-actin between two actin subunits (see figure above). The levels of cofilin are shown in 'd' above. 4 indicates 40% and 1 indicates 10% by volume of cofilin. The silver portion of image 'd' is actin. The cofilin binding site includes subdomain 2. The twist in the structure causes strain at the actin-actin contact site. Four actin histidines near the cofilin binding site may be needed for cofilin/actin interaction, but pH sensitivity alone may not be enough of an explanation for the levels of interaction encountered. Cofilin is accommodated in ADP-F actin because of increased flexibility in this form of actin. Binding by both cofilin and ADF(destrin) causes the crossover length of the filament to be reduced. Therefore, strains increase filament dynamics and the level of filament fragmentation observed.
# Function
Cofilin is a ubiquitous actin-binding factor required for the reorganization of actin filaments. ADF/Cofilin family members bind G-actin monomers and depolymerize actin filaments through two mechanisms: severing and increasing off-rate for actin monomers from the pointed end. "Older" ADP/ADP-Pi actin filaments free of tropomyosin and proper pH are required for cofilin to function effectively. In the presence of readily available ATP-G-actin cofilin speeds-up actin polymerization via its actin-severing activity (providing free barbed ends for furtherer polymerization and nucleation by Arp2/3 complex). As a long-lasting in vivo effect, cofilin recycles older ADP-F-actin, helping cell to maintain ATP-G-actin pool for sustained motlity. pH, phosphorylation and phosphoinositides regulate cofilin’s binding and associating activity with actin
## What Cofilin Functions with
The Arp2/3 complex and cofilin work together to reorganize the actin filaments in the cytoskeleton. Arp 2/3, an actin binding proteins complex, binds to the side of ATP-F-actin near the growing barbed end of the filament, causing nucleation of a new F-actin branch, while cofilin-driven depolymerization takes place after dissociating from the Arp2/3 complex. They also work together to reorganize microtubules in order to traffic more proteins by vesicle to continue the growth of filaments.
Cofilin also binds with other proteins such as myosin, tropomyosin, α-actinin, gelsolin and scruin. These proteins compete with cofilin for actin binding.
## In a Model Organism
ADF/cofilins are found in ruffling membranes and at the leading edge of mobile cells. In particular, ADF/cofilin promotes disassembly of the filament at the rear of the brush in Xenopus laevis lamellipodia, a protrusion from fibroblast cells characterized by actin networks. Subunits are added to barbed ends and lost from rear-facing pointed ends. Increasing the rate constant, k, for actin dissociation from the pointed ends was found to sever actin filaments. Through this experimentation, it was found that ATP or ADP-Pi are probably involved in binding to actin filaments. | Cofilin
ADF/cofilin is a family of actin-binding proteins which disassembles actin filaments.
Actin-binding proteins regulate assembly and disassembly of actin filaments[1]. Cofilin, a member of the ADF/cofilin family is actually a protein with 70% sequence homology to ADF, making it part of the ADF/cofilin family of small ADP-binding proteins [2]. The protein binds to actin monomers and filaments, G actin and F actin, respectively[3]. Cofilin causes depolymerization at the minus end of filaments, thereby preventing their reassembly. The protein is known to sever actin filaments by creating more positive ends on filament fragments[1]. Cofilin/ADF(destrin) is likely to sever F-actin without capping [2] and prefers ADP-actin. These monomers can be recycled by profilin, activating monomers to go back into filament form again by an ADP-to-ATP exchange. ATP-actin is then available for assembly [1].
# Structure
Cofilin alters F-actin structure to make it twisted. The structure is a helix, proposed to bind G-actin. ADF/Destrin fits better with a twist in F-actin between two actin subunits (see figure above). The levels of cofilin are shown in 'd' above. 4 indicates 40% and 1 indicates 10% by volume of cofilin. The silver portion of image 'd' is actin. The cofilin binding site includes subdomain 2. The twist in the structure causes strain at the actin-actin contact site. Four actin histidines near the cofilin binding site may be needed for cofilin/actin interaction, but pH sensitivity alone may not be enough of an explanation for the levels of interaction encountered. Cofilin is accommodated in ADP-F actin because of increased flexibility in this form of actin. Binding by both cofilin and ADF(destrin) causes the crossover length of the filament to be reduced. Therefore, strains increase filament dynamics and the level of filament fragmentation observed[2].
# Function
Cofilin is a ubiquitous actin-binding factor required for the reorganization of actin filaments. ADF/Cofilin family members bind G-actin monomers and depolymerize actin filaments through two mechanisms: severing[4] and increasing off-rate for actin monomers from the pointed end[5]. "Older" ADP/ADP-Pi actin filaments free of tropomyosin and proper pH are required for cofilin to function effectively. In the presence of readily available ATP-G-actin cofilin speeds-up actin polymerization via its actin-severing activity (providing free barbed ends for furtherer polymerization and nucleation by Arp2/3 complex)[6]. As a long-lasting in vivo effect, cofilin recycles older ADP-F-actin, helping cell to maintain ATP-G-actin pool for sustained motlity. pH, phosphorylation and phosphoinositides regulate cofilin’s binding and associating activity with actin[3]
## What Cofilin Functions with
The Arp2/3 complex and cofilin work together to reorganize the actin filaments in the cytoskeleton. Arp 2/3, an actin binding proteins complex, binds to the side of ATP-F-actin near the growing barbed end of the filament, causing nucleation of a new F-actin branch[6], while cofilin-driven depolymerization takes place after dissociating from the Arp2/3 complex[1]. They also work together to reorganize microtubules in order to traffic more proteins by vesicle to continue the growth of filaments[7].
Cofilin also binds with other proteins such as myosin, tropomyosin, α-actinin, gelsolin and scruin. These proteins compete with cofilin for actin binding[2].
## In a Model Organism
ADF/cofilins are found in ruffling membranes and at the leading edge of mobile cells[5]. In particular, ADF/cofilin promotes disassembly of the filament at the rear of the brush in Xenopus laevis lamellipodia, a protrusion from fibroblast cells characterized by actin networks. Subunits are added to barbed ends and lost from rear-facing pointed ends. Increasing the rate constant, k, for actin dissociation from the pointed ends was found to sever actin filaments. Through this experimentation, it was found that ATP or ADP-Pi are probably involved in binding to actin filaments[7]. | https://www.wikidoc.org/index.php/Cofilin | |
df84168220813345673729bd98cc28ce00562743 | wikidoc | Tacrine | Tacrine
# Overview
Tacrine is a parasympathomimetic and a centrally acting cholinesterase inhibitor (anticholinesterase). It was the first centrally-acting cholinesterase inhibitor approved for the treatment of Alzheimer's disease, and was marketed under the trade name Cognex. Tacrine was first synthesised by Adrien Albert at the University of Sydney.
# Clinical use
Tacrine was the prototypical cholinesterase inhibitor for the treatment of Alzheimer's disease. Studies have found that it may have a small beneficial effect on cognition and other clinical measures, though adequate study data is limited and the clinical relevance of these findings is unclear.
The use of tacrine is limited by poor oral bioavailability, the necessity for four-times daily dosing, and considerable adverse drug reactions (including nausea, diarrhea, urinary incontinence and hepatotoxicity) such that few patients could tolerate therapeutic doses.
Other newer cholinesterase inhibitors, such as donepezil, are now preferred over tacrine.
# Overdosage/Toxicity
As stated above, overdosage of tacrine may giva rise to severe side effects such as nausea, vomiting, salivation, sweating, bradycardia, hypotension, collapse, and colvulsions. Tertiary anticholinergics, such as atropine, may be used as an antidote for overdose.
Major form of metabolism is in the liver via hydroxylation of benzylic carbon by CYP450. This forms the major metabolite 1-hydroxy-tacrine (velnacrine) which is still active. | Tacrine
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
# Overview
Tacrine is a parasympathomimetic and a centrally acting cholinesterase inhibitor (anticholinesterase). It was the first centrally-acting cholinesterase inhibitor approved for the treatment of Alzheimer's disease, and was marketed under the trade name Cognex. Tacrine was first synthesised by Adrien Albert at the University of Sydney.
# Clinical use
Tacrine was the prototypical cholinesterase inhibitor for the treatment of Alzheimer's disease. Studies have found that it may have a small beneficial effect on cognition and other clinical measures, though adequate study data is limited and the clinical relevance of these findings is unclear.[1][2]
The use of tacrine is limited by poor oral bioavailability, the necessity for four-times daily dosing, and considerable adverse drug reactions (including nausea, diarrhea, urinary incontinence and hepatotoxicity) such that few patients could tolerate therapeutic doses.[3]
Other newer cholinesterase inhibitors, such as donepezil, are now preferred over tacrine.
# Overdosage/Toxicity
As stated above, overdosage of tacrine may giva rise to severe side effects such as nausea, vomiting, salivation, sweating, bradycardia, hypotension, collapse, and colvulsions. Tertiary anticholinergics, such as atropine, may be used as an antidote for overdose.
Major form of metabolism is in the liver via hydroxylation of benzylic carbon by CYP450. This forms the major metabolite 1-hydroxy-tacrine (velnacrine) which is still active. | https://www.wikidoc.org/index.php/Cognex | |
b75e9764f38dc148e4437084b34c614aa48cb10a | wikidoc | Cold fX | Cold fX
Cold-fX is a natural cold and flu supplement claimed to strengthen the immune system. Health Canada recently approved a comprehensive treatment claim for Cold-fX, stating it "helps reduce the frequency, severity, and duration of cold & flu symptoms by boosting the immune system." It is believed to be the first medicine in Canada approved to fight colds and flu by boosting the immune system.
# The Discovery
A team of 25 international scientists in the field of phytomedicines and natural health products from the University of Alberta formed a company in 1992 to develop products for disease prevention. The team looked for ways to apply natural medicines of the East to the rigor and standardization of Western science.
These scientists identified a group of molecules in North American Ginseng (Panax quinquefolius) that produced the strongest immune-boosting effect of all the natural sources they had studied. A U.S. patent was granted for Cold-fX in 2002. In 1995, the scientists also developed an internationally recognized technology called ChemBioPrint that ensures that each capsule delivers precise chemical identity and biological activity consistently from batch to batch. This technology is an industry first for meaningful standardization.
# Clinical Evidence
Seven clinical trials have shown that COLD-fX is safe, and supports its intended use. Scientific studies have been published in nine peer-reviewed medical journals, including the Canadian Medical Association Journal. Some of the Cold-fX clinical trial findings include:
- significantly enhanced the body’s first line of defense: the Natural Killer (NK) and Macrophage immune cells
- significantly enhanced production of cytokines which are critical to activate the body’s second line of defense, the T-lymphocytes
- reduced the relative risk of recurrent colds and the flu
- significantly reduced the severity and duration of cold and flu symptoms
- was safe and effective in strengthening the immune system
In addition, International Olympic Committee (IOC) protocol testing demonstrated that Cold-fX did not contain or induce any banned substances. Five Canadian universities and a major U.S. medical centre are now conducting clinical trials and scientific studies on COLD-fX.
# Medical Recognition
Since its launch into the U.S., COLD-fX has received several reviews within the health/medical community:
- The University of California’s UC Berkeley Wellness Letter lauded COLD-fX for its “well designed” clinical trials, “promising results” and recent stamp of approval from Health Canada in a review of 60 nutritional supplements taken from a list of 29,000 products currently available in the U.S..
- The Centre for Science in the Public Interest,recently conducted a comprehensive medical review of 10 popular natural cold remedies. A leading public health watchdog and consumer advocacy group, it regularly publishes the Nutrition Action Healthletter, which is mailed to 900,000 subscribers in the United States and Canada. Its recent review concluded that “…Cold-fX is the only remedy we found with any evidence that it might improve your chances of getting through the cold and flu season without coming down with something.”
- The American Botanical Council (ABC), North America’s leading nonprofit research and education organization on herbal medicines, issued a report prepared by leading U.S. cold and flu experts concluding that Cold-fX demonstrated “impressive” benefits to users.
# Athlete Usage
Through the years, the popularity of COLD-fX has grown, helped in a major way by athlete endorsements. Over 300 elite Canadian athletes use COLD-fX regularly and 27 professional hockey teams and several football teams have also used the product. Company spokespeople include: Olympic Gold Medalist Clara Hughes, Hockey Legend Mark Messier, and Canadian hockey commentator Don Cherry, who were all approached by the company after they made it known that they were using COLD-fX. Other celebrities who have identified themselves as COLD-fX users include internationally renowned author Margaret Atwood, gifted theatrical vocalist Michael Burgess, Canadian Idol winner Eva Avila, actor Colin Mochrie and TV star and comedian Rick Mercer. | Cold fX
Template:Advert
Cold-fX is a natural cold and flu supplement claimed to strengthen the immune system. Health Canada recently approved a comprehensive treatment claim for Cold-fX, stating it "helps reduce the frequency, severity, and duration of cold & flu symptoms by boosting the immune system." It is believed to be the first medicine in Canada approved to fight colds and flu by boosting the immune system.
# The Discovery
A team of 25 international scientists in the field of phytomedicines and natural health products from the University of Alberta formed a company in 1992 to develop products for disease prevention. The team looked for ways to apply natural medicines of the East to the rigor and standardization of Western science.
These scientists identified a group of molecules in North American Ginseng (Panax quinquefolius) that produced the strongest immune-boosting effect of all the natural sources they had studied. A U.S. patent was granted for Cold-fX in 2002. In 1995, the scientists also developed an internationally recognized technology called ChemBioPrint that ensures that each capsule delivers precise chemical identity and biological activity consistently from batch to batch. This technology is an industry first for meaningful standardization.
# Clinical Evidence
Seven clinical trials have shown that COLD-fX is safe, and supports its intended use. Scientific studies have been published in nine peer-reviewed medical journals, including the Canadian Medical Association Journal. Some of the Cold-fX clinical trial findings include:
- significantly enhanced the body’s first line of defense: the Natural Killer (NK) and Macrophage immune cells
- significantly enhanced production of cytokines which are critical to activate the body’s second line of defense, the T-lymphocytes
- reduced the relative risk of recurrent colds and the flu
- significantly reduced the severity and duration of cold and flu symptoms
- was safe and effective in strengthening the immune system
In addition, International Olympic Committee (IOC) protocol testing demonstrated that Cold-fX did not contain or induce any banned substances. Five Canadian universities and a major U.S. medical centre are now conducting clinical trials and scientific studies on COLD-fX.
# Medical Recognition
Since its launch into the U.S., COLD-fX has received several reviews within the health/medical community:
- The University of California’s UC Berkeley Wellness Letter lauded COLD-fX for its “well designed” clinical trials, “promising results” and recent stamp of approval from Health Canada in a review of 60 nutritional supplements taken from a list of 29,000 products currently available in the U.S..
- The Centre for Science in the Public Interest,recently conducted a comprehensive medical review of 10 popular natural cold remedies. A leading public health watchdog and consumer advocacy group, it regularly publishes the Nutrition Action Healthletter, which is mailed to 900,000 subscribers in the United States and Canada. Its recent review concluded that “…Cold-fX is the only remedy we found with any evidence that it might improve your chances of getting through the cold and flu season without coming down with something.”
- The American Botanical Council (ABC), North America’s leading nonprofit research and education organization on herbal medicines, issued a report prepared by leading U.S. cold and flu experts concluding that Cold-fX demonstrated “impressive” benefits to users.
# Athlete Usage
Through the years, the popularity of COLD-fX has grown, helped in a major way by athlete endorsements. Over 300 elite Canadian athletes use COLD-fX regularly and 27 professional hockey teams and several football teams have also used the product. Company spokespeople include: Olympic Gold Medalist Clara Hughes, Hockey Legend Mark Messier, and Canadian hockey commentator Don Cherry, who were all approached by the company after they made it known that they were using COLD-fX. Other celebrities who have identified themselves as COLD-fX users include internationally renowned author Margaret Atwood, gifted theatrical vocalist Michael Burgess, Canadian Idol winner Eva Avila, actor Colin Mochrie and TV star and comedian Rick Mercer. | https://www.wikidoc.org/index.php/Cold_fX | |
f89a4098a76390c92fa9b9e8532a70979c703506 | wikidoc | Colicin | Colicin
A colicin is a type of bacteriocin.
Colicins are composed of three globular domains. One domain regulates the target and binds to the receptor on the sensitive cell. The second is involved with translocation, co-opting the machinery of the target cell. The third is the 'killing' domain and may produce a pore in the target cell membrane, or act as a nuclease to chop up the DNA or RNA of the target cell. Because they target specific receptors and use specific translocation machinery, cells can make themselves resistant to the colicin by repressing or deleting the genes for these proteins. Such resistant cells may suffer the lack of a key nutrient (such as iron or vitamin B) but benefit by not being killed. Colicins exhibit a '1-hit killing kinetic' which doesn't necessarily mean a single molecule is sufficient to kill, but certainly that it only takes a small number. In his Nobel Laureate speech, Salvador E. Luria, 1969, speculated that colicins could only be this toxic by causing a domino effect that destabilized the cell membrane He was not entirely correct, but pore-forming colicins do de-polarize the membrane and thus eliminate the energy source for the cell. The colicins are highly effective toxins.
Virtually all colicins are carried on plasmids. There are two general classes of colicinogenic plasmids, large, low-copy number plasmids, and small high copy number plasmids. The larger plasmids carry other genes as well as the colicin operon. The colicin operons are generally organized with several major genes. These include an immunity gene, a colicin structural gene, and a BRP (bacteriocin release protein), or lysis, gene. The immunity gene is often produced constitutively, while the BRP is generally produced only as a read-through of the stop codon on the colicin structural gene. The colicin itself is repressed by the SOS response and may be regulated in other ways as well.
Research indicates that retaining the colicin plasmid is very important for cells that live with their relatives, because if a cell loses the immunity gene, it quickly becomes subject to destruction by circulating colicin. At the same time, colicin is only released from a producing cell by the use of the lysis protein, which results in that cell's death. This suicidal production mechanism would appear to be very costly, except for the fact that it is regulated by the SOS response, which responds to significant DNA damage. In short, colicin production may only occur in terminally-ill cells. Still these matters require further research. | Colicin
A colicin is a type of bacteriocin.
Colicins[1] are composed of three globular domains. One domain regulates the target and binds to the receptor on the sensitive cell. The second is involved with translocation, co-opting the machinery of the target cell. The third is the 'killing' domain and may produce a pore in the target cell membrane, or act as a nuclease to chop up the DNA or RNA of the target cell. Because they target specific receptors and use specific translocation machinery, cells can make themselves resistant to the colicin by repressing or deleting the genes for these proteins. Such resistant cells may suffer the lack of a key nutrient (such as iron or vitamin B) but benefit by not being killed. Colicins exhibit a '1-hit killing kinetic' which doesn't necessarily mean a single molecule is sufficient to kill, but certainly that it only takes a small number. In his Nobel Laureate speech, Salvador E. Luria, 1969, speculated that colicins could only be this toxic by causing a domino effect that destabilized the cell membrane [2] He was not entirely correct, but pore-forming colicins do de-polarize the membrane and thus eliminate the energy source for the cell. The colicins are highly effective toxins.
Virtually all colicins are carried on plasmids. There are two general classes of colicinogenic plasmids, large, low-copy number plasmids, and small high copy number plasmids. The larger plasmids carry other genes as well as the colicin operon. The colicin operons are generally organized with several major genes. These include an immunity gene, a colicin structural gene, and a BRP (bacteriocin release protein), or lysis, gene. The immunity gene is often produced constitutively, while the BRP is generally produced only as a read-through of the stop codon on the colicin structural gene. The colicin itself is repressed by the SOS response and may be regulated in other ways as well.
Research indicates that retaining the colicin plasmid is very important for cells that live with their relatives, because if a cell loses the immunity gene, it quickly becomes subject to destruction by circulating colicin. At the same time, colicin is only released from a producing cell by the use of the lysis protein, which results in that cell's death. This suicidal production mechanism would appear to be very costly, except for the fact that it is regulated by the SOS response, which responds to significant DNA damage. In short, colicin production may only occur in terminally-ill cells. Still these matters require further research. | https://www.wikidoc.org/index.php/Colicin | |
93bece5b3453c6f42fadeeeab8f6833d944cee0e | wikidoc | Colloid | Colloid
# Overview
A Colloid or colloidal dispersion is a type of heterogeneous mixture. A colloid consists of two separate phases: a dispersed phase and a continuous phase. In a colloid, the dispersed phase is made of tiny particles or droplets that are distributed evenly throughout the continuous phase. The size of the dispersed phase particles are between 1 nm and 1000 nm in at least one dimension. Homogeneous mixtures with a dispersed phase in this size range may be called colloidal aerosols, colloidal emulsions, colloidal foams, colloidal dispersions or hydrosols. The dispersed phase particles or droplets are largely affected by the surface chemistry present in the colloid.
Because the size of the dispersed phase may be hard to measure, and because colloids look like solutions, colloids are sometimes characterized by their properties. For example, if a colloid has a solid phase dispersed in a liquid, the solid particles will not pass through a membrane, whereas the dissolved ions or molecules of a solution will pass through a membrane. In other words, dissolved components will diffuse through a membrane through which dispersed colloidal particles will not.
Some colloids are translucent because of the Tyndall effect, which is the scattering of light by particles in the colloid. Other colloids may be opaque or have a slight color.
Many familiar substances, including butter, milk, cream, aerosols (fog, smog, smoke), asphalt, inks, paints, glues, and sea foam are colloids. This field of study was introduced in 1861 by Scottish scientist Thomas Graham.
# Classification of colloids
Colloids can be classified as follows:
# Interaction between colloid particles
The following forces play an important role in the interaction of colloid particles:
- Excluded Volume Repulsion: This refers to the impossibility of any overlap between hard particles.
- Electrostatic interaction: Colloidal particles often carry an electrical charge and therefore attract or repel each other. The charge of both the continuous and the dispersed phase, as well as the mobility of the phases are factors affecting this interaction.
- van der Waals forces: This is due to interaction between two dipoles which are either permanent or induced. Even if the particles do not have a permanent dipole, fluctuations of the electron density gives rise to a temporary dipole in a particle. This temporary dipole induces a dipole in particles nearby. The temporary dipole and the induced dipoles are then attracted to each other. This is known as van der Waals force and is always present, is short range and is attractive.
- Entropic forces: According to the second law of thermodynamics, a system progresses to a state in which entropy is maximized. This can result in effective forces even between hard spheres.
- Steric forces between polymer-covered surfaces or in solutions containing non-adsorbing polymer can modulate interparticle forces, producing an additional repulsive steric stabilization force or attractive depletion force between them.
# Stabilization of a colloidal dispersion
Stabilization serves to prevent colloids from aggregating. Steric stabilization and electrostatic stabilization are the two main mechanisms for colloid stabilization. Electrostatic stabilization is based on the mutual repulsion of like electrical charges. Different phases generally have different charge affinities, so that a charge double-layer forms at any interface. Small particle sizes lead to enormous surface areas, and this effect is greatly amplified in colloids. In a stable colloid, mass of a dispersed phase is so low that its buoyancy or kinetic energy is too little to overcome the electrostatic repulsion between charged layers of the dispersing phase. The charge on the dispersed particles can be observed by applying an electric field: all particles migrate to the same electrode and therefore must all have the same sign charge!
# Destabilizing a colloidal dispersion
Unstable colloidal dispersions form flocs as the particles aggregate due to interparticle attractions. In this way photonic glasses can be grown. This can be accomplished by a number of different methods:
- Removal of the electrostatic barrier that prevents aggregation of the particles. This can be accomplished by the addition of salt to a suspension or changing the pH of a suspension to effectively neutralize or "screen" the surface charge of the particles in suspension. This removes the repulsive forces that keep colloidal particles separate and allows for coagulation due to van der Waals forces.
- Addition of a charged polymer flocculant. Polymer flocculants can bridge individual colloidal particles by attractive electrostatic interactions. For example, negatively charged colloidal silica particles can be flocculated by the addition of a positively charged polymer.
- Addition of nonadsorbed polymers called depletants that cause aggregation due to entropic effects.
- Physical deformation of the particle (e.g. stretching) may increase the van der Waals forces more than stabilization forces (such as electrostatic) resulting coagulation of colloids at certain orientations.
Unstable colloidal suspensions of low volume fraction form clustered liquid suspensions wherein individual clusters of particles fall to the bottom of the suspension (or float to the top if the particles are less dense than the suspending medium) once the clusters are of sufficient size for the Brownian forces that work to keep the particles in suspension to be overcome by gravitational forces. However, colloidal suspensions of higher volume fraction form colloidal gels with viscoelastic properties. Viscoelastic colloidal gels such as toothpaste flow like liquids under shear but maintain their shape when shear is removed. It is for this reason that toothpaste can be squeezed from a toothpaste tube, but stays on the toothbrush after it is applied.
# Measuring intensity of colloids
The intensity of colloids can be measured by a UV-Visable spectophotometer.
# Colloids as a model system for atoms
In physics, colloids are an interesting model system for atoms. Micron-scale colloidal particles are large enough to be observed by optical techniques such as confocal microscopy. Many of the forces that govern the structure and behavior of matter such as excluded volume interactions or electrostatic forces govern the structure and behavior of colloidal suspensions. For example, the same techniques that can be used to model ideal gases can be used to model the behavior of a hard sphere colloidal suspension. Additionally, phase transitions in colloidal suspensions can be studied in real time using optical techniques and are analogous to phase transitions in liquids.
# Colloids in biology
In the early 20th century, before enzymology was well understood, colloids were thought to be the key to the operation of enzymes; i.e., the addition of small quantities of an enzyme to a quantity of water would, in some fashion yet to be specified, subtly alter the properties of the water so that it would break down the enzyme's specific substrate, such as a solution of ATPase breaking down ATP. Furthermore, life itself was explainable in terms of the aggregate properties of all the colloidal substances that make up an organism. As more detailed knowledge of biology and biochemistry developed, of course, the colloidal theory was replaced by the macromolecular theory, which explains an enzyme as a collection of identical huge molecules that act as very tiny machines, freely moving about between the water molecules of the solution and individually operating on the substrate, no more mysterious than a factory full of machinery. The properties of the water in the solution are not altered, other than the simple osmotic changes that would be caused by the presence of any solute. | Colloid
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
# Overview
A Colloid or colloidal dispersion is a type of heterogeneous mixture. A colloid consists of two separate phases: a dispersed phase and a continuous phase. In a colloid, the dispersed phase is made of tiny particles or droplets that are distributed evenly throughout the continuous phase. The size of the dispersed phase particles are between 1 nm and 1000 nm in at least one dimension. Homogeneous mixtures with a dispersed phase in this size range may be called colloidal aerosols, colloidal emulsions, colloidal foams, colloidal dispersions or hydrosols. The dispersed phase particles or droplets are largely affected by the surface chemistry present in the colloid.
Because the size of the dispersed phase may be hard to measure, and because colloids look like solutions, colloids are sometimes characterized by their properties. For example, if a colloid has a solid phase dispersed in a liquid, the solid particles will not pass through a membrane, whereas the dissolved ions or molecules of a solution will pass through a membrane. In other words, dissolved components will diffuse through a membrane through which dispersed colloidal particles will not.
Some colloids are translucent because of the Tyndall effect, which is the scattering of light by particles in the colloid. Other colloids may be opaque or have a slight color.
Many familiar substances, including butter, milk, cream, aerosols (fog, smog, smoke), asphalt, inks, paints, glues, and sea foam are colloids. This field of study was introduced in 1861 by Scottish scientist Thomas Graham.
# Classification of colloids
Colloids can be classified as follows:
# Interaction between colloid particles
The following forces play an important role in the interaction of colloid particles:
- Excluded Volume Repulsion: This refers to the impossibility of any overlap between hard particles.
- Electrostatic interaction: Colloidal particles often carry an electrical charge and therefore attract or repel each other. The charge of both the continuous and the dispersed phase, as well as the mobility of the phases are factors affecting this interaction.
- van der Waals forces: This is due to interaction between two dipoles which are either permanent or induced. Even if the particles do not have a permanent dipole, fluctuations of the electron density gives rise to a temporary dipole in a particle. This temporary dipole induces a dipole in particles nearby. The temporary dipole and the induced dipoles are then attracted to each other. This is known as van der Waals force and is always present, is short range and is attractive.
- Entropic forces: According to the second law of thermodynamics, a system progresses to a state in which entropy is maximized. This can result in effective forces even between hard spheres.
- Steric forces between polymer-covered surfaces or in solutions containing non-adsorbing polymer can modulate interparticle forces, producing an additional repulsive steric stabilization force or attractive depletion force between them.
# Stabilization of a colloidal dispersion
Stabilization serves to prevent colloids from aggregating. Steric stabilization and electrostatic stabilization are the two main mechanisms for colloid stabilization. Electrostatic stabilization is based on the mutual repulsion of like electrical charges. Different phases generally have different charge affinities, so that a charge double-layer forms at any interface. Small particle sizes lead to enormous surface areas, and this effect is greatly amplified in colloids. In a stable colloid, mass of a dispersed phase is so low that its buoyancy or kinetic energy is too little to overcome the electrostatic repulsion between charged layers of the dispersing phase. The charge on the dispersed particles can be observed by applying an electric field: all particles migrate to the same electrode and therefore must all have the same sign charge!
# Destabilizing a colloidal dispersion
Unstable colloidal dispersions form flocs as the particles aggregate due to interparticle attractions. In this way photonic glasses can be grown. This can be accomplished by a number of different methods:
- Removal of the electrostatic barrier that prevents aggregation of the particles. This can be accomplished by the addition of salt to a suspension or changing the pH of a suspension to effectively neutralize or "screen" the surface charge of the particles in suspension. This removes the repulsive forces that keep colloidal particles separate and allows for coagulation due to van der Waals forces.
- Addition of a charged polymer flocculant. Polymer flocculants can bridge individual colloidal particles by attractive electrostatic interactions. For example, negatively charged colloidal silica particles can be flocculated by the addition of a positively charged polymer.
- Addition of nonadsorbed polymers called depletants that cause aggregation due to entropic effects.
- Physical deformation of the particle (e.g. stretching) may increase the van der Waals forces more than stabilization forces (such as electrostatic) resulting coagulation of colloids at certain orientations.
Unstable colloidal suspensions of low volume fraction form clustered liquid suspensions wherein individual clusters of particles fall to the bottom of the suspension (or float to the top if the particles are less dense than the suspending medium) once the clusters are of sufficient size for the Brownian forces that work to keep the particles in suspension to be overcome by gravitational forces. However, colloidal suspensions of higher volume fraction form colloidal gels with viscoelastic properties. Viscoelastic colloidal gels such as toothpaste flow like liquids under shear but maintain their shape when shear is removed. It is for this reason that toothpaste can be squeezed from a toothpaste tube, but stays on the toothbrush after it is applied.
# Measuring intensity of colloids
The intensity of colloids can be measured by a UV-Visable spectophotometer.
# Colloids as a model system for atoms
In physics, colloids are an interesting model system for atoms. Micron-scale colloidal particles are large enough to be observed by optical techniques such as confocal microscopy. Many of the forces that govern the structure and behavior of matter such as excluded volume interactions or electrostatic forces govern the structure and behavior of colloidal suspensions. For example, the same techniques that can be used to model ideal gases can be used to model the behavior of a hard sphere colloidal suspension. Additionally, phase transitions in colloidal suspensions can be studied in real time using optical techniques and are analogous to phase transitions in liquids.
# Colloids in biology
In the early 20th century, before enzymology was well understood, colloids were thought to be the key to the operation of enzymes; i.e., the addition of small quantities of an enzyme to a quantity of water would, in some fashion yet to be specified, subtly alter the properties of the water so that it would break down the enzyme's specific substrate, such as a solution of ATPase breaking down ATP. Furthermore, life itself was explainable in terms of the aggregate properties of all the colloidal substances that make up an organism. As more detailed knowledge of biology and biochemistry developed, of course, the colloidal theory was replaced by the macromolecular theory, which explains an enzyme as a collection of identical huge molecules that act as very tiny machines, freely moving about between the water molecules of the solution and individually operating on the substrate, no more mysterious than a factory full of machinery. The properties of the water in the solution are not altered, other than the simple osmotic changes that would be caused by the presence of any solute. | https://www.wikidoc.org/index.php/Colloid | |
a8b69af223275df9b2e198ee82d2c80b202f4292 | wikidoc | Comfrey | Comfrey
For the place, see Comfrey, Minnesota
Comfrey (also comphrey) is an important herb in organic gardening, having many medicinal and fertiliser uses.
# Description
Comfrey (Symphytum officinale L.) is a perennial herb of the family Boraginaceae with a black, turnip-like root and large, hairy broad leaves that bears small bell-shaped white, cream, purple or pink flowers. It is native to Europe, growing in damp, grassy places, and is widespread throughout the British Isles on river banks and ditches. Comfrey has long been recognised by both organic gardeners and herbalists for its great usefulness and versatility; of particular interest is the "Bocking 14" cultivar of Russian Comfrey (Symphytum x uplandicum). This strain was developed during the 1950s by Lawrence D Hills, the founder of the Henry Doubleday Research Association (the organic gardening organisation itself named after the Quaker pioneer who first introduced Russian Comfrey into Britain in the 1910s) following trials at Bocking, near Braintree, the original home of the organisation.
Other species include:
- Symphytum asperum, Prickly Comfrey, Rough Comfrey (synonym: S. asperrimum)
- Symphytum bulbosum, Bulbous Comfrey
- Symphytum caucasicum, Caucasian Comfrey
- Symphytum grandiflorum, Creeping Comfrey (synonym: S. ibericum)
- Symphytum orientale, White Comfrey
- Symphytum tauricum, Crimean Comfrey
- Symphytum tuberosum, Tuberous Comfrey
- Symphytum x uplandicum, Russian Comfrey, Healing Herb, Blackwort, Bruisewort, Wallwort, Gum Plant. (S. asperum x officinale, synonym: S. peregrinum)
# Propagation
Bocking 14 is sterile, and therefore will not set seed (one of its advantages over other cultivars as it will not spread out of control), thus is propagated from root cuttings. The gardener can produce their own 'offsets' from mature, strongly growing plants by driving a spade horizontally through the leaf clumps about 3 inches below the soil surface. This removes the crown which can then be split into pieces. The original plant will quickly recover, and each piece can be replanted with the growing points just below the soil surface, and will quickly grow into new plants. When choosing plants to divide ensure that they are strong healthy specimens with no signs of rust or mildew. When dividing comfrey plants take care not to spread root fragments around, or dispose of on the compost heap as each can re-root, and comfrey can be a very difficult plant to get rid of. Offsets can also be purchased by mail order from specialist nurseries in order to initially build up a stock of plants.
