nirantk/geneticsQA-train huggingface dataset:
Question: Can administration of the thyrotropin releasing hormone reduce fatigue in cancer patients?

Context:
TRH administration was associated with significant improvement (p < 0.05) in fatigue levels as measured by the Visual Analog Scale-Energy (VAS-E), was associated with significant (p < 0.05) improvement in sleep disturbances and improved quality of life. 
This decrease in CRP level with TRH administration was associated with improvement in energy levels as measured by the VAS-E. 
In the present pilot, randomized, placebo-controlled, crossover study, we investigated the efficacy and safety of TRH as a treatment for CF.
TRH administration was associated with significant improvement in fatigue level as measured by the VAS-E, the fatigue and vigor subscales of the POMS, and the fatigue subscale of FACIT-F (p < 0.05). 
TRH administration was efficacious, safe, and tolerable in the treatment of CF with a positive impact on quality of life. These results provide a crucial impetus for pursuing TRH therapeutics to treat CF.
Thyrotropin-releasing hormone can relieve cancer-related fatigue: hypothesis and preliminary observations.
Global assessment using both subjective and objective parameters showed that TRH exerted clear anti-fatigue effects in four of the six TRH treatments. 
These initial findings support the proposal that TRH can ameliorate cancer-related fatigue.

Answer: yes, in cancer patients, thyrotropin releasing hormone (TRH) administration was associated with significant improvement in cancer related fatigue levels as measured by the Visual Analog Scale-Energy, fatigue and vigor subscales of the POMS, and the fatigue subscale of FACIT-F. TRH administration was safe and tolerable in the treatment of cancer-related with a positive impact on quality of life, suggesting the need for further studies investigating TRH for treatment of fatigue in cancer patients.
Exact answer: yes
Question: Is transcapillary  albumin escape altered in diabetic patients?

Context:
On the contrary, altered TERalb and increased carotid artery intimal thickness are shown by all hypertensive type 2 diabetic patients, both with normal and altered patterns of AER.
Altered systemic capillary permeability characterizes insulin-resistant hypertensive patients with Metabolic Syndrome.
TERalb is increased in normo-albuminuric type 1 diabetic patients. 

Answer: An altered TERalb is present in type 2 diabetic patients, both with normal and altered patterns of AER.
TERalb is increased also in normo-albuminuric type 1 diabetic patients.
Exact answer: yes
Question: Does the Oncotype DX test work with paraffin embedded tissues?

Context:
The Oncotype-DX Breast Cancer Assay (Genomic Health, Redwood City, CA) quantifies gene expression for 21 genes in breast cancer tissue by performing reverse transcription polymerase chain reaction (RT-PCR) on formalin-fixed paraffin-embedded (FFPE) tumour blocks that are obtained during initial surgery (lumpectomy, mastectomy, or core biopsy) of women with early breast cancer that is newly diagnosed.
Oncotype DXtrade mark, is a diagnostic test comprised of a 21-gene assay applied to paraffin-embedded breast cancer tissue, which allows physicians to predict subgroups of hormone-receptor-positive, node-negative patients who may benefit from hormonal therapy alone or require adjuvant chemotherapy to attain the best survival outcome.
Oncotype DX is a clinically validated, high-complexity, multianalyte reverse transcription-PCR genomic test that predicts the likelihood of breast cancer recurrence in early-stage, node-negative, estrogen receptor-positive breast cancer. 
We therefore investigated the analytical performance of the assay.
Assays used a pooled RNA sample from fixed paraffin-embedded tissues to evaluate the analytical performance of a 21-gene panel with respect to amplification efficiency, precision, linearity, and dynamic range, as well as limits of detection and quantification.
One such strategy is the 21-gene assay (Oncotype DX), which is currently in commercial use in the USA. One advantage of this test is the use of paraffin-embedded blocks instead of previous methods, which required fresh frozen tissue. 
We used paraffin-embedded core biopsies from a completed phase II trial to identify genes that correlate with response to primary chemotherapy. 
In addition to the individual genes, the correlation of the Oncotype DX Recurrence Score with pCR was examined
RNA was extracted from paraffin blocks
to develop the 21-gene Recurrence Score assay (Oncotype DX)

Answer: Yes, the Oncotype DX test works with paraffin embedded tissue.
Exact answer: yes
Question: Where does TORC1 sequester during heat stress?

