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http://www.ncbi.nlm.nih.gov/pubmed/31799626,http://www.ncbi.nlm.nih.gov/pubmed/31462144,http://www.ncbi.nlm.nih.gov/pubmed/31712269,http://www.ncbi.nlm.nih.gov/pubmed/31865463,http://www.ncbi.nlm.nih.gov/pubmed/33075123 | Are Toll-like receptors (TLRs) induced by microbes? | Yes,
Gram-negative bacteria and endogenous molecules coordinate to trigger inflammatory cascades via Toll-like receptor 4 to induce excessive expression of cytokines such as tumor necrosis factor-α and to activate NLRP3 inflammasome, a multiprotein complex that processes pro-interleukin-1β into its mature form. |
http://www.ncbi.nlm.nih.gov/pubmed/27843457,http://www.ncbi.nlm.nih.gov/pubmed/30651550,http://www.ncbi.nlm.nih.gov/pubmed/21364924,http://www.ncbi.nlm.nih.gov/pubmed/22396543 | What is a decoy exosome? | exosomes display a large repertoire of tumor antigens that induce autoantibodies and exert a decoy function against complement-mediated cytotoxicity. |
http://www.ncbi.nlm.nih.gov/pubmed/32859770,http://www.ncbi.nlm.nih.gov/pubmed/16155434,http://www.ncbi.nlm.nih.gov/pubmed/11886578,http://www.ncbi.nlm.nih.gov/pubmed/31998320,http://www.ncbi.nlm.nih.gov/pubmed/24141560,http://www.ncbi.nlm.nih.gov/pubmed/20067169,http://www.ncbi.nlm.nih.gov/pubmed/19209651,http://www.ncbi.nlm.nih.gov/pubmed/28654435,http://www.ncbi.nlm.nih.gov/pubmed/28941526,http://www.ncbi.nlm.nih.gov/pubmed/31937334,http://www.ncbi.nlm.nih.gov/pubmed/21087811,http://www.ncbi.nlm.nih.gov/pubmed/22428294,http://www.ncbi.nlm.nih.gov/pubmed/16037773,http://www.ncbi.nlm.nih.gov/pubmed/27690672,http://www.ncbi.nlm.nih.gov/pubmed/33223079 | Can you summarize Myasthenia Gravis? | Myasthenia gravis (MG) is a neuromuscular disease which affects the central nervous system, dorsal root ganglia of the spinal cord, heart and in certain cases the pancreas. Two thirds of MG cases result from sporadic genetic mutations, not inheritance, but their offspring may inherit it from them.Myasthenia gravis (MG) is a neuromuscular disease resulting from a disorder of the central nervous system. Pathogenesis is still unknown and temporal lobe has been thought to take part in the epileptogenesis. MG can be symptomatic of focal cortical malformation, in which there is intraepithelial (usually intraepidermal) infiltration by neoplastic cells showing glandular differentiation. Clinical symptoms occur first after an age of approximately 30 years. Main manifestations include cognitive decline, parkinsonism, features of spinocerebellar degeneration, and peripheralMyasthenia gravis is a rare and invalidating disease affecting the neuromuscular junction of voluntary muscles. The classical form of this autoimmune disease is characterized by the presence of antibodies against the most abundant protein in the neuromuscular junction, the nicotinic acetylcholine receptor.Myasthenia gravis is a rare and invalidating disease affecting the neuromuscular junction of voluntary muscles. The classical form of this autoimmune disease is characterized by the presence of antibodies against the most abundant protein in the neuromuscular junction, the nicotinic acetylcholine receptor. Other variants of the disease involve autoimmune attack of non-receptor scaffolding proteins or enzymes essential for building or maintaining the integrity of this peripheral synapse.Myasthenia gravis (MG) is a neuromuscular disease resulting from a disorder of the extrapyramidal system. Pathogenesis is still unknown and temporal lobe has been thought to take part in the pathogenesis. MG can be symptomatic of focal cortical malformation, and few cases were reported. Clinical symptoms occur first after an age of approximately 30 years. Main manifestations include central nervous system (CNS) and retinal haemangioblastomas, endolymphatic sac tumors, clear-cell renal cell carcinomas (RCC), phaeoch |
http://www.ncbi.nlm.nih.gov/pubmed/22470656,http://www.ncbi.nlm.nih.gov/pubmed/25017277,http://www.ncbi.nlm.nih.gov/pubmed/10465109,http://www.ncbi.nlm.nih.gov/pubmed/1853883,http://www.ncbi.nlm.nih.gov/pubmed/15772095,http://www.ncbi.nlm.nih.gov/pubmed/12107442,http://www.ncbi.nlm.nih.gov/pubmed/29866251,http://www.ncbi.nlm.nih.gov/pubmed/16418967,http://www.ncbi.nlm.nih.gov/pubmed/10802661,http://www.ncbi.nlm.nih.gov/pubmed/25635170,http://www.ncbi.nlm.nih.gov/pubmed/6495304,http://www.ncbi.nlm.nih.gov/pubmed/9467007,http://www.ncbi.nlm.nih.gov/pubmed/12026212,http://www.ncbi.nlm.nih.gov/pubmed/8985498,http://www.ncbi.nlm.nih.gov/pubmed/22090721,http://www.ncbi.nlm.nih.gov/pubmed/3314666 | What 3 disorders are commonly associated with Kaufman-McKusick syndrome? | McKusick-Kaufman syndrome (MKKS) is a rare, recessively inherited syndrome reported mainly in young children. It is characterised by vaginal atresia with hydrometrocolpos, postaxial polydactyly, and congenital heart defect.Clinical symptoms of Kaufman-McKusick syndrome (KM) include postaxial polydactyly, hydrometrocolpos, and congenital heart disease.Mekusick-Kusick syndrome is a rare autosomal recessive disorder characterized by the triad of hydrometrocolpos, postaxial polydactyly, and congenital heart disease.McKusick-Kaufman Syndrome (MKKS) is a rare, recessively inherited syndrome reported mainly in young children. It is characterised by vaginal atresia with hydrometrocolpos, postaxial polydactyly, and congenital heart defect.MKKS) is one of rare syndromes which presents as polydactyly, hydrometrocolpos (HMC) and cardiac anomalies.McKusick-Kaufman syndrome (MKKS) is a rare, recessively inherited syndrome reported mainly in young children and is characterised by vaginal atresia with hydrometrocolpos, postaxial polydactyly, and congenital heart defect.The Kaufman-McKusick syndrome (MK 23670) AKA McKusik-Kaufman syndrome, is a rare autosomal recessive disorder characterized by the triad of hydrometrocolpos, postaxial polydactyly, and congenital heart disease |
http://www.ncbi.nlm.nih.gov/pubmed/21153754,http://www.ncbi.nlm.nih.gov/pubmed/26336217,http://www.ncbi.nlm.nih.gov/pubmed/11296828,http://www.ncbi.nlm.nih.gov/pubmed/25236960,http://www.ncbi.nlm.nih.gov/pubmed/12938010,http://www.ncbi.nlm.nih.gov/pubmed/31943036,http://www.ncbi.nlm.nih.gov/pubmed/14500917,http://www.ncbi.nlm.nih.gov/pubmed/27473852,http://www.ncbi.nlm.nih.gov/pubmed/25035799,http://www.ncbi.nlm.nih.gov/pubmed/21028959,http://www.ncbi.nlm.nih.gov/pubmed/20101443,http://www.ncbi.nlm.nih.gov/pubmed/30914054,http://www.ncbi.nlm.nih.gov/pubmed/32327327,http://www.ncbi.nlm.nih.gov/pubmed/23077588,http://www.ncbi.nlm.nih.gov/pubmed/31887120,http://www.ncbi.nlm.nih.gov/pubmed/32723642,http://www.ncbi.nlm.nih.gov/pubmed/29448923,http://www.ncbi.nlm.nih.gov/pubmed/28173840,http://www.ncbi.nlm.nih.gov/pubmed/33010631,http://www.ncbi.nlm.nih.gov/pubmed/14570115,http://www.ncbi.nlm.nih.gov/pubmed/17089744,http://www.ncbi.nlm.nih.gov/pubmed/23444797,http://www.ncbi.nlm.nih.gov/pubmed/25333277,http://www.ncbi.nlm.nih.gov/pubmed/12422585,http://www.ncbi.nlm.nih.gov/pubmed/26586535,http://www.ncbi.nlm.nih.gov/pubmed/30207871,http://www.ncbi.nlm.nih.gov/pubmed/19184580,http://www.ncbi.nlm.nih.gov/pubmed/25434042,http://www.ncbi.nlm.nih.gov/pubmed/31720842,http://www.ncbi.nlm.nih.gov/pubmed/16350531,http://www.ncbi.nlm.nih.gov/pubmed/30079309,http://www.ncbi.nlm.nih.gov/pubmed/27263092,http://www.ncbi.nlm.nih.gov/pubmed/33059172,http://www.ncbi.nlm.nih.gov/pubmed/31031164,http://www.ncbi.nlm.nih.gov/pubmed/23975565,http://www.ncbi.nlm.nih.gov/pubmed/19998007,http://www.ncbi.nlm.nih.gov/pubmed/12880241,http://www.ncbi.nlm.nih.gov/pubmed/27286701,http://www.ncbi.nlm.nih.gov/pubmed/33002807 | Is Ixodes a species of tick? | Ixodes is a family of hard ticks.tick, Ixodes ricinusYes, Ixodes is a species of tick.ixodid ticks hard ticks (family Ixodidae) |
http://www.ncbi.nlm.nih.gov/pubmed/32459621,http://www.ncbi.nlm.nih.gov/pubmed/30676276,http://www.ncbi.nlm.nih.gov/pubmed/28279942,http://www.ncbi.nlm.nih.gov/pubmed/29987197,http://www.ncbi.nlm.nih.gov/pubmed/29502883,http://www.ncbi.nlm.nih.gov/pubmed/26282413,http://www.ncbi.nlm.nih.gov/pubmed/25726133,http://www.ncbi.nlm.nih.gov/pubmed/32790662,http://www.ncbi.nlm.nih.gov/pubmed/31668935,http://www.ncbi.nlm.nih.gov/pubmed/30969148,http://www.ncbi.nlm.nih.gov/pubmed/21730079,http://www.ncbi.nlm.nih.gov/pubmed/21219741,http://www.ncbi.nlm.nih.gov/pubmed/33134040,http://www.ncbi.nlm.nih.gov/pubmed/29322859,http://www.ncbi.nlm.nih.gov/pubmed/32461409 | What is the active ingredient in the most common hand sanitizer? | Evaluation of a benzalkonium chloride hand sanitizer in reducing transient Staphylococcus aureus bacterial skin contamination in health care workers.The active ingredient is isopropyl alcohol, which is an alcohol-based hand sanitizer.The active ingredients in most hand sanitizers include ethanol, benzalkonium chloride, isopropanol, alcohol, bzk, 70% ethanol and soap.The active ingredient in the most common hand sanitizer is ethanol, benzalkonium chloride, isopropanol, alcohol, bzk, 70% ethanol.While there is a new commercially available hand sanitizer using 0.12% benzalkonium chloride (BZK) as the active ingredient in hand sanitizer, most hand sanitizers are 70-80% ethanol-based or 75% isopropanol |
http://www.ncbi.nlm.nih.gov/pubmed/31785606 | Which was the first oral drug for the treatment of multiple sclerosis by the US Food and Drug Administration (FDA)? | FTY720 (Fingolimod) was approved as the first oral drug for the treatment of multiple sclerosis by the US Food and Drug Administration (FDA) in 2010. |
http://www.ncbi.nlm.nih.gov/pubmed/30776422 | Which S1P receptors does fingolimod bind to? | Pharmacologically, fingolimod has been characterized as a non-selective agonist of all of the S1P receptors (S1PR), with the exception of S1P2. |
http://www.ncbi.nlm.nih.gov/pubmed/30776422 | What was fingolimod synthesized from? | FTY720 (fingolimod, Gilenya®) was synthesized from myriocin, one of the metabolites of the fungus Isaria sinclairii known from traditional Chinese medicine for its antibacterial and energy boosting effect. |
http://www.ncbi.nlm.nih.gov/pubmed/29938336 | What does fingolimod do to the grey matter of the brain? | Fingolimod has been shown to reduce/prevent both focal and diffuse grey matter (GM) damage in active multiple sclerosis. The percentage of patients with new cortical lesions (CL) (13.5 vs. 89%, p < 0.001) and the percentage of GM volume change was lower in the fingolimod treated group (p < 0.001). The regional analysis revealed that the treated group had also less volume loss in thalamus, caudatus, globus pallidus, cingulate cortex, and hippocampus (p < 0.001), as well as in, cerebellum, superior frontal gyrus, and insular-long gyrus (p < 0.05). |
http://www.ncbi.nlm.nih.gov/pubmed/22494956 | What doses of fingolimod were administered during the FREEDOMS trial? | In the FREEDOMS trial fingolimod was administered at 0.5mg or 1.25mg doses. |
http://www.ncbi.nlm.nih.gov/pubmed/22494956 | How many patients were enrolled in the FREEDOMS clinical trial? | FREEDOMS study, a randomised, double-blind study included 1272 patients with relapsing-remitting MS. |
http://www.ncbi.nlm.nih.gov/pubmed/14871168,http://www.ncbi.nlm.nih.gov/pubmed/23747003,http://www.ncbi.nlm.nih.gov/pubmed/21221669,http://www.ncbi.nlm.nih.gov/pubmed/32091988,http://www.ncbi.nlm.nih.gov/pubmed/32250472,http://www.ncbi.nlm.nih.gov/pubmed/28629634,http://www.ncbi.nlm.nih.gov/pubmed/19273924,http://www.ncbi.nlm.nih.gov/pubmed/17986501,http://www.ncbi.nlm.nih.gov/pubmed/31889644,http://www.ncbi.nlm.nih.gov/pubmed/18786893,http://www.ncbi.nlm.nih.gov/pubmed/10732662,http://www.ncbi.nlm.nih.gov/pubmed/8098852,http://www.ncbi.nlm.nih.gov/pubmed/19039478,http://www.ncbi.nlm.nih.gov/pubmed/27333537,http://www.ncbi.nlm.nih.gov/pubmed/539757,http://www.ncbi.nlm.nih.gov/pubmed/30838249,http://www.ncbi.nlm.nih.gov/pubmed/27064462,http://www.ncbi.nlm.nih.gov/pubmed/16690695,http://www.ncbi.nlm.nih.gov/pubmed/9163399,http://www.ncbi.nlm.nih.gov/pubmed/28017248 | What is blepharospasm? | The neurophysiological disruptions underlying blepharospasm, a disabling movement disorder characterized by increased blinking and involuntary muscle spasms of the eyelid, remain poorly understood.Yes, blepharospasm is an adult-onset dystonia typically present at rest and exacerbated by bright light, stress and voluntary movements of eyes and eyelids.Blepharospasm is a type of focal dystonia depicted by periodic and spontaneous closure of the orbicularis oculi and surrounding muscles.Blepharospasm (BL) is characterized by involuntary closures of the eyelids due to spasms of the orbicularis oculi muscle.Blepharospasm is a type of focal dystonia. It is a movement disorder characterized by periodic and spontaneous closure of the orbicularis oculi muscle and surrounding muscles.Blepharospasm is a type of focal dystonia. It's a movement disorder characterized by periodic and spontaneous closure of the orbicularis oculi muscle and surrounding muscles.Blepharospasm is a type of focal dystonia. It's a movement disorder characterized by periodic and spontaneous closure of the orbicularis oculi and surrounding muscles.Blepharospasm means involuntary twitching, blinking or closure of the eyelids resulting from any cause. |
