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[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo determine whether the nucleic acid amplification (NAA) test on specimens collected by bronchoscopy improves the diagnostic accuracy of pulmonary tuberculosis (PTB) in sputum-negative patients. Bronchoscopy was performed among smear-negative PTB suspects to collect respiratory specimens to assess the efficacy and accuracy of the Amplified Mycobacterium Tuberculosis Direct (AMTD) test in the diagnosis of PTB. In 105 PTB suspects, 80 were finally excluded, of whom two were false-AMTD-positive. PTB (n = 25) was diagnosed in 10 patients culture-positive for Mycobacterium Tuberculosis (7/105 bronchial wash/bronchoalveolar lavage [BW/BAL] specimens, 6/315 expectorated sputum specimens [2 positive in 2 patients; 1 positive in 2 patients], and one with both), and in 15 patients with improvement after anti-tuberculosis treatment. Among the 25 PTB patients, 20 were AMTD-positive, of whom four were culture-positive. Three AMTD-negative patients were culture-positive. The sensitivity and specificity of AMTD were respectively 80.0% and 97.5%. The diagnostic yield was higher in respiratory specimens obtained at bronchoscopy and measured by AMTD than in conventional sputum or BW/BAL culture.\n\nQuestion:\nDo nucleic acid amplification test and bronchoscopy improve the diagnostic accuracy of smear-negative tuberculosis?\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:\nVenous thromboembolic disease (VTD) is a recently recognized complication of thalidomide in combination therapy for patients with multiple myeloma (MM). The authors assessed the frequency of VTD and its risk factors in 612 consecutive patients with plasma cell dyscrasia (PCD) who were evaluated and followed from 1991 to 2001. In the current study, 404 patients were diagnosed with multiple myeloma (MM), 174 with monoclonal gammopathy of undetermined significance (MGUS), and 34 with other forms (excluding amyloidosis). Univariable correlates of VTD were assessed using Kaplan-Meier analysis and Cox proportional hazards analysis. The authors identified several univariable correlates of VTD in patients with MGUS, including a family and medical history of VTD, immobility, low serum albumin level, and high leukocyte count. Patients with MGUS with immunoglobulin (Ig) G monoclonal immunoglobulin were found to be less prone to develop VTD. In patients with MM, a family and medical history of VTD and the presence of a hypercoagulable state were factors identified in univariable analysis to be associated with an increased risk of VTD. In patients with MM, for each unit increase in serum albumin, the risk of VTD was lower. The type of the treatment regimen did not appear to correlate with the development of VTD.\n\nQuestion:\nAre monoclonal gammopathy of undetermined significance and multiple myeloma associated with an increased incidence of venothromboembolic 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:\nInfantile hemangiomas (IHs) are the most common tumor of infancy, yet there are no Food and Drug Administration-approved therapeutics to date. Recently, the nonselective β-adrenergic-blocker propranolol has been shown to be a safe and effective means of treating IHs, although its mechanism has yet to be elucidated. We have previously demonstrated that propranolol induces early and incomplete adipogenesis in stem cells derived from hemangiomas. We hypothesize that propranolol promotes dysregulated adipogenesis via the improper regulation of adipogenic genes. Hemangioma stem cells (HemSCs) isolated from resected IH specimens were treated with adipogenic medium for 1 or 4 days in either propranolol or vehicle. Cell death was measured by the incorporation of annexin V and propidium iodide by flow cytometry. Adipogenesis was assessed by visualizing lipid droplet formation by Oil Red O staining. Proadipogenic genes C/EBPα, C/EBPβ, C/EBPδ, PPARδ, PPARγ, RXRα, and RXRγ were analyzed by quantitative reverse transcription and polymerase chain reaction. Hemangioma stem cells treated with propranolol increased lipid droplet formation compared to vehicle-treated cells indicating increased adipogenesis. Cell death as measured by FACS analysis indicated that the propranolol-treated cells died due to necrosis and not apoptosis. During adipogenesis, transcript levels of PPARδ, PPARγ, C/EBPβ, and C/EBPδ were significantly increased (P<0.01) in propranolol-treated cells relative to control cells. In contrast, RXRα and RXRγ levels were significantly decreased (P<0.05), and C/EBPα, a gene required for terminal adipocyte differentiation, was strongly suppressed by propranolol when compared to vehicle-treated cells (P<0.01).\n\nQuestion:\nDoes propranolol promote accelerated and dysregulated adipogenesis in hemangioma stem 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:\nThe consensus statements for eosinophilic oesophagitis recommend that ambulatory pH monitoring is one means of determining if gastro-oesophageal reflux is the cause of oesophageal eosinophilia and should guide pharmacological therapy. To evaluate prospectively the accuracy of pH monitoring as a predictor of endoscopic, histological and symptomatic response in patients with oesophageal eosinophilia. We conducted a prospective trial in which patients with oesophageal eosinophilic infiltration with ≥15 eos/hpf underwent a 24-h pH study and were placed in one of two treatment arms for 6 weeks based on positive or negative results. Patients with abnormal acid exposure were treated with esomeprazole 40 mg twice daily and others were treated with oral viscous budesonide 1 g twice daily. Response to treatment was assessed by oesophageal histology (<5 eos/hpf) and symptoms. A total of 51 patients were enrolled in the study. The average patient age was 39 years and 31 patients (61%) were male. The average number of eosinophils per hpf, prior to study enrolment was 41.2 (range 15-140, s.d. 27.7). Nineteen (37%) had positive pH studies and 32 (63%) had negative pH studies. Eighteen patients completed treatment with esomeprazole. Only eleven (61%) had histological response and, of these eleven, five (46%) had symptomatic improvement. A total of 28 patients with normal acid exposure completed treatment with budesonide. Only 16 (57%) had histological and 11 (69%) had symptomatic improvement.\n\nQuestion:\nDo results of ambulatory pH monitoring reliably predict response to therapy in patients with eosinophilic oesophagitis?\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 the relation between patient survival and incrementally increasing percentages of fluorescence in situ hybridization-determined complete loss of chromosome 3 (monosomy 3) and gain of chromosome 8q in primary uveal melanoma cells. Clinicopathological factors were related to disease-free survival. Fluorescence in situ hybridization was performed using probes on chromosomes 1, 3, 6, and 8. The percentages of UM cells with monosomy 3 or chromosome 8q gain were classified in groups with incrementally increasing percentages and related to disease-free survival. Correlations between clinical factors and cytogenetic aberrations were also analyzed. Two-hundred twenty choroidal and ciliary body melanomas were analyzed. The following proved to be significant predictors of survival in univariate analysis: older patient age (P = 0.003); large tumor diameter (P < 0.001); mixed cell type (P = 0.001); presence of closed microvascular loops (P < 0.001); loss of chromosome 1p (P = 0.006); monosomy 3 (P < 0.001); gain of 6p (P < 0.001); and gain of chromosome 8q (P < 0.001). Multivariate Cox analysis displayed monosomy 3 (Hazard ratio [HR] 2.83, P = 0.002) and gain of chromosome 8q (HR 3.13, P = 0.002) as the most important independent prognostic factors of poor survival, followed by older patient age (HR 1.02, P = 0.017). Increasing percentages of monosomy 3 and gain of chromosome 8q in tumor cells showed a correlation with worse prognosis (Log-rank test 49.9 and 40.4, both P < 0.001) and increased number of additional copies of 8q correlated with shorter disease-free interval (Log-rank test 45.7, P < 0.001).\n\nQuestion:\nDo higher percentage of FISH-determined monosomy 3 and 8q amplification in uveal melanoma cells relate to poor patient prognosis?\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:\nBlockade of the mineralocorticoid receptor (MR) in patients with chronic kidney disease (CKD) improves surrogate cardiovascular outcomes, such as left ventricular mass. Animal models of renal disease support a pathological role of mineralocorticoids, in the context of a high sodium intake. We aimed to assess the regulation of mineralocorticoid biosynthesis in patients with CKD. Seventy patients with CKD stages 3/4 and 30 patients with essential hypertension (EH) were recruited. Patients underwent detailed clinical phenotyping, drug history and biochemical assessment. Patients completed a 24-h urine collection for measurement of urinary tetrahydroaldosterone (THALDO) and tetrahydrocorticosterone (THDOC) excretion rates (measured using gas chromatography-mass spectrometry) and urinary electrolytes. The factors which correlated significantly with THALDO and THDOC excretion were entered into linear regression models. Patients with EH and CKD were well matched with no significant differences in gender, age or weight. The mean estimated glomerular filtration rate (eGFR) in CKD patients was 38.6/min/1.73 m(2). The mean urinary excretion rates of THALDO, THDOC and 24-h urinary sodium (24-h USod) were not significantly different between CKD and EH patients. The level of renal function did not correlate with THALDO or THDOC excretion. In patients with CKD, 24-h USodium (r = 0.614, P < 0.001) and 24-h UPotassium (r = 0.538, P < 0.001) were positively correlated with THALDO excretion. On multivariate linear regression analysis, 24-h USod was the strongest independent predictor (P = 0.004) of THALDO and THDOC excretion in CKD. In patients with EH, no relationship was seen between mineralocorticoid excretion and 24-h urinary sodium excretion.\n\nQuestion:\nIs urinary sodium excretion the main determinant of mineralocorticoid excretion rates in patients with chronic kidney 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:\nTo examine factors related to long-term psychological functioning in political ex-prisoners who had been subjected to systematic torture. The psychological status of 55 tortured political activists, 55 nontortured political activists, and 55 subjects with no history of torture or political activism was assessed using Structured Clinical Interview for DSM-III for psychiatric assessment, Semi-structured Interview for Survivors of Torture, and other self-rated and assessor-rated measures of anxiety, depression, and posttraumatic stress disorder (PTSD). Correlational and multiple regression analyses were used to assess the independent effects of precaptivity, captivity, and postcaptivity variables as predictors of long-term psychological status among the torture survivors. Istanbul, Turkey. Number of lifetime and current PTSD symptoms, and scores on the Beck Depression Inventory, Hamilton Depression Rating, Hamilton Anxiety Scale, and State-Trait Anxiety Inventory. Effect of captivity experience on various life areas (eg, family and social, economic, and employment status) and other postcaptivity psychosocial stressors were associated with PTSD symptoms, anxiety, and depression. Perceived severity of torture was related to PTSD symptoms but not to anxiety or depression. Lack of social support predicted anxiety and depression but not PTSD. Family history of psychiatric illness correlated with higher scores on most measures. Impact of captivity experience on family was the strongest predictor of PTSD symptoms.