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http://www.ncbi.nlm.nih.gov/pubmed/24991914,http://www.ncbi.nlm.nih.gov/pubmed/24466013,http://www.ncbi.nlm.nih.gov/pubmed/25380933,http://www.ncbi.nlm.nih.gov/pubmed/24434184,http://www.ncbi.nlm.nih.gov/pubmed/25007710,http://www.ncbi.nlm.nih.gov/pubmed/24980542,http://www.ncbi.nlm.nih.gov/pubmed/25636143,http://www.ncbi.nlm.nih.gov/pubmed/25404658,http://www.ncbi.nlm.nih.gov/pubmed/26131357 | Is Fibroblast Growth Factor 23 a phosphaturic hormone? | Yes, fbroblast growth factor 23 (FGF23) is a phosphaturic hormone. |
http://www.ncbi.nlm.nih.gov/pubmed/23830918,http://www.ncbi.nlm.nih.gov/pubmed/18579285,http://www.ncbi.nlm.nih.gov/pubmed/20577896,http://www.ncbi.nlm.nih.gov/pubmed/23357260,http://www.ncbi.nlm.nih.gov/pubmed/21114588,http://www.ncbi.nlm.nih.gov/pubmed/15302871,http://www.ncbi.nlm.nih.gov/pubmed/25549223,http://www.ncbi.nlm.nih.gov/pubmed/19828453,http://www.ncbi.nlm.nih.gov/pubmed/18672025,http://www.ncbi.nlm.nih.gov/pubmed/21953325,http://www.ncbi.nlm.nih.gov/pubmed/21352421,http://www.ncbi.nlm.nih.gov/pubmed/20153362,http://www.ncbi.nlm.nih.gov/pubmed/20031162,http://www.ncbi.nlm.nih.gov/pubmed/14551156,http://www.ncbi.nlm.nih.gov/pubmed/19062038,http://www.ncbi.nlm.nih.gov/pubmed/22505926,http://www.ncbi.nlm.nih.gov/pubmed/18045538,http://www.ncbi.nlm.nih.gov/pubmed/18719379,http://www.ncbi.nlm.nih.gov/pubmed/14702756,http://www.ncbi.nlm.nih.gov/pubmed/20670956 | Which type of cell death is known as anoikis? | Anoikis (Greek for Homelessness) is a programmed cell death induced upon cell detachment from extracellular matrix, behaving as a critical mechanism in preventing adherent-independent cell growth and attachment to an inappropriate matrix, thus avoiding colonizing of distant organs. Anoikis is important in the normal physiologic development of the human body, as well as in disease states. Adhesion to structural glycoproteins of the extracellular matrix is necessary for survival of the differentiated adherent cells. Cancer cells harbor anoikis resistance allowing spread to occur.Ano?kis is defined as programmed cell death induced by the loss of cell/matrix interactions. Adhesion to structural glycoproteins of the extracellular matrix is necessary for survival of the differentiated adherent cells in the cardiovascular system, including endothelial cells, smooth muscle cells, fibroblasts, and cardiac myocytes.Developed organs display strict spatial organization of differentiated cells which is required for proper organ function. One important device that prevents tissue disorganization is the death of cells that lose anchorage to their native matrix, a signal that indicates potential loss of proper tissue context. Termed anoikis (Greek for Homelessness), this form of cell death is a specialized form of apoptosis. |
http://www.ncbi.nlm.nih.gov/pubmed/19593760,http://www.ncbi.nlm.nih.gov/pubmed/15556149,http://www.ncbi.nlm.nih.gov/pubmed/22075452,http://www.ncbi.nlm.nih.gov/pubmed/18855935,http://www.ncbi.nlm.nih.gov/pubmed/15678087,http://www.ncbi.nlm.nih.gov/pubmed/22119380,http://www.ncbi.nlm.nih.gov/pubmed/21672583,http://www.ncbi.nlm.nih.gov/pubmed/15703202,http://www.ncbi.nlm.nih.gov/pubmed/17310075,http://www.ncbi.nlm.nih.gov/pubmed/16842776,http://www.ncbi.nlm.nih.gov/pubmed/15878358,http://www.ncbi.nlm.nih.gov/pubmed/16497099,http://www.ncbi.nlm.nih.gov/pubmed/11877314,http://www.ncbi.nlm.nih.gov/pubmed/19423954,http://www.ncbi.nlm.nih.gov/pubmed/20447431,http://www.ncbi.nlm.nih.gov/pubmed/17727839,http://www.ncbi.nlm.nih.gov/pubmed/16495765,http://www.ncbi.nlm.nih.gov/pubmed/15231867,http://www.ncbi.nlm.nih.gov/pubmed/23441899,http://www.ncbi.nlm.nih.gov/pubmed/21903118,http://www.ncbi.nlm.nih.gov/pubmed/16960421,http://www.ncbi.nlm.nih.gov/pubmed/11408549 | The small molecule SEA0400 is an inhibitor of which ion antiporter/exchanger? | The effects of SEA0400, a selective inhibitor of the Na(+)/Ca(2+) exchanger (NCX), on Na(+)-dependent Ca(2+) uptake and catecholamine (CA) release were examined in bovine adrenal chromaffin cells that were loaded with Na(+) by treatment with ouabain and veratridine. SEA0400 inhibited Na(+)-dependent (45)Ca(2+) uptake and CA release, with the IC(50) values of 40 and 100 nM, respectively. SEA0400 is a selective inhibitor of the Na(+)/Ca(2+) exchanger having equal potencies to suppress both the forward and reverse mode operation of the Na(+)/Ca(2+) exchanger. SEA0400 (2-[4-[(2,5-difluorophenyl)methoxy] phenoxy]-5-ethoxyaniline), is a selective NCX inhibitor in vivo. |
http://www.ncbi.nlm.nih.gov/pubmed/11174389,http://www.ncbi.nlm.nih.gov/pubmed/21382296,http://www.ncbi.nlm.nih.gov/pubmed/20676476,http://www.ncbi.nlm.nih.gov/pubmed/22670867,http://www.ncbi.nlm.nih.gov/pubmed/23130293,http://www.ncbi.nlm.nih.gov/pubmed/23016555,http://www.ncbi.nlm.nih.gov/pubmed/20137753,http://www.ncbi.nlm.nih.gov/pubmed/22438235,http://www.ncbi.nlm.nih.gov/pubmed/23786947,http://www.ncbi.nlm.nih.gov/pubmed/7529964,http://www.ncbi.nlm.nih.gov/pubmed/12204004,http://www.ncbi.nlm.nih.gov/pubmed/7525736 | What is Piebaldism? | Piebaldism is a rare autosomal dominant disorder of melanocyte development characterized by a congenital white forelock and multiple symmetrical stable hypopigmented or depigmented macules. |
http://www.ncbi.nlm.nih.gov/pubmed/23506900 | Which SLC family is FLVCR1 a member of? | Feline leukemia virus subgroup C receptor (FLVCR1) is a member of the SLC49 family. |
http://www.ncbi.nlm.nih.gov/pubmed/23326395,http://www.ncbi.nlm.nih.gov/pubmed/20545919,http://www.ncbi.nlm.nih.gov/pubmed/21836758,http://www.ncbi.nlm.nih.gov/pubmed/23755286,http://www.ncbi.nlm.nih.gov/pubmed/23363496,http://www.ncbi.nlm.nih.gov/pubmed/18318945 | Is amoxicillin used for treatment of malnutrition in children? | Yes, amoxicillin is used for treatment of malnutrition in children. |
http://www.ncbi.nlm.nih.gov/pubmed/22771813,http://www.ncbi.nlm.nih.gov/pubmed/21903140,http://www.ncbi.nlm.nih.gov/pubmed/25258168,http://www.ncbi.nlm.nih.gov/pubmed/23707377,http://www.ncbi.nlm.nih.gov/pubmed/22325091,http://www.ncbi.nlm.nih.gov/pubmed/24991043,http://www.ncbi.nlm.nih.gov/pubmed/25241055,http://www.ncbi.nlm.nih.gov/pubmed/25047666,http://www.ncbi.nlm.nih.gov/pubmed/25017744,http://www.ncbi.nlm.nih.gov/pubmed/22922128,http://www.ncbi.nlm.nih.gov/pubmed/25039297,http://www.ncbi.nlm.nih.gov/pubmed/25502749,http://www.ncbi.nlm.nih.gov/pubmed/21574955 | Where are the orexigenic peptides synthesized? | The orexigenic peptides are sythesized in the hypothalamus. |
http://www.ncbi.nlm.nih.gov/pubmed/23152537,http://www.ncbi.nlm.nih.gov/pubmed/22787460,http://www.ncbi.nlm.nih.gov/pubmed/24651717,http://www.ncbi.nlm.nih.gov/pubmed/17126871,http://www.ncbi.nlm.nih.gov/pubmed/24623435,http://www.ncbi.nlm.nih.gov/pubmed/24345943,http://www.ncbi.nlm.nih.gov/pubmed/24859335 | What is the mechanism of action of APOBEC3G cytidine deaminase to inhibit HIV-1 replication? | During reverse transcription, APOBEC3G deaminates dC to dU in nascent minus-strand viral DNA, resulting in G-to-A hypermutation in the plus strand DNA to inhibit replication of HIV-1, due to viral cDNA degradation, production of non-functional proteins, formation of undesired stop codons and decreased viral protein synthesis. In an additional line of antiviral defense, APOBEC3G induces deamination of the apical loop cytidine of the trans-activation response (TAR) element, a short stem-loop RNA structure required for binding of elongation factors during HIV-1 transcription elongation, resulting in accumulation of short viral transcripts and production of lower amounts of full-length HIV-1 transcripts in Vif-deficient HIV-1-infected cells. |
http://www.ncbi.nlm.nih.gov/pubmed/22036144,http://www.ncbi.nlm.nih.gov/pubmed/19149237,http://www.ncbi.nlm.nih.gov/pubmed/16532398,http://www.ncbi.nlm.nih.gov/pubmed/18350553,http://www.ncbi.nlm.nih.gov/pubmed/23378396,http://www.ncbi.nlm.nih.gov/pubmed/22236433,http://www.ncbi.nlm.nih.gov/pubmed/20434027,http://www.ncbi.nlm.nih.gov/pubmed/20499091,http://www.ncbi.nlm.nih.gov/pubmed/23405946,http://www.ncbi.nlm.nih.gov/pubmed/17569396,http://www.ncbi.nlm.nih.gov/pubmed/15833158,http://www.ncbi.nlm.nih.gov/pubmed/22121116,http://www.ncbi.nlm.nih.gov/pubmed/16104114,http://www.ncbi.nlm.nih.gov/pubmed/24339369,http://www.ncbi.nlm.nih.gov/pubmed/10911992 | Which inherited disorder is known to be caused by mutations in the NEMO gene? | Incontinentia pigmenti (IP) is a rare neurocutaneous disorder with a frequency of 1 in 50,000 newborn, and is associated with mutations in IKBKG gene (NEMO) in Xq28, inherited as an X-linked dominant traitIncontinentia pigmenti (IP) or Bloch-Sulzberger syndrome (BSS) is a rare neurocutaneous disorder with a frequency of 1 in 50,000 newborn, and is associated with mutations in IKBKG gene (NEMO) in Xq28, inherited as an X-linked dominant trait. |
http://www.ncbi.nlm.nih.gov/pubmed/24515121 | What is ISMARA? | ISMARA (Integrated System for Motif Activity Response Analysis) is a web-based tool that models gene expression or chromatin modifications in terms of genome-wide predictions of regulatory sites. Given only gene expression or chromatin state data across a set of samples as input, ISMARA identifies the key TFs and miRNAs driving expression/chromatin changes and makes detailed predictions regarding their regulatory roles. These include predicted activities of the regulators across the samples, their genome-wide targets, enriched gene categories among the targets, and direct interactions between the regulators. |
http://www.ncbi.nlm.nih.gov/pubmed/22980730,http://www.ncbi.nlm.nih.gov/pubmed/21909922,http://www.ncbi.nlm.nih.gov/pubmed/23313222,http://www.ncbi.nlm.nih.gov/pubmed/22751350,http://www.ncbi.nlm.nih.gov/pubmed/17712138 | Is it possible to purify pseudopodia to be used for proteomic analysis? | Pseudopodia can be purified, using different strategies, in order to be used in proteomic studies. |
http://www.ncbi.nlm.nih.gov/pubmed/19251627,http://www.ncbi.nlm.nih.gov/pubmed/17481916 | Where does TDP43 localize in ALS neurons? | In control motor neurons, TDP43 was almost exclusively nuclear, whereas in ALS spinal motor neurons, TDP43 was predominantly localized to the cytosol and not the nucleus. In control motor neurons, TDP43 was almost exclusively nuclear, whereas in ALS spinal motor neurons, TDP43 was predominantly localized to the cytosol and not the nucleus. |
http://www.ncbi.nlm.nih.gov/pubmed/16339652,http://www.ncbi.nlm.nih.gov/pubmed/21532337,http://www.ncbi.nlm.nih.gov/pubmed/17108004,http://www.ncbi.nlm.nih.gov/pubmed/18844071,http://www.ncbi.nlm.nih.gov/pubmed/12032775,http://www.ncbi.nlm.nih.gov/pubmed/20959602,http://www.ncbi.nlm.nih.gov/pubmed/15542823,http://www.ncbi.nlm.nih.gov/pubmed/15920471 | List interaction partners for the protein GATA1. | GATA-1 interact with factor Gfi-1b, the repressive MeCP1 complex, the chromatin remodeling ACF/WCRF complex, FOG-1, TAL-1, Ldb-1 and LMO2-C.GATA1 interacts with the essential hematopoietic factor Gfi-1b, the repressive MeCP1 complex, the chromatin remodeling ACF/WCRF complex, in addition to the known GATA-1/FOG-1 and GATA-1/TAL-1 complexes. Ldb1 is a known partners of GATA1. LMO2-C can bind endogenous GATA1. Novel transcription factor binding partners for PIAS3 include GATA1. Combinatorial interactions occurre between RUNX1 and its coregulator GATA1. Ski interacts with GATA1. GATA-1 interacts with multiple proteins including FOG-1, EKLF, SP1, CBP/p300 and PU.1. |
http://www.ncbi.nlm.nih.gov/pubmed/23784309,http://www.ncbi.nlm.nih.gov/pubmed/23688559,http://www.ncbi.nlm.nih.gov/pubmed/24068255,http://www.ncbi.nlm.nih.gov/pubmed/23772048,http://www.ncbi.nlm.nih.gov/pubmed/24037988,http://www.ncbi.nlm.nih.gov/pubmed/23651738,http://www.ncbi.nlm.nih.gov/pubmed/23982684,http://www.ncbi.nlm.nih.gov/pubmed/24177031,http://www.ncbi.nlm.nih.gov/pubmed/24004079,http://www.ncbi.nlm.nih.gov/pubmed/24261510,http://www.ncbi.nlm.nih.gov/pubmed/23720266,http://www.ncbi.nlm.nih.gov/pubmed/24291500,http://www.ncbi.nlm.nih.gov/pubmed/24091600,http://www.ncbi.nlm.nih.gov/pubmed/23609136,http://www.ncbi.nlm.nih.gov/pubmed/24064762,http://www.ncbi.nlm.nih.gov/pubmed/23811326,http://www.ncbi.nlm.nih.gov/pubmed/23861371,http://www.ncbi.nlm.nih.gov/pubmed/23824184,http://www.ncbi.nlm.nih.gov/pubmed/24089008,http://www.ncbi.nlm.nih.gov/pubmed/23680185,http://www.ncbi.nlm.nih.gov/pubmed/24041925,http://www.ncbi.nlm.nih.gov/pubmed/24211198 | Is farnesoid X receptor (FXR) a nuclear receptor? | Yes, farnesoid X receptor (FXR) is a nuclear receptor. |
http://www.ncbi.nlm.nih.gov/pubmed/18296106,http://www.ncbi.nlm.nih.gov/pubmed/20407219,http://www.ncbi.nlm.nih.gov/pubmed/11893489,http://www.ncbi.nlm.nih.gov/pubmed/19234522,http://www.ncbi.nlm.nih.gov/pubmed/21901086,http://www.ncbi.nlm.nih.gov/pubmed/16951256,http://www.ncbi.nlm.nih.gov/pubmed/21383063,http://www.ncbi.nlm.nih.gov/pubmed/17851762,http://www.ncbi.nlm.nih.gov/pubmed/19131518,http://www.ncbi.nlm.nih.gov/pubmed/12202754,http://www.ncbi.nlm.nih.gov/pubmed/19607843,http://www.ncbi.nlm.nih.gov/pubmed/21700704,http://www.ncbi.nlm.nih.gov/pubmed/23777805,http://www.ncbi.nlm.nih.gov/pubmed/16094454,http://www.ncbi.nlm.nih.gov/pubmed/23319141,http://www.ncbi.nlm.nih.gov/pubmed/20703100,http://www.ncbi.nlm.nih.gov/pubmed/17613284,http://www.ncbi.nlm.nih.gov/pubmed/23365640,http://www.ncbi.nlm.nih.gov/pubmed/19896956,http://www.ncbi.nlm.nih.gov/pubmed/22122340,http://www.ncbi.nlm.nih.gov/pubmed/22493515,http://www.ncbi.nlm.nih.gov/pubmed/22331172,http://www.ncbi.nlm.nih.gov/pubmed/16760674,http://www.ncbi.nlm.nih.gov/pubmed/22253857 | What histone variants play a role in the DNA damage reponse? | Mostly H2A.X, but H2A.Z and H1R have also been associated to DNA damage |
http://www.ncbi.nlm.nih.gov/pubmed/18002293,http://www.ncbi.nlm.nih.gov/pubmed/18002454,http://www.ncbi.nlm.nih.gov/pubmed/20925563,http://www.ncbi.nlm.nih.gov/pubmed/21250829,http://www.ncbi.nlm.nih.gov/pubmed/17272161,http://www.ncbi.nlm.nih.gov/pubmed/20875149,http://www.ncbi.nlm.nih.gov/pubmed/21971974,http://www.ncbi.nlm.nih.gov/pubmed/15718654,http://www.ncbi.nlm.nih.gov/pubmed/23529100,http://www.ncbi.nlm.nih.gov/pubmed/19163770,http://www.ncbi.nlm.nih.gov/pubmed/20597833 | List tele monitoring applications of miniaturised sensors | Home-polysomnography (HPSG)
Body weight
Blood pressure control
Heart failure control
Vital signs - disaster relief, dangerous outdoor sports and adventure monitoring, and antiterrorism activities.