Context:
Transient sequestration of TORC1 into stress granules during heat stress.
Here we report that TORC1 signaling upon heat stress is regulated by stress granules (SGs), which are cytoplasmic foci formed under certain stresses. Ectopic formation of SGs achieved by Pbp1 overexpression in unstressed cells sequesters TORC1 in this compartment, thereby blunting TORC1 signaling
Upon heat stress, a physiological SG-inducing condition, TORC1 is also recruited to SGs, which delays reactivation of TORC1 signaling during recovery from heat stress
TORC1 reactivation is directed through SG disassembly, suggesting that SGs act as a key determinant for TORC1 reactivation during recovery from heat stress
Upon heat stress, a physiological SG-inducing condition, TORC1 is also recruited to SGs, which delays reactivation of TORC1 signaling during recovery from heat stress.
Here we report that TORC1 signaling upon heat stress is regulated by stress granules (SGs), which are cytoplasmic foci formed under certain stresses.
Here we report that TORC1 signaling upon heat stress is regulated by stress granules (SGs), which are cytoplasmic foci formed under certain stresses. Ectopic formation of SGs achieved by Pbp1 overexpression in unstressed cells sequesters TORC1 in this compartment, thereby blunting TORC1 signaling. Upon heat stress, a physiological SG-inducing condition, TORC1 is also recruited to SGs, which delays reactivation of TORC1 signaling during recovery from heat stress. 
Ectopic formation of SGs achieved by Pbp1 overexpression in unstressed cells sequesters TORC1 in this compartment, thereby blunting TORC1 signaling. Upon heat stress, a physiological SG-inducing condition, TORC1 is also recruited to SGs, which delays reactivation of TORC1 signaling during recovery from heat stress.
Here we report that TORC1 signaling upon heat stress is regulated by stress granules (SGs), which are cytoplasmic foci formed under certain stresses. Ectopic formation of SGs achieved by Pbp1 overexpression in unstressed cells sequesters TORC1 in this compartment, thereby blunting TORC1 signaling.
Upon heat stress, a physiological SG-inducing condition, TORC1 is also recruited to SGs, which delays reactivation of TORC1 signaling during recovery from heat stress. Moreover, TORC1 reactivation is directed through SG disassembly, suggesting that SGs act as a key determinant for TORC1 reactivation during recovery from heat stress.
Although TORC1 signaling is repressed by various stresses in yeast, the underlying mechanisms remain elusive. Here we report that TORC1 signaling upon heat stress is regulated by stress granules (SGs), which are cytoplasmic foci formed under certain stresses.
Here we report that TORC1 signaling upon heat stress is regulated by stress granules (SGs), which are cytoplasmic foci formed under certain stresses.
Upon heat stress, a physiological SG-inducing condition, TORC1 is also recruited to SGs, which delays reactivation of TORC1 signaling during recovery from heat stress.

Answer: Upon heat stress, TORC1 is recruited to stress granules.
Question: Which drugs may interfere thyroxine absorption?

Context:
ommonly used drugs, such as bile acid sequestrants, ferrous sulphate, sucralfate, calcium carbonate, aluminium-containing antacids, phosphate binders, raloxifene and proton-pump inhibitors, have also been shown to interfere with the absorption of levothyroxine
Hypothyroid patients taking sevelamer hydrochloride or chromium picolinate should be advised to separate the time of ingestion of these drugs from their thyroid hormone preparation by several hours.

Answer: bile acid sequestrants, ferrous sulphate, sucralfate, calcium carbonate, aluminium-containing antacids, phosphate binders, raloxifene and proton-pump inhibitors, have also been shown to interfere with the absorption of levothyroxine
sevelamer hydrochloride or chromium picolinate should be advised to separate the time of ingestion of these drugs from their thyroid hormone preparation by several hours
Exact answer: bile acide sequestrant, ferrous sulphate, sucralfate, Calcium carbonate, aluminium-containing antacids, raloxifene, proton pump inhibithors, sevelamer, chromium picolinate
Question: What is the Shelterin complex?

