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http://www.ncbi.nlm.nih.gov/pubmed/30268152,http://www.ncbi.nlm.nih.gov/pubmed/18988810,http://www.ncbi.nlm.nih.gov/pubmed/25918552,http://www.ncbi.nlm.nih.gov/pubmed/11562346,http://www.ncbi.nlm.nih.gov/pubmed/11845212,http://www.ncbi.nlm.nih.gov/pubmed/12853484,http://www.ncbi.nlm.nih.gov/pubmed/16204191 | How is Slc22a3 imprinted? | Two novel imprinted genes, Slc22a2 and Slc22a3 are described here that lie 110 and 155 kb 3' to Igf2r and that are not overlapped by the Air transcript but are regulated by the Igf2r-ICE, as previously shown for Igf2r. A bidirectional silencer for a 400-kilobase region that contains three imprinted, maternally expressed protein-coding genes (Igf2r/Slc22a2/Slc22a3) has been shown by targeted deletion to be located in a sequence of 3.7 kilobases, which also contains the promoter for the imprinted, paternally expressed non-coding Air RNA. Silencing of the paternal allele of three imprinted genes (Igf2r, Slc22a2 and Slc22a3) requires cis expression of the Air RNAcis expression of the air rnaSilencing of the paternal allele of three imprinted genes (Igf2r, Slc22a2 and Slc22a3) requires cis expression of the Air RNA.Epigenetic mechanisms restrict the expression of imprinted genes to one parental allele in diploid cells. At the Igf2r/Air imprinted cluster on mouse chromosome 17, paternal-specific expression of the Air noncoding RNA has been shown to silence three genes in cis: Igf2r, Slc22a2, and Slc22a3. |
http://www.ncbi.nlm.nih.gov/pubmed/29659825 | What are the effects of 14-3-3 dimers on Tau phosphorylation? | 14-3-3 dimers regulate steady-state phosphorylation of both wild-type and the R406W mutant Tau, but they are not essential for toxicity of either variant. Furthermore, recruitment of dimers on accumulating wild- type Tau increases its steady- state levels ostensibly by occluding access to proteases in a phosphorylated-dependent manner.The 14-3-3 dimers regulate steady-state phosphorylation of both wild-type and mutant Tau proteins.14-3-3 dimers regulate steady-state phosphorylation of both wild-type and the R406W mutant Tau, but they are not essential for toxicity of either variant.14-3-3 dimers have two contrasting effects on Tau phosphorylation: (i) they increase the rate of Tau is phosphorylated by cAMP-dependent protein kinase and (ii) they prevent the relaxation of the autophagic state of Tau.Proteomic, biochemical and genetic evidence demonstrate that both Drosophila 14-3-3 proteins interact with human wild-type and mutant Tau on multiple sites irrespective of their phosphorylation state. 14-3-3 dimers regulate steady-state phosphorylation of both wild-type and the R406W mutant Tau, but they are not essential for toxicity of either variant. Moreover, 14-3-3 elevation itself is not pathogenic, but recruitment of dimers on accumulating wild-type Tau increases its steady-state levels ostensibly by occluding access to proteases in a phosphorylation-dependent manner.Neurodegenerative dementias collectively known as Tauopathies involve aberrant phosphorylation and aggregation of the neuronal protein Tau. The largely neuronal 14-3-3 proteins are also elevated in the central nervous system (CNS) and cerebrospinal fluid of Tauopathy patients, suggesting functional linkage. Proteomic, biochemical and genetic evidence demonstrate that both Drosophila 14-3-3 proteins interact with human wild-type and mutant Tau on multiple sites irrespective of their phosphorylation state. 14-3-3 dimers regulate steady-state phosphorylation of both wild-type and the R406W mutant Tau, but they are not essential for toxicity of either variant. Moreover, 14-3-3 elevation itself is not pathogenic, but recruitment of dimers on accumulating wild-type Tau increases its steady-state levels ostensibly by occluding access to proteases in a phosphorylation-dependent manner. In contrast, the R406W mutant, which lacks a putative 14-3-3 binding site, responds differentially to elevation of each 14-3-3 isoform. Although excess 14-3-3z stabilizes the mutant protein, elevated D14-3-3e has a destabilizing effect probably because of altered 14-3-3 dimer composition.Proteomic, biochemical and genetic evidence demonstrate that both Drosophila 14-3-3 proteins interact with human wild-type and mutant Tau on multiple sites irrespective of their phosphorylation state. 14-3-3 dimers regulate steady-state phosphorylation of both wild-type and the R406W mutant Tau, but they are not essential for toxicity of either variant. Moreover, 14-3-3 elevation itself is not pathogenic, but recruitment of dimers on accumulating wild-type Tau increases its steady-state levels ostensibly by occluding access to proteases in a phosphorylation-dependent manner. In contrast, the R406W mutant, which lacks a putative 14-3-3 binding site, responds differentially to elevation of each 14-3-3 isoform. Although excess 14-3-3z stabilizes the mutant protein, elevated D14-3-3e has a destabilizing effect probably because of altered 14-3-3 dimer composition.Proteomic, biochemical and genetic evidence demonstrate that both Drosophila 14-3-3 proteins interact with human wild-type and mutant Tau on multiple sites irrespective of their phosphorylation state. 14-3-3 dimers regulate steady-state phosphorylation of both wild-type and the R406W mutant Tau, but they are not essential for toxicity of either variant. |
http://www.ncbi.nlm.nih.gov/pubmed/22383797,http://www.ncbi.nlm.nih.gov/pubmed/23136880,http://www.ncbi.nlm.nih.gov/pubmed/23672610,http://www.ncbi.nlm.nih.gov/pubmed/26341110,http://www.ncbi.nlm.nih.gov/pubmed/26209625,http://www.ncbi.nlm.nih.gov/pubmed/9730885,http://www.ncbi.nlm.nih.gov/pubmed/27669440,http://www.ncbi.nlm.nih.gov/pubmed/19687229 | Is the tyrosine kinase BTK implicated in autoimmunity? | Autoimmunity, hypersensitivity to B cell receptor (BCR) cross-linking, and splenomegaly caused by myeloerythroid hyperplasia were alleviated by Btk deficiency in lyn-/- mice. Augmented TLR9-induced Btk activation in PIR-B-deficient B-1 cells provokes excessive autoantibody production and autoimmunity. Autoimmunity was fully dependent on Btk kinase activity, because Btk inhibitor treatment (PCI-32765) could normalize B-cell activation and differentiation, and because autoantibodies were absent in Btk transgenic mice overexpressing a kinase inactive Btk mutant.Yes, Bruton's tyrosine kinase (BTK) is implicated in autoimmunity.Autoimmunity was fully dependent on Btk kinase activity, because Btk inhibitor treatment (PCI-32765) could normalize B-cell activation and differentiation, and because autoantibodies were absent in BtAutoimmunity was fully dependent on Btk kinase activity, because Btk inhibitor treatment (PCI-32765) could normalize B-cell activation and differentiation, and because autoantibodies were absent in Btk transgenic mice overexpressing a kinase inactive Btk mutant. Given the phenotype of affected patients, namely lack of B-lymphocytes and plasma cells with the ensuing inability to mount humoral immune responses, BTK inhibitors were anticipated to have beneficial effects on antibody-mediated pathologies, such as autoimmunityyes, BTK Signaling in B Cell Differentiation and AutoimmunityBruton's tyrosine kinase (Btk) is a proximal transducer of the BCR signal that allows for B-cell activation and differentiation. Recently, selective inhibition of Btk by PCI-32765 has shown promise in limiting activity of multiple cells types in various models of cancer and autoimmunity.Autoimmunity was fully dependent on Btk kinase activity, because Btk inhibitor treatment (PCI-32765) could normalize B-cell activation and differentiation, and because autoantibodies were absent in Btk transgenic mice overexpressing a kinase inactive Btk mutant.Yes, variants of the tyrosine kinase BTK may be implicated in autoimmunity.Yes, tyrosine kinase BTK is implicated in autoimmunity. |
http://www.ncbi.nlm.nih.gov/pubmed/26186194,http://www.ncbi.nlm.nih.gov/pubmed/29054129,http://www.ncbi.nlm.nih.gov/pubmed/27552850 | What is the BioPlex network? | Protein interactions form a network whose structure drives cellular function and whose organization informs biological inquiry. BioPlex contains 23,744 interactions among 7,668 proteins with 86% previously undocumented. BioPlex accurately depicts known complexes, attaining 80%-100% coverage for most CORUM complexes. The network readily subdivides into communities that correspond to complexes or clusters of functionally related proteins. More generally, network architecture reflects cellular localization, biological process, and molecular function, enabling functional characterization of thousands of proteins. Network structure also reveals associations among thousands of protein domains, suggesting a basis for examining structurally related proteins. BioPlex, in combination with other approaches, can be used to reveal interactions of biological or clinical significance. For example, mutations in the membrane protein VAPB implicated in familial amyotrophic lateral sclerosis perturb a defined community of interactors.BioPlex accurately depicts known complexes, attaining 80%-100% coverage for most CORUM complexes. The network readily subdivides into communities that correspond to complexes or clusters of functionally related proteins. More generally, network architecture reflects cellular localization, biological process, and molecular function, enabling functional characterization of thousands of proteins. Network structure also reveals associations among thousands of protein domains, suggesting a basis for examining structurally related proteins. Finally, BioPlex, in combination with other approaches, can be used to reveal interactions of biological or clinical significance. For example, mutations in the membrane protein VAPB implicated in familial amyotrophic lateral sclerosis perturb a defined community of interactors. |
http://www.ncbi.nlm.nih.gov/pubmed/28887402 | Which algorithm has been developed for detecting expansions of tandem repeats? | Identifying large expansions of short tandem repeats (STRs), such as those that cause amyotrophic lateral sclerosis (ALS) and fragile X syndrome, is challenging for short-read whole-genome sequencing (WGS) data. A solution to this problem is an important step toward integrating WGS into precision medicine. For that purpose, ExpansionHunter has been developed as a software tool that, using PCR-free WGS short- read data, can genotype repeats at the locus of interest, even if the expanded repeat is larger than the read length.Identifying large expansions of short tandem repeats (STRs), such as those that cause amyotrophic lateral sclerosis (ALS) and fragile X syndrome, is challenging for short-read whole-genome sequencing (WGS) data. A solution to this problem is an important step toward integrating WGS into precision medicine. ExpansionHunter has been developed as a tool which using PCR-free WGS short-read data, can genotype repeats at the locus of interest, even if the expanded repeat is larger than the read length. ExpansionHunter can be used to accurately detect known pathogenic repeat expansions and provides researchers with a tool that can be used to identify new pathogenic repeat expansions. |
http://www.ncbi.nlm.nih.gov/pubmed/30013295,http://www.ncbi.nlm.nih.gov/pubmed/30362966,http://www.ncbi.nlm.nih.gov/pubmed/30053385,http://www.ncbi.nlm.nih.gov/pubmed/29926311,http://www.ncbi.nlm.nih.gov/pubmed/30459509 | Which clotting factor is in the Andexxa? | Andexxa(r) is a first-in-class recombinant modified factor Xa protein. It is available to reverse life-threatening or uncontrolled bleeding with the factor Xa inhibitors apixaban and rivaroxaban. |
http://www.ncbi.nlm.nih.gov/pubmed/25263161,http://www.ncbi.nlm.nih.gov/pubmed/24812327,http://www.ncbi.nlm.nih.gov/pubmed/22196727,http://www.ncbi.nlm.nih.gov/pubmed/25506399,http://www.ncbi.nlm.nih.gov/pubmed/26832418 | How are nucleosome posisitions correlated with sites of 5'-methyl-cytosine (5mC) or 5-hydroxy-methyl-cytosine (5hmC)? | We find that Mbd3 and Brg1 antagonistically regulate a common set of genes by regulating promoter nucleosome occupancy. outside of CpG islands most CpGs are methylated, and the average methylation density oscillates so that it is highest in the linker region between nucleosomes we have investigated nucleosome organization around hypomethylated regions (HMRs)Nucleosomes are enriched at hypomethylated region (HMR) boundaries. The mostly unmethylated CpG islands have reduced nucleosome occupancy. Outside of CpG islands most CpGs are methylated, and the average methylation density oscillates so that it is highest in the linker region between nucleosomes.Using this global approach, we observe the dependency of nucleosome positioning upon the 5'-methyl-cytosine (5mC) methylation seems to function together with exonic nucleosomes and H3K36me3 for the proper splicing of transcripts with different expression levels. Using a novel bioinformatics pipeline, we show a striking anti-correlation between nucleosomic positioning and 5-hydroxymethylation at CTCF regions that is not present at promoters. Transcription, histone modifications, and DNA methylation alter this "ground state"outside of CpG islands most CpGs are methylated, and the average methylation density oscillates so that it is highest in the linker region between nucleosomes |