Telemetric fetal home monitoring system for recording the trans-abdominal fetal heart signal and the uterine contractions
Vital signs - electrocardiograms (ECGs), temperature (T), and oxygen saturation (SaO2) , breath rate
Step-counting for tele-rehabilitation
Detection of falls in elderly |
http://www.ncbi.nlm.nih.gov/pubmed/22962458,http://www.ncbi.nlm.nih.gov/pubmed/23193254 | How are ultraconserved elements called when they form clusters? | Ultraconserved non-coding elements (UCNEs) are organized as large clusters, so-called gene regulatory blocks (GRBs) around key developmental genes. Their molecular functions and the reasons for their high degree of conservation remain enigmatic. |
http://www.ncbi.nlm.nih.gov/pubmed/24565001,http://www.ncbi.nlm.nih.gov/pubmed/25161229,http://www.ncbi.nlm.nih.gov/pubmed/16317079,http://www.ncbi.nlm.nih.gov/pubmed/18990722,http://www.ncbi.nlm.nih.gov/pubmed/16895928,http://www.ncbi.nlm.nih.gov/pubmed/16280084,http://www.ncbi.nlm.nih.gov/pubmed/24497970,http://www.ncbi.nlm.nih.gov/pubmed/16706726,http://www.ncbi.nlm.nih.gov/pubmed/15176478,http://www.ncbi.nlm.nih.gov/pubmed/23934932,http://www.ncbi.nlm.nih.gov/pubmed/23557376 | What is the basis of the methodology of "functional class scoring" (FCS) for the analysis of gene expression data? | The second method, "functional class scoring" (FCS), examines the statistical distribution of individual gene scores among all genes in the gene ontology class and does not involve an initial gene selection step.Functional class scoring (FCS), examines the statistical distribution of individual gene scores among all genes in the gene ontology class and does not involve an initial gene selection step. It consists of a semi-supervised method exploring both the expression pattern and the functional annotation of the genes.The second method, "functional class scoring" (FCS), examines the statistical distribution of individual gene scores among all genes in the gene ontology class and does not involve an initial gene selection step. |
http://www.ncbi.nlm.nih.gov/pubmed/23690510,http://www.ncbi.nlm.nih.gov/pubmed/21915623,http://www.ncbi.nlm.nih.gov/pubmed/17467634,http://www.ncbi.nlm.nih.gov/pubmed/20301577,http://www.ncbi.nlm.nih.gov/pubmed/18536931,http://www.ncbi.nlm.nih.gov/pubmed/22999068,http://www.ncbi.nlm.nih.gov/pubmed/21910241,http://www.ncbi.nlm.nih.gov/pubmed/22106044,http://www.ncbi.nlm.nih.gov/pubmed/23678275,http://www.ncbi.nlm.nih.gov/pubmed/23313911,http://www.ncbi.nlm.nih.gov/pubmed/22120178,http://www.ncbi.nlm.nih.gov/pubmed/21307850,http://www.ncbi.nlm.nih.gov/pubmed/21700933,http://www.ncbi.nlm.nih.gov/pubmed/18250309,http://www.ncbi.nlm.nih.gov/pubmed/21878566,http://www.ncbi.nlm.nih.gov/pubmed/23580742,http://www.ncbi.nlm.nih.gov/pubmed/19916019,http://www.ncbi.nlm.nih.gov/pubmed/24215710,http://www.ncbi.nlm.nih.gov/pubmed/19001023,http://www.ncbi.nlm.nih.gov/pubmed/21685391,http://www.ncbi.nlm.nih.gov/pubmed/22990809,http://www.ncbi.nlm.nih.gov/pubmed/23299782 | What is the Timothy syndrome? | Timothy syndrome is a multisystem disorder characterized by cardiac, hand/foot, facial, and neurodevelopmental features. The two forms are type 1 (classic) and type 2, a rare form caused by mutations in a transcript variant of the same gene. Cardiac findings include a rate-corrected QT interval of between 480 ms and 700 ms and congenital heart defects (patent ductus arteriosus, patent foramen ovale, ventricular septal defect, tetralogy of Fallot, hypertrophic cardiomyopathy). Hand/foot findings are unilateral or bilateral cutaneous syndactyly variably involving fingers two (index), three (middle), four (ring), and five (little) and bilateral cutaneous syndactyly of toes two and three. Facial findings include flat nasal bridge, low-set ears, thin upper lip, and round face. Neuropsychiatric involvement includes global developmental delays and autism spectrum disorders. Ventricular tachyarrhythmia is the leading cause of death, followed by infection and complications of intractable hypoglycemia. Average age of death is 2.5 years. |
http://www.ncbi.nlm.nih.gov/pubmed/20451171,http://www.ncbi.nlm.nih.gov/pubmed/20627960,http://www.ncbi.nlm.nih.gov/pubmed/8673125,http://www.ncbi.nlm.nih.gov/pubmed/15728667,http://www.ncbi.nlm.nih.gov/pubmed/12390248,http://www.ncbi.nlm.nih.gov/pubmed/24376213,http://www.ncbi.nlm.nih.gov/pubmed/12559496,http://www.ncbi.nlm.nih.gov/pubmed/25686609,http://www.ncbi.nlm.nih.gov/pubmed/19598128 | Which disease has been associated to a disruptive ALX1 protein? | Disruption of ALX1 causes extreme microphthalmia and severe facial clefting: expanding the spectrum of autosomal-recessive ALX-related frontonasal dysplasia. |
http://www.ncbi.nlm.nih.gov/pubmed/22943432,http://www.ncbi.nlm.nih.gov/pubmed/18174224,http://www.ncbi.nlm.nih.gov/pubmed/12775843,http://www.ncbi.nlm.nih.gov/pubmed/15843685 | How many selenoproteins are encoded in the human genome? | 25. 15kDa, DI1, DI2, DI3, GPx1, GPx2, GPx3, GPx4, GPx6, SelH, SelI, SelK, SelM, SelN, SelO, SelP, SelR, SelS, SPS2, SelT, TR1, TR2, TR3, SelV and SelW. |
http://www.ncbi.nlm.nih.gov/pubmed/16540652,http://www.ncbi.nlm.nih.gov/pubmed/22039045,http://www.ncbi.nlm.nih.gov/pubmed/20937825,http://www.ncbi.nlm.nih.gov/pubmed/23417847,http://www.ncbi.nlm.nih.gov/pubmed/17446433,http://www.ncbi.nlm.nih.gov/pubmed/19704022 | In which process Src, Cortactin and MT1-MMP are playing an essential role? | Src was shown to be required for invadopodia formation and function, whereas Cortactin was found to regulate cofilin and N-WASp activities to control the stages of invadopodium assembly and maturation. Finally, membrane type 1 matrix metalloproteinase (MT1-MMP) was demostrated as the key invadopodial enzyme responsible for gelatin matrix degradation in cancer cells. |
http://www.ncbi.nlm.nih.gov/pubmed/8371105,http://www.ncbi.nlm.nih.gov/pubmed/16738130,http://www.ncbi.nlm.nih.gov/pubmed/24333410,http://www.ncbi.nlm.nih.gov/pubmed/8175878,http://www.ncbi.nlm.nih.gov/pubmed/9169867 | In which yeast chromosome does the rDNA cluster reside? | Chromosome XII context is important for rDNA function in yeastThe rDNA cluster in Saccharomyces cerevisiae is located 450 kb from the left end and 610 kb from the right end of chromosome XII and consists of approximately 150 tandemly repeated copies of a 9.1 kb rDNA unit.Condensation of a unique region of chromosome XVI and the highly repetitive ribosomal DNA (rDNA) cluster from chromosome XII were also examined in budding yeast. The rDNA cluster in Saccharomyces cerevisiae is located 450 kb from the left end and 610 kb from the right end of chromosome XII and consists of approximately 150 tandemly repeated copies of a 9.1 kb rDNA unit. However, in cells arrested in late mitosis (M) by a cdc15 mutation, the unique DNA appeared decondensed while the repetitive rDNA region appeared condensed, suggesting that the condensation state of separate regions of the genome may be regulated differently. Finally our FISH method provides a new tool to analyze centromeres, telomeres, and gene expression in budding yeast. |
http://www.ncbi.nlm.nih.gov/pubmed/19140108,http://www.ncbi.nlm.nih.gov/pubmed/22086232,http://www.ncbi.nlm.nih.gov/pubmed/23521559,http://www.ncbi.nlm.nih.gov/pubmed/20150322,http://www.ncbi.nlm.nih.gov/pubmed/24380394,http://www.ncbi.nlm.nih.gov/pubmed/17612397 | Which is the underlying mechanism for exon skipping used to treat Duchenne muscular dystrophy? | Antisense-mediated exon skipping therapy is a promising therapeutic approach that uses short DNA-like molecules called antisense oligonucleotides (AOs) to skip over/splice out the mutated part of the gene to produce a shortened but functional dystrophin protein. Many Duchenne Muscular Dystrophy patients need exon skipping of multiple exons in order to restore the reading frame, depending on how many base pairs the mutated exon(s) and adjacent exons have.Antisense-mediated exon skipping therapy is a promising therapeutic approach that uses short DNA-like molecules called antisense oligonucleotides (AOs) to skip over/splice out the mutated part of the gene to produce a shortened but functional dystrophin protein Antisense-mediated exon skipping therapy is a promising therapeutic approach that uses short DNA-like molecules called antisense oligonucleotides (AOs) to skip over/splice out the mutated part of the gene to produce a shortened but functional dystrophin proteinAntisense oligonucleotides (AONs) that bind to complementary sequences of the dystrophin pre-mRNA to induce skipping of the targeted exon by modulating pre-mRNA splicing are promising therapeutic agents for DMD. In addition, multiple exon skipping could be used to select deletions that optimize the functionality of the truncated dystrophin protein. Theoretically, multiple exon skipping could be used to treat approximately 90%, 80%, and 98% of DMD patients with deletion, duplication, and nonsense mutations, respectively. One major challenge has been its limited applicability. |
http://www.ncbi.nlm.nih.gov/pubmed/20382391,http://www.ncbi.nlm.nih.gov/pubmed/22021278,http://www.ncbi.nlm.nih.gov/pubmed/21751368,http://www.ncbi.nlm.nih.gov/pubmed/22728655,http://www.ncbi.nlm.nih.gov/pubmed/15058572,http://www.ncbi.nlm.nih.gov/pubmed/23210603,http://www.ncbi.nlm.nih.gov/pubmed/22265351 | What is the advantage of using long nano columns in proteomics? | The longer the columns, the longer gradients are applied and finally more proteins (increased peak capacity) are identified in a complex proteomic experiment |
http://www.ncbi.nlm.nih.gov/pubmed/11069892,http://www.ncbi.nlm.nih.gov/pubmed/17670945,http://www.ncbi.nlm.nih.gov/pubmed/15870297,http://www.ncbi.nlm.nih.gov/pubmed/24778232,http://www.ncbi.nlm.nih.gov/pubmed/18178375,http://www.ncbi.nlm.nih.gov/pubmed/11081625,http://www.ncbi.nlm.nih.gov/pubmed/15137940,http://www.ncbi.nlm.nih.gov/pubmed/15309048,http://www.ncbi.nlm.nih.gov/pubmed/18079700,http://www.ncbi.nlm.nih.gov/pubmed/9990856,http://www.ncbi.nlm.nih.gov/pubmed/22677545 | During which stage of the cell cycle is cohesin deposited on the yeast genome? | In the budding yeast, cohesin is loaded onto the chromosome during the late G1 phase, establishes sister chromatid cohesion concomitant with DNA replication, and dissociates by the telophase.In the budding yeast, cohesin is loaded onto the chromosome during the late G1 phase, establishes sister chromatid cohesion concomitant with DNA replication, and dissociates by the telophase. Cohesin association with G1 chromosomes requires continued activity of the cohesin loader Mis4/Ssl3, suggesting that repeated loading cycles maintain cohesin binding. In mammalian cells, cohesin binding to chromatin is dynamic in G1, but becomes stabilized during S-phase. Instead, we find that cohesin stability increases at the time of S-phase in a reaction that can be uncoupled from DNA replication. Budding yeast Scc1p/Mcd1p, an essential subunit, is cleaved and dissociates from chromosomes in anaphase, leading to sister chromatid separation. |
