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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nBrain natriuretic peptide (BNP) is a cardiac hormone mainly synthesized in ventricles and its expression is markedly increased in ventricular hypertrophy that involves the accumulation of extracellular matrix proteins, such as fibronectin (Fn). We recently reported that Fn signaling stimulated BNP secretion accompanied by hypertrophic responses in vitro. To elucidate the regulatory mechanism for BNP gene transcription, we examined cis-acting elements downstream of Fn signaling in rat ventricular myocytes transfected with either the -1812 human BNP-luciferase reporter gene (-1812hBNP/Luc) or one of several truncated forms. A strong cis-repressor element was identified between -552 and -522 in myocytes plated on uncoated dishes. This region contains a neuron-restrictive silencer element (NRSE)-like element (NRSE(BNP)) that is 90% homologous with the NRSE consensus sequence. Neuron-restrictive silencer factor (NRSF) is known to bind to NRSE and to silence transcription of genes containing NRSE. Deletion of NRSE(BNP) and dominant negative NRSF markedly increased the reporter activity in transfected cells, suggesting that the NRSE/NRSF system silences basal BNP gene transcription. When myocytes were cultured on Fn-coated dishes, the reporter activity of -1812hBNP/Luc was increased by approximately 600% compared with that on uncoated dishes. Interestingly, truncation from -552 to -522 reduced the Fn-inducible reporter activity. Moreover, deletion of NRSE(BNP) and dominant negative NRSF also inhibited the Fn-inducible reporter activity. Electrophoretic mobility shift assays showed that Fn signaling inhibited the binding activity of NRSF to NRSE(BNP).\n\nQuestion:\nDoes fibronectin signaling stimulate BNP gene transcription by inhibiting neuron-restrictive silencer element-dependent repression?\n\nAnswer:",
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"content": "yes",
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIntermittent pneumatic compression (IPC) has been shown, by duplex, to increase popliteal artery flow in normal legs and in legs with superficial femoral artery occlusion. The objective of this study was to see if IPC improves distal circulation in legs with severe infra-popliteal disease. Sixteen chronically ischemic legs with arteriographically demonstrated crural or pedal disease were studied during compression with an ArtAssist compression-device. This device delivers rapid compression of the foot and calf. Cutaneous laser-Doppler flux was measured continuously at the dorsal aspect of the distal forefoot. The findings were compared to those in thirteen normal controls of similar age. In ischemic legs, the spontaneous changes in skin-flux are minimal: mean resting flux in sitting position was 0.87 +/- 0.46 AU (Arbitrary Units). Upon activation of the compression device the maximum flux increased to 4.55 +/- 1.35 AU. The difference was statistically significant (p < 0.001). This response was similar to that in normal controls.\n\nQuestion:\nDoes rapid intermittent compression increase skin circulation in chronically ischemic legs with infra-popliteal arterial obstruction?\n\nAnswer:",
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"content": "yes",
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMast cells are involved in early- and late-phase reactions by releasing vasoactive molecules, proteases, and cytokines. Certain histamine-1 receptor antagonists and other antiallergic drugs seem to inhibit the release of mediators from rat and human mast cells. Azelastine and olopatadine are antiallergic agents present in the ophthalmic solutions azelastine hydrochloride (Optivar, Asta Medica/Muro Pharmaceuticals, Tewksbury, MA), and olopatadine hydrochloride (Patanol, Alcon Laboratories, Fort Worth, TX), respectively. We investigated the effect of these drugs on interleukin-6 (IL-6), tryptase, and histamine release from cultured human mast cells (CHMCs). CHMCs were grown from human umbilical cord blood-derived CD34+ cells in the presence of stem cell factor and IL-6 for 14 to 16 weeks. Sensitized CHMCs were pretreated with various concentrations of azelastine or olopatadine for 5 minutes. CHMCs were then challenged with anti-immunoglobulin E, and the released mediators were quantitated. The greatest inhibition of mediator release was seen with 24 microM azelastine; this level of inhibition was matched with the use of 133 microM olopatadine. At this concentration, these drugs inhibited IL-6 release by 83% and 74%, tryptase release by 55% and 79%, and histamine release by 41% and 45%, respectively. Activated CHMCs were characterized by numerous filopodia that were inhibited by both drugs as shown by electron microscopy.\n\nQuestion:\nIs azelastine more potent than olopatadine n inhibiting interleukin-6 and tryptase release from human umbilical cord blood-derived cultured mast cells?\n\nAnswer:",
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"content": "yes",
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nLong-term β-adrenergic receptor (β-AR) blockade reduces mortality in patients with heart failure. Chronic sympathetic hyperactivity in heart failure causes sustained β-AR activation, and this can deplete Ca(2+) in endoplasmic reticulum (ER) leading to ER stress and subsequent apoptosis. We tested the effect of β-AR blockers on ER stress pathway in experimental model of heart failure. ER chaperones were markedly increased in failing hearts of patients with end-stage heart failure. In Sprague-Dawley rats, cardiac hypertrophy and heart failure was induced by abdominal aortic constriction or isoproterenol subcutaneous injection. Oral β-AR blockers treatment was performed in therapy groups. Cardiac remodeling and left ventricular function were analyzed in rats failing hearts. After 4 or 8 weeks of banding, rats developed cardiac hypertrophy and failure. Cardiac expression of ER chaperones was significantly increased. Similar to the findings above, sustained isoproterenol infusion for 2 weeks induced cardiac hypertrophy and failure with increased ER chaperones and apoptosis in hearts. β-AR blockers treatment markedly attenuated these pathological changes and reduced ER stress and apoptosis in failing hearts. On the other hand, β-AR agonist isoproterenol induced ER stress and apoptosis in cultured cardiomyocytes. β-AR blockers largely prevented ER stress and protected myocytes against apoptosis. And β-AR blockade significantly suppressed the overactivation of CaMKII in isoproterenol-stimulated cardiomyocytes and failing hearts in rats.\n\nQuestion:\nDoes β-AR blockers suppress ER stress in cardiac hypertrophy and heart failure?\n\nAnswer:",
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"content": "yes",
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nParkin is recruited to defective mitochondria to promote degradation by an autophagy mechanism (mitophagy). VDACs specifically interact with Parkin on defective mitochondria and are required for efficient targeting of Parkin to mitochondria and subsequent mitophagy.\n\nQuestion:\nDo voltage-dependent anion channels ( VDACs ) recruit Parkin to defective mitochondria to promote mitochondrial autophagy?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nEnterohemorrhagic Escherichia coli (EHEC) are major foodborne pathogens that constitute a serious public health threat, mainly in young children. Shiga toxins (Stx) are the main virulence determinants of EHEC pathogenesis but adhesins like intimin (eae) and Long polar fimbriae (Lpf) also contribute to infection. The TNO GastroIntestinal Model (TIM) was used for a comparative study of EHEC O157:H7 survival and virulence under adult and child digestive conditions. Survival kinetics in the in vitro digestive tract were determined by plating while bacterial viability was assessed by flow cytometry analysis. Expression of stx, eae, and lpf genes was followed by reverse transcriptase-quantitative PCR (RT-qPCR) and Stx production was measured by ELISA (enzyme-linked immunosorbent assay). Upon gastrointestinal passage, a higher amount of viable cells was found in the simulated ileal effluents of children compared to that of adults (with 34 and 6% of viable cells, respectively). Expression levels of virulence genes were up to 125-fold higher in children. Stx was detected only in child ileal effluents.\n\nQuestion:\nDo increased EHEC survival and virulence gene expression indicate an enhanced pathogenicity upon simulated pediatric gastrointestinal conditions?\n\nAnswer:",
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"content": "yes",
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe postulated that combinations of C and E vitamins modulate the antioxidant network and blocks survivin gene expression in androgen-responsive and non-responsive human prostate cancer cell (HPCC) lines. ALVA-101 and DU-145 cell growth and apoptosis were estimated using the Cell Titer 96 AQ and cell death detection ELISA. Reverse transcription-polymerase chain reaction, Western blot and electrophoretic mobility shift assay were used to quantify survivin mRNA, protein, nuclear factor kappa B (NF-kappaB), and activator protein-1 (AP-1). All the tested combinations of vitamins C and E (25-100 microM, 72 hr) reduced cell growth (4-83%). Vitamin C enhanced the growth suppressive effect of vitamin E. Apoptosis was enhanced (25-45%) (vitamins = 100 microM, 24 hr). Survivin mRNA was decreased (26-29%) (vitamins = 250 microM, 24 hr), and survivin protein was decreased (>90%) (vitamins = 100 microM, 72 hr). NF-kappaB and AP-1 activities were increased (vitamins = 100 microM, 24 hr).\n\nQuestion:\nDoes combination therapy with vitamins C plus E inhibit survivin and human prostate cancer cell growth?\n\nAnswer:",
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"content": "yes",
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe arrival of tacrolimus has drastically improved AALDLT recipients' survival. However, little data of tacrolimus have been reported concerning its effects on lipid metabolism for AALDLT recipients. Out aim was to investigate the relationship between tacrolimus blood concentration and lipid metabolism in AALDLT recipients. The pre and postoperative data of 77 adult patients receiving AALDLT between 2002 and December 2007 were retrospectively reviewed. The postoperative immune suppressive regimen was prednisone with tacrolimus ± mycophenolate mofetil. Prednisone was withdrawn within the first postoperative month. Blood lipids and tacrolimus concentration were detected at the first, third, and sixth month during follow-up. Episodes of acute rejection were diagnosed based on biopsy. Overall prevalence of post-transplantation hyperlipidemia was 29.9% (23/77) at the sixth postoperative month. The patients were divided into two groups, the hyperlipidemia group and the ortholipidemia group. In the 23 patients with hyperlipidemia, 15 (65%) were hypercholesterolemia, five (22%) were hypertriglyceridemia, and three (13%) patients had both hypercholesterolemia and hypertriglyceridemia. In univariate analysis, only tacrolimus blood concentration at the third and sixth post-transplantation months showed significant difference (8.7 ± 2.1 vs. 6.9 ± 3.2, p = 0.013; 9.2 ± 2.7 vs. 7.3 ± 3.8, p = 0.038, respectively). In multivariate logistic analysis, only two factors appear to be risk factors, namely, tacrolimus blood concentration at the third and sixth post-transplantation months (8.7 ± 2.1 vs. 6.9 ± 3.2, p = 0.043; 9.2 ± 2.7 vs. 7.3 ± 3.8 p = 0.035, respectively).\n\nQuestion:\nIs higher tacrolimus blood concentration related to hyperlipidemia in living donor liver transplantation recipients?\n\nAnswer:",
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"content": "yes",
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nGemcitabine monotherapy is the standard palliative chemotherapy for pancreatic adenocarcinoma. Gemcitabine requires plasma membrane nucleoside transporter proteins to efficiently enter cells and exert it cytotoxicity. In vitro studies have demonstrated that deficiency of human equilibrative nucleoside transporter 1 (hENT1), the most widely abundant and distributed nucleoside transporter in human cells, confers resistance to gemcitabine toxicity, but the distribution and abundance of nucleoside transporters in normal and malignant pancreatic tissue is unknown. We studied tumor blocks from normal pancreas and 21 Alberta patients with gemcitabine-treated pancreatic cancer. Immunohistochemistry on the formalin-fixed, paraffin-embedded tissues was performed with specific hENT1 and human Concentrative Nucleoside Transporter 3 monoclonal antibodies and scored by a pathologist blinded to clinical outcomes. hENT1 was detected in normal Langerhan cells and lymphocytes but not in normal glandular elements. Patients in whom all adenocarcinoma cells had detectable hENT1 had significantly longer median survivals from gemcitabine initiation than those for whom hENT1 was absent in a proportion (10 to 100%) of adenocarcinoma cells (median survival, 13 versus 4 months, P = 0.01). Immunohistochemistry for human Concentrative Nucleoside Transporter 3 revealed moderate to high-intensity staining in all adenocarcinoma tissue samples.\n\nQuestion:\nIs the absence of human equilibrative nucleoside transporter 1 associated with reduced survival in patients with gemcitabine-treated pancreas adenocarcinoma?\n\nAnswer:",
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"content": "yes",
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMeasuring HbA1c blood levels allows us to assess average glycaemia in individuals during the preceding 6-8 weeks. There is a clear association between increasing risk of complications with higher HbA1c values and a significant risk reduction of the complications with lower HbA1c values. The performance of South African laboratories in an External Quality Assurance scheme for HbA1c is reported.\n\nQuestion:\nDoes evaluation of HbA1C result in an external quality assessment scheme in South Africa?\n\nAnswer:",
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe serine/threonine kinase Aurora-A (Aur-A) is a proto-oncoprotein overexpressed in a wide range of human cancers. Overexpression of Aur-A is thought to be caused by gene amplification or mRNA overexpression. However, recent evidence revealed that the discrepancies between amplification of Aur-A and overexpression rates of Aur-A mRNA were observed in breast cancer, gastric cancer, hepatocellular carcinoma, and ovarian cancer. We found that aggressive head and neck cancers exhibited overexpression and stabilization of Aur-A protein without gene amplification or mRNA overexpression. Here we tested the hypothesis that aberration of the protein destruction system induces accumulation and consequently overexpression of Aur-A in cancer. Aur-A protein was ubiquitinylated by APC(Cdh1) and consequently degraded when cells exited mitosis, and phosphorylation of Aur-A on Ser51 was observed during mitosis. Phosphorylation of Aur-A on Ser51 inhibited its APC(Cdh1)-mediated ubiquitylation and consequent degradation. Interestingly, constitutive phosphorylation on Ser51 was observed in head and neck cancer cells with protein overexpression and stabilization. Indeed, phosphorylation on Ser51 was observed in head and neck cancer tissues with Aur-A protein overexpression. Moreover, an Aur-A Ser51 phospho-mimetic mutant displayed stabilization of protein during cell cycle progression and enhanced ability to cell transformation.\n\nQuestion:\nDoes constitutive phosphorylation of aurora-a on ser51 induce its stabilization and consequent overexpression in cancer?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAs many as 20-30% of women report an inability to orgasm during sexual intercourse. Some female sexual problems have been reported to cluster with psychological and social problems. Underlying personality type may play a role in the development or maintenance of such problems. The aim of this study was to investigate whether certain domains of personality are associated with female coital orgasmic infrequency. To our knowledge this is the first such study in a large unselected population. A total of 2632 women (mean age 51) from the TwinsUK registry completed questionnaires relating to personality and sexual behavior. Personality domains were assessed using the validated Ten-Item Personality Index (TIPI). Coital orgasmic frequency was measured using a seven-point Likert scale. Using logistic regression, we investigated whether variations in five domains of personality are associated with female coital orgasmic infrequency. Discordant twin analysis was used to verify findings. Introversion (odds ratio [OR] 2.5, 95% confidence interval [CI] 1.7-3.7), emotional instability (OR 2.0, 95% CI 1.3-3.1), and not being open to new experience (OR 2.4, 95% CI 1.6-3.6) were significantly associated with orgasmic infrequency, whereas indices of agreeableness and conscientiousness were not significantly associated with orgasm frequency.\n\nQuestion:\nAre normal variations in personality associated with coital orgasmic infrequency in heterosexual women : a population-based study?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSevere burn injury leads to marked catabolism and decreased lean mass, which can impair healing. Anabolic agents can attenuate net catabolism. Our purpose was to determine whether the testosterone analog, oxandrolone, given during the acute post burn period decreased the degree of nitrogen loss and loss of body weight while also increasing the healing rate of a skin donor site. Patients with burns between 40% and 70% of body surface were studied. A randomized double-blinded placebo-controlled study design was used. Patients were given oxandrolone 20 mg/day (n = 11) or a placebo 20 mg/day (n = 9) beginning between days 2 and 3 post burn. Net nitrogen balance and the healing time of a standardized donor site were measured. Patients were monitored until transferred to a burn rehabilitation facility, an average time period of 33 +/- 9 days. Mean burn size was 49 +/- 8% for placebo and 53 +/- 9% of total body surface for the oxandrolone group. Smoke inhalation was present in approximately 50% of patients in both groups. All patients survived the burn injury. Net weight loss was 8 +/- 3.1 kg in the placebo group compared with 3 +/- 1.9 kg in the oxandrolone group, a statistically significant decrease. Net daily nitrogen loss over a 3-week period (days 7 to 28) was 13 +/- 4 g in placebo treated compared with 4 +/- 1.9 g for the oxandrolone group, a statistically significant decrease. The healing time of a standardized donor site, decreased from the placebo group value of 13 +/- 3 days to 9 +/- 2 days for oxandrolone treated patients, a significant improvement. No major liver dysfunction, or other complication attributable to an anabolic steroid was seen in either group.\n\nQuestion:\nDo the anticatabolic and wound healing effects of the testosterone analog oxandrolone after severe burn injury?\n\nAnswer:",
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"content": "yes",