http://www.ncbi.nlm.nih.gov/pubmed/28315543,http://www.ncbi.nlm.nih.gov/pubmed/31002008,http://www.ncbi.nlm.nih.gov/pubmed/29177842,http://www.ncbi.nlm.nih.gov/pubmed/28213365,http://www.ncbi.nlm.nih.gov/pubmed/26609205,http://www.ncbi.nlm.nih.gov/pubmed/30445951,http://www.ncbi.nlm.nih.gov/pubmed/27431756,http://www.ncbi.nlm.nih.gov/pubmed/26197742,http://www.ncbi.nlm.nih.gov/pubmed/30350179,http://www.ncbi.nlm.nih.gov/pubmed/31489588,http://www.ncbi.nlm.nih.gov/pubmed/27568360,http://www.ncbi.nlm.nih.gov/pubmed/28977993 | Which drugs are included in the drug LONSURF? | Lonsurf includes trifluridine and tipiracil. It is a novel oral anti-tumor agent combining an anti-neoplastic thymidine-based nucleoside analogue (trifluridine) with a thymidine phosphorylase inhibitor (tipiracil hydrochloride) presents a new treatment option for metastatic colorectal cancer patients refractory or intolerant to standard therapies. |
http://www.ncbi.nlm.nih.gov/pubmed/28629370,http://www.ncbi.nlm.nih.gov/pubmed/30452341,http://www.ncbi.nlm.nih.gov/pubmed/29469551,http://www.ncbi.nlm.nih.gov/pubmed/27449572,http://www.ncbi.nlm.nih.gov/pubmed/22616356,http://www.ncbi.nlm.nih.gov/pubmed/20415555,http://www.ncbi.nlm.nih.gov/pubmed/18852208,http://www.ncbi.nlm.nih.gov/pubmed/29998537 | What is 23andMe? | We first take a look at how personal genomics services, exemplified by the company 23andMe,23andMe is a genetic testing company which offers personal genetic services. |
http://www.ncbi.nlm.nih.gov/pubmed/18088248 | Is induction of interferon by TLR7 higher in males? | Yes. TLR7 activation correlates with induction of interferon more strongly in males.Yes. TLR7 induction of interferon is higher in males than in females.variations of tlr7 impair the immune response to hcv and imply a gender-specific effectVariations of TLR7 impair the immune response to HCV and imply a gender-specific effect of this X-chromosomal variation. Within the group of female patients with chronic HCV-infection, c.32T was predictive of an unfavourable outcome of interferon-alpha therapy. |
http://www.ncbi.nlm.nih.gov/pubmed/28413388,http://www.ncbi.nlm.nih.gov/pubmed/22918543,http://www.ncbi.nlm.nih.gov/pubmed/28850717,http://www.ncbi.nlm.nih.gov/pubmed/15521676,http://www.ncbi.nlm.nih.gov/pubmed/30148086,http://www.ncbi.nlm.nih.gov/pubmed/31666445 | Cushing's disease is associated with a tumor in what part of the body? | Cushing's disease is associated with a tumor in the pituitary glandCushing's disease is associated with a tumor in the pituitary gland.Cushing's disease (CD) is a rare endocrine disorder associated with increased serum levels of cortisol secreted due to an underlying tumour in pituitary.Most cases of Cushing's syndrome are due to increased adrenocorticotropic hormone production from a pituitary adenoma, |
http://www.ncbi.nlm.nih.gov/pubmed/27425792 | Which was the first genetically modified organism (GMO) to be used as vaccine? | The first genetically modified organism to be used as vaccine was the live oral cholera vaccine CVD 103-HgR or vaxchora. |
http://www.ncbi.nlm.nih.gov/pubmed/29674518,http://www.ncbi.nlm.nih.gov/pubmed/22162947,http://www.ncbi.nlm.nih.gov/pubmed/23618393,http://www.ncbi.nlm.nih.gov/pubmed/29072575,http://www.ncbi.nlm.nih.gov/pubmed/23651476,http://www.ncbi.nlm.nih.gov/pubmed/22028627,http://www.ncbi.nlm.nih.gov/pubmed/26351520,http://www.ncbi.nlm.nih.gov/pubmed/28155083,http://www.ncbi.nlm.nih.gov/pubmed/27932493,http://www.ncbi.nlm.nih.gov/pubmed/29478809,http://www.ncbi.nlm.nih.gov/pubmed/26840484 | How does PRDM9 recognize the specific DNA motifs for meiotic recombination? | The PRDM9 gene encodes a protein with a highly variable tandem-repeat zinc finger (ZF) DNA-binding domain that plays a key role in determining sequence-specific hotspots of meiotic recombination genome wide. The long zinc finger domain of PRDM9 forms a highly stable and long-lived complex with its DNA recognition sequence.The long zinc finger domain of PRDM9 forms a highly stable and long-lived complex with its DNA recognition sequence. In many organisms, recombination occurs at limited sites, termed 'hotspots', whose positions in mammals are determined by PR domain member 9 (PRDM9), a long-array zinc-finger and chromatin-modifier protein. |
http://www.ncbi.nlm.nih.gov/pubmed/28182010,http://www.ncbi.nlm.nih.gov/pubmed/22049153,http://www.ncbi.nlm.nih.gov/pubmed/24616567,http://www.ncbi.nlm.nih.gov/pubmed/29945115,http://www.ncbi.nlm.nih.gov/pubmed/29404887,http://www.ncbi.nlm.nih.gov/pubmed/29511456,http://www.ncbi.nlm.nih.gov/pubmed/24472607,http://www.ncbi.nlm.nih.gov/pubmed/29524580,http://www.ncbi.nlm.nih.gov/pubmed/27900011,http://www.ncbi.nlm.nih.gov/pubmed/25907560,http://www.ncbi.nlm.nih.gov/pubmed/28678919 | Which micro-RNAs (miR) are associated with the human cycloxygenase-2 (COX-2) gene promoter? | MicroRNA-16, miRNA-128, miR-26b, icroRNA-26a, MicroRNA-146b-3p, microRNA-137, mi R-146a, mir-143-5p,microRNA-101, microRNAs-142-3 p, mi r-146p, mir-128 and miR -128 were found to be associated with the human cycloxygenase-2 (COX-2) gene promoter.miR-146a, miR-203, miRNA-124a, microRNA-155, miRS-146b, miS-146c, miG-145, miRP-148a, let-7b, siRNA-181, miRNAs-152, miN-182, mir-223, myosin heavy chain, are associated with the human cycloxygenase-2 (COX-2) gene promoter We also report the following miRNA associations with the COX- 2 gene promoters: miCENP-1,Recently, the human cycloxygenase-2 (COX-2) gene promoter has a microRNA (miR) promoter region that is highly expressed in non-cancer cells and is associated with the cell cycle. MicroRNA-16, miRNA-128, microRNA-26a, miRNAs-142-3p, miR-144, mi R-146b-3 p, mir-146a, icroRNA- 26a, -26b,microRNA-137, mi r-146 a, mir-143-5p,miR-16 was shown to bind the COX-2 3'-UTR and inhibit COX-2 expression by promoting rapid mRNA decay. miR-143-5p directly targets COX-2. The NF-kB family member RelB regulates microRNA miR-146a to suppress cigarette smoke-induced COX-2 protein expression in lung fibroblasts. TargetScan analysis predicted COX-2 as a target of miR-26a and miR-26b. miR-26a/-26b decreased luciferase activity associated with COX-2-3'-UTR. microRNA-142-3p inhibits apoptosis and inflammation induced by bleomycin through down-regulation of Cox-2 in MLE-12 cells. MicroRNA-144 is regulated by CP2 and decreases COX-2 expression and PGE2 production in mouse ovarian granulosa cells. The down-regulation of microRNA-137 contributes to the up-regulation of retinoblastoma cell proliferation and invasion by regulating COX-2/PGE2 signaling. MicroRNA-128 inhibits proliferation and invasion of glioma cells by targeting COX-2. Altered expression of miR-146b-3p is closely related to the progression and development of DCMI mediating the RAF/P38MAPK/COX-2 signal transduction pathway. MicroRNA-101 inhibits angiogenesis via COX-2 in endometrial carcinoma.The following micro-RNAs (miRNAs) have been associated with the human cycloxygenase-2 (COX-2) gene promoter: microRNA-16, miRNA-128, micro RNA-26a, miR-142-3p, mir-144, mi r-146b-3 p, mir-16), mir-26b, icroRNA-26 a, MicroRNA-146 b-3P, mir-146a, mir -143-5p, mir microRNA-137, mir--MicroRNA |
http://www.ncbi.nlm.nih.gov/pubmed/28900497,http://www.ncbi.nlm.nih.gov/pubmed/29290287,http://www.ncbi.nlm.nih.gov/pubmed/28849027,http://www.ncbi.nlm.nih.gov/pubmed/30142809,http://www.ncbi.nlm.nih.gov/pubmed/21982471,http://www.ncbi.nlm.nih.gov/pubmed/25607111,http://www.ncbi.nlm.nih.gov/pubmed/25265358 | What percentage of patients of nasopharyngeal carcinoma (NPC) develop recurrent disease? | 1.04% of patients with nasopharyngeal carcinoma develop recurrent disease. The overall recurrence rate is 75%.The overall recurrence rate was 75% in HPV negative patients and 11% in HPV positive ones. Disease recurred in a spared parotid gland in three patients (1.04%). |
http://www.ncbi.nlm.nih.gov/pubmed/18389088,http://www.ncbi.nlm.nih.gov/pubmed/19436611,http://www.ncbi.nlm.nih.gov/pubmed/22777229,http://www.ncbi.nlm.nih.gov/pubmed/23793314,http://www.ncbi.nlm.nih.gov/pubmed/28874907,http://www.ncbi.nlm.nih.gov/pubmed/18041900,http://www.ncbi.nlm.nih.gov/pubmed/17350985,http://www.ncbi.nlm.nih.gov/pubmed/18341664,http://www.ncbi.nlm.nih.gov/pubmed/16940066,http://www.ncbi.nlm.nih.gov/pubmed/28533232 | What classes of drugs does Retapamulin belong to? | Retapamulin is a member of the pleuromutilin family of antibiotics.Pleuromutilins have a potential to be developed as a new class of antibiotics for use in humans. This class includes valnemulin, tiamulin, and retapamulin.Retapamulin belongs to the class of gentamycin-resistant antibiotics. |
http://www.ncbi.nlm.nih.gov/pubmed/28398597,http://www.ncbi.nlm.nih.gov/pubmed/26990079,http://www.ncbi.nlm.nih.gov/pubmed/29608575,http://www.ncbi.nlm.nih.gov/pubmed/31492652,http://www.ncbi.nlm.nih.gov/pubmed/27144850,http://www.ncbi.nlm.nih.gov/pubmed/28765121,http://www.ncbi.nlm.nih.gov/pubmed/31492651,http://www.ncbi.nlm.nih.gov/pubmed/30930775,http://www.ncbi.nlm.nih.gov/pubmed/29500302,http://www.ncbi.nlm.nih.gov/pubmed/28783871,http://www.ncbi.nlm.nih.gov/pubmed/29125718,http://www.ncbi.nlm.nih.gov/pubmed/26239599,http://www.ncbi.nlm.nih.gov/pubmed/30043658,http://www.ncbi.nlm.nih.gov/pubmed/27049060 | What is the mechanism of action of ozanimod? | Ozanimod is a specific and potent small molecule modulator of the sphingosine 1-phosphate receptor 1 (S1PR1) and receptor 5 (S1PR5), which has shown therapeutic benefit in clinical trials of relapsing multiple sclerosis and ulcerative colitis. |
http://www.ncbi.nlm.nih.gov/pubmed/25572401,http://www.ncbi.nlm.nih.gov/pubmed/11900484,http://www.ncbi.nlm.nih.gov/pubmed/8875948,http://www.ncbi.nlm.nih.gov/pubmed/16620374,http://www.ncbi.nlm.nih.gov/pubmed/29510059,http://www.ncbi.nlm.nih.gov/pubmed/29931674,http://www.ncbi.nlm.nih.gov/pubmed/23384311,http://www.ncbi.nlm.nih.gov/pubmed/29226950,http://www.ncbi.nlm.nih.gov/pubmed/15936998,http://www.ncbi.nlm.nih.gov/pubmed/26149933 | What are Syndecans? | Syndecans are transmembrane proteoglycans with heparan and chondroitin sulfate chains attached to their extracellular domain. Like many proteoglycans, they interact with a large number of ligands, such as growth factors, adhesion receptors, soluble small molecules, proteinases, and other extracellular matrix proteins to initiate downstream signaling pathways. Syndecans play a major role in inflammation, mainly by regulating leukocyte extravasation and cytokine function.Syndecans are important mediators of signalling by transmitting external stimuli into the cells. Syndecans (SDCs) are a family of heparan sulfate proteoglycans (HSPGs) glycoproteins ubiquitously expressed on the cell surfaces and extracellular matrix of all mammalian tissues Syndecans are transmembrane proteoglycans that, together with integrins, control cell interactions with extracellular matrix components. Syndecans are transmembrane proteoglycans that, together with integrins, control cell interactions with extracellular matrix components. |
http://www.ncbi.nlm.nih.gov/pubmed/29566102,http://www.ncbi.nlm.nih.gov/pubmed/8604012,http://www.ncbi.nlm.nih.gov/pubmed/15274332,http://www.ncbi.nlm.nih.gov/pubmed/21743962,http://www.ncbi.nlm.nih.gov/pubmed/25290568,http://www.ncbi.nlm.nih.gov/pubmed/16317716 | What is chemokinesis? | Chemokinesis is chemically prompted kinesis, a motile response of unicellular prokaryotic or eukaryotic organisms to chemicals that cause the cell to make some kind of change in their migratory/swimming behaviour. |