# Cultivation
The comfrey bed should be well prepared by weeding thoroughly, and dressing with manure if available. Offsets should be planted 2-3 feet apart with the growing points just below the surface, whilst root segments should be buried about 2 inches deep. Keep the bed well watered until the young plants are established. Comfrey should not be harvested in its first season as it needs to become established. Any flowering stems should be removed as these will weaken the plants in its first year. Comfrey should also be regularly watered until well established.
Comfrey is a fast growing plant, producing huge amounts of leaf during the growing season, hence is very nitrogen hungry. Although it will continue to grow no matter what, it will benefit from the addition of animal manure applied as a mulch, and can also be mulched with other nitrogen rich materials such as lawn mowings, and is one of the few plants that will tolerate the application of fresh urine diluted 50:50 with water, although this should not be regularly added as it may increase salt levels in the soil and have adverse effects on soil life such as worms. Mature comfrey plants can be harvested up to four or five times a year. They are ready for cutting when about 2 feet high, and, depending on seasonal conditions, this is usually in mid-Spring. Comfrey will rapidly regrow, and will be ready for further cutting about 5 weeks later. It is said that the best time to cut comfrey is shortly before flowering, for this is when it is at its most potent in terms of the nutrients that it offers. Comfrey can continue growing into mid-Autumn, but it is not advisable to continue taking cuttings after early Autumn in order to allow the plants to build up winter reserves. As the leaves die back and break down in winter, nutrients and minerals are transported back to the roots for use the following spring.
Comfrey should be harvested by using either shears a sickle or a scythe to cut the plant about 2 inches above the ground, taking care handling it because the leaves and stems are covered in hairs that can irritate the skin. It is advisable to wear gloves when handling comfrey. Despite being sterile, Bocking 14 Russian Comfrey will steadily increase in size. It is therefore advisable to split it up every few years (and at the same time propagate more plants that can be shared with fellow gardeners!). It is however difficult to remove comfrey once established as it is very deep rooting, and any fragments left in the soil will regrow. Rotovation can be successful, but may take several seasons. The best way to eradicate comfrey is to very carefully dig it out, removing as much of the root as possible. This is best done in hot, dry summer weather, wherein the dry conditions will help to kill off any remaining root stumps. Comfrey is generally trouble free once established, although weaker or stressed plants can suffer from comfrey rust or mildew. Both are fungal diseases, although they rarely seriously reduce plant growth and thus do not generally require control. However infected plants should not be used for propagation purposes.
# Medicinal uses
Dorothy Hall writes that 'Russian comfrey and garlic could together, according to natural health usage, almost halve the present ills of western civilisation' . An extravagant claim perhaps, but comfrey did indeed have a wealth of medicinal uses in bygone days. Contemporary herbalists view comfrey as an ambivalent and controversial herb that may offer therapeutic benefits but at the potential risk of liver toxicity.
One of its country names for comfrey was 'knitbone', a reminder of its traditional use in healing. Modern science confirms that comfrey can influence the course of bone ailments. The herb contains allantoin, a cell proliferant that speeds up the natural replacement of body cells. Comfrey was used to treat a wide variety of ailments ranging from bronchial problems, broken bones, sprains, arthritis, gastric and varicose ulcers, severe burns, acne and other skin conditions. It was reputed to have bone and teeth building properties in children, and have value in treating 'many female disorders'. In past times comfrey baths were popular to repair the hymen and thus 'restore virginity'. Constituents of comfrey also include mucilage, steroidal saponins, tannins, pyrrolizidine alkaloids, inulin, vitamin B12 and proteins.
Internal usage of comfrey should be avoided because it contains hepatotoxic pyrrolizidine alkaloids (PAs) (Note, there are also non-hepatotoxic pyrrolizidine alkaloids.). Use of comfrey can, because of these PAs, lead to veno-occlusive disease (VOD). VOD can in turn lead to liver failure, and comfrey, taken in extreme amounts, has been implicated in at least one death. In 2001, the United States Food and Drug Administration issued a warning against internal usage of herbal products containing comfrey.
Symphytine, one of the PAs in comfrey, causes cancer in rats.This was injection of the pure alkaloid. The whole plant has also been shown to induce precancerous changes in rats.
# Fertilizer uses
Comfrey is a particularly valuable source of fertility to the organic gardener. It is very deep rooted and acts as a dynamic accumulator, mining a host of nutrients from the soil. These are then made available through its fast growing leaves (up to 4-5 pounds per plant per cut) which, lacking fibre, quickly break down to a thick black liquid. There is also no risk of nitrogen robbery when comfrey is dug into the soil as the C:N ratio of the leaves is lower than that of well-rotted compost. Comfrey is an excellent source of potassium, an essential plant nutrient needed for flower, seeds and fruit production. Its leaves contain 2-3 times more potassium than farmyard manure, mined from deep in the subsoil, tapping into reserves that would not normally be available to plants.
There are various ways in which comfrey can be utilised as a fertiliser, these include:
- Comfrey for potatoes - freshly cut comfrey should be wilted for a day or two, then laid along potato trenches about 2 inches deep. Avoid using flowering stems as these can root. The leaves will rapidly break down and supply potassium rich fertiliser for the developing potato plants.
- Comfrey as a compost activator- include 2-3 inch deep layers of comfrey in the compost heap to encourage bacterial activity and help to heat the heap. Comfrey should not be added in quantity as it will quickly break down into a dark sludgey liquid that needs to be balanced with more fibrous, carbon rich material.
- Comfrey liquid fertiliser- can be produced by either rotting leaves down in rainwater for 4-5 weeks to produce a ready to use 'comfrey tea', or by stacking dry leaves under a weight in a container with a hole in the base. When the leaves decompose a thick black comfrey concentrate is collected. This must be diluted at 15:1 before use.
- Comfrey as a mulch- a 2 inch layer of comfrey leaves placed around a crop will slowly break down and release plant nutrients. it is especially useful for crops that need extra potassium, such as tomatoes, and also fruit bushes like gooseberries and currants.
- Comfrey potting mixture- originally devised using peat, environmental awareness has led to a leaf mold-based alternative being adopted instead. Two year old, well decayed leaf mold should be used, this will absorb the nutrient-rich liquid released by the decaying comfrey.
- In a black plastic sack alternate 3-4 inch layers of leaf mould and chopped comfrey leaves. Add a little dolomitic limestone to slightly raise pH. Leave for between 2-5 months depending on the season, checking that it does not dry out or become too wet. The mixture is ready when the comfrey leaves have rotted and are no longer visible. Use as a general potting compost, although it is too strong for seedlings. | Comfrey
For the place, see Comfrey, Minnesota
Comfrey (also comphrey) is an important herb in organic gardening, having many medicinal and fertiliser uses.
# Description
Comfrey (Symphytum officinale L.) is a perennial herb of the family Boraginaceae with a black, turnip-like root and large, hairy broad leaves that bears small bell-shaped white, cream, purple or pink flowers. It is native to Europe, growing in damp, grassy places, and is widespread throughout the British Isles on river banks and ditches. Comfrey has long been recognised by both organic gardeners and herbalists for its great usefulness and versatility; of particular interest is the "Bocking 14" cultivar of Russian Comfrey (Symphytum x uplandicum). This strain was developed during the 1950s by Lawrence D Hills, the founder of the Henry Doubleday Research Association (the organic gardening organisation itself named after the Quaker pioneer who first introduced Russian Comfrey into Britain in the 1910s) following trials at Bocking, near Braintree, the original home of the organisation.
Other species include:
- Symphytum asperum, Prickly Comfrey, Rough Comfrey (synonym: S. asperrimum)
- Symphytum bulbosum, Bulbous Comfrey
- Symphytum caucasicum, Caucasian Comfrey
- Symphytum grandiflorum, Creeping Comfrey (synonym: S. ibericum)
- Symphytum orientale, White Comfrey
- Symphytum tauricum, Crimean Comfrey
- Symphytum tuberosum, Tuberous Comfrey
- Symphytum x uplandicum, Russian Comfrey, Healing Herb, Blackwort, Bruisewort, Wallwort, Gum Plant. (S. asperum x officinale, synonym: S. peregrinum)
# Propagation
Bocking 14 is sterile, and therefore will not set seed (one of its advantages over other cultivars as it will not spread out of control), thus is propagated from root cuttings. The gardener can produce their own 'offsets' from mature, strongly growing plants by driving a spade horizontally through the leaf clumps about 3 inches below the soil surface. This removes the crown which can then be split into pieces. The original plant will quickly recover, and each piece can be replanted with the growing points just below the soil surface, and will quickly grow into new plants. When choosing plants to divide ensure that they are strong healthy specimens with no signs of rust or mildew. When dividing comfrey plants take care not to spread root fragments around, or dispose of on the compost heap as each can re-root, and comfrey can be a very difficult plant to get rid of. Offsets can also be purchased by mail order from specialist nurseries in order to initially build up a stock of plants.
# Cultivation
The comfrey bed should be well prepared by weeding thoroughly, and dressing with manure if available. Offsets should be planted 2-3 feet apart with the growing points just below the surface, whilst root segments should be buried about 2 inches deep. Keep the bed well watered until the young plants are established. Comfrey should not be harvested in its first season as it needs to become established. Any flowering stems should be removed as these will weaken the plants in its first year. Comfrey should also be regularly watered until well established.
Comfrey is a fast growing plant, producing huge amounts of leaf during the growing season, hence is very nitrogen hungry. Although it will continue to grow no matter what, it will benefit from the addition of animal manure applied as a mulch, and can also be mulched with other nitrogen rich materials such as lawn mowings, and is one of the few plants that will tolerate the application of fresh urine diluted 50:50 with water, although this should not be regularly added as it may increase salt levels in the soil and have adverse effects on soil life such as worms. Mature comfrey plants can be harvested up to four or five times a year. They are ready for cutting when about 2 feet high, and, depending on seasonal conditions, this is usually in mid-Spring. Comfrey will rapidly regrow, and will be ready for further cutting about 5 weeks later. It is said that the best time to cut comfrey is shortly before flowering, for this is when it is at its most potent in terms of the nutrients that it offers. Comfrey can continue growing into mid-Autumn, but it is not advisable to continue taking cuttings after early Autumn in order to allow the plants to build up winter reserves. As the leaves die back and break down in winter, nutrients and minerals are transported back to the roots for use the following spring.
Comfrey should be harvested by using either shears a sickle or a scythe to cut the plant about 2 inches above the ground, taking care handling it because the leaves and stems are covered in hairs that can irritate the skin. It is advisable to wear gloves when handling comfrey. Despite being sterile, Bocking 14 Russian Comfrey will steadily increase in size. It is therefore advisable to split it up every few years (and at the same time propagate more plants that can be shared with fellow gardeners!). It is however difficult to remove comfrey once established as it is very deep rooting, and any fragments left in the soil will regrow. Rotovation can be successful, but may take several seasons. The best way to eradicate comfrey is to very carefully dig it out, removing as much of the root as possible. This is best done in hot, dry summer weather, wherein the dry conditions will help to kill off any remaining root stumps. Comfrey is generally trouble free once established, although weaker or stressed plants can suffer from comfrey rust or mildew. Both are fungal diseases, although they rarely seriously reduce plant growth and thus do not generally require control. However infected plants should not be used for propagation purposes.
# Medicinal uses
Dorothy Hall writes that 'Russian comfrey and garlic could together, according to natural health usage, almost halve the present ills of western civilisation' [1]. An extravagant claim perhaps, but comfrey did indeed have a wealth of medicinal uses in bygone days. Contemporary herbalists view comfrey as an ambivalent and controversial herb that may offer therapeutic benefits but at the potential risk of liver toxicity.
One of its country names for comfrey was 'knitbone', a reminder of its traditional use in healing. Modern science confirms that comfrey can influence the course of bone ailments. [2] [3] [4] [5] The herb contains allantoin, a cell proliferant that speeds up the natural replacement of body cells. Comfrey was used to treat a wide variety of ailments ranging from bronchial problems, broken bones, sprains, arthritis, gastric and varicose ulcers, severe burns, acne and other skin conditions. It was reputed to have bone and teeth building properties in children, and have value in treating 'many female disorders'. In past times comfrey baths were popular to repair the hymen and thus 'restore virginity'. Constituents of comfrey also include mucilage, steroidal saponins, tannins, pyrrolizidine alkaloids, inulin, vitamin B12 and proteins.
Internal usage of comfrey should be avoided because it contains hepatotoxic pyrrolizidine alkaloids (PAs) (Note, there are also non-hepatotoxic pyrrolizidine alkaloids.). Use of comfrey can, because of these PAs, lead to veno-occlusive disease (VOD). VOD can in turn lead to liver failure, and comfrey, taken in extreme amounts, has been implicated in at least one death.[citation needed] In 2001, the United States Food and Drug Administration issued a warning against internal usage of herbal products containing comfrey. [6]
Symphytine, one of the PAs in comfrey, causes cancer in rats.[citation needed]This was injection of the pure alkaloid. The whole plant has also been shown to induce precancerous changes in rats. [7]
# Fertilizer uses
Comfrey is a particularly valuable source of fertility to the organic gardener. It is very deep rooted and acts as a dynamic accumulator, mining a host of nutrients from the soil. These are then made available through its fast growing leaves (up to 4-5 pounds per plant per cut) which, lacking fibre, quickly break down to a thick black liquid. There is also no risk of nitrogen robbery when comfrey is dug into the soil as the C:N ratio of the leaves is lower than that of well-rotted compost. Comfrey is an excellent source of potassium, an essential plant nutrient needed for flower, seeds and fruit production. Its leaves contain 2-3 times more potassium than farmyard manure, mined from deep in the subsoil, tapping into reserves that would not normally be available to plants.
There are various ways in which comfrey can be utilised as a fertiliser, these include:
- Comfrey for potatoes - freshly cut comfrey should be wilted for a day or two, then laid along potato trenches about 2 inches deep. Avoid using flowering stems as these can root. The leaves will rapidly break down and supply potassium rich fertiliser for the developing potato plants.
- Comfrey as a compost activator- include 2-3 inch deep layers of comfrey in the compost heap to encourage bacterial activity and help to heat the heap. Comfrey should not be added in quantity as it will quickly break down into a dark sludgey liquid that needs to be balanced with more fibrous, carbon rich material.
- Comfrey liquid fertiliser- can be produced by either rotting leaves down in rainwater for 4-5 weeks to produce a ready to use 'comfrey tea', or by stacking dry leaves under a weight in a container with a hole in the base. When the leaves decompose a thick black comfrey concentrate is collected. This must be diluted at 15:1 before use.
- Comfrey as a mulch- a 2 inch layer of comfrey leaves placed around a crop will slowly break down and release plant nutrients. it is especially useful for crops that need extra potassium, such as tomatoes, and also fruit bushes like gooseberries and currants.
- Comfrey potting mixture- originally devised using peat, environmental awareness has led to a leaf mold-based alternative being adopted instead. Two year old, well decayed leaf mold should be used, this will absorb the nutrient-rich liquid released by the decaying comfrey.
- In a black plastic sack alternate 3-4 inch layers of leaf mould and chopped comfrey leaves. Add a little dolomitic limestone to slightly raise pH. Leave for between 2-5 months depending on the season, checking that it does not dry out or become too wet. The mixture is ready when the comfrey leaves have rotted and are no longer visible. Use as a general potting compost, although it is too strong for seedlings. | https://www.wikidoc.org/index.php/Comfrey | |
70bec39ef0789fb7e4d7a2863bbd58d2eb269e82 | wikidoc | Mixture | Mixture
# Overview
In chemistry, a mixture is a substance made by combining two or more different materials without chemical reaction occurring. The objects do not bond together in a mixture. A mixture can usually be separated back into its original components. Some examples of mixtures are: fruit salad,ocean water and soil, some examples of heterogeneous mixtures are salt water, iron fillings, sulfur and salt mixed with sand. Mixtures are the product of a mechanical blending or mixing of chemical substances like elements and compounds, without chemical bonding or other chemical change, so that each ingredient substance retains it's own chemical properties and makeup.
While there are no chemical changes in a mixture, physical properties of a mixture, such as its melting point, may differ from those of its components. Mixtures can usually be separated by any mechanical means.
Mixtures are either homogeneous or heterogeneous.
# Homogeneous Mixtures
Homogeneous mixtures are mixtures that have definite, consistent properties. Particles are uniformly spread. For example, any amount of a given mixture has the same composition and properties. Examples are solutions and some alloys (but not all). A homogeneous mixture is a uniform mixture consisting of only one phase. Examples are gasoline and margarine.
## Solutions
A solution is when a homogeneous mixture of one or more substances (the solutes) dissolved in another substance (the solvent). Solutions have all particles within the size of atoms, small molecules or small ions, less than 1 nanometer (nm) in all dimensions. A common example would be a solid dissolving into a liquid (i.e. salt or sugar dissolving in water or gold into mercury). Liquids dissolve into one another, and sometimes liquids dissolve into gases, for example water vapor and the atmosphere. Common examples include fountain drinks, where carbon dioxide is trapped in the liquid through carbonation. Several solution properties collectively called colligative properties change as a function of solute concentration. Solubility is a compound property.
## Colloidal Dispersions
Colloids are another type of homogeneous mixture in which the particles of one or more components have at least one dimension in the range of 1 to 1000nm, larger than those in a solution but smaller than those in a suspension. In general, a colloid or colloidal dispersion is a substance with components of one or two phases. It creates the Tyndall effect when light passes through it. A colloid will not settle if left to sit. Jelly, milk, blood, paint, fog, and glue are examples of colloid dispersions.
# Heterogeneous Mixtures
Heterogeneous mixtures are mixtures with inconsistent, non-uniform composition. The parts of a heterogeneous composition can be mechanically separated from each other. Examples include salad, trail mix and granite.
## Suspensions
A heterogeneous mixture in which the particles, of at least one component is larger than 1μm (1000nm) in at least one dimension, larger than colloidal particles. Unlike colloids, suspensions will eventually settle. An example of a suspension would be sand in water. Particles of suspensions exhibit the Tyndall effect, that is, they are big enough to disperse light. | Mixture
# Overview
In chemistry, a mixture is a substance made by combining two or more different materials without chemical reaction occurring. The objects do not bond together in a mixture. A mixture can usually be separated back into its original components. Some examples of mixtures are: fruit salad,ocean water and soil, some examples of heterogeneous mixtures are salt water, iron fillings, sulfur and salt mixed with sand. Mixtures are the product of a mechanical blending or mixing of chemical substances like elements and compounds, without chemical bonding or other chemical change, so that each ingredient substance retains it's own chemical properties and makeup.[1]
While there are no chemical changes in a mixture, physical properties of a mixture, such as its melting point, may differ from those of its components. Mixtures can usually be separated by any mechanical means.
Mixtures are either homogeneous or heterogeneous.
# Homogeneous Mixtures
Homogeneous mixtures are mixtures that have definite, consistent properties. Particles are uniformly spread. For example, any amount of a given mixture has the same composition and properties. Examples are solutions and some alloys (but not all). A homogeneous mixture is a uniform mixture consisting of only one phase. Examples are gasoline and margarine.
## Solutions
A solution is when a homogeneous mixture of one or more substances (the solutes) dissolved in another substance (the solvent). Solutions have all particles within the size of atoms, small molecules or small ions, less than 1 nanometer (nm) in all dimensions.[2] A common example would be a solid dissolving into a liquid (i.e. salt or sugar dissolving in water or gold into mercury). Liquids dissolve into one another, and sometimes liquids dissolve into gases, for example water vapor and the atmosphere. Common examples include fountain drinks, where carbon dioxide is trapped in the liquid through carbonation. Several solution properties collectively called colligative properties change as a function of solute concentration. Solubility is a compound property.
## Colloidal Dispersions
Colloids are another type of homogeneous mixture in which the particles of one or more components have at least one dimension in the range of 1 to 1000nm, larger than those in a solution but smaller than those in a suspension.[2] In general, a colloid or colloidal dispersion is a substance with components of one or two phases. It creates the Tyndall effect when light passes through it. A colloid will not settle if left to sit. Jelly, milk, blood, paint, fog, and glue are examples of colloid dispersions.
# Heterogeneous Mixtures
Heterogeneous mixtures are mixtures with inconsistent, non-uniform composition. The parts of a heterogeneous composition can be mechanically separated from each other. Examples include salad, trail mix and granite.
## Suspensions
A heterogeneous mixture in which the particles, of at least one component is larger than 1μm (1000nm) in at least one dimension, larger than colloidal particles.[2] Unlike colloids, suspensions will eventually settle. An example of a suspension would be sand in water. Particles of suspensions exhibit the Tyndall effect, that is, they are big enough to disperse light. | https://www.wikidoc.org/index.php/Complex_mixtures | |
27e9485fe9f18580480c2663e4c1537d8420fd17 | wikidoc | Conatus | Conatus
Conatus (Template:PronEng; Latin: effort; endeavor; impulse, inclination, tendency; undertaking; striving) is a term used in early philosophies of psychology and metaphysics to refer to an innate inclination of a thing to continue to exist and enhance itself. This "thing" may be mind, matter or a combination of both. Over the millennia, many different definitions and treatments have been formulated by philosophers. The most important of these include the seventeenth century philosophers René Descartes, Baruch Spinoza, and Gottfried Leibniz, along with their Empiricist contemporary Thomas Hobbes. The conatus may refer to the instinctual "will to live" of animals or to various metaphysical theories of motion and inertia. Often the concept is associated with God's will in a pantheist view of Nature. The concept may be broken up into separate definitions for the mind and body, or even split up when discussing centrifugal force or inertia.
The history of the term conatus is that of a series of subtle tweaks in meaning and clarifications of scope developed over the course of two and a half millennia. After its formulation in ancient Greece, successive philosophers to adopt the term put their own personal twist on the concept, each developing the term differently such that it now has no concrete and universally accepted definition. The earliest authors to discuss conatus wrote primarily in Latin, and therefore used it not only as a technical term but as a common word and in a general sense. Conatus is, of course, more than simply a Latin participle. In archaic texts, the more technical usage is difficult to discern from the more common one, and they are also hard to differentiate in translation. In English translations, the term is italicized when used in the technical sense or translated and followed by conatus in brackets. Today, conatus is rarely used in the technical sense, since modern physics and evolutionary biology use concepts such as inertia and conservation of momentum that have superseded it. It has, however, been a notable influence on nineteenth and twentieth-century thinkers such as Friedrich Nietzsche, Louis Dumont and Arthur Schopenhauer.
# Classical origins
The Latin conatus comes from the verb conari, which is usually translated into English as, "to endeavor"; but the concept of the conatus was first developed by the Stoics (333–264 BCE) and Peripatetics (c. 335 BCE) before the Common Era. These groups used the word Template:Polytonic (hormê, translated in Latin by impetus) to describe the movement of the soul towards an object, and from which a physical act results . Classical thinkers, Marcus Tullius Cicero (106–43 BCE) and Diogenes Laertius (c. 235 BCE), expanded this principle to include an aversion to destruction, but continued to limit its application to the motivations of non-human animals. Diogenes Laertius, for example, specifically denied the application of the term to plants. Before the Renaissance, Thomas Aquinas (c. 1225–1274 CE), Duns Scotus (c. 1266–1308 CE) and Dante Alighieri (1265–1321 CE) expressed similar sentiments using the Latin words vult, velle or appetit as synonyms of conatus; indeed, all four terms may be used to translate the original Greek Template:Polytonic. Around 1700, Telesius and Campanella extended the ancient Greek notions and applied them to all objects, animate and inanimate.
First Aristotle, then Cicero and Laertius each alluded to a connection between the conatus and other emotions. In their view, the former induces the latter. They maintained that humans do not wish to do something because they think it "good", but rather they think it "good" because they want to do it. In other words, the cause of human desire is the natural inclination of a body to augment itself in accordance with the principles of the conatus.
# Medieval views
There is a traditional connection between conatus and motion itself. Aquinas and Abravanel (1265–1321) both related the concept directly to that which Augustine (354–430 CE) saw to be the "natural movements upward and downward or with their being balanced in an intermediate position" described in his De Civitate Dei, (c. 520 CE). They called this force that causes objects to rise or fall, "amor naturalis", or "natural love".
In the 6th century, John Philoponus (c. 490–c. 570 CE) criticized Aristotle's view of motion, noting the inconsistency between Aristotle's discussion of projectiles, where the medium of aether keeps projectiles going, and his discussion of the void, where there is no such medium and hence a body's motion should be impossible. Philoponus proposed that motion was not maintained by the action of some surrounding medium but by some property, or conatus implanted in the object when it was set in motion. This was not the modern concept of inertia, for there was still the need for an inherent power to keep a body in motion. This view was strongly opposed by Averroës and many scholastic philosophers who supported Aristotle. The Aristotelian view was also challenged in the Islamic world. For example, Ibn al-Haytham (Alhazen) seems to have supported Philoponus' views, while he developed a concept similar to inertia. His contemporary Avicenna also developed a concept similar to momentum.
Later, Jean Buridan (1300–1358) rejected the notion that this motion-generating property, which he named impetus, dissipated spontaneously. Buridan's position was that a moving object would be arrested by the resistance of the air and the weight of the body which would oppose its impetus. He also maintained that impetus increased with speed; thus, his initial idea of impetus was similar in many ways to the modern concept of momentum. Despite the obvious similarities to more modern ideas of inertia, Buridan saw his theory as only a modification to Aristotle's basic philosophy, maintaining many other peripatetic views, including the belief that there was still a fundamental difference between an object in motion and an object at rest. Buridan also maintained that impetus could be not only linear, but also circular in nature, causing objects such as celestial bodies to move in a circle.
# In Descartes
In the first half of the seventeenth century, René Descartes (1596–1650) began to develop a more modern, materialistic concept of the conatus, describing it as "an active power or tendency of bodies to move, expressing the power of God." Whereas the ancients used the term in a strictly anthropomorphic sense similar to voluntary "endeavoring" or "struggling" to achieve certain ends, and medieval Scholastic philosophers developed a notion of conatus as a mysterious intrinsic property of things, Descartes uses the term in a somewhat more mechanistic sense. More specifically, for Descartes, in contrast to Buridan, movement and stasis are two states of the same thing, not different things. Although there is much ambiguity in Descartes' notion of conatus, one can see here the beginnings of a move away from the attribution of desires and intentions to nature and its workings toward a more scientific and modern view.
Descartes rejects the teleological, or purposive, view of the material world that was dominant in the West from the time of Aristotle. The mind is not viewed by Descartes as part of the material world, and hence is not subject to the strictly mechanical laws of nature. Motion and rest, on the other hand, are properties of the interactions of matter according to eternally fixed mechanical laws. God only sets the whole thing in motion at the start, and later does not interfere except to maintain the dynamical regularities of the mechanical behavior of bodies. Hence there is no real teleology in the movements of bodies since the whole thing reduces to the law-governed collisions and their constant reconfigurations. The conatus is just the tendency of bodies to move when they collide with each other. God may set this activity in motion, but thereafter no new motion or rest can be created or destroyed.
Descartes specifies two varieties of the conatus: conatus a centro and conatus recedendi. Conatus a centro, or "tendency towards the center", is used by Descartes as a theory of gravity; conatus recendendi, or "tendency away from the center", represents the centrifugal forces. These tendencies are not to be thought of in terms of animate dispositions and intentions, nor as inherent properties or "forces" of things, but rather as a unifying, external characteristic of the physical universe itself which God has bestowed.
Descartes, in developing his First Law of Nature, also invokes the idea of a conatus se movendi, or "conatus of self-preservation". This law is a generalization of the principle of inertia, which was developed and experimentally demonstrated earlier by Galileo. The principle was formalized by Isaac Newton and made into the first of his three Laws of Motion fifty years after the death of Descartes. Descartes' version states: "Each thing, insofar as in it lies, always perseveres in the same state, and when once moved, always continues to move."
# In Hobbes
## Conatus and the psyche
Thomas Hobbes (1588–1679), too, worked off of the previous notions of the conatus principle. However, he criticized the previous definitions for failing to explain the origin of motion. Working toward this end became the primary focus of Hobbes' work in this area. Indeed, Hobbes "reduces all the cognitive functions of the mind to variations of its conative functions".
Furthermore, Hobbes describes emotion as the beginning of motion and the will as the sum of all emotions. This "will" forms the conatus of a body and its physical manifestation is the perceived "will to survive". In order that living beings may thrive, Hobbes says, "they seek peace and fight anything that threatens this peace". Hobbes also equates this conatus with "imagination", and states that a change in the conatus, or will, is the result of "deliberation".
## Conatus and physics
As in his psychological theory, Hobbes's physical conatus is an infinitesimal unit of motion. It is the beginning of motion: an inclination in a specified direction. The concept of impetus, as used by Hobbes, is defined in terms of this physical conatus. It is “a measure of the conatus exercised by a moving body over the course of time”. Resistance is caused by a contrary conatus; force is this motion plus “the magnitude of the body”. Hobbes also uses the word conatus to refer to the "restorative forces" which may cause springs, for example, to contract or expand. Hobbes claims there is some force inherent in these objects that inclines them to return to their previous state. Today, science attributes this phenomenon to material elasticity.
# In Spinoza
Spinoza (1632–1677) applies the idea of a conatus to the human body, psyche and both simultaneously, using a different term for each. When referring to psychological manifestations of the concept, he uses the term voluntas (will). When referring to the overarching concept, he uses the word appetitus (appetite). When referring to the bodily impulse, he uses the plain term conatus. Sometimes he expands the term and uses the whole phrase, conatus sese conservandi (the striving for self-preservation).
Spinoza asserts the existence of this general principle of a conatus in attempting to explain the "self-evident" truth that "nothing can be destroyed except by an external cause". To him, it is self-evident that "the definition of anything affirms, and does not negate, the thing's essence." This resistance to self-destruction is formulated by Spinoza in terms of a human striving to continue to exist; and conatus is the word he most often uses to describe this force.
In Spinoza's world-view, this principle is applicable to all things, and furthermore constitutes the very essence of objects, including the human mind and morals, for these are but finite modes of God. As he states in the Ethics (1677), the conatus is of "indefinite time"; it lasts as long as the object does. Spinoza uses conatus to describe an inclination of things to increase in power; rather than just continuing to exist statically, all beings must strive towards perfection. Further, all existing things act if and only if such action maintains or augments their existence. Spinoza also uses the term conatus to refer to rudimentary concepts of inertia, as Descartes had earlier. Since a thing cannot be destroyed without the action of external forces, motion and rest, too, exist indefinitely until disturbed.
## Psychological manifestation
The concept of the conatus, as used in Baruch Spinoza's philosophy of psychology, is derived from sources both ancient and medieval. Spinoza reformulates principles that the Stoics, Cicero, Laertius, and especially Hobbes and Descartes developed. One significant change he makes to Hobbes' theory is his belief that the conatus ad motum, (conatus to motion), is not mental, but material.
Spinoza, with his determinism, believes that man and nature must be unified under a consistent set of laws; God and nature are one, and there is no free will. Contrary to most philosophers of his time and in accordance with most of those of the present, Spinoza rejects the dualistic assumption that mind, intentionality, ethics and freedom are to be treated as things separate from the natural world of physical objects and events. His goal is to provide a unified explanation of all these things within a naturalistic framework, and his notion of conatus is central to this project. For example, an action is "free", for Spinoza, only if it arises from the essence and conatus of an entity. There can be no absolute, unconditioned freedom of the will, since all events in the natural world, including human actions and choices, are determined in accord with the natural laws of the universe, which are inescapable. However, an action can still be free in the sense that it is not constrained or otherwise subject to external forces.
Human beings are thus an integral part of nature. Spinoza explains seemingly irregular human behaviour as really "natural" and rational and motivated by this principle of the conatus. In the process, he replaces the notion of free will with the conatus, a principle that can be applied to all of nature and not just man.
### Emotions and affects
Spinoza's view of the relationship between the conatus and the human affects is not clear. Firmin DeBrabander, assistant professor of philosophy at the Maryland Institute College of Art, and Antonio Damasio, professor of neuroscience at the University of Southern California, both argue that the human affects arise from the conatus and the perpetual drive toward perfection. Indeed, Spinoza states in his Ethics that happiness, specifically, "consists in the human capacity to preserve itself." This "endeavor" is also characterized by Spinoza as the "foundation of virtue". Conversely, a person is saddened by anything that opposes his conatus.
The late David Bidney (1908–1987), professor at Yale University, disagrees. Bidney closely associates "desire", a primary affect, with the conatus principle of Spinoza. This view is backed by the Scholium of IIIP9 of the Ethics which states, "...Between appetite and desire there is no difference, except that desire is generally related to men insofar as they are conscious of the appetite. So desire can be defined as appetite together with consciousness of the appetite." According to Bidney, this desire is controlled by the other affects, pleasure and pain, and thus the conatus strives towards that which causes joy and avoids that which produces pain. Arthur Schopenhauer (1788–1860) agrees with Bidney in interpretation, but states in The World as Will and Representation (1819) that he disagrees with Spinoza because "according to the whole of my fundamental view, all this is a reversal of the true relation. The will is first and original; knowledge is merely added to it as an instrument belonging to the phenomenon of the will."
# In Leibniz
Gottfried Leibniz (1646–1716) was a student of Erhard Weigel (1625–1699) and learned of the conatus principle from him and from Hobbes, though Weigel used the word tendentia (Latin: tendency). Specifically, Leibniz uses the word conatus in his Exposition and Defence of the New System (1695) to describe a notion similar that of Hobbes, but he differentiates between the conatus of the body and soul, the first of which may only travel in a straight line by its own power, and the latter of which may "remember" more complicated motions.
For Leibniz, the problem of motion comes to a resolution of the paradox of Zeno.
Since motion is continuous, space must be infinitely divisible. In order for anything to begin moving at all, there must be some mind-like, voluntaristic property or force inherent in the basic constituents of the universe that propels them. This conatus is a sort of instantaneous or "virtual" motion that all things possess, even when they are static. Motion, meanwhile, is just the summation of all the conatuses that a thing has, along with the interactions of things. The conatus is to motion as a point is to space. The problem with this view is that an object that collides with another would not be able to bounce back, if the only force in play were the conatus. Hence, Leibniz was forced to postulate the existence of an aether that kept objects moving and allowed for elastic collisions. Leibniz' concept of a mind-like memory-less property of conatus, coupled with his rejection of atoms, eventually led to his theory of monads.
Leibniz also uses his concept of a conatus in developing the principles of the integral calculus, adapting the meaning of the term, in this case, to signify a mathematical analog of Newton's accelerative "force". By summing an infinity of such conatuses (i.e., what is now called integration), Leibniz could measure the effect of a continuous force. He defines impetus as the result of a continuous summation of the conatus of a body, just as the vis viva (or "living force") is the sum of the inactive vis mortua.