\n\nQuestion:\nDo factors related to long-term traumatic stress responses in survivors of torture in Turkey?\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 US Environmental Protection Agency voluntary phased-out residential use of chlorpyrifos in 2001. In contrast, in Costa Rica, chlorpyrifos-treated bags are increasingly used to protect banana and plantain fruits from insects and to fulfill product standards, even in populated areas. To evaluate children's exposure to chlorpyrifos in villages situated nearby banana plantations and plantain farms in Costa Rica. The study targeted two villages with use of chlorpyrifos-treated bags in nearby banana plantations and plantain farms and one village with mainly organic production. For 140 children from these villages, mostly indigenous Ngäbe and Bribri, parent-interviews and urine samples (n=207) were obtained. Urinary 3,5,6-trichloro-2-pyridinol (TCPy) levels were measured as a biomarker for chlorpyrifos exposure. In the banana and plantain village also environmental contamination to chlorpyrifos was explored. Children from the banana and plantain villages had statistically significant higher urinary TCPy concentrations than children from the referent village; 2.6 and 2.2 versus 1.3μg/g creatinine, respectively. Chlorpyrifos was detected in 30% of the environmental samples as well as in 92% of the hand/foot wash samples. For more than half of the children their estimated intake exceeded the US EPA chronic population adjusted dose. For some, the acute population adjusted dose and the chronic reference dose were also exceeded.\n\nQuestion:\nDo indigenous children living nearby plantations with chlorpyrifos-treated bags have elevated 3,5,6-trichloro-2-pyridinol ( TCPy ) urinary concentrations?\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:\nCognitive impairment is a common finding in end-stage renal disease patients on chronic hemodialysis, but data on the associated factors are still scanty. The present study evaluated the association between cognitive function and left ventricular systolic function in hemodialysis patients. We enrolled 72 patients admitted to the Hemodialysis Unit of the Catholic University, Rome. Cognitive performance was evaluated using the Mini Mental State Examination (MMSE); a cutoff of 24 was used to diagnose cognitive impairment. Left ventricular ejection fraction (LVEF) was assessed by echocardiography. Multivariable linear and logistic regressions were adopted to assess the adjusted association between cognitive performance and LVEF. Also, linear discriminant analysis was performed to ascertain the cutoff level of LVEF which best predicted cognitive impairment. Cognitive impairment was found in 37 (51 %) patients. According to linear regression, MMSE was independently associated with LVEF (B = 0.06; 95 % CI = 0.01-0.12; P = 0.040). Logistic regression confirmed the inverse association between LVEF and cognitive impairment (OR = 0.87; 95 % CI = 0.78-0.98; P = 0.022). In linear discriminant analysis, the LVEF cutoff level that best predicted cognitive impairment was ≤51 %.\n\nQuestion:\nIs cognitive performance associated with left ventricular function in older chronic hemodialysis patients : result of a pilot 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:\nMimetic peptides of apolipoprotein A-I (apoA-I) present a new strategy for promoting the biological activity of high density lipoproteins (HDL). This study aimed to compare the anti-inflammatory effects of ETC-642, a new apoA-I mimetic peptide, with discoidal reconstituted HDL (rHDL). New Zealand White rabbits (n=42) received daily infusions of saline, rHDL or discoidal complexes of an amphipathic peptide, ETC-642 (1-30 mg/kg), prior to insertion of non-occlusive carotid collars. Human coronary artery endothelial cells (HCAECs) were pre-incubated with ETC-642 or rHDL before TNF-α stimulation. Monocyte adhesion was investigated by pre-incubating HCAECs with rHDL or ETC-642, stimulating with TNF-α and incubating with THP-1 monocytes. Infusion of ETC-642 resulted in dose-dependent reductions of collar-induced expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in the artery wall (p<0.05). Pre-incubation of HCAECs with ETC-642 and rHDL reduced TNF-α-induced THP-1 monocyte adhesion (p<0.01). Furthermore, ETC-642 and rHDL treatment reduced TNF-α induced mRNA levels of inflammatory markers VCAM-1, fractalkine, MCP-1 and the p65 subunit of NF-κB (p<0.05).\n\nQuestion:\nDoes the apolipoprotein A-I mimetic peptide ETC-642 exhibit anti-inflammatory properties that are comparable to high density lipoproteins?\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 describe the phenotype consistent with axonal Charcot-Marie-Tooth disease type 2 (CMT2) in 4 families with a c.197G>T (p.(Gly66Val)) variant in CHCHD10. We sequenced the CHCHD10 gene in a cohort of 107 families with CMT2 of unknown etiology. The patients were characterized by clinical examination and electroneuromyography. Muscle MRI and biopsy of the muscle or nerve were performed in selected cases. Neuropathologic autopsy was performed in 1 case. The c.197G>T variant in CHCHD10 was found in 6 families, 4 of which included multiple individuals available for detailed clinical study. Variants in this gene have recently been associated with amyotrophic lateral sclerosis-frontotemporal dementia, mitochondrial myopathy, or spinal muscular atrophy Jokela type (SMAJ), but not with CMT2. Our patients had a late-onset distal axonal neuropathy with motor predominance, progressing to involve sensory nerves. Neurophysiologic and neuropathologic studies confirmed the diagnosis of sensorimotor axonal neuropathy with no loss of anterior horn neurons. Muscle biopsies showed occasional cytochrome c oxidase-negative fibers, combined with small amounts of mitochondrial DNA deletions.\n\nQuestion:\nDoes cHCHD10 variant p. ( Gly66Val ) cause axonal Charcot-Marie-Tooth 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:\nThere is scarce information in the literature about a possible association between atopy and certain clinical manifestations of NSAID sensitivity. (1) To evaluate the prevalence of atopy in patients proved to be sensitive to cyclooxygenase inhibitors. (2) To assess cross-reactivity to two alternative NSAIDs, paracetamol (acetaminophen) and nimesulide. NSAID-sensitive patients attending an allergy clinic and unselected controls were prick tested with inhalant allergens. Oral challenges with NSAIDs were carried out by the single-blinded (SBOC) method. Clinical data about personal and family history of allergic and atopic diseases were obtained by a careful review of the medical records and by direct questioning by experienced allergists. Fifty patients had positive SBOCs to the suspected NSAID and only these were studied. A personal history of atopic diseases was present in 41 patients (82%) and 7 controls (14.5%), and a family history in 24 patients (48%) and 6 controls (12.5%). Prick skin tests with aeroallergens were positive in 39 of 45 patients tested (86.6%) and in 14 of 48 controls (29.1%), (P = .0001). Skin test positivity rates were higher in patients with cutaneous challenge reactions who responded to only one NSAID (single reactors) in comparison to cross-reactors (P = .04). The most frequent clinical manifestations of NSAID sensitivity were (1) cutaneous (angioedema, urticaria) in 34 patients, (2) blended (cutaneous plus respiratory) in 12, (3) respiratory in 3, and (4) anaphylactoid in 1. Aspirin, pyrazolone, paracetamol, and ibuprofen were the drugs more frequently implicated in these reactions. Cross-sensitivity with paracetamol and nimesulide were 32% and 25%, respectively.\n\nQuestion:\nIs atopy a risk factor for non-steroidal anti-inflammatory drug sensitivity?\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:\nEzrin is highly expressed in skin cancer and promotes tumor metastasis. Ezrin serves as a promising target for anti-metastasis therapy. The aim of this study is to determine if the flavonoid bacailein inhibits the metastasis of skin cancer cells through Ezrin. Cells from a cutaneous squamous carcinoma cell line, A431, were treated with baicalein at 0-60 μM to establish the non-cytotoxic concentration (NCC) range for baicalein. Following treatment with baicalein within this range, total Ezrin protein (both phosphorylated and unphosphorylated forms) and phosphorylated-Ezrin (phos-Ezrin) were detected by western blotting, and Ezrin RNA was detected in A431 cells using reverse transcription-polymerase chain reaction (RT-PCR). Thereafter, the motility and invasiveness of A431 cells following baicalein treatment were determined using wound-healing and Boyden chamber invasion assays. Short-interfering RNA (si-RNA) specifically targeting Ezrin was transfected into A431 cells, and a si-RNA Ezrin-A431 cell line was established by G418 selection. This stable cell line was transiently transfected with Ezrin and mutant Ezrin plasmids, and its motility and invasiveness was subsequently determined to clarify whether bacailein inhibits these processes through Ezrin. We determined the range of NCCs for baicalein to be 2.5-40 μM in A431 cells. Baicalein displayed a dose- and time-dependent inhibition of expressions of total Ezrin and phos-Ezrin within this range NCCs. In addition, it exerted this inhibitory effect through the reduction of Ezrin RNA transcript. Baicalein also inhibited the motility and invasiveness of A431 skin carcinoma cells within the range of NCCs, in a dose- and time-dependent manner. A431 cell motility and invasiveness were inhibited by 73% and 80% respectively when cells were treated with 20 μM baicalein. However, the motility and invasiveness of A431 cells containing the Ezrin mutant were not effectively inhibited by baicalein.\n\nQuestion:\nDoes baicalein mediate inhibition of migration and invasiveness of skin carcinoma through Ezrin in A431 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:\nFor a variety of reasons, many patients abruptly discontinue statin therapy. The present analysis was conducted to determine whether the risk of cardiovascular outcomes increases after withdrawal of statin therapy in a stable cardiac population. In the Treating to New Target (TNT) study, 2 doses of atorvastatin (10 and 80 mg once daily) are being used in a double-blind parallel-group design. Of the 18,468 patients screened for study participation, 16,619 entered a dietary lead-in/drug-washout period, and of these, 15,432 eligible participants began treatment with atorvastatin 10 mg/d on an open-label basis. Of the subjects who entered the dietary lead-in/drug-washout period, 57% were receiving prior statin therapy. During the 6-week drug-washout period, there were 24 primary events (defined as coronary heart disease death, nonfatal myocardial infarction, resuscitated cardiac arrest, and fatal or nonfatal stroke); throughout the subsequent 8-week open-label period, there were 31 primary events. This equated to monthly Kaplan-Meier event rates of 0.20% during washout and 0.26% in the open-label phase. Event rates were therefore similar during the 2 phases.