http://www.ncbi.nlm.nih.gov/pubmed/22670134,http://www.ncbi.nlm.nih.gov/pubmed/11738860,http://www.ncbi.nlm.nih.gov/pubmed/11269512,http://www.ncbi.nlm.nih.gov/pubmed/11402105,http://www.ncbi.nlm.nih.gov/pubmed/12111643,http://www.ncbi.nlm.nih.gov/pubmed/19495527,http://www.ncbi.nlm.nih.gov/pubmed/11960578,http://www.ncbi.nlm.nih.gov/pubmed/18332345,http://www.ncbi.nlm.nih.gov/pubmed/23449173,http://www.ncbi.nlm.nih.gov/pubmed/21982064,http://www.ncbi.nlm.nih.gov/pubmed/22982301,http://www.ncbi.nlm.nih.gov/pubmed/10577905,http://www.ncbi.nlm.nih.gov/pubmed/18337588,http://www.ncbi.nlm.nih.gov/pubmed/10767337,http://www.ncbi.nlm.nih.gov/pubmed/17089071,http://www.ncbi.nlm.nih.gov/pubmed/11462237,http://www.ncbi.nlm.nih.gov/pubmed/11524741,http://www.ncbi.nlm.nih.gov/pubmed/17387578,http://www.ncbi.nlm.nih.gov/pubmed/11055898,http://www.ncbi.nlm.nih.gov/pubmed/11313756 | Which is the neurodevelopmental disorder associated to mutations in the X- linked gene mecp2? | The neurodevelopmental disorder named Rett syndrome, originally termed as cerebroatrophic hyperammonemia. Although most exclusively affects females, has also been found in male patients. |
http://www.ncbi.nlm.nih.gov/pubmed/11014014,http://www.ncbi.nlm.nih.gov/pubmed/21568724,http://www.ncbi.nlm.nih.gov/pubmed/3287769,http://www.ncbi.nlm.nih.gov/pubmed/22210556,http://www.ncbi.nlm.nih.gov/pubmed/8120524 | What is the treatment of Riedel disease (thyroiditis)? | Riedel thyroiditis is a rare disorder related to a systemic extracervical fibrotic process of unknown origin. The tratment of choice is the surgical treatment: Corticosteroids may be also useful |
http://www.ncbi.nlm.nih.gov/pubmed/23508100 | What is the link between Dax1 and Esrrb? | Dax1 associates with Esrrb and regulates its function in embryonic stem cellsDax1 associates with Esrrb and regulates its function in embryonic stem cells. |
http://www.ncbi.nlm.nih.gov/pubmed/23228017,http://www.ncbi.nlm.nih.gov/pubmed/24908540,http://www.ncbi.nlm.nih.gov/pubmed/21521775,http://www.ncbi.nlm.nih.gov/pubmed/23443805,http://www.ncbi.nlm.nih.gov/pubmed/24495750,http://www.ncbi.nlm.nih.gov/pubmed/21976540,http://www.ncbi.nlm.nih.gov/pubmed/25023489,http://www.ncbi.nlm.nih.gov/pubmed/22180308,http://www.ncbi.nlm.nih.gov/pubmed/24238094,http://www.ncbi.nlm.nih.gov/pubmed/23010851,http://www.ncbi.nlm.nih.gov/pubmed/23339124,http://www.ncbi.nlm.nih.gov/pubmed/26070683,http://www.ncbi.nlm.nih.gov/pubmed/23041231,http://www.ncbi.nlm.nih.gov/pubmed/23400739,http://www.ncbi.nlm.nih.gov/pubmed/24448819,http://www.ncbi.nlm.nih.gov/pubmed/22230479,http://www.ncbi.nlm.nih.gov/pubmed/24556040 | What is dovitinib? | Dovitinib (TKI258) is a tyrosine kinase receptor inhibitor with potent activity against fibroblast growth factor receptor (FGFR) and vascular endothelial growth factor receptor (VEGFR). |
http://www.ncbi.nlm.nih.gov/pubmed/10984715,http://www.ncbi.nlm.nih.gov/pubmed/17131053,http://www.ncbi.nlm.nih.gov/pubmed/16987878,http://www.ncbi.nlm.nih.gov/pubmed/15743670,http://www.ncbi.nlm.nih.gov/pubmed/15734684 | Are DNA helicases involved in progeroid syndromes? | Yes, mutations in genes coding for DNA helicases were found to induce progeroid syndromes, such as Werner syndrome (WS) or Bloom syndrome (BS). |
http://www.ncbi.nlm.nih.gov/pubmed/20805989,http://www.ncbi.nlm.nih.gov/pubmed/20973886,http://www.ncbi.nlm.nih.gov/pubmed/18657870,http://www.ncbi.nlm.nih.gov/pubmed/15963485,http://www.ncbi.nlm.nih.gov/pubmed/23462278,http://www.ncbi.nlm.nih.gov/pubmed/16377649,http://www.ncbi.nlm.nih.gov/pubmed/16887493,http://www.ncbi.nlm.nih.gov/pubmed/21619467,http://www.ncbi.nlm.nih.gov/pubmed/22134047,http://www.ncbi.nlm.nih.gov/pubmed/20495659,http://www.ncbi.nlm.nih.gov/pubmed/19248196,http://www.ncbi.nlm.nih.gov/pubmed/15006940,http://www.ncbi.nlm.nih.gov/pubmed/22647661,http://www.ncbi.nlm.nih.gov/pubmed/22771606,http://www.ncbi.nlm.nih.gov/pubmed/24305596,http://www.ncbi.nlm.nih.gov/pubmed/20507559,http://www.ncbi.nlm.nih.gov/pubmed/18619827,http://www.ncbi.nlm.nih.gov/pubmed/11215996,http://www.ncbi.nlm.nih.gov/pubmed/17868431,http://www.ncbi.nlm.nih.gov/pubmed/23708532,http://www.ncbi.nlm.nih.gov/pubmed/24299143,http://www.ncbi.nlm.nih.gov/pubmed/22209594,http://www.ncbi.nlm.nih.gov/pubmed/12877652,http://www.ncbi.nlm.nih.gov/pubmed/23772662,http://www.ncbi.nlm.nih.gov/pubmed/16326150,http://www.ncbi.nlm.nih.gov/pubmed/23601567,http://www.ncbi.nlm.nih.gov/pubmed/18045887,http://www.ncbi.nlm.nih.gov/pubmed/10443811,http://www.ncbi.nlm.nih.gov/pubmed/23471596,http://www.ncbi.nlm.nih.gov/pubmed/18420865,http://www.ncbi.nlm.nih.gov/pubmed/19717480,http://www.ncbi.nlm.nih.gov/pubmed/18367951,http://www.ncbi.nlm.nih.gov/pubmed/12540328 | List the diseases for which there are point-of-care breath tests | Point of care breath tests are available for lung cancer, pulmonary embolism, respiratory distress syndrome, methanol intoxication, kidney diseases, liver diseases, Helicobacter pylori infection, asthma, sepsis, heart failure, diabetes and tuberculosis. |
http://www.ncbi.nlm.nih.gov/pubmed/10634397,http://www.ncbi.nlm.nih.gov/pubmed/10598711,http://www.ncbi.nlm.nih.gov/pubmed/12508658,http://www.ncbi.nlm.nih.gov/pubmed/18493720,http://www.ncbi.nlm.nih.gov/pubmed/16172741,http://www.ncbi.nlm.nih.gov/pubmed/16167532,http://www.ncbi.nlm.nih.gov/pubmed/16078111,http://www.ncbi.nlm.nih.gov/pubmed/22822048,http://www.ncbi.nlm.nih.gov/pubmed/17235567,http://www.ncbi.nlm.nih.gov/pubmed/10946906,http://www.ncbi.nlm.nih.gov/pubmed/12904990 | Is there association of matrix metalloproteinases with behaviour of pituitary adenomas? | Yes, there is evidence to suggest that matrix metalloproteinases are associated with more aggressive of pituitary adenomas. |
http://www.ncbi.nlm.nih.gov/pubmed/14741203,http://www.ncbi.nlm.nih.gov/pubmed/11164046,http://www.ncbi.nlm.nih.gov/pubmed/16957730,http://www.ncbi.nlm.nih.gov/pubmed/8380072,http://www.ncbi.nlm.nih.gov/pubmed/8365659,http://www.ncbi.nlm.nih.gov/pubmed/20657178,http://www.ncbi.nlm.nih.gov/pubmed/22649084,http://www.ncbi.nlm.nih.gov/pubmed/24244123,http://www.ncbi.nlm.nih.gov/pubmed/8570657,http://www.ncbi.nlm.nih.gov/pubmed/16709275,http://www.ncbi.nlm.nih.gov/pubmed/16924405,http://www.ncbi.nlm.nih.gov/pubmed/18366680,http://www.ncbi.nlm.nih.gov/pubmed/17720933,http://www.ncbi.nlm.nih.gov/pubmed/23046686,http://www.ncbi.nlm.nih.gov/pubmed/23100362,http://www.ncbi.nlm.nih.gov/pubmed/12967275,http://www.ncbi.nlm.nih.gov/pubmed/18302772,http://www.ncbi.nlm.nih.gov/pubmed/19305500,http://www.ncbi.nlm.nih.gov/pubmed/2247152,http://www.ncbi.nlm.nih.gov/pubmed/4448362,http://www.ncbi.nlm.nih.gov/pubmed/22661327,http://www.ncbi.nlm.nih.gov/pubmed/23028310,http://www.ncbi.nlm.nih.gov/pubmed/9369098 | What is the evolutionary process described by the "Muller's ratchet" model? | The vast majority of mutations are deleterious and are eliminated by purifying selection. Yet in finite populations, purifying selection cannot completely prevent the accumulation of deleterious mutations. Muller's ratchet is a paradigmatic model for the accumulation of deleterious mutations in a population of finite size, due to genetic drift. Muller's ratchet suggests that population bottlenecks, which may constrain the genetic diversity of a population, could lead to extinction of all individuals with the least number of deleterious mutations, due to a stochastic fluctuation. When the most-fit class of genotypes is lost, it is lost irreversibly. |
http://www.ncbi.nlm.nih.gov/pubmed/23023377,http://www.ncbi.nlm.nih.gov/pubmed/24100469,http://www.ncbi.nlm.nih.gov/pubmed/20015528 | Which heat shock protein is found to be upregulated during Hsp90 inhibition? | HSP90 inhibition was found to be associated with induction of HSP70 expression. |
http://www.ncbi.nlm.nih.gov/pubmed/25510705,http://www.ncbi.nlm.nih.gov/pubmed/25852445,http://www.ncbi.nlm.nih.gov/pubmed/21567906,http://www.ncbi.nlm.nih.gov/pubmed/26043501,http://www.ncbi.nlm.nih.gov/pubmed/23190751,http://www.ncbi.nlm.nih.gov/pubmed/14571271,http://www.ncbi.nlm.nih.gov/pubmed/24192683,http://www.ncbi.nlm.nih.gov/pubmed/22012791,http://www.ncbi.nlm.nih.gov/pubmed/16232326,http://www.ncbi.nlm.nih.gov/pubmed/21834033,http://www.ncbi.nlm.nih.gov/pubmed/20420030,http://www.ncbi.nlm.nih.gov/pubmed/16010675 | Which gene is responsible for the development of Sotos syndrome? | Sotos syndrome (SoS) is a multiple anomaly, congenital disorder characterized by overgrowth, macrocephaly, distinctive facial features and variable degree of intellectual disability. Haploinsufficiency of the NSD1 gene at 5q35.3, arising from 5q35 microdeletions, point mutations, and partial gene deletions, accounts for a majority of patients with SoS.Sotos syndrome is a well-known overgrowth syndrome characterized by excessive growth during childhood, macrocephaly, distinctive facial appearance and learning disability. This disorder is caused by mutations or deletions in NSD1 gene |
http://www.ncbi.nlm.nih.gov/pubmed/10551340,http://www.ncbi.nlm.nih.gov/pubmed/24240086 | What is the name for anorexia in gymnasts? | Anorexia athletica |
http://www.ncbi.nlm.nih.gov/pubmed/23452283,http://www.ncbi.nlm.nih.gov/pubmed/20962313,http://www.ncbi.nlm.nih.gov/pubmed/19692182,http://www.ncbi.nlm.nih.gov/pubmed/22548949,http://www.ncbi.nlm.nih.gov/pubmed/18544105,http://www.ncbi.nlm.nih.gov/pubmed/14633808,http://www.ncbi.nlm.nih.gov/pubmed/22717271,http://www.ncbi.nlm.nih.gov/pubmed/21658195,http://www.ncbi.nlm.nih.gov/pubmed/18285809,http://www.ncbi.nlm.nih.gov/pubmed/19015731,http://www.ncbi.nlm.nih.gov/pubmed/21470081,http://www.ncbi.nlm.nih.gov/pubmed/21663527,http://www.ncbi.nlm.nih.gov/pubmed/22150921,http://www.ncbi.nlm.nih.gov/pubmed/23311886,http://www.ncbi.nlm.nih.gov/pubmed/22606369,http://www.ncbi.nlm.nih.gov/pubmed/23026519,http://www.ncbi.nlm.nih.gov/pubmed/23533188,http://www.ncbi.nlm.nih.gov/pubmed/17607661,http://www.ncbi.nlm.nih.gov/pubmed/21818838,http://www.ncbi.nlm.nih.gov/pubmed/21977923,http://www.ncbi.nlm.nih.gov/pubmed/21454797,http://www.ncbi.nlm.nih.gov/pubmed/22008274,http://www.ncbi.nlm.nih.gov/pubmed/22150870 | Is Vitamin D deficiency in pregnant women associated with gestational diabetes? | Yes, there are multiple studies reporting an association between low VitD in pregnancy and impaired glucose tolerance, but it is not entirely clear if this translates directly to the increased risk of Gestational diabetes or via maternal obesity and/or genetic polymorphisms. |
http://www.ncbi.nlm.nih.gov/pubmed/19804685,http://www.ncbi.nlm.nih.gov/pubmed/10172049,http://www.ncbi.nlm.nih.gov/pubmed/23336348,http://www.ncbi.nlm.nih.gov/pubmed/7579782,http://www.ncbi.nlm.nih.gov/pubmed/12450926,http://www.ncbi.nlm.nih.gov/pubmed/11772304,http://www.ncbi.nlm.nih.gov/pubmed/11778213,http://www.ncbi.nlm.nih.gov/pubmed/17656661,http://www.ncbi.nlm.nih.gov/pubmed/2689138,http://www.ncbi.nlm.nih.gov/pubmed/23727456,http://www.ncbi.nlm.nih.gov/pubmed/11794977,http://www.ncbi.nlm.nih.gov/pubmed/23251746,http://www.ncbi.nlm.nih.gov/pubmed/1641820,http://www.ncbi.nlm.nih.gov/pubmed/9385884,http://www.ncbi.nlm.nih.gov/pubmed/15532135,http://www.ncbi.nlm.nih.gov/pubmed/10581997,http://www.ncbi.nlm.nih.gov/pubmed/7549071,http://www.ncbi.nlm.nih.gov/pubmed/23463740,http://www.ncbi.nlm.nih.gov/pubmed/11919252,http://www.ncbi.nlm.nih.gov/pubmed/8521760 | What are the indications for alteplase? | Intravenous alteplase (recombinant tissue plasminogen activator) is the only approved thrombolytic agent at present indicated for acute ischaemic stoke.
