nirantk/geneticsQA-train huggingface dataset:
Question: How is active neurotoxin of Clostridium botulinum detected?

Context:
The neurotoxin detection is based on the mouse lethality assay. 
which could be shown by bioassay to produce biologically active type B toxin in culture.
Human induced pluripotent stem cells (hiPSC) hold great promise for providing various differentiated cell models for in vitro toxigenicity testing. 
A direct comparison of BoNT detection using primary rat spinal cord cells and hiPSC-derived neurons showed equal or increased sensitivity
BoNT/A intoxication studies demonstrate that the hiPSC-derived neurons reproducibly and quantitatively detect biologically active BoNT/A with high sensitivity (EC(50) ∼0.3 U).
 these data suggest that neurons derived from hiPSCs provide an ideal and highly sensitive platform for BoNT potency determination, neutralizing antibody detection and for mechanistic studies.
Detection of botulinum neurotoxin-A activity in food by peptide cleavage assay.
his study reports the successful use of an enzymatic assay employing an internally quenched fluorogenic peptide as a fast, simple and inexpensive alternative to the mouse bioassay. 
BoNT endopeptidase assays
in vivo mouse bioassay has for years been the 'gold standard' assay used for this purpose
Cell-based assays are currently the only in vitro alternative that detect fully functional BoNTs in a single assay and have been utilized for years for research purposes.
mouse bioassay (MBA) is traditionally used to confirm the presence of toxin in serum or food
A novel FDC (functional dual coating) microtitre plate immuno-biochemical assay,
This report demonstrates a novel assay that utilises the endopeptidase activity of the toxin to detect Botulinum neurotoxin in a pharmaceutical sample. The cleaving of SNAP-25 is monitored via UV-Visible spectroscopy with a limit of detection of 373 fg/mL and has been further developed into a high throughput method using a microplate reader detecting down to 600 fg/mL of active toxin. 

Answer: Active neurotoxin of Clostridium botulinum can be detected by:
mouse lethality assay
by mass spectrometry
bioassay
differentiated cell models
peptide cleavage assay
FDC (functional dual coating) microtitre plate immuno-biochemical assay
endopeptidase activity monitored via UV-Visible spectroscopy
Exact answer: mouse lethality assay
by mass spectrometry
bioassay
differentiated cell models
peptide cleavage assay
FDC (functional dual coating) microtitre plate immuno-biochemical assay
endopeptidase activity monitored via UV-Visible spectroscopy
Question: The protein NONO forms heterodimers. With which proteins?

Context:
The paraspeckle component 1 (PSPC1) and non-POU-domain-containing octamer-binding protein (NONO) heterodimer is an essential structural component of paraspeckles,
PSPC1-NONO heterodimer.
Crystallization of a paraspeckle protein PSPC1-NONO heterodimer
difficult heterodimeric complex of two human proteins, paraspeckle component 1 (PSPC1) and non-POU domain-containing octamer-binding protein (NONO), that are involved in gene regulation and the structural integrity of nuclear bodies termed paraspeckles is described.
SFPQ (PSF) and NONO (p54) are nuclear proteins that interact with each other and have diverse roles in nucleic acids metabolism. The SFPQ/NONO heterodimer was previously found to enhance DNA strand break rejoining in vitro.
We identified a heterodimer, p54nrb and PSF,
P54nrb forms a heterodimer with PSP1 that localizes to paraspeckles in an RNA-dependent manner.
e demonstrated that the PSF heterodimer partner, p54nrb (non-POU-domain-containing, octamer binding protein), can also function as a transcription corepressor, independent of PSF.
The PSPC1/NONO heterodimer has a right-handed antiparallel coiled-coil
Structure of the heterodimer of human NONO and paraspeckle protein component 1

Answer: The protein NONO forms heterodimers with PSPC1, SFPQ.
Exact answer: PSPC1, SFPQ
Question: To which family does the Zika virus belong?

Context:
Zika virus (ZIKV; genus Flavivirus, family Flaviviridae) 

Answer: The Zika virus belongs to the family Flaviviridae.
Exact answer: Flaviviridae
Question: What is the effect of Allopurinol on asphyxia in neonates?

