anand-s/m_qalm huggingface dataset:
Question: Which syndrome is associated with mutant DVL1?
Answer: Mutations in DVL1 cause an osteosclerotic form of Robinow syndrome.
Question: What is the LINCS Program?
Answer: The Library of Integrated Network-based Cellular Signatures (LINCS) is an NIH Common Fund program that catalogs how human cells globally respond to chemical, genetic, and disease perturbations.
Question: What is the LINCS Program?
Answer: The National Institutes of Health library of Integrated Network-based Cellular Signatures (LINCS) program is generating extensive multidimensional data sets, including biochemical, genome-wide transcriptional, and phenotypic cellular response signatures to a variety of small-molecule and genetic perturbations with the goal of creating a sustainable, widely applicable, and readily accessible systems biology knowledge resource.
Question: What is the LINCS Program?
Answer: To fill this gap, recently, the LINCS program generated almost 1.3 million profiles for over 40,000 drug and genetic perturbations for over 70 different human cell types, including meta information about the experimental conditions and cell lines The Library of Integrated Network-based Cellular Signatures (LINCS) program is a national consortium funded by the NIH to generate a diverse and extensive reference library of cell-based perturbation-response signatures, along with novel data analytics tools to improve our understanding of human diseases at the systems level
Question: What is the LINCS Program?
Answer: The National Institutes of Health Library of Integrated Network-based Cellular Signatures (LINCS) program is generating extensive multidimensional data sets, including biochemical, genome-wide transcriptional, and phenotypic cellular response signatures to a variety of small-molecule and genetic perturbations with the goal of creating a sustainable, widely applicable, and readily accessible systems biology knowledge resource. To fill this gap, recently, the LINCS program generated almost 1.3 million profiles for over 40,000 drug and genetic perturbations for over 70 different human cell types, including meta information about the experimental conditions and cell lines
Question: What is the LINCS Program?
Answer: The library of Integrated Network-based Cellular Signatures (LINCS) program is a national consortium funded by the NIH to generate a diverse and extensive reference library of cell-based perturbation-response signatures, along with novel data tools to improve our understanding of human diseases at the systems level.
Question: What is the LINCS Program?
Answer: The Library of Integrated Network-based Cellular Signatures (LINCS) program is a national consortium funded by the NIH to generate a diverse and extensive reference library of cell-based perturbation-response signatures, along with novel data analytics tools to improve our understanding of human diseases at the systems level. It has generated almost 1.3 million profiles for over 40,000 drug and genetic perturbations for over 70 different human cell types, including meta information about the experimental conditions and cell lines.
Question: What is the LINCS Program?
Answer: The Library of Integrated Network-Based Cellular Signatures (LINCS) is an NIH Common Fund program that catalogs how human cells globally respond to chemical, genetic, and disease perturbations The Library of Integrated Network-based Cellular Signatures (LINCS) program is a national consortium funded by the NIH to generate a diverse and extensive reference library of cell-based perturbation-response signatures, along with novel data analytics tools to improve our understanding of human diseases at the systems level
Question: What can Nothobranchius furzeri be used as a model system for?
Answer: N. furzeri an interesting model system to investigate the effects of experimental manipulations on longevity and age-related pathologies.
N. furzeri could represent a model system for studying the genetic control of life-history traits in natural populations.
N. furzeri could be a very useful model for comparative genomics of aging.
It can be employed to test the effects of experimental manipulation on aging and apharmacological research.
Question: Which protein is found to be mutated in Friedreich's ataxia?
Answer: It is generally accepted that Friedreich's ataxia (FRDA) is caused by a deficiency in frataxin expression, a mitochondrial protein involved in iron homeostasis, which mainly affects the brain, dorsal root ganglia of the spinal cord, heart and in certain cases the pancreas
Question: Which protein is found to be mutated in Friedreich's ataxia?
Answer: It is generally accepted that Friedreich's ataxia (FRDA) is caused by a deficiency in frataxin expression, a mitochondrial protein involved in iron homeostasis, which mainly affects the brain, dorsal root ganglia of the spinal cord, heart and in certain cases the pancreas.
Question: Which disease is treated with ZMapp?
Answer: ZMapp is a combination of antibodies for treatment of Ebola virus disease.
Question: Which disease is treated with ZMapp?
Answer: Vectored delivery of the ZMapp antibody cocktail (c2G4, c4G7, and c13C6) by using recombinant adeno-associated viruses (rAAVs) is useful for preventive immunization against Ebola virus infection.