Context:
Human telomeres are associated with the shelterin complex which consists of six telomere-associated proteins that specifically bind to telomeric DNA. Alterations or removal of individual shelterin components would lead to telomere uncapping and telomere dysfunction, resulting in cellular senescence and transformation to a malignant state.
Telomeres interact with numerous proteins, including components of the shelterin complex, whose alteration, similarly to proliferation-induced telomere shortening, initiates cellular senescence.
Telomere repeat binding factor TRF2 is a member of shelterin complex with an important role in protecting and stabilizing chromosomal ends.
In human, the shelterin complex binds TTAGGG DNA repeats and provides capping to chromosome ends.
Shelterin Protects Chromosome Ends by Compacting Telomeric Chromatin.
Telomeres, repetitive DNA sequences at chromosome ends, are shielded against the DNA damage response (DDR) by the shelterin complex. 
Telomeres need to be protected by the shelterin complex to avoid junctions occurring between chromosomes while failing topoisomerases or clustered DNA damage processing may produce double-strand breaks, thus requiring swift repair to avoid cell death.
A multiprotein complex known as shelterin prevents recognition of telomeric sequences as sites of DNA damage. 

Answer: Human telomeres are associated with the shelterin complex which consists of six telomere-associated proteins that specifically bind to telomeric DNA. Alterations or removal of individual shelterin components would lead to telomere uncapping and telomere dysfunction, resulting in cellular senescence and transformation to a malignant state.
Question: Which are the best treatment options to treat Helicobacter pylori?

Context:
Triple therapy, which has been the mainstay of treatment in many countries over the last decade, now has suboptimal results in many parts of the world.
equential therapy and quadruple therapy (either bismuth-based or non-bismuth-based) are the best current options to replace initial treatment with triple therapy.
olecular tests can be used to detect H. pylori and clarithromycin and/or fluoroquinolone resistance in gastric biopsies without necessitating culture. In regions of high clarithromycin resistance, such as France, sequential treatment or bismuth-containing quadruple therapies are replacing standard triple therapies for the first-line empirical treatment.
The evidence in favour of bismuth compounds for treating infected children is still not clear.
Chitosan microspheres with multiple Eudragit L100 cores were easily prepared by a new emulsification/coagulation encapsulating method.
the multi-core chitosan microspheres could serve as a satisfactory vehicle for stomach-specific delivery of hydrophilic antibiotics.
Treatment consisted of a one-week regimen containing a PPI twice daily, amoxicillin (A) 1 g twice daily and rifabutin (R) 300 mg once daily (PPI-AR).
Pretreatment antibiotic susceptibility to metronidazole, clarithromycin and A was evaluated using a validated epsilometer test.
four different strategies for prevention of rebleeding in patients with peptic ulcer hemorrhage: 1) test for H. pylori and treatment, if positive; 2) proton pump inhibitor maintenance; 3) no preventive treatment; 4) empirical H. pylori eradication immediately after bleeding.
Empirical H. pylori eradication was the dominant strategy: its estimated rate of recurrent bleeding was lower (6.1%) than those of strategies 1 (7.4%), 2 (11.1%), and 3 (18.4%) and it was the least expensive strategy. The results remained stable when variables were changed inside a wide range of plausible values.
In patients with bleeding peptic ulcer, empirical treatment of H. pylori infection immediately after feeding is restarted is the most cost-effective strategy for preventing recurrent hemorrhage.

Answer: The best treatment options  for eradication of Helicobacter pylori involve triple or quadruple drugs therapy with different types of antibiotics.
Bismuth may be also an additional option. Proton pump inhibitors are also included in treatment.
The more effective drug list includes: amoxicillin, claritromycin, metronidazole rifabutin.
Also chitosan microspheres with Eudragit L100 have been tested.
Exact answer: amoxicillin, metronidazole, claritromycin, Proton pump inhibithors, rifabutin, Eudragit L100
Question: To what extent does HPV vaccination reduce the risk for cervical cancer?