Based on the work of Kepler and probably Descartes, Leibniz develops a model of planetary motion based on the conatus principle, the idea of aether and a fluid vortex. This theory is expounded in the work Tentamen de motuum coelestium causis (1689). According to Leibniz, Kepler's analysis of elliptical orbits into a circular and a radial component can be explained by a "harmonic vortex" for the circular motion combined with a centrifugal force and gravity, both of which are examples of conatus, to account for the radial motion. Leibniz later defines the term monadic conatus, as the "state of change" through which his monads perpetually advance.
# Related usages and terms
Several other uses of the term conatus, apart from the primary ones mentioned above, have been formulated by various philosophers over the centuries. There are also some important related terms and concepts which have, more or less, similar meanings and usages. Giambattista Vico (1668–1744) defined conatus as the essence of human society, and also, in a more traditional, hylozoistic sense, as the generating power of movement which pervades all of nature. Nearly a century after the beginnings of modern science, Vico, inspired by Neoplatonism, explicitly rejected the principle of inertia and the laws of motion of the new physics. For him, nature was composed neither of atoms, as in the dominant view, nor of extension, as in Descartes, but of metaphysical points animated by a conatus principle provoked by God.
Arthur Schopenhauer (1788–1860) developed a philosophy that contains a principle notably similar to that of Hobbes's conatus. This principle, Wille zum Leben, or "Will to Live", described the specific phenomenon of an organism's self-preservation instinct. Schopenhauer qualified this, however, by suggesting that the Will to Live is not limited in duration. Rather, "the will wills absolutely and for all time", across generations. Friedrich Nietzsche (1844–1900), an early disciple of Schopenhauer, developed a separate principle which comes out of a rejection of the primacy of Schopenhauer's Will to Live and other notions of self-preservation. He called his version the Will to Power, or Wille zur Macht. Nietzsche criticized Spinoza's conatus principle, arguing that if true, it would allegedly favour a stagnant Universe. He thought "the opposite is true"; every organism strives not to just to persevere, but to "become more" than it is and to exert its creative strength. Spinoza's conatus, however, was much more alike to such an understanding than to simple self-preservation, as it was akin to empowerment.
Sigmund Freud (1856–1939), greatly depended on Spinoza's formulation of the conatus principle as a system of self preservation, though he never cited him directly in any of his published works. Around the same time, Henri Bergson (1859–1941), developed the principle of the élan vital, or "vital impulse", which was thought to aid in the evolution of organisms. This concept, which implies a fundamental driving force behind all life, is reminiscent of the conatus principle of Spinoza and others.
The cultural anthropologist Louis Dumont (1911–1988), described a cultural conatus built directly upon Spinoza's seminal definition in IIIP3 of his Ethics. The principle behind this derivative concept states that any given culture, "tends to persevere in its being, whether by dominating other cultures or by struggling against their domination."
# Modern significance
## Physical
After the advent of Newtonian physics, the concept of a conatus of all physical bodies was largely superseded by the principle of inertia and conservation of momentum. As Bidney states, "It is true that logically desire or the conatus is merely a principle of inertia ... the fact remains, however, that this is not Spinoza's usage". Likewise, conatus was used by many philosophers to describe other concepts which have slowly been made obsolete. Conatus recendendi, for instance, became the centrifugal force, and gravity is used where conatus a centro had been previously. Today, the topics with which conatus dealt are matters of science and are thus subject to inquiry by the scientific method.
## Biological
The archaic concept of conatus is today being reconciled with modern biology by scientists such as Antonio Damasio. . The conatus of today, however, is explained in terms of chemistry and neurology where, before, it was a matter of metaphysics and theurgy. This concept may be "constructed so as to maintain the coherence of a living organism's structures and functions against numerous life-threatening odds". This conatus is similar to modern notions of the libido in the Jungian sense, and the animal directive of self preservation.
### Systems theory
The Spinozistic conception of a conatus was a historical precursor to modern theories of autopoiesis in biological systems. In systems theory and the sciences in general, the concept of a conatus may be related to the phenomenon of emergence, whereby complex systems may spontaneously form from a multiplicity of more simple structures. The self-regulating and self-maintaining properties of biological and even social systems may thus be considered modern versions of Spinoza's conatus principle. ; however, the scope of the idea is definitely narrower today without the religious implications of the earlier variety.
# Citations
- ↑ Traupman 1966, p. 52
- ↑ Jump up to: 2.0 2.1 2.2 2.3 2.4 LeBuffe 2006
- ↑ Jump up to: 3.0 3.1 Wolfson 1934, p. 202
- ↑ Schopenhauer 1958, p. 357
- ↑ Jump up to: 5.0 5.1 5.2 Kollerstrom 1999, pp. 331–356
- ↑ Leibniz 1989, p. 118
- ↑ Clement of Alexandria, in SVF, III, 377; Cicero, De Officiis, I, 132; Seneca the Younger, Epistulae morales ad Lucilium, 113, 23
- ↑ Wolfson 1934, pp. 196,199,202
- ↑ Wolfson 1934, p. 204
- ↑ Wolfson 1934, pp. 197,200
- ↑ Sorabji 1988, pp. 227,228
- ↑ Leaman 1997
- ↑ Sabra 1994, pp. 133–136
- ↑ Salam & 1984 (1987), pp. 179–213
- ↑ Jump up to: 15.0 15.1 Sayili 1987, pp. 447–482
- ↑ Grant 1964, pp. 265–292>
- ↑ Jump up to: 17.0 17.1 17.2 Pietarinen 2000
- ↑ Garber 1992, pp. 150,154
- ↑ Goukroger 1980, pp. 178–179
- ↑ Grant 1981, pp. 140–44
- ↑ Gueroult 1980, pp. 120–34
- ↑ Garber 1992, pp. 180,184
- ↑ Wolfson 1934, p. 201
- ↑ Blackwell 1966, p. 220
- ↑ Bidney 1962, p. 91
- ↑ Schmitter 2006
- ↑ Hobbes & III, xiv, 2
- ↑ Jesseph 2006, p. 22
- ↑ Jesseph 2006, p. 35
- ↑ Osler 2001, pp. 157–61
- ↑ Wolfson 1934, p. 199
- ↑ Allison 1975, p. 126
- ↑ Duff 1903, chp. VII
- ↑ Spinoza, 1677 & Book III Prop 4
- ↑ Spinoza 1677, p. 66
- ↑ Allison 1975, p. 124
- ↑ Jump up to: 37.0 37.1 Lin 2004, p. 4
- ↑ Spinoza 1677, pp. 66–7
- ↑ Allison 1975, p. 126
- ↑ Allison 1975, p. 125
- ↑ Morgan 2006, p. ix
- ↑ Bidney 1962, p. 93
- ↑ Jarrett 1991, pp. 470–475
- ↑ Lachterman 1978
- ↑ Jump up to: 45.0 45.1 Allison 1975, p. 125
- ↑ Dutton 2006, chp. 5
- ↑ DeBrabander 2007, p. 20–1
- ↑ Damasio 2003, p. 170
- ↑ Damasio 2003, pp. 138–9
- ↑ Bidney 1962, p. 87
- ↑ Schopenhauer 1958, p. 292
- ↑ Leibniz 1988, p. 135
- ↑ Jump up to: 54.0 54.1 54.2 Gillespie 1971, pp. 159–161
- ↑ Jump up to: 55.0 55.1 Carlin 2004, pp. 365–379
- ↑ Duchesneau 1998, pp. 88–89
- ↑ Arthur 1994, sec. 3
- ↑ Goulding 2005, p. 22040
- ↑ Vico 1710, pp. 180–186
- ↑ Landucci 2004, pp. 1174,1175
- ↑ Rabenort 1911, p. 16
- ↑ Schopenhauer 1958, p. 568
- ↑ Durant & Durant 1963, chp. IX
- ↑ Damasio 2003, p. 260
- ↑ Bidney 1962, p. 398
- ↑ Schrift 2006, p. 13
- ↑ Polt 1996
- ↑ Bidney 1962, p. 88
- ↑ Bidney 1962
- ↑ Damasio 2003, p. 37
- ↑ Damasio 2003, p. 36
- ↑ Ziemke 2007, pp. 6
- ↑ Sandywell 1996, pp. 144–5
- ↑ Matthews 1991, pp. 110
# Bibliography
- Allison, Henry E. (1975), Benedict de Spinoza, San Diego: Twayne Publishers, ISBN 0-8057-2853-8.mw-parser-output cite.citation{font-style:inherit}.mw-parser-output q{quotes:"\"""\"""'""'"}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-lock-free a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-limited a,.mw-parser-output .cs1-lock-registration a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-subscription a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{display:none;font-size:100%}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}
- Arthur, Richard (1994), "Space and relativity in Newton and Leibniz", The British Journal for the Philosophy of Science, 45 (1): 219&ndash, 240, Thomson Gale Document Number:A16109468
- Arthur, Richard (1998), "Cohesion, Division and Harmony: Physical Aspects of Leibniz's Continuum Problem (1671–1686)", Perspectives on Science, 6 (1): 110&ndash, 135, Thomson Gale Document Number:A54601187
- Bidney, David (1962), The Psychology and Ethics of Spinoza: A Study in the History and Logic of Ideas, New York: Russell & RussellCS1 maint: Date and year (link)
- Blackwell, Richard J. (1966), "Descartes' Laws of Motion", Isis, 57 (2): 220&ndash, 234
- Carlin, Lawrence (2004), "Leibniz on Conatus, Causation, and Freedom", Pacific Philosophical Quarterly, 85 (4): 365&ndash, 379 Text " doi:10.1111/j.1468-0114.2004.00205.x
" ignored (help)
- Damasio, Antonio R. (2003), Looking for Spinoza: Joy, Sorrow, and the Feeling, Florida: Harcourt, ISBN 0-15-100557-5
- DeBrabander, Firmin (March 15, 2007), Spinoza and the Stoics: Power, Politics and the Passions, London; New York: Continuum International Publishing Group, ISBN 0-826-49393-9CS1 maint: Date and year (link)
- Duchesneau, Francois (Spring–Summer 1998), "Leibniz's Theoretical Shift in the Phoranomus and Dynamica de Potentia", Perspectives on Science, 6 (2): 77&ndash, 109, Thomson Gale Document Number: A54601186CS1 maint: Date and year (link) CS1 maint: Date format (link)
- Duff, Robert Alexander (1903), Spinoza's Political and Ethical Philosophy, J. Maclehose and Sons, retrieved 2007-03-19
- Durant, Will; Durant, Ariel (1963), "XXII: Spinoza: 1632–77", The Story of Civilization, 8, New York: Simon & Schuster, retrieved 2007-03-29
- Dutton, Blake D. (2006), "Benedict De Spinoza", The Internet Encyclopedia of Philosophy, retrieved 2007-01-15
- Garber, D. (1992), Descartes' Metaphysical Physics, Chicago: University of Chicago Press, ISBN 0-226-28217-1
- Gillespie, Charles S. (1971), "Leibniz, Gottfried Wilhelm", Dictionary of Scientific Biography, New York, retrieved 2007-03-27
- Goukroger, S. (1980), Descartes: Philosophy, Mathematics and Physics., Sussex: Harvester Press., ISBN 0-389-20084-0
- Goulding, Jay (2005), Horowitz, Maryanne, ed., "Society", New Dictionary of the History of Ideas, Detroit: Charles Scribner's Sons, 5, Thomson Gale Document Number:CX3424300736
- Grant, Edward (1964), "Motion in the Void and the Principle of Inertia in the Middle Ages", Isis, 55 (3): 265&ndash, 292
- Grant, Edward (1981), Much Ado About Nothing: Theories of Space and Vacuum from the Middle Ages to the Scientific Revolution., Cambridge: Cambridge University Press, ISBN 0-521-22983-9
- Gueroult, Martial (1980), "The Metaphysics and Physics of Force in Descartes", Descartes: Philosophy, Mathematics and Physics, Sussex: Harvester Press Unknown parameter |Editor= ignored (|editor= suggested) (help)
- Hobbes, Thomas (1998), De Corpore, New York: Oxford Publishing Company, ISBN 0-192-83682-X Check date values in: |year= / |date= mismatch (help)
- Jarrett, C. (1991), "Spinoza's Denial of Mind-Body Interaction and the Explanation of Human Action", The Southern Journal of Philosophy, 29 (4): 465&ndash, 486
- Jesseph, Doug (2006), "Hobbesian Mechanics" (PDF), Oxford Studies in Early Modern Philosophy, 3, ISBN 9-780-19920394-9, retrieved 2007-03-10
- Kollerstrom, Nicholas (1999), "How Newton Failed to Discover the Law of Gravity", Annals of Science, 59: 331&ndash, 356, retrieved 2007-01-15
- Lachterman, D. (1978), Robert Shahan; J.I. Biro., eds., The Physics of Spinoza's Ethics in Spinoza: New Perspectives, Norman: University of Oklahoma Press
- Landucci, Sergio (2004), "Vico, Giambattista", in Gianni Vattimo, Enciclopedia Garzantine della Filosofia, Milan: Garzanti Editore, ISBN 88-11-50515-1
- Leaman, Olivier (1997), Averroes and his philosophy, Richmond, Surrey: Curzon Press, ISBN 0-7007-0675-5
- LeBuffe, Michael (2006-03-20), "Spinoza's Psychological Theory", Stanford Encyclopedia of Philosophy, Edward N. Zalta (ed.), retrieved 2007-01-15CS1 maint: Date and year (link)
- Leibniz, Gottfried Wilhelm, Freiherr von (December 31, 1988), "Exposition and Defence of the New System", in Morris, Mary, M.A., Leibniz: Philosophical Writings, J.M. Dent & Sons, p. 136, ISBN 0-460-87045-9 Check date values in: |year=, |year= / |date= mismatch (help)
- Leibniz, Gottfried Wilhelm, Freiherr von (1695/1989), Ariew, Roger; Garber, Daniel, eds., Philosophical essays, Indianapolis: Hackett Pub. Co., ISBN 0-872-20063-9 Check date values in: |year=, |date= (help)CS1 maint: Date and year (link)
- Lin, Martin (2004), "Spinoza's Metaphysics of Desire: IIIP6D" (PDF), Archiv für Geschichte der Philosophie, 86 (1): 21&ndash, 55, retrieved 2007-03-10
- Matthews, Freya (1991), The Ecological Self, Routledge, ISBN 0415107970
- Morgan, Michael L. (2006), The Essential Spinoza, Indianapolis/Cambridge: Hackett Publishing Company, Inc., p. ix, ISBN 0-87220-803-6
- Osler, Margaret J. (2001), "Whose ends? Teleology in early modern natural philosophy", Osiris, 16: 151&ndash, 168, Thomson Gale Document Number:A80401149
- Pietarinen, Juhani (2000-08-08), "Hobbes, Conatus and the Prisoner's Dilemma", Stanford Encyclopedia of Philosophy, retrieved 2007-01-15CS1 maint: Date and year (link)
- Polt, Richard (1996), "German Ideology: From France to Germany and Back.", The Review of Metaphysics, 49 (3), Thomson Gale Document Number:A18262679
- Rabenort, William Louis (1911), Spinoza as Educator (PDF), New York City: Teachers College, Columbia University, retrieved 2007-03-24
- Sabra, A. I. (1994), The astronomical origin of Ibn al-Haytham’s concept of experiment, Paris: Aldershot Variorum, ISBN 0-86078-435-5
- Salam, Abdus (1984 (1987)), Lai, C. H., ed., Ideals and Realities: Selected Essays of Abdus Salam, Singapore: World Scientific Check date values in: |year= (help)
- Sandywell, Barry (1996), Reflexivity and the Crisis of Western Reason, 1: Logological Investigations, London and New York: Routledge, pp. 144&ndash, 5, ISBN 0415087562
- Sayili, A. (1987), "Ibn Sīnā and Buridan on the Motion of the Projectile", Annals of the New York Academy of Sciences, 500 (1)
- Schmitter, Amy M. (2006), "Hobbes on the Emotions", Stanford Encyclopedia of Philosophy, retrieved 2006-03-04
- Schopenhauer, Arthur (1958), Payne, E.F.J., ed., The World as Will and Representation, 1, Clinton, Massachusetts: The Colonial Press Inc.CS1 maint: Date and year (link)
- Schrift, Alan D. (2006), Twentieth-Century French Philosophy: Key Themes and Thinkers, Blackwell Publishing, ISBN 9-781-40513218-3
- Sorabji, Richard (1988), Matter, Space, and Motion: Theories in Antiquity and their Sequel, London: Duckworth
- Spinoza, Baruch (2005), Curley, Edmund, ed., Ethics, New York: Penguin Classics, pp. 144&ndash, 146, ISBN 0-140-43571-9 Check date values in: |year= / |date= mismatch (help)
- Traupman, John C. (1966), The New Collegiate Latin & English Dictionary, New York: Bantam Books, ISBN 0-553-25329-8
- Vico, Giambattista (1710), L.M. Palmer, ed., De antiquissima Italiorum sapientia ex linguae originibus eruenda librir tres, Ithaca: Cornell University Press Check date values in: |year= / |date= mismatch (help)
- Wolfson, Harry Austryn (1934), The Philosophy of Spinoza, Cambridge, Massachusetts: Harvard University Press, ISBN 0-674-66595-3
- Ziemke, Tom (2007), Chella, A.; Manzotti, R., eds., "What's life got to do with it?", Artificial Consciousness, Exeter, UK: Imprint Academic, retrieved 2007-05-27
# Further reading
- Ariew, Roger (2003), Historical dictionary of Descartes and Cartesian philosophy, Lanham, Md. ; Oxford: Scarecrow PressCS1 maint: Date and year (link)
- Bernstein, Howard R. (1980), "Conatus, Hobbes, and the Young Leibniz", Studies in History and Philosophy of Science, 11: 167–81CS1 maint: Date and year (link)
- Bove, Laurent (1992), L'affirmation absolue d'une existence essai sur la stratégie du conatus Spinoziste, Université de Lille III: Lille, OCLC 57584015CS1 maint: Date and year (link)
- Caird, Edward (1892), Essays on Literature and Philosophy: Glasgow, J. Maclehose and sons, retrieved 2007-03-20
- Carlin, Laurence (December 2004), "Leibniz on Conatus, causation and freedom", Pacific Philosophical Quarterly, 85 (4): 365–79, ISSN 0279-0750CS1 maint: Date and year (link)
- Chamberland, Jacques (September 2000), Duchesneau, Francois, ed., "Les conatus chez Thomas Hobbes", The Review of Metaphysics, Université de Montreal, 54 (1)CS1 maint: Date and year (link)
- Deleuze, Gilles (1988), Spinoza: Practical Philosophy, City Lights Book
- Garber, Daniel (1994), "Descartes and Spinoza on Persistence and Conatus", Studia Spinozana, Walther & Walther, 10CS1 maint: Date and year (link)
- Garret, D. (2002), Koistinen, Olli; Biro, John, eds., "Spinoza's Conatus Argument", Spinoza: Metaphysical Themes, Oxford: Oxford University Press
- Leibniz, Gottfried Wilhelm; Gerhardt, K.; Langley, Alfred Gideon (1896), Langley, Alfred Gideon, ed., New Essays Concerning Human Understanding, Macmillan & Co., ltd., retrieved 2007-03-19
- Lyon, Georges (1893), La philosophie de Hobbes, F. Alean, retrieved 2007-03-19
- Montag, Warren (1999), Bodies, Masses, Power: Spinoza and his Contemporaries, New York: Verso, ISBN 1-85984-701-3
- Rabouin, David (June/July 2000), "Entre Deleuze et Foucault : Le jeu du désir et du pouvoir", Critique: 637&ndash, 638 Check date values in: |date= (help)CS1 maint: Date and year (link)
- Schrijvers, M. (1999), Yovel, Yirmiyahu, ed., "The Conatus and the Mutual Relationship Between Active and Passive Affects in Spinoza", Desire and Affect: Spinoza as Psychologist, New York: Little Room Press
- Schulz, O. (1995), "Schopenhauer's Ethik - die Konzequenz aus Spinoza's Metaphysik?", Schopenhauer-Jahrbuch, 76: 133&ndash, 149, ISSN 0080-6935CS1 maint: Date and year (link)
- Steinberg, Diane (Spring 2005), "Belief, Affirmation, and the Doctrine of Conatus in Spinoza", Southern Journal of Philosophy, 43 (1): 147&ndash, 158, ISSN 0038-4283
- Tuusvuori, Jarkko S. (March 2000), Nietzsche & Nihilism: Exploring a Revolutionary Conception of Philosophical Conceptuality, University of Helsinki, ISBN 951-45-9135-6CS1 maint: Date and year (link)
- Wendell, Rich (1997), Spinoza's Conatus doctrine: existence, being, and suicide, Waltham, Mass., OCLC 37542442CS1 maint: Date and year (link)
- Youpa, A. (2003), "Spinozistic Self-Preservation", The Southern Journal of Philosophy, 41 (3): 477&ndash, 490
he:קונאטוס
sv:Conatus Template:Link FA | Conatus
Template:Two other uses
Conatus (Template:PronEng; Latin: effort; endeavor; impulse, inclination, tendency; undertaking; striving) is a term used in early philosophies of psychology and metaphysics to refer to an innate inclination of a thing to continue to exist and enhance itself.[1] This "thing" may be mind, matter or a combination of both. Over the millennia, many different definitions and treatments have been formulated by philosophers. The most important of these include the seventeenth century philosophers René Descartes, Baruch Spinoza, and Gottfried Leibniz, along with their Empiricist contemporary Thomas Hobbes.[2] The conatus may refer to the instinctual "will to live" of animals or to various metaphysical theories of motion and inertia.[3] Often the concept is associated with God's will in a pantheist view of Nature.[2][4] The concept may be broken up into separate definitions for the mind and body, or even split up when discussing centrifugal force or inertia.[5]
The history of the term conatus is that of a series of subtle tweaks in meaning and clarifications of scope developed over the course of two and a half millennia. After its formulation in ancient Greece, successive philosophers to adopt the term put their own personal twist on the concept, each developing the term differently such that it now has no concrete and universally accepted definition.[3] The earliest authors to discuss conatus wrote primarily in Latin, and therefore used it not only as a technical term but as a common word and in a general sense. Conatus is, of course, more than simply a Latin participle. In archaic texts, the more technical usage is difficult to discern from the more common one, and they are also hard to differentiate in translation. In English translations, the term is italicized when used in the technical sense or translated and followed by conatus in brackets.[6] Today, conatus is rarely used in the technical sense, since modern physics and evolutionary biology use concepts such as inertia and conservation of momentum that have superseded it. It has, however, been a notable influence on nineteenth and twentieth-century thinkers such as Friedrich Nietzsche, Louis Dumont and Arthur Schopenhauer.
# Classical origins
The Latin conatus comes from the verb conari, which is usually translated into English as, "to endeavor"; but the concept of the conatus was first developed by the Stoics (333–264 BCE) and Peripatetics (c. 335 BCE) before the Common Era. These groups used the word Template:Polytonic (hormê, translated in Latin by impetus) to describe the movement of the soul towards an object, and from which a physical act results [7]. Classical thinkers, Marcus Tullius Cicero (106–43 BCE) and Diogenes Laertius (c. 235 BCE), expanded this principle to include an aversion to destruction, but continued to limit its application to the motivations of non-human animals[citation needed]. Diogenes Laertius, for example, specifically denied the application of the term to plants. Before the Renaissance, Thomas Aquinas (c. 1225–1274 CE), Duns Scotus (c. 1266–1308 CE) and Dante Alighieri (1265–1321 CE) expressed similar sentiments using the Latin words vult, velle or appetit as synonyms of conatus; indeed, all four terms may be used to translate the original Greek Template:Polytonic. Around 1700, Telesius and Campanella extended the ancient Greek notions and applied them to all objects, animate and inanimate.[8]
First Aristotle, then Cicero and Laertius each alluded to a connection between the conatus and other emotions. In their view, the former induces the latter. They maintained that humans do not wish to do something because they think it "good", but rather they think it "good" because they want to do it[citation needed]. In other words, the cause of human desire is the natural inclination of a body to augment itself in accordance with the principles of the conatus.[9]
# Medieval views
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There is a traditional connection between conatus and motion itself. Aquinas and Abravanel (1265–1321) both related the concept directly to that which Augustine (354–430 CE) saw to be the "natural movements upward and downward or with their being balanced in an intermediate position" described in his De Civitate Dei, (c. 520 CE). They called this force that causes objects to rise or fall, "amor naturalis", or "natural love".[10]
In the 6th century, John Philoponus (c. 490–c. 570 CE) criticized Aristotle's view of motion, noting the inconsistency between Aristotle's discussion of projectiles, where the medium of aether keeps projectiles going, and his discussion of the void, where there is no such medium and hence a body's motion should be impossible. Philoponus proposed that motion was not maintained by the action of some surrounding medium but by some property, or conatus implanted in the object when it was set in motion. This was not the modern concept of inertia, for there was still the need for an inherent power to keep a body in motion.[11] This view was strongly opposed by Averroës and many scholastic philosophers who supported Aristotle.[12] The Aristotelian view was also challenged in the Islamic world. For example, Ibn al-Haytham (Alhazen) seems to have supported Philoponus' views,[13] while he developed a concept similar to inertia.[14] His contemporary Avicenna also developed a concept similar to momentum.[15]
Later, Jean Buridan (1300–1358) rejected the notion that this motion-generating property, which he named impetus, dissipated spontaneously. Buridan's position was that a moving object would be arrested by the resistance of the air and the weight of the body which would oppose its impetus. He also maintained that impetus increased with speed; thus, his initial idea of impetus was similar in many ways to the modern concept of momentum. Despite the obvious similarities to more modern ideas of inertia, Buridan saw his theory as only a modification to Aristotle's basic philosophy, maintaining many other peripatetic views, including the belief that there was still a fundamental difference between an object in motion and an object at rest. Buridan also maintained that impetus could be not only linear, but also circular in nature, causing objects such as celestial bodies to move in a circle.[16]
# In Descartes
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In the first half of the seventeenth century, René Descartes (1596–1650) began to develop a more modern, materialistic concept of the conatus, describing it as "an active power or tendency of bodies to move, expressing the power of God."[17] Whereas the ancients used the term in a strictly anthropomorphic sense similar to voluntary "endeavoring" or "struggling" to achieve certain ends, and medieval Scholastic philosophers developed a notion of conatus as a mysterious intrinsic property of things, Descartes uses the term in a somewhat more mechanistic sense.[18] More specifically, for Descartes, in contrast to Buridan, movement and stasis are two states of the same thing, not different things. Although there is much ambiguity in Descartes' notion of conatus, one can see here the beginnings of a move away from the attribution of desires and intentions to nature and its workings toward a more scientific and modern view.[19]
Descartes rejects the teleological, or purposive, view of the material world that was dominant in the West from the time of Aristotle. The mind is not viewed by Descartes as part of the material world, and hence is not subject to the strictly mechanical laws of nature. Motion and rest, on the other hand, are properties of the interactions of matter according to eternally fixed mechanical laws. God only sets the whole thing in motion at the start, and later does not interfere except to maintain the dynamical regularities of the mechanical behavior of bodies. Hence there is no real teleology in the movements of bodies since the whole thing reduces to the law-governed collisions and their constant reconfigurations.[20] The conatus is just the tendency of bodies to move when they collide with each other. God may set this activity in motion, but thereafter no new motion or rest can be created or destroyed.[21]
Descartes specifies two varieties of the conatus: conatus a centro and conatus recedendi. Conatus a centro, or "tendency towards the center", is used by Descartes as a theory of gravity; conatus recendendi, or "tendency away from the center", represents the centrifugal forces.[5] These tendencies are not to be thought of in terms of animate dispositions and intentions, nor as inherent properties or "forces" of things, but rather as a unifying, external characteristic of the physical universe itself which God has bestowed.[22]
Descartes, in developing his First Law of Nature, also invokes the idea of a conatus se movendi, or "conatus of self-preservation".[23] This law is a generalization of the principle of inertia, which was developed and experimentally demonstrated earlier by Galileo. The principle was formalized by Isaac Newton and made into the first of his three Laws of Motion fifty years after the death of Descartes. Descartes' version states: "Each thing, insofar as in it lies, always perseveres in the same state, and when once moved, always continues to move."[24]
# In Hobbes
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## Conatus and the psyche
Thomas Hobbes (1588–1679), too, worked off of the previous notions of the conatus principle. However, he criticized the previous definitions for failing to explain the origin of motion. Working toward this end became the primary focus of Hobbes' work in this area. Indeed, Hobbes "reduces all the cognitive functions of the mind to variations of its conative functions".[25]
Furthermore, Hobbes describes emotion as the beginning of motion and the will as the sum of all emotions. This "will" forms the conatus of a body[17] and its physical manifestation is the perceived "will to survive".[2] In order that living beings may thrive, Hobbes says, "they seek peace and fight anything that threatens this peace".[17] Hobbes also equates this conatus with "imagination", and states that a change in the conatus, or will, is the result of "deliberation".[26]
## Conatus and physics
As in his psychological theory, Hobbes's physical conatus is an infinitesimal unit of motion. It is the beginning of motion: an inclination in a specified direction. The concept of impetus, as used by Hobbes, is defined in terms of this physical conatus. It is “a measure of the conatus exercised by a moving body over the course of time”.[28] Resistance is caused by a contrary conatus; force is this motion plus “the magnitude of the body”.[29] Hobbes also uses the word conatus to refer to the "restorative forces" which may cause springs, for example, to contract or expand. Hobbes claims there is some force inherent in these objects that inclines them to return to their previous state. Today, science attributes this phenomenon to material elasticity.[30]
# In Spinoza
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Spinoza (1632–1677) applies the idea of a conatus to the human body, psyche and both simultaneously, using a different term for each.[31] When referring to psychological manifestations of the concept, he uses the term voluntas (will). When referring to the overarching concept, he uses the word appetitus (appetite). When referring to the bodily impulse, he uses the plain term conatus.[32] Sometimes he expands the term and uses the whole phrase, conatus sese conservandi (the striving for self-preservation).[33]
Spinoza asserts the existence of this general principle of a conatus in attempting to explain the "self-evident" truth that "nothing can be destroyed except by an external cause".[34] To him, it is self-evident that "the definition of anything affirms, and does not negate, the thing's essence."[35] This resistance to self-destruction is formulated by Spinoza in terms of a human striving to continue to exist; and conatus is the word he most often uses to describe this force.[36]
In Spinoza's world-view, this principle is applicable to all things, and furthermore constitutes the very essence of objects, including the human mind and morals, for these are but finite modes of God.[37] As he states in the Ethics (1677), the conatus is of "indefinite time"; it lasts as long as the object does.[38] Spinoza uses conatus to describe an inclination of things to increase in power; rather than just continuing to exist statically, all beings must strive towards perfection.[39] Further, all existing things act if and only if such action maintains or augments their existence.[37] Spinoza also uses the term conatus to refer to rudimentary concepts of inertia, as Descartes had earlier.[2] Since a thing cannot be destroyed without the action of external forces, motion and rest, too, exist indefinitely until disturbed.[40]
## Psychological manifestation
The concept of the conatus, as used in Baruch Spinoza's philosophy of psychology, is derived from sources both ancient and medieval. Spinoza reformulates principles that the Stoics, Cicero, Laertius, and especially Hobbes and Descartes developed.[41] One significant change he makes to Hobbes' theory is his belief that the conatus ad motum, (conatus to motion), is not mental, but material.[42]
Spinoza, with his determinism, believes that man and nature must be unified under a consistent set of laws; God and nature are one, and there is no free will. Contrary to most philosophers of his time and in accordance with most of those of the present, Spinoza rejects the dualistic assumption that mind, intentionality, ethics and freedom are to be treated as things separate from the natural world of physical objects and events.[43] His goal is to provide a unified explanation of all these things within a naturalistic framework, and his notion of conatus is central to this project. For example, an action is "free", for Spinoza, only if it arises from the essence and conatus of an entity. There can be no absolute, unconditioned freedom of the will, since all events in the natural world, including human actions and choices, are determined in accord with the natural laws of the universe, which are inescapable. However, an action can still be free in the sense that it is not constrained or otherwise subject to external forces.[44]
Human beings are thus an integral part of nature.[45] Spinoza explains seemingly irregular human behaviour as really "natural" and rational and motivated by this principle of the conatus.[46] In the process, he replaces the notion of free will with the conatus, a principle that can be applied to all of nature and not just man.[45]
### Emotions and affects
Spinoza's view of the relationship between the conatus and the human affects is not clear. Firmin DeBrabander, assistant professor of philosophy at the Maryland Institute College of Art, and Antonio Damasio, professor of neuroscience at the University of Southern California, both argue that the human affects arise from the conatus and the perpetual drive toward perfection.[47] Indeed, Spinoza states in his Ethics that happiness, specifically, "consists in the human capacity to preserve itself." This "endeavor" is also characterized by Spinoza as the "foundation of virtue".[48] Conversely, a person is saddened by anything that opposes his conatus.[49]
The late David Bidney (1908–1987), professor at Yale University, disagrees. Bidney closely associates "desire", a primary affect, with the conatus principle of Spinoza. This view is backed by the Scholium of IIIP9 of the Ethics which states, "...Between appetite and desire there is no difference, except that desire is generally related to men insofar as they are conscious of the appetite. So desire can be defined as appetite together with consciousness of the appetite."[2] According to Bidney, this desire is controlled by the other affects, pleasure and pain, and thus the conatus strives towards that which causes joy and avoids that which produces pain.[50] Arthur Schopenhauer (1788–1860) agrees with Bidney in interpretation, but states in The World as Will and Representation (1819) that he disagrees with Spinoza because "according to the whole of my fundamental view, all this is a reversal of the true relation. The will is first and original; knowledge is merely added to it as an instrument belonging to the phenomenon of the will."[51]
# In Leibniz
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Gottfried Leibniz (1646–1716) was a student of Erhard Weigel (1625–1699) and learned of the conatus principle from him and from Hobbes, though Weigel used the word tendentia (Latin: tendency).[52] Specifically, Leibniz uses the word conatus in his Exposition and Defence of the New System (1695) to describe a notion similar that of Hobbes, but he differentiates between the conatus of the body and soul, the first of which may only travel in a straight line by its own power, and the latter of which may "remember" more complicated motions.[53]
For Leibniz, the problem of motion comes to a resolution of the paradox of Zeno.
