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http://www.ncbi.nlm.nih.gov/pubmed/25087078 | Describe the genetic determinants of common epilepsies | Genetic determinants of common epilepsies are defined as the interaction of mutations in one of two unlinked genes, SCN1 and SCN2, which code for the proteins hamartin and epilepticin, respectively. Disruption of these genes has been found to be associated with epileptic encephalopathies, but it is not entirely clear if this translates directly to the increased risk for epilepsy or via epigenetic changes.The epilepsies are a clinically heterogeneous group of neurological disorders. Despite strong evidence for heritability, genome-wide association studies have had little success in identification of risk loci associated with epilepsy, probably because of relatively small sample sizes and insufficient power. Meta-analysis of an all-epilepsy cohort identified loci at 2q24.3 (p=8·71 × 10(-10)), implicating SCN1A, and at 4p15.1 (p=5·44 × 10(-9)), harbouring PCDH7, which encodes a protocadherin molecule. For the cohort of genetic generalised epilepsy, a single signal at 2p16.1 (p=9·99 × 10(-9)), implicating VRK2 or FANCL was noted. Data suggest that specific loci can act pleiotropically raising risk for epilepsy broadly, or can have effects limited to a specific epilepsy subtype. |
http://www.ncbi.nlm.nih.gov/pubmed/32087818,http://www.ncbi.nlm.nih.gov/pubmed/33148815 | Should nerinetide be used for treatment of ischaemic stroke? | Nerinetide did not improve the proportion of ischemic stroke patients achieving good clinical outcomes after endovascular thrombectomy compared with patients receiving placebo. |
http://www.ncbi.nlm.nih.gov/pubmed/16247561,http://www.ncbi.nlm.nih.gov/pubmed/24661745,http://www.ncbi.nlm.nih.gov/pubmed/11985619 | What is the role of alcohol acyl transferases in fruit aroma? | Volatile esters, a major class of compounds contributing to the aroma of many fruit, are synthesized by alcohol acyl-transferases (AAT).
The expression of all Cm-AAT genes is up-regulated during ripening and inhibited in antisense ACC oxidase melons and in fruit treated with the ethylene antagonist 1-methylcyclopropene (1-MCP), indicating a positive regulation by ethylene. |
http://www.ncbi.nlm.nih.gov/pubmed/24056835,http://www.ncbi.nlm.nih.gov/pubmed/20531124,http://www.ncbi.nlm.nih.gov/pubmed/32985914,http://www.ncbi.nlm.nih.gov/pubmed/24869848,http://www.ncbi.nlm.nih.gov/pubmed/31542731,http://www.ncbi.nlm.nih.gov/pubmed/29369656,http://www.ncbi.nlm.nih.gov/pubmed/29188542,http://www.ncbi.nlm.nih.gov/pubmed/32631267,http://www.ncbi.nlm.nih.gov/pubmed/31305235,http://www.ncbi.nlm.nih.gov/pubmed/29440704,http://www.ncbi.nlm.nih.gov/pubmed/21706238,http://www.ncbi.nlm.nih.gov/pubmed/29615267,http://www.ncbi.nlm.nih.gov/pubmed/26973544,http://www.ncbi.nlm.nih.gov/pubmed/25836972,http://www.ncbi.nlm.nih.gov/pubmed/32913802 | What is Hikikomori syndrome? | The 'Hikikomori' syndrome (HS) consists of prolonged and severe social withdrawal.Hikikomori syndrome is a Japanese culture-bound syndrome and a serious social withdrawal in Japan. It is a condition in which a subject locks himself/self into a house for a prolonged period of time for the period of 6 months or more, with no evident psychosis.Hikikomori syndrome is a Japanese culture-bound syndrome and a serious social problem in Japan. It is a condition in which a subject locks himself/self into a house for a prolonged period of time for the period of 6 months or more, with no evident psychosis.Hikikomori syndrome is a Japanese culture-bound syndrome and a serious social problem in Japan. It's a condition in which a subject locks himself/self into a house for a prolonged period of time for the period of 6 months or more, with no evident psychosis.Hikikomori is a clinical condition in which a subject locks himself/herself into his/her own house for more than 6 months.Hikikomori syndrome is a Japanese culture-bound syndrome and a serious social withdrawal in Japan. It's a condition in which a subject locks himself/self into a house for a prolonged period of time for the period of 6 months or more, with no evident psychosis. |
http://www.ncbi.nlm.nih.gov/pubmed/25118508,http://www.ncbi.nlm.nih.gov/pubmed/8988166,http://www.ncbi.nlm.nih.gov/pubmed/8988167,http://www.ncbi.nlm.nih.gov/pubmed/15923834,http://www.ncbi.nlm.nih.gov/pubmed/10094188,http://www.ncbi.nlm.nih.gov/pubmed/11314068,http://www.ncbi.nlm.nih.gov/pubmed/10649491,http://www.ncbi.nlm.nih.gov/pubmed/9215678,http://www.ncbi.nlm.nih.gov/pubmed/17868088,http://www.ncbi.nlm.nih.gov/pubmed/16502419,http://www.ncbi.nlm.nih.gov/pubmed/15735646,http://www.ncbi.nlm.nih.gov/pubmed/28521820,http://www.ncbi.nlm.nih.gov/pubmed/9259286,http://www.ncbi.nlm.nih.gov/pubmed/12221714,http://www.ncbi.nlm.nih.gov/pubmed/19483581,http://www.ncbi.nlm.nih.gov/pubmed/12116251,http://www.ncbi.nlm.nih.gov/pubmed/28220539,http://www.ncbi.nlm.nih.gov/pubmed/11772178,http://www.ncbi.nlm.nih.gov/pubmed/22628249,http://www.ncbi.nlm.nih.gov/pubmed/21814570,http://www.ncbi.nlm.nih.gov/pubmed/24585549,http://www.ncbi.nlm.nih.gov/pubmed/16251895,http://www.ncbi.nlm.nih.gov/pubmed/11248247,http://www.ncbi.nlm.nih.gov/pubmed/19952666,http://www.ncbi.nlm.nih.gov/pubmed/17437280,http://www.ncbi.nlm.nih.gov/pubmed/22569119,http://www.ncbi.nlm.nih.gov/pubmed/15880747,http://www.ncbi.nlm.nih.gov/pubmed/14513358,http://www.ncbi.nlm.nih.gov/pubmed/30040876,http://www.ncbi.nlm.nih.gov/pubmed/21811467,http://www.ncbi.nlm.nih.gov/pubmed/19860490,http://www.ncbi.nlm.nih.gov/pubmed/29663378,http://www.ncbi.nlm.nih.gov/pubmed/20125191,http://www.ncbi.nlm.nih.gov/pubmed/19863427 | Which gene is primarily associated with the Saethre-Chotzen syndrome? | Saethre-Chotzen syndrome is a craniosynostosis syndrome that is rarely diagnosed prenatally . It is caused by cytogenetic deletions or mutations of the TWIST1 gene . Of the 37 patients with classic features of the syndrome, the overall detection rate for TWIST mutations was 68% . Increased risk for developmental delay is associated with TWIST deletions .Saethre-Chotzen syndrome is an autosomalomal, dominantly inherited craniosynostosis caused by mutations in the basic helix-loop-helix transcription factor gene TWIST1 . The majority of patients have mutations in TWIST gene, which codes for a basic helx-loix-loge transcription factor .Saethre-Chotzen syndrome (SCS), one of the most common forms of syndromic craniosynostosis (premature fusion of the cranial sutures), results from haploinsufficiency of TWIST1, caused by deletions of the entire gene or loss-of-function variants within the coding region.We have evaluated TWIST, a basic helix-loop-helix transcription factor, as a candidate gene for this condition because its expression pattern and mutant phenotypes in Drosophila and mouse are consistent with the Saethre-Chotzen phenotype. Mutations of the TWIST gene in the Saethre-Chotzen syndrome.It is caused by cytogenetic deletions or mutations of the TWIST1 gene. We have evaluated TWIST, a basic helix-loop-helix transcription factor, as a candidate gene for this condition because its expression pattern and mutant phenotypes in Drosophila and mouse are consistent with the Saethre-Chotzen phenotype.Autosomal dominant mutations in the gene encoding the basic helix-loop-helix transcription factor Twist1 are associated with limb and craniofacial defects in humans with Saethre-Chotzen syndrome.Saethre-Chotzen syndrome is a craniosynostosis syndrome that is rarely diagnosed prenatally. We have evaluated TWIST, a basic helix-loop-helix transcription factor, as a candidate gene for this condition because its expression pattern and mutant phenotypes in Drosophila and mouse are consistent with the Saethre-Chotzen phenotype.It is caused by cytogenetic deletions or mutations of the TWIST1 gene.Saethre-Chotzen syndrome is a craniosynostosis syndrome that is rarely diagnosed prenatally. It is caused by cytogenetic deletions or mutations of the TWIST1 gene. We have evaluated TWIST, a basic helix-loop-helix transcription factor, as a candidate gene for this condition because its expression pattern and mutant phenotypes in Drosophila and mouse are consistent with the Saethre-Chotzen phenotype.Saethre-Chotzen syndrome is an autosomal, dominantly inherited craniosynostosis caused by mutations in the basic helix-loop-helix transcription factor gene TWIST1 . The majority of patients have mutations in TWIST gene on chromosome 7p21 . The most common cause of the syndrome is loss-of-function mutations in a genetic mutation in the TWIST 1 gene . The patient is a heterozygous carrier of the pathogenic variant c.415C>A .Saethre-Chotzen syndrome (SCS) is a multiple congenital anomaly-mental retardation complex caused by mutations in the TWIST1 gene (transcription factor Xa, also known as T-box-binding protein 1).The Saethre-Chotzen syndrome is an autosomal, dominantly inherited craniosynostosis caused by mutations in the basic helix-loop-helix transcription factor gene TWIST1 . The majority of patients with the syndrome have mutations in TWIST gene . In 55 patients with features of the syndrome, 11% detected to have deletions by real-time gene dosage analysis .Mutations in the TWIST1 gene, encoding the syntaxin binding protein 1, have been described as the cause of the Saethre-Chotzen syndrome.Saethre-Chotzen syndrome (SCS) is a multiple congenital anomaly-mental retardation complex caused by mutations in the TWIST1 gene. |
http://www.ncbi.nlm.nih.gov/pubmed/31969328 | List 4 targeted synthetic DMARDs that are JAK inhibitors. | Targeted synthetic (ts) DMARDs that are Janus kinase (JAK) inhibitors include tofacitinib, baricitinib, filgotinib, upadacitinib. |
http://www.ncbi.nlm.nih.gov/pubmed/30269739,http://www.ncbi.nlm.nih.gov/pubmed/27476169 | Which microRNAs are involved in targeting CYLD in triple negative breast cancer? | Mir-182 and miR-301b are involved in targeting CYLD in triple negative breast cancer.MicroRNA-301b promotes cell proliferation and apoptosis resistance in triple-negative breast cancer by targeting CYLD. Knockdown of miR-182 up-regulates the expression of cylindromatosis (CYLD) deubiquitinase, which promotes the formation of death-inducing signaling complex (DISC) and subsequent caspase-8 activation in TNF-α-treated BT-549 cells. |
http://www.ncbi.nlm.nih.gov/pubmed/32682484,http://www.ncbi.nlm.nih.gov/pubmed/32376237 | Which drugs were tested in the candor trial? | CANDOR trial investigated carfilzomib, dexamethasone, and daratumumab for patients with relapsed or refractory multiple myeloma. |
http://www.ncbi.nlm.nih.gov/pubmed/33252734,http://www.ncbi.nlm.nih.gov/pubmed/31940802,http://www.ncbi.nlm.nih.gov/pubmed/31172377 | Which are the parts of a flaggelum? | The bacterial flagellum is a supramolecular motility machine consisting of the basal body, the hook, and the filament.
