nirantk/geneticsQA-train huggingface dataset:
Question: Which microRNAs are involved in exercise adaptation?

Context:
Some miRNAs as miR-1, miR-133 and miR-208a are highly expressed in the heart and strongly associated with the development of cardiac hypertrophy. Recent data indicate that these miRNAs as well as miR-206 change their expression quickly in response to physical activity.
the miR-494 content significantly decreased after endurance exercise in C57BL/6J mice, accompanied by an increase in expression of mtTFA and Foxj3 proteins. These results suggest that miR-494 regulates mitochondrial biogenesis by downregulating mtTFA and Foxj3 during myocyte differentiation and skeletal muscle adaptation to physical exercise.
1) c-miRNA up-regulated by acute exercise before and after sustained training (miR-146a and miR-222), (2) c-miRNA responsive to acute exercise before but not after sustained training (miR-21 and miR-221), (3) c-miRNA responsive only to sustained training (miR-20a),
MicroRNA 1 expression was decreased independent of the training modality, and was paralleled by an increased expression of IGF-1 representing a potential target.
we investigated the expression of these myomiRs, including miR-1, miR-133a, miR-133b and miR-206 in muscle biopsies from vastus lateralis of healthy young males (n = 10) in relation to a hyperinsulinaemic–euglycaemic clamp as well as acute endurance exercise before and after 12 weeks of endurance training.
In resting biopsies, endurance training for 12 weeks decreased basal expression of all four myomiRs (P < 0.05)
These results suggest that miR-494 regulates mitochondrial biogenesis by downregulating mtTFA and Foxj3 during myocyte differentiation and skeletal muscle adaptation to physical exercise.

Answer: miR-1, miR-133, miR-208a, miR-206, miR-494, miR-146a, miR-222, miR-21, miR-221, miR-20a, miR-133a, miR-133b, miR-23, miR-107 and miR-181 are involved in exercise adaptation
Exact answer: miR-1, miR-133, miR-208a, miR-206, miR-494, miR-146a, miR-222, miR-21, miR-221, miR-20a, miR-133a, miR-133b, miR-23, miR-107, miR-181
Question: What is the indication for valbenazine?

Context:
VMAT2 inhibitors (e.g. deutetrabenazine and valbenazine) have been studied in the treatment of HD-related chorea, tardive dyskinesia and tics associated with Tourette syndrome.
Valbenazine granted breakthrough drug status for treating tardive dyskinesia.
The FDA lowered approval hurdles for valbenazine due to a successful Phase II trial, which showed a distinctive improvement in tardive dyskinesia symptoms during valbenazine administration. 

Answer: Valbenazine granted breakthrough drug status for treating tardive dyskinesia.
Exact answer: Valbenazine granted breakthrough drug status for treating tardive dyskinesia.
Question: What is the effect of a defective CLN3 gene?

Context:
Juvenile neuronal ceroid lipofuscinosis (Batten disease) is a neurodegenerative disorder caused by defective function of the lysosomal membrane glycoprotein CLN3. 
human CLN3 that is defective in Batten disease, localizes to the vacuole
JNCL results from mutations in CLN3 on chromosome 16p12.1.
Mutations in the CLN3 gene, which encodes a lysosomal membrane protein, are responsible for the neurodegenerative disorder juvenile Batten disease.
Batten disease [juvenile-onset neuronal ceroid lipofuscinosis (JNCL)], the most common progressive encephalopathy of childhood, is caused by mutations in a novel lysosomal membrane protein (CLN3) with unknown function.
the human CLN3 gene that is defective in Batten disease,
ln3 was recently identified as the gene defective in juvenile Batten disease, an inherited neurodegenerative disease of childhood
Batten disease (juvenile-onset neuronal ceroid lipofuscinosis, JNCL), the most common neurodegenerative disorder of childhood, is caused by mutations in a recently identified gene ( CLN3 ) localized to chromosome 16p11.2-12.1. 

