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http://www.ncbi.nlm.nih.gov/pubmed/25677180 | Does deletion of cohesin change gene expression? | The conditional deletion of cohesin from noncycling thymocytes preserved enhancer position, H3K27ac, H4K4me1, and enhancer transcription, but weakened interactions between enhancers. Interestingly, ~ 50% of deregulated genes reside in the vicinity of enhancer elements, suggesting that cohesin regulates gene expression through spatial clustering of enhancer elements.Yes. Deletion of cohesin inhibits gene expression at multiple points within the genome and in different genomic regions.The conditional deletion of cohesin from noncycling thymocytes preserved enhancer position, H3K27ac, H4K4me1, and enhancer transcription, but weakened interactions between enhancers. 50% of deregulated genes reside in the vicinity of enhancer elements, suggesting that cohesin regulates gene expression through spatial clustering of enhancer elements.We propose a model for cohesin-dependent gene regulation in which spatial clustering of enhancer elements acts as a unified mechanism for both enhancer-promoter "connections" and "insulation.". The conditional deletion of cohesin from noncycling thymocytes preserved enhancer position, H3K27ac, H4K4me1, and enhancer transcription, but weakened interactions between enhancers. Interestingly, ~ 50% of deregulated genes reside in the vicinity of enhancer elements, suggesting that cohesin regulates gene expression through spatial clustering of enhancer elements.Interestingly, ~ 50% of deregulated genes reside in the vicinity of enhancer elements, suggesting that cohesin regulates gene expression through spatial clustering of enhancer elements. We propose a model for cohesin-dependent gene regulation in which spatial clustering of enhancer elements acts as a unified mechanism for both enhancer-promoter "connections" and "insulation."Yes. Numerous studies have demonstrated that deletion of cohesin reduces gene expression at multiple points within the genome. |
http://www.ncbi.nlm.nih.gov/pubmed/30153633,http://www.ncbi.nlm.nih.gov/pubmed/29515123 | Do MAIT cells have a role in multiple myeloma? | Yes, MAIT cells may represent new immunotherapeutic targets for treatment of Multiple Myeloma and other malignanciesYes, MAIT cells have a role in multiple myeloma.Yes. Mucosal-associated invariant T cells (MAIT cells) play a key role in the pathogenesis of multiple myeloma. |
http://www.ncbi.nlm.nih.gov/pubmed/24412048,http://www.ncbi.nlm.nih.gov/pubmed/30156440 | What is ProSavin? | ProSavin, a lentiviral vector based gene therapy aimed at restoring local and continuous dopamine production in patients with advanced Parkinson's disease. It has been shown to be well tolerated in a Phase I/II first-in-human study, with significant improvements in motor behavior from baseline at 1 year. Moderate improvements in motor behavior over baseline continued to be reported in the majority of patients who could still be evaluated up to 5 years of follow-up. |
http://www.ncbi.nlm.nih.gov/pubmed/30169995 | Are stretch enhancers transcribed more than super-enhancers? | No. Super-enhancers are transcriptionally more active and cell type-specific than stretch enhancers.No. Super-enhancers are transcriptionally more active and cell type-specific than stretch enhancers. Importantly, most of the stretch enhancers that are distinct from super-enhancers do not show an association with cell identity genes, are less active, and more likely to be poised enhancers. |
http://www.ncbi.nlm.nih.gov/pubmed/25282031 | What is Q-SYMBIO? | Q-SYMBIO is a randomised, double-blind, multicentre trial with focus on SYMptoms, BIomarker status [Brain-Natriuretic Peptide (BNP)], and long-term Outcome [hospitalisations/mortality] that assessed coenzyme Q10 as adjunctive treatment of chronic heart failure. METHOD: Patients with moderate to severe HF were randomly assigned in a 2-year prospective trial to either CoQ10 100 mg 3 times daily or placebo, in addition to standard therapy. The primary short-term endpoints at 16 weeks were changes in New York Heart Association (NYHA) functional classification, 6-min walk test, and levels of N-terminal pro-B type natriuretic peptide. The primary long-term endpoint at 2 years was composite major adverse cardiovascular events as determined by a time to first event analysis. CONCLUSION: Long-term CoQ10 treatment of patients with chronic HF is safe, improves symptoms, and reduces major adverse cardiovascular events. |
http://www.ncbi.nlm.nih.gov/pubmed/18854353,http://www.ncbi.nlm.nih.gov/pubmed/23760082,http://www.ncbi.nlm.nih.gov/pubmed/28855971,http://www.ncbi.nlm.nih.gov/pubmed/28914604,http://www.ncbi.nlm.nih.gov/pubmed/30096364,http://www.ncbi.nlm.nih.gov/pubmed/24550742,http://www.ncbi.nlm.nih.gov/pubmed/25255084,http://www.ncbi.nlm.nih.gov/pubmed/19468298 | What is the function of the NIPBL factor in genome conformation? | The NIPBL protein stimulates cohesin's ABC-like ATPase and is essential for loading cohesin onto chromosomes.. NIPBL recruits histone deacetylases to mediate local chromatin modifications.NIPBL loads cohesin onto chromatin. The NIPBL protein is required for the loading of cohesin onto chromatin. A cohesin-loading factor (NIPBL) is one of important regulatory factors in the maintenance of 3D genome organization and function, by interacting with a large number of factors, e.g. cohesion, CCCTC-binding factor (CTCF) or cohesin complex component. The mechanism of this gene regulation remains unclear, but NIPBL and cohesin have been reported to affect long-range chromosomal interactions, both independently and through interactions with CTCF.The Cohesin loading factor NIPBL recruits histone deacetylases to mediate local chromatin modifications. |
http://www.ncbi.nlm.nih.gov/pubmed/26024342,http://www.ncbi.nlm.nih.gov/pubmed/23463177,http://www.ncbi.nlm.nih.gov/pubmed/30479770,http://www.ncbi.nlm.nih.gov/pubmed/27705549,http://www.ncbi.nlm.nih.gov/pubmed/26418833,http://www.ncbi.nlm.nih.gov/pubmed/30618090,http://www.ncbi.nlm.nih.gov/pubmed/26161391,http://www.ncbi.nlm.nih.gov/pubmed/28685333,http://www.ncbi.nlm.nih.gov/pubmed/28910456,http://www.ncbi.nlm.nih.gov/pubmed/23714495,http://www.ncbi.nlm.nih.gov/pubmed/27462362,http://www.ncbi.nlm.nih.gov/pubmed/8394641 | Is mesothelioma caused by asbestos exposure? | Yes, mesothelioma is caused by asbestos exposure.Yes, mesothelioma is a hard to treat malignant neoplasia caused by asbestos exposure.Yes, mesothelioma is a type of malignant mesothelial cancer caused by asbestos exposure.Yes, mesothelioma is caused by exposure to asbestos.Exposure to asbestos can cause malignant mesothelioma 30-40 years after exposure. |
http://www.ncbi.nlm.nih.gov/pubmed/14707219,http://www.ncbi.nlm.nih.gov/pubmed/28191331,http://www.ncbi.nlm.nih.gov/pubmed/24153118,http://www.ncbi.nlm.nih.gov/pubmed/14522060 | Which diagnostic test is approved for coronavirus infection screening? | Real-time reverse transcription-PCR (rRT-PCR) is mostly used as the lab test for screening coronaviral infection. |
http://www.ncbi.nlm.nih.gov/pubmed/28012176 | What is Xanamem? | UE2343 was identified as a potent, orally bioavailable, brain-penetrant 11b-HSD1 inhibitor and selected for clinical studies. Reducing glucocorticoid exposure in the brain via intracellular inhibition of the cortisol-regenerating enzyme 11b-hydroxysteroid dehydrogenase type 1 (11b-HSD1) has emerged as a therapeutic strategy to treat cognitive impairment in early Alzheimer's disease (AD). UE2343 is safe, well tolerated and reaches the brain at concentrations predicted to inhibit 11b-HSD1. UE2343 is therefore a suitable candidate to test the hypothesis that 11b-HSD1 inhibition in brain improves memory in patients with AD. |
http://www.ncbi.nlm.nih.gov/pubmed/25159739,http://www.ncbi.nlm.nih.gov/pubmed/29500295,http://www.ncbi.nlm.nih.gov/pubmed/24078215,http://www.ncbi.nlm.nih.gov/pubmed/25717032 | Can nrf2 activation lead to resistance to radiotherapy? | Resistance to chemoradiotherapy is a major obstacle to successful treatment of glioblastoma. Recently, the role of NF-E2-related factor 2 (Nrf2) in enhancing chemoradiation sensitivity has been reported in several types of cancers. Blocking Nrf2 activation may be a promising method enhancing chemoradiation sensitivity of glioblastoma cells. |
http://www.ncbi.nlm.nih.gov/pubmed/29749606 | Are there interactions between short and long noncoding RNAs? | Yes. Short RNAs and long noncoding RNAs (lncRNAs) interact with each other with reciprocal consequences for their fates and functions.It is now evident that noncoding RNAs play key roles in regulatory networks determining cell fate and behavior, in a myriad of different conditions, and across all species. Among these noncoding RNAs are short RNAs, such as MicroRNAs, snoRNAs, and Piwi-interacting RNAs, and the functions of those are relatively well understood. Other noncoding RNAs are longer, and their modes of action and functions are also increasingly explored and deciphered. Short RNAs and long noncoding RNAs (lncRNAs) interact with each other with reciprocal consequences for their fates and functions. LncRNAs serve as precursors for many types of small RNAs and, therefore, the pathways for small RNA biogenesis can impinge upon the fate of lncRNAs. In addition, lncRNA expression can be repressed by small RNAs, and lncRNAs can affect small RNA activity and abundance through competition for binding or by triggering small RNA degradation.Yes. Short RNAs and long noncoding RNAs interact with each other with reciprocal consequences for their fates and functions. |
http://www.ncbi.nlm.nih.gov/pubmed/31050693,http://www.ncbi.nlm.nih.gov/pubmed/27116335,http://www.ncbi.nlm.nih.gov/pubmed/31114933,http://www.ncbi.nlm.nih.gov/pubmed/28640105,http://www.ncbi.nlm.nih.gov/pubmed/29326440,http://www.ncbi.nlm.nih.gov/pubmed/30122982,http://www.ncbi.nlm.nih.gov/pubmed/30018031,http://www.ncbi.nlm.nih.gov/pubmed/28277830,http://www.ncbi.nlm.nih.gov/pubmed/29568360,http://www.ncbi.nlm.nih.gov/pubmed/29356698,http://www.ncbi.nlm.nih.gov/pubmed/26673799,http://www.ncbi.nlm.nih.gov/pubmed/30652516,http://www.ncbi.nlm.nih.gov/pubmed/29903896,http://www.ncbi.nlm.nih.gov/pubmed/26586345,http://www.ncbi.nlm.nih.gov/pubmed/29573941,http://www.ncbi.nlm.nih.gov/pubmed/28611198,http://www.ncbi.nlm.nih.gov/pubmed/29210065,http://www.ncbi.nlm.nih.gov/pubmed/29155017,http://www.ncbi.nlm.nih.gov/pubmed/30117021 | Which molecule is inhibited by encorafenib? | Encorafenib is a BRAF inhibitor. It is a promising therapy for metastatic or inoperable melanoma with a BRAF mutation. |