The axial structure of the flagellum consists of the rod, hook, junction, filament, and cap. |
http://www.ncbi.nlm.nih.gov/pubmed/32574385,http://www.ncbi.nlm.nih.gov/pubmed/13776765,http://www.ncbi.nlm.nih.gov/pubmed/1163864 | Why are male calico cats rare? | The tortoiseshell coat color is characteristic to female cats, and its occurrence in tomcats is very rare and associated with the presence of an additional copy of X chromosome.The tortoishell coat colour is characteristic to female cats, and its occurrence in tom cats is very rare and associated with chromosome abnormalities. |
http://www.ncbi.nlm.nih.gov/pubmed/23607685,http://www.ncbi.nlm.nih.gov/pubmed/20657840,http://www.ncbi.nlm.nih.gov/pubmed/29234104,http://www.ncbi.nlm.nih.gov/pubmed/29332143,http://www.ncbi.nlm.nih.gov/pubmed/27709008,http://www.ncbi.nlm.nih.gov/pubmed/18462375,http://www.ncbi.nlm.nih.gov/pubmed/30191603,http://www.ncbi.nlm.nih.gov/pubmed/25043045,http://www.ncbi.nlm.nih.gov/pubmed/25263553 | Which master regulator drives liver development? | Hepatocyte nuclear factor (HNF)4α regulates fetal liver development.The HNF4α plays a major role in liver development, but it's not the only factor. There's a lot of other factors that play a role, but that's the big one. |
http://www.ncbi.nlm.nih.gov/pubmed/28644160 | Are there small molecule CGRPs under development for the treatment of migraine? | Yes, there are several small molecule CGRPs under development for the treatment of migraine. |
http://www.ncbi.nlm.nih.gov/pubmed/25607358 | Which subcortical brain structure is influenced the most by common genetic variants? | The highly complex structure of the human brain is strongly shaped by genetic influences. Subcortical brain regions form circuits with cortical areas to coordinate movement, learning, memory and motivation, and altered circuits can lead to abnormal behaviour and disease. Five novel genetic variants influencing the volumes of the putamen and caudate nucleus were identified. These variants show specific volumetric effects on brain structures rather than global effects across structures. The strongest effects were found for the putamen, where a novel intergenic locus with replicable influence on volume (rs945270; P = 1.08 × 10(-33); 0.52% variance explained) showed evidence of altering the expression of the KTN1 gene in both brain and blood tissue.Common genetic variants influence human subcortical brain structures. The strongest effects are found for the putamen and caudate nucleus, where a novel intergenic locus with replicative influence on volume and the intracranial volume derived from magnetic resonance images of 30,717 individuals from 50 cohort.Common genetic variants influence human subcortical brain structures. The strongest effects are found for the putamen, where a novel intergenic locus with replicable influence on volume (rs945330; P = 1.08 × 10(-33); 0.52% variance explained. In caudate nucleus scientists have identified five novel genetic variants influenced the volumes of putamen and caudated nucleus.The putamen is the most affected by common genetic variants. It is the subcortical brain structure responsible for learning, memory and motivation.The putamen is the most influenced by common genetic variants. It is the subcortical brain structure responsible for learning, memory and motivation.Common genetic variants influence human subcortical brain structures. The strongest effects are found for the putamen, where a novel intergenic locus with replicable influence on volume (rs945280; P = 1.08 × 10(-33); 0.52% variance explained) showed evidence of altering the expression of theKTN1 gene in both brain and blood tissue. Variants affecting putamen volume clustered near developmental genes that regulate apoptosis, axon guidance and vesicle transport.The putamen is the most influenced by common genetic variants. It is the subcortical brain structure responsible for learning and memory consolidation.Common genetic variants influence human subcortical brain structures. The strongest effects are found for the putamen and caudate nucleus, where a novel intergenic locus with replicable influence on volume and intracranial volume have been identified.The putamen is the most affected by common genetic variants. It is the subcortical brain structure responsible for learning and memory consolidation. |
http://www.ncbi.nlm.nih.gov/pubmed/31792921,http://www.ncbi.nlm.nih.gov/pubmed/32521132,http://www.ncbi.nlm.nih.gov/pubmed/33043761,http://www.ncbi.nlm.nih.gov/pubmed/32034693,http://www.ncbi.nlm.nih.gov/pubmed/31994716,http://www.ncbi.nlm.nih.gov/pubmed/30847674,http://www.ncbi.nlm.nih.gov/pubmed/33275677,http://www.ncbi.nlm.nih.gov/pubmed/32592692,http://www.ncbi.nlm.nih.gov/pubmed/30726693,http://www.ncbi.nlm.nih.gov/pubmed/33139979 | Givosiran is used for treatment of which disease? | Givosiran is approved for treatment of porphyria. |
http://www.ncbi.nlm.nih.gov/pubmed/31709696,http://www.ncbi.nlm.nih.gov/pubmed/31722348,http://www.ncbi.nlm.nih.gov/pubmed/18039527 | List mediators that are released from mast cells? | tryptase
histamine
heparin proteoglycan
chymase
cytokines
2,3-dinor-11β-PGF2α
leukotriene (LT)E4 |
http://www.ncbi.nlm.nih.gov/pubmed/18078364,http://www.ncbi.nlm.nih.gov/pubmed/15517958,http://www.ncbi.nlm.nih.gov/pubmed/7651715,http://www.ncbi.nlm.nih.gov/pubmed/2303880,http://www.ncbi.nlm.nih.gov/pubmed/1746228,http://www.ncbi.nlm.nih.gov/pubmed/3054653,http://www.ncbi.nlm.nih.gov/pubmed/3890003,http://www.ncbi.nlm.nih.gov/pubmed/24902834 | What is Exencephaly? | Exencephaly is a type of cephalic disorder wherein the brain is located outside of the skullexencephaly, a failure of the cranial neural folds to close which leads to degeneration of the exposed brain tissue termed anencephaly. .exencephaly, a failure of the cranial neural folds to close which leads to degeneration of the exposed brain tissue termed anencephaly. |
http://www.ncbi.nlm.nih.gov/pubmed/20357716,http://www.ncbi.nlm.nih.gov/pubmed/24078163,http://www.ncbi.nlm.nih.gov/pubmed/20173393,http://www.ncbi.nlm.nih.gov/pubmed/17578885,http://www.ncbi.nlm.nih.gov/pubmed/17088083,http://www.ncbi.nlm.nih.gov/pubmed/10359811,http://www.ncbi.nlm.nih.gov/pubmed/9832419,http://www.ncbi.nlm.nih.gov/pubmed/8662983,http://www.ncbi.nlm.nih.gov/pubmed/10668912,http://www.ncbi.nlm.nih.gov/pubmed/10371192,http://www.ncbi.nlm.nih.gov/pubmed/9644096,http://www.ncbi.nlm.nih.gov/pubmed/30548217,http://www.ncbi.nlm.nih.gov/pubmed/11126333,http://www.ncbi.nlm.nih.gov/pubmed/9664082,http://www.ncbi.nlm.nih.gov/pubmed/10395191,http://www.ncbi.nlm.nih.gov/pubmed/15813957,http://www.ncbi.nlm.nih.gov/pubmed/17020651,http://www.ncbi.nlm.nih.gov/pubmed/9877261,http://www.ncbi.nlm.nih.gov/pubmed/9137980,http://www.ncbi.nlm.nih.gov/pubmed/17935818,http://www.ncbi.nlm.nih.gov/pubmed/11334412,http://www.ncbi.nlm.nih.gov/pubmed/9278582,http://www.ncbi.nlm.nih.gov/pubmed/7678183,http://www.ncbi.nlm.nih.gov/pubmed/30165404,http://www.ncbi.nlm.nih.gov/pubmed/18339717,http://www.ncbi.nlm.nih.gov/pubmed/15009470,http://www.ncbi.nlm.nih.gov/pubmed/7926300,http://www.ncbi.nlm.nih.gov/pubmed/7738205,http://www.ncbi.nlm.nih.gov/pubmed/9335502,http://www.ncbi.nlm.nih.gov/pubmed/9792545,http://www.ncbi.nlm.nih.gov/pubmed/26113076,http://www.ncbi.nlm.nih.gov/pubmed/8899294 | What is the role of TNF in obesity? | The role of TNF in obesity is not fully understood, but it is thought to play a major role in adipose tissue formation and fat storage. TNF-alpha is a protein that has been shown to increase fat storage in fat cells. It is also thought to have a role in insulin resistance.The role of TNF in obesity is not fully understood, but it is thought to play a major role in adipose tissue formation and fat storage. TNF-alpha is a protein that has been shown to increase fat storage in fat cells. It also has a role in insulin resistance, which is a major factor in obesity.TNF, acting via its receptors, is a major contributor to obesity-associated insulin resistance.Macrophage TNF-alpha contributes to insulin resistance and hepatic steatosis in diet-induced obesity.TNFalpha gene overexpression induces insulin resistance. TNF-alpha is associated with obesity |
http://www.ncbi.nlm.nih.gov/pubmed/32266704 | Is eptinezumab a small molecule? | No, eptinezumab is a humanized monoclonal antibody. |
http://www.ncbi.nlm.nih.gov/pubmed/29218892,http://www.ncbi.nlm.nih.gov/pubmed/29960671,http://www.ncbi.nlm.nih.gov/pubmed/24399358,http://www.ncbi.nlm.nih.gov/pubmed/26747746,http://www.ncbi.nlm.nih.gov/pubmed/33044802,http://www.ncbi.nlm.nih.gov/pubmed/31471575,http://www.ncbi.nlm.nih.gov/pubmed/32470572,http://www.ncbi.nlm.nih.gov/pubmed/28617224,http://www.ncbi.nlm.nih.gov/pubmed/28426957,http://www.ncbi.nlm.nih.gov/pubmed/32501580,http://www.ncbi.nlm.nih.gov/pubmed/32198361,http://www.ncbi.nlm.nih.gov/pubmed/29764998 | Describe the Enhancing NeuroImaging Genetics through Meta-Analysis (ENIGMA) Consortium | The Enhancing NeuroImaging Genetics through Meta-Analysis (ENIGMA) Consortium is a collaborative network of researchers working together on a range of large-scale studies that integrate data from 70 institutions worldwide. Organized into Working Groups that tackle questions in neuroscience, genetics, and medicine, ENIGMA studies have analyzed neuroimaging data from over 12,826 subjects. In addition, data from 12,171 individuals were provided by the CHARGE consortium for replication of findings, in a total of 24,997 subjects. By meta-analyzing results from many sites, ENIGMA has detected factors that affect the brain that no individual site could detect on its own, and that require larger numbers of subjects than any individual neuroimaging study has currently collected. ENIGMA's first project was a genome-wide association study identifying common variants in the genome associated with hippocampal volume or intracranial volume. Continuing work is exploring genetic associations with subcortical volumes (ENIGMA2) and white matter microstructure (ENIGMA-DTI). Working groups also focus on understanding how schizophrenia, bipolar illness, major depression and attention deficit/hyperactivity disorder (ADHD) affect the brain.The Enhancing NeuroImaging Genetics through Meta-Analysis (ENIGMA) Consortium is a collaborative network of researchers working together on a range of large-scale studies that integrate data from 70 institutions worldwide. Organized into Working Groups that tackle questions in neuroscience, genetics, and medicine, ENIGMA studies have analyzed neuroimaging data from over 12,826 subjects. In addition, data from 12,171 individuals were provided by the CHARGE consortium for replication of findings, in a total of 24,997 subjects. By meta-analyzing results from many sites, ENIGMA has detected factors that affect the brain that no individual site could detect on its own, and that require larger numbersThe ENIGMA Consortium is a global team science effort, now including over 800 scientists spread across 340 institutions in 35 countries, with the shared goal of understanding disease and genetic influences on the brain.The Enhancing NeuroImaging genetics through Meta-Analysis (ENIGMA) Consortium is a collaborative network of researchers working together on a range of large-scale studies that integrate data from 70 institutions worldwide. Organized into Working groups that tackle questions in neuroscience, genetics, and medicine, ENIGMA studies have analyzed neuroimaging data from over 12,826 subjects. In addition, data from 12,189 individuals have been provided by the Charcot-Marie-Tooth [CMT] Consortium for replication of findings, in a total of 24,997 subjects.The ENIGMA Consortium is a collaborative network of researchers working together on a range of large-scale studies that integrate data from 70 institutions worldwide. Organized into Working Groups that tackle questions in neuroscience, genetics, and medicine, EnIGMA studies have analyzed neuroimaging data from over 12,826 subjects. By meta-analyzing results from many sites, they have detected factors that affect the brain that no individual site could detect on their own, and that require larger numbers of subjects than any individual study has currently collected.The ENIGMA Consortium is a collaborative network of researchers working together on a range of large-scale studies that integrate data from 70 institutions worldwide. Organized into Working Groups that tackle questions in neuroscience, genetics, and medicine, EnIGMA studies have analyzed neuroimaging data from over 12,826 subjects. By meta-analyzing results from many sites, the consortium has detected factors that affect the brain that no individual site could detect on its own.The ENIGMA Consortium is a collaborative network of researchers working together on a range of large-scale studies that integrate data from 70 institutions worldwide. Organized into Working Groups that tackle questions in neuroscience, genetics, and medicine, EnIGMA studies have analyzed neuroimaging data from over 12,826 subjects. By meta-analyzing results from many sites, they have detected factors that affect the brain that no individual site could detect on its own, and that require larger numbers of subjects than any individual study has currently collected.The ENIGMA Consortium is a collaborative network of researchers working together on a range of large-scale studies that integrate data from 70 institutions worldwide. Organized into Working Groups that tackle questions in neuroscience, genetics, and medicine, EnIGMA studies have analyzed neuroimaging data from over 12,826 subjects. By meta-analyzing results from many sites, they have detected factors that affect the brain that no individual site could detect on their own. |
http://www.ncbi.nlm.nih.gov/pubmed/29719809,http://www.ncbi.nlm.nih.gov/pubmed/32897035 | Inhaled Molgramostim can be used for treatment of which disease? | Inhaled Molgramostim was shown to be effective for Autoimmune Pulmonary Alveolar Proteinosis. |
http://www.ncbi.nlm.nih.gov/pubmed/15590064,http://www.ncbi.nlm.nih.gov/pubmed/28440436,http://www.ncbi.nlm.nih.gov/pubmed/21131363,http://www.ncbi.nlm.nih.gov/pubmed/29408340,http://www.ncbi.nlm.nih.gov/pubmed/16210453,http://www.ncbi.nlm.nih.gov/pubmed/27318360 | Which are the main functions of the annexin family? | Annexins are required for membrane organization and membrane transport events required for the establishment/maintenance of epithelial polarity.
An association of annexins with ion channels, as membrane-guiding auxiliary proteins or modulators of channel activity.