Food and Drug Administration approval of alteplase for central venous catheter (CVC) occlusions.
Alteplase is now firmly established as a treatment of choice in the management of acute myocardial infarction. The efficacy of intravenous alteplase in the treatment of pulmonary thromboembolism has also been established and appears to be similar to that of streptokinase and urokinase in this indication and in arterial thrombotic occlusion. However, its use in this latter indication and in other vascular disorders has not been as extensively documented.
Preliminary data suggest efficacy of alteplase of deep vein thrombosis and arterial thrombotic occlusion. |
http://www.ncbi.nlm.nih.gov/pubmed/23755307,http://www.ncbi.nlm.nih.gov/pubmed/24101133,http://www.ncbi.nlm.nih.gov/pubmed/23987506,http://www.ncbi.nlm.nih.gov/pubmed/21615688,http://www.ncbi.nlm.nih.gov/pubmed/17052209,http://www.ncbi.nlm.nih.gov/pubmed/22926523,http://www.ncbi.nlm.nih.gov/pubmed/15371409,http://www.ncbi.nlm.nih.gov/pubmed/18823331,http://www.ncbi.nlm.nih.gov/pubmed/24018045,http://www.ncbi.nlm.nih.gov/pubmed/12479806,http://www.ncbi.nlm.nih.gov/pubmed/10769183,http://www.ncbi.nlm.nih.gov/pubmed/21401930,http://www.ncbi.nlm.nih.gov/pubmed/23267331,http://www.ncbi.nlm.nih.gov/pubmed/23431403,http://www.ncbi.nlm.nih.gov/pubmed/25352726,http://www.ncbi.nlm.nih.gov/pubmed/24278035,http://www.ncbi.nlm.nih.gov/pubmed/17785185,http://www.ncbi.nlm.nih.gov/pubmed/16038799,http://www.ncbi.nlm.nih.gov/pubmed/19560418,http://www.ncbi.nlm.nih.gov/pubmed/12133899,http://www.ncbi.nlm.nih.gov/pubmed/21829671,http://www.ncbi.nlm.nih.gov/pubmed/20051520,http://www.ncbi.nlm.nih.gov/pubmed/19200235,http://www.ncbi.nlm.nih.gov/pubmed/11940661,http://www.ncbi.nlm.nih.gov/pubmed/15547943,http://www.ncbi.nlm.nih.gov/pubmed/22776333,http://www.ncbi.nlm.nih.gov/pubmed/21268275,http://www.ncbi.nlm.nih.gov/pubmed/23763998,http://www.ncbi.nlm.nih.gov/pubmed/15118098,http://www.ncbi.nlm.nih.gov/pubmed/19563921,http://www.ncbi.nlm.nih.gov/pubmed/23788642 | List scaffold proteins of the ERK signaling pathway. | Originally identified in yeast, scaffold proteins are now recognized to contribute to the specificity of MEK/ERK pathways in mammalian cells. These scaffolds include kinase suppressor of Ras (KSR), beta-arrestin, MEK partner-1 (MP-1), Sef and IQ motif-containing GTPase-activating protein 1(IQGAP1). Human disc-large homolog (hDlg) acts as a MEK2-specific scaffold protein for the ERK signaling pathway. Two scaffold proteins, caveolin-1 and IQGAP1, are required for phosphorylation of the actin associated pool of extracellular signal regulated kinase 1 and 2 (ERK1/2). Several 14-3-3 isotypes bind to protein kinase C (PKC)-zeta and facilitate coupling of PKC-zeta to Raf-1 an event that boosts the mitogen-activated protein kinase (ERK) pathway.kinase suppressor of Ras 1
MEK Partner 1
Beta-arrestin
IQ motif containing GTPase-activating protein 1
kinase suppressor of Ras 2
mitogen-activated protein kinase organizer 1 |
http://www.ncbi.nlm.nih.gov/pubmed/21846773,http://www.ncbi.nlm.nih.gov/pubmed/18367714,http://www.ncbi.nlm.nih.gov/pubmed/22815530,http://www.ncbi.nlm.nih.gov/pubmed/20838592,http://www.ncbi.nlm.nih.gov/pubmed/23302691,http://www.ncbi.nlm.nih.gov/pubmed/22133874,http://www.ncbi.nlm.nih.gov/pubmed/23357425,http://www.ncbi.nlm.nih.gov/pubmed/23393137,http://www.ncbi.nlm.nih.gov/pubmed/21378119,http://www.ncbi.nlm.nih.gov/pubmed/20679393,http://www.ncbi.nlm.nih.gov/pubmed/18413740,http://www.ncbi.nlm.nih.gov/pubmed/21559294,http://www.ncbi.nlm.nih.gov/pubmed/17616512,http://www.ncbi.nlm.nih.gov/pubmed/22737219,http://www.ncbi.nlm.nih.gov/pubmed/22134929,http://www.ncbi.nlm.nih.gov/pubmed/20071334,http://www.ncbi.nlm.nih.gov/pubmed/22328086,http://www.ncbi.nlm.nih.gov/pubmed/23033272,http://www.ncbi.nlm.nih.gov/pubmed/22210859,http://www.ncbi.nlm.nih.gov/pubmed/19173286,http://www.ncbi.nlm.nih.gov/pubmed/19322801,http://www.ncbi.nlm.nih.gov/pubmed/18437543,http://www.ncbi.nlm.nih.gov/pubmed/17371843,http://www.ncbi.nlm.nih.gov/pubmed/22140515,http://www.ncbi.nlm.nih.gov/pubmed/17890317,http://www.ncbi.nlm.nih.gov/pubmed/20547750,http://www.ncbi.nlm.nih.gov/pubmed/16999741,http://www.ncbi.nlm.nih.gov/pubmed/19626461,http://www.ncbi.nlm.nih.gov/pubmed/22088914,http://www.ncbi.nlm.nih.gov/pubmed/16236173,http://www.ncbi.nlm.nih.gov/pubmed/15962389,http://www.ncbi.nlm.nih.gov/pubmed/19576953,http://www.ncbi.nlm.nih.gov/pubmed/19386473,http://www.ncbi.nlm.nih.gov/pubmed/18974146,http://www.ncbi.nlm.nih.gov/pubmed/17182866,http://www.ncbi.nlm.nih.gov/pubmed/16575165,http://www.ncbi.nlm.nih.gov/pubmed/17929180,http://www.ncbi.nlm.nih.gov/pubmed/21549127,http://www.ncbi.nlm.nih.gov/pubmed/18544619 | Which are the families of mammalian DNA-(cytosine-5)-methyltransferases? | DNA (cytosine-5)-methyltransferases catalyze the specific transfer of a methyl group to the C5 position of cytosine residues in DNA. Three families of DNA (cytosine-5)-methyltransferases have been identified in mammals: DNMT1, DNMT2 and DNMT3 (including DNMT3a, DNMT3b and DNMT3L isoforms). All of them share homologous catalytic domains. DNMT1 is the ���maintenance” methyltransferase family. DNMT1 is specific for hemi-methylated DNA and ensures the faithful transmission of DNA methylation patterns in every replication cycle. DNMT3 is required for de novo methylation of DNA. DNMT3 targets unmethylated DNA and is responsible for the establishment of new methylation patterns. Dnmt2, in contrast to all other mammalian DNA (cytosine-5)-methyltransferases, does not possess a large N-terminal regulatory domain. The DNA methylation activity of DNMT2 is still controversial. |
http://www.ncbi.nlm.nih.gov/pubmed/22406018,http://www.ncbi.nlm.nih.gov/pubmed/18636276,http://www.ncbi.nlm.nih.gov/pubmed/10697412 | Which classes of endogenous retroelements are known to date? | Endogenous retroelements fall into two distinct classes: retrotransposons containing LTRs (Long Terminal Repeats), and retrostransposons lacking LTRs. |
http://www.ncbi.nlm.nih.gov/pubmed/23701638,http://www.ncbi.nlm.nih.gov/pubmed/25102374,http://www.ncbi.nlm.nih.gov/pubmed/16565563,http://www.ncbi.nlm.nih.gov/pubmed/17904063 | What is the association between proBNP serum concentrations and stroke outcomes? | ProBNP serum concentrations are elevated in stroke patients relative to healthy controls. Greater proBNP serum concentrations are associated with greater stroke severity and with increased risk for unfvorable functional outcomes. |
http://www.ncbi.nlm.nih.gov/pubmed/19026781,http://www.ncbi.nlm.nih.gov/pubmed/18980972,http://www.ncbi.nlm.nih.gov/pubmed/24040281,http://www.ncbi.nlm.nih.gov/pubmed/20631058,http://www.ncbi.nlm.nih.gov/pubmed/19954516,http://www.ncbi.nlm.nih.gov/pubmed/22821416,http://www.ncbi.nlm.nih.gov/pubmed/22966008,http://www.ncbi.nlm.nih.gov/pubmed/25617436,http://www.ncbi.nlm.nih.gov/pubmed/15520282,http://www.ncbi.nlm.nih.gov/pubmed/24077602,http://www.ncbi.nlm.nih.gov/pubmed/9214638,http://www.ncbi.nlm.nih.gov/pubmed/25680271,http://www.ncbi.nlm.nih.gov/pubmed/21892963,http://www.ncbi.nlm.nih.gov/pubmed/23688634 | What is the effect that EZH2 has on chromatin? | Ezh1 and Ezh2 maintain repressive chromatin through different mechanismsEz that catalyzes di- and trimethylation of histone H3 lysine 27 (H3K37me2/3), marks repressive to transcription. The mammalian homologs Ezh1 and Ezh2 form similar PRC2 complexes but exhibit contrasting repressive roles. PRC2-Ezh2 catalyzes H3K27me2/3 and its knockdown affects global H3K27me2/3 levels. EZH2 thus maintains chromatin in a repressive state. |
http://www.ncbi.nlm.nih.gov/pubmed/24173036,http://www.ncbi.nlm.nih.gov/pubmed/17477493,http://www.ncbi.nlm.nih.gov/pubmed/22248020,http://www.ncbi.nlm.nih.gov/pubmed/22870189,http://www.ncbi.nlm.nih.gov/pubmed/24255646,http://www.ncbi.nlm.nih.gov/pubmed/21934668,http://www.ncbi.nlm.nih.gov/pubmed/22499706,http://www.ncbi.nlm.nih.gov/pubmed/17592629,http://www.ncbi.nlm.nih.gov/pubmed/22522655,http://www.ncbi.nlm.nih.gov/pubmed/21554688 | Does Chromatin Immunoprecipitation (ChIP) show a bias for highly expressed loci? | Several issues in the processing and analysis of ChIP-chip data have not been resolved fully, including the effect of background (mock control) subtraction and normalization within and across arrays. We detected a chromatin-state bias: open chromatin regions yielded higher coverage, which led to false positives if not corrected. The localization of unrelated proteins, including the entire silencing complex, to the most highly transcribed genes was highly suggestive of a technical issue with the immunoprecipitations. |
http://www.ncbi.nlm.nih.gov/pubmed/17298950,http://www.ncbi.nlm.nih.gov/pubmed/12657640,http://www.ncbi.nlm.nih.gov/pubmed/23671930,http://www.ncbi.nlm.nih.gov/pubmed/18331728,http://www.ncbi.nlm.nih.gov/pubmed/21516109 | Is clathrin involved in E-cadherin endocytosis? | E-cadherin is a central component of the adherens junction in epithelial cells and continuously undergoes endocytosis via clathrin-coated vesicles and/or caveolae depending on the cell type. |
http://www.ncbi.nlm.nih.gov/pubmed/21054594,http://www.ncbi.nlm.nih.gov/pubmed/22386826,http://www.ncbi.nlm.nih.gov/pubmed/21591526 | What are the generic versions of Viagra | Sildenafil Citrate and Elonza in Thailand are the generic versions of Viagra |
http://www.ncbi.nlm.nih.gov/pubmed/16339652,http://www.ncbi.nlm.nih.gov/pubmed/15920471,http://www.ncbi.nlm.nih.gov/pubmed/16888367,http://www.ncbi.nlm.nih.gov/pubmed/19196479 | List GATA-1 interacting partners as discovered with the help of the biotinylation tagging approach. | Our work describes, for the first time, distinct GATA-1 interactions with the essential hematopoietic factor Gfi-1b, the repressive MeCP1 complex, and the chromatin remodeling ACF/WCRF complex, in addition to the known GATA-1/FOG-1 and GATA-1/TAL-1 complexesUsing a biotinylation tagging/proteomics approach in erythroid cells, we describe distinct GATA-1 interactions with the essential hematopoietic factor Gfi-1b, the repressive MeCP1 complex and the chromatin remodeling ACF/WCRF complex, in addition to the known GATA-1/FOG-1 and GATA-1/TAL-1 complexes The biotinylation tagging approach revealed, for the first time, distinct GATA-1 interactions with the essential hematopoietic factor Gfi-1b, the repressive MeCP1 complex, and the chromatin remodeling ACF/WCRF complex, in addition to the known GATA-1/FOG-1 and GATA-1/TAL-1 complexes. |
http://www.ncbi.nlm.nih.gov/pubmed/7874122,http://www.ncbi.nlm.nih.gov/pubmed/22723857,http://www.ncbi.nlm.nih.gov/pubmed/17146684,http://www.ncbi.nlm.nih.gov/pubmed/20157369,http://www.ncbi.nlm.nih.gov/pubmed/15841484,http://www.ncbi.nlm.nih.gov/pubmed/17178205 | Which diseases are associated with Alu element insertion? | Diseases associated with Alu element insertion are the following: myotonic dystrophy type 2, Friedreich ataxia, spinocerebellar ataxia type 10, autosomal dominant optic atrophy, Menkes disease, hyper-IgM with immunodeficiency syndrome (HIGM), and anterior pituitary aplasia. |