http://www.ncbi.nlm.nih.gov/pubmed/31951127,http://www.ncbi.nlm.nih.gov/pubmed/32935287,http://www.ncbi.nlm.nih.gov/pubmed/31043521 | Explain the action of Balovaptan. | Balovaptan is a low-molecular-weight, orally active, hydrophilic non-peptide molecule that blocks Vasopressin-1a. It is approved for the treatment of autism spectrum disorders (ASD).Balovaptan is an investigational vasopressin 1a receptor antagonist that has been evaluated for improvement of social communication and interaction.Balovaptan, an orally administered selective vasopressin V1a receptor antagonist which can penetrate the blood brain barrier.Yes, Balovaptan, an investigational vasopressin 1a receptor antagonist that has been evaluated for improvement of social communication and interaction.Balovaptan is an orally administered selective vasopressin V1a receptor antagonis. Balovaptan has been evaluated for improvement of social communication and interaction.Balovaptan is an orally administered small molecule that binds to mTORC1 and inhibits activation of the mTOR signalling pathway. It is approved for treatment of children with autism spectrum disorders.Balovaptan is a low-molecular-weight, orally active, hydrophilic non-peptide dual antagonist of both the V1a and V2a receptors that is approved for the treatment of autism spectrum disorders (ASD) in children and adults with intellectual disability. |
http://www.ncbi.nlm.nih.gov/pubmed/19890158,http://www.ncbi.nlm.nih.gov/pubmed/12573901,http://www.ncbi.nlm.nih.gov/pubmed/21705716,http://www.ncbi.nlm.nih.gov/pubmed/12505450,http://www.ncbi.nlm.nih.gov/pubmed/17622711,http://www.ncbi.nlm.nih.gov/pubmed/32891999,http://www.ncbi.nlm.nih.gov/pubmed/32777607,http://www.ncbi.nlm.nih.gov/pubmed/22470480,http://www.ncbi.nlm.nih.gov/pubmed/30359670,http://www.ncbi.nlm.nih.gov/pubmed/17689037,http://www.ncbi.nlm.nih.gov/pubmed/27089241,http://www.ncbi.nlm.nih.gov/pubmed/25619032,http://www.ncbi.nlm.nih.gov/pubmed/28774890,http://www.ncbi.nlm.nih.gov/pubmed/24171222,http://www.ncbi.nlm.nih.gov/pubmed/26821503,http://www.ncbi.nlm.nih.gov/pubmed/32861950,http://www.ncbi.nlm.nih.gov/pubmed/27177772,http://www.ncbi.nlm.nih.gov/pubmed/29874946,http://www.ncbi.nlm.nih.gov/pubmed/30257398,http://www.ncbi.nlm.nih.gov/pubmed/27641926,http://www.ncbi.nlm.nih.gov/pubmed/12387626,http://www.ncbi.nlm.nih.gov/pubmed/12767684,http://www.ncbi.nlm.nih.gov/pubmed/33049673,http://www.ncbi.nlm.nih.gov/pubmed/33049674 | what is the effect of Bisphenol A in the body? | Bisphenol A (BPA) is an endocrine-disruptor compound that exhibits estrogenic activitBPA is considered an endocrine disruptor and several studies have proposed a relationship between exposure to BPA and the appearance of adverse health effects, such as cancer, infertility, diabetes, and obesity, among others.Bisphenol A is an endocrine-disruptor compound, that exhibits estrogenic activity, can affect male fertility, and can modulate the immune response to infections. It is also associated with increased risk of obesity and diabetes.Bisphenol A (BPA) is an endocrine disruptor that modulates the immune response to infections. |
http://www.ncbi.nlm.nih.gov/pubmed/30632771,http://www.ncbi.nlm.nih.gov/pubmed/32260553,http://www.ncbi.nlm.nih.gov/pubmed/31998446,http://www.ncbi.nlm.nih.gov/pubmed/16440601 | List the main proteins found in human saliva. | Amylases
Cystatins
Immunoglobulins
Mucins |
http://www.ncbi.nlm.nih.gov/pubmed/32913038 | Is HbA1c an ideal biomarker of well-controlled diabetes? | No. The HbA1c is a biomarker with a central role in the diagnosis and follow-up of patients with diabetes mellitus, although not a perfect one. It is associated with high morbidity and mortality, and is not an ideal biomarker for assessment of well-controlled diabetes.No. HbA1c is a biomarker with a central role in the diagnosis and follow-up of patients with diabetes, although not a perfect one. Common comorbidities encountered in patients with diabetes mellitus, such as renal insufficiency, high output states (iron deficiency anaemia, haemolytic anaemia, haemoglobinopathies and pregnancy) and intake of specific drugs could compromise the sensitivity and specificity of the biomarker. COVID-19 pandemic poses a pressing challenge for the diabetic population, since maintaining optimal blood glucose control is key to reduce morbidity and mortality rates.No, HbA1c is not an ideal biomarker of well-controlled diabetes.No. The HbA1c is a biomarker with a central role in the diagnosis and follow-up of patients with diabetes mellitus, although not a perfect one. It is associated with poor prognosis in patients with type 2 diabetes and is an ideal biomarker for the diagnosis of Type 2 diabetes. |
http://www.ncbi.nlm.nih.gov/pubmed/31684860 | Which tool has been developed for microRNA-target enrichment and network-based analysis? | MIENTURNET (MicroRNA ENrichment TURned NETwork) is a web tool that receives in input a list of miRNAs or mRNAs and tackles the problem of prioritizing miRNA-target interactions by performing a statistical analysis followed by a fully featured network-based visualization and analysis. The statistics is used to assess the significance of an over-representation of miRNA-target interactions and then MIENTURNET filters based on the statistical significance associated with each miRNA-target interaction. In addition, the holistic approach of the network theory is used to infer possible evidences of miRNA regulation by capturing emergent properties of the miRNA-target regulatory network that would be not evident through a pairwise analysis of the individual components.MIENTURNET (MicroRNA ENrichment TURned NETwork) is an interactive web tool for microRNA-target enrichment and network-based analysis.MIENTURNET is a web tool for microRNA-target enrichment and network-based analysis. MIENTURNET offers the possibility to consistently perform both statistical and network-based analyses. |
http://www.ncbi.nlm.nih.gov/pubmed/30497369 | List example genes that SWIM tool has identified and which are down-regulated in glioblastoma | SWIM is a software able to unveil a small pool of genes - called switch genes - critically associated with drastic changes in cell phenotype. Applying SWIM to the expression profiling of glioblastoma stem-like cells and conventional glioma cell lines identifies switch genes related to stem-like phenotype. SWIM identifies 171 switch genes that are all down-regulated in glioblastoma stem-like cells. This list encompasses genes like CAV1, COL5A1, COL6A3, FLNB, HMMR, ITGA3, ITGA5, MET, SDC1, THBS1, and VEGFC, involved in "ECM-receptor interaction" and "focal adhesion" pathways.This list encompasses genes like CAV1, COL5A1, COL6A3, FLNB, HMMR, ITGA3, ITGA5, MET, SDC1, THBS1, and VEGFC, involved in "ECM-receptor interaction" and "focal adhesion" pathways.SWIM tool has identified and which genes are down-regulated in glioblastoma. These include the genes: itga3, hmmr, sox2, cav1, itga5, thbs1, sdc1, col6a3, col5a1 and sall2.SWIM tool has identified and which genes are down-regulated in glioblastoma and which are important for tumorigenesis: met, vegfc, flnb, itga3, hmmr, sox2, cav1, itGA5, thbs1, sdc1, col6a3, col5a1 and sall2.SWIM identifies 171 switch genes that are all down-regulated in glioblastoma stem-like cells. This list encompasses genes like CAV1, COL5A1, COL6A3, FLNB, HMMR, ITGA3, ITGA5, MET, SDC1, THBS1, and VEGFC, involved in "ECM-receptor interaction" and "focal adhesion" pathways |
http://www.ncbi.nlm.nih.gov/pubmed/28317894 | Describe SWItchMiner (SWIM) | SWItchMiner (SWIM) is a wizard-like software implementation of a procedure, previously described, able to extract information contained in complex networks. Specifically, SWIM allows unearthing the existence of a new class of hubs, called "fight-club hubs", characterized by a marked negative correlation with their first nearest neighbors. Among them, a special subset of genes, called "switch genes", appears to be characterized by an unusual pattern of intra- and inter-module connections that confers them a crucial topological role, interestingly mirrored by the evidence of their clinic-biological relevance.SWItchMiner (SWIM) is a wizard-like software implementation of a procedure, previously described, able to extract information contained in complex networks. SWIM allows unearthing the existence of a new class of hubs, called "fight-club hubs", characterized by a marked negative correlation with their first nearest neighbors. |
http://www.ncbi.nlm.nih.gov/pubmed/27476701 | What promotes amyloid-peptide beta 42 (Aβ42) accumulation in neuroblastoma cells? | The apolipoprotein (apo) E4 isoform is the strongest risk factor for late-onset Alzheimer's disease (AD). ApoE4 is more susceptible to proteolysis than apoE2 and apoE3 isoforms and carboxyl-terminal truncated apoE4 forms have been found in AD patients' brain. A specific apoE4 fragment, apoE4-165, promotes amyloid-peptide beta 42 (Aβ42) accumulation in human neuroblastoma SK-N-SH cells and increased intracellular reactive oxygen species formation, two events considered to occur early in AD pathogenesis.The amyloid-peptide beta 42 (Aβ42) accumulates in neuroblastoma cells due to a protein called apoE4-165, which is an apolipoprotein (APOE4). This protein is the most common protein responsible for late-onset Alzheimer disease. |
http://www.ncbi.nlm.nih.gov/pubmed/31752933 | Which method has been developed for detection of ATAC-seq or ChIP-seq signals with DNA methylation? | EpiMethylTag is a fast, low- input, low sequencing depth method that combines ATAC-seq or ChIP-seq (M-ATAC or M-ChIP) with bisulfite conversion, to simultaneously examine accessibility/TF binding and methylation on the same DNA.EpiMethyl tag is a method that combines ATAC-seq or ChIP-seq (M-ATAC or M-ChIP) with bisulfite conversion, to simultaneously examine accessibility/TF binding and methylation on the same DNA.Activation of regulatory elements is thought to be inversely correlated with DNA methylation levels. However, it is difficult to determine whether DNA methylation is compatible with chromatin accessibility or transcription factor (TF) binding if assays are performed separately. EpiMethylTag is a fast, low-input, low sequencing depth method that combines ATAC-seq or ChIP-seq (M-ATAC or M-ChIP) with bisulfite conversion, to simultaneously examine accessibility/TF binding and methylation on the same DNA.EpiMethyl tag is a fast, low- input, low sequencing depth method that combines ATAC-seq or ChIP-seq (M-ATAC or M-ChIP) with bisulfite conversion, to simultaneously examine accessibility/TF binding and methylation on the same DNA.EpiMethylTag is a fast, low- input, low sequencing depth method that combines ATAC-seq or ChIP-seq (M-ATAC or M-ChIP) with bisulfite conversion to simultaneously examine accessibility/TF binding and methylation on the same DNA.EpiMethyl tag is a technology that combines ATAC-seq or ChIP-seq (M-ATAC or M-ChIP) with bisulfite conversion, to simultaneously examine accessibility/TF binding and methylation on the same DNA. |
http://www.ncbi.nlm.nih.gov/pubmed/31548608 | Which protein is involved in the organization and regulation of pluripotency-associated three-dimensional enhancer networks? | KLF4 is involved in the organization and regulation of pluripotency-associated three-dimensional enhancer networks.KLF4 is involved in the organization and regulation of pluripotency-associated three-dimensional enhancer networks. Cell fate transitions are accompanied by global transcriptional, epigenetic and topological changes driven by transcription factors. Inducible depletion of KLF factors in PSCs caused a genome-wide decrease in enhancer connectivity.KLF4 is involved in the organization and regulation of pluripotency-associated three-dimensional enhancers networks.KLF4 is involved in the organization and regulation of pluripotency-associated three-dimensional enhancer networks. How transcription factors orchestrate the complex molecular changes around their target gene loci remains incompletely understood.KLF4 is involved in the organization and regulation of pluripotency-associated enhancer networks. How transcription factors orchestrate the complex molecular changes around their target gene loci remains incompletely understood. |
http://www.ncbi.nlm.nih.gov/pubmed/31974377,http://www.ncbi.nlm.nih.gov/pubmed/31557134,http://www.ncbi.nlm.nih.gov/pubmed/31995643,http://www.ncbi.nlm.nih.gov/pubmed/31692367 | Where is the agouti-related peptide expressed? | Function. Agouti-related protein is expressed primarily in the adrenal gland, subthalamic nucleus, and hypothalamus, with lower levels of expression in the testis, kidneys, and lungs.The agouti-related peptide is expressed in neurons in the hypothalamus. |
http://www.ncbi.nlm.nih.gov/pubmed/27088854,http://www.ncbi.nlm.nih.gov/pubmed/31750240,http://www.ncbi.nlm.nih.gov/pubmed/26083752,http://www.ncbi.nlm.nih.gov/pubmed/29604362 | What is the function of ketohexokinase-A? | The central fructose-metabolising enzyme is ketohexokinase (KHK), which exists in two isoforms: KHK-A and KHK-C. |
http://www.ncbi.nlm.nih.gov/pubmed/15037093,http://www.ncbi.nlm.nih.gov/pubmed/10772900 | Are the major royal jelly proteins similar to the yellow proteins? | Yes,
Major royal jelly proteins (named MRJP1-5) of honeybee (Apis mellifera), yellow proteins of Drosophila, together with putative proteins found in several bacteria, form a protein family termed the MRJP/yellow family. |
http://www.ncbi.nlm.nih.gov/pubmed/32689928,http://www.ncbi.nlm.nih.gov/pubmed/32211023 | Which R packages have been developed for studying TADs? | TADCompare is an R Package for differential and temporal analysis of Topologically Associated Domains. SpectralTAD is an R package for defining a hierarchy of topologically associated domains using spectral clustering.TADCompare is a method for differential analysis of boundaries of interacting domains between two or more Hi-C datasets. SpectralTAD is a method for defining a hierarchy of topologically associated domains using spectral clustering. |