Last but not least, some annexins seem to work as extracellular autocrine modulators of receptor function under different physiological conditions. |
http://www.ncbi.nlm.nih.gov/pubmed/31015813,http://www.ncbi.nlm.nih.gov/pubmed/30558674,http://www.ncbi.nlm.nih.gov/pubmed/31436592,http://www.ncbi.nlm.nih.gov/pubmed/32284271,http://www.ncbi.nlm.nih.gov/pubmed/29457489,http://www.ncbi.nlm.nih.gov/pubmed/20113211,http://www.ncbi.nlm.nih.gov/pubmed/32305975,http://www.ncbi.nlm.nih.gov/pubmed/30179221,http://www.ncbi.nlm.nih.gov/pubmed/22024532,http://www.ncbi.nlm.nih.gov/pubmed/32999027,http://www.ncbi.nlm.nih.gov/pubmed/23839657,http://www.ncbi.nlm.nih.gov/pubmed/25144544,http://www.ncbi.nlm.nih.gov/pubmed/16977285,http://www.ncbi.nlm.nih.gov/pubmed/28426274,http://www.ncbi.nlm.nih.gov/pubmed/31339679,http://www.ncbi.nlm.nih.gov/pubmed/33294953,http://www.ncbi.nlm.nih.gov/pubmed/29720364,http://www.ncbi.nlm.nih.gov/pubmed/31061027,http://www.ncbi.nlm.nih.gov/pubmed/24834646,http://www.ncbi.nlm.nih.gov/pubmed/17326312,http://www.ncbi.nlm.nih.gov/pubmed/27189459,http://www.ncbi.nlm.nih.gov/pubmed/22086893 | Please list the 2 vaccines for herpes zoster(shingles) | live attenuated zoster vaccine (Zostavax®) and live attenuates herpes zoster (Shingles) are effective for treatment of infections with herpesZoster(shingles).live attenuated zoster vaccine (Zostavax; also known as shingles vaccine) is effective for prevention of infections with herpes zoster virus (VZV).Shingrix is a recombinant adjuvant subunit vaccine.The are 2 vaccines for herpes zoster, adjuvated recombinant vaccines and a live attenuated vaccine. |
http://www.ncbi.nlm.nih.gov/pubmed/21620332,http://www.ncbi.nlm.nih.gov/pubmed/10843807,http://www.ncbi.nlm.nih.gov/pubmed/24820954,http://www.ncbi.nlm.nih.gov/pubmed/13677319,http://www.ncbi.nlm.nih.gov/pubmed/26415210,http://www.ncbi.nlm.nih.gov/pubmed/22732409,http://www.ncbi.nlm.nih.gov/pubmed/16469316,http://www.ncbi.nlm.nih.gov/pubmed/15325254,http://www.ncbi.nlm.nih.gov/pubmed/21860604 | What is a likely origin of intronless genes? | More than half of SEGs identified in most of the species have at least one ortholog multiple exon gene in the same genome, which provides insight to their possible origin by retrotranspositionThere is strong support for the idea that retrotransposition followed by tandem duplications is the most probable event that can explain the expansion of intronless or single-exon genes (SEG) in eukaryotic organisms. More than half of SEGs identified in most of the species have at least one ortholog multiple exon gene in the same genome, which provides insight to their possible origin by retrotransposition.The origin of intronless genes is most likely retrotranspositionIntronless genes (IGs) constitute approximately 3% of the human genome. Their origin is likely to be retrotransposition due to loss-of-function mutations or duplication.Genes without introns are a characteristic feature of prokaryotes, but there are still a number of intronless genes in eukaryotes. Most of these genes may have originated from retrotransposition rather than lineage-specific expansions of repeat elements. |
http://www.ncbi.nlm.nih.gov/pubmed/31660152 | Which company developed ivosidenib? | Ivosidenib has been developed by Agios Pharmaceuticals. |
http://www.ncbi.nlm.nih.gov/pubmed/32511357 | Is the apilimod inhibitor effective against SARS-CoV-2? | To identify therapeutics that can be repurposed as SARS-CoV-2 antivirals, a library of known drugs encompassing approximately 12,000 clinical-stage or FDA-approved small molecules were profiled. In a study the identification of 30 known drugs that inhibit viral replication was reportedd. Of these, six were characterized for cellular dose-activity relationships, and showed effective concentrations likely to be commensurate with therapeutic doses in patients. These include the PIKfyve kinase inhibitor Apilimod, cysteine protease inhibitors MDL-28170, Z LVG CHN2, VBY-825, and ONO 5334, and the CCR1 antagonist MLN-3897. Since many of these molecules have advanced into the clinic, the known pharmacological and human safety profiles of these compounds will accelerate their preclinical and clinical evaluation for COVID-19 treatment.Yes, apilimod inhibition is effective for treatment of SARS-CoV-2. |
http://www.ncbi.nlm.nih.gov/pubmed/31764959,http://www.ncbi.nlm.nih.gov/pubmed/33049114 | Is Lanabecestat effective for Alzheimer's disease? | No. Treatment with lanabecestat was well tolerated and did not slow cognitive or functional decline of Alzheimer's disease patients. |
http://www.ncbi.nlm.nih.gov/pubmed/31928996,http://www.ncbi.nlm.nih.gov/pubmed/31820985,http://www.ncbi.nlm.nih.gov/pubmed/31896590,http://www.ncbi.nlm.nih.gov/pubmed/31980485,http://www.ncbi.nlm.nih.gov/pubmed/31991682 | How is the STING protein activated? | During DNA virus infections, detection of cytosolic DNA by the cGAS-STING pathway leads to activation of IFN-β. |
http://www.ncbi.nlm.nih.gov/pubmed/12376615,http://www.ncbi.nlm.nih.gov/pubmed/15947578,http://www.ncbi.nlm.nih.gov/pubmed/26361338,http://www.ncbi.nlm.nih.gov/pubmed/12441927,http://www.ncbi.nlm.nih.gov/pubmed/25992184,http://www.ncbi.nlm.nih.gov/pubmed/31065438,http://www.ncbi.nlm.nih.gov/pubmed/18670269,http://www.ncbi.nlm.nih.gov/pubmed/7900601,http://www.ncbi.nlm.nih.gov/pubmed/11110923,http://www.ncbi.nlm.nih.gov/pubmed/30396206,http://www.ncbi.nlm.nih.gov/pubmed/29372343,http://www.ncbi.nlm.nih.gov/pubmed/1417404,http://www.ncbi.nlm.nih.gov/pubmed/17981554,http://www.ncbi.nlm.nih.gov/pubmed/21496837,http://www.ncbi.nlm.nih.gov/pubmed/11779979,http://www.ncbi.nlm.nih.gov/pubmed/25106899,http://www.ncbi.nlm.nih.gov/pubmed/20017327,http://www.ncbi.nlm.nih.gov/pubmed/11598245,http://www.ncbi.nlm.nih.gov/pubmed/12751862,http://www.ncbi.nlm.nih.gov/pubmed/10751849,http://www.ncbi.nlm.nih.gov/pubmed/15663674,http://www.ncbi.nlm.nih.gov/pubmed/31644405,http://www.ncbi.nlm.nih.gov/pubmed/19357382,http://www.ncbi.nlm.nih.gov/pubmed/32902841,http://www.ncbi.nlm.nih.gov/pubmed/12418770,http://www.ncbi.nlm.nih.gov/pubmed/25571196,http://www.ncbi.nlm.nih.gov/pubmed/9480582,http://www.ncbi.nlm.nih.gov/pubmed/22335865,http://www.ncbi.nlm.nih.gov/pubmed/22357170,http://www.ncbi.nlm.nih.gov/pubmed/7944863,http://www.ncbi.nlm.nih.gov/pubmed/12441926,http://www.ncbi.nlm.nih.gov/pubmed/18423723,http://www.ncbi.nlm.nih.gov/pubmed/15749505,http://www.ncbi.nlm.nih.gov/pubmed/26905020,http://www.ncbi.nlm.nih.gov/pubmed/29696193 | Explain the use of Radio Frequency Ablation as a treatment | Radio-frequency ablation (RFA) is a promising minimal-invasive treatment option for treatment of, cancer, pain, tissue hyperplasia and cardiac arrhythmias cancer, triggering tissue necrosis and results in reduced tumor volumes.Radiofrequency ablation is a simple, safe, and effective treatment option for the treatment of castration-resistant ovarian cancer.Radio frequency ablation is used in the treatment of infertility. |
http://www.ncbi.nlm.nih.gov/pubmed/25173347,http://www.ncbi.nlm.nih.gov/pubmed/23378146,http://www.ncbi.nlm.nih.gov/pubmed/28089983,http://www.ncbi.nlm.nih.gov/pubmed/32427982,http://www.ncbi.nlm.nih.gov/pubmed/25600850,http://www.ncbi.nlm.nih.gov/pubmed/26449852,http://www.ncbi.nlm.nih.gov/pubmed/21748861,http://www.ncbi.nlm.nih.gov/pubmed/17330303,http://www.ncbi.nlm.nih.gov/pubmed/19772784,http://www.ncbi.nlm.nih.gov/pubmed/24339425,http://www.ncbi.nlm.nih.gov/pubmed/30402934,http://www.ncbi.nlm.nih.gov/pubmed/31590930,http://www.ncbi.nlm.nih.gov/pubmed/32669456,http://www.ncbi.nlm.nih.gov/pubmed/29578196,http://www.ncbi.nlm.nih.gov/pubmed/16978395,http://www.ncbi.nlm.nih.gov/pubmed/28676129,http://www.ncbi.nlm.nih.gov/pubmed/32475078,http://www.ncbi.nlm.nih.gov/pubmed/21204103,http://www.ncbi.nlm.nih.gov/pubmed/30368562,http://www.ncbi.nlm.nih.gov/pubmed/15901635,http://www.ncbi.nlm.nih.gov/pubmed/24955759,http://www.ncbi.nlm.nih.gov/pubmed/23950187,http://www.ncbi.nlm.nih.gov/pubmed/24599677,http://www.ncbi.nlm.nih.gov/pubmed/19849865,http://www.ncbi.nlm.nih.gov/pubmed/30168272,http://www.ncbi.nlm.nih.gov/pubmed/23818710,http://www.ncbi.nlm.nih.gov/pubmed/19635732,http://www.ncbi.nlm.nih.gov/pubmed/20459619,http://www.ncbi.nlm.nih.gov/pubmed/29955927,http://www.ncbi.nlm.nih.gov/pubmed/17611990,http://www.ncbi.nlm.nih.gov/pubmed/25530992,http://www.ncbi.nlm.nih.gov/pubmed/27870649,http://www.ncbi.nlm.nih.gov/pubmed/25031546,http://www.ncbi.nlm.nih.gov/pubmed/26414115,http://www.ncbi.nlm.nih.gov/pubmed/25143522,http://www.ncbi.nlm.nih.gov/pubmed/26200604,http://www.ncbi.nlm.nih.gov/pubmed/24983407,http://www.ncbi.nlm.nih.gov/pubmed/22673898 | What does "28" stand for in the Disease Activity Score DAS28? | It stands for the Disease Activity Score 28 Joint Index (DAS28). It’s basically a measure of how active a patient is in regards to how active they are in relation to the DAS28. The 28 joint DAS (28 joints) is a way to measure how active the patient is compared to other people with the same disease.DAS28 is a subjective Disease Activity Score in Rheumatoid Arthritis patients that checks 28 individual joints. In order to further dissect this issue, we numerically and graphically modeled 28-joint disease activity scale (DAS28), simplified disease activity index (SDAI), and clinical disease activity index (CDAI) by three-dimensional (3D) plotting. The 28-joint DAS (DAS28), clinical disease activity index (CDAI) and simplified disease activity index (SDAI) are indices frequently used to assess disease activity in RA patients.It stands for the Disease Activity Score 28 Joint Index (DAS28). It’s a measure of how active a patient is in regards to how active they are in relation to the DAS28. The 28 joint DAS (28 joints) is the highest score.In order to further dissect this issue, we numerically and graphically modeled 28-joint disease activity scale (DAS28), simplified disease activity index (SDAI), and clinical disease activity index (CDAI) by three-dimensional (3D) plotting.It stands for the Disease Activity Score 28 Joint Index (DAS28). It’s basically a measure of how active a patient is in regards to how active they are in relation to the DAS28. The 28 joint DAS (28 joints) is a way to measure how active the patient is compared to other patients with the same disease.It stands for the Disease Activity Score 28 Joint Index (DAS28). It’s a measure of how active a patient is in regards to how active they are in relation to the DAS28. |
http://www.ncbi.nlm.nih.gov/pubmed/32728595 | What is EPICCURE? | EPICCURE is an ongoing randomized, double-blind, placebo-controlled study of the safety of AZD8601 in patients with moderately decreased left ventricular function (ejection fraction 30%-50%) undergoing elective coronary artery bypass surgery. EPICCURE combines high-efficiency delivery with quantitative targeting and follow-up for robust assessment of the safety and exploratory efficacy of VEGF-A mRNA angiogenesis (ClinicalTrials.gov: NCT03370887). |
http://www.ncbi.nlm.nih.gov/pubmed/31701148 | List updates for JASPAR 2020 | JASPAR (http://jaspar.genereg.net) is an open-access database of curated, non-redundant transcription factor (TF)-binding profiles stored as position frequency matrices (PFMs) for TFs across multiple species in six taxonomic groups. In this 8th release of JASPAR, the CORE collection has been expanded with 245 new PFMs (169 for vertebrates, 42 for plants, 17 for nematodes, 10 for insects, and 7 for fungi), and 156 PFMs were updated (125 for vertebrates, 28 for plants and 3 for insects). This collection has a dedicated web form to engage the community in the curation of unvalidated TF-binding profiles.JASPAR (http://jaspar.genereg.net) is an open-access database of curated, non-redundant transcription factor (TF)-binding profiles stored as position frequency matrices (PFMs) for TFs across multiple species in six taxonomic groups. In this 8th release of JASPAR, the CORE collection has been expanded with 245 new PFMs (169 for vertebrates, 42 for plants, 17 for nematodes, 10 for insects, and 7 for fungi), and 156 PFMs were updated (125 for vertebrates, 28 for plants and 3 for insects). These new profiles represent an 18% expansion compared to the previous release. JASPAR 2020 comes with a novel collection of unvalidated TF-binding profiles for which curators did not find orthogonal supporting evidence in the literature. This collection has a dedicated web form to engage the community in the curation of unvalidated TF-binding profiles. Moreover, a Q&A forum was created to ease the communication between the user community and JASPAR curators. Finally, the genomic tracks, inference tool, and TF-binding profile similarity clusters were updated.JASPAR (http://jaspar.genereg.net) is an open-access database of curated, non-redundant transcription factor (TF)-binding profiles stored as position frequency matrices (PFMs) for TFs across multiple species in six taxonomic groups. In this 8th release of JASPAR, the CORE collection has been expanded with 245 new PFMs (169 for vertebrates, 42 for plants, 17 for nematodes, 10 for insects, and 7 for fungi), and 156 PFMs were updated (125 for vertebrates, 28 for plants and 3 for insects). These new profiles represent an 18% expansion compared to the previous release. This collection has a dedicated web form to engage the community in the curation of unvalidated TF-binding profiles.JASPAR (http://jaspar.genereg.net) is an open-access database of curated, non-redundant transcription factor (TF)-binding profiles stored as position frequency matrices (PFMs) for TFs across multiple species in six taxonomic groups. In this 8th release of JASPAR, the CORE collection has been expanded with 245 new PFMs (169 for vertebrates, 42 for plants, 17 for nematodes, 10 for insects, and 7 for fungi), and 156 PFMs were updated (125 for vertebrates, 28 for plants and 3 for insects). These new profiles represent an 18% expansion compared to the previous release.JASPAR (http://jaspar.genereg.net) is an open-access database of curated, non-redundant transcription factor (TF)-binding profiles stored as position frequency matrices (PFMs) for TFs across multiple species in six taxonomic groups. In this 8th release of JASPAR, the CORE collection has been expanded with 245 new PFMs (169 for vertebrates, 42 for plants, 17 for nematodes, 10 for insects, and 7 for fungi), and 156 PFMs were updated (125 for vertebrates, 28 for plants and 3 for insects). JASPAR 2020 comes with a novel collection of unvalidated TF-binding profiles for which our curators did not find orthogonal supporting evidence in the literature. |