http://www.ncbi.nlm.nih.gov/pubmed/18449558,http://www.ncbi.nlm.nih.gov/pubmed/8290959,http://www.ncbi.nlm.nih.gov/pubmed/17478517,http://www.ncbi.nlm.nih.gov/pubmed/16640774,http://www.ncbi.nlm.nih.gov/pubmed/18682829,http://www.ncbi.nlm.nih.gov/pubmed/19557188 | Approximately how many recombination hotspots have been found in the yeast genome? | In the fission yeast genome DSBs are located within 194 prominent peaks separated on average by 65-kbp intervals of DNA that are largely free of DSBs. |
http://www.ncbi.nlm.nih.gov/pubmed/24035588,http://www.ncbi.nlm.nih.gov/pubmed/21060967,http://www.ncbi.nlm.nih.gov/pubmed/25479728,http://www.ncbi.nlm.nih.gov/pubmed/24794627,http://www.ncbi.nlm.nih.gov/pubmed/23197849,http://www.ncbi.nlm.nih.gov/pubmed/21464439,http://www.ncbi.nlm.nih.gov/pubmed/21755313,http://www.ncbi.nlm.nih.gov/pubmed/24577791,http://www.ncbi.nlm.nih.gov/pubmed/22512788,http://www.ncbi.nlm.nih.gov/pubmed/25059784,http://www.ncbi.nlm.nih.gov/pubmed/24469711,http://www.ncbi.nlm.nih.gov/pubmed/24784583,http://www.ncbi.nlm.nih.gov/pubmed/24911883,http://www.ncbi.nlm.nih.gov/pubmed/24554704,http://www.ncbi.nlm.nih.gov/pubmed/22820846 | How could iPSCs be used for the treatment of diabetes? | One of the promising approaches to cure diabetes is to use induced PCSs (iPSCs) and to differentiate them into insulin-secreting β cells. The induction of iPSC differentiation into insulin-secreting cells can be achieved in several ways, such as with the use of microRNAs, or adenoviral transfection with selected genes. |
http://www.ncbi.nlm.nih.gov/pubmed/19467292,http://www.ncbi.nlm.nih.gov/pubmed/11092556,http://www.ncbi.nlm.nih.gov/pubmed/17470795,http://www.ncbi.nlm.nih.gov/pubmed/8344267,http://www.ncbi.nlm.nih.gov/pubmed/24251578,http://www.ncbi.nlm.nih.gov/pubmed/8601283,http://www.ncbi.nlm.nih.gov/pubmed/23788723,http://www.ncbi.nlm.nih.gov/pubmed/8955902,http://www.ncbi.nlm.nih.gov/pubmed/11839807,http://www.ncbi.nlm.nih.gov/pubmed/17715293,http://www.ncbi.nlm.nih.gov/pubmed/23603359,http://www.ncbi.nlm.nih.gov/pubmed/23783574,http://www.ncbi.nlm.nih.gov/pubmed/10334333,http://www.ncbi.nlm.nih.gov/pubmed/9256076,http://www.ncbi.nlm.nih.gov/pubmed/15791204,http://www.ncbi.nlm.nih.gov/pubmed/22209284,http://www.ncbi.nlm.nih.gov/pubmed/17901054,http://www.ncbi.nlm.nih.gov/pubmed/8602359,http://www.ncbi.nlm.nih.gov/pubmed/23614019,http://www.ncbi.nlm.nih.gov/pubmed/8634917,http://www.ncbi.nlm.nih.gov/pubmed/19179357,http://www.ncbi.nlm.nih.gov/pubmed/20385601,http://www.ncbi.nlm.nih.gov/pubmed/10567350 | What is the name of the stem loop present in the 3' end of genes encoding for selenoproteins? | SECIS (selenocysteine insertion sequence) |
http://www.ncbi.nlm.nih.gov/pubmed/21257635,http://www.ncbi.nlm.nih.gov/pubmed/19189080,http://www.ncbi.nlm.nih.gov/pubmed/1636917,http://www.ncbi.nlm.nih.gov/pubmed/23155249,http://www.ncbi.nlm.nih.gov/pubmed/10150552,http://www.ncbi.nlm.nih.gov/pubmed/10502909,http://www.ncbi.nlm.nih.gov/pubmed/11575340,http://www.ncbi.nlm.nih.gov/pubmed/19589243,http://www.ncbi.nlm.nih.gov/pubmed/12500519,http://www.ncbi.nlm.nih.gov/pubmed/10853884,http://www.ncbi.nlm.nih.gov/pubmed/2212256,http://www.ncbi.nlm.nih.gov/pubmed/22991132,http://www.ncbi.nlm.nih.gov/pubmed/19448211,http://www.ncbi.nlm.nih.gov/pubmed/15960715,http://www.ncbi.nlm.nih.gov/pubmed/12392590,http://www.ncbi.nlm.nih.gov/pubmed/16741692,http://www.ncbi.nlm.nih.gov/pubmed/15891317,http://www.ncbi.nlm.nih.gov/pubmed/22577917,http://www.ncbi.nlm.nih.gov/pubmed/15774043,http://www.ncbi.nlm.nih.gov/pubmed/19046459,http://www.ncbi.nlm.nih.gov/pubmed/15959548,http://www.ncbi.nlm.nih.gov/pubmed/10757567 | Is Propofol used for short-term sedation? | Yes. Propofol is the most frequently used sedating agent for patients with expected duration of ICU admission less than 24 hours. There are numerous studies of its efficacy and comparisons with other sedatives. |
http://www.ncbi.nlm.nih.gov/pubmed/21122287,http://www.ncbi.nlm.nih.gov/pubmed/22405852,http://www.ncbi.nlm.nih.gov/pubmed/9129142,http://www.ncbi.nlm.nih.gov/pubmed/9950430 | Which proteins are the different members of the NF-kappaB family of transcription factors? | Nuclear factor kappa B (NFκB) is a dimeric transcription factor comprised of five family members RelA (p65), RelB, c-Rel, NF-kB1/p50 and NF-kB2/p52. |
http://www.ncbi.nlm.nih.gov/pubmed/17464171,http://www.ncbi.nlm.nih.gov/pubmed/22232210,http://www.ncbi.nlm.nih.gov/pubmed/20955959,http://www.ncbi.nlm.nih.gov/pubmed/6807787,http://www.ncbi.nlm.nih.gov/pubmed/11972401,http://www.ncbi.nlm.nih.gov/pubmed/22982575 | What are the symptoms of Rotor syndrome? | Rotor syndrome is characterized by conjugated hyperbilirubinemia, coproporphyrinuria, and near-absent hepatic uptake of anionic diagnostics. |
http://www.ncbi.nlm.nih.gov/pubmed/22326677,http://www.ncbi.nlm.nih.gov/pubmed/22022255,http://www.ncbi.nlm.nih.gov/pubmed/22955974,http://www.ncbi.nlm.nih.gov/pubmed/19710184,http://www.ncbi.nlm.nih.gov/pubmed/19656867,http://www.ncbi.nlm.nih.gov/pubmed/16440002,http://www.ncbi.nlm.nih.gov/pubmed/22056773,http://www.ncbi.nlm.nih.gov/pubmed/19185575,http://www.ncbi.nlm.nih.gov/pubmed/23638305,http://www.ncbi.nlm.nih.gov/pubmed/21264352,http://www.ncbi.nlm.nih.gov/pubmed/20631007,http://www.ncbi.nlm.nih.gov/pubmed/11602343 | Does splicing occur co-transcriptionally? | The consensus view, based on four organisms, is that the majority of splicing events take place co-transcriptionally in most cells and tissues. RNA processing events that take place on the transcribed pre-mRNA include capping, splicing, editing, 3' processing, and polyadenylation. Most of these processes occur co-transcriptionally while the RNA polymerase II (Pol II) enzyme is engaged in transcriptional elongation. |
http://www.ncbi.nlm.nih.gov/pubmed/24296066,http://www.ncbi.nlm.nih.gov/pubmed/12719540,http://www.ncbi.nlm.nih.gov/pubmed/19678910,http://www.ncbi.nlm.nih.gov/pubmed/24269346,http://www.ncbi.nlm.nih.gov/pubmed/24060313,http://www.ncbi.nlm.nih.gov/pubmed/22675075,http://www.ncbi.nlm.nih.gov/pubmed/24158830,http://www.ncbi.nlm.nih.gov/pubmed/24048932,http://www.ncbi.nlm.nih.gov/pubmed/21249368,http://www.ncbi.nlm.nih.gov/pubmed/19594452,http://www.ncbi.nlm.nih.gov/pubmed/16451554,http://www.ncbi.nlm.nih.gov/pubmed/18556259,http://www.ncbi.nlm.nih.gov/pubmed/24050263,http://www.ncbi.nlm.nih.gov/pubmed/24055287,http://www.ncbi.nlm.nih.gov/pubmed/18988631,http://www.ncbi.nlm.nih.gov/pubmed/24222505,http://www.ncbi.nlm.nih.gov/pubmed/24296044 | List the existing methods for genetic manipulation of cells. | Genetic engineering, also called genetic modification, is the direct manipulation of an organism's genome using biotechnology. New DNA may be inserted in the host genome by first isolating and copying the genetic material of interest using molecular cloning methods to generate a DNA sequence, or by synthesizing the DNA, and then inserting this construct into the host organism. Genes may be removed, or "knocked out", using a nuclease. Gene targeting is a different technique that uses homologous recombination to change an endogenous gene, and can be used to delete a gene, remove exons, add a gene, or introduce point mutations. Based on results there are developed many methods for genetic manipulation of cells such as Microinjection, electroporation, liposomes and via viral vectors.The existing methods for genetic manipulation of cells include Agrobacterium-mediated or direct delivery methods, as well as methods using plant artificial chromosomes, site-directed plasmid mutagenesis, combined use of Red/ET recombination and unique restriction site elimination, Bacterial artificial chromosomes (BACs), direct in vitro transposition of viral genomes with a BAC cassette, and subsequent recovery in Escherichia coli, as well as transformation-competent artificial chromosome (TAC)-based acceptor vector, by exploiting the CreloxP recombination system and homing endonucleases. |
http://www.ncbi.nlm.nih.gov/pubmed/18562508,http://www.ncbi.nlm.nih.gov/pubmed/21366911,http://www.ncbi.nlm.nih.gov/pubmed/23197667,http://www.ncbi.nlm.nih.gov/pubmed/23124791,http://www.ncbi.nlm.nih.gov/pubmed/12376881,http://www.ncbi.nlm.nih.gov/pubmed/15764028,http://www.ncbi.nlm.nih.gov/pubmed/23331685,http://www.ncbi.nlm.nih.gov/pubmed/20413685,http://www.ncbi.nlm.nih.gov/pubmed/22359549,http://www.ncbi.nlm.nih.gov/pubmed/21440544,http://www.ncbi.nlm.nih.gov/pubmed/22561409 | Are there clinical trials on stem cells in multiple sclerosis | Yes. Human multipotent mesenchymal stem cell (MSC) therapies are currently being tested in clinical trials for multiple sclerosis. Several small pilot clinical trials in subjects with advanced MS have demonstrated that MSC administration is safe and provided an early signal of clinical effectiveness. The current aim of clinicians and scientists interested in the development of MSC-based strategies for the treatment of MS is to have the ultimate demonstration in large clinical trials that MSC can inhibit CNS inflammation and foster tissue repair. |
http://www.ncbi.nlm.nih.gov/pubmed/11726552 | Which SWI/SNF protein complex subunit has been demonstrated to interact with the FANCA gene product? | The Fanconi anemia protein FANCA has been shown to interact with the brm-related gene 1 (BRG1) product. BRG1 is a subunit of the SWI/SNF complex, which remodels chromatin structure through a DNA-dependent ATPase activity.FANCA was demonstrated to associate with the endogenous SWI/SNF complexFANCA may recruit the SWI/SNF complex to target genes, thereby enabling coupled nuclear functions such as transcription and DNA repair |
http://www.ncbi.nlm.nih.gov/pubmed/23465540,http://www.ncbi.nlm.nih.gov/pubmed/20559422,http://www.ncbi.nlm.nih.gov/pubmed/20080197,http://www.ncbi.nlm.nih.gov/pubmed/25842866,http://www.ncbi.nlm.nih.gov/pubmed/20439430,http://www.ncbi.nlm.nih.gov/pubmed/26302790,http://www.ncbi.nlm.nih.gov/pubmed/23392610,http://www.ncbi.nlm.nih.gov/pubmed/23124062,http://www.ncbi.nlm.nih.gov/pubmed/17872506,http://www.ncbi.nlm.nih.gov/pubmed/25336588,http://www.ncbi.nlm.nih.gov/pubmed/23625890,http://www.ncbi.nlm.nih.gov/pubmed/25313140,http://www.ncbi.nlm.nih.gov/pubmed/24288375,http://www.ncbi.nlm.nih.gov/pubmed/26472911,http://www.ncbi.nlm.nih.gov/pubmed/21764773,http://www.ncbi.nlm.nih.gov/pubmed/21775629,http://www.ncbi.nlm.nih.gov/pubmed/18809914,http://www.ncbi.nlm.nih.gov/pubmed/24939875,http://www.ncbi.nlm.nih.gov/pubmed/26279487,http://www.ncbi.nlm.nih.gov/pubmed/23132912,http://www.ncbi.nlm.nih.gov/pubmed/24178563 | Are piRNAs involved in gene silencing? | Piwi induces piRNA-guided transcriptional silencing and establishment of a repressive chromatin state. piRNA-guided slicing of transposon transcripts enforces their transcriptional silencing via specifying the nuclear piRNA repertoire. Transcriptional silencing implies a piRNA-mediated formation of repressive chromatin which diminishes the transcriptional capacity of the target locus. |