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis study investigates the combined effects of gemcitabine and trabectedin (ecteinascidin 743) in two pancreatic cancer cell lines and proposes a pharmacodynamic (PD) model to quantify their pharmacological interactions. Effects of gemcitabine and trabectedin upon the pancreatic cancer cell lines MiaPaCa-2 and BxPC-3 were investigated using cell proliferation assays. Cells were exposed to a range of concentrations of the two drugs, alone and in combination. Viable cell numbers were obtained daily over 5 days. A model incorporating nonlinear cytotoxicity, transit compartments, and an interaction parameter ψ was used to quantify the effects of the individual drugs and combinations. Simultaneous fitting of temporal cell growth profiles for all drug concentrations provided reasonable cytotoxicity parameter estimates (the cell killing rate constant K max and the sensitivity constant KC50) for each drug. The interaction parameter ψ was estimated as 0.806 for MiaPaCa-2 and 0.843 for BxPC-3 cells, suggesting that the two drugs exert modestly synergistic effects.\n\nQuestion:\nDoes pharmacodynamic modeling of combined chemotherapeutic effects predict synergistic activity of gemcitabine and trabectedin in pancreatic cancer cells?\n\nAnswer:",
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"content": "yes",
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nNuclear factor-kappa B (NF-kappaB) is a transcription factor for a wide range of proinflammatory mediators while heat shock factor-1 (HSF-1) transcribes stress proteins that protect against cellular damage. Both are attractive therapeutic targets, undergoing investigation in other acute inflammatory conditions, such as sepsis. To evaluate the role of the transcription factors NF-kappaB and HSF-1 in human acute pancreatitis and their relationship to cytokine/chemokine production, disease severity and outcome. Twenty-four patients with acute pancreatitis and 12 healthy controls. Peripheral blood mononuclear cells were isolated. NF-kappaB and HSF-1 were measured by electrophoretic mobility shift assay. Soluble tumor necrosis factor (TNF) receptor II and interleukin-8 were measured by ELISA. Acute physiology scores (APS), APACHE II scores and final Atlanta designations of severity were also determined. Systemic NF-kappaB activation occurs in acute pancreatitis compared to healthy controls (P=0.004). However, there was no significant difference between those with mild and severe disease (P=0.685). Systemic activation of HSF-1 was observed in acute pancreatitis compared to healthy controls although this did not reach statistical significance (P=0.053). Activation, however, was greatest in those who had a final Atlanta designation of mild pancreatitis compared to those who had a severe attack of acute pancreatitis (P=0.036). Furthermore, HSF-1 was inversely correlated with acute physiology score (APS; r=-0.49, P=0.019) and APACHE II score (r=-0.47, P=0.026).\n\nQuestion:\nAre heat shock factor-1 and nuclear factor-kappaB systemically activated in human acute pancreatitis?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nBiomarkers of micronutrient status are needed to best define deficiencies and excesses of essential nutrients. We evaluated several supporting biomarkers of vitamin A status in Zambian children to determine whether any of the biomarkers were consistent with high liver retinol stores determined by using retinol isotope dilution (RID). A randomized, placebo-controlled, biofortified maize efficacy trial was conducted in 140 rural Zambian children from 4 villages. A series of biomarkers were investigated to better define the vitamin A status of these children. In addition to the assessment of total-body retinol stores (TBSs) by using RID, tests included analyses of serum carotenoids, retinyl esters, and pyridoxal-5'-phosphate (PLP) by using high-pressure liquid chromatography, retinol-binding protein by using ELISA, and alanine aminotransferase (ALT) activity by using a colorimetric assay. Children (n = 133) were analyzed quantitatively for TBSs by using RID. TBSs, retinyl esters, some carotenoids, and PLP differed by village site. Serum carotenoids were elevated above most nonintervened reference values for children. α-Carotene, β-carotene, and lutein values were >95th percentile from children in the US NHANES III, and 13% of children had hypercarotenemia (defined as total carotenoid concentration >3.7 μmol/L). Although only 2% of children had serum retinyl esters >10% of total retinol plus retinyl esters, 16% of children had >5% as esters, which was consistent with high liver retinol stores. Ratios of serum retinol to retinol-binding protein did not deviate from 1.0, which indicated full saturation. ALT activity was low, which was likely due to underlying vitamin B-6 deficiency, which was confirmed by very low serum PLP concentrations.\n\nQuestion:\nAre high provitamin A carotenoid serum concentrations , elevated retinyl esters , and saturated retinol-binding protein in Zambian preschool children consistent with the presence of high liver vitamin A stores?\n\nAnswer:",
"role": "user"
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"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo determine whether serum levels of 2 Wnt signaling antagonists, Frizzled-related protein (FRP) and Dkk-1, are associated with the development and progression of radiographic hip osteoarthritis (RHOA). Pelvic radiographs were obtained a mean of 8.3 years apart in 5,928 Caucasian women >or=65 years of age who were enrolled in the Study of Osteoporotic Fractures. Random sampling of this cohort was performed, with approximately 180 subjects per group assigned to 2 nested case-control studies on RHOA incidence and progression. Baseline serum levels of FRP and Dkk-1 were measured by capture enzyme-linked immunosorbent assay. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated using logistic regression analyses with adjustment for potential covariates. There were no differences in serum levels of FRP and Dkk-1 between case subjects with incidence or progression of RHOA and their respective control subjects. There was a trend for higher baseline serum levels of FRP to be associated with a reduced risk of incident RHOA (age-adjusted OR 0.59 [95% CI 0.32-1.09], P = 0.09 for women in the highest quartile versus women in the lowest quartile). There was no association of serum levels of FRP with progression of RHOA. Serum levels of Dkk-1 did not correlate with incident RHOA. However, higher serum levels of Dkk-1 were associated with diminished risk of RHOA progression (age-adjusted OR 0.43 [95% CI 0.23-0.79], P = 0.007 for women in the highest quartile compared with women in the lowest quartile).\n\nQuestion:\nAre wnt signaling antagonists potential prognostic biomarkers for the progression of radiographic hip osteoarthritis in elderly Caucasian women?\n\nAnswer:",
"role": "user"
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"content": "yes",
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMultidimensional impairment of older patients may influence the clinical outcome of diseases. The aim of this study was to evaluate whether a Multidimensional Prognostic Index (MPI) based on a comprehensive geriatric assessment predicts short-term mortality in older patients with heart failure. In this prospective study with a 1-month follow-up, 376 patients aged 65 and older with a diagnosis of heart failure were enrolled. A standardized comprehensive geriatric assessment that included information on functional (activities of daily living and instrumental activities of daily living), cognitive (Short Portable Mental Status Questionnaire), and nutritional status (Mini Nutritional Assessment), as well as on risk of pressure sore (Exton-Smith Scale), comorbidities (Cumulative Illness Rating Scale Index), medications, and social support network, was used to calculate the MPI for mortality using a previously validated algorithm. The New York Heart Association, the Enhanced Feedback for Effective Cardiac Treatment, and the Acute Decompensated Heart Failure National Registry regression model scores were also calculated. Higher MPI values were significantly associated with higher 30-day mortality, both in men (MPI-1, 2.8%; MPI-2, 15.3%; MPI-3, 47.4%; P=0.000) and women (MPI-1, 0%; MPI-2, 6.5%; MPI-3, 14.6%; P=0.011). The discrimination of the MPI was also good, with areas under the receiver operating characteristic curves (men: 0.83; 95% CI, 0.75 to 0.90; women: 0.80; 95% CI, 0.71 to 0.89) greater than receiver operating characteristic areas of New York Heart Association (men: 0.63; 95% CI, 0.57 to 0.69; P=0.015; women: 0.65; 95% CI, 0.55 to 0.75; P=0.064), Enhanced Feedback for Effective Cardiac Treatment (men: 0.69; 95% CI, 0.58 to 0.79; P=0.045; women: 0.71; 95% CI, 0.55 to 0.87; P=0.443), and Acute Decompensated Heart Failure National Registry scores (men: 0.65; 95% CI, 0.52 to 0.78; P=0.023; women: 0.67; 95% CI, 0.49 to 0.83, P=0.171).\n\nQuestion:\nDoes multidimensional Prognostic Index based on a comprehensive geriatric assessment predict short-term mortality in older patients with heart failure?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo investigate the mechanisms underpinning modifications in glucose homeostasis and insulin sensitivity 24 h after a bout of resistance exercise (RE) with or without protein ingestion. Twenty-four healthy males were assigned to a control (CON; n = 8), exercise (EX; n = 8) or exercise plus protein condition (EX+PRO; n = 8). Muscle biopsy and blood samples were obtained at rest for all groups and immediately post-RE (75% 1RM, 8×10 repetitions of leg-press and extension exercise) for EX and EX+PRO only. At 24 h post-RE (or post-resting biopsy for CON), a further muscle biopsy was obtained. Participants then consumed an oral glucose load (OGTT) containing 2 g of [U-¹³C] glucose during an infusion of 6, 6-[²H₂] glucose. Blood samples were obtained every 10 min for 2 h to determine glucose kinetics. EX+PRO ingested an additional 25 g of intact whey protein with the OGTT. A final biopsy sample was obtained at the end of the OGTT. Fasted plasma glucose and insulin were similar for all groups and were not different immediately post- and 24 h post-RE. Following RE, muscle glycogen was 26±8 and 19±6% lower in EX and EX+PRO, respectively. During OGTT, plasma glucose AUC was lower for EX and EX+PRO (75.1±2.7 and 75.3±2.8 mmol·L⁻¹∶120 min, respectively) compared with CON (90.6±4.1 mmol·L⁻¹∶120 min). Plasma insulin response was 13±2 and 21±4% lower for EX and CON, respectively, compared with EX+PRO. Glucose disappearance from the circulation was ∼12% greater in EX and EX+PRO compared with CON. Basal 24 h post-RE and insulin-stimulated PAS-AS160/TBC1D4 phosphorylation was greater for EX and EX+PRO.\n\nQuestion:\nAre beneficial effects of resistance exercise on glycemic control further improved by protein ingestion?\n\nAnswer:",
"role": "user"
},
{
"content": "no",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nElevated low density lipoproteins (LDL)-cholesterol and homocysteine levels have both been found to be associated with an increased risk for atherosclerotic vascular disease. To assess the effects of elevated homocysteine levels in hypercholesterolemic subjects on endothelial function, we examined basal and stimulated nitric oxide (NO) mediated vasodilation in the forearm vascular bed in hypercholesterolemic subjects with normal or elevated homocysteine levels. Twenty-seven white subjects (age: 48 +/- 12 years) with elevated LDL-cholesterol (> or = 160 mg/dl) were divided into two groups with normal (n = 11) or mildly elevated (n = 16) homocysteine plasma concentration. We used strain gauge plethysmography to measure changes in forearm blood flow in response to intraarterial administration of increasing doses of acetylcholine (3, 12, 24, 48 microg/min), sodium nitroprusside (200, 800, 3200 ng/min), and N-monomethyl L-arginine (L-NMMA) (1, 2, 4 micromol/min). Total homocysteine plasma concentrations were determined by high performance liquid chromatography fluorimetry. Endothelium independent vascular relaxation tested by i.a. sodium nitroprusside and changes in forearm blood flow after i.a. L-NMMA indicating basal production and release of nitric oxide were similar between the two groups with normal or elevated homocysteine levels. In contrast, endothelium dependent vasodilation as assessed by the administration of i.a. acetylcholine differed between the groups with normal or elevated homocysteine levels for all doses tested (MANOVA P < 0.01: ACH 48 microg/min: 480 +/- 237% with normal vs 234 +/- 130% with elevated homocysteine; P < 0.002). This was significant even after taking possible covariates such as age, blood pressure, body mass index, LDL-, high density lipoproteins (HDL)-cholesterol, and trigylcerides into account (MANOVA P < 0.02).\n\nQuestion:\nDo mildly elevated homocysteine concentrations impair endothelium dependent vasodilation in hypercholesterolemic patients?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe TM4SF10 gene encodes a putative four-transmembrane domains protein of unknown function termed Brain Cell Membrane Protein 1 (BCMP1), and is abundantly expressed in the brain. This gene is located on the short arm of human chromosome X at p21.1. The hypothesis that mutations in the TM4SF10 gene are associated with impaired brain function was investigated by sequencing the gene in individuals with hereditary X-linked mental retardation (XLMR). The coding region (543 bp) of TM4SF10, including intronic junctions, and the long 3' untranslated region (3 233 bp), that has been conserved during evolution, were sequenced in 16 male XLMR patients from 14 unrelated families with definite, or suggestive, linkage to the TM4SF10 gene locus, and in 5 normal males. Five sequence changes were identified but none was found to be associated with the disease. Two of these changes correspond to previously known SNPs, while three other were novel SNPs in the TM4SF10 gene.\n\nQuestion:\nDoes tM4SF10 gene sequencing in XLMR patients identify common polymorphisms but no disease-associated mutation?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo investigate the incidence of major adverse cardiac events (MACEs) after discharge from the emergency department (ED) with unspecified chest pain and the predictive value of cardiovascular risk factors included in HEART score. This was a register-based retrospective cohort study including all patients discharged with the diagnosis 'unspecified chest pain' from Swedish EDs between 2006-2013. Diagnosis and drug prescriptions were collected from national registers and the association to the occurrence of MACE was studied with logistic regression and category-free net reclassification improvement (cNRI). Out of 74,329 included patients 619 (0.8%) experienced MACE within 30 days of discharge from the ED. Hypertension (odds ratio (OR) 4.74, 95% confidence interval (CI) 4.02-5.59), diabetes mellitus (3.76, 3.10-4.57), hyperlipidaemia (1.92, 1.51-2.44), and earlier cardiovascular disease (CVD) were all associated with MACE. The addition of hypertension to a risk factor model improved net reclassification (cNRI 53%, 95% CI 29-67%). The variables age (A) (1 point OR 7.01, 95% CI 4.79-10.26, 2 points OR 23.57, 95% CI 16.35-33.97) and risk factors (R) (1 point OR 3.76, 95% CI 3.05-4.63, 2 points OR 10.94, 95% CI 8.96-13.38) in HEART score were both independently associated with MACE with a combination area under the curve (AUC) of 0.8.\n\nQuestion:\nDoes hypertension predict major adverse cardiac events after discharge from the emergency department with unspecified chest pain?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHigh-dose therapy (HDT) is currently under investigation for patients with advanced low-grade non-Hodgkin lymphoma (NHL). We report on the toxicity of a modified HDT that combines total-body irradiation (TBI) with involved-field irradiation (IF-RT) for patients with bulky disease or residual lymphomas > 2 cm after induction chemotherapy. 41 patients received HDT which consisted of high-dose cyclophosphamide and fractionated TBI (6 x 2 Gy) followed by autologous stem cell transplantation. Eleven patients received IF-RT prior to TBI, three patients had already received another radiotherapy treatment prior to HDT. After a medium follow-up of 19 months we observed an overall survival rate of 100%, and a relapse-free survival rate of 78%. Severe toxicity was observed only in one patient who developed a myelodysplastic syndrome, and another patient who showed signs of pneumonitis. About two thirds of the patients claimed minor toxicity of grade I-II according the LENT-SOMA scale, predominantly as a decrease in concentration, reduced sexual functioning, and musculo-skeletal pain. Correspondingly, laboratory tests showed grade I-II changes of blood counts, liver enzymes, hormone levels, and lung function. There was no excess toxicity in the patients who received IF-RT additional to TBI.\n\nQuestion:\nDoes involved-field irradiation in combination with total-body irradiation ( TBI ) increase short-term toxicity compared to TBI alone in patients with advanced-stage low-grade non-Hodgkin lymphoma?\n\nAnswer:",
"role": "user"
},
{
