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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:\nPrions and amyloid-β (Aβ) oligomers trigger neurodegeneration by hijacking a poorly understood cellular signal mediated by the prion protein (PrP) at the plasma membrane. In early zebrafish embryos, PrP-1-dependent signals control cell-cell adhesion via a tyrosine phosphorylation-dependent mechanism. Here we report that the Src family kinases (SFKs) Fyn and Yes act downstream of PrP-1 to prevent the endocytosis and degradation of E-cadherin/β-catenin adhesion complexes in vivo. Accordingly, knockdown of PrP-1 or Fyn/Yes cause similar zebrafish gastrulation phenotypes, whereas Fyn/Yes expression rescues the PrP-1 knockdown phenotype. We also show that zebrafish and mouse PrPs positively regulate the activity of Src kinases and that these have an unexpected positive effect on E-cadherin-mediated cell adhesion. Interestingly, while PrP knockdown impairs β-catenin adhesive function, PrP overexpression enhances it, thereby antagonizing its nuclear, wnt-related signaling activity and disturbing embryonic dorsoventral specification. The ability of mouse PrP to influence these events in zebrafish embryos requires its neuroprotective, polybasic N-terminus but not its neurotoxicity-associated central region. Remarkably, human Aβ oligomers up-regulate the PrP-1/SFK/E-cadherin/β-catenin pathway in zebrafish embryonic cells, mimicking a PrP gain-of-function scenario.\n\nQuestion:\nIs activation of zebrafish Src family kinases by the prion protein an amyloid-β-sensitive signal that prevents the endocytosis and degradation of E-cadherin/β-catenin complexes in vivo?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nPreterm births are a major cause of neonatal morbidity and mortality, and represent an important public health issue. About 30% of preterm births are due to medical conditions of the mother or the fetus, among \"which preeclampsia plays a major role. We have previously reported that maternal periodontal disease enhances the risk for preterm delivery and preeclampsia. Our current objective was to determine whether maternal periodontal disease increases the risk for preterm delivery among preeclamptic women. Women were enrolled prior to their twenty-sixth week of gestation. Periodontal status was assessed at baseline and defined as healthy, mild, or moderate/severe. Repeat examinations were performed at delivery to assess changes in periodontal status. A cohort of 1,020 women was studied, 47 of whom had preeclampsia. A strong association between periodontal disease status at enrollment and rate of premature delivery was observed among preeclamptic women after adjusting for the major risk factors for preterm delivery, including maternal race; age; marital status; WIC (women, infants, children program) or food stamps; insurance; previous preterm delivery; and chorioamnionitis. Among preeclamptic women, 49.3% with mild periodontal disease and 82.6% with moderate to severe disease delivered preterm (hazard ratios [HR] 4.11 and 11.0, respectively). Periodontal disease worsening during pregnancy in preeclamptic women was also associated with an increased risk of preterm births (HR 8.44).\n\nQuestion:\nDoes periodontal disease increase the risk of preterm delivery among preeclamptic women?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 seminoma class of testicular germ cell tumor (TGCT) are characterized by a morphological resemblance to primordial germ cells (PGCs) or gonocytes, and chromosome duplications at 12p. Recently, it was determined that human embryonic stem cells (hESCs) express genes in common with PGCs, and that three of these genes, GDF3, STELLAR, and NANOG, are located on 12p. The current study was designed to identify whether expression of these 12p genes were elevated in seminoma relative to normal testis, and to determine whether elevated expression was unique to seminoma. Real-time polymerase chain reaction (PCR) and immunohistochemistry were used to assess gene expression in seminoma samples relative to normal testis and endpoint PCR was used to identify the presence or absence of these genes in breast carcinoma. GDF3 expression was increased in eight of nine seminomas compared with normal testis, whereas NANOG, OCT4, or both were expressed at the highest levels in seminoma compared with all other markers analyzed. In addition, the NANOG protein was expressed in the majority of seminoma cells. The adult meiotic germ cell markers BOULE and TEKT1 were undetectable in seminoma, whereas the embryonic and adult germ cell markers DAZL and VASA were significantly reduced. Analysis of these markers in breast carcinoma and the MCF7 breast carcinoma cell line revealed that a core hESC-transcriptional profile could be identified consisting of OCT4, NANOG, STELLAR, and GDF3 and that NANOG protein could be detected in breast carcinoma.\n\nQuestion:\nAre human embryonic stem cell genes OCT4 , NANOG , STELLAR , and GDF3 expressed in both seminoma and breast carcinoma?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 identify molecular biologic differences between two gastric adenocarcinoma subgroups presenting different prognoses through the analysis of microRNA and protein expression. Array technologies were used to generate 1146 microRNAs and 124 proteins expression profiles of samples from 60 patients with gastric cancer. For the integrative analysis, we used established mRNA expression data published in our previous study. Whole mRNA expression levels were acquired from microarray data for 60 identical gastric cancer patients. Two gastric adenocarcinoma subgroups with distinct mRNA expression profiles presented distinctly different prognoses. MicroRNA and protein expression patterns were compared between gastric cancer tissue and normal gastric tissue and between two different prognostic groups. Aberrantly expressed microRNA, associated mRNA, and protein in patients with poor-prognosis gastric cancer were validated by quantitative reverse transcription polymerase chain reaction and immunochemistry in independent patients. We obtained the expression data of 1146 microRNAs and 124 cancer-related proteins. Four microRNAs were aberrantly expressed in the two prognostic groups and in cancer vs non-cancer tissues (P < 0.05). In the poor-prognosis group, miR-196b, miR-135b, and miR-93 were up-regulated and miR-29c* was down-regulated. miR-196b expression positively correlated with Homeobox A10 (HOXA10) expression (r = 0.726, P < 0.001), which was significantly increased in poor-prognosis patients (P < 0.001). Comparing gastric cancer with non-cancer tissues, 46/124 proteins showed differential expression (P < 0.05); COX2 (P < 0.001) and cyclin B1 (P = 0.017) were clearly over-expressed in the poor-prognosis group.\n\nQuestion:\nDo overexpression of miR-196b and HOXA10 characterize a poor-prognosis gastric cancer subtype?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nTreatment of rheumatoid arthritis (RA) should aim at full remission. The aims of this study were to define: (1) how many patients reached ultrasound power Doppler (US-PD) remission in a cohort of patients with early RA (ERA) compared with longstanding RA (LSRA); (2) possible predictors of US-PD remission; and (3) how many patients with and without US-PD remission relapsed after 1 year of follow-up in ERA and LSRA. 48 patients with ERA and 46 with LSRA with disease activity score <1.6 underwent US assessment. Six hand and wrist joints were studied for active synovitis. 56.2% of patients with ERA and 50.0% of those with LSRA fulfilled American College of Rheumatology (ACR) remission criteria. 43.7% of patients with ERA and 17.4% of those with LSRA had no evidence of synovitis at US evaluation. Using a stricter clinical definition of remission (ie, ACR criteria), US evaluation confirmed clinical remission in 66.7% of patients with ERA and 26.1% of those with LSRA. Early disease was predictive of clinical US remission. 20.0% of patients with RA who had a negative PD signal at the US evaluation had a flare during the 12-month follow-up period compared with 47.1% of patients who had a positive PD signal.\n\nQuestion:\nDoes clinical and ultrasonographic remission determine different chances of relapse in early and long standing rheumatoid arthritis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nUrocortin II (UcnII) is a neuropeptide that binds with high affinity to the corticotropin-releasing hormone receptor 2 (CRHR2) in peripheral tissues. UcnII is synthesised in the intestine, but its role in human intestinal inflammation is largely unknown. Responses of human colonic epithelial cells expressing CRHR2 to stimulation by UcnII were measured using ELISA, western blot analysis, real-time reverse transcription-PCR (RT-PCR) and interleukin (IL)8 promoter activity. Expression levels of CRHR2 and UcnII in human colitis were determined by immunofluorescence and real-time RT-PCR in mucosal biopsies from patients with Crohn's and ulcerative colitis, and in human intestinal xenografts after exposure to Clostridium difficile toxin A. It is reported here that expression of CRHR2 mRNA and protein in human colonic epithelial cells (HT-29) are increased by exposure to C difficile toxin A or tumour necrosis factor (TNF)alpha. Stimulation of non-transformed NCM460 colonocytes overexpressing CRHR2alpha receptor with UcnII resulted in a time- and concentration-dependent increase in IL8 production. UcnII stimulation also led to activation of nuclear factor-kappaB (NF-kappaB) and mitogen-acivated protein (MAP) kinase in these cells, as evidenced by degradation of IkappaBalpha and phosphorylation of the p65 subunit of NF-kappaB and extracellularly regulated kinase (ERK) 1/2. Furthermore, expression of UcnII and CRHR2 mRNA was increased in mucosal samples of patients with inflammatory bowel disease, and after exposure of human intestinal xenografts to C difficile toxin A.\n\nQuestion:\nDoes urocortin II mediate pro-inflammatory effects in human colonocytes via corticotropin-releasing hormone receptor 2alpha?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nGranulocyte/macrophage colony-stimulating factor (GM-CSF) autoantibodies (GMAb) are strongly associated with idiopathic pulmonary alveolar proteinosis (PAP) and are believed to be important in its pathogenesis. However, levels of GMAb do not correlate with disease severity and GMAb are also present at low levels in healthy individuals. Our primary objective was to determine whether human GMAb would reproduce PAP in healthy primates. A secondary objective was to determine the concentration of GMAb resulting in loss of GM-CSF signaling in vivo (i.e., critical threshold). Nonhuman primates (Macaca fascicularis) were injected with highly purified, PAP patient-derived GMAb in dose-ranging (2.2-50 mg) single and multiple administration studies, and after blocking antihuman immunoglobulin immune responses, in chronic administration studies maintaining serum levels greater than 40 microg/ml for up to 11 months. GMAb blocked GM-CSF signaling causing (1) a milky-appearing bronchoalveolar lavage fluid containing increased surfactant lipids and proteins; (2) enlarged, foamy, surfactant-filled alveolar macrophages with reduced PU.1 and PPARgamma mRNA, and reduced tumor necrosis factor-alpha secretion; (3) pulmonary leukocytosis; (4) increased serum surfactant protein-D; and (5) impaired neutrophil functions. GM-CSF signaling varied inversely with GMAb concentration below a critical threshold of 5 microg/ml, which was similar in lungs and blood and to the value observed in patients with PAP.\n\nQuestion:\nDo patient-derived granulocyte/macrophage colony-stimulating factor autoantibodies reproduce pulmonary alveolar proteinosis in nonhuman primates?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nIt has been well established that high serum levels of interleukin-8 (IL-8) in ovarian cancer result in a poor clinical outcome. Thus, the aim of this study was investigating the role of IL-8 in ovarian cancer development. Two human ovarian cancer cell lines (SKOV3 and OVCAR3) were cocultured with IL-8 (100 ng/L) for 24 h, then cell migration was determined by transwell assay. Epithelial-mesenchymal transition (EMT)-associated proteins including E-cadherin and β-catenin, and phosphorylation status of β-catenin were investigated by Western blot analysis. After treatment with IL-8 (100 ng/L) for 24 h, transwell assay result showed that the number of migrated ovarian cells increased significantly. Western blot analysis revealed that protein levels of E-cadherin were decreased, while that of β-catenin were elevated both in IL-8 pretreated SKOV3 and OVCAR3 cells. We further found that phosphorylation status of β-catenin were elevated either in cytoplasm or in nucleus of these two ovarian cancer cell lines after treatment with IL-8 for 24 h.\n\nQuestion:\nDoes interleukin-8 promote human ovarian cancer cell migration by epithelial-mesenchymal transition induction in vitro?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 Notch signalling in human epithelial cancers is of immense interest. In this study, we examine the interplay between Notch signalling and RhoC, a well-established molecular factor in metastasis. By linking the function of Notch and RhoC, we further strengthen the notion that there is a pro-oncogenic role of Notch signalling in human cervical cancers. RhoC protein expression in cervical carcinoma cell lines was assessed by western blotting. Using CaSki and SiHa cells (cervical carcinoma cells lines), we show that RhoC contributes to wound healing, invasion and migration, anoikis resistance, colony formation, in vitro tube formation and tumour formation. Immunohistochemical studies were carried out to assess the co-expression of RhoC, pAkt and Notch1 in clinical sections. An assessment of the changes associated with epithelial-to-mesenchymal transition (EMT) shows that both Notch1 and RhoC have similar phenotypic contribution to EMT. Rho activity assessment on Notch1 inhibition with DAPT shows decreased RhoC activity. We further show that constitutively active RhoC rescues the phenotypic effect of Notch1 inactivation, and a comparison of Notch1 with RhoC expression shows an overlap between the two proteins in the same areas of the tissue.\n\nQuestion:\nDoes notch1 regulate the functional contribution of RhoC to cervical carcinoma progression?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 grain aphid, Sitobion avenae Fabricius (Hemiptera: Aphididae), is an important pest of cereal crops. Pesticides are the main method for control but carry the risk of selecting for resistance. In response to reports of reduced efficacy of pyrethroid sprays applied to S. avenae, field samples were collected and screened for mutations in the voltage-gated sodium channel, the primary target site for pyrethroids. Aphid mobility and mortality to lambda-cyhalothrin were measured in coated glass vial bioassays. A single amino acid substitution (L1014F) was identified in the domain IIS6 segment of the sodium channel from the S. avenae samples exhibiting reduced pyrethroid efficacy. Bioassays on aphids heterozygous for the kdr mutation (SR) or homozygous for the wild-type allele (SS) showed that those carrying the mutation had significantly lower susceptibility to lambda-cyhalothrin.\n\nQuestion:\nIs a mutation ( L1014F ) in the voltage-gated sodium channel of the grain aphid , Sitobion avenae , associated with resistance to pyrethroid insecticides?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nMutational inactivation of the von Hippel-Lindau (VHL) tumor suppressor gene has been linked to hereditary as well as sporadic clear cell renal carcinomas. The product of the VHL gene, pVHL, acts to target hypoxia-inducible factor alpha (HIF-alpha) subunits for ubiquitination and subsequent degradation. Using an RNA interference approach to lower levels of HIF-2alpha in two different renal cell lines that lack functional pVHL, we have tested the contribution of HIF-2alpha toward cellular pVHL activities. Knockdown of HIF-2alpha resulted in cell cycle arrest of renal cells that were grown on collagen I, indicating that this pVHL function is dependent on HIF-2alpha regulation. However, cellular morphological changes and downregulation of integrins alpha5 and beta1, which were seen upon pVHL replacement, were not faithfully phenocopied by HIF-2alpha reduction. Moreover, fibronectin deposition and expression of renal cell differentiation markers were observed in cells containing replaced pVHL, but not in HIF-2alpha knockdown cells, indicating that these pVHL functions may occur independently of HIF-2alpha downregulation.\n\nQuestion:\nIs hIF-2alpha downregulation in the absence of functional VHL sufficient for renal cell differentiation?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "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:\nIn this study, we aimed at investigating the involvement of the warmth-sensitive channel - TRPV4 (in vitro sensitive to temperatures in the range of approx. 24-34 °C) - on the thermoregulatory mechanisms in rats. We treated rats with a chemical selective agonist (RN-1747) and two antagonists (RN-1734 and HC-067047) of the TRPV4 channel and measured core body temperature, metabolism, heat loss index and preferred ambient temperature. Our data revealed that chemical activation of TRPV4 channels by topical application of RN-1747 on the skin leads to hypothermia and this effect was blocked by the pre-treatment with the selective antagonist of this channel. Intracerebroventricular treatment with RN-1747 did not cause hypothermia, indicating that the observed response was indeed due to activation of TRPV4 channels in the periphery. Intravenous blockade of this channel with HC-067047 caused an increase in core body temperature at ambient temperature of 26 and 30 °C, but not at 22 and 32 °C. At 26 °C, HC-067047-induced hyperthermia was accompanied by increase in oxygen consumption (an index of thermogenesis), while chemical stimulation of TRPV4 increased tail heat loss, indicating that these two autonomic thermoeffectors in the rat are modulated through TRPV4 channels. Furthermore, rats chemically stimulated with TRPV4 agonist choose colder ambient temperatures and cold-seeking behaviour after thermal stimulation (28-31 °C) was inhibited by TRPV4 antagonist.\n\nQuestion:\nDoes tRPV4 activate autonomic and behavioural warmth-defence responses in Wistar rats?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 appendicitis (AA) is a common indication for urgent abdominal surgery. CA-125 glycoprotein antigen is a non-specific marker for epithelial ovarian cancer; CA-125 serum levels also increased in the conditions of peritoneal inflammation. The aim of this study was to examine the correlation between serum CA-125 levels and AA. All emergency department (ED) patients with suspected AA were prospectively enrolled in the study. The serum level of CA-125 was checked in every patient on arrival to the ED in addition to the routine clinical and laboratory evaluation. Data regarding demographic, clinical, radiological, operative and pathological features were analysed. One hundred consecutive patients (48 males) were enrolled in the study. We found a statistically significant correlation between CA-125 levels in males and the severity of appendicitis as described in the operative and pathology reports (P = 0.008 and P = 0.02, respectively). In addition, we observed a trend towards higher levels of CA-125 in males with AA compared with males without AA (9.9 ± 4.7 versus 7.8 ± 3.2 U/mL, respectively; P = 0.09).