Answer: Mutations in the CLN3 gene, which encodes a lysosomal membrane protein, are responsible for the neurodegenerative disorder juvenile Batten disease.
Exact answer: Batten disease, juvenile-onset neuronal ceroid lipofuscinosis, JNCL
Question: List available genetic multicolor cell labeling techiniques in Drosophila

Context:
Flybow: genetic multicolor cell labeling for neural circuit analysis in Drosophila melanogaster.
To facilitate studies of neural network architecture and formation, we generated three Drosophila melanogaster variants of the mouse Brainbow-2 system, called Flybow. Sequences encoding different membrane-tethered fluorescent proteins were arranged in pairs within cassettes flanked by recombination sites. Flybow combines the Gal4-upstream activating sequence binary system to regulate transgene expression and an inducible modified Flp-FRT system to drive inversions and excisions of cassettes. This provides spatial and temporal control over the stochastic expression of one of two or four reporters within one sample. Using the visual system, the embryonic nervous system and the wing imaginal disc, we show that Flybow in conjunction with specific Gal4 drivers can be used to visualize cell morphology with high resolution. Finally, we demonstrate that this labeling approach is compatible with available Flp-FRT-based techniques, such as mosaic analysis with a repressible cell marker; this could further support the genetic analysis of neural circuit assembly and function.
Drosophila Brainbow: a recombinase-based fluorescence labeling technique to subdivide neural expression patterns.
We developed a multicolor neuron labeling technique in Drosophila melanogaster that combines the power to specifically target different neural populations with the label diversity provided by stochastic color choice. This adaptation of vertebrate Brainbow uses recombination to select one of three epitope-tagged proteins detectable by immunofluorescence. Two copies of this construct yield six bright, separable colors. We used Drosophila Brainbow to study the innervation patterns of multiple antennal lobe projection neuron lineages in the same preparation and to observe the relative trajectories of individual aminergic neurons. Nerve bundles, and even individual neurites hundreds of micrometers long, can be followed with definitive color labeling. We traced motor neurons in the subesophageal ganglion and correlated them to neuromuscular junctions to identify their specific proboscis muscle targets. The ability to independently visualize multiple lineage or neuron projections in the same preparation greatly advances the goal of mapping how neurons connect into circuits.
Brainbow: new resources and emerging biological applications for multicolor genetic labeling and analysis.

Answer: Flybow and Drosophila Brainbow.
Exact answer: Flybow, Drosophila Brainbow
Question: Can we use platelet biomarkers to study Alzheimer's disease?

Context:
Platelet biomarkers in Alzheimer's disease.
platelets are the most important source of circulating forms of the amyloid precursor protein and other important proteins such as Tau and glycogen synthase kinase-3B.
Alternative plasma and platelet measures are described,
The success of these studies led to the application of platelet proteomics to the study of several pathologies where platelets play a fundamental role. Those include platelet-related disorders, such as storage pool disease, gray platelet syndrome, and Quebec platelet disorder; diseases where unwanted platelet activation is highly relevant, such as thrombosis and cardiovascular disease; and other diseases, such as cystic fibrosis, uremia, or Alzheimer's disease. 

Answer: Yes, platelet biomarkers can be used to study Alzheimer's disease.
Exact answer: yes
Question: Name the major classes of small  non coding RNAs in mammalians?

Context:
Some of these RNA classes, in particular microRNAs and snoRNAs, undergo maturation processes that lead to the production of shorter RNAs.

Answer: microRNAs (miRNAs), small nuclear RNAs (snRNAs), small nucleolar RNAs (snoRNAs) are the major classes of small non coding RNAs. Recently, thanks mostly to massively parallel sequencing technologies, other classes of small RNAs have been discovered, such as piRNAs and scaRNAs.
Exact answer: miRNA, snRNA, snoRNAs, scaRNAs, piRNAS
Question: By which methods can we evaluate the reliability of a phylogenetic tree?

Context:
For robustness evaluation, we apply bootstrap and jackknife techniques to input data.
An alignment confidence score capturing robustness to guide tree uncertainty.
We build on the widely used bootstrap method for perturbing the phylogenetic tree.
SuperTRI: A new approach based on branch support analyses of multiple independent data sets for assessing reliability of phylogenetic inferences.
To overcome these limitations, we propose a new approach, called SuperTRI, which is based on the branch support analyses of the independent data sets, and where the reliability of the nodes is assessed using three measures: the supertree Bootstrap percentage and two other values calculated from the separate analyses: the mean branch support (mean Bootstrap percentage or mean posterior probability) and the reproducibility index.
In contrast to other similar software, the program FreeTree (available at http://www.natur.cuni.cz/~flegr/programs/freetree or http://ijs.sgmjournals.org/content/vol51/issue3/) can also assess the robustness of the tree topology by bootstrap, jackknife or operational taxonomic unit-jackknife analysis.
Unlike any previous tool for inferring phylogenies from rearrangement data, TIBA uses novel methods of robustness estimation to provide support values for the edges in the inferred tree.
Fast and accurate phylogenetic reconstruction from high-resolution whole-genome data and a novel robustness estimator.
Moreover, whereas phylogenetic analyses from sequence data are deemed incomplete unless bootstrapping scores (a measure of confidence) are given for each tree edge, no equivalent to bootstrapping exists for rearrangement-based phylogenetic analysis.
We also describe a novel approach to estimate the robustness of results-an equivalent to the bootstrapping analysis used in sequence-based phylogenetic reconstruction.
The standard deviation also suggests the reliability level of the branch order.
Assessment of the reliability of a given phylogenetic hypothesis is an important step in phylogenetic analysis.
The reliability of the phylogenetic trees was probed with the bootstrapping of 100 replicates of the original sequence alignments.