Question: Which is the defective protein causing the lysosomal storage disease Fabry?
Answer: Anderson-Fabry disease (referred to as Fabry disease) is an X-linked disorder characterized by a deficiency of the lysosomal enzyme alpha-galactosidase A and the subsequent accumulation in various tissues of globotriaosylceramide (Gb(3)), the main substrate of the defective enzyme.
Question: Which gene has been implicated in Majeed Syndrome?
Answer: Homozygous mutations in LPIN2 are responsible for the syndrome of chronic recurrent multifocal osteomyelitis and congenital dyserythropoietic anaemia (Majeed syndrome).
Question: Which gene has been implicated in Majeed Syndrome?
Answer: Genetic alteration of LPIN2 in humans is known to cause Majeed syndrome.
Question: As of September 2018, what machine learning algorithm is used to for cardiac arrhythmia detection from a  short single-lead ECG recorded by a wearable device?
Answer: Support Vector machines( SVM) can be used for cardiac arrhythmia detection in from an ECG recorded by a wearable device.
Question: As of September 2018, what machine learning algorithm is used to for cardiac arrhythmia detection from a  short single-lead ECG recorded by a wearable device?
Answer: SVM approach for cardiac arrhythmias detection in short single-lead ECG recorded by a wearable device
Question: What is the most common feature of the Doege–Potter syndrome?
Answer: Doege-Potter syndrome is a paraneoplastic syndrome characterized by hypoglycemia secondary to a solitary fibrous tumor of the pleura.
Question: Which library is used for fixed-length approximate string matching?
Answer: libFLASM is a free open-source C++ software library for solving fixed-length approximate string matching under both the edit and the Hamming distance models.
Question: Which algorithm has been proposed for efficient storage of WGS variant calls?
Answer: Whole-genome sequencing (WGS) data are being generated at an unprecedented rate. Analysis of WGS data requires a flexible data format to store the different types of DNA variation. Variant call format (VCF) is a general text-based format developed to store variant genotypes and their annotations. However, VCF files are large and data retrieval is relatively slow. 'SeqArray' is a new WGS variant data format implemented in the R/Bioconductor package for storing variant calls in an array-oriented manner which provides the same capabilities as VCF, but with multiple high compression options and data access using high-performance parallel computing.
Question: When was Afrezza approved by the FDA?
Answer: Afrezza was approved by the FDA in June 2014.
Question: Which signalling pathway is involved in Tuberous Sclerosis?
Answer: Tuberous Sclerosis is a multisystem genetic disorder caused by mutation in TSC1 or TSC2 gene, that leads to hyperactivation of the mTOR signalling pathway, and subsequent dysregulation of cell growth control.
Question: What fruit causes Jamaican vomiting sickness?
Answer: Jamaican Vomiting Sickness is caused by ingestion of the unripe arils of the Ackee fruit, its seeds and husks.
Question: What is the inheritance pattern of Hunter disease or mucopolysaccharidosis II?
Answer: X- linked recessive
Question: What disease is treated with BIVV001?
Answer: BIVV001 fusion protein has been developed as Factor VIII replacement therapy for hemophilia A
Question: PBT2 has been tested for which disorder?
Answer: PBT2 has been tested for treatment of Alzheimer's disease.
Question: Which protein is encoded by the protein APOBEC3C?
Answer: The gene APOBEC3C codes for: apolipoprotein B mRNA editing enzyme catalytic polypeptide-like 3C
Question: Which E3 ubiquitin ligase mediates the ubiquitination and degradation of the interferon receptor type 1 (IFNAR1)?
Answer: Ubiquitination and degradation of the IFNAR1 (interferon alpha receptor 1) subunit of the type I interferon (IFN) receptor is mediated by the SCFbeta-Trcp (Skp1-Cullin1-F-box protein beta transducin repeat-containing protein) E3 ubiquitin ligase in a phosphorylation-dependent manner.
Question: Which E3 ubiquitin ligase mediates the ubiquitination and degradation of the interferon receptor type 1 (IFNAR1)?
Answer: Ubiquitination, endocytosis, and lysosomal degradation of the IFNAR1 (interferon alpha receptor 1) subunit of the type I interferon (IFN) receptor is mediated by the SCFbeta-Trcp (Skp1-Cullin1-F-box protein beta transducin repeat-containing protein) E3 ubiquitin ligase in a phosphorylation-dependent manner.