http://www.ncbi.nlm.nih.gov/pubmed/26938566,http://www.ncbi.nlm.nih.gov/pubmed/27928945,http://www.ncbi.nlm.nih.gov/pubmed/26398764,http://www.ncbi.nlm.nih.gov/pubmed/28716890,http://www.ncbi.nlm.nih.gov/pubmed/27713030,http://www.ncbi.nlm.nih.gov/pubmed/22284190,http://www.ncbi.nlm.nih.gov/pubmed/28914550,http://www.ncbi.nlm.nih.gov/pubmed/23827161,http://www.ncbi.nlm.nih.gov/pubmed/12479803 | What cellular process is JAK/STAT involved in? | The Janus Kinase/Signal Transducers and Activators of Transcription (JAK/STAT) signaling pathway is utilized by numerous cytokines and interferons, and is essential for the development and function of both innate and adaptive immunity.The serine/threonine kinase JAK/STAT is a major regulator of Janus kinase activity and plays a critical role in regulating the ubiquitin/proinflammatory signaling pathway.JAK/STAT is a master regulator of immunityJAK/STAT is involved in the regulation of immunity |
http://www.ncbi.nlm.nih.gov/pubmed/22492363,http://www.ncbi.nlm.nih.gov/pubmed/18447746,http://www.ncbi.nlm.nih.gov/pubmed/23406732,http://www.ncbi.nlm.nih.gov/pubmed/30661338,http://www.ncbi.nlm.nih.gov/pubmed/2790826,http://www.ncbi.nlm.nih.gov/pubmed/31502516,http://www.ncbi.nlm.nih.gov/pubmed/1646072,http://www.ncbi.nlm.nih.gov/pubmed/26094363 | What is the link between dental x-ray and brain tumor risk? | There is data to suggest that dental x-ray can be associated with significantly increased risk of meningiomas and gliomas. However, some studies failed to demonstrate an association between dental x-rays and brain tumor risk. |
http://www.ncbi.nlm.nih.gov/pubmed/22423021,http://www.ncbi.nlm.nih.gov/pubmed/2851185,http://www.ncbi.nlm.nih.gov/pubmed/7707626,http://www.ncbi.nlm.nih.gov/pubmed/22796685,http://www.ncbi.nlm.nih.gov/pubmed/16397431,http://www.ncbi.nlm.nih.gov/pubmed/8920706,http://www.ncbi.nlm.nih.gov/pubmed/24422678,http://www.ncbi.nlm.nih.gov/pubmed/28442435,http://www.ncbi.nlm.nih.gov/pubmed/27443593,http://www.ncbi.nlm.nih.gov/pubmed/19995190,http://www.ncbi.nlm.nih.gov/pubmed/15502699,http://www.ncbi.nlm.nih.gov/pubmed/22702319,http://www.ncbi.nlm.nih.gov/pubmed/26263200,http://www.ncbi.nlm.nih.gov/pubmed/22119590,http://www.ncbi.nlm.nih.gov/pubmed/9015114,http://www.ncbi.nlm.nih.gov/pubmed/22431803,http://www.ncbi.nlm.nih.gov/pubmed/19931717,http://www.ncbi.nlm.nih.gov/pubmed/21504245,http://www.ncbi.nlm.nih.gov/pubmed/8752295,http://www.ncbi.nlm.nih.gov/pubmed/11389295,http://www.ncbi.nlm.nih.gov/pubmed/27522178,http://www.ncbi.nlm.nih.gov/pubmed/25680314,http://www.ncbi.nlm.nih.gov/pubmed/20661105,http://www.ncbi.nlm.nih.gov/pubmed/30046133,http://www.ncbi.nlm.nih.gov/pubmed/28340179,http://www.ncbi.nlm.nih.gov/pubmed/29102168,http://www.ncbi.nlm.nih.gov/pubmed/9949951,http://www.ncbi.nlm.nih.gov/pubmed/31023829,http://www.ncbi.nlm.nih.gov/pubmed/28369477 | Is there a vaccine for rotavirus? | yes, rotavirus pentavalent vaccine (RotaTeq(r)) as a sole vaccineEffectiveness of rotavirus pentavalent vaccine rotavirus pentavalent vaccine (RotaTeq(r)) as a sole vaccinesafety and immunogenicity of pentavalent rotavirus vaccine (rv5 )Yes, there is a vaccine against rotavirus infection that is approved for Europe, Canada and Australia.Yes, there is a human neonatal rotavirus vaccine against serogroup B Rotavirus.Effectiveness of rotavirus pentavalent vaccineYes, there is a 4-component vaccine against capsular rotavirus vaccine.Yes, there is a pentavalent vaccine for RotavirusYes, there is a human neonatal rotavirus vaccine.High effectiveness of RotaTeq as the sole rotavirus vaccine in a universal immunization programme was demonstrated in a high-income country. rotavirus pentavalent vaccine (RotaTeq(r)) as a sole vaccine |
http://www.ncbi.nlm.nih.gov/pubmed/29212226 | Which T-UCR has been implicated in prostate cancer? | Transcribed ultraconserved region Uc.63+ promotes resistance to docetaxel through regulation of androgen receptor signaling in prostate cancer. Docetaxel is the standard chemotherapy for metastatic castration-resistant prostate cancer ( CRPC). However, nearly all patients ultimately become refractory due to the development of docetaxel resistance.The transcribed ultraconserved regions (T-UCRs) are a novel class of non-coding RNAs that are absolutely conserved across species and are involved in carcinogenesis including prostate cancer (PC). Quantitative real-time polymerase chain reaction analysis revealed that the expression of T-UCR Uc.63+ was increased in PC tissues. MTT assay and wound healing assay revealed that Uc.63+ was involved in cell growth and cell migration. miR-130b was predicted to have binding sites within the Uc.63+ sequence. The expression of miR-130b was significantly disturbed by the overexpression or knockdown of Uc.63+. Overexpression of Uc.63+ increased the expression of AR and its downstream molecule PSA and promoted resistance to docetaxel through AR regulation. In patients treated with docetaxel, the expression of serum Uc.63+ in the docetaxel-resistant patients was higher than that in the docetaxel-sensitive patients (P = 0.011). Moreover, Kaplan-Meier analysis showed that the high expression of serum Uc.63+ correlated with a worse prognosis (P = 0.020). |
http://www.ncbi.nlm.nih.gov/pubmed/28461162 | Is BNN20 involved in Parkinson's disease? | Yes. Neurotrophic factors are among the most promising treatments aiming at slowing or stopping and even reversing Parkinson's disease (PD). BNN-20 has been suggested as an important neuroprotective agent acting through the TrkB neurotrophin receptor pathway, mimicking the action of the endogenous neurotrophin BDNF. Thus BNN-20 could be proposed for treatment of PD.Yes. BNN20 is an important neuroprotective agent acting through the TrkB neurotrophin receptor pathway that has been implicated in numerous pathologies including inflammatory diseases, cancer, viral infection, and neurodegenerative diseases such as amyotrophic lateral sclerosis and Parkinson's disease.Yes. BNN20 is involved in the development of Parkinson's disease. It is a member of the intramembrane-tumor necrosis factor-a (ITF-a) family of transcription factors that are dysregulated in several neurodegenerative diseases such as amyotrophic lateral sclerosis, frontotemporal degeneration, axonal injury, late-onset cerebellar ataxia, and multiple sclerosis.Yes. BNN20 could be proposed as a therapeutic for PD. BNN-20 administration to Weaver/NGL mice induced a strong NF-kB-dependent transcriptional response in the brain as detected by bioluminescence imaging, which was abolished by co-administration of the TrkB inhibitor ANA-12 |
http://www.ncbi.nlm.nih.gov/pubmed/24150941,http://www.ncbi.nlm.nih.gov/pubmed/19922872 | Which domain of the MOZ/MYST3 protein complex associates with histone H3? | The double PHD finger domain of MOZ/MYST3 induces a-helical structure of the histone H3 tailThe double PHD finger domain of MOZ/MYST3 induces a-helical structure of the histone H3 tail to facilitate acetylation and methylation sampling and modification In addition to sampling H3 and H4 modification status, we show that the DPF cooperates with the MYST domain to promote H3K9 and H3K14 acetylation, although not if H3K4 is trimethylatedMOZ/MYST3 complex associates with histone H3 with high affinity and specificity. Both proteins share a PHD finger domain.The double PHD finger domain of MOZ/MYST3 induces a-helical structure of the histone H3 tail to facilitate acetylation and methylation sampling and modification.In conclusion, our data show that Moz regulates H3K9 acetylation at Hox gene loci and that RA can act independently of Moz to establish specific Hox gene expression boundaries. The double PHD finger domain of MOZ/MYST3 induces a-helical structure of the histone H3 tail to facilitate acetylation and methylation sampling and modificationMOZ/MYST3 complex associates with histone H3 with PHD finger domain.ere we report novel insights into histone H3 tail structure in complex with the double PHD finger (DPF) of the lysine acetyltransferase MOZ/MYST3/KAT6A.ere we report novel insights into histone H3 tail structure in complex with the double PHD finger (DPF) of the lysine acetyltransferase MOZ/MYST3/KAT6A. In addition to sampling H3 and H4 modification status, we show that the DPF cooperates with the MYST domain to promote H3K9 and H3K14 acetylation, although not if H3K4 is trimethylatedIn conclusion, our data show that Moz regulates H3K9 acetylation at Hox gene loci and that RA can act independently of Moz to establish specific Hox gene expression boundaries. The double PHD finger domain of MOZ/MYST3 induces a-helical structure of the histone H3 tail to facilitate acetylation and methylation sampling and modification ere we report novel insights into histone H3 tail structure in complex with the double PHD finger (DPF) of the lysine acetyltransferase MOZ/MYST3/KAT6A. |
http://www.ncbi.nlm.nih.gov/pubmed/26222134 | Which company sells the drug Afrezza since 2015? | Afrezza has been marketed by Sanofi since February 2015. |
http://www.ncbi.nlm.nih.gov/pubmed/29053389 | Is there a role for MRPL53 in cancer? | No. MRPL53 is a new candidate gene for orofacial clefting identified using an eQTL approach. |
http://www.ncbi.nlm.nih.gov/pubmed/29212226 | Does Uc.63+ promote sensitivity to treatment in prostate cancer? | No. Overexpression of Uc.63+ increases the expression of AR and its downstream molecule PSA and promotes resistance to docetaxel through AR regulation. In patients treated with docetaxel, the expression of serum Uc.63+ in the docetaxel-resistant patients is higher than that in the docetaxel-sensitive patients (P = 0.011). Moreover, Kaplan-Meier analysis indicates that the high expression of serum Uc.63+ correlated with a worse prognosis (P = 0.020).No. Transcribed ultraconserved region Uc.63+ promotes resistance to docetaxel through regulation of androgen receptor signaling in prostate cancer. Moreover, high expression of serum Uc63+ correlated with a worse prognosis (P = 0.020) in patients treated with copropane versus placebo.No. Transcribed ultraconserved region Uc.63+ promotes resistance to docetaxel through regulation of androgen receptor signaling in prostate cancer. In contrast, Uc-63+ enhances sensitivity to treatment in other types of prostate cancer |
http://www.ncbi.nlm.nih.gov/pubmed/27936183 | What is the gene PTENP? | PTEN pseudogene (PTENp) acts as an endogenous RNA, which regulates its parental gene by competitively binding to the 3' UTR of PTEN gene in the human. |
http://www.ncbi.nlm.nih.gov/pubmed/30130840,http://www.ncbi.nlm.nih.gov/pubmed/25823689,http://www.ncbi.nlm.nih.gov/pubmed/22994082,http://www.ncbi.nlm.nih.gov/pubmed/15603341,http://www.ncbi.nlm.nih.gov/pubmed/26894632,http://www.ncbi.nlm.nih.gov/pubmed/7752802,http://www.ncbi.nlm.nih.gov/pubmed/23511035,http://www.ncbi.nlm.nih.gov/pubmed/8649955,http://www.ncbi.nlm.nih.gov/pubmed/19462421,http://www.ncbi.nlm.nih.gov/pubmed/30353757,http://www.ncbi.nlm.nih.gov/pubmed/26985865,http://www.ncbi.nlm.nih.gov/pubmed/24981894,http://www.ncbi.nlm.nih.gov/pubmed/19821197,http://www.ncbi.nlm.nih.gov/pubmed/26642816,http://www.ncbi.nlm.nih.gov/pubmed/24742079,http://www.ncbi.nlm.nih.gov/pubmed/17168120 | Rachmilewitz Index is used for which diseases? | Rachmilewitz Index is used for assessment of endoscopic disease activity of patients with ulcerative colitis. |
http://www.ncbi.nlm.nih.gov/pubmed/27100959,http://www.ncbi.nlm.nih.gov/pubmed/28475676 | List angiotensin-converting-enzyme inhibitors. | captopril
enalapril
lisinopril
ramipril |
http://www.ncbi.nlm.nih.gov/pubmed/28941963 | How does androgen deprivation therapy affect pain perception? | There were no significant changes in pain thresholds, ratings, or other response to quantitative sensory tests over the 6-month course of the study. Clinical pain did not differ between test and control groups, and no changes from baseline were observed in their group. |
http://www.ncbi.nlm.nih.gov/pubmed/28359728,http://www.ncbi.nlm.nih.gov/pubmed/27884812 | What is OAC CHV? | The Open Access and Collaborative Consumer Health Vocabulary (OAC CHV), which contains health-related terms used by lay consumers,The Open Access and Collaborative Consumer Health Vocabulary (OAC CHV), contains health-related terms used by lay consumers. |
http://www.ncbi.nlm.nih.gov/pubmed/28949931,http://www.ncbi.nlm.nih.gov/pubmed/29182052 | What is known about autosomal dominant Alzheimer’s disease? | The first autosomal dominant mutation in the amyloid precursor protein (APP) gene was described in 1991. Later, AD was also associated with mutated early-onset (presenilin 1/2, PSEN1/2 and APP) and late-onset (apolipoprotein E, ApoE) genes. Genome-wide association and linkage analysis studies with identified multiple genomic areas have implications for the treatment of AD.