\n\nQuestion:\nIs there no evidence for an increase in acute coronary syndromes after short-term abrupt discontinuation of statins in stable cardiac 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:\nPrevious research has reported no effect of exercise modality (aerobic vs. resistance) on energy intake (EI). However, the relatively low energy cost of resistance training, the absence of total energy expenditure (TEE) measurements and the short duration of these studies justify further investigation. To evaluate the effects of exercise modality on EI, TEE, non-exercise activity thermogenesis (NEAT) and post-exercise energy compensation (PEEC) measured acutely, as well as for 10 and 34 h following exercise. Eight men and 8 women participated in three randomized crossover sessions: aerobic-based exercise, resistance-based exercise, and sedentary control. Exercise energy expenditure (ExEE) was continuously measured (indirect calorimetry) throughout the exercise sessions, which were designed to produce an isocaloric ExEE of 4 kcal/kg body weight. TEE and EI were monitored for 34 h post-exercise with biaxial accelerometers and a validated food menu, respectively. There were no differences in EI between exercise modalities acutely, as well as 10 and 34 h following exercise. However, a modality by sex interaction was noted for acute EI. Men ate more after the resistance than after the aerobic session (1567±469; 1255±409 kcal, respectively; P=0.034), while no differences were seen in women (568±237; 648±270 kcal, respectively; P=NS). No differences in TEE, NEAT and PEEC were found 10h and 34 h post-exercise, while a positive correlation (r=0.897; P<0.01) was found between both modalities across participants for PEEC.\n\nQuestion:\nDo resistance and aerobic exercises affect post-exercise energy compensation in normal weight men and women?\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 majority of patients with non-alcoholic fatty liver disease (NAFLD) have simple steatosis. A minority, however, present with non-alcoholic steatohepatitis (NASH), a condition that can lead to advanced fibrosis and cirrhosis. The frequencies of NASH and fibrosis among patients with NAFLD and sustained elevation of liver function tests (LFT) are uncertain. Our aim was to estimate these frequencies. We characterize a population with NAFLD, with special emphasis on insulin resistance and the metabolic syndrome, and study possible predictors for different stages of the disease. All referred patients with sustained elevation of LFT, radiological evidence or clinical suspicion of fatty liver, and absence of other liver disease, were invited to participate in our study in the period June 2002 to December 2004. Of 129 patients who met the inclusion criteria, 88 underwent liver biopsy. NAFLD was verified in 83 of them. Among these patients, 59 (71%) had the metabolic syndrome, 41 (49%) had NASH and 36 (43%) had fibrosis. Abnormal glucose tolerance (T2DM or impaired glucose tolerance) was the only independent risk factor for NASH (OR: 3.14; 95% CI: 1.20-8.23). Independent predictors for fibrosis were abnormal glucose tolerance (OR: 3.83; 95% CI: 1.29-11.40) and body mass index (OR: 1.20; 95% CI: 1.06-1.36) per kg/m2.\n\nQuestion:\nIs abnormal glucose tolerance a predictor of steatohepatitis and fibrosis in patients with non-alcoholic fatty liver 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:\nPrevious studies have demonstrated that positive blood culture could contribute to poorer outcomes in patients with pneumonia. However, the impact of positive blood culture on the outcomes of patients with sepsis-induced acute respiratory distress syndrome (ARDS) has not been evaluated. An observational study that prospectively screened 4861 patients admitted to medical or surgical intensive care units (ICUs) of a tertiary referral centre was performed. Among 4861 admitted patients, 146 diagnosed with sepsis-induced ARDS were enrolled (mean age: 66.1 years). Lower PaO2 /FiO2 , decreased respiratory system compliance, and higher lung injury scores (LIS) on the day of ARDS diagnosis were associated with positive blood cultures (n = 68) rather than negative blood cultures (n = 78). There was no relationship between positive blood culture and in-hospital mortality. Kaplan-Meier estimates also revealed that positive blood culture was not associated with 60-day mortality but with an increased length of stay in the hospital and in the ICU (P = 0.007 and P = 0.016, respectively). Using multivariate logistic regression, higher LIS was independently associated with positive blood culture. In addition, chronic pulmonary disease, lower platelet count, higher LIS, and the development of shock on the diagnosis of ARDS, were independent risk factors for in-hospital mortality.\n\nQuestion:\nIs positive blood culture associated with increased mortality in patients with sepsis-induced acute respiratory distress syndrome?\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:\nAlthough the repositioning maneuvers are usually very effective in patients with BPPV, some patients still complain residual dizziness. Danhong injection (DHI), a traditional Chinese medicine, can effectively dilate blood vessels and improve microcirculation, and has been proven to be effective in improving cervical vertigo and posterior circulation ischemic vertigo. The aim of this study was to evaluate the effects of DHI on residual dizziness after successful repositioning treatment in patients with BPPV. Eighty-six patients with BPPV were randomized into two treatment groups, DHI group and non DHI group. The DHI group received the same repositioning treatment as the non-DHI group, with the addition of DHI therapy. The durations of residual dizziness of DHI group and non-DHI group were compared. In addition, the scores of the dizziness handicap inventory of these two groups were calculated. The durations of residual dizziness of DHI group were shorter than that of non-DHI group. There were no significant differences in the scores of dizziness handicap inventory in the first week between these two groups, and there were much significant differences in the second, the fourth, the sixth and eighth weeks.\n\nQuestion:\nDoes danhong enhance recovery from residual dizziness after successful repositioning treatment in patients with benign paroxysmal positional vertigo?\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:\nIntroduction of the yellow obese gene (A(y)) into mice (KKAy) results in obesity and diabetes by 5 weeks of age. Using this model of type 2 diabetes, we evaluated male and female 6- to 8-month-old wild-type (WT, n=10) and KKAy (n=22) mice subjected to myocardial infarction (MI) and sacrificed at day (d) 7. Despite similar infarct sizes (50% ± 4% for WT and 49% ± 2% for KKAy, P=not significant), the 7d post-MI survival was 70% (n=7/10) in WT mice and 45% (n=10/22) in KKAy mice (P<.05). Plasma glucose levels were 1.4-fold increased in KKAy mice at baseline compared to WT (P<.05). Glucose levels did not change in WT mice but decreased 38% in KKAy post-MI (P<.05). End-diastolic and end-systolic dimensions post-MI were smaller and fractional shortening improved in the KKAy (5% ± 1% in WT and 10% ± 2% in KKAy, P<.05 for all). The improved cardiac function in KKAy was accompanied by reduced macrophage numbers and collagen I and III levels (both P<.05). Griffonia (Bandeiraea) simplicifolia lectin-I staining for vessel density demonstrated fewer vessels in KKAy infarcts (5.9% ± 0.5%) compared to WT infarcts (7.3% ± 0.1%, P<.05).\n\nQuestion:\nDo obese and diabetic KKAy mice show increased mortality but improved cardiac function following 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:\n\"Chimney\" techniques used to extend landing zones for endovascular aortic repair (chEVAR) have been increasingly reported; however, concerns about durability and patency remain. The purpose of this analysis was to examine midterm outcomes of chEVAR. All patients at the University of Florida treated with chEVAR were reviewed. Major adverse events (MAEs) were recorded and defined as any chimney stent thrombosis, type Ia endoleak in follow-up, reintervention, 30-day/in-hospital death, or ≥25% decrease in estimated glomerular filtration rate after discharge. Primary end points included chimney stent patency and freedom from MAE. Secondary end points included complications and long-term survival. From 2008 to 2012, 41 patients (age ± standard deviation, 73 ± 8 years; male, 66% [n = 27]) were treated with a total of 76 chimney stents (renal, n = 51; superior mesenteric artery, n = 16; celiac artery, n = 9) for a variety of indications: juxtarenal, 42% (n = 17, one rupture), suprarenal, 17% (n = 7), and thoracoabdominal aneurysm, 17% (n = 7); aortic anastomotic pseudoaneurysm, 15% (n = 6; three ruptures); type Ia endoleak after EVAR, 7% (n = 3); and atheromatous disease, 2% (n = 1). Two patients had a single target vessel abandoned because of cannulation failure, and one had a type Ia endoleak at case completion (technical success, 93%). Intraoperative complications occurred in seven patients (17%), including graft maldeployment with unplanned mesenteric chimney (n = 2) and access vessel injury requiring repair (n = 5). Major postoperative complications developed in 20% (n = 8). The 30-day mortality and in-hospital mortality were 5% (n = 2) and 7% (n = 3), respectively. At median follow-up of 18.2 months (range, 1.4-41.5 months), 28 of 33 patients (85%) with available postoperative imaging experienced stabilization or reduction of abdominal aortic aneurysm sac diameters. Nine patients (32%) developed endoleak at some point during follow-up (type Ia, 7% [n = 3]; type II, 10% [n = 4]; indeterminate, 7% [n = 3]), and one patient underwent open, surgical conversion. The estimated probability of freedom from reintervention (±standard error mean) was 96% ± 4% at both 1 year and 3 years. Primary patency of all chimney stents was 88% ± 5% and 85% ± 5% at 1 year and 3 years, respectively. Corresponding freedom from MAEs was 83% ± 7% and 57% ± 10% at 1 year and 3 years. The actuarial estimated survival for all patients at 1 year and 5 years was 85% ± 6% and 65% ± 8%, respectively.\n\nQuestion:\nDoes critical analysis of results after chimney endovascular aortic aneurysm repair raise cause for concern?\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:\nOptimal training intensity and the adequate exercise level for physical fitness is one of the most important interests of coaches and sports physiologists. The aim of this study was to investigate the validity of the Narita et al target heart rate equation for the adequate exercise training level in sedentary young boys. Forty two sedentary young boys (19.07±1.16 years) undertook a blood lactate transition threshold maximal treadmill test to volitional exhaustion with continuous respiratory gas measurements according to the Craig method. The anaerobic threshold (AT) of the participants then was calculated using the Narita target heart rate equation. Hopkin's spreadsheet to obtain confidence limit and the chance of the true difference between gas measurements and Narita target heart rate equation revealed that the Narita equation most likely underestimates the measured anaerobic threshold in sedentary young boys (168.76±15 vs. 130.08±14.36) (Difference ±90% confidence limit: 38.1±18). Intraclass correlation coefficient (ICC) showed a poor agreement between the criterion method and Narita equation (ICC= 0.03).