http://www.ncbi.nlm.nih.gov/pubmed/33207093 | Was golimumab tested for diabetes? | Yes, among children and young adults with newly diagnosed overt type 1 diabetes, golimumab resulted in better endogenous insulin production and less exogenous insulin use than placebo. |
http://www.ncbi.nlm.nih.gov/pubmed/31956030,http://www.ncbi.nlm.nih.gov/pubmed/31704836,http://www.ncbi.nlm.nih.gov/pubmed/29463567 | Is G3BP1 found in stress granules? | Yes,
RAS GTPase-activating protein-binding protein (G3BP1) is an RNA-binding protein that is essential for assembling stress granules. |
http://www.ncbi.nlm.nih.gov/pubmed/30548460,http://www.ncbi.nlm.nih.gov/pubmed/1791375,http://www.ncbi.nlm.nih.gov/pubmed/32799251,http://www.ncbi.nlm.nih.gov/pubmed/3736130,http://www.ncbi.nlm.nih.gov/pubmed/27931782,http://www.ncbi.nlm.nih.gov/pubmed/25027075,http://www.ncbi.nlm.nih.gov/pubmed/32046343,http://www.ncbi.nlm.nih.gov/pubmed/22752073,http://www.ncbi.nlm.nih.gov/pubmed/27267192,http://www.ncbi.nlm.nih.gov/pubmed/29127216,http://www.ncbi.nlm.nih.gov/pubmed/8471783,http://www.ncbi.nlm.nih.gov/pubmed/31834988,http://www.ncbi.nlm.nih.gov/pubmed/19823665,http://www.ncbi.nlm.nih.gov/pubmed/17664768,http://www.ncbi.nlm.nih.gov/pubmed/8459803,http://www.ncbi.nlm.nih.gov/pubmed/31014187,http://www.ncbi.nlm.nih.gov/pubmed/16429102,http://www.ncbi.nlm.nih.gov/pubmed/18769635,http://www.ncbi.nlm.nih.gov/pubmed/23666920,http://www.ncbi.nlm.nih.gov/pubmed/1590260,http://www.ncbi.nlm.nih.gov/pubmed/14582653,http://www.ncbi.nlm.nih.gov/pubmed/21251803,http://www.ncbi.nlm.nih.gov/pubmed/22121285,http://www.ncbi.nlm.nih.gov/pubmed/24122691,http://www.ncbi.nlm.nih.gov/pubmed/33087645 | What is Progeria? | Hutchinson-Gilford progeria syndrome is a segmental premature aging disease causing patient death by early teenage years from cardiovascular dysfunction.Progeria is a rare genetic premature ageing disorder.Progeria is a rare genetic disorder that causes premature aging and early death in the first or second decade of life, usually secondary cardiovascular events (myocardial infarction and stroke).Progeria is a rare genetic disorder, characterized by premature aging and early death in the first or second decade of life, usually secondary cardiovascular events (myocardial infarction and stroke).Hutchinson-Gilford Progeria Syndrome (HGPS) is a premature aging disorder caused by mutations in LMNA, which encodes the nuclear scaffold proteins lamin A and C . In HGPS and related progerias, processing of prelamin A is blocked at a critical step mediated by the zinc metalloprotease ZMPSTE24 .Hirschford Progeria Syndrome (HGPS) is a segmental premature aging disease causing patient death by early teenage years from cardiovascular dysfunction.Progeria is a rare genetic disorder, characterized by progressive premature aging and early death in the first or second decade of life, usually secondary cardiovascular events (myocardial infarction and stroke).Progeria is a genetic disorder that causes premature aging and early death in the first or second decade of life, usually secondary cardiovascular events (myocardial infarction and stroke).Hutchinson-Gilford Progeria Syndrome (HGPS) is a segmental premature aging disease causing patient death by early teenage years from cardiovascular dysfunction |
http://www.ncbi.nlm.nih.gov/pubmed/32978617 | Describe CrossICC | CrossICC is an R package designed for the unsupervised clustering of gene expression data from multiple datasets/platforms without the requirement of batch effect adjustment. CrossICC utilizes an iterative strategy to derive the optimal gene signature and cluster numbers from a consensus similarity matrix generated by consensus clustering.CrossICC is an R package designed for the unsupervised clustering of gene expression data from multiple datasets/platforms without the requirement of batch effect adjustment. CrossICC utilizes an iterative strategy to derive the optimal gene signature and cluster numbers from a consensus similarity matrix generated by consensus clustering. The package also provides abundant functions to visualize the identified subtypes and evaluate subtyping performance. The package is implemented in R and available at GitHub (https://github.com/bioinformatist/CrossICC) and Bioconductor (http://bioconductor.org/packages/release/bioc/html/CrossICC.html) under the GPL v3 License. |
http://www.ncbi.nlm.nih.gov/pubmed/28025025,http://www.ncbi.nlm.nih.gov/pubmed/32088716,http://www.ncbi.nlm.nih.gov/pubmed/28926607,http://www.ncbi.nlm.nih.gov/pubmed/30171161,http://www.ncbi.nlm.nih.gov/pubmed/30356804,http://www.ncbi.nlm.nih.gov/pubmed/26203193,http://www.ncbi.nlm.nih.gov/pubmed/26634965,http://www.ncbi.nlm.nih.gov/pubmed/29437893,http://www.ncbi.nlm.nih.gov/pubmed/29779093,http://www.ncbi.nlm.nih.gov/pubmed/31665733,http://www.ncbi.nlm.nih.gov/pubmed/32945624,http://www.ncbi.nlm.nih.gov/pubmed/28320854,http://www.ncbi.nlm.nih.gov/pubmed/32910349,http://www.ncbi.nlm.nih.gov/pubmed/26325557,http://www.ncbi.nlm.nih.gov/pubmed/29668577,http://www.ncbi.nlm.nih.gov/pubmed/33099609,http://www.ncbi.nlm.nih.gov/pubmed/30825073,http://www.ncbi.nlm.nih.gov/pubmed/26902493,http://www.ncbi.nlm.nih.gov/pubmed/33179798,http://www.ncbi.nlm.nih.gov/pubmed/31583611,http://www.ncbi.nlm.nih.gov/pubmed/33107592,http://www.ncbi.nlm.nih.gov/pubmed/31283930,http://www.ncbi.nlm.nih.gov/pubmed/24621652,http://www.ncbi.nlm.nih.gov/pubmed/25678098,http://www.ncbi.nlm.nih.gov/pubmed/28577743,http://www.ncbi.nlm.nih.gov/pubmed/26095025,http://www.ncbi.nlm.nih.gov/pubmed/27431783,http://www.ncbi.nlm.nih.gov/pubmed/32890415,http://www.ncbi.nlm.nih.gov/pubmed/32729974,http://www.ncbi.nlm.nih.gov/pubmed/31655812 | Which receptor is blocked by Finerenone? | Finerenone is a nonsteroidal mineralocorticoid receptor antagonist. |
http://www.ncbi.nlm.nih.gov/pubmed/33057672,http://www.ncbi.nlm.nih.gov/pubmed/30892111,http://www.ncbi.nlm.nih.gov/pubmed/30088449 | Is colistin an antibiotic? | Yes,
colistin is an antibiotic. |
http://www.ncbi.nlm.nih.gov/pubmed/22870473,http://www.ncbi.nlm.nih.gov/pubmed/20953198,http://www.ncbi.nlm.nih.gov/pubmed/18071945,http://www.ncbi.nlm.nih.gov/pubmed/33262810,http://www.ncbi.nlm.nih.gov/pubmed/32365119,http://www.ncbi.nlm.nih.gov/pubmed/31164961,http://www.ncbi.nlm.nih.gov/pubmed/20402381,http://www.ncbi.nlm.nih.gov/pubmed/31809899,http://www.ncbi.nlm.nih.gov/pubmed/20065633,http://www.ncbi.nlm.nih.gov/pubmed/29952844,http://www.ncbi.nlm.nih.gov/pubmed/24155139,http://www.ncbi.nlm.nih.gov/pubmed/23844337,http://www.ncbi.nlm.nih.gov/pubmed/30021477,http://www.ncbi.nlm.nih.gov/pubmed/19368420,http://www.ncbi.nlm.nih.gov/pubmed/16102523,http://www.ncbi.nlm.nih.gov/pubmed/31796986,http://www.ncbi.nlm.nih.gov/pubmed/33269653,http://www.ncbi.nlm.nih.gov/pubmed/20305672,http://www.ncbi.nlm.nih.gov/pubmed/28841363,http://www.ncbi.nlm.nih.gov/pubmed/22334272,http://www.ncbi.nlm.nih.gov/pubmed/33264466 | Is Tocilizumab (Actemra) used to block/antagonize the IL-6 receptor? | yes, tocilizumab (actemra) is used to block/antagonize the il-6 receptor.Yes. Tocilizumab (Actemra) is an anti-IL-6 receptor antagonist. It is a monoclonal antibody against the receptor.Tocilizumab is an IL-6 receptor antagonist.yes, tocilizumab (actemra) is an approved humanized monoclonal antibody that blocks the il-6 receptor. |
http://www.ncbi.nlm.nih.gov/pubmed/29706548,http://www.ncbi.nlm.nih.gov/pubmed/29754816,http://www.ncbi.nlm.nih.gov/pubmed/29300120,http://www.ncbi.nlm.nih.gov/pubmed/31780627,http://www.ncbi.nlm.nih.gov/pubmed/16292342,http://www.ncbi.nlm.nih.gov/pubmed/27224481,http://www.ncbi.nlm.nih.gov/pubmed/29079757,http://www.ncbi.nlm.nih.gov/pubmed/29140466,http://www.ncbi.nlm.nih.gov/pubmed/31753851,http://www.ncbi.nlm.nih.gov/pubmed/27210764,http://www.ncbi.nlm.nih.gov/pubmed/29472443,http://www.ncbi.nlm.nih.gov/pubmed/30100265 | Is the process of DNA loop-extrusion independent of ATP? | The process of DNA loop-extrusion is not independent of ATP. It is dependent on the energy of ATP hydrolysis.Yes, a single condensin complex is able to extrude tens of kilobase pairs of DNA, using the energy of ATP hydrolysis.The DNA-organizing mechanism of condensin depends on the energy of ATP hydrolysis but how this activity specifically promotes proper compaction and segregation of chromosomes during mitosis remains poorly understood. |
http://www.ncbi.nlm.nih.gov/pubmed/31650711 | What is the effect of carbamazepine on CYP3A4? | Carbamazepine is an inducer of CYP3A4. |
http://www.ncbi.nlm.nih.gov/pubmed/28854598 | Is there an upper limit on the functional fraction of the human genome? | Mutational load considerations lead to the conclusion that the functional fraction within the human genome cannot exceed 25%, and is probably considerably lower.yes, there is an upper limit on the functional fraction of the human genome. |
http://www.ncbi.nlm.nih.gov/pubmed/25102676,http://www.ncbi.nlm.nih.gov/pubmed/9313351,http://www.ncbi.nlm.nih.gov/pubmed/9788648,http://www.ncbi.nlm.nih.gov/pubmed/15559411,http://www.ncbi.nlm.nih.gov/pubmed/29233830,http://www.ncbi.nlm.nih.gov/pubmed/28290978 | What is Couvelaire Uterus? | Couvelaire uterus is hematic infiltration uterine myometrium due to the formation of a massive hematoma. It is charecterised by dark purple patches with ecchymosis and indurations. |
http://www.ncbi.nlm.nih.gov/pubmed/31875531,http://www.ncbi.nlm.nih.gov/pubmed/32265471,http://www.ncbi.nlm.nih.gov/pubmed/30509897,http://www.ncbi.nlm.nih.gov/pubmed/32476384,http://www.ncbi.nlm.nih.gov/pubmed/32106631,http://www.ncbi.nlm.nih.gov/pubmed/33256196 | What protein is Otof gene encoding? | The OTOF gene encodes otoferlin, a critical protein at the synapse of auditory sensory cells, the inner hair cells (IHCs)The OTOF gene encodes otoferlin, a critical protein at the synapse of auditory sensory cells, the inner hair cells (IHCs). In the absence of otoferlin, signal transmission of IHCs fails due to impaired release of synaptic vesicles at the IHC synapse.The OTOF gene encodes otoferlin, a critical protein at the synapse of auditory sensory cells, the inner hair cells (IHCs). |
http://www.ncbi.nlm.nih.gov/pubmed/20181940,http://www.ncbi.nlm.nih.gov/pubmed/31828519,http://www.ncbi.nlm.nih.gov/pubmed/28779577,http://www.ncbi.nlm.nih.gov/pubmed/21762783,http://www.ncbi.nlm.nih.gov/pubmed/31811514,http://www.ncbi.nlm.nih.gov/pubmed/27044749,http://www.ncbi.nlm.nih.gov/pubmed/25895534,http://www.ncbi.nlm.nih.gov/pubmed/23777386,http://www.ncbi.nlm.nih.gov/pubmed/30202079,http://www.ncbi.nlm.nih.gov/pubmed/26574187,http://www.ncbi.nlm.nih.gov/pubmed/31844927,http://www.ncbi.nlm.nih.gov/pubmed/32748016,http://www.ncbi.nlm.nih.gov/pubmed/31264907,http://www.ncbi.nlm.nih.gov/pubmed/32589951,http://www.ncbi.nlm.nih.gov/pubmed/31484786 | What is hypercapnia? | Hypercapnia is also known as High CO2 retention. |
http://www.ncbi.nlm.nih.gov/pubmed/30154186 | What is TSA-Seq used for? | TSA-Seq provides a "cytological ruler" for estimating mean chromosomal distances from nuclear speckles genome-wide and for predicting several Mbp chromosome trajectories between nuclear compartments without sophisticated computational modeling.TSA-Seq is a new mapping method capable of providing a "cytological ruler" for estimating mean mean distance distances from nuclear speckles genome-wide and for predicting several MbP chromosome trajectories between nuclear compartments.TSA-Seq is used as a cytological ruler to calculate relative distances between nuclear elements in 3D genome organization maps.yes, tsa-seq is a new mapping method capable of providing a cytological ruler for estimating mean chromosomal distances from nuclear speckles genome-wide and for predicting several mbp chromosome trajectories between nuclear compartments without sophisticated computational modeling.tsa-seq is a new mapping method capable of providing a "cytological ruler" for estimating mean chromosomal distances from nuclear speckles genome-wide and for predicting several Mbp chromosome trajectories between nuclear compartments without sophisticated computational modeling.we describe TSA-Seq, a new mapping method capable of providing a "cytological ruler" for estimating mean chromosomal distances from nuclear speckles genome-wide and for predicting several Mbp chromosome trajectories between nuclear compartments without sophisticated computational modeling |
http://www.ncbi.nlm.nih.gov/pubmed/22827758 | Does the HercepTest use a polycloncal or monoclonal antibody? | The HercepTest uses a polyclonal antibody. |
http://www.ncbi.nlm.nih.gov/pubmed/30503854 | Describe participants' experiences from the 100,000 genomes project | Interviewees' decisions to participate in 100 kG P were based on interpersonal and institutional trust in the NHS, and on an investment in improving care for the future. Interviewees relied upon receiving good ongoing NHS care for managing their own or their child's rare disease, but they worried about what their relationships with NHS healthcare professionals would be like in future. A few participants worried about whether Genomics England's biorepository would remain protected and an asset of the NHS. |
