anand-s/m_qalm huggingface dataset:
Question: What is the mode of inheritance of Acromicric dysplasia?
Answer: Acromicric dysplasia has an autosomal dominant mode of inheritance
Question: Which drug is benserazide usually co-administered with?
Answer: Co-administration of L-Dopa with carbidopa or benserazide is the most effective symptomatic treatment for Parkinson Disease (PD).
Question: What is a potential side effect for Tymlos?
Answer: Possible bone cancer (osteosarcoma). During animal drug testing, TYMLOS caused some rats to develop a bone cancer called osteosarcoma.
Question: When are itaconic acid levels elevated?
Answer: Itaconic acid levels are elevetad in immune defence.
Question: Which receptor is inhibited by Tivozanib?
Answer: Tivozanib is a selective inhibitor of vascular endothelial growth factor receptors (VEGFRs) 1, 2 and 3 tyrosine kinases.
Question: Which receptors can be evaluated with the [18F]altanserin?
Answer: 5-HT2A (5-hydroxytryptamine type 2a) receptor can be evaluated with the [18F]altanserin.
Question: Which is the master oncogenic transcription factor in T-cell acute lymphoblastic leukemia?
Answer: The oncogenic transcription factor TAL1/SCL induces an aberrant transcriptional program in T-Cell Acute lymphoblastic Leukemia (T-ALL) cells.
Question: Which is the master oncogenic transcription factor in T-cell acute lymphoblastic leukemia?
Answer: The oncogenic transcription factor TAL1/SCL induces an aberrant transcriptional program in T-cell acute lymphoblastic leukemia (T-ALL) cells.
Question: Which is the master oncogenic transcription factor in T-cell acute lymphoblastic leukemia?
Answer: The oncogenic transcription factor TAL1/SCL induces an aberrant transcriptional program in T-cell Acute lymphoblastic Leukemia (T-ALL) cells. It's not the master transcription factor, it's the oncogene.
Question: Which is the master oncogenic transcription factor in T-cell acute lymphoblastic leukemia?
Answer: The oncogenic transcription factor TAL1/SCL induces an aberrant transcriptional program in T-cell Acute lymphoblastic Leukemia (T-ALL) cells.
Question: Which syndrome is associated to SAMHD1 gene mutations?
Answer: Mutations in the SAMHD1 gene that cause the severe autoimmune disease, Aicardi-Goutieres syndrome (AGS).
Question: Which is the methyl donor of histone methyltransferases?
Answer: The major methyl donor of histone methyltransferases (HMTs) is S-adenosyl-L–methionine (SAM, AdoMet).
Question: Which tool has been developed for coverage calculation for genomes?
Answer: Mosdepth is a command-line tool for rapidly calculating genome-wide sequencing coverage. It measures depth from BAM or CRAM files at either each nucleotide position in a genome or for sets of genomic regions. Genomic regions may be specified as either a BED file to evaluate coverage across capture regions, or as a fixed-size window as required for copy-number calling. Mosdepth uses a simple algorithm that is computationally efficient and enables it to quickly produce coverage summaries.
Question: Which tool has been developed for coverage calculation for genomes?
Answer: Mosdepth is a new command-line tool for rapidly calculating genome-wide sequencing coverage. It measures depth from BAM or CRAM files at either each nucleotide position in a genome or for sets of genomic regions.
Question: Centor criteria are used for which disease?
Answer: Centor criteria were developed to diagnose streptococcal pharyngitis.
Question: Which is the branch site consensus sequence in U12-dependent introns?
Answer: The branch site consensus sequence in U12-dependent introns is UUCCUUAAC.
Question: What is the effect of thapsigargin treatment?
Answer: Thapsigargin is an endoplasmic stress inducer. 	It is a sarcoplasmic/endoplasmic Ca(2+)-ATPase (SERCA) inhibitor.
Question: Which is the relation between coffee consumption and stroke risk?
Answer: The coffee paradox in stroke: Increased consumption linked with fewer strokes.
Question: In what phase of clinical trials is crenezumab? (November 2017)
Answer: Crenezumab is undergoing phase III clinical trials.
Question: What disease is associated with mutations in the MECP2 transcription factor?
Answer: mutations in the methyl-cpg-binding protein-2 gene (mecp2) are commonly associated with rett syndrome
Question: What disease is associated with mutations in the MECP2 transcription factor?
Answer: Mutations in the MECP2 transcription factor, which codes for the transcription factor ECE1, have been found to be associated with Rett syndrome.