The Dominantly Inherited Alzheimer Network, an international family-clustered registry to study autosomal dominant Alzheimer disease which is a rare form of Alzheimer disease caused by mutations in any of the three genes including the amyloid precursor protein, presenilin 1 and presenilin 2. |
http://www.ncbi.nlm.nih.gov/pubmed/29749240,http://www.ncbi.nlm.nih.gov/pubmed/17901676,http://www.ncbi.nlm.nih.gov/pubmed/17990901,http://www.ncbi.nlm.nih.gov/pubmed/24321428,http://www.ncbi.nlm.nih.gov/pubmed/27065378,http://www.ncbi.nlm.nih.gov/pubmed/25067791,http://www.ncbi.nlm.nih.gov/pubmed/17874088,http://www.ncbi.nlm.nih.gov/pubmed/28866069,http://www.ncbi.nlm.nih.gov/pubmed/28095086 | List characteristic features of the Revesz syndrome. | Revesz syndrome is characterized by retinopathy, aplastic anemia, nail dystrophy, and cerebellar hypoplasia. |
http://www.ncbi.nlm.nih.gov/pubmed/28274826 | Does BNN27 promote memory loss? | No. The novel dehydroepiandrosterone (DHEA) derivative BNN27 counteracts delay-dependent and scopolamine-induced recognition memory deficits in rats. |
http://www.ncbi.nlm.nih.gov/pubmed/28874668 | Are genomic regulatory blocks (GRBs) any different than TADs? | No, clusters of CNEs (GRBs) strongly coincide with topological organisation, predicting the boundaries of hundreds of topologically associating domains (TADs) in human and Drosophila. The set of TADs that are associated with high levels of noncoding conservation exhibit distinct properties compared to TADs devoid of extreme noncoding conservation. The close correspondence between extreme noncoding conservation and TADs suggests that these TADs are ancient, revealing a regulatory architecture conserved over hundreds of millions of years. |
http://www.ncbi.nlm.nih.gov/pubmed/27593814,http://www.ncbi.nlm.nih.gov/pubmed/24926928 | Are Spinal Intradural Primary Malignant Peripheral Nerve Sheath Tumors(MPNST) rare in neurofibromatosis patients? | Spinal intradural primary malignant peripheral nerve sheath tumors (MPNST) are rare in patients without neurofibromatosis.No, Spinal Intradural Primary Malignant Peripheral Nerve Sheath Tumors(MPNST) rare in patients without neurofibromatosis.yes, Primary malignant peripheral nerve sheath tumors (MPNSTs) are extremely rare in patients without a history of neurofibromatosis; only 18 cases have been reported in the English-language literature to this point. |
http://www.ncbi.nlm.nih.gov/pubmed/22789508 | What does MVA85A stand for? | MVA85A is the Modified Vaccinia virus Ankara expressing Antigen 85A. |
http://www.ncbi.nlm.nih.gov/pubmed/25726088 | Can MVA85A confer immunity against smallpox? | No MVA85A is a candidate tuberculosis vaccine. |
http://www.ncbi.nlm.nih.gov/pubmed/21330447 | Is MLL3 part of the ASCOM complex? | Yes |
http://www.ncbi.nlm.nih.gov/pubmed/24667640,http://www.ncbi.nlm.nih.gov/pubmed/24839356,http://www.ncbi.nlm.nih.gov/pubmed/30462889 | What are the effects of CAMK4 inhibition? | Here, we present evidence that the calcium/calmodulin-dependent protein kinase IV (CaMK4) is increased and required during Th17 cell differentiation. Inhibition of CaMK4 reduced Il17 transcription through decreased activation of the cAMP response element modulator a (CREM-a) and reduced activation of the AKT/mTOR pathway, which is known to enhance Th17 differentiation. CAMK4 knockdown and kinase-dead mutant inhibited crocin-mediated HO-1 expression, Nrf2 activation, and phosphorylation of Akt, indicating that HO-1 expression is mediated by CAMK4 and that Akt is a downstream mediator of CAMK4 in crocin signalingCaMK4 inhibition has potential as a therapeutic strategy for Th17-driven autoimmune diseases.CaMK4-dependent activation of AKT/mTOR and CREM-a underlies autoimmunity-associated Th17 imbalance Here, we present evidence that the calcium/calmodulin-dependent protein kinase IV (CaMK4) is increased and required during Th17 cell differentiation. Inhibition of CaMK4 reduced Il17 transcription through decreased activation of the cAMP response element modulator a (CREM-a) and reduced activation of the AKT/mTOR pathway, which is known to enhance Th17 differentiation.Inhibition of CaMK4 reduced Il17 transcription through decreased activation of the cAMP response element modulator a (CREM-a) and reduced activation of the AKT/mTOR pathway, which is known to enhance Th17 differentiation. |
http://www.ncbi.nlm.nih.gov/pubmed/25352100,http://www.ncbi.nlm.nih.gov/pubmed/28422453 | List cohesinopathies | Roberts syndrome (RBS), Cornelia de Lange Syndrome (CdLS), Warsaw Breakage Syndrome (WABS) and Chronic Atrial and Intestinal Dysrhythmia (CAID) syndrome. |
http://www.ncbi.nlm.nih.gov/pubmed/29610169,http://www.ncbi.nlm.nih.gov/pubmed/30175727,http://www.ncbi.nlm.nih.gov/pubmed/29116687 | Which protein is mutated in Erythropoietic Protoporphyria? | Erythropoietic protoporphyria (EPP) is a rare inherited disorder of the heme biosynthesis pathway resulting in the accumulation of protoporphyrins in the blood, erythrocytes, and other tissues. Because of a gene mutation in the FECH gene, ferrochelatase, the enzyme involved in the final step of heme synthesis, is deficient in these patients. |
http://www.ncbi.nlm.nih.gov/pubmed/11894017,http://www.ncbi.nlm.nih.gov/pubmed/12757409,http://www.ncbi.nlm.nih.gov/pubmed/12431965 | Is marimastat effective for small-cell lung cancer? | No. Marimastat is not effective for small-cell lung cancer. |
http://www.ncbi.nlm.nih.gov/pubmed/11197692,http://www.ncbi.nlm.nih.gov/pubmed/11607787,http://www.ncbi.nlm.nih.gov/pubmed/11169260,http://www.ncbi.nlm.nih.gov/pubmed/10395102,http://www.ncbi.nlm.nih.gov/pubmed/11196716 | Which part of the TNFR2 gene is genetically associated with Systemic Lupus Erythematosus? | There is a TNFR2 3' flanking region polymorphism in systemic lupus erythematosus.A TNFR2 3' flanking region polymorphism in systemic lupus erythematosus.A tnfr2 3' flanking region polymorphism in systemic lupus erythematosus has been shown to be significantly associated with selenocytoplasmic lupus erythematotosus. No transmission distortion was observed for tnpr2-196r allele. |
http://www.ncbi.nlm.nih.gov/pubmed/28931371 | What is VISMapper? | VISMapper is a vector integration site analysis web server to analyze next-generation sequencing data for retroviral vector integration sites. VISMapper can be found at: http://vismapper.babelomics.org.The possibility of integrating viral vectors to become a persistent part of the host genome makes them a crucial element of clinical gene therapy. However, viral integration has associated risks, such as the unintentional activation of oncogenes that can result in cancer. Therefore, the analysis of integration sites of retroviral vectors is a crucial step in developing safer vectors for therapeutic use. VISMapper is a vector integration site analysis web server to analyze next-generation sequencing data for retroviral vector integration sites. VISMapper can be found at: http://vismapper.babelomics.org. |
http://www.ncbi.nlm.nih.gov/pubmed/23745112,http://www.ncbi.nlm.nih.gov/pubmed/26611895 | What is Taupathy? | Tauopathies are a group of neurodegenerative disorders with accumulation of three-repeat (3R) or four-repeat (4R) Tau protein.Tauopathies are a group of neurodegenerative disorders with accumulation of three-repeat (3R) or four-repeat (4R) TauTaupathy is a progressive neurodegenerative disease of the central nervous system caused by autosomal recessive mutations in the Tau (amyloid precursor protein 1) gene.Taupathy is an autosomal-dominant neurodegenerative disease characterized by the progressive degeneration of substantia nigra pars compacta (SNpc) dopaminergic neurones and is characterized by loss of motor, sensory, and sensory function. |
http://www.ncbi.nlm.nih.gov/pubmed/28104361,http://www.ncbi.nlm.nih.gov/pubmed/20676809,http://www.ncbi.nlm.nih.gov/pubmed/24888810,http://www.ncbi.nlm.nih.gov/pubmed/23826179,http://www.ncbi.nlm.nih.gov/pubmed/21907495,http://www.ncbi.nlm.nih.gov/pubmed/21102589,http://www.ncbi.nlm.nih.gov/pubmed/21717907 | Is Figitumumab effective for non-small cell lung cancer? | No. Phase III trials of the anti-insulin-like growth factor-1 receptor (IGF1R) antibody figitumumab in non-small cell lung cancer (NSCLC) patients have been discontinued owing to lack of survival benefit. Adding figitumumab to standard chemotherapy also failed to increase overall survival in patients with advanced nonadenocarcinoma NSCLC. |
http://www.ncbi.nlm.nih.gov/pubmed/27153606,http://www.ncbi.nlm.nih.gov/pubmed/29745839,http://www.ncbi.nlm.nih.gov/pubmed/28413689,http://www.ncbi.nlm.nih.gov/pubmed/31258549,http://www.ncbi.nlm.nih.gov/pubmed/27796074,http://www.ncbi.nlm.nih.gov/pubmed/25609570 | The LINCS L1000 data set contains gene expression data for drug treated human cells, yes or no? | The Library of Integrated Network-based Cellular Signatures (LINCS) L1000 dataset measures changes in GE before and after treatment of human cells with over 20 000 small-molecule compounds including most of the FDA-approved drugs.yes, The Library of Integrated Network-based Cellular Signatures (LINCS) L1000 big data provide gene expression profiles induced by over 10 000 compounds, shRNAs, and kinase inhibitors using the L1000 platform.TheLINCS L1000 data set contains gene expression data for drug treated human cells, yes |
http://www.ncbi.nlm.nih.gov/pubmed/24728596,http://www.ncbi.nlm.nih.gov/pubmed/20736486,http://www.ncbi.nlm.nih.gov/pubmed/29780651,http://www.ncbi.nlm.nih.gov/pubmed/29039102,http://www.ncbi.nlm.nih.gov/pubmed/29056305,http://www.ncbi.nlm.nih.gov/pubmed/28951472,http://www.ncbi.nlm.nih.gov/pubmed/24672024,http://www.ncbi.nlm.nih.gov/pubmed/31039345,http://www.ncbi.nlm.nih.gov/pubmed/23217619 | What is a cytokine storm? | A cytokine storm is an undesirable elevation of cytokine levels, as may occur in response to a drug or a device, may lead to severe side effects such as systemic inflammatory response syndrome.Cytokine storm is a poorly explained clinical entity caused by an undesired and aggrandized immune system response leading to unregulated activation of the proinflammatory cascade, often contributing to multisystem organ failure and even deathCytokine storm is a poorly understood clinical entity caused by an undesired and ag grandized immune system response leading to unregulated activation of the proinflammatory cascade, often contributing to multisystem organ failure and even death. |
http://www.ncbi.nlm.nih.gov/pubmed/27899579 | Which database exists that contains regulatory SNPs which affect predicted transcription factor binding site affinity? | SNP2TFBS is a computational resource intended to support researchers investigating the molecular mechanisms underlying regulatory variation in the human genome. The database essentially consists of a collection of text files providing specific annotations for human single nucleotide polymorphisms (SNPs), namely whether they are predicted to abolish, create or change the affinity of one or several transcription factor (TF) binding sites. A SNP's effect on TF binding is estimated based on a position weight matrix (PWM) model for the binding specificity of the corresponding factor.SNP2TFBS is a computational resource intended to support researchers investigating the molecular mechanisms underlying regulatory variation in the human genome. The database essentially consists of a collection of text files providing specific annotations for human single nucleotide polymorphisms (SNPs), namely whether they are predicted to abolish, create or change the affinity of one or several transcription factor (TF) binding sites.SN2TFBS is a computational resource intended to support researchers investigating the molecular mechanisms underlying regulatory variation in the human genome. The database essentially consists of a collection of text files providing specific annotations for human single nucleotide polymorphisms (SNPs), namely whether they are predicted to abolish, create or change the affinity of one or several transcription factor (TF) binding sites. A SNP's effect on TF binding is estimated based on a position weight matrix (PWM) model for the binding specificity of the corresponding factor.SNP2TFBS is a computational resource intended to support researchers investigating the molecular mechanisms underlying regulatory variation in the human genome. The database essentially consists of a collection of text files providing specific annotations for human single nucleotide polymorphisms (SNPs), namely whether they are predicted to abolish, create or change the affinity of one or several transcription factor (TF) binding sites. A SNP's effect on TF binding is estimated based on a position weight matrix (PWM) model for the binding specificity of the corresponding factor. These data files are regenerated at regular intervals by an automatic procedure that takes as input a reference genome, a comprehensive SNP catalogue and a collection of PWMs. SNP2TFBS is also accessible over a web interface, enabling users to view the information provided for an individual SNP, to extract SNPs based on various search criteria, to annotate uploaded sets of SNPs or to display statistics about the frequencies of binding sites affected by selected SNPs. |