http://www.ncbi.nlm.nih.gov/pubmed/25938943,http://www.ncbi.nlm.nih.gov/pubmed/26616563,http://www.ncbi.nlm.nih.gov/pubmed/25695508,http://www.ncbi.nlm.nih.gov/pubmed/29531215,http://www.ncbi.nlm.nih.gov/pubmed/25122612,http://www.ncbi.nlm.nih.gov/pubmed/29979818,http://www.ncbi.nlm.nih.gov/pubmed/30224643,http://www.ncbi.nlm.nih.gov/pubmed/30010637 | What is the basis of the capture Hi-C experimental protocol? | Capture Hi-C (CHi-C) allows high-resolution analysis of targeted regions of the genome by incorporating a sequence capture step into a Hi-C protocol. Capture Hi-C (CHi-C) enriches standard Hi-C libraries for regions of biological interest, for example by specifically targeting gene promoters, aiding identification of biologically significant chromatin interactions compared to conventional Hi-C, for an equivalent number of sequence readsChromosome conformation capture implemented in Hi-C allows for genome-wide agnostic characterization of chromatin contacts.Capture Hi-C (CHi-C), which, by incorporating a sequence capture step into a Hi-C protocol, allows high-resolution analysis of targeted regions of the genome. To address this, Capture Hi-C (CHi-C) enriches standard Hi-C libraries for regions of biological interest, for example by specifically targeting gene promoters, aiding identification of biologically significant chromatin interactions compared to conventional Hi-C, for an equivalent number of sequence reads We use Capture Hi-C to investigate, for the first time, the interactions between associated variants for four autoimmune diseases and their functional targets in B- and T-cell lines. We developed Promoter Capture Hi-C (PCHi-C) to enable the genome-wide detection of distal promoter-interacting regions (PIRs), for all promoters in a single experiment. Here we use high-throughput chromosome conformation capture techniques (Hi-C) for 19,023 promoter fragments to catalog the regulatory landscape of colorectal cancer in cell lines, mapping CREs and integrating these with whole-genome sequence and expression data from The Cancer Genome Atlas7,8 Here we use Capture Hi-C (CHi-C), an adapted genome conformation assay, to examine the long-range interactions of almost 22,000 promoters in 2 human blood cell types. Chromosome conformation capture implemented in Hi-C allows for genome-wide agnostic characterization of chromatin contacts. Capture Hi-C (CHi-C), which, by incorporating a sequence capture step into a Hi-C protocol, allows high-resolution analysis of targeted regions of the genome. Here we develop a capture Hi-C (cHi-C) approach to allow an agnostic characterization of these physical interactions on a genome-wide scale. Here we use Capture Hi-C (CHi-C), an adapted genome conformation assay, to examine the long-range interactions of almost 22,000 promoters in 2 human blood cell types.Capture Hi-C (CHi-C), which, by incorporating a sequence capture step into a Hi-C protocol, allows high-resolution analysis of targeted regions of the genome. Here we use Capture Hi-C (CHi-C), an adapted genome conformation assay, to examine the long-range interactions of almost 22,000 promoters in 2 human blood cell types. Here we use high-throughput chromosome conformation capture techniques (Hi-C) for 19,023 promoter fragments to catalog the regulatory landscape of colorectal cancer in cell lines, mapping CREs and integrating these with whole-genome sequence and expression data from The Cancer Genome Atlas7,8 To address this, Capture Hi-C (CHi-C) enriches standard Hi-C libraries for regions of biological interest, for example by specifically targeting gene promoters, aiding identification of biologically significant chromatin interactions compared to conventional Hi-C, for an equivalent number of sequence reads We developed Promoter Capture Hi-C (PCHi-C) to enable the genome-wide detection of distal promoter-interacting regions (PIRs), for all promoters in a single experiment. Here, we use Capture Hi-C (CHi-C) to annotate 63 loci; we identify 110 putative target genes at 33 loci. |
http://www.ncbi.nlm.nih.gov/pubmed/28914604 | What is the role of Scc2/Nipbl? | Scc2 (Nipbl) stimulates cohesin's ABC-like ATPase and is essential for loading cohesin onto chromosomes. Scc2 also binds dynamically to chromatin, principally through an association with cohesin. Scc2's movement within chromatin is consistent with a 'stop-and-go' or 'hopping' motion. A low diffusion coefficient, a low stoichiometry relative to cohesin, and a high affinity for chromosomal cohesin enables Scc2 to move rapidly from one chromosomal cohesin complex to another, performing a function distinct from loading. |
http://www.ncbi.nlm.nih.gov/pubmed/15717219,http://www.ncbi.nlm.nih.gov/pubmed/9016531,http://www.ncbi.nlm.nih.gov/pubmed/10764678,http://www.ncbi.nlm.nih.gov/pubmed/7585875 | What is the chromosomal location of the LDL receptor gene associated with autosomal dominant Familial Hypercholesterolemia? | Familial hypercholesterolemia (FH) is an autosomal dominant inherited metabolic disorder resulting in advanced vascular atherosclerosis and premature death, primarily from coronary artery disease. The primary defect is a mutation in the gene encoding for the plasma LDL receptor located on the short arm of chromosome 19Mutations in the LDLr gene (LDLR), which is located on chromosome 19, cause familial hypercholesterolemiaThe chromosomal location of the LDL receptor gene associated with autosomal dominant Familial Hypercholesterolemia is chromosome 19q13.3.Familial hypercholesterolemia (FH) is an autosomal dominant inherited metabolic disorder resulting in advanced vascular atherosclerosis and premature death, primarily from coronary artery disease. The primary defect is a mutation in the gene encoding for the plasma LDL receptor located on the short arm of chromosome 19.The primary defect is a mutation in the gene encoding for the plasma LDL receptor located on the short arm of chromosome 19. |
http://www.ncbi.nlm.nih.gov/pubmed/29277576,http://www.ncbi.nlm.nih.gov/pubmed/28956068,http://www.ncbi.nlm.nih.gov/pubmed/18171695,http://www.ncbi.nlm.nih.gov/pubmed/28184302 | Can brain derived exosomes carry APP molecules? | Yes,
small lipid vesicles called exosomes, secreted in the extracellular milieu by cortical neurons, carry endogenous APP |
http://www.ncbi.nlm.nih.gov/pubmed/8896256,http://www.ncbi.nlm.nih.gov/pubmed/28535153,http://www.ncbi.nlm.nih.gov/pubmed/7480642,http://www.ncbi.nlm.nih.gov/pubmed/25034478,http://www.ncbi.nlm.nih.gov/pubmed/11309438,http://www.ncbi.nlm.nih.gov/pubmed/25088201 | List the most common cancers after a radiation exposure? | well-known increase in leukaemia, increases in solid cancer such as cancers of the lung, breast, stomach and thyroid have also been demonstrated. |
http://www.ncbi.nlm.nih.gov/pubmed/21257795,http://www.ncbi.nlm.nih.gov/pubmed/10512874,http://www.ncbi.nlm.nih.gov/pubmed/23382076,http://www.ncbi.nlm.nih.gov/pubmed/28505153,http://www.ncbi.nlm.nih.gov/pubmed/29792825 | Which are the main G1/S transcription factors in yeast? | MBF/SBF is the major transcriptional repressor of G1/S genes in Saccharomyces cerevisiae.The G(1)/S transition is a critical control point for cell proliferation and involves essential transcription complexes termed SBF and MBF in Saccharomyces cerevisiae or MBF in Schizosaccharomyces pombe. Over 200 G1/S genes are regulated by either one of the two TF complexes, SBF and MBF, which bind to specific DNA binding sequences, SCB and MCB, respectively.MBF and SBF are two members of bHLH-PAS-containing family of transcription factors that represent theG1/S transcription factors in Saccharomyces cerevisiaeWe previously isolated the SKN7 gene in a screen designed to isolate new components of the G1-S cell cycle transcription machinery in budding yeast. We have now found that Skn7 associates with Mbp1, the DNA-binding component of the G1-S transcription factor DSC1/MBF In Saccharomyces cerevisiae, G1/S transcription factors MBF and SBF regulate a large family of genes important for entry to the cell cycle and DNA replication and repair.To understand how commitment to cell division in late G1 phase (Start) is controlled by growth and nutrients in budding yeast, we determined the absolute concentrations of the G1/S transcription factors SBF (composed of Swi4 and Swi6) and MBF (composed of Mbp1 and Swi6), the transcriptional repressor Whi5, and the G1 cyclins, Cln1 and Cln2, in single live yeast cells using scanning number and brightness (sN&B) microscopy. We previously isolated the SKN7 gene in a screen designed to isolate new components of the G1-S cell cycle transcription machinery in budding yeast. In Saccharomyces cerevisiae, G1/S transcription factors MBF and SBF regulate a large family of genes important for entry to the cell cycle and DNA replication and repair.To understand how commitment to cell division in late G1 phase (Start) is controlled by growth and nutrients in budding yeast, we determined the absolute concentrations of the G1/S transcription factors SBF (composed of Swi4 and Swi6) and MBF (composed of Mbp1 and Swi6), the transcriptional repressor Whi5, and the G1 cyclins, Cln1 and Cln2, in single live yeast cells using scanning number and brightness (sN&B) microscopy. We previously isolated the SKN7 gene in a screen designed to isolate new components of the G1-S cell cycle transcription machinery in budding yeast.MBF and SBF consist of a common component, Swi6, and a DNA-specific binding protein, Mbp1 and Swi4, respectively. We have now found that Skn7 associates with Mbp1, the DNA-binding component of the G1- S transcription factor DSC1/ MBF. Over 200 G1/S genes are regulated by either one of the two TF complexes, SBF and MBF, which