Question: What disease is associated with mutations in the MECP2 transcription factor?
Answer: Mutations in the methyl-CpG-binding protein-2 gene (MECP2) are commonly associated with Rett syndrome. Mutations in the MECP2 gene cause the neurodevelopmental disorder Rett syndrome (RTT).
Question: What disease is associated with mutations in the MECP2 transcription factor?
Answer: Mutations in the methyl-CpG-binding protein-2 gene (MECP2) are commonly associated with Rett syndrome.
Question: What disease is associated with mutations in the MECP2 transcription factor?
Answer: Mutations in the MECP2 gene cause the neurodevelopmental disorder Rett syndrome (RTT).
Question: What disease is associated with mutations in the MECP2 transcription factor?
Answer: Rett syndrome (RS) is a debilitating neurological disorder affecting mostly girls with heterozygous mutations in the gene encoding the methyl-CpG-binding protein MeCP2 on the X chromosome
Question: What disease is associated with mutations in the MECP2 transcription factor?
Answer: Mutations in the MECP2 transcription factor, which encodes the cellular iron exporter ferroportin, are associated with Rett syndrome.
Question: Which genomic positions are preferentially selected for transposon insertion?
Answer: Preferential integration occurs in non-coding DNA and heterochromatin. A preference for structural features in the target DNA associated with DNA flexibility (Twist, Tilt, Rise, Roll, Shift, and Slide) was also observed.
Question: What is the usual HER-2 status in breast cancer associated with Li-Fraumeni syndrome?
Answer: In up to two thirds of breast cancer patients associated with Li-Fraumeni syndrome, the HER-2 status was found to be positive.
Question: What is the origin of human breast milk bacteria?
Answer: It is believed that certain bacteria from the maternal gastrointestinal tract could translocate through a mechanism involving mononuclear immune cells, migrate to the mammary glands via an endogenous cellular route (the bacterial entero-mammary pathway), and subsequently colonize the gastrointestinal tract of the breast-fed neonate
Question: What is the function of HDAC  proteins?
Answer: Histone deacetylases influence diverse cellular processes and may contribute to tumor development and progression by multiple mechanisms. Histone deacetylases prevent the relaxation of chromatin, and positively or negatively regulate transcription.
Question: What is the function of HDAC  proteins?
Answer: Histone deacetylases (HDACs) prevent the relaxation of chromatin, and positively or negatively regulate transcription and thus cellular processes
Question: What methodology does the FoundationOne CDx test use?
Answer: FoundationOne CDx is a next generation sequencing (NGS) based test.
Question: What are DMARDs?
Answer: To determine the utility of ultrasonography in guiding modification of disease-modifying anti-rheumatic drug (DMARD) and steroid therapy for inflammatory arthritis (IA)
Question: What are DMARDs?
Answer: DMARDs are Disease Modifying anti-rheumatic drugs (DMARD).
Question: What are DMARDs?
Answer: Treatment with disease-modifying antirheumatic drugs (DMARDs)
Question: What are DMARDs?
Answer: Treatment with disease-modifying antirheumatic drugs (DMARDs) was 61% (claims data)
Question: What are DMARDs?
Answer: Treatment with disease-modifying antirheumatic drugs (DMARDs) was 61% (claims data) and
Question: Which R package can infer protein-protein interactions via thermal proximity coaggregation (TPCA)?
Answer: Rtpca is an R package implemented methods for inferring protein-protein interactions (PPIs) based on thermal proteome profiling experiments of a single condition or in a differential setting via an approach called thermal proximity coaggregation. It offers user-friendly tools to explore datasets for their PPI predictive performance and easily integrates with available R packages.
Question: Which R package can infer protein-protein interactions via thermal proximity coaggregation (TPCA)?
Answer: Rtpca is an R package implemented methods for inferring protein-protein interactions (PPIs) based on thermal proteome profiling experiments of a single condition or in a differential setting via an approach called Thermal proximity coaggregation. It offers user-friendly tools to explore datasets for their PPI predictive performance and easily integrates with available R packages.
Question: Which R package can infer protein-protein interactions via thermal proximity coaggregation (TPCA)?
Answer: Rtpca is an R package implementing methods for inferring protein-protein interactions based on thermal proteome profiling experiments of a single condition or in a differential setting via an approach called thermal proximity coaggregation (TPCA). Rtpca can be used for high-throughput intracellular monitoring of protein complex dynamics.
Question: Which R package can infer protein-protein interactions via thermal proximity coaggregation (TPCA)?