http://www.ncbi.nlm.nih.gov/pubmed/28968644 | Which R package has been developed for MS-based label-free phosphoproteomics? | Phosphonormalizer is an R package for normalization of MS-based label-free phosphoproteomics.Phosphonormalizer is a commonly used normalization approach in mass spectrometry-based label-free proteomics. It scales the peptide abundances to have the same median intensities, based on an assumption that the majority of abundances remain the same across the samples.Global centering-based normalization is a commonly used normalization approach in mass spectrometry-based label-free proteomics. It scales the peptide abundances to have the same median intensities, based on an assumption that the majority of abundances remain the same across the samples. However, especially in phosphoproteomics, this assumption can introduce bias, as the samples are enriched during sample preparation which can mask the underlying biological changes. To address this possible bias, phosphopeptides quantified in both enriched and non-enriched samples can be used to calculate factors that mitigate the bias. Phosphonormalizer is an R package for normalizing enriched samples in label-free mass spectrometry-based phosphoproteomics.Phosphonormalizer is an R package for MS-based label-free phosphoproteomics based on mass spectrometry-based normalization. It scales the peptide abundances to have the same median intensities, based on an assumption that the majority of abundances remain the same across the samples. |
http://www.ncbi.nlm.nih.gov/pubmed/30319619,http://www.ncbi.nlm.nih.gov/pubmed/25459578,http://www.ncbi.nlm.nih.gov/pubmed/26288733 | Is there a vaccine for peanut allergy? | Yes, there is a vaccine for peanut allergy.yes, there is currently a vaccine being tested for peanut allergies. |
http://www.ncbi.nlm.nih.gov/pubmed/22546085,http://www.ncbi.nlm.nih.gov/pubmed/27712624,http://www.ncbi.nlm.nih.gov/pubmed/31375588,http://www.ncbi.nlm.nih.gov/pubmed/29329682,http://www.ncbi.nlm.nih.gov/pubmed/30065095,http://www.ncbi.nlm.nih.gov/pubmed/23865689,http://www.ncbi.nlm.nih.gov/pubmed/23763835,http://www.ncbi.nlm.nih.gov/pubmed/29778200,http://www.ncbi.nlm.nih.gov/pubmed/25701212,http://www.ncbi.nlm.nih.gov/pubmed/29478397,http://www.ncbi.nlm.nih.gov/pubmed/26656689 | The virus that causes FIP, Feline Infectious Peritonitis belongs to what family? | The virus that causes FIP, Feline Infectious Peritonitis belongs to the family coronavirus.Feline coronavirus (fcov) is an etiological agent that causes a benign enteric illness and the fatal systemic disease feline infectious peritonitis (fip).Feline coronavirus (FCoV) is an etiological agent that causes a benign enteric illness and the fatal systemic disease feline infectious peritonitis (FIP)Feline Infectious Peritonitis (FIP) belongs to the family of coronavirus.Feline infectious peritonitis (FIP) is a common and highly lethal coronavirus disease of domestic cats.Feline infectious peritonitis (FIP) is a common and highly lethal coronavirus disease of domestic catsFeline Infectious Peritonitis virus (FIP) belongs to the coronavirus family of the genus Flavivirus which cause central nervous system disease.Feline infectious peritonitis (FIP) is a cat virus caused by a member of the coronavirus family coronaviruses. |
http://www.ncbi.nlm.nih.gov/pubmed/29307884,http://www.ncbi.nlm.nih.gov/pubmed/29455535,http://www.ncbi.nlm.nih.gov/pubmed/28918421,http://www.ncbi.nlm.nih.gov/pubmed/29056305 | What is a "cytokine storm"? | During infectious processes, the production of inflammatory cytokines including tumor necrosis factor (TNF), interleukin-1b (IL-1b), gamma interferon (IFNg) and chemokines orchestrates the anti-infectious innate immune response. However, an overzealous production, leading up to a cytokine storm, can be deleterious and contributes to mortality consecutive to sepsis or toxic shock syndrome. |
http://www.ncbi.nlm.nih.gov/pubmed/29601563,http://www.ncbi.nlm.nih.gov/pubmed/25034562 | Is golimumab effective for sarcoidosis? | No, golimumab is not effective for treatment of sarcoidosis. |
http://www.ncbi.nlm.nih.gov/pubmed/26487711,http://www.ncbi.nlm.nih.gov/pubmed/27082314,http://www.ncbi.nlm.nih.gov/pubmed/29190287,http://www.ncbi.nlm.nih.gov/pubmed/30356097,http://www.ncbi.nlm.nih.gov/pubmed/30102747 | Is SARS virus interacting with ACE2 encoded protein? | Yes,
The infection of target cells by the SARS CoV is mediated through the interaction of the viral Spike (S) protein (1255 amino acids) and its cellular receptor, angiotensin-converting enzyme 2 (ACE2). |
http://www.ncbi.nlm.nih.gov/pubmed/22149703 | What is Soluvia? | Soluvia(tm) by Becton Dickinson is a microinjection system for intradermal delivery of vaccines. |
http://www.ncbi.nlm.nih.gov/pubmed/22280883,http://www.ncbi.nlm.nih.gov/pubmed/24209771,http://www.ncbi.nlm.nih.gov/pubmed/24707494,http://www.ncbi.nlm.nih.gov/pubmed/26822958,http://www.ncbi.nlm.nih.gov/pubmed/27027316,http://www.ncbi.nlm.nih.gov/pubmed/23964891,http://www.ncbi.nlm.nih.gov/pubmed/19889934,http://www.ncbi.nlm.nih.gov/pubmed/30691609 | Is the FIP virus thought to be a mutated strain for the Feline enteric Coronavirus? | yes, Feline infectious peritonitis (FIP) results from mutations in the viral genome during a common feline enteric coronavirus (FECV) infection.Yes. The FIP virus is a mutated strain of the Feline enteric Coronavirus (FECV) causing infectious peritonitis and neoplasia Feline infectious peritonitis (FIP) results from mutations in the viral genome during a common feline enteric coronavirus (FECV) infection. Feline infectious peritonitis (FIP) results from mutations in the viral genome during a common feline enteric coronavirus (FECV) infection.Feline infectious peritonitis (FIP) results from mutations in the viral genome during a common feline enteric coronavirus (FECV) infection.Yes. The FIP virus is a mutated strain of the Feline enteric coronavirus (FECV) infects cats, and is thought to be a newly identified strain with heterozygous mutations that create a K27M amino acid substitution. |
http://www.ncbi.nlm.nih.gov/pubmed/25847946,http://www.ncbi.nlm.nih.gov/pubmed/9886398 | Does SATB1 regulate the RAG1 and RAG2 genes? | SATB1 binds to the ASE and Rag promoters, facilitating inclusion of Rag2 in the chromatin hub and the loading of RNA polymerase II to both the Rag1 and Rag2 promoters.An anti-silencer- and SATB1-dependent chromatin hub regulates Rag1 and Rag2 gene expressionHigh level expression of the Xlr nuclear protein in immature thymocytes and colocalization with the matrix-associated region-binding SATB1 protein Its onset preceded the rearrangement of TCR genes, as Xlr expression was conserved in thymus cells from RAG1(0/0) mice. An anti-silencer- and SATB1-dependent chromatin hub regulates Rag1 and Rag2 gene expression during thymocyte development. SATB1 binds to the ASE and Rag promoters, facilitating inclusion of Rag2 in the chromatin hub and the loading of RNA polymerase II to both the Rag1 and Rag2 promoters. SATB1 binds to the ASE and Rag promoters, facilitating inclusion of Rag2 in the chromatin hub and the loading of RNA polymerase II to both the Rag1 and Rag2 promoters. Our results provide a novel framework for understanding ASE function and demonstrate a novel role for SATB1 as a regulator of Rag locus organization and gene expression in DP thymocytes.An anti-silencer- and SATB1-dependent chromatin hub regulates Rag1 and Rag2 gene expression during thymocyte development. Its onset preceded the rearrangement of TCR genes, as Xlr expression was conserved in thymus cells from RAG1(0/0) mice. SATB1 binds to the ASE and Rag promoters, facilitating inclusion of Rag2 in the chromatin hub and the loading of RNA polymerase II to both the Rag1 and Rag2 promoters.An anti-silencer- and SATB1-dependent chromatin hub regulates Rag1 and Rag2 gene expression during thymocyte development. SATB1 binds to the ASE and Rag promoters, facilitating inclusion of Rag2 in the chromatin hub and the loading of RNA polymerase II to both the Rag1 and Rag2 promoters. |
http://www.ncbi.nlm.nih.gov/pubmed/6226660,http://www.ncbi.nlm.nih.gov/pubmed/7171565,http://www.ncbi.nlm.nih.gov/pubmed/1893943 | What is the main difference between nascent and mature chromatin? | Nascent chromatin is created after transcription and is mostly lacking histone modifications and H1, which makes it more prone to digestion by DNaseI. Like normal nascent chromatin, chromatin labeled for brief periods (0.5-1 min) in the presence of butyrate was more sensitive to digestion with DNase I and micrococcal nuclease than control bulk chromatin. 17, 4275 [1989]) it was shown that when replication occurs in the presence of sodium butyrate (thereby inhibiting histone deacetylation), nascent chromatin fails to mature fully and instead remains preferentially sensitive to DNaseI, more soluble in magnesium, and depleted of histone H1 (relative to mature chromatin).The nascent and mature forms of chromatin differ in two aspects of their histone modifications: polycistronic messengers are expressed as a sequence of individual nucleosomes only in mature chromatin, and the nucleosome is involved in both transcription and repair processes. The second class of nascent DNA is distinguished from the nucleosomal component by its insolubility, lack of discernible nucleosomal organization, and dependence on protein synthesis to attain typical subunit structure Like normal nascent chromatin, chromatin labeled for brief periods (0.5-1 min) in the presence of butyrate was more sensitive to digestion with DNase I and micrococcal nuclease than control bulk chromatin. 17, 4275 [1989]) it was shown that when replication occurs in the presence of sodium butyrate (thereby inhibiting histone deacetylation), nascent chromatin fails to mature fully and instead remains preferentially sensitive to DNaseI, more soluble in magnesium, and depleted of histone H1 (relative to mature chromatin). Incubation of mature chromatin in butyrate for 1 h did not induce DNase I sensitivity: therefore, the presence of sodium butyrate was required during replication to preserve the increased digestibility of nascent chromatin DNA In a previous study (Perry and Annunziato, Nucleic Acids Res. Within 10 min of DNA synthesis, the spacing of mature chromatin is established; the spacing maturation can occur in the absence of protein synthesis. this class of nascent chromatin exhibits a shortened repeat length of approximately 165 bp, as opposed to the 288-bp repeat of bulk chromatin.Mature and nascent chromatin differ in two aspects of their histone modifications: polycistronic messengers are expressed as a sequence of individual nucleosomes only in mature cells, and they are preferentially expressed in the later stages of cell development.In a previous study (Perry and Annunziato, Nucleic Acids Res. 17, 4275 [1989]) it was shown that when replication occurs in the presence of sodium butyrate (thereby inhibiting histone deacetylation), nascent chromatin fails to mature fully and instead remains preferentially sensitive to DNaseI, more soluble in magnesium, and depleted of histone H1 (relative to mature chromatin). |