bind to specific DNA binding sequences, SCB and MCB, respectively. In Saccharomyces cerevisiae, G1/S transcription factors MBF and SBF regulate a large family of genes important for entry to the cell cycle and DNA replication and repair.MBF and SBF consist of a common component, Swi6, and a DNA-specific binding protein, Mbp1 and Swi4, respectively. We have now found that Skn7 associates with Mbp1, the DNA-binding component of the G1-S transcription factor DSC1/MBF. Over 200 G1/S genes are regulated by either one of the two TF complexes, SBF and MBF, which bind to specific DNA binding sequences, SCB and MCB, respectively. In Saccharomyces cerevisiae, G1/S transcription factors MBF and SBF regulate a large family of genes important for entry to the cell cycle and DNA replication and repair.To understand how commitment to cell division in late G1 phase (Start) is controlled by growth and nutrients in budding yeast, we determined the absolute concentrations of the G1/S transcription factors SBF (composed of Swi4 and Swi6) and MBF (composed of Mbp1 and Swi6), the transcriptional repressor Whi5, and the G1 cyclins, Cln1 and Cln2, in single live yeast cells using scanning number and brightness (sN&B) microscopy. We previously isolated the SKN7 gene in a screen designed to isolate new components of the G1-S cell cycle transcription machinery in budding yeast. The G(1)/S transition is a critical control point for cell proliferation and involves essential transcription complexes termed SBF and MBF in Saccharomyces cerevisiae or MBF in Schizosaccharomyces pombeIn Saccharomyces cerevisiae, G1/S transcription factors MBF and SBF regulate a large family of genes important for entry to the cell cycle and DNA replication and repair. MBF and SBF consist of a common component, Swi6, and a DNA-specific binding protein, Mbp1 and Swi4, respectively. Over 200 G1/S genes are regulated by either one of the two TF complexes, SBF and MBF, which bind to specific DNA binding sequences, SCB and MCB, respectively. |
http://www.ncbi.nlm.nih.gov/pubmed/29154924,http://www.ncbi.nlm.nih.gov/pubmed/28902419,http://www.ncbi.nlm.nih.gov/pubmed/29454332,http://www.ncbi.nlm.nih.gov/pubmed/12091366,http://www.ncbi.nlm.nih.gov/pubmed/11517631,http://www.ncbi.nlm.nih.gov/pubmed/19342478,http://www.ncbi.nlm.nih.gov/pubmed/22099368,http://www.ncbi.nlm.nih.gov/pubmed/18293685,http://www.ncbi.nlm.nih.gov/pubmed/24054178,http://www.ncbi.nlm.nih.gov/pubmed/20609690,http://www.ncbi.nlm.nih.gov/pubmed/25075539,http://www.ncbi.nlm.nih.gov/pubmed/28541873,http://www.ncbi.nlm.nih.gov/pubmed/23418762,http://www.ncbi.nlm.nih.gov/pubmed/29134618,http://www.ncbi.nlm.nih.gov/pubmed/29423808 | What is Hemochromatosis? | Hereditary hemochromatosis (HH) is a group of genetic iron overload disorders that manifest with various symptoms, including hepatic dysfunction, diabetes, and cardiomyopathy.Hereditary hemochromatosis (HH) is a genetic disorder of iron metabolism that may lead to iron overload. |
http://www.ncbi.nlm.nih.gov/pubmed/30222019,http://www.ncbi.nlm.nih.gov/pubmed/30079523,http://www.ncbi.nlm.nih.gov/pubmed/29895698 | What molecules are the multidrug transporter MDR3 targeting? | Multidrug-resistant P-glycoprotein 3 (MDR3) is a phospholipid translocator. |
http://www.ncbi.nlm.nih.gov/pubmed/29321253 | What is the role of the Hof1-Cyk3 interaction in yeast? | In Saccharomyces cerevisiae, it is well established that Hof1, Cyk3, and Inn1 contribute to septum formation and cytokinesis. There is also evidence that they interact physically.In Saccharomyces cerevisiae, it is well established that Hof1, Cyk3, and Inn1 contribute to septum formation and cytokinesis. Hof1 and Cyk3 interact physically and the interaction 1) is mediated by a direct binding of the Hof1 SH3 domain to a proline-rich motif in Cyk3; 2) occurs specifically at the time of cytokinesis but is independent of the (hyper)phosphorylation of both proteins that occurs at about the same time; 3) is dispensable for the normal localization of both proteins; 4) is essential for normal primary-septum formation and a normal rate of cleavage-furrow ingression; and 5) becomes critical for growth when either Inn1 or the type II myosin Myo1 (a key component of the contractile actomyosin ring) is absent. The similarity in phenotype between cyk3[?] mutants and mutants specifically lacking the Hof1-Cyk3 interaction suggests that the interaction is particularly important for Cyk3 function, but it may be important for Hof1 function as well. |
http://www.ncbi.nlm.nih.gov/pubmed/31106887,http://www.ncbi.nlm.nih.gov/pubmed/23974871,http://www.ncbi.nlm.nih.gov/pubmed/27154412,http://www.ncbi.nlm.nih.gov/pubmed/26073755,http://www.ncbi.nlm.nih.gov/pubmed/29604126,http://www.ncbi.nlm.nih.gov/pubmed/25041099 | List features of the SAM syndrome. | SAM syndrome is characterized by severe dermatitis, multiple allergies and metabolic wasting. It is caused by mutations in the desmoglein 1 gene (DSG1). |
http://www.ncbi.nlm.nih.gov/pubmed/11301301,http://www.ncbi.nlm.nih.gov/pubmed/28432608,http://www.ncbi.nlm.nih.gov/pubmed/26445214 | What does the Smith–Waterman algorithm do? | The Smith-Waterman algorithm performs local sequence alignments. |
http://www.ncbi.nlm.nih.gov/pubmed/24729451,http://www.ncbi.nlm.nih.gov/pubmed/24047082,http://www.ncbi.nlm.nih.gov/pubmed/18408014,http://www.ncbi.nlm.nih.gov/pubmed/28179318,http://www.ncbi.nlm.nih.gov/pubmed/24118100,http://www.ncbi.nlm.nih.gov/pubmed/10629043,http://www.ncbi.nlm.nih.gov/pubmed/8049444,http://www.ncbi.nlm.nih.gov/pubmed/29306014,http://www.ncbi.nlm.nih.gov/pubmed/9548713,http://www.ncbi.nlm.nih.gov/pubmed/27590341 | Is SATB1 positioned close to AT-rich sequences? | Yes, SATB1 is preferentially located at the start of an AT-rich sequence and is associated with other, more diffuse AT- rich sequences in the genome.Special AT-rich sequence-binding protein 1 (SATB1), a DNA-binding protein expressed predominantly in thymocytes, recognizes an ATC sequence context that consists of a cluster of sequence stretches with well-mixed A's, T's, and C's without G's on one strand. SATB1 (special AT-rich sequence-binding protein-1) provides a key link between DNA loop organization, chromatin modification/remodeling, and association of transcription factors at matrix attachment regions (MARs).Special AT-rich sequence-binding protein 1 (SATB1), a DNA-binding protein expressed predominantly in thymocytes, recognizes an ATC sequence context that consists of a cluster of sequence stretches with well-mixed A's, T's, and C's without G's on one strand.We have purified and identified one of the core factors as the matrix attachment region (MAR) binding protein, SATB1, which is known to bind to AT-rich sequences with a high propensity to unwind |
http://www.ncbi.nlm.nih.gov/pubmed/25298803,http://www.ncbi.nlm.nih.gov/pubmed/20465815 | Describe the Java Adverse Drug Event (JADE) tool | The Java Adverse Drug event (Jade) is a tool for medical researchers to explore adverse drug events using health insurance plans and drug-drug interactions.The Java Adverse Drug Event (JADE) tool enables the analysis of prescribed drugs in connection with diagnoses from hospital stays. It can support physicians during their planning of clinical trials by showing the occurrences of adverse drug events with population based information. |
http://www.ncbi.nlm.nih.gov/pubmed/29661758,http://www.ncbi.nlm.nih.gov/pubmed/29658845,http://www.ncbi.nlm.nih.gov/pubmed/30393621,http://www.ncbi.nlm.nih.gov/pubmed/27610613,http://www.ncbi.nlm.nih.gov/pubmed/31066582,http://www.ncbi.nlm.nih.gov/pubmed/31195357 | Which drugs were tested in the CheckMate 227 clinical trial? | CheckMate-227 clinical trial tested ipilimumab plus nivolumab for the treatment of non-small cell lung cancer. |
http://www.ncbi.nlm.nih.gov/pubmed/15939070,http://www.ncbi.nlm.nih.gov/pubmed/9108791,http://www.ncbi.nlm.nih.gov/pubmed/29152572 | What is known about PAI-1 in longevity in humans? | Plasminogen activator inhibitor-1 (PAI-1) has been shown to be a key component of the senescence-related secretome and a direct mediator of cellular senescence. In murine models of accelerated aging, genetic deficiency and targeted inhibition of PAI-1 protect against aging-like pathology and prolong life span. However, the role of PAI-1 in human longevity remains unclear.
, in centenarians there was a significantly higher frequency of the 4G allele and of the homozygous 4G4G genotype associated with high PAI-1 levels. Since high PAI-1 is considered a predictor of recurrent myocardial infarction in young men, it is intriguing that the corresponding genetic marker is more frequent in centenarians who have escaped major age-related atherothrombotic disease and reached the extreme limits of human life. Homozygosity for the 4G allele, despite its association with impaired fibrinolysis, is compatible with successful aging. |
http://www.ncbi.nlm.nih.gov/pubmed/25552600,http://www.ncbi.nlm.nih.gov/pubmed/17307426,http://www.ncbi.nlm.nih.gov/pubmed/29878903,http://www.ncbi.nlm.nih.gov/pubmed/25527624,http://www.ncbi.nlm.nih.gov/pubmed/29499335,http://www.ncbi.nlm.nih.gov/pubmed/29452166,http://www.ncbi.nlm.nih.gov/pubmed/22672501,http://www.ncbi.nlm.nih.gov/pubmed/28526884,http://www.ncbi.nlm.nih.gov/pubmed/27737949 | Does metformin alleviate atherosclerosis? | Yes. Metformin has been shown to decrease frequency of atherosclerosis-associated adverse effects in statin-intolerant patients and to slow the pathogenesis of type 2 diabetes mellitus.Metformin Suppresses Diabetes-Accelerated Atherosclerosis via the Inhibition of Drp1-Mediated Mitochondrial Fission.Yes. Metformin has been shown to decrease frequency of atherosclerosis-associated adverse effects in statin-intolerant patients and to slow the pathogenesis of type 2 diabetes.Coupled with their proven good safety profile these findings could translate into a significant clinical benefit. Our results suggest that metformin impeded the progression of atherosclerosis, possibly by suppressing macrophage infiltration and inflammatory responses.Metformin ameliorates the progression of atherosclerosis via suppressing macrophage infiltration and inflammatory responses Our results suggest that metformin impeded the progression of atherosclerosis, possibly by suppressing macrophage infiltration and inflammatory responses.Yes. Metformin has been shown in a number of clinical trial to prevent and attenuate atherosclerosis.Several recently completed randomized clinical trials have reported effects of metformin on surrogate measures of atherosclerotic vascular disease. Metformin ameliorates the progression of atherosclerosis via suppressing macrophage infiltration and inflammatory response. |