\n\nQuestion:\nDo elevations of serum CA-125 predict severity of acute appendicitis in males?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\n15-Deoxy-Δ-prostaglandin (15d-PG)J(2) is an electrophilic oxidant that dilates the coronary vasculature. This lipid can adduct to redox active protein thiols to induce oxidative posttranslational modifications that modulate protein and tissue function. To investigate the role of oxidative protein modifications in 15d-PGJ(2)-mediated coronary vasodilation and define the distal signaling pathways leading to enhanced perfusion. Proteomic screening with biotinylated 15d-PGJ(2) identified novel vascular targets to which it adducts, most notably soluble epoxide hydrolase (sEH). 15d-PGJ(2) inhibited sEH by specifically adducting to a highly conserved thiol (Cys521) adjacent to the catalytic center of the hydrolase. Indeed a Cys521Ser sEH \"redox-dead\" mutant was resistant to 15d-PGJ(2)-induced hydrolase inhibition. 15d-PGJ(2) dilated coronary vessels and a role for hydrolase inhibition was supported by 2 structurally different sEH antagonists each independently inducing vasorelaxation. Furthermore, 15d-PGJ(2) and sEH antagonists also increased coronary effluent epoxyeicosatrienoic acids consistent with their vasodilatory actions. Indeed 14,15-EET alone induced relaxation and 15d-PGJ(2)-mediated vasodilation was blocked by the EET receptor antagonist 14,15-epoxyeicosa-5(Z)-enoic acid (14,15-EEZE). Additionally, the coronary vasculature of sEH-null mice was basally dilated compared to wild-type controls and failed to vasodilate in response to 15d-PGJ(2). Coronary vasodilation to hypoxia in wild-types was accompanied by 15d-PGJ(2) adduction to and inhibition of sEH. Consistent with the importance of hydrolase inhibition, sEH-null mice failed to vasodilate during hypoxia.\n\nQuestion:\nDoes redox regulation of soluble epoxide hydrolase by 15-deoxy-delta-prostaglandin J2 control coronary hypoxic vasodilation?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nDespite early promise as a means of reducing the inflammatory response to surgery and subsequent organ damage, the evidence of the clinical value of leukocyte filtration remains equivocal. Three hundred patients presenting for routine coronary artery bypass surgery were randomized to a total leukocyte filtration group (filters in five different locations) and a control group with a standard 40-mum filter in the bypass return line only. Data on efficacy and safety of leukocyte filtration were collected by research and postoperative care staff who were blinded to the mode of filtration. Leukofiltration achieved a transient fall in white cells immediately after surgery (p = 0.07) and a sustained fall in platelets, which was still significant on the second postoperative day (p = 0.0001). However, there were no significant differences in postoperative hospital stay, the primary outcome variable (p = 0.35), in ICU stay (p = 0.92), or mortality (p = 1.0). There were no differences in postoperative cardiac status including cardiac output (p = 0.16), inotrope (p = 0.93) or balloon pump (p = 0.48) requirement, or 24-hour troponin (p = 0.60). Similarly there were no differences in pulmonary or renal function (intubation time (p = 0.83), respiratory index (p = 0.19) rise in creatinine (p = 0.13) or hemofiltration (1.0)). Leukofitration was not associated with a statistically significant increase in bleeding or requirement for blood or blood products. It was associated with a decrease approaching significance (p = 0.1) in number and severity of postoperative wound infections. Three filters were blocked during use but were changed without incident or compromise to patient safety.\n\nQuestion:\nDoes total leukocyte control for elective coronary bypass surgery improve short-term outcome?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "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 compare silicone-hydrogel, poly(2-hydroxyethyl methacrylate) (pHEMA), and phosphorylcholine-coated (PC-C) contact lenses in terms of their susceptibility to biofilm formation by Staphylococcus epidermidis and Pseudomonas aeruginosa. Laboratory investigation. Biofilm formation on colonized test lenses was evaluated with confocal microscopy and in vitro antibiotic susceptibility assays. The results of the latter assays were compared with those performed on planktonic cultures of the same organism. For both microorganisms, sessile colonies on silicone-hydrogel and pHEMA lenses displayed lower antibiotic susceptibility than their planktonic counterparts. In contrast, the susceptibility of cultures growing on PC-C lenses was comparable with that for planktonic cultures. In particular, minimum inhibitory concentration for Tazocin (piperacillin plus tazobactam; Wyeth Pharmaceuticals, Aprilia, Italy; S. epidermidis) and gentamicin (P. aeruginosa) was identical, either in the presence of PC-C support or in planktonic cultures (Tazocin, </= 0.2 mug/ml; gentamicin, 0.4 mug/ml). Minimum inhibitory concentration for imipenem (P. aeruginosa) was two-fold higher for PC-C lenses (0.4 mug/ml) with respect to planktonic cultures (0.2 mug/ml). Confocal microscopy of lenses colonized for 24 hours with P. aeruginosa green fluorescent protein-expressing cells revealed a sessile colonization on silicone-hydrogel lens and a few isolated bacterial cells scattered widely over the surface of the PC-C lens.\n\nQuestion:\nDoes phosphorylcholine impair susceptibility to biofilm formation of hydrogel contact lenses?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 novel T helper (Th) cell lineage, Th17, that exclusively produces the proinflammatory cytokine interleukin 17 (IL17) has been reported to play important roles in various inflammatory diseases. IL23 is also focused upon for its potential to promote Th17. Here, the roles of the IL23/IL17 axis in inflammatory bowel diseases such as ulcerative colitis (UC) and Crohn's disease (CD) were investigated. Mucosal samples were obtained from surgically resected specimens (controls, n = 12; UC, n = 17; CD, n = 22). IL17 production by isolated peripheral blood (PB) and lamina propria (LP) CD4(+) cells was examined. Quantitative PCR amplification was performed to determine the mRNA expression levels of IL17, interferon gamma (IFNgamma), IL23 receptor (IL23R) and retinoic acid-related orphan receptor gamma (RORC) in LP CD4(+) cells, and IL12 family members, such as IL12p40, IL12p35 and IL23p19, in whole mucosal specimens. The effects of exogenous IL23 on IL17 production by LP CD4(+) cells were also examined. IL17 production was higher in LP CD4(+) cells than in PB. Significant IL17 mRNA upregulation in LP CD4(+) cells was found in UC, while IFNgamma was increased in CD. IL23R and RORC were upregulated in LP CD4(+) cells isolated from both UC and CD. IL17 production was significantly increased by IL23 in LP CD4(+) cells from UC but not CD. Upregulated IL23p19 mRNA expression was correlated with IL17 in UC and IFNgamma in CD.\n\nQuestion:\nDoes iL23 differentially regulate the Th1/Th17 balance in ulcerative colitis and Crohn 's disease?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 designed to test the hypothesis that the level of aortic blood pressure affects the rate and extent of coronary thrombolysis induced by intracoronary administration of recombinant tissue-type plasminogen activator (rt-PA). Although many studies have confirmed the efficacy of thrombolytic therapy in the treatment of acute myocardial infarction, the effects of altered blood pressure on coronary thrombolysis have not been studied. Because the aortic pressure represents the coronary artery inflow pressure, first principles predict that changes in blood pressure will affect the delivery of the thrombolytic agent and thus affect thrombolysis. The effects of large changes in blood pressure on coronary thrombolysis were studied in a canine model. Coronary thrombosis was induced by injection of radioactive blood clot through a catheter placed in the left anterior descending coronary artery. Subsequently, 24 dogs were classified into three groups of 8 dogs each: Group 1 dogs underwent phlebotomy to adjust systolic blood pressure to 130 mm Hg; Group 2 dogs underwent phlebotomy to decrease systolic blood pressure to 75 mm Hg. Dogs in Group 3 also underwent phlebotomy to achieve a systolic blood pressure of 75 mm Hg and then received norepinephrine to increase this pressure to 130 mm Hg. After adjustment in blood pressure, all dogs received an infusion of rt-PA (0.25 mg/kg body weight) over 30 min through the left anterior descending artery catheter. In a fourth group of six dogs, the effect of altered blood pressure on the rate of coronary thrombolysis was assessed. In dogs in Groups 1 and 3, the rate and extent of coronary thrombolysis were significantly increased compared with values in Group 2. In each of the six Group 4 dogs the rate of coronary thrombolysis increased when norepinephrine increased systolic blood pressure from 75 to 130 mm Hg.\n\nQuestion:\nDoes marked systemic hypotension depress coronary thrombolysis induced by intracoronary administration of recombinant tissue-type plasminogen activator?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 was a planned substudy from the European observational Sepsis Occurrence in Acutely ill Patients (SOAP) study to investigate the possible impact of insulin-treated diabetes on morbidity and mortality in ICU patients. The SOAP study was a cohort, multicenter, observational study which included data from all adult patients admitted to one of 198 participating ICUs from 24 European countries during the study period. For this substudy, patients were classified according to whether or not they had a known diagnosis of insulin-treated diabetes mellitus. Outcome measures included the degree of organ dysfunction/failure as assessed by the sequential organ failure assessment (SOFA) score, the occurrence of sepsis syndromes and organ failure in the ICU, hospital and ICU length of stay, and all cause hospital and ICU mortality. Of the 3147 patients included in the SOAP study, 226 (7.2%) had previously diagnosed insulin-treated diabetes mellitus. On admission, patients with insulin-treated diabetes were older, sicker, as reflected by higher simplified acute physiology system II (SAPS II) and SOFA scores, and more likely to be receiving hemodialysis than the other patients. During the ICU stay, more patients with insulin-treated diabetes required renal replacement therapy (hemodialysis or hemofiltration) than other patients. There were no significant differences in ICU or hospital lengths of stay or in ICU or hospital mortality between patients with or without insulin-treated diabetes. Using a Cox proportional hazards regression analysis with hospital mortality censored at 28-days as the dependent factor, insulin-treated diabetes was not an independent predictor of mortality.\n\nQuestion:\nIs insulin-treated diabetes associated with increased mortality in critically ill patients?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "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:\nIdentifying indirect markers of the physiology or neuroendocrinology of a primate can provide a powerful tool to scientists. Anecdotal descriptions and recent experimental evidence suggests that the colorful sexual skin in adult male vervet monkeys (Cercopithecus aethiops sabaeus) might be sensitive to social changes, including dominance relationships, which could be related to serotonergic activity. The present study examined whether individual differences in scrotal coloration were related to cisternal cerebrospinal fluid concentrations of 5-hydroxyindoleacetic acid (CSF 5-HIAA) in a captive population of vervet monkeys. Darkly colored males had relatively higher CSF 5-HIAA concentrations than paler males, and scrotal color hue was also related CSF 5-HIAA concentrations.\n\nQuestion:\nAre secondary sexual coloration and CSF 5-HIAA correlated in vervet monkeys ( Cercopithecus aethiops sabaeus )?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nColonoscopy, the \"gold standard\" screening test for colorectal cancer (CRC), has known diagnostic limitations. Advances in endoscope technology have focused on improving mucosal visualisation. In addition to increased angle of view and resolution features, recent colonoscopes have non-white-light optics, such as narrow band imaging (NBI), to enhance image contrast. We aimed to study the neoplasia diagnostic characteristics of NBI, by comparing the neoplasm miss rate when the colonoscopy was performed under NBI versus white light (WL). Randomised controlled trial. US Veterans hospital. Elective colonoscopy adults. We randomly assigned patients to undergo a colonoscopic examination using NBI or WL. All patients underwent a second examination using WL, as the reference standard. The primary end point was the difference in the neoplasm miss rate, and secondary outcome was the neoplasm detection rate. In 276 tandem colonoscopy patients, there was no significant difference of miss or detection rates between NBI or WL colonoscopy techniques. Of the 135 patients in the NBI group, 17 patients (12.6%; 95% confidence interval (CI) 7.5 to 19.4%) had a missed neoplasm, as compared with 17 of the 141 patients (12.1%; 95% CI 7.2 to 18.6%) in the WL group, with a miss rate risk difference of 0.5% (95% CI -7.2 to 8.3). 130 patients (47%) had at least one neoplasm. Missed lesions with NBI showed similar characteristics to those missed with WL. All missed neoplasms were tubular adenomas, the majority (78%) was < or = 5 mm and none were larger than 1 cm (one-sided 95% CI up to 1%). Nonpolypoid lesions represented 35% (13/37) of missed neoplasms.\n\nQuestion:\nDo a randomised tandem colonoscopy trial of narrow band imaging versus white light examination to compare neoplasia miss rates?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 was to determine the effects of quercetin on homocysteine (Hcy) metabolism and hepatic antioxidant status in high methionine (Met)-fed rats. Rats were fed for 6 wk the following diets: control, 1.0% Met, 1.0% Met and 0.1% quercetin, 1.0% Met and 0.5% quercetin, 1.0% Met and 2.5% quercetin-supplemented diets. Serum Hcy, Met, cysteine, serine, taurine, glutathione (GSH), quercetin and its metabolites, and activities of alanine transaminase (ALT) and aspartate transaminase (AST) were assayed. Hepatic malondialdehyde, GSH and carbonyls, and activity of superoxide dismutase and ferric-reducing antioxidant power also were measured. Serum Hcy was increased significantly after Met treatment and decreased after quercetin supplementation. Meanwhile, serum taurine was increased and serine decreased. However, the content of GSH in serum and liver was decreased in the quercetin-supplemented groups and activities of serum ALT and AST were enhanced in the 1.0% Met and 2.5% quercetin-supplemented groups.\n\nQuestion:\nDoes quercetin reduce serum homocysteine level in rats fed a methionine-enriched diet?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 open reading frames of subAB genes and their flanking regions of 18 food-borne Shiga toxin-producing E. coli (STEC) strains were analyzed. All but one subAB open reading frames (ORF) were complete in all STEC strains. The subAB1 genes of nine STEC strains were located on large plasmids. The subAB2 allele (here designated subAB2-1), which was recently described by others to be present in the Subtilase-Encoding PAI (SE-PAI) was found in 6 STEC strains. A new chromosomal subAB2 variant, designated subAB2-2 was detected in 6 strains and was linked to a chromosomal gene hypothetically encoding an outer membrane efflux protein (OEP). Three STEC strains contained both subAB2 variants. DNA analysis indicated sequence conservation in the plasmid-located alleles and sequence heterogeneity among the chromosomal subAB2 genes.\n\nQuestion:\nDoes molecular analysis of subtilase cytotoxin genes of food-borne Shiga toxin-producing Escherichia coli reveal a new allelic subAB variant?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nApproximately one-quarter of patients with Barcelona Clinic Liver Cancer (BCLC) stage 0/A hepatocellular carcinoma (HCC) suffer from tumor relapse within the first year after surgical resection. Little data is available for inflammatory indices, including neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and prognostic nutritional index (PNI), in predicting the clinical outcome of patients with very early/early stage HCC who underwent curative surgery. A retrospective cohort study of 324 patients with BCLC stage 0/A primary HCC undergoing surgical resection was conducted to investigate the prognostic impacts of NLR, PLR, and PNI. The low-PNI group (<45) had an adverse overall survival (1-year survival rate of 92 vs. 97 %; 5-year survival rate of 57 vs. 82 %; p < 0.001) and disease-free survival (1-year survival rate of 69 vs. 85 %; 5-year survival rate of 39 vs. 63 %; p < 0.001). It was an independent predictor for disease-specific death, and early and late tumor relapses, with hazard ratios of 2.78 (p < 0.001), 1.82 (p = 0.011), and 2.55 (p = 0.013), respectively. Neither NLR nor PLR had any prognostic significance.\n\nQuestion:\nDoes prognostic Nutritional Index ( PNI ) predict Tumor Recurrence of Very Early/Early Stage Hepatocellular Carcinoma After Surgical Resection?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nIn the era of early reperfusion therapy, life-threatening ventricular arrhythmias (VA) remain common after recanalization of an occluded coronary artery. Experimental studies reported that angiotensin-converting (ACE) inhibitors suppress reperfusion-induced VA. However, whether ACE inhibitors lower the incidence of reperfusion clinical VA is unknown. We examined the effects of low doses of intracoronary (i.c.) enalaprilat (EN) as an adjunct to direct percutaneous coronary interventions (PCI) on reperfusion VA in the acute phase of myocardial infarction (MI). We randomly assigned 22 patients with a first acute MI, who underwent successful direct PCI, to EN, 50 mug, i.c., or placebo (PL), administered immediately after reperfusion. VA were manually edited and counted from 24-hour Holter recordings begun upon hospital admission. There were no significant between-groups differences in clinical characteristics. Mean RR interval before and after PCI, and the incidence of VA before PCI were similar in both groups. After PCI the incidence of reperfusion-induced VA was significantly lower in the EN-treated group (VPB/h: PL 29.9 +/- 12 vs EN 43.2 +/- 42, P < 0.05; couplets/h: EN 0.9 +/- 0.7 vs PL 4.1 +/- 5.0, P < 0.01; triplets/h: EN 0.3 +/- 0.2 vs PL 1.2 +/- 1.5, P < 0.05; ventricular tachycardia/h: EN 0.3 +/- 0.1 vs PL 0.8 +/- 0.5, P < 0.01).