Context:
Potential neuroprotective strategies targeting different pathways leading to neuronal cell death in response to hypoxic-ischemic insult have been investigated: hypothermia, erythropoietin, iminobiotin, deferioxamine, magnesium, allopurinol, xenon, melatonin and statins.
Allopurinol reduces the formation of free radicals, thereby potentially limiting the amount of hypoxia-reperfusion damage.
There were no differences in long-term outcome between the allopurinol-treated infants and controls. However, subgroup analysis of the moderately asphyxiated group showed significantly less severe adverse outcome in the allopurinol-treated infants compared with controls (25% vs 65%; RR 0.40, 95%CI 0.17 to 0.94).
The reported data may suggest a (neuro)protective effect of neonatal allopurinol treatment in moderately asphyxiated infants.
The asphyxiated newborns treated with allopurinol had better neurologic and neurodevelopmental outcome at 12 or more months of age.
In newborn infants, allopurinol is being tested as a free radical scavenger to prevent brain damage caused by reperfusion and oxygenation after perinatal hypoxia and ischemia (birth asphyxia).
Early postnatal allopurinol does not improve short term outcome after severe birth asphyxia.
The analysis showed an unaltered (high) mortality and morbidity in the infants treated with allopurinol.
Allopurinol treatment started postnatally was too late to reduce the early reperfusion induced free radical surge.
One randomized trial of allopurinol showed short-term benefits but was too small to test death or disability.
No toxic side effects of ALLO were detected.
This study suggests a beneficial effect of ALLO treatment on free radical formation, CBV, and electrical brain activity, without toxic side effects.

Answer: Allopurinol was shown in a number of clinical trial to be safe and effective for treatment of neonatal asphyxia. Allopurinol  improves short-term and long-term clinical outcomes of neonatal asphyxia. Allopurinol should be administered as soon as possible. Postulated mechanism of allopurinol action in this setting is prevention of hypoxia-perfusion injury by reduction of free radical formation.
Question: Which are the most under-represented oligonucleotides in higher eukaryote genomes?

Context:
Unusual frequencies of certain alternating purine-pyrimidine runs in natural DNA sequences
Octanucleotides are the most deficient, occurring at only 60% of the frequency expected in random sequences. An unexpectedly high proportion of these octamers consists of alternating tetramers with the repeat structure (PuPyPuPy)2 or (PyPuPyPu)2
For dinucleotides, TA is almost universally under-represented, with the exception of vertebrate mitochondrial genomes, and CG is strongly under-represented in vertebrates and in mitochondrial genomes
For trinucleotides, GCA.TGC tends to be under-represented in phage, human viral, and eukaryotic sequences, and CTA.TAG is strongly under-represented in many prokaryotic, eukaryotic, and viral sequences
The dinucleotide CpG is significantly under-represented in vertebrate DNA and is usually methylated
One such pattern recognition system is based on unmethylated CpG dinucleotides in particular sequence contexts (CpG motifs); these motifs are common in bacterial DNA but are under-represented ("CpG suppression") and methylated in vertebrate DNA
We argue that the significant under-represented motif pattern of CpG in an AU context--which is found in both the ssRNA viruses and innate genes, and has decreased throughout the history of H1N1 influenza replication in humans--is immunostimulatory and has been selected against during the co-evolution of viruses and host innate immune genes

Answer: The oligonucleotides containing the CG and TA dinucleotide are generally under-represented in higher eukaryote genomes
TpA is the most underepresented dinucleotide followed closely by CpG. For trinucleotides, GCA/TGC tends to be under-represented in phage, human viral, and eukaryotic sequences, and CTA/TAG is strongly under-represented in many prokaryotic, eukaryotic, and viral sequences. For higher lengts alternating Purine/Pyrimidine tracts are underepresented up to 60%.
Oligonucleotides containing CG and TA dinucleoides
Exact answer: TA
CG
(PuPy)n
GCA/TGC
CTA/TAG
Question: Is the circadian clock involved in ribosome biogenesis?