Answer: Rtpca is an R package implementing methods for inferring protein-protein interactions based on thermal proteome profiling experiments of a single condition or in a differential setting via an approach called thermal proximity coaggregation (TPCA). Rtpca was reported to be able to integrate downloaded protein/protein interaction information from different online databases with private data to construct new and personalized interaction networks.
Question: Which R package can infer protein-protein interactions via thermal proximity coaggregation (TPCA)?
Answer: Rtpca is an R package implementing methods for inferring protein-protein interactions based on thermal proteome profiling experiments of a single condition or in a differential setting via an approach called thermal proximity coaggregation (TPCA).
Question: Which R package can infer protein-protein interactions via thermal proximity coaggregation (TPCA)?
Answer: Rtpca is an R package implementing methods for inferring protein-protein interactions based on thermal proteome profiling experiments of a single condition or in a differential setting via an approach called thermal proximity coaggregation (TPCA). It offers user-friendly tools to explore datasets for their protein-protein interaction predictive performance and easily integrates with available R packages.
Question: Which R package can infer protein-protein interactions via thermal proximity coaggregation (TPCA)?
Answer: Rtpca is an R package implementing methods for inferring protein-protein interactions based on thermal proteome profiling experiments of a single condition or in a differential setting via an approach called thermal proximity coaggregation (TPCA)
Question: Which R package can infer protein-protein interactions via thermal proximity coaggregation (TPCA)?
Answer: Rtpca is an R package for differential thermal proximity coaggregation analysis. It is based on a model of thermal proximity (TFD) analysis performed by combining multiple layers of TSSs with TSSS (TSC) and TSSF (TSS-FANCA) data.
Question: Which R package can infer protein-protein interactions via thermal proximity coaggregation (TPCA)?
Answer: Rtpca is an R package implementing methods for inferring protein-protein interactions (PPIs) based on thermal proteome profiling experiments of a single condition or in a differential setting via an approach called thermal proximity coaggregation.
Question: Which R package can infer protein-protein interactions via thermal proximity coaggregation (TPCA)?
Answer: Rtpca is an R package implemented methods for inferring protein-protein interactions (PPIs) based on thermal proteome profiling experiments of a single condition or in a differential setting via an approach called Thermal proximity coaggregation (TPCA). It offers user-friendly tools to explore datasets for their PPI predictive performance and easily integrates with available R packages.
Question: Which R package can infer protein-protein interactions via thermal proximity coaggregation (TPCA)?
Answer: Rtpca is an R package implemented methods for inferring protein-protein interactions (PPIs) based on Thermal proteome profiling experiments or in a differential setting via an approach called Thermal proximity coaggregation. It offers user-friendly tools to explore datasets for their PPI predictive performance and easily integrates with available R packages.
Question: Which R package can infer protein-protein interactions via thermal proximity coaggregation (TPCA)?
Answer: Rtpca is an R package implementing methods for inferring protein-protein interactions based on thermal proteome profiling experiments of a single condition or in a differential setting via an approach called thermal proximity coaggregation (TPCA) It offers user-friendly tools to explore datasets for their protein-protein interaction predictive performance and easily integrates with available R packages.
Question: Which enzyme is deficient in Wolman disease?
Answer: Deficiency of lysosomal acid lipase (LAL) causes Wolman disease.
Question: ROSIER scale is used for which disorder?
Answer: ROSIER (Recognition of Stroke in the Emergency Room) scale was developed as a stroke recognition tool on suspected patients in the prehospital setting.
Question: In what proportion of children with heart failure has Enalapril been shown to be safe and effective?
Answer: In children with heart failure evidence of the effect of enalapril is empirical. Enalapril was clinically safe and effective in 50% to 80% of for children with cardiac failure secondary to congenital heart malformations before and after cardiac surgery,  impaired ventricular function , valvar regurgitation,  congestive cardiomyopathy,  , arterial hypertension, life-threatening arrhythmias coexisting with circulatory insufficiency.   
ACE inhibitors have shown a transient beneficial effect on heart failure due to anticancer drugs and possibly a beneficial effect in muscular dystrophy-associated cardiomyopathy, which deserves further studies.
Question: Which syndrome is caused by dysfunction of the ciliary ARMC9/TOGARAM1 protein?
Answer: Dysfunction of the ciliary ARMC9/TOGARAM1 protein module causes Joubert syndrome.
Question: Which syndrome is caused by dysfunction of the ciliary ARMC9/TOGARAM1 protein?
Answer: Dysfunction of the ciliary ARMC9/TOGARAM1 protein causes Joubert syndrome.