http://www.ncbi.nlm.nih.gov/pubmed/14597637,http://www.ncbi.nlm.nih.gov/pubmed/19121308,http://www.ncbi.nlm.nih.gov/pubmed/24818808,http://www.ncbi.nlm.nih.gov/pubmed/16923723,http://www.ncbi.nlm.nih.gov/pubmed/7721763 | List representatives of the major fungal hypoxanthine-adenine-guanine transporter families. | AzgA and Fcy21p are prototypes of the two major fungal hypoxanthine-adenine-guanine transporter families. |
http://www.ncbi.nlm.nih.gov/pubmed/11973622,http://www.ncbi.nlm.nih.gov/pubmed/9764818,http://www.ncbi.nlm.nih.gov/pubmed/9284737,http://www.ncbi.nlm.nih.gov/pubmed/11324313,http://www.ncbi.nlm.nih.gov/pubmed/9192898,http://www.ncbi.nlm.nih.gov/pubmed/9885824,http://www.ncbi.nlm.nih.gov/pubmed/12668632,http://www.ncbi.nlm.nih.gov/pubmed/9473110,http://www.ncbi.nlm.nih.gov/pubmed/16294336,http://www.ncbi.nlm.nih.gov/pubmed/11106284,http://www.ncbi.nlm.nih.gov/pubmed/17638907,http://www.ncbi.nlm.nih.gov/pubmed/10321971,http://www.ncbi.nlm.nih.gov/pubmed/9700200,http://www.ncbi.nlm.nih.gov/pubmed/11409869,http://www.ncbi.nlm.nih.gov/pubmed/10652334,http://www.ncbi.nlm.nih.gov/pubmed/10822229,http://www.ncbi.nlm.nih.gov/pubmed/22753894,http://www.ncbi.nlm.nih.gov/pubmed/15013219,http://www.ncbi.nlm.nih.gov/pubmed/10790203,http://www.ncbi.nlm.nih.gov/pubmed/8896569,http://www.ncbi.nlm.nih.gov/pubmed/10027003,http://www.ncbi.nlm.nih.gov/pubmed/18970938 | Which proteins have been identified as RET ligands? | RET is activated by members of the glial cell line-derived neurotrophic factor (GDNF) family of ligands, which include GDNF, neurturin, artemin, and persephin.The RET proto-oncogene encodes a receptor tyrosine kinase, which is activated by members of the glial cell line-derived neurotrophic factor (GDNF) family of ligands, which include GDNF, neurturin (NRTN), artemin (ARTN), and persephin (PSPN). |
http://www.ncbi.nlm.nih.gov/pubmed/23690191,http://www.ncbi.nlm.nih.gov/pubmed/22963789,http://www.ncbi.nlm.nih.gov/pubmed/17355169,http://www.ncbi.nlm.nih.gov/pubmed/22018328,http://www.ncbi.nlm.nih.gov/pubmed/23664599,http://www.ncbi.nlm.nih.gov/pubmed/23874116,http://www.ncbi.nlm.nih.gov/pubmed/23275730,http://www.ncbi.nlm.nih.gov/pubmed/23483616,http://www.ncbi.nlm.nih.gov/pubmed/22171972,http://www.ncbi.nlm.nih.gov/pubmed/23282778,http://www.ncbi.nlm.nih.gov/pubmed/23065279 | Which substances are dangerous to g6PD deficient individuals? | Antimalarial drugs (primaquine, pamaquine, chloriquine), fava beans, sulfonamides, some antibiotics( nalidixic acid, nitrofurantoin, isoniazid, dapsone, and furazolidone) and henna |
http://www.ncbi.nlm.nih.gov/pubmed/20129283,http://www.ncbi.nlm.nih.gov/pubmed/22984773,http://www.ncbi.nlm.nih.gov/pubmed/21397042,http://www.ncbi.nlm.nih.gov/pubmed/18341814,http://www.ncbi.nlm.nih.gov/pubmed/15863661,http://www.ncbi.nlm.nih.gov/pubmed/22529811,http://www.ncbi.nlm.nih.gov/pubmed/10727653,http://www.ncbi.nlm.nih.gov/pubmed/19377070,http://www.ncbi.nlm.nih.gov/pubmed/19648062,http://www.ncbi.nlm.nih.gov/pubmed/17442746,http://www.ncbi.nlm.nih.gov/pubmed/11420310,http://www.ncbi.nlm.nih.gov/pubmed/24317018,http://www.ncbi.nlm.nih.gov/pubmed/22277643,http://www.ncbi.nlm.nih.gov/pubmed/17675083,http://www.ncbi.nlm.nih.gov/pubmed/22490985,http://www.ncbi.nlm.nih.gov/pubmed/20609320,http://www.ncbi.nlm.nih.gov/pubmed/15851320,http://www.ncbi.nlm.nih.gov/pubmed/17081365,http://www.ncbi.nlm.nih.gov/pubmed/23538271,http://www.ncbi.nlm.nih.gov/pubmed/12693506,http://www.ncbi.nlm.nih.gov/pubmed/19345130,http://www.ncbi.nlm.nih.gov/pubmed/11748104,http://www.ncbi.nlm.nih.gov/pubmed/17399644,http://www.ncbi.nlm.nih.gov/pubmed/15877619,http://www.ncbi.nlm.nih.gov/pubmed/11960580,http://www.ncbi.nlm.nih.gov/pubmed/14625171,http://www.ncbi.nlm.nih.gov/pubmed/23085483,http://www.ncbi.nlm.nih.gov/pubmed/17141278,http://www.ncbi.nlm.nih.gov/pubmed/12051963,http://www.ncbi.nlm.nih.gov/pubmed/18599870,http://www.ncbi.nlm.nih.gov/pubmed/17075016,http://www.ncbi.nlm.nih.gov/pubmed/19272188,http://www.ncbi.nlm.nih.gov/pubmed/19406494,http://www.ncbi.nlm.nih.gov/pubmed/15277732,http://www.ncbi.nlm.nih.gov/pubmed/11823453,http://www.ncbi.nlm.nih.gov/pubmed/10690282,http://www.ncbi.nlm.nih.gov/pubmed/10664447,http://www.ncbi.nlm.nih.gov/pubmed/15338453,http://www.ncbi.nlm.nih.gov/pubmed/11786529,http://www.ncbi.nlm.nih.gov/pubmed/11150514,http://www.ncbi.nlm.nih.gov/pubmed/16325048,http://www.ncbi.nlm.nih.gov/pubmed/21321465 | Which mutations of SCN5A gene are implicated in Brugada syndrome? | The following mutations of SCN5A gene have been linked to Brugada syndrome:I137M, p.W1095X; c.3284G>A, R27H, E901K, G1743R, V728I, N1443S, E1152X, c.664C>T; p.Arg222X, Ala2>Thr, Ala735, Ala735>Thr, Val1340>Ile, IVS18-1G>A, E1784K (14x), F861WfsX90 (11x), D356N (8x), G1408R (7x), G400A, H558R, W822X, Q55X, V95I, A1649V, delF1617, c.4810+3_4810+6dupGGGT, K1527R, A1569P, R367H, A735V, R1192Q, D1795. |
http://www.ncbi.nlm.nih.gov/pubmed/25852445,http://www.ncbi.nlm.nih.gov/pubmed/2347353,http://www.ncbi.nlm.nih.gov/pubmed/12807965,http://www.ncbi.nlm.nih.gov/pubmed/2319581,http://www.ncbi.nlm.nih.gov/pubmed/22715272,http://www.ncbi.nlm.nih.gov/pubmed/24670087,http://www.ncbi.nlm.nih.gov/pubmed/21484993,http://www.ncbi.nlm.nih.gov/pubmed/16232326,http://www.ncbi.nlm.nih.gov/pubmed/21834047,http://www.ncbi.nlm.nih.gov/pubmed/26043501,http://www.ncbi.nlm.nih.gov/pubmed/23239432 | What is Sotos syndrome? | Sotos syndrome is a well-known overgrowth syndrome characterized by excessive growth during childhood, macrocephaly, distinctive facial appearance and learning disabilitySotos syndrome is a rare genetic disorder with a distinct phenotypic spectrum including excessive growth during childhood, macrocephaly, distinctive facial appearance and learning disability. |
http://www.ncbi.nlm.nih.gov/pubmed/23921808 | What is the CRAPome database? | The CRAPome is a contaminant repository for affinity purification-mass spectrometry data. |
http://www.ncbi.nlm.nih.gov/pubmed/23046909,http://www.ncbi.nlm.nih.gov/pubmed/22992327,http://www.ncbi.nlm.nih.gov/pubmed/19357145,http://www.ncbi.nlm.nih.gov/pubmed/23728690,http://www.ncbi.nlm.nih.gov/pubmed/24323793 | List all articles on network meta-analysis for smoking cessation | Cardiovascular events associated with smoking cessation pharmacotherapies: a network meta-analysis.
Pharmacological interventions for smoking cessation: an overview and network meta-analysis
Effectiveness and cost-effectiveness of computer and other electronic aids for smoking cessation: a systematic review and network meta-analysis.
Smoking cessation interventions in COPD: a network meta-analysis of randomised trials. |
http://www.ncbi.nlm.nih.gov/pubmed/23400593,http://www.ncbi.nlm.nih.gov/pubmed/23808545,http://www.ncbi.nlm.nih.gov/pubmed/24900694,http://www.ncbi.nlm.nih.gov/pubmed/22753001,http://www.ncbi.nlm.nih.gov/pubmed/23084521,http://www.ncbi.nlm.nih.gov/pubmed/24869939,http://www.ncbi.nlm.nih.gov/pubmed/24309210,http://www.ncbi.nlm.nih.gov/pubmed/21391905,http://www.ncbi.nlm.nih.gov/pubmed/25082860,http://www.ncbi.nlm.nih.gov/pubmed/24812409 | Can RG7112 inhibit MDM2? | Yes, RG7112 is a small molecule MDM2 antagonist. |
http://www.ncbi.nlm.nih.gov/pubmed/23876036,http://www.ncbi.nlm.nih.gov/pubmed/21144965,http://www.ncbi.nlm.nih.gov/pubmed/23298923,http://www.ncbi.nlm.nih.gov/pubmed/22371104,http://www.ncbi.nlm.nih.gov/pubmed/19132191,http://www.ncbi.nlm.nih.gov/pubmed/23964817,http://www.ncbi.nlm.nih.gov/pubmed/23557519,http://www.ncbi.nlm.nih.gov/pubmed/22655676,http://www.ncbi.nlm.nih.gov/pubmed/23547865,http://www.ncbi.nlm.nih.gov/pubmed/23683607,http://www.ncbi.nlm.nih.gov/pubmed/19601856,http://www.ncbi.nlm.nih.gov/pubmed/23487517,http://www.ncbi.nlm.nih.gov/pubmed/23086101,http://www.ncbi.nlm.nih.gov/pubmed/24650612,http://www.ncbi.nlm.nih.gov/pubmed/19996630,http://www.ncbi.nlm.nih.gov/pubmed/21892216,http://www.ncbi.nlm.nih.gov/pubmed/22742650,http://www.ncbi.nlm.nih.gov/pubmed/23394539,http://www.ncbi.nlm.nih.gov/pubmed/20124518,http://www.ncbi.nlm.nih.gov/pubmed/22680641,http://www.ncbi.nlm.nih.gov/pubmed/19739042,http://www.ncbi.nlm.nih.gov/pubmed/19297154,http://www.ncbi.nlm.nih.gov/pubmed/19644596,http://www.ncbi.nlm.nih.gov/pubmed/24344662,http://www.ncbi.nlm.nih.gov/pubmed/20520539,http://www.ncbi.nlm.nih.gov/pubmed/21047577,http://www.ncbi.nlm.nih.gov/pubmed/22564122 | Which clotting factor is inhibited by betrixaban? | Betrixaban is an orally administered direct clotting factor Xa inhibitor. |
http://www.ncbi.nlm.nih.gov/pubmed/16304365,http://www.ncbi.nlm.nih.gov/pubmed/20022637 | Which are the most frequent syndromes associated with inherited bone marrow failure? | The inherited bone marrow failure syndromes (IBMFS) are a heterogeneous group of genetic disorders that share the inability of the bone marrow to produce an adequate number of blood cells. The 4 most frequent syndromes are Fanconi anemia (FA), dyskeratosis congenita (DC), Diamond-Blackfan anemia (DBA), and Shwachman-Diamond syndrome (SDS) The inherited bone marrow failure syndromes (IBMFS) are a heterogeneous group of genetic disorders that share the inability of the bone marrow to produce an adequate number of blood cells. The 4 most frequent syndromes are Fanconi anemia (FA), dyskeratosis congenita (DC), Diamond-Blackfan anemia (DBA), and Shwachman-Diamond syndrome (SDS). |
http://www.ncbi.nlm.nih.gov/pubmed/20513550,http://www.ncbi.nlm.nih.gov/pubmed/23697028,http://www.ncbi.nlm.nih.gov/pubmed/21143108,http://www.ncbi.nlm.nih.gov/pubmed/23411863,http://www.ncbi.nlm.nih.gov/pubmed/21413253,http://www.ncbi.nlm.nih.gov/pubmed/24056028,http://www.ncbi.nlm.nih.gov/pubmed/23967358,http://www.ncbi.nlm.nih.gov/pubmed/21199140,http://www.ncbi.nlm.nih.gov/pubmed/23523817,http://www.ncbi.nlm.nih.gov/pubmed/22999801,http://www.ncbi.nlm.nih.gov/pubmed/21723310,http://www.ncbi.nlm.nih.gov/pubmed/20874041,http://www.ncbi.nlm.nih.gov/pubmed/16913829,http://www.ncbi.nlm.nih.gov/pubmed/15705322,http://www.ncbi.nlm.nih.gov/pubmed/22594140,http://www.ncbi.nlm.nih.gov/pubmed/24027319,http://www.ncbi.nlm.nih.gov/pubmed/18645665,http://www.ncbi.nlm.nih.gov/pubmed/22264275,http://www.ncbi.nlm.nih.gov/pubmed/23980723,http://www.ncbi.nlm.nih.gov/pubmed/22377581,http://www.ncbi.nlm.nih.gov/pubmed/22897918,http://www.ncbi.nlm.nih.gov/pubmed/22966141,http://www.ncbi.nlm.nih.gov/pubmed/23740065,http://www.ncbi.nlm.nih.gov/pubmed/16707042,http://www.ncbi.nlm.nih.gov/pubmed/23133693 | How is yellow fever virus transmitted? | Yellow fever virus is transmitted by mosquitoes and is restricted to Africa, Central and South America and the Caribbean.
Yellow fever virus is a flavivirus, and there is only one antigenic type. It was taken to the Americas by the early slave traders, and nowadays reported in Africa, America, Asia and Europe. Yellow fever virus is transmitted by two different cycles:
-from human to human by the mosquito Aedes aegypti; which is well-adapted to breeding around human habitations; the infection can be maintained in this way as ‘urban’ yellow fever.
-from infected monkeys to humans by mosquitoes such as Haemagogus. This is ‘jungle’ yellow fever and is seen in Africa and South America.