Context:
The circadian clock coordinates ribosome biogenesis.
Here we show that the circadian clock exerts its function also through the regulation of mRNA translation. Namely, the circadian clock influences the temporal translation of a subset of mRNAs involved in ribosome biogenesis by controlling the transcription of translation initiation factors as well as the clock-dependent rhythmic activation of signaling pathways involved in their regulation. Moreover, the circadian oscillator directly regulates the transcription of ribosomal protein mRNAs and ribosomal RNAs. Thus the circadian clock exerts a major role in coordinating transcription and translation steps underlying ribosome biogenesis.
Namely, the circadian clock influences the temporal translation of a subset of mRNAs involved in ribosome biogenesis by controlling the transcription of translation initiation factors as well as the clock-dependent rhythmic activation of signaling pathways involved in their regulation
The circadian clock coordinates ribosome biogenesis
Here we show that the circadian clock exerts its function also through the regulation of mRNA translation
Here we show that the circadian clock exerts its function also through the regulation of mRNA translation. Namely, the circadian clock influences the temporal translation of a subset of mRNAs involved in ribosome biogenesis by controlling the transcription of translation initiation factors as well as the clock-dependent rhythmic activation of signaling pathways involved in their regulation.

Answer: Yes. The circadian clock coordinates ribosome biogenesis. It influences the temporal translation of a subset of mRNAs involved in ribosome biogenesis by controlling the transcription of translation initiation factors as well as the clock-dependent rhythmic activation of signaling pathways involved in their regulation.
Exact answer: yes
Question: Is LPS a microbial product?

Context:
and microbial translocation [lipopolysaccaride (LPS), microbial 16S rDNA and sCD14] 
Lipopolysaccharide sensing an important factor in the innate immune response to Gram-negative bacterial infections
bacterial lipopolysaccharide (LPS)
sterile bacterial wall lipopolysaccharide (LPS) to investigate the changes in innate lung microbiota

Answer: Yes, the lipopolysaccharide (LPS) is a component of the bacterial cell wall.
Exact answer: yes
Question: Which is the third subunit of the TSC1-TSC2 complex upstream of mTORC1?

Context:
The tuberous sclerosis complex (TSC) tumor suppressors form the TSC1-TSC2 complex, which limits cell growth in response to poor growth conditions. Through its GTPase-activating protein (GAP) activity toward Rheb, this complex inhibits the mechanistic target of rapamycin (mTOR) complex 1 (mTORC1), a key promoter of cell growth.
Here, we identify and biochemically characterize TBC1D7 as a stably associated and ubiquitous third core subunit of the TSC1-TSC2 complex. We demonstrate that the TSC1-TSC2-TBC1D7 (TSC-TBC) complex is the functional complex that senses specific cellular growth conditions and possesses Rheb-GAP activity.
TBC1D7 knockdown decreases the association of TSC1 and TSC2 leading to decreased Rheb-GAP activity, without effects on the localization of TSC2 to the lysosome.
Like the other TSC-TBC components, TBC1D7 knockdown results in increased mTORC1 signaling, delayed induction of autophagy, and enhanced cell growth under poor growth conditions.

Answer: TBC1D7 was identified as a stably associated and ubiquitous third core subunit of the TSC1-TSC2 complex. It was demonstrated that TSC1-TSC2-TBC1D7 (TSC-TBC) is the functional complex that senses specific cellular growth conditions and possesses Rheb-GAP activity to negatively regulate mTORC1 activity. In agreement with this, TBC1D7 knockdown was shown to result in increased mTORC1 signaling, delayed induction of autophagy, and enhanced cell growth under poor growth conditions.
Exact answer: TBC1D7
Question: Is triadin involved in cardiac function?

Context:
Junctin (JCN), a 26-kd sarcoplasmic reticulum (SR) transmembrane protein, forms a quaternary protein complex with the ryanodine receptor, calsequestrin, and triadin in the SR lumen of cardiac muscle. Within this complex, calsequestrin, triadin, and JCN appear to be critical for normal regulation of ryanodine receptor-mediated calcium (Ca) release.
Recent studies have uncovered functional roles of both JCN and triadin in the mouse heart, using transgenic overexpression strategies, which exhibit varying phenotypes including mild SR structural alterations, prolongation of Ca transient decay, impaired relaxation, and cardiac hypertrophy and/or heart failure.
Triadin is involved in the regulation of cardiac excitation-contraction coupling. 
Thus the maintenance of triadin expression is essential for normal SR Ca cycling and contractile function.
Ca2+ release from the cardiac junctional sarcoplasmic reticulum (SR) is regulated by a complex of proteins, including the ryanodine receptor (RyR), calsequestrin (CSQ), junctin (JCN), and triadin 1 (TRD).
Impaired sarcoplasmic reticulum (SR) Ca release has been suggested to contribute to the depressed cardiac function in heart failure. The release of Ca from the SR may be regulated by the ryanodine receptor, triadin, junctin, calsequestrin, and a histidine-rich, Ca-binding protein (HRC).