http://www.ncbi.nlm.nih.gov/pubmed/25141962,http://www.ncbi.nlm.nih.gov/pubmed/26390925,http://www.ncbi.nlm.nih.gov/pubmed/29947933,http://www.ncbi.nlm.nih.gov/pubmed/29983028,http://www.ncbi.nlm.nih.gov/pubmed/29953370 | List side effects of radiation therapy? | radiation-induced tumors
radiation necrosis
microangiopathy
progressive leukencephalopathy
pneumonitis
disturbance of the blood-brain barrier
radionecrosis of brain tissue
radiogenic liver damage
mucositis
colitis
osteitis
osteoradionecrosis
myositis
Radiation-induced fibrosis
Acute skin reactions |
http://www.ncbi.nlm.nih.gov/pubmed/26301869,http://www.ncbi.nlm.nih.gov/pubmed/25591463,http://www.ncbi.nlm.nih.gov/pubmed/7904067,http://www.ncbi.nlm.nih.gov/pubmed/1533274,http://www.ncbi.nlm.nih.gov/pubmed/28382035,http://www.ncbi.nlm.nih.gov/pubmed/29677476,http://www.ncbi.nlm.nih.gov/pubmed/10882415,http://www.ncbi.nlm.nih.gov/pubmed/2573519,http://www.ncbi.nlm.nih.gov/pubmed/10761920 | Are CD8+ (cytotoxic) T cells and CD4+ Helper T cells generated in the thyroid and express the T-cell receptor? | Through positive selection, double-positive cells in the thymus differentiate into CD4(+) or CD8(+) T single-positive cells that subsequently develop into different types of effective T cells, such as T-helper and cytotoxic T lymphocyte cells, These two cell types are derived from common precursors in the thymus.no, CD8+ (cytotoxic) T cells, like CD4+ Helper T cells, are generated in the thymus not the thyroid and express the T-cell receptor.The CD4(+) helper versus CD8(+) cytotoxic T-cell fate decision serves as an excellent model to study binary fate decision processes. These two cell types are derived from common precursors in the thymus. |
http://www.ncbi.nlm.nih.gov/pubmed/7886456,http://www.ncbi.nlm.nih.gov/pubmed/29764950,http://www.ncbi.nlm.nih.gov/pubmed/29432909,http://www.ncbi.nlm.nih.gov/pubmed/15610081,http://www.ncbi.nlm.nih.gov/pubmed/25539656,http://www.ncbi.nlm.nih.gov/pubmed/16583309,http://www.ncbi.nlm.nih.gov/pubmed/29446491,http://www.ncbi.nlm.nih.gov/pubmed/8341988 | What bacteria is associated with Gastric cancer and peptic ulcers? | Helicobacter pylori (H. pylori), a gram-negative microaerophilic bacterial pathogen that colonizes the stomachs of more than half of all humans, is linked to chronic gastritis, peptic ulcers and gastric cancer.Peptic ulcer and gastric cancer are caused by the same bacteria, Helicobacter pylori. |
http://www.ncbi.nlm.nih.gov/pubmed/28642124,http://www.ncbi.nlm.nih.gov/pubmed/28986324,http://www.ncbi.nlm.nih.gov/pubmed/17472569,http://www.ncbi.nlm.nih.gov/pubmed/20668093,http://www.ncbi.nlm.nih.gov/pubmed/30583877,http://www.ncbi.nlm.nih.gov/pubmed/27400454,http://www.ncbi.nlm.nih.gov/pubmed/30358836,http://www.ncbi.nlm.nih.gov/pubmed/22383888,http://www.ncbi.nlm.nih.gov/pubmed/21177255,http://www.ncbi.nlm.nih.gov/pubmed/25656686,http://www.ncbi.nlm.nih.gov/pubmed/31695145,http://www.ncbi.nlm.nih.gov/pubmed/26079385,http://www.ncbi.nlm.nih.gov/pubmed/25034271,http://www.ncbi.nlm.nih.gov/pubmed/26642438,http://www.ncbi.nlm.nih.gov/pubmed/28334749,http://www.ncbi.nlm.nih.gov/pubmed/27721240,http://www.ncbi.nlm.nih.gov/pubmed/29403030,http://www.ncbi.nlm.nih.gov/pubmed/31529216,http://www.ncbi.nlm.nih.gov/pubmed/23576953,http://www.ncbi.nlm.nih.gov/pubmed/28497201,http://www.ncbi.nlm.nih.gov/pubmed/29125980,http://www.ncbi.nlm.nih.gov/pubmed/25035419,http://www.ncbi.nlm.nih.gov/pubmed/23372043 | Is Huntington's disease is caused by expansion of a CTG repeat in the HTT gene on Chromosome 4? | No, Huntington's disease is caused by expansion of a CAG repeat (not CTG) in the HTT gene on Chromosome 4.Huntington's disease (HD) is caused by a CAG repeat expansion that encodes a polyglutamine (polyQ) expansion in the HD disease protein, huntingtin (HTT).Huntington disease (HD) is a dominantly inherited disorder caused by a CAG expansion mutation in the huntingtin (HTT) gene, |
http://www.ncbi.nlm.nih.gov/pubmed/23826567,http://www.ncbi.nlm.nih.gov/pubmed/26865172,http://www.ncbi.nlm.nih.gov/pubmed/19404956,http://www.ncbi.nlm.nih.gov/pubmed/15331626,http://www.ncbi.nlm.nih.gov/pubmed/25262961,http://www.ncbi.nlm.nih.gov/pubmed/24890515,http://www.ncbi.nlm.nih.gov/pubmed/19859718,http://www.ncbi.nlm.nih.gov/pubmed/20856225 | What is the purpose of the 123 dihydrorhodamine assay? | detection of inheritance pattern in thirty-three mexican males with chronic granulomatous diseaseDihydrorhodamine assays measure oxidative bursts and are used to quantify cell activation via respiratory bursts. Nitroblue-tetrazolium dye reduction test and 123 dihydro-rhodamine assay by flow cytometry are the screening tests for Chronic Granulomatous Disease.Dihydrorhodamine assay (DRB) is a simple, reliable, and valid method for studying oxidative stress, in particular oxidative stress and reactive oxygen species.We detected the female relatives within the families of male patients with CGD, and carried out the 123 dihydrorhodamine (DHR) assay in all female participants. Detection of inheritance pattern in thirty-three Mexican males with chronic granulomatous disease through 123 dihydrorhodamine assay. |
http://www.ncbi.nlm.nih.gov/pubmed/30088677,http://www.ncbi.nlm.nih.gov/pubmed/30360969,http://www.ncbi.nlm.nih.gov/pubmed/27993829,http://www.ncbi.nlm.nih.gov/pubmed/27993828,http://www.ncbi.nlm.nih.gov/pubmed/28622463,http://www.ncbi.nlm.nih.gov/pubmed/30360970,http://www.ncbi.nlm.nih.gov/pubmed/27988142,http://www.ncbi.nlm.nih.gov/pubmed/25681059,http://www.ncbi.nlm.nih.gov/pubmed/28838249,http://www.ncbi.nlm.nih.gov/pubmed/29566740,http://www.ncbi.nlm.nih.gov/pubmed/26693854 | What is the mode of action of filgotinib? | Filgotinib is an oral selective Janus kinase 1 (JAK1) inhibitor. It has been tested in patients with rheumatoid arthritis and Chroni's disease, and has been shown to be effective.Filgotinib (GLPG0634) is a selective inhibitor of Janus kinase 1 (JAK1) currently in development for the treatment of rheumatoid arthritis and Crohn's disease.Filgotinib is an oral selective JAK inhibitor. It works by inhibiting JAK1.Filgotinib (GLPG0634) is a selective inhibitor of Janus kinase 1 (JAK1).Filgotinib (GS-6034, formerly GLPG0634) is an oral, selective Janus kinase 1 (JAK1) inhibitor that showed early response and sustained efficacy in patients with rheumatoid arthritis and with Crohn's disease. Effect of filgotinib, a selective JAK 1 inhibitor, with and without methotrexate in patients with rheumatoid arthritis: patient-reported outcomes.Filgotinib is an oral selective JAK1 inhibitor. It has been tested in patients with rheumatoid arthritis and Chroni's disease, and has been shown to be safe and efficacious.Efficacy and safety of filgotinib, a selective Janus kinase 1 inhibitor,Selective inhibition of JAK-1 with filgotinib shows initial efficacy in RA with an encouraging safety profile in these exploratory studies. The selectivity of filgotinib for JAK1 may have theoretical advantages in terms of limiting toxicity. |
http://www.ncbi.nlm.nih.gov/pubmed/29413175,http://www.ncbi.nlm.nih.gov/pubmed/31286142,http://www.ncbi.nlm.nih.gov/pubmed/2881213,http://www.ncbi.nlm.nih.gov/pubmed/22119622,http://www.ncbi.nlm.nih.gov/pubmed/25356969,http://www.ncbi.nlm.nih.gov/pubmed/14526190,http://www.ncbi.nlm.nih.gov/pubmed/15764008,http://www.ncbi.nlm.nih.gov/pubmed/28927719,http://www.ncbi.nlm.nih.gov/pubmed/29134321,http://www.ncbi.nlm.nih.gov/pubmed/11723754 | Is Huntington's disease caused by a dominate or recessive gene? | Huntington's Disease (HD) is an autosomal dominant neurodegenerative diseaseHuntington's disease is caused by an autosomal dominant gene.Huntington's disease (HD) is an inherited NDD caused by autosomal-dominant expanded CAG trinucleotide repeat mutation in the gene coding for Huntingtin (Htt). |
http://www.ncbi.nlm.nih.gov/pubmed/26054767 | What is RiboTag profiling? | RiboTag is a flexible tool for measuring the translational state of targeted cells in heterogeneous cell cultures.Ribo tag is a flexible tool for measuring the translational state of targeted cells in heterogeneous cell types and organisms. It is a simple, sensitive, rapid and relatively cheap method for integrative epigenomic profiling. The method can be used to identify endogenous and ectopically expressed ribosomal RNAs (RP), which are then analyzed using a simple two-step protocol with 500-50,000 cells and reveals the interplay between genomic locations of ubiquitously expressed proteins.RiboTag is a flexible tool for measuring the translational state of targeted cells in heterogeneous cell cultures. RiboTag immunoprecipitation is capable of recovering high integrity RNA from small numbers of transfected cells that can then be interrogated by a variety of methods (e.g., RT-qPCR, PCR array, RNA-Seq) and compared with basal RNA expression of the entire culture. Co-transfection of RiboTag with small hairpin RNA (shRNA) constructs can validate and accurately assess the degree of gene expression knockdown. |
http://www.ncbi.nlm.nih.gov/pubmed/12381708,http://www.ncbi.nlm.nih.gov/pubmed/8707402,http://www.ncbi.nlm.nih.gov/pubmed/10408177,http://www.ncbi.nlm.nih.gov/pubmed/15378499 | Is there an increased risk of meningiomas in atomic bomb survivors? | Yes, the incidence of meningiomas is increased in atomic bomb survivors. |
http://www.ncbi.nlm.nih.gov/pubmed/30216534 | What is foliglurax? | Foliglurax is a positive allosteric modulator of the metabotropic glutamate receptor 4. Foliglurax induced a robust and dose-dependent reversal of parkinsonian motor symptoms in macaques, including bradykinesia, tremor, posture, and mobility. Moreover, PXT002331 strongly decreased dyskinesia severity, thus having therapeutic efficacy on both parkinsonian motor impairment and l-dopa-induced dyskinesia. It was the first compound of its class to enter phase IIa clinical trials. |