Question: What is liquid liquid phase transition?
Answer: The influence of membrane-free microcompartments resulting from crowding-induced liquid/liquid phase separation (LLPS) on the dynamic spatial organization of FtsZ, the main component of the bacterial division machinery, has been studied using several LLPS systems.
Question: Which is the main protein in brown adipose tissue (BAT) active in thermogenesis?
Answer: Uncoupling protein 1 (UCP1) is the hallmark protein responsible for cold- and diet-induced thermogenesis in brown adipose tissue (BAT).
Question: How many times is CLAST faster than BLAST?
Answer: was capable of identifying sequence similarities ~80.8 times faster than blast and 9.6 times faster than blat .
Question: How many times is CLAST faster than BLAST?
Answer: CLAST was capable of identifying sequence similarities ~80.8 times faster than BLAST and 9.6 times faster than BLAT.
Question: How many times is CLAST faster than BLAST?
Answer: CLAST was capable of identifying sequence similarities ~80.8 times faster than BLAST and 9.6 times faster than BLAT
Question: How many times is CLAST faster than BLAST?
Answer: clast was capable of identifying sequence similarities ~80.8 times faster than blast and 9.6 times faster than blat.
Question: How many times is CLAST faster than BLAST?
Answer: CLAST is capable of identifying sequence similarities ~80.8 times faster than BLAST
Question: What type of enzyme is peroxiredoxin 2 (PRDX2)?
Answer: Peroxiredoxin 2 (PRDX2) is an antioxidant enzyme that uses cysteine residues to decompose peroxides. 
Peroxiredoxin-2 (PRDX2), an enzyme reducing hydrogen peroxide and lipid peroxides 
Peroxiredoxin 2 (Prx2) is a thiol-dependent peroxidase.
Question: Which is the genetic lesion associated with Huntington’s disease?
Answer: The genetic lesion associated with Huntington's disease is a CAG trinucleotide repeat expansion in the HD (or HTT) gene.
Question: Which disease can be diagnosed with the "probe to bone" test?
Answer: Probe-to-bone test is used for the diagnosis of diabetic foot osteomyelitis. The test has good sensitivity and specificity. Other diagnostic tests of diabetic foot osteomyelitis are plain films and magnetic resonance imaging.
Question: What is the microgenderome?
Answer: The sexually dimorphic microbiome has been termed the 'microgenderome'.
Question: Which histone mark distinguishes active from inactive enhancers?
Answer: Histone H3K27ac separates active from poised enhancers and predicts developmental state . In contrast, elements of the second class 'poised enhancers' are linked to genes inactive in hESCs . They are involved in orchestrating early steps in embryogenesis, such as gastrulation, mesoderm formation and neurulation .
Question: Which histone mark distinguishes active from inactive enhancers?
Answer: Enhancers cause a high level of transcription and activation of chromatin structure at target genes . Individual chromatin marks, such as H3K27ac, have been identified to distinguish active from inactive enhancers . In contrast, elements of the second class, which we term 'poised enhancers', are distinguished by the absence of H327ac and enrichment of histone H3 lysine 27 trimethylation .
Question: Which histone mark distinguishes active from inactive enhancers?
Answer: Conversion of inactive enhancers to an active state is marked by accumulation of H3K4me1 and H3K27ac histone marks.
Question: Which histone mark distinguishes active from inactive enhancers?
Answer: Hyperacetylation of histones H3 and H4, a mark of active chromatin, is established broadly across target loci by enhancers that function over long distances . In contrast, elements of the second class 'poised enhancers' are distinguished by the absence of H3K27ac and enrichment of histone H3 lysine 27 trimethylation . They are linked to genes inactive in hESCs and instead are involved in orchestrating early steps in embryogenesis, such as gastrulation and mesoderm formation .
Question: Which histone mark distinguishes active from inactive enhancers?
Answer: Monomethylation of histone H3 on Lys 27 (H3K27) is associated with active and inactive enhancers, respectively. An enhancer chromatin state signature associated withactive enhancers may be defined by high levels of H3 K27 acetylation, nucleosome displacement, hypersensitivity to sonication, and strong suppression of enhancer activity by DNase I.
Question: Which histone mark distinguishes active from inactive enhancers?