Answer: Yes, triadin is involved in the regulation of cardiac excitation-contraction coupling.
Exact answer: yes
Question: Has proteomics been used in the study of the dry eye syndrome?

Context:
Tear proteomic analysis of patients with type 2 diabetes and dry eye syndrome by two-dimensional nano-liquid chromatography coupled with tandem mass spectrometry.
Dry eye syndrome in diabetic patients is associated with aberrant expression of tear proteins, and the findings could lead to identification of novel pathways for therapeutic targeting and new diagnostic markers.
 2D electrophoresis (2DE) and Differential gel electrophoresis (DIGE) was done to identify differentially expressed proteins. 
Two dimensional electrophoretic analysis of human tears: collection method in dry eye syndrome.
Identification of tear fluid biomarkers in dry eye syndrome using iTRAQ quantitative proteomics.
This study demonstrated that iTRAQ technology combined with 2D-nanoLC-nanoESI-MS/MS quantitative proteomics is a powerful tool for biomarker discovery.

Answer: Yes, tears obtained from patients with the dry eye syndrome have been analyzed using different proteomic technologies.
Exact answer: yes
Question: Which are currently available software tools for detecting rare codon clusters in coding sequences?

Context:
Our program Sherlocc, detects statistically relevant conserved rare codon clusters and produces a user-friendly HTML output.
LaTcOm: a web server for visualizing rare codon clusters in coding sequences
We present LaTcOm, a new web tool, which offers several alternative methods for 'rare codon cluster' (RCC) identification
three RCC detection schemes are implemented: the recently described %MinMax algorithm and a simplified sliding window approach, along with a novel modification of a linear-time algorithm for the detection of maximally scoring subsequences tailored to the RCC detection problem
The PAUSE software has been developed as a new tool to study translational control over protein targeting. This makes it possible to correlate the position of clusters of rare codons in a gene, predicted to cause a translational pause, with the position of hydrophobic stretches in the encoded protein, predicted to span a membrane or to act as a cleavable signal for targeting to the secretory pathway.

Answer: Rare codon clusters (RCCs) correspond to regions along mRNA sequences where among the possible choices of synonymous codons those  with lower usage are observed. Due to the fact that relative codon frequencies have been shown to correlate with their cognate tRNA frequencies, RCCs indicate possible translational attenuation sites. A few tools specific for this task have been described in the literature, namely: LaTcOm, %MinMax, PAUSE, Sherlocc, Sliding Window (RiboTempo)
Exact answer: LaTcOm, %MinMax, PAUSE, Sherlocc, Sliding Window, RiboTempo
Question: Is cytisine superior to nicotine replacement therapy for smoking cessation?

Context:
The effectiveness of cytisine for continuous abstinence was superior to that of nicotine-replacement therapy at 1 week, 2 months, and 6 months. In a prespecified subgroup analysis of the primary outcome, cytisine was superior to nicotine-replacement therapy among women and noninferior among men.
CONCLUSIONS: When combined with brief behavioral support, cytisine was found to be superior to nicotine-replacement therapy in helping smokers quit smoking, but it was associated with a higher frequency of self-reported adverse events.

Answer: Yes, one clinical trial that directly compared smoking cessation rates with cytisine versus nicotine replacement therapy reported that cytisine was  superior to nicotine-replacement therapy in helping smokers quit smoking, but it was associated with a higher frequency of self-reported adverse events.
Exact answer: yes
Question: What is situs inversus?