Since motion is continuous, space must be infinitely divisible. In order for anything to begin moving at all, there must be some mind-like, voluntaristic property or force inherent in the basic constituents of the universe that propels them. This conatus is a sort of instantaneous or "virtual" motion that all things possess, even when they are static. Motion, meanwhile, is just the summation of all the conatuses that a thing has, along with the interactions of things. The conatus is to motion as a point is to space.[54] The problem with this view is that an object that collides with another would not be able to bounce back, if the only force in play were the conatus. Hence, Leibniz was forced to postulate the existence of an aether that kept objects moving and allowed for elastic collisions. Leibniz' concept of a mind-like memory-less property of conatus, coupled with his rejection of atoms, eventually led to his theory of monads.[55]
Leibniz also uses his concept of a conatus in developing the principles of the integral calculus, adapting the meaning of the term, in this case, to signify a mathematical analog of Newton's accelerative "force". By summing an infinity of such conatuses (i.e., what is now called integration), Leibniz could measure the effect of a continuous force.[54] He defines impetus as the result of a continuous summation of the conatus of a body, just as the vis viva (or "living force") is the sum of the inactive vis mortua.[56]
Based on the work of Kepler and probably Descartes, Leibniz develops a model of planetary motion based on the conatus principle, the idea of aether and a fluid vortex. This theory is expounded in the work Tentamen de motuum coelestium causis (1689).[54] According to Leibniz, Kepler's analysis of elliptical orbits into a circular and a radial component can be explained by a "harmonic vortex" for the circular motion combined with a centrifugal force and gravity, both of which are examples of conatus, to account for the radial motion.[55] Leibniz later defines the term monadic conatus, as the "state of change" through which his monads perpetually advance.[57]
# Related usages and terms
Several other uses of the term conatus, apart from the primary ones mentioned above, have been formulated by various philosophers over the centuries. There are also some important related terms and concepts which have, more or less, similar meanings and usages. Giambattista Vico (1668–1744) defined conatus as the essence of human society,[58] and also, in a more traditional, hylozoistic sense, as the generating power of movement which pervades all of nature.[59] Nearly a century after the beginnings of modern science, Vico, inspired by Neoplatonism, explicitly rejected the principle of inertia and the laws of motion of the new physics. For him, nature was composed neither of atoms, as in the dominant view, nor of extension, as in Descartes, but of metaphysical points animated by a conatus principle provoked by God.[60]
Arthur Schopenhauer (1788–1860) developed a philosophy that contains a principle notably similar to that of Hobbes's conatus. This principle, Wille zum Leben, or "Will to Live", described the specific phenomenon of an organism's self-preservation instinct.[61] Schopenhauer qualified this, however, by suggesting that the Will to Live is not limited in duration. Rather, "the will wills absolutely and for all time", across generations.[62] Friedrich Nietzsche (1844–1900), an early disciple of Schopenhauer, developed a separate principle which comes out of a rejection of the primacy of Schopenhauer's Will to Live and other notions of self-preservation. He called his version the Will to Power, or Wille zur Macht.[63] Nietzsche criticized Spinoza's conatus principle, arguing that if true, it would allegedly favour a stagnant Universe. He thought "the opposite is true"; every organism strives not to just to persevere, but to "become more" than it is and to exert its creative strength. Spinoza's conatus, however, was much more alike to such an understanding than to simple self-preservation, as it was akin to empowerment[citation needed].
Sigmund Freud (1856–1939), greatly depended on Spinoza's formulation of the conatus principle as a system of self preservation, though he never cited him directly in any of his published works.[64][65] Around the same time, Henri Bergson (1859–1941), developed the principle of the élan vital, or "vital impulse", which was thought to aid in the evolution of organisms. This concept, which implies a fundamental driving force behind all life, is reminiscent of the conatus principle of Spinoza and others.[66]
The cultural anthropologist Louis Dumont (1911–1988), described a cultural conatus built directly upon Spinoza's seminal definition in IIIP3 of his Ethics. The principle behind this derivative concept states that any given culture, "tends to persevere in its being, whether by dominating other cultures or by struggling against their domination."[67]
# Modern significance
## Physical
After the advent of Newtonian physics, the concept of a conatus of all physical bodies was largely superseded by the principle of inertia and conservation of momentum. As Bidney states, "It is true that logically desire or the conatus is merely a principle of inertia ... the fact remains, however, that this is not Spinoza's usage".[68] Likewise, conatus was used by many philosophers to describe other concepts which have slowly been made obsolete. Conatus recendendi, for instance, became the centrifugal force, and gravity is used where conatus a centro had been previously.[5] Today, the topics with which conatus dealt are matters of science and are thus subject to inquiry by the scientific method.[69]
## Biological
The archaic concept of conatus is today being reconciled with modern biology by scientists such as Antonio Damasio. . The conatus of today, however, is explained in terms of chemistry and neurology where, before, it was a matter of metaphysics and theurgy.[70] This concept may be "constructed so as to maintain the coherence of a living organism's structures and functions against numerous life-threatening odds".[71] This conatus is similar to modern notions of the libido in the Jungian sense, and the animal directive of self preservation.
### Systems theory
The Spinozistic conception of a conatus was a historical precursor to modern theories of autopoiesis in biological systems.[72] In systems theory and the sciences in general, the concept of a conatus may be related to the phenomenon of emergence, whereby complex systems may spontaneously form from a multiplicity of more simple structures. The self-regulating and self-maintaining properties of biological and even social systems may thus be considered modern versions of Spinoza's conatus principle. [73]; however, the scope of the idea is definitely narrower today without the religious implications of the earlier variety.[74]
# Citations
- ↑ Traupman 1966, p. 52
- ↑ Jump up to: 2.0 2.1 2.2 2.3 2.4 LeBuffe 2006
- ↑ Jump up to: 3.0 3.1 Wolfson 1934, p. 202
- ↑ Schopenhauer 1958, p. 357
- ↑ Jump up to: 5.0 5.1 5.2 Kollerstrom 1999, pp. 331–356
- ↑ Leibniz 1989, p. 118
- ↑ Clement of Alexandria, in SVF, III, 377; Cicero, De Officiis, I, 132; Seneca the Younger, Epistulae morales ad Lucilium, 113, 23
- ↑ Wolfson 1934, pp. 196,199,202
- ↑ Wolfson 1934, p. 204
- ↑ Wolfson 1934, pp. 197,200
- ↑ Sorabji 1988, pp. 227,228
- ↑ Leaman 1997
- ↑ Sabra 1994, pp. 133–136
- ↑ Salam & 1984 (1987), pp. 179–213
- ↑ Jump up to: 15.0 15.1 Sayili 1987, pp. 447–482
- ↑ Grant 1964, pp. 265–292>
- ↑ Jump up to: 17.0 17.1 17.2 Pietarinen 2000
- ↑ Garber 1992, pp. 150,154
- ↑ Goukroger 1980, pp. 178–179
- ↑ Grant 1981, pp. 140–44
- ↑ Gueroult 1980, pp. 120–34
- ↑ Garber 1992, pp. 180,184
- ↑ Wolfson 1934, p. 201
- ↑ Blackwell 1966, p. 220
- ↑ Bidney 1962, p. 91
- ↑ Schmitter 2006
- ↑ Hobbes & III, xiv, 2
- ↑ Jesseph 2006, p. 22
- ↑ Jesseph 2006, p. 35
- ↑ Osler 2001, pp. 157–61
- ↑ Wolfson 1934, p. 199
- ↑ Allison 1975, p. 126
- ↑ Duff 1903, chp. VII
- ↑ Spinoza, 1677 & Book III Prop 4
- ↑ Spinoza 1677, p. 66
- ↑ Allison 1975, p. 124
- ↑ Jump up to: 37.0 37.1 Lin 2004, p. 4
- ↑ Spinoza 1677, pp. 66–7
- ↑ Allison 1975, p. 126
- ↑ Allison 1975, p. 125
- ↑ Morgan 2006, p. ix
- ↑ Bidney 1962, p. 93
- ↑ Jarrett 1991, pp. 470–475
- ↑ Lachterman 1978
- ↑ Jump up to: 45.0 45.1 Allison 1975, p. 125
- ↑ Dutton 2006, chp. 5
- ↑ DeBrabander 2007, p. 20–1
- ↑ Damasio 2003, p. 170
- ↑ Damasio 2003, pp. 138–9
- ↑ Bidney 1962, p. 87
- ↑ Schopenhauer 1958, p. 292
- ↑
- ↑ Leibniz 1988, p. 135
- ↑ Jump up to: 54.0 54.1 54.2 Gillespie 1971, pp. 159–161
- ↑ Jump up to: 55.0 55.1 Carlin 2004, pp. 365–379
- ↑ Duchesneau 1998, pp. 88–89
- ↑ Arthur 1994, sec. 3
- ↑ Goulding 2005, p. 22040
- ↑ Vico 1710, pp. 180–186
- ↑ Landucci 2004, pp. 1174,1175
- ↑ Rabenort 1911, p. 16
- ↑ Schopenhauer 1958, p. 568
- ↑ Durant & Durant 1963, chp. IX
- ↑ Damasio 2003, p. 260
- ↑ Bidney 1962, p. 398
- ↑ Schrift 2006, p. 13
- ↑ Polt 1996
- ↑ Bidney 1962, p. 88
- ↑ Bidney 1962
- ↑ Damasio 2003, p. 37
- ↑ Damasio 2003, p. 36
- ↑ Ziemke 2007, pp. 6
- ↑ Sandywell 1996, pp. 144–5
- ↑ Matthews 1991, pp. 110
# Bibliography
Template:Sisterlinks
- Allison, Henry E. (1975), Benedict de Spinoza, San Diego: Twayne Publishers, ISBN 0-8057-2853-8.mw-parser-output cite.citation{font-style:inherit}.mw-parser-output q{quotes:"\"""\"""'""'"}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-lock-free a{background:url("https://upload.wikimedia.org/wikipedia/commons/thumb/6/65/Lock-green.svg/9px-Lock-green.svg.png")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-limited a,.mw-parser-output .cs1-lock-registration a{background:url("https://upload.wikimedia.org/wikipedia/commons/thumb/d/d6/Lock-gray-alt-2.svg/9px-Lock-gray-alt-2.svg.png")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-subscription a{background:url("https://upload.wikimedia.org/wikipedia/commons/thumb/a/aa/Lock-red-alt-2.svg/9px-Lock-red-alt-2.svg.png")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{display:none;font-size:100%}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}
- Arthur, Richard (1994), "Space and relativity in Newton and Leibniz", The British Journal for the Philosophy of Science, 45 (1): 219&ndash, 240, Thomson Gale Document Number:A16109468
- Arthur, Richard (1998), "Cohesion, Division and Harmony: Physical Aspects of Leibniz's Continuum Problem (1671–1686)", Perspectives on Science, 6 (1): 110&ndash, 135, Thomson Gale Document Number:A54601187
- Bidney, David (1962), The Psychology and Ethics of Spinoza: A Study in the History and Logic of Ideas, New York: Russell & RussellCS1 maint: Date and year (link)
- Blackwell, Richard J. (1966), "Descartes' Laws of Motion", Isis, 57 (2): 220&ndash, 234
- Carlin, Lawrence (2004), "Leibniz on Conatus, Causation, and Freedom", Pacific Philosophical Quarterly, 85 (4): 365&ndash, 379 Text " doi:10.1111/j.1468-0114.2004.00205.x
" ignored (help)
- Damasio, Antonio R. (2003), Looking for Spinoza: Joy, Sorrow, and the Feeling, Florida: Harcourt, ISBN 0-15-100557-5
- DeBrabander, Firmin (March 15, 2007), Spinoza and the Stoics: Power, Politics and the Passions, London; New York: Continuum International Publishing Group, ISBN 0-826-49393-9CS1 maint: Date and year (link)
- Duchesneau, Francois (Spring–Summer 1998), "Leibniz's Theoretical Shift in the Phoranomus and Dynamica de Potentia", Perspectives on Science, 6 (2): 77&ndash, 109, Thomson Gale Document Number: A54601186CS1 maint: Date and year (link) CS1 maint: Date format (link)
- Duff, Robert Alexander (1903), Spinoza's Political and Ethical Philosophy, J. Maclehose and Sons, retrieved 2007-03-19
- Durant, Will; Durant, Ariel (1963), "XXII: Spinoza: 1632–77", The Story of Civilization, 8, New York: Simon & Schuster, retrieved 2007-03-29
- Dutton, Blake D. (2006), "Benedict De Spinoza", The Internet Encyclopedia of Philosophy, retrieved 2007-01-15
- Garber, D. (1992), Descartes' Metaphysical Physics, Chicago: University of Chicago Press, ISBN 0-226-28217-1
- Gillespie, Charles S. (1971), "Leibniz, Gottfried Wilhelm", Dictionary of Scientific Biography, New York, retrieved 2007-03-27
- Goukroger, S. (1980), Descartes: Philosophy, Mathematics and Physics., Sussex: Harvester Press., ISBN 0-389-20084-0
- Goulding, Jay (2005), Horowitz, Maryanne, ed., "Society", New Dictionary of the History of Ideas, Detroit: Charles Scribner's Sons, 5, Thomson Gale Document Number:CX3424300736
- Grant, Edward (1964), "Motion in the Void and the Principle of Inertia in the Middle Ages", Isis, 55 (3): 265&ndash, 292
- Grant, Edward (1981), Much Ado About Nothing: Theories of Space and Vacuum from the Middle Ages to the Scientific Revolution., Cambridge: Cambridge University Press, ISBN 0-521-22983-9
- Gueroult, Martial (1980), "The Metaphysics and Physics of Force in Descartes", Descartes: Philosophy, Mathematics and Physics, Sussex: Harvester Press Unknown parameter |Editor= ignored (|editor= suggested) (help)
- Hobbes, Thomas (1998), De Corpore, New York: Oxford Publishing Company, ISBN 0-192-83682-X Check date values in: |year= / |date= mismatch (help)
- Jarrett, C. (1991), "Spinoza's Denial of Mind-Body Interaction and the Explanation of Human Action", The Southern Journal of Philosophy, 29 (4): 465&ndash, 486
- Jesseph, Doug (2006), "Hobbesian Mechanics" (PDF), Oxford Studies in Early Modern Philosophy, 3, ISBN 9-780-19920394-9, retrieved 2007-03-10
- Kollerstrom, Nicholas (1999), "How Newton Failed to Discover the Law of Gravity", Annals of Science, 59: 331&ndash, 356, retrieved 2007-01-15
- Lachterman, D. (1978), Robert Shahan; J.I. Biro., eds., The Physics of Spinoza's Ethics in Spinoza: New Perspectives, Norman: University of Oklahoma Press
- Landucci, Sergio (2004), "Vico, Giambattista", in Gianni Vattimo, Enciclopedia Garzantine della Filosofia, Milan: Garzanti Editore, ISBN 88-11-50515-1
- Leaman, Olivier (1997), Averroes and his philosophy, Richmond, Surrey: Curzon Press, ISBN 0-7007-0675-5
- LeBuffe, Michael (2006-03-20), "Spinoza's Psychological Theory", Stanford Encyclopedia of Philosophy, Edward N. Zalta (ed.), retrieved 2007-01-15CS1 maint: Date and year (link)
- Leibniz, Gottfried Wilhelm, Freiherr von (December 31, 1988), "Exposition and Defence of the New System", in Morris, Mary, M.A., Leibniz: Philosophical Writings, J.M. Dent & Sons, p. 136, ISBN 0-460-87045-9 Check date values in: |year=, |year= / |date= mismatch (help)
- Leibniz, Gottfried Wilhelm, Freiherr von (1695/1989), Ariew, Roger; Garber, Daniel, eds., Philosophical essays, Indianapolis: Hackett Pub. Co., ISBN 0-872-20063-9 Check date values in: |year=, |date= (help)CS1 maint: Date and year (link)
- Lin, Martin (2004), "Spinoza's Metaphysics of Desire: IIIP6D" (PDF), Archiv für Geschichte der Philosophie, 86 (1): 21&ndash, 55, retrieved 2007-03-10
- Matthews, Freya (1991), The Ecological Self, Routledge, ISBN 0415107970
- Morgan, Michael L. (2006), The Essential Spinoza, Indianapolis/Cambridge: Hackett Publishing Company, Inc., p. ix, ISBN 0-87220-803-6
- Osler, Margaret J. (2001), "Whose ends? Teleology in early modern natural philosophy", Osiris, 16: 151&ndash, 168, Thomson Gale Document Number:A80401149
- Pietarinen, Juhani (2000-08-08), "Hobbes, Conatus and the Prisoner's Dilemma", Stanford Encyclopedia of Philosophy, retrieved 2007-01-15CS1 maint: Date and year (link)
- Polt, Richard (1996), "German Ideology: From France to Germany and Back.", The Review of Metaphysics, 49 (3), Thomson Gale Document Number:A18262679
- Rabenort, William Louis (1911), Spinoza as Educator (PDF), New York City: Teachers College, Columbia University, retrieved 2007-03-24
- Sabra, A. I. (1994), The astronomical origin of Ibn al-Haytham’s concept of experiment, Paris: Aldershot Variorum, ISBN 0-86078-435-5
- Salam, Abdus (1984 (1987)), Lai, C. H., ed., Ideals and Realities: Selected Essays of Abdus Salam, Singapore: World Scientific Check date values in: |year= (help)
- Sandywell, Barry (1996), Reflexivity and the Crisis of Western Reason, 1: Logological Investigations, London and New York: Routledge, pp. 144&ndash, 5, ISBN 0415087562
- Sayili, A. (1987), "Ibn Sīnā and Buridan on the Motion of the Projectile", Annals of the New York Academy of Sciences, 500 (1)
- Schmitter, Amy M. (2006), "Hobbes on the Emotions", Stanford Encyclopedia of Philosophy, retrieved 2006-03-04
- Schopenhauer, Arthur (1958), Payne, E.F.J., ed., The World as Will and Representation, 1, Clinton, Massachusetts: The Colonial Press Inc.CS1 maint: Date and year (link)
- Schrift, Alan D. (2006), Twentieth-Century French Philosophy: Key Themes and Thinkers, Blackwell Publishing, ISBN 9-781-40513218-3
- Sorabji, Richard (1988), Matter, Space, and Motion: Theories in Antiquity and their Sequel, London: Duckworth
- Spinoza, Baruch (2005), Curley, Edmund, ed., Ethics, New York: Penguin Classics, pp. 144&ndash, 146, ISBN 0-140-43571-9 Check date values in: |year= / |date= mismatch (help)
- Traupman, John C. (1966), The New Collegiate Latin & English Dictionary, New York: Bantam Books, ISBN 0-553-25329-8
- Vico, Giambattista (1710), L.M. Palmer, ed., De antiquissima Italiorum sapientia ex linguae originibus eruenda librir tres, Ithaca: Cornell University Press Check date values in: |year= / |date= mismatch (help)
- Wolfson, Harry Austryn (1934), The Philosophy of Spinoza, Cambridge, Massachusetts: Harvard University Press, ISBN 0-674-66595-3
- Ziemke, Tom (2007), Chella, A.; Manzotti, R., eds., "What's life got to do with it?", Artificial Consciousness, Exeter, UK: Imprint Academic, retrieved 2007-05-27
# Further reading
- Ariew, Roger (2003), Historical dictionary of Descartes and Cartesian philosophy, Lanham, Md. ; Oxford: Scarecrow PressCS1 maint: Date and year (link)
- Bernstein, Howard R. (1980), "Conatus, Hobbes, and the Young Leibniz", Studies in History and Philosophy of Science, 11: 167–81CS1 maint: Date and year (link)
- Bove, Laurent (1992), L'affirmation absolue d'une existence essai sur la stratégie du conatus Spinoziste, Université de Lille III: Lille, OCLC 57584015CS1 maint: Date and year (link)
- Caird, Edward (1892), Essays on Literature and Philosophy: Glasgow, J. Maclehose and sons, retrieved 2007-03-20
- Carlin, Laurence (December 2004), "Leibniz on Conatus, causation and freedom", Pacific Philosophical Quarterly, 85 (4): 365–79, ISSN 0279-0750CS1 maint: Date and year (link)
- Chamberland, Jacques (September 2000), Duchesneau, Francois, ed., "Les conatus chez Thomas Hobbes", The Review of Metaphysics, Université de Montreal, 54 (1)CS1 maint: Date and year (link)
- Deleuze, Gilles (1988), Spinoza: Practical Philosophy, City Lights Book
- Garber, Daniel (1994), "Descartes and Spinoza on Persistence and Conatus", Studia Spinozana, Walther & Walther, 10CS1 maint: Date and year (link)
- Garret, D. (2002), Koistinen, Olli; Biro, John, eds., "Spinoza's Conatus Argument", Spinoza: Metaphysical Themes, Oxford: Oxford University Press
- Leibniz, Gottfried Wilhelm; Gerhardt, K.; Langley, Alfred Gideon (1896), Langley, Alfred Gideon, ed., New Essays Concerning Human Understanding, Macmillan & Co., ltd., retrieved 2007-03-19
- Lyon, Georges (1893), La philosophie de Hobbes, F. Alean, retrieved 2007-03-19
- Montag, Warren (1999), Bodies, Masses, Power: Spinoza and his Contemporaries, New York: Verso, ISBN 1-85984-701-3
- Rabouin, David (June/July 2000), "Entre Deleuze et Foucault : Le jeu du désir et du pouvoir", Critique: 637&ndash, 638 Check date values in: |date= (help)CS1 maint: Date and year (link)
- Schrijvers, M. (1999), Yovel, Yirmiyahu, ed., "The Conatus and the Mutual Relationship Between Active and Passive Affects in Spinoza", Desire and Affect: Spinoza as Psychologist, New York: Little Room Press
- Schulz, O. (1995), "Schopenhauer's Ethik - die Konzequenz aus Spinoza's Metaphysik?", Schopenhauer-Jahrbuch, 76: 133&ndash, 149, ISSN 0080-6935CS1 maint: Date and year (link)
- Steinberg, Diane (Spring 2005), "Belief, Affirmation, and the Doctrine of Conatus in Spinoza", Southern Journal of Philosophy, 43 (1): 147&ndash, 158, ISSN 0038-4283
- Tuusvuori, Jarkko S. (March 2000), Nietzsche & Nihilism: Exploring a Revolutionary Conception of Philosophical Conceptuality, University of Helsinki, ISBN 951-45-9135-6CS1 maint: Date and year (link)
- Wendell, Rich (1997), Spinoza's Conatus doctrine: existence, being, and suicide, Waltham, Mass., OCLC 37542442CS1 maint: Date and year (link)
- Youpa, A. (2003), "Spinozistic Self-Preservation", The Southern Journal of Philosophy, 41 (3): 477&ndash, 490
Template:Featured article
he:קונאטוס
sv:Conatus Template:Link FA
Template:WH
Template:WS | https://www.wikidoc.org/index.php/Conatus | |
41db23ceaaba126ef3a8a32519e2524e1c824de8 | wikidoc | Concave | Concave
The word concave means curving in or hollowed inward. The term is most commonly used to refer to:
- Concave lens, a lens with inward-curving (concave) surfaces.
- Concave polygon, a polygon which is not convex.
- Concave function, a type of function which is related to convex functions.
- Concave mirror
In addition, the term concave upwards is used for convex functions, and concave downwards for concave functions. | Concave
The word concave means curving in or hollowed inward. The term is most commonly used to refer to:
- Concave lens, a lens with inward-curving (concave) surfaces.
- Concave polygon, a polygon which is not convex.
- Concave function, a type of function which is related to convex functions.
- Concave mirror
In addition, the term concave upwards is used for convex functions, and concave downwards for concave functions. | https://www.wikidoc.org/index.php/Concave | |
56c553f27bda19713984c7bd5d581b4a3970f416 | wikidoc | Cooking | Cooking
Cooking is the act of preparing food for eating by the application of heat. It encompasses a vast range of methods, tools and combinations of ingredients to alter the flavor or digestibility of food. It is the general preparation process of selecting, measuring and combining of ingredients in an ordered procedure in an effort to achieve the desired result. Factors affecting the final outcome include the variability of ingredients, ambient conditions, tools, and the skill of the individual doing the actual cooking.
The diversity of cooking worldwide is a reflection of the myriad nutritional, aesthetic, agricultural, economic, cultural, social and religious considerations that impact upon it.
Applying heat to a food usually, though not always, chemically transforms it, thus changing its flavor, texture, consistency, appearance, and nutritional properties. There is archaeological evidence of roasted foodstuffs, both animal and vegetable, in human (Homo erectus) campsites dating from the earliest known use of fire, some 800,000 years ago. Other methods of cooking that involve the boiling of liquid in a receptacle have been practiced at least since the 10th millennium BC, with the introduction of pottery.
# Effects of cooking
## Proteins
Edible animal material, including muscle, offal, milk and egg white, contains substantial amounts of protein. Almost all vegetable matter (in particular legumes and seeds) also includes proteins, although generally in smaller amounts. These may also be a source of essential amino acids. When proteins are heated they become de-natured and change texture. In many cases, this causes the structure of the material to become softer or more friable - meat becomes cooked. In some cases, proteins can form more rigid structures, such as the coagulation of albumen in egg whites. The formation of a relatively rigid but flexible matrix from egg white provides an important component of much cake cookery, and also underpins many desserts based on meringue.
## Liquids
Cooking often involves water which is frequently present as other liquids, both added in order to immerse the substances being cooked (typically water, stock or wine), and released from the foods themselves. Liquids are so important to cooking that the name of the cooking method used may be based on how the liquid is combined with the food, as in steaming, simmering, boiling, braising and blanching. Heating liquid in an open container results in rapidly increased evaporation, which concentrates the remaining flavor and ingredients - this is a critical component of both stewing and sauce making.
## Fat
Fats and oils come from both animal and plant sources. In cooking, fats provide tastes and textures. When used as the principal cooking medium (rather than water), they also allow the cook access to a wide range of cooking temperatures. Common oil-cooking techniques include sauteing, stir-frying, and deep-frying. Commonly used fats and oils include butter; olive oil; vegetable oils such as sunflower oil, corn oil, and safflower oil; animal fats such as lard, schmaltz, and beef fat (both dripping and tallow); and seed oils such as rapeseed oil (Canola or mustard oil), sesame oil, soybean oil, and peanut oil. The inclusion of fats tends to add flavour to cooked food, even though the taste of the oil on its own is often unpleasant. This fact has encouraged the popularity of high fat foods, many of which are classified as junk food.
## Carbohydrates
Cooking include simple sugars such as glucose (from table sugar) and fructose (from fruit), and starches from sources such as cereal flour, rice, arrowroot, potato. The interaction of heat and carbohydrate is complex.
Long-chain sugars such as starch tend to break down into more simple sugars when cooked, while simple sugars can form syrups. If sugars are heated so that all water of crystallisation is driven off, then caramelisation starts, with the sugar undergoing thermal decomposition with the formation of carbon, and other breakdown products producing caramel. Similarly, the heating of sugars and proteins elicits the Maillard reaction, a basic flavor-enhancing technique.
An emulsion of starch with fat or water can, when gently heated, provide thickening to the dish being cooked. In European cooking, a mixture of butter and flour called a roux is used to thicken liquids to make stews or sauces. In Asian cooking, a similar effect is obtained from a mixture of rice or corn starch and water. These techniques rely on the properties of starches to create simpler mucilaginous saccharides during cooking, which causes the familiar thickening of sauces. This thickening will break down, however, under additional heat.
# Food safety
If heat is used in the preparation of food, this can kill or inactivate potentially harmful organisms including bacteria and viruses. The effect will depend on temperature, cooking time, and technique used. The temperature range from 41°F to 135°F (5°C to 57°C) is the "food danger zone." Between these temperatures bacteria can grow rapidly. Under optimal conditions, E. coli, for example, can double in number every twenty minutes. The food may not appear any different or spoiled but can be harmful to anyone who eats it. Meat, poultry, dairy products, and other prepared food must be kept outside of the "food danger zone" to remain safe to eat. Refrigeration and freezing do not kill bacteria, but only slow their growth. When cooling hot food, it shouldn't be left on the side or in a blast chiller (an appliance used to quickly cool food) for more than 90 minutes.
Cutting boards are a potential breeding ground for bacteria, and can be quite hazardous unless safety precautions are taken. Plastic cutting boards are less porous than wood and have conventionally been assumed to be far less likely to harbor bacteria. This has been debated, and some research have shown wooden boards are far better. Washing and sanitizing cutting boards is highly recommended, especially after use with raw meat, poultry, or seafood. Hot water and soap followed by a rinse with an antibacterial cleaner (dilute bleach is common in a mixture of 1 tablespoon per gallon of water, as at that dilution it is considered food safe, though some professionals choose not to use this method because they believe it could taint some foods), or a trip through a dishwasher with a "sanitize" cycle, are effective methods for reducing the risk of illness due to contaminated cooking implements.
# Science of cooking
The application of scientific knowledge to cooking and gastronomy has become known as molecular gastronomy. This is a subdiscipline of food science. Important contributions have been made by scientists, chefs and authors such as Herve This (chemist), Nicholas Kurti (physicist), Peter Barham (physicist), Harold McGee (author), Shirley Corriher (biochemist, author), Heston Blumenthal (chef), Ferran Adria (chef), Robert Wolke (chemist, author) and Pierre Gagnaire (chef).
## The culinary triangle
The culinary triangle is a concept thought up by Claude Lévi-Strauss involving three types of cooking; these are boiling, roasting, and smoking, usually done to meats.
The boiling of meat is looked at as a cultural way of cooking because it uses a receptacle to hold water, therefore it is not completely natural. It is also the most preferred way to cook due to the fact that neither any of the meat or its juices are lost. In most cultures, this form of cooking is most represented by women and is served domestically to small closed groups, such as families. Roasting of meat is a natural way of cooking because it uses no receptacle. It is done by directly exposing the meat to the fire. It is most commonly offered to guests and is associated with men in many cultures. As opposed to boiling, meat can lose some parts, thus it is also associated with destruction and loss. Smoking meat is also a natural way of cooking. It is also done without a receptacle and in the same way as roasting. It is a slower method of roasting, however, which makes it somewhat like boiling. | Cooking
Template:Otheruses4
Cooking is the act of preparing food for eating by the application of heat. It encompasses a vast range of methods, tools and combinations of ingredients to alter the flavor or digestibility of food. It is the general preparation process of selecting, measuring and combining of ingredients in an ordered procedure in an effort to achieve the desired result. Factors affecting the final outcome include the variability of ingredients, ambient conditions, tools, and the skill of the individual doing the actual cooking.
The diversity of cooking worldwide is a reflection of the myriad nutritional, aesthetic, agricultural, economic, cultural, social and religious considerations that impact upon it.
Applying heat to a food usually, though not always, chemically transforms it, thus changing its flavor, texture, consistency, appearance, and nutritional properties. There is archaeological evidence of roasted foodstuffs, both animal and vegetable, in human (Homo erectus) campsites dating from the earliest known use of fire, some 800,000 years ago[citation needed]. Other methods of cooking that involve the boiling of liquid in a receptacle have been practiced at least since the 10th millennium BC, with the introduction of pottery.[citation needed]
# Effects of cooking
## Proteins
Edible animal material, including muscle, offal, milk and egg white, contains substantial amounts of protein. Almost all vegetable matter (in particular legumes and seeds) also includes proteins, although generally in smaller amounts. These may also be a source of essential amino acids. When proteins are heated they become de-natured and change texture. In many cases, this causes the structure of the material to become softer or more friable - meat becomes cooked. In some cases, proteins can form more rigid structures, such as the coagulation of albumen in egg whites. The formation of a relatively rigid but flexible matrix from egg white provides an important component of much cake cookery, and also underpins many desserts based on meringue.
## Liquids
Cooking often involves water which is frequently present as other liquids, both added in order to immerse the substances being cooked (typically water, stock or wine), and released from the foods themselves. Liquids are so important to cooking that the name of the cooking method used may be based on how the liquid is combined with the food, as in steaming, simmering, boiling, braising and blanching. Heating liquid in an open container results in rapidly increased evaporation, which concentrates the remaining flavor and ingredients - this is a critical component of both stewing and sauce making.
## Fat
Fats and oils come from both animal and plant sources. In cooking, fats provide tastes and textures. When used as the principal cooking medium (rather than water), they also allow the cook access to a wide range of cooking temperatures. Common oil-cooking techniques include sauteing, stir-frying, and deep-frying. Commonly used fats and oils include butter; olive oil; vegetable oils such as sunflower oil, corn oil, and safflower oil; animal fats such as lard, schmaltz, and beef fat (both dripping and tallow); and seed oils such as rapeseed oil (Canola or mustard oil), sesame oil, soybean oil, and peanut oil. The inclusion of fats tends to add flavour to cooked food, even though the taste of the oil on its own is often unpleasant. This fact has encouraged the popularity of high fat foods, many of which are classified as junk food.
## Carbohydrates
Cooking include simple sugars such as glucose (from table sugar) and fructose (from fruit), and starches from sources such as cereal flour, rice, arrowroot, potato. The interaction of heat and carbohydrate is complex.
Long-chain sugars such as starch tend to break down into more simple sugars when cooked, while simple sugars can form syrups. If sugars are heated so that all water of crystallisation is driven off, then caramelisation starts, with the sugar undergoing thermal decomposition with the formation of carbon, and other breakdown products producing caramel. Similarly, the heating of sugars and proteins elicits the Maillard reaction, a basic flavor-enhancing technique.
An emulsion of starch with fat or water can, when gently heated, provide thickening to the dish being cooked. In European cooking, a mixture of butter and flour called a roux is used to thicken liquids to make stews or sauces. In Asian cooking, a similar effect is obtained from a mixture of rice or corn starch and water. These techniques rely on the properties of starches to create simpler mucilaginous saccharides during cooking, which causes the familiar thickening of sauces. This thickening will break down, however, under additional heat.
# Food safety
Template:Mainarticle
If heat is used in the preparation of food, this can kill or inactivate potentially harmful organisms including bacteria and viruses. The effect will depend on temperature, cooking time, and technique used. The temperature range from 41°F to 135°F (5°C to 57°C) is the "food danger zone." Between these temperatures bacteria can grow rapidly. Under optimal conditions, E. coli, for example, can double in number every twenty minutes. The food may not appear any different or spoiled but can be harmful to anyone who eats it. Meat, poultry, dairy products, and other prepared food must be kept outside of the "food danger zone" to remain safe to eat. Refrigeration and freezing do not kill bacteria, but only slow their growth. When cooling hot food, it shouldn't be left on the side or in a blast chiller (an appliance used to quickly cool food) for more than 90 minutes.