Answer: We demonstrate that UTX, in a demethylase activity-independent manner, facilitates conversion of inactive enhancers in embryonic stem cells to an active (H3K4me1+/H3K27ac+) state by recruiting and coupling the enzymatic functions of MLL4 and p300. This work reveals a previously unrecognized cooperativity among enhancer-associated chromatin modulators, including a unique function for UTX, in establishing an "active enhancer landscape" and defines a detailed mechanism for the joint deposition of H3K4me1 and H3K27ac.
Question: Which disorder has been approved for treatment with Alk inhibitors?
Answer: Anaplastic lymphoma kinase (ALK) rearrangement is detected in 3-7% of patients with non-small-cell lung cancer. Crizotinib is an ALK inhibitor, which was approved in 2011 for the treatment of ALK-positive lung cancer.
Question: Which disorder has been approved for treatment with Alk inhibitors?
Answer: Crizotinib was approved to treat anaplastic lymphoma kinase (ALK)-positive non-small cell lung cancer (NSCLC) by the Food and Drug Administration in 2011
Question: Which yeast genes encode for condensin?
Answer: Smc2-Smc4 forms the core of the Saccharomyces cerevisiae condensin, which promotes metaphase chromosome compaction . Both SMC2 and SMC4 are essential for chromosome transmission in anaphase . Smc 2-8 suppresses catenanes accumulation, mitotic arrest and growth defects induced by histone depletion at semi-permissive temperature .
Question: Which yeast genes encode for condensin?
Answer: Smc2/4 forms the core of the Saccharomyces cerevisiae condensin, which promotes metaphase chromosome compaction
Question: Which yeast genes encode for condensin?
Answer: Condensin Smc2-Smc4 Dimers Are Flexible and Dynamic. Here, we probe the topology of Smc2-Smc4 dimers of the S. cerevisiae condensin complex with high-speed atomic force microscopy (AFM) in liquid Interestingly, SAC activation is suppressed by the absence of Top2 and Smc2, an essential component of condensin.
Question: Do A-type lamins bind euchromatin or heterochromatin?
Answer: These data reveal that the domain encoded by exon 9 is important to maintain telomere homeostasis and heterochromatin structure but does not play a role in DNA repair, thus pointing to other exons in the lamin A tail as responsible for the genomic instability phenotype in Lmna(Δ8-11/Δ8-11) mice
Question: Do A-type lamins bind euchromatin or heterochromatin?
Answer: Comparative genomic hybridization (CGH) analyses of microdissected blebs, fluorescence in situ hybridization (FISH), and immunofluorescence localization of modified histones demonstrate that gene-rich euchromatin associates with the LA/C blebs. On the other hand, the domain encoded by exon 9 is important to maintain telomere homeostasis and heterochromatin structure but does not play a role in DNA repair, thus pointing to other exons in the lamin A tail as responsible for the genomic instability phenotype in Lmna(Δ8-11/Δ8-11) mice
Question: Which protein is the main inhibitor of protein phosphatase 1 (PP1)?
Answer: Inhibitor 1 (I-1) is a protein inhibitor of protein phosphatase 1 (PP1), a major eukaryotic Ser/Thr phosphatase. Nonphosphorylated I-1 is inactive, whereas phosphorylated I-1 is a potent PP1 inhibitor.
Question: Which protein is the main inhibitor of protein phosphatase 1 (PP1)?
Answer: Protein Phosphatase-1 is restrained by its endogenous inhibitor, protein phosphatase inhibitor-1 (PPI-1). Inhibition of the protein phosphatase 1, by inhibitor-1, significantly increases cardiac contractility and calcium handling. Inhibitor-1 becomes a potent inhibitor of protein phosphatase 1 when phosphorylated by cAMP-dependent protein kinase.
Question: Which gene has been found to be mutant in Lesch-Nyhan Disease patients?
Answer: Lesch-Nyhan Disease (LND) is the result of mutations in the X-linked gene encoding the purine metabolic enzyme, hypoxanthine guanine phosphoribosyl transferase (HPRT).
Question: Which is the mass-tag that reveal the ubiquitination of a lysine residue?
Answer: Lys-ɛ-Gly-Gly (K-ɛ-GG) is the remnant produced by trypsin digestion of proteins having ubiquitinated lysine side chains.
Question: Where does gemtuzumab ozogamicin bind?
Answer: Gemtuzumab ozogamicin binds to CD33
Question: What is the indication for prophylactic use of antibiotics in COPD?
Answer: In a subset of patients with severe disease and prone to developing infections prophylactic use of antibiotics may reduce number of exacerbations and improve social and health care costs.