http://www.ncbi.nlm.nih.gov/pubmed/24038889 | What is the genetic basis for Cornelia de Lange's syndrome? | Mutations in five genes (NIPBL, SMC1A, SMC3, RAD21, and HDAC8), all regulators or structural components of cohesin, have been identified.Approximately 60% of Cornelia de Lange Syndrome (CdLS) cases are due to NIPBL mutations, 5% caused by mutations in SMC1A, RAD21, and HDAC8 and one proband was found to carry a mutation in SMC3. Mutations in five genes (NIPBL, SMC1A, SMC3, RAD21, and HDAC8), all regulators or structural components of cohesin, have been identified.Mutations in five genes (NIPBL, SMC1A, SMC3, RAD21, and HDAC8), all regulators or structural components of cohesin, have been identified. 60% of CdLS cases are due to NIPBL mutations, 5% caused by mutations in SMC1A, RAD21, and HDAC8 and one proband was found to carry a mutation in SMC3. |
http://www.ncbi.nlm.nih.gov/pubmed/30343431,http://www.ncbi.nlm.nih.gov/pubmed/30430918,http://www.ncbi.nlm.nih.gov/pubmed/30459840 | Are gut microbiota profiles altered by irradiation? | Yes, Irradiation profoundly impacted gut microbiota profiles |
http://www.ncbi.nlm.nih.gov/pubmed/27699239,http://www.ncbi.nlm.nih.gov/pubmed/29440769,http://www.ncbi.nlm.nih.gov/pubmed/27283895,http://www.ncbi.nlm.nih.gov/pubmed/29721382,http://www.ncbi.nlm.nih.gov/pubmed/26851185,http://www.ncbi.nlm.nih.gov/pubmed/27846884 | Is TIM-3 a target for cancer immunotherapy in NSCLC? | Yes. Furthermore, TIM-3 and CEACAM1 were strongly expressed simultaneously during long-term CIK culture and showed a significant and mutually positive correlation.Yes, TIM-3 has shown promising results in early phases of trials in NSCLC patients and can be a target for cancer immunotherapy.Yes, TIM-3 has emerged as an important target of cancer immunotherapy because of its preferential expression in NSCLC cell lines and its presence in 90% of tumors. (PMID: 21494614) We have developed a cancer vaccine in whichtim-3 is fused with dendritic cells resulting in the presentation of tumor antigens in the context of DC-mediated costimulation. This (CT)n element has been shown to induce poly(ADP-ribose) polymerase activation, and it has also been suggested thatTim-3 may act as a tumor suppressor gene, thus making it a potential therapeutic target of CDKN2A/PD- Our results imply that implementing combined treatment on CIK cells before transfusion via antibodies targeting PD-L1, LAG-3, TIM-3, and CEACAM-1 might improve the efficiency of CIK therapy for NSCLC patients. Furthermore, TIM-3 and CEACAM1 were strongly expressed simultaneously during long-term CIK culture and showed a significant and mutually positive correlation.Implementing combined treatment on CIK cells before transfusion via antibodies targeting PD-L1, LAG-3, TIM-3, and CEACAM-1 might improve the efficiency of CIK therapy for NSCLC patients. Our results imply that implementing combined treatment on CIK cells before transfusion via antibodies targeting PD-L1, LAG-3, TIM-3, and CEACAM-1 might improve the efficiency of CIK therapy for NSCLC patients. Cytometric profiling identified an immunologically "hot" cluster with abundant CD8+ T cells expressing high levels of PD-1 and TIM-3 and an immunologically "cold" cluster with lower relative abundance of CD8+ T cells and expression of inhibitory markers |
http://www.ncbi.nlm.nih.gov/pubmed/25376608 | How does LB-100 affect the DDR proteins (BRCA1, Chk2, and γH2AX)? | LB100 induced constitutive hyperphosphorylation of DDR proteins (BRCA1, Chk2, and gH2AX). |
http://www.ncbi.nlm.nih.gov/pubmed/29609813,http://www.ncbi.nlm.nih.gov/pubmed/28884707,http://www.ncbi.nlm.nih.gov/pubmed/29625810 | What particles is Hadron therapy using? | Hadron therapy is using proton beams. |
http://www.ncbi.nlm.nih.gov/pubmed/29850618,http://www.ncbi.nlm.nih.gov/pubmed/21576205,http://www.ncbi.nlm.nih.gov/pubmed/29321042,http://www.ncbi.nlm.nih.gov/pubmed/28830352 | Does an interferon (IFN) signature exist for SLE patients? | Interferon type I (IFN-I) plays a pivotal role in the pathogenesis of SLE. An IFN-I score (positive or negative), as a measure of IFN-I activation, is assessed using the expression values of IFN-I signature genes (IFI44, IFI44L, IFIT1, Ly6e, MxA, IFITM1) in CD14+ monocytes of cSLE patients and healthy controls (HCs). |
http://www.ncbi.nlm.nih.gov/pubmed/30082684 | Is AND-1/Ctf4 essential for proliferation? | Yes. AND-1 fork protection function prevents fork resection and is essential for proliferation.Yes. AND-1/Ctf4 bridges the CMG helicase and DNA polymerase alpha, facilitating replication. AND-1 depletion is incompatible with proliferation, owing to cells accumulating in G2 with activated DNA damage checkpoint. Replication without AND-1 causes fork speed slow-down and accumulation of long single-stranded DNA (ssDNA) gaps at the replication fork junction, with these regions being converted to DNA double strand breaks (DSBs) in G2. |
http://www.ncbi.nlm.nih.gov/pubmed/26780618,http://www.ncbi.nlm.nih.gov/pubmed/29549631,http://www.ncbi.nlm.nih.gov/pubmed/30312216,http://www.ncbi.nlm.nih.gov/pubmed/26838744 | Does the BRAFV600E mutation have an effect on clinical response to radioiodine therapy? | Yes, it has been suggested that patients with papillary thyroid cancer (PTC) harbouring the BRAF(V600E) mutation have a worse prognosis. |
http://www.ncbi.nlm.nih.gov/pubmed/29199006 | Which phosphatase is inhibited by LB-100? | LB-100 is a phosphatase 2A inhibitor |
http://www.ncbi.nlm.nih.gov/pubmed/29564954 | What are the most common side effects of amantadine ER? | The most common side effects of amantadine ER are hallucination, dizziness, orthostatic hypotension and pedal edema. |
http://www.ncbi.nlm.nih.gov/pubmed/25687811,http://www.ncbi.nlm.nih.gov/pubmed/21097454,http://www.ncbi.nlm.nih.gov/pubmed/25003065,http://www.ncbi.nlm.nih.gov/pubmed/19520879,http://www.ncbi.nlm.nih.gov/pubmed/24964430,http://www.ncbi.nlm.nih.gov/pubmed/3782278 | Which symptoms comprise Abdominal aortic aneurysm rupture Triad? | Classic triad of Abdominal aortic aneurysm rupture include shock, acute abdominal pain, and pulsatile abdominal mass. |
http://www.ncbi.nlm.nih.gov/pubmed/20051279,http://www.ncbi.nlm.nih.gov/pubmed/16937455,http://www.ncbi.nlm.nih.gov/pubmed/12752575,http://www.ncbi.nlm.nih.gov/pubmed/29237697,http://www.ncbi.nlm.nih.gov/pubmed/17880814,http://www.ncbi.nlm.nih.gov/pubmed/20200814,http://www.ncbi.nlm.nih.gov/pubmed/30501443,http://www.ncbi.nlm.nih.gov/pubmed/17880786,http://www.ncbi.nlm.nih.gov/pubmed/12497758,http://www.ncbi.nlm.nih.gov/pubmed/27555148,http://www.ncbi.nlm.nih.gov/pubmed/29383495,http://www.ncbi.nlm.nih.gov/pubmed/26354489,http://www.ncbi.nlm.nih.gov/pubmed/29874194,http://www.ncbi.nlm.nih.gov/pubmed/29866068,http://www.ncbi.nlm.nih.gov/pubmed/16938764,http://www.ncbi.nlm.nih.gov/pubmed/29255950,http://www.ncbi.nlm.nih.gov/pubmed/29492088,http://www.ncbi.nlm.nih.gov/pubmed/27698338,http://www.ncbi.nlm.nih.gov/pubmed/23056690,http://www.ncbi.nlm.nih.gov/pubmed/21073617,http://www.ncbi.nlm.nih.gov/pubmed/29334914,http://www.ncbi.nlm.nih.gov/pubmed/16197535 | List symptoms of Allgrove syndrome. | The classical clinical triad of the Allgrove syndrome includes alacrima, achalasia and adrenal insufficiency. It can be also associated with progressive peripheral neuropathy. |
http://www.ncbi.nlm.nih.gov/pubmed/28376128,http://www.ncbi.nlm.nih.gov/pubmed/29734786,http://www.ncbi.nlm.nih.gov/pubmed/29337289 | What is water radiolysis? | Water radiolysis involves chemical decomposition of the water molecule into free radicals after exposure to ionizing radiation. These free radicals have deleterious effects on normal cell physiology. |
http://www.ncbi.nlm.nih.gov/pubmed/29564954,http://www.ncbi.nlm.nih.gov/pubmed/29777529 | How do the plasma concentrations of amantadine extended release and amantadine immediate release compare? | When it is given at bedtime, it reaches plasma concentration approximately twice the level achieved by amantadine immediate release.When it is given at bedtime, it reaches plasma concentration approximately twice the level achieved by amantadine immediate release. PK modeling suggested the recommended daily ADS-5102 dosage (274 mg qhs) resulted in 1.4- to 2.0-fold higher amantadine plasma concentrations during the day versus amantadine IR. |
http://www.ncbi.nlm.nih.gov/pubmed/27083490 | Is the BAGEL algorithm used for arrayed CRISPR screens? | No. BAGEL (Bayesian Analysis of Gene EssentiaLity) is a supervised learning method for analyzing pooled library gene knockout screens. It offers significantly greater sensitivity than current methods, while computational optimizations reduce runtime by an order of magnitude. |
http://www.ncbi.nlm.nih.gov/pubmed/30279159,http://www.ncbi.nlm.nih.gov/pubmed/30040677,http://www.ncbi.nlm.nih.gov/pubmed/29343987,http://www.ncbi.nlm.nih.gov/pubmed/23696773,http://www.ncbi.nlm.nih.gov/pubmed/30926557,http://www.ncbi.nlm.nih.gov/pubmed/29634597,http://www.ncbi.nlm.nih.gov/pubmed/29148921 | What is included in the LACE Index? | The LACE index is a simple tool that includes 4 parameters: Length of stay, Acuity of admission, Comorbidity, and Emergency visits in the previous 6 months. It is used to predict early re-admission after hospital discharge. |
http://www.ncbi.nlm.nih.gov/pubmed/2202240,http://www.ncbi.nlm.nih.gov/pubmed/15219296,http://www.ncbi.nlm.nih.gov/pubmed/22463973,http://www.ncbi.nlm.nih.gov/pubmed/24791662,http://www.ncbi.nlm.nih.gov/pubmed/7492037,http://www.ncbi.nlm.nih.gov/pubmed/14585449 | Which drugs are included in GI cocktail? | "GI cocktail" is a mixture of liquid antacid, viscous lidocaine, and an anticholinergic. |
http://www.ncbi.nlm.nih.gov/pubmed/30308485 | Is AZD5153 active in prostate cancer? | Yes, AZD5153 was shown to be effective in treatment of prostate cancer.Yes. AZD5153, a novel BRD4 inhibitor, inhibits prostate cancer cell growth in vitro and in vivo. AZD5153 induced apoptosis activation and cell cycle arrest in prostate cancer cells. AZD5153 was non-cytotoxic to the prostate epithelial cells. |