\n\nQuestion:\nDoes narita target heart rate equation underestimate the predicted adequate exercise level in sedentary young boys?\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 difference of the dose distribution in clinical target volume and organ at risk (OAR) between coplanar decile field intensity-modulated radiotherapy (IMRT) and conventional three-dimensional conformal radiotherapy (3D-CRT) for postoperative radiotherapy of cervical cancer. Ten postoperative patients with cervical cancer were selected randomly to undergo CT scan and planning target volume (PTV) and OAR contouring. 3D-CRT and coplanar decile IMRT planning was performed for each patient with a prescribed dose of 50 Gy. The homogeneity index (HI), conformity index (CI), maximum dose, minimum dose, mean dose of PTV, and irradiated volume of OARs were calculated and the results were compared. 5-field IMRT, 7-field IMRT and 9-field IMRT plans had a significant better conformity index (CI) of PTV compared with 3D-CRT (P<0.05) . Compared with 3D-CRT plans , V30, V40, and V50 of the bladder, V50 of the small bowel, and V30, V40, and V50 of the rectum in the coplanar decile IMRT plans were all significantly reduced (P<0.05) but showed no significant differences among the IMRT plans (P>0.05).\n\nQuestion:\nDo [ Dosimetric study of postoperative 3-dimensional conformal radiotherapy and coplanar decile intensity-modulated radiotherapy for cervical 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:\nEpinephrine added to local anesthetic agents for spinal anesthesia is frequently used to prolong the duration of anesthesia. Epinephrine stimulates the alpha-adrenoceptor, and it is known that the alpha2-adrenoceptor agonists have a central inhibitory effect. We investigated the effect of intrathecal epinephrine during propofol sedation with spinal anesthesia, using a bispectral index (BIS) monitor. Twenty adult patients, scheduled for spinal anesthesia, were allocated to the control group ( n = 10) or epinephrine group ( n = 10). Patients in the control group received 14 mg of tetracaine, whereas the epinephrine group received 14 mg of tetracaine and 0.2 mg of epinephrine. Immediately after the pinprick test, propofol was administered at 0.5 mg x kg(-1) by infusion for the initial dose, then continuously at 2 mg x kg(-1) x h(-1) in both groups. BIS scores were recorded before subarachnoid block, and then every 5 min for 90 min after subarachnoid block. There were significant differences in the BIS score between the two groups at 45-55 min and at 60-70 min after subarachnoid block.\n\nQuestion:\nDoes addition of epinephrine to intrathecal tetracaine augment depression of the bispectral index during intraoperative propofol sedation?\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 purpose of this study was to investigate whether the amount of intracoronary attenuation influences the diagnostic accuracy of MDCT coronary angiography in the detection of clinically significant stenosis. One hundred twenty patients in sinus rhythm with suspected coronary artery disease who underwent MDCT of the heart and conventional coronary angiography were retrospectively selected. The population was divided into two groups depending on median (326 H) coronary vascular enhancement (i.e., low attenuation and high attenuation). The diagnostic accuracy of MDCT for the detection of clinically significant coronary artery lesions (> or = 50% lumen reduction) in both groups was compared with that of quantitative coronary angiography. The sensitivity of MDCT was 90% and 93% for the low- and high-attenuation groups, respectively. The specificity was 95% and 97%.\n\nQuestion:\nDoes higher intracoronary attenuation improve diagnostic accuracy in MDCT coronary angiography?\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:\nAcknowledging that eosinophilic esophagitis (EoE) is a disease with variable involvement throughout the oesophagus, studies have suggested a minimum of five biopsies to diagnose EoE. Although it is accepted that furrows and exudates appear to represent areas of inflammation, no research to date has looked specifically at EoE endoscopic findings to see if eosinophilic infiltrate correlates with specific endoscopic findings. To evaluate the distribution of eosinophils in EoE and determine whether endoscopic appearances predict the degree of eosinophilia at various locations of the oesophagus. We performed a prospective cross sectional study of EoE (treated and untreated) patients to study the distribution of eosinophils according to endoscopic findings. The oesophagus of 10 EoE patients were biopsied up to 32 times in a circumferential manner. The mucosal changes were documented at the site of each biopsy. Histological determination of eosinophil counts and related histopathology of the oesophagus were then correlated with endoscopic findings. Similar biopsy assessments were made in treated (resolved) EoE patients (n = 6) to determine the permanence of specific endoscopic appearances. A total of 16 patients were biopsied (10 EoE, 6 treated EoE). A total of 432 biopsies were obtained in all with 294 biopsies from 10 EoE subjects. Eosinophil density was increased distally in the majority of EoE patients. Biopsies performed in areas of exudates and furrows demonstrated higher eosinophil counts. Lines and normal-appearing oesophagi in EoE subjects were not commonly associated with elevated eosinophil counts (>15 eos/HPF). Rings alone without associated furrows or plaques did not demonstrate elevated eosinophil counts and were seen in resolved EoE (Rx-EoE) as well as in active EoE patients.\n\nQuestion:\nDo endoscopic appearance and location dictate diagnostic yield of biopsies in eosinophilic oesophagitis?\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 establish the human colorectal cancer cell model SW620/PAR4D with inducible suppression of proteinase activated receptor 4 (PAR4) expression, and investigate the role PAR4 plays in the proliferation and migration of cancer cells. A human colorectal cancer cell line with tetracycline-inducible expression regulatory system, namely SW620/Tet-on, was established; inducible expression lentiviral vector with artificial microRNA targeting PAR4, pLVX-Tight-Puro-PAR4-miR, was constructed and transfected into SW620/Tet-on to make an inducible PAR4-suppressed cell model SW620/PAR4D. Western blotting was used to confirm the suppression of PAR4 expression after the doxycycline (DOX) treatment. CCK-8 assay was used to evaluate the impact of suppressed PAR4 expression on cell proliferation, and wound-healing assay was used to analyze the migration of the cells. The SW620/PAR4D cell model was established successfully. Suppression of PAR4 expression by DOX treatment had no significant impact on the growth/proliferation of SW620/PAR4D cells, but markedly inhibited the cell migration.\n\nQuestion:\nDoes [ Downregulation of proteinase activated receptor 4 inhibit migration of SW620 human colorectal 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:\nWe have identified a novel cancer/testis antigen, TRAG-3, (Taxol Resistance Associated Gene-3) that was initially discovered in search for new genes involved in drug resistance by differential display. Early study of TRAG-3 revealed minimal to absent expression in various normal tissues and over-expression in many carcinoma cell lines including several melanoma lines. Northern and RT-PCR technologies were used to evaluate TRAG-3 expression in numerous cell lines and tumor tissue. Analysis of a wider panel of normal tissues, 32 melanoma cell lines and 4 malignant melanomas demonstrates TRAG-3 expression in 25 of the 32 melanoma cell lines (78%) and four of four of the malignant melanoma tumors (100%). Of the additional eight normal tissues screened, expression was present in normal testis but absent in all other tissues. RT-PCR evaluation of TRAG-3 reveals two transcripts in many carcinoma cell lines with sequencing of these products demonstrating the 799 bp TRAG-3 transcript and a second alternatively spliced transcript, TRAG-3long TRAG-3 maps to band Xq28 within a MAGE gene complex, however sequence analysis demonstrates that TRAG-3 is not homologous to other known cancer/testis antigens.\n\nQuestion:\nIs tRAG-3 , a novel cancer/testis antigen , overexpressed in the majority of melanoma cell lines and malignant melanoma?\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:\nRed cell distribution width (RDW) is a variability of red cell sizes and has been associated with outcomes in many clinical settings. Its prognostic value in intensive care unit (ICU) has been reported but requires confirmation. The study aimed to investigate the role of RDW in predicting hospital mortality in critically ill patients. This is a retrospective study conducted in a 24-bed ICU of a tertiary teaching hospital. Data on demographic characteristics and laboratory measurements were collected from medical information database. Baseline variables were compared between survivors and nonsurvivors. The primary endpoint was hospital mortality; and ICU length of stays (LOS) were compared between patients with RDW >14.8% and ≤14.8%. The predictive value of RDW was also measured using receiver operating characteristic (ROC) curves. Two-sided P<0.05 was considered to be statistically significant. A total of 1,539 patients were enrolled during study period, including 1,084 survivors and 455 nonsurvivors. In univariate analysis, variables such as age, sex, primary diagnosis, C-reactive protein (CRP), RDW and albumin were significantly associated with hospital mortality. RDW remained significantly associated with mortality after adjustment for sex, age, Charlson index albumin and CRP, with an odds ratio of 1.1 (95% CI: 1.03-1.16). Diagnostic performance of RDW in predicting mortality appeared to be suboptimal (AU-ROC: 0.62). Changes in RDW during a short follow up period were not associated with mortality.\n\nQuestion:\nIs red cell distribution width associated with hospital mortality in unselected critically ill 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:\nThymidylate synthase (TYMS) expression in lung cancer tissue affects the therapeutic efficacy of pemetrexed (PMT). TYMS protein expression is primarily assessed using immunohistochemistry (IHC), but this method is not suitable for accurate quantitative analysis. It is not known whether the analysis of TYMS gene copy number using fluorescence in situ hybridization (FISH) is a useful method for assessment of TYMS expression. The participants were patients with chemo-naïve advanced NSCLC treated with PMT plus carboplatin (CBDCA) in prospective clinical phase II study. TYMS expression was evaluated in 40 patients by gene copy number and protein expression using FISH and IHC. Therapeutic efficacy was evaluated by investigating the response rate (RR), disease control rate (DCR), progression-free survival (PFS), and overall survival (OS). TYMS gene amplification was detected in 8 patients (32 %) among 25 patients who could be evaluated for TYMS gene copy number. There were no patients with complete or partial response in the TYMS amplified group. RR and DCR were lower in the TYMS amplified group compared with the TYMS unamplified group (0 versus 35.3 %, p = 0.0539, 62.5 versus 94.1 %, p = 0.0443). PFS and OS were reduced in the TYMS amplified group. The analysis of TYMS gene copy number had higher sensitivity and specificity compared with TYMS protein expression (76.2 versus 50.0 %, 75.0 versus 66.7 %).