\n\nQuestion:\nDo low doses of intracoronary enalaprilat suppress reperfusion-associated ventricular arrhythmias after primary percutaneous coronary interventions for acute myocardial infarction?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 speech perception outcomes as related to a reduction in the number of functional electrodes postimplantation and to determine the effect of electrode reduction on subsequent device failure. Retrospective review. Tertiary academic referral center. Of 1,520 children and adults with full insertions of the Advanced Bionics, Med El, and Nucleus devices, 15 (1%) were patients. Patients were included in the study if all electrodes were functional at initial stimulation, but the number of electrodes in use was subsequently reduced at follow-up programming sessions. Exclusion criteria included partial and split-array electrode insertions. Patients with bilateral severe to profound sensorineural hearing loss underwent either unilateral or bilateral cochlear implantation. Postimplantation speech perception tests obtained with a full complement of functional electrodes were performed and the results compared to those obtained with 1 or more electrodes removed from the user program. Electrode deactivation was also correlated with device failure.\n\nQuestion:\nDo the effects of cochlear implant electrode deactivation on speech perception and in predicting device failure?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 underlying the suppression of somatostatin dependent reflexes in Helicobacter pylori infection are not fully determined. The H pylori product N alpha-methylhistamine and inflammatory mediators such as tumour necrosis factor-alpha (TNF-alpha) may be responsible for the alterations in somatostatin release. To examine the effect of N alpha-methylhistamine on somatostatin release from cultured somatostatin-secreting D-cells. Rabbit fundic D-cells were obtained by collagenase-EDTA digestion and enriched by centrifugal elutriation and cultured for 40 hours. The effects of N alpha-methylhistamine on somatostatin release soon after stimulation (two hours) and after more prolonged exposure (24 hours) were assessed. N alpha-Methylhistamine (1 nM-1 microM) had no effect on basal or carbachol or adrenaline stimulated release over two hours. Similarly with prolonged exposure no effect on somatostatin cell content or release was identified. In contrast, TNF-alpha (24 hours) led to a dose dependent fall in both somatostatin content and release.\n\nQuestion:\nDoes the histamine H3 receptor agonist N alpha-methylhistamine produced by Helicobacter pylori alter somatostatin release from cultured rabbit fundic D-cells?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "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 risk factors for unexplained falls in older community-dwelling individuals. Prospective cohort study. Community population, Sydney, Australia. Older adults (N = 529; mean age 79.8 ± 4.4, 52.2% female). Participants provided information demographic, medical, and medication characteristics and completed cardiovascular (tilt table test, pulse wave velocity), cognitive, and sensorimotor assessments at baseline. Falls were then recorded in monthly fall diaries for 12 months. Unexplained fallers (UFs) were those who reported falls due to a blackout, dizziness, feeling faint, or \"found themselves suddenly on the ground.\" Of the 523 participants available at follow-up, 238 (45.5%) reported one or more falls; 35 participants fulfilled the definition of UFs. UFs were more likely than balance-related fallers (BFs) (n = 203) and nonfallers (n = 291) to have orthostatic hypotension (39.4%, 20.5% and 22.4%, respectively) and depressive symptoms (24.2%, 10.1%, and 7.9% respectively). More UFs (88.6%) than BFs (70.9%) had injurious falls. A multivariate logistic regression model revealed that depressive symptoms and orthostatic hypotension were significant and independent determinants of UF status.\n\nQuestion:\nDo depressive Symptoms and Orthostatic Hypotension Are Risk Factors for Unexplained Falls in Community-Living Older People?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 retrospective study was to investigate the relationship between progression of carotid intima-media thickness (cIMT) and cardiovascular events in Japanese patients with type 2 diabetes mellitus (T2DM) and free of history of cardiovascular events. Patients with T2DM (n=342) without history of cardiovascular events whose cIMT was assessed more than twice by ultrasonography were recruited and followed up for cardiovascular events. During a mean follow-up of 7.6 years, 56 (16.4%) cardiovascular events (27 coronary events and 29 cerebrovascular events) were recorded. Multivariate analysis with the Cox proportional hazard model identified cIMT progression as a significant determinant of cardiovascular events, with a hazard ratio (HR) of 2.24 (95% confidence interval; CI, 1.25-4.03, P<0.01), in addition to baseline cIMT. The Kaplan-Meier curves also showed significantly higher event rate in patients with high cIMT progression compared with those with low cIMT progression (log-rank χ(2)=6.65; P<0.01). Furthermore, the combination of high baseline cIMT and high cIMT progression was a significant predictor of cardiovascular events.\n\nQuestion:\nDoes carotid intima-media thickness progression predict cardiovascular events in Japanese patients with type 2 diabetes?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 peritoneum is progressively denuded of its mesothelial cell monolayer in patients on continuous ambulatory peritoneal dialysis (CAPD). These alterations of the mesothelium cause membrane dysfunction and progressive peritoneal fibrosis. Integrins regulate cell motility and play an important role in wound healing. We investigated the effects of high glucose on the regeneration process of the peritoneal mesothelial cell monolayer using cultured rat peritoneal mesothelial cells (RPMC). The effects of glucose or mannitol on the regeneration of RPMC and formation of focal adhesions were examined by in vitro wound healing assay and immunocytochemistry, respectively. Activities of focal adhesion kinase (FAK) and its downstream p130Cas were examined by Western blotting. Effects of wild-type and dominant-negative FAK on RPMC migration were examined by a transient transfection assay. Cell migration over fibronectin (FN) was clearly inhibited in culture media containing high glucose (28 to 140 mmol/L). RPMC formed focal adhesions on FN in the presence of a regular glucose concentration (5.6 mmol/L); however, tyrosine phosphorylation of FAK and p130Cas and formation of focal adhesions observed by FAK and vinculin staining were substantially inhibited by high glucose. Mannitol also induced significant inhibitory effects, but these were milder than those of glucose. Transfection of dominant-negative FAK inhibited cell migration in a regular glucose concentration, whereas overexpression of wild-type FAK abrogated glucose-induced inhibition of cell migration.\n\nQuestion:\nDo high glucose levels inhibit focal adhesion kinase-mediated wound healing of rat peritoneal mesothelial cells?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 effect of experimental tumor bearing on acute inflammation models in rats. Four and 7 days after Walker tumor implantation in the right armpit, carrageenan or dextran- induced edema in the contralateral paw, carrageenan induced neutrophil migration into peritoneal cavities, cutaneous vascular permeability induced by bradykinin, histamine, serotonin, substance P, capsaicin or compound 48/80, and mesenteric mast cell degranulation induced by compound 48/80 were evaluated. The control group did not receive tumor implantation. Statistical analysis was performed using one way analysis of variance (ANOVA) followed by the Bonferroni test. On the 7(th) day after tumor inoculation, there were significant decreases in both carrageenan and dextran- induced paw edema. Tumor bearing did not change the neutrophil infiltration induced by carrageenan. There were decreases in cutaneous vascular permeability induced by compound 48/80, serotonin or bradykinin, but not that induced by histamine, substance P. A significant inhibition of mesenteric mast cell degranulation induced by compound 48/80 was observed, on the 4(th) and 7(th) days after tumor inoculation.\n\nQuestion:\nDoes tumor bearing decrease systemic acute inflammation in rats -- role of mast cell degranulation?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nIL-1beta is a proinflammatory cytokine driving joint inflammation as well as systemic signs of inflammation, such as fever and acute phase protein production. ACZ885, a fully human monoclonal antibody that neutralizes the bioactivity of human IL-1beta, was generated to study the potent and long-lasting neutralization of IL-1beta in mechanistic animal models as well as in a proof-of-concept study in patients with rheumatoid arthritis (RA). The mouse IL-1 receptor cross-reacts with human IL-1beta, and it was demonstrated that ACZ885 can completely suppress IL-1beta-mediated joint inflammation and cartilage destruction in mice. This observation prompted us to study the safety, tolerability and pharmacodynamic activity of ACZ885 in RA patients in a small proof-of-concept study--the first to be conducted in humans. Patients with active RA despite treatment with stable doses of methotrexate were enrolled in this dose escalation study. The first 32 patients were split into four cohorts of eight patients each (six were randomly assigned to active treatment and two to placebo). ACZ885 doses were 0.3, 1, 3 and 10 mg/kg, administered intravenously on days 1 and 15. To explore efficacy within 6 weeks of treatment, an additional 21 patients were randomly assigned to the 10 mg/kg cohort, resulting in a total of 20 patients dosed with 10 mg/kg and 15 patients treated with placebo. There was clinical improvement (American College of Rheumatology 20% improvement criteria) at week 6 in the 10 mg/kg treatment group; however, this did not reach statistical significance (P = 0.085). A statistically significant reduction in disease activity score was observed after 4 weeks in the 10 mg/kg group. Onset of action was rapid, because most responders exhibited improvement in their symptoms within the first 3 weeks. C-reactive protein levels decreased in patients treated with ACZ885 within 1 week. ACZ885 was well tolerated. Three patients receiving ACZ885 developed infectious episodes that required treatment. No anti-ACZ885 antibodies were detected during the study.\n\nQuestion:\nIs the human anti-IL-1 beta monoclonal antibody ACZ885 effective in joint inflammation models in mice and in a proof-of-concept study in patients with rheumatoid arthritis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nHistorically, alpha-fetoprotein (AFP) levels in insulin-dependent diabetes (IDDM) have shown an approximately 20% decrement, and a correction factor is used to standardize multiples of the median (MOMs). With new laboratory methods and improved precision, we sought to re-evaluate the correctness of this approach. Consecutive biochemical screens were conducted among 60,287 nondiabetic patients and 307 patients with IDDM. Analyses were conducted in one laboratory, and comparisons were made with use of standard formula weight adjustments including a 20% correction factor for IDDM. Patients were then stratified according to maternal weight. Nondiabetic patients averaged 1.00 MOM, IDDM patients 0.91 MOM with no adjustments, 0.96 MOM adjusting for weight only, and 1.20 MOM adjusting for weight and diabetes status. To explain the \"overcorrection,\" analysis by maternal weight showed significant overrepresentation of IDDM patients at 175 pounds or above. In fact, the mean weight in pounds for nondiabetic subjects was 151 +/- 35 and for those with IDDM 174 +/- 52 (P <.001). With use of an upper limit weight cutoff of 200 pounds, results are within 4% of normal.\n\nQuestion:\nDoes correction for insulin-dependent diabetes in maternal serum alpha-fetoprotein testing have outlived its usefulness?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 common missense variant of the CDKN2A gene (A148T) predisposes to malignant melanoma in Poland. An association between malignant melanoma and breast cancer has been reported in several families with CDKN2A mutations, To determine whether this variant also predisposes to breast cancer. Genotyping was undertaken in 4209 cases of breast cancer, unselected for family history, from 18 hospitals throughout Poland and in 3000 controls. The odds ratio (OR) associated with the CDKN2A allele for women diagnosed with breast cancer before the age of 50 was 1.5 (p = 0.002) and after age 50 it was 1.3 (p = 0.2). The effect was particularly strong for patients diagnosed at or before the age of 30 (OR = 3.8; p = 0.0002).\n\nQuestion:\nDoes a common variant of CDKN2A ( p16 ) predispose to breast cancer?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 sustain cell growth, cancer cells exhibit an altered metabolism characterized by increased lipogenesis. Stearoyl-CoA desaturase-1 (SCD-1) catalyzes the production of monounsaturated fatty acids that are essential for membrane biogenesis, and is required for cell proliferation in many cancer cell types. Although estrogen is required for the proliferation of many estrogen-sensitive breast carcinoma cells, it is also a repressor of SCD-1 expression in liver and adipose. The current study addresses this apparent paradox by investigating the impact of estrogen on SCD-1 expression in estrogen receptor-α-positive breast carcinoma cell lines. MCF-7 and T47D mammary carcinomas cells and immortalized MCF-10A mammary epithelial cells were hormone-starved then treated or not with 17β-estradiol. SCD-1 activity was assessed by measuring cellular monounsaturated/saturated fatty acid (MUFA/SFA) ratios, and SCD-1 expression was measured by qPCR, immunoblot, and immunofluorescence analyses. The role of SCD-1 in cell proliferation was measured following treatment with the SCD-1 inhibitor A959372 and following SCD-1 silencing using siRNA. The involvement of IGF-1R on SCD-1 expression was measured using the IGF-1R antagonist AG1024. The expression of SREBP-1c, a transcription factor that regulates SCD-1, was measured by qPCR, and by immunoblot analyses. 17β-estradiol significantly induced cell proliferation and SCD-1 activity in MCF-7 and T47D cells but not MCF-10A cells. Accordingly, 17β-estradiol significantly increased SCD-1 mRNA and protein expression in MCF-7 and T47D cells compared to untreated cells. Treatment of MCF-7 cells with 4-OH tamoxifen or siRNA silencing of estrogen receptor-α largely prevented 17β-estradiol-induced SCD-1 expression. 17β-estradiol increased SREBP-1c expression and induced the mature active 60 kDa form of SREBP-1. The selective SCD-1 inhibitor or siRNA silencing of SCD-1 blocked the 17β-estradiol-induced cell proliferation and increase in cellular MUFA/SFA ratios. IGF-1 also induced SCD-1 expression, but to a lesser extent than 17β-estradiol. The IGF-1R antagonist partially blocked 17β-estradiol-induced cell proliferation and SCD-1 expression, suggesting the impact of 17β-estradiol on SCD-1 expression is partially mediated though IGF-1R signaling.\n\nQuestion:\nDoes 17β-estradiol induce stearoyl-CoA desaturase-1 expression in estrogen receptor-positive breast cancer cells?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nPostoperative blood loss after prostate surgery is thought to be associated with an increase in urinary fibrinolytic activity. Tranexamic acid (TXA) is both a potent inhibitor of plasminogen and urokinase activators and a low molecular weight substance that is excreted unchanged in the urinary tract and can be administered both orally and intravenously. We investigated the effect of TXA on the amount of blood loss during transurethral resection of the prostate (TURP). Forty patients with registry numbers ending in even numbers were allocated to the treatment group; those ending in odd numbers were used as controls and received no treatment. The treatment group received 10 mg/kg TXA by intravenous infusion during the first half hour of the operation, while the control group of patients received no medication. Serum hemoglobin was measured before and after surgery. The volume and hemoglobin concentration of the irrigation fluid, resected prostate weight, and duration of resection were recorded. The mean loss of hemoglobin per gram of resected prostate tissue was 1.25 g in the TXA group and 2.84 g in the control group. Total hemoglobin loss in the irrigating fluid and hemoglobin loss per 1 gram of prostate tissue was lower in the group of patients given TXA than in the control group (p = 0.018 and p <0.001).\n\nQuestion:\nDoes tranexamic acid decrease blood loss during transurethral resection of the prostate ( TUR -P )?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 analgesic effect of oral sucrose in newborn infants undergoing painful procedures is generally accepted. For blood sampling, some studies have shown that venepuncture (VP) is less painful than heel lance (HL). To determine the least painful and most effective method among blood sampling by VP or HL with or without sucrose. Randomised, double blind, placebo controlled trial. A total of 100 healthy, full term newborn infants being screened for inborn errors of metabolism were randomly allocated to one of four experimental groups (25 infants in each). Intervention and Seven specially trained nurses took turns to carry out blood sampling two minutes after administration of oral sucrose or water. Neonatal pain was assessed by the neonatal facial coding system (NFCS), as well as by crying. Without sucrose, the NFCS score was higher in the HL group than the VP group during blood sampling (median 58 v 23, p<0.001). Oral sucrose significantly reduced the score of the HL group (58 v 47, p<0.01) and also tended to reduce the score of the VP group (23 v 2, p<0.1). However, the HL with sucrose group still had a higher score than the VP without sucrose group (47 v 23, p<0.01). Crying and the total procedure time showed the same trends as the NFCS score.\n\nQuestion:\nIs venepuncture preferable to heel lance for blood sampling in term neonates?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 compare 4-year changes in cognitive performance among elderly subjects according to category of fasting blood glucose (FBG) using American Diabetes Association criteria. Subjects without any detectable cognitive dysfunction were selected from the Epidemiology of Vascular Aging (EVA) Study, a cohort of community-dlwelling people aged 59-71 years at baseline. They were classified into glucose categories (normal, impaired fasting glucose [IFG], or diabetic) based on FBG values or known diabetes. Their cognitive abilities were assessed by a global test (Mini Mental Status Examination [MMSE]) and eight domain-specific tests, and they were reassessed 4 years later. Serious cognitive worsening was defined as a score evolution into the worst 15% of the sample's distribution of score differences (4-year score minus baseline score) for each test. At baseline, age-, sex-, and education-adjusted scores for all cognitive tests except one were similar across glucose categories. After 4 years, diabetic subjects had a lower performance on all tests except the MMSE, with differences reaching statistical significance on four tests. Adjusted odds ratios for serious worsening over 4 years in diabetic subjects, with reference to normal subjects, were >2 for four tests (P < 0.05) and bordering this value for two others (P < 0.09). Further adjustment for blood pressure or potential cognition-affecting substances (alcohol, tobacco, and medications) did not modify these results.