http://www.ncbi.nlm.nih.gov/pubmed/30194661,http://www.ncbi.nlm.nih.gov/pubmed/30570832,http://www.ncbi.nlm.nih.gov/pubmed/30774352,http://www.ncbi.nlm.nih.gov/pubmed/28579415,http://www.ncbi.nlm.nih.gov/pubmed/31695514,http://www.ncbi.nlm.nih.gov/pubmed/31650182,http://www.ncbi.nlm.nih.gov/pubmed/33045114,http://www.ncbi.nlm.nih.gov/pubmed/29476499,http://www.ncbi.nlm.nih.gov/pubmed/32702363,http://www.ncbi.nlm.nih.gov/pubmed/31971678 | What is the role of elagolix in treatment of uterine fibroids? | Elagolix is approved for the treatment of moderate to severe pain caused by endometriosis. Elagolix is also effective for heavy bleeding caused by uterine fibroids. |
http://www.ncbi.nlm.nih.gov/pubmed/32571852,http://www.ncbi.nlm.nih.gov/pubmed/31939628,http://www.ncbi.nlm.nih.gov/pubmed/32393641,http://www.ncbi.nlm.nih.gov/pubmed/32154838,http://www.ncbi.nlm.nih.gov/pubmed/32579963 | Where is the organ of Corti located? | The cochlea, a coiled structure located in the ventral region of the inner ear, acts as the primary structure for the perception of sound. Along the length of the cochlear spiral is the organ of Corti, a highly derived and rigorously patterned sensory epithelium that acts to convert auditory stimuli into neural impulses. |
http://www.ncbi.nlm.nih.gov/pubmed/31429610,http://www.ncbi.nlm.nih.gov/pubmed/17596951,http://www.ncbi.nlm.nih.gov/pubmed/30332547,http://www.ncbi.nlm.nih.gov/pubmed/31589483,http://www.ncbi.nlm.nih.gov/pubmed/15906073,http://www.ncbi.nlm.nih.gov/pubmed/25127047,http://www.ncbi.nlm.nih.gov/pubmed/33060522,http://www.ncbi.nlm.nih.gov/pubmed/32068467 | What eye disease(s) are associated with ocular toxoplasmosis? | Retinochoroiditis is the most frequent manifestation of congenital toxoplasmosis Infectious uveitis accounted for 37% of posterior uveitis cases of which toxoplasmosis was the most common cause. Toxoplasmosis was the most common cause of posterior uveitis (60%)A large percentage of posterior and infectious uveitis is associate with toxoplasmosis. Retinochoroiditis is associated with congenital toxoplasmosis.the most frequent manifestation of congenital toxoplasmosis is retinochoroiditis.Retinochoroiditis is the most frequent manifestation of congenital toxoplasmosisyes, ocular toxoplasmosis is associated with retinochoroiditis.Toxoplasmosis was the most common cause of posterior uveitis (60%) Retinochoroiditis is the most frequent manifestation of congenital toxoplasmosis Infectious uveitis accounted for 37% of posterior uveitis cases of which toxoplasmosis was the most common cause.The eye disease(s) associated with ocular toxoplasmosis are:1) ocular syphthalmia, 2) retinochoroiditis, 3) juvenile idiopathic arthritis and4) chorioretinitis.Toxoplasmosis was the most common cause of posterior uveitis (60%) for infectious uveritis, herpetic iridocyclitis, ocular toxoplasmosa, and bacterial endophthalmitis increased in patients with congenital tasma.Diseases associated with ocular toxoplasmosis are ocular syphilis, retinochoroiditis, juvenile idiopathic arthritis and chorioretinitis.Diseases associated with ocular toxoplasmosis are:1) ocular syphilis, 2) retinochoroiditis, 3) juvenile idiopathic arthritis and4) chorioretinitis.Ocular toxoplasmosis (OTS) is a rare but life threatening complication of ocular syphilis, which is followed by retinochoroiditis, juvenile idiopathic arthritis and chorioretinitis. |
http://www.ncbi.nlm.nih.gov/pubmed/20382830,http://www.ncbi.nlm.nih.gov/pubmed/19740764,http://www.ncbi.nlm.nih.gov/pubmed/19712444,http://www.ncbi.nlm.nih.gov/pubmed/12075352,http://www.ncbi.nlm.nih.gov/pubmed/17174523,http://www.ncbi.nlm.nih.gov/pubmed/23668349,http://www.ncbi.nlm.nih.gov/pubmed/18218978,http://www.ncbi.nlm.nih.gov/pubmed/12949121,http://www.ncbi.nlm.nih.gov/pubmed/24429814,http://www.ncbi.nlm.nih.gov/pubmed/24931407 | Which eukaryote genomes contain operons? | Genes in nematode and ascidian genomes frequently occur in operons such genes comprise 15-20% of the coding genome for Caenorhabditis elegans and Ciona intestinalis We find that birth-death models of operon evolution reasonably describe the relative abundance of operons of different sizes in the C. elegans and Ciona genomes and generate predictions about the number of monocistronic, nonoperon genes that likely participate in the birth-death processThe eukaryote genomes contain operons, which can be classified into boader families based, particularly, on the presence of other types of genes. Operons have been found to be present in the following genomes: caenorhabditis elegans, ciona, c. elegans, trichinella spiralis, trichuris muris and ciona intestinalis. Operons have also been reported to exist in the non-coding regions of the human and plant genomes.Genes in nematode and ascidian genomes frequently occur in operons. Such genes comprise 15-20% of the coding genome for Caenorhabditis elegans and Ciona intestinalis. The organization of genes into operons, clusters of genes that are co-transcribed to produce polycistronic pre-mRNAs, is a trait found in a wide range of eukaryotic groups, including multiple animal phyla.Operons are widespread in prokaryotes, but are uncommon in eukaryotes, except nematode worms, where approximately 15% of genes reside in over 1100 operons in the model organism Caenorhabditis elegansOperons are widespread in prokaryotes, but are uncommon in eukaryotes, except nematode worms, where approximately 15% of genes reside in over 1100 operons in the model organism Caenorhabditis elegans. Birth-death models of operon evolution reasonably describe the relative abundance of operons of different sizes in the C. elegans and Ciona genomes |
http://www.ncbi.nlm.nih.gov/pubmed/32557339 | What has capmatinib received FDA approval for in 2020? | In May 2020, oral capmatinib received its first global approval in the USA for the treatment of adults with metastatic non-small cell lung cancer (NSCLC) whose tumours have a mutation that leads to MET exon 14 skipping, as detected by an FDA-approved test. |
http://www.ncbi.nlm.nih.gov/pubmed/30404778,http://www.ncbi.nlm.nih.gov/pubmed/31305534 | Is SLIC-CAGE used for quantification of translation? | No. Cap analysis of gene expression (CAGE) is a method used for single-nucleotide resolution detection of RNA polymerase II transcription start sites (TSSs). Accurate detection of TSSs enhances identification and discovery of core promoters. In addition, active enhancers can be detected through signatures of bidirectional transcription initiation. Described here is a protocol for performing super-low input carrier-CAGE (SLIC-CAGE). The SLIC adaptation of the CAGE protocol minimizes RNA losses by artificially increasing the RNA amount through use of an in vitro transcribed RNA carrier mix that is added to the sample of interest, thus enabling library preparation from nanogram-amounts of total RNA (i.e., thousands of cells).No, the super-low input carrier-CAGE (SLIC-Cage) is not used for quantification of translation. |
http://www.ncbi.nlm.nih.gov/pubmed/31785177,http://www.ncbi.nlm.nih.gov/pubmed/21327862,http://www.ncbi.nlm.nih.gov/pubmed/33080729,http://www.ncbi.nlm.nih.gov/pubmed/31728883,http://www.ncbi.nlm.nih.gov/pubmed/24560760 | Does hypofractionated radiotherapy offers any benefit for DIPG? | No. Hypofractionated radiotherapy does not offers benefit when compared to conventional fractionated radiation therapy for DIPG. |
http://www.ncbi.nlm.nih.gov/pubmed/23200860,http://www.ncbi.nlm.nih.gov/pubmed/15976441,http://www.ncbi.nlm.nih.gov/pubmed/15911624 | What is the function of the stard10 protein? | STARD10, a member of the steroidogenic acute regulatory protein (StAR)-related lipid transfer (START) protein family, is highly expressed in the liver and has been shown to transfer phosphatidylcholine. |
http://www.ncbi.nlm.nih.gov/pubmed/17664768,http://www.ncbi.nlm.nih.gov/pubmed/28660486,http://www.ncbi.nlm.nih.gov/pubmed/17028399,http://www.ncbi.nlm.nih.gov/pubmed/22971867,http://www.ncbi.nlm.nih.gov/pubmed/27617860,http://www.ncbi.nlm.nih.gov/pubmed/29149836,http://www.ncbi.nlm.nih.gov/pubmed/32360386,http://www.ncbi.nlm.nih.gov/pubmed/21365542,http://www.ncbi.nlm.nih.gov/pubmed/32596971,http://www.ncbi.nlm.nih.gov/pubmed/3228132,http://www.ncbi.nlm.nih.gov/pubmed/32528764,http://www.ncbi.nlm.nih.gov/pubmed/17375009,http://www.ncbi.nlm.nih.gov/pubmed/27931782,http://www.ncbi.nlm.nih.gov/pubmed/19432833,http://www.ncbi.nlm.nih.gov/pubmed/16598422,http://www.ncbi.nlm.nih.gov/pubmed/16838330,http://www.ncbi.nlm.nih.gov/pubmed/17219342,http://www.ncbi.nlm.nih.gov/pubmed/19875478,http://www.ncbi.nlm.nih.gov/pubmed/33087645 | Is progeria caused by an autosomal recessive gene? | Yes. Progeria is caused by an autosomal recessive gene.yes, progeria is caused by an autosomal recessive gene. |
http://www.ncbi.nlm.nih.gov/pubmed/16164218,http://www.ncbi.nlm.nih.gov/pubmed/18680684,http://www.ncbi.nlm.nih.gov/pubmed/30701218,http://www.ncbi.nlm.nih.gov/pubmed/25381481,http://www.ncbi.nlm.nih.gov/pubmed/19707417,http://www.ncbi.nlm.nih.gov/pubmed/29752913,http://www.ncbi.nlm.nih.gov/pubmed/23928807,http://www.ncbi.nlm.nih.gov/pubmed/24774505,http://www.ncbi.nlm.nih.gov/pubmed/29171393,http://www.ncbi.nlm.nih.gov/pubmed/21744772,http://www.ncbi.nlm.nih.gov/pubmed/24069534,http://www.ncbi.nlm.nih.gov/pubmed/15379777,http://www.ncbi.nlm.nih.gov/pubmed/16255652,http://www.ncbi.nlm.nih.gov/pubmed/22540283,http://www.ncbi.nlm.nih.gov/pubmed/19128982,http://www.ncbi.nlm.nih.gov/pubmed/28516879 | What is the target of adalimumab? | adalimumab is an anti-tumour necrosis factor (tf)-α antibody.Adalimumab is a fully human monoclonal antibody directed against tumor necrosis factor-alpha, a central cytokine in the immune response in psoriasis that has already been shown to be an effective target for therapy. Targeted drugs against key pathogenetic molecules such as TNF-alpha have significantly improved outcomes in rheumatoid arthritis (RA). They are widely used in clinical practice and drug registries give us information to support their use.Adalimumab is a fully human anti-TNF-alpha IgG1-κ monoclonal antibody.Adalimumab is a fully human monoclonal antibody against TNF-alpha.The objective of this study was to assess the relative importance of local versus systemic interactions between adalimumab and tumour necrosis factor (TNF)-α in rheumatoid arthritis (RA), identify localization of the site of adalimumab action and assess the efficacy of local (intra-articular) versus systemic adalimumab administration for treatment of RAAdalimumab is a monoclonal antibody that targets TNF-alpha, a central cytokine in the immune response in psoriasis that has been linked to autoimmune disease.Adalimumab is a fully human anti-TNF-alpha monoclonal antibody.Adalimumab is a fully human monoclonal antibody directed against tumor necrosis factor-alpha, a central cytokine in the immune response in psoriasis that has already been shown to be an effective target for therapy.Adalimumab is a human anti-TNFα monoclonal antibody that has been reported to demonstrate clinical efficacy and safety, resulting in reversal of epidermal hyperplasia and cutaneous inflammation. The major pathway of TNFα elimination from the synovial fluid (∼77% for subcutaneous administration, and ∼72% for intravenous and intra-articular administration of adgalimumab 40 mg) is interaction with adalumumab, which reaches the joints following local or systemic administration. |
http://www.ncbi.nlm.nih.gov/pubmed/28696420 | Which gene is implicated in the metabolism of codeine, and its polymorphisms in the mother can pose a risk to breastfeeding children? | Mothers with a CYP2D6 ultrarapid metabolizer phenotype may expose their infants to risk of adverse events when taking codeine while breastfeeding, by producing more of the active metabolite, morphine. |
http://www.ncbi.nlm.nih.gov/pubmed/27478875 | Describe the role of epidermal CYLD inactivation in sebaceous and basaloid skin tumors | Epidermal CYLD inactivation sensitizes mice to the development of sebaceous and basaloid skin tumors. Epidermal cyld inactivation also inhibits the growth of epidermal cell lines, leading to development of skin tumors in the early phase of the disease.Epidermal CYLD inactivation sensitizes mice to the development of sebaceous and basaloid skin tumors. The deubiquitinase-encoding gene Cyld displays a dominant genetic linkage to a wide spectrum of skin-appendage tumors, which could be collectively designated as CYLD mutant-syndrome (CYLDm-syndrome).Epidermal CYLD inactivation sensitizes mice to the development of sebaceous and basaloid skin tumors.The deubiquitinase-encoding CYLDM gene is a dominant genetic linkage to a wide spectrum of skin-appendage tumors, which could be collectively designated as CYLD mutant-syndrome (CYLDM-Syndrome). It's a dominant gene in the basaloid and sebaceous regions of the epidermis, which is the outermost layer of the skin. When it's mutated, it can lead to a variety of skin tumors.The deubiquitinase-encoding gene Cyld displays a dominant genetic linkage to a wide spectrum of skin-appendage tumors, which could be collectively designated as CYLD mutant-syndrome (CYLDm-syndrome). Despite recent advances, little is understood about the molecular mechanisms responsible for this painful and difficult-to-treat skin disease. Epidermal CYLD inactivation sensitizes mice to the development of sebaceous and basaloid skin tumors. |
http://www.ncbi.nlm.nih.gov/pubmed/31899702,http://www.ncbi.nlm.nih.gov/pubmed/32611216,http://www.ncbi.nlm.nih.gov/pubmed/32670869,http://www.ncbi.nlm.nih.gov/pubmed/32888407,http://www.ncbi.nlm.nih.gov/pubmed/31677848,http://www.ncbi.nlm.nih.gov/pubmed/31099671,http://www.ncbi.nlm.nih.gov/pubmed/31648957,http://www.ncbi.nlm.nih.gov/pubmed/32740094 | Describe the mechanism of action of Lisocabtagene maraleucel. | Lisocabtagene maraleucel is an autologous, CD19-directed, chimeric antigen receptor (CAR) T-cell product. |