\n\nQuestion:\nDoes thymidylate synthase gene amplification predict pemetrexed resistance in patients with advanced non-small cell lung 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:\nThis study aimed at correlating maternal blood glucose levels with DNA damage levels in the offspring of women with diabetes or mild gestational hyperglycemia (MGH). Based on oral glucose tolerance test results and glycemic profiles, 56 pregnant women were allocated into 3 groups: nondiabetes, MGH, and diabetes. The offspring of these women (56 infants) were also evaluated. Maternal peripheral blood and umbilical cord blood samples were collected and processed for biochemical and DNA damage analysis by the comet assay. A positive correlation between maternal blood glucose mean and increased offspring DNA damage levels was observed. Hyperglycemia played a role in offspring DNA damage, but other diabetes-induced complications were also involved.\n\nQuestion:\nIs increased DNA Damage Related to Maternal Blood Glucose Levels in the Offspring of Women With Diabetes and Mild Gestational Hyperglycemia?\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 usefulness of transcranial Doppler CO2 reactivity (CO2R) for prediction of ipsilateral ischemic stroke in carotid artery stenosis and occlusion with a meta-analysis of prospective studies based on individual patient data. We searched Medline, Biosis Previews, Science Citation Index, The Cochrane Library, and EMBASE for studies in which patients with severe carotid artery stenosis or occlusion underwent Doppler CO2R testing (inhalation of CO2 or breath-holding) and were prospectively followed for ipsilateral ischemic stroke. Individual data from 754 patients from 9 studies were included. We used percentage cerebral blood flow velocity increase (pCi) during hypercapnia as the primary CO2R measure, and defined impaired reactivity as pCi <20% increase. In a multiple regression model, impaired CO2R was independently associated with an increased risk of ipsilateral ischemic stroke (hazard ratio [HR] 3.69; confidence interval [CI] 2.01, 6.77; p < 0.0001). Risk prediction was similar for recently symptomatic vs asymptomatic patients. Using continuous values of pCi, a significant association between decreasing pCi and increasing risk of ipsilateral stroke was found: HR of 1.64 (95% CI 1.33, 2.02; p < 0.0001) per 10% decrease in pCi. For patients with asymptomatic internal carotid artery stenosis only (n = 330), a comparable stroke risk prediction was found: increasing HR 1.95 (95% CI 1.26, 3.04; p = 0.003) per 10% decrease in pCi.\n\nQuestion:\nDoes cerebrovascular reactivity predict stroke in high-grade carotid artery 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:\nWe hypothesized that deregulated corepressor actions, with associated histone deacetylation activity, epigenetically suppressed vitamin D receptor (VDR) responsiveness and drives resistance towards 1alpha,25-dihydroxyvitamin D(3). Profiling, transcriptional, and proliferation assays were undertaken in 1alpha,25(OH)(2)D(3)-sensitive MCF-12A nonmalignant breast epithelial cells, a panel of breast cancer cell lines, and a cohort of primary breast cancer tumors (n = 21). Elevated NCoR1 mRNA levels correlated with suppressed regulation of VDR target genes and the ability of cells to undergo arrest in G(1) of the cell cycle. A similar increased ratio of corepressor mRNA to VDR occurred in matched primary tumor and normal cells, noticeably in estrogen receptor alpha-negative (n = 7) tumors. 1alpha,25(OH)(2)D(3) resistance in cancer cell lines was targeted by cotreatments with either 1alpha,25(OH)(2)D(3) or a metabolically stable analogue (RO-26-2198) in combination with either trichostatin A (TSA; histone deacetylation inhibitor) or 5-aza-2'-deoxycytidine (DNA methyltransferase inhibitor). Combinations of vitamin D(3) compounds with TSA restored VDR antiproliferative signaling (target gene regulation, cell cycle arrest, and antiproliferative effects in liquid culture) to levels which were indistinguishable from MCF-12A cells.\n\nQuestion:\nDoes altered nuclear receptor corepressor expression attenuate vitamin D receptor signaling in 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:\nUveal melanoma (UM) cells and neurohormone-producing cells both originate from the neural crest. Somatostatin receptors subtype 2 (SSTR2) are over-expressed in several tumors, often from neuroendocrine origin, and synthetic antagonists like octreotide and octreotate are being used as diagnostic or therapeutic agents. We investigated the SSTR2 expression in UM, and determined whether this expression was related to prognosis of the disease. UM cell lines and fresh primary UM samples were tested for SSTR2 expression by autoradiography (AR) using 125I-Tyr3-octreotate. Furthermore, UM cell lines were analyzed for SSTR2 mRNA expression with quantitative real-time RT-PCR. Using AR, cell-surface SSTR2 expression was demonstrated in two UM metastatic cell lines, but no expression was detected in three cell lines derived from primary UM. However, all primary and metastatic UM cell lines showed mRNA expression levels for SSTR2 using quantitative real-time RT-PCR. Only three of 14 primary UM demonstrated moderate SSTR2 expression, and this expression was not significantly associated with tumor-free survival or any tested prognostic factor.\n\nQuestion:\nIs expression of the SST receptor 2 in uveal melanoma a prognostic marker?\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:\nInterstitial cells of Cajal (ICC) are distributed with smooth muscle throughout the gastrointestinal tract and are involved in regulating motility. ICC were recently discovered in the wall of the human gallbladder. This study sought to determine whether ICC are present in human bile ducts. Biliary tract samples were obtained from several sources: surgical specimens (n = 16, 11 women, mean age 61 years); archival post-mortem specimen (n = 1, 86 years, man); and cadavers (n = 2, 68 and 80 years, men). Paraffin-embedded sections (3 microm) from the gallbladder (fundus, body and neck) and both extrahepatic and intrahepatic bile ducts were investigated. A double immunofluorescence protocol using polyclonal and monoclonal c-kit antibodies and mast cell tryptase was used to distinguish c-kit-positive cells with typical ICC morphology from c-kit-positive mast cells. Small bowel samples were used as positive controls. ICC in the gallbladder were confirmed by ultrastructural study. c-kit-positive cells with characteristic ICC morphology were identified in the subepithelial and muscular layers of the gallbladder and extrahepatic bile ducts. They were most prominent within the muscle layer of the extrahepatic bile ducts where they were organized into loosely arranged laminae running parallel to circular smooth muscle fibers. ICC were not found in intrahepatic bile ducts.\n\nQuestion:\nAre interstitial cells of Cajal present in human extrahepatic bile ducts?\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 scientific literature contains many examples where DNA sequence analyses have been used to provide definitive answers to phylogenetic problems that traditional (non-DNA based) approaches alone have failed to resolve. One notable example concerns the rhinoceroses, a group for which several contradictory phylogenies were proposed on the basis of morphology, then apparently resolved using mitochondrial DNA fragments. In this study we report the first complete mitochondrial genome sequences of the extinct ice-age woolly rhinoceros (Coelodonta antiquitatis), and the threatened Javan (Rhinoceros sondaicus), Sumatran (Dicerorhinus sumatrensis), and black (Diceros bicornis) rhinoceroses. In combination with the previously published mitochondrial genomes of the white (Ceratotherium simum) and Indian (Rhinoceros unicornis) rhinoceroses, this data set putatively enables reconstruction of the rhinoceros phylogeny. While the six species cluster into three strongly supported sister-pairings: (i) The black/white, (ii) the woolly/Sumatran, and (iii) the Javan/Indian, resolution of the higher-level relationships has no statistical support. The phylogenetic signal from individual genes is highly diffuse, with mixed topological support from different genes. Furthermore, the choice of outgroup (horse vs tapir) has considerable effect on reconstruction of the phylogeny. The lack of resolution is suggestive of a hard polytomy at the base of crown-group Rhinocerotidae, and this is supported by an investigation of the relative branch lengths.\n\nQuestion:\nDoes analysis of complete mitochondrial genomes from extinct and extant rhinoceroses reveal lack of phylogenetic resolution?\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:\nEndovascular therapy is an alternative for the treatment of AIS resulting from large intracranial arterial occlusions that depends on the use of iodinated RCM. The risk of RCM-mediated AKI following endovascular therapy for AIS may be different from that following coronary interventions because patients may not have identical risk factors. All consecutive patients with large-vessel AIS undergoing endovascular therapy were prospectively recorded. We recorded the baseline kidney function, and RCM-AKI was assessed according to the AKIN criteria at 48 hours after RCM administration. We compared the rate of RCM-AKI 48 hours after the procedure and sought to determine whether any preexisting factors increased the risk of RCM-AKI. We identified 99 patients meeting inclusion criteria. The average volume of contrast was 189 ± 71 mL, and the average creatinine change was -4.6% at 48 hours postangiography. There were 3 patients with RCM-AKI. Although all 3 patients died as a result of their strokes, return to baseline creatinine levels occurred before death. There was a trend toward higher rates of premorbid diabetes mellitus, chronic renal insufficiency, preadmission statin and NSAID use, and a higher serum creatinine level on admission for the RCM-AKI group. The volume of procedural contrast was similar between groups (those with and those without RCM-AKI) (P = .5).\n\nQuestion:\nIs the risk of acute radiocontrast-mediated kidney injury following endovascular therapy for acute ischemic stroke low?\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 obstetric handoff quality differs morning versus evening, weekend versus weekday, or based on provider type. Using the American College of Obstetricians and Gynecologists (ACOG) handoff guidelines, we developed an observational tool to assess whether handoffs included its 8 recommended elements. We observed handoffs between attending obstetricians, Obstetrics and Gynecology residents, labor and delivery nurses, and certified nurse midwives. Observation times included a balance of morning, evening, weekdays, and weekends. Participants were blinded to the study objectives. We defined high-quality handoffs as those that included 7 of the 8 recommended ACOG elements. A total of 425 inpatient handoffs were observed: 233 (55%) were morning handoffs and 189 (45%) were evening; 251 (59%) were on weekdays and 171 (41%) on weekends. Of the handoffs observed, 201 (48%) were presented by residents, 139 (33%) by nurses, 56 (13%) by attending obstetricians, and 26 (6%) by midwives. Only 169 (40%) of all handoffs met criteria for high quality. A greater percentage of all morning handoffs met criteria as compared to evening handoffs (45% vs. 34%, p < 0.05). There was no significant difference between the overall percentage of weekday and weekend handoffs meeting criteria (39% vs. 42%, p = 0.48). Residents had a higher percentage of high-quality handoffs as compared to nurses (55% vs. 32%, p < 0.001).