Question: Which syndrome is caused by dysfunction of the ciliary ARMC9/TOGARAM1 protein?
Answer: Joubert syndrome (JBTS) is a recessive neurodevelopmental disorder caused by dysfunction of the ciliary ARMC9/TOGARAM1 protein.
Question: Which syndrome is caused by dysfunction of the ciliary ARMC9/TOGARAM1 protein?
Answer: Dysfunction of the ciliary ARMC9/TOGARAM1 protein module causes Joubert syndrome. All known JBTS genes encode proteins involved in the structure or function of primary cilia, ubiquitous antenna-like organelles essential for cellular signal transduction.
Question: Which syndrome is caused by dysfunction of the ciliary ARMC9/TOGARAM1 protein?
Answer: Joubert syndrome is a rare autosomal recessive disorder caused by dysfunction of the ciliary ARMC9/TOGARAM1 protein.
Question: Which syndrome is caused by dysfunction of the ciliary ARMC9/TOGARAM1 protein?
Answer: Dysfunction of the ciliary ARMC9/TOGARAM1 protein module causes Joubert syndrome. Joubert syndrome (JBTS) is a recessive neurodevelopmental ciliopathy characterized by a pathognomonic hindbrain malformation.
Question: Which syndrome is caused by dysfunction of the ciliary ARMC9/TOGARAM1 protein?
Answer: Joubert syndrome (JBTS) is a rare autosomal recessive disorder caused by dysfunction of the ciliary ARMC9/TOGARAM1 protein.
Question: What is the function of the stard10 protein?
Answer: 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.
Question: GV1001 vaccine targets which enzyme?
Answer: GV1001 is a 16-amino-acid vaccine peptide derived from the human telomerase reverse transcriptase sequence. It has been developed as a vaccine against various cancers.
Question: What promotes amyloid-peptide beta 42 (Aβ42) accumulation in neuroblastoma cells?
Answer: The apolipoprotein (apo) E4 isoform is the strongest risk factor for late-onset Alzheimer's disease (AD). ApoE4 is more susceptible to proteolysis than apoE2 and apoE3 isoforms and carboxyl-terminal truncated apoE4 forms have been found in AD patients' brain. A specific apoE4 fragment, apoE4-165, promotes amyloid-peptide beta 42 (Aβ42) accumulation in human neuroblastoma SK-N-SH cells and increased intracellular reactive oxygen species formation, two events considered to occur early in AD pathogenesis.
Question: What promotes amyloid-peptide beta 42 (Aβ42) accumulation in neuroblastoma cells?
Answer: The amyloid-peptide beta 42 (Aβ42) accumulates in neuroblastoma cells due to a protein called apoE4-165, which is an apolipoprotein (APOE4). This protein is the most common protein responsible for late-onset Alzheimer disease.
Question: Mutation of which gene is associated with Achondroplasia?
Answer: Achondroplasia is due to mutations in the fibroblast growth factor receptor 3 (FGFR3) gene.
Question: What is the Pfam database?
Answer: The Pfam database provides a collection of curated protein families.
Question: Which inherited disorder is known to be caused by mutations in the NEMO gene?
Answer: Incontinentia pigmenti (IP) is a rare neurocutaneous disorder with a frequency of 1 in 50,000 newborn, and is associated with mutations in IKBKG gene (NEMO) in Xq28, inherited as an X-linked dominant trait
Question: Which inherited disorder is known to be caused by mutations in the NEMO gene?
Answer: Incontinentia pigmenti (IP) or Bloch-Sulzberger syndrome (BSS) is a rare neurocutaneous disorder with a frequency of 1 in 50,000 newborn, and is associated with mutations in IKBKG gene (NEMO) in Xq28, inherited as an X-linked dominant trait.
Question: Which cloud-based platform has been developed for comparing GWAS?
Answer: EasyGWAS is a cloud-based platform for comparing the results of Genome-Wide Association Studies (GWAS).
Question: Which cloud-based platform has been developed for comparing GWAS?
Answer: The ever- growing availability of high-quality genotypes for a multitude of species has enabled researchers to explore the underlying genetic architecture of complex phenotypes at an unprecedented level of detail using genome-wide association studies (GWAS). The systematic comparison of results obtained from GWAS of different traits opens up new possibilities, including the analysis of pleiotropic effects. In order to facilitate the simple comparison of GWAS results, easyGWAS has been developed as a powerful, species-independent online resource for computing, storing, sharing, annotating, and comparing GWAS.