http://www.ncbi.nlm.nih.gov/pubmed/32531423,http://www.ncbi.nlm.nih.gov/pubmed/32975655,http://www.ncbi.nlm.nih.gov/pubmed/30585561,http://www.ncbi.nlm.nih.gov/pubmed/31750954,http://www.ncbi.nlm.nih.gov/pubmed/32539280 | What is the cause of the Kleefstra syndrome? | Mutations in the Euchromatic Histone Methyltransferase 1 (EHMT1) gene cause Kleefstra syndrome, a rare form of intellectual disability (ID) with strong autistic traits and sensory processing deficits. |
http://www.ncbi.nlm.nih.gov/pubmed/29620626,http://www.ncbi.nlm.nih.gov/pubmed/33178308,http://www.ncbi.nlm.nih.gov/pubmed/31852126,http://www.ncbi.nlm.nih.gov/pubmed/33014527,http://www.ncbi.nlm.nih.gov/pubmed/32190087,http://www.ncbi.nlm.nih.gov/pubmed/31574849,http://www.ncbi.nlm.nih.gov/pubmed/33010179,http://www.ncbi.nlm.nih.gov/pubmed/30681588,http://www.ncbi.nlm.nih.gov/pubmed/31399459,http://www.ncbi.nlm.nih.gov/pubmed/32506848,http://www.ncbi.nlm.nih.gov/pubmed/31383431,http://www.ncbi.nlm.nih.gov/pubmed/32280270,http://www.ncbi.nlm.nih.gov/pubmed/29890806,http://www.ncbi.nlm.nih.gov/pubmed/31277532,http://www.ncbi.nlm.nih.gov/pubmed/26345906 | Is acupotomy used to treat muscle stiffness? | Yes. Acupotomy has been widely used to treat nerve entrapment syndrome. URL_0Acupotomy has been used to treat frozen shoulder, cervical spondylosis, third lumbar vertebrae transverse process syndrome, trigger finger, knee osteoarthritis, and lumbar spinal stenosis. |
http://www.ncbi.nlm.nih.gov/pubmed/24998386,http://www.ncbi.nlm.nih.gov/pubmed/27773677,http://www.ncbi.nlm.nih.gov/pubmed/29157917,http://www.ncbi.nlm.nih.gov/pubmed/29209056,http://www.ncbi.nlm.nih.gov/pubmed/31211995,http://www.ncbi.nlm.nih.gov/pubmed/31209209,http://www.ncbi.nlm.nih.gov/pubmed/26240385,http://www.ncbi.nlm.nih.gov/pubmed/24824069,http://www.ncbi.nlm.nih.gov/pubmed/27742736,http://www.ncbi.nlm.nih.gov/pubmed/28575439,http://www.ncbi.nlm.nih.gov/pubmed/33176147 | Which is the role of mediator in genome organization? | Mediator binds to boundaries of chromosomal interaction domains and to proteins involved in DNA looping, RNA metabolism, chromatin remodeling, and actin assembly.Mediator, in addition to binding Pol II promoters, occupies chromosomal interacting domain (CID) boundaries and that Mediator in chromatin associates with proteins that have been shown to interact with CID boundaries, such as Sth1, Ssu72 and histone H4. Together with architectural proteins and transcriptional regulators, such as CTCF and Mediator, respectively, it contributes to genome organization at different scales and thereby affects transcription, DNA replication, and locus rearrangement.mediator binds to boundaries of chromosomal interaction domains and to proteins involved in dna looping, rna metabolism, chromatin remodeling, and actin assembly.. mediator is a multi-unit molecular complex that plays a key role in transferring signals from transcriptional regulators to rna polymerase ii in eukaryotes.Mediator plays a significant role in higher-order genome organization. Mediator, in addition to binding Pol II promoters, occupies chromosomal interacting domain (CID) boundaries and that Mediator in chromatin associates with proteins that have been shown to interact with CID boundaries, such as Sth1, Ssu72 and histone H4 |
http://www.ncbi.nlm.nih.gov/pubmed/30550780 | Which two antibodies directed towards the CGRP ligand, were approved by the FDA in September 2018. | Two antibodies, fremanezumab and galcanezumab, directed towards the CGRP ligand, were approved by the FDA in September 2018. |
http://www.ncbi.nlm.nih.gov/pubmed/26860319 | Describe LowMACA | LowMACA (Low frequency Mutations Analysis via Consensus Alignment) is a method that combines the mutations of various proteins sharing the same functional domains to identify conserved residues that harbor clustered mutations in multiple sequence alignments. LowMACA is designed to visualize and statistically assess potential driver mutations through the identification of their mutational hotspots. Low MACA is an R package available at http://www.bioconductor.org/packages/release/bioc/html/LowMCCC.html.LowMACA is a software for the identification of gain-of-function mutations in putative oncogenic families, increasing the amount of information on functional domains and their possible role in cancer. In this context LowMACA emphasizes the role of genes mutated at low frequency otherwise undetectable by classical single gene analysis.LowMACA is a computational tool for the analysis and visualization of somatic mutation data in cancer.LowMACA (Low frequency Mutations Analysis via Consensus Alignment) is a software for the identification of gain-of-function mutations in putative oncogenic families, increasing the amount of information on functional domains and their possible role in cancer. In this context LowMACA emphasizes the role of genes mutated at low frequency otherwise undetectable by classical single gene analysis. LowMACA is an R package available at http://www.bioconductor.org/packages/release/bioc/html/LowMACA.html. It is also available as a GUI standalone downloadable at: https://cgsb.genomics.iit.it/wiki/projects/LowMACA.LowMACA (Low frequency Mutations Analysis via Consensus Alignment) is a method that combines the mutations of various proteins sharing the same functional domains to identify conserved residues that harbor clustered mutations in multiple sequence alignments. LowMACA is designed to visualize and statistically assess potential driver mutations through the identification of their mutational hotspots.LowMACA (Low frequency Mutations Analysis via Consensus Alignment) is a method that combines the mutations of various proteins sharing the same functional domains to identify conserved residues that harbor clustered mutations in multiple sequence alignments. LowMACA is exploiting protein family analysis for the identification of rare driver mutations in cancer.LowMACA (Low frequency Mutations Analysis via Consensus Alignment) is a method that combines the mutations of various proteins sharing the same functional domains to identify conserved residues that harbor clustered mutations in multiple sequence alignments. LowMACA is designed to visualize and statistically assess potential driver genes through the identification of their mutational hotspots. It is an R package available at http://www.bioconductor.org/packages/release/bioc/html/ lowMACA.html.LowMACA is designed to visualize and statistically assess potential driver genes through the identification of their mutational hotspots.LowMACA is a software that combines the mutations of various proteins sharing the same domains to identify conserved residues that harbor clustered mutations in multiple sequence alignments. |
http://www.ncbi.nlm.nih.gov/pubmed/33092190,http://www.ncbi.nlm.nih.gov/pubmed/33107072,http://www.ncbi.nlm.nih.gov/pubmed/30985372,http://www.ncbi.nlm.nih.gov/pubmed/30604390,http://www.ncbi.nlm.nih.gov/pubmed/29695594,http://www.ncbi.nlm.nih.gov/pubmed/30539801,http://www.ncbi.nlm.nih.gov/pubmed/33090003,http://www.ncbi.nlm.nih.gov/pubmed/30632834,http://www.ncbi.nlm.nih.gov/pubmed/24453078,http://www.ncbi.nlm.nih.gov/pubmed/32757523 | Is ofatumumab effective for multiple sclerosis? | Ofatumumab, a fully human anti-CD20 monoclonal antibody, is effective for relapsing forms of multiple sclerosis. |
http://www.ncbi.nlm.nih.gov/pubmed/31852220,http://www.ncbi.nlm.nih.gov/pubmed/30847765,http://www.ncbi.nlm.nih.gov/pubmed/31768941 | List proteins that promotes calcification. | tissue nonspecific alkaline phosphatase (TNAP)
matrix Gla protein (MGP)
fibroblast growth factor-23 (FGF-23)
matrix metalloproteinases |
http://www.ncbi.nlm.nih.gov/pubmed/32799325,http://www.ncbi.nlm.nih.gov/pubmed/32020557,http://www.ncbi.nlm.nih.gov/pubmed/19939188,http://www.ncbi.nlm.nih.gov/pubmed/31932515,http://www.ncbi.nlm.nih.gov/pubmed/30725283,http://www.ncbi.nlm.nih.gov/pubmed/28644160,http://www.ncbi.nlm.nih.gov/pubmed/31096904,http://www.ncbi.nlm.nih.gov/pubmed/32173558,http://www.ncbi.nlm.nih.gov/pubmed/31020659,http://www.ncbi.nlm.nih.gov/pubmed/32058712 | Please list 3 small molecule CGRP-Receptor antagonists for migraine | Rimegepant and ubrogepant have been developed for acute migraine treatment, while atogepant is studied for migraine prophylaxis. |
http://www.ncbi.nlm.nih.gov/pubmed/28459980,http://www.ncbi.nlm.nih.gov/pubmed/12836700,http://www.ncbi.nlm.nih.gov/pubmed/15126414,http://www.ncbi.nlm.nih.gov/pubmed/12594514,http://www.ncbi.nlm.nih.gov/pubmed/25908670,http://www.ncbi.nlm.nih.gov/pubmed/19594930,http://www.ncbi.nlm.nih.gov/pubmed/18604285,http://www.ncbi.nlm.nih.gov/pubmed/12902158,http://www.ncbi.nlm.nih.gov/pubmed/27799339 | What are the two types of duplicated genes in the yeast S. cerevisiae? | Yeast genes are duplicated both via the whole genome duplication and via smaller scale duplications. The genome of the budding yeast contains 50% of protein-coding genes that are paralogs, including 457 pairs of duplicated genes coming probably from an ancient whole genome duplication.The mechanism of duplication matters, with whole-genome duplicates being more transcriptionally altered than small-scale duplicates. |
http://www.ncbi.nlm.nih.gov/pubmed/31110049 | Why is fingolimod considered a prodrug? | FTY720/fingolimod, is considered a prodrug because it requires in vivo phosphorylation to its active phosphorylated form. |
http://www.ncbi.nlm.nih.gov/pubmed/26913608,http://www.ncbi.nlm.nih.gov/pubmed/17245340,http://www.ncbi.nlm.nih.gov/pubmed/18687985,http://www.ncbi.nlm.nih.gov/pubmed/33015525 | Is there a role for Dickkopf-1 (DKK1) in prostate cancer? | Yes. Dickkopf-1 (DKK1) expression is increased in double-negative prostate cancer (DNPC) relative to prostate-specific antigen (PSA)-expressing Metastatic castration-resistant prostate cancer (mCRPC).Yes, Dickkopf-1 (DKK-1) stimulated prostate cancer growth and metastasis and inhibited bone formation in osteoblastic bone metastases. |
http://www.ncbi.nlm.nih.gov/pubmed/25290383,http://www.ncbi.nlm.nih.gov/pubmed/25404776,http://www.ncbi.nlm.nih.gov/pubmed/15454768,http://www.ncbi.nlm.nih.gov/pubmed/18799938,http://www.ncbi.nlm.nih.gov/pubmed/25629563,http://www.ncbi.nlm.nih.gov/pubmed/23095268,http://www.ncbi.nlm.nih.gov/pubmed/31725667,http://www.ncbi.nlm.nih.gov/pubmed/25332621,http://www.ncbi.nlm.nih.gov/pubmed/17721227,http://www.ncbi.nlm.nih.gov/pubmed/18092253,http://www.ncbi.nlm.nih.gov/pubmed/20460342,http://www.ncbi.nlm.nih.gov/pubmed/1395299,http://www.ncbi.nlm.nih.gov/pubmed/8938781,http://www.ncbi.nlm.nih.gov/pubmed/27615056,http://www.ncbi.nlm.nih.gov/pubmed/32700372,http://www.ncbi.nlm.nih.gov/pubmed/32530103,http://www.ncbi.nlm.nih.gov/pubmed/16721483,http://www.ncbi.nlm.nih.gov/pubmed/33083429,http://www.ncbi.nlm.nih.gov/pubmed/32490041,http://www.ncbi.nlm.nih.gov/pubmed/18284939,http://www.ncbi.nlm.nih.gov/pubmed/24942018,http://www.ncbi.nlm.nih.gov/pubmed/18836937,http://www.ncbi.nlm.nih.gov/pubmed/8819627,http://www.ncbi.nlm.nih.gov/pubmed/29095073,http://www.ncbi.nlm.nih.gov/pubmed/20671836,http://www.ncbi.nlm.nih.gov/pubmed/25006951,http://www.ncbi.nlm.nih.gov/pubmed/2093257,http://www.ncbi.nlm.nih.gov/pubmed/8246062,http://www.ncbi.nlm.nih.gov/pubmed/28211222,http://www.ncbi.nlm.nih.gov/pubmed/16296204,http://www.ncbi.nlm.nih.gov/pubmed/28590380,http://www.ncbi.nlm.nih.gov/pubmed/28852852,http://www.ncbi.nlm.nih.gov/pubmed/26000180,http://www.ncbi.nlm.nih.gov/pubmed/15662330,http://www.ncbi.nlm.nih.gov/pubmed/17306128,http://www.ncbi.nlm.nih.gov/pubmed/31970256,http://www.ncbi.nlm.nih.gov/pubmed/22677741 | What is Hemophilic Pseudotumor? | Hemophilic Pseudotumor is a rare complication of hemophilia. It is an encapsulated haematoma in patients with haemophilia which has a tendency to progress and produce clinical symptoms related to its anatomical location. The lesion most frequently occurs in the long bones, pelvis, small bones of the hands and feet, or rarely in the maxillofacial region. |
http://www.ncbi.nlm.nih.gov/pubmed/31354448,http://www.ncbi.nlm.nih.gov/pubmed/28648677,http://www.ncbi.nlm.nih.gov/pubmed/32478741 | What is the aim of the TRAP method? | The translating ribosome affinity purification (TRAP) method is used to obtain obtain translatome data. |
http://www.ncbi.nlm.nih.gov/pubmed/32999027,http://www.ncbi.nlm.nih.gov/pubmed/31399377,http://www.ncbi.nlm.nih.gov/pubmed/33067034,http://www.ncbi.nlm.nih.gov/pubmed/31423396,http://www.ncbi.nlm.nih.gov/pubmed/30145235,http://www.ncbi.nlm.nih.gov/pubmed/33163688,http://www.ncbi.nlm.nih.gov/pubmed/32862397,http://www.ncbi.nlm.nih.gov/pubmed/31258310,http://www.ncbi.nlm.nih.gov/pubmed/30370455,http://www.ncbi.nlm.nih.gov/pubmed/32606264,http://www.ncbi.nlm.nih.gov/pubmed/31400911 | The Shingrix vaccine is used to prevent what disease? | Shingrix is a 4-component vaccine against capsular herpes zoster (4CZV), which has recently been licensed in Europe, Canada and Australia.the shingrix vaccine is used for the prevention of herpes zoster and postherpetic neuralgia.Shingrix vaccine is used for prevention of herpes zoster.The Shingrix vaccine is used for prevention of herpes zoster.The Shingrix vaccine prevents Postherpetic neuralgia, also known as Shingles, which is caused by herpes zoster (HZ) |