Answer: The methods for assessing the robustness/reliability of the topology of the inferred phylogenetic trees are: the widely used bootstrap method and the jackknife method.
In contrast to other similar software, the program FreeTree (available at http://www.natur.cuni.cz/~flegr/programs/freetree or http://ijs.sgmjournals.org/content/vol51/issue3/) can also assess the robustness of the tree topology by bootstrap, jackknife or operational taxonomic unit-jackknife analysis. (PMID: 11411692)
Exact answer: bootstrap, jackknife
Question: What is the treatment of acute myocarditis?

Context:
ibuprofen 400 mg twice a day as therapy
Acute fulminant myocarditis commonly manifests itself as severe, rapidly progressive hemodynamic deterioration and circulatory collapse that may be resistant to high doses of inotropic agents and steroids and to mechanical support by intra-aortic balloon pump
the TandemHeart percutaneous ventricular assist device, can enable patients to recover in a few days.
he authors report a typical case of fulminating myocarditis with electromechanical dissociation, which recovered completely after a period of circulatory assistance.
To clarify the effects of Astragalus Membranaceus (AM) combined with taurine and/or coenzyme Q10(CoQ10) on coxsackievirus B3 (CVB3) murine myocarditis
AM, taurine and CoQ10 have some curative effects on CVB3 murine myocarditis, AM combined with taurine and CoQ10 is the best.

Answer: Treatment of acute myocarditis includes antiinflammatory drugs like ibuoprofen and steroids, inotropic agents and mechanical support (intra-aortic ballon pump). TandemHeart percutaneous ventricular assist device may be used in some, more compromised, patients for few days.
Exact answer: antiinflammatory steroid and non steroid drugs, inotropic agents, mechanical support
Question: What is plantar fasciitis

Context:
Plantar fascia (PF) disorders commonly cause heel pain and disability
Plantar fasciitis (PF) is a common foot complaint, affects both active sportsmen and physically inactive middle age group. It is believed that PF results from degenerative changes rather than inflammation
Plantar fasciitis (PF) is present in 10% of the population and is the most common cause of plantar heel pain
Plantar fasciitis, a chronic degenerative process that causes medial plantar heel pain, is responsible for approximately 1 million physician visits each year
Plantar fasciitis (PF)is the most common cause of plantar heel pain
Plantar fasciitis is the most common cause of heel pain and is estimated to affect 2 million people in the United States alone.For adults suffering from plantar fasciitis, are foot orthoses a viable treatment option to reduce pain
Plantar fasciitis: a degenerative process (fasciosis) without inflammation.
BACKGROUND: Plantar fasciitis is a common foot disorder that impacts many functional activities.
The second purpose was to determine whether chronic plantar fasciitis is accompanied by atrophy of plantar intrinsic foot muscles and tibialis posterior.METHODS: Magnetic resonance images were taken bilaterally in eight subjects with unilateral plantar fasciitis.
Plantar fasciitis, a common injury in runners, has been speculated to be associated with weakness of the intrinsic foot muscles
Although plantar fasciitis is the most common cause of heel pain,
Plantar fasciitis, a self-limiting condition, is a common cause of heel pain in adults. It affects more than 1 million persons per year, and two-thirds of patients with plantar fasciitis will seek care from their family physician
Plantar fasciitis is a common cause of heel pain and is the result of a degenerative process of the plantar fascia at its calcaneal attachment.