http://www.ncbi.nlm.nih.gov/pubmed/32573705 | Which bioconductor tool has been developed for accessing bacterial regulatory networks? | The Regutools R package to facilitates programmatic access to RegulonDB data in computational biology. regutools gives researchers the possibility of writing reproducible workflows with automated queries to RegulonDB. The regutools package serves as a bridge between RegulonDB data and the Bioconductor ecosystem by reusing the data structures and statistical methods powered by other Bioconductor packages.RegulonDB has collected, harmonized and centralized data from hundreds of experiments for nearly two decades and is considered a point of reference for transcriptional regulation in Escherichia coli K12. The regutools package serves as a bridge between RegulonDB data and the Bioconductor ecosystem by reusing the data structures and statistical methods powered by other Bioconductor packages. |
http://www.ncbi.nlm.nih.gov/pubmed/32384687,http://www.ncbi.nlm.nih.gov/pubmed/32518251,http://www.ncbi.nlm.nih.gov/pubmed/31965987,http://www.ncbi.nlm.nih.gov/pubmed/32134461 | Is the Apis mellifera genome available? | Yes,
the Apis mellifera genome is available since 2006. |
http://www.ncbi.nlm.nih.gov/pubmed/8855341,http://www.ncbi.nlm.nih.gov/pubmed/23113340,http://www.ncbi.nlm.nih.gov/pubmed/18974556,http://www.ncbi.nlm.nih.gov/pubmed/31669315,http://www.ncbi.nlm.nih.gov/pubmed/10215406,http://www.ncbi.nlm.nih.gov/pubmed/27415035,http://www.ncbi.nlm.nih.gov/pubmed/32129495,http://www.ncbi.nlm.nih.gov/pubmed/22197188,http://www.ncbi.nlm.nih.gov/pubmed/25438602,http://www.ncbi.nlm.nih.gov/pubmed/12021248,http://www.ncbi.nlm.nih.gov/pubmed/26510092,http://www.ncbi.nlm.nih.gov/pubmed/32270509,http://www.ncbi.nlm.nih.gov/pubmed/21204798,http://www.ncbi.nlm.nih.gov/pubmed/9392583,http://www.ncbi.nlm.nih.gov/pubmed/25088311 | What genes is implicated in myotonic goats and other nondystrophic myotonias? | The gene encoding clcn1, mBNl1, gcic-1, scn4a, clc-1 and dmpk are implicated in myotonic goats and other nondystrophic myotonias.The following genes are implicated in myotonic goats and other nondystrophic myotonias: clcn1 (also known as mbnl1), gcic-1, scn4a, clc-1 and dmpk.The genes that are implicated in myotonic goats and other nondystrophic myotonias are clcn1, mbnl1, gcic-1, scn4a, clc-1 and dmpk.Myotonic goats and other Nondystrophic myotonic myotonias are caused by mutations in either the CLCN1 gene or the SCN4A gene.The gene encoding clcn1 (also known as clc-1), gcic-1, scn4a, and dmpk is implicated in myotonic goats and other nondystrophic myotoniasThe nondystrophic myotonias are rare muscle hyperexcitability disorders caused by gain-of-function mutations in the SCN4A gene or loss-of-function mutations in the CLCN1 gene. In goats, the gCIC-1 protein encoded by the CLCN1 gene, is affected .The nondystrophic myotonias are rare muscle hyperexcitability disorders caused by gain-of-function mutations in the SCN4A gene or loss-of-function mutations in the CLCN1 geneThe gene encoding clcn1, mphanl1, gcic-1, scn4a, clc-1 and dmpk are implicated in myotonic goats and other nondystrophic myotoniasMyotonic goats and other Nondystrophic Myotonias are caused by mutations in either the CLCN1 gene in Myotonia congenita or in the SCN4A gene in S4A. |
http://www.ncbi.nlm.nih.gov/pubmed/31192604 | Has the olive tree pollen proteome been studied? | Yes,
Olive pollen is a major allergenic source worldwide due to its extensive cultivation. We have combined available genomics data with a comprehensive proteomics approach to get the annotated olive tree (Olea europaea L.) pollen proteome and define its complex allergenome. |
http://www.ncbi.nlm.nih.gov/pubmed/31838186,http://www.ncbi.nlm.nih.gov/pubmed/32044971,http://www.ncbi.nlm.nih.gov/pubmed/32939719,http://www.ncbi.nlm.nih.gov/pubmed/32239671 | Is cadherin a plasma membrane marker? | Yes,
cadherin is a plasma membrane protein marker. |
http://www.ncbi.nlm.nih.gov/pubmed/32187532 | What impacts stability of genomic imprinting in mouse pluripotent stem cells? | A susceptibility locus on chromosome 13 profoundly impacts the stability of genomic imprinting in mouse pluripotent stem cells. |
http://www.ncbi.nlm.nih.gov/pubmed/32616740,http://www.ncbi.nlm.nih.gov/pubmed/31961458,http://www.ncbi.nlm.nih.gov/pubmed/32154231,http://www.ncbi.nlm.nih.gov/pubmed/32642925,http://www.ncbi.nlm.nih.gov/pubmed/32538627 | What are the end products of the shikimate pathway? | The shikimate pathway responsible for the generation of aromatic amino acids |
http://www.ncbi.nlm.nih.gov/pubmed/16682449 | What are the uber-operons? | Uber-operons are groups of functionally or transcriptionally related operons, whose gene sets are conserved across multiple reference genomes. Many of the uber-operons correspond to parts of known regulons or biological pathways or are involved in highly related biological processes based on their Gene Ontology (GO) assignments. |
http://www.ncbi.nlm.nih.gov/pubmed/27822311,http://www.ncbi.nlm.nih.gov/pubmed/22003227 | Which key gene is involved in syndromic obesity phenotype of patients with 1p21.3 microdeletions? | MIR137 is the key gene mediator of the syndromic obesity phenotype of patients with 1p21. 3 microdeletions.MIR137 is the key gene mediator of the syndromic obesity phenotype of patients with 1p21.3 microdeletions.The MIR137 gene. It is the one that is responsible for the obesity phenotype of patients with 1p21.3 microdeletions.The MIR137 gene. It is the one that is responsible for the obesity phenotype of patients carrying 1p21.3 microdeletions.Deletions in the long arm of chromosome 1 have been described in patients with a phenotype consisting primarily of obesity, intellectual disability and autism-spectrum disorder. MIR137 is suggested as the mediator of the obesity phenotype of patients carrying 1p21.3 microdeletions. |
http://www.ncbi.nlm.nih.gov/pubmed/20702648,http://www.ncbi.nlm.nih.gov/pubmed/10971110,http://www.ncbi.nlm.nih.gov/pubmed/15557761,http://www.ncbi.nlm.nih.gov/pubmed/26221547,http://www.ncbi.nlm.nih.gov/pubmed/16845600,http://www.ncbi.nlm.nih.gov/pubmed/16311416,http://www.ncbi.nlm.nih.gov/pubmed/17574308,http://www.ncbi.nlm.nih.gov/pubmed/10710275 | Is cabergoline used for treatment of the Nelson's syndrome ? | Yes, cabergoline has been shown to be effective for treatment of the Nelson's syndrome. |
http://www.ncbi.nlm.nih.gov/pubmed/31907968,http://www.ncbi.nlm.nih.gov/pubmed/31908009,http://www.ncbi.nlm.nih.gov/pubmed/31904283 | Are mucins glycosylated proteins? | Yes,
Many members of the mucin family are evolutionarily conserved and are often aberrantly expressed and glycosylated in various benign and malignant pathologies leading to tumor invasion, metastasis, and immune evasion. |
http://www.ncbi.nlm.nih.gov/pubmed/3618059,http://www.ncbi.nlm.nih.gov/pubmed/25526716,http://www.ncbi.nlm.nih.gov/pubmed/15605660,http://www.ncbi.nlm.nih.gov/pubmed/19534294,http://www.ncbi.nlm.nih.gov/pubmed/32174033,http://www.ncbi.nlm.nih.gov/pubmed/22492102,http://www.ncbi.nlm.nih.gov/pubmed/32477509,http://www.ncbi.nlm.nih.gov/pubmed/24740988,http://www.ncbi.nlm.nih.gov/pubmed/23997744,http://www.ncbi.nlm.nih.gov/pubmed/19756731,http://www.ncbi.nlm.nih.gov/pubmed/31634868,http://www.ncbi.nlm.nih.gov/pubmed/16558255,http://www.ncbi.nlm.nih.gov/pubmed/28447963,http://www.ncbi.nlm.nih.gov/pubmed/24422297,http://www.ncbi.nlm.nih.gov/pubmed/21845587,http://www.ncbi.nlm.nih.gov/pubmed/29218119,http://www.ncbi.nlm.nih.gov/pubmed/31632712,http://www.ncbi.nlm.nih.gov/pubmed/28718333,http://www.ncbi.nlm.nih.gov/pubmed/31736403,http://www.ncbi.nlm.nih.gov/pubmed/18050074,http://www.ncbi.nlm.nih.gov/pubmed/23799199,http://www.ncbi.nlm.nih.gov/pubmed/28824352,http://www.ncbi.nlm.nih.gov/pubmed/10918251,http://www.ncbi.nlm.nih.gov/pubmed/21320832,http://www.ncbi.nlm.nih.gov/pubmed/32082444,http://www.ncbi.nlm.nih.gov/pubmed/12475522,http://www.ncbi.nlm.nih.gov/pubmed/33141768,http://www.ncbi.nlm.nih.gov/pubmed/28928252,http://www.ncbi.nlm.nih.gov/pubmed/23113142,http://www.ncbi.nlm.nih.gov/pubmed/33151661,http://www.ncbi.nlm.nih.gov/pubmed/6756339,http://www.ncbi.nlm.nih.gov/pubmed/19280893 | Is carpal tunnel syndrome a type of nerve entrapment? | Carpal tunnel syndrome (CTS) is the most frequent entrapment neuropathy in humans.Carpal tunnel syndrome (CTS) is a type of nerve entrapment due to compression of the nerve root extraforaminally between the wrist and the wrist at the carpal tunnel.Carpal tunnel syndrome is a neuropathy resulting from compression of the median nerve as it passes through a narrow tunnel in the wrist on its way to the hand.Carpal tunnel syndrome (CTS) is the most common focal entrapment mononeuropathy, comprising medium nerve chronic inflammation and fibrosis.Carpal tunnel syndrome (CTS) is a focal compressive neuropathy of the central nervous system causing hemorrhage-prone multiple lumen vascular malformation and very severe neurological consequencesCarpal tunnel syndrome (CTS) is an entrapment neuropathy accounting for up to 90% of nerve compression syndromesCarpal tunnel syndrome (CTS) is a type of nerve entrapment due to compression of the nerve root ganglion as it travels through the wrist at the carpal tunnel. |
http://www.ncbi.nlm.nih.gov/pubmed/23940102,http://www.ncbi.nlm.nih.gov/pubmed/23395106,http://www.ncbi.nlm.nih.gov/pubmed/23587911 | What is the main manifestation of Liebenberg syndrome? | Liebenberg syndrome (MIM 186550) is a very rare autosomal dominant condition characterized by three main features: dysplasia of all of the bony components of the elbow joint, abnormalities in the shape of carpal bones, and brachydactyly.Liebenberg syndrome (MIM 186550) is a very rare autosomal dominant condition characterized by dysplasia of all of the bony components of the elbow joint, abnormalities in the shape of carpal bones, and brachydactyly . It is caused by a deletion upstream to the PITX1 gene resulting in transformation of the upper limbs to reflect lower limb characteristics .People who are affected by Liebenberg Syndrome suffer from three main symptoms: Dysplasia (improper formation) of the bony components of the elbow. Abnormal shape of carpal bones. Brachydactyly, a symptom where the fingers and toes are shorter than normal.Liebenberg syndrome (MIM 186550) is a very rare autosomal dominant condition . It is characterized by dysplasia of all of the bony components of the elbow joint, abnormalities in the shape of carpal bones, and brachydactyly . We speculate that the area of deletion contains a regulatory sequence that suppresses the expression of PITX1 in the upper limb buds .Liebenberg syndrome (MIM 186550) is a very rare autosomal dominant condition characterized by three main features: dysplasia of all of the bony components of the elbow joint, abnormalities in the shape of carpal bones, and brachydactyly |
http://www.ncbi.nlm.nih.gov/pubmed/31660152 | Which IDH inhibitors by Agios Pharmaceuticals have been approved by the FDA? | Enasidenib and ivosidenib, the IDH2 and IDH1 inhibitors developed by Agios Pharmaceuticals, have been approved by the Food and Drug Administration |
http://www.ncbi.nlm.nih.gov/pubmed/32094342 | What is RADICL-seq? | Mammalian genomes encode tens of thousands of noncoding RNAs. Most noncoding transcripts exhibit nuclear localization and several have been shown to play a role in the regulation of gene expression and chromatin remodeling. To investigate the function of such RNAs, methods to massively map the genomic interacting sites of multiple transcripts have been developed; however, these methods have some limitations. RNA And DNA Interacting Complexes Ligated and sequenced (RADICL-seq) is a technology that maps genome-wide RNA-chromatin interactions in intact nuclei. RADICL-seq is a proximity ligation-based methodology that reduces the bias for nascent transcription, while increasing genomic coverage and unique mapping rate efficiency compared with existing methods. RADICL-seq identifies distinct patterns of genome occupancy for different classes of transcripts as well as cell type-specific RNA-chromatin interactions, and highlights the role of transcription in the establishment of chromatin structure.RADICL-seq is a technology that maps genome-wide RNA-chromatin interactions in intact nuclei. It identifies distinct patterns of genome occupancy for different classes of transcripts as well as cell type-specific RNA- chromatin interactions, and highlights the role of transcription in the establishment of chromatin structure.RADICL-seq is a technology that maps genome-wide RNA-chromatin interactions in intact nuclei. It is a proximity ligation-based methodology that reduces the bias for nascent transcription, while increasing genomic coverage and unique mapping rate efficiency compared with existing methods. RADICL -seq identifies distinct patterns of genome occupancy for different classes of transcripts as well as cell type-specific RNA- chromatin interactions, and highlights the role of transcription in the establishment of chromatin structure. |
http://www.ncbi.nlm.nih.gov/pubmed/29680938,http://www.ncbi.nlm.nih.gov/pubmed/31465299,http://www.ncbi.nlm.nih.gov/pubmed/31401630,http://www.ncbi.nlm.nih.gov/pubmed/33085861 | Which disease is treated with Anti–Siglec-8 Antibody? | Anti-Siglec-8 Antibody was shown to be effective for Eosinophilic Gastritis and Duodenitis. It is also undergoing clinical investigation for treatment of allergic, inflammatory, and proliferative diseases. |
http://www.ncbi.nlm.nih.gov/pubmed/12957828,http://www.ncbi.nlm.nih.gov/pubmed/14521626,http://www.ncbi.nlm.nih.gov/pubmed/12111545,http://www.ncbi.nlm.nih.gov/pubmed/30915128 | What is known about mammalian melatonin receptors? | Melatonin receptors MT1 and MT2 (genes officially named MTNR1A and MTNR1B, respectively) play crucial roles in melatonin-mediated regulation of circadian rhythms, the immune system, and control of reproduction in seasonally breeding animals.