\n\nQuestion:\nDoes handoff quality for obstetrical inpatients vary depending on time of day and provider type?\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:\nMyelinating Schwann cells compartmentalize their outermost layer to form actin-rich channels known as Cajal bands. Herein we investigate changes in Schwann cell architecture and cytoplasmic morphology in a novel mouse model of carpal tunnel syndrome. Chronic nerve compression (CNC) injury was created in wild-type and slow-Wallerian degeneration (Wld(S) ) mice. Over 12 weeks, nerves were electrodiagnostically assessed, and Schwann cell morphology was thoroughly evaluated. A decline in nerve conduction velocity and increase in g-ratio is observed without early axonal damage. Schwann cells display shortened internodal lengths and severely disrupted Cajal bands. Quite surprisingly, the latter is reconstituted without improvements to nerve conduction velocity.\n\nQuestion:\nDoes chronic nerve compression alter Schwann cell myelin architecture in a murine 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:\nHippocampal pathology has been proposed to underlie clinical, functional and cognitive impairments in schizophrenia. The hippocampus is a highly plastic brain region; examining change in volume, or change bilaterally, over time, can advance understanding of the substrate of recovery in psychosis. Magnetic resonance imaging and outcome data were collected at baseline and 6-year follow-up in 42 first-episode psychosis subjects and 32 matched controls, to investigate whether poorer outcomes are associated with loss of global matter and hippocampal volumes. Bilateral hippocampal increase (BHI) over time, as a marker of hippocampal plasticity was hypothesized to be associated with better outcomes. Regression analyses were performed on: (i) clinical and functional outcomes with grey matter volume change and BHI as predictor variables; and (ii) cognitive outcome with BHI as predictor. BHI was present in 29% of psychosis participants. There was no significant grey matter loss over time in either patient or control groups. Less severe illness course and lesser symptom severity were associated with BHI, but not with grey matter change. Employment and global function were associated with BHI and with less grey matter loss. Superior delayed verbal recall was also associated with BHI.\n\nQuestion:\nIs bilateral hippocampal increase following first-episode psychosis associated with good clinical , functional and cognitive outcomes?\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:\nGlioblastoma multiforme (GBM) is an incurable malignant glioma which is very resistant to radiation and alkylating agent-based chemotherapy. Necrosis is a hallmark for GBM and the layer surrounding necrotic area is packed with cells which are now believed to be those migrating out of the necrotic area. Oxidative stress is a condition that GBM cells encounter in the necrotic zone, which is one of the stressful conditions that GBM cells need to resist in order to survive. Our previous studies revealed that low PAX6 expression is a favorable molecular trait for survival acquired by GBM cells because PAX6 could suppress cell invasion and tumorigenicity. Since detachment of cells from GBM is an early event for cell migration and subsequent invasion, we examined whether PAX6 is involved in cell survival after detachment. PAX6 over-expression was achieved in glioma cells transiently (by adenoviral-mediated transient over-expression) or stably (by the establishment of stable cell lines after transfection). The effect of PAX6 over-expression on the survival and growth of glioma cells after detachment from the culture was determined. Our data revealed that GBM cells (with their low PAX6 levels) survived the detachment procedure well. However, PAX6 over-expression attenuated GBM cell recovery of growth after detachment-induced stress. Importantly, intracellular reactive oxygen species (ROS) levels increased following cell detachment and that PAX6 over-expressing cells retained higher level of ROS than control cells. This may be partially responsible for the impaired growth rate after cell detachment. Addition of anti-oxidant improved the cell viability of PAX6 over-expressing cells, but did not restore their ability to proliferate.\n\nQuestion:\nDoes pAX6 increase glioma cell susceptibility to detachment and oxidative stress?\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 effect of nicardipine (Nic) on the cytoplasmic free calcium concentration ([Ca2+]i) in thymocytes and on the proliferation of thymus lymphocytes from mice in vitro. The [Ca2+]i was measured by loading cells with the fluorescent dye Fura-2. The lymphocyte proliferation was determined by [3H] thymidine incorporation. Nic 1-30 mumol . L-1 elevated [Ca2+]i of resting thymocytes with the percentages of its increase 43%-192% and 12%-148% in the presence and absence of extracellular Ca2+ respectively. Mitogen Con A 5 mg . L-1 also released Ca2+ from intracellular stores. Nic decreased the enhancement of [Ca2+]i induced by Con A. The IC50 (mumol . L-1) was 26.8 (95% limit: 24.8-29.0) and approximated to 10 in the presence and absence of extracellular Ca2+ respectively. Nic 1-30 mumol . L-1 did not stimulate the proliferation of resting lymphocytes from mouse thymuses (P > 0.05), but inhibited the proliferation when the lymphocytes had been stimulated by Con A (P < 0.01).\n\nQuestion:\nDoes nicardipine enhance cytoplasmic calcium concentration in mouse thymocytes 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:\nA small supernumerary marker chromosome is often seen in patients with developmental disorders. Prior to array-based comparative genomic hybridization markers were rarely genotyped end to end. In this study, a valid genotype-to-phenotype correlation was possible because the supernumerary marker chromosomes were fully characterized by array-based comparative genomic hybridization in a genome-wide analysis. Ten consecutive de novo small supernumerary marker chromosome cases were systematically genotyped using G-banding, C-banding, AgNOR staining, whole-genome array-based comparative genomic hybridization, and fluorescence in situ hybridization. Among 10 small supernumerary marker chromosome cases studied, 4 (40%) were not identified by array-based comparative genomic hybridization because of low-level mosaicism or because they lacked euchromatin. One case (10%) was a simple pericentromeric marker extending from 5p13.3 to 5q11.2. Five (50%) markers showed unexpected complexity. Two cases had markers that were derivative acrocentric (AgNOR+) chromosomes with the euchromatin from chromosomes 18p or 19p. Each of the other three cases with complex markers had unusual characteristics including a marker from noncontiguous segments of chromosome 19q, a highly complex rearrangement involving a chromosome 20 homolog as well as the small supernumerary marker chromosome, and a mosaic duplication of a proximal 8p marker.\n\nQuestion:\nDoes a systematic analysis of small supernumerary marker chromosomes using array CGH expose unexpected complexity?\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 primary objective was to evaluate whether addition of enteral iron supplementation will facilitate a systemic erythropoietic effect when feeding erythropoietin (Epo) to suckling rats. A secondary objective was to confirm that iron does not alter the previous finding that enteral Epo exerts local trophic effects on the small intestine. Four-day-old Sprague-Dawley rats underwent gastrostomy and were fed a cow's milk-based rat milk substitute for 8 days. We studied rats fed rat milk substitute alone (control), enteral Epo 425 U x kg(-1) x day(-1), and enteral Epo 1700 U x kg(-1) x day(-1), and the effects of oral iron sulfate (Fe) therapy (6 mg x kg(-1) x day(-1)). Blood was collected to measure hemoglobin (Hb), reticulocytes, red cell indices, and zinc protoporphyrin/heme. To confirm previous work describing trophic effects of enteral Epo on the intestine, duodenal villous height was measured. Hb levels in control (84 +/- 1 g/L) were similar to Epo 425 (87 +/- 1 g/L). Hb levels in control+Fe (97 +/- 1 g/L), Epo 425+Fe (97 +/- 1 g/L), and Epo 1700 (94 +/- 1 g/L) were higher than control, P < 0.001, but mean Hb level in Epo 1700+Fe was higher (105 +/- 1 g/L) than the other groups, P < 0.003. Mean cell volume was higher in rats receiving iron supplementation, compared with those without iron, P < 0.005. Duodenal villous height was taller in Epo 1700+Fe compared with control + Fe, P < 0.01.\n\nQuestion:\nDo enteral erythropoietin and iron stimulate erythropoiesis in suckling 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:\nLow birth weight has been associated with metabolic and vascular diseases, but the precise mechanism is debated. Adiponectin is one of the key molecules in metabolic disease, and a decrease in level precedes the onset of type 2 diabetes and development of atherosclerosis. Our aim is to examine whether low birth weight is associated with adiponectin concentration in adult. We conducted a population-based cross-sectional study of 2277 subjects (1661 men and 616 women) aged 35 to 66 years who had their self-reported birth weights and adiponectin concentrations measured as adults. After adjusting for potential confounders, including age, sex, current body mass index (BMI), smoking status, alcohol consumption, and exercise, geometric mean adiponectin levels were 6.63, 6.45, 6.86, 7.05, 6.75, and 7.22 microg/mL for subjects with birth weights less than 2500, 2500 to less than 2800, 2800 to less than 3000, 3000 to less than 3200, 3200 to less than 3500, and greater than 3500 g, respectively. A positive association was found between birth weight and adiponectin concentration (trend p = 0.002). Stratified by current BMI of 25 kg/m2, a positive association was not observed for subjects with a BMI less than 25 kg/m2, but was pronounced in those with a BMI of 25 kg/m2 or greater.\n\nQuestion:\nIs low birth weight associated with reduced adiponectin concentration in adult?\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 presents fungi and their characteristics identified from burn patients at a major Chinese burn centre. All burns patients admitted to our Burn Research Institute from 2003 to 2006 inclusive were included in this study. Once fungal infection was suspected clinically, samples including wound tissue, blood, urine, stool and sputum were harvested for the culture of yeast. The sensitivities of the identified yeast were determined and the positive samples and cases were analysed. Out of a total of 3909 cases, 467 patients were clinically suspected of fungal infection, of which 1970 samples were taken for yeast culture. A total of 38 samples and 36 patients tested positive. The three most positive samples were urine, blood and catheter. Candida tropicalis was identified as the most common yeast type (42.1%), followed by Candida albicans (31.6%), Candida famata (T. Famata) (10.5%) and Candida glabrata (T. Glabrata) (7.9%). Except for C. galbrata, most of the yeast strains found in the study were sensitive to the routine antimycotic agents. There were eight deaths in the 36 positive patients. As much as 83.3% of the positive cases suffered burns of more than 50% total body surface area (TBSA) and half of the positive cases were greater than 80% TBSA. A total of 78.95% of the positive samples were taken from patients after 2 weeks post-burn injury.