http://www.ncbi.nlm.nih.gov/pubmed/19798443,http://www.ncbi.nlm.nih.gov/pubmed/29728561,http://www.ncbi.nlm.nih.gov/pubmed/30659116,http://www.ncbi.nlm.nih.gov/pubmed/22547675,http://www.ncbi.nlm.nih.gov/pubmed/24782529,http://www.ncbi.nlm.nih.gov/pubmed/24555990,http://www.ncbi.nlm.nih.gov/pubmed/30384843,http://www.ncbi.nlm.nih.gov/pubmed/24637637,http://www.ncbi.nlm.nih.gov/pubmed/25945750,http://www.ncbi.nlm.nih.gov/pubmed/28688038,http://www.ncbi.nlm.nih.gov/pubmed/23476027,http://www.ncbi.nlm.nih.gov/pubmed/28636597,http://www.ncbi.nlm.nih.gov/pubmed/29358235,http://www.ncbi.nlm.nih.gov/pubmed/11259603,http://www.ncbi.nlm.nih.gov/pubmed/30442760,http://www.ncbi.nlm.nih.gov/pubmed/23894480,http://www.ncbi.nlm.nih.gov/pubmed/24681131 | What is the function of HP1a in the nucleus? | Heterochromatin protein 1 (HP1) is an abundant component of heterochromatin, a highly condensed compartment of the nucleus that comprises a major fraction of complex genomes.Drosophila heterochromatin-associated protein 1 (HP1) is an abundant component of heterochromatin, a highly condensed compartment of the nucleus that comprises a major fraction of complex genomes.Heterochromatin protein 1 (HP1) was first described in Drosophila melanogaster as a heterochromatin associated protein required for epigenetic gene silencing. |
http://www.ncbi.nlm.nih.gov/pubmed/22458939,http://www.ncbi.nlm.nih.gov/pubmed/26043724 | Has AZD9668 been tested in clinical trials? | Yes, AZD9668 has been tested in clinical trials. |
http://www.ncbi.nlm.nih.gov/pubmed/32718982,http://www.ncbi.nlm.nih.gov/pubmed/33211864 | Which class of genomic elements was assessed as part of the FANTOM6 project? | Long noncoding RNAs (lncRNAs) constitute the majority of transcripts in the mammalian genomes, and yet, their functions remain largely unknown. As part of the FANTOM6 project, the expression of 285 lncRNAs was systematically knocked down in human dermal fibroblasts. Cellular growth, morphological changes, and transcriptomic responses were quantified using Capped Analysis of Gene Expression (CAGE).The functional annotation of the mammalian genome 6 (FANTOM6) project aims to systematically map all human long noncoding RNAs (lncRNAs) in a gene-dependent manner through dedicated efforts from national and international teams |
http://www.ncbi.nlm.nih.gov/pubmed/31939447,http://www.ncbi.nlm.nih.gov/pubmed/31939448,http://www.ncbi.nlm.nih.gov/pubmed/30213452,http://www.ncbi.nlm.nih.gov/pubmed/32112738,http://www.ncbi.nlm.nih.gov/pubmed/32416073,http://www.ncbi.nlm.nih.gov/pubmed/32499235,http://www.ncbi.nlm.nih.gov/pubmed/31017739,http://www.ncbi.nlm.nih.gov/pubmed/32376724,http://www.ncbi.nlm.nih.gov/pubmed/33004770,http://www.ncbi.nlm.nih.gov/pubmed/32256049,http://www.ncbi.nlm.nih.gov/pubmed/32623573,http://www.ncbi.nlm.nih.gov/pubmed/32602470,http://www.ncbi.nlm.nih.gov/pubmed/32411597,http://www.ncbi.nlm.nih.gov/pubmed/33087333,http://www.ncbi.nlm.nih.gov/pubmed/32762583,http://www.ncbi.nlm.nih.gov/pubmed/31420358,http://www.ncbi.nlm.nih.gov/pubmed/33154554,http://www.ncbi.nlm.nih.gov/pubmed/31238988,http://www.ncbi.nlm.nih.gov/pubmed/33299330,http://www.ncbi.nlm.nih.gov/pubmed/30242068,http://www.ncbi.nlm.nih.gov/pubmed/31313098,http://www.ncbi.nlm.nih.gov/pubmed/31039052,http://www.ncbi.nlm.nih.gov/pubmed/32776600,http://www.ncbi.nlm.nih.gov/pubmed/33092443,http://www.ncbi.nlm.nih.gov/pubmed/33097476,http://www.ncbi.nlm.nih.gov/pubmed/33241036,http://www.ncbi.nlm.nih.gov/pubmed/32064977,http://www.ncbi.nlm.nih.gov/pubmed/32530632,http://www.ncbi.nlm.nih.gov/pubmed/33063473,http://www.ncbi.nlm.nih.gov/pubmed/33194624,http://www.ncbi.nlm.nih.gov/pubmed/33052760 | Which molecule is targeted by Camrelizumab? | Camrelizumab is a humanised antibody that targets programmed death-1 (PD-1) ligand.Camrelizumab is PD-1 (programmed cell death-1 receptor) inhibitor that is used for treatment of cancer. |
http://www.ncbi.nlm.nih.gov/pubmed/31945610,http://www.ncbi.nlm.nih.gov/pubmed/31938053,http://www.ncbi.nlm.nih.gov/pubmed/32012706,http://www.ncbi.nlm.nih.gov/pubmed/31894855,http://www.ncbi.nlm.nih.gov/pubmed/31909985,http://www.ncbi.nlm.nih.gov/pubmed/31967154 | What is a foam cell? | Foam cell, a hallmark of atherosclerosis, is prominently derived from monocyte-differentiated macrophage, and vascular smooth muscle cells (VSMCs) through unlimitedly phagocytizing oxidized low-density lipoprotein (oxLDL). Therefore, the inhibition of monocyte adhesion to endothelium and uptake of oxLDL might be a breakthrough point for retarding atherosclerosis. |
http://www.ncbi.nlm.nih.gov/pubmed/17143099,http://www.ncbi.nlm.nih.gov/pubmed/19940267,http://www.ncbi.nlm.nih.gov/pubmed/20195425,http://www.ncbi.nlm.nih.gov/pubmed/26402985,http://www.ncbi.nlm.nih.gov/pubmed/27870723,http://www.ncbi.nlm.nih.gov/pubmed/33194498,http://www.ncbi.nlm.nih.gov/pubmed/17700359,http://www.ncbi.nlm.nih.gov/pubmed/12426921,http://www.ncbi.nlm.nih.gov/pubmed/16575599,http://www.ncbi.nlm.nih.gov/pubmed/15849374,http://www.ncbi.nlm.nih.gov/pubmed/11869826,http://www.ncbi.nlm.nih.gov/pubmed/15269925 | What class of drugs frequently has muscle pain and other muscle toxicities such as mysositis and rhabdomyolysis as a side effect? | Muscular complaints are known side-effects of statin therapy, ranging from myalgia to clinically important myositis and rhabdomyolysis.3-hydroxy-3-methylglutaryl coenzyme A reductase reductase inhibitors (statins) are generally well tolerated, with statin-associated muscle symptoms (SAMS) the most common side effect (~10%) seen in statin users.The most commonly experienced side-effect of statin medication is muscle painA class of drug called a statin. It's a drug that works by reducing the amount of cholesterol in the body, which is what causes muscle fatigue.statins are generally well tolerated, with statin-associated muscle symptoms (sams) the most common side effect (~10%) seen in statin users.Statin use has been associated with an increased risk of glucocorticoid-induced rhabdomyolysis as well as with adverse effects such as mysositis and hypercholesterolemia.3-hydroxy-3-methylglutaryl coenzyme A reductase reductase inhibitors, a class of drugs called statins are generally well tolerated, with statin-associated muscle symptoms (SAMS) such as muscle pain, myositis, and rarely rhabdomyolysis, the most common side effect (~10%) seen in statin users. |
http://www.ncbi.nlm.nih.gov/pubmed/29973939,http://www.ncbi.nlm.nih.gov/pubmed/15225217,http://www.ncbi.nlm.nih.gov/pubmed/21975932,http://www.ncbi.nlm.nih.gov/pubmed/16998902,http://www.ncbi.nlm.nih.gov/pubmed/12957874,http://www.ncbi.nlm.nih.gov/pubmed/23347175,http://www.ncbi.nlm.nih.gov/pubmed/29558695,http://www.ncbi.nlm.nih.gov/pubmed/17182123,http://www.ncbi.nlm.nih.gov/pubmed/32235336,http://www.ncbi.nlm.nih.gov/pubmed/19838011,http://www.ncbi.nlm.nih.gov/pubmed/14500551,http://www.ncbi.nlm.nih.gov/pubmed/30152848,http://www.ncbi.nlm.nih.gov/pubmed/23727390,http://www.ncbi.nlm.nih.gov/pubmed/20656683,http://www.ncbi.nlm.nih.gov/pubmed/10974035,http://www.ncbi.nlm.nih.gov/pubmed/15647278,http://www.ncbi.nlm.nih.gov/pubmed/29892481,http://www.ncbi.nlm.nih.gov/pubmed/29710466,http://www.ncbi.nlm.nih.gov/pubmed/32334267,http://www.ncbi.nlm.nih.gov/pubmed/23741316,http://www.ncbi.nlm.nih.gov/pubmed/10611754,http://www.ncbi.nlm.nih.gov/pubmed/15184872,http://www.ncbi.nlm.nih.gov/pubmed/12297674,http://www.ncbi.nlm.nih.gov/pubmed/26956486,http://www.ncbi.nlm.nih.gov/pubmed/19352540,http://www.ncbi.nlm.nih.gov/pubmed/17513865,http://www.ncbi.nlm.nih.gov/pubmed/20603212,http://www.ncbi.nlm.nih.gov/pubmed/24129565,http://www.ncbi.nlm.nih.gov/pubmed/19030025,http://www.ncbi.nlm.nih.gov/pubmed/18322180,http://www.ncbi.nlm.nih.gov/pubmed/15192102,http://www.ncbi.nlm.nih.gov/pubmed/21095583 | Which cytokine molecule activates SMADs? | SMADs are activated by Transforming growth factor beta (TGF beta)smads are activated by transforming growth factor-β (tgf-β).SMADs are activated by Transforming growth factor beta (TGF-β)TGF-β1 effects appear to be mediated through the canonical Smad pathway.SMADs are activated by Transforming growth factor beta (TGF beta).In an NEC animal model, oral administration of the isoform TGF-β1 activated the downstream effector Smad2 in intestine and significantly reduced NEC incidence Transcription factor specificity protein 1 modulates TGFβ1/Smad signaling to negatively regulate SIGIRR expression by human M1 macrophages stimulated with substance P.The protein expression of TGF‑β1/mothers against decapentaplegic homolog (Smad) and phosphoinositide 3‑kinase (PI3K)/protein kinase B (AKT) signaling pathways was evaluated by western blotting regulates the ERK/MAPK pathway independent of the SMAD pathwayActivated SMADs are phosphorylated by TGF-β superfamily type I receptors at two serine residues at an S-M/V-S motif at their extreme C-terminus. Once phosphorylated, activated R-SMADs form complexes with SMAD4, which accumulate in the nucleus where they activate or repress transcription. |
http://www.ncbi.nlm.nih.gov/pubmed/30243889,http://www.ncbi.nlm.nih.gov/pubmed/33185331 | What is the Oncomine Dx Target test? | The Oncomine Dx Target Test (ODxTT) is a next-generation sequencing-based companion diagnostic test, that could facilitate access to multiple biomarker testing using small tissue samples to support therapy decisions for patients with advanced NSCLC. |
http://www.ncbi.nlm.nih.gov/pubmed/22504421,http://www.ncbi.nlm.nih.gov/pubmed/24361131 | What are common variants at 12q14 and 12q24 associated with? | Common variants at 12q14 and 12q24 are associated with hippocampal volume. Aging is associated with reductions in hippocampal volume that are accelerated by Alzheimer's disease and vascular risk factors.Common variants at 12q14 and 12q24 are associated with hippocampal volume. As we age, our hippocampus (the part of the brain that is responsible for memory and cognition) becomes less and less efficient at storing information. As a result, the volume of the hippocampus shrinks.Common variants at 12q14 and 12q24 are associated with hippocampal volume.Aging is associated with reductions in hippocampal volume that are accelerated by Alzheimer's disease and vascular risk factors. Common variants at 12q14 and 12q24 are associated with hippocampal volume. |
http://www.ncbi.nlm.nih.gov/pubmed/32955176,http://www.ncbi.nlm.nih.gov/pubmed/33097477,http://www.ncbi.nlm.nih.gov/pubmed/33004338 | Which mutation is targeted by Sotorasib? | Sotorasib is a small molecule that selectively and irreversibly targets KRASG12C. |
http://www.ncbi.nlm.nih.gov/pubmed/32132707,http://www.ncbi.nlm.nih.gov/pubmed/32132706 | When is DELE1 exiting the mitochondrion? | Mitochondrial stress stimulates OMA1-dependent cleavage of DELE1 and leads to the accumulation of DELE1 in the cytosol. |
http://www.ncbi.nlm.nih.gov/pubmed/25398052,http://www.ncbi.nlm.nih.gov/pubmed/27290837,http://www.ncbi.nlm.nih.gov/pubmed/31147753,http://www.ncbi.nlm.nih.gov/pubmed/30656919,http://www.ncbi.nlm.nih.gov/pubmed/29334628,http://www.ncbi.nlm.nih.gov/pubmed/21943201,http://www.ncbi.nlm.nih.gov/pubmed/31965514,http://www.ncbi.nlm.nih.gov/pubmed/28698599,http://www.ncbi.nlm.nih.gov/pubmed/21816947,http://www.ncbi.nlm.nih.gov/pubmed/30578505,http://www.ncbi.nlm.nih.gov/pubmed/29650680,http://www.ncbi.nlm.nih.gov/pubmed/31698098,http://www.ncbi.nlm.nih.gov/pubmed/29534263,http://www.ncbi.nlm.nih.gov/pubmed/21679365,http://www.ncbi.nlm.nih.gov/pubmed/28625504,http://www.ncbi.nlm.nih.gov/pubmed/20097287,http://www.ncbi.nlm.nih.gov/pubmed/29281629,http://www.ncbi.nlm.nih.gov/pubmed/29303074,http://www.ncbi.nlm.nih.gov/pubmed/25388584,http://www.ncbi.nlm.nih.gov/pubmed/22169048,http://www.ncbi.nlm.nih.gov/pubmed/30867380,http://www.ncbi.nlm.nih.gov/pubmed/26540106,http://www.ncbi.nlm.nih.gov/pubmed/25599087 | What is a ciliopathy? | A ciliopathy is any genetic disorder that affects the cellular cilia or the cilia anchoring structures, the basal bodies, or ciliary functionCiliopathy is a rare disorder of the central nervous system characterized by defects in ciliary motility, endocytosis, and photoreceptors.ciliopathies are a group of disorders caused by a defect in ciliogenesis, ciliary protein trafficking.Ciliopathies are a group of disorders caused by a defect in ciliogenesis, ciliary protein trafficking. |
http://www.ncbi.nlm.nih.gov/pubmed/11242054,http://www.ncbi.nlm.nih.gov/pubmed/27733730,http://www.ncbi.nlm.nih.gov/pubmed/16222246,http://www.ncbi.nlm.nih.gov/pubmed/19788305,http://www.ncbi.nlm.nih.gov/pubmed/17406994,http://www.ncbi.nlm.nih.gov/pubmed/11859155,http://www.ncbi.nlm.nih.gov/pubmed/12897054,http://www.ncbi.nlm.nih.gov/pubmed/17172865,http://www.ncbi.nlm.nih.gov/pubmed/17542647,http://www.ncbi.nlm.nih.gov/pubmed/19880879,http://www.ncbi.nlm.nih.gov/pubmed/23166515,http://www.ncbi.nlm.nih.gov/pubmed/11242053,http://www.ncbi.nlm.nih.gov/pubmed/22514736,http://www.ncbi.nlm.nih.gov/pubmed/18926834,http://www.ncbi.nlm.nih.gov/pubmed/11882902,http://www.ncbi.nlm.nih.gov/pubmed/22815475,http://www.ncbi.nlm.nih.gov/pubmed/12068920 | Which histone mark is recognized by HP1? | h3k9me3 is the major histone mark that is recognized by hp1.Here, we present structural, energetic, and mutational analyses of the complex between the Drosophila HP1 chromodomain and the histone H3 tail with a methyllysine at residue 9, a modification associated with epigenetic silencing Methylation of histone H3 lysine 9 creates a binding site for HP1 proteins.Histone H3 at lysine 9 trimethylation (H3K9me3)Histone H3 at lysine 9 (H3K9me3)Methylation of histone H3 lysine 9 creates a binding site for HP1 proteins. We show that methylated lysine 9 of histone H3 (Me9H3) is a marker of heterochromatin in divergent animal species.HP1 can bind with high affinity to histone H3 methylated at lysine 9 but not at lysine 4. Methylation of lysine 9 in histone H3 is recognized by heterochromatin protein 1 (HP1), which directs the binding of other proteins to control chromatin structure and gene expression.Methylation of lysine 9 in histone H3 is recognized by heterochromatin protein 1 (HP1), which directs the binding of other proteins to control chromatin structure and gene expression.Methylation of histone H3 lysine 9 creates a binding site for HP1 proteins. Here we show that mammalian methyltransferases that selectively methylate histone H3 on lysine 9 (Suv39h HMTases) generate a binding site for HP1 proteins--a family of heterochromatic adaptor molecules implicated in both gene silencing and supra-nucleosomal chromatin structure. |