http://www.ncbi.nlm.nih.gov/pubmed/30214018 | Is GRG5 involved only in late embryonic mouse development? | No. Groucho related gene 5 (GRG5) is a multifunctional protein that has been implicated in both early and late embryonic mouse development. |
http://www.ncbi.nlm.nih.gov/pubmed/29855508,http://www.ncbi.nlm.nih.gov/pubmed/29644336 | Are astronauts in higher risk for developing cancer? | No significant associations between space radiation dose and mortality were found using logistic regression with an internal reference group, adjusting for medical radiation. |
http://www.ncbi.nlm.nih.gov/pubmed/30194661,http://www.ncbi.nlm.nih.gov/pubmed/29889764,http://www.ncbi.nlm.nih.gov/pubmed/29335207,http://www.ncbi.nlm.nih.gov/pubmed/28737050,http://www.ncbi.nlm.nih.gov/pubmed/25249568,http://www.ncbi.nlm.nih.gov/pubmed/29946962,http://www.ncbi.nlm.nih.gov/pubmed/19033369,http://www.ncbi.nlm.nih.gov/pubmed/28525302,http://www.ncbi.nlm.nih.gov/pubmed/31749075,http://www.ncbi.nlm.nih.gov/pubmed/30320043,http://www.ncbi.nlm.nih.gov/pubmed/28255765,http://www.ncbi.nlm.nih.gov/pubmed/30303923,http://www.ncbi.nlm.nih.gov/pubmed/29476499,http://www.ncbi.nlm.nih.gov/pubmed/28323948,http://www.ncbi.nlm.nih.gov/pubmed/30551159 | Describe the mechanism of action of a drug Elagolix. | Elagolix is a novel, orally active, non-peptide, competitive gonadotropin-releasing hormone (GnRH) receptor antagonist. It is in development for the management of endometriosis with associated pain and heavy menstrual bleeding due to uterine fibroids. |
http://www.ncbi.nlm.nih.gov/pubmed/30102092,http://www.ncbi.nlm.nih.gov/pubmed/29889589,http://www.ncbi.nlm.nih.gov/pubmed/29096837,http://www.ncbi.nlm.nih.gov/pubmed/27271183,http://www.ncbi.nlm.nih.gov/pubmed/29124482,http://www.ncbi.nlm.nih.gov/pubmed/26848137,http://www.ncbi.nlm.nih.gov/pubmed/30403015,http://www.ncbi.nlm.nih.gov/pubmed/29842811,http://www.ncbi.nlm.nih.gov/pubmed/28300080,http://www.ncbi.nlm.nih.gov/pubmed/29547399,http://www.ncbi.nlm.nih.gov/pubmed/31350288,http://www.ncbi.nlm.nih.gov/pubmed/28209220,http://www.ncbi.nlm.nih.gov/pubmed/31032598,http://www.ncbi.nlm.nih.gov/pubmed/30596391 | Describe mechanism of action of volanesorsen. | Volanesorsen, is an antisense oligonucleotid that inhibits the production of the Apo C-III which is crucial in regulating TGs metabolism because it inhibits lipoprotein lipase (LPL) and hepatic lipase activity but also hepatic uptake of TGs-rich particles. It has been shown to decrease TGs by 70-80%. |
http://www.ncbi.nlm.nih.gov/pubmed/28544809,http://www.ncbi.nlm.nih.gov/pubmed/28298046,http://www.ncbi.nlm.nih.gov/pubmed/28849326 | What is the cyberknife used for? | CyberKnife(r) is a robotic stereotactic radiotherapy system |
http://www.ncbi.nlm.nih.gov/pubmed/29251678,http://www.ncbi.nlm.nih.gov/pubmed/28474297,http://www.ncbi.nlm.nih.gov/pubmed/29081841,http://www.ncbi.nlm.nih.gov/pubmed/29327913,http://www.ncbi.nlm.nih.gov/pubmed/30073633,http://www.ncbi.nlm.nih.gov/pubmed/29322231,http://www.ncbi.nlm.nih.gov/pubmed/29397193,http://www.ncbi.nlm.nih.gov/pubmed/27810860,http://www.ncbi.nlm.nih.gov/pubmed/29911447,http://www.ncbi.nlm.nih.gov/pubmed/28994564,http://www.ncbi.nlm.nih.gov/pubmed/27717299,http://www.ncbi.nlm.nih.gov/pubmed/30293481,http://www.ncbi.nlm.nih.gov/pubmed/28299955 | Is Niraparib effective for ovarian cancer? | Yes. Niraparib is an oral poly(ADP ribose) polymerase (PARP) inhibitor that is approved by the United States Food and Drug Administration and the European Medicines Agency for the maintenance treatment of women with recurrent ovarian cancer who are in complete or partial response to platinum-based chemotherapy. |
http://www.ncbi.nlm.nih.gov/pubmed/29186335,http://www.ncbi.nlm.nih.gov/pubmed/31583637 | Which portal has been developed to explore protein-protein interactions in cancer cell lines? | The OncoPPi Portal has been developed as an interactive web resource that allows investigators to access, manipulate and interpret a high-quality cancer-focused network of protein-protein interactions (PPIs) experimentally detected in cancer cell lines. To facilitate prioritization of PPIs for further biological studies, this resource combines network connectivity analysis, mutual exclusivity analysis of genomic alterations, cellular co-localization of interacting proteins and domain-domain interactions. Estimates of PPI essentiality allow users to evaluate the functional impact of PPI disruption on cancer cell proliferation. Furthermore, connecting the OncoPPi network with the approved drugs and compounds in clinical trials enables discovery of new tumor dependencies to inform strategies to interrogate undruggable targets like tumor suppressors. The OncoPPi Portal serves as a resource for the cancer research community to facilitate discovery of cancer targets and therapeutic development. |
http://www.ncbi.nlm.nih.gov/pubmed/24023392,http://www.ncbi.nlm.nih.gov/pubmed/17383248 | Are genes that escape X-chromosome inactivation related to mental impairment? | Yes. Genes that escape X-inactivation in humans have high intraspecific variability in expression, are associated with mental impairment but are not slow evolving.Yes, most of the X-chromosome inactivation genes shown to be associated with mental retardation are those encoding transcription factors involved in intellectual disability, such as X-linked Na(+) /H(+) exchanger 2 (NHE2), Sox 10, Endothelin-3 (EDN3) and SOX10. Some X- chromosome inactivation gene variants are associated with intellectual disability but not others.Genes that escape X-inactivation in humans have high intraspecific variability in expression, are associated with mental impairment but are not slow evolving. The newly described escape genes cluster on the X chromosome in the same chromosomal regions as the previously known escapees. There is an excess of escaping genes associated with mental retardation, consistent with this being a common phenotype of polyX phenotypes. |
http://www.ncbi.nlm.nih.gov/pubmed/12923522,http://www.ncbi.nlm.nih.gov/pubmed/12826600,http://www.ncbi.nlm.nih.gov/pubmed/12002677,http://www.ncbi.nlm.nih.gov/pubmed/29496966,http://www.ncbi.nlm.nih.gov/pubmed/23934081,http://www.ncbi.nlm.nih.gov/pubmed/27239700,http://www.ncbi.nlm.nih.gov/pubmed/30032211,http://www.ncbi.nlm.nih.gov/pubmed/29773831,http://www.ncbi.nlm.nih.gov/pubmed/30194269 | Which biological process takes place in nuclear speckles? | Speckles are subnuclear structures that are enriched in pre-messenger RNA splicing factors and are located in the interchromatin regions of the nucleoplasm of mammalian cells. They serve as splicing factor storage sites and play important roles in regulation of pre-mRNA splicing. |
http://www.ncbi.nlm.nih.gov/pubmed/29706538,http://www.ncbi.nlm.nih.gov/pubmed/27226577 | What is the effect of HMGB2 loss on CTCF clustering? | Depletion of the abundant HMGB2 protein occurs early on the path to senescence and coincides with the dramatic spatial clustering of CTCF. Knocking down HMGB2 suffices for senescence-induced CTCF clustering and for loop reshuffling, while ectopically expressing HMGB2 rescues these effects. |
http://www.ncbi.nlm.nih.gov/pubmed/28039265 | Has LB-100 been tested in clinical trials? | Yes, a phase I trial has been performed to assess the safety, tolerability, and potential activity of LB-100, a first-in-class small-molecule inhibitor of protein phosphatase 2A (PP2A) in adult patients with progressive solid tumors. |
http://www.ncbi.nlm.nih.gov/pubmed/25476604,http://www.ncbi.nlm.nih.gov/pubmed/25428347 | Which algorithms have been developed for analysing CRISPR/Cas9 knockout screens data? | HiTSelect and MAGeCK (Model-based Analysis of Genome-wide CRISPR/Cas9 Knockout) |
http://www.ncbi.nlm.nih.gov/pubmed/17179481,http://www.ncbi.nlm.nih.gov/pubmed/9209408 | Which cells are affected in radiation-induced leukemias? | Hemopoietic stem cells, the possible target cells for radiation-induced leukemias. |
http://www.ncbi.nlm.nih.gov/pubmed/29670566,http://www.ncbi.nlm.nih.gov/pubmed/24035927,http://www.ncbi.nlm.nih.gov/pubmed/30363378,http://www.ncbi.nlm.nih.gov/pubmed/18543333,http://www.ncbi.nlm.nih.gov/pubmed/23346238,http://www.ncbi.nlm.nih.gov/pubmed/28805568,http://www.ncbi.nlm.nih.gov/pubmed/28122431,http://www.ncbi.nlm.nih.gov/pubmed/30108543,http://www.ncbi.nlm.nih.gov/pubmed/29542093,http://www.ncbi.nlm.nih.gov/pubmed/15778909,http://www.ncbi.nlm.nih.gov/pubmed/28980176,http://www.ncbi.nlm.nih.gov/pubmed/28770096,http://www.ncbi.nlm.nih.gov/pubmed/29644334,http://www.ncbi.nlm.nih.gov/pubmed/28290191,http://www.ncbi.nlm.nih.gov/pubmed/17702633,http://www.ncbi.nlm.nih.gov/pubmed/21163736,http://www.ncbi.nlm.nih.gov/pubmed/16258207,http://www.ncbi.nlm.nih.gov/pubmed/29215823,http://www.ncbi.nlm.nih.gov/pubmed/23323136,http://www.ncbi.nlm.nih.gov/pubmed/20347841,http://www.ncbi.nlm.nih.gov/pubmed/16763974 | PDQ39 questionnaires is design for which disease? | PDQ39 is Parkinson's Disease Questionnaire that is used for assessment of quality of life in patients with Parkinson's Disease. |
http://www.ncbi.nlm.nih.gov/pubmed/30151703,http://www.ncbi.nlm.nih.gov/pubmed/29726787 | Is palbociclib effective for glioblastoma? | No. In a clinical trial palbociclib monotherapy was not an effective treatment for recurrent glioblastoma. |
http://www.ncbi.nlm.nih.gov/pubmed/30387809,http://www.ncbi.nlm.nih.gov/pubmed/29077914,http://www.ncbi.nlm.nih.gov/pubmed/29577948 | List five proteins with antioxidant properties? | thioredoxin 1 (Trx1),
peroxiredoxin 1 (Prx1),
GSH reductase (GSR),
phosphatase and tensin homolog (PTEN)
superoxide dismutase (SOD) |
http://www.ncbi.nlm.nih.gov/pubmed/30244834 | Does the Mcm2-Ctf4-Polα axis play a role in transfer of histones to leading strand DNA at the replication forks? | No, the Mcm2-Ctf4-Pola axis facilitates parental histone H3-H4 transfer to lagging strands. |