Yellow fever is not transmitted directly from human to human by day-to-day contact, but transmission from ill patients to healthcare workers has been reported, notably after needlestick injury. |
http://www.ncbi.nlm.nih.gov/pubmed/22615265,http://www.ncbi.nlm.nih.gov/pubmed/23389753,http://www.ncbi.nlm.nih.gov/pubmed/23312927,http://www.ncbi.nlm.nih.gov/pubmed/21748501,http://www.ncbi.nlm.nih.gov/pubmed/23821689,http://www.ncbi.nlm.nih.gov/pubmed/24103671,http://www.ncbi.nlm.nih.gov/pubmed/23634730,http://www.ncbi.nlm.nih.gov/pubmed/22177763,http://www.ncbi.nlm.nih.gov/pubmed/20352166,http://www.ncbi.nlm.nih.gov/pubmed/23953907,http://www.ncbi.nlm.nih.gov/pubmed/20858186,http://www.ncbi.nlm.nih.gov/pubmed/22308807,http://www.ncbi.nlm.nih.gov/pubmed/23810130,http://www.ncbi.nlm.nih.gov/pubmed/23460104,http://www.ncbi.nlm.nih.gov/pubmed/23657589,http://www.ncbi.nlm.nih.gov/pubmed/22353706,http://www.ncbi.nlm.nih.gov/pubmed/23790307,http://www.ncbi.nlm.nih.gov/pubmed/22008738,http://www.ncbi.nlm.nih.gov/pubmed/22669799 | Are there any specific antidotes for dabigatran? | No specific antidote currently exists for dabigatran |
http://www.ncbi.nlm.nih.gov/pubmed/25870109 | What is the outcome of TAF10 interacting with the GATA1 transcription factor? | TAF10 Interacts with the GATA1 Transcription Factor and Controls Mouse Erythropoiesis. |
http://www.ncbi.nlm.nih.gov/pubmed/18403482 | How does TNF affect thyroid hormone receptors? | TNF-alpha inhibits the T3-induced expression of thyroid hormone receptor-beta |
http://www.ncbi.nlm.nih.gov/pubmed/22366995,http://www.ncbi.nlm.nih.gov/pubmed/25124187,http://www.ncbi.nlm.nih.gov/pubmed/24342634,http://www.ncbi.nlm.nih.gov/pubmed/26139286,http://www.ncbi.nlm.nih.gov/pubmed/21659436,http://www.ncbi.nlm.nih.gov/pubmed/23548324,http://www.ncbi.nlm.nih.gov/pubmed/24794971,http://www.ncbi.nlm.nih.gov/pubmed/25232168,http://www.ncbi.nlm.nih.gov/pubmed/24392752,http://www.ncbi.nlm.nih.gov/pubmed/25498089,http://www.ncbi.nlm.nih.gov/pubmed/23267668 | Which ones are the ESKAPE organisms? | The 6 ESKAPE pathogens are Enterococcus faecium, Staphylococcus aureus, Klebsiella pneumoniae, Acinetobacter baumannii, Pseudomonas aeruginosa, and Enterobacter species. |
http://www.ncbi.nlm.nih.gov/pubmed/22027573,http://www.ncbi.nlm.nih.gov/pubmed/21521775,http://www.ncbi.nlm.nih.gov/pubmed/24238094 | What is the effect of dovitinib on the cell cycle? | Dovitinib triggers a G2 /M arrest. It promotes a delay in mitotic exit in a subset of cells, causing the cells to undergo mitotic slippage. Higher concentrations of Dovitinib induce a G2 arrest similar to the G2 DNA damage checkpoint. |
http://www.ncbi.nlm.nih.gov/pubmed/19417143 | What is the involvement of PDGFRB in metastatic medulloblastoma? | Platelet-derived growth factor (PDGF) receptor B (PDGFRB) expression was shown to correlate with metastatic medulloblastoma, while PDGFRB tyrosine kinase activity was demonstrated to be critical for migration and invasion of medulloblastoma cells possibly by transactivating EGFR. |
http://www.ncbi.nlm.nih.gov/pubmed/15110149,http://www.ncbi.nlm.nih.gov/pubmed/23123322,http://www.ncbi.nlm.nih.gov/pubmed/2726431,http://www.ncbi.nlm.nih.gov/pubmed/21718716,http://www.ncbi.nlm.nih.gov/pubmed/18538346,http://www.ncbi.nlm.nih.gov/pubmed/25377479,http://www.ncbi.nlm.nih.gov/pubmed/21979103,http://www.ncbi.nlm.nih.gov/pubmed/17214508,http://www.ncbi.nlm.nih.gov/pubmed/15194743,http://www.ncbi.nlm.nih.gov/pubmed/10779321 | What is known as Calcium Induced Calcium Release (CICR) and its role in cardiomyocyte contractility? | the cicr mechanism has been understood mainly based on binding of cytosolic ca(2+) with ryanodine receptors (ryrs) and inducing ca(2+) release from the sarcoplasmic reticulum (sr). l-type ca(2+) channels activate ryrs to produce cicr in smooth muscle cells in the form of ca(2+) sparks and propagated ca(2+) waves. in heart cells, a tight coupling between the gating of single l-type ca(2+) channels and ryanodine receptors (ryrs) underlies calcium release. the importance of ca-induced ca release in excitation-contraction coupling in the heart. waves of calcium-induced calcium release occur in a variety of cell types and have been implicated in the origin of cardiac arrhythmias. in mammals, ca(2+) influx as l-type ca(2+) current (ica) triggers the release of ca(2+) from sarcoplasmic reticulum (sr) and ca(2+)-induced ca(2+) release (cicr) is critical for excitation-contraction coupling. Cardiomyocyte contraction depends on rapid changes in intracellular Ca(2+). Ca(2+) influx as L-type Ca(2+) current (ICa) triggers the release of Ca(2+) from sarcoplasmic reticulum (SR) and Ca(2+)-induced Ca(2+) release (CICR) is critical for excitation-contraction coupling. Calcium-induced calcium-release in cardiac myocytes takes place in spatially restricted regions known as dyads, where discrete patches of junctional sarcoplasmic reticulum tightly associate with the t-tubule membrane. Calcium-induced calcium release (CICR) has been observed in cardiac myocytes as elementary calcium release events (calcium sparks) associated with the opening of L-type Ca(2+) channels. Waves of calcium-induced calcium release occur in a variety of cell types and have been implicated in the origin of cardiac arrhythmias. |
http://www.ncbi.nlm.nih.gov/pubmed/7656507,http://www.ncbi.nlm.nih.gov/pubmed/9353417,http://www.ncbi.nlm.nih.gov/pubmed/9577836,http://www.ncbi.nlm.nih.gov/pubmed/6249092,http://www.ncbi.nlm.nih.gov/pubmed/1224004,http://www.ncbi.nlm.nih.gov/pubmed/6817377,http://www.ncbi.nlm.nih.gov/pubmed/7965768,http://www.ncbi.nlm.nih.gov/pubmed/2895008 | What is the action of molindone? | Molindone is a short-acting antipsychotic.
Molindone, along with other antipsychotic drugs which elicit little or no Parkinsonism, bind more loosely than dopamine to D2 receptors. Compared to the tightly bound antipsychotic drugs, the more loosely bound antipsychotics generally require higher clinical doses, require fewer days for clinical adjustment, but may dissociate from the D2 receptor more rapidly and could lead to clinical relapse somewhat earlier than that found with the traditional tightly bound antipsychotic drugs.
Molindone is D2-selective in vitro and has a dual D1-D2 receptor profile in vivo.
Molindone can selectively block the presynaptic DA receptors.
Molindone causes a statistically significant up-regulation of both the long and short isoforms of the D2 receptor mRNAs in the prefrontal and temporal cortex, but has no effect on D4 mRNA levels in either cortical or striatal tissue.
Molindone elevates Fos-like immunoreactivity (FLI) in the dorsolateral striatum.
Molindone exhibits selectivity for cortical serotonin-stimulated cyclase versus dopamine-stimulated cyclase.
Molindone in low intravenous doses (0.4-0.8 mg/kg) was found to reverse d-amphetamine and apomorphine induced depression of DA neurons and to block apomorphine induced depression of these cells. Molindone was also found to increase dopamine synthesis and dihydroxyphenylactic acid levels in the striatum and olfacotry tubercles. In all of these respects molindone behaves identically to most classical neuroleptics. However, unlike most antipsychotic drugs previously tested, molindone failed to increase the baseline firing rate of DA cells and blocked haloperidol induced increases in DA neuron activity. In this regard molindone most closely resembles thioridazine and clozapine. |
http://www.ncbi.nlm.nih.gov/pubmed/22812510,http://www.ncbi.nlm.nih.gov/pubmed/21764456,http://www.ncbi.nlm.nih.gov/pubmed/21300429,http://www.ncbi.nlm.nih.gov/pubmed/21288197,http://www.ncbi.nlm.nih.gov/pubmed/22266315,http://www.ncbi.nlm.nih.gov/pubmed/24311790,http://www.ncbi.nlm.nih.gov/pubmed/24155099,http://www.ncbi.nlm.nih.gov/pubmed/22769588,http://www.ncbi.nlm.nih.gov/pubmed/23190643,http://www.ncbi.nlm.nih.gov/pubmed/23926106,http://www.ncbi.nlm.nih.gov/pubmed/19228121,http://www.ncbi.nlm.nih.gov/pubmed/24308939,http://www.ncbi.nlm.nih.gov/pubmed/24206177,http://www.ncbi.nlm.nih.gov/pubmed/24531476 | What is the function of the enzymes known as dual specificity phoshpatases (DUSPs)? | DUSPs (dual-specificity phosphatases) are a heterogeneous group of protein phosphatases that can dephosphorylate both phosphotyrosine and phosphoserine/phosphothreonine residues within the one substrate. DUSPs have been implicated as major modulators of critical signalling pathways that are dysregulated in various diseases. DUSPs can be divided into six subgroups on the basis of sequence similarity that include slingshots, PRLs (phosphatases of regenerating liver), Cdc14 phosphatases (Cdc is cell division cycle), PTENs (phosphatase and tensin homologues deleted on chromosome 10), myotubularins, MKPs (mitogen-activated protein kinase phosphatases) and atypical DUSPs.Dual-specificity protein phosphatases participate in signal transduction pathways inactivating mitogen-activated protein kinases (MAP kinases).
Dual-specificity phosphatases (DUSPs) dephosphorylate phosphotyrosine and phosphoserine/phosphothreonine residues on target MAPKs.
These signaling pathways are of critical importance in the regulation of numerous biological processes, including cell proliferation, differentiation and development. |
http://www.ncbi.nlm.nih.gov/pubmed/17445666,http://www.ncbi.nlm.nih.gov/pubmed/11490298,http://www.ncbi.nlm.nih.gov/pubmed/20432327,http://www.ncbi.nlm.nih.gov/pubmed/20438565,http://www.ncbi.nlm.nih.gov/pubmed/18335255,http://www.ncbi.nlm.nih.gov/pubmed/23427760,http://www.ncbi.nlm.nih.gov/pubmed/21895933,http://www.ncbi.nlm.nih.gov/pubmed/11002301,http://www.ncbi.nlm.nih.gov/pubmed/22903482,http://www.ncbi.nlm.nih.gov/pubmed/19238399,http://www.ncbi.nlm.nih.gov/pubmed/19901837,http://www.ncbi.nlm.nih.gov/pubmed/18499168,http://www.ncbi.nlm.nih.gov/pubmed/14511039,http://www.ncbi.nlm.nih.gov/pubmed/8813311 | How is bladder wall thickness measured? | Ultrasound |
http://www.ncbi.nlm.nih.gov/pubmed/19692615,http://www.ncbi.nlm.nih.gov/pubmed/20350302,http://www.ncbi.nlm.nih.gov/pubmed/22710916,http://www.ncbi.nlm.nih.gov/pubmed/22018341,http://www.ncbi.nlm.nih.gov/pubmed/23278303,http://www.ncbi.nlm.nih.gov/pubmed/19527190,http://www.ncbi.nlm.nih.gov/pubmed/22778845,http://www.ncbi.nlm.nih.gov/pubmed/20634579 | LY450139 is investigational name of which drug? | LY450139 is investigational name of Semagacestat. It is a γ-secretase inhibitor developed for treatment for Alzheimer's disease. Chemical name of LY450139 is hydroxylvaleryl monobenzocaprolactam. |
http://www.ncbi.nlm.nih.gov/pubmed/21249951,http://www.ncbi.nlm.nih.gov/pubmed/20385018,http://www.ncbi.nlm.nih.gov/pubmed/11524346,http://www.ncbi.nlm.nih.gov/pubmed/23601912,http://www.ncbi.nlm.nih.gov/pubmed/24073031 | Are there any Decision support systems for chronic pain management ? | Yes, there is a variety of decision support systems for chronic pain management.Clinical decision support systems are promising tools for improving behavioral medicine care for chronic pain.The use of a computer-based decision support system facilitates primary care physicians' management of chronic pain. |
http://www.ncbi.nlm.nih.gov/pubmed/8485579,http://www.ncbi.nlm.nih.gov/pubmed/22132985,http://www.ncbi.nlm.nih.gov/pubmed/22042773,http://www.ncbi.nlm.nih.gov/pubmed/15571229,http://www.ncbi.nlm.nih.gov/pubmed/23691025,http://www.ncbi.nlm.nih.gov/pubmed/20159777,http://www.ncbi.nlm.nih.gov/pubmed/15277709,http://www.ncbi.nlm.nih.gov/pubmed/22157001,http://www.ncbi.nlm.nih.gov/pubmed/1483694,http://www.ncbi.nlm.nih.gov/pubmed/6853716,http://www.ncbi.nlm.nih.gov/pubmed/8851475,http://www.ncbi.nlm.nih.gov/pubmed/2875930,http://www.ncbi.nlm.nih.gov/pubmed/23046577,http://www.ncbi.nlm.nih.gov/pubmed/754871,http://www.ncbi.nlm.nih.gov/pubmed/9799086,http://www.ncbi.nlm.nih.gov/pubmed/20544510,http://www.ncbi.nlm.nih.gov/pubmed/15140374,http://www.ncbi.nlm.nih.gov/pubmed/7228031,http://www.ncbi.nlm.nih.gov/pubmed/2671903,http://www.ncbi.nlm.nih.gov/pubmed/3384338,http://www.ncbi.nlm.nih.gov/pubmed/4624352,http://www.ncbi.nlm.nih.gov/pubmed/24075303,http://www.ncbi.nlm.nih.gov/pubmed/24001192,http://www.ncbi.nlm.nih.gov/pubmed/7586656,http://www.ncbi.nlm.nih.gov/pubmed/204459,http://www.ncbi.nlm.nih.gov/pubmed/11336982 | Which gene has been found to be mutant in Lesch-Nyhan Disease patients? | Lesch-Nyhan Disease (LND) is the result of mutations in the X-linked gene encoding the purine metabolic enzyme, hypoxanthine guanine phosphoribosyl transferase (HPRT). |
http://www.ncbi.nlm.nih.gov/pubmed/2461933,http://www.ncbi.nlm.nih.gov/pubmed/12819771,http://www.ncbi.nlm.nih.gov/pubmed/22561085,http://www.ncbi.nlm.nih.gov/pubmed/23086207,http://www.ncbi.nlm.nih.gov/pubmed/20936105,http://www.ncbi.nlm.nih.gov/pubmed/18693240,http://www.ncbi.nlm.nih.gov/pubmed/17440941,http://www.ncbi.nlm.nih.gov/pubmed/164278,http://www.ncbi.nlm.nih.gov/pubmed/196592,http://www.ncbi.nlm.nih.gov/pubmed/15292170,http://www.ncbi.nlm.nih.gov/pubmed/10747987,http://www.ncbi.nlm.nih.gov/pubmed/23236167,http://www.ncbi.nlm.nih.gov/pubmed/17640894,http://www.ncbi.nlm.nih.gov/pubmed/14633678,http://www.ncbi.nlm.nih.gov/pubmed/6282265,http://www.ncbi.nlm.nih.gov/pubmed/22624060,http://www.ncbi.nlm.nih.gov/pubmed/18852888,http://www.ncbi.nlm.nih.gov/pubmed/20303346,http://www.ncbi.nlm.nih.gov/pubmed/18393372,http://www.ncbi.nlm.nih.gov/pubmed/16086857,http://www.ncbi.nlm.nih.gov/pubmed/21958314,http://www.ncbi.nlm.nih.gov/pubmed/11309147,http://www.ncbi.nlm.nih.gov/pubmed/8123667,http://www.ncbi.nlm.nih.gov/pubmed/18790802,http://www.ncbi.nlm.nih.gov/pubmed/21736313,http://www.ncbi.nlm.nih.gov/pubmed/21782458,http://www.ncbi.nlm.nih.gov/pubmed/21779408 | Which is the methyl donor of histone methyltransferases? | The major methyl donor of histone methyltransferases (HMTs) is S-adenosyl-L–methionine (SAM, AdoMet). |
http://www.ncbi.nlm.nih.gov/pubmed/20179156,http://www.ncbi.nlm.nih.gov/pubmed/22412940,http://www.ncbi.nlm.nih.gov/pubmed/20502635,http://www.ncbi.nlm.nih.gov/pubmed/16915236,http://www.ncbi.nlm.nih.gov/pubmed/22075116 | How are human accelerated regions (HAR) defined? | Human accelerated regions (HAR) are defined as previously slowly evolving regions of the genome that have evolved most quickly along the human lineage. These represent genomic regions that are conserved among vertebrates but have accumulated substitutions on the human lineage at an accelerated rate. |
http://www.ncbi.nlm.nih.gov/pubmed/19386850,http://www.ncbi.nlm.nih.gov/pubmed/20534805,http://www.ncbi.nlm.nih.gov/pubmed/22553235,http://www.ncbi.nlm.nih.gov/pubmed/20686438,http://www.ncbi.nlm.nih.gov/pubmed/22796889,http://www.ncbi.nlm.nih.gov/pubmed/20960935,http://www.ncbi.nlm.nih.gov/pubmed/20237104,http://www.ncbi.nlm.nih.gov/pubmed/17594211,http://www.ncbi.nlm.nih.gov/pubmed/18070960,http://www.ncbi.nlm.nih.gov/pubmed/17227206,http://www.ncbi.nlm.nih.gov/pubmed/22383444,http://www.ncbi.nlm.nih.gov/pubmed/20649801,http://www.ncbi.nlm.nih.gov/pubmed/20542902,http://www.ncbi.nlm.nih.gov/pubmed/23114438 | Carbapenemase-producing gram-negative bacteria is a major health concern because their resistance to antibiotics.