\n\nQuestion:\nDo yeast from burn patients at a major burn centre of China?\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:\nMesenchymal stem cells (MSCs) have the ability to migrate to lesion sites and undergo differentiation into functional tissues. Although this function may be important for tissue regeneration after radiation therapy, the influence of ionizing radiation (IR) on cellular survival and the functional aspects of differentiation and stem cell characteristics of MSCs have remained largely unknown. Radiation sensitivity of human primary MSCs from healthy volunteers and primary human fibroblast cells was examined, and cellular morphology, cell cycle effects, apoptosis, and differentiation potential after exposure to IR were assessed. Stem cell gene expression patterns after exposure to IR were studied using gene arrays. MSCs were not more radiosensitive than human primary fibroblasts, whereas there were considerable differences regarding radiation sensitivity within individual MSCs. Cellular morphology, cytoskeletal architecture, and cell motility were not markedly altered by IR. Even after high radiation doses up to 10 Gy, MSCs maintained their differentiation potential. Compared to primary fibroblast cells, MSCs did not show an increase in irradiation-induced apoptosis. Gene expression analyses revealed an upregulation of various genes involved in DNA damage response and DNA repair, but expression of established MSC surface markers appeared only marginally influenced by IR.\n\nQuestion:\nDo mesenchymal stem cells retain their defining stem cell characteristics after exposure to ionizing radiation?\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 have observed prolonged survival in patients undergoing vaccine reinduction after resection of recurrent metastatic melanoma and adjuvant polyvalent allogenic cell vaccine (PACV) immunotherapy. We hypothesized that reinduction with a more intensive vaccine regimen would re-stimulate specific immune responses that were correlated with survival after recurrence. From 1996 to 1998, 194 patients developed recurrence during adjuvant PACV (CancerVax vaccine) treatment after resection of metastatic melanoma. Recurrent disease was treated with or without vaccine reinduction. Reinduction regimen entailed an increased vaccine frequency and coadministration of two doses of bacille Calmette-Guérin (BCG). PACV Delayed-type hypersensitivity (DTH) responses were prospectively recorded. Survival was defined as the interval from recurrence to death. Ninety-four patients underwent reinduction immunotherapy. DTH responses to PACV before recurrence increased significantly after reinduction therapy (P =.0001). The median survival time was 37 months for reinduced patients and 17 months for other patients. On multivariate analysis, reinduction status remained a significant prognostic variable (P =.0277). In the reinduction group, there was a significant correlation between PACV DTH responses and survival (P =.0178).\n\nQuestion:\nDoes active immunotherapy by reinduction with a polyvalent allogeneic cell vaccine correlate with improved survival in recurrent metastatic melanoma?\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 decline in cognitive test scores in elderly persons can signal the beginning of a descent into dementia or may indicate only a short-term cognitive disturbance. It would be clinically useful to distinguish between the two outcomes and to identify characteristics of each. Four hundred thirty-seven community-dwelling elderly persons were given the Mini-Mental State Examination (MMSE) annually for an average of 7 years. A low score between baseline and final MMSE was identified. A low score 3 or more points lower than baseline score indicated cognitive decline. This decline was called persistent if the final MMSE score was also at least 3 points lower than baseline MMSE score; otherwise, the decline was considered transient. Twenty participants (4.6%) experienced a persistent cognitive decline, 67 participants (15.3%) experienced a transient cognitive decline. Presence of the apolipoprotein epsilon4 allele was significantly associated with persistent cognitive decline (age-adjusted odd ratio [OR] = 11.46, p < .0001) but not with transient cognitive decline (age-adjusted OR = 1.53, p = .219). Incorrect answers on the orientation part of the MMSE at the time of cognitive decline was associated with persistent decline compared to transient decline (age-adjusted OR = 3.58, p = .058).\n\nQuestion:\nAre apolipoprotein epsilon4 allele and problems with orientation associated with a persistent decline in cognition in community-dwelling elderly persons?\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 magnitude and longevity of synaptic activity-induced changes in synaptic efficacy is quantified by measuring evoked responses whose potentiation requires gene transcription to persist for more than 2-3 hours. While miniature EPSCs (mEPSCs) are also increased in amplitude and/or frequency during long-term potentiation (LTP), it is not known how long such changes persist or whether gene transcription is required. We use whole-cell patch clamp recordings from dissociated hippocampal cultures to characterise for the first time the persistence and transcription dependency of mEPSC upregulation during synaptic potentiation. The persistence of recurrent action potential bursting in these cultures is transcription-, translation- and NMDA receptor-dependent thus providing an accessible model for long-lasting plasticity. Blockade of GABAA-receptors with bicuculline for 15 minutes induced action potential bursting in all neurons and was maintained in 50-60% of neurons for more than 6 hours. Throughout this period, the frequency but neither the amplitude of mEPSCs nor whole-cell AMPA currents was markedly increased. The transcription blocker actinomycin D abrogated, within 2 hours of burst induction, both action potential bursting and the increase in mEPSCs. Reversible blockade of action potentials during, but not after this 2 hour transcription period suppressed the increase in mEPSC frequency and the recovery of burst activity at a time point 6 hours after induction.\n\nQuestion:\nDoes a transcription-dependent increase in miniature EPSC frequency accompany late-phase plasticity in cultured hippocampal neurons?\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 assess the role of uterine activity on fetal outcome. Intrauterine pressure (IUP) recordings from consecutive term singleton, vaginal deliveries collected between June 1, 1993, and July 1, 2004, were analyzed. One thousand four hundred thirty-three recordings were included. IUP data were obtained using HP 8040A and HP M1350 cardiotocographs. For each recording the uterine contraction curve was analyzed, and the following contraction parameters were determined: relaxation time; contraction duration, frequency, amplitude, and surface; Montevideo units; and active planimeter units and contraction frequency. IUP recordings and contraction parameters from deliveries ending with an umbilical artery pH of 7.11 or less were compared with those ending with an umbilical artery pH of 7.12 or greater. Statistical analyses were performed using Student's t test and logistic regression. An umbilical artery pH 7.11 or less at birth is associated with significant more uterine activity during the first and second stage of labor.\n\nQuestion:\nDoes elevated uterine activity increase the risk of fetal acidosis at birth?\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:\nRecently described, aggressive B-cell lymphomas with genetic abnormalities involving MYC and BCL2 have been shown to have a poor prognosis when treated with regimens for diffuse large B-cell lymphomas. Similar data on cases with concurrent MYC and BCL6 translocation are still scant. Moreover, little is known regarding the morphologic and immunophenotypic characteristics of these cases, which further complicates their identification. This study describes six cases of aggressive B-cell lymphoma with translocations involving MYC and BCL6. Six cases of large B-cell lymphoma with translocation involving MYC and BCL6 confirmed by fluorescence in situ were identified. The morphologic, immunophenotypic, and clinical features of the cases were examined. All the patients were older women, and in 50% of cases, the presentation was extranodal. In two cases, the liver was involved at presentation. A starry-sky pattern was a constant feature of the cases in which the morphology could be reliably assessed. Five of six cases had an immunophenotype corresponding to the germinal center B cells, and only one was positive for BCL2, an immunophenotype reminiscent of that of Burkitt lymphoma.\n\nQuestion:\nDo aggressive B-cell lymphomas with translocations involving BCL6 and MYC have distinct clinical-pathologic characteristics?\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 hemodialysis (HD) patients, the plasma brain natriuretic peptide (BNP) level is associated with left ventricular dysfunction and patients' survival. Malnutrition is common in HD patients, it is associated with inflammation and contributes to the high incidence of cardiovascular (CV) disease in this setting (malnutrition-inflammation-atherosclerosis syndrome). In a cross-sectional study, we assessed the relationship between predialysis plasma BNP level and nutritional markers in chronic HD patients. Of 210 patients receiving HD treatment in our unit, 51 patients who were treated with three times weekly long-hour HD (5-8 h/session) for at least 6 months (mean age 65.8 +/- 15.0 years; F/M ratio 23/28; vintage 71.3 +/- 71.9 months; BMI 24.9 +/- 5.9; session time 6.9 +/- 1.3 h; percentage of diabetic patients 31%) were studied before a mid-week HD session for nutritional markers (plasma albumin 35.3 +/- 3.7 g/l; prealbumin 0.36 +/- 0.09 g/l; CRP 15.3 +/- 14.7 mg/l; nPNA 1.29 +/- 0.29 g/kg/day) and plasma BNP (246.9 +/- 252.2 ng/l, normal <100 ng/l, Bayer(R) kit). The interdialytic weight gain was 2.1 +/- 1.0 kg. In the last 3 months prior to the commencement of the study, the patients' dry weight varied by +0.17 +/- 1.9 kg. Predialysis plasma BNP levels did not differ according to gender and the presence of diabetes. It was not correlated with age and vintage but was found to be negatively associated with the session time (r = -0.34, p = 0.018). Several nutritional markers were negatively correlated with BNP levels: prealbumin (r = -0.46, p = 0.001), BMI (r = -0.33, p = 0.018), nPNA (r = -0.46, p = 0.002). The plasma albumin relationship with the BNP level was close to significance (p = -0.26, p = 0.070). The 3-month dry weight variation was also negatively correlated with BNP levels (r = -0.34, p = 0.018). With multiple stepwise regression analysis, prealbumin and session time remained significant (respectively p = 0.004 and 0.01). BNP levels were higher in a subgroup of malnourished patients (n = 12) (400 +/- 405 vs. 202 +/- 166 ng/l, p = 0.03) than in patients who did not meet the malnutrition criteria (34 patients). They were not correlated with CRP levels, interdialytic weight gain, or predialysis MAP.