Answer: Plantar fascia (PF) disorders like plantar fasciitis commonly cause heel pain and disability and are thought to be degenerative rather than inflammatory in nature
Exact answer: heel pain
Question: Which value of nuchal translucency thickness is set as the threshold for high-risk for Down Syndrome?

Context:
Combined prenatal screening was always positive for Down syndrome when NT thickness exceeded 4.0 mm
In women aged 35 to 37 years, combined prenatal screening was always positive when NT exceeded 2.8 mm, 3.0 mm, and 3.4 mm at 11, 12, and 13 weeks of gestation, respectively
NT is physiological for a measurement < 3 mm but the incidence of chromosomal abnormalities (essentially trisomies 21, 18 and 13) increases when NT > or = 3 mm

Answer: NT is physiological for a measurement < 3 mm but the incidence of chromosomal abnormalities (essentially trisomies 21, 18 and 13) increases when NT > or = 3 mm. As women aged, this upper NT threshold value changed according to gestational age. In women aged 35 to 37 years, combined prenatal screening was always positive when NT exceeded 2.8 mm, 3.0 mm, and 3.4 mm at 11, 12, and 13 weeks of gestation, respectively.
Exact answer: 3mm
Question: What is Path2PPI?

Context:
Path2PPI: an R package to predict protein-protein interaction networks for a set of proteins
We introduce Path2PPI, a new R package to identify protein-protein interaction (PPI) networks for fully sequenced organisms for which nearly none PPI are known. Path2PPI predicts PPI networks based on sets of proteins from well-established model organisms, providing an intuitive visualization and usability. It can be used to combine and transfer information of a certain pathway or biological process from several reference organisms to one target organism.
: We introduce Path2PPI, a new R package to identify protein-protein interaction (PPI) networks for fully sequenced organisms for which nearly none PPI are known.
Path2PPI predicts PPI networks based on sets of proteins from well-established model organisms, providing an intuitive visualization and usability.

Answer: Path2PPI is an R package to identify protein-protein interaction (PPI) networks for fully sequenced organisms for which nearly none PPI are known. Path2PPI predicts PPI networks based on sets of proteins from well-established model organisms, providing an intuitive visualization and usability. It can be used to combine and transfer information of a certain pathway or biological process from several reference organisms to one target organism.
Question: How are lincRNA affecting the regulation of gene expression?

Context:
We detected a considerable number of cis expression quantitative trait loci (cis-eQTLs) and demonstrated that the genetic regulation of lincRNA expression is independent of the regulation of neighboring protein-coding genes.
We observe biases in lincRNA genomic locations and expression profiles that are consistent with some of these lincRNAs being involved in the regulation of neighboring protein-coding genes with developmental functions.
In this issue of Developmental Cell, Wang et al. (2013) find that linc-RoR maintains human embryonic stem cell self-renewal by functioning as a sponge to trap miR-145, thus regulating core pluripotency factors Oct4, Nanog, and Sox2
Enrichment of expressed lincRNA promoters in enhancer marks provides an additional argument for the involvement of lincRNAs in the regulation of transcription in cis. 
Together, these findings suggest that lincRNA-p21 is an important player in the regulation of the Warburg effect and also implicate lincRNA-p21 as a valuable therapeutic target for cancer.
Our findings implicate a novel RNA gene, lincRNA AC068718.1, as risk factor for PTSD in women and add to emerging evidence that non-coding RNA genes may play a crucial role in shaping the landscape of gene regulation with putative pathological effects that lead to phenotypic differences.
Taken together, our results imply that mdig is involved in the regulation of H3K9me3 to influence the heterochromatin structure of the genome and the expression of genes important for cell growth or transformation.
ndogenous miRNA sponge lincRNA-RoR regulates Oct4, Nanog, and Sox2 in human embryonic stem cell self-renewal.
Here, we demonstrate that a lincRNA, linc-RoR, may function as a key competing endogenous RNA to link the network of miRNAs and core TFs, e.g., Oct4, Sox2, and Nanog.
We suggest that linc-RoR forms a feedback loop with core TFs and miRNAs to regulate ESC maintenance and differentiation.
ammalian long intergenic noncoding RNAs (lincRNAs) are best known for modulating transcription.
Our findings uncover a role for lincRNA as a posttranscriptional inhibitor of translation.