"content": "no",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo evaluate the effect of hyperbaric oxygen therapy (HBOT) on superoxide dismutase 2 (SOD2) expression pattern after the cortical stab injury (CSI). CSI was performed on 88 male Wistar rats, divided into control, sham, lesioned, and HBO groups. HBOT protocol was the following: pressure applied was 2.5 absolute atmospheres, for 60 minutes, once a day for consecutive 3 or 10 days. The pattern of SOD2 expression and cellular localization was analyzed using real-time polymerase chain reaction, Western blot, and double-label fluorescence immunohistochemistry. Neurons undergoing degeneration were visualized with Fluoro-Jade®B. CSI induced significant transient increase in SOD2 protein levels at day 3 post injury, which was followed by a reduction toward control levels at post-injury day 10. At the same time points, mRNA levels for SOD2 in the injured cortex were down-regulated. Exposure to HBO for 3 days considerably down-regulated SOD2 protein levels in the injured cortex, while after 10 days of HBOT an up-regulation of SOD2 was observed. HBOT significantly increased mRNA levels for SOD2 at both time points compared to the corresponding L group, but they were still lower than in controls. Double immunofluorescence staining revealed that 3 days after CSI, up-regulation of SOD2 was mostly due to an increased expression in reactive astrocytes surrounding the lesion site. HBOT attenuated SOD2 expression both in neuronal and astroglial cells. Fluoro-Jade®B labeling showed that HBOT significantly decreased the number of degenerating neurons in the injured cortex.\n\nQuestion:\nDoes hyperbaric oxygenation alter temporal expression pattern of superoxide dismutase 2 after cortical stab injury in rats?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nA variety of surgical approaches used to treat primary oral cavity tumors are described to delineate the technique and rationale behind each treatment choice. Size, location, proximity to bone, lymph node status, histology, and prior treatment considerations are employed to determine the most appropriate surgical approach for primary oral cavity tumors. Oncologic outcomes and physical function show the best results from surgical treatment of many primary oral cavity, but necessitates careful selection of surgical approach.\n\nQuestion:\nDoes surgical approach to the oral cavity primary and neck?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCoeliac disease is an autoimmune enteropathy characterized by an enhanced permeability of the intestinal epithelial barrier. In epithelial cells paracellular permeability is regulated by intercellular tight junction. The cytoplasmic protein ZO-1 interacts directly with F-actin and plays a pivotal role in the structural and functional organization of tight junction. The aim of this study was to investigate the expression and localization of ZO-1 in the intestinal mucosa of coeliac patients. Twenty patients with active coeliac disease, seven of whom underwent a repeat biopsy following a gluten-free diet and 27 control subjects, were studied. In all subjects, three biopsies were obtained from distal duodenum during upper gastrointestinal endoscopy. ZO-1 protein localization and levels were detected by immunofluorescence followed by confocal microscopy analysis and immunoblotting. ZO-1 mRNA expression was assessed by RT-PCR. F-actin distribution was also investigated. In patients with active coeliac disease, both ZO-1 protein levels and mRNA were clearly reduced. Cytoskeletal organization was disrupted with F-actin staining concentrated at the subcortical and basal surface regions. Abnormalities in ZO-1 expression and actin organization were reversed after a gluten-free diet.\n\nQuestion:\nIs transcriptional downregulation of tight junction protein ZO-1 in active coeliac disease reversed after a gluten-free diet?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nRecent observational studies have shown therapeutic benefits of acetylsalicylic acid (ASA) in several types of cancer. We examined whether ASA exerts antitumor activity in esophageal adenocarcinoma (EAC). Human EAC cells (OE33) were treated with ASA (0-5 mM) to evaluate proliferation, apoptosis, and migration. In vivo model: OE33-derived tumors were subcutaneously implanted into athymic mice which were allocated to ASA (5 or 50 mg/kg/day)/vehicle (5-6 animals/group). Tumor growth was assessed every 2-3 days, and after 40 days, mice were euthanized. Plasma drug levels were determined by high-performance liquid chromatography. Histological and immunohistochemical (Ki67, activated caspase-3) analysis of tumors were performed. The effect of ASA on tumor prostaglandin E2 (PGE2) levels was also evaluated. In vitro cell proliferation and migration were significantly inhibited while apoptosis increased (p < 0.05) by ASA. Although ASA did not induce tumor remission, tumor progression was significantly lower in ASA-treated mice when compared to non-treated animals (478 % in mice treated with 5 mg/kg/day ASA vs. 2696 % control; 748 % in mice treated with 50 mg/kg/day ASA vs. 2670 % control). Maximum tumor inhibition was 92 and 85 %, respectively. This effect was associated with a significant decrease of proliferation index in tumors. ASA 5 mg/kg/day did not modify tumor PGE2 levels. Whereas tumor PGE2 content in mice treated with ASA 50 mg/kg was lower than in control mice, the difference was not significant.\n\nQuestion:\nDoes acetylsalicylic Acid exhibit Antitumor Effects in Esophageal Adenocarcinoma Cells In Vitro and In Vivo?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nConditional gene activation is an efficient strategy for studying gene function in genetically modified animals. Among the presently available gene switches, the tetracycline-regulated system has attracted considerable interest because of its unique potential for reversible and adjustable gene regulation. To investigate whether the ubiquitously expressed Gt(ROSA)26Sor locus enables uniform DOX-controlled gene expression, we inserted the improved tetracycline-regulated transcription activator iM2 together with an iM2 dependent GFP gene into the Gt(ROSA)26Sor locus, using gene targeting to generate ROSA26-iM2-GFP (R26t1Δ) mice. Despite the presence of ROSA26 promoter driven iM2, R26t1Δ mice showed very sparse DOX-activated expression of different iM2-responsive reporter genes in the brain, mosaic expression in peripheral tissues and more prominent expression in erythroid, myeloid and lymphoid lineages, in hematopoietic stem and progenitor cells and in olfactory neurons.\n\nQuestion:\nDoes tetracycline-controlled transgene activation using the ROSA26-iM2-GFP knock-in mouse strain permit GFP monitoring of DOX-regulated transgene-expression?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo study the action mechanism of a Chinese herbal mixture PC-SPES II inducing the apoptosis of androgen independent prostate adenocarcinoma cell line (PC-3). The growth of PC-3 was shown by MTT. Immunofluorescence staining of acridine orange (AO) and flow cytometry were used to detect the apoptosis. The expressions of the apoptosis-related proteins were analyzed with their monoclonal or polyclonal antibodies after Western blotting. PC-SPES II not only inhibited the growth of PC-3 cells but also induced their death. The apoptosis of PC-3 cells treated with PC-SPES II was detected by immunofluorescence staining of AO and flow cytometry, which showed the apoptotic cells to be (29.8 +/- 5.6)%, but the untreated control cells (0.06 +/- 0.014)%, (P < 0.01). The expression of Bcl-2 and Bcl-xL, two antiapoptosis proteins, was decreased while Bax, a pro apoptosis protein, was elevated in the cells treated with PC-SPES II as compared with the untreated control (P < 0.01). Accordingly, the expression of the activated fragments of caspase-3 was also increased (P < 0.01).\n\nQuestion:\nDoes [ Chinese herbal medicine PC-SPES II induce the apoptosis of androgen-independent prostate carcinoma cell line PC-3 ]?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nRodent alpha(2A)-adrenoceptors bind the classical alpha(2)-antagonists yohimbine and rauwolscine with lower affinity than the human alpha(2A)-adrenoceptor. A serine-cysteine difference in the fifth transmembrane helix (TM; position 5.43) partially explains this, but all determinants of the interspecies binding selectivity are not known. Molecular models of alpha(2A)-adrenoceptors suggest that the second extracellular loop (XL2) folds above the binding cavity and may participate in antagonist binding. Amino acids facing the binding cavity were identified using molecular models: side chains of residues 5.43 in TM5 and xl2.49 and xl2.51 in XL2 differ between the mouse and human receptors. Reciprocal mutations were made in mouse and human alpha(2A)-adrenoceptors at positions 5.43, xl2.49 and xl2.51, and tested with a set of thirteen chemically diverse ligands in competition binding assays. Reciprocal effects on the binding of yohimbine and rauwolscine in human and mouse alpha(2A)-adrenoceptors were observed for mutations at 5.43, xl2.49 and xl2.51. The binding profile of RS-79948-197 was reversed only by the XL2 substitutions.\n\nQuestion:\nDoes the second extracellular loop of alpha2A-adrenoceptors contribute to the binding of yohimbine analogues?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nProcurement of coagulation factor concentrates (CFCs) for the treatment of haemophilia is a vital process that determines the quantity and quality of factor replacement therapy. The aim of this study was to examine the different tender and procurement systems used in Europe for the procurement of CFCs and the outcomes produced by the various systems. The survey questionnaire consisted of 30 items and explored various aspects of the procurement process including the prices of CFCs. In 2014, the survey was sent out by the European Haemophilia Consortium (EHC) to 45 national haemophilia patient organizations affiliated to the EHC in all European countries as well as to a designated clinician familiar with the procurement process. The survey was completed by 38 European countries. Nineteen countries use a tender process, 17 an alternative procurement process and 2 use a combination of methods. A wide variety of agencies and individuals are involved in the process. Factors associated with optimum outcome and lower prices include a tender process with a specific legal framework and a tender board including haemophilia clinicians and patient organization representatives. Safety was reported as the most important selection criterion but given the safety profile of almost all currently licensed products, price was the main criterion used in many countries.\n\nQuestion:\nDoes survey of coagulation factor concentrate tender and procurement procedures in 38 European Countries?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAlthough survival rates have improved for patients receiving implantable continuous flow left ventricular assist devices (I-CF LVAD), postoperative exercise tolerance levels are not necessarily satisfactory. We enrolled 51 patients who had received an I-CF LVAD and underwent follow-up between 2006 and 2014; all patients underwent cardiopulmonary exercise testing 3 months following surgery: 26 (51%) patients achieved peak oxygen consumption (PV̇O2) ≥14 ml·kg(-1)·min(-1)and had significantly lower readmission rates for cardiovascular events than those with PV̇O2<14 ml·kg(-1)·min(-1)during 2 years of LVAD treatment (17 vs. 43%, P=0.033). Uni- and multivariate logistic regression analyses showed that the preoperative serum albumin (S-ALB) level was an independent predictor for PV̇O2≥14 ml·kg(-1)·min(-1)at 3 months (P=0.023, odds ratio 6.132). Patients with persistently normal S-ALB levels during the perioperative period had the lowest preoperative serum C-reactive protein level (S-CRP, 0.7±0.9 mg/dl), and the majority (77%) showed improved exercise tolerance. Conversely, patients with persistently low S-ALB levels during this period had the highest preoperative S-CRP level (2.8±1.2 mg/dl) and did not achieve the test endpoint.\n\nQuestion:\nDoes perioperative Hypoalbuminemia affect Improvement in Exercise Tolerance After Left Ventricular Assist Device Implantation?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTraumatic events in early life are associated with an increased risk of psychiatric diseases in adulthood. 5-hydroxytryptamine (5-HT)(1A) receptors play a pivotal role in the 5-HTergic mechanisms associated with the etiology of stress-related disorders. The goal of the present study was to investigate whether juvenile stress influences emotional control via postsynaptic 5-HT(1A) receptor in the hippocampus and amygdala using contextual fear conditioning test in adult rats. The rats were subjected to aversive footshock (FS) during the third week of the postnatal period (3wFS group). During the postadolescent period (10-14 weeks postnatal), experiments were performed. The systemic administration of the 5-HT(1A) receptor agonist R-(+)-8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) (0.2 mg/kg, i.p.) attenuated the freezing behavior in the non-FS group, but not in the 3wFS group. The bilateral local injection of 8-OH-DPAT (1 μg/side) into the amygdala decreased the freezing behavior in the non-FS group and the 3wFS group. However, the local injection of 8-OH-DPAT (1 μg/side) into the hippocampus decreased the freezing behavior in the non-FS group, but not in the 3wFS group. In a 5-HT(1A) receptor binding study, the Bmax of the 3wFS group decreased in the dorsal hippocampus, but not the amygdala in comparison with the non-FS group.\n\nQuestion:\nDoes juvenile stress attenuate the dorsal hippocampal postsynaptic 5-HT1A receptor function in adult rats?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nJAK2V617F occurs in approximately 93% of patients with polycythemia vera and approximately 50% of patients with either primary myelofibrosis or essential thrombocythemia. Chromosomal abnormalities are detected in 50% of patients with primary myelofibrosis, 29% with polycythemia vera, and 8% to 10% with essential thrombocythemia. The relationship between the presence of such chromosomal abnormalities and the JAK2V617 allele burden, and the role that each of these genetic events play in the origins and progression of the myeloproliferative neoplasms (MPNs), remain unclear. Individual hematopoietic colonies were assayed in vitro from the CD34(+) cells of six JAK2V617F-positive MPN patients with marker chromosomal abnormalities. Colonies were simultaneously analyzed for JAK2 genotype and chromosomal abnormalities. Among the 248 colonies assayed from cultures containing 500 CD34(+) cells, chromosomal abnormalities were detected in 5% of colonies with wild-type JAK2, 32% of JAK2V617F heterozygous colonies and 56% of JAK2V617F homozygous colonies. Overall, 92% of chromosomally abnormal colonies were also JAK2V617F homozygous. Although 54 colonies contained wild-type JAK2 exclusively, 4 of these colonies were characterized by chromosomal abnormalities.\n\nQuestion:\nDo clonal analyses define the relationships between chromosomal abnormalities and JAK2V617F in patients with Ph-negative myeloproliferative neoplasms?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMethamphetamine use disorders (MUD) are associated with severe health effects and psychiatric comorbidities, but little is known about the health care utilization of patients with MUD. The goal of this study was to describe health service use among veterans with MUD relative to a group of veterans with an alcohol use disorder (AUD). Using Veterans Affairs (VA) administrative data, we identified 718 patients who were diagnosed with MUD and had confirmatory drug testing. Data were compared with those of 744 patients who had diagnoses of an AUD also with confirmatory testing. We examined diagnoses and medical utilization for 5 years after their index date. Patients with MUD and laboratory-confirmed recent use were younger and more likely to be diagnosed with a mood disorder, posttraumatic stress disorder, and a psychotic-spectrum disorder (all P values < 0.05). After statistical controls, patients with MUD were more likely to have an inpatient hospitalization (80% vs 70%, odds ratio [OR] = 1.8; 95% confidence interval [CI] = 1.4-2.3), discharge from an inpatient admission against medical advice (23.4% vs 8.3%, OR = 2.6, 95% CI = 1.9-3.7), receive care at 3 or more VA medical centers (13.1% vs 5.4%, OR = 2.3, 95% CI = 1.5-3.5), have a behavioral flag in the medical record (5.6% vs 1.1%, OR = 4.6, 95% CI = 2.1-10.6), and have more total missed appointments in the 5-year study period (M = 33.1 vs M = 23.5, P < 0.001).\n\nQuestion:\nDo comparison of health service use among veterans with methamphetamine versus alcohol use disorders?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nOver the years, en bloc spondylectomy has proven its efficacy in controlling spinal tumors and improving survival rates. However, there are few reports of large series that critically evaluate the results of multilevel en bloc spondylectomies for spinal neoplasms. Using data from a large spine tumor center, we answered the following questions: (1) Does multilevel total en bloc spondylectomy result in acceptable function, survival rates, and local control in spinal neoplasms? (2) Is reconstruction after this procedure feasible? (3) What complications are associated with this procedure? (4) is it possible to achieve adequate surgical margins with this procedure? We retrospectively investigated 38 patients undergoing multilevel total en bloc spondylectomy by a single surgeon (AL) from 1994 to 2011. Indications for this procedure were primary spinal sarcomas, solitary metastases, and aggressive primary benign tumors involving multiple segments of the thoracic or lumbar spine. Patients had to be medically fit and have no visceral metastases. Analysis was by chart and radiographic review. Margin quality was classified into intralesional, marginal, and wide. Radiographs, MR images, and CT scans were studied for local recurrence. Graft healing and instrumentation failures at subsequent followup were assessed. Complications were divided into major or minor and further classified as intraoperative and early and late postoperative. We evaluated the oncologic status using cumulative disease-specific and metastases-free survival analysis. Minimum followup was 24 months (mean, 39 months; range, 24-124 months). Of the 38 patients, 34 (89%) were alive and walking without support at final followup. Thirty-one (81%) had no evidence of disease. Two patients died postoperatively and another two died of systemic disease (without local recurrence). Only three patients (8%) had a local recurrence. There were 14 major complications and 22 minor complications in 25 patients (65%). Only one patient required revision of implants secondary to mechanical failure. Two cases of cage subsidence were noted but had no clinical significance. Wide margins were achieved in nine patients (23%), marginal in 25 (66%), and intralesional in four (11%).\n\nQuestion:\nIs multilevel en bloc spondylectomy for tumors of the thoracic and lumbar spine challenging but rewarding?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAmiloride derivatives, commonly used for their diuretic and antihypertensive properties, can also cause a sustained but reversible decrease of intracellular pH (pHi). Using dimethyl amiloride (DMA) on normal rodent pancreatic islets, we previously demonstrated the critical influence of islet pHi on insulin secretion. Nutrient-stimulated insulin secretion (NSIS) requires a specific pHi-range, and is dramatically enhanced by forced intracellular acidification with DMA. Furthermore, DMA can enable certain non-secretagogues to stimulate insulin secretion, and induce time-dependent potentiation (TDP) of insulin release in mouse islets where this function is normally absent. The present study was performed to determine whether pHi-manipulation could correct the secretory defect in islets isolated from mice with type 2 diabetes. Using two mouse models of type 2 diabetes, we compared a) pHi-regulation, and b) NSIS with and without treatment with amiloride derivatives, in islets isolated from diabetic mice and wild type mice. A majority of the islets from the diabetic mice showed a slightly elevated basal pHi and/or poor recovery from acid/base load. DMA treatment produced a significant increase of NSIS in islets from the diabetic models. DMA also enabled glucose to induce TDP in the islets from diabetic mice, albeit to a lesser degree than in normal islets.\n\nQuestion:\nDo amiloride derivatives enhance insulin release in pancreatic islets from diabetic mice?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