\n\nQuestion:\nAre changes in cognitive abilities over a 4-year period unfavorably affected in elderly diabetic subjects : results of the Epidemiology of Vascular Aging Study?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nQuantifying chromosomal instability (CIN) has both prognostic and predictive clinical utility in breast cancer. In order to establish a robust and clinically applicable gene expression-based measure of CIN, we assessed the ability of four qPCR quantified genes selected from the 70-gene Chromosomal Instability (CIN70) expression signature to stratify outcome in patients with grade 2 breast cancer. AURKA, FOXM1, TOP2A and TPX2 (CIN4), were selected from the CIN70 signature due to their high level of correlation with histological grade and mean CIN70 signature expression in silico. We assessed the ability of CIN4 to stratify outcome in an independent cohort of patients diagnosed between 1999 and 2002. 185 formalin-fixed, paraffin-embedded (FFPE) samples were included in the qPCR measurement of CIN4 expression. In parallel, ploidy status of tumors was assessed by flow cytometry. We investigated whether the categorical CIN4 score derived from the CIN4 signature was correlated with recurrence-free survival (RFS) and ploidy status in this cohort. We observed a significant association of tumor proliferation, defined by Ki67 and mitotic index (MI), with both CIN4 expression and aneuploidy. The CIN4 score stratified grade 2 carcinomas into good and poor prognostic cohorts (mean RFS: 83.8±4.9 and 69.4±8.2 months, respectively, p = 0.016) and its predictive power was confirmed by multivariate analysis outperforming MI and Ki67 expression.\n\nQuestion:\nDoes the CIN4 chromosomal instability qPCR classifier define tumor aneuploidy and stratifies outcome in grade 2 breast cancer?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 objective of the study was to study the etiology of and factors determining the emergency department disposition of infants sustaining burn injuries. A retrospective chart review was performed on all patients 12 months or younger with a burn injury presenting to our emergency department over a 5-year period. We collected the chief complaint and diagnosis, patient demographics, and circumstances surrounding the burn injury from the emergency department charts. Univariable statistics, multiple imputation, and multivariable regression were performed to determine differences between races and factors leading to admission. During the study period, 344 patients meeting inclusion criteria were treated in our emergency department. Scalds (53.2%) and contact burns (39.8%) were the most common causes of burns among the study group. Significant differences were observed between races for mechanism of burn, interhospital transport, and total body surface area affected (P < 0.05). White patients were more likely to have higher body surface affected and to be transferred from another facility (P < 0.05). Increased severity of burn, burns located on the hand, and concern for abuse resulted in higher likelihood of admission (P < 0.01). No significant differences in disposition or mechanism of burn were present between English-speaking and non-English-speaking patients.\n\nQuestion:\nDo epidemiology and disposition of burn injuries among infants presenting to a tertiary-care pediatric emergency department?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nPrimary nasal epithelium of house dust mite allergic individuals is in a permanently activated inflammatory transcriptional state. To investigate whether a deregulated expression of EGR-1 and/or DUSP-1, two potential negative regulators of pro-inflammatory responses, could contribute to the activation of the inflammatory state. We silenced the expression of EGR-1 or DUSP-1 in the airway epithelial cell line NCI-H292. The cell lines were stimulated in a 24-h time course with the house dust mite allergen or poly(I:C). RNA expression profiles of cytokines were established using q-PCR and protein levels were determined in supernatants with ELISA. The shRNA-mediated gene silencing reduced expression levels of EGR-1 by 92% (p<0.0001) and of DUSP-1 by 76% (p<0.0001). Both mutant cells lines showed an increased and prolonged response to the HDM allergen. The mRNA induction of IL-6 was 4.6 fold (p=0.02) and 2.4 fold higher (p=0.01) in the EGR-1 and DUSP-1 knock-down, respectively when compared to the induced levels in the control cell line. For IL-8, the induction levels were 4.6 fold (p=0.01) and 13.0 (p=0.001) fold higher. The outcome was largely similar, yet not identical at the secreted protein levels. Furthermore, steroids were able to suppress the poly(I:C) induced cytokine levels by 70-95%.\n\nQuestion:\nAre eGR-1 and DUSP-1 important negative regulators of pro-allergic responses in airway epithelium?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 to what degree environmental exposure (childhood trauma, urbanicity, cannabis use, and discrimination) impacts symptom connectivity using both continuous and categorical measures of psychopathology. Outcomes were continuous symptom dimensions of self-reported psychopathology using the Self-report Symptom Checklist-90-R in 3021 participants from The Early Developmental Stages of the Psychopathology (EDSP) study and binary DSM-III-R categories of mental disorders and a binary measure of psychotic symptoms in 7076 participants from The Netherlands Mental Health Survey and Incidence Study (NEMESIS-1). For each symptom dimension in the EDSP and mental disorder in the NEMESIS-1 as the dependent variable, regression analyses were carried out including each of the remaining symptom dimensions/mental disorders and its interaction with cumulative environmental risk load (the sum score of environmental exposures) as independent variables. All symptom dimensions in the EDSP and related diagnostic categories in the NEMESIS-1 were strongly associated with each other, and environmental exposures increased the degree of symptom connectivity in the networks in both cohorts.\n\nQuestion:\nDoes exposure to environmental factors increase connectivity between symptom domains in the psychopathology network?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nVaccination of chimpanzees against hepatitis C virus (HCV) using T-cell-based vaccines targeting nonstructural proteins has not resulted in the same levels of control and clearance as those seen in animals reexposed after HCV clearance. We hypothesized that the outcome of infection depends on the different subtypes of activated T cells. We used multicolor flow cytometry to evaluate activation (CD38+/HLA-DR+) and proliferation (Ki67+/Bcl-2-low) profiles of CD4+ and CD8+ T cells in peripheral blood before and after challenge in chimpanzees vaccinated using DNA/adenovirus, mock-vaccinated, and chimpanzees that had spontaneously cleared infection (rechallenged). The frequencies of activated or proliferating CD8+ T cells peaked at 2 weeks postchallenge in the vaccinated and rechallenged animals, coinciding with reductions in viral titers. However, the magnitude of the responses did not correlate with outcome or sustained control of viral replication. In contrast, proliferation of the CD8+ T cells coexpressing HLA-DR either with or without CD38 expression was significantly higher at challenge in animals that rapidly cleared HCV and remained so throughout the follow-up period.\n\nQuestion:\nDoes hepatitis C virus clearance correlate with HLA-DR expression on proliferating CD8+ T cells in immune-primed chimpanzees?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nResponse to therapy in canine exocrine pancreatic insufficiency (EPI) varies considerably, making it difficult to determine prognosis for individual patients. Response to initial treatment (RIT) and survival are affected by signalment, clinical variables, and therapeutic regimen employed. Client-owned dogs diagnosed with EPI between 1990 and 2002 were included in this study. The study comprised a retrospective, questionnaire-based review. One hundred seventy-eight completed questionnaires were returned. RIT was good in 60% of treated dogs, partial in 17%, and poor in 23%. On univariate analysis, dogs that received antibiotics (P = .037) or had high serum folate concentration (P = .037) had a poorer RIT. On multivariate analysis, there were no strong predictors of good RIT. Nineteen percent of treated dogs were euthanized within 1 year, but overall median survival time for treated dogs was 1919 days. No clear benefit of changing to a fat-restricted diet could be demonstrated, but marked hypocobalaminemia (< 100 ng/L) was associated with shorter survival (P = .012). Use of uncoated pancreatic enzyme supplements, antibacterials, or H2 antagonists was not associated with longer survival. Breed, sex, age at diagnosis ( < or = 4 years or > 4 years), and clinical signs at diagnosis also made no difference.\n\nQuestion:\nIs prognostic factors in canine exocrine pancreatic insufficiency : prolonged survival likely if clinical remission is achieved?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 the present study was to investigate the relationship between atherosclerotic progression rate as measured by carotid artery IMT during very long-term follow-up in clinically healthy men and a number of baseline risk factors of potential importance for atherosclerosis progression including apoA-I, apoB, apoB/apoA-I ratio, other lipid variables including LDL particle size, body composition variables, blood pressure, smoking, fasting blood glucose and insulin, and also hsCRP. Low-density lipoprotein (LDL) is associated with increased carotid IMT progression rate during long-term follow-up, whereas the relationship between newer biomarkers such as apoB/apoA-I ratio and carotid artery IMT progression rate has been less investigated. 58-year-old men identified by screening in the community (n=391) with varying degrees of obesity and insulin sensitivity were examined with high-resolution B-mode ultrasound at baseline and after 3, and 8.9 years of follow-up (n=305 investigated after 8.9 years). The carotid arteries were examined bilaterally, and the mean intima-thickness was calculated for 10mm sections of the composite of common carotid arteries and bulbs (IMT(composite)). Serum levels of apoB and apoA-I were measured using a turbidimetric method. Uni- and multi-variable analyses were performed to study the relationship between carotid IMT(composite) progression rate and risk factors. In a multi-variable analysis including all baseline variables only the apoB/apoA-I ratio (p=0.003; beta=0.181, standard error=0.003) and serum insulin (p=0.026; beta=-0.133, standard error=0.000) was significantly related to IMT(composite) progression rate.\n\nQuestion:\nIs high apoB/apoA-I ratio associated with increased progression rate of carotid artery intima-media thickness in clinically healthy 58-year-old men : experiences from very long-term follow-up in the AIR study?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nMelatonin may attenuate organ damage via direct antioxidative properties, and was recently demonstrated to reduce cardiac and hepatic injury through receptor-dependent effects. However, the relevance of an isolated activation of melatonin receptors for organ protection, excluding direct antioxidant effects, has not been established yet. This study was designed to investigate whether therapy with melatonin receptor agonist and hypnotic substance ramelteon may improve liver function, hepatic perfusion, and hepatic integrity after hemorrhagic shock in rat. Prospective, randomized, controlled study. University research laboratory. Male Sprague-Dawley rats (n = 10 per group). Animals underwent hemorrhagic shock (mean arterial pressure 35 +/- 5 mm Hg for 90 mins) and were resuscitated with shed blood and Ringer's lactate (2 hrs). At the end of shock, animals were treated with ramelteon (1.0 mg/kg intravenously), melatonin receptor antagonist luzindole plus ramelteon (each 1.0 mg/kg intravenously), or vehicle. In vitro, ramelteon displayed no relevant antioxidant capacity in an 2,2'-Azino-bis-(3-ethylbenzthiazoline-6-sulfonic acid) assay, compared with melatonin. In vivo, liver function was assessed by plasma disappearance rate of indocyanine green, and intravital microscopy was performed for evaluation of hepatic perfusion index, nicotinamide adenine dinucleotide phosphate autofluorescence, and hepatic integrity. Compared with vehicle controls, ramelteon therapy significantly improved plasma disappearance rate of indocyanine green (7.89 +/- 2.12% vs. 13.67 +/- 2.51%; p = 0.006), hepatic perfusion index (352.04 +/- 111.78 pl/sec/mm vs. 848.81 +/- 181.38 pl/sec/mm; p = 0.002), nicotinamide adenine dinucleotide phosphate autofluorescence and hepatocellular injury. Coadministration of luzindole abolished the protective effect of ramelteon with respect to liver function and nicotinamide adenine dinucleotide phosphate autofluorescence.\n\nQuestion:\nDoes selective activation of melatonin receptors with ramelteon improve liver function and hepatic perfusion after hemorrhagic shock in rat?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 compare qualitative and quantitative measures of the contrast-enhanced dual-echo Dixon technique with the commonly used standard three-dimensional (3D) gradient echo (spectrally selective fat suppression) technique (SS-FS) in breast MRI exams (bMRI). A total of 19 women, with prescheduled bMRI exam, were recruited to our study between 2006 and 2008. Dixon and standard SS-SF techniques were used on both breasts of each patient. Image quality was rated in five categories: fat suppression quality, fat suppression uniformity, lesion margin clarity, lesion visibility, and axillary visibility. For quantitative assessment, we calculated the signal-to-noise ratio (SNR) and contrast-to-noise ratio (CNR) of lesion to breast, SNR efficiency, and CNR efficiency. Of 19 patients evaluated, 13 had a primary breast malignancy and 6 had benign lesions or negative exams. Dixon images were rated higher in four of five qualitative categories (P < 0.0001) and required a shorter scan time. Dixon images yielded significantly higher SNR (43.8) and CNR (40.1) values than did 3DGRE images (SNR = 34.8, CNR = 25.3; P < 0.05). SNR efficiency (36.30) and CNR efficiency (33.79) values for Dixon images were also higher than were 3DGRE images (SNR efficiency =25.7, CNR efficiency = 19.1; P < 0.05).\n\nQuestion:\nDo fast three-dimensional dual echo dixon technique improves fat suppression in breast MRI?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 feasibility of seeding adipose-derived stem cells (ADSCs) onto bladder acellular matrix grafts (BAMGs) for bladder reconstruction in a rabbit model. Autologous ADSCs were isolated, expanded and identified by flow cytometry. In the experimental group, ADSCs were seeded onto BAMGS for reconstructing bladder defects in 12 male rabbits. Unseeded BAMGs were used for bladder reconstruction in the control group of 12 rabbits. Cystography was performed at 4, 12 and 24 weeks after grafts implantation. Following cystography, the animals were killed and grafts were harvested; H&E and immunohistochemical staining were performed with cytokeratin AE1/AE3, smooth muscle alpha-actin and S-100 markers. Flow cytometry demonstrated that the ADSCs expressed CD90, CD44, CD105, CD166 and CD34, but not CD45 or CD106. The cells demonstrated good biocompatibility with BAMGs. At 24 weeks, in the experimental group, the reconstructed bladders reached a mean volume of 94.68 +/- 3.31% of the pre-cystectomy bladder capacity. Complete regeneration of smooth muscle and nerve tissue was evident. Regenerated SMCs, urothelium and nerve cells stained positively for alpha-smooth muscle actin, AE1/AE3 and S-100. In the control group, the mean bladder volume was 69.33 +/- 5.05% of the pre-cystectomy volume; histologically, the control group was characterized by multi-layered urothelium without evidence for organized muscle or nerve tissue.\n\nQuestion:\nDo bladder reconstruction with adipose-derived stem cell-seeded bladder acellular matrix grafts improve morphology composition?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 role of Janus kinase-signal transducers and activators of transcription (JAK-STAT) pathway in platelet-derived growth factor (PDGF) induced proliferation in activated pancreatic stellate cells (PSCs). PSCs were isolated from rat pancreas tissue, and used in their culture-activated, myofibroblast-like phenotype. STAT-specific binding activity was assessed by electrophoretic mobility shift assay. Activation of Src, JAK2, STAT1, STAT3, and ERK was determined by Western blotting using anti-phospho-specific antibodies. Cell proliferation was assessed by measuring the incorporation of 5-bromo-2'-deoxyuridine. PDGF-BB induced STAT-specific binding activity, and activation of Src, JAK2, STAT1, STAT3, and ERK. Ethanol and acetaldehyde at clinically relevant concentrations decreased basal activation of JAK2 and STAT3. PDGF-induced activation of STAT1 and STAT3 was inhibited by a Src inhibitor PP1 and a JAK2 inhibitor AG490, whereas PDGF-induced activation of ERK was inhibited by PP1, and not by AG490. PDGF-induced proliferation was inhibited by PP1 and AG490 as well as by STAT3 antisense oligonucleotide.\n\nQuestion:\nIs activation of JAK-STAT pathway required for platelet-derived growth factor-induced proliferation of pancreatic stellate cells?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 bioequivalence of esomeprazole MUPS 40 mg tablets administered with and without a hard gelatine capsule. Bioequivalence of the esomeprazole MUPS 40 mg tablet administered without (Reference) and with a hard gelatine capsule (Test) was evaluated using a randomized, two-period crossover study. In each study period 49 healthy male Caucasian subjects received a single oral dose of 40 mg esomeprazole. Blood samples were collected at specified time intervals, and serum was separated and analyzed for esomeprazole concentrations using a validated HPLC-MS method. The primary parameters were AUC (extent of absorption) and Cmax (rate of absorption). The time-to-peak plasma concentration, tmax, and the elimination half-life, t1/2, were determined as secondary characteristics. Point estimates and 90%-confidence intervals were obtained for the ratio of the population medians of Test and Reference, using a multiplicative model and a parametric analysis except in the case of tmax, where an additive model and a non-parametric analysis was used. Bioequivalence of Test and Reference was concluded if the 90%-confidence intervals were entirely within the predefined equivalence ranges. The AUC(0-infinity) and Cmax-ratios (Test/Reference) were 1.00 and 1.01, respectively. The 90%-confidence intervals for AUC(0-infinity) (0.94-1.06) and Cmax (0.93-1.09) of these ratios were within the predefined equivalence range of 0.80-1.25 and 0.75-1.33, respectively. The ratios and 90%-confidence intervals of the secondary characteristics t1/2 and tmax were also within the respective predefined equivalence ranges. Both esomeprazole formulations were well tolerated and safe.