Context:
The success of HPV vaccination as a major public health prevention opportunity, however, will entirely depend on efficient infrastructures to deliver the vaccines and on the acceptance by individuals, parents and health care providers.
The most effective strategy therein was vaccination of 12-year-olds, plus a temporary 12-24-year-old catch-up program covering both sexes; whereby HPV 6/11/16/18-related cervical cancer, high-grade cervical precancer, and genital wart incidence was reduced by 84-98% during year 50 following vaccine introduction
the introduction of cervical screening programs, the incidence and mortality of cervical cancer has been drastically reduced
On the assumption that the vaccine provided lifelong immunity, the cost-effectiveness ratio of vaccination of 12-year-old girls was $43,600 per quality-adjusted life-year (QALY) gained, as compared with the current screening practice
Vaccine efficacy in prevention of CIN 2 or higher lesions in HPV 16 or HPV 18 negative women, who received all vaccination doses, ranges between 98% and 100%
Life expectancy gained from vaccination is 13.04 years and average Quality Adjusted Life Years saved (QALYs) is 24.4 in vaccinated vs 6.29 in unvaccinated
Organized vaccination programs against HPV have the potential to prevent about 70% of cervical cancers and the vast majority of the other HPV-related conditions. 
However, existing data strongly suggests that as many as 440,000 cervical cancer cases and 220,000 deaths due to this malignancy will be prevented with the establishment of an effective worldwide HPV immunization program
Prophylactic HPV vaccination against HPV 16 and 18 has been shown to be highly effective in preventing HPV related malignancy in clinical trials
Nevertheless women up to 45 years of age have been shown to exhibit strong immune responses to the bivalent HPV vaccine which might be expected to reduce the risk of HPV re-infection and address the second peak of HPV related malignancy in later life, evident over 45 years of age
Reduced costs, simple vaccine regimes and strengthening vaccine delivery platforms for adolescents should eventually facilitate HPV vaccine introduction in developing countries.
Besides cost, there are several socio-cultural and ethical issues involved with the implementation of already developed vaccines including the acceptability of HPV vaccination by preadolescent girls and their parents in India.

Answer: The most effective strategy therein was vaccination of 12-year-olds, plus a temporary 12-24-year-old catch-up program covering both sexes; whereby HPV 6/11/16/18-related cervical cancer, high-grade cervical precancer, and genital wart incidence was reduced by 84-98% during year 50 following vaccine introduction. Vaccine efficacy in prevention of CIN 2 or higher lesions in HPV 16 or HPV 18 negative women, who received all vaccination doses, ranges between 98% and 100%
Exact answer: Cervical precancer and similar neoplasias were reduced by 84-100%
Question: List signaling molecules (ligands) that interact with the receptor EGFR?

Context:
the epidermal growth factor receptor (EGFR) ligands, such as epidermal growth factor (EGF) and amphiregulin (AREG)
 EGFR ligands epidermal growth factor (EGF), amphiregulin (AREG) and transforming growth factor alpha (TGFα)
 EGFR and its ligand EGF 
Among EGFR ligands, heparin-binding EGF-like growth factor, TGF-α and Betacellulin (BTC) are produced in the tumor microenvironment of FDC-S at RNA level. 
. Plasma amphiregulin (AR), epidermal growth factor (EGF), transforming growth factor-α, and heparin binding-EGF were assessed by ELISA in 45 chemorefractory mCRC patients
Among EGFR ligands, heparin-binding epidermal growth factor (HB-EGF)
 Of the six known EGFR ligands, transforming growth factor alpha (TGFα) was expressed more highly in triple-negative breast tumors than in tumors of other subtypes.
the 7 known EGFR ligands (EGF, betacellulin, epiregulin, heparin-binding EGF, transforming growth factor-α [TGF-α], amphiregulin, and epigen) 
EGFR ligands based on the two affinity classes: EGF>HB-EGF>TGF-α>BTC>EPR>EPG>AR
In this article, however, we demonstrate that PEPD directly binds to and activates epidermal growth factor receptor (EGFR),
four EGFR ligands (AR, HB-EGF, TGF-α, and EREG) 
Epidermal growth factor (EGF) family peptides are ligands for the EGF receptor (EGFR). 
oluble amphiregulin (AR), transforming growth factor alpha (TGFα), neuregulin 2 beta, and epigen stimulate greater EGFR coupling to cell proliferation and DNA synthesis than do EGF, betacellulin, heparin-binding EGF-like growth factor, and epiregulin
Here, we demonstrate that histamine releases 2 EGFR ligands, amphiregulin and heparin-binding epidermal growth factor-like growth factor (HB-EGF), from airway epithelial cells.
mammalian EGFR ligands including EGF, TGF-α (TGFα), amphiregulin (AREG), heparin-binding EGF-like growth factor (HB-EGF), betacellulin, epiregulin, and epigen.