http://www.ncbi.nlm.nih.gov/pubmed/30504800 | What is AZD8601? | AZD8601 is a modified mRNA encoding vascular endothelial growth factor A (VEGF-A). Sequential dosing of AZD8601 improves vascularization and tissue oxygenation of the wound bed, leading to accelerated re-epithelialization during the early phase of diabetic wound healing. |
http://www.ncbi.nlm.nih.gov/pubmed/27866048 | List critical regions for 7p22.1 microduplication syndrome | 7p22.1 microduplication syndrome is mainly characterized by developmental and speech delay, craniofacial dysmorphism and skeletal abnormalities. The minimal critical region includes two OMIM genes: ACTB and RNF216.7p22.1 microduplication syndrome is mainly characterized by developmental and speech delay, craniofacial dysmorphisms and skeletal abnormalities. The minimal critical region includes two OMIM genes: ACTB and RNF216. |
http://www.ncbi.nlm.nih.gov/pubmed/32144719,http://www.ncbi.nlm.nih.gov/pubmed/32005279,http://www.ncbi.nlm.nih.gov/pubmed/31825192,http://www.ncbi.nlm.nih.gov/pubmed/29037983,http://www.ncbi.nlm.nih.gov/pubmed/31047804,http://www.ncbi.nlm.nih.gov/pubmed/32058843,http://www.ncbi.nlm.nih.gov/pubmed/31843763,http://www.ncbi.nlm.nih.gov/pubmed/32469182,http://www.ncbi.nlm.nih.gov/pubmed/33118153,http://www.ncbi.nlm.nih.gov/pubmed/31087550,http://www.ncbi.nlm.nih.gov/pubmed/32917537,http://www.ncbi.nlm.nih.gov/pubmed/31574081,http://www.ncbi.nlm.nih.gov/pubmed/31047803,http://www.ncbi.nlm.nih.gov/pubmed/30351177,http://www.ncbi.nlm.nih.gov/pubmed/29703841 | Which molecules are targeted by Trastuzumab Deruxtecan? | Trastuzumab deruxtecan is a HER2-directed antibody and DNA topoisomerase I inhibitor conjugate being developed for the treatment of HER2-expressing solid tumours, including breast cancer, gastric cancer, colorectal cancer and non-small cell lung cancer |
http://www.ncbi.nlm.nih.gov/pubmed/28031292,http://www.ncbi.nlm.nih.gov/pubmed/21625540,http://www.ncbi.nlm.nih.gov/pubmed/22522442,http://www.ncbi.nlm.nih.gov/pubmed/25274842 | What is the function of the HSJ1 proteins? | HSJ1 is a neuronal enriched member of the HSP40/DNAJ co-chaperone family. |
http://www.ncbi.nlm.nih.gov/pubmed/14642738,http://www.ncbi.nlm.nih.gov/pubmed/9399013,http://www.ncbi.nlm.nih.gov/pubmed/9399012,http://www.ncbi.nlm.nih.gov/pubmed/9170337,http://www.ncbi.nlm.nih.gov/pubmed/9399017,http://www.ncbi.nlm.nih.gov/pubmed/14743270,http://www.ncbi.nlm.nih.gov/pubmed/32752932,http://www.ncbi.nlm.nih.gov/pubmed/11200789,http://www.ncbi.nlm.nih.gov/pubmed/31889312,http://www.ncbi.nlm.nih.gov/pubmed/9660035,http://www.ncbi.nlm.nih.gov/pubmed/15992000,http://www.ncbi.nlm.nih.gov/pubmed/9725543,http://www.ncbi.nlm.nih.gov/pubmed/12083998,http://www.ncbi.nlm.nih.gov/pubmed/31593739,http://www.ncbi.nlm.nih.gov/pubmed/10473025,http://www.ncbi.nlm.nih.gov/pubmed/10640260,http://www.ncbi.nlm.nih.gov/pubmed/16575626,http://www.ncbi.nlm.nih.gov/pubmed/9071267,http://www.ncbi.nlm.nih.gov/pubmed/11594437,http://www.ncbi.nlm.nih.gov/pubmed/10210888,http://www.ncbi.nlm.nih.gov/pubmed/18028032 | What is the indication for zolmitriptan? | Development of a novel zolmitriptan intracutaneous microneedle system (Qtrypta™) for the acute treatment of migraineZolmitriptan is an effective medicine used in the treatment of migraine.zolmitriptan is approved for the treatment of migraine.zolmitriptan is approved for migraine treatment. |
http://www.ncbi.nlm.nih.gov/pubmed/20382830,http://www.ncbi.nlm.nih.gov/pubmed/16752214,http://www.ncbi.nlm.nih.gov/pubmed/27631780,http://www.ncbi.nlm.nih.gov/pubmed/12386927,http://www.ncbi.nlm.nih.gov/pubmed/12075352,http://www.ncbi.nlm.nih.gov/pubmed/25936768,http://www.ncbi.nlm.nih.gov/pubmed/19204375,http://www.ncbi.nlm.nih.gov/pubmed/18218978,http://www.ncbi.nlm.nih.gov/pubmed/21177958 | What percentage of C. elegans genes reside in operons? | Nearly 15% of the ~20,000 C. elegans genes are contained in operons, multigene clusters controlled by a single promoter. Our evidence indicates that the genome contains at least 1,000 operons, 2 8 genes long, that contain about 15% of all C. elegans genes.Nearly 15% of the ~20,000 C. elegans genes are contained in operons, multigene clusters controlled by a single promoter.Approximately 15% of the genes in C. elegans are operons.Nearly 15% of the ~20,000 C. elegans genes are contained in operons, multigene clusters controlled by a single promoter. Both methods indicate that the pre-mRNAs of about 70% of Caenorhabditis elegans genes are trans-spliced and as many as a quarter are transcribed in these operons.about 15% of genes in Caenorhabditis elegans, a model organism belonging to Nematoda, reside in operons (Blumenthal et al. 2002; Blumenthal and Gleason 2003). For two reasons, nematode and prokaryotic operons are believed to have separate origins.Our evidence indicates that the genome contains at least 1,000 operons, 2 8 genes long, that contain about 15% of all C. elegans genes. Nearly 15% of the ~20,000 C. elegans genes are contained in operons, multigene clusters controlled by a single promoter.Our data indicate that 15% of the genes in C. elegans reside in operons.Approximately 15% of the genes in C. elegans are located in operons, of which at least 15% are known to date.Nearly 15% of the ~20,000 C. elegans genes are contained in operons, multigene clusters controlled by a single promoter. Our evidence indicates that the genome contains at least 1,000 operons, 2 8 genes long, that contain about 15% of all C. elegans genes. Because operons account for about 15% of the genes in C. elegans, this lower duplication frequency might place a large constraint on the plasticity of the genome.Nearly 15% of the ~20,000 C. elegans genes are contained in operons, multigene clusters controlled by a single promoter. Because operons account for about 15% of the genes in C. elegans, this lower duplication frequency might place a large constraint on the plasticity of the genome.Our evidence indicates that the genome contains at least 1,000 operons, 2 8 genes long, that contain about 15% of all C. elegans genes. Because operons account for about 15% of the genes in C. elegans, this lower duplication frequency might place a large constraint on the plasticity of the genome.Approximately 15% of the genes in C. elegans are located in operons.About 15% of all C. elegans genes reside in operons. URL_0 > Nearly 15 percent of the ~20,000 C. Elegans genes are contained in operon, multigene clusters controlled by a single promoter.Evidence indicates that the genome of C. elegans contains at least 1,000 operons, 2 8 genes long, that contain about 15% of all C. elegans genes. |
http://www.ncbi.nlm.nih.gov/pubmed/29938336 | What is the most advanced phase of clinical trial that fingolimod has entered? | Fingolimod has been assessed in phase IV clinical trials. |
http://www.ncbi.nlm.nih.gov/pubmed/29403011,http://www.ncbi.nlm.nih.gov/pubmed/29403012 | What is caused by a gain-of-function mutation in CLCN2? | A gain-of-function mutation in the CLCN2 chloride channel gene causes primary aldosteronism, which is the most common and curable form of arterial hypertension.A gain-of-function mutation in the CLCN2 chloride channel gene causes primary aldosteronism. A gain-of-function mutation in the CLCN2 chloride channel gene causes primary aldosteronism. The leukodystrophy of Glialcam, which is encoded in the gene, is associated with dysregulated extracellular ion homeostasis, and abnormal RPE cell function.Primary aldosteronism is a rare autosomal dominant disorder caused by gain-of-function mutations in CLCN2 and clinically characterized by severe intrauterine and post-natal growth retardationA gain-of-function mutation in the CLCN2 chloride channel gene causes primary aldosteronism.Primary aldosteronism is an autosomal dominant disorder caused by gain-of-function mutations in CLCN2.A gain-of-function mutation in the CLCN2 chloride channel gene causes primary aldosteronism. Primary aldosteronism is the most common and curable form of secondary arterial hypertension.Primary aldosteronism is the most common and curable form of secondary arterial hypertension. A gain-of-function mutation in the CLCN2 chloride channel gene causes primary aldosteronism. |
http://www.ncbi.nlm.nih.gov/pubmed/32558178,http://www.ncbi.nlm.nih.gov/pubmed/32901611,http://www.ncbi.nlm.nih.gov/pubmed/28412960,http://www.ncbi.nlm.nih.gov/pubmed/32622397 | Which treatments were compared in the UNBLOCS trial? | The UNBLOCS trial compared thulium laser transurethral vaporesection of the prostate versus transurethral resection of the prostate for men with lower urinary tract symptoms or urinary retention. |
http://www.ncbi.nlm.nih.gov/pubmed/30700556,http://www.ncbi.nlm.nih.gov/pubmed/29217730,http://www.ncbi.nlm.nih.gov/pubmed/31939155,http://www.ncbi.nlm.nih.gov/pubmed/30820596 | Which are the ligands of the Roundabout (Robo) receptors? | Roundabouts comprise a family of single-pass transmembrane receptors facilitating this process upon interaction with the soluble extracellular ligand Slit protein family emanating from the midline. |
http://www.ncbi.nlm.nih.gov/pubmed/27246282,http://www.ncbi.nlm.nih.gov/pubmed/18840491,http://www.ncbi.nlm.nih.gov/pubmed/23549999,http://www.ncbi.nlm.nih.gov/pubmed/32926943,http://www.ncbi.nlm.nih.gov/pubmed/20670626,http://www.ncbi.nlm.nih.gov/pubmed/20064520,http://www.ncbi.nlm.nih.gov/pubmed/23348107,http://www.ncbi.nlm.nih.gov/pubmed/29867758,http://www.ncbi.nlm.nih.gov/pubmed/31812674,http://www.ncbi.nlm.nih.gov/pubmed/31790683,http://www.ncbi.nlm.nih.gov/pubmed/27349533,http://www.ncbi.nlm.nih.gov/pubmed/30333302,http://www.ncbi.nlm.nih.gov/pubmed/22649563,http://www.ncbi.nlm.nih.gov/pubmed/19770291,http://www.ncbi.nlm.nih.gov/pubmed/19210293,http://www.ncbi.nlm.nih.gov/pubmed/23638144,http://www.ncbi.nlm.nih.gov/pubmed/20738704,http://www.ncbi.nlm.nih.gov/pubmed/31729619 | What is the function of kisspeptin in the brain? | Kisspeptin is a neuropeptide that plays an integral role in the regulation of energy intake and reproduction by acting centrally on the hypothalamus-pituitary-gonadal axis. It is the most potent factor known to induce GnRH release. Kisspeptin preserves mitochondrial function by inducing mitophagy and autophagy in aging rat brain hippocampus Kisspeptin is a neuropeptide that plays an integral role in the regulation of energy intake and reproduction by acting centrally on the hypothalamus-pituitary-gonadal axisThe function of kisspeptin in the brain is not really known, but it plays an integral role in the regulation of hunger, sex, and reproduction. Kisspeptin is the most potent factor known to induce GnRH release in Mice. URL_0 Kisspeptin is the most potent factor known to induce GnRH release. Kisspeptin preserves mitochondrial function by inducing mitophagy and autophagy in aging rat brain hippocampusKisspeptin is a neuropeptide that plays an integral role in the regulation of energy intake and reproduction by acting centrally on the hypothalamus-pituitary-gonadal axis. Kisspeptin also preserves mitochondrial function by inducing mitophagy and autophagy in aging rat brain.kisspeptin preserves mitochondrial function by inducing mitophagy and autophagy in aging rat brain hippocampus and human neuronal cell line. Kisspeptin is the most potent factor known to induce GnRH release. Kisspeptin preserves mitochondrial function by inducing mitophagy and autophagy in aging rat brain hippocampus Kisspeptin is a neuropeptide that plays an integral role in the regulation of energy intake and reproduction by acting centrally on the hypothalamus-pituitary-gonadal axis Intraperitoneal Treatment of Kisspeptin Suppresses Appetite and Energy Expenditure and Alters Gastrointestinal Hormones in Mice.Kisspeptin is a leptin-like protein that exerts important effects on the regulation of food intake and energy expenditure by interacting with the glucocorticoid receptor in the brain.Kisspeptin is a neuropeptide that plays an integral role in the regulation of energy intake and reproduction by acting centrally on the hypothalamus-pituitary-gonadal axis. |
http://www.ncbi.nlm.nih.gov/pubmed/20824089,http://www.ncbi.nlm.nih.gov/pubmed/19036726,http://www.ncbi.nlm.nih.gov/pubmed/17267691,http://www.ncbi.nlm.nih.gov/pubmed/18223644,http://www.ncbi.nlm.nih.gov/pubmed/16908534,http://www.ncbi.nlm.nih.gov/pubmed/18454139,http://www.ncbi.nlm.nih.gov/pubmed/20026622,http://www.ncbi.nlm.nih.gov/pubmed/16790525,http://www.ncbi.nlm.nih.gov/pubmed/25544848,http://www.ncbi.nlm.nih.gov/pubmed/15939376,http://www.ncbi.nlm.nih.gov/pubmed/24489122,http://www.ncbi.nlm.nih.gov/pubmed/26296469,http://www.ncbi.nlm.nih.gov/pubmed/19845468,http://www.ncbi.nlm.nih.gov/pubmed/15494369,http://www.ncbi.nlm.nih.gov/pubmed/22713603,http://www.ncbi.nlm.nih.gov/pubmed/21304588 | Is Nanog repressed in pluripotent stem cells? | The homeobox gene Nanog is a key intrinsic determinant of self renewal in embryonic stem (ES) cells, and its repression leads ES cells to selectively differentiate into primitive endoderm.No. The homeobox gene Nanog is a key intrinsic determinant of self renewal in embryonic stem (ES) cells, and its repression leads ES cells to selectively differentiate into primitive endoderm.Aggregation of embryonic stem cells induces Nanog repression and primitive endoderm differentiation The homeobox gene Nanog is a key intrinsic determinant of self renewal in embryonic stem (ES) cells, and its repression leads ES cells to selectively differentiate into primitive endoderm. |
http://www.ncbi.nlm.nih.gov/pubmed/31537107,http://www.ncbi.nlm.nih.gov/pubmed/31899602,http://www.ncbi.nlm.nih.gov/pubmed/31758661,http://www.ncbi.nlm.nih.gov/pubmed/29136283,http://www.ncbi.nlm.nih.gov/pubmed/32020557 | What is the mode of administration of Ubrogepant? | Ubrogepant (MK-1602) is administered orally. |