http://www.ncbi.nlm.nih.gov/pubmed/30188887,http://www.ncbi.nlm.nih.gov/pubmed/21249180,http://www.ncbi.nlm.nih.gov/pubmed/16877759,http://www.ncbi.nlm.nih.gov/pubmed/30414923,http://www.ncbi.nlm.nih.gov/pubmed/25348714 | Is CTCF bound at nucleosome free regions? | yes, robust inter-nucleosomal interactions exist around transcription start site (TSS), transcription termination sites (TTS) or around CTCF binding sitesnucleosome occupancy at nucleosome-free regions (NFRs), many of which are located at sites occupied by the multivalent factors Ctcf and cohesin.robust inter-nucleosomal interactions exist around transcription start site (TSS), transcription termination sites (TTS) or around CTCF binding sitesNucleosome occupancy at nucleosome-free regions (nfrs), many of which are located at sites occupied by the multivalent factors ctcf and cohesin. This general architectural change correlate with enhanced binding of ct cf and more pronounced insulation across chromatin boundaries in lineage-committed cells.Nucleosome occupancy is reduced at nucleosome-free regions (NFRs), many of which are located at sites occupied by the multivalent factors CTCF and cohesin. Robust inter-nucleosomal interactions exist around transcription start site (TSS), transcription termination sites (TTS) or around CTCF binding sites |
http://www.ncbi.nlm.nih.gov/pubmed/26288836,http://www.ncbi.nlm.nih.gov/pubmed/22702336,http://www.ncbi.nlm.nih.gov/pubmed/28409734,http://www.ncbi.nlm.nih.gov/pubmed/16278210,http://www.ncbi.nlm.nih.gov/pubmed/31088925,http://www.ncbi.nlm.nih.gov/pubmed/22027222,http://www.ncbi.nlm.nih.gov/pubmed/21247388,http://www.ncbi.nlm.nih.gov/pubmed/22216088,http://www.ncbi.nlm.nih.gov/pubmed/28860152,http://www.ncbi.nlm.nih.gov/pubmed/28317148 | Is bortezomib a Proteasome inhibitor? | The proteasome inhibitor bortezomib is effective for a variety of tumors, but not for GBM. Proteasome inhibitor bortezomibYes, bortezomib is a Proteasome inhibitor.Yes, bortezomib is a potent and specific reversible ubiquitin/proteasome inhibitor.yes, The proteasome-inhibitor bortezomibYes bortezomib is a Proteasome inhibitor.proteasome inhibitor bortezomibThe proteasome inhibitor bortezomib is effective for a variety of tumors, but not for gbm.Proteasome inhibitor bortezomib |
http://www.ncbi.nlm.nih.gov/pubmed/29674518,http://www.ncbi.nlm.nih.gov/pubmed/19997497,http://www.ncbi.nlm.nih.gov/pubmed/24634223,http://www.ncbi.nlm.nih.gov/pubmed/23190393,http://www.ncbi.nlm.nih.gov/pubmed/30161134,http://www.ncbi.nlm.nih.gov/pubmed/29478809 | Is PRDM9 essential for meiosis? | PRDM9 is essential for the progression through early meiotic prophase, including double strand break repair, homologous chromosome pairing, and sex body formation during spermatogenesis.In aggregate, our data indicate that domains typically involved in regulation of gene expression do not serve that role in PRDM9, but are likely involved in setting the proper chromatin environment for initiation and completion of homologous recombination. PRDM9 Methyltransferase Activity Is Essential for Meiotic DNA Double-Strand Break Formation at Its Binding Sites.yes, Our findings do not identify the nature of the underlying DNA sequences, but argue against the proposed role of Prdm9 as an essential transcription factor in mouse meiosisPrdm9, is a meiosis-specific protein that trimethylates h3k4 and controls the activation of recombination hot spots. It is an essential enzyme in the progression of early meiotic prophase.Yes. PRDM9 is an evolutionarily conserved protein that is essential for meiosis.In many eukaryotes, sites of meiotic recombination, also called hotspots, are regions of accessible chromatin, but in many vertebrates, their location follows a distinct pattern and is specified by PR domain-containing protein 9 (PRDM9). PRDM9 Methyltransferase Activity Is Essential for Meiotic DNA Double-Strand Break Formation at Its Binding Sites.Yes, PRDM9 is essential for meiosis.Yes. PRDM9 is an RNA-binding protein that is essential for meiosis.Yes. PRDM9 is an essential factor for meiosis.PRDM9 Methyltransferase Activity Is Essential for Meiotic DNA Double-Strand Break Formation at Its Binding Sites.PRDM9 is essential for the progression through early meiotic prophase, including double strand break repair, homologous chromosome pairing, and sex body formation during spermatogenesis. PRDM9 (PR domain-containing protein 9) is a meiosis-specific protein that trimethylates H3K4 and controls the activation of recombination hot spots. |
http://www.ncbi.nlm.nih.gov/pubmed/10644436,http://www.ncbi.nlm.nih.gov/pubmed/9425238,http://www.ncbi.nlm.nih.gov/pubmed/10508587 | What is particular about the mouse Fxy gene's chromosomal position? | We have previously described a gene, Fxy , that spans the pseudoautosomal boundary in mice such that the first three exons of the gene are located on the X chromosome, but the remainder of the gene is located on both X and Y chromosomes. The Fxy gene in mice is also located on the X chromosome but spans the pseudoautosomal boundary in this species.The gene Fxy (also known as MID1 [7]) spans the pseudoautosomal boundary (PAB) in the laboratory mouse (Mus musculus domesticus, C57BL/6) such that the 5' three exons of the gene are located on the X chromosome but the seven exons encoding the carboxy-terminal two-thirds of the protein are located within the PAR and are therefore present on both the X and Y chromosomesWe have previously described a gene, Fxy , that spans the pseudoautosomal boundary in mice such that the first three exons of the gene are located on the X chromosome, but the remainder of the gene is located on both X and Y chromosomes. The mouse fxy gene spans the pseudoautosomal boundary in mice such that the first three exons of the gene are located on the x chromosome, but the remainder is located on both x and y chromosomes.The gene Fxy (also known as MID1) spans the pseudoautosomal boundary (PAB) in the laboratory mouse (Mus musculus domesticus, C57BL/6) such that the 5' three exons of the gene are located on the X chromosome but the seven exons encoding the carboxy-terminal two-thirds of the protein are located within the PAR and are therefore present on both the X and Y chromosomes.The Fxy gene in mice is also located on the X chromosome but spans the pseudoautosomal boundary in this species. Here we describe a gene closely related to FXY/MID1, called FXY2, which also maps to the X chromosome within Xq22 |
http://www.ncbi.nlm.nih.gov/pubmed/16401852 | Should Pentoxifylline be used for treatment of amyotrophic lateral sclerosis? | No. Pentoxifylline is not beneficial in amyotrophic lateral sclerosis and should be avoided in patients treated with riluzole. |
http://www.ncbi.nlm.nih.gov/pubmed/9439081,http://www.ncbi.nlm.nih.gov/pubmed/23575833,http://www.ncbi.nlm.nih.gov/pubmed/18988199,http://www.ncbi.nlm.nih.gov/pubmed/2101731,http://www.ncbi.nlm.nih.gov/pubmed/28168704 | What does a PET (Positron Excitation Tomography) measure? | Positron Excitation Tomography (PET) is a simple, reliable, and valid method of assessing brain activity in patients with Parkinson's disease (PD).Positron emission tomography pet (pet) is used to measure changes in regional brain glucose metabolism. It is used for the quantitative measurement of regional cerebral flow in awake rats.Positron emission tomography (PET) allows the quantitative measurement of regional cerebral flow (rCBF) in humans in quantitative termsPositron Excitation Tomography (PET) is a method that uses photoreactive nucleotides (Percutaneous Transluminal Angioplasty) to detect structural changes in the central nervous system (CNS) following ischemic injury.Positron emission tomography (PET) is used to measure differences in metabolism in different tissues.Positron Excitation Tomography (PET) is a method that allows for quantitative assessment of brain injury conditions such as multiple system atrophy.Positron emission tomography (PET) with [(18)F]2-fluoro-2-deoxy-D-glucose was used to measure changes in regional brain glucose metabolism |
http://www.ncbi.nlm.nih.gov/pubmed/28797215,http://www.ncbi.nlm.nih.gov/pubmed/25869804 | Is the CADM2 gene associated with differences in information processing speed? | Yes, genetic variation in the CADM2 gene is associated with individual differences in information processing speed.Yes. Genetic variation in the CADM2 gene is associated with individual differences in information processing speed.Yes, changes in the CADM2 gene have been associated with differences in information processing speed. |
http://www.ncbi.nlm.nih.gov/pubmed/27354700 | What is GeneCodeq? | The exponential reduction in cost of genome sequencing has resulted in a rapid growth of genomic data. Most of the entropy of short read data lies not in the sequence of read bases themselves but in their Quality Scores-the confidence measurement that each base has been sequenced correctly. Lossless compression methods are now close to their theoretical limits and hence there is a need for lossy methods that further reduce the complexity of these data without impacting downstream analyses. GeneCodeq is a Bayesian method inspired by coding theory for adjusting quality scores to improve the compressibility of quality scores without adversely impacting genotyping accuracy.The exponential reduction in cost of genome sequencing has resulted in a rapid growth of genomic data. Most of the entropy of short read data lies not in the sequence of read bases themselves but in their Quality scores-the confidence measurement that each base has been sequenced correctly. Lossless compression methods are now close to their theoretical limits and hence there is a need for lossy methods that further reduce the complexity of these data without impacting downstream analyses. GeneCodeq is a Bayesian method inspired by coding theory for adjusting quality scores to improve the compressibility of quality scores without adversely impacting genotyping accuracy.The exponential reduction in cost of genome sequencing has resulted in a rapid growth of genomic data. Most of the entropy of short read data lies not in the sequence of read bases themselves but in their Quality Scores-the confidence measurement that each base has been sequenced correctly. Lossless compression methods are now close to their theoretical limits and hence there is a need for lossy methods that further reduce the complexity of these data without impacting downstream analyses. GeneCodeq is a Bayesian method inspired by coding theory for adjusting quality scores to improve the compressibility of quality scores without adversely impacting genotyping accuracy. The method leverages a corpus of k-mers to reduce the entropy of the quality scores and thereby the compressibility of these data (in FASTQ or SAM/BAM/CRAM files), resulting in compression ratios that significantly exceeds those of other methods. |
http://www.ncbi.nlm.nih.gov/pubmed/30171077,http://www.ncbi.nlm.nih.gov/pubmed/27313464,http://www.ncbi.nlm.nih.gov/pubmed/28833116,http://www.ncbi.nlm.nih.gov/pubmed/26514815 | Is Nivolumab (Opdivo) a PD-L1 inhibitor? | No, Nivolumab (Opdivo) is a PD-1 inhibitor.Fatal Myocarditis Following Treatment with the PD-1 Inhibitor Nivolumab |
http://www.ncbi.nlm.nih.gov/pubmed/15159491,http://www.ncbi.nlm.nih.gov/pubmed/17980667,http://www.ncbi.nlm.nih.gov/pubmed/16193258,http://www.ncbi.nlm.nih.gov/pubmed/16638021,http://www.ncbi.nlm.nih.gov/pubmed/18802797 | Does clinical trial data support the use of minocycline for amyotrophic lateral sclerosis? | No. Available clinical trial data suggest that minocycline does not improve prognosis and functional status, and has a harmful effect on patients with amyotrophic lateral sclerosis. |
http://www.ncbi.nlm.nih.gov/pubmed/29518372,http://www.ncbi.nlm.nih.gov/pubmed/28684288,http://www.ncbi.nlm.nih.gov/pubmed/29181712,http://www.ncbi.nlm.nih.gov/pubmed/28766167,http://www.ncbi.nlm.nih.gov/pubmed/29616307 | What are apoptotic bodies? | Extracellular vesicles (EVs) are membrane-bound vesicles released into the extracellular space by almost all types of cells. EVs can cross the physiological barriers, and a variety of biological fluids are enriched in them. EVs are a heterogeneous population of vesicles, including exosomes, microvesicles, and apoptotic bodies.