Cutting boards are a potential breeding ground for bacteria, and can be quite hazardous unless safety precautions are taken. Plastic cutting boards are less porous than wood and have conventionally been assumed to be far less likely to harbor bacteria.[1] This has been debated, and some research have shown wooden boards are far better.[2] Washing and sanitizing cutting boards is highly recommended, especially after use with raw meat, poultry, or seafood. Hot water and soap followed by a rinse with an antibacterial cleaner (dilute bleach is common in a mixture of 1 tablespoon per gallon of water, as at that dilution it is considered food safe, though some professionals choose not to use this method because they believe it could taint some foods), or a trip through a dishwasher with a "sanitize" cycle, are effective methods for reducing the risk of illness due to contaminated cooking implements.[2]
# Science of cooking
The application of scientific knowledge to cooking and gastronomy has become known as molecular gastronomy. This is a subdiscipline of food science. Important contributions have been made by scientists, chefs and authors such as Herve This (chemist), Nicholas Kurti (physicist), Peter Barham (physicist), Harold McGee (author), Shirley Corriher (biochemist, author), Heston Blumenthal (chef), Ferran Adria (chef), Robert Wolke (chemist, author) and Pierre Gagnaire (chef).
## The culinary triangle
The culinary triangle is a concept thought up by Claude Lévi-Strauss involving three types of cooking; these are boiling, roasting, and smoking, usually done to meats.[3]
The boiling of meat is looked at as a cultural way of cooking because it uses a receptacle to hold water, therefore it is not completely natural. It is also the most preferred way to cook due to the fact that neither any of the meat or its juices are lost. In most cultures, this form of cooking is most represented by women and is served domestically to small closed groups, such as families. Roasting of meat is a natural way of cooking because it uses no receptacle. It is done by directly exposing the meat to the fire. It is most commonly offered to guests and is associated with men in many cultures. As opposed to boiling, meat can lose some parts, thus it is also associated with destruction and loss. Smoking meat is also a natural way of cooking. It is also done without a receptacle and in the same way as roasting. It is a slower method of roasting, however, which makes it somewhat like boiling. | https://www.wikidoc.org/index.php/Cooking | |
5df040ee0eeccdb8d59b4ebad33ffe80fd5d1f23 | wikidoc | Copepod | Copepod
Copepods are a group of small crustaceans found in the sea and nearly every freshwater habitat and they constitute the biggest source of protein in the oceans. Many species are planktonic, but more are benthic, and some continental species may live in limno-terrestrial habitats and other wet terrestrial places, such as swamps, under leaf fall in wet forests, bogs, springs, ephemeral ponds and puddles, damp moss, or water-filled recesses (phytotelmata) of plants such as bromeliads and pitcher plants. Many live underground in marine and freshwater caves, sinkholes, or stream beds. Copepods are sometimes used as bioindicators (see particle (ecology)).
# Ecology
Planktonic copepods are important to global ecology and the carbon cycle; They are usually the dominant members of the zooplankton, and are major food organisms for small fish, whales, seabirds and other crustaceans such as krill in the ocean and in fresh water. Some scientists say they form the largest animal biomass on earth. They compete for this title with Antarctic krill (Euphausia superba). Because of their smaller size and relatively faster growth rates, however, and because they are more evenly distributed throughout more of the world's oceans, copepods almost certainly contribute far more to the secondary productivity of the world's oceans, and to the global ocean carbon sink than krill, and perhaps than all other groups of organisms together. The surface layers of the oceans are currently believed to be the world's largest carbon sink, absorbing about 2 billion tonnes of carbon a year, the equivalent to perhaps a third of human carbon emissions, thus reducing their impact. Many planktonic copepods feed near the surface at night, then sink into deeper water during the day to avoid visual predators. Their moulted exoskeletons, faecal pellets and respiration at depth all bring carbon to the deep sea.
Some copepods are parasitic and have strongly modified bodies. They attach themselves to fish, sharks, marine mammals, and many kinds of invertebrates such as molluscs, tunicates, or corals. They live as endo- or ectoparasites on fish or invertebrates in fresh water as well as in marine environments.
# Characteristics
Copepods are typically 1 millimetre (0.0393700787 in) to 2 millimetres (0.0787401574 in) long, with a teardrop shaped body and large antennae. Although like other crustaceans they have an armoured exoskeleton, they are so small that in most species this armour, and the entire body, is almost totally transparent. Copepods have a single eye, usually bright red and in the centre of the transparent head. Some polar copepods reach 1 (0.393700787 ). Most of the smaller copepods feed directly on phytoplankton, catching cells singly, but a few of the larger species are predators of their smaller relatives. Herbivorous copepods, particularly those in rich cold seas, store up energy from their food as oil droplets while they feed in the spring and summer plankton blooms. These droplets may take up over half of the volume of the body in polar species.
Many species have neurons surrounded by myelin, which is very rare among invertebrates (other examples are some annelids and malacostracan crustaceans like palaemonid shrimp and penaeids). Even rarer is the fact that the myelin is highly organized, resembling the well-organized wrapping found in vertebrates (Gnathostomata).
Some copepods are very evasive and can jump with extreme speed over a few millimeters (warning: takes some time to load to the correct speed):
This scene was scanned with the ecoSCOPE, an underwater high speed microscope. Very little is known about the details of these kinds of predator/prey interactions, in spite of their importance for global processes, because copepods are difficult to keep in the laboratory and lose most of their escape capacity, and herring are very fast, alert and evasive organisms and flee from normal camera systems or scuba divers.
# Classification
Copepods form a subclass belonging to the subphylum Crustacea (crustaceans). Some authors consider the copepods to be a full class. The group contains ten orders with some 14,000 described species. A scientist that studies copepods is a copepodologist.
# Water supply
Copepods are sometimes found in the public mains water supply, especially systems where the water is not filtered, such as New York City and Boston, Massachusetts. This is not usually a problem in treated water supplies. In some tropical countries, such as Peru and Bangladesh, a correlation has been found between copepods and cholera in untreated water, because the cholera bacteria attach to the surfaces of planktonic animals. The risk of cholera from infected water can be reduced by filtering out the copepods (and other matter), for example with a cloth filter. | Copepod
Copepods are a group of small crustaceans found in the sea and nearly every freshwater habitat and they constitute the biggest source of protein in the oceans.[1] Many species are planktonic, but more are benthic, and some continental species may live in limno-terrestrial habitats and other wet terrestrial places, such as swamps, under leaf fall in wet forests, bogs, springs, ephemeral ponds and puddles, damp moss, or water-filled recesses (phytotelmata) of plants such as bromeliads and pitcher plants. Many live underground in marine and freshwater caves, sinkholes, or stream beds. Copepods are sometimes used as bioindicators (see particle (ecology)).
# Ecology
Planktonic copepods are important to global ecology and the carbon cycle; They are usually the dominant members of the zooplankton, and are major food organisms for small fish, whales, seabirds and other crustaceans such as krill in the ocean and in fresh water. Some scientists say they form the largest animal biomass on earth. They compete for this title with Antarctic krill (Euphausia superba). Because of their smaller size and relatively faster growth rates, however, and because they are more evenly distributed throughout more of the world's oceans, copepods almost certainly contribute far more to the secondary productivity of the world's oceans, and to the global ocean carbon sink than krill, and perhaps than all other groups of organisms together. The surface layers of the oceans are currently believed to be the world's largest carbon sink, absorbing about 2 billion tonnes of carbon a year, the equivalent to perhaps a third of human carbon emissions, thus reducing their impact. Many planktonic copepods feed near the surface at night, then sink into deeper water during the day to avoid visual predators. Their moulted exoskeletons, faecal pellets and respiration at depth all bring carbon to the deep sea.
Some copepods are parasitic[2][3] and have strongly modified bodies. They attach themselves to fish, sharks, marine mammals, and many kinds of invertebrates such as molluscs, tunicates, or corals. They live as endo- or ectoparasites on fish or invertebrates in fresh water as well as in marine environments.
# Characteristics
Copepods are typically 1 millimetre (0.0393700787 in) to 2 millimetres (0.0787401574 in) long, with a teardrop shaped body and large antennae. Although like other crustaceans they have an armoured exoskeleton, they are so small that in most species this armour, and the entire body, is almost totally transparent. Copepods have a single eye, usually bright red and in the centre of the transparent head. Some polar copepods reach 1 (0.393700787 ). Most of the smaller copepods feed directly on phytoplankton, catching cells singly, but a few of the larger species are predators of their smaller relatives. Herbivorous copepods, particularly those in rich cold seas, store up energy from their food as oil droplets while they feed in the spring and summer plankton blooms. These droplets may take up over half of the volume of the body in polar species.
Many species have neurons surrounded by myelin, which is very rare among invertebrates (other examples are some annelids and malacostracan crustaceans like palaemonid shrimp and penaeids). Even rarer is the fact that the myelin is highly organized, resembling the well-organized wrapping found in vertebrates (Gnathostomata).
Some copepods are very evasive and can jump with extreme speed over a few millimeters (warning: takes some time to load to the correct speed):
This scene was scanned with the ecoSCOPE, an underwater high speed microscope. Very little is known about the details of these kinds of predator/prey interactions, in spite of their importance for global processes, because copepods are difficult to keep in the laboratory and lose most of their escape capacity, and herring are very fast, alert and evasive organisms and flee from normal camera systems or scuba divers.
# Classification
Copepods form a subclass belonging to the subphylum Crustacea (crustaceans). Some authors consider the copepods to be a full class. The group contains ten orders with some 14,000 described species. A scientist that studies copepods is a copepodologist.
# Water supply
Copepods are sometimes found in the public mains water supply, especially systems where the water is not filtered, such as New York City and Boston, Massachusetts. This is not usually a problem in treated water supplies. In some tropical countries, such as Peru and Bangladesh, a correlation has been found between copepods and cholera in untreated water, because the cholera bacteria attach to the surfaces of planktonic animals. The risk of cholera from infected water can be reduced by filtering out the copepods (and other matter), for example with a cloth filter. | https://www.wikidoc.org/index.php/Copepod | |
49873edd9ea2e864cf7dc64972e5ebcc74fd0c23 | wikidoc | Steroid | Steroid
# Overview
A steroid is a terpenoid lipid characterized by a carbon skeleton with four fused rings, generally arranged in a 6-6-6-5 fashion.
Steroids can vary by the functional groups attached to these rings and the oxidation state of the rings. Hundreds of distinct steroids are found in plants, animals, and fungi. All steroids are biosynthetically derived either from the sterol lanosterol (animals and fungi) or the sterol cycloartenol (plants). Both sterols are derived from the cyclization of the triterpene squalene.
# Origin
Steroids include estrogen (US spelling) or oestrogen (UK/AUS spelling), progesterone and testosterone. Oestrogen and progesterone are made primarily in the ovary and in the placenta during pregnancy and testosterone in the testes. Certain neurons and glia in the central nervous system (CNS) express the enzymes that are required for the local synthesis of pregnane neurosteroids, either de novo or from peripherally derived sources.
# Classification
## Taxonomical/Functional
Some of the common categories of steroids:
- Animal steroids
Insect steroids
Ecdysteroids such as ecdysterone
Vertebrate steroids
Steroid hormones
Sex steroids are a subset of sex hormones that produce sex differences or support reproduction. They include androgens, estrogens, and progestagens.
Corticosteroids include glucocorticoids and mineralocorticoids. Glucocorticoids regulate many aspects of metabolism and immune function, whereas mineralocorticoids help maintain blood volume and control renal excretion of electrolytes.
Anabolic steroids are a class of steroids that interact with androgen receptors to increase muscle and bone synthesis. There are natural and synthetic anabolic steroids. In popular language the word "steroids" usually refers to anabolic steroids.
Cholesterol which modulates the fluidity of cell membranes and is the principle constituent of the plaques implicated in atherosclerosis.
- Insect steroids
Ecdysteroids such as ecdysterone
- Ecdysteroids such as ecdysterone
- Vertebrate steroids
Steroid hormones
Sex steroids are a subset of sex hormones that produce sex differences or support reproduction. They include androgens, estrogens, and progestagens.
Corticosteroids include glucocorticoids and mineralocorticoids. Glucocorticoids regulate many aspects of metabolism and immune function, whereas mineralocorticoids help maintain blood volume and control renal excretion of electrolytes.
Anabolic steroids are a class of steroids that interact with androgen receptors to increase muscle and bone synthesis. There are natural and synthetic anabolic steroids. In popular language the word "steroids" usually refers to anabolic steroids.
Cholesterol which modulates the fluidity of cell membranes and is the principle constituent of the plaques implicated in atherosclerosis.
- Steroid hormones
Sex steroids are a subset of sex hormones that produce sex differences or support reproduction. They include androgens, estrogens, and progestagens.
Corticosteroids include glucocorticoids and mineralocorticoids. Glucocorticoids regulate many aspects of metabolism and immune function, whereas mineralocorticoids help maintain blood volume and control renal excretion of electrolytes.
Anabolic steroids are a class of steroids that interact with androgen receptors to increase muscle and bone synthesis. There are natural and synthetic anabolic steroids. In popular language the word "steroids" usually refers to anabolic steroids.
- Sex steroids are a subset of sex hormones that produce sex differences or support reproduction. They include androgens, estrogens, and progestagens.
- Corticosteroids include glucocorticoids and mineralocorticoids. Glucocorticoids regulate many aspects of metabolism and immune function, whereas mineralocorticoids help maintain blood volume and control renal excretion of electrolytes.
- Anabolic steroids are a class of steroids that interact with androgen receptors to increase muscle and bone synthesis. There are natural and synthetic anabolic steroids. In popular language the word "steroids" usually refers to anabolic steroids.
- Cholesterol which modulates the fluidity of cell membranes and is the principle constituent of the plaques implicated in atherosclerosis.
- Plant steroids
Phytosterols
Brassinosteroids
- Phytosterols
- Brassinosteroids
- Fungus steroids
Ergosterols
- Ergosterols
## Structural
It is also possible to classify steroids based upon their chemical composition.
# See Also
- List of steroid abbreviations | Steroid
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
# Overview
A steroid is a terpenoid lipid characterized by a carbon skeleton with four fused rings, generally arranged in a 6-6-6-5 fashion.
Steroids can vary by the functional groups attached to these rings and the oxidation state of the rings. Hundreds of distinct steroids are found in plants, animals, and fungi. All steroids are biosynthetically derived either from the sterol lanosterol (animals and fungi) or the sterol cycloartenol (plants). Both sterols are derived from the cyclization of the triterpene squalene.[1]
# Origin
Steroids include estrogen (US spelling) or oestrogen (UK/AUS spelling), progesterone and testosterone. Oestrogen and progesterone are made primarily in the ovary and in the placenta during pregnancy and testosterone in the testes. Certain neurons and glia in the central nervous system (CNS) express the enzymes that are required for the local synthesis of pregnane neurosteroids, either de novo or from peripherally derived sources.
# Classification
## Taxonomical/Functional
Some of the common categories of steroids:
- Animal steroids
Insect steroids
Ecdysteroids such as ecdysterone
Vertebrate steroids
Steroid hormones
Sex steroids are a subset of sex hormones that produce sex differences or support reproduction. They include androgens, estrogens, and progestagens.
Corticosteroids include glucocorticoids and mineralocorticoids. Glucocorticoids regulate many aspects of metabolism and immune function, whereas mineralocorticoids help maintain blood volume and control renal excretion of electrolytes.
Anabolic steroids are a class of steroids that interact with androgen receptors to increase muscle and bone synthesis. There are natural and synthetic anabolic steroids. In popular language the word "steroids" usually refers to anabolic steroids.
Cholesterol which modulates the fluidity of cell membranes and is the principle constituent of the plaques implicated in atherosclerosis.
- Insect steroids
Ecdysteroids such as ecdysterone
- Ecdysteroids such as ecdysterone
- Vertebrate steroids
Steroid hormones
Sex steroids are a subset of sex hormones that produce sex differences or support reproduction. They include androgens, estrogens, and progestagens.
Corticosteroids include glucocorticoids and mineralocorticoids. Glucocorticoids regulate many aspects of metabolism and immune function, whereas mineralocorticoids help maintain blood volume and control renal excretion of electrolytes.
Anabolic steroids are a class of steroids that interact with androgen receptors to increase muscle and bone synthesis. There are natural and synthetic anabolic steroids. In popular language the word "steroids" usually refers to anabolic steroids.
Cholesterol which modulates the fluidity of cell membranes and is the principle constituent of the plaques implicated in atherosclerosis.
- Steroid hormones
Sex steroids are a subset of sex hormones that produce sex differences or support reproduction. They include androgens, estrogens, and progestagens.
Corticosteroids include glucocorticoids and mineralocorticoids. Glucocorticoids regulate many aspects of metabolism and immune function, whereas mineralocorticoids help maintain blood volume and control renal excretion of electrolytes.
Anabolic steroids are a class of steroids that interact with androgen receptors to increase muscle and bone synthesis. There are natural and synthetic anabolic steroids. In popular language the word "steroids" usually refers to anabolic steroids.
- Sex steroids are a subset of sex hormones that produce sex differences or support reproduction. They include androgens, estrogens, and progestagens.
- Corticosteroids include glucocorticoids and mineralocorticoids. Glucocorticoids regulate many aspects of metabolism and immune function, whereas mineralocorticoids help maintain blood volume and control renal excretion of electrolytes.
- Anabolic steroids are a class of steroids that interact with androgen receptors to increase muscle and bone synthesis. There are natural and synthetic anabolic steroids. In popular language the word "steroids" usually refers to anabolic steroids.
- Cholesterol which modulates the fluidity of cell membranes and is the principle constituent of the plaques implicated in atherosclerosis.
- Plant steroids
Phytosterols
Brassinosteroids
- Phytosterols
- Brassinosteroids
- Fungus steroids
Ergosterols
- Ergosterols
## Structural
It is also possible to classify steroids based upon their chemical composition.
# See Also
- List of steroid abbreviations | https://www.wikidoc.org/index.php/Corticosteriod | |
21887a42c3356814d11f7142c29c1f8c91f2e980 | wikidoc | Covance | Covance
Covance Inc. (Template:Nyse), formerly Hazleton Laboratories America, Inc., with headquarters in Princeton, New Jersey, provides drug development and animal testing services. According to its website, it is one of the largest companies of its kind in the world, with annual revenues of over $1 billion, operations in 20 countries, and over 8,000 employees worldwide. It provides the world's largest central laboratory network, and employs a global team of clinical trial professionals and cardiac safety experts. It became a publicly traded company after being spun off by Corning, Inc. in 1997.
Under the name Covance Research Products Inc. (CRP), based in Denver, Pennsylvania, the company also deals in the import and sale of laboratory animals. It is the single largest importer of primates in the U.S. and the world's largest breeder of laboratory dogs. It owns two dog-breeding facilities, two primate centers, and a rabbit-breeding facility.
The company has been the subject of controversy following allegations of primate abuse in its laboratories in Germany and the United States, and in connection with a potential outbreak of the Ebola virus.
# History of Covance
In the late 1980s and early 1990s, Corning Incorporated acquired numerous best-of-class drug development companies, some with roots dating back to the 1940s. In January 1997, Corning spun off these businesses as one publicly traded, independent company called Covance Inc..
The company's primary focus is serving the pharmaceutical and biotech industries. It provides testing services to the environmental, food, and nutritional supplement industries, and provides custom antibody products and services to the research community for neurological disorders. It also offers cell type-specific marker antibodies for neuroscience; suites of products for both Alzheimer’s and Parkinson’s disease; and an online antibody store including phospho-specific and secondary antibodies.
# Ebola virus
In October 1989, 100 cynomolgus macaques (Macaca fascicularis) were imported from Mindanao Island in the Philippines through Amsterdam and New York to Hazleton Research Products' (now Covance), Primate Quarantine Unit in Reston, Virginia. A second shipment from the same supplier arrived on November 8. Shortly afterwards, some of the monkeys were found to have carried the Ebola.
In January 1990, the same Philippines supplier sent a shipment of 100 macaques to Hazleton's Texas Primate Center in Alice, Texas and another 100 Hazleton's Reston Unit. Between February 1 and March 15, 46 of 52 monkeys in one of the quarantine rooms died, showing the same symptoms as before. The Centers for Disease Control decided the monkeys were infected with simian hemorrhagic fever and Ebola.
In March 1996, 100 macaques from the same supplier were shipped to Hazleton in Alice, Texas. Two monkeys tested positive for the Ebola virus.
# Alleged primate abuse
## Münster, Germany
In 2004, German journalist Friedrich Mülln, working undercover at the German Covance facility in Münster, Europe's largest primate-testing center, obtained photographs, video, and other evidence of alleged abuse of monkeys and other non-human primates. The laboratory in Münster specializes in reproduction toxicology and primate toxicology, which includes testing on pregnant primates. The company is responsible for around half the primate experiments in Germany.
The undercover footage shows staff making monkeys dance in time to blaring pop music, handling them roughly, and screaming at them. The monkeys are shown isolated in small wire cages with little or no natural light and no environmental enrichment, and living with high noise levels caused by staff shouting and playing the radio.
Primatologist Dr. Jane Goodall described the living conditions of the monkeys as "horrendous," and told the British Union for the Abolition of Vivisection (BUAV) that to see them "crazed with boredom, and sadness probably, is deeply, deeply disturbing." Primatologist Stephen Brend told BUAV that using monkeys in such a stressed state is "bad science" and that trying to extrapolate useful data in such circumstances is an "untenable proposition."
The ensuing publicity in Germany gave rise to the "Close Covance" (Covance Schliessen) animal rights campaign there, as well as campaigns launched in Britain by the BUAV, and in America by PETA.
According to the European Biomedical Research Association, the local authorities in Munster inspected Covance after the video footage was shown on German television, and insisted that Covance install video cameras to monitor staff working with primates. Covance appealed through the courts, which decided that video monitoring would infringe the rights of the staff. The public prosecutor's office also viewed the film and questioned witnesses. The prosecutor's office concluded that Covance "had not rendered themselves liable to prosecution," thus clearing Covance of all charges. Covance maintains that the editing of the footage exaggerated the evidence.
After parts of Mülln's footage were shown on German television and in major newspapers, Covance filed a lawsuit, leading a German court to forbid further distribution of the material. The publication ban led to major protests from animal-rights advocates and anti-censorship activists. A first ruling confirming Covance's claims was partially reverted by a higher court's ruling that the right of the public to be informed on the subject prevailed over the company's privacy rights. The video footage may now be displayed publicly, albeit not in the form of the existing television edition, but it may not be used by animal-rights groups.
## Vienna, Virginia
People for the Ethical Treatment of Animals (PETA) found similar conditions in Covance's Vienna, Virginia lab during an undercover investigation in 2004-5.
A former study director at the Covance facility in Vienna, Virginia in the U.S., who worked there from 2002 to 2004, told city officials in Chandler, Arizona, that Covance was dissecting monkeys in its Vienna laboratory while the animals were still alive and able to feel pain.
The allegations were uncovered as part of an open-records request made by PETA in November 2006. The employee had earlier approached the city with her concerns when she learned that Covance planned to build a new laboratory in Chandler.
She alleged that three monkeys in the Vienna laboratory had pushed themselves up on their elbows and had gasped for breath after their eyes had been removed, and while their intestines were being removed during necropsies. When she expressed concern at the next study directors' meeting, the employee says she was told that it was just a reflex. She told city officials that she believed such movements were not reflexes but suggested "botched euthanasia performed by inadequately trained personnel." She says that she was ridiculed and subjected to thinly veiled threats when she contacted her supervisors about the issue.
In June 2005, Covance filed a lawsuit against PETA and its former employee for fraud, breach of employee contract, and "conspiracy to harm the company's business by deceitfully infiltrating and videotaping the company's Vienna, Virginia facility." Covance and PETA agreed to a settlement in which PETA accepted a five-year ban on any attempts to infiltrate Covance facilities.
In a March 2006 statement, Covance announced that inspections of the Vienna, Virginia facility by the Food & Drug Administration (FDA) “resulted in no findings to substantiate any claims made against the facility.” Inspections by the United States Department of Agriculture (USDA) resulted in sixteen citations ranging, according to Covance, from "administrative issues to scope of veterinary authority." The company agreed to pay a settlement of $8,720.
# Expansion
In recent years, Covance continued its expansion with acquisitions of drug development companies. Notably, in August 2005, Covance acquired GFI Clinical Services, an 80-bed clinical pharmacology business, from West Pharmaceutical Services, Inc. in order to expand the company’s Phase I clinical research offerings.
In May 2006, Covance also acquired Signet Laboratories, Inc., which is a provider of monoclonal antibodies used in the research of cancer, infectious disease and neurodegenerative disease. | Covance
Template:Infobox Company
Covance Inc. (Template:Nyse), formerly Hazleton Laboratories America, Inc., with headquarters in Princeton, New Jersey, provides drug development and animal testing services. According to its website, it is one of the largest companies of its kind in the world, with annual revenues of over $1 billion, operations in 20 countries, and over 8,000 employees worldwide. It provides the world's largest central laboratory network, and employs a global team of clinical trial professionals and cardiac safety experts.[1] It became a publicly traded company after being spun off by Corning, Inc. in 1997.
Under the name Covance Research Products Inc. (CRP), based in Denver, Pennsylvania, the company also deals in the import and sale of laboratory animals. It is the single largest importer of primates in the U.S. and the world's largest breeder of laboratory dogs.[citation needed] It owns two dog-breeding facilities, two primate centers, and a rabbit-breeding facility.
The company has been the subject of controversy following allegations of primate abuse in its laboratories in Germany and the United States, and in connection with a potential outbreak of the Ebola virus.
# History of Covance
In the late 1980s and early 1990s, Corning Incorporated acquired numerous best-of-class drug development companies, some with roots dating back to the 1940s. In January 1997, Corning spun off these businesses as one publicly traded, independent company called Covance Inc..
The company's primary focus is serving the pharmaceutical and biotech industries. It provides testing services to the environmental, food, and nutritional supplement industries, and provides custom antibody products and services to the research community for neurological disorders. It also offers cell type-specific marker antibodies for neuroscience; suites of products for both Alzheimer’s and Parkinson’s disease; and an online antibody store including phospho-specific and secondary antibodies.
# Ebola virus
In October 1989, 100 cynomolgus macaques (Macaca fascicularis) were imported from Mindanao Island in the Philippines through Amsterdam and New York to Hazleton Research Products' (now Covance), Primate Quarantine Unit in Reston, Virginia. A second shipment from the same supplier arrived on November 8. Shortly afterwards, some of the monkeys were found to have carried the Ebola.[2]
In January 1990, the same Philippines supplier sent a shipment of 100 macaques to Hazleton's Texas Primate Center in Alice, Texas and another 100 Hazleton's Reston Unit. Between February 1 and March 15, 46 of 52 monkeys in one of the quarantine rooms died, showing the same symptoms as before. The Centers for Disease Control decided the monkeys were infected with simian hemorrhagic fever and Ebola.[2]
In March 1996, 100 macaques from the same supplier were shipped to Hazleton in Alice, Texas. Two monkeys tested positive for the Ebola virus.[2][3]
# Alleged primate abuse
## Münster, Germany
In 2004, German journalist Friedrich Mülln, working undercover at the German Covance facility in Münster, Europe's largest primate-testing center, obtained photographs, video, and other evidence of alleged abuse of monkeys and other non-human primates. The laboratory in Münster specializes in reproduction toxicology and primate toxicology, which includes testing on pregnant primates. The company is responsible for around half the primate experiments in Germany.[citation needed]
The undercover footage shows staff making monkeys dance in time to blaring pop music, handling them roughly, and screaming at them. The monkeys are shown isolated in small wire cages with little or no natural light and no environmental enrichment, and living with high noise levels caused by staff shouting and playing the radio.[4]
Primatologist Dr. Jane Goodall described the living conditions of the monkeys as "horrendous," and told the British Union for the Abolition of Vivisection (BUAV) that to see them "crazed with boredom, and sadness probably, is deeply, deeply disturbing." Primatologist Stephen Brend told BUAV that using monkeys in such a stressed state is "bad science" and that trying to extrapolate useful data in such circumstances is an "untenable proposition."[4]
The ensuing publicity in Germany gave rise to the "Close Covance" (Covance Schliessen) animal rights campaign there, as well as campaigns launched in Britain by the BUAV, and in America by PETA.
According to the European Biomedical Research Association, the local authorities in Munster inspected Covance after the video footage was shown on German television, and insisted that Covance install video cameras to monitor staff working with primates.[5] Covance appealed through the courts, which decided that video monitoring would infringe the rights of the staff. The public prosecutor's office also viewed the film and questioned witnesses. The prosecutor's office concluded that Covance "had not rendered themselves liable to prosecution," thus clearing Covance of all charges. Covance maintains that the editing of the footage exaggerated the evidence.[5]
After parts of Mülln's footage were shown on German television and in major newspapers, Covance filed a lawsuit, leading a German court to forbid further distribution of the material. The publication ban led to major protests from animal-rights advocates and anti-censorship activists. A first ruling confirming Covance's claims was partially reverted by a higher court's ruling that the right of the public to be informed on the subject prevailed over the company's privacy rights. The video footage may now be displayed publicly, albeit not in the form of the existing television edition, but it may not be used by animal-rights groups.
## Vienna, Virginia
Template:Animal testing
People for the Ethical Treatment of Animals (PETA) found similar conditions in Covance's Vienna, Virginia lab during an undercover investigation in 2004-5.[6]
A former study director at the Covance facility in Vienna, Virginia in the U.S., who worked there from 2002 to 2004, told city officials in Chandler, Arizona, that Covance was dissecting monkeys in its Vienna laboratory while the animals were still alive and able to feel pain.
The allegations were uncovered as part of an open-records request made by PETA in November 2006. The employee had earlier approached the city with her concerns when she learned that Covance planned to build a new laboratory in Chandler. [2]
She alleged that three monkeys in the Vienna laboratory had pushed themselves up on their elbows and had gasped for breath after their eyes had been removed, and while their intestines were being removed during necropsies. When she expressed concern at the next study directors' meeting, the employee says she was told that it was just a reflex. She told city officials that she believed such movements were not reflexes but suggested "botched euthanasia performed by inadequately trained personnel." She says that she was ridiculed and subjected to thinly veiled threats when she contacted her supervisors about the issue.[7]
In June 2005, Covance filed a lawsuit against PETA and its former employee for fraud, breach of employee contract, and "conspiracy to harm the company's business by deceitfully infiltrating and videotaping the company's Vienna, Virginia facility." Covance and PETA agreed to a settlement in which PETA accepted a five-year ban on any attempts to infiltrate Covance facilities. [8]
In a March 2006 statement, Covance announced that inspections of the Vienna, Virginia facility by the Food & Drug Administration (FDA) “resulted in no findings to substantiate any claims made against the facility.” Inspections by the United States Department of Agriculture (USDA) resulted in sixteen citations ranging, according to Covance, from "administrative issues to scope of veterinary authority." The company agreed to pay a settlement of $8,720. [3]
# Expansion
In recent years, Covance continued its expansion with acquisitions of drug development companies. Notably, in August 2005, Covance acquired GFI Clinical Services, an 80-bed clinical pharmacology business, from West Pharmaceutical Services, Inc. in order to expand the company’s Phase I clinical research offerings. [4]
In May 2006, Covance also acquired Signet Laboratories, Inc., which is a provider of monoclonal antibodies used in the research of cancer, infectious disease and neurodegenerative disease. [5] | https://www.wikidoc.org/index.php/Covance | |
d1ce7b1cd19c783c381fedfb156ccdcce60fbb30 | wikidoc | Cowlick | Cowlick
A cowlick appears when the growth direction of the hair forms a spiral pattern. The hair in a cowlick either stands straight up or lies at an extreme angle and seems to be always at odds with the style in which the rest of the hair is worn. They can show up anywhere. The most common site is in the crown like the one belonging to Carl "Alfalfa" Switzer of the “Our Gang” comedy series of the 1930s and 1940s, or on Dennis the Menace.
The term cowlick dates from the late 16th century, when Richard Haydocke used it in his translation of Lomazzo: "The lockes or plaine feakes of haire called cow-lickes, are made turning upwards." Also, the Latin word "calyx" is often pronounced this way and literally means a whorled look or appearance on something, and the "cowlick" always has a whorled appearance.
# Management
Many people find Cowlicks to be extremely irritating, as they often conflict with the desired hairstyle. There are several methods of taming the unruly cowlick. For most people, a combination of the right hairstyle, length, product used, and styling technique can overcome the appearance. For people more serious about cowlick management, more drastic measures may be used. Electrology, waxing, and even cosmetic surgery can be used to more permanently correct the cowlick. | Cowlick
Template:Inappropriate tone
A cowlick appears when the growth direction of the hair forms a spiral pattern. The hair in a cowlick either stands straight up or lies at an extreme angle and seems to be always at odds with the style in which the rest of the hair is worn. They can show up anywhere. The most common site is in the crown like the one belonging to Carl "Alfalfa" Switzer of the “Our Gang” comedy series of the 1930s and 1940s, or on Dennis the Menace.[1]
The term cowlick dates from the late 16th century, when Richard Haydocke used it in his translation of Lomazzo: "The lockes or plaine feakes of haire called cow-lickes, are made turning upwards." Also, the Latin word "calyx" is often pronounced this way and literally means a whorled look or appearance on something, and the "cowlick" always has a whorled appearance. [2]
# Management
Many people find Cowlicks to be extremely irritating, as they often conflict with the desired hairstyle. There are several methods of taming the unruly cowlick. For most people, a combination of the right hairstyle, length, product used, and styling technique can overcome the appearance. For people more serious about cowlick management, more drastic measures may be used. Electrology, waxing, and even cosmetic surgery can be used to more permanently correct the cowlick.[3] | https://www.wikidoc.org/index.php/Cowlick | |
c85d31257110949b5c29bc89cdd782b52e4bf1b0 | wikidoc | Cricoid | Cricoid
The cricoid cartilage, or simply cricoid (from the Greek krikoeides meaning "ring-shaped"), is the only complete ring of cartilage around the trachea.
# Location
It sits just inferior to the thyroid cartilage in the neck, and is joined to it medially by the median cricothyroid ligament and postero-laterally by the cricothyroid joints. Inferior to it are the rings of cartilage around the trachea (which are not continuous - rather they are C-shaped with a gap posteriorly). The cricoid is joined to the first tracheal ring by the cricotracheal ligament, and this can be felt as a more yielding area between the firm thyroid cartilage and firmer cricoid.
It is also anatomically related to the thyroid gland; although the thyroid isthmus is inferior to it, the two lobes of the thyroid extend superiorly on each side of the cricoid as far as the thyroid cartilage above it.
The posterior part of the cricoid is slightly broader than the anterior and lateral parts, and is called the lamina, while the anterior part is the band; this may be the reason for the common comparison made between the cricoid and a signet ring.