Question: What type of sequences do enhancers evolve from?
Answer: Studies have identified enhancers that were pivotal for morphological divergence and highlighted how novel genetic networks shaping form emerged from pre-existing ones.Most of the recently evolved enhancers arise from ancestral dna exaptation , rather than lineage-specific expansions of repeat elements.
Question: What type of sequences do enhancers evolve from?
Answer: Recently evolved enhancers arise from ancestral DNA exaptation, rather than lineage-specific expansions of repeat elements.
Question: What type of sequences do enhancers evolve from?
Answer: Most of the recently evolved enhancers arise from ancestral DNA exaptation, rather than lineage-specific expansions of repeat elements. The sequences of some gene regulatory elements diverge considerably, even between closely related species.
Question: What type of sequences do enhancers evolve from?
Answer: The trend is one of high divergence of cis-regulatory elements between species, possibly compensated by extensive creation and loss of regulatory elements and rewiring of their target genes.  Most of the recently evolved enhancers arise from ancestral DNA exaptation, rather than lineage-specific expansions of repeat elements.
Question: How many copies of TP53 does the elephant genome contain?
Answer:   Here, we show that the elephant genome encodes 20 copies of the tumor suppressor gene TP53 and that the increase in TP53 copy number occurred coincident with the evolution of large body sizes, the evolution of extreme sensitivity to genotoxic stress, and a hyperactive TP53 signaling pathway in the elephant (Proboscidean) lineage. While humans have 1 copy (2 alleles) of TP53, African elephants have at least 20 copies (40 alleles), including 19 retrogenes (38 alleles) with evidence of transcriptional activity measured by reverse transcription polymerase chain reaction.
Question: How many copies of TP53 does the elephant genome contain?
Answer:  Here, we show that the elephant genome encodes 20 copies of the tumor suppressor gene TP53 and that the increase in TP53 copy number occurred coincident with the evolution of large body sizes, the evolution of extreme sensitivity to genotoxic stress, and a hyperactive TP53 signaling pathway in the elephant (Proboscidean) lineage. While humans have 1 copy (2 alleles) of TP53, African elephants have at least 20 copies (40 alleles), including 19 retrogenes (38 alleles) with evidence of transcriptional activity measured by reverse transcription polymerase chain reaction.
Question: How many copies of TP53 does the elephant genome contain?
Answer: Here, we show that the elephant genome encodes 20 copies of the tumor suppressor gene TP53 and that the increase in TP53 copy number occurred coincident with the evolution of large body sizes, the evolution of extreme sensitivity to genotoxic stress, and a hyperactive TP53 signaling pathway in the elephant (Proboscidean) lineage. While humans have 1 copy (2 alleles) of TP53, African elephants have at least 20 copies (40 alleles), including 19 retrogenes (38 alleles) with evidence of transcriptional activity measured by reverse transcription polymerase chain reaction.
Question: How many copies of TP53 does the elephant genome contain?
Answer: 20
Question: How many copies of TP53 does the elephant genome contain?
Answer: Here, we show that the elephant genome encodes 20 copies of the tumor suppressor gene TP53 and that the increase in TP53 copy number occurred coincident with the evolution of large body sizes, the emergence of extreme sensitivity to genotoxic stress, and a hyperactive TP53 signaling pathway.
Question: How many copies of TP53 does the elephant genome contain?
Answer: While humans have 1 copy (2 alleles) of TP53, African elephants have at least 20 copies (40 alleles), including 19 retrogenes (38 alleles) with evidence of transcriptional activity measured by reverse transcription polymerase chain reaction.
Question: How many copies of TP53 does the elephant genome contain?
Answer: In the elephant genome, TP53 is encoded by 20 copies.
Question: How many copies of TP53 does the elephant genome contain?
Answer: Here, we show that the elephant genome encodes 20 copies of the tumor suppressor gene TP53 and that the increase in TP53 copy number occurred coincident with the evolution of large body sizes, the evolution of extreme sensitivity to genotoxic stress, and a hyperactive TP53 signaling pathway in the elephant (Proboscidean) lineage.
Question: How many copies of TP53 does the elephant genome contain?
Answer: The elephant genome encodes 20 copies of the tumor suppressor gene tp53 and that the evolution of large body sizes, the evolves of extreme sensitivity to genotoxic stress, and a hyperactive tp53 signaling pathway in the elephant (proboscidean) lineage have at least 20 copies (40 alleles), including 19 retrogenes (38 alleles) with evidence of transcriptional activity measured by reverse transcription polymerase chain reaction.