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] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nChronic Myeloid Leukaemia (CML) is caused by the BCR/ABL1 fusion gene. Both the presence and the levels of BCR/ABL1 expression seem to be critical for CML progression from chronic phase (CP) to blast crisis (BC). After the oncogenic translocation, the BCR/ABL1 gene is under the transcriptional control of BCR promoter but the molecular mechanisms involved in the regulation of oncogene expression are mostly unknown. A region of 1443bp of the functional BCR promoter was studied for transcription factor binding sites through in-silico analysis and Chromatin Immunoprecipitation experiments. BCR and BCR/ABL1 expression levels were analysed in CML cell lines after over-expression or silencing of MYC transcription factor. A luciferase reporter assay was used to confirm its activity on BCR promoter. In the present study we demonstrate that MYC and its partner MAX bind to the BCR promoter, leading to up-regulation of BCR and BCR/ABL1 at both transcriptional and protein levels. Accordingly, silencing of MYC expression in various BCR/ABL1 positive cell lines causes significant downregulation of BCR and BCR/ABL1, which consequently leads to decreased proliferation and induction of cell death.\n\nQuestion:\nAre bCR/ABL1 and BCR under the transcriptional control of the MYC oncogene?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nBone marrow-derived mesenchymal stem cells (BMSCs) can reduce liver fibrosis. Apart from the paracrine mechanism by which the antifibrotic effects of BMSCs inhibit activated hepatic stellate cells (HSCs), the effects of direct interplay and juxtacrine signaling between the two cell types are poorly understood. The purpose of this study was to explore the underlying mechanisms by which BMSCs modulate the function of activated HSCs. We used BMSCs directly and indirectly co-culture system with HSCs to evaluate the anti-fibrosis effect of BMSCs. Cell proliferation and activation were examined in the presence of BMSCs and HGF. c-met was knockdown in HSCs to evaluate the effect of HGF secreted by BMSCs. The TLR4 and Myeloid differentiation primary response gene 88(MyD88) mRNA levels and the NF-kB pathway activation were determined by real-time PCR and western blotting analyses. The effect of BMSCs on HSCs activation was investigated in vitro in either MyD88 silencing or overexpression in HSCs. Liver fibrosis in rats fed CCl(4) with and without BMSCs supplementation was compared. Histopathological examinations and serum biochemical tests were compared between the two groups. BMSCs remarkably inhibited the proliferation and activation of HSCs by interfering with LPS-TLR4 pathway through a cell-cell contact mode that was partially mediated by HGF secretion. The NF-kB pathway is involved in HSCs activation inhibition by BMSCs. MyD88 over expression reduced the BMSC inhibition of NF-kB luciferase activation. BMSCs protected liver fibrosis in vivo.\n\nQuestion:\nDo hGF and direct mesenchymal stem cells contact synergize to inhibit hepatic stellate cells activation through TLR4/NF-kB pathway?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo establish three-dimension finite element model of mandible with two kinds of Replace implant, and to study stress of implant and abutment. The data of components of the dental implant was measured, cross section of the mandible was scanned by spiral CT and image reconstruction technique was conducted. Three-dimension finite element analysis software UG and MSC. Marc/Mentat were used to built the conjunction model and bone model of two implant systems. Axial loading (200N) and 30 degrees oblique loading (100N) were applied on the models respectively, the stress distribution patterns of the implant and abutment of two implant systems were analyzed. The peak stress district was concentrated on the structure of the implant cervix, which was more obviously displayed on the Replace Select implant. The peak stress of oblique loading was higher than that of axial loading. The peak stress on the implant cervix of Replace Select implant was higher than that of Replace External Hex implant in all loadings.\n\nQuestion:\nDo [ Three-dimension finite element analyses of interior stress of two kinds of Replace implant ]?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPulmonary fibrosis is a progressive disease with only few treatment options available at the moment. Recently, the nucleoside uridine has been shown to exert anti-inflammatory effects in different animal models, e.g. in acute lung injury or bronchial asthma. Therefore, we investigated the influence of uridine supplementation on inflammation and fibrosis in the classical bleomycin model. Male C57BL/6 mice received an intratracheal injection of bleomycin on day 0 and were treated intraperitoneally with uridine or vehicle. The degree of inflammation and fibrosis was assessed at different time points. Uridine administration resulted in attenuated inflammation, as demonstrated by reduced leukocytes and pro-inflammatory cytokines in the broncho-alveolar lavage (BAL) fluid. Furthermore, collagen deposition in the lung interstitium was also reduced by uridine supplementation. Similar results were obtained in a model in which animals received repeated intraperitoneal bleomycin injections. In addition uridine inhibited collagen and TGF-ß synthesis by primary lung fibroblasts, the release of pro-inflammatory cytokines by human lung epithelial cells, as well as the production of reactive oxygen species by human neutrophils.\n\nQuestion:\nDoes uridine supplementation exert anti-inflammatory and anti-fibrotic effects in an animal model of pulmonary fibrosis?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
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] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
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{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe role of polymorphonuclear neutrophils in pulmonary host defense is well recognized. The influence of a pre-existing inflammation driven by neutrophils (neutrophilic inflammation) on the airway epithelial response toward pro-inflammatory exogenous triggers, however, is still poorly addressed. Therefore, the aim of the present study is to investigate the effect of neutrophils on lipopolysaccharide (LPS)-induced pro-inflammatory signaling in lung epithelial cells. Additionally, underlying signaling pathways are examined. Human bronchial epithelial cells (BEAS-2B) were co-incubated with human peripheral blood neutrophils or bone-marrow derived neutrophils from either C57BL/6J wild type or nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase deficient (p47(phox-/-)) mice. Upon stimulation with LPS, interleukin (IL)-8 production and reactive oxygen species (ROS) generation were measured. Additionally, activation of the extracellular signal-regulated kinases (ERK) 1/2 and nuclear factor (NF)-κB signaling pathways was analyzed. Our studies show that the presence of neutrophils synergistically increases LPS-induced IL-8 and ROS production by BEAS-2B cells without inducing cytotoxicity. The observed IL-8 response to endotoxin increases in proportion to time, LPS-concentration and the number of neutrophils present. Moreover, this synergistic IL-8 production strongly correlated with the chemotactic properties of the co-incubations and significantly depended on a functional neutrophilic NADPH oxidase. The presence of neutrophils also augments LPS-induced phosphorylation of ERK1/2 and IκBα as well as NF-κB RelA DNA binding activity in BEAS-2B cells.\n\nQuestion:\nDo neutrophils augment LPS-mediated pro-inflammatory signaling in human lung epithelial cells?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe occurrence of inflammatory bowel disease (IBD) is higher in Western countries and is increasing worldwide. The incidence of IBDs is about nearly 20-fold in Western countries than Asia and has risen in Taiwan over the past few decades. Epidemiological studies have demonstrated an increased risk of colorectal cancer (CRC) in patients with IBD. The prevalence of IBD as well as IBD-associated CRC is changing and the risk of CRC in patients with IBD appears to be greater in Western countries, but CRC risk in IBD patients is less well understood in low endemic areas, such as Asia. This population-based cohort study collected data from the Taiwan Health Insurance Research Database (from January 1998 to December 2011). In total, 10 650 patients with confirmed diagnosis of IBD served as the IBD cohort and 42 600 non-IBD subjects were enrolled. Cox proportional hazards regression was used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) were used to assess the risk of CRC. The incidence of CRC was slightly lower in the IBD cohort compared with that in the non-IBD cohort (0.94 vs. 1.13 per 1000 person-years), with an adjusted HR of 0.99 (95% CI: 0.71-1.37). More than four hospitalizations were associated with a significantly higher risk of CRC in IBD patients in the Cox model (adjusted HR = 3.48, 95% CI: 1.59-7.63).\n\nQuestion:\nIs the risk of colorectal cancer related to frequent hospitalization of IBD in an Asian population : results from a nationwide study?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nOropharyngeal dysphagia is an important disability that occurs after stroke; it contributes to aspiration pneumonia and death, and current modalities for rehabilitation of dysphagia have uncertain efficacy. We therefore examined the role of pharyngeal electrical stimulation (PES) in expediting human swallowing recovery after experimental (virtual) and actual (stroke) brain lesions. First, healthy subjects (n = 13) were given 1-Hz repetitive transcranial magnetic stimulation to induce a unilateral virtual lesion in pharyngeal motor cortex followed by active or sham (control) PES. Motor-evoked potentials and swallow accuracy were recorded before and after the lesion to assess PES response. Thereafter, 50 acute dysphagic stroke patients underwent either a dose-response study, to determine optimal parameters for PES (n = 22), or were assigned randomly to groups given either active or sham (control) PES (n = 28). The primary end point was the reduction of airway aspiration at 2 weeks postintervention. In contrast to sham PES, active PES reversed the cortical suppression induced by the virtual lesion (F(7,70) = 2.7; P = .015) and was associated with improvement in swallowing behavior (F(3,42) = 5; P = .02). After stroke, 1 PES treatment each day (U = 8.0; P = .043) for 3 days (U = 10.0) produced improved airway protection compared with controls (P = .038). Active PES also reduced aspiration (U = 54.0; P = .049), improved feeding status (U = 58.0; P = .040), and resulted in a shorter time to hospital discharge (Mantel-Cox log-rank test, P = 0.038).\n\nQuestion:\nDoes adjunctive functional pharyngeal electrical stimulation reverse swallowing disability after brain lesions?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAseptic abscesses syndrome (AA) is an inflammatory disease in which non-infectious deep abscesses develop; these respond quickly to corticosteroids. AA is associated with Crohn disease (CD) in 57% of cases and with neutrophilic dermatosis (ND) in 20%. Pyoderma gangrenosum is usually a sporadic ND. A hereditary autosomal dominant syndromic kind of pyoderma gangrenosum, the PAPA syndrome, is linked to mutations in the CD2BP1/PSTPIP1 gene. We systematically screened this gene in French AA patients. One microsatellite (CCTG)n with 3 alleles was identified in the promoter. The longest form (CCTG)7 was significantly more frequent in AA patients than in French controls (P = 0.0154). We also found an association of the (CCTG)7 allele with CD in French patients (P = 0.0351). This association was not found in a sample of Indian patients.\n\nQuestion:\nIs longest form of CCTG microsatellite repeat in the promoter of the CD2BP1/PSTPIP1 gene associated with aseptic abscesses and with Crohn disease in French patients?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAcute liver failure (ALF) is a syndrome characterized by an intense systemic inflammatory response (SIRS) and multi-organ system failure (MOSF). Platelet-derived microparticles increase in proportion to the severity of the SIRS and MOSF, and are associated with poor outcome. We investigated whether patients with ALF develop thrombocytopenia in proportion to the SIRS, MOSF, and poor outcome. In a retrospective study, we collected data on the post-admission platelet counts of 1598 patients included in the ALF Study Group Registry from 1998 through October 2012. We investigated correlations between platelet counts and clinical features of ALF, laboratory test results, and outcomes. Of the patients studied, 752 (47%) survived without liver transplantation, 390 (24%) received liver transplants, and 517 (32%) died. In patients with SIRS, platelet counts decreased 2 to 7 days after admission, compared with patients without SIRS (P ≤ .001). Patients with abnormal levels of creatinine, phosphate, lactate, or bicarbonate had significantly lower platelet counts than patients with normal levels of these laboratory values (all P ≤ .001). The decrease in platelets during days 1 to 7 after admission was proportional to the grade of hepatic encephalopathy and requirement for vasopressor and renal replacement therapy. Although platelet numbers decreased after admission in the overall population, platelets were significantly lower 2 to 7 days after admission in patients with outcomes of death or liver transplantation than in patients who made spontaneous recoveries and survived. In contrast, international normalized ratios over time were not associated with SIRS, laboratory test results associated with poor outcomes, grade of hepatic encephalopathy, or requirement for renal replacement therapy.\n\nQuestion:\nDoes thrombocytopenia be Associated With Multi-organ System Failure in Patients With Acute Liver Failure?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nUnderstanding patterns of biodiversity is a longstanding challenge in ecology. Similar to other biotic groups, arthropod community structure can be shaped by deterministic and stochastic processes, with limited understanding of what moderates the relative influence of these processes. Disturbances have been noted to alter the relative influence of deterministic and stochastic processes on community assembly in various study systems, implicating ecological disturbances as a potential moderator of these forces. Using a disturbance gradient along a 5-year chronosequence of insect-induced tree mortality in a subalpine forest of the southern Rocky Mountains, Colorado, USA, we examined changes in community structure and relative influences of deterministic and stochastic processes in the assembly of aboveground (surface and litter-active species) and belowground (species active in organic and mineral soil layers) arthropod communities. Arthropods were sampled for all years of the chronosequence via pitfall traps (aboveground community) and modified Winkler funnels (belowground community) and sorted to morphospecies. Community structure of both communities were assessed via comparisons of morphospecies abundance, diversity, and composition. Assembly processes were inferred from a mixture of linear models and matrix correlations testing for community associations with environmental properties, and from null-deviation models comparing observed vs. expected levels of species turnover (Beta diversity) among samples. Tree mortality altered community structure in both aboveground and belowground arthropod communities, but null models suggested that aboveground communities experienced greater relative influences of deterministic processes, while the relative influence of stochastic processes increased for belowground communities. Additionally, Mantel tests and linear regression models revealed significant associations between the aboveground arthropod communities and vegetation and soil properties, but no significant association among belowground arthropod communities and environmental factors.\n\nQuestion:\nDo aboveground and belowground arthropods experience different relative influences of stochastic versus deterministic community assembly processes following disturbance?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo determine whether objective measures of sleep correlate with plasma levels of the proinflammatory cytokine interleukin (IL)-6 and the procoagulant marker fibrin D-dimer in caregivers of patients with dementia. Cross-sectional study. Subjects' homes. Sixty-four community-dwelling spousal caregivers (69% women, mean age+/-standard deviation 72+/-9) and 36 sex-matched noncaregiving controls. All participants underwent in-home full-night polysomnography. Demographic and lifestyle factors, depression, diseases, and medication that could affect inflammation, coagulation, and sleep were controlled for in analyses regressing sleep variables and caregiver status and their interaction on plasma levels of IL-6 and D-dimer. Caregivers had higher levels of D-dimer (781+/-591 vs 463+/-214 ng/mL, P=.001) and IL-6 (1.42+/-1.52 vs 0.99+/-0.86 pg/mL, P<.06) and lower levels of total sleep time (369+/-70 vs 393+/-51 minutes, P=.049) and sleep efficiency (77+/-11 vs 82+/-9%, P=.04) than controls. After controlling for age and body mass index, longer wake time after sleep onset (change in coefficient of determination (DeltaR2)=0.039, P=.04) and the interaction between caregiver status and higher apnea-hypopnea index (DeltaR2=0.054, P=.01) were predictors of IL-6. Controlling for age, caregiver status independently predicted D-dimer levels (DeltaR2=0.047, P=.01). Controlling for age and caregiver status, lower sleep efficiency (DeltaR2=0.032, P=.03) and the interaction between caregiver status and more Stage 2 sleep (DeltaR2=0.037, P=.02) independently predicted plasma D-dimer levels.\n\nQuestion:\nIs poor sleep associated with higher plasma proinflammatory cytokine interleukin-6 and procoagulant marker fibrin D-dimer in older caregivers of people with Alzheimer 's disease?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo study the effect of using lamivudine to prevent fulminant hepatic failure (FHF) in patients with chronic hepatitis B. 164 patients were randomly put into a conventional supporting treatment control group and a lamivudine treatment group. In the latter, 82 patients were given lamivudine orally at a dose of 100 mg every day besides the support care which was also given to the control group. The rate of deterioration to chronic severe hepatitis in the lamivudine treatment group was significantly lower than that of the control group (23.2% vs. 46.3%, P < 0.01). 52.6% (20/38) with chronic severe hepatitis in the control group died. Only 26.3% (5/19) in the lamivudine treatment group succumbed to terminal liver disease (P < 0.01). There was a significant difference between the two groups in regards to the complication incidence of gastrointestinal bleeding, infections, hepatic coma, and kidney failure (P < 0.05). In addition, the recovery of liver function and liver fibrosis, and the rates of HBeAg loss and seroconversion in the lamivudine treatment group were better than those in the control group. Furthermore, the serum HBV DNA levels decreased more rapidly and continued to be substantially suppressed in the lamivudine treatment group.\n\nQuestion:\nDoes [ Lamivudine administration prevent fulminant hepatic failure in patients with severe chronic hepatitis B ]?