# Function
The function of the cricoid is to provide attachments for the various muscles, cartilages, and ligaments involved in opening and closing the airway and in speech production.
# Composition
It is made of hyaline cartilage, and so can become calcified or even ossified, particularly in old age.
# Clinical significance
When intubating a patient under general anesthesia prior to surgery, the anesthesiologist will press on the cricoid cartilage to compress the esophagus behind it so as to prevent gastric reflux from occurring.
Gastric reflux could cause aspiration if this is not done considering the general anesthesia can cause relaxation of the gastro-esophageal sphincter allowing stomach contents to ascend through the esophagus into the trachea.
# Additional images
- Larynx
- Tracheotomy neck profile
Tracheotomy neck profile
- Muscles of the pharynx and cheek.
- The cartilages of the larynx. Posterior view.
- Ligaments of the larynx. Posterior view.
- Sagittal section of the larynx and upper part of the trachea.
- Coronal section of larynx and upper part of trachea.
- The entrance to the larynx, viewed from behind.
- Muscles of larynx. Side view. Right lamina of thyroid cartilage removed.
- Muscles of the larynx, seen from above.
- Sagittal section of nose mouth, pharynx, and larynx.
- Front view of neck. | Cricoid
Template:Infobox Anatomy
The cricoid cartilage, or simply cricoid (from the Greek krikoeides meaning "ring-shaped"), is the only complete ring of cartilage around the trachea.
# Location
It sits just inferior to the thyroid cartilage in the neck, and is joined to it medially by the median cricothyroid ligament and postero-laterally by the cricothyroid joints. Inferior to it are the rings of cartilage around the trachea (which are not continuous - rather they are C-shaped with a gap posteriorly). The cricoid is joined to the first tracheal ring by the cricotracheal ligament, and this can be felt as a more yielding area between the firm thyroid cartilage and firmer cricoid.
It is also anatomically related to the thyroid gland; although the thyroid isthmus is inferior to it, the two lobes of the thyroid extend superiorly on each side of the cricoid as far as the thyroid cartilage above it.
The posterior part of the cricoid is slightly broader than the anterior and lateral parts, and is called the lamina, while the anterior part is the band; this may be the reason for the common comparison made between the cricoid and a signet ring.
# Function
The function of the cricoid is to provide attachments for the various muscles, cartilages, and ligaments involved in opening and closing the airway and in speech production.
# Composition
It is made of hyaline cartilage, and so can become calcified or even ossified, particularly in old age.
# Clinical significance
When intubating a patient under general anesthesia prior to surgery, the anesthesiologist will press on the cricoid cartilage to compress the esophagus behind it so as to prevent gastric reflux from occurring.
Gastric reflux could cause aspiration if this is not done considering the general anesthesia can cause relaxation of the gastro-esophageal sphincter allowing stomach contents to ascend through the esophagus into the trachea.
# Additional images
- Larynx
- Tracheotomy neck profile
Tracheotomy neck profile
- Muscles of the pharynx and cheek.
- The cartilages of the larynx. Posterior view.
- Ligaments of the larynx. Posterior view.
- Sagittal section of the larynx and upper part of the trachea.
- Coronal section of larynx and upper part of trachea.
- The entrance to the larynx, viewed from behind.
- Muscles of larynx. Side view. Right lamina of thyroid cartilage removed.
- Muscles of the larynx, seen from above.
- Sagittal section of nose mouth, pharynx, and larynx.
- Front view of neck. | https://www.wikidoc.org/index.php/Cricoid | |
a7fe520137a6549d4fe90b19c026bd2bd718f8df | wikidoc | Crystal | Crystal
In chemistry, mineralogy, and materials science, a crystal is a solid in which the constituent atoms, molecules, or ions are packed in a regularly ordered, repeating pattern extending in all three spatial dimensions.
The word crystal originates from the Greek word κρύσταλλος (krystallos) meaning clear ice, as it was thought to be an especially solid form of water. The word once referred particularly to quartz, or "rock crystal".
Most metals encountered in everyday life are polycrystals. Crystals are often symmetrically intergrown to form crystal twins.
# Crystal structure
Which crystal structure the fluid will form depends on the chemistry of the fluid, the conditions under which it is being solidified, and also on the ambient pressure. The process of forming a crystalline structure is often referred to as crystallization.
While the cooling process usually results in the generation of a crystalline material, under certain conditions, the fluid may be frozen in a noncrystalline state. In most cases, this involves cooling the fluid so rapidly that atoms cannot travel to their lattice sites before they lose mobility. A noncrystalline material, which has no long-range order, is called an amorphous, vitreous, or glassy material. It is also often referred to as an amorphous solid, although there are distinct differences between solids and glasses: most notably, the process of forming a glass does not release the latent heat of fusion. For this thermodynamic reason, many scientists consider glassy materials to be viscous liquids rather than solids, although this is a controversial topic; see the entry on glass for more details.
Crystalline structures occur in all classes of materials, with all types of chemical bonds. Almost all metal exists in a polycrystalline state; amorphous or single-crystal metals must be produced synthetically, often with great difficulty. Ionically bonded crystals can form upon solidification of salts, either from a molten fluid or when it condenses from a solution. Covalently bonded crystals are also very common, notable examples being diamond, silica, and graphite. Polymer materials generally will form crystalline regions, but the lengths of the molecules usually prevents complete crystallization. Weak Van der Waals forces can also play a role in a crystal structure; for example, this type of bonding loosely holds together the hexagonal-patterned sheets in graphite.
Most crystalline materials have a variety of crystallographic defects. The types and structures of these defects can have a profound effect on the properties of the materials.
# Other meanings and characteristics
Since the initial discovery, made in 1982 by Dan Shechtman, the acceptance of the concept and the word quasicrystal have led the International Union of Crystallography to redefine the term crystal to mean 'any solid having an essentially discrete diffraction diagram', thereby shifting the essential attribute of crystallinity from position space to Fourier space. Within the family of crystals one distinguishes between traditional crystals, which are periodic on the atomic scale, and aperiodic crystals which are not. This broader definition adopted in 1996 reflects the current understanding that microscopic periodicity is a sufficient but not a necessary condition for crystallinity.
While the term "crystal" has a precise meaning within materials science and solid-state physics, colloquially "crystal" refers to solid objects that exhibit well-defined and often pleasing geometric shapes. In this sense of the word, many types of crystals are found in nature. The shape of these crystals is dependent on the types of molecular bonds between the atoms to determine the structure, as well as on the conditions under which they formed. Snowflakes, diamonds, and common salt are common examples of crystals.
Some crystalline materials may exhibit special electrical properties such as the ferroelectric effect or the piezoelectric effect. Additionally, light passing through a crystal is often refracted or bent in different directions, producing an array of colors; crystal optics is the study of these effects. In periodic dielectric structures a range of unique optical properties can be expected as sawed in photonic crystals.
Crystallography is the scientific study of crystals and crystal formation.
# Crystalline rocks
Inorganic matter, if free to take that physical state in which it is most stable, always tends to crystallize. Crystalline rock masses have consolidated from aqueous solution or from molten magma. The vast majority of igneous rocks belong to this group and the degree of crystallization depends primarily on the conditions under which they solidified. Such rocks as granite, which have cooled very slowly and under great pressures, have completely crystallized, but many lavas were poured out at the surface and cooled very rapidly; in this latter group a small amount of amorphous or glassy matter is frequent. Other crystalline rocks, the evaporites such as rock salt, gypsum and some limestones have been deposited from aqueous solution, mostly owing to evaporation in arid climates. Still another group, the metamorphic rocks which includes the marbles, mica-schists and quartzites; are recrystallized, that is to say, they were at first fragmental rocks, like limestone, shale and sandstone and have never been in a molten condition nor entirely in solution. The high temperature and pressure conditions of metamorphism have acted on them erasing their original structures, and inducing recrystallization in the solid state. | Crystal
In chemistry, mineralogy, and materials science, a crystal is a solid in which the constituent atoms, molecules, or ions are packed in a regularly ordered, repeating pattern extending in all three spatial dimensions.
The word crystal originates from the Greek word κρύσταλλος (krystallos) meaning clear ice, as it was thought to be an especially solid form of water.[citation needed] The word once referred particularly to quartz, or "rock crystal".
Most metals encountered in everyday life are polycrystals.[citation needed] Crystals are often symmetrically intergrown to form crystal twins.
# Crystal structure
Which crystal structure the fluid will form depends on the chemistry of the fluid, the conditions under which it is being solidified, and also on the ambient pressure. The process of forming a crystalline structure is often referred to as crystallization.
While the cooling process usually results in the generation of a crystalline material, under certain conditions, the fluid may be frozen in a noncrystalline state. In most cases, this involves cooling the fluid so rapidly that atoms cannot travel to their lattice sites before they lose mobility. A noncrystalline material, which has no long-range order, is called an amorphous, vitreous, or glassy material. It is also often referred to as an amorphous solid, although there are distinct differences between solids and glasses: most notably, the process of forming a glass does not release the latent heat of fusion. For this thermodynamic reason, many scientists consider glassy materials to be viscous liquids rather than solids, although this is a controversial topic; see the entry on glass for more details.
Crystalline structures occur in all classes of materials, with all types of chemical bonds. Almost all metal exists in a polycrystalline state; amorphous or single-crystal metals must be produced synthetically, often with great difficulty. Ionically bonded crystals can form upon solidification of salts, either from a molten fluid or when it condenses from a solution. Covalently bonded crystals are also very common, notable examples being diamond, silica, and graphite. Polymer materials generally will form crystalline regions, but the lengths of the molecules usually prevents complete crystallization. Weak Van der Waals forces can also play a role in a crystal structure; for example, this type of bonding loosely holds together the hexagonal-patterned sheets in graphite.
Most crystalline materials have a variety of crystallographic defects. The types and structures of these defects can have a profound effect on the properties of the materials.
# Other meanings and characteristics
Since the initial discovery, made in 1982 by Dan Shechtman, the acceptance of the concept and the word quasicrystal have led the International Union of Crystallography to redefine the term crystal to mean 'any solid having an essentially discrete diffraction diagram', thereby shifting the essential attribute of crystallinity from position space to Fourier space. Within the family of crystals one distinguishes between traditional crystals, which are periodic on the atomic scale, and aperiodic crystals which are not. This broader definition adopted in 1996 reflects the current understanding that microscopic periodicity is a sufficient but not a necessary condition for crystallinity.
While the term "crystal" has a precise meaning within materials science and solid-state physics, colloquially "crystal" refers to solid objects that exhibit well-defined and often pleasing geometric shapes. In this sense of the word, many types of crystals are found in nature. The shape of these crystals is dependent on the types of molecular bonds between the atoms to determine the structure, as well as on the conditions under which they formed. Snowflakes, diamonds, and common salt are common examples of crystals.
Some crystalline materials may exhibit special electrical properties such as the ferroelectric effect or the piezoelectric effect. Additionally, light passing through a crystal is often refracted or bent in different directions, producing an array of colors; crystal optics is the study of these effects. In periodic dielectric structures a range of unique optical properties can be expected as sawed in photonic crystals.
Crystallography is the scientific study of crystals and crystal formation.
# Crystalline rocks
Inorganic matter, if free to take that physical state in which it is most stable, always tends to crystallize. Crystalline rock masses have consolidated from aqueous solution or from molten magma. The vast majority of igneous rocks belong to this group and the degree of crystallization depends primarily on the conditions under which they solidified. Such rocks as granite, which have cooled very slowly and under great pressures, have completely crystallized, but many lavas were poured out at the surface and cooled very rapidly; in this latter group a small amount of amorphous or glassy matter is frequent. Other crystalline rocks, the evaporites such as rock salt, gypsum and some limestones have been deposited from aqueous solution, mostly owing to evaporation in arid climates. Still another group, the metamorphic rocks which includes the marbles, mica-schists and quartzites; are recrystallized, that is to say, they were at first fragmental rocks, like limestone, shale and sandstone and have never been in a molten condition nor entirely in solution. The high temperature and pressure conditions of metamorphism have acted on them erasing their original structures, and inducing recrystallization in the solid state.[1] | https://www.wikidoc.org/index.php/Crystal | |
24553540daf0fd386e11e9151033a77ee7b6129a | wikidoc | Cubilin | Cubilin
Cubilin is a protein that in humans is encoded by the CUBN gene.
# Function
Cubilin (CUBN) acts as a receptor for intrinsic factor-vitamin B12 complexes. The role of receptor is supported by the presence of 27 CUB domains. Cubilin shows a restricted mode of expression according to protein profiling and transcriptomics analyses, and is essentially only present in the kidneys and small intestine. Mutations in CUBN may play a role in autosomal recessive megaloblastic anemia. A complex of amnionless and cubilin forms the cubam receptor.
It can be found in the proximal tubule forming part complexes with megalin; the function of these complexes is reabsorptive and can be inhibited by sodium maleate.
# Clinical significance
Cubilin is a potential diagnostic and prognostic cancer biomarker for kidney cancer. Based on patient survival data, high levels of cubilin in tumor cells is a favourable prognostic biomarker in renal cell carcinoma. | Cubilin
Cubilin is a protein that in humans is encoded by the CUBN gene.[1][2][3]
# Function
Cubilin (CUBN) acts as a receptor for intrinsic factor-vitamin B12 complexes. The role of receptor is supported by the presence of 27 CUB domains. Cubilin shows a restricted mode of expression according to protein profiling and transcriptomics analyses[4], and is essentially only present in the kidneys and small intestine[5]. Mutations in CUBN may play a role in autosomal recessive megaloblastic anemia.[3] A complex of amnionless and cubilin forms the cubam receptor.
It can be found in the proximal tubule forming part complexes with megalin; the function of these complexes is reabsorptive and can be inhibited by sodium maleate.[6]
# Clinical significance
Cubilin is a potential diagnostic and prognostic cancer biomarker for kidney cancer[7]. Based on patient survival data, high levels of cubilin in tumor cells is a favourable prognostic biomarker in renal cell carcinoma[8][9]. | https://www.wikidoc.org/index.php/Cubilin | |
6051b8fbba265ad17694f2bd3757335942992277 | wikidoc | Dactyly | Dactyly
Synonyms and keywords: webbing of the digits
# Overview
In biology, dactyly is the arrangement of digits (fingers and toes) on the hands, feet, or sometimes wings of a tetrapod animal. It comes from the Greek word δακτυλος = "finger".
# Classification
Sometimes the ending "-dactylia" is used. The derived adjectives end with "-dactyl" or "-dactylous".
## Pentadactyly
Pentadactyly (from Greek pente-="five" plus δακτυλος = "finger") is the condition of having five digits on each limb. It appears that all land vertebrates are descended from an ancestor with a pentadactyl limb, although many species have now lost or transformed some or all of their digits by the process of evolution. Despite the individual variations listed below, the relationship to the original five-digit 'model' can be traced. This phenomenon featured in the work of Charles Darwin who noteably said; "What could be more curious than that the hand of man formed for grasping, that of a mole, for digging, the leg of a horse, the paddle of a porpoise and the wing of a bat, should all be constructed on the same pattern and should include similar bones and in the same relative positions?" Darwin was suggesting that the pentadactyl limb represents some of the strongest evidence for the theory of evolution as it indicates a common ancestry for all land vertebrates.
## Tetradactyly
Tetradactyly (from Greek tetra-="four" plus δακτυλος = "finger") is the condition of having four digits on a limb, as in many amphibians and birds. Some mammals also exhibit tetradactyly (for example the hind limbs of dogs and cats).
## Tridactyly
Tridactyly (from Greek tri- = "three" plus δακτυλος = "finger") is the condition of having three digits on a limb, as in the Rhinoceros and ancestors of the horse such as Protohippus and Hipparion. These belong to the Perissodactyla. Some birds also have three toes.
## Didactyly
Didactyly (from Greek di-="two" plus δακτυλος = "finger") or bidactyly is the condition of having two digits on each limb, as in the Two-toed Sloth, Choloepus didactylus. In humans this name is used for an abnormality in which the middle digits are missing, leaving only the thumb and fifth finger. Cloven-hoofed mammals (such as deer, sheep and cattle - 'Artiodactyla') walk on two digits.
## Monodactyly
Monodactyly (from Greek monos- = "one" plus δακτυλος = "finger") is the condition of having a single digit on a limb, as in modern horses. These belong to the Perissodactyla.
## Syndactyly
Syndactyly (from Greek συν- = "together" plus δακτυλος = "finger") is a condition where two or more digits are fused together. It occurs normally in some mammals, such as the siamang. It occurs as an unusual condition in humans.
Syndactyly can be simple or complex. In simple syndactyly, adjacent fingers or toes are joined by soft tissue. In complex syndactyly, the bones of adjacent digits are fused. The kangaroo exhibits complex syndactyly.
Simple syndactyly can be full or partial, and is present at birth (congenital). In early human fetal development, webbing (syndactyly) of the toes and fingers is normal. At about 16 weeks of gestation, apoptosis takes place and an enzyme dissolves the tissue between the fingers and toes, and the webbing disappears. In some fetuses, this process does not occur completely between all fingers or toes and some residual webbing remains. The exact cause is not known. In cases, this condition appears to be hereditary.
In the case of human feet, syndactyly does not affect the function of the foot or toes and does not interfere with walking or swimming or any other activities. Although webbing of the fingers usually does not affect the function of the hand, it can impair function of the fingers. Surgery may be performed to separate webbed fingers or toes. As with any surgery, there are risks of complications. This procedure involves local anesthesia with a sedative and can be done just with a local without the sedative for adults if desired. In addition to the incision between the toes, sometimes it is necessary to remove some skin from elsewhere on the body to graft into the newly exposed space between the toes.
In the case of webbed toes, surgical separation is a purely cosmetic operation with no medical benefits.
## Polydactyly
Polydactyly (from Greek πολυ- = "many" plus δακτυλος = "finger") (or hyperdactyly, from Greek hyper- = "too many" plus δακτυλος = "finger") is when a limb has more than five digits. This can be:-
- As a result of congenital abnormality in a normally pentadactyl animal. Polydactyly is very common among domestic cats.
- Normality in some early tetrapod aquatic animals, such as Acanthostega gunnari (Jarvik 1952), which is one of an increasing number of genera of stem-tetrapods known from the Upper Devonian, which are providing insights into the appearance of tetrapods and the origin of limbs with digits. For more information, see polydactyly.
## Hypodactyly
Hypodactyly (from Greek hypo- = "too few" plus δακτυλος = "finger") is having too few digits when not caused by an amputation.
## Ectrodactyly
Ectrodactyly is the congenital absence of all or part of one or more fingers or toes. This term is used for a range of conditions from aphalangia (in which some of the phalanges or finger bones are missing), to adactyly (the absence of a digit).
A fusing of almost all digits on all of the hands and feet is ectrodactyly. News anchor Bree Walker is probably the best-known person with this condition, which affects about one in 91,000 people. It is conspicuously more common in the Vadoma in Zimbabwe.
de:Syndaktylie
he:דקטיליה
nl:Syndactylie
sr:Синдактилија
fi:Syndaktylia
sv:Syndaktyli | Dactyly
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Synonyms and keywords: webbing of the digits
# Overview
In biology, dactyly is the arrangement of digits (fingers and toes) on the hands, feet, or sometimes wings of a tetrapod animal. It comes from the Greek word δακτυλος = "finger".
# Classification
Sometimes the ending "-dactylia" is used. The derived adjectives end with "-dactyl" or "-dactylous".
## Pentadactyly
Pentadactyly (from Greek pente-="five" plus δακτυλος = "finger") is the condition of having five digits on each limb. It appears that all land vertebrates are descended from an ancestor with a pentadactyl limb, although many species have now lost or transformed some or all of their digits by the process of evolution. Despite the individual variations listed below, the relationship to the original five-digit 'model' can be traced. This phenomenon featured in the work of Charles Darwin who noteably said; "What could be more curious than that the hand of man formed for grasping, that of a mole, for digging, the leg of a horse, the paddle of a porpoise and the wing of a bat, should all be constructed on the same pattern and should include similar bones and in the same relative positions?" Darwin was suggesting that the pentadactyl limb represents some of the strongest evidence for the theory of evolution as it indicates a common ancestry for all land vertebrates.
## Tetradactyly
Tetradactyly (from Greek tetra-="four" plus δακτυλος = "finger") is the condition of having four digits on a limb, as in many amphibians and birds. Some mammals also exhibit tetradactyly (for example the hind limbs of dogs and cats).
## Tridactyly
Tridactyly (from Greek tri- = "three" plus δακτυλος = "finger") is the condition of having three digits on a limb, as in the Rhinoceros and ancestors of the horse such as Protohippus and Hipparion. These belong to the Perissodactyla. Some birds also have three toes.
## Didactyly
Didactyly (from Greek di-="two" plus δακτυλος = "finger") or bidactyly is the condition of having two digits on each limb, as in the Two-toed Sloth, Choloepus didactylus. In humans this name is used for an abnormality in which the middle digits are missing, leaving only the thumb and fifth finger. Cloven-hoofed mammals (such as deer, sheep and cattle - 'Artiodactyla') walk on two digits.
## Monodactyly
Monodactyly (from Greek monos- = "one" plus δακτυλος = "finger") is the condition of having a single digit on a limb, as in modern horses. These belong to the Perissodactyla.
## Syndactyly
Syndactyly (from Greek συν- = "together" plus δακτυλος = "finger") is a condition where two or more digits are fused together. It occurs normally in some mammals, such as the siamang. It occurs as an unusual condition in humans.
Syndactyly can be simple or complex. In simple syndactyly, adjacent fingers or toes are joined by soft tissue. In complex syndactyly, the bones of adjacent digits are fused. The kangaroo exhibits complex syndactyly.
Simple syndactyly can be full or partial, and is present at birth (congenital). In early human fetal development, webbing (syndactyly) of the toes and fingers is normal. At about 16 weeks of gestation, apoptosis takes place and an enzyme dissolves the tissue between the fingers and toes, and the webbing disappears. In some fetuses, this process does not occur completely between all fingers or toes and some residual webbing remains. The exact cause is not known. In cases, this condition appears to be hereditary.
In the case of human feet, syndactyly does not affect the function of the foot or toes and does not interfere with walking or swimming or any other activities. Although webbing of the fingers usually does not affect the function of the hand, it can impair function of the fingers. Surgery may be performed to separate webbed fingers or toes. As with any surgery, there are risks of complications. This procedure involves local anesthesia with a sedative and can be done just with a local without the sedative for adults if desired. In addition to the incision between the toes, sometimes it is necessary to remove some skin from elsewhere on the body to graft into the newly exposed space between the toes.
In the case of webbed toes, surgical separation is a purely cosmetic operation with no medical benefits.
## Polydactyly
Polydactyly (from Greek πολυ- = "many" plus δακτυλος = "finger") (or hyperdactyly, from Greek hyper- = "too many" plus δακτυλος = "finger") is when a limb has more than five digits. This can be:-
- As a result of congenital abnormality in a normally pentadactyl animal. Polydactyly is very common among domestic cats.
- Normality in some early tetrapod aquatic animals, such as Acanthostega gunnari (Jarvik 1952), which is one of an increasing number of genera of stem-tetrapods known from the Upper Devonian, which are providing insights into the appearance of tetrapods and the origin of limbs with digits. For more information, see polydactyly.
## Hypodactyly
Hypodactyly (from Greek hypo- = "too few" plus δακτυλος = "finger") is having too few digits when not caused by an amputation.
## Ectrodactyly
Ectrodactyly is the congenital absence of all or part of one or more fingers or toes. This term is used for a range of conditions from aphalangia (in which some of the phalanges or finger bones are missing), to adactyly (the absence of a digit).
A fusing of almost all digits on all of the hands and feet is ectrodactyly. News anchor Bree Walker is probably the best-known person with this condition, which affects about one in 91,000 people. It is conspicuously more common in the Vadoma in Zimbabwe.
de:Syndaktylie
he:דקטיליה
nl:Syndactylie
sr:Синдактилија
fi:Syndaktylia
sv:Syndaktyli
Template:WikiDoc Sources | https://www.wikidoc.org/index.php/Cutaneous_syndactyly | |
de7de59a9e298554aabb62fb980c165f188aaf05 | wikidoc | Cuticle | Cuticle
# Overview
In biology, the term cuticle or cuticula is given to a variety of tough but flexible, non-mineral outer coverings of an organism, or part of an organism, that provide protection. They are non-homologous, differing in their origin, structure and chemical composition.
# In human anatomy
In human anatomy, cuticle refers to the dead layers of epidermal cells or keratinocytes that produce the horn protein keratin, to the strip of dead skin cells at the base and sides of the fingernail, the eponychium and also to the superficial layer of overlapping cells covering the hair shaft (cuticula pili) that locks the hair into its follicle.
# In invertebrate zoology
In zoology, the invertebrate cuticle or cuticula is a multi-layered structure outside the epidermis of many invertebrates, notably roundworms and arthropods, in which it forms an exoskeleton.
The main structural components of the nematode cuticle are proteins, highly cross-linked collagens and specialised insoluble proteins known as "cuticlins", together with glycoproteins and lipids. .
The main structural component of arthropod cuticle is a polysaccharide, chitin, composed of N-acetylglucosamine units, together with proteins and lipids.
# In botany
In botany, plant cuticles are protective waxy coverings produced by the epidermal cells of leaves, young shoots and all other aerial plant organs.
The main structural components of plant cuticles are the unique polymers cutin and/or cutan, impregnated with wax.
The cuticles of plants function as permeability barriers for water and water-soluble materials. The cuticle both prevents plant surfaces from becoming wet and helps to prevent plants from drying out. Xerophytic plants such as Cactus have very thick cuticles to help them survive in their arid climates. Plants that live in range of sea's spray also tend to have thicker cuticles, to protect them from the toxic effects of salt. | Cuticle
# Overview
In biology, the term cuticle or cuticula is given to a variety of tough but flexible, non-mineral outer coverings of an organism, or part of an organism, that provide protection. They are non-homologous, differing in their origin, structure and chemical composition.
# In human anatomy
In human anatomy, cuticle refers to the dead layers of epidermal cells or keratinocytes that produce the horn protein keratin, to the strip of dead skin cells at the base and sides of the fingernail, the eponychium and also to the superficial layer of overlapping cells covering the hair shaft (cuticula pili) that locks the hair into its follicle.
# In invertebrate zoology
In zoology, the invertebrate cuticle or cuticula is a multi-layered structure outside the epidermis of many invertebrates, notably roundworms[1] and arthropods, in which it forms an exoskeleton.
The main structural components of the nematode cuticle are proteins, highly cross-linked collagens and specialised insoluble proteins known as "cuticlins", together with glycoproteins and lipids. [2].
The main structural component of arthropod cuticle is a polysaccharide, chitin, composed of N-acetylglucosamine units, together with proteins and lipids.
# In botany
In botany, plant cuticles are protective waxy coverings produced by the epidermal cells of leaves, young shoots and all other aerial plant organs.
The main structural components of plant cuticles are the unique polymers cutin and/or cutan, impregnated with wax.
The cuticles of plants function as permeability barriers for water and water-soluble materials. The cuticle both prevents plant surfaces from becoming wet and helps to prevent plants from drying out. Xerophytic plants such as Cactus have very thick cuticles to help them survive in their arid climates. Plants that live in range of sea's spray also tend to have thicker cuticles, to protect them from the toxic effects of salt. | https://www.wikidoc.org/index.php/Cuticle | |
62dfbb5959d2103a3d9ea497b401e5b154de9e0e | wikidoc | Cyanate | Cyanate
# Overview
The cyanate ion is an anion consisting of one oxygen atom, one carbon atom, and one nitrogen atom, −, in that order, and possesses 1 unit of negative charge, borne mainly by the nitrogen atom. In organic compounds the cyanate group is a functional group.
The structure of cyanate can be considered to resonate between two canonical forms:
The resonance hybrid resulting from these two contributory structures can be represented as
The cyanate ion is isoelectronic with carbon dioxide, and so shares its linear shape.
The cyanate ion is an ambident nucleophile in nucleophilic substitution because it can react to form an alkyl cyanate R-OCN (exception) or an alkyl isocyanate R-NCO (rule). Aryl cyanates (C6H5OCN) can be formed by a reaction of phenol with cyanogen chloride (ClCN) in the presence of a base.
Cyanates are salts or esters of cyanic acid, for example potassium cyanate (KOCN) or methyl cyanate.
The cyanate ion is relatively non-toxic in comparison with cyanides. Use of this fact is made in cyanide decontamination processes where a permanganate oxidation converts toxic cyanide to safer cyanate.
The fulminate ion − has the same chemical formula but a different structure — it is a structural isomer of cyanate.
ar:سيانات
de:Cyansäure#Cyanate
lv:Cianāti
sv:Cyanater | Cyanate
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
# Overview
The cyanate ion is an anion consisting of one oxygen atom, one carbon atom, and one nitrogen atom, [OCN]−, in that order, and possesses 1 unit of negative charge, borne mainly by the nitrogen atom. In organic compounds the cyanate group is a functional group.
The structure of cyanate can be considered to resonate between two canonical forms:
The resonance hybrid resulting from these two contributory structures can be represented as
The cyanate ion is isoelectronic with carbon dioxide, and so shares its linear shape.
The cyanate ion is an ambident nucleophile in nucleophilic substitution because it can react to form an alkyl cyanate R-OCN (exception) or an alkyl isocyanate R-NCO (rule). Aryl cyanates (C6H5OCN) can be formed by a reaction of phenol with cyanogen chloride (ClCN) in the presence of a base.
Cyanates are salts or esters of cyanic acid, for example potassium cyanate (KOCN) or methyl cyanate.
The cyanate ion is relatively non-toxic in comparison with cyanides. Use of this fact is made in cyanide decontamination processes where a permanganate oxidation converts toxic cyanide to safer cyanate.
The fulminate ion [ONC]− has the same chemical formula but a different structure — it is a structural isomer of cyanate.
Template:Functional Groups
Template:Inorganic compounds of carbon
ar:سيانات
de:Cyansäure#Cyanate
lv:Cianāti
sv:Cyanater | https://www.wikidoc.org/index.php/Cyanate | |
70687684c0610b941bf1d6a2d74f9ec3d39f7243 | wikidoc | Cyanide | Cyanide
A cyanide is any chemical compound that contains the cyano group (C≡N), which consists of a carbon atom triple-bonded to a nitrogen atom. Cyanide specifically is the anion CN-. Many organic compounds feature cyanide as a functional group; these are called nitriles in IUPAC nomenclature (for example, CH3CN is referred to by the names acetonitrile or ethanenitrile per IUPAC, but occasionally it is labeled using the common name methyl cyanide). Of the many kinds of cyanide compounds, some are gases, others are solids or liquids. Those that can release the cyanide ion CN- are highly toxic.
The word "cyanide" comes from the Greek word for "blue", in reference to hydrogen cyanide, which was called Blausäure ("blue acid") in German after its preparation by acid treatment of Prussian blue.
# Appearance and odor
Hydrogen cyanide (HCN) is a colorless gas with a faint bitter almond-like odor. Most people can smell hydrogen cyanide; however, due to an apparent genetic trait, some individuals cannot detect the odor of HCN. Sodium cyanide and potassium cyanide are both white powders with a bitter almond-like odor in damp air, due to the presence of hydrogen cyanide formed by hydrolysis:
# Occurrence
Cyanides are produced by certain bacteria, fungi, and algae and are found in a number of foods and plants. Cyanide is found, although in small amounts, in apple seeds, mangoes and almonds. In plants, cyanides are usually bound to sugar molecules in the form of cyanogenic glycosides and serve the plant as defense against herbivores. Cassava roots (aka manioc), an important potato-like food grown in tropical countries (and the base from which tapioca is made), contains cyanogenic glycosides.
The Fe-only and -hydrogenase enzymes contain cyanide ligands at their active sites. The biosynthesis of cyanide in the -hydrogenases proceeds from carbamoylphosphate, which converts to cysteinyl thiocyanate, the CN- donor.
Hydrogen cyanide is a product of certain kinds of pyrolysis and consequently it occurs in the exhaust of internal combustion engines, tobacco smoke, and certain plastics, especially those derived from acrylonitrile.
# Coordination chemistry
Cyanide is considered, in a broad sense, to be the most potent ligand for many transition metals. The very high affinities of metals for cyanide can be attributed to its negative charge, compactness, and ability to engage in π-bonding. Well known complexes include:
- hexacyanides 3− (M = Ti, V, Cr, Mn, Fe, Co), which are octahedral in shape;
- the tetracyanides, 2− (M = Ni, Pd, Pt), which are square planar in their geometry;
- the dicyanides − (M = Cu, Ag, Au), which are linear in geometry.
The deep blue pigment Prussian blue, used in the making of blueprints, is derived from iron cyanide complexes (hence the name cyanide, from cyan, a shade of blue). Prussian blue can produce hydrogen cyanide when exposed to acids.
# Organic synthesis
Because of its high nucleophilicity, cyanide is readily introduced into organic molecules by displacement of a halide group (i.e. the chloride on methyl chloride). Organic cyanides are generally called nitriles. Thus, CH3CN can be methyl cyanide but more commonly is referred to as acetonitrile. In organic synthesis, cyanide is used as a C-1 synthon. I.e., it can be used to lengthen a carbon chain by one, while retaining the ability to be functionalized.
- RCN + 2 H2O → RCOOH + NH3 (Hydrolysis under reflux with mineral acid catalyst), or
- RCN + 0.5 LiAlH4 + (second step) 2 H2O → RCH2NH2 + 0.5 LiAl(OH)4 (under reflux in dry ether, followed by addition of H2O)
An alternative method for introducing cyanide is via the process of hydrocyanation, whereby hydrogen cyanide and alkenes combine:
RCH=CH2 + HCN → RCH(CN)CH3
Metal catalysts are required for such reactions.
# Applications
Potassium ferrocyanide is used to achieve a blue colour on cast bronze sculptures during the final finishing stage of the sculpture. On its own, it will produce a very dark shade of blue and is often mixed with other chemicals to achieve the desired tint and hue. It is applied using a torch and paint brush while wearing the standard safety equipment used for any patina application: rubber gloves, safety glasses, and a respirator. The actual amount of cyanide in the mixture varies according to the recipes used by each foundry.
## Medical uses
The cyanide compound sodium nitroprusside is occasionally used in emergency medical situations to produce a rapid decrease in blood pressure in humans; it is also used as a vasodilator in vascular research. The molecule of Vitamin B12 usually also contains cyanide. During World War I, a copper cyanide compound was briefly used by Japanese physicians for the treatment of tuberculosis and leprosy.