\n\nQuestion:\nAre esomeprazole MUPS 40 mg tablets and esomeprazole MUPS 40 mg tablets encapsulated in hard gelatine bioequivalent?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 explore the views of hospitalised school-aged children with complex healthcare needs related to spiritual care. This could help inform national policies and raise awareness of the impact that a stay in an acute paediatric hospital can have on the spiritual needs of some of the children who use the NHS. Pictures used in previous (US) studies were used to facilitate story telling, enabling children to talk about concepts that may not have emerged through direct conversation. A convenience sample of five hospitalised children were presented with the pictures one at a time and asked open-ended questions about each picture. Data analysis involved identifying emerging themes from the transcriptions using a grounded theory approach. The main themes to emerge from the interview data were: the role of the child's relationships with family, friends and healthcare professionals; the impact of the hospital environment on the child; coping with invasive procedures; belief--children's views about their health and belief system.\n\nQuestion:\nDoes spiritual needs of children with complex healthcare need in hospital?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nSerum response factor (SRF) is a transcription factor that binds to a CarG box motif within the serum response element of genes that are expressed in response to mitogens. SRF plays essential roles in muscle and nervous system development; however, little is known about the role of SRF during liver growth and function. To examine the function of SRF in the liver, we generated mice in which the Srf gene was specifically disrupted in hepatocytes. The survival of mice lacking hepatic SRF activity was lower than that of control mice; moreover, surviving mutant mice had lower blood glucose and triglyceride levels compared with control mice. In addition, Srf(loxP/loxP)AlfpCre mice were smaller and had severely depressed levels of serum insulin-like growth factor 1 (IGF-1). Srf-deficient livers were also smaller than control livers, and liver cell proliferation and viability were compromised. Gene array analysis of SRF depleted livers revealed a reduction in many messenger RNAs, including those encoding components of the growth hormone/IGF-1 pathway, cyclins, several metabolic regulators, and cytochrome p450 enzymes.\n\nQuestion:\nIs hepatocyte expression of serum response factor essential for liver function , hepatocyte proliferation and survival , and postnatal body growth in mice?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 sensory nerve neuropeptide substance P (SP) regulates cardiac fibrosis in rodents under pressure overload conditions. Interestingly, SP induces transient increased expression of specific genes in isolated rat cardiac fibroblasts, without resultant changes in cell function. This suggests that SP 'primes' fibroblasts, but does not directly activate them. We investigated whether these unusual findings are specific to rodent fibroblasts or are translatable to a larger animal model more closely related to humans. We compared the effects of SP on genes associated with extracellular matrix (ECM) regulation, cell-cell adhesion, cell-matrix adhesion and ECM in cardiac fibroblasts isolated from a non-human primate and Sprague-Dawley rats. We found that rodent and non-human primate cardiac fibroblasts showed similar responses in genes that relate to ECM regulation and cell adhesion in response to SP. There were large discrepancies in ECM component genes, however, this did not result in collagen or laminin synthesis in rat or non-human primate fibroblasts in response to SP.\n\nQuestion:\nDo non-human primate and rat cardiac fibroblasts show similar extracellular matrix-related and cellular adhesion gene responses to substance P?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 most musculoskeletal illness is managed by primary care providers, and not by surgeons, evidence suggests that primary care physicians may receive inadequate training in musculoskeletal medicine. We evaluated the musculoskeletal knowledge and self-perceived confidence of fully trained, practicing academic primary care physicians and tested the following hypotheses: (1) a relationship exists between a provider's musculoskeletal knowledge and self-perceived confidence, (2) demographic variables are associated with differences in the knowledge-confidence relationship, and (3) specific education or training affects a provider's musculoskeletal knowledge and clinical confidence. An examination of basic musculoskeletal knowledge and a 10-point Likert scale assessing self-perceived confidence were administered to family practice, internal medicine, and pediatric faculty at a large, regional, academic primary care institution serving both rural and urban populations across a five-state region. Subspecialty physicians were excluded. Individual examination scores and self-reported confidence scores were correlated and compared with demographic variables. One hundred and five physicians participated. Ninety-two physicians adequately completed the musculo-skeletal knowledge examination. Fifty-nine (64%) of the ninety-two physicians scored < 70%. Higher examination scores were associated with male gender (p = 0.01) and participation in a musculoskeletal course (p = 0.009). Practitioners who took elective courses demonstrated higher scores compared with those who took required courses (p = 0.014). Greater musculoskeletal confidence was associated with the number of years in clinical practice (p = 0.045), male gender (p = 0.01), residency training in family practice (p < 0.00001), and prior participation in a musculoskeletal course (p = 0.0004). Physicians demonstrated greater confidence with medical issues than with musculoskeletal issues (mean confidence scores, 8.3 and 5.1, respectively; p < 0.00001). Higher scores for musculoskeletal knowledge correlated significantly with increasing levels of musculoskeletal confidence (r = 0.416, p < 0.0001).\n\nQuestion:\nDo important demographic variables impact the musculoskeletal knowledge and confidence of academic primary care physicians?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 biliary cirrhosis could induce pancreatic dysfunction such as modifications in endothelial nitric oxide synthase(eNOS) expression and whether the regulation of eNOS could be altered by the regulatory proteins caveolin and heat shock protein 90 (Hsp90), as well as by the modifications of calmodulin binding to eNOS. Immunoprecipitations and Western blotting analysis were performed in pancreas isolated from sham and cirrhotic rats. Pancreatic injury was minor in cirrhotic rats but eNOS expression importantly decreased with the length (and the severity) of the disease. Because co-immunoprecipitation of eNOS with both Hsp90 and caveolin similarly decreased in cirrhotic rats, eNOS activity was not modified by this mechanism. In contrast, cirrhosis decreased the calmodulin binding to eNOS with a concomitant decrease in eNOS activity.\n\nQuestion:\nIs endothelial nitric oxide synthase regulation altered in pancreas from cirrhotic rats?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nEndothelial nitric oxide synthase (eNOS) gene variations have been linked to a higher risk for cardiovascular diseases (CVD) by unknown mechanisms. Our aim was to determine if two single nucleotide polymorphisms (SNPs) located in NOS3 (E298D and i19342) interfere with microvascular endothelial function (MEF) and/or oxidative stress during the postprandial state. MEF was assessed with laser Doppler flowmetry at baseline and 2, 4, 6 and 8 h after ingestion of a single fatty meal (60% fat, 15% proteins and 25% carbohydrates) by 40 healthy young males. Oxidative stress was measured by nitrites/nitrates and oxidized LDL (LDL-ox) concentrations in fasting and postprandial states. Postprandial MEF was impaired in the carriers of minor alleles of the SNPs (global mean 60.99% Vs 87.25%, p = 0.016 for i19342; 63.62% Vs 95.71%, p = 0.011 for E298D). Carriers of E298D showed a higher LDL-ox at fasting and postprandial measures, and lower nitrites/nitrates at fasting.\n\nQuestion:\nDo gene variations of nitric oxide synthase regulate the effects of a saturated fat rich meal on endothelial function?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nInhibition of cyclooxygenase-2 has been proposed to be a potential mechanism for the chemoprevention of gastrointestinal tumors by nonsteroidal anti-inflammatory drugs. This study investigates the mechanisms by which the cyclooxygenase-2 inhibitor SC236 induces apoptosis of gastric cancer cell lines and its downstream signaling pathway. Two gastric cancer cell lines, AGS and MKN28, were treated with SC236 and assessed for cell growth and apoptosis. The involvement of mitogen-activated protein kinase and Akt kinase/protein kinase B (Akt/PKB) pathways and their downstream signalings were studied in the AGS cell line. SC236 treatment induced apoptosis in gastric cancer cells and caused activation of p38 and stress-activated protein kinase/jun kinase, but down-regulated Akt/PKB. The specific p38 inhibitor SB203580 and the dominant-negative stress-activated protein kinase/jun kinase both failed, while the constitutively active form of Akt/PKB was able to block SC236-induced apoptosis. SC236-induced apoptosis was coupled with release of cytochrome c and activation of caspases.\n\nQuestion:\nDoes inhibition of Akt/PKB by a COX-2 inhibitor induce apoptosis in gastric cancer cells?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nMutations in the retinitis pigmentosa GTPase regulator (RPGR) gene are a frequent cause of X-linked retinitis pigmentosa. The RPGR transcript undergoes complex alternative splicing to express both constitutive (Rpgr(ex1-19)) and Rpgr(ORF15) variants. Because functional studies of Rpgr suggest a role in intracellular protein trafficking through the connecting cilia, the goal of this study was to identify potential binding partners for Rpgr(ORF15) and to identify the domains on whirlin necessary for Rpgr binding. The C-terminus of mouse Rpgr(ORF15) was used as bait in a yeast two-hybrid system. Whirlin expression was analyzed using RT-PCR and Western blot analysis. Protein-protein interactions were confirmed using in vitro binding assays and coimmunoprecipitation. Subcellular colocalization was analyzed using immunohistochemistry on retinal cryosections. Yeast two-hybrid analysis identified whirlin, a PDZ-scaffold protein, as a putative binding partner for Rpgr(ORF15). The RPGR(ORF15)-whirlin interaction was confirmed using in vitro binding assays and coimmunoprecipitation from retinal tissue, and both proteins were shown to colocalize in the photoreceptor connecting cilia in vivo. Results from RT-PCR, Western blot analysis, and immunocytochemistry demonstrated that whirlin expressed multiple isoforms in photoreceptors with variable subcellular localization.\n\nQuestion:\nDoes rpgrORF15 connect to the usher protein network through direct interactions with multiple whirlin isoforms?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 epidermal growth factor receptor (EGFR) is overexpressed in colorectal cancer (CRC), and is correlated with poor prognosis, making it an attractive target for monoclonal antibody (mAb) therapy. A component of the therapeutic efficacy of IgG1 mAbs is their stimulation of antibody-dependent cellular cytotoxicity (ADCC) by natural killer (NK) cells bearing the CD16 receptor. As NK cells are functionally impaired in cancer patients and may be further compromised upon chemotherapy, it is crucial to assess whether immunotherapeutic strategies aimed at further enhancing ADCC are viable. CRC patients before, during and after chemotherapy were immunophenotyped by flow cytometry for major white blood cell populations. ADCC-independent NK cell functionality was assessed in cytotoxicity assays against K562 cells. ADCC-dependent killing of EGFR(+) A431 cancer cells by NK cells was measured with a degranulation assay where ADCC was induced by GA201, an anti-EGFR mAb glyco-engineered to enhance ADCC. Here, we confirm the observation that NK cells in cancer patients are dysfunctional. However, GA201 was able to induce robust NK cell-dependent cytotoxicity in CRC patient NK cells, effectively overcoming their impairment.\n\nQuestion:\nDoes glyco-engineered anti-EGFR mAb elicit ADCC by NK cells from colorectal cancer patients irrespective of chemotherapy?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 interleukin-6 (IL-6) stimulates rat muscle satellite cell proliferation in culture, and if so, to clarify the signalling mechanisms. Primary satellite cells were isolated from thirty male F344 rats, 11 weeks of age. IL-6 at concentrations of 0.01, 0.1, 1, 10 or 100 ng/ml was added to culture media. IL-6 at 0.01-1 ng/ml induced dose-dependent increase in cell proliferation. After treatment with 1 ng/ml IL-6, cell proliferation increased by 31%, and p-STAT3(+) /MyoD(+) cells increased in number compared to those in control media (P < 0.05). Inhibitors of JAK2 (AG 490) and STAT3 (STAT3 peptide) blocked the increase in BrdUrd(+) cell numbers at 6 h post stimulation with 1 ng/ml IL-6 (P < 0.05). Furthermore, cyclin D1 mRNA expression and cyclin D1(+) /MyoD(+) cell numbers significantly increased in cultures treated with 1 ng/ml IL-6 compared to those in control media (P < 0.05). In contrast, treatment with 10 and 100 ng/ml IL-6 did not stimulate cell proliferation. Treatment with 10 ng/ml IL-6 induced greater SOCS3 mRNA expression than with 1 ng/ml IL-6 and control media. Moreover, co-localization of SOCS3 and myogenin was observed after treatment with 10 ng/ml IL-6.\n\nQuestion:\nIs interleukin-6-induced satellite cell proliferation regulated by induction of the JAK2/STAT3 signalling pathway through cyclin D1 targeting?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 root of Bupleurum falcatum L. (BF) has been used in traditional Korean and Chinese medicines for over 2000 years to treat infections, fever, and chronic liver diseases. Among the many active compounds in BF ethanol extract (BFE), saikosaponins exert pharmacological activities including anti-inflammatory effects. Activated microglial cells release a variety of pro-inflammatory substances, leading to neuronal cell death and neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease. The aim of the present study was to investigate the mechanism of the anti-neuroinflammatory effects of BFE using lipopolysaccharide (LPS)-stimulated microglial cells and LPS-intraperitoneal injected C57BL/6 mice. Dried roots of BF were extracted with 70% ethanol (tenfold volume) on a stirring plate for 24h at room temperature to prepare BFE. Pure saikosaponins (SB3, SB4, and SD) were prepared by solvent extraction and column chromatography fractionation. BV2 murine microglial cells were treated with BFE or saikosaponins for 4h and stimulated with LPS. Generation of nitric oxide (NO), inflammatory cytokines, and reactive oxygen species (ROS) from activated microglial cells were monitored. The effects of BFE on NF-κB activation were determined using RT-PCR, reporter assay, and immunostaining. The in vivo effects of BFE were also assessed by immunohistochemical staining of tissue sections from LPS-injected mouse brains. Treatment with BFE or saikosaponins dose-dependently attenuated LPS-induced production of NO, iNOS mRNA, and ROS by 30-50%. They reduced LPS-mediated increases in the mRNA levels of IL-6, IL-1β, and TNF-α by approximately 30-70% without affecting cell viability, and decreased LPS-mediated NF-κB activity via reducing p65/RELA mRNA, transcriptional activity, and nuclear localization of NF-κB. BFE also reduced LPS-induced activation of microglia and astrocytes in the hippocampus and substantia nigra of LPS-injected mice.\n\nQuestion:\nDo ethanol extract of Bupleurum falcatum and saikosaponins inhibit neuroinflammation via inhibition of NF-κB?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 retrospective study was undertaken to provide data on occurrence, significance and therapy of ventricular tachyarrhythmia (VT) clusters (VTCs) in patients with dilated cardiomyopathy (DCM) and implantable cardioverter defibrillators (ICDs). Data on the clinical significance of VTCs are lacking in patients with DCM and ICDs. Baseline characteristics of 106 consecutive patients with DCM and ICDs were prospectively collected, and chart reviews and episode data retrospectively analyzed. A VTC was defined as > or =3 sustained VTs/24 h. During a mean follow-up of 33+/-23 months, 73 patients (68.9%) had recurrent VT or ventricular fibrillation (VF), 43 patients (40.6%) suffered only single VTs and 30 patients (28.3%) experienced 52 clusters of VTs. Actuarial survival free of VT or VF was 44.6%, 33.0% and 26.5%, and survival free of VTC was 77.3%, 72.2% and 67.1% after one, two and three years, respectively. Independent predictors of VT clusters were heart failure before ICD implantation (p = 0.033), presenting monomorphic VT (p = 0.044), EF <0.40 (p = 0.014) and inducible mVT, especially with right bundle branch block and superior axis configuration (p<0.001). Survival free of recurrent VTCs was 50.8%, 38.1% and 19.0% after one, two and three years, respectively. Once a VTC had occurred, only 56.7%, 46.4%, 30.9% and 15.5% of patients survived and were not transplanted after one, two, three and four years, respectively. Survival was even more reduced if a VTC was associated with cardiac decompensation: 65.6% and 21.9% after one and two years, respectively.\n\nQuestion:\nDo clusters of ventricular tachycardias signify impaired survival in patients with idiopathic dilated cardiomyopathy and implantable cardioverter defibrillators?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nAllergic rhinitis (AR) precedes and is often associated with bronchial asthma. Indeed, local and systemic inflammations in both conditions are very similar. Cysteinyl-leukotrienes (cys-LTs) are generated during early- and late-phase allergic reactions and induce smooth-muscle contraction, microvascular leakage, and mucous hypersecretion. Cys-LTs are detected in exhaled breath condensate (EBC) of asthmatics and regardless of bronchial symptoms, they are also found in EBC of rhinitic patients. To evaluate cys-LTs in EBC of allergic patients and to assess the activity of nasal fluticasone propionate (FP) on EBC cys-LTs levels. Cys-LTs coefficient of variation (CV) was evaluated from different EBC in 5 healthy volunteers. Cys-LTs levels from EBCs in 13 healthy controls and 56 allergic rhinitic (n=31) and rhinitic/asthmatic (n=25) patients were also evaluated at baseline. Subsequently patients were randomized to receive either FP 100 microg/day per nostril or placebo for 2 weeks and then re-evaluated for EBC cys-LTs. The CV was 14.12%. EBC cys-LTs in allergic patients were significantly higher than in healthy subjects (70.9 vs. 20.6 pg/mL (median), P<0.05), while it did not differ between asthmatic/rhinitic and purely rhinitic patients. Treatment significantly reduced cys-LTs (from 93.6 to 19.9 pg/mL, P<0.001). This effect was evident both in asthmatic/rhinitic and in rhinitic patients.