Apoptotic bodies are generated on apoptotic cell shrinkage and death. |
http://www.ncbi.nlm.nih.gov/pubmed/25485886 | Is the drug Exubera currently (March 2020) available? | No, Exubera has been discontinued due to suboptimal market acceptance. |
http://www.ncbi.nlm.nih.gov/pubmed/22922743,http://www.ncbi.nlm.nih.gov/pubmed/26861626 | What is the function of the ISW1 and CHD1 remodellers in yeast chromatin? | eviction of h1Chd1 and chd1 atp-dependent chromatin remodelers compete to set nucleosome spacing in vivo.The ISW1 and CHD1 ATP-dependent chromatin remodelers compete to set nucleosome spacing in vivo. CHD1 and ISW1 compete to set the spacing on most genes, such that CHD1 dominates genes with shorter spacing and ISW1 dominates genes with longer spacing.In vitro, the three known yeast nucleosome spacing enzymes (CHD1, ISW1 and ISW2) form arrays with different spacing.The ISW1 and CHD1 ATP-dependent chromatin remodelers compete to set nucleosome spacing in vivoWe propose that CHD1 directs short spacing, resulting in eviction of H1 and chromatin unfolding, whereas ISW1 directs longer spacing, allowing H1 to bind and condense the chromatinCHD1 and ISW1 compete to set the spacing on most genes, such that CHD1 dominates genes with shorter spacing and ISW1 dominates genes with longer spacingThe ISW1 and CHD1 ATP-dependent chromatin remodelers compete to set nucleosome spacing in vivo In vitro, the three known yeast nucleosome spacing enzymes (CHD1, ISW1 and ISW2) form arrays with different spacing. CHD1 and ISW1 compete to set the spacing on most genes, such that CHD1 dominates genes with shorter spacing and ISW1 dominates genes with longer spacing |
http://www.ncbi.nlm.nih.gov/pubmed/10639091,http://www.ncbi.nlm.nih.gov/pubmed/1540967,http://www.ncbi.nlm.nih.gov/pubmed/16650867,http://www.ncbi.nlm.nih.gov/pubmed/31652722,http://www.ncbi.nlm.nih.gov/pubmed/9665145,http://www.ncbi.nlm.nih.gov/pubmed/29043625,http://www.ncbi.nlm.nih.gov/pubmed/26089209,http://www.ncbi.nlm.nih.gov/pubmed/20079875,http://www.ncbi.nlm.nih.gov/pubmed/6445538,http://www.ncbi.nlm.nih.gov/pubmed/29787435,http://www.ncbi.nlm.nih.gov/pubmed/29956296,http://www.ncbi.nlm.nih.gov/pubmed/7683090,http://www.ncbi.nlm.nih.gov/pubmed/23948232 | Are breaks in double stranded DNA associated with ionizing radiation? | Yes, double-strand breaks in double stranded DNA may be associated with ionizing radiation risk.Yes, breaks in double stranded DNA are associated with ionizing radiation. |
http://www.ncbi.nlm.nih.gov/pubmed/19145669,http://www.ncbi.nlm.nih.gov/pubmed/20518663,http://www.ncbi.nlm.nih.gov/pubmed/20921829,http://www.ncbi.nlm.nih.gov/pubmed/24597745,http://www.ncbi.nlm.nih.gov/pubmed/25536554,http://www.ncbi.nlm.nih.gov/pubmed/7029300,http://www.ncbi.nlm.nih.gov/pubmed/26436129,http://www.ncbi.nlm.nih.gov/pubmed/22077339 | As of 2019, what type of cancer is commonly associated with ionizing radiation | Ionizing radiation is commonly associated with lung cancer, prostate cancer, breast cancer, cervical intraepithelial neoplasia and oral squamous cell carcinoma.Exposure to ionizing radiation increases the risk for thyroid and breast cancer and leukemia as well as others such as osteosarcoma.Breast cancer, multiple myeloma, leukaemia and osteosarcoma are commonly associated with ionizing radiation.Breast cancer, multiple myeloma, leukaemia and osteosarcoma are examples of cancers that are commonly associated with ionizing radiation.Because latency period for different nosological forms of radiation-induced malignant tumors varies widely, profound attention in further studies should be drawn not only to thyroid, breast cancers and leukemia, but also to malignancies with longer latent period: lung, stomach, colon, ovary, urinary bladder, kidney cancer and multiple myeloma.By contrast, osteosarcoma may be caused by external or internal ionizing radiation,radiation- induced breast cancer |
http://www.ncbi.nlm.nih.gov/pubmed/27760321 | Is KAT2A involved in Acute myeloid leukemia (AML)? | Yes. The KAT2A gene encodes a receptor tyrosine kinase that is frequently mutated in human acute myeloid leukemia (AML). Activating mutations in Kat2A in response to aberrations in TRAIL can lead to TRAIL-1 activation, resulting in the up-regulation of key AML genes, such as TGFb1, NF-kB, Akt, IKK-1, FOXO1, ERK1/2 and c-Myc.Yes, KAT2A inhibition demonstrated anti-AML activity by inducing myeloid differentiation and apoptosis, and suppressed the growth of primary human AMLs of diverse genotypes while sparing normal hemopoietic stem-progenitor cells. |
http://www.ncbi.nlm.nih.gov/pubmed/29881221,http://www.ncbi.nlm.nih.gov/pubmed/29575996,http://www.ncbi.nlm.nih.gov/pubmed/18432151,http://www.ncbi.nlm.nih.gov/pubmed/29571089,http://www.ncbi.nlm.nih.gov/pubmed/17161602,http://www.ncbi.nlm.nih.gov/pubmed/30347291,http://www.ncbi.nlm.nih.gov/pubmed/29664850,http://www.ncbi.nlm.nih.gov/pubmed/17260610,http://www.ncbi.nlm.nih.gov/pubmed/31587271,http://www.ncbi.nlm.nih.gov/pubmed/28705637,http://www.ncbi.nlm.nih.gov/pubmed/28716514 | What is Idiopathic toe walking? | Idiopathic toe walking is a pathological gait pattern in which children older than 3 years walk on their tip toes with no contact between the heels and the ground. |
http://www.ncbi.nlm.nih.gov/pubmed/22895958,http://www.ncbi.nlm.nih.gov/pubmed/22229310,http://www.ncbi.nlm.nih.gov/pubmed/21270788,http://www.ncbi.nlm.nih.gov/pubmed/23496672,http://www.ncbi.nlm.nih.gov/pubmed/24894625 | Is NicVAX vaccine effective for smoking cessation? | No. NicVAX vaccine failed to meet the primary endpoint in two large phase III studies, although the correlation of higher abstinence rates in subjects with higher immunity to nicotine was observed. The nicotine vaccine, NicVAX, does not appear to improve the chances of stopping smoking when given in addition to varenicline and behavioural support. |
http://www.ncbi.nlm.nih.gov/pubmed/29545067,http://www.ncbi.nlm.nih.gov/pubmed/28861122,http://www.ncbi.nlm.nih.gov/pubmed/26788129 | Does natalizumab improve disease course of secondary progressive multiple sclerosis? | No. Atalizumab treatment for secondary progressive multiple sclerosis did not reduce progression on the primary multicomponent disability endpoint in part 1, but it did reduce progression on its upper-limb component. |
http://www.ncbi.nlm.nih.gov/pubmed/29441009,http://www.ncbi.nlm.nih.gov/pubmed/27697018,http://www.ncbi.nlm.nih.gov/pubmed/27995573,http://www.ncbi.nlm.nih.gov/pubmed/20826658,http://www.ncbi.nlm.nih.gov/pubmed/22009441,http://www.ncbi.nlm.nih.gov/pubmed/20678581,http://www.ncbi.nlm.nih.gov/pubmed/23552370 | Before 2019, what neurologic diseases are associated with the tau protein? | Tau proteins are involved in the pathogenesis of multiple sclerosis and amyotrophic lateral sclerosis.Both Alzheimer's Disease and Multiple Sclerosis are associated with tau protein |
http://www.ncbi.nlm.nih.gov/pubmed/19117896 | What is the difference between Daptacel and Pentacel? | Pentacel is a combination vaccine equivalent to the combination of Daptacel, IPOL and ActHIB vaccines. |
http://www.ncbi.nlm.nih.gov/pubmed/17327465,http://www.ncbi.nlm.nih.gov/pubmed/28944315 | AhR ligands are attractive drug targets for pharmaceutical development due to their induction of Cyp1a1, yes or no? | Yes, there is little evidence to support the indiscriminate exclusion of AhR activators/Cyp1a1 inducers from early drug developmental pipelines. |
http://www.ncbi.nlm.nih.gov/pubmed/21266479,http://www.ncbi.nlm.nih.gov/pubmed/19410542,http://www.ncbi.nlm.nih.gov/pubmed/25813039,http://www.ncbi.nlm.nih.gov/pubmed/22122340,http://www.ncbi.nlm.nih.gov/pubmed/18268003 | Does the chromatin remodeling complex, RSC target H2A.Z nucleosomes? | H2A.Z probably helps RSC in keeping the gene nucleosome-free.H2A.Z probably helps RSC in keeping the gene nucleosome-freYes, the chromatin remodeling complex, RSC, uses H2A. Z nucleosomes to remodel chromatin.yes, Accordingly, the absence of SWR-C or histone H2A.Z results in compromised chromatin remodeling and impaired gene expression in the absence of RSC and H3K4 methylation.H2A.Z probably helps RSC in keeping the gene nucleosome-fre Accordingly, the absence of SWR-C or histone H2A.Z results in compromised chromatin remodeling and impaired gene expression in the absence of RSC and H3K4 methylation. |
http://www.ncbi.nlm.nih.gov/pubmed/29801788,http://www.ncbi.nlm.nih.gov/pubmed/28581409,http://www.ncbi.nlm.nih.gov/pubmed/29141565,http://www.ncbi.nlm.nih.gov/pubmed/30360725,http://www.ncbi.nlm.nih.gov/pubmed/30136132,http://www.ncbi.nlm.nih.gov/pubmed/23796837,http://www.ncbi.nlm.nih.gov/pubmed/29671693,http://www.ncbi.nlm.nih.gov/pubmed/25400428,http://www.ncbi.nlm.nih.gov/pubmed/27389300 | List radioprotection agents. | Amifostine
CAPE
Melanin
Melatonin
Metformin
Tea polyphenols
alpha-2-macroglobulin |
http://www.ncbi.nlm.nih.gov/pubmed/30024617,http://www.ncbi.nlm.nih.gov/pubmed/15851481,http://www.ncbi.nlm.nih.gov/pubmed/29388727 | What is the effect of Satb1 knock-out in mice? | inhibited cell viability and migrationWhile T cell growth in vitro, Satb1 knockdown was found to be effective in vivo by inhibiting T cell proliferation and activating apoptosis in a subset of T cellsknock-out of Satb1 significantly inhibited cell viability and migration, and promoted Schwann cells apoptosis.SATB1 is essential for maintaining TCR responsiveness during the induction and effector phases and may provide a novel therapeutic target for T cell-mediated autoimmune diseases. knock-out of Satb1 significantly inhibited cell viability and migration, and promoted Schwann cells apoptosis.Knock-out of Satb1 significantly inhibited cell viability and migration, and promoted Schwann cells apoptosis. |
http://www.ncbi.nlm.nih.gov/pubmed/20183917 | Has ZP-PTH been tested in a phase II clinical trial? | Yes, ZP-PTH was successfully tested in a phase II clinical trial for the treatment of post-menopausal women with osteoporosis. |
http://www.ncbi.nlm.nih.gov/pubmed/26928551,http://www.ncbi.nlm.nih.gov/pubmed/26600192 | PH motifs in which genes endow breast cancer growth? | Although emerging roles of protease-activated receptor1&2 (PAR1&2) in cancer are recognized, their underlying signalling events are poorly understood. Signal-binding motifs in PAR1&2 are critical for breast cancer growth. This occurs via the association of the pleckstrin homology (PH) domain with Akt/PKB as a key signalling event of PARs. Other PH-domain signal-proteins such as Etk/Bmx and Vav3 also associate with PAR1 and PAR2 through their PH domains. PAR1 and PAR2 bind with priority to Etk/Bmx. A point mutation in PAR2, H349A, but not in R352A, abrogates PH-protein association and is sufficient to markedly reduce PAR2-instigated breast tumour growth in vivo and placental extravillous trophoblast (EVT) invasion in vitro. Similarly, the PAR1 mutant hPar1-7A, which is unable to bind the PH domain, reduces mammary tumours and EVT invasion, endowing these motifs with physiological significance and underscoring the importance of these previously unknown PAR1 and PAR2 PH-domain-binding motifs in both pathological and physiological invasion processes. |
http://www.ncbi.nlm.nih.gov/pubmed/29254557,http://www.ncbi.nlm.nih.gov/pubmed/29429063,http://www.ncbi.nlm.nih.gov/pubmed/29047019,http://www.ncbi.nlm.nih.gov/pubmed/28557577 | What is herd immunity? | Vaccines are very effective in providing individual and community (herd) immunity against a range of diseases.