Context:
Situs inversus totalis is a relatively rare condition and is an autosomal recessive congenital defect in which an abdominal and/or thoracic organ is positioned as a "mirror image" of the normal position in the sagittal plane.
Situs inversus totalis (SIT) represents a total vertical transposition of the thoracic and abdominal organs which are arranged in a mirror image reversal of the normal positioning.
The patient had dextrocardia situs inversus totalis with a mirror-image reversal of the thoracic and abdominal organs.
Situs inversus totalis (SIT) is characterized by complete mirroring of gross cardiac anatomy and position combined with an incompletely mirrored myofiber arrangement, being normal at the apex but inverted at the base of the left ventricle (LV).
Situs inversus totalis is a rare congenital anomaly with a complete mirror image of the thoracic and abdominal organs. 
 Situs inversus totalis (SIT) is an uncommon congenital syndrome, which refers to a reversal mirror-image of the normal thoracoabdominal organs position.

Answer: Situs inversus totalis is a rare congenital anomaly with a complete mirror image of the thoracic and abdominal organs.
Exact answer: Situs inversus totalis is a rare congenital anomaly with a complete mirror image of the thoracic and abdominal organs.
Question: What is the typical outer diameter of microtubules (tubulin heterodimers)?

Context:
microtubules are highly anisotropic structures built from tubulin heterodimers. They are hollow cylindrical shells with a ∼ 25 nm outer diameter
single microtubules (diameter 25 nm
The individual microtubules measured about 24 nm in outer diameter
Microtubules are hollow tubes some 25 nm in diameter participating in the eukaryotic cytoskeleton.
Microtubule assembly is accompanied by hydrolysis of GTP associated with beta-tubulin so that microtubules consist principally of "GDP-tubulin" stabilized by a short "GTP cap." Microtubules are polar, cylindrical structures some 25 nm in diameter.
They are hollow cylindrical shells with a ∼ 25 nm outer diameter and are tens of microns long
Microtubule assembly is accompanied by hydrolysis of GTP associated with beta-tubulin so that microtubules consist principally of "GDP-tubulin" stabilized by a short "GTP cap." Microtubules are polar, cylindrical structures some 25 nm in diameter
Microtubules are hollow tubes some 25 nm in diameter participating in the eukaryotic cytoskeleton

Answer: Microtubules are highly anisotropic structures built from tubulin heterodimers. They are hollow cylindrical shells with a ∼ 25 nm (24nm - 25nm) outer diameter.
Exact answer: 24nm - 25 nm
Question: What role does the SHH-Gli pathway play in brain growth and medulloblastoma, in relation to WNT signaling and potential therapy with cyclopamine?

Context:
148a having potential tumor/metastasis suppressive activity were found to be overexpressed in the WNT signaling associated medulloblastomas", "The requirement for SHH-Gli signaling in the growth of the mouse brain, together with the ability of inappropriate pathway activation in the cerebellum to cause medulloblastomas, and the inhibition of the growth of a number of brain tumors with cyclopamine, a SHH signaling inhibitor, underscores the critical role of the SHH-GLI pathway in brain growth and tumor formation", "Aberrant activation of the Hedgehog (Hh) and Wnt developmental pathways is associated with medulloblastoma, but deregulation of other molecular pathways, including insulin-like growth factor (IGF) signaling, has also been implicated in the pathogenesis of the tumor", "Distinctive microRNA signature of medulloblastomas associated with the WNT signaling pathway."]
148a having potential tumor/metastasis suppressive activity were found to be overexpressed in the WNT signaling associated medulloblastomas", "The requirement for SHH-Gli signaling in the growth of the mouse brain, together with the ability of inappropriate pathway activation in the cerebellum to cause medulloblastomas, and the inhibition of the growth of a number of brain tumors with cyclopamine, a SHH signaling inhibitor, underscores the critical role of the SHH-GLI pathway in brain growth and tumor formation", "Aberrant activation of the Hedgehog (Hh) and Wnt developmental pathways is associated with medulloblastoma, but deregulation of other molecular pathways, including insulin-like growth factor (IGF) signaling, has also been implicated in the pathogenesis of the tumor", "Distinctive microRNA signature of medulloblastomas associated with the WNT signaling pathway."]

Answer: The SHH-Gli pathway plays a critical role in brain growth and tumor formation, particularly in medulloblastomas associated with WNT signaling. Inappropriate pathway activation in the cerebellum can lead to medulloblastomas, and the growth of brain tumors can be inhibited with cyclopamine, a SHH signaling inhibitor.