\n\nQuestion:\nDoes intranasal steroid reduce exhaled bronchial cysteinyl leukotrienes in allergic patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nIt has been suggested that arnica can reduce postoperative edema and ecchymosis associated with cosmetic surgical procedures and improve outcome. Despite a high incidence of arnica use among upper blepharoplasty patients, evidence to support its treatment effect is lacking. The authors performed a randomized, double-blind, placebo-controlled trial to investigate the efficacy of arnica ointment after upper blepharoplasty. One hundred thirty-six bilateral upper blepharoplasty patients were randomized between arnica ointment 10% and placebo ointment. In both study arms, one periorbital area was designated as the treatment side (either arnica or placebo ointment), and the contralateral side served as an untreated (no ointment) internal control. As the primary endpoint, the overall periorbital appearance as based on light photography and judged by a medical and nonmedical panel, was assessed after 3 days, 7 days, and 6 weeks. Secondary endpoints were swelling, ecchymosis, erythema, pain, and patient satisfaction with recovery and outcome. There was no significant difference between arnica and placebo in overall judgment of periorbital appearance 3 days, 7 days, and 6 weeks after surgery. Furthermore, swelling, ecchymosis, erythema, pain, and patient satisfaction with recovery and outcome did not differ between arnica and placebo. Postoperative outcome in untreated eyelids was not different from eyelids treated with either arnica or placebo on any of the studied outcome measures.\n\nQuestion:\nDoes arnica Ointment 10 % Improve Upper Blepharoplasty Outcome : A Randomized , Placebo-Controlled Trial?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "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 pro-inflammatory cytokine interferon gamma (IFNγ), a key player in various neurological diseases, was recently shown to induce a dysregulated phenotype in neural stem/precursor cells (NSPCs) that is characterized by the simultaneous expression of glial and neuronal markers and irregular electrophysiological properties. Thus far, the mechanisms of this phenomenon have remained unclear. To determine if binding of the signal transducers and activators of transcription (Stat 1) to the sonic hedgehog (SHH) promoter is important for this phenomenon to occur, chromatin immunoprecipitation and pharmacological inhibition studies were performed. We report here that the activation of both the Stat 1 and SHH pathways is necessary to elicit the dysregulated phenotype.\n\nQuestion:\nAre interferon gamma and sonic hedgehog signaling required to dysregulate murine neural stem/precursor cells?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nPancreatic cancer has an extremely dismal clinical course and high fatality rate. Knowing that, adipokines could regulate insulin resistance, inflammation, immunity and carcinogenesis. Accordingly, an understanding of adipokines in relation to pancreatic cancer could be useful to improve disease outcome. We aimed to determine serum retinol binding protein-4 (RBP-4) and neutophil gelatinase-associated lipocalin (NGAL) levels in pancreatic cancer patients. Moreover, we assessed their association with tumor severity and with each other. A total of 23 pancreatic cancer patients and 20 healthy controls were enrolled. Fifteen of the pancreatic cancer patients underwent Whipple resection and were examined before and after operation. Serum glucose, insulin, lipid profile, CA19-9, RBP-4 and NGAL were estimated by ELISA. Significant elevation in serum concentrations of RBP-4 (64.4 ± 5.6 ng/ml) and NGAL (142(80-235) ng/ml) at p < 0.001 was found in pancreatic cancer patients. Both RBP-4 and NGAL were significantly lower after operation than before operation. Moreover, NGAL was elevated in advanced pathological T stage. Interestingly, RBP-4 and NGAL levels were positively correlated (r = 0.484, p = 0.05) and they are associated with some of the lipid profile parameters.\n\nQuestion:\nAre serum retinol binding protein-4 and neutrophil gelatinase-associated lipocalin interrelated in pancreatic cancer patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nPostmenopausal women undergoing chronic hemodialysis are at risk of uremic bone disease and postmenopausal osteoporosis. There are few reports discussing the effects of raloxifene hydrochloride on chronic hemodialysis patients. We investigated whether differences in the effects of raloxifene on bone mineral density (BMD) are dependent on the level of intact parathyroid hormone (iPTH). 47 postmenopausal hemodialysis patients with osteoporosis were divided into two groups, i.e. Group A, with treatment, and Group B, without treatment by raloxifene hydrochloride (60 mg/day, three times per week) for 1 year. We evaluated the changes in BMD at the distal one-third of the radial bone and aortic calcification index (ACI) by plain abdominal computerized tomography. Furthermore, we compared the BMD and ACI results for patients with similar iPTH levels within each group. After 1 year of raloxifene treatment, patients with iPTH levels of < 250 pg/ml in Group A showed significantly less BMD deterioration than similar patients in Group B (A: -0.31 +/- 1.7% vs. B: -3.71 +/- 0.7%, p = 0.04). However, raloxifene showed no difference in patients with iPTH levels of > or = 250 pg/ml in the two groups (A: -3.49 +/- 0.7% vs. B: -6.10 +/- 1.9%, p = 0.09). Among the patients with iPTH levels of < 250 pg/ml, changes in the ACI values were 1.30 +/- 0.3% for Group A and 1.67 +/- 1.0% for Group B. Among the patients with iPTH levels of (3) 250 pg/ml, the ACI values were 2.58 +/- 0.7% for Group A and 3.01 +/- 1.2% for Group B.\n\nQuestion:\nDoes raloxifene ameliorate progressive bone loss in postmenopausal dialysis patients with controlled parathyroid hormone levels?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 growing body of evidence identifies the renin-angiotensin system as a key factor in the onset and progression of renal damage in chronic partial obstruction, which often represents a complex diagnostic challenge. A prospective study was undertaken to evaluate the role of captopril mercaptoacetyltriglycine-3 (MAG-3) renography as an early diagnostic test of obstruction. We report the results in a subgroup of children who underwent surgical correction for pyeloureteral obstruction. Pyeloplasty was performed in 12 patients, including 10 males, 2 to 72 months old (median age 7) with unilateral hydronephrosis, including normal renal function and blood pressure. Basal and captopril enhanced diuretic renography with 99mtechnetium MAG-3 was performed within 24 hours using the same hydration and diuretic stimulus (0.75 mg./kg. furosemide), and 0.75 mg./kg. captopril was administered orally 60 to 90 minutes before scintigraphy. No adverse effects or modifications of the blood pressure were observed after captopril administration. The diuretic response was deeply worsened by angiotensin converting enzyme inhibition in each hydronephrotic kidney even when the basal study was only slightly abnormal (15-minute washout basal -27 +/- 16%, after captopril -9 +/- 13, p <0.005). After surgical correction the diuretic washout during angiotensin inhibition appeared normal in all patients (15-minute washout -56 +/- 14%). Separate renal function and parenchymal transit of MAG-3 were not modified by angiotensin converting enzyme inhibition, preoperatively or postoperatively.\n\nQuestion:\nDoes angiotensin converting enzyme inhibition worsen the excretory phase of diuretic renography for obstructive hydronephrosis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nCisplatin is a widely used gastric cancer (GC) chemotherapy; however, genetic factors regulating GC responses to cisplatin remain obscure. Identifying genes regulating cisplatin resistance could aid clinicians in tailoring treatments, by distinguishing cisplatin sensitive patients from those who might benefit from alternative platinum therapies, and highlight novel targeted strategies for overcoming cisplatin resistance. Here integrated epigenomics is applied to identify genes associated with GC cisplatin resistance. 20 GC cell lines were subjected to gene expression profiling, DNA methylation profiling and drug response assays. The molecular data were integrated to identify genes highly expressed and unmethylated specifically in cisplatin-resistant lines. Candidate genes were functionally tested by several in vitro and in vivo assays. Clinical impact of candidate genes was also assessed in a cohort of 197 GC patients. Epigenomic analysis identified bone morphogenetic protein 4 (BMP4) as an epigenetically regulated gene highly expressed in cisplatin-resistant lines. Functional assays confirmed that BMP4 is necessary and sufficient for the expression of several prooncogenic traits, likely mediated through stimulation of the epithelial-mesenchymal transition. In primary tumours, BMP4 promoter methylation levels were inversely correlated with BMP4 expression, and patients with high BMP4-expressing tumours exhibited significantly worse prognosis. Therapeutically, targeted genetic inhibition of BMP4 caused significant sensitisation of GC cells to cisplatin. Notably, BMP4-expressing GCs also did not exhibit cross resistance to oxaliplatin.\n\nQuestion:\nDoes integrated epigenomics identify BMP4 as a modulator of cisplatin sensitivity in gastric cancer?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nCentral adiposity has been implicated as a risk factor for Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC), possibly promoting the progression from inflammation to metaplasia and neoplasia. We performed a systematic review and meta-analysis of studies to evaluate the association between central adiposity and erosive esophagitis (EE), BE, and EAC, specifically exploring body mass index (BMI)-independent and gastroesophageal reflux (GERD)-independent effects of central adiposity on the risk of these outcomes. We performed a systematic search of multiple databases through March 2013. Studies were included if they reported effect of central adiposity (visceral adipose tissue area, waist-hip ratio, and/or waist circumference) on the risk of EE, BE, and EAC. Summary adjusted odds ratio (aOR) estimates with 95% confidence intervals (CIs), comparing highest category of adiposity with the lowest category of adiposity, were calculated by using random-effects model. Forty relevant articles were identified. Compared with patients with normal body habitus, patients with central adiposity had a higher risk of EE (19 studies; aOR, 1.87; 95% CI, 1.51-2.31) and BE (17 studies; aOR, 1.98; 95% CI, 1.52-2.57). The association between central adiposity and BE persisted after adjusting for BMI (5 studies; aOR, 1.88; 95% CI, 1.20-2.95). Reflux-independent association of central adiposity and BE was observed in studies that used GERD patients as controls or adjusted for GERD symptoms (11 studies; aOR, 2.04; 95% CI, 1.44-2.90). In 6 studies, central adiposity was associated with higher risk of EAC (aOR, 2.51; 95% CI, 1.54-4.06), compared with normal body habitus.\n\nQuestion:\nIs central adiposity associated with increased risk of esophageal inflammation , metaplasia , and adenocarcinoma : a systematic review and meta-analysis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nIn surgical graft replacement of the descending aorta graft, one-lung ventilation (OLV) is required to provide adequate surgical view and to allow removal of blood from the left lung. It is best to use a double-lumen tube (DLT) to assure OLV but it is sometimes difficult to place the left-sided DLT due to thoracic aneurysm or the dissection lumen. We retrospectively investigated tracheobronchial anatomy by chest X-ray and chest computed tomography (CT) in 29 cases of descending aorta replacement to determine how best to manage difficult placement of the left-sided DLT. From our database of 29 patients who had undergone descending aorta replacement between February 1, 2005, and December 31, 2009, we investigated the association between difficulty in placing the left-sided DLT and tracheobronchial anatomy by chest X-ray and CT. We could not place a left-sided DLT in 3 of 29 cases. Two of these cases were planned surgery for aortic aneurysm and the other was an emergency operation for acute aortic dissection. We could manage the two cases safely using a right-sided DLT. We compared chest X-ray and chest CT images of these 3 cases with the other 26 cases and found that compression of the tracheobronchial tree was prevalent in the cases of difficult placement of the left-sided DLT.\n\nQuestion:\nIs [ Difficulty in left-sided double-lumen tube placement in patients undergoing surgical graft replacement of the descending aorta predicted from tracheobronchial compression ]?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nProbiotic bacteria have a beneficial effect on intestinal inflammation. In this study, we have examined the effect of lactic acid and commensal Gram positive (+) bacteria conditioned media (CM) on tumour necrosis factor alpha (TNF-alpha) release and the mechanisms involved. Lipopolysaccharide (LPS) induced TNF-alpha secretion by peripheral blood mononuclear cells or the THP-1 cell line was monitored in the presence or absence of bacteria CM obtained from two probiotic strains, Bifidobacterium breve (Bb) and Streptococcus thermophilus (St), and three commensal bacterial strains (Bifidobacterium bifidum, Ruminococcus gnavus, and unidentified Streptococcus). Bb and St bacteria CM were allowed to cross filter grown intestinal epithelial cell monolayers (HT29-19A) to assess intestinal transport of active bacterial products. These products were characterised and their effect on LPS binding to THP-1 cells and nuclear factor kappa B (NF kappa B) activation assessed. Dose dependent inhibition of LPS induced TNF-alpha secretion was noted for both probiotic bacteria CM (64% and 71% inhibition for Bb and St, respectively) and to a lesser extent commensal bacteria CM (21-32% inhibition). Active products from Bb and St were resistant to digestive enzymes and had a molecular mass <3000 Da. Their inhibitory effect was preserved after transepithelial transport across intestinal cell monolayers, mainly in inflammatory conditions. LPS-FITC binding to THP-1 cells and NF kappa B activation were significantly inhibited by Bb and St CM.\n\nQuestion:\nDo lactic acid bacteria secrete metabolites retaining anti-inflammatory properties after intestinal transport?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nIn preclinical reports, restriction of dietary methionine intake was shown to enhance metabolic flexibility, improve lipid profiles, and reduce fat deposition. The present report is the outcome of a \"proof of concept\" study to evaluate the efficacy of dietary methionine restriction (MR) in humans with metabolic syndrome. Twenty-six obese subjects (six male and 20 female) meeting criteria for metabolic syndrome were randomized to a diet restricted to 2 mg methionine/kg body weight per day and were provided capsules containing either placebo (n = 12) or 33 mg methionine/kg body weight per day (n = 14). Energy expenditure, body composition, insulin sensitivity, and biomarkers of metabolic syndrome were measured before and after 16 wk on the respective diets. Insulin sensitivity and biomarkers of metabolic syndrome improved comparably in both dietary groups. Rates of energy expenditure were unaffected by the diets, but dietary MR produced a significant increase in fat oxidation (MR, 12.1 ± 6.0% increase; control, 8.1 ± 3.3% decrease) and reduction in intrahepatic lipid content (MR liver/spleen attenuation ratio, 8.1 ± 3.3% increase; control ratio, 2.2 ± 2.1% increase) that was independent of the comparable reduction in weight and adiposity that occurred in both groups.\n\nQuestion:\nDoes dietary methionine restriction increase fat oxidation in obese adults with metabolic syndrome?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nVisceral obesity is shown to be a predictor of morbidity and mortality. We evaluated the association of measurements of generalized adiposity and visceral fat area (VFA), with abnormalities of metabolic syndrome (MS). Seventy-six women (47.9 +/- 9.2 years) with BMI of 38.7 +/- 5.4 kg/m(2) underwent anthropometric measurements, laboratory procedures, bioeletrical impedance, and abdominal computed tomography (CT) scan. Diagnosis of MS was based on the presence of abdominal obesity and at least two of the following components: hypertension, dyslipidemia, and glucose intolerance and/or hyperinsulinemia. BMI was correlated with both components of adipose tissue--subcutaneous (r = 0.66, P < 0.01) and VFA (r = 0.33, P < 0.02)--and leptin levels (r = 0.38, P < 0.01). In contrast, VFA was correlated with 2-h glucose and insulin levels (r = 0.32 and 0.35, P < 0.05, respectively), triglyceride, HDL cholesterol, and uric acid (r = 0.33, -0.34 and 0.24, P < 0.05, respectively). Subjects with high VFA, matched for BMI, showed greater plasma glucose area under the curve (621 +/- 127 vs. 558 +/- 129 mg x h(-1) x dl(-1), P < 0.05), 2-h insulin (804 +/- 599 vs. 579 +/- 347 pmol/l, P < 0.05), and uric acid levels (0.33 +/- 0.07 vs. 0.26 +/- 0.06 mmol/l, P < 0.05) than subjects with low VFA. In logistic regression analysis, waist circumference, VFA, and 2-h insulin were identified as independent predictors of MS. Receiver operating characteristic curve analysis pointed out the values of 104 cm for waist circumference (58.1% specificity, 84.1% sensitivity), 158.5 cm(2) for VFA (78.1% specificity, 52.3% sensitivity), and 559.8 pmol/l for 2-h insulin (71.9% specificity, 69.8% sensitivity); the presence of at least two of the three variables resulted in a degree of concordance of 76%.\n\nQuestion:\nDoes two-hour insulin determination improve the ability of abdominal fat measurement to identify risk for the metabolic syndrome?