http://www.ncbi.nlm.nih.gov/pubmed/12021881,http://www.ncbi.nlm.nih.gov/pubmed/29864562,http://www.ncbi.nlm.nih.gov/pubmed/22874530,http://www.ncbi.nlm.nih.gov/pubmed/619442,http://www.ncbi.nlm.nih.gov/pubmed/30295882,http://www.ncbi.nlm.nih.gov/pubmed/21156709,http://www.ncbi.nlm.nih.gov/pubmed/31384940,http://www.ncbi.nlm.nih.gov/pubmed/8956889 | What is Scalp cirsoid aneurysms? | Cirsoid aneurysms are rare arteriovenous malformations of the scalp, which are usually of congenital etiology. They often present as an enlarging pulsatile scalp mass. |
http://www.ncbi.nlm.nih.gov/pubmed/28769756,http://www.ncbi.nlm.nih.gov/pubmed/26311780,http://www.ncbi.nlm.nih.gov/pubmed/27854160,http://www.ncbi.nlm.nih.gov/pubmed/19961535,http://www.ncbi.nlm.nih.gov/pubmed/23676464,http://www.ncbi.nlm.nih.gov/pubmed/21225301,http://www.ncbi.nlm.nih.gov/pubmed/23261988,http://www.ncbi.nlm.nih.gov/pubmed/26189928,http://www.ncbi.nlm.nih.gov/pubmed/23649844,http://www.ncbi.nlm.nih.gov/pubmed/30697589,http://www.ncbi.nlm.nih.gov/pubmed/31143934,http://www.ncbi.nlm.nih.gov/pubmed/25701871,http://www.ncbi.nlm.nih.gov/pubmed/16951681,http://www.ncbi.nlm.nih.gov/pubmed/30949481 | Which gene is frequently involved in autosomal dominant adult-onset demyelinating leukodystrophy (ADLD)? | Autosomal dominant leukodystrophy (ADLD) is an adult onset demyelinating disorder that is caused by duplications of the lamin B1 (LMNB1) gene. |
http://www.ncbi.nlm.nih.gov/pubmed/30220974,http://www.ncbi.nlm.nih.gov/pubmed/30327309 | What is the radiation-induced CD8 lymphocyte apoptosis (RILA) assay used for? | Radiation-induced lymphocyte apoptosis (RILA) has been suggested as a predictive assay for adverse late reactions after radiotherapy. |
http://www.ncbi.nlm.nih.gov/pubmed/29116076 | What are the puQTLs (promoter-usage Quantitative Trait Loci)? | The identification of genetic variants affecting gene expression, namely expression quantitative trait loci (eQTLs), has contributed to the understanding of mechanisms underlying human traits and diseases. The majority of these variants map in non-coding regulatory regions of the genome and their identification remains challenging. Regulatory variants associated with promoter usage (puQTLs) and enhancer activity (eaQTLs) have been mapped from 154 EBV-transformed lymphoblastoid cell lines, derived from unrelated individuals. There are five categories of genes associated with puQTLs, distinguishing single from multi-promoter genes. Among multi-promoter genes, puQTL effects are either specific to a single promoter or to multiple promoters with variable effect orientations. Regulatory variants associated with opposite effects on different mRNA isoforms suggest compensatory mechanisms occurring between alternative promoters. |
http://www.ncbi.nlm.nih.gov/pubmed/29932419,http://www.ncbi.nlm.nih.gov/pubmed/26970625,http://www.ncbi.nlm.nih.gov/pubmed/27285123,http://www.ncbi.nlm.nih.gov/pubmed/27979994,http://www.ncbi.nlm.nih.gov/pubmed/28275002,http://www.ncbi.nlm.nih.gov/pubmed/21106759 | Which is the main epigenetic difference between poised and constitutive enhancers? | We find that histone H3K27ac distinguishes active enhancers from inactive/poised enhancer elements containing H3K4me1 alone.Histone H3K27ac separates active from poised enhancers and predicts developmental state.. The poised enhancer signature, involving H3K4me1 and low levels of H3K27ac, has been reported to mark inactive enhancers that are poised for future activation.. Histone H3K27ac separates active from poised enhancers and predicts developmental state.. We find that histone H3K27ac distinguishes active enhancers from inactive/poised enhancer elements containing H3K4me1 alone.. These chromatin domains, mostly constitutive, may have been used as genomic niches where novel regulations could evolve due to both the preexistence of a structural backbone poised to integrate novel regulatory inputs, and a highly adaptive transcriptional readout. These results support a model in which the PRC2 complex is redistributed to poised enhancers in H3.3K27M mutant cells and contributes to tumorigenesis in part by locally enhancing H3K27me3, and hence silencing of tumor suppressor genesHistone H3K27ac distinguishes active enhancers from inactive/poised enhancer elements containing H3K4me1 alone. |
http://www.ncbi.nlm.nih.gov/pubmed/27699276 | What is PRL3-zumab? | PRL3-zumab is a first-in-class humanized antibody (PRL3-zumab) against PRL-3, an intracellular tumor-associated phosphatase upregulated in multiple human cancers, for unconventional cancer immunotherapies. PRL3-zumab specifically blocked PRL-3+, but not PRL-3-, orthotopic gastric tumors. In this setting, PRL3-zumab had better therapeutic efficacy as a monotherapy, rather than simultaneous combination with 5-fluorouracil or 5-fluorouracil alone. PRL3-zumab could also prevent PRL-3+ tumor recurrence. Mechanistically, we found that intracellular PRL-3 antigens could be externalized to become "extracellular oncotargets" that serve as bait for PRL3-zumab binding to potentially bridge and recruit immunocytes into tumor microenvironments for killing effects on cancer cells.PRL3-zumab is a humanized monoclonal antibody specific for the epithelial-cell-associated phosphatase 3 (PRL-3) protein. It is approved for treatment of non-small cell lung carcinoma, adenocarcinoma of the stomach and gastroesophageal Junction, and recurrent glioblastoma. |
http://www.ncbi.nlm.nih.gov/pubmed/29716948,http://www.ncbi.nlm.nih.gov/pubmed/28287096,http://www.ncbi.nlm.nih.gov/pubmed/23252559,http://www.ncbi.nlm.nih.gov/pubmed/25908516,http://www.ncbi.nlm.nih.gov/pubmed/28383032,http://www.ncbi.nlm.nih.gov/pubmed/23818763,http://www.ncbi.nlm.nih.gov/pubmed/25895472,http://www.ncbi.nlm.nih.gov/pubmed/27771610,http://www.ncbi.nlm.nih.gov/pubmed/28971328,http://www.ncbi.nlm.nih.gov/pubmed/25591799,http://www.ncbi.nlm.nih.gov/pubmed/24295377,http://www.ncbi.nlm.nih.gov/pubmed/27128461,http://www.ncbi.nlm.nih.gov/pubmed/29547835,http://www.ncbi.nlm.nih.gov/pubmed/23013465,http://www.ncbi.nlm.nih.gov/pubmed/24019545,http://www.ncbi.nlm.nih.gov/pubmed/27853960,http://www.ncbi.nlm.nih.gov/pubmed/30084668,http://www.ncbi.nlm.nih.gov/pubmed/23701975,http://www.ncbi.nlm.nih.gov/pubmed/23679664,http://www.ncbi.nlm.nih.gov/pubmed/27128217,http://www.ncbi.nlm.nih.gov/pubmed/21976547,http://www.ncbi.nlm.nih.gov/pubmed/22493422 | Which receptor is inhibited by Tivozanib? | Tivozanib is a selective inhibitor of vascular endothelial growth factor receptors (VEGFRs) 1, 2 and 3 tyrosine kinases. |
http://www.ncbi.nlm.nih.gov/pubmed/26305296,http://www.ncbi.nlm.nih.gov/pubmed/24717404,http://www.ncbi.nlm.nih.gov/pubmed/31327649,http://www.ncbi.nlm.nih.gov/pubmed/25106801,http://www.ncbi.nlm.nih.gov/pubmed/29788192 | Can discharge destinations be accurately predicted using the Risk Assessment and Prediction Tool (RAPT)? | Yes. The Risk Assessment and Prediction Tool (RAPT) appears to be a valuable predictor of discharge destination after orthopedic surgery and neurosurgical procedures. |
http://www.ncbi.nlm.nih.gov/pubmed/27984732 | What is Perturb-seq? | Perturb-seq is a technique that combines single-cell RNA sequencing (RNA-seq) and clustered regularly interspaced short palindromic repeats (CRISPR)-based perturbations to perform many such assays in a pool. Perturb-seq accurately identifies individual gene targets, gene signatures, and cell states affected by individual perturbations and their genetic interactions. By decomposing many high content measurements into the effects of perturbations, their interactions, and diverse cell metadata, Perturb-seq dramatically increases the scope of pooled genomic assays. |
http://www.ncbi.nlm.nih.gov/pubmed/21051355 | What is the content of the REPAIRtoire database? | The REPAIRtoire database collects and organizes the following types of information: (i) DNA damage linked to environmental mutagenic and cytotoxic agents, (ii) pathways comprising individual processes and enzymatic reactions involved in the removal of damage, (iii) proteins participating in DNA repair and (iv) diseases correlated with mutations in genes encoding DNA repair proteins. REPAIRtoire provides also links to publications and external databases. |
http://www.ncbi.nlm.nih.gov/pubmed/29532440 | Has amantadine ER been approved by the FDA? | Yes, amantadine ER is an US FDA-approved treatment. |
http://www.ncbi.nlm.nih.gov/pubmed/31171773 | Can PRL3-zumab inhibit PRL3+ cancer cells in vitro and in vivo? | PRL3-zumab specifically inhibits PRL3+ cancer cells in vivo, but not in vitro. |
http://www.ncbi.nlm.nih.gov/pubmed/25808775,http://www.ncbi.nlm.nih.gov/pubmed/30442398,http://www.ncbi.nlm.nih.gov/pubmed/30345741,http://www.ncbi.nlm.nih.gov/pubmed/19410375,http://www.ncbi.nlm.nih.gov/pubmed/20155985 | How rare are CTCs (circulating tumour cells) in the plasma of patients? | Circulating tumour cells (CTCs) are significantly rare entity in the blood of patients with non-small cell lung cancer (NSCLC) patients as well as in other types of cancer. Small-cell lung cancer cells are typically quiescent, whereas CTCs can be up-regulated in response to radiation or chemical agents and may contribute to tumorigenesis as an endogenous red cell marker.extremely lowHowever, largely because of the extremely low number of CTCs (as low as 1 in 10(9) hematologic cells) in the blood of patients, effective detection and separation of the rare cells remain a tremendous challenge.However, largely because of the extremely low number of CTCs (as low as 1 in 10(9) hematologic cells) in the blood of patients, effective detection and separation of the rare cells remain a tremendous challenge. However, selective capture and quantification of CTCs from whole blood was still full of challenge due to the extremely scare number of CTCs.We have focused on breast cancer as most clinical studies on CTC detection so far have been done in these patients. However, largely because of the extremely low number of CTCs (as low as 1 in 10(9) hematologic cells) in the blood of patients, effective detection and separation of the rare cells remain a tremendous challenge.CTCs are of extremely low number (as low as 1 in 10(9) hematologic cells) in the blood of patients.However, largely because of the extremely low number of CTCs (as low as 1 in 10(9) hematologic cells) in the blood of patients, effective detection and separation of the rare cells remain a tremendous challenge. This study reports a microfluidic-based optical sensing device for label-free detection of circulating tumor cells (CTCs), a rare cell species in blood circulation. |