The melatonin receptor family is a small group of receptors within the G protein-coupled receptor (GPCR) superfamily. The group comprises of three subtypes which bind melatonin and one member, the melatonin related receptor (MRR), that shares >40% sequence identity with the other melatonin receptors but does not bind melatonin. |
http://www.ncbi.nlm.nih.gov/pubmed/25590404,http://www.ncbi.nlm.nih.gov/pubmed/25218063,http://www.ncbi.nlm.nih.gov/pubmed/6633857,http://www.ncbi.nlm.nih.gov/pubmed/26564444,http://www.ncbi.nlm.nih.gov/pubmed/23112757,http://www.ncbi.nlm.nih.gov/pubmed/29770996,http://www.ncbi.nlm.nih.gov/pubmed/21795094,http://www.ncbi.nlm.nih.gov/pubmed/31528602,http://www.ncbi.nlm.nih.gov/pubmed/33111505,http://www.ncbi.nlm.nih.gov/pubmed/26361024,http://www.ncbi.nlm.nih.gov/pubmed/8862623,http://www.ncbi.nlm.nih.gov/pubmed/25339593,http://www.ncbi.nlm.nih.gov/pubmed/27086438,http://www.ncbi.nlm.nih.gov/pubmed/15021236 | What is holoprosencephaly? | Holoprosencephaly (HPE) is a congenital defect of the brain, median structures, and face resulting from an incomplete cleavage of the primitive brain during early embryogenesis . The most common developmental defect is characterized by inadequate or absent midline division of the forebrain into cerebral hemispheres with concomitant midline facial defects in the majority of cases .Holoprosencephaly (HPE) is a congenital defect of the brain, median structures, and face resulting from an incomplete cleavage of the primitive brain during early embryogenesis.Holoprosencephaly is a congenital defect of the brain, median structures, and face resulting from incomplete incomplete cleavage of the primitive brain during early embryogenesis. Holoprosencephaly (HPE) is a congenital defect of the brain, median structures, and face resulting from an incomplete cleavage of the primitive brain during early embryogenesis. |
http://www.ncbi.nlm.nih.gov/pubmed/24583034,http://www.ncbi.nlm.nih.gov/pubmed/18956012,http://www.ncbi.nlm.nih.gov/pubmed/28573150,http://www.ncbi.nlm.nih.gov/pubmed/30176986,http://www.ncbi.nlm.nih.gov/pubmed/19783418,http://www.ncbi.nlm.nih.gov/pubmed/15081359,http://www.ncbi.nlm.nih.gov/pubmed/12100893,http://www.ncbi.nlm.nih.gov/pubmed/19059466,http://www.ncbi.nlm.nih.gov/pubmed/18000541,http://www.ncbi.nlm.nih.gov/pubmed/25336612,http://www.ncbi.nlm.nih.gov/pubmed/27466320,http://www.ncbi.nlm.nih.gov/pubmed/33229432,http://www.ncbi.nlm.nih.gov/pubmed/11234018 | What is the effect of notch in the division of neural progenitor cells in Drosophila? | The Notch pathway mediates the differentiation of neural progenitor cells in Drosophila. It's an important part of the development of neural stem cells, which are the cells that make up the brain. Notch/HES signaling and MIR-9 signaling are very important for the homeostasis of neural cells. It is thought that notch activation is responsible for the growth of neurons.Canonical Notch signaling has diverse functions during nervous system development and is critical for neural progenitor self-renewal, timing of differentiation and specification of various cell fates. In the adult mammalian brain niches for neural stem cells are maintained, which enable a steady-state neurogenesis. This process is tightly regulated by multiple niche factors, including Notch and NF-κB signaling. As a result of Notch activation, neuronal differentiation is inhibited in neighboring cells and they remain neural progenitor cells.Notch signaling is an evolutionarily conserved mechanism, used to regulate cell fate decisions. Disruption of Notch signaling causes neuronal progenitor cell self-renewal, a hallmark of systemic lupus erythematosus (SLE), and leads to premature differentiation of them into the erythroid lineage.Canonical Notch signaling has diverse functions during nervous system development and is critical for neural progenitor self-renewal, timing of differentiation and specification of various cell fates In the adult mammalian brain niches for neural stem cells are maintained, which enable a steady-state neurogenesis. This process is tightly regulated by multiple niche factors, including Notch and NF-?B signaling. As a result of Notch activation, neuronal differentiation is inhibited in neighboring cells and they remain neural progenitor cells.The Notch pathway mediates the differentiation of neural progenitor cells in Drosophila. It's an important part of the development of neural stem cells, which are the cells that make up the brain. Notch/HES signaling and MIR-9 signaling are very important for the homeostasis of neural cells. |
http://www.ncbi.nlm.nih.gov/pubmed/30091218 | In what clinical trials has SAR425899 been tested? | Subcutaneous administrations of SAR425899 were tested in two randomized, placebo-controlled, double-blind clinical trials. In the first trial, healthy overweight volunteers (body mass index [BMI] 25-30 kg/m2 ; n = 32) received single-ascending doses (0.01-0.1 mg) of SAR425899 or placebo. In the second, a multiple-ascending-dose trial (NCT02411825), healthy normal- to overweight volunteers (BMI 20-30 kg/m2 ; n = 40) and overweight/obese patients with T2D (BMI 28-42 kg/m2 ; n = 36) received daily doses of SAR425899 or placebo over 21 or 28 days, respectively. |
http://www.ncbi.nlm.nih.gov/pubmed/25157153 | Is there a link between rare variants in PPARG and type 1 diabetes? | No. Rare variants in PPARG with decreased activity in adipocyte differentiation are associated with increased risk of type 2 diabetes.No. Rare variants in PPARG with decreased activity in adipocyte differentiation are associated with increased risk of type 2 diabetes |
http://www.ncbi.nlm.nih.gov/pubmed/31229240,http://www.ncbi.nlm.nih.gov/pubmed/31420495,http://www.ncbi.nlm.nih.gov/pubmed/30926949,http://www.ncbi.nlm.nih.gov/pubmed/32440095,http://www.ncbi.nlm.nih.gov/pubmed/31862477,http://www.ncbi.nlm.nih.gov/pubmed/30825104,http://www.ncbi.nlm.nih.gov/pubmed/32535390,http://www.ncbi.nlm.nih.gov/pubmed/32251854,http://www.ncbi.nlm.nih.gov/pubmed/31602563,http://www.ncbi.nlm.nih.gov/pubmed/31258629,http://www.ncbi.nlm.nih.gov/pubmed/31213500,http://www.ncbi.nlm.nih.gov/pubmed/33143617,http://www.ncbi.nlm.nih.gov/pubmed/31240240,http://www.ncbi.nlm.nih.gov/pubmed/31848580,http://www.ncbi.nlm.nih.gov/pubmed/32306101,http://www.ncbi.nlm.nih.gov/pubmed/32943455 | What is the mechanisms of action of pexidartinib? | Pexidartinib is small-molecule tyrosine kinase inhibitor that has strong selectivity against colony-stimulating factor 1 receptor. |
http://www.ncbi.nlm.nih.gov/pubmed/30914205,http://www.ncbi.nlm.nih.gov/pubmed/32041354,http://www.ncbi.nlm.nih.gov/pubmed/31903844,http://www.ncbi.nlm.nih.gov/pubmed/31584206,http://www.ncbi.nlm.nih.gov/pubmed/31852826,http://www.ncbi.nlm.nih.gov/pubmed/32492702,http://www.ncbi.nlm.nih.gov/pubmed/31936048 | List pore forming toxins. | cytolysin A
α-hemolysin
Streptolysin O
pneumolysin
listeriolysin
leukocidin
Glabralysin |
http://www.ncbi.nlm.nih.gov/pubmed/28475860,http://www.ncbi.nlm.nih.gov/pubmed/28007623,http://www.ncbi.nlm.nih.gov/pubmed/31935506,http://www.ncbi.nlm.nih.gov/pubmed/31813957,http://www.ncbi.nlm.nih.gov/pubmed/24838796,http://www.ncbi.nlm.nih.gov/pubmed/29914387,http://www.ncbi.nlm.nih.gov/pubmed/30980591,http://www.ncbi.nlm.nih.gov/pubmed/29725259,http://www.ncbi.nlm.nih.gov/pubmed/31282990,http://www.ncbi.nlm.nih.gov/pubmed/31465303,http://www.ncbi.nlm.nih.gov/pubmed/24705355,http://www.ncbi.nlm.nih.gov/pubmed/30891914,http://www.ncbi.nlm.nih.gov/pubmed/31816409,http://www.ncbi.nlm.nih.gov/pubmed/32803813,http://www.ncbi.nlm.nih.gov/pubmed/26194542,http://www.ncbi.nlm.nih.gov/pubmed/27573763,http://www.ncbi.nlm.nih.gov/pubmed/26932671,http://www.ncbi.nlm.nih.gov/pubmed/32083401,http://www.ncbi.nlm.nih.gov/pubmed/24240169 | What syndrome is associated with mutations in lysine methyltransferase 2D KMT2D? | Mutations in lysine methyltransferase 2D (KMT2D) gene, which encodes the catalytic core of a multisubunit chromatin remodeling enzyme, are responsible for the neurodegenerative disorder Kabuki syndrome.Mutations in lysine methyltransferase 2D (KMT2D) cause Kabuko syndrome.Kabuki syndrome (KS) is commonly caused by mutations in the histone-modifying enzyme lysine methyltransferase 2D (KMT2D).Mutations in the lysine methyltransferase 2D (KMT2D) gene, which encodes the alpha-subunit of the kappaB gene, are associated with the autosomal dominant hemophagocytic syndrome type 4 or Ferroportin syndrome.Kabuki syndrome is a rare autosomal dominant disorder caused by mutations in the lysine methyltransferase 2D (KMT2D) gene. |
http://www.ncbi.nlm.nih.gov/pubmed/11515490,http://www.ncbi.nlm.nih.gov/pubmed/23633205,http://www.ncbi.nlm.nih.gov/pubmed/10458450,http://www.ncbi.nlm.nih.gov/pubmed/20850730,http://www.ncbi.nlm.nih.gov/pubmed/27693263,http://www.ncbi.nlm.nih.gov/pubmed/8110760,http://www.ncbi.nlm.nih.gov/pubmed/10564874,http://www.ncbi.nlm.nih.gov/pubmed/21147889,http://www.ncbi.nlm.nih.gov/pubmed/24383016,http://www.ncbi.nlm.nih.gov/pubmed/3489839,http://www.ncbi.nlm.nih.gov/pubmed/8001864,http://www.ncbi.nlm.nih.gov/pubmed/1944596,http://www.ncbi.nlm.nih.gov/pubmed/17663907,http://www.ncbi.nlm.nih.gov/pubmed/20511729,http://www.ncbi.nlm.nih.gov/pubmed/8302780,http://www.ncbi.nlm.nih.gov/pubmed/20132346,http://www.ncbi.nlm.nih.gov/pubmed/8768837 | Does steroid 5A-Reductase deficiency lead to hermaphroditism? | Yes, steroid 5A-reductase deficiency can lead to hermaphroditism.5α steroid reductase deficiency (5αSRD) is an autosomal recessive enzymatic deficiency and mutations in the 5α steroid reductase type 2 gene (SRD5A2) result in male pseudohermaphrodism caused by decreased dihydrotestosterone (DHT) synthesis. The diagnosis of steroid-5-alpha-reductase deficiency is rarely considered by the paediatrician.Yes, steroid 5A-reductase deficiency is a rare autosomal recessive disorder.Yes, steroid 5A-Reductase deficiency is associated with hermaphroditism.5α steroid reductase deficiency (5αSRD) is an autosomal recessive enzymatic deficiency and mutations in the 5α steroid reductase type 2 gene (SRD5A2) result in male pseudohermaphrodism caused by decreased dihydrotestosterone (DHT) synthesis.Male pseudo hermaphroditism caused by steroid 5 alpha reductase deficiency is a rare autosomal recessive disorder. This enzyme catalyses the conversion of testosterone to dihydrotestosterone (DHT) in genital tissue.Yes, steroid 5A-reductase deficiency is associated with hermaphroditism. |
http://www.ncbi.nlm.nih.gov/pubmed/32011192,http://www.ncbi.nlm.nih.gov/pubmed/31758661,http://www.ncbi.nlm.nih.gov/pubmed/32648856 | Has ubrogepant entered clinical phase III trials? | Yes, ubrogepant has entered phase III trials. |
http://www.ncbi.nlm.nih.gov/pubmed/32268280 | How many nucleotides long is the HOTAIR CNE? | The HOTAIR CNE is a 32-nucleotide long conserved noncoding elementHOTAIR was proposed to regulate either HoxD cluster genes in trans or HoxC cluster genes in cis, a mechanism that remains unclear. A 32-nucleotide conserved noncoding element (CNE) was identified as HOTAIR ancient sequence that likely originated at the root of vertebrate.The HOTAIR element is a 32-nucleotide conserved noncoding element |