We argue that individuals who have access to vaccines and for whom vaccination is not medically contraindicated have a moral obligation to contribute to the realisation of herd immunity by being vaccinated. |
http://www.ncbi.nlm.nih.gov/pubmed/28320635 | Are multipotent adult progenitor cells effective for treatment of stroke? | No. There was no difference between the multipotent adult progenitor cell group and placebo groups in global stroke recovery at day 90. Further clinical trials evaluating the efficacy of the intervention in an earlier time window after stroke (<36 h) are planned. |
http://www.ncbi.nlm.nih.gov/pubmed/28349074,http://www.ncbi.nlm.nih.gov/pubmed/29465579,http://www.ncbi.nlm.nih.gov/pubmed/29968175 | List the stages/types of Multiple Sclerosis. | Multiple sclerosis presents with different phenotypes, most commonly a relapsing-remitting course and, less frequently, a progressive accumulation of disability from disease onset (primary progressive multiple sclerosis). The majority of people with relapsing-remitting multiple sclerosis, after a variable time, switch to a stage characterised by gradual neurological worsening known as secondary progressive multiple sclerosis.Multiple Sclerosis (MS) is divided into three stages: primary progressive, relapsing-remitting, relapping-Remitting MS, and secondary progressive MS.Multiple Sclerosis can be classified into four different stages (A to C), with different types of neurodegenerative disorders such as primary, chronic, relapsing-remitting and progressive forms.Multiple Sclerosis (MS) is a multisystem disorder, which can be classified into primary progressive, relapsing-remitting, relapping-remoting and non-progressive stages. |
http://www.ncbi.nlm.nih.gov/pubmed/29779852,http://www.ncbi.nlm.nih.gov/pubmed/31285147,http://www.ncbi.nlm.nih.gov/pubmed/28885860 | What is known about Opicinumab for multiple sclerosis? | Opicinumab is a new Anti lingo 1 monoclonal antibody that is tested in relapsing remitting multiple sclerosis. The anti-LINGO-1 trial showed that the drug is safe and tolerable. A future phase II trial will provide more insights regarding the compound. |
http://www.ncbi.nlm.nih.gov/pubmed/30915717,http://www.ncbi.nlm.nih.gov/pubmed/29512131,http://www.ncbi.nlm.nih.gov/pubmed/29143550,http://www.ncbi.nlm.nih.gov/pubmed/29956883,http://www.ncbi.nlm.nih.gov/pubmed/28910968,http://www.ncbi.nlm.nih.gov/pubmed/27886126,http://www.ncbi.nlm.nih.gov/pubmed/29447988,http://www.ncbi.nlm.nih.gov/pubmed/31495497 | What is the target of Inebilizumab? | Inebilizumab is an anti-CD19 antibody with enhanced antibody-dependent cell-mediated cytotoxicity against B cells, is currently being evaluated in multiple sclerosis and neuromyelitis optica. |
http://www.ncbi.nlm.nih.gov/pubmed/29685815,http://www.ncbi.nlm.nih.gov/pubmed/31171755,http://www.ncbi.nlm.nih.gov/pubmed/27801990 | Is eculizumab effective for Guillain-Barré syndrome? | In a clinical trial eculizumab did not achieve primary outcome for Guillain-Barre syndrome. However, because this was a small study without statistical comparison with the placebo group, the efficacy and safety of eculizumab could be investigated in larger, randomised controlled trials. |
http://www.ncbi.nlm.nih.gov/pubmed/30139826,http://www.ncbi.nlm.nih.gov/pubmed/29580266,http://www.ncbi.nlm.nih.gov/pubmed/30017199,http://www.ncbi.nlm.nih.gov/pubmed/30185782,http://www.ncbi.nlm.nih.gov/pubmed/30185825 | List Mcl-1 inhibitors. | A-1210477
S63845 |
http://www.ncbi.nlm.nih.gov/pubmed/29022289,http://www.ncbi.nlm.nih.gov/pubmed/22475795,http://www.ncbi.nlm.nih.gov/pubmed/24779013,http://www.ncbi.nlm.nih.gov/pubmed/30544615,http://www.ncbi.nlm.nih.gov/pubmed/28884441,http://www.ncbi.nlm.nih.gov/pubmed/28889353,http://www.ncbi.nlm.nih.gov/pubmed/31803515,http://www.ncbi.nlm.nih.gov/pubmed/24914338 | Autophagy is the process where a virus obtains nutrients from it's host, yes or no? | No, autophagy is important in cellular homeostasis for the cell survival mechanism and is involved apoptosis.Autophagy is a cellular survival pathway that is necessary for the degradation of cellular constituents such as long-lived proteins and damaged organelles.Autophagy is important in cellular homeostasis for the cell survival mechanism. |
http://www.ncbi.nlm.nih.gov/pubmed/26080409 | What is the basis of the methidiumpropyl-EDTA sequencing (MPE-seq) method? | MPE-seq (methidiumpropyl-EDTA sequencing) is a new method for the genome-wide characterization of chromatin that involves the digestion of nuclei with MPE-Fe(II) followed by massively parallel sequencing of the whole genome. Like micrococcal nuclease (MNase), MNase preferentially cleaves the linker DNA between nucleosomes. However, there are differences in the cleavage of nuclear chromatin by MP e-seq relative to MNase. Moreover, unlike MNase, MPe-seq cleaves nuclear DNAMethidiumpropyl-EDTA sequencing (MPE-seq) is a method for the genome-wide characterization of chromatin that involves the digestion of nuclei withMPE-Fe(II) followed by massively parallel sequencing. MPE-seq unlike MNase-seq cleaves nuclear DNA with little sequence bias and thus provides a unique and straightforward means for the genome-wide analysis of chromatin structure with minimal DNA sequence bias.digestion of nuclei withmpe-fe(ii)methidiumpropyl-EDTA sequencing (MPE-seq), a method for the genome-wide characterization of chromatin that involves the digestion of nuclei withMPE-Fe(II) followed by massively parallel sequencing. MPE-seq provides a unique and straightforward means for the genome-wide analysis of chromatin structure with minimal DNA sequence bias.Methidiumpropyl-edta sequencing is a method for the genome-wide characterization of chromatin that involves the digestion of nuclei withmpe-fe (ii) followed by massively parallel sequencing. Mpe-seq provides a unique and straightforward means for theome-wide analysis of chromat structure with minimal dna sequence bias.The methidiumpropyl-EDTA sequencing (MPE-seq) method uses a GpC methyltransferase (M. CviPI) and next generation sequencing to generate a high resolution footprint of nucleosome structure using less than 1 million cells while retaining endogenous DNA fragments from the same DNA strand. methidiumpropyl-EDTA sequencing (MPE-seq), a method for the genome-wide characterization of chromatin that involves the digestion of nuclei withMPE-Fe(II) followed by massively parallel sequencing. MPE-seq provides a unique and straightforward means for the genome-wide analysis of chromatin structure with minimal DNA sequence bias. methidiumpropyl-EDTA sequencing (MPE-seq), a method for the genome-wide characterization of chromatin that involves the digestion of nuclei withMPE-Fe(II) followed by massively parallel sequencing. MPE-seq provides a unique and straightforward means for the genome-wide analysis of chromatin structure with minimal DNA sequence bias.methidiumpropyl-EDTA sequencing (MPE-seq), a method for the genome-wide characterization of chromatin that involves the digestion of nuclei withMPE-Fe(II) followed by massively parallel sequencing.methidiumpropyl-EDTA sequencing (MPE-seq), a method for the genome-wide characterization of chromatin that involves the digestion of nuclei withMPE-Fe(II) followed by massively parallel sequencing. methidiumpropyl-EDTA sequencing (MPE-seq), a method for the genome-wide characterization of chromatin that involves the digestion of nuclei withMPE-Fe(II) followed by massively parallel sequencing. MPE-seq provides a unique and straightforward means for the genome-wide analysis of chromatin structure with minimal DNA sequence bias. |
http://www.ncbi.nlm.nih.gov/pubmed/29436336 | Name two rotavirus vaccines. | Two rotavirus vaccines licensed for global use are RotaTeq and Rotarix. |
http://www.ncbi.nlm.nih.gov/pubmed/17504899,http://www.ncbi.nlm.nih.gov/pubmed/24596594,http://www.ncbi.nlm.nih.gov/pubmed/27729837,http://www.ncbi.nlm.nih.gov/pubmed/17347996 | Does CXorf21 escape X chromosome inactivation? | CXORF21 belongs to a set of X-linked differentially expressed genes that show verbal cognition-gene expression correlations may establish a causal link between these genes, neurodevelopment, and language function.Examination of X-linked DEGs, such as GTPBP6, TAF9L, and CXORF21, that show verbal cognition-gene expression correlations may establish a causal link between these genes, neurodevelopment, and language function.yes, Examination of X-linked DEGs, such as GTPBP6, TAF9L, and CXORF21, that show verbal cognition-gene expression correlations may establish a causal link between these genes, neurodevelopment, and language function. |
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