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis work aims to study the associations, if any, of hyperuricemia, gout, and menopause status in the US population. Using multiyear data from the National Health and Nutrition Examination Survey, we performed unmatched comparisons and one to three age-matched comparisons of women aged 20 to 70 years with and without hyperuricemia (serum urate ≥6 mg/dL). Analyses were performed using survey-weighted multiple logistic regression and conditional logistic regression, respectively. Overall, there were 1,477 women with hyperuricemia. Age and serum urate were significantly correlated. In unmatched analyses (n = 9,573 controls), postmenopausal women were older, were heavier, and had higher prevalence of renal impairment, hypertension, diabetes, and hyperlipidemia. In multivariable regression, after accounting for age, body mass index, glomerular filtration rate, and diuretic use, menopause was associated with hyperuricemia (odds ratio, 1.36; 95% CI, 1.05-1.76; P = 0.002). In corresponding multivariable regression using age-matched data (n = 4,431 controls), the odds ratio for menopause was 0.94 (95% CI, 0.83-1.06). Current use of hormone therapy was not associated with prevalent hyperuricemia in both unmatched and matched analyses.\n\nQuestion:\nIs aging , not menopause , associated with higher prevalence of hyperuricemia among older women?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nClara cell 10-kDa protein (CC10) is a multifunctional protein with anti-inflammatory and immunomodulatory effects. Induction of CC10 expression by gene transfection may possess potential therapeutic effect. Nuclear factor κB (NF-κB) plays a key role in the inflammatory processes of airway diseases. To investigate potential therapeutic effect of CC10 gene transfection in controlling airway inflammation and the underlying intracellular mechanisms, in this study, we constructed CC10 plasmid and transfected it into bronchial epithelial cell line BEAS-2B cells and CC10 knockout mice. In BEAS-2B cells, CC10's effect on interleukin (IL)-1β induced IL-8 expression was explored by means of RT-PCR and ELISA and its effect on NF-κB classical signaling pathway was studied by luciferase reporter, western blot, and immunoprecipitation assay. The effect of endogenous CC10 on IL-1β evoked IL-8 expression was studied by means of nasal explant culture. In mice, CC10's effect on IL-1β induced IL-8 and nuclear p65 expression was examined by immunohistochemistry. First, we found that the CC10 gene transfer could inhibit IL-1β induced IL-8 expression in BEAS-2B cells. Furthermore, we found that CC10 repressed IL-1β induced NF-κB activation by inhibiting the phosphorylation of IκB-α but not IκB kinase-α/β in BEAS-2B cells. Nevertheless, we did not observe a direct interaction between CC10 and p65 subunit in BEAS-2B cells. In nasal explant culture, we found that IL-1β induced IL-8 expression was inversely correlated with CC10 levels in human sinonasal mucosa. In vivo study revealed that CC10 gene transfer could attenuate the increase of IL-8 and nuclear p65 staining in nasal epithelial cells in CC10 knockout mice evoked by IL-1β administration.\n\nQuestion:\nDoes clara cell 10-kDa protein gene transfection inhibit NF-κB activity in airway epithelial cells?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
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] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe mechanisms producing hemodynamic changes during epidural anesthesia are incompletely understood. The role of capacitance changes in the splanchnic venous bed can be clarified by comparing blocks of differing segmental distributions. Specifically, we speculated that blocks that include the innervation to the mesenteric circulation alter hemodynamics, sympathetic activity, and venous capacitance to a greater extent than blocks without blockade of sympathetic nerves to this critical vascular bed. Rabbits were studied during alpha-chloralose anesthesia and mechanical ventilation. Sympathetic efferent nerve activity to the mesenteric vessels was measured by surgically placed electrodes, and mesenteric vein diameter was measured by videomicroscopy. Heart rate and mean arterial pressure were monitored by intraarterial cannulation. Responses were compared after administration of epidural lidocaine using a dose and catheter level that limited anesthetic to lumbar levels (lumbar group) or thoracic levels (thoracic group). In addition, hemodynamic responses were recorded after thoracolumbar block in animals receiving alpha-chloralose but breathing spontaneously (spontaneous ventilation group) and in awake animals (awake group). Mean arterial pressure decreased 38.3 +/- 5.8% in the thoracic group but only 16.5 +/- 2.8 in the lumbar group. Sympathetic efferent nerve activity decreased in the thoracic group but increased in the lumbar group. An increase in vein diameter followed thoracic epidural anesthesia, but venoconstriction was observed after lumbar epidural block. The addition of intravenous sedation with alpha-chloralose did not increase the hypotensive effect of epidural anesthesia in this model.\n\nQuestion:\nDoes region of epidural blockade determine sympathetic and mesenteric capacitance effects in rabbits?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis study assessed whether aging is associated with progressive endothelial dysfunction, whether the pattern of any age-related decline in vascular health is different in men and women and whether any gender difference is consistent with known changes in hormonal status. Coronary and cerebrovascular disease are much less common in young and middle-aged women compared with men, although the gender difference in death from atherosclerosis is less marked after the menopause. Endothelial dysfunction is an early event in atherogenesis and is important in dynamic plaque stenosis in later life. The effect of aging on endothelial function in men and women, however, is not well known. We used high resolution ultrasound to study endothelium-dependent and endothelium-independent vascular responses. Brachial artery physiology was investigated in 238 subjects (103 men, 135 women; mean [+/- SD] age 38 +/- 17 years, range 15 to 72) with no known risk factors for atherosclerosis. The responses to reactive hyperemia (flow-mediated dilation, which is endothelium dependent) and to glyceryl trinitrate (an endothelium-independent dilator) were assessed for all the subjects and then for men and women separately. On multivariate analysis for the whole group, reduced flow-mediated dilation was related to older age (r = -0.34, p < 0.0001). In men, flow-mediated dilation was preserved in subjects aged < or = 40 years but declined thereafter at 0.21%/year. In women, flow-mediated dilation was stable until the early 50s, after which it declined at 0.49%/year (p = 0.002 compared with men). In contrast, there was no significant change in the glyceryl trinitrate response with aging in either gender.\n\nQuestion:\nIs aging associated with endothelial dysfunction in healthy men years before the age-related decline in women?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAlterations in the production of the beta-galactoside binding protein galectin-3 and of MUC2 intestinal mucin have been independently correlated with the malignant behavior of human colon cancer cells. MUC2 mucin is a major ligand for galectin-3, and colon cancer cells that differ quantitatively in MUC2 expression may also vary in expression of galectin-3. The current study was designed to investigate the relationship between galectin-3 production and MUC2 mucin synthesis by human colon cancer cells. The effect of galectin-3 on MUC2 mucin production was assessed by stable transfection of sense and antisense galectin-3 expression constructs under the control of constitutive or tetracycline-inducible promoters into human colon cancer cells. Galectin-3 and MUC2 expression were determined by fluorescence-activated cell sorter (cell surface galectin-3), Western and Northern analysis (galectin-3, MUC2), and gel filtration of secreted high-weight glycoprotein (MUC2). In vitro results were confirmed in vivo by analysis of cecal xenografts in athymic mice. Colon cancer cells with high levels of galectin-3 also had high levels of MUC2 mucin, whereas those with low galectin-3 levels had low MUC2 levels. Alterations in galectin-3 levels by expression of sense or antisense galectin-3 constructs resulted in parallel alterations of MUC2 protein and RNA. Induction of antisense to galectin-3 in vivo was associated with decreases in both galectin-3 and MUC2 protein in cecal xenografts.\n\nQuestion:\nIs expression of human intestinal mucin modulated by the beta-galactoside binding protein galectin-3 in colon cancer?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPrevious studies have demonstrated that the immunosuppressant FK506 provides neuroprotection in experimental brain injury and suggest that this action may be mediated by suppression of neuronal nitric oxide synthase activation that occurs after ischemic depolarization. We sought to determine whether FK506 reduces histological injury after middle cerebral artery occlusion (MCAO) in the rat and whether the neuroprotective effect is mediated via suppression of in vivo nitric oxide (NO) production during ischemia or early reperfusion. Under controlled conditions of normoxia, normocarbia, and normothermia, halothane-anesthetized male Wistar rats were subjected to 2 hours of MCAO by the intraluminal occlusion technique in a blinded, randomized experimental trial. Ipsilateral parietal cortical laser-Doppler flowmetry was monitored throughout ischemia. Animals were randomly assigned to 4 pretreatment groups: intravenous FK506 0.3 mg/kg or 1. 0 mg/kg, vehicle (cremaphor), or an equivalent volume of saline administered 30 minutes before MCAO. Infarction volume was assessed by a triphenyltetrazolium chloride staining at 22 hours of reperfusion. In separate experiments, microdialysis probes were placed bilaterally into the striatum. Rats were perfused with artificial cerebrospinal fluid containing 3 micromol/L [14C]- L-arginine for 3 hours and then subjected to 2 hours of right MCAO. Intravenous 0.3 mg/kg FK506 or cremaphor was given 30 minutes before right MCAO. Right-left differences between [14C]-L-citrulline in the effluent were assumed to reflect differences in NO production. All values are mean+/-SE. FK506 at 0.3 mg/kg reduced infarction volume in cortex: 40+/-12 mm3 compared with saline (109+/-15 mm3) and cremaphor vehicle (148+/-23) (P<0.05). Striatal infarction was also reduced by low-dose FK506: 16+/-4 mm3 versus 36+/-4 mm3 and 34+/-4 mm3 in saline and vehicle groups, respectively (P<0.05). High-dose treatment reduced infarction volume in cortex (61+/-14 mm3, P<0.05 from saline and vehicle groups) and in striatum (22+/-5 mm3, P<0.05 from saline and vehicle groups). [14C]-L-citrulline recovery via microdialysis was markedly enhanced in ischemic compared with nonischemic striatum. However, ischemia-evoked [14C]-L-citrulline recovery was not different in FK506-treated rats compared with vehicle-treated animals.\n\nQuestion:\nDoes neuroprotective FK506 alter in vivo nitric oxide production during ischemia and early reperfusion in rats?\n\nAnswer:",
"role": "user"
},
{
"content": "no",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo evaluate potential differences at a molecular level between KRAS mutant tumors (MT) and KRAS wild-type (WT) pancreatic tumors and the biological and prognostic significance of different KRAS mutations. Expression of a panel of 29 genes was analyzed in KRAS WT and MT tumors. Effects of KRAS mutation and gene expression levels were assessed on patients' survival. MUC6 (p = 0.009), HGF (p = 0.011), VEGFR-2 (p = 0.020) and VEGFB (p = 0.026) were significantly more expressed and SMAD4 was less suppressed (p = 0.003) in WT KRAS. Contrariwise, SHH (p = 0.012) and IHH (p = 0.031) were more expressed in MT KRAS patients. No OS difference was found between WT and MT KRAS tumors.\n\nQuestion:\nIs kRAS mutation status associated with specific pattern of genes expression in pancreatic adenocarcinoma?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHirsutism is most often caused by polycystic ovary syndrome (PCOS). PCOS patients are characterized by insulin resistance, abdominal obesity and low-grade inflammation. Insulin sensitizing treatment reduces the inflammatory state, but the effect on serum levels of migration inhibitor factor (MIF), monocyte chemoattractant protein (MCP)-1 and macrophage inflammatory protein (MIP)-1alpha have not been evaluated before in PCOS. Plasma chemokine levels (MCP-1, MIP-1alpha and MIF) were measured in two study designs. (i) 51 hirsute patients and 63 matched controls and (ii) 30 PCOS patients before and after randomized treatment with 30 mg pioglitazone/placebo for 16 weeks. Clinical evaluations and whole body DXA-scans were performed in all participants. Hirsute patients (n = 51) had significantly increased MCP-1 [121 (15-950) vs. 81 (18-365) pg/ml; P < 0.05] and MIP-1alpha[179 (8-4202) vs. 103 (4-1598) pg/ml; P < 0.05] than controls of matched body composition [geometric mean (-2SD to +2SD)]. In PCOS (n = 30), MCP-1, MIP-1alpha and MIF correlated positively with central fat mass. A BMI independent positive association was found between MIF and free testosterone (r = 0.49, P = 0.01) in PCOS. Pioglitazone treatment significantly improved insulin sensitivity without affecting testosterone, body composition, MCP-1, MIP-1alpha and MIF levels.\n\nQuestion:\nAre plasma monocyte chemoattractant protein-1 ( MCP-1 ) and macrophage inflammatory protein-1alpha increased in patients with polycystic ovary syndrome ( PCOS ) and associated with adiposity , but unaffected by pioglitazone treatment?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe recessive disorder trimethylaminuria is caused by defects in the FMO3 gene, and may be associated with hypertension. We investigated whether common polymorphisms of the FMO3 gene confer an increased risk for elevated blood pressure and/or essential hypertension. FMO3 genotypes (E158K, V257M, E308G) were determined in 387 healthy subjects with ambulatory systolic and diastolic blood pressure measurements, and in a cardiovascular disease population of 1649 individuals, 691(41.9%) of whom had a history of hypertension requiring drug treatment. Haplotypes were determined and their distribution noted. There was no statistically significant association found between any of the 4 common haplotypes and daytime systolic blood pressure in the healthy population (p = 0.65). Neither was a statistically significant association found between the 4 common haplotypes and hypertension status among the cardiovascular disease patients (p = 0.80).\n\nQuestion:\nDo polymorphisms of the Flavin containing monooxygenase 3 ( FMO3 ) gene predispose to essential hypertension in Caucasians?\n\nAnswer:",
"role": "user"
},
{
"content": "no",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe current obesity epidemic is attributed to complex interactions between genetic and environmental factors. However, a limited number of cases, especially those with early-onset severe obesity, are linked to single gene defects. Rapid-onset obesity with hypothalamic dysfunction, hypoventilation and autonomic dysregulation (ROHHAD) is one of the syndromes that presents with abrupt-onset extreme weight gain with an unknown genetic basis. To identify the underlying genetic etiology in a child with morbid early-onset obesity, hypoventilation, and autonomic and behavioral disturbances who was clinically diagnosed with ROHHAD syndrome. Design/Setting/Intervention: The index patient was evaluated at an academic medical center. Whole-exome sequencing was performed on the proband and his parents. Genetic variants were validated by Sanger sequencing. We identified a novel de novo nonsense mutation, c.3265 C>T (p.R1089X), in the retinoic acid-induced 1 (RAI1) gene in the proband. Mutations in the RAI1 gene are known to cause Smith-Magenis syndrome (SMS). On further evaluation, his clinical features were not typical of either SMS or ROHHAD syndrome.\n\nQuestion:\nDoes whole exome sequencing identify RAI1 mutation in a morbidly obese child diagnosed with ROHHAD syndrome?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTissue type plasminogen activator (tPA) functions as a fibrinolytic factor in the blood and has unique roles in the nervous system. However, the role of tPA in the olfactory epithelium (OE) is still unclear. Generally, surgical ablation of the olfactory bulb (bulbectomy) triggers degeneration followed by regeneration of OE. In this experimental study, we investigated the role of tPA in OE regeneration. Wild-type (WT) mice and tPA-knockout (tPA(-/-) ) mice were subjected to bulbectomy. Reverse-transcription polymerase chain reaction (RT-PCR), in situ hybridization, and immunohistochemical examination was done to detect tPA expression in the olfactory bulb and OE. Cellular proliferation and apoptosis was also monitored in the OE. Before bulbectomy, tPA was found to be expressed in the olfactory bulb and OE. OE degenerated to a similar extent in both strains between 0 and 3 days after bulbectomy. However, OE was thicker and contained more cells in tPA(-/-) mice than in WT mice at 7 days after bulbectomy. Moreover, the number of apoptotic bodies was reduced and the number of proliferating cells was increased in the OE of tPA(-/-) mice compared to WT mice, after bulbectomy. Transmission electron microscopy revealed continuous degeneration of the OE for up to 7 days after bulbectomy in WT mice. In contrast, we observed some intact olfactory vesicles and almost normal supporting cells in the OE of tPA(-/-) mice, at 7 days after bulbectomy.\n\nQuestion:\nDoes tissue plasminogen activator deficiency promote early phase regeneration in the olfactory epithelium after bulbectomy?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nESCC is a life-threatening disease due to invasion and metastasis in the early stage. Great efforts had been made to detect the molecular mechanisms which led to the invasion and metastasis in ESCC. Recent evidence had suggested that deregulation of miR-424-5p took an important role in cancers. However, its role and functional mechanism in ESCC had seldom been elucidated. The expression levels of miR-424-5p were detected in ESCC tissues and cell lines by real-time PCR methods. Then, the invasion, metastasis and proliferation ability of ESCC cell lines transfected with miR-424-5p mimics were analyzed separately by transwell invasion assay, wound healing assay and cell proliferation assay. Finally, the target gene of miR-424-5p was studied and verified by luciferase activity assay. And the role of miR-424-5p in EMT was also investigated by real-time PCR and western blot assay. We showed that the expression levels of miR-424-5p were decreased both in ESCC tissues and cell lines. Furthermore, the expression levels of miR-424-5p were negatively linked to lymph node metastasis in ESCC tissues. Restoration of miR-424-5p in EC-1 cells by using miR-424-5p mimics could decrease the invasion, metastasis and proliferation of EC-1 cells, indicating its role in inhibition on the invasion and metastasis ability of ESCC cells and tissues. In addition, we demonstrated that SMAD7 was a specific target gene for miR-424-5p by luciferase activity assay and miR-424-5p could not only negatively regulate SMAD7 expression but also participate in EMT via SMAD7, because overexpression of SMAD7 could partly enhance the miR-424-5p anti-EMT function.