Answer: The 7 known EGFR ligands  are: epidermal growth factor (EGF), betacellulin (BTC), epiregulin (EPR), heparin-binding EGF (HB-EGF), transforming growth factor-α [TGF-α], amphiregulin (AREG) and epigen (EPG).
Exact answer: epidermal growth factor, betacellulin, epiregulin, heparin-binding epidermal growth factor, transforming growth factor-α, amphiregulin, epigen
Question: Which genes code for the alpha subunit of the DNA polymerase III in most Firmicutes?

Context:
PolC co-evolves with RNA degradation enzymes that are present only in the A+T-rich Firmicutes clade
Bacterial genomes displaying a strong bias between the leading and the lagging strand of DNA replication encode two DNA polymerases III, DnaE and PolC, rather than a single one.
SGD, PAS, and polC are all features associated with a group of low-GC, gram-positive bacteria (Firmicutes)
PAS is a characteristic of organisms with a heterodimeric DNA polymerase III alpha-subunit constituted by polC and dnaE
Bacterial DNA polymerase III, the primary complex of DNA replication, consists of PolC and DnaE. PolC is conserved in Gram-positive bacteria, especially in the Firmicutes with low GC content, whereas DnaE is widely conserved in most Gram-negative and Gram-positive bacteria.
PolC-PolE DNA polymerases
We conclude that PAS is a characteristic of organisms with a heterodimeric DNA polymerase III alpha-subunit constituted by polC and dnaE, which may play a direct role in the maintenance of SGD.
Furthermore, SGD, PAS, and polC are all features associated with a group of low-GC, gram-positive bacteria (Firmicutes)
In contrast, PolC co-evolves with RNA degradation enzymes that are present only in the A+T-rich Firmicutes clade, suggesting at least two origins for the degradosome.
A method for the construction of in frame substitutions in operons: deletion of the essential Escherichia coli holB gene coding for a subunit of the DNA polymerase III holoenzyme.

Answer: Bacterial DNA polymerase III is the primary complex of DNA replication. In most Firmicutes, which are low-GC, gram-positive bacteria, the alpha subunit of their DNA polymerase III is encoded by polC and dnaE. DnaE is widely conserved in most bacteria, while PolC is present mainly in Firmicutes clade.
Exact answer: dnaE, polC
Question: Which cellular processes are regulated by Nanog?

Context:
critical for the regulation of cancer stem cells.
the effect of FAK and Nanog cross-regulation on cancer cell morphology, invasion, and growth that plays a significant role in carcinogenesis
Nanog-like regulates endoderm formation
In mammalian embryonic stem cells, the acquisition of pluripotency is dependent on Nanog
we identified a zebrafish Nanog ortholog and found that its knockdown impaired endoderm formation
establishes a role for Nanog-like in regulating the formation of the extraembryonic tissue required for endoderm induction
Nanog regulates molecules involved in stemness and cell cycle-signaling pathway for maintenance of pluripotency
Nanog, a key transcription factor in the maintenance of pluripotency of embryonic stem (ES) and embryonal carcinoma (EC) cells
Nanog, a positive regulator of ESC proliferation and G1/S transition
Nanog is a stem cell transcription factor required for self-renewal and for maintaining pluripotency
NANOG regulates glioma stem cells
We find that NANOG modulates gliomasphere clonogenicity, CD133(+) stem cell cell behavior and proliferation
NANOG is essential for GBM tumourigenicity
Nanog regulates primordial germ cell migration
Nanog mediates PGC migration by regulating Cxcr4b expression
Nanog regulates proliferation during early fish development.
Nanog is necessary for S-phase transition and proliferation in the developing embryo
our results demonstrate that NANOG, a cell-fate regulatory molecule known to be important for ESC self-renewal, also plays a novel role in tumor development
the self-renewal gene NANOG regulates human tumor development
The emerging picture is one in which Oct4 and Nanog control a cascade of pathways that are intricately connected to govern pluripotency, self-renewal, genome surveillance and cell fate determination
the pluripotency sustaining factor nanog

Answer: The pluripotency sustaining factor Nanog, controls a cascade of pathways that are intricately connected to govern pluripotency, self-renewal, genome surveillance and cell fate determination. Elevated expression of Nanog has also been reported to result in clonal expansion of murine ESCs, but it also plays a role in tumor development. A positive regulator of cell proliferation, it is essential for G1 to S transition in human embryonic stem cells while it regulates primordial germ cell migration.
Exact answer: cell proliferation, pluripotency, cell fate determination, G1 to S transition, germ cell migration, tumour development