Question: Which approach was used to diagnose a patient with Cutis Verticis Gyrata-Intellectual Disability (CVG-ID) syndrome?
Answer: Magnetic Resonance Imaging (MRI)
Question: Which disorder is rated by Palmini classification?
Answer: Palmini classification system is used for classification of focal cortical dysplasia.
Question: How long in bp is the human pseudoautosomal region 2 (PAR2)?
Answer: The human pseudoautosomal region 2 (PAR2), which is located in the long arm of chromosome 9 (LTR6B) and consists of 32 exons, is320-kb long.
Question: How long in bp is the human pseudoautosomal region 2 (PAR2)?
Answer: The 320-kb human pseudoautosomal region 2 (PAR2) at the tips of the long arms of the X and Y chromosomes is thought to have been duplicated onto the Y chromosome recently in primate evolution
Question: How long in bp is the human pseudoautosomal region 2 (PAR2)?
Answer: The human pseudoautosomal region 2 (PAR2) is 320-kb long.
Question: Which company developed opdivo?
Answer: Opdivo or nivolumab was developed by Bristol-Myers Squibb.
Question: What is caused by a gain-of-function mutation in CLCN2?
Answer: 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.
Question: What is caused by a gain-of-function mutation in CLCN2?
Answer: A gain-of-function mutation in the CLCN2 chloride channel gene causes primary aldosteronism.
Question: What is caused by a gain-of-function mutation in CLCN2?
Answer: 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.
Question: What is caused by a gain-of-function mutation in CLCN2?
Answer: 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 retardation
Question: What is caused by a gain-of-function mutation in CLCN2?
Answer: Primary aldosteronism is an autosomal dominant disorder caused by gain-of-function mutations in CLCN2.
Question: What is caused by a gain-of-function mutation in CLCN2?
Answer: 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.
Question: What is caused by a gain-of-function mutation in CLCN2?
Answer: 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.
Question: What is the exoproteome?
Answer: Exoproteomics aims at describing and quantifying the proteins found outside of the cells.
Question: Which is the enzymatic activity of nardilysin?
Answer: Nardilysin (N-arginine dibasic convertase; Nrdc) is a metalloendopeptidase of the M16 family that promotes ectodomain shedding of the precursor forms of various growth factors and cytokines by enhancing the protease activities of a disintegrin and metalloproteinase (ADAM) proteins.
Question: Which is the most widely used model for the study of multiple sclerosis (MS)?
Answer: Experimental autoimmune encephalomyelitis (EAE) is a classical, conventional and widely recognized animal model for studying multiple sclerosis (MS). EAE is the best available model for the inflammatory processes that occur in MS, and for the disease process. A less commonly used model is that of Theiler's murine encephalomyelitis virus (TMEV).
Question: How rare are CTCs (circulating tumour cells) in the plasma of patients?
Answer: Circulating tumour cells (CTCs) are significantly rare entity in the blood of patients with non-small cell lung cancer (NSCLC) patients as well as in other types of cancer. Small-cell lung cancer cells are typically quiescent, whereas CTCs can be up-regulated in response to radiation or chemical agents and may contribute to tumorigenesis as an endogenous red cell marker.
Question: How rare are CTCs (circulating tumour cells) in the plasma of patients?
Answer: extremely low
Question: How rare are CTCs (circulating tumour cells) in the plasma of patients?
Answer: However, largely because of the extremely low number of CTCs (as low as 1 in 10(9) hematologic cells) in the blood of patients, effective detection and separation of the rare cells remain a tremendous challenge.
Question: How rare are CTCs (circulating tumour cells) in the plasma of patients?
Answer: However, largely because of the extremely low number of CTCs (as low as 1 in 10(9) hematologic cells) in the blood of patients, effective detection and separation of the rare cells remain a tremendous challenge. However, selective capture and quantification of CTCs from whole blood was still full of challenge due to the extremely scare number of CTCs.
Question: How rare are CTCs (circulating tumour cells) in the plasma of patients?
Answer: We have focused on breast cancer as most clinical studies on CTC detection so far have been done in these patients. However, largely because of the extremely low number of CTCs (as low as 1 in 10(9) hematologic cells) in the blood of patients, effective detection and separation of the rare cells remain a tremendous challenge.
Question: How rare are CTCs (circulating tumour cells) in the plasma of patients?
Answer: CTCs are of extremely low number (as low as 1 in 10(9) hematologic cells) in the blood of patients.