http://www.ncbi.nlm.nih.gov/pubmed/32941089,http://www.ncbi.nlm.nih.gov/pubmed/30595352,http://www.ncbi.nlm.nih.gov/pubmed/28726523,http://www.ncbi.nlm.nih.gov/pubmed/28162143,http://www.ncbi.nlm.nih.gov/pubmed/31931470 | What symptoms are included in the narcolepsy pentad? | Narcolepsy is a chronic sleep disorder characterized by a pentad of excessive daytime sleepiness (EDS), cataplexy, sleep paralysis, hypnagogic/hypnopompic hallucinations, and disturbed nocturnal sleep. |
http://www.ncbi.nlm.nih.gov/pubmed/32003015,http://www.ncbi.nlm.nih.gov/pubmed/30632962,http://www.ncbi.nlm.nih.gov/pubmed/33053358 | What is the function of osteolectin? | C-type lectin domain family 11 member A (Clec11a), also known as stem cell growth factor (SCGF), C-type lectin superfamily member 3 (CLECSF3), or osteolectin was initially identified as a growth factor for hematopoietic progenitor cells. |
http://www.ncbi.nlm.nih.gov/pubmed/32144062,http://www.ncbi.nlm.nih.gov/pubmed/24809246,http://www.ncbi.nlm.nih.gov/pubmed/28413074,http://www.ncbi.nlm.nih.gov/pubmed/30386759,http://www.ncbi.nlm.nih.gov/pubmed/29768983,http://www.ncbi.nlm.nih.gov/pubmed/23817232,http://www.ncbi.nlm.nih.gov/pubmed/22914430,http://www.ncbi.nlm.nih.gov/pubmed/28533721,http://www.ncbi.nlm.nih.gov/pubmed/25608845,http://www.ncbi.nlm.nih.gov/pubmed/25176974,http://www.ncbi.nlm.nih.gov/pubmed/25711946,http://www.ncbi.nlm.nih.gov/pubmed/24651227,http://www.ncbi.nlm.nih.gov/pubmed/28948652,http://www.ncbi.nlm.nih.gov/pubmed/29050526,http://www.ncbi.nlm.nih.gov/pubmed/895593,http://www.ncbi.nlm.nih.gov/pubmed/32092196,http://www.ncbi.nlm.nih.gov/pubmed/19088593,http://www.ncbi.nlm.nih.gov/pubmed/27113690,http://www.ncbi.nlm.nih.gov/pubmed/29808279,http://www.ncbi.nlm.nih.gov/pubmed/26837253,http://www.ncbi.nlm.nih.gov/pubmed/23594433,http://www.ncbi.nlm.nih.gov/pubmed/32094031,http://www.ncbi.nlm.nih.gov/pubmed/23406535,http://www.ncbi.nlm.nih.gov/pubmed/25789816,http://www.ncbi.nlm.nih.gov/pubmed/19806801 | What is ECMO? | Extracorporeal membrane oxygenation (ECMO) is an increasingly prevalent treatment for acute respiratory failure (ARF)The method of extracorporeal membrane oxygenation (VA-ECMO) has developed from being used as a 'rescue therapy' to become an accepted treatment option for patients with acute lung failure.Extracorporeal membrane oxygenation (ECMO) is an increasingly prevalent treatment for acute respiratory failure (ARF) and is used to treat severe symptoms of Covid-19 as well as other cases of severe respiratory and/or circulatory failure over periods of several days to several weeksExtracorporeal membrane oxygenation (ECMO) is an increasingly prevalent treatment for acute respiratory failure (ARF). |
http://www.ncbi.nlm.nih.gov/pubmed/15634937,http://www.ncbi.nlm.nih.gov/pubmed/9862363,http://www.ncbi.nlm.nih.gov/pubmed/9754557,http://www.ncbi.nlm.nih.gov/pubmed/9743333,http://www.ncbi.nlm.nih.gov/pubmed/7930846,http://www.ncbi.nlm.nih.gov/pubmed/1537372,http://www.ncbi.nlm.nih.gov/pubmed/8181531,http://www.ncbi.nlm.nih.gov/pubmed/8040305,http://www.ncbi.nlm.nih.gov/pubmed/18521959,http://www.ncbi.nlm.nih.gov/pubmed/10753498,http://www.ncbi.nlm.nih.gov/pubmed/7843228,http://www.ncbi.nlm.nih.gov/pubmed/12594250,http://www.ncbi.nlm.nih.gov/pubmed/16777955,http://www.ncbi.nlm.nih.gov/pubmed/2599002 | Which diseases are associated with the Yaa gene? | The Y-linked autoimmune accelerating gene mutation (yaa), first discovered in the BXSB mouse strain, is known to accelerate spontaneous autoantibody production and subsequent development of lupus disease. It has also been shown to be associated with various autoimmune conditions such as lupus-like syndrome, collagen induced arthrits and glomerulonephritis.Diseases associated with the Yaa gene include aids, systemic lupus erythematosus, maids, rheumatoid arthritis, arthritis, l upus nephritis, murine acquired immunodeficiency syndrome, and lupUS-like nephitis.The Yaa gene-mediated acceleration of murine lupus: Yaa- T cells from non-autoimmune mice collaborate with Yaa+ B cells to produce Lupus autoantibodies in vivo.The Y-linked autoimmune accelerating gene mutation (yaa), first discovered in the BXSB mouse strain, is known to accelerate spontaneous autoantibody production and subsequent development of lupus disease.Diseases associated with the Yaa gene include aids, systemic lupus erythematosus,maids, rheumatoid arthritis, arthritis, l upus nephritis, murine acquired immunodeficiency syndrome, lUPus-like nephitis and other inflammatory bowel diseases.Diseases associated with the Yaa gene include aids, systemic lupus erythematosus,maids, rheumatoid arthritis, l upus nephritis, murine acquired immunodeficiency syndrome, lUPus and lupUS-like nephitis.F1 mice, a model in which the lupus-like autoimmune syndrome observed in male mice is associated with the presence of an as yet unidentified Y chromosome-linked autoimmune acceleration gene, Yaa. Yaa is a Y-chromosome-linked gene that accelerates autoimmune diseases in some autoimmune-prone strains of mice The role of the Yaa gene in lupus syndrome The Y chromosome-linked "autoimmune accelerating" yaa gene suppresses collagen-induced arthritisYaa is a Y-chromosome-linked gene that accelerates autoimmune diseases in some autoimmune-prone strains of mice . BXSB mice spontaneously develop a lupus-like syndrome that is accelerated by the Yaa gene . Yaa mice bearing the NZB chromosome 13 locus displayed increased serum gp70 production, but not glomerulonephritis .Diseases associated with the Yaa gene include aids, systemic lupus erythematosus, maids, rheumatoid arthritis, arthritis, l upus nephritis, murine acquired immunodeficiency syndrome, and lUPus-like nephitis.Diseases associated with the Yaa gene include aids, systemic lupus erythematosus,maids, rheumatoid arthritis, l upus nephritis and murine acquired immunodeficiency syndrome. |
http://www.ncbi.nlm.nih.gov/pubmed/30095981 | Which receptors does bimagrumab block? | Bimagrumab blocks the activin type II receptors. |
http://www.ncbi.nlm.nih.gov/pubmed/31187503,http://www.ncbi.nlm.nih.gov/pubmed/32522499 | Are PDXK mutations linked to polyneuropathy? | Yes, PDXK mutations are linked to polyneuropathy.Yes, PDXK mutations are associated with autosomal recessive polyneuropathy.Yes. PDXK mutations cause polyneuropathy responsive to pyridoxal 5'-phosphate supplementation.Yes, PDXK mutations are associated with delayed polyneuropathy.Yes, point mutations in PDXK gene may be associated with peripheral neuropathy. |
http://www.ncbi.nlm.nih.gov/pubmed/31807039,http://www.ncbi.nlm.nih.gov/pubmed/32135514,http://www.ncbi.nlm.nih.gov/pubmed/29217288,http://www.ncbi.nlm.nih.gov/pubmed/32945632,http://www.ncbi.nlm.nih.gov/pubmed/30004857,http://www.ncbi.nlm.nih.gov/pubmed/32762233,http://www.ncbi.nlm.nih.gov/pubmed/29103968,http://www.ncbi.nlm.nih.gov/pubmed/30481100,http://www.ncbi.nlm.nih.gov/pubmed/28585615,http://www.ncbi.nlm.nih.gov/pubmed/31553054,http://www.ncbi.nlm.nih.gov/pubmed/33037118,http://www.ncbi.nlm.nih.gov/pubmed/32146152,http://www.ncbi.nlm.nih.gov/pubmed/28375787,http://www.ncbi.nlm.nih.gov/pubmed/31286802,http://www.ncbi.nlm.nih.gov/pubmed/31940998,http://www.ncbi.nlm.nih.gov/pubmed/30021426,http://www.ncbi.nlm.nih.gov/pubmed/29540084 | Is avelumab effective for urothelial carcinoma? | Yes. Avelumab is an anti-programmed death-ligand 1 monoclonal antibody that is approved for the treatment of urothelial carcinoma. |
http://www.ncbi.nlm.nih.gov/pubmed/17726681,http://www.ncbi.nlm.nih.gov/pubmed/30973132,http://www.ncbi.nlm.nih.gov/pubmed/31034157 | What tissues have been studied by circadian proteomics? | Retina
Liver |
http://www.ncbi.nlm.nih.gov/pubmed/33278107,http://www.ncbi.nlm.nih.gov/pubmed/33300011,http://www.ncbi.nlm.nih.gov/pubmed/32925547,http://www.ncbi.nlm.nih.gov/pubmed/32463092,http://www.ncbi.nlm.nih.gov/pubmed/33042918,http://www.ncbi.nlm.nih.gov/pubmed/32631771,http://www.ncbi.nlm.nih.gov/pubmed/33180935,http://www.ncbi.nlm.nih.gov/pubmed/32953455,http://www.ncbi.nlm.nih.gov/pubmed/32532619,http://www.ncbi.nlm.nih.gov/pubmed/32755212,http://www.ncbi.nlm.nih.gov/pubmed/33263635,http://www.ncbi.nlm.nih.gov/pubmed/32935083,http://www.ncbi.nlm.nih.gov/pubmed/33055501,http://www.ncbi.nlm.nih.gov/pubmed/32946801,http://www.ncbi.nlm.nih.gov/pubmed/32827525,http://www.ncbi.nlm.nih.gov/pubmed/33042116,http://www.ncbi.nlm.nih.gov/pubmed/33011038,http://www.ncbi.nlm.nih.gov/pubmed/32496723,http://www.ncbi.nlm.nih.gov/pubmed/33180050,http://www.ncbi.nlm.nih.gov/pubmed/33110725,http://www.ncbi.nlm.nih.gov/pubmed/33083367,http://www.ncbi.nlm.nih.gov/pubmed/33243303,http://www.ncbi.nlm.nih.gov/pubmed/32923992,http://www.ncbi.nlm.nih.gov/pubmed/32837148,http://www.ncbi.nlm.nih.gov/pubmed/33295957,http://www.ncbi.nlm.nih.gov/pubmed/32839782,http://www.ncbi.nlm.nih.gov/pubmed/32493734,http://www.ncbi.nlm.nih.gov/pubmed/33269352,http://www.ncbi.nlm.nih.gov/pubmed/33263756,http://www.ncbi.nlm.nih.gov/pubmed/32975439,http://www.ncbi.nlm.nih.gov/pubmed/32995826,http://www.ncbi.nlm.nih.gov/pubmed/32966765,http://www.ncbi.nlm.nih.gov/pubmed/33217259,http://www.ncbi.nlm.nih.gov/pubmed/32511374 | Is MIS-C or Multisystem Inflammatory syndrome in children a complication of Covid-19? | Is MIS-C or Multisystem Inflammatory Syndrome in children a complication of Covid-19? Yes, it is.Multisystem Inflammatory syndrome AKA MIS-C is a complication of Covid-19 infection in children.Multisystem inflammatory syndrome in children (MIS-C) is a complication of Covid-19, clinically characterized by severe chronic inflammation in the central nervous system of children and adolescents. |
http://www.ncbi.nlm.nih.gov/pubmed/27662874,http://www.ncbi.nlm.nih.gov/pubmed/30448228,http://www.ncbi.nlm.nih.gov/pubmed/28533025,http://www.ncbi.nlm.nih.gov/pubmed/27662872,http://www.ncbi.nlm.nih.gov/pubmed/32060325,http://www.ncbi.nlm.nih.gov/pubmed/3299107,http://www.ncbi.nlm.nih.gov/pubmed/26319018,http://www.ncbi.nlm.nih.gov/pubmed/29378668,http://www.ncbi.nlm.nih.gov/pubmed/3462718,http://www.ncbi.nlm.nih.gov/pubmed/26864944,http://www.ncbi.nlm.nih.gov/pubmed/2218723,http://www.ncbi.nlm.nih.gov/pubmed/31824865,http://www.ncbi.nlm.nih.gov/pubmed/26219400,http://www.ncbi.nlm.nih.gov/pubmed/20393465,http://www.ncbi.nlm.nih.gov/pubmed/3031599,http://www.ncbi.nlm.nih.gov/pubmed/25578728,http://www.ncbi.nlm.nih.gov/pubmed/24599251,http://www.ncbi.nlm.nih.gov/pubmed/2986013 | Which RNA polymerase transcribes enhancer RNAs? | Analogously to mRNAs, the non-protein-encoding enhancer RNAs are synthesized by RNA Pol II and post-transcriptionally modified by addition of a 5'-cap and a 3'-poly (A) tail.Enhancers are bound by sequence-specific transcription factors, which in turn facilitate the cooperative binding of chromatin remodeling enzymes, histone modifying enzymes, other co-factors, and ultimately the RNA polymerase II complex (RNA pol II). Both the target genes and the enhancers are transcribed by RNA pol II.Analogously to mRNAs, the non-protein-encoding enhancer RNAs are synthesized by RNA Pol II and post-transcriptionally modified by addition of a 5'-cap and a 3'-poly (A) tail. Recent evidence indicates that miRNA genes are transcribed by RNA polymerase II (Pol II)Enhancer RNAs (eRNAs) are a group of lncRNAs transcribed from enhancers by RNA Polymerase II.Analogously to mRNAs, the non-protein-encoding enhancers are synthesized by RNA polymerase II and post-transcriptionally modified by addition of a 5'-cap and a 3'-poly (A) tail. Recent evidence indicates that miRNA genes are transcribed by RNA Pol II (Pol II)Because the transcripts of most enhancer genes are the products of type-II RNA polymerase, enhancer RNA Pol II (Pol II) has a poly(A) tail and appears in expressed sequence tags (EST). Analogously to mRNAs, the non-protein-encoding enhancer RNAs (ncRNAs) are synthesized by RNAPol II and post-transcriptionally modified by addition of a 5'-cap and a 3'-poly (A) tails.Because the transcripts of most enhancers are the products of type-II RNA polymerase, enhancer RNA Pol II (Pol II) has a poly(A) tail and appears in expressed sequence tags (EST). Analogously to mRNAs, the non-protein-encoding enhancer RNAs are synthesized by RNAPol II and post-transcriptionally modified by addition of a 5'-cap and a 3'-poly ( A) tail.The enhancer produced an eRNA, termed AS1eRNA, that enhanced DHRS4-AS1 transcription by mediating the spatial interactions of the enhancer and DHRS4-AS1 promoter in cooperation with RNA polymerase II and p300/CBP. |