\n\nQuestion:\nDoes miR-424-5p participate in esophageal squamous cell carcinoma invasion and metastasis via SMAD7 pathway mediated EMT?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAccumulation of advanced glycation end products (AGEs) contributes to the development of diabetic ulcers. Recent evidence indicates that AGEs administration enhanced autophagy in many cell types. As a positive trigger of autophagy, the effect of AGEs on autophagy in skin tissues and fibroblasts remains unknown. Skin tissues were isolated from Spreqne-Dawley rats and immunohistochemical staining was performed to analyze the location of LC3 and FOXO1 in skin tissues. Then primary cultured foreskin fibroblast cells with treated with AGEs and the effect of AGEs on autophagy was investigated. Protein level expressions of LC3, Beclin-1 and FOXO1 in fibroblasts were analyzed by Western blotting. Autophagic flux is detected with autophagy inhibitor chloroquine and mRFP-GFP-LC3 tandem construct. Compared with skin from normal rats, immunohistochemical staining shows a predominant LC3 localization in fibroblasts cytoplasm in diabetic rats. Elevated expression of FOXO1 also existed in diabetic rats dermis fibroblasts when compared with normal rats in immunohistochemical analysis. In human skin fibroblasts cells, AGEs administration stimulated the autophagy related LC3-II/LC3-I and Beclin-1 expressions and increased autophagy flux. In mRFP-GFP-LC3 puncta formation assays, both autolysosome and autophagosome were increased in human fibroblasts after treatment with AGEs. Fibroblasts exposed to AGEs also have increased FOXO1 expression compared with control group.\n\nQuestion:\nDo aGEs trigger autophagy in diabetic skin tissues and fibroblasts?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo determine whether patients with treated depression but no other risk factors for coronary heart disease (CHD) have abnormal arterial endothelial function, an abnormality that is common to other acquired risk factors for CHD. Case-control study. Secondary care departments of cardiology and psychiatry in a single centre and the surrounding community. Patients with treated depression and matched healthy controls, aged 18-55 years, without conventional acquired risk factors for CHD. These were recruited from local community mental health clinics, general practices, and patient support groups, and through posters placed in public areas of the hospital. Patients had major depression as defined in the American Psychiatric Association's Diagnostic and statistical manual of mental disorders, fourth edition. Fifteen patients and 12 controls were recruited, and 12 patients and 10 controls completed the study. Brachial artery flow mediated dilatation and baroreflex sensitivity. Arterial endothelial function measured by flow mediated dilatation was impaired in depression (mean (SEM) -0.7% (1.7%)) compared with controls (5.7% (0.9%), p = 0.005 by non-paired t test). Baroreflex sensitivity did not differ significantly between the groups.\n\nQuestion:\nIs arterial endothelial function impaired in treated depression?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWhile several studies have reported a link between the presence of gout and adverse cardiovascular (CV) events in the general population, none has addressed the question of whether the mortality risk of patients with gout is influenced by disease severity. We applied survival analysis methodology to prospectively collected data on clinical and radiographic measures of disease severity and mortality in a specialty clinic based cohort of 706 patients with gout (1992-2008). Standardised mortality ratios (SMR) were calculated to assess the magnitude of excess mortality among patients with gout compared with the underlying general population. Mean follow-up was 47 months. Tophaceous deposition was present in 30.5% of patients; >4 joints were involved in 34.6% of cases. Mean annual flare rate was 3.4. Arterial hypertension (41.2%), hyperlipidaemia (42.2%), diabetes mellitus (20.1%), renal function impairment (26.6%) and a previous CV event (25.3%) were recorded. 64 (9.1%) patients died, death being attributed to vascular causes in 38 (59%) patients. SMR for gout patients was 2.37 (95% CI 1.82 to 3.03), 1.57 (1.18 to 2.05) and 4.50 (2.06 to 8.54) overall, and in men and women, respectively. The presence of tophi and the highest baseline serum urate (SU) levels were independently associated with a higher risk of mortality, in addition to age, loop diuretic use and a history of a previous vascular event. In the multivariable survival regression models, with time varying covariates, the presence of tophi remained a significant mortality risk after adjustment for baseline SU levels (1.98; 1.24 to 3.20).\n\nQuestion:\nAre tophaceous gout and high level of hyperuricaemia both associated with increased risk of mortality in patients with gout?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHepatic artery thrombosis (HAT) after orthotopic liver transplantation (OLT) is associated with significant morbidity and mortality. Factor V Leiden (FVL) mutation is the most common genetic defect that predisposes to thrombosis. The reconstruction of hepatic artery with arterial graft is a documented risk factor for HAT. However, the relationship among FVL mutation, arterial graft, and HAT remains to be determined. We randomly genotyped 485 patients who underwent OLT from April 2002 to January 2011 and studied the incidence of Hepatic artery thrombosis in the presence of FVL mutation. Of 485 patients, 21 patients (4.3%) developed HAT (13 male, 8 female); 10 patients (4 male, 6 female) were heterozygous for the FVL mutation. The incidences of HAT in patients without versus with the FVL mutation were 3.8% and 30% (P = .007). Of patients with HAT, 8 hepatic arteries were reconstructed with infrarenal aortic conduits. All 3 patients (100%) with vs 5 (28%) without FVL who received arterial grafts developed HAT (P = .042).\n\nQuestion:\nIs factor V Leiden mutation a risk factor for hepatic artery thrombosis in liver transplantation?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo examine associations between quantitatively measured retinal vessel caliber and the 10-year incidence of primary open-angle glaucoma (OAG). Population-based cohort study. The Blue Mountains Eye Study examined 3654 persons at baseline and 2461 persons at either 5 years, 10 years, or both times. After excluding 44 subjects with OAG at baseline, 2417 participants at risk of OAG at the 5- or 10-year examinations were included. Retinal vessel calibers of baseline retinal photographs were measured using a computer-based program and summarized as central retinal artery and vein equivalents (CRAE, CRVE). Incident OAG was defined as the development of typical glaucomatous visual field loss combined with matching optic disc rim thinning and an enlarged cup-to-disc (C:D) ratio of >0.7 or C:D asymmetry between the 2 eyes (≥0.3) at either the 5- or 10-year examination. Generalized estimating equation models were used to account for correlation between eyes while adjusting for glaucoma risk characteristics including intraocular pressure (IOP) or ocular perfusion pressure (OPP). We assessed the 10-year incidence of OAG. There were 82 persons (104 eyes) who developed incident OAG over the 10-year follow-up. After adjusting for age, sex, family history of glaucoma, smoking, diabetes, hypertension, hypercholesterolemia, body mass index, spherical equivalent refraction, and C:D ratio, narrower CRAE was associated with higher risk of incident OAG (adjusted odds ratio [OR], 1.77; 95% confidence interval [CI], 1.12-2.79, per standard deviation decrease in CRAE). This association persisted after further adjustment for IOP (adjusted OR, 1.87; 95% CI, 1.14-3.05) or OPP (adjusted OR, 1.76; 95% CI, 1.11-2.78), and remained significant when analyses were confined to eyes with IOP<20 mmHg and C:D ratio<0.6 at baseline. There were no independent associations between CRVE and incident OAG.\n\nQuestion:\nIs retinal vessel caliber associated with the 10-year incidence of glaucoma : the Blue Mountains Eye Study?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nDuring active (or REM) sleep, infant mammals exhibit myoclonic twitches of skeletal muscles throughout the body, generating jerky, discrete movements of the distal limbs. Hundreds of thousands of limb twitches are produced daily, and sensory feedback from these movements is a substantial driver of infant brain activity, suggesting that they contribute to motor learning and sensorimotor integration. It is not known whether the production of twitches is random or spatiotemporally structured, or whether the patterning of twitching changes with age; such information is critical for understanding how twitches contribute to development. We used high-speed videography and 3D motion tracking to assess the spatiotemporal structure of twitching at forelimb joints in 2- and 8-day-old rats. At both ages, twitches exhibited highly structured spatiotemporal properties at multiple timescales, including synergistic and multijoint movements within and across forelimbs. Hierarchical cluster analysis and latent class analysis revealed developmental changes in twitching quantity and patterning. Critically, we found evidence for a selectionist process whereby movement patterns at the early age compete for retention and expression over development.\n\nQuestion:\nDoes spatiotemporal structure of REM sleep twitching reveal developmental origins of motor synergies?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis study was aimed at examining a separate or combined effect of tamoxifen and tranilast drugs on growth and proliferation of breast cancer cells. Breast cancer is one of the most common cancers and the second leading cause of cancer death among women worldwide. Tamoxifen is the most widely used anti-estrogen for the treatment of breast cancer. Studies show that a combination therapy with other drugs enhances the activity of tamoxifen. Tranilast is an anti-inflammatory drug. We hypothesize that tranilast plus tamoxifen can work synergistically and help getting better result from this anticancer drug. Two breast cancer cell lines, MCF-7 and MDA-MB-231, were treated with graduated concentrations of tamoxifen and tranilast alone or in combination at 24, 48 or 72 hours for MCF-7, and 48 hours for MDA-MB-231 cells. We used the MTT assay and lactate dehydrogenase leakage (LDH) assay to evaluate cell viability and cytotoxicity, respectively. In both ER-positive and ER-negative breast cancer cell lines, the combination of tranilast and tamoxifen was more effective in growth inhibition than single drug exposure.\n\nQuestion:\nDo tamoxifen and tranilast show a synergistic effect against breast cancer in vitro?\n\nAnswer:",
"role": "user"
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{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe Japan Geriatrics Society published a guideline on the decision-making process for health care for the elderly in June 2012, noting that withholding or withdrawing feeding tubes are treatment options that should be discussed during the decision-making process. Arguments against the guideline posit that the insertion of a percutaneous endoscopic gastrostomy (PEG) tube feeding may improve quality of life (QOL) for elderly adults and their relatives. The aim of the present study was to explore (a) expected outcomes with PEG tube placement and (b) outcomes from PEG tube feeding in long-term care settings among elderly adults with advanced dementia in Japan. This study was conducted using a cross-sectional study design. A total of 381 hospitals and 985 long-term care facilities provided sets of completed questionnaires. There were 1 199 hospital patients and 2 160 long-term care patients aged 65 years or older with PEG tube placement included in the analysis. The nurses or physicians at each hospital provided information on the level of dementia at the time of PEG tube placement and on the expected outcomes of PEG tube feeding for elderly hospital patients. The nurses or other direct care workers at each facility provided information on the level of dementia and outcomes from PEG tube feeding for the long-term care patients. In the hospital patient group, 62.9% of patients had advanced dementia. PEG tube feeding was expected to prolong survival for 51.1% of hospital patients with advanced dementia. Improved QOL was expected for 39.1% of them. In the long-term care patient group, 61.7% of patients had advanced dementia. The rate of patients enjoying their own lives was lower in long-term care patients who had advanced dementia (4.2%) than in the other patients (16.4%). Approximately 60% of relatives reported satisfaction with the QOL of the patients, both in the long-term care patients with advanced dementia and the other patients.\n\nQuestion:\nAre percutaneous endoscopic gastrostomy ( PEG ) tubes placed in elderly adults in Japan with advanced dementia regardless of expectation of improvement in quality of life?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nEarly animal studies of the therapeutic mechanisms of vagus nerve stimulation (VNS) suggested that seizure suppression requires maximal activation of small, unmyelinated vagal C fibers. However, effective therapeutic stimulation parameters appear to be subthreshold for these fibers in humans, and there are no clinical reports of the autonomic side effects that would be expected if these fibers were maximally activated. We report here that selective destruction of C fibers with capsaicin does not affect VNS-induced seizure suppression in rats. Rats were pretreated with capsaicin or vehicle in three injections over a 2-day period. A cuff electrode was later implanted on the left cervical vagus nerve. Two days after surgery, VNS was given to half of the capsaicin- and vehicle-treated rats. The remaining rats were connected to the stimulator but did not receive VNS. Thirty seconds after VNS onset, seizures were induced by pentylenetetrazol (PTZ), and seizure severity was measured. Two days later, the reciprocal VNS treatment was given, and PTZ-induced seizure severity was again measured. VNS effectively reduced seizure severity in both capsaicin- and vehicle-treated rats as compared with their non-VNS baselines.\n\nQuestion:\nDoes destruction of peripheral C-fibers alter subsequent vagus nerve stimulation-induced seizure suppression in rats?\n\nAnswer:",
"role": "user"
},
{
"content": "no",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo assess the impact of early (dry) and late (wet/neovascular and/or atrophic) forms of AMD on panretinal function. Light- and dark-adapted full-field ERG recordings were obtained over a 5-log-unit intensity range from both eyes of 25 patients with unilateral wet AMD. Fellow eyes showed various signs of dry AMD ranging from multiple medium-sized drusen to noncentral geographic atrophy. The leading edges of rod-isolated ERG a-waves were fitted to a quantitative model of phototransduction. ERG a- and b-wave amplitudes and implicit times were compared between wet and dry AMD eyes and from non-AMD eyes of age-matched subjects. A quantitative and objective assessment of dark adaptation was achieved by recording the recovery of the pure rod b-wave (postsynaptic depolarization of rod bipolar cells); b-wave amplitudes were measured at 120-second intervals for 20 minutes and normalized to the amplitude recorded at t = 20 minutes. Delays in mixed a- and b-wave implicit times were recorded in both wet and dry AMD eyes. Time required to reach 50% of fully recovered responses was delayed in all wet and dry AMD eyes independently of dry AMD severity in the fellow eye. Generalized cone dysfunction and slower activation of the rod phototransduction cascade was noted in a subgroup of patients with advanced features of dry AMD in the fellow eye.\n\nQuestion:\nDo subjects with unilateral neovascular AMD have bilateral delays in rod-mediated phototransduction activation kinetics and in dark adaptation recovery?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPlatelet-derived growth factor-BB plays a role in the development of vascular and lymphatic vessels in tumors. In this study plasma levels of platelet-derived growth factor-BB were assessed preoperatively in patients with adenomas and colorectal cancer to determine whether platelet-derived growth factor-BB is a useful marker or prognostic indicator. Patients with adenomas and colorectal cancer undergoing resection were assessed. Clinical and pathologic data and preoperative blood samples were collected. Plasma platelet-derived growth factor-BB levels (median, 95 percent confidence interval for median) were determined and the Kruskal-Wallis test and Mann-Whitney U test were used for analysis. One hundred seventy-nine patients were studied (91 with colorectal cancer, 88 with adenomas). Preoperative colorectal cancer platelet-derived growth factor-BB levels were higher (1,771.1 pg/ml; confidence intervals, 1,429-2,065) than in the benign neoplasm group (1083 pg/ml; confidence intervals, 933-1,192, P < 0.001). In patients with colorectal cancer, a direct relationship was noted between platelet-derived growth factor-BB levels and disease severity. Despite the increase in platelet-derived growth factor-BB noted with increasing stage, the differences between the Stages 1, 2, 3, and 4 groups were not significant.\n\nQuestion:\nIs platelet-derived growth factor ( subtype BB ) elevated in patients with colorectal carcinoma?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAlthough several approaches for identification and isolation of carcinoma cells with tumour initiating properties have been established, enrichment of a population of pure and viable tumour-initiating cells (TICs) is still problematic. This study investigated possibilities to isolate a population of cancer cells with tumour initiating properties based on their adherence properties, rather than expression of defined markers or clonogenicity. Several human cell lines derived from oral dysplasia and oral squamous cell carcinoma (OSCC), as well as primary cells derived from patients with OSCC were allowed to adhere to collagen IV-coated dishes sequentially. Rapid adherent cells (RAC), middle adherent cells (MAC) and late adherent cells (LAC) were then harvested and further investigated for their morphology, stem cell-like properties and molecular profile while grown in vitro and tongue xenotransplantation in NOD-SCID mice at serial dilutions. RAC showed significantly higher colony forming efficiency (p<0.05), sphere forming ability, greater migration ability (p<0.05), exhibited longer G2 phase and displayed higher expression of integrin β1 and other stem-cell related molecules as compared to MAC and LAC. RAC induced tongue tumours in NOD-SCID mice with the highest incidence. These tumours were also bigger and metastasised more frequently in loco-regional lymph nodes than MAC and LAC.\n\nQuestion:\nDoes rapid adherence to collagen IV enrich for tumour initiating cells in oral cancer?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nEndogenous IL-17 is needed for the Ag sensitization that results in murine allergic asthma, a Th2-mediated disease. Here, we aimed to investigate the role IL-17 plays in the development of murine experimental allergic conjunctivitis (EC) which is also a Th2-mediated disease. To induce EC, wild-type (WT) and IL-17-deficient (IL-17 KO) mice on the BALB/c and C57BL/6 backgrounds were immunized with ragweed (RW) in alum and challenged with RW in eye drops. Alternatively, EC was induced by adoptively transferring RW-primed splenocytes followed by challenge with RW-containing eye drops. Twenty-four hours after the RW challenge, the conjunctivas and spleens were harvested for histological analyses and cytokine assays, respectively. The WT and IL-17 KO mice on both backgrounds did not differ in terms of the severity of actively induced EC, as evaluated by the conjunctival eosinophil infiltration. They also did not differ with regard to the phenotypes of the inflammatory cells infiltrating the conjunctivas, although primed IL-17 KO splenocytes stimulated in vitro with RW extract did produce significantly higher amounts of IL-4, IL-13 and IFN-gamma than WT splenocytes. Reciprocal adoptive transfer experiments also demonstrated that the IL-17 from both the donor splenocytes and the recipient mice is not involved in the development of EC.\n\nQuestion:\nDoes endogenous IL-17 play a significant role in the development of experimental murine allergic conjunctivitis?\n\nAnswer:",