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nMeasurement of proteolytic activity in feces is a traditional method for the diagnosis of exocrine pancreatic insufficiency (EPI). A drawback of this method is the occurrence of falsely low results that may lead to a false-positive diagnosis of EPI. We hypothesized that intestinal loss of serum proteinase inhibitors in protein-losing enteropathy (PLE) may inhibit fecal proteolytic activity and be a potential source of false low results. The objective of this study was to determine the effect of PLE on fecal proteolytic activity in dogs. Fecal proteolytic activity was measured using a radial diffusion casein digestion assay in 12 samples from 4 clinically healthy control dogs and 30 samples from 16 dogs with PLE. Gastrointestinal protein loss was assessed using an ELISA to determine fecal canine alpha 1-proteinase inhibitor concentration. The relationship between the concentration of canine alpha 1-proteinase inhibitor in the feces and the diameter cleared in the casein digestion assay was determined. The mean clearing diameter was compared between control dogs and dogs with PLE. A significant negative correlation was observed between fecal canine alpha1-proteinase inhibitor concentration and casein clearing diameter (P <.001, Pearson r =.6317, r2 =.3999). Mean clearing diameter was significantly lower in dogs with PLE than in control dogs (12.63 vs 16.83 mm, P <.001, two-tailed Student's t-test).\n\nQuestion:\nIs protein-losing enteropathy in dogs associated with decreased fecal proteolytic activity?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nAn important inter-individual variability in the response of insulin sensitivity following a fish oil supplementation has been observed. The objective was to examine the associations between single nucleotide polymorphisms (SNPs) within sterol regulatory element binding transcription factor 1 (SREBF1) gene and the response of insulin sensitivity to a fish oil supplementation. Participants (n = 210) were recruited in the greater Quebec City area and followed a 6-week fish oil supplementation protocol (5 g/day: 1.9-2.2 g EPA; 1.1 g DHA). Insulin sensitivity was assessed by the quantitative insulin sensitivity check index (QUICKI). Three tag SNPs (tSNPs) within SREBF1 gene were genotyped according to TAQMAN methodology. Three tSNPs (rs12953299, rs4925118 and rs4925115) covered 100% of the known genetic variability within SREBF1 gene. None of the three tSNPs was associated with either baseline fasting insulin concentrations (rs12953299, rs4925118 and rs4925115) (p = 0.29, p = 0.20 and p = 0.70, respectively) or QUICKI (p = 0.20, p = 0.18 and p = 0.76, respectively). The three tSNPs (rs12953299, rs4925118 and rs4925115) were associated with differences in the response of plasma insulin levels (p = 0.01, p = 0.005 and p = 0.004, respectively) and rs12953299 as well as rs4925115 were associated with the insulin sensitivity response (p = 0.009 and p = 0.01, respectively) to the fish oil supplementation, independently of the effects of age, sex and BMI.\n\nQuestion:\nDo sREBF1 gene variations modulate insulin sensitivity in response to a fish oil supplementation?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 the prognostic significance of lumican and decorin, two abundant small leucine-rich proteoglycans in breast tissue stroma. Lumican and decorin expression was examined in a cohort of 140 invasive breast carcinomas by Western blot analysis. All cases were axillary lymph node-negative and treated by adjuvant endocrine therapy. Lumican and decorin expression was highly correlated (r = 0.45, P < 0.0001), but although low levels of lumican were associated with large tumor size (P = 0.0496), negative estrogen receptor (P = 0.0024) and progesterone receptor status (P = 0.0116), and increased host inflammatory response (P = 0.0077), low decorin levels were associated only with large tumor size (P = 0.0496). However, using univariate analysis, low levels of lumican and decorin were both associated with a shorter time to progression (P = 0.0013 and 0.0262) and poorer survival (P = 0.001 and 0.0076). In multivariate analysis using the Cox regression model, low decorin was also shown to be an independent predictive factor for recurrence (hazard ratio 2.25: 95% confidence interval 1-5, P = 0.047) and survival (hazard ratio 3.39: 95% confidence interval 1.2-9.6, P = 0.021).\n\nQuestion:\nIs reduced expression of the small leucine-rich proteoglycans , lumican , and decorin associated with poor outcome in node-negative invasive breast cancer?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 role of P and its nuclear receptor PR in the growth of ectopic uterine tissue of mice with or without a disrupted PR gene. Animal study. Academic medical center. Female wild-type (WT) and transgenic knockout mice for P receptor (PRKO). Endometriosis was induced in the following groups of ovariectomized adult mice: [1] untreated WT, [2] estradiol (E(2))-treated WT, [3] P-treated WT, [4] E(2) + P-treated WT, [5] untreated PRKO, [6] E(2)-treated PRKO, and [7] E(2) + P-treated PRKO (n = 5 in each group). The size of ectopic uterine tissue in WT and PRKO mice were compared between the groups subjected to treatments with P or E(2). Tissue proliferating cell nuclear antigen (PCNA) levels were compared among these groups. Treatment with P only significantly decreased the size of WT ectopic uterine tissue. The untreated PRKO ectopic uterine tissue was significantly larger than WT tissue. Estradiol increased the size of ectopic uterine tissues, and this E(2)-dependent growth could be suppressed by P in WT tissues but not in PRKO tissues. Finally, the hormone-dependent changes in ectopic uterine tissue size were accompanied by comparable alterations in PCNA levels.\n\nQuestion:\nAre intact progesterone receptors essential to counteract the proliferative effect of estradiol in a genetically engineered mouse model of endometriosis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nIntegral to the function and morphology of the epithelium is the lattice of cell-cell junctions known as adherens junctions (AJs). AJ stability and plasticity relies on E-Cadherin exocytosis and endocytosis. A mechanism regulating E-Cadherin (E-Cad) exocytosis to the AJs has implicated proteins of the exocyst complex, but mechanisms regulating E-Cad endocytosis from the AJs remain less well understood. Here we show that Cdc42, Par6, or aPKC loss of function is accompanied by the accumulation of apical E-Cad intracellular punctate structures and the disruption of AJs in Drosophila epithelial cells. These punctate structures derive from large and malformed endocytic vesicles that emanate from the AJs; a phenotype that is also observed upon blocking vesicle scission in dynamin mutant cells. We demonstrate that the Drosophila Cdc42-interacting protein 4 (Cip4) is a Cdc42 effector that interacts with Dynamin and the Arp2/3 activator WASp in Drosophila. Accordingly, Cip4, WASp, or Arp2/3 loss of function also results in defective E-Cadherin endocytosis.\n\nQuestion:\nDo drosophila Cip4 and WASp define a branch of the Cdc42-Par6-aPKC pathway regulating E-cadherin endocytosis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nDespite tremendous progress in understanding the mechanisms of constitutive and alternative splicing, an important and widespread step along the gene expression pathway, our ability to deliberately regulate gene expression at this step remains rudimentary. The present study was performed to investigate whether a theophylline-dependent \"splice switch\" that sequesters the branchpoint sequence (BPS) within RNA-theophylline complex can regulate alternative splicing. We constructed a series of pre-mRNAs in which the BPS was inserted within theophylline aptamer. We show that theophylline-induced sequestering of BPS inhibits pre-mRNA splicing both in vitro and in vivo in a dose-dependent manner. Several lines of evidence suggest that theophylline-dependent inhibition of splicing is highly specific, and thermodynamic stability of RNA-theophylline complex as well as the location of BPS within this complex affects the efficiency of splicing inhibition. Finally, we have constructed an alternative splicing model pre-mRNA substrate in which theophylline caused exon skipping both in vitro and in vivo, suggesting that a small molecule-RNA interaction can modulate alternative splicing.\n\nQuestion:\nDoes ligand-induced sequestering of branchpoint sequence allow conditional control of splicing?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 if caesarean section (CS) increases the risk for childhood asthma and gastroenteritis with reference made to children born with vaginal delivery (VD). Retrospective study of data from linked Swedish medical service registers--Medical Birth Registry (MBR) and Hospital Discharge Registry (HDR). Data were obtained from women without any background/perinatal morbidity noted, and from children without any neonatal complications. Children that had reached at least 1 year of age and were found in the HDR were considered as cases, whereas children not found in the HDR or hospitalized for other causes than asthma or gastroenteritis were defined as controls. Odds ratios (OR) stratified for year of birth, maternal age, parity and smoking in early pregnancy were calculated. Investigations were made comparing the risk for in hospital treatment for asthma or gastroenteritis in CS children and in VD siblings of CS children. The overall inpatient morbidity in CS and VD children were also investigated. The OR for asthma in CS children was 1.31 [95% confidence interval (CI) 1.23-1.40]. The same OR, 1.31, was found for gastroenteritis (95% CI 1.24-1.38). The OR for CS children having experienced both asthma and gastroenteritis was further increased (1.74, 95% CI 1.36-2.23). The risk for asthma in VD siblings of CS children was not significantly increased, whereas VD siblings experienced a slightly increased risk for gastroenteritis. CS children had an increased overall in hospital morbidity when compared to VD children.\n\nQuestion:\nDoes caesarean section increase the risk of hospital care in childhood for asthma and gastroenteritis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 relationship between maternal thyroid function at each pregnancy trimester and neonatal screening results. Overt maternal thyroid dysfunction during gestation is associated with poor neonatal thyroid function. However, research on the relationship between suboptimal maternal thyroid function (assessed at three trimesters) and neonatal thyroid screening outcome is scarce. Prospective follow-up study during three trimesters of gestation in 886 Dutch Caucasian healthy pregnant women followed from 12-week gestation until term delivery (>37 weeks) and their neonates. The relation between neonatal data from the Congenital Hypothyroidism (CH) screening and maternal thyroid determinants [TSH, FT4 and thyroid peroxidase (TPO)-Ab] assessed at 12-, 24- and 36-week gestation. Boys have lower screening TT4 levels and their mothers have higher TSH levels at 24- and 36-week gestation. Higher maternal TSH levels (>97·5th percentile, as defined in 810 women without TPO-Ab at 12 weeks) at one or more times during pregnancy (O.R: 2·26, 95% CI: 1·20-4·29) and lower gestational age (O.R: 1·22, 95% CI: 1·05-1·41) are independently related to lower screening TT4 levels.\n\nQuestion:\nAre neonatal thyroid screening results related to gestational maternal thyroid function?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 examined the association between disturbed sleep and poorer daytime function in older women. Observational study. 2,889 women, mean age 83.5 years, participating in the 2002-2004 examination of the Study of Osteoporotic Fractures. N/A. Participants wore actigraphs for an average +/- SD of 4.1 +/- 0.83 24-hour periods. Actigraphy measured sleep variables were total sleep time and hours awake after sleep onset during the night and daytime napping behavior. Neuromuscular performance measurements included gait speed, chair stands, and grip strength. Functional limitations were assessed as self-reported difficulty with one or more of 6 instrumental activities of daily living (IADL). In fully adjusted, multivariable models, women who slept <6 hours per night walked 3.5% slower than those who slept 6.0-6.8 hours. Those who slept > or =7.5 hours took 4.1% longer to complete 5 chair stands than those who slept 6.8-7.5 hours. With higher wake after sleep onset (> or =1.6 hours compared to <0.7 hours) gait speed was 9.1% slower; it took 7.6% longer to complete 5 chair stands, and odds of functional limitation were 1.8 (95% CI: 1.4, 2.4) higher. Women with 1.0-1.8 hours of daytime sleep had higher odds (1.4 [95% CI: 1.1, 1.8]) of a functional limitation than those with <0.5 hours. Sleep variables did not appear to be associated with grip strength.\n\nQuestion:\nIs poor sleep associated with poorer physical performance and greater functional limitations in older women?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nLactase phlorizin hydrolase (LPH) activity is high in infants but declines 80%-90% before adulthood in most mammals, including humans. However, 95% of whites show autosomal dominant inheritance of a lifelong high lactose digesting capacity (LDC). This study attempted to clarify the molecular mechanism(s) of this phenomenon (posttranslational vs. pretranslational). A race- and sex-balanced cohort (n = 20) was studied, and lactose tolerance and levels of jejunal lactase protein, activity, and messenger RNA (mRNA) were measured. These data confirm that black heritage predicts low LDC, and white heritage predicts high LDC. Lactase breath hydrogen and determination of lactase/sucrase ratio (L/S) from jejunal biopsy specimens divide the group by high and low LDC phenotypes concordantly. All subjects with an L/S ratio > 0.5 had immunodetectable LPH protein and measurably higher LPH mRNA levels than the remaining subjects. LPH mRNA levels are highly correlated with lactase specific activity (r = 0.80) and L/S ratio (r = 0.88).\n\nQuestion:\nIs the polymorphic expression of lactase in adults regulated at the messenger RNA level?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nLipoprotein(a) [Lp(a)] is an independent risk factor for aortic valve stenosis and aortic valve calcification (AVC) in the general population. In this study, we determined the association between AVC and both plasma Lp(a) levels and apolipoprotein(a) [apo(a)] kringle IV repeat polymorphisms in asymptomatic statin-treated patients with heterozygous familial hypercholesterolaemia (FH). A total of 129 asymptomatic heterozygous FH patients (age 40-69 years) were included in this study. AVC was detected using computed tomography scanning. Lp(a) concentration and apo(a) kringle IV repeat number were measured using immunoturbidimetry and immunoblotting, respectively. Univariate and multivariate logistic regression were used to assess the association between Lp(a) concentration and the presence of AVC. Aortic valve calcification was present in 38.2% of patients, including three with extensive AVC (>400 Agatston units). Lp(a) concentration was significantly correlated with gender, number of apo(a) kringle IV repeats and the presence and severity of AVC, but not with coronary artery calcification (CAC). AVC was significantly associated with plasma Lp(a) level, age, body mass index, blood pressure, duration of statin use, cholesterol-year score and CAC score. After adjustment for all significant covariables, plasma Lp(a) concentration remained a significant predictor of AVC, with an odds ratio per 10-mg dL(-1) increase in Lp(a) concentration of 1.11 (95% confidence interval 1.01-1.20, P = 0.03).\n\nQuestion:\nAre lipoprotein ( a ) levels associated with aortic valve calcification in asymptomatic patients with familial hypercholesterolaemia?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nLacritin is a tear glycoprotein with prosecretory, prosurvival, and mitogenic properties. We examined lacritin levels in the tears of Sjögren's syndrome (SS) patients and explored the therapeutic potential of topical lacritin for the treatment of keratoconjunctivitis sicca. Tears from healthy controls (n = 14) and SS patients (n = 15) were assayed for lacritin using a C-terminal antibody. In a paired-eye study, autoimmune regulator (Aire) knockout (KO) mice (n = 7) were treated three times daily for 21 days with 10 μL of 4 μM lacritin (left eye) or vehicle (PBS) control (right eye). Tear secretion and ocular surface integrity were assessed at baseline and after treatment. Immunohistochemical staining of CD4+ T cells, cytokeratin-10 (K10), and cytokeratin-12 (K12) expression in the cornea and CD4+ T cell infiltration in the lacrimal glands were assessed. Lacritin monomer (421.8 ± 65.3 ng [SS] vs. 655.8 ± 118.9 ng [controls]; P = 0.05) and C-terminal fragment protein (125 ± 34.1 ng [SS] vs. 399.5 ± 84.3 ng [controls]; P = 0.008) per 100 μL of tear eluate were significantly lower in SS patients. In Aire KO mice treated with lacritin, tear secretion increased by 46% (13.0 ± 3.5 mm vs. 8.9 ± 2.9 mm; P = 0.01) and lissamine green staining score significantly decreased relative to baseline (-0.417 ± 0.06 vs. 0.125 ± 0.07; P = 0.02). Expression of K10 but not K12 in the cornea was significantly decreased in lacritin-treated eyes. Focal CD4+ T cell infiltration of the lacrimal glands was significantly reduced on the lacritin-treated side versus the untreated side.\n\nQuestion:\nIs topical administration of lacritin a novel therapy for aqueous-deficient dry eye disease?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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:\nSpecific aspects of care have been identified as important in order to provide high-quality care for patients with diabetes, including the need for patients to understand their condition. Little research has specifically explored the views and understanding of older people with diabetes in primary care. To explore views on quality of diabetes care and to gauge patients' understanding of their condition in order to identify areas for improvement in care. During August and September 2012, 13 semi-structured interviews were held with people with diabetes aged over 75 years, recruited from an inner-city general practice. The interviews focused on three areas: (1) their understanding of diabetes, (2) their views on the information they had received, and (3) their views on the quality of their care. The qualitative data were analysed using N-Vivo and techniques derived from framework analysis. A basic understanding of diabetes was shared among the responders, but certain gaps were identified, notably misunderstandings regarding hypoglycaemia and diabetic coma. Information was valued most if given in person; written information may not be impactful. Educational input attenuated over time and patients did not actively seek updating. Personal care was appreciated, but many patients expressed a desire to be kept better informed about their treatment.\n\nQuestion:\nIs ' A one-to-one thing better than a thousand books ' : views and understanding of older people with diabetes?