List the most frequent carbapenemases found in Enterobacteriaceae. | The most frequent carbapenemases in Enterobacteriaceae are OXA-48, KPC, VIM, NDM, IMP, SME, NMC, GES, IMI and MBL. |
http://www.ncbi.nlm.nih.gov/pubmed/19561171,http://www.ncbi.nlm.nih.gov/pubmed/22962458,http://www.ncbi.nlm.nih.gov/pubmed/21619633,http://www.ncbi.nlm.nih.gov/pubmed/20080751,http://www.ncbi.nlm.nih.gov/pubmed/19374772,http://www.ncbi.nlm.nih.gov/pubmed/18047696,http://www.ncbi.nlm.nih.gov/pubmed/22666536,http://www.ncbi.nlm.nih.gov/pubmed/17387144,http://www.ncbi.nlm.nih.gov/pubmed/17989259,http://www.ncbi.nlm.nih.gov/pubmed/22722344,http://www.ncbi.nlm.nih.gov/pubmed/23193254,http://www.ncbi.nlm.nih.gov/pubmed/19698106,http://www.ncbi.nlm.nih.gov/pubmed/22234889,http://www.ncbi.nlm.nih.gov/pubmed/19969543 | How are GRBs (Genomic Regulatory Blocks) defined? | Genomic regulatory blocks (GRBs) are chromosomal regions spanned by highly conserved non-coding elements (HCNEs), most of which serve as regulatory inputs of one target gene in the region. The target genes are most often transcription factors involved in embryonic development and differentiation. GRBs often contain extensive gene deserts, as well as additional 'bystander' genes intertwined with HCNEs but whose expression and function are unrelated to those of the target gene.Genomic regulatory blocks are chromosomal regions spanned by long clusters of highly conserved noncoding elements devoted to long-range regulation of developmental genes, often immobilizing other, unrelated genes into long-lasting syntenic arrangements. Integrating sequence conservation, gene expression data, gene function, epigenetic marks, and other genomic features, we provide extensive evidence that many conserved ancient linkages involve (1) the coordinated transcription of neighboring genes, or (2) genomic regulatory blocks (GRBs) in which transcriptional enhancers controlling developmental genes are contained within nearby bystander genes. Although gene order in hox and other gene clusters has long been known to be conserved because of shared regulatory sequences or overlapping transcriptional units, the chromosomal areas found through insertional hotspots contain only one or a few developmental regulatory genes as well as phylogenetically unrelated genes. In addition, we generated ChIP-seq data for key histone modifications in zebrafish embryos, which provided further evidence of putative GRBs in embryonic development.Genomic regulatory blocks (GRBs) are chromosomal regions spanned by highly conserved non-coding elements (HCNEs), most of which serve as regulatory inputs of one target gene in the region. |
http://www.ncbi.nlm.nih.gov/pubmed/18062802,http://www.ncbi.nlm.nih.gov/pubmed/17525482,http://www.ncbi.nlm.nih.gov/pubmed/23210566,http://www.ncbi.nlm.nih.gov/pubmed/21542403,http://www.ncbi.nlm.nih.gov/pubmed/9745455,http://www.ncbi.nlm.nih.gov/pubmed/16712668,http://www.ncbi.nlm.nih.gov/pubmed/19826964,http://www.ncbi.nlm.nih.gov/pubmed/19177457,http://www.ncbi.nlm.nih.gov/pubmed/15991157,http://www.ncbi.nlm.nih.gov/pubmed/21678021,http://www.ncbi.nlm.nih.gov/pubmed/7641404,http://www.ncbi.nlm.nih.gov/pubmed/21422799,http://www.ncbi.nlm.nih.gov/pubmed/22199277,http://www.ncbi.nlm.nih.gov/pubmed/20152359 | What is the gene frequently mutated in Multiple endocrine neoplasia 2 (MEN2) and Hisrchsprung disease? | The Ret gene may have gain of mutation functions in MEN2 cancer as well as loss of function mutations in Hirschprung disease. |
http://www.ncbi.nlm.nih.gov/pubmed/20860157,http://www.ncbi.nlm.nih.gov/pubmed/22801312,http://www.ncbi.nlm.nih.gov/pubmed/21193437,http://www.ncbi.nlm.nih.gov/pubmed/17047599,http://www.ncbi.nlm.nih.gov/pubmed/19664240,http://www.ncbi.nlm.nih.gov/pubmed/21246178,http://www.ncbi.nlm.nih.gov/pubmed/17174235,http://www.ncbi.nlm.nih.gov/pubmed/16170691,http://www.ncbi.nlm.nih.gov/pubmed/22051823,http://www.ncbi.nlm.nih.gov/pubmed/17947214,http://www.ncbi.nlm.nih.gov/pubmed/18700964,http://www.ncbi.nlm.nih.gov/pubmed/19417170,http://www.ncbi.nlm.nih.gov/pubmed/22574099,http://www.ncbi.nlm.nih.gov/pubmed/20386670,http://www.ncbi.nlm.nih.gov/pubmed/24367719,http://www.ncbi.nlm.nih.gov/pubmed/20333604,http://www.ncbi.nlm.nih.gov/pubmed/12668828,http://www.ncbi.nlm.nih.gov/pubmed/15618076 | Which are the clinical characteristics of isolated Non-compaction cardiomyopathy? | The clinical characteristics of isolated Non-compaction cardiomyopathy are excessively thickened endocardial layer with deep intertrabecular recesses (with ratio of non-compacted to compacted myocardium >2), heart failure, syncope, ventricular arrhythmias, stroke, pulmonary hypertension, complete left branch conductive block, sick sinus syndrome and paroxysmal supraventricular tachycardia |
http://www.ncbi.nlm.nih.gov/pubmed/23328393,http://www.ncbi.nlm.nih.gov/pubmed/24685159 | What is STARR-seq? | STARR-seq is a method to directly and quantitatively assess enhancer activity for millions of candidates from arbitrary sources of DNA, which enables screens across entire genomes. When applied to the Drosophila genome, STARR-seq identifies thousands of cell type-specific enhancers across a broad continuum of strengths, links differential gene expression to differences in enhancer activity, and creates a genome-wide quantitative enhancer map. This map reveals the highly complex regulation of transcription, with several independent enhancers for both developmental regulators and ubiquitously expressed genes. STARR-seq can be used to identify and quantify enhancer activity in other eukaryotes, including humans. |
http://www.ncbi.nlm.nih.gov/pubmed/16738309,http://www.ncbi.nlm.nih.gov/pubmed/16213499,http://www.ncbi.nlm.nih.gov/pubmed/20670405,http://www.ncbi.nlm.nih.gov/pubmed/14608463,http://www.ncbi.nlm.nih.gov/pubmed/20937776,http://www.ncbi.nlm.nih.gov/pubmed/12082075,http://www.ncbi.nlm.nih.gov/pubmed/17570398,http://www.ncbi.nlm.nih.gov/pubmed/18195046,http://www.ncbi.nlm.nih.gov/pubmed/18936163 | In which genomic positions is the histone variant macroH2A enriched? | macroH2A1 is enriched on the inactive X chromosome in female mammalian cells, where it functions to maintain gene silencing. The transcribed regions of most active genes are depleted of macroH2A, often in sharply localized domains that show depletion of 4-fold or more relative to bulk mouse liver chromatin. This repressor activity of marcroH2A is further supported by the substantial and relatively uniform macroH2A1 enrichment along the inactive X chromosome, which averages 4-fold. In addition to localizing to the MCB, macroH2A accumulates at a perinuclear structure centered at the centrosome |
http://www.ncbi.nlm.nih.gov/pubmed/17535870,http://www.ncbi.nlm.nih.gov/pubmed/9781936,http://www.ncbi.nlm.nih.gov/pubmed/10445678,http://www.ncbi.nlm.nih.gov/pubmed/7598731 | Does amiodarone affect thyroid hormone receptors in the myocardium? | Yes |
http://www.ncbi.nlm.nih.gov/pubmed/9694666,http://www.ncbi.nlm.nih.gov/pubmed/8576966,http://www.ncbi.nlm.nih.gov/pubmed/16343813,http://www.ncbi.nlm.nih.gov/pubmed/12815945,http://www.ncbi.nlm.nih.gov/pubmed/12167372,http://www.ncbi.nlm.nih.gov/pubmed/9395063 | From which sequence does the Alu repeat originate from? | The presence of Alu-like structural motifs supports the hypothesis of the monophyletic origin of Alu and B1 repeats, i.e., from a common 7SL RNA-derived retroposing monomeric element, The origin of Alu subfamilies in human populations may be related to evolution of chromosome Y. |
http://www.ncbi.nlm.nih.gov/pubmed/11154546,http://www.ncbi.nlm.nih.gov/pubmed/23969004,http://www.ncbi.nlm.nih.gov/pubmed/2533403,http://www.ncbi.nlm.nih.gov/pubmed/16943469,http://www.ncbi.nlm.nih.gov/pubmed/23096483,http://www.ncbi.nlm.nih.gov/pubmed/8457417,http://www.ncbi.nlm.nih.gov/pubmed/21511940,http://www.ncbi.nlm.nih.gov/pubmed/24156003,http://www.ncbi.nlm.nih.gov/pubmed/19830065,http://www.ncbi.nlm.nih.gov/pubmed/18596536,http://www.ncbi.nlm.nih.gov/pubmed/19547821,http://www.ncbi.nlm.nih.gov/pubmed/19646556,http://www.ncbi.nlm.nih.gov/pubmed/19037900,http://www.ncbi.nlm.nih.gov/pubmed/20624239 | Abnormality in which vertebral region is important in the Bertolotti's syndrome? | Lumbosacral vertebral region is implicated in the Bertolotti's syndrome. Lumbosacral transitional vertebra is an anatomical variation of the fifth lumbar vertebra in which an enlarged transverse process can form a joint or fusion with the sacrum or ilium. Patients often complain of intractable sciatica that arises from impingement of the nerve root extraforaminally by compression caused by the enlarged transverse process. |
http://www.ncbi.nlm.nih.gov/pubmed/23794183,http://www.ncbi.nlm.nih.gov/pubmed/22771841,http://www.ncbi.nlm.nih.gov/pubmed/23981693 | What does iBAQ stand for in proteomic analysis? | iBAQ stands for intensity-based absolute quantification. |
http://www.ncbi.nlm.nih.gov/pubmed/23334259,http://www.ncbi.nlm.nih.gov/pubmed/25274603,http://www.ncbi.nlm.nih.gov/pubmed/23558880,http://www.ncbi.nlm.nih.gov/pubmed/24614665,http://www.ncbi.nlm.nih.gov/pubmed/24510469,http://www.ncbi.nlm.nih.gov/pubmed/24917414,http://www.ncbi.nlm.nih.gov/pubmed/24858181 | Which is the main target of the anti-arrhythmic activity of flecainide? | Flecainide is a class 1c antiarrhythmic that acts by blocking sodium channels and is used mainly in the treatment of supraventricular arrhythmias. |
http://www.ncbi.nlm.nih.gov/pubmed/18455802,http://www.ncbi.nlm.nih.gov/pubmed/20926779,http://www.ncbi.nlm.nih.gov/pubmed/23820669,http://www.ncbi.nlm.nih.gov/pubmed/23532677,http://www.ncbi.nlm.nih.gov/pubmed/17560116,http://www.ncbi.nlm.nih.gov/pubmed/22039709,http://www.ncbi.nlm.nih.gov/pubmed/22134702,http://www.ncbi.nlm.nih.gov/pubmed/18430565,http://www.ncbi.nlm.nih.gov/pubmed/18622044,http://www.ncbi.nlm.nih.gov/pubmed/20730619,http://www.ncbi.nlm.nih.gov/pubmed/16499159,http://www.ncbi.nlm.nih.gov/pubmed/20668933,http://www.ncbi.nlm.nih.gov/pubmed/17389455,http://www.ncbi.nlm.nih.gov/pubmed/18274800,http://www.ncbi.nlm.nih.gov/pubmed/17024559,http://www.ncbi.nlm.nih.gov/pubmed/21568669,http://www.ncbi.nlm.nih.gov/pubmed/23555069,http://www.ncbi.nlm.nih.gov/pubmed/20560106,http://www.ncbi.nlm.nih.gov/pubmed/18773293,http://www.ncbi.nlm.nih.gov/pubmed/22403173,http://www.ncbi.nlm.nih.gov/pubmed/19951746,http://www.ncbi.nlm.nih.gov/pubmed/21159857,http://www.ncbi.nlm.nih.gov/pubmed/19826181 | Does thyroid hormone affect cardiac remodeling? | TH affects cardiac remodeling |
http://www.ncbi.nlm.nih.gov/pubmed/23567243,http://www.ncbi.nlm.nih.gov/pubmed/22147197,http://www.ncbi.nlm.nih.gov/pubmed/24296129,http://www.ncbi.nlm.nih.gov/pubmed/18023967,http://www.ncbi.nlm.nih.gov/pubmed/20444961,http://www.ncbi.nlm.nih.gov/pubmed/19331169,http://www.ncbi.nlm.nih.gov/pubmed/17671211,http://www.ncbi.nlm.nih.gov/pubmed/24147344,http://www.ncbi.nlm.nih.gov/pubmed/24064966,http://www.ncbi.nlm.nih.gov/pubmed/20446899,http://www.ncbi.nlm.nih.gov/pubmed/22834967 | What is the effect of ROS on cyclin B1? | Reactive oxygen species (ROS) production is able to cause growth arrest at the G2-M checkpoint of the cell cycle, partly by deregulation of Cyclin B1 expression. |
http://www.ncbi.nlm.nih.gov/pubmed/23791700,http://www.ncbi.nlm.nih.gov/pubmed/23466233,http://www.ncbi.nlm.nih.gov/pubmed/23440335,http://www.ncbi.nlm.nih.gov/pubmed/23629709,http://www.ncbi.nlm.nih.gov/pubmed/24154738,http://www.ncbi.nlm.nih.gov/pubmed/23453230,http://www.ncbi.nlm.nih.gov/pubmed/21694902,http://www.ncbi.nlm.nih.gov/pubmed/23896281,http://www.ncbi.nlm.nih.gov/pubmed/24165192,http://www.ncbi.nlm.nih.gov/pubmed/23745769,http://www.ncbi.nlm.nih.gov/pubmed/23230455,http://www.ncbi.nlm.nih.gov/pubmed/23431163,http://www.ncbi.nlm.nih.gov/pubmed/23384816,http://www.ncbi.nlm.nih.gov/pubmed/23454058,http://www.ncbi.nlm.nih.gov/pubmed/23688081,http://www.ncbi.nlm.nih.gov/pubmed/23896953,http://www.ncbi.nlm.nih.gov/pubmed/21331152 | Are there any HCV replication inhibitors available? | Chronic hepatitis C virus (HCV) infection is a worldwide health problem causing serious complications, such as liver cirrhosis and hepatoma. Small interfering RNAs (siRNAs) and short hairpin RNAs (shRNAs) have been reported to suppress gene expression significantly. HCV seems a suitable candidate for targets of siRNAs, as HCV is a positive single-strand RNA virus and replicates in the cytoplasm. Based on results, nowadays there are few HCV replication inhibitors such as GS-563253, PSI-6130, NA-808, BMS-790052, GS-9132 and BMS-788329. |
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