"role": "user"
},
{
"content": "no",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIncreased urine secretion of peptides has been found in celiac disease, probably resulting from increased intestinal uptake of peptides caused by damage to the small gut mucosa. High-performance liquid chromatography of low-molecular-weight peptides in the urine was performed over 6 months, before and after a gluten-free diet was instituted in children who clinically improved while consuming the diet. A significant decrease of peptide levels was observed in children consuming the gluten-free diet. Certain peptide peaks thought to be gluten related decreased the most after the patients began the diet.\n\nQuestion:\nDoes gluten-free diet decrease urinary peptide levels in children with celiac disease?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe compare the effects of postinjury administration of allopregnanolone, a metabolite of progesterone, to progesterone in an animal model of transient middle cerebral artery occlusion. Focal cerebral ischemia was induced in age-matched, adult, male, Sprague-Dawley rats by using an intraluminal filament and suture method to occlude the right middle cerebral artery. After 120 minutes of middle cerebral artery occlusion, the occluding filament was withdrawn to allow reperfusion. Laser-Doppler flowmetry was used to monitor cerebral blood flow for the entire 2-hour period of occlusion and for 5 minutes after reperfusion. Animals subjected to middle cerebral artery occlusion received injections of allopregnanolone (8 mg/kg, n=6), progesterone (8 mg/kg, n=6) and vehicle (2-hydroxypropyl-beta-cyclodextrin, n=7) at 2 hours (intraperitoneally 5 minutes before reperfusion) and 6 hours (subcutaneously) postocclusion. Brains were removed at 72 hours post-middle cerebral artery occlusion, sectioned into coronal slices, and stained with 2,3,5-triphenyltetrazolium chloride (TTC). In a blinded analysis, infarct volume was calculated by using computer-aided morphometry to measure brain areas not stained with TTC. After progesterone or allopregnanolone treatment, stained sections revealed a significant reduction in cortical, caudate-putamen, and hemispheric infarct volumes (percentage of contralateral structure) compared with vehicle-injected controls. Cortical infarction (percentage of contralateral cortex) was 37.47%+/-10.57% (vehicle), 25.49%+/-7.38% (progesterone; P<.05 from vehicle), and 11.40%+/-7.09% (allopregnanolone; P<.05 from vehicle; P<.05 from progesterone). Caudate-putamen infarction (percentage of contralateral caudate-putamen) was 78.02%+/-22.81% (vehicle), 48.41%+/-22.44% (progesterone; P<.05 from vehicle), and 50.44%+/-10.90% (allopregnanolone; P<.05 from vehicle). Total hemispheric infarction (percentage of contralateral hemisphere) was 24.37%+/-6.69% (vehicle), 15.95%+/-3.59% (progesterone; P<.05 from vehicle), and 11.54%+/-3.71% (allopregnanolone; P<.05 from vehicle). No significant differences in cerebral blood flow between groups and time points during ischemia and early reperfusion were observed, suggesting that the relative ischemic insult was equivalent among all groups.\n\nQuestion:\nIs allopregnanolone , a progesterone metabolite , more effective than progesterone in reducing cortical infarct volume after transient middle cerebral artery occlusion?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo establish a novel, sensitive and high-throughput gelatinolytic assay to define new inhibitors and compare domain deletion mutants of gelatinase B/matrix metalloproteinase (MMP)-9. Fluorogenic Dye-quenched (DQ)™-gelatin was used as a substrate and biochemical parameters (substrate and enzyme concentrations, DMSO solvent concentrations) were optimized to establish a high-throughput assay system. Various small-sized libraries (ChemDiv, InterBioScreen and ChemBridge) of heterocyclic, drug-like substances were tested and compared with prototypic inhibitors. First, we designed a test system with gelatin as a natural substrate. Second, the assay was validated by selecting a novel pyrimidine-2,4,6-trione (barbiturate) inhibitor. Third, and in line with present structural data on collagenolysis, it was found that deletion of the O-glycosylated region significantly decreased gelatinolytic activity (k(cat)/k(M) ± 40% less than full-length MMP-9).\n\nQuestion:\nDoes gelatin degradation assay reveal MMP-9 inhibitors and function of O-glycosylated domain?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nProlonged air leakage is common after lung resection. We observed that during deep inspiration some patients were able to empty the water-seal of commercial chest drainage systems and retract air back into the chest tube, which subsequently escaped during the following expiration, mimicking \"true\" air leakage. This led us to perform in vitro and in vivo pressure measurements in chest tube systems and investigate possible relationships with \"false\" air. Commercially available one- and three-chamber drainage systems were used as models for large and small water-seals, respectively. Digital pressure measurements were performed in vitro and in ten selected patients with clinical suspicion of reverse airflow. Repeated measurements in the laboratory demonstrated that in three-chamber chest drainage systems with small water-seals a negative pressure below -30.4 cmH(2)O led to emptying of the water-seal with retrograde flow of air. Retrograde airflow was not possible in one-chamber chest drainage systems. In vivo measurements demonstrated that six of ten highly selected patients were able to create negative pressures below -30.4 cmH(2)O during deep inspiration.\n\nQuestion:\nDoes reverse airflow in certain chest drain may be misinterpreted as prolonged air leakage?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo determine the incidence of second malignancies among patients with Hodgkin's lymphoma (HL) treated with autologous hematopoietic stem cell transplantation (AHSCT) compared with patients receiving conventional therapy alone and to identify potential risk factors for their occurrence. We analyzed data on 1,732 consecutive patients with HL treated at the British Columbia Cancer Agency from 1976 to 2001, including 202 patients undergoing AHSCT. The median follow-up duration was 9.8 years for the whole cohort, 9.7 years for those patients treated with conventional therapy, and 7.8 years from AHSCT. The cumulative incidence of developing any second malignancy 15 years after therapy for HL was 9% (risk ratio = 3.5; P < .001); however, the incidence did not differ between those patients receiving conventional therapy alone compared with those undergoing AHSCT (10% and 8%, respectively; P = .48). In multivariate analysis, the only factor significantly associated with an increased risk of developing any second neoplasm or solid tumor was age > or = 35 years (P < .0001). An increased risk of therapy-induced acute myeloid leukemia and therapy-induced myelodysplastic syndrome was seen for patients aged > or = 35 years (P = .03) and stage III/IV (P = .04).\n\nQuestion:\nDoes high-dose therapy and autologous hematopoietic stem-cell transplantation increase the risk of second neoplasms for patients with Hodgkin 's lymphoma : a comparison of conventional therapy alone versus conventional therapy followed by autologous hematopoietic stem-cell transplantation?\n\nAnswer:",
"role": "user"
},
{
"content": "no",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nActivated protein C (APC) is known to protect animals from sepsis. Endogenous protein C is important in protection. It is unknown whether the cytoprotective or anticoagulant properties of protein C (PC) are responsible for the protective effect of endogenous PC. To determine if signaling by endogenous activated protein C contributes to survival in sepsis. We used an immunochemical approach to either block all of the known activities of protein C using mAb MPC1609 or, alternatively, selectively block the anticoagulant activity of activated protein C while sparing some of its cytoprotective activities using mAb MAPC1591. MPC1609 blocked APC binding to endothelium whereas MAPC1591 enhanced binding. MPC1609 prevented APC protection of endothelial barrier function whereas MAPC1591 did not. Injection of MPC1609, but not MAPC1591, with a sublethal dose of lipopolysaccharide (LPS) caused lethality. At 18 h, the mice injected with MPC1609 plus LPS had much higher interleukin-6 (IL-6) levels than mice injected with LPS alone or LPS plus MPC1591. In these mice treated with LPS plus MPC1609, higher blood urea nitrogen (BUN) and creatinine levels suggested that an acute renal failure might contribute to a slow clearance of IL-6.\n\nQuestion:\nIs endogenous activated protein C signaling critical to protection of mice from lipopolysaccaride-induced septic shock?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nGlucocorticoids (GCs), such as prednisolone, are associated with adverse metabolic effects, including glucose intolerance and diabetes. In contrast to the well known GC-induced insulin resistance, the effects of GCs on beta-cell function are less well established. We assessed the acute and short-term effects of prednisolone treatment on beta-cell function in healthy men. A randomised, double-blind, placebo-controlled trial consisting of two protocols was conducted. In protocol 1 (n=6), placebo and a single dose of 75 mg of prednisolone were administered. In protocol 2 (n=23), participants received 30 mg of prednisolone daily or placebo for 15 days. Both empirical and model-based parameters of beta-cell function were calculated from glucose, insulin and C-peptide concentrations obtained during standardised meal tests before and during prednisolone treatment (protocols 1 and 2), and 1 day after cessation of treatment (protocol 2). Seventy-five milligrams of prednisolone acutely increased the area under the postprandial glucose curve (AUC(gluc); P=0.005), and inhibited several parameters of beta-cell function, including AUC(c-pep)/AUC(gluc) ratio (P=0.004), insulinogenic index (P=0.007), glucose sensitivity (P=0.02) and potentiation factor ratio (PFR; P=0.04). A 15-day treatment with prednisolone increased AUC(gluc) (P<0.001), despite augmented C-peptide secretion (P=0.05). beta-cell function parameters were impaired, including the fasting insulin secretory tone (P=0.02) and PFR (P=0.007).\n\nQuestion:\nDo acute and 2-week exposure to prednisolone impair different aspects of beta-cell function in healthy men?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCoronary heart disease remains a significant clinical problem, and new therapies are needed especially for patients with refractory angina for whom the current therapies do not provide sufficient relief. The aim of this study was to find out if angiogenic gene therapy using new members of the vascular endothelial growth factor (VEGF) family, VEGF-B Intramyocardial adenoviral (Ad) VEGF-B AdVEGF-B\n\nQuestion:\nDo adVEGF-B186 and AdVEGF-DΔNΔC induce angiogenesis and increase perfusion in porcine myocardium?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCancer-testis antigens are among the new promising biomarkers, especially for targeted therapy. Aberrant and specific expression of these proteins has been reported in some tumor tissues. Also understanding their differential role in normal and cancer tissues may introduce them as new candidates for biomarker in cancer. AKAP3 expression was investigated in 162 tumors, normal adjacent and normal tissues of the breast with Real-Time PCR. Also the correlation between the gene expression and clinico-pathologic features of the tumors and treatment regimen was evaluated. There was an association between lack of AKAP3 expression in tumor tissues and triple negative status (p=. 03). There was also a correlation between lack of this marker and tumor size (p = .01) and stage (p = .04). Lack of AKAP3 in normal adjacent tissues was associated with poor prognosis. Kaplan Meier plot demonstrated a remarkable better 5-year disease free survival in AKAP3 positive normal adjacent group.\n\nQuestion:\nDoes aKAP3 correlate with triple negative status and disease free survival in breast cancer?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe aim of this study is to investigate the clinicopathological and prognostic values of miR-149 expression and its roles in colorectal cancer (CRC) progression. qRT-PCR was performed to detect miR-149 expression in CRC cell lines or tissues. Also, the clinical significance of miR-149 expression was investigated. The study further explored whether miR-149 inhibits migration and invasion of CRC cells by targeting the mammalian Forkhead Box M1 (FOXM1). miR-149 was significantly downregulated in CRC tissues, and low miR-149 expression was observed to be significantly correlated with lymph node or distant metastasis and advanced TNM stage of CRC patients. Patients with low miR-149 expression showed poorer prognosis than those with high miR-149 expression, and multivariate analyses indicated that status of miR-149 expression might be an independent prognostic factor. Gain- and loss - of - function assays indicated that miR-149 significantly inhibited growth, migration and invasion of CRC cells by targeting FOXM1. Furthermore, FOXM1 was significantly uiregulated in CRC tissues and inversely correlated with miR-149 expression.\n\nQuestion:\nDoes microRNA-149 suppress colorectal cancer cell migration and invasion by directly targeting forkhead box transcription factor FOXM1?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe investigated the anticancer effect of AE (1,8-dihydroy-3-[hydroxymethyl]-anthraquione) in the T24 human bladder cancer cell line (Food Industry Research and Development Institute, Hsinchu, Taiwan) by studying apoptosis regulation. AE, which is purified from aloe vera leaves, has been reported to have antitumor activity. Cell viability, cell cycle and apoptosis were determined by flow cytometric methods. Levels of cyclins, cyclin-dependent kinase 1 and other enzyme were examined by Western blotting methods. AE inhibited cell viability, and induced G2/M arrest and apoptosis in T24 cells. AE increased the levels of Wee1 and cdc25c, and may have led to inhibition of the levels of cyclin-dependent kinase 1 and cyclin B1, which cause G2/M arrest. AE induced p53 expression and was accompanied by the induction of p21 and caspase-3 activation, which was associated with apoptosis. In addition, AE was associated with a marked increase in Fas/APO1 receptor and Bax expression but it inhibited Bcl-2 expression.\n\nQuestion:\nDoes aloe-emodin induce apoptosis in T24 human bladder cancer cells through the p53 dependent apoptotic pathway?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nLater life metabolic dysfunction is a well-recognized consequence of being born small for gestational age (SGA). This study has applied metabolomics to identify whether there are changes in these pathways in prepubertal short SGA children and aimed to compare the intracellular and extracellular metabolome in fibroblasts derived from healthy children and SGA children with postnatal growth impairment. Skin fibroblast cell lines were established from eight SGA children (age 1.8-10.3 y) with failure of catch-up growth and from three healthy control children. Confluent cells were incubated in serum-free media and the spent growth medium (metabolic footprint), and intracellular metabolome (metabolic fingerprint) were analyzed by gas-chromatography mass spectrometry. Nineteen metabolites were significantly altered between SGA and control cell lines. The greatest fold difference (FD) was seen for alanine (fingerprint FD, SGA: control 0.3, P = 0.01 and footprint FD = 0.19, P = 0.01), aspartic acid (fingerprint FD = 5.21, P = 0.01), and cystine (footprint FD = 1.66, P = 0.02). Network analysis of the differentially expressed metabolites predicted inhibition of insulin as well as growth (ERK) signaling in SGA cells.\n\nQuestion:\nAre metabolites involved in glycolysis and amino acid metabolism altered in short children born small for gestational age?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe reverse mode of Na An osmotic minipump was implanted for administration of Ang II in Sprague-Dawley rats, and blood pressure, as well as NCX1 expression, in the aorta was measured. VSMCs were cultured to verify that Ang II-upregulated NCX1 expression is dependent on activation of NF-κB and contributes to Ca Ang II-upregulated NCX1 expression in rat aortas (2.1-fold at day 6) and VSMCs (1.7-fold at 24 hours) and NF-κB knockdown and p38 mitogen-activated protein kinase (MAPK) inhibitor resulted in 2.1- and 2.0-fold decreases in Ang II-upregulated NCX1 expression in VSMCs. KB-R7943 (an inhibitor of NCX1 reversal) and NCX1 knockdown decreased Ang II-induced Ca\n\nQuestion:\nDoes nF-κB-Dependent Upregulation of NCX1 Induced by Angiotensin II contribute to Calcium Influx in Rat Aortic Smooth Muscle Cells?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMetastasis is a major reason for poor prognosis in patients with cancer, including hepatocellular carcinoma (HCC). A salient feature is the ability of cancer cells to colonize different organs. Long non-coding RNAs (lncRNAs) play important roles in numerous cellular processes, including metastasis. In this study, the lncRNA expression profiles of two HCC cell lines, one with high potential for metastasis to the lung (HCCLM3) and the other to lymph nodes (HCCLYM-H2) were assessed using the Arraystar Human LncRNA Array v2.0, which contains 33,045 lncRNAs and 30,215 mRNAs. Coding-non-coding gene co-expression (CNC) networks were constructed and gene set enrichment analysis (GSEA) was performed to identify lncRNAs with potential functions in organ-specific metastasis. Levels of two representative lncRNAs and one representative mRNA, RP5-1014O16.1, lincRNA-TSPAN8 and TSPAN8, were further detected in HCC cell lines with differing metastasis potential by qRT-PCR. Using microarray data, we identified 1,482 lncRNAs and 1,629 mRNAs that were differentially expressed (≥1.5 fold-change) between the two HCC cell lines. The most upregulated lncRNAs in H2 were RP11-672F9.1, RP5-1014O16.1, and RP11-501G6.1, while the most downregulated ones were lincRNA-TSPAN8, lincRNA-CALCA, C14orf132, NCRNA00173, and CR613944. The most upregulated mRNAs in H2 were C15orf48, PSG2, and PSG8, while the most downregulated ones were CALCB, CD81, CD24, TSPAN8, and SOST. Among them, lincRNA-TSPAN8 and TSPAN8 were found highly expressed in high lung metastatic potential HCC cells, while lowly expressed in no or low lung metastatic potential HCC cells. RP5- 1014O16.1 was highly expressed in high lymphatic metastatic potential HCC cell lines, while lowly expressed in no lymphatic metastatic potential HCC cell lines.