## Mining
Gold and silver cyanides are among the very few soluble forms of these metals, and cyanides are thus used in mining as well as electroplating, metallurgy, jewelry, and photography. In the so-called cyanide process, finely ground high-grade ore is mixed with the cyanide (concentration of about two kilogram NaCN per tonne); low-grade ores are stacked into heaps and sprayed with cyanide solution (concentration of about one kilogram NaCN per ton). The precious-metal cations are complexed by the cyanide anions to form soluble derivatives, e.g. − and −.
Silver is less "noble" than gold and often occurs as the sulfide, in which case redox is not invoked (no O2 is required), instead a displacement reaction occurs:
The "pregnant liquor" containing these ions is separated from the solids, which are discarded to a tailing pond or spent heap, the recoverable gold having been removed. The metal is recovered from the "pregnant solution" by reduction with zinc dust or by adsorption onto activated carbon. This process can result in environmental and health problems. Aqueous cyanide is hydrolyzed rapidly, especially in sunlight. It can mobilize some heavy metals such as mercury if present. Gold can also be associated with arsenopyrite (FeAsS), which is similar to iron pyrite (fool's gold), wherein half of the sulfur atoms are replaced by arsenic. Au-containing arsenopyrite ores are similarly reactive toward cyanide.
## Fishing
Cyanides are illegally used to capture live fish near coral reefs for the aquarium and seafood markets. This fishing occurs mainly in the Philippines, Indonesia and the Caribbean to supply the 2 million marine aquarium owners in the world. In this method, a diver uses a large, needleless syringe to squirt a cyanide solution into areas where the fish are hiding, stunning them so that they can be easily gathered. Many fish caught in this fashion die immediately, or in shipping. Those that survive to find their way into pet stores often die from shock, or from massive digestive damage. The high concentrations of cyanide on reefs on which this has occurred has resulted in cases of cyanide poisoning among local fishermen and their families, as well as irreversible damage to the coral reefs themselves and other marine life in the area.
Environmental organizations are critical of the practice, as are some aquarists and aquarium dealers, to prevent the trade of illegally-caught aquarium fish. The Marine Aquarium Council (Headquarters: Honolulu, Hawaii) has created a certification in which the tropical fish are caught legally with nets only. To ensure authenticity, "MAC-Certified marine organisms bear the MAC-Certified label on the tanks and boxes in which they are kept and shipped." MAC Certification.
Magnesium cyanide is also used in some countries illegally to stun and harvest streamlined fish.
## Fumigation
Cyanides are used as insecticides for the fumigating of ships. In the past cyanide salts have and still are in some places being used as rat poison, and for killing ants.
# Chemical tests for cyanide
### Prussian blue
The formation of Prussian blue can be used as a test for inorganic cyanide, for instance in the sodium fusion test. Typically, iron(II) sulfate is added to a solution suspected of containing cyanide, such as the filtrate from the sodium fusion test. The resulting mixture is acidified with mineral acid. The formation of Prussian blue is a positive result for cyanide.
### para-benzoquinone in DMSO
A solution of para-benzoquinone in DMSO reacts with cyanide to form a cyanophenol, which is fluorescent. Illumination with a UV light gives a green/blue glow if the test is positive.
### Copper and an aromatic amine
As used by fumigators to detect hydrogen cyanide, copper(II) salt and an aromatic amine such as benzidine is added to the sample, as an alternative to the benzidine an alternative amine di-(4,4-bis-dimethylaminophenyl) methane can be used. A positive test gives a blue colour. Copper(I) cyanide is poorly soluble. By sequestering the copper(I) the copper(II) is rendered a stronger oxidant. The copper, in a cyanide facilitated oxidation, converts the amine into a coloured compound. The Nernst equation explains this process. Another good example of such chemistry is the way in which the saturated calomel reference electrode (SCE) works. The copper, in a cyanide facilitated, oxidation converts the amine into a coloured compound.
### Pyridine - Barbituric Acid Colorimetry
A sample containing cyanide is purged with air from a boiling acid solution into a basic absorber solution. The cyanide salt absorbed in the basic solution is buffered at pH 4.5 and then reacted with chlorine to form cyanogen chloride. The cyanogen chloride formed couples pyridine with barbituric acid to form a strongly colored red dye that is proportional to cyanide concentration. This colorimetric method following distillation is the basis for most regulatory methods (for instance EPA 335.4) used to analyze cyanide in water, wastewater, and contaminated soils. Distillation followed by colorimetric methods, however, have been found to be prone to interferences from thiocyanate, nitrate, thiosulfate, sulfite, and sulfide that can result in both positive and negative bias. It has been recommended by the USEPA (MUR March 12, 2007) that samples containing these compounds be analyzed by Gas-Diffusion Flow Injection Analysis - Amperometry.
### Gas Diffusion Flow Injection Analysis - Amperometry
Instead of distilling, the sample is injected into an acidic stream where the HCN formed is passed under a hydrophobic gas diffusion membrane that selectively allows only HCN to pass through. The HCN that passes through the membrane is absorbed into a basic carrier solution that transports the CN to an amperometric detector that accurately measures cyanide concentration with high sensitivity. Sample pretreatment determined by acid reagents, ligands, or preliminary UV irradiation allow cyanide speciation of free cyanide, available cyanide, and total cyanide respectively. These relative simplicity of these flow injection analysis methods limit the interference experienced by the high heat of distillation and also prove to be cost effective since time consuming distillations are not required.
# Toxicity
Many cyanide-containing compounds are highly toxic, but some are not. Prussian blue, with an approximate formula Fe7(CN)18 is the blue of blue prints and is administered orally as an antidote to poisoning by thallium and Caesium-137. The most dangerous cyanides are hydrogen cyanide (HCN) and salts derived from it, such as potassium cyanide (KCN) and sodium cyanide (NaCN), among others. Also some compounds readily release HCN or the cyanide ion, such as trimethylsilyl cyanide (CH3)3SiCN upon contact with water and cyanoacrylates upon pyrolysis.
Cyanide is an inhibitor of the enzyme cytochrome c oxidase (also known as aa3) in the fourth complex of the electron transport chain (found in the membrane of the mitochondria of eukaryotic cells.) It attaches to the iron within this protein. The binding of cyanide to this cytochrome prevents transport of electrons from cytochrome c oxidase to oxygen. As a result, the electron transport chain is disrupted, meaning that the cell can no longer aerobically produce ATP for energy. Tissues that mainly depend on aerobic respiration, such as the central nervous system and the heart, are particularly affected. Antidotes to cyanide poisoning include hydroxocobalamin and sodium nitrite which release the cyanide from the cytochrome system, and rhodanase, which is an enzyme occurring naturally in mammals that combines serum cyanide with thiosulfate, producing comparatively harmless thiocyanate.
Cyanides have been used as a poison many times throughout history. Its most infamous application was the use of hydrogen cyanide by the Nazi regime in Germany for mass murder in some gas chambers during the Holocaust. Cyanide has been used for murder, as in the case of Grigori Rasputin. It has also been used for suicide. Some notable cases are Erwin Rommel, Eva Braun, Wallace Carothers, Hermann Göring, Heinrich Himmler, Alan Turing, Odilo Globocnik, Adolf Hitler (in combination with a gunshot), residents of Jim Jones' the People's Temple in Jonestown and the LTTE (they use it to kill themselves if they are captured by Armed forces). | Cyanide
Template:Otheruses1
A cyanide is any chemical compound that contains the cyano group (C≡N), which consists of a carbon atom triple-bonded to a nitrogen atom. Cyanide specifically is the anion CN-. Many organic compounds feature cyanide as a functional group; these are called nitriles in IUPAC nomenclature (for example, CH3CN is referred to by the names acetonitrile or ethanenitrile per IUPAC, but occasionally it is labeled using the common name methyl cyanide). Of the many kinds of cyanide compounds, some are gases, others are solids or liquids. Those that can release the cyanide ion CN- are highly toxic.
The word "cyanide" comes from the Greek word for "blue", in reference to hydrogen cyanide, which was called Blausäure ("blue acid") in German after its preparation by acid treatment of Prussian blue.[1]
# Appearance and odor
Hydrogen cyanide (HCN) is a colorless gas with a faint bitter almond-like odor. Most people can smell hydrogen cyanide; however, due to an apparent genetic trait, some individuals cannot detect the odor of HCN.[2] Sodium cyanide and potassium cyanide are both white powders with a bitter almond-like odor in damp air, due to the presence of hydrogen cyanide formed by hydrolysis:
# Occurrence
Cyanides are produced by certain bacteria, fungi, and algae and are found in a number of foods and plants. Cyanide is found, although in small amounts, in apple seeds, mangoes and almonds.[3] In plants, cyanides are usually bound to sugar molecules in the form of cyanogenic glycosides and serve the plant as defense against herbivores. Cassava roots (aka manioc), an important potato-like food grown in tropical countries (and the base from which tapioca is made), contains cyanogenic glycosides[4][5].
The Fe-only and [NiFe]-hydrogenase enzymes contain cyanide ligands at their active sites. The biosynthesis of cyanide in the [NiFe]-hydrogenases proceeds from carbamoylphosphate, which converts to cysteinyl thiocyanate, the CN- donor. [6]
Hydrogen cyanide is a product of certain kinds of pyrolysis and consequently it occurs in the exhaust of internal combustion engines, tobacco smoke, and certain plastics, especially those derived from acrylonitrile.[citation needed]
# Coordination chemistry
Cyanide is considered, in a broad sense, to be the most potent ligand for many transition metals. The very high affinities of metals for cyanide can be attributed to its negative charge, compactness, and ability to engage in π-bonding. Well known complexes include:
- hexacyanides [M(CN)6]3− (M = Ti, V, Cr, Mn, Fe, Co), which are octahedral in shape;
- the tetracyanides, [M(CN)4]2− (M = Ni, Pd, Pt), which are square planar in their geometry;
- the dicyanides [M(CN)2]− (M = Cu, Ag, Au), which are linear in geometry.
The deep blue pigment Prussian blue, used in the making of blueprints, is derived from iron cyanide complexes (hence the name cyanide, from cyan, a shade of blue). Prussian blue can produce hydrogen cyanide when exposed to acids.
# Organic synthesis
Because of its high nucleophilicity, cyanide is readily introduced into organic molecules by displacement of a halide group (i.e. the chloride on methyl chloride). Organic cyanides are generally called nitriles. Thus, CH3CN can be methyl cyanide but more commonly is referred to as acetonitrile. In organic synthesis, cyanide is used as a C-1 synthon. I.e., it can be used to lengthen a carbon chain by one, while retaining the ability to be functionalized.
- RCN + 2 H2O → RCOOH + NH3 (Hydrolysis under reflux with mineral acid catalyst), or
- RCN + 0.5 LiAlH4 + (second step) 2 H2O → RCH2NH2 + 0.5 LiAl(OH)4 (under reflux in dry ether, followed by addition of H2O)
An alternative method for introducing cyanide is via the process of hydrocyanation, whereby hydrogen cyanide and alkenes combine:
RCH=CH2 + HCN → RCH(CN)CH3
Metal catalysts are required for such reactions.
# Applications
Potassium ferrocyanide is used to achieve a blue colour on cast bronze sculptures during the final finishing stage of the sculpture. On its own, it will produce a very dark shade of blue and is often mixed with other chemicals to achieve the desired tint and hue. It is applied using a torch and paint brush while wearing the standard safety equipment used for any patina application: rubber gloves, safety glasses, and a respirator. The actual amount of cyanide in the mixture varies according to the recipes used by each foundry.
## Medical uses
The cyanide compound sodium nitroprusside is occasionally used in emergency medical situations to produce a rapid decrease in blood pressure in humans; it is also used as a vasodilator in vascular research. The molecule of Vitamin B12 usually also contains cyanide. During World War I, a copper cyanide compound was briefly used by Japanese physicians for the treatment of tuberculosis and leprosy.[7]
## Mining
Gold and silver cyanides are among the very few soluble forms of these metals, and cyanides are thus used in mining as well as electroplating, metallurgy, jewelry, and photography. In the so-called cyanide process, finely ground high-grade ore is mixed with the cyanide (concentration of about two kilogram NaCN per tonne); low-grade ores are stacked into heaps and sprayed with cyanide solution (concentration of about one kilogram NaCN per ton). The precious-metal cations are complexed by the cyanide anions to form soluble derivatives, e.g. [Au(CN)2]− and [Ag(CN)2]−.
Silver is less "noble" than gold and often occurs as the sulfide, in which case redox is not invoked (no O2 is required), instead a displacement reaction occurs:
The "pregnant liquor" containing these ions is separated from the solids, which are discarded to a tailing pond or spent heap, the recoverable gold having been removed. The metal is recovered from the "pregnant solution" by reduction with zinc dust or by adsorption onto activated carbon. This process can result in environmental and health problems. Aqueous cyanide is hydrolyzed rapidly, especially in sunlight. It can mobilize some heavy metals such as mercury if present. Gold can also be associated with arsenopyrite (FeAsS), which is similar to iron pyrite (fool's gold), wherein half of the sulfur atoms are replaced by arsenic. Au-containing arsenopyrite ores are similarly reactive toward cyanide.
## Fishing
Cyanides are illegally used to capture live fish near coral reefs for the aquarium and seafood markets. This fishing occurs mainly in the Philippines, Indonesia and the Caribbean to supply the 2 million marine aquarium owners in the world. In this method, a diver uses a large, needleless syringe to squirt a cyanide solution into areas where the fish are hiding, stunning them so that they can be easily gathered. Many fish caught in this fashion die immediately, or in shipping. Those that survive to find their way into pet stores often die from shock, or from massive digestive damage. The high concentrations of cyanide on reefs on which this has occurred has resulted in cases of cyanide poisoning among local fishermen and their families, as well as irreversible damage to the coral reefs themselves and other marine life in the area.
Environmental organizations are critical of the practice, as are some aquarists and aquarium dealers, to prevent the trade of illegally-caught aquarium fish. The Marine Aquarium Council (Headquarters: Honolulu, Hawaii) has created a certification in which the tropical fish are caught legally with nets only. To ensure authenticity, "MAC-Certified marine organisms bear the MAC-Certified label on the tanks and boxes in which they are kept and shipped." MAC Certification.
Magnesium cyanide is also used in some countries illegally to stun and harvest streamlined fish.
## Fumigation
Cyanides are used as insecticides for the fumigating of ships. In the past cyanide salts have and still are in some places being used as rat poison, and for killing ants.
# Chemical tests for cyanide
### Prussian blue
The formation of Prussian blue can be used as a test for inorganic cyanide, for instance in the sodium fusion test. Typically, iron(II) sulfate is added to a solution suspected of containing cyanide, such as the filtrate from the sodium fusion test. The resulting mixture is acidified with mineral acid. The formation of Prussian blue is a positive result for cyanide.
### para-benzoquinone in DMSO
A solution of para-benzoquinone in DMSO reacts with cyanide to form a cyanophenol, which is fluorescent. Illumination with a UV light gives a green/blue glow if the test is positive.
### Copper and an aromatic amine
As used by fumigators to detect hydrogen cyanide, copper(II) salt and an aromatic amine such as benzidine is added to the sample, as an alternative to the benzidine an alternative amine di-(4,4-bis-dimethylaminophenyl) methane can be used. A positive test gives a blue colour. Copper(I) cyanide is poorly soluble. By sequestering the copper(I) the copper(II) is rendered a stronger oxidant. The copper, in a cyanide facilitated oxidation, converts the amine into a coloured compound. The Nernst equation explains this process. Another good example of such chemistry is the way in which the saturated calomel reference electrode (SCE) works. The copper, in a cyanide facilitated, oxidation converts the amine into a coloured compound.
### Pyridine - Barbituric Acid Colorimetry
A sample containing cyanide is purged with air from a boiling acid solution into a basic absorber solution. The cyanide salt absorbed in the basic solution is buffered at pH 4.5 and then reacted with chlorine to form cyanogen chloride. The cyanogen chloride formed couples pyridine with barbituric acid to form a strongly colored red dye that is proportional to cyanide concentration. This colorimetric method following distillation is the basis for most regulatory methods (for instance EPA 335.4) used to analyze cyanide in water, wastewater, and contaminated soils. Distillation followed by colorimetric methods, however, have been found to be prone to interferences from thiocyanate, nitrate, thiosulfate, sulfite, and sulfide that can result in both positive and negative bias. It has been recommended by the USEPA (MUR March 12, 2007) that samples containing these compounds be analyzed by Gas-Diffusion Flow Injection Analysis - Amperometry.[8]
### Gas Diffusion Flow Injection Analysis - Amperometry
Instead of distilling, the sample is injected into an acidic stream where the HCN formed is passed under a hydrophobic gas diffusion membrane that selectively allows only HCN to pass through. The HCN that passes through the membrane is absorbed into a basic carrier solution that transports the CN to an amperometric detector that accurately measures cyanide concentration with high sensitivity. Sample pretreatment determined by acid reagents, ligands, or preliminary UV irradiation allow cyanide speciation of free cyanide, available cyanide, and total cyanide respectively. These relative simplicity of these flow injection analysis methods limit the interference experienced by the high heat of distillation and also prove to be cost effective since time consuming distillations are not required.
# Toxicity
Many cyanide-containing compounds are highly toxic, but some are not. Prussian blue, with an approximate formula Fe7(CN)18 is the blue of blue prints and is administered orally as an antidote to poisoning by thallium and Caesium-137. The most dangerous cyanides are hydrogen cyanide (HCN) and salts derived from it, such as potassium cyanide (KCN) and sodium cyanide (NaCN), among others. Also some compounds readily release HCN or the cyanide ion, such as trimethylsilyl cyanide (CH3)3SiCN upon contact with water and cyanoacrylates upon pyrolysis.[citation needed]
Cyanide is an inhibitor of the enzyme cytochrome c oxidase (also known as aa3) in the fourth complex of the electron transport chain (found in the membrane of the mitochondria of eukaryotic cells.) It attaches to the iron within this protein. The binding of cyanide to this cytochrome prevents transport of electrons from cytochrome c oxidase to oxygen. As a result, the electron transport chain is disrupted, meaning that the cell can no longer aerobically produce ATP for energy. Tissues that mainly depend on aerobic respiration, such as the central nervous system and the heart, are particularly affected. Antidotes to cyanide poisoning include hydroxocobalamin and sodium nitrite which release the cyanide from the cytochrome system, and rhodanase, which is an enzyme occurring naturally in mammals that combines serum cyanide with thiosulfate, producing comparatively harmless thiocyanate.
Cyanides have been used as a poison many times throughout history. Its most infamous application was the use of hydrogen cyanide by the Nazi regime in Germany for mass murder in some gas chambers during the Holocaust. Cyanide has been used for murder, as in the case of Grigori Rasputin. It has also been used for suicide. Some notable cases are Erwin Rommel, Eva Braun, Wallace Carothers, Hermann Göring, Heinrich Himmler, Alan Turing, Odilo Globocnik, Adolf Hitler (in combination with a gunshot), residents of Jim Jones' the People's Temple in Jonestown and the LTTE (they use it to kill themselves if they are captured by Armed forces). | https://www.wikidoc.org/index.php/Cyanide | |
4066564610b8fe453a8eda65f87a289c59d9149a | wikidoc | Cycling | Cycling
Cycling is the use of bicycles, unicycles, tricycles, quadricycles and other similar wheeled human powered vehicles (HPVs) as a means of transport, a form of recreation or a sport. It is done on roads and paths, across open country, through tunnels, over bridges, on snow, or even over ice (icebiking).
# Introduction
As a sport, cycling is governed internationally by the Union Cycliste Internationale in Switzerland (for upright bicycles) and by the International Human Powered Vehicle Association (for other HPVs, or human-powered vehicles). Cycling for transport and touring is promoted on a European level by the European Cyclists' Federation, with associated members from Great Britain, Japan and elsewhere. Regular conferences on cycling for transport are held under the auspices of Velo City; global conferences are coordinated by Velo Mondial .
## Equipment
In many countries, the most commonly used vehicle for road transport is a utility bicycle. These have frames with so-called relaxed geometry, protecting the rider from shocks from the road, and easing low speeds steering. Road bikes tend to have a more upright shape and a shorter wheelbase, which make the bike more mobile but harder to ride slowly. The design, coupled with low or dropped handlebars, requires the rider to bend forward more, which reduces air resistance at high speed.
The price of a new bicycle can range from US$50 to more than US$20,000, depending on quality, type and weight (the most exotic road bicycles can weigh as little as 3.2kg (7 lb)) ). Being measured for a bike and taking it for a test ride are recommended before buying.
The drivetrain components of the bike should also be considered. A middle grade dérailleur is sufficient for a beginner, although many utility bikes come equipped with hub gears. If the rider plans a significant amount of hillclimbing, a triple-crank (three chainrings) front gear system may be preferred. Otherwise, the relatively lighter and less expensive two chainrings may be better.
Many road bikes include clipless pedals to which special shoes attach via a cleat, permitting the rider to pull on the pedals as well as push. Other possible accessories for the bicycle include locks, mudguards (UK)/fenders (US), luggage carriers and pannier bags, water bottles and bottle cages.
For basic maintenance and repairs, cyclists can choose to carry a pump, a spare inner tube, a CO2 cartridge, a puncture repair kit and tyre levers. Cycling can be more efficient and comfortable with special shoes, gloves, and shorts. In wet weather, riding can be more tolerable with waterproof clothes, such as cape, jacket, trousers and overshoes.
Items legally required in some jurisdictions, or voluntarily adopted for safety reasons, include bicycle helmets, generator or battery operated lighting, and audible signaling devices such as a bell or horn. Extras include studded tires and a bicycle computer.
## Skills
Learning to ride efficiently and safely in traffic is important. In the United Kingdom, many primary school children take the Cycling Proficiency Test, to help them travel more safely. However, the Cycling Proficiency Test has now been superseded, for children, by 'Bikeability' and the National Standards for Cycle Training. In countries such as the Netherlands, where cycling is popular, cyclists sometimes ride in bike lanes at the side of or separate from, the main highway. Many primary schools participate in the national road test in which children individually complete a circuit on roads near the school while being observed by testers.
# Types of cycling
## City
Cyclists and motorists make different demands on road design which may lead to conflicts. Some jurisdictions give priority to motorised traffic, for example setting up one-way street systems, free-right turns, high capacity roundabouts, and slip roads. Others may apply traffic restraint measures to limit the impact of motorised transport. In the former cases, cycling has tended to decline while in the latter it has tended to be maintained. Occasionally, extreme measures against cycling may occur. In Shanghai, where bicycles were once the dominant mode of transport, bicycle travel on a few city roads was banned temporarily in December 2003.
In areas in which cycling is popular and encouraged, cycle-parking facilities using bicycle stands, lockable mini-garages, and patrolled cycle parks are used to reduce theft. Local governments promote cycling by permitting the carriage of bicycles on public transport or by providing external attachment devices on public transport vehicles. Conversely, an absence of secure cycle-parking is a recurring complaint by cyclists from cities with low modal share of cycling.
Extensive bicycle path systems may be found in some cities. Such dedicated paths often have to be shared with in-line skaters, scooters, skateboarders, and pedestrians. Segregating bicycle and automobile traffic in cities has met with mixed success, both in terms of safety and bicycle promotion. At some point the two streams of traffic inevitably intersect, often in a haphazard and congested fashion. Studies have demonstrated that, due to the high incidence of accidents at these sites, some such segregated schemes can actually increase the number of car-bike collisions.
Bicycles are considered a sustainable mode of transport, especially suited for urban use and relatively shorter distances when used for transport (compared to recreation). Case studies and good practices (from European cities and some world-wide examples) that promote and stimulate this kind of functional cycling in cities can be found at Eltis, Europe's portal for local transport.
In the Netherlands bicycle paths are widespread and are (in the cities) not allowed for scooters. Cyclists in the Netherlands are well protected as the law assumes the stronger participant (i.e. the car) guilty party in all accidents involving weaker traffic unless evidence of the opposite is provided. Furthermore, drivers know to expect bikes, which are plentiful and treat traffic rules more as guidelines. Due to these issues the number of car-bike collisions with serious consequences is not alarmingly high in the Netherlands
## Commercial
The postal services of many countries have long relied on bicycles. The British Royal Mail first started using bicycles in 1880; now bicycle delivery fleets include 37,000 in the UK, 25,700 in Germany, 10,500 in Hungary and 7000 in Sweden. The London Ambulance Service has recently introduced bicycling paramedics, who can often get to the scene of an incident in Central London more quickly than a motorised ambulance.
Late in the 20th century, urban police bicycles became more common, as the mobility of car-borne officers was increasingly limited by traffic congestion and pedestrianisation.
Bicycles enjoy substantial use as general delivery vehicles in many countries. In the UK and North America, generations of teenagers have got their first jobs delivering newspapers by bicycle. London has many delivery companies that use bicycles with trailers. Most cities in the West, and many outside it, support a sizeable and visible industry of cycle couriers who deliver documents and small packages. In India, many of Mumbai's Dabbawalas use bicycles to deliver home cooked lunches to the city’s workers. In Bogotá, Colombia the city’s largest bakery recently replaced most of its delivery trucks with bicycles. Even the car industry uses bicycles. At the huge Mercedes-Benz factory in Sindelfingen, Germany workers use bicycles, colour-coded by department, to move around the factory.
## Recreational
Bicycles are used for recreation at all ages. Bicycle touring, also known as cyclotourism, involves touring and exploration or sightseeing by bicycle for leisure. A brevet or randonnée is an organized long-distance ride.
One popular Dutch pleasure is the enjoyment of relaxed cycling in the countryside of the Netherlands. The land is very flat and full of public bicycle trails where cyclists aren't bothered by cars and other traffic, which makes it ideal for cycling recreation. Many Dutch people subscribe every year to an event called fietsvierdaagse — four days of organised cycling through the local environment. Paris-Brest-Paris (PBP), which began in 1891, is the oldest bicycling event still run on a regular basis on the open road, covers over 1200 km and imposes a 90-hour time limit. Similar if smaller institutions exist in many countries.
Many cycling clubs hold organized rides in which bicyclists of all levels participate. The typical organized ride starts with a large group of riders, called the mass, bunch or even peloton. This will thin out over the course of the ride. Many riders choose to ride together in groups of the same skill level to take advantage of drafting.
Most organized rides, for example Cyclosportives, Challenge Rides or reliability trials, and hill climbs (Hillclimbing (cycling)) include registration requirements and will provide information either through the mail or online concerning start times and other requirements. Rides usually consist of 25, 50 and 100 mile routes, each with a certain number of rest stops that usually include refreshments, first aid and maintenance tools.
Mountain biking grew in the late 20th century, including recreation and racing.
## Racing
Shortly after the introduction of bicycles, competitions developed independently in many parts of the world. Early races involving boneshaker style bicycles were predictably fraught with injuries. Large races became popular during the 1890s "Golden Age of Cycling", with events across Europe, and in the U.S. and Japan as well. At one point, almost every major city in the US had a velodrome or two for track racing events. However since the middle of the 20th Century cycling has become a minority sport in the US whilst in Continental Europe it continues to be a major sport, particularly in France, Belgium and Italy. The most famous of all bicycle races is the Tour de France. This began in 1903, and continues to capture the attention of the sporting world.
In 1899, Mile-a-Minute Murphy became the first man to ride a bicycle a mile in under a minute.
As the bicycle evolved its various forms, different racing formats developed. Road races may involve both team and individual competition, and are contested in various ways. They range from the one-day road race, criterium, and time trial to multi-stage events like the Tour de France and its sister events which make up cycling's Grand Tours. Recumbent bicycles were banned from bike races in 1934 after Marcel Berthet set a new hour record in his Velodyne streamliner (49.992 km on 18 November 1933). Track bicycles are used for track cycling in Velodromes , while cyclo-cross races are held on rugged outdoor terrain. In the past decade, mountain bike racing has also reached international popularity and is even an Olympic sport.
Professional racing organizations place limitations on the bicycles that can be used in the races that they sanction. For example, the Union Cycliste Internationale, the governing body of international cycle sport (which sanctions races such as the Tour de France), decided in the late 1990s to create additional rules which prohibit racing bicycles weighing less than 6.8 kilograms (14.96 pounds). The UCI rules also effectively ban some bicycle frame innovations (such as the recumbent bicycle) by requiring a double triangle structure.
## War
The bicycle is not suited for combat, but it has been used as a method of reconnaissance as well as transporting soldiers and supplies to combat zones. In this it has taken over many of the function of horses in warfare. Bicycles were used in the Second Boer War, where both sides used them for scouting. In World War I, France and Germany used bicycles to move troops. In its 1937 invasion of China, Japan employed some 50,000 bicycle troops, and similar forces were instrumental in Japan's march or "roll" through Malaysia in World War II. Germany used bicycles again in World War II, while the British employed airborne "Cycle-commandos" with folding bikes.
In the Vietnam War, communist forces used bicycles extensively as cargo carriers along the Ho Chi Minh Trail. There are reports of mountain bicycles being used in scouting by U.S. Special Forces in the U.S. invasion of Afghanistan and in subsequent battles against the Taliban. British troops, designated Light Bicycle Infantry LBI, used bicycles to patrol in Basra, Iraq in January 2005.
The last country known to maintain a regiment of bicycle troops was Switzerland, who disbanded their final unit in 2003.
# Activism
Two broad and correlated themes run in bicycle activism: one is about advocating the bicycle as an alternative mode of transport, and the other is about the creation of conditions to permit and/or encourage bicycle use, both for utility and recreative cycling. Although the first, which emphasizes the potential for energy and resource conservation and health benefits gained from cycling versus automobile use, is relatively undisputed, the second is target of much debate.
It is generally agreed that improved local and inter-city rail services and other methods of mass transportation (including greater provision for cycle carriage on such services) create conditions to encourage bicycle use. However, there are different opinions on the role of the use of segregated cycle facilities and other items of the cycling infrastructure in building bicycle-friendly cities and roads.
Some bicycle activists (including some traffic management advisers) seek the construction of segregated cycle facilities for journeys of all lengths. Other activists, especially those from the more established tradition, view the safety, practicality, and intent of many segregated cycle facilities with suspicion. They favour a more holistic approach based on the 4 'E's; education (of everyone involved), encouragement (to apply the education), enforcement (to protect the rights of others), and engineering (to facilitate travel while respecting every person's equal right to do so). In some cases this opposition has a more ideological basis: some members of the Vehicular Cycling movement oppose segregated public facilities, such as on-street bike lanes, on principle. Some groups offer training courses to help cyclists integrate themselves with other traffic. This is part of the ongoing cycle path debate.
Critical Mass is an event typically held on the last Friday of every month in cities around the world where bicyclists take to the streets en masse. While the ride was originally founded with the idea of drawing attention to how unfriendly the city was to bicyclists, the leaderless structure of Critical Mass makes it impossible to assign it any one specific goal. In fact, the purpose of Critical Mass is not formalized beyond the direct action of meeting at a set location and time and traveling as a group through city streets.
Midnight Ridazz is a massive established bicycle ride in Los Angeles based on recreational activism. The ride incorporates themes and ride routes designed to maximize fun and comraderie without any overt political agenda that might fracture the group of diverse riders. The one goal of Midnight Ridazz is to have fun riding a bike and thus inspire others to ride and have fun as well.
There is a long-running cycle helmet debate among activists. The most heated controversy surrounds the topic of compulsory helmet use.
# Associations
Cyclists form associations, both for specific interests (trails development, road maintenance, urban design, racing clubs, touring clubs, etc.) and for more global goals (energy conservation, pollution reduction, promotion of fitness). Some bicycle clubs and national associations became prominent advocates for improvements to roads and highways. In the United States, the League of American Wheelmen lobbied for the improvement of roads in the last part of the 19th century, founding and leading the national Good Roads Movement. Their model for political organization, as well as the paved roads for which they argued, facilitated the growth of the automobile.
# Health
Bicycles are commonly used by people seeking to improve their fitness and cardiovascular health. In this regard, bicycling is especially helpful for those with arthritis of the lower limbs and who are unable to pursue sports such as running that involve more impact to joints such as the knees. Furthermore, since cycling can be used as a form of transportation, there can be less demand for self-discipline to maintain the exercise because of the practical purpose of the activity.
Cycling while seated is a relatively non-weight bearing exercise that, like swimming, does little to promote bone density. Cycling up and out of the saddle, on the other hand, does a better job by transferring more of the rider's body weight to the legs. However, excessive cycling while standing can cause knee damage. It used to be thought that cycling while standing was less energy efficient, but recent research has proven this not to be true. There is no wasted energy from cycling while standing.
Cycling on a stationary cycle is frequently advocated as a suitable exercise for rehabilitation particularly for lower limb injury due to the low impact that it has on the joints. In particular cycling is commonly used within knee rehabilitation programs.
## Benefits
The physical exercise gained from cycling is generally linked with increased health and well-being. According to the World Health Organisation, physical inactivity is second only to tobacco smoking as a health risk in developed countries, and this is associated with many tens of billions of dollars of healthcare costs. The WHO's report suggests that increasing physical activity is a public health 'best buy', and that cycling is a 'highly suitable activity' for this purpose. The charity Sustrans reports that investment in cycling provision can give a 20:1 return from health and other benefits. It has been estimated that, on average, approximately 20 life-years are gained from the health benefits of road bicycling for every life-year lost through injury.
## Injuries
Cycling is not generally considered as a high-risk activity. In the UK, casualty rates per kilometre are comparable with walking, but are higher than for car occupants. Most cycle deaths result from a collision with a car or heavy goods vehicle. A Danish study in 2000 concluded that cycling to work was linked to a 40% reduction in mortality rate; this included all causes of death, including road deaths.
Injuries can be divided into two types:
- Physical trauma (extrinsic)
- Overuse (intrinsic).
Acute physical trauma includes injuries to the head and extremities resulting from falls and collisions. Since a large percentage of the collisions between motor and pedal vehicles occur at night, bicycle lighting is required for safety when bicycling at night.
The most common cycling overuse injury occurs in the knees, affecting cyclists at all levels. These are caused by many factors:
- Incorrect bicycle fit or adjustment, particularly the saddle.
- Incorrect adjustment of clipless pedals.
- Too many hills, or too many miles, too early in the training season.
- Poor training preparation for long touring rides.
- Selecting too high a gear. A lower gear for uphill climb protects the knees, even though your muscles are well able to handle a higher gear.
Overuse injuries, including chronic nerve damage at weight bearing locations, can occur as a result of repeatedly riding a bicycle for extended periods of time. Damage to the ulnar nerve in the palm, carpal tunnel in the wrist, the genitourinary tract or bicycle seat neuropathy may result from overuse.
Note that overuse is a relative term, and capacity varies greatly between individuals. Someone starting out in cycling must be careful to increase length and frequency of cycling sessions slowly, starting for example at an hour or two per day, or a hundred miles or kilometers per week. Muscular pain is a normal by-product of the training process, but joint pain and numbness are early signs of overuse injury.