http://www.ncbi.nlm.nih.gov/pubmed/32319039 | Name the three phase 3, randomized, double-blind, placebo-controlled that assessed galcanezumab? | Galcanezumab has been assessed in the phase 3, randomized, double-blind, placebo-controlled EVOLVE-1, EVOLVE-2 and REGAIN studies. |
http://www.ncbi.nlm.nih.gov/pubmed/31796516 | Is co-loss of BRCA2-RB1 associated with better prognosis for prostate cancer patients? | No. Co-loss of BRCA2-RB1 in human prostate cancer cells induces an epithelial-to-mesenchymal transition, which is associated with invasiveness and a more aggressive disease phenotype. |
http://www.ncbi.nlm.nih.gov/pubmed/32473356,http://www.ncbi.nlm.nih.gov/pubmed/33202219 | Which drugs were investigated in the ALPHEUS trial? | ALPHEUS study examined if ticagrelor was superior to clopidogrel in reducing periprocedural myocardial necrosis in stable coronary patients undergoing high-risk elective percutaneous coronary intervention (PCI). |
http://www.ncbi.nlm.nih.gov/pubmed/31709696,http://www.ncbi.nlm.nih.gov/pubmed/31858758,http://www.ncbi.nlm.nih.gov/pubmed/31853339 | Which cell secretes the enzyme tryptase? | Degranulation of mast cells (MCs) releases several mediators such as vascular endothelial growth factor (VEGF), chymase, tryptase, histamine, and cytokines. |
http://www.ncbi.nlm.nih.gov/pubmed/31755155,http://www.ncbi.nlm.nih.gov/pubmed/23517232,http://www.ncbi.nlm.nih.gov/pubmed/29576423,http://www.ncbi.nlm.nih.gov/pubmed/12084297,http://www.ncbi.nlm.nih.gov/pubmed/10575270,http://www.ncbi.nlm.nih.gov/pubmed/26032289,http://www.ncbi.nlm.nih.gov/pubmed/27241256,http://www.ncbi.nlm.nih.gov/pubmed/28488840,http://www.ncbi.nlm.nih.gov/pubmed/26000263,http://www.ncbi.nlm.nih.gov/pubmed/31900581,http://www.ncbi.nlm.nih.gov/pubmed/4412271,http://www.ncbi.nlm.nih.gov/pubmed/6342739,http://www.ncbi.nlm.nih.gov/pubmed/18976938,http://www.ncbi.nlm.nih.gov/pubmed/15281319,http://www.ncbi.nlm.nih.gov/pubmed/7016300,http://www.ncbi.nlm.nih.gov/pubmed/31307960,http://www.ncbi.nlm.nih.gov/pubmed/24064971,http://www.ncbi.nlm.nih.gov/pubmed/19957324,http://www.ncbi.nlm.nih.gov/pubmed/12057150,http://www.ncbi.nlm.nih.gov/pubmed/178234,http://www.ncbi.nlm.nih.gov/pubmed/30893148,http://www.ncbi.nlm.nih.gov/pubmed/9259090,http://www.ncbi.nlm.nih.gov/pubmed/27960233,http://www.ncbi.nlm.nih.gov/pubmed/1244548,http://www.ncbi.nlm.nih.gov/pubmed/8573479,http://www.ncbi.nlm.nih.gov/pubmed/19967427,http://www.ncbi.nlm.nih.gov/pubmed/28807024,http://www.ncbi.nlm.nih.gov/pubmed/32577059,http://www.ncbi.nlm.nih.gov/pubmed/25794874 | What disease does BCG immunotherapy used to treat? | Bacillus Calmette-Guérin (BCG) immunotherapy is used for treatment of bladder cancer.Bacillus Calmette- Guérin (BCG) immunotherapy is used for treatment of bladder cancer.Bacillus Calmette- Guérin (BCG) immunotherapy is used in the treatment of bladder cancer.BCG immunotherapy is the choice of care for high-grade non-muscle invasive bladder cancer (NMIBC) after transurethral resection.BCG immunotherapy is the choice of care for high-grade non-muscle invasive bladder cancer.Bacillus Calmette-guérin (BCG) immunotherapy is used in the treatment of bladder cancer. |
http://www.ncbi.nlm.nih.gov/pubmed/27410265,http://www.ncbi.nlm.nih.gov/pubmed/26151332,http://www.ncbi.nlm.nih.gov/pubmed/21311219,http://www.ncbi.nlm.nih.gov/pubmed/25071008,http://www.ncbi.nlm.nih.gov/pubmed/19462008,http://www.ncbi.nlm.nih.gov/pubmed/25754661,http://www.ncbi.nlm.nih.gov/pubmed/27630184,http://www.ncbi.nlm.nih.gov/pubmed/18974828,http://www.ncbi.nlm.nih.gov/pubmed/26564795,http://www.ncbi.nlm.nih.gov/pubmed/23706298 | Which epigenetic marks are deposited by PRC1? | PRC2 induces histone H3 lysine 27 (H3K27) trimethylation (H3K27me3), which is subsequently read by PRC1 that further catalyzes H2A monoubiquitination (H2Aub1), creating a transcriptional silent chromatin conformation.H2A monoubiquitination (H2Aub1), catalyzed by Polycomb-Repressive Complex1 (PRC1) is a key epigenetic mark in Polycomb silencing . Stable X chromosome inactivation involves the PRC1 Polycomb complex and requires histone MACROH2A1 and the CULLIN3/SPOP ubiquitin E3 ligase .Histone H2A monoubiquitination (H2Aub1), catalyzed by Polycomb-Repressive Complex1 (PRC1), is a key epigenetic mark in Polycomb silencing . Stable X chromosome inactivation involves the PRC1 Polycomb complex and requires histone MACROH2A1 and the CULLIN3/SPOP ubiquitin E3 ligase . |
http://www.ncbi.nlm.nih.gov/pubmed/30651064 | Does erenumab target the calcitonin gene-related peptide? | No, erenumab targets the calcitonin gene-related peptide receptor. |
http://www.ncbi.nlm.nih.gov/pubmed/26754677 | Which key gene is involved in interstitial 6q25 microdeletion syndrome? | Interstitial deletions of the long arm of chromosome 6 are rare. Clinically, these deletions are considered to be part of a unique microdeletion syndrome associated with intellectual disability and speech impairment, typical dysmorphic features, structural anomalies of the brain, microcephaly, and non-specific multiple organ anomalies. ARID1B is the key gene behind 6q microdeletion syndrome.Interstitial 6q25 microdeletion syndrome (ICS) is a rare autosomal dominant disorder characterized by loss-of-function mutations of the ARID1B gene and severe intrauterine and post-natal growth retardationThe critical region for the interstitial 6q microdeletion phenotype was mapped to 6q24-6q25, particularly the 6q25.3 region containing the genes ARID1B and ZDHHC14.Interstitial 6q25 microdeletion syndrome (IL-6q25) is a rare autosomal dominant disorder caused by mutations in the ARID1B gene, which encodes a major regulator of heme oxygenase 1 (HMOX1), resulting in a loss of a ubiquitously expressed protein, gigaxonin.Interstitial 6q25 microdeletion syndrome (IPS) is a rare autosomal dominant disorder characterized by loss-of-function mutations in the ARID1B gene, which encodes a major regulator of heme oxygenase 1 (HMOX1), and many other genes involved in heme catabolism.Interstitial 6q25 microdeletion syndrome (ICS) is a rare autosomal recessive genetic disorder characterized by loss-of-function mutations in the ARID1B gene, which encodes a major regulator of heme oxygenase activity. |
http://www.ncbi.nlm.nih.gov/pubmed/32897034 | Brensocatib was tested for treatment of which disease? | Brensocatib was tested for bronchiectasis. Brensocatib in patients with bronchiectasis was associated with improvements in bronchiectasis clinical outcomes. |
http://www.ncbi.nlm.nih.gov/pubmed/11274192,http://www.ncbi.nlm.nih.gov/pubmed/21489137,http://www.ncbi.nlm.nih.gov/pubmed/18723604,http://www.ncbi.nlm.nih.gov/pubmed/17384198,http://www.ncbi.nlm.nih.gov/pubmed/12244050 | What is the function of the protein Cuf1? | Cuf1 is a copper-sensing transcription factor. |
http://www.ncbi.nlm.nih.gov/pubmed/28588308,http://www.ncbi.nlm.nih.gov/pubmed/32132243 | How many groups of viruses exist in the Baltimore Classification? | There are seven "Baltimore classes" (BCs) that define the major features of virus reproduction.seven "Baltimore classes" (BCs) that define the major features of virus reproductionThe Baltimore Classification system consists of seven classes (A, B, C, D, E, F, G, C and D) that are classified into seven different regions based on sequence similarity. |
http://www.ncbi.nlm.nih.gov/pubmed/22363428,http://www.ncbi.nlm.nih.gov/pubmed/14695408,http://www.ncbi.nlm.nih.gov/pubmed/15378020,http://www.ncbi.nlm.nih.gov/pubmed/29763912,http://www.ncbi.nlm.nih.gov/pubmed/24671437,http://www.ncbi.nlm.nih.gov/pubmed/20142103,http://www.ncbi.nlm.nih.gov/pubmed/11044603,http://www.ncbi.nlm.nih.gov/pubmed/14695885,http://www.ncbi.nlm.nih.gov/pubmed/20161711,http://www.ncbi.nlm.nih.gov/pubmed/21811562,http://www.ncbi.nlm.nih.gov/pubmed/18505732,http://www.ncbi.nlm.nih.gov/pubmed/21861760,http://www.ncbi.nlm.nih.gov/pubmed/17295608,http://www.ncbi.nlm.nih.gov/pubmed/30216540,http://www.ncbi.nlm.nih.gov/pubmed/28849121,http://www.ncbi.nlm.nih.gov/pubmed/26880631,http://www.ncbi.nlm.nih.gov/pubmed/20543981,http://www.ncbi.nlm.nih.gov/pubmed/20618428,http://www.ncbi.nlm.nih.gov/pubmed/29165387,http://www.ncbi.nlm.nih.gov/pubmed/24520934,http://www.ncbi.nlm.nih.gov/pubmed/23261660 | What is the effect of Dkk1 in Wnt signaling? | Transcriptional silencing of the Wnt-antagonist DKK1 is a secreted protein that antagonizes Wnt signaling and plays essential roles in vertebrate embryogenesis.DKK1 is a secreted protein that antagonizes Wnt signaling and plays essential roles in vertebrate embryogenesis.DKK1 is a secreted protein that inhibits WNT signaling and plays essential roles in vertebrate embryogenesis.DKK1 is a secreted protein that antagonizes Wnt signaling and plays essential roles in vertebrate embryogenesis including head induction, skeletal development, and limb patterning. |
http://www.ncbi.nlm.nih.gov/pubmed/27167138,http://www.ncbi.nlm.nih.gov/pubmed/30095981,http://www.ncbi.nlm.nih.gov/pubmed/29226558,http://www.ncbi.nlm.nih.gov/pubmed/29566437 | What is bimagrumab | Bimagrumab is a fully human monoclonal antibody that blocks the activin type II receptors, preventing the activity of myostatin and other negative skeletal muscle regulators. |
http://www.ncbi.nlm.nih.gov/pubmed/21159646,http://www.ncbi.nlm.nih.gov/pubmed/29380674,http://www.ncbi.nlm.nih.gov/pubmed/27335255,http://www.ncbi.nlm.nih.gov/pubmed/28334731,http://www.ncbi.nlm.nih.gov/pubmed/31575759 | List orally bioavailable MPS1 kinase inhibitors | 1 h-pyrrolo [3,2-c] pyridine, cct271850, nms-p715, 4-aminopyrazalo,bos172722 and cct251455.1 h-pyrrolo [3,2-c] pyridine, cct271850, nms-p715, 4-aminopyrazolo, bos172722, cCT251455.MPS1 kinase is a key regulator of the spindle assembly checkpoint (SAC), a mitotic mechanism specifically required for proper chromosomal alignment and segregation. It has been found aberrantly overexpressed in a wide range of human tumors and is necessary for tumoral cell proliferation. CCT251455, BOS172722, CCT271850, 4-(4-aminopyrazolo[1,5-a][1,3,5]triazin-8-yl)benzamides and NMS-P715 are orally bioavailable MPS1 kinase inhibitors.1 h-pyrrolo [3,2-c] pyridine, cct271850, nms-p715, 4-aminopyrazolo, bos172722 and cct251455 are orally bioavailable MPS1 kinase inhibitors.1 h-pyrrolo [3,2-c] pyridine, cct271850, nms-p715, 4-aminopyrazola,bos172722 and cct251455 are orally bioavailable MPS1 kinase inhibitors. |
http://www.ncbi.nlm.nih.gov/pubmed/28868186,http://www.ncbi.nlm.nih.gov/pubmed/17240596 | Can radiosurgery be used for the DNET tumors? | Yes, radiosurgery is used for the DNET (Dysembryoplastic neuroepithelial) tumors. However, the level of evidence is limited. |