\n\nQuestion:\nAre long non-coding RNAs differentially expressed in hepatocellular carcinoma cell lines with differing metastatic potential?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nDurability of plate fixation is important in delayed union. Although locking plates result in stronger constructs, it is not known if locking affects the fatigue life of a plate. Two locking screws on either side of the nonunion could decrease working length and increase strain in the plate. However, the reinforcing effect of the locking head on the plate may compensate, so that it is unclear whether locking reduces fatigue life. We determined whether locking screws, compression screws, and locking buttons reduce or increase the fatigue life of a plate. We tested fatigue life of four constructs using an eight-hole locking plate in a segmental defect model: (1) all locking screws (Locked; n = 5); (2) all compression screws (Unlocked; n = 5); (3) six compression screws with two locking buttons in the central holes (Button; n = 6); and (4) six compression screws with two open central holes (Open; n = 6). The Button group had the longest fatigue life (1.3 million cycles). There was no difference between the Locked and Unlocked groups. All of the constructs failed by fracture of the plates through a screw hole adjacent to the defect.\n\nQuestion:\nDo locking buttons increase fatigue life of locking plates in a segmental bone defect model?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCongenital heart disease (CHD) is a cardinal feature of X chromosome monosomy, or Turner syndrome (TS). Haploinsufficiency for gene(s) located on Xp have been implicated in the short stature characteristic of the syndrome, but the chromosomal region related to the CHD phenotype has not been established. We used cardiac MRI to diagnose cardiovascular abnormalities in four non-mosaic karyotype groups based on 50-metaphase analyses: 45,X (n=152); 46,X,del(Xp) (n=15); 46,X,del(Xq) (n=4); and 46,X,i(Xq) (n=14) from peripheral blood cells. Bicuspid aortic valves (BAV) were found in 52/152 (34%) 45,X study subjects and aortic coarctation (COA) in 19/152 (12.5%). Isolated anomalous pulmonary veins (APV) were detected in 15/152 (10%) for the 45,X study group, and this defect was not correlated with the presence of BAV or COA. BAVs were present in 28.6% of subjects with Xp deletions and COA in 6.7%. APV were not found in subjects with Xp deletions. The most distal break associated with the BAV/COA trait was at cytologic band Xp11.4 and ChrX:41,500 000. One of 14 subjects (7%) with the 46,X,i(Xq) karyotype had a BAV and no cases of COA or APV were found in this group. No cardiovascular defects were found among four patients with Xq deletions.\n\nQuestion:\nAre bicuspid aortic valve and aortic coarctation linked to deletion of the X chromosome short arm in Turner syndrome?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMost human pancreatic adenocarcinoma cells do not express somatostatin receptors, and somatostatin does not inhibit the growth of these cancers. We have demonstrated previously that somatostatin inhibits the growth of pancreatic cancers expressing somatostatin receptor subtype-2 (SSTR2), but not receptor-negative cancers. SSTR2 expression may be an important tumor-suppressor pathway that is lost in human pancreatic cancer. We hypothesized that SSTR2 gene transfer would restore the growth-inhibitory response of human pancreatic cancer to somatostatin. Palpable human pancreatic adenocarcinoma tumors were established on the backs of nude mice by subcutaneous injection of cultured cells (Panc-1). The animals were divided into 5 groups (n = 10/group). Group I served as an untreated control. Group II received an intramuscular injection of the long-acting somatostatin analogue Sandostatin LAR. Group III received Lac-Z expressing adenovirus via intraperitoneal injection. Group IV received SSTR2 expressing adenovirus via intraperitoneal injection. Group V received SSTR2 expressing adenovirus via intraperitoneal injection and an intramuscular injection of Sandostatin LAR. The rate of tumor growth was assessed with calipers. After 28 days, the animals were anesthetized and exsanguanated, and the tumors were excised and weighed. Plasma somatostatin and octreotide levels were measured by radioimmunoassay. Expression of cell-surface somatostatin-receptor protein and known tumor-suppressor proteins was determined by reverse transcriptase-polymerase chain reaction, Western blot, and immunohistochemistry. Systemic delivery of SSTR2-expressing adenovirus by intraperitoneal injection resulted in expression of SSTR2 protein in the subcutaneous human pancreatic cancers. Final tumor weight was significantly decreased in the groups expressing SSTR2 receptors compared to the other 3 groups. Treatment with Sandostatin LAR increased plasma octreotide levels as determined by radioimmunoassay, but had no significant effect on tumor growth. Western blot analysis revealed an up-regulation of the cyclin-dependent kinase inhibitors p27 and p16 in the SSTR2 transfected tumors.\n\nQuestion:\nDoes somatostatin receptor gene transfer inhibit established pancreatic cancer xenografts?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe current study compared 3 groups of adolescents identified in an emergency department (ED) following an alcohol-related event: (1) alcohol-positive adolescents scoring at or above the clinical cutoff on a measure of problematic drinking, the Adolescent Drinking Inventory (ADI) (n = 45); (2) alcohol-positive adolescents scoring below the clinical cutoff on the ADI (n = 68), and (3) alcohol-negative adolescents (n = 64). We examined whether these 3 groups of adolescents differed on measures of substance use as well as psychosocial factors. Participants were recruited as part of a larger clinical trial. Alcohol-positive adolescents were recruited from a level I regional trauma center for treatment related to an alcohol-related incident. Alcohol-negative adolescents were recruited from the ED and the community. The data reported here were from the baseline adolescent and parent assessments. Before completing assessments, adolescents were required to pass a brief mental status examination. Adolescents in the alcohol-positive, high-ADI group reported significantly more substance use, peer substance use, and peer tolerance of substance use than adolescents in the alcohol-positive, low-ADI group followed by adolescents in the alcohol-negative group. Adolescents in the alcohol-positive, high-ADI group reported significantly less parental supervision than adolescents in the other 2 groups.\n\nQuestion:\nDoes alcohol use history differentiate adolescents treated in the emergency department after an alcohol-related incident?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCited2 (CBP/p300-interacting transactivators with glutamic acid (E) and aspartic acid (D)-rich tail 2) is a member of a new family of transcriptional modulators. Cited2 null embryos exhibit hyaloid hypercellularity consisting of aberrant vasculature in the eye. The purpose of the study is to address whether abnormal lenticular development is a primary defect of Cited2 deletion and whether deletion of hypoxia inducible factor (HIF)-1α or an HIF-1α target gene, vascular endothelial growth factor (VEGF), could rescue abnormal hyaloid vascular system (HVS) in Cited2 deficient adult eyes. Le-Cre specific Cited2 knockout (Cited2(CKO)) mice with or without deletion of HIF-1α or VEGF were generated by standard Cre-Lox methods. Eyes collected from six-eight weeks old mice were characterized by Real Time PCR and immunohistological staining. Cited2(CKO) mice had smaller lenses, abnormal lens stalk formation, and failed regression of the HVS in the adult eye. The eye phenotype had features similar to persistent hyperplastic primary vitreous (PHPV), a human congenital eye disorder leading to abnormal lenticular development. Deletion of HIF-1α or VEGF in Cited2 knockout eyes partially rescued the abnormal HVS but had no effect on the smaller lens and abnormal lens stalk differentiation. Intravitreal injection of Topotecan (TPT), a compound that inhibits HIF-1α expression, partially eliminated HVS defects in Cited2(CKO) lenses.\n\nQuestion:\nDoes deletion of HIF-1α partially rescue the abnormal hyaloid vascular system in Cited2 conditional knockout mouse eyes?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nNuclear factor kappaB (NFkappaB) is an inducible and ubiquitously expressed transcription factor which is involved in cell survival, differentiation and growth and, thus, has also been implicated in tumor formation and development. Research on the effect of NFkappaB in inhibiting cancer cell growth, however, remains controversial. We investigated the effects of overexpressed IkappaBalpha on the proliferation of the human lung cancer cell line H460 in vitro and in vivo using IkappaBalpha-expressing adenovirus. The results suggested that the infection of AdIkappaBalpha blocked NFkappaB activity in H460 cells and significantly inhibited cell proliferation by inducing apoptosis. An in vivo study showed the tumor incidence to be significantly lower in mice implanted with H460 cells infected with AdIkappaBa. For established H460 tumor, the intratumoral injection of AdIkappaBalpha also inhibited the tumor growth due to both a blockade of the NFkappaB activity and an inhibition of the VEGF expression.\n\nQuestion:\nDoes gene transfer of inhibitor kappaB in human lung cancer cell line NCI-H460 inhibit tumorigenesis and angiogenesis in vivo?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo clarify the endocrine mechanisms underlying the outcome of different ovulation induction regimens with gonadotropins and GnRH agonists (GnRH-a). Prospective study. Reproductive Endocrinology Center, University of Bologna. Forty eumenorrheic women randomly assigned to four groups of 10 subjects each. Ovulation induction regimens: group A, purified FSH only; group B, purified FSH and flare-up GnRH-a; group C, purified FSH and long GnRH-a; and group D, hMG and long GnRH-a. Pelvic ultrasound and hormone levels in daily serum samples and in follicular fluid drawn immediately before hCG administration. Exogenous gonadotropin dose did not differ among groups. Group B had fewer preovulatory follicles than group C. Group B had higher serum LH, FSH, E2, P, T, and follicular fluid LH, E2, T, and alpha-inhibin than groups C and/or D. Groups C and D did not differ.\n\nQuestion:\nDo different gonadotropin and leuprorelin ovulation induction regimens markedly affect follicular fluid hormone levels and folliculogenesis?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nNeural networks supporting encoding of new information are affected early in the course of Alzheimer disease (AD). Functional magnetic resonance imaging (fMRI) studies in AD have reported decreased medial temporal lobe (MTL) activation when comparing novel versus repeated stimuli. It is, however, unclear whether this finding is related to a failure of normal suppression of MTL activity to repeated stimuli in AD. Twenty-nine healthy older subjects comprising a comparison group (OC) and 15 mild AD patients underwent fMRI during an associative memory paradigm in an academic medical center. The task consisted of blocks of Novel and Repeated face-name pairs and visual Fixation. To reveal neural correlates of processing repeatedly presented stimuli, Repeated blocks were contrasted to Fixation. AD patients demonstrated greater activation during Repeated stimuli in the MTL and in prefrontal and superior parietal cortices, compared with OC. In contrast, OC showed greater parietal task-induced deactivation than AD. Increased MTL activity during Repeated was correlated with more impaired parietal deactivation and poorer performance of the postscan recognition memory test of encoding the face-name pairs.\n\nQuestion:\nIs impaired medial temporal repetition suppression related to failure of parietal deactivation in Alzheimer disease?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nOxidative stress (OS) is enhanced in hemodialysis (HD) patients. Lipid peroxidation and oxidative damage to glycids, proteins and nucleic acids are the main consequences of OS and are associated with increased cardiovascular risk. Vitamin E and glutathione peroxidase (GSH-Px) represent the main antioxidant systems in human cells. Selenium (Se), bound to the active sites of GSH-Pxs, plays a critical role in this antioxidant defence system. Statins are widely used and extensively investigated in the prevention of cardiovascular disease, notably in high-risk subjects. Several studies show antioxidant effects of statins not related to their lipid-lowering action. Our study aimed to compare serum Se concentration in ESRD patients on maintenance HD and in homogeneous healthy subjects and to investigate whether chronic treatment with statins may interfere with serum Se concentration in HD patients. A total of 103 HD patients and 69 healthy subjects were enrolled; HD patients were divided into patients who were not treated with statins (group A) and patients who assumed statins since 6 months at least (group B). Serum Se was determined by atomic absorption spectrometry. Serum Se was significantly lower in HD patients of group A compared with healthy subjects (81.65+/-19.66 Vs. 96.47+/-15.62 mcg/L, p<0.0040). However, in HD patients who assumed statins serum, Se was significantly higher than in HD patients who did not (111.83+/-18.82 vs. 81.65+/-19.66 mcg/L, p<0.0001).\n\nQuestion:\nDoes chronic treatment with statins increase the availability of selenium in the antioxidant defence systems of hemodialysis patients?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nEndometrial cancer incidence is increasing in industrialised countries. High body mass index (BMI, kg m(-2)) is associated with higher risk for disease. We wanted to investigate if BMI is related to clinico-pathological characteristics, hormone receptor status in primary tumour, and disease outcome in endometrial cancer. In total, 1129 women primarily treated for endometrial carcinoma at Haukeland University Hospital during 1981-2009 were studied. Body mass index was available for 949 patients and related to comprehensive clinical and histopathological data, hormone receptor status in tumour, treatment, and follow-up. High BMI was significantly associated with low International Federation of Gynaecology and Obstetrics (FIGO) stage, endometrioid histology, low/intermediate grade, and high level of progesterone receptor (PR) mRNA by qPCR (n=150; P=0.02) and protein expression by immunohistochemistry (n=433; P=0.003). In contrast, oestrogen receptor (ERα) status was not associated with BMI. Overweight/obese women had significantly better disease-specific survival (DSS) than normal/underweight women in univariate analysis (P=0.035). In multivariate analysis of DSS adjusting for age, FIGO stage, histological subtype, and grade, BMI showed no independent prognostic impact.\n\nQuestion:\nIs high BMI significantly associated with positive progesterone receptor status and clinico-pathological markers for non-aggressive disease in endometrial cancer?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTumour-associated lymphangiogenesis was identified as an important clinical determinant for the prognosis of hepatocellular carcinoma (HCC) and significantly influences patient survival. However, in this context, little is known about regulation of lymphangiogenesis by hypoxia-inducible factors (HIF). In HCC, mainly HIF-1α was positively correlated with lymphatic invasion and metastasis, whereas a defined role of HIF-2α is missing. We created a stable knockdown (k/d) of HIF-1α and HIF-2α in HepG2 cells and generated co-cultures of HepG2 spheroids with embryonic bodies. This constitutes an in vitro tumour model mimicking the cancer microenvironment and allows addressing the role of distinct HIF isoforms in regulating HCC lymphangiogenesis. In co-cultures with a HIF-2α k/d, lymphangiogenesis was significantly increased, whereas the k/d of HIF-1α showed no effect. The HIF-2α-dependent lymphangiogenic phenotype was confirmed in vivo using matrigel plug assays with supernatants of HIF-2α k/d HepG2 cells. We identified and verified insulin-like growth factor binding protein 1 (IGFBP1) as a HIF-2α target gene. The potential of HepG2 cells to induce lymphangiogenesis in two independent functional assays was significantly enhanced either by a k/d of HIF-2α or by silencing IGFBP1. Moreover, we confirmed IGF as a potent pro-lymphatic growth factor with IGFBP1 being its negative modulator.\n\nQuestion:\nDoes hIF-2α attenuate lymphangiogenesis by up-regulating IGFBP1 in hepatocellular carcinoma?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.
| [
{
"content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThere are several reports regarding intraductal papillary mucinous neoplasms (IPMNs) detected after the occurrence of acute pancreatitis. Although the presence of symptoms is regarded as a factor for predicting malignant IPMNs, there have been few reports demonstrating whether a history of acute pancreatitis is a predictor of malignancy. The aim of this study was to evaluate the relationship between a history of acute pancreatitis and clinicopathological features of IPMNs including the papillary subtype. The data of 150 IPMNs resected between 1990 and 2009 were retrospectively reviewed. They were classified into IPMNs with or without history of acute pancreatitis, and then the clinicopathological features were compared between the 2 groups. Nineteen (13%) of the 150 patients had a history of acute pancreatitis. Nine of them had repeated episodes of pancreatitis; however, severe pancreatitis was uncommon. The diameter of the main pancreatic duct of the pancreatitis group was significantly larger than that of the nonpancreatitis group (p = 0.04). The pancreatitis group had a significantly higher frequency of carcinoma derived from IPMNs than the nonpancreatitis group (p = 0.03). The incidence of intestinal-type IPMNs in the pancreatitis group was significantly higher than that in the nonpancreatitis group (p < 0.001).\n\nQuestion:\nIs a history of acute pancreatitis in intraductal papillary mucinous neoplasms of the pancreas a potential predictive factor for malignant papillary subtype?\n\nAnswer:",
"role": "user"
},
{
"content": "yes",
"role": "assistant"
}
] | 0 |
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