Cycling has been linked to sexual impotence due to pressure on the perineum from the seat, but fitting a proper sized seat prevents this effect. In extreme cases, Pudendal Nerve Entrapment can be a source of intractable perineal pain. Some cyclists with induced pudendal nerve pressure neuropathy gained relief from improvements in saddle position and riding techniques.
The National Institute for Occupational Safety and Health (NIOSH) has investigated the potential health effects of prolonged bicycling in police bicycle patrol units, including the possibility that some bicycle saddles exert excessive pressure on the urogenital area of cyclists, restricting blood flow to the genitals. NIOSH is currently investigating whether saddles developed without protruding noses (which remove the pressure from the urogenital area) will alleviate any potential health problems.
Riding a Recumbent bicycle or quadricycle where ergonomic principles are more closely respected will largely address these health issues, particularly those related to chronic nerve damage at weight bearing locations, simply because the body is supported in the normal sitting position.
Also your back can suffer from strain; this can be induced by pushing big gears, incorrect positioning on the bike, poor core strength and a poor riding style.
# Notes
- ↑ "Bicycling Life"
- ↑ Union Cycliste International (2003). "UCI Cycling Regulations" (PDF). Retrieved 2006-08-04..mw-parser-output cite.citation{font-style:inherit}.mw-parser-output q{quotes:"\"""\"""'""'"}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-lock-free a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-limited a,.mw-parser-output .cs1-lock-registration a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-subscription a{background:url("")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{display:none;font-size:100%}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}
- ↑ Osteoporos Int., Low bone mineral density in highly trained male master cyclists. 2003 Aug;14(8):644-9 (PMID 12856112)
- ↑ "Sit or Stand: Tradeoffs in Efficiency?". . November 212006. Retrieved 2006-11-28. Check date values in: |date= (help); External link in |publisher= (help)
- ↑ "Cycling for Knee Rehabilitation".
- ↑ "Overweight and Obesity: Economic Consequences". Centers for Disease Control and Prevention (cdc.gov).
- ↑ "A PHYSICALLY ACTIVE LIFE THROUGH EVERYDAY TRANSPORT" (PDF). World health Organisation.
- ↑ "How transport can save the NHS". sustrans.org.uk.
- ↑ British Medical Association. Cycling: Towards Health and Safety. Oxford University Press. ISBN 0-19-286151-4. Unknown parameter |coauthors= ignored (help)
- ↑ "COMPARATIVE RISK OF DIFFERENT ACTIVITIES". magma.ca.
- ↑ "Cycling in Great Britain". Department of Transport.
- ↑ "All-Cause Mortality Associated With Physical Activity During Leisure Time, Work, Sports, and Cycling to Work". Archives of Internal Medicine.
- ↑ "Knee Pain in Cycling: New Twist on an old Injury". BioMechanics. July/August, 1996. Retrieved 2006-11-24. Check date values in: |date= (help)
- ↑ Eur Urol., Bicycling related urogenital disorders. 2005 Mar;47(3):277-86 (PMID 15716187)
- ↑ "Bicycle Seat Neuropathy, follow up". eMedicine. February 8, 2006. Retrieved 2006-03-20. Check date values in: |date= (help)
- ↑ "Cycle of despair". BBC News.
- ↑ "Cycling linked to impotence". BBC News.
- ↑ Am J Phys Med Rehabil., Pudendal nerve entrapment as source of intractable perineal pain. 2003 Jun;82(6):479-84. (PMID 12820792)
- ↑ Clin Exp Neurol., Bicycling induced pudendal nerve pressure neuropathy. 1991;28:191-6. (PMID 1821826)
- ↑ "NIOSH -Bicycle Saddles and Reproductive Health". United States National Institute for Occupational Safety and Health. Retrieved 2007-10-10. | Cycling
Cycling is the use of bicycles, unicycles, tricycles, quadricycles and other similar wheeled human powered vehicles (HPVs) as a means of transport, a form of recreation or a sport. It is done on roads and paths, across open country, through tunnels, over bridges, on snow, or even over ice (icebiking).
# Introduction
As a sport, cycling is governed internationally by the Union Cycliste Internationale in Switzerland (for upright bicycles) and by the International Human Powered Vehicle Association (for other HPVs, or human-powered vehicles). Cycling for transport and touring is promoted on a European level by the European Cyclists' Federation, with associated members from Great Britain, Japan and elsewhere. Regular conferences on cycling for transport are held under the auspices of Velo City; global conferences are coordinated by Velo Mondial [2].
## Equipment
Template:Globalize
In many countries, the most commonly used vehicle for road transport is a utility bicycle. These have frames with so-called relaxed geometry, protecting the rider from shocks from the road, and easing low speeds steering. Road bikes tend to have a more upright shape and a shorter wheelbase, which make the bike more mobile but harder to ride slowly. The design, coupled with low or dropped handlebars, requires the rider to bend forward more, which reduces air resistance at high speed.
The price of a new bicycle can range from US$50 to more than US$20,000[3], depending on quality, type and weight (the most exotic road bicycles can weigh as little as 3.2kg (7 lb)) [4]). Being measured for a bike and taking it for a test ride are recommended before buying.
The drivetrain components of the bike should also be considered. A middle grade dérailleur is sufficient for a beginner, although many utility bikes come equipped with hub gears. If the rider plans a significant amount of hillclimbing, a triple-crank (three chainrings) front gear system may be preferred. Otherwise, the relatively lighter and less expensive two chainrings may be better.
Many road bikes include clipless pedals to which special shoes attach via a cleat, permitting the rider to pull on the pedals as well as push. Other possible accessories for the bicycle include locks, mudguards (UK)/fenders (US), luggage carriers and pannier bags, water bottles and bottle cages.
For basic maintenance and repairs, cyclists can choose to carry a pump, a spare inner tube, a CO2 cartridge, a puncture repair kit and tyre levers. Cycling can be more efficient and comfortable with special shoes, gloves, and shorts. In wet weather, riding can be more tolerable with waterproof clothes, such as cape, jacket, trousers and overshoes.
Items legally required in some jurisdictions, or voluntarily adopted for safety reasons, include bicycle helmets, generator or battery operated lighting, and audible signaling devices such as a bell or horn. Extras include studded tires and a bicycle computer.
## Skills
Learning to ride efficiently and safely in traffic is important. In the United Kingdom, many primary school children take the Cycling Proficiency Test, to help them travel more safely. However, the Cycling Proficiency Test has now been superseded, for children, by 'Bikeability' and the National Standards for Cycle Training. In countries such as the Netherlands, where cycling is popular, cyclists sometimes ride in bike lanes at the side of or separate from, the main highway. Many primary schools participate in the national road test in which children individually complete a circuit on roads near the school while being observed by testers.
# Types of cycling
## City
Cyclists and motorists make different demands on road design which may lead to conflicts. Some jurisdictions give priority to motorised traffic, for example setting up one-way street systems, free-right turns, high capacity roundabouts, and slip roads. Others may apply traffic restraint measures to limit the impact of motorised transport. In the former cases, cycling has tended to decline while in the latter it has tended to be maintained. Occasionally, extreme measures against cycling may occur. In Shanghai, where bicycles were once the dominant mode of transport, bicycle travel on a few city roads was banned temporarily in December 2003.
In areas in which cycling is popular and encouraged, cycle-parking facilities using bicycle stands, lockable mini-garages, and patrolled cycle parks are used to reduce theft. Local governments promote cycling by permitting the carriage of bicycles on public transport or by providing external attachment devices on public transport vehicles. Conversely, an absence of secure cycle-parking is a recurring complaint by cyclists from cities with low modal share of cycling.
Extensive bicycle path systems may be found in some cities. Such dedicated paths often have to be shared with in-line skaters, scooters, skateboarders, and pedestrians. Segregating bicycle and automobile traffic in cities has met with mixed success, both in terms of safety and bicycle promotion. At some point the two streams of traffic inevitably intersect, often in a haphazard and congested fashion. Studies have demonstrated that, due to the high incidence of accidents at these sites, some such segregated schemes can actually increase the number of car-bike collisions.[1]
Bicycles are considered a sustainable mode of transport, especially suited for urban use and relatively shorter distances when used for transport (compared to recreation). Case studies and good practices (from European cities and some world-wide examples) that promote and stimulate this kind of functional cycling in cities can be found at Eltis, Europe's portal for local transport.
In the Netherlands bicycle paths are widespread and are (in the cities) not allowed for scooters. Cyclists in the Netherlands are well protected as the law assumes the stronger participant (i.e. the car) guilty party in all accidents involving weaker traffic unless evidence of the opposite is provided. Furthermore, drivers know to expect bikes, which are plentiful and treat traffic rules more as guidelines. Due to these issues the number of car-bike collisions with serious consequences is not alarmingly high in the Netherlands
## Commercial
The postal services of many countries have long relied on bicycles. The British Royal Mail first started using bicycles in 1880; now bicycle delivery fleets include 37,000 in the UK, 25,700 in Germany, 10,500 in Hungary and 7000 in Sweden. The London Ambulance Service has recently introduced bicycling paramedics, who can often get to the scene of an incident in Central London more quickly than a motorised ambulance.
Late in the 20th century, urban police bicycles became more common, as the mobility of car-borne officers was increasingly limited by traffic congestion and pedestrianisation.
Bicycles enjoy substantial use as general delivery vehicles in many countries. In the UK and North America, generations of teenagers have got their first jobs delivering newspapers by bicycle. London has many delivery companies that use bicycles with trailers. Most cities in the West, and many outside it, support a sizeable and visible industry of cycle couriers who deliver documents and small packages. In India, many of Mumbai's Dabbawalas use bicycles to deliver home cooked lunches to the city’s workers. In Bogotá, Colombia the city’s largest bakery recently replaced most of its delivery trucks with bicycles. Even the car industry uses bicycles. At the huge Mercedes-Benz factory in Sindelfingen, Germany workers use bicycles, colour-coded by department, to move around the factory.
## Recreational
Bicycles are used for recreation at all ages. Bicycle touring, also known as cyclotourism, involves touring and exploration or sightseeing by bicycle for leisure. A brevet or randonnée is an organized long-distance ride.
One popular Dutch pleasure is the enjoyment of relaxed cycling in the countryside of the Netherlands. The land is very flat and full of public bicycle trails where cyclists aren't bothered by cars and other traffic, which makes it ideal for cycling recreation. Many Dutch people subscribe every year to an event called fietsvierdaagse — four days of organised cycling through the local environment. Paris-Brest-Paris (PBP), which began in 1891, is the oldest bicycling event still run on a regular basis on the open road, covers over 1200 km and imposes a 90-hour time limit. Similar if smaller institutions exist in many countries.
Many cycling clubs hold organized rides in which bicyclists of all levels participate. The typical organized ride starts with a large group of riders, called the mass, bunch or even peloton. This will thin out over the course of the ride. Many riders choose to ride together in groups of the same skill level to take advantage of drafting.
Most organized rides, for example Cyclosportives, Challenge Rides or reliability trials, and hill climbs (Hillclimbing (cycling)) include registration requirements and will provide information either through the mail or online concerning start times and other requirements. Rides usually consist of 25, 50 and 100 mile routes, each with a certain number of rest stops that usually include refreshments, first aid and maintenance tools.
Mountain biking grew in the late 20th century, including recreation and racing.
## Racing
Shortly after the introduction of bicycles, competitions developed independently in many parts of the world. Early races involving boneshaker style bicycles were predictably fraught with injuries. Large races became popular during the 1890s "Golden Age of Cycling", with events across Europe, and in the U.S. and Japan as well. At one point, almost every major city in the US had a velodrome or two for track racing events. However since the middle of the 20th Century cycling has become a minority sport in the US whilst in Continental Europe it continues to be a major sport, particularly in France, Belgium and Italy. The most famous of all bicycle races is the Tour de France. This began in 1903, and continues to capture the attention of the sporting world.
In 1899, Mile-a-Minute Murphy became the first man to ride a bicycle a mile in under a minute.
As the bicycle evolved its various forms, different racing formats developed. Road races may involve both team and individual competition, and are contested in various ways. They range from the one-day road race, criterium, and time trial to multi-stage events like the Tour de France and its sister events which make up cycling's Grand Tours. Recumbent bicycles were banned from bike races in 1934 after Marcel Berthet set a new hour record in his Velodyne streamliner (49.992 km on 18 November 1933). Track bicycles are used for track cycling in Velodromes , while cyclo-cross races are held on rugged outdoor terrain. In the past decade, mountain bike racing has also reached international popularity and is even an Olympic sport.
Professional racing organizations place limitations on the bicycles that can be used in the races that they sanction. For example, the Union Cycliste Internationale, the governing body of international cycle sport (which sanctions races such as the Tour de France), decided in the late 1990s to create additional rules which prohibit racing bicycles weighing less than 6.8 kilograms (14.96 pounds). The UCI rules also effectively ban some bicycle frame innovations (such as the recumbent bicycle) by requiring a double triangle structure.[2]
## War
The bicycle is not suited for combat, but it has been used as a method of reconnaissance as well as transporting soldiers and supplies to combat zones. In this it has taken over many of the function of horses in warfare. Bicycles were used in the Second Boer War, where both sides used them for scouting. In World War I, France and Germany used bicycles to move troops. In its 1937 invasion of China, Japan employed some 50,000 bicycle troops, and similar forces were instrumental in Japan's march or "roll" through Malaysia in World War II. Germany used bicycles again in World War II, while the British employed airborne "Cycle-commandos" with folding bikes.
In the Vietnam War, communist forces used bicycles extensively as cargo carriers along the Ho Chi Minh Trail. There are reports of mountain bicycles being used in scouting by U.S. Special Forces in the U.S. invasion of Afghanistan and in subsequent battles against the Taliban. British troops, designated Light Bicycle Infantry LBI, used bicycles to patrol in Basra, Iraq in January 2005.
The last country known to maintain a regiment of bicycle troops was Switzerland, who disbanded their final unit in 2003.
# Activism
Two broad and correlated themes run in bicycle activism: one is about advocating the bicycle as an alternative mode of transport, and the other is about the creation of conditions to permit and/or encourage bicycle use, both for utility and recreative cycling. Although the first, which emphasizes the potential for energy and resource conservation and health benefits gained from cycling versus automobile use, is relatively undisputed, the second is target of much debate.
It is generally agreed that improved local and inter-city rail services and other methods of mass transportation (including greater provision for cycle carriage on such services) create conditions to encourage bicycle use. However, there are different opinions on the role of the use of segregated cycle facilities and other items of the cycling infrastructure in building bicycle-friendly cities and roads.
Some bicycle activists (including some traffic management advisers) seek the construction of segregated cycle facilities for journeys of all lengths. Other activists, especially those from the more established tradition, view the safety, practicality, and intent of many segregated cycle facilities with suspicion. They favour a more holistic approach based on the 4 'E's; education (of everyone involved), encouragement (to apply the education), enforcement (to protect the rights of others), and engineering (to facilitate travel while respecting every person's equal right to do so). In some cases this opposition has a more ideological basis: some members of the Vehicular Cycling movement oppose segregated public facilities, such as on-street bike lanes, on principle. Some groups offer training courses to help cyclists integrate themselves with other traffic. This is part of the ongoing cycle path debate.
Critical Mass is an event typically held on the last Friday of every month in cities around the world where bicyclists take to the streets en masse. While the ride was originally founded with the idea of drawing attention to how unfriendly the city was to bicyclists, the leaderless structure of Critical Mass makes it impossible to assign it any one specific goal. In fact, the purpose of Critical Mass is not formalized beyond the direct action of meeting at a set location and time and traveling as a group through city streets.
Midnight Ridazz is a massive established bicycle ride in Los Angeles based on recreational activism. The ride incorporates themes and ride routes designed to maximize fun and comraderie without any overt political agenda that might fracture the group of diverse riders. The one goal of Midnight Ridazz is to have fun riding a bike and thus inspire others to ride and have fun as well.
There is a long-running cycle helmet debate among activists. The most heated controversy surrounds the topic of compulsory helmet use.
# Associations
Cyclists form associations, both for specific interests (trails development, road maintenance, urban design, racing clubs, touring clubs, etc.) and for more global goals (energy conservation, pollution reduction, promotion of fitness). Some bicycle clubs and national associations became prominent advocates for improvements to roads and highways. In the United States, the League of American Wheelmen lobbied for the improvement of roads in the last part of the 19th century, founding and leading the national Good Roads Movement. Their model for political organization, as well as the paved roads for which they argued, facilitated the growth of the automobile.
# Health
Bicycles are commonly used by people seeking to improve their fitness and cardiovascular health. In this regard, bicycling is especially helpful for those with arthritis of the lower limbs and who are unable to pursue sports such as running that involve more impact to joints such as the knees. Furthermore, since cycling can be used as a form of transportation, there can be less demand for self-discipline to maintain the exercise because of the practical purpose of the activity.
Cycling while seated is a relatively non-weight bearing exercise that, like swimming, does little to promote bone density.[3] Cycling up and out of the saddle, on the other hand, does a better job by transferring more of the rider's body weight to the legs. However, excessive cycling while standing can cause knee damage. It used to be thought that cycling while standing was less energy efficient, but recent research has proven this not to be true. There is no wasted energy from cycling while standing.[4]
Cycling on a stationary cycle is frequently advocated as a suitable exercise for rehabilitation particularly for lower limb injury due to the low impact that it has on the joints. In particular cycling is commonly used within knee rehabilitation programs. [5]
## Benefits
The physical exercise gained from cycling is generally linked with increased health and well-being. According to the World Health Organisation, physical inactivity is second only to tobacco smoking as a health risk in developed countries, and this is associated with many tens of billions of dollars of healthcare costs.[6] The WHO's report[7] suggests that increasing physical activity is a public health 'best buy', and that cycling is a 'highly suitable activity' for this purpose. The charity Sustrans reports that investment in cycling provision can give a 20:1 return from health and other benefits.[8] It has been estimated that, on average, approximately 20 life-years are gained from the health benefits of road bicycling for every life-year lost through injury.[9]
## Injuries
Cycling is not generally considered as a high-risk activity.[10] In the UK, casualty rates per kilometre are comparable with walking, but are higher than for car occupants. Most cycle deaths result from a collision with a car or heavy goods vehicle.[11] A Danish study in 2000 concluded that cycling to work was linked to a 40% reduction in mortality rate; this included all causes of death, including road deaths.[12]
Injuries can be divided into two types:
- Physical trauma (extrinsic)
- Overuse (intrinsic).
Acute physical trauma includes injuries to the head and extremities resulting from falls and collisions. Since a large percentage of the collisions between motor and pedal vehicles occur at night, bicycle lighting is required for safety when bicycling at night.
The most common cycling overuse injury occurs in the knees, affecting cyclists at all levels. These are caused by many factors:[13]
- Incorrect bicycle fit or adjustment, particularly the saddle.
- Incorrect adjustment of clipless pedals.
- Too many hills, or too many miles, too early in the training season.
- Poor training preparation for long touring rides.
- Selecting too high a gear. A lower gear for uphill climb protects the knees, even though your muscles are well able to handle a higher gear.
Overuse injuries, including chronic nerve damage at weight bearing locations, can occur as a result of repeatedly riding a bicycle for extended periods of time. Damage to the ulnar nerve in the palm, carpal tunnel in the wrist, the genitourinary tract[14] or bicycle seat neuropathy[15] may result from overuse.
Note that overuse is a relative term, and capacity varies greatly between individuals. Someone starting out in cycling must be careful to increase length and frequency of cycling sessions slowly, starting for example at an hour or two per day, or a hundred miles or kilometers per week. Muscular pain is a normal by-product of the training process, but joint pain and numbness are early signs of overuse injury.
Cycling has been linked to sexual impotence due to pressure on the perineum from the seat, but fitting a proper sized seat prevents this effect.[16][17] In extreme cases, Pudendal Nerve Entrapment can be a source of intractable perineal pain.[18] Some cyclists with induced pudendal nerve pressure neuropathy gained relief from improvements in saddle position and riding techniques.[19]
The National Institute for Occupational Safety and Health (NIOSH) has investigated the potential health effects of prolonged bicycling in police bicycle patrol units, including the possibility that some bicycle saddles exert excessive pressure on the urogenital area of cyclists, restricting blood flow to the genitals. NIOSH is currently investigating whether saddles developed without protruding noses (which remove the pressure from the urogenital area) will alleviate any potential health problems.[20]
Riding a Recumbent bicycle or quadricycle where ergonomic principles are more closely respected will largely address these health issues, particularly those related to chronic nerve damage at weight bearing locations, simply because the body is supported in the normal sitting position.
Also your back can suffer from strain; this can be induced by pushing big gears, incorrect positioning on the bike, poor core strength and a poor riding style.
# Notes
- ↑ "Bicycling Life"
- ↑ Union Cycliste International (2003). "UCI Cycling Regulations" (PDF). Retrieved 2006-08-04..mw-parser-output cite.citation{font-style:inherit}.mw-parser-output q{quotes:"\"""\"""'""'"}.mw-parser-output code.cs1-code{color:inherit;background:inherit;border:inherit;padding:inherit}.mw-parser-output .cs1-lock-free a{background:url("https://upload.wikimedia.org/wikipedia/commons/thumb/6/65/Lock-green.svg/9px-Lock-green.svg.png")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-limited a,.mw-parser-output .cs1-lock-registration a{background:url("https://upload.wikimedia.org/wikipedia/commons/thumb/d/d6/Lock-gray-alt-2.svg/9px-Lock-gray-alt-2.svg.png")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-lock-subscription a{background:url("https://upload.wikimedia.org/wikipedia/commons/thumb/a/aa/Lock-red-alt-2.svg/9px-Lock-red-alt-2.svg.png")no-repeat;background-position:right .1em center}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration{color:#555}.mw-parser-output .cs1-subscription span,.mw-parser-output .cs1-registration span{border-bottom:1px dotted;cursor:help}.mw-parser-output .cs1-hidden-error{display:none;font-size:100%}.mw-parser-output .cs1-visible-error{display:none;font-size:100%}.mw-parser-output .cs1-subscription,.mw-parser-output .cs1-registration,.mw-parser-output .cs1-format{font-size:95%}.mw-parser-output .cs1-kern-left,.mw-parser-output .cs1-kern-wl-left{padding-left:0.2em}.mw-parser-output .cs1-kern-right,.mw-parser-output .cs1-kern-wl-right{padding-right:0.2em}
- ↑ Osteoporos Int., Low bone mineral density in highly trained male master cyclists. 2003 Aug;14(8):644-9 (PMID 12856112)
- ↑ "Sit or Stand: Tradeoffs in Efficiency?". [1]. November 212006. Retrieved 2006-11-28. Check date values in: |date= (help); External link in |publisher= (help)
- ↑ "Cycling for Knee Rehabilitation".
- ↑ "Overweight and Obesity: Economic Consequences". Centers for Disease Control and Prevention (cdc.gov).
- ↑ "A PHYSICALLY ACTIVE LIFE THROUGH EVERYDAY TRANSPORT" (PDF). World health Organisation.
- ↑ "How transport can save the NHS". sustrans.org.uk.
- ↑ British Medical Association. Cycling: Towards Health and Safety. Oxford University Press. ISBN 0-19-286151-4. Unknown parameter |coauthors= ignored (help)
- ↑ "COMPARATIVE RISK OF DIFFERENT ACTIVITIES". magma.ca.
- ↑ "Cycling in Great Britain". Department of Transport.
- ↑ "All-Cause Mortality Associated With Physical Activity During Leisure Time, Work, Sports, and Cycling to Work". Archives of Internal Medicine.
- ↑ "Knee Pain in Cycling: New Twist on an old Injury". BioMechanics. July/August, 1996. Retrieved 2006-11-24. Check date values in: |date= (help)
- ↑ Eur Urol., Bicycling related urogenital disorders. 2005 Mar;47(3):277-86 (PMID 15716187)
- ↑ "Bicycle Seat Neuropathy, follow up". eMedicine. February 8, 2006. Retrieved 2006-03-20. Check date values in: |date= (help)
- ↑ "Cycle of despair". BBC News.
- ↑ "Cycling linked to impotence". BBC News.
- ↑ Am J Phys Med Rehabil., Pudendal nerve entrapment as source of intractable perineal pain. 2003 Jun;82(6):479-84. (PMID 12820792)
- ↑ Clin Exp Neurol., Bicycling induced pudendal nerve pressure neuropathy. 1991;28:191-6. (PMID 1821826)
- ↑ "NIOSH -Bicycle Saddles and Reproductive Health". United States National Institute for Occupational Safety and Health. Retrieved 2007-10-10. | https://www.wikidoc.org/index.php/Cycling | |
46880f20a92fc2b2f46b6d53881f296f69c8eb78 | wikidoc | Cypress | Cypress
# Overview
Cypress is the name applied to many plants in the cypress family Cupressaceae, which is a conifer of northern temperate regions. Most cypress species are trees, while a few are shrubs. Most plants bearing the common name cypress are in the genera Cupressus and Chamaecyparis, but several other genera in the family also carry the name.
Cupressus sempervirens is famous for its longevity, and has been a popular garden plant for thousands of years.
The word "cypress" is derived from Old French "cipres", which was imported from Latin "cyparissus," the latinisation of the Greek κυπάρισσος (kyparissos).
- African Cypress (Widdringtonia species)
- Bald, Pond, and Montezuma Cypresses (Taxodium species, native to North America)
- Chinese Swamp Cypress (Glyptostrobus pensilis)
- Cordilleran Cypress (Austrocedrus chilensis)
- Cypress (Callitropsis species)
- Cypress (Cupressus species)
- Cypress-pines (Actinostrobus species)
- Cypress-pines (Callitris species)
- "False" Cypress (Chamaecyparis species)
- Fujian Cypress (Fokienia hodginsii)
- Guaitecas Cypress (Pilgerodendron uviferum)
- Patagonian Cypress (Fitzroya cupressoides)
- Sargent Cypress (Cupressus sargentii)
- Siberian Cypress (Microbiota decussata)
The Cupressaceae family also contains 13-16 other genera (not listed above) that as of yet do not bear cypress in their common names.
The word cypress is also used as a descriptor for the angiosperm vine in the bindweed family Convolvulaceae, known as the Cypress vine (Ipomoea quamoclit).
The plant called "summer cypress" is Bassia scoparia (Amaranthaceae). | Cypress
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
# Overview
Cypress is the name applied to many plants in the cypress family Cupressaceae, which is a conifer of northern temperate regions. Most cypress species are trees, while a few are shrubs. Most plants bearing the common name cypress are in the genera Cupressus and Chamaecyparis, but several other genera in the family also carry the name.
Cupressus sempervirens is famous for its longevity, and has been a popular garden plant for thousands of years.
The word "cypress" is derived from Old French "cipres", which was imported from Latin "cyparissus," the latinisation of the Greek κυπάρισσος (kyparissos).[1][2]
- African Cypress (Widdringtonia species)
- Bald, Pond, and Montezuma Cypresses (Taxodium species, native to North America)
- Chinese Swamp Cypress (Glyptostrobus pensilis)
- Cordilleran Cypress (Austrocedrus chilensis)
- Cypress (Callitropsis species)
- Cypress (Cupressus species)
- Cypress-pines (Actinostrobus species)
- Cypress-pines (Callitris species)
- "False" Cypress (Chamaecyparis species)
- Fujian Cypress (Fokienia hodginsii)
- Guaitecas Cypress (Pilgerodendron uviferum)
- Patagonian Cypress (Fitzroya cupressoides)
- Sargent Cypress (Cupressus sargentii)
- Siberian Cypress (Microbiota decussata)
The Cupressaceae family also contains 13-16 other genera (not listed above) that as of yet do not bear cypress in their common names.
The word cypress is also used as a descriptor for the angiosperm vine in the bindweed family Convolvulaceae, known as the Cypress vine (Ipomoea quamoclit).
The plant called "summer cypress" is Bassia scoparia (Amaranthaceae). | https://www.wikidoc.org/index.php/Cypress | |
e0c447025d3f1708208ab8bb436d73d6e8773ca6 | wikidoc | Cystine | Cystine
Cystine is the amino acid formed when of a pair of cysteine molecules are joined by a disulfide bond. It is described by the formula (SCH2CH(NH2)CO2H)2. It is a colorless solid, and melts at 247-249 °C. It was discovered in 1810 by William Hyde Wollaston but was not recognized as a component of proteins until it was isolated from the horn of a cow in 1899. Through formation of disulfide bonds within and between protein molecules, cystine is a significant determinant of the tertiary structure of most proteins. Disulfide bonding, along with hydrogen bonding and hydrophobic interactions is partially responsible for the formation of the gluten matrix in bread. Human hair contains approximately 5% cystine by mass.
# Properties
The disulfide link is readily reduced to give the corresponding thiol, cysteine. This reaction is typically effected with thiols such as mercaptoethanol or dithiothreitol.
# Nutritional sources
Supplemental N-acetyl cysteine is claimed to be a source of cystine, but the dose of this supplement is limited by side effects. One of the richest nutritional sources of cystine in the diet is undenatured whey proteins from milk. The disulfide-bonded cystine is not digested or significantly hydrolized by the stomach, but is transported by the blood stream to the tissues of the body. Here, within the cells of the body, the weak disulfide bond is cleaved to give cysteine, from which glutathione can be synthesized.
### In animal feed
Disulfide bonds can be broken at temperatures above about 150 °C, especially at low moisture levels (below about 20%).
# Side effects
Nutritional sources of cystine are virtually free of the toxic side effects associated with the single molecule of cysteine, N-acetyl cysteine. The greatest dietary source of cystine is bio-active, unpasteurized or low-heat pasteurized undenatured whey proteins. | Cystine
Template:NatOrganicBox
Cystine is the amino acid formed when of a pair of cysteine molecules are joined by a disulfide bond. It is described by the formula (SCH2CH(NH2)CO2H)2. It is a colorless solid, and melts at 247-249 °C. It was discovered in 1810 by William Hyde Wollaston but was not recognized as a component of proteins until it was isolated from the horn of a cow in 1899.[1] Through formation of disulfide bonds within and between protein molecules, cystine is a significant determinant of the tertiary structure of most proteins. Disulfide bonding, along with hydrogen bonding and hydrophobic interactions is partially responsible for the formation of the gluten matrix in bread. Human hair contains approximately 5% cystine by mass.[2]
# Properties
The disulfide link is readily reduced to give the corresponding thiol, cysteine. This reaction is typically effected with thiols such as mercaptoethanol or dithiothreitol.
# Nutritional sources
Supplemental N-acetyl cysteine is claimed to be a source of cystine, but the dose of this supplement is limited by side effects. One of the richest nutritional sources of cystine in the diet is undenatured whey proteins from milk. The disulfide-bonded cystine is not digested or significantly hydrolized by the stomach, but is transported by the blood stream to the tissues of the body. Here, within the cells of the body, the weak disulfide bond is cleaved to give cysteine, from which glutathione can be synthesized.
### In animal feed
Disulfide bonds can be broken at temperatures above about 150 °C, especially at low moisture levels (below about 20%)[3].
# Side effects
Nutritional sources of cystine are virtually free of the toxic side effects associated with the single molecule of cysteine, N-acetyl cysteine. The greatest dietary source of cystine is bio-active, unpasteurized or low-heat pasteurized undenatured whey proteins.[citation needed] | https://www.wikidoc.org/index.php/Cystine | |
82572a2c12f310edc23671c9e5e167e13079eea8 | wikidoc | Cytosol | Cytosol
The cytosol (cf. cytoplasm, which also includes the organelles) is the internal fluid of the cell, and a portion of cell metabolism occurs here. Proteins within the cytosol play an important role in signal transduction pathways and glycolysis. They also act as intracellular receptors and form part of the ribosomes, enabling protein synthesis.
In prokaryotes, all chemical reactions take place in the cytosol. In eukaryotes, the cytosol surrounds the cell organelles; this is collectively called cytoplasm. In plants, the amount of cytosol can be reduced because of the large tonoplast (central vacuole) that takes up most of the cell interior volume. The portion of cytosol in the nucleus is called nucleohyaloplasm.
The cytosol also surrounds the cytoskeleton, which is made of fibrous proteins (e.g. microfilaments, microtubules, and intermediate filaments). In many organisms, the cytoskeleton maintains the shape of the cell, anchors organelles, and controls internal movement of structures (e.g. transport vesicles).
The cytosol is a "soup" with free-floating particles, but is highly organized on the molecular level. As the concentration of soluble molecules increases within the cytosol, an osmotic gradient builds up toward the outside of the cell. Water flows into the cell, making the cell bigger. To prevent the cell from bursting apart, molecular pumps in the plasma membrane, the cytoskeleton, the tonoplast or the cell wall (if present), are used to counteract the osmotic pressure.
Cytosol mostly consists of water, dissolved ions, small molecules, and large water-soluble molecules (such as protein). It contains about 20% to 30% protein.
Normal human cytosolic pH is (roughly) 7.0 (i.e. neutral), whereas the pH of the extracellular fluid is 7.4. | Cytosol
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
The cytosol (cf. cytoplasm, which also includes the organelles) is the internal fluid of the cell, and a portion of cell metabolism occurs here. Proteins within the cytosol play an important role in signal transduction pathways and glycolysis. They also act as intracellular receptors and form part of the ribosomes, enabling protein synthesis.
In prokaryotes, all chemical reactions take place in the cytosol. In eukaryotes, the cytosol surrounds the cell organelles; this is collectively called cytoplasm. In plants, the amount of cytosol can be reduced because of the large tonoplast (central vacuole) that takes up most of the cell interior volume. The portion of cytosol in the nucleus is called nucleohyaloplasm.
The cytosol also surrounds the cytoskeleton, which is made of fibrous proteins (e.g. microfilaments, microtubules, and intermediate filaments). In many organisms, the cytoskeleton maintains the shape of the cell, anchors organelles, and controls internal movement of structures (e.g. transport vesicles).
The cytosol is a "soup" with free-floating particles, but is highly organized on the molecular level. As the concentration of soluble molecules increases within the cytosol, an osmotic gradient builds up toward the outside of the cell. Water flows into the cell, making the cell bigger. To prevent the cell from bursting apart, molecular pumps in the plasma membrane, the cytoskeleton, the tonoplast or the cell wall (if present), are used to counteract the osmotic pressure.
Cytosol mostly consists of water, dissolved ions, small molecules, and large water-soluble molecules (such as protein). It contains about 20% to 30% protein.
Normal human cytosolic pH is (roughly) 7.0 (i.e. neutral), whereas the pH of the extracellular fluid is 7.4. | https://www.wikidoc.org/index.php/Cytosol |
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