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 studies have focused on the diagnostic and prognostic significance of CD24 and CD44 expression in human cancers. This study aimed to explore changes in CD44 and CD24 expression levels in patients with gastric cancer and to assess their prognostic values. CD44 and CD24 expression levels were investigated immunohistochemically in tumor samples from 290 patients with non-cardia gastric adenocarcinoma, of whom 77 had paired adjacent normal gastric mucosa. CD24 and CD44 mRNA levels were determined by quantitative polymerase chain reaction in 34 patients. Serum anti-Helicobacter pylori IgG was detected by enzyme-linked immunosorbent assay. Relationships between CD44 and CD24 protein expression levels and tumor parameters were analyzed and their prognostic values were evaluated by Cox proportional hazards models. CD24 and CD44 expression levels were significantly higher in patients with gastric cancer compared with those in paired controls (45.5% vs. 0.0%, and 61.0% vs. 0.0%, P < 0.001). Among 290 patients, the overall survival rate was significantly higher in CD44(-) compared with CD44(+) patients (log-rank test, P = 0.035). However, there was no significant correlation between CD24 expression and overall survival time (log-rank test, P = 0.115). Multivariate regression analysis indicated that positive CD44 expression (P = 0.029), TNM staging (P < 0.001), and lymphovascular invasion (P = 0.016), but not CD24 expression (P = 0.065), were independent prognostic factors in gastric cancer.\n\nQuestion:\nIs cD44 but not CD24 expression related to poor prognosis in non-cardia adenocarcinoma of the stomach?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 compare the incidence of hepatitis B virus (HBV)-associated membranous nephropathy (HBVMN) before and after universal HBV vaccination and to identify factors underlying the change. This study included 471 hospitalized children with nephrotic syndrome (NS) and 488 long-term follow-up hepatitis B surface antigen (HBsAg)-carrier children. Horizontal transmission (negative maternal HBsAg status) of HBVMN and HBV was assessed, and the incidence of HBVMN was compared before and after initiation of the universal HBV vaccination program started in 1984. The frequency of HBVMN in children with NS was 11.6% between 1974 and 1984, 4.5% between 1984 and 1994, 2.1% between 1994 and 2004, and 0% between 2004 and 2009. Similarly, the number of HBsAg-seropositive children with NS (mainly via horizontal infection) decreased after universal vaccination. The prevaccination frequency of HBV horizontal transmission in chronic HBsAg carriers from the general population was 36.5% compared with 5% in the postvaccination period. The incidence of HBVMN in these carriers revealed a parallel decline.\n\nQuestion:\nDoes universal hepatitis B vaccination reduce childhood hepatitis B virus-associated membranous nephropathy?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 Mediterranean diet (MedD) has long been associated with lower incidence of cardiovascular disease. Little information is available on association between MedD, vitamins intake and arrhythmias. We sought to investigate the relationship between adherence to MedD, antioxidants intake and spontaneous conversion of atrial fibrillation (AF). A group of 800 subjects was included in a case-control study; 400 of them had a first detected episode of AF. Nutritional parameters were assessed by a self-administered food frequency validated questionnaire and completed by an interviewer-administered 7 days diet recall. Adherence to MedD was evaluated using the Mediterranean Score and intake of antioxidants from food was calculated. Adherence to the Med Diet was lower in patients that developed AF compared to control (mean Med Score: 22.3 ± 3.1 vs 27.9 ± 5.6; p < 0.001). The median value was 23.5 (Q1-Q3 range 23-30) in patients with AF and 27.4 (Q1-Q3 range 26-33). The estimated intake of total antioxidants was lower in patients with AF (13.5 ± 8.3 vs 18.2 ± 9.4 mmol/d; p < 0.001). Patients in the highest quartile of Mediterranean Score had higher probability of spontaneous conversion of atrial fibrillation (OR1.9; 95%CI 1.58-2.81). High levels of antioxidants intake were also associated with an increasing probability of spontaneous conversion of arrhythmia (O.R. 1.8; 95%CI 1.56-2.99; P < 0.01).\n\nQuestion:\nDo adherence to Mediterranean diet and intake of antioxidants influence spontaneous conversion of atrial fibrillation?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 explore whether EEG and MRI abnormalities in the \"healthy\" hemisphere influence seizure and cognitive outcome after functional hemispherectomy. This is a retrospective consecutive cohort study of 43 children who underwent functional hemispherectomy between 1994 and 2008. Results of preoperative EEG recordings were reviewed for the existence of (inter)ictal epileptic or background abnormalities in the contralateral hemisphere. Preoperative MRIs were reexamined for the existence of unequivocal contralateral abnormalities. Postoperative seizure status was assessed, and of 34 children, IQ or mental developmental index (MDI) scores were obtained preoperatively and postoperatively. Seizure freedom was defined as Engel 1A. Contralateral EEG and MRI abnormalities were studied in relation to seizure and cognitive outcome. Thirty-three children achieved seizure freedom (77%). Of the 11 patients with contralateral MRI abnormalities, only 45% were seizure free, compared with 88% of the 32 patients without contralateral MRI lesions (p = 0.030). Children with contralateral MRI abnormalities more often were severely retarded after surgery (MDI/IQ <55; 90% vs 42%, p = 0.030). Postoperative MDI/IQ scores improved in none of the children with, but in 38% of those without contralateral MRI abnormalities (p = 0.034). Contralateral epileptic or background EEG abnormalities did not affect seizure outcome or postoperative cognitive performance. Four of 6 children with bilateral epileptic encephalopathy reached seizure freedom.\n\nQuestion:\nDo contralateral MRI abnormalities affect seizure and cognitive outcome after hemispherectomy?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 value of C-reactive protein concentrations in the assessment of prognosis in patients with advanced lymphoma has not been clearly defined. Patients with a diagnosis of non-Hodgkin's lymphoma (n = 108) and Hodgkin's lymphoma, (n = 39) and who had measurements of C-reactive protein were studied retrospectively and the data was reviewed over 8 years. Median survival, from the time of sampling, was 7.4 months. On univariate analysis there was a significant relationship between the duration of cancer specific survival and tumour type (p < 0.05), circulating concentrations of albumin (p < 0.001) and C-reactive protein (p < 0.001). In contrast, only C-reactive protein concentration was a predictor of death from intercurrent disease (p < 0.05). On multivariate analysis, C-reactive protein concentration remained a strong independent predictor of both death from cancer and intercurrent disease (p < 0.001). The hazard ratio associated with a unit increase in stratified C-reactive protein concentration was 8.18 (95% CI 4.80 - 13.95) for cancer specific death and 2.11 (95% CI 1.22 - 3.64) for intercurrent death.\n\nQuestion:\nDoes the systemic inflammatory response predict overall and cancer specific survival in patients with malignant lymphoma?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 was to investigate whether fatty and clear cell areas in large regenerative nodules (LRN), dysplastic nodules (DN), and hepatocellular carcinoma (HCC) show higher degree of genomic mutation compared to non-fatty/clear cell area in the same nodule or non-lesional tissue. We examined 22 nodular lesions (9 HCC, 5 DN and 8 LRN) from seven cirrhotic livers removed at transplantation. Frozen sections were used for manual microdissection of areas with fatty/clear cell change. DNA from microdissected tissue was amplified using arbitrarily primed polymerase chain reaction (AP-PCR), and PCR products were run on polyacrilamide gel generating a \"fingerprint\" band pattern. Autoradiographs were analysed using Adobe Photoshop version 6.0. Fingerprints from lesional tissue were compared to reference tissue and the total number of bands in excess or defect was calculated and divided by the total number of bands identified, obtaining the genomic damage fraction (GDF). Increasing GDF average values were seen from cirrhotic liver (0.13+/-0.04), to LRN (0.16+/-0.1), DN (0.28+/-0.08) and HCC (0.30+/-0.07). A statistically significant difference in GDF values was documented between cirrhotic liver and DN (p=0.008) and HCC (p=0.005) and between HCC and LRN (p=0.02). No significant difference was documented between DN and HCC, and between LRN and cirrhotic liver. Eleven nodules containing fat/clear cell areas were compared to the other 11 nodules without fat/clear cell areas. The GDF was not different between the two groups: 0.29+/-0.11 versus 0.25+/-0.12; p=0.5. The average value of genomic damage fraction between fat/clear cell areas (0.29+/-0.11) and no fat/clear cell areas (0.25+/-0.1) within the same nodules were not significantly different (p=0.11).\n\nQuestion:\nIs genomic alteration associated with fatty and clear cell change in hepatocellular carcinomas and its precursor nodular lesions in cirrhotic liver?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "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:\nCulturing Helicobacter pylori (Hp) has a low sensitivity rate, and is affected by factors such as the number of biopsies, transport, and culture conditions. Hp detection is also influenced by omeprazole, antibiotics, bismuth salts, or benzocaine use. Disinfection procedures based on glutaraldehyde are highly effective in eliminating any Hp contamination of endoscopic equipment. However, the possibility that some residual glutaraldehyde present in biopsy forceps after decontamination could affect Hp viability has not yet been investigated. Antral specimens from 25 patients with active gastric or duodenal ulcer obtained with three forceps (sterilized with ethylene oxide, glutaraldehyde, or glutaraldehyde-phenolate) were streaked on appropriate media, and results of culture evaluated. Helicobacter pylori was isolated in 17 patients. Positivity of culture was independent of the way the forceps were sterilized, and the number of colonies (mean +/- SD) was similar for the three types of forceps (475 +/- 312, 533 +/- 242, and 550 +/- 225 colony-forming units [CFUs] for ethylene oxide, glutaraldehyde, and glutaraldehyde-phenolate, respectively). Moreover, the incubation time since isolation was also similar (6.0 +/- 1.3, 5.8 +/- 1.2, and 5.7 +/- 1.2 days for ethylene oxide, glutaraldehyde, and glutaraldehyde-phenolate disinfected forceps, respectively).\n\nQuestion:\nDoes biopsy forceps disinfection technique influence Helicobacter pylori culture?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "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 variations in the plasma metabolomic profile of endometriosis patients as a consequence of pathophysiologic alterations associated with this disorder. Prospective study. For each subject, a plasma sample was collected after overnight fasting and before surgery. University medical center. The clinical cohort included 50 endometriosis patients, diagnosed at early (n = 6) and advanced (n = 44) stages of the disease, and 23 healthy women. All volunteers underwent diagnostic laparoscopy to visually confirm the presence or absence of endometriotic lesions. Metabolomic profiling of plasma samples based on Comparative identification of metabolites present in plasma from endometriosis patients and healthy women. The plasma metabolomic profile of endometriosis patients was characterized by increased concentration of valine, fucose, choline-containing metabolites, lysine/arginine, and lipoproteins and decreased concentration of creatinine compared with healthy women. Metabolic alterations identified in the plasma metabolomic profile of endometriosis patients correlate with pathophysiologic events previously described in the progression of this disease.\n\nQuestion:\nDo pathophysiologic processes have an impact on the plasma metabolomic signature of endometriosis patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 whether clinical improvement observed after deep brain stimulation (DBS) of the globus pallidus internus (GPi) in cervical dystonia (CD) is paralleled by the normalisation of temporal discrimination thresholds (TDTs), a marker of abnormal sensory processing in CD. TDT was tested in 11 patients with CD after they received DBS and was compared with TDT scores from 24 patients with CD and a group of 61 controls. A clear clinical response to GPi-DBS was demonstrated (total Toronto Western Spasmodic Torticollis Rating Scale scores fell from 50 to 18; P < 0.001). In contrast, TDT remained abnormal in the CD-DBS group (P < 0.001) and was not significantly different from the abnormal TDT range observed in CD.\n\nQuestion:\nDoes pallidal stimulation for cervical dystonia correct abnormal temporal discrimination?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "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:\nPortal vein ligation (PVL) and portal vein embolization (PVE) are used to induce hypertrophy of the future remnant liver before major liver resection. The aim of our study was to compare the hypertrophy response of the liver after PVL versus PVE in a rabbit model. Twenty rabbits were divided into an embolization group (n = 10) and a ligation group (n = 10). Both groups were divided in 2 subgroups of 5 rabbits that were humanely killed after days 7 and 14. The portal vein branches to the 3 cranial liver lobes (80% of the liver) were occluded. Regeneration of the caudal liver lobe was measured using volumetry based on computed tomography on days 3, 7, 10, and 14. Immunohistochemistry for Ki-67 and RAM11 was performed to quantify proliferating cells and macrophages. In addition, tissue tumor necrosis factor-α and interleukin-6 were assessed. The caudal liver volume increased over time in both groups (P < .001), but this increase was greater after PVE than after PVL (P = .001) with a mean degree of hypertrophy of 15% ± 4% and 20% ± 2%, respectively. When comparing the groups on the separate time points, a difference was found on days 10 and 14 (P = .008 and P = .016, respectively). These data were confirmed by Ki-67 staining, which showed a greater number of proliferating hepatocytes on day 7 after embolization (P = .016). Cytokine analysis of liver tissue did not show significant differences between the ligation and embolization groups on days 7 and 14.\n\nQuestion:\nDoes portal vein embolization induce more liver regeneration than portal vein ligation in a standardized rabbit model?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 pathophysiology of acute kidney injury (AKI) after cardiac surgery is not completely understood. Recent evidence suggests a pivotal role for the endothelium in AKI. In experimental models of AKI, the endothelial specific receptor Tie2 with its ligands Angiopoietin (Ang) 1 and Ang2 are deranged. This study investigates their status after cardiac surgery, and a possible relation between angiopoietins and AKI. From a cohort of 541 patients that underwent cardiac surgery, blood and urine was collected at 5 predefined time points. From this cohort we identified 21 patients who had at least 50% post-operative serum creatinine increase (AKI). We constructed a control group (n = 21) using propensity matching. Systemic levels of Ang1, Ang2, and sTie2 were measured in plasma and the AKI markers albumin, kidney injury molecule-1 (KIM-1) and N-acetyl-beta-D-glucosaminidase (NAG) were measured in the urine. Ang2 plasma levels increased over time in AKI (from 4.2 to 11.6 ng/ml) and control patients (from 3.0 to 6.7 ng/ml). Ang2 levels increased 1.7-fold more in patients who developed AKI after cardiac surgery compared to matched control patients. Plasma levels of sTie2 decreased 1.6-fold and Ang1 decreased 3-fold over time in both groups, but were not different between AKI and controls (Ang1 P = 0.583 and sTie2 P = 0.679). Moreover, we found a positive correlation between plasma levels of Ang2 and urinary levels of NAG.\n\nQuestion:\nDoes angiopoietin/Tie2 Dysbalance be Associated with Acute Kidney Injury after Cardiac Surgery Assisted by Cardiopulmonary Bypass?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 prevalence of both low testosterone levels and depression increases with age. Currently, there is no consensus regarding the existence of an association. Our study analyses the cross-sectional association of testosterone levels with depressive symptoms and its prospective association with the development of incident depressive symptoms. Longitudinal population-based study; based on the data of the Longitudinal Aging Study Amsterdam (LASA) including 608 men aged >or=65 years (median age 75.6 years). Linear and logistic regression between total and free testosterone levels and depressive symptoms as measured by the Center of Epidemiologic Studies Depression (CES-D) scale, taking into account medical and lifestyle factors. Cox Proportional Hazards model was used to assess incident depressive symptoms. Unadjusted linear regression between square-root transformed CES-D scores and free testosterone levels showed a significant inverse association as a continuous variable (beta = -0.10, P < 0.05), lowest quartile compared to highest (beta = 0.12, P < 0.05) and with a threshold value of 170 pmol/l (beta = 0.13, P < 0.05). The results remained significant for the group below threshold after adjustment for all confounders (beta = 0.09, P < 0.05). Cox Proportional Hazards Model showed a decreased risk for incident depressive symptoms for men with higher free testosterone levels [HR = 0.997 CI (0.995-1.000)]. Men with the threshold value below 220 pmol/l were at increased risk of incident depressive symptoms [HR = 1.989 CI (1.173-3.374)].\n\nQuestion:\nAre low free testosterone levels associated with prevalence and incidence of depressive symptoms in older men?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "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 existing caries risk factors in preschool children and to illustrate their caries risk profiles graphically with aid of a computer-based program. All 2-year-old children from a small town in northern Sweden were invited and 87% (n = 125) accepted to participate. Data was collected with a questionnaire concerning the child's normal diet and sugar consumption. Special care was taken to note the intake of sweet drinks and sugary between-meal products. Questions on general health and medication, toothbrushing frequency with parental help and use of fluorides were also included. The caries prevalence was recorded with mirror and probe and the level of oral mutans streptococci was enumerated with a chair-side technique. The obtained data were computerised in a risk assessment program (Cariogram) and a graphical profile of each child was constructed. The caries prevalence was 6%, and 18% had detectable levels of oral mutans streptococci. The sugar consumption was strikingly high with 82% and 97% having ice cream and sweets once a week or more often. In 22% of the families, toothbrushing with parental help was not a daily routine. Of the children, 51% displayed a low chance (0-20%) of avoiding caries in the future. The frequency of sugar consumption was the most pertinent factor in the children's caries risk profiles.\n\nQuestion:\nDo caries risk profiles in two-year-old children from northern Sweden?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]