http://www.ncbi.nlm.nih.gov/pubmed/19610053,http://www.ncbi.nlm.nih.gov/pubmed/24737302,http://www.ncbi.nlm.nih.gov/pubmed/26498171,http://www.ncbi.nlm.nih.gov/pubmed/24119926 | What is gamma sterilization used for? | Gamma sterilization of bone allografts is used as a gold standard method to provide safety against disease transmission. Also, gamma (g)-sterilization has been commonly employed for wide range of products as indicated by the pharmacopoeias. |
http://www.ncbi.nlm.nih.gov/pubmed/22713214,http://www.ncbi.nlm.nih.gov/pubmed/27883218,http://www.ncbi.nlm.nih.gov/pubmed/21151129,http://www.ncbi.nlm.nih.gov/pubmed/16009131,http://www.ncbi.nlm.nih.gov/pubmed/25707489,http://www.ncbi.nlm.nih.gov/pubmed/16087863,http://www.ncbi.nlm.nih.gov/pubmed/20610384,http://www.ncbi.nlm.nih.gov/pubmed/23771556 | Does Estrogen lead to forkhead FoxA1 activation? | The pioneer transcription factor FoxA1 plays an important role in estrogen signaling by opening closed chromatin and promoting recruitment of the estrogen receptor to its target regions in DNA.We showed that CTCF acts upstream of the "pioneer" factor FOXA1 in determining the genomic response to estrogen.The pioneer transcription factor FoxA1 plays an important role in estrogen signaling by opening closed chromatin and promoting recruitment of the estrogen receptor to its target regions in DNAYes, estrogen-induced transcriptional activation of FoxA1 is tightly regulated by estrogen receptor tyrosine kinase and enhances Forkhead protein expression.Yes, induction of forkhead FoxA1 activation by estrogen seems to result in increased expression of the ERK2/ERK1 pathway in breast cancer cells. (PMID: 21494614) We also find that the testis-specific variant of the FOXA1 gene, which encodes the triggering receptor encoded by exon 9 on estrogen, is recruited to kinetochores and contributes to estrogen-induced silencing of NF-kappaB activation at the mating-type locus. ( PMID: 20160027) |
http://www.ncbi.nlm.nih.gov/pubmed/12034848,http://www.ncbi.nlm.nih.gov/pubmed/12812979,http://www.ncbi.nlm.nih.gov/pubmed/16473935 | What is detected by the UV-damaged DNA-binding protein (UV-DDB) complex? | Upon UV irradiation of primate cells, UV-DDB associates tightly with chromatin and is involved in global genomic nucleotide excision repair (NER) in mammalian cells. |
http://www.ncbi.nlm.nih.gov/pubmed/29687260,http://www.ncbi.nlm.nih.gov/pubmed/29155416,http://www.ncbi.nlm.nih.gov/pubmed/30053275 | What is the current regulation of eye lens radiation exposure? | The reduction of the dose limit for eye lens from 150 to 20 mSv yr-1 must be implemented by EU member states by February 2018. Consequently, there is a requirement for all employers engaged with work with ionising radiation to have appropriate monitoring arrangements in place by this date to demonstrate that they can meet this new limit for all workers. Eye lens dose is conventionally monitored by specific dosemeters worn near the eye.
The yearly ocular lens dose, particularly for interventionists dealing with complex interventions, could cross the permitted yearly limit set by the new Euratom directive. Therefore, X-ray safety glasses would become mandatory for complex radiological vascular interventions. |
http://www.ncbi.nlm.nih.gov/pubmed/17724121,http://www.ncbi.nlm.nih.gov/pubmed/28039207,http://www.ncbi.nlm.nih.gov/pubmed/20407419,http://www.ncbi.nlm.nih.gov/pubmed/21811608,http://www.ncbi.nlm.nih.gov/pubmed/12802065 | Does association with the nuclear pore promote gene silencing? | MicroRNA (miRNA)-guided mRNA repression, mediated by the miRNA-induced silencing complex (miRISC), is an important component of post-transcriptional gene silencing. The nucleoporin Nup358 plays an important role in this process |
http://www.ncbi.nlm.nih.gov/pubmed/17358192,http://www.ncbi.nlm.nih.gov/pubmed/23077526,http://www.ncbi.nlm.nih.gov/pubmed/12386005 | Which methods are used for genome segmentation of gene expression data? | Most of the used methods are variations of Markov Models such as Markov Chain Monte Carlo (MCMC) or Combinatorial methods.We use piecewise constant intensity models with varying number of pieces, and show how a reversible jump Markov Chain Monte Carlo (RJMCMC) method can be used to obtain a posteriori distribution on the intensity of the patterns along the genome.We use piecewise constant intensity models with varying number of pieces, and show how a reversible jump Markov Chain Monte Carlo (RJMCMC) method can be used to obtain a posteriori distribution on the intensity of the patterns along the genome. We introduce Markov models for segmentation of symbolic sequences, extending a segmentation procedure based on the Jensen-Shannon divergence that has been introduced earlier. Our method is based on a combinatorial genome segmentation solely using information on combinations of epigenetic marks.. We introduce Markov models for segmentation of symbolic sequences, extending a segmentation procedure based on the Jensen-Shannon divergence that has been introduced earlier.. Our method is based on a combinatorial genome segmentation solely using information on combinations of epigenetic marks.. We use piecewise constant intensity models with varying number of pieces, and show how a reversible jump Markov Chain Monte Carlo (RJMCMC) method can be used to obtain a posteriori distribution on the intensity of the patterns along the genome.reversible jump markov chain monte carlo (rjmcmc) methodWe use piecewise constant intensity models with varying number of pieces, and show how a reversible jump Markov Chain Monte Carlo (RJMCMC) method can be used to obtain a posteriori distribution on the intensity of the patterns along the genome. We introduce Markov models for segmentation of symbolic sequences, extending a segmentation procedure based on the Jensen-Shannon divergence that has been introduced earlier. |
http://www.ncbi.nlm.nih.gov/pubmed/28427155,http://www.ncbi.nlm.nih.gov/pubmed/26287404,http://www.ncbi.nlm.nih.gov/pubmed/24878056,http://www.ncbi.nlm.nih.gov/pubmed/26087256,http://www.ncbi.nlm.nih.gov/pubmed/29273685,http://www.ncbi.nlm.nih.gov/pubmed/30575804,http://www.ncbi.nlm.nih.gov/pubmed/28467880,http://www.ncbi.nlm.nih.gov/pubmed/29744034,http://www.ncbi.nlm.nih.gov/pubmed/30215690,http://www.ncbi.nlm.nih.gov/pubmed/27346786,http://www.ncbi.nlm.nih.gov/pubmed/29847668,http://www.ncbi.nlm.nih.gov/pubmed/25105999 | Which receptor is inhibited by Teprotumumab? | Teprotumumab is a monoclonal inhibitory antibody targeting IGF-1 receptor. |
http://www.ncbi.nlm.nih.gov/pubmed/28974143,http://www.ncbi.nlm.nih.gov/pubmed/29403087,http://www.ncbi.nlm.nih.gov/pubmed/26074087,http://www.ncbi.nlm.nih.gov/pubmed/29105242,http://www.ncbi.nlm.nih.gov/pubmed/28676261 | What is the cause of the disease Xeroderma Pigmentosum? | Mutations in the ERCC1 or ERCC4 genes cause a remarkable array of rare inherited human disorders including specific forms of xeroderma pigmentosum. Individuals with NER-defective xeroderma pigmentosum (XP), in which bulky DNA lesions are not efficiently removed, are cancer-prone and suffer neurodegeneration. |
http://www.ncbi.nlm.nih.gov/pubmed/18846913,http://www.ncbi.nlm.nih.gov/pubmed/27142149,http://www.ncbi.nlm.nih.gov/pubmed/21772695,http://www.ncbi.nlm.nih.gov/pubmed/21927854,http://www.ncbi.nlm.nih.gov/pubmed/31022456,http://www.ncbi.nlm.nih.gov/pubmed/29501639,http://www.ncbi.nlm.nih.gov/pubmed/23105706,http://www.ncbi.nlm.nih.gov/pubmed/26474772,http://www.ncbi.nlm.nih.gov/pubmed/21254745 | List Alkaptonuria Triad. | Alkaptonuria is a rare inherited genetic disorder of tyrosine metabolism characterized by a triad of homogentisic aciduria, ochronosis, and arthritis. |
http://www.ncbi.nlm.nih.gov/pubmed/25376608 | Can LB-100 sensitize ovarian carcinoma to cisplatin? | Yes, LB100 sensitizes ovarian carcinoma cells to cisplatin-mediated cytotoxicity. |
http://www.ncbi.nlm.nih.gov/pubmed/29312798,http://www.ncbi.nlm.nih.gov/pubmed/27447964 | List T-UCRs that have been implicated in breast cancer | Long non-coding RNAs (lncRNAs) are transcripts longer than 200 bp with no protein-coding capacity. Transcribed ultraconserved regions (T-UCRs) are a type of lncRNA and are conserved among human, chick, dog, mouse and rat genomes. These sequences are involved in cancer biology and tumourigenesis. Overexpression of one specific T-UCRs named uc.63 is associated with bad outcome in luminal A subtype of breast cancer patients. Uc.38 negatively regulates the expression of the pre-B-cell leukaemia homeobox 1 (PBX1) protein and subsequently affects the expression of Bcl-2 family members, ultimately inducing breast cancer cell apoptosis. |
http://www.ncbi.nlm.nih.gov/pubmed/28588271 | How many different miRNAs can be upregulated by LB-100? | LB-100 has been reported to upregulate one miRNA, namely miR-181b-1. |
http://www.ncbi.nlm.nih.gov/pubmed/28382457,http://www.ncbi.nlm.nih.gov/pubmed/26640143,http://www.ncbi.nlm.nih.gov/pubmed/30323869 | Which T-UCRs have been implicated in gastric cancer? | Uc.160 is significantly down-regulated in gastric carcinomas and can inhibit the tumor growth both in vitro and in vivo, suggesting that uc.160 may be used as a diagnostic marker and therapeutic target of gastric malignancies. Uc.416+A is overexpressed in GC and is associated with cell growth through the regulation of IGFBP6 (insulin-like growth factor-binding protein 6) in gastric cancer (GC). |
http://www.ncbi.nlm.nih.gov/pubmed/29420200,http://www.ncbi.nlm.nih.gov/pubmed/30588322,http://www.ncbi.nlm.nih.gov/pubmed/28130918,http://www.ncbi.nlm.nih.gov/pubmed/29644080,http://www.ncbi.nlm.nih.gov/pubmed/29644082,http://www.ncbi.nlm.nih.gov/pubmed/29460699,http://www.ncbi.nlm.nih.gov/pubmed/27663753 | Which disease can be treated with Anifrolumab? | Anifrolumab is a type I interferon (IFN) receptor antagonist that has been shown to be effective for moderate-to-severe systemic lupus erythematosus (SLE). |