Answer: lincRNA may function either as modulators of epigenetic mark deposition or as endogenous antagonists for microRNA binding. A lincRNA, linc-RoR, may function as a key competing endogenous RNA to link the network of miRNAs and core TFs, e.g., Oct4, Sox2, and Nanog. Mdig is involved in the regulation of H3K9me3 to influence the heterochromatin structure of the genome and the expression of genes important for cell growth or transformation. Observed biases in lincRNA genomic locations and expression profiles are consistent with some of these lincRNAs being involved in the regulation of neighboring protein-coding genes with developmental functions.
Question: What is the function of the mammalian gene Irg1?

Context:
IRG1 is highly upregulated in murine ANA-1 macrophages by several proinflammatory cytokines and Toll-like receptor (TLR) agonists, as well as in spleen and lung of Listeria monocytogenes or Toxoplasma gondii infected mice, respectively
The proinflammatory cytokine-induced IRG1 protein associates with mitochondria
multiple genes induced by Borrelia burgdorferi in macrophages to regulate Lyme disease inflammation
One of these genes, IRG1, was confirmed by single nucleotide polymorphism analysis to be involved in susceptibility. Its precise mechanism remains to be elucidated, although the analysis of gene expression data suggests it has a role in apoptosis.
Murine immune-responsive gene 1 (IRG1) plays significant roles in embryonic implantation and neurodegeneration
the IRG1 gene is differentially expressed in human fetal PBMCs and LPS-stimulated adult PBMCs.
we identified the immune-responsive gene 1 (IRG1), which was expressed substantially higher in lipopolysaccharide (LPS)-stimulated than in MAP-infected murine macrophage cell lines.
The inhibitor also blocked induction by LIF of several LIF-regulated genes in the LE including Irg1, which has been shown previously to be essential for implantation.
Immune-responsive gene 1 is a novel target of progesterone receptor and plays a critical role during implantation in the mouse.
our studies identified Irg1 as a novel target of PR in the pregnant uterus and also revealed that it is a critical regulator of the early events leading to implantation
 This resulted in the identification of one novel P4-regulated gene that had been previously found in lipopolysaccharide-stimulated macrophages and called immune response gene-1 (Irg1) and which is the mammalian ortholog of the bacterial gene encoding methylcitrate dehydratase
the mammalian ortholog of methylcitrate dehydratase (immune response gene 1)
Here we report the isolation of a complementary DNA representing a novel gene, interferon-regulated gene 1 (IRG1). T
Here we report the isolation of a complementary DNA representing a novel gene, interferon-regulated gene 1 (IRG1). This gene exhibits significant homology to interferon (IFN)-alpha/beta-inducible human genes p27 and 6-16, indicating that these genes may belong to the same family
The level of IRG1 mRNA again rose transiently on day 4 immediately preceding implantation.
Although the functional roles of IRG1 and p27 remain unclear, we describe for the first time, identification of a gene family regulated by IFNalpha in both rodent and human uteri
Hence, the induction of IRG1 by LPS is mediated by tyrosine kinase and protein kinase C pathway.

Answer: Human IRG1 and mouse Irg1 mediates antiviral and antimicrobial immune responses, without its exact role having been elucidated. Irg1 has been suggested to have a role in apoptosis and to play a significant role in embryonic implantation. Irg1 is reported as the mammalian ortholog of methylcitrate dehydratase.
Question: Why are insulators necessary in gene therapy vectors?

Context:
hromatin insulators separate active transcriptional domains and block the spread of heterochromatin in the genome. Studies on the chicken hypersensitive site-4 (cHS4) element, a prototypic insulator, have identified CTCF and USF-1/2 motifs in the proximal 250 bp of cHS4, termed the "core", which provide enhancer blocking activity and reduce position effects.
An attractive solution to the problem of oncogene activation is the inclusion of insulators/enhancer-blockers in the viral vectors.
We propose the incorporation of chromatin insulators in the design of gene therapy vectors to overcome the problem of position effects. Chromatin insulators are protein-binding DNA elements that lack intrinsic promoter/enhancer activity but shelter genes from transcriptional influence of surrounding chromatin.
The design and incorporation of effective chromatin insulator sequences in the next generation of gene therapy vectors should lead to improved and more predictable expression of therapeutic transgenes and constitute an important step toward clinically effective gene therapy.

Answer: a) They inhibit oncogene activation upon vector integration and b) They maximize the probability of vector expression upon integration in heterochromatinic regions
The presence of insulators in gene therapy vectors is necessary because these elements have the ability to help overcome the problem of position effects, caused due to random integration of the therapeutic genes in the host cell genome.