http://www.ncbi.nlm.nih.gov/pubmed/30672882,http://www.ncbi.nlm.nih.gov/pubmed/31049923,http://www.ncbi.nlm.nih.gov/pubmed/33186243,http://www.ncbi.nlm.nih.gov/pubmed/32758517 | What are commensal bacteria? | The gut microbiota is composed of a large number of microbes, usually regarded as commensal bacteria. Maintenance of the commensal bacteria that comprise the gut microbiome is essential to both gut and systemic health. |
http://www.ncbi.nlm.nih.gov/pubmed/31740281,http://www.ncbi.nlm.nih.gov/pubmed/29073101,http://www.ncbi.nlm.nih.gov/pubmed/31924266,http://www.ncbi.nlm.nih.gov/pubmed/30509212,http://www.ncbi.nlm.nih.gov/pubmed/24838796,http://www.ncbi.nlm.nih.gov/pubmed/29725259,http://www.ncbi.nlm.nih.gov/pubmed/31282990,http://www.ncbi.nlm.nih.gov/pubmed/27028180,http://www.ncbi.nlm.nih.gov/pubmed/31935506,http://www.ncbi.nlm.nih.gov/pubmed/25934606,http://www.ncbi.nlm.nih.gov/pubmed/32817139,http://www.ncbi.nlm.nih.gov/pubmed/31883305 | What disease is associate with defects in both the KDM6A (lysine specific demethylase 6A) and KMT2D (lysine methyltransferase 2D) | Over the last 20 years, mutations in five key COMPASS complex genes have been linked to three human congenital syndromes: Kabuki syndrome (type 1 [KMT2D] and 2 [KDM6A]Kabuki syndrome is a rare genetic disorder, caused by mutation in the KMT2D or KDM6A genes, which affects several organs in the majority of patients, among which are the eyes. |
http://www.ncbi.nlm.nih.gov/pubmed/20581311,http://www.ncbi.nlm.nih.gov/pubmed/19796237,http://www.ncbi.nlm.nih.gov/pubmed/23024276,http://www.ncbi.nlm.nih.gov/pubmed/23382991,http://www.ncbi.nlm.nih.gov/pubmed/25940801,http://www.ncbi.nlm.nih.gov/pubmed/29973462,http://www.ncbi.nlm.nih.gov/pubmed/26267538,http://www.ncbi.nlm.nih.gov/pubmed/29382715,http://www.ncbi.nlm.nih.gov/pubmed/16751774 | Which transcription factor regulates emergency granulopoiesis? | The transcription factor CCAAT/enhancer binding protein β (C/EBPβ) plays critical roles in the differentiation and proliferation of hematopoietic stem cells.The transcription factor CCAAT/enhancer binding protein β (C/EBPβ) plays critical roles in emergency granulopoiesis, but the precise developmental stages in which C/EBPalpha is required are unknown . 'Steady-state' granulopsis is absolutely dependent on the C/ EBPalpha transcription factor .The transcription factor CCAAT/enhancer binding protein β (C/EBPβ) plays critical roles in the differentiation and proliferation of hematopoietic stem cells. It is a transcription factor required for emergency granulopoiesis.Differentiation and proliferation of hematopoietic stem cells are regulated by C/EBPβ, a transcription factor required for emergency granulopoiesis. Granulopoiesis during emergency situations, such as infection, is dependent on C/EBPβ.These data suggest a critical function for C/EBPbeta in emergency granulopoiesis, which demands both differentiation and proliferation of granulocyte precursors.The transcription factor CCAAT/enhancer binding protein β (C/EBPβ) plays critical roles in the differentiation and proliferation of hematopoietic stem cells. There is no definitive role of the transcription factor in emergency granulopoiesis.The transcription factor CCAAT/enhancer binding protein β (C/EBPβ) regulates the differentiation and proliferation of hematopoietic stem cells. |
http://www.ncbi.nlm.nih.gov/pubmed/32266704 | When did eptinezumab get its first FDA approval? | In February 2020, eptinezumab was approved in the USA for the preventive treatment of migraine in adults. |
http://www.ncbi.nlm.nih.gov/pubmed/32098967 | Which database exists that contains regulatory sites for splicing in human basal ganglia? | Braineacv2 has been identified as a database that contains regulatory sites for splicing in human basal ganglia.Genome-wide association studies have generated an increasing number of common genetic variants associated with neurological and psychiatric disease risk. An improved understanding of the genetic control of gene expression in human brain is vital considering this is the likely modus operandum for many causal variants. However, human brain sampling complexities limit the explanatory power of brain-related expression quantitative trait loci (eQTL) and allele-specific expression (ASE) signals. Disease-relevant regulatory loci were identified, finding that splicing eQTLs are enriched for regulatory information of neuron-specific genes, that ASEs provide cell-specific regulatory information with evidence for cellular specificity, and that incomplete annotation of the brain transcriptome limits interpretation of risk loci for neuropsychiatric disease. This resource of regulatory data is accessible through http://braineacv2.inf.um.es/.Braineacv2 is a database that contains regulatory sites for splicing in human basal ganglia. |
http://www.ncbi.nlm.nih.gov/pubmed/31738372 | Should minocycline be used for mild Alzheimer disease? | No. Minocycline did not delay the progress of cognitive or functional impairment in people with mild Alzheimer disease during a 2-year period. |
http://www.ncbi.nlm.nih.gov/pubmed/30917630,http://www.ncbi.nlm.nih.gov/pubmed/31733200,http://www.ncbi.nlm.nih.gov/pubmed/31710896,http://www.ncbi.nlm.nih.gov/pubmed/31756255 | What is pyroptosis? | Pyroptosis is an inflammatory form of cell death triggered by certain inflammasomes, leading to the cleavage of gasdermin D (GSDMD) and activation of inactive cytokines like IL-18 and IL-1β. Pyroptosis has been reported to be closely associated to some diseases like atherosclerosis and diabetic nephropathy. Recently, some studies found that pyroptosis can influence the proliferation, invasion and metastasis of tumor, which regulated by some non-coding RNAs and other molecules. |
http://www.ncbi.nlm.nih.gov/pubmed/16877472,http://www.ncbi.nlm.nih.gov/pubmed/21210977,http://www.ncbi.nlm.nih.gov/pubmed/16982009,http://www.ncbi.nlm.nih.gov/pubmed/18453083,http://www.ncbi.nlm.nih.gov/pubmed/19933162,http://www.ncbi.nlm.nih.gov/pubmed/22844100,http://www.ncbi.nlm.nih.gov/pubmed/17943122,http://www.ncbi.nlm.nih.gov/pubmed/12615007,http://www.ncbi.nlm.nih.gov/pubmed/20869033,http://www.ncbi.nlm.nih.gov/pubmed/19913122,http://www.ncbi.nlm.nih.gov/pubmed/17568388,http://www.ncbi.nlm.nih.gov/pubmed/16434598,http://www.ncbi.nlm.nih.gov/pubmed/16374835,http://www.ncbi.nlm.nih.gov/pubmed/17033966,http://www.ncbi.nlm.nih.gov/pubmed/21356867,http://www.ncbi.nlm.nih.gov/pubmed/14685227,http://www.ncbi.nlm.nih.gov/pubmed/19286890,http://www.ncbi.nlm.nih.gov/pubmed/15454560,http://www.ncbi.nlm.nih.gov/pubmed/17922574,http://www.ncbi.nlm.nih.gov/pubmed/22319179,http://www.ncbi.nlm.nih.gov/pubmed/15587301 | What is a HapMap | HapMap is a international effort for creating an annotated haplotype map of the world’s most commonhaplotype sequences.HapMap provides linkage disequilibrium information on a sample of 3.7 million SNPs that can be used for tag SNP selection in whole-genome association studies.A haplotype map (HapMap)is aimed at describing these variation patterns across the entire genome and has been recently developed by the International HapMap Consortium. HapMap characterizes over 3.1 million human single nucleotide polymorphisms (SNPs) genotyped in 270 individuals from four geographically diverse populations and includes 25-35% of common SNP variation in the populations surveyed.The "HapMap" project is now underway to characterize patterns of LD in the human genome.The HapMap haplotype map project aims to systematically map all human haplotypes, chromosome by chromosome, in a gene-dependent manner through dedicated efforts from national and international teams.The HapMap haplotype map project aims to systematically map all human haplotypes, chromosome by chromosome, in a gene-rich manner through dedicated efforts from national and international teams.The International Haplotype Map Project (HapMap) is an international effort for creating an annotated haplotype map of the human genome using protein sequences and other genomic data.A HapMap is a map of the human genome. It's a 3.1 million human single nucleotide polymorphisms (SNPs) that can be genotyped and mapped. |
http://www.ncbi.nlm.nih.gov/pubmed/24117170,http://www.ncbi.nlm.nih.gov/pubmed/21330172,http://www.ncbi.nlm.nih.gov/pubmed/21876555,http://www.ncbi.nlm.nih.gov/pubmed/30272327,http://www.ncbi.nlm.nih.gov/pubmed/29123266,http://www.ncbi.nlm.nih.gov/pubmed/29455655,http://www.ncbi.nlm.nih.gov/pubmed/25368021,http://www.ncbi.nlm.nih.gov/pubmed/25622896,http://www.ncbi.nlm.nih.gov/pubmed/25892968,http://www.ncbi.nlm.nih.gov/pubmed/28851812,http://www.ncbi.nlm.nih.gov/pubmed/28466252,http://www.ncbi.nlm.nih.gov/pubmed/23623921,http://www.ncbi.nlm.nih.gov/pubmed/17437280,http://www.ncbi.nlm.nih.gov/pubmed/21502402,http://www.ncbi.nlm.nih.gov/pubmed/29477381,http://www.ncbi.nlm.nih.gov/pubmed/19373776,http://www.ncbi.nlm.nih.gov/pubmed/30265861,http://www.ncbi.nlm.nih.gov/pubmed/29452232,http://www.ncbi.nlm.nih.gov/pubmed/23364532,http://www.ncbi.nlm.nih.gov/pubmed/20689556,http://www.ncbi.nlm.nih.gov/pubmed/27524420,http://www.ncbi.nlm.nih.gov/pubmed/19863427 | Which cancer types are associated with mutations in the TWIST1 gene? | Loss-of-function mutations of TWIST1, a catalytic component of polycomb repressive complex 1, are observed in ~\n10% of all human cancers, including gastric, non-small cell lung, breast ductal carcinoma, nonsmall cell lung cancer, prostate cancer, ovarian cancer, breast tumor, papillary thyroid cancer, and gastric cancer.Cancer is caused by uncontrolled cell division. Mutations in TWIST1 are associated with breast cancer, prostate cancer, lung cancer, and skin cancer.Cancer is caused by uncontrolled cell division. Mutations in TWIST1 are associated with breast cancer, prostate cancer, lung cancer, and lung cancer.TWIST1, an epithelial-mesenchymal transition (EMT) transcription factor, is critical for oncogene-driven non-small cell lung cancer (NSCLC) tumorigenesis. STAT3 mediates TGF-β1-induced TWIST1 expression and prostate cancer invasion. Phosphorylation of serine 68 of Twist1 by MAPKs stabilizes Twist1 protein and promotes breast cancer cell invasiveness. The Transcription Factor ETV5 Mediates BRAFV600E-Induced Proliferation and TWIST1 Expression in Papillary Thyroid Cancer Cells.Cancer is caused by uncontrolled cell division. Mutations in TWIST1 are associated with breast cancer, prostate cancer, and lung cancer.Cancer is caused by uncontrolled cell division. Mutations in TWIST1 are associated with breast cancer, prostate cancer, lung cancer, and prostate cancer.Loss-of-function mutations of TWIST1, a catalytic component of polycomb repressive complex 1 (PRC1), are observed in ~\n10% of patients with gastric, non-small cell lung, breast ductal carcinomas, nonsmall cell lung cancer, prostate cancer, ovarian cancer, breast tumor, papillary thyroid cancer, and gastric cancer.Loss-of-function mutations of TWIST1, a catalytic component of polycomb repressive complex 1 (PRC1), are observed in ~\n10% of patients with gastric, non-small cell lung, breast ductal carcinomas, nonsmall cell lung cancer, prostate cancer, female breast cancer, ovarian cancer, breast tumor, papillary thyroid cancer, and gastric cancer.Loss-of-function mutations of TWIST1, a catalytic component of polycomb repressive complex 1 (PRC1), are observed in ~\n10% of patients with gastric, non-small cell lung, breast ductal carcinomas, nonsmall cell lung cancer, prostate cancer, ovarian cancer, breast tumor, papillary thyroid cancer, cervical cancer, adenoid cystic carcinoma, salivary gland neoplasms. |
http://www.ncbi.nlm.nih.gov/pubmed/31761834 | What did the RESILIENT study investigate? | A global, randomized, double-blind placebo-controlled study was conducted to confirm that BYM338 (bimagrumab), an anti-activin type II receptor antibody, improves motor function in patients with sporadic inclusion body myositis after 52 weeks' treatment consisting of intravenous administration every 4 weeks at doses of 10, 3, and 1 mg/kg. |
http://www.ncbi.nlm.nih.gov/pubmed/16104532,http://www.ncbi.nlm.nih.gov/pubmed/1605172,http://www.ncbi.nlm.nih.gov/pubmed/21415981,http://www.ncbi.nlm.nih.gov/pubmed/23263974,http://www.ncbi.nlm.nih.gov/pubmed/2647685,http://www.ncbi.nlm.nih.gov/pubmed/18097325,http://www.ncbi.nlm.nih.gov/pubmed/23767207,http://www.ncbi.nlm.nih.gov/pubmed/11399382,http://www.ncbi.nlm.nih.gov/pubmed/32190437,http://www.ncbi.nlm.nih.gov/pubmed/23738162,http://www.ncbi.nlm.nih.gov/pubmed/22233953,http://www.ncbi.nlm.nih.gov/pubmed/21850657,http://www.ncbi.nlm.nih.gov/pubmed/30447150,http://www.ncbi.nlm.nih.gov/pubmed/32699732,http://www.ncbi.nlm.nih.gov/pubmed/16616715,http://www.ncbi.nlm.nih.gov/pubmed/29123569,http://www.ncbi.nlm.nih.gov/pubmed/12423834,http://www.ncbi.nlm.nih.gov/pubmed/9360410,http://www.ncbi.nlm.nih.gov/pubmed/29270999,http://www.ncbi.nlm.nih.gov/pubmed/1821908,http://www.ncbi.nlm.nih.gov/pubmed/25512716,http://www.ncbi.nlm.nih.gov/pubmed/22574558,http://www.ncbi.nlm.nih.gov/pubmed/1171419,http://www.ncbi.nlm.nih.gov/pubmed/10775033,http://www.ncbi.nlm.nih.gov/pubmed/8427289,http://www.ncbi.nlm.nih.gov/pubmed/16913442,http://www.ncbi.nlm.nih.gov/pubmed/7863389,http://www.ncbi.nlm.nih.gov/pubmed/12745043,http://www.ncbi.nlm.nih.gov/pubmed/26634125,http://www.ncbi.nlm.nih.gov/pubmed/17525362,http://www.ncbi.nlm.nih.gov/pubmed/29340125,http://www.ncbi.nlm.nih.gov/pubmed/19665681,http://www.ncbi.nlm.nih.gov/pubmed/33024522,http://www.ncbi.nlm.nih.gov/pubmed/30072561,http://www.ncbi.nlm.nih.gov/pubmed/4038757,http://www.ncbi.nlm.nih.gov/pubmed/12753286,http://www.ncbi.nlm.nih.gov/pubmed/10541941,http://www.ncbi.nlm.nih.gov/pubmed/12938786 | List features of the Thrombotic Thrombocytopenic Purpura pentad. | Thrombotic thrombocytopenic purpura (TTP) is typically characterized by the symptomatic pentad of fever, thrombocytopenia, microangiopathic hemolytic anemia, neurologic abnormalities, and renal failure. |
http://www.ncbi.nlm.nih.gov/pubmed/32865304,http://www.ncbi.nlm.nih.gov/pubmed/33068633,http://www.ncbi.nlm.nih.gov/pubmed/33241206,http://www.ncbi.nlm.nih.gov/pubmed/32984947 | What are organoids? | Organoids are 3D physiological in vitro structures that recapitulate morphological and functional features of in vivo tissues and offer significant advantages over traditional cell culture methods. |
http://www.ncbi.nlm.nih.gov/pubmed/33008506,http://www.ncbi.nlm.nih.gov/pubmed/20664247,http://www.ncbi.nlm.nih.gov/pubmed/32923741,http://www.ncbi.nlm.nih.gov/pubmed/17458494,http://www.ncbi.nlm.nih.gov/pubmed/31579938,http://www.ncbi.nlm.nih.gov/pubmed/31408270,http://www.ncbi.nlm.nih.gov/pubmed/29173661,http://www.ncbi.nlm.nih.gov/pubmed/19837283,http://www.ncbi.nlm.nih.gov/pubmed/17119144 | List 3 therapeutic uses for botulism toxin. | Botulinum toxin injections are effective in relieving focal spasticity resulting from upper motor neuron injuries, migraine headaches, over active bladder and to relieve pain in the Sacroiliac Joint. |
http://www.ncbi.nlm.nih.gov/pubmed/23040478,http://www.ncbi.nlm.nih.gov/pubmed/28288968,http://www.ncbi.nlm.nih.gov/pubmed/18347094,http://www.ncbi.nlm.nih.gov/pubmed/30115631,http://www.ncbi.nlm.nih.gov/pubmed/29513567,http://www.ncbi.nlm.nih.gov/pubmed/21685889,http://www.ncbi.nlm.nih.gov/pubmed/29299140,http://www.ncbi.nlm.nih.gov/pubmed/23658527 | What is the role of Tcf3 in the maintenance of pluripotency? | Tcf3 is an integral component of the core regulatory circuitry of ES cells, which includes an autoregulatory loop involving the pluripotency regulators. Tcf3 co-occupies promoters throughout the genome in association with the pluripotency regulators Oct4 and Nanog. Tcf3 down-regulation modulates the lineage differentiation potential of mouse embryonic stem cells through Wnt signaling. Tcf3 down-regulation is a necessary step towards Wnt-mediated suppression of differentiation. Depletion of Tcf3 enables the maintenance of undifferentiated mouse ESCs.The maintenance of pluripotency in mouse embryonic stem cells relies on a transcriptional network that is fuelled by the activity of three transcription factors (Nanog, Oct4 and Sox2) and balanced by the repressive activity of Tcf3 . We uncover a key role for post-translational regulation in the maintenance of pliospotency .The maintenance of pluripotency in mouse embryonic stem cells relies on a transcriptional network that is fuelled by the activity of three transcription factors (Nanog, Oct4 and Sox2) and balanced by the repressive activity of Tcf3 . We found that down-regulation of Tlf3, a member of the Tcf/Lef family, represents a specific response to Wnt activation in ESCs . Further studies revealed that T cell factor 3 ( TCF3) is a potential downstream target of TERRA .The maintenance of pluripotency in mouse embryonic stem cells relies on a transcriptional network that is fuelled by the activity of three transcription factors (Nanog, Oct4 and Sox2) and balanced by the repressive activity of Tcf3 . A recent report shows that β-catenin modulates the effect of TERRA in mESC maintenance . |
http://www.ncbi.nlm.nih.gov/pubmed/27269043,http://www.ncbi.nlm.nih.gov/pubmed/28644160,http://www.ncbi.nlm.nih.gov/pubmed/31758661,http://www.ncbi.nlm.nih.gov/pubmed/29136283 | What pathological condition is MK-1602 used for? | MK-1602 has been assessed in clinical trials for the acute treatment of migraine. |
http://www.ncbi.nlm.nih.gov/pubmed/28067910 | Is there an association of alterations in ADCY7 and ulcerative colitis? | Yes. Genome-wide analyses indicate a association between mutations in ACVR1 and ulcerative colitis due to loss-of-function mutations in ADCY7.Yes. Sequencing analysis showed an association between mutations in ADCY7 and ulcerative colitis patients and high psychopathic traits.Yes. Genome-wide analyses indicate an association of alterations in ADCY7 and ulcerative colitis. Mutations in exon 2 interfere with the synthesis of the full-length isoform of CDKN2A and lead to the production of a shortened isoform, with significant morbidity and mortality.Yes, there is an association of alterations in ADCY7 and ulcerative colitis.To further resolve the genetic architecture of the inflammatory bowel diseases ulcerative colitis and Crohn's disease, whole genomes of 4,280 patients were sequenced at low coverage and compared to 3,652 previously sequenced population controls across 73.5 million variants. A 0.6% frequency missense variant in ADCY7 was discovered that doubles the risk of ulcerative colitis. |
http://www.ncbi.nlm.nih.gov/pubmed/32797372,http://www.ncbi.nlm.nih.gov/pubmed/33011853,http://www.ncbi.nlm.nih.gov/pubmed/32228250,http://www.ncbi.nlm.nih.gov/pubmed/32333898,http://www.ncbi.nlm.nih.gov/pubmed/32306778,http://www.ncbi.nlm.nih.gov/pubmed/31774956,http://www.ncbi.nlm.nih.gov/pubmed/32731771,http://www.ncbi.nlm.nih.gov/pubmed/32348222,http://www.ncbi.nlm.nih.gov/pubmed/33301078,http://www.ncbi.nlm.nih.gov/pubmed/30623348,http://www.ncbi.nlm.nih.gov/pubmed/32304439,http://www.ncbi.nlm.nih.gov/pubmed/33059216,http://www.ncbi.nlm.nih.gov/pubmed/33167776 | What is the mechanism of action of satralizumab? | Satralizumab is a humanized anti-interleukin-6 (IL-6) receptor monoclonal recycling antibody that has been approved for the treatment of neuromyelitis optica spectrum disorder (NMOSD). |
http://www.ncbi.nlm.nih.gov/pubmed/31837357,http://www.ncbi.nlm.nih.gov/pubmed/33300069,http://www.ncbi.nlm.nih.gov/pubmed/31729101,http://www.ncbi.nlm.nih.gov/pubmed/32195770 | Are mucin overexpression associated with disease? | Yes,
mucins are overexpressed in various malignancies and inflammations. |
http://www.ncbi.nlm.nih.gov/pubmed/6431778,http://www.ncbi.nlm.nih.gov/pubmed/17001700,http://www.ncbi.nlm.nih.gov/pubmed/15301825,http://www.ncbi.nlm.nih.gov/pubmed/28050387 | What are the 4 types of holoprosencephaly? | Holoprosencephaly is a rare congenital disorder which results from failure of cleavage or incomplete differentiation of the forebrain structures at various levels or to various degrees . Depending on the degree of involvement, it is classified into 4 types: Alobar, Semilobar, Lobar, and Middle interhemispheric fusion variant .Holoprosencephaly is a rare congenital disorder which results from failure of cleavage or incomplete differentiation of the forebrain structures at various levels or to various degrees. Depending on the degree of involvement, it is classified into 4 types: Alobar, Semilobar, Lobar and Middle interhemispheric fusion variant.The 4 types of holoprosencephaly is a rare congenital disorder which results from failure of cleavage or incomplete differentiation of the foremost structures at various levels or to varying degrees. Depending on the degree of involvement, it is divided into 4 types: Alobar, Halilobar, Lobar and Middle interhemispheric fusion variant.4 types of holoprosencephaly have been described: lobar, alobar, interhemispheric, sacral, and cerebellar.The 4 types of holoprosencephaly is a rare congenital disorder which results from failure of cleavage or incomplete differentiation of the foremost structures at various levels or to varying degrees. Depending on the degree of involvement, it is broken down into 4 types: Alobar, Halilobar, Lobar and Middle interhemispheric fusion variant.Four types of holoprosencephaly have been described: lobar, alobar, interhemispheric, and sacral. (PMID: 22990134) |
http://www.ncbi.nlm.nih.gov/pubmed/26904946,http://www.ncbi.nlm.nih.gov/pubmed/16100111,http://www.ncbi.nlm.nih.gov/pubmed/12783798,http://www.ncbi.nlm.nih.gov/pubmed/10811823,http://www.ncbi.nlm.nih.gov/pubmed/25300489,http://www.ncbi.nlm.nih.gov/pubmed/12719426,http://www.ncbi.nlm.nih.gov/pubmed/11846874,http://www.ncbi.nlm.nih.gov/pubmed/10749931,http://www.ncbi.nlm.nih.gov/pubmed/10485849 | Which yeast genes encode for condensin? | Smc2-Smc4 forms the core of the Saccharomyces cerevisiae condensin, which promotes metaphase chromosome compaction . Both SMC2 and SMC4 are essential for chromosome transmission in anaphase . Smc 2-8 suppresses catenanes accumulation, mitotic arrest and growth defects induced by histone depletion at semi-permissive temperature .Smc2/4 forms the core of the Saccharomyces cerevisiae condensin, which promotes metaphase chromosome compactionCondensin Smc2-Smc4 Dimers Are Flexible and Dynamic. Here, we probe the topology of Smc2-Smc4 dimers of the S. cerevisiae condensin complex with high-speed atomic force microscopy (AFM) in liquid Interestingly, SAC activation is suppressed by the absence of Top2 and Smc2, an essential component of condensin. |
http://www.ncbi.nlm.nih.gov/pubmed/28240610 | What is another name for the drug AMG334? | AMG334 is also called erenumab. |