\n\nQuestion:\nIs the plasma level of brain natriuretic peptide increased in malnourished hemodialysis 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:\nMen are more susceptible to gastric cancer (GC) than women. However, the genetic factors associated with the sex difference are not well understood. Chemokines have been shown to modulate tumor behavior, and the sex-specific effect of the chemokine polymorphisms on the host susceptibility to several diseases has been reported. We aimed to determine the role of chemokine polymorphisms on host susceptibility to GC, with special interest on their sex-specific effect. A hospital-based case-control study, including 177 patients with GC and 217 age-matched unaffected healthy controls, was performed in three major tertiary care hospitals. Genotyping for regulated upon activation, normal T-cell expressed and secreted (RANTES) -403 A/G and -28 C/G, CC chemokine receptor 5 (CCR5) deletion, and CCR2-V64I was performed using peripheral blood DNA. The RANTES -403 GA and AA genotypes were independently associated with a 2.3-fold reduced risk of developing GC (OR=0.44, 95% CI 0.22-0.90, P=0.025) compared with GG genotype in women, but not in men. The RANTES -28C/G and CCR2-V64I polymorphisms were not associated with different risk of developing GC. The tumor stage, histological features, and survival rate were not different when stratified by RANTES -403 and -28 and CCR2-V64I genotypes.\n\nQuestion:\nIs rANTES-403 polymorphism associated with reduced risk of gastric cancer in 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 equilibrium between endothelial apoptosis and endothelial renewal is altered in acute coronary syndromes and may be related to differences in the beneficial effects of angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists (angiotensin receptor blockers). We evaluated the effect of treatment on endothelial function in post-myocardial infarction (MI) patients treated with perindopril (group 2, n = 16) or valsartan (group 3, n = 17) at baseline and after 7, 15, and 30 days and in normal controls (group 1, n = 20). Endothelial apoptosis was determined by cultivating serum samples in vitro with human umbilical vein endothelial cells (HUVECs), while endothelial renewal was assessed by mobilization of CD34+ bone marrow cells. At baseline, post-MI patients had significantly elevated rates of apoptosis (16.6 ± 5.0% and 16.5 ± 8.4% in groups 2 and 3, respectively [both p = 0.01] vs 1.6 ± 0.7% in group 1), which declined in group 2 (10.5 ± 4.4% at 30 days, p = 0.04), but not in group 3. Similar results and trends were found for the Bax/Bcl-2 ratio. CD34+ mobilization was significantly increased in group 2 (3.0 ± 1.0 at baseline to 6.2 ± 1.6 at 15 days, p = 0.03), whereas in group 3 CD34+ mobilization did not change significantly. The findings in group 2 were accompanied by an increase in vascular endothelial growth factor at 15 days, and a reduction in tumor necrosis factor-α and its soluble receptors, versus no change in group 3. Similar findings were observed for angiotensin II and bradykinin.\n\nQuestion:\nDoes aCE inhibition modulate endothelial apoptosis and renewal via endothelial progenitor cells in patients with acute coronary syndromes?\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 study was to assess if QT dispersion and RR interval on the standard 12-lead electrocardiogram (ECG) predict cardiac death and late arrhythmic events in postinfarction patients with low left ventricular ejection fraction (LVEF). QT dispersion on a standard electrocardiogram (ECG) is a measure of repolarization inhomogeneity, but its prognostic meaning in myocardial infarction (MI) survivors is unclear, especially in patients with left ventricular dysfunction. RR interval has been shown to predict mortality in post-MI patients, but its prognostic power has not been compared with other noninvasive risk factors. Retrospective cohort study. Ninety patients were identified, from a series of 547 consecutive postinfarction patients admitted to our institution for phase II cardiac rehabilitation, as having a LVEF of <0.40 at two-dimensional echocardiography (mean LVEF 0.35+/-0.04; range 0.20-0.39). QT dispersion and RR interval were analyzed on the admission 12-lead electrocardiogram, 20+/-10 (range 8-45) days after MI, using specially designed software. Additional risk markers were collected from clinical variables, signal-averaged ECG and Holter recording. During 24+/-18 (range 1-63) months of follow-up, 10 of 90 patients (11%) died, all from cardiac causes, and there were 18 late arrhythmic events, defined as sudden death or the occurrence of a sustained ventricular arrhythmia > or =5 days after the index MI. QT interval and dispersion were not significantly prolonged in patients who died compared to survivors and not significantly different between patients with and without arrhythmic events. Mean RR interval from standard ECG was significantly shorter in patients with both cardiac death (682+/-99 vs. 811+/-134 ms; P=0.004) and arrhythmic events (720+/-100 vs. 818+/-139 ms; P=0.006). A Cox proportional hazards model identified RR interval from standard ECG (P<0.001) and a history of more than one MI (P=0.002) as significant predictors of cardiac death independent of thrombolytic therapy, LVEF, filtered QRS complex duration at signal-averaged ECG, mean RR and its standard deviation at 24-h Holter monitoring.\n\nQuestion:\nIs prognosis in myocardial infarction survivors with left ventricular dysfunction predicted by electrocardiographic RR interval but not QT dispersion?\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:\nMore than 90% of house dust mite-allergic patients are sensitized to the major Dermatophagoides pteronyssinus allergen, Der p 2. The aim of this study was to develop and characterize an allergy vaccine based on carrier-bound Der p 2 peptides, which should allow reducing IgE- and T-cell-mediated side-effects during specific immunotherapy (SIT). Five Der p 2 peptides (P1-P5) were synthesized and analyzed regarding IgE reactivity and allergenic activity. Lymphoproliferative and cytokine responses induced with Der p 2 and Der p 2 peptides were determined in peripheral blood mononuclear cells from mite-allergic patients. Der p 2-specific IgG antibodies induced with carrier-bound Der p 2 peptides in mice and rabbits were tested for their capacity to inhibit IgE binding and basophil activation in allergic patients. Of five overlapping peptides (P1-P5) covering the Der p 2 sequence, two peptides (P2 and P4) were identified, which showed no relevant IgE reactivity, allergenic activity, and induced lower Der p 2-specific T-cell activation than Der p 2. However, when coupled to a carrier, P2 and P4 induced Der p 2-specific IgG antibodies in animals, which inhibited allergic patients' IgE binding to the allergen and allergen-induced basophil activation similar as antibodies induced with Der p 2.\n\nQuestion:\nDo carrier-bound nonallergenic Der p 2 peptides induce IgG antibodies blocking allergen-induced basophil activation 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:\nHistopathologic evidence of fibrosis on surgical lung biopsy has been associated with reduced survival in patients with hypersensitivity pneumonitis (HP). Changes of pulmonary fibrosis detected on CT may also correlate with prognosis in patients with HP. We identified 69 consecutive patients with HP diagnosed between January 1997 and December 2002 at Mayo Clinic, Rochester, MN. Patients were stratified into fibrotic and nonfibrotic groups based on the CT findings. Fibrosis was defined by the presence of irregular linear opacities, traction bronchiectasis, or honeycombing. Of 69 patients, 26 were classified as fibrotic and 43 as nonfibrotic. Patients in the fibrotic group were older, had longer symptom duration, were more likely to have crackles on auscultation, more likely to be exposed to avian antigen, and had greater restrictive lung impairment (p<0.05 for all comparisons). There were 11 deaths in the fibrotic group and 1 death in the nonfibrotic group (p<0.0001). In the regression analysis, CT evidence of fibrosis, more severe pulmonary function abnormalities, and the presence of crackles on auscultation were predictive of reduced survival (p<0.05 for all). The presence as well as the extent of fibrosis on CT was associated with increased mortality. The age-adjusted hazard ratio for mortality in patients with fibrosis was 4.6 (95% confidence interval, 2.0 to 20.1; p<0.0001).\n\nQuestion:\nDo high-resolution CT findings of parenchymal fibrosis correlate with prognosis in hypersensitivity pneumonitis?\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:\nOur aim was to evaluate the ultrastructure of human metaphase II oocytes subjected to slow freezing and fixed after thawing at different intervals during post-thaw rehydration. Samples were studied by light and transmission electron microscopy. We found that vacuolization was present in all cryopreserved oocytes, reaching a maximum in the intermediate stage of rehydration. Mitochondria-smooth endoplasmic reticulum (M-SER) aggregates decreased following thawing, particularly in the first and intermediate stages of rehydration, whereas mitochondria-vesicle (MV) complexes augmented in the same stages. At the end of rehydration, vacuoles and MV complexes both diminished and M-SER aggregates increased again. Cortical granules (CGs) were scarce in all cryopreserved oocytes, gradually diminishing as rehydration progressed.\n\nQuestion:\nDoes freeze/thaw stress induce organelle remodeling and membrane recycling in cryopreserved human mature oocytes?\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:\nResistance to conventional antiestrogens is a major cause of treatment failure and, ultimately, death in breast cancer. The objective of the study was to identify small-molecule estrogen receptor (ER)-α antagonists that work differently from tamoxifen and other selective estrogen receptor modulators. Based on in silico screening of a pharmacophore database using a computed model of the BRCA1-ER-α complex (with ER-α liganded to 17β-estradiol), we identified a candidate group of small-molecule compounds predicted to bind to a BRCA1-binding interface separate from the ligand-binding pocket and the coactivator binding site of ER-α. Among 40 candidate compounds, six inhibited estradiol-stimulated ER-α activity by at least 50% in breast carcinoma cells, with IC50 values ranging between 3 and 50 μM. These ER-α inhibitory compounds were further studied by molecular and cell biological techniques. The compounds strongly inhibited ER-α activity at concentrations that yielded little or no nonspecific toxicity, but they produced only a modest inhibition of progesterone receptor activity. Importantly, the compounds blocked proliferation and inhibited ER-α activity about equally well in antiestrogen-sensitive and antiestrogen-resistant breast cancer cells. Representative compounds disrupted the interaction of BRCA1 and ER-α in the cultured cells and blocked the interaction of ER-α with the estrogen response element. However, the compounds had no effect on the total cellular ER-α levels.\n\nQuestion:\nAre small-molecule `` BRCA1-mimetics '' antagonists of estrogen receptor-α?\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 structure and function of chromatin can be altered by modifications to histone. Histone acetylation in vivo is a dynamic reversible process governed by histone acetyltransferases (HATs) and histone deacetylases (HDACs). HDAC6 is a unique isoform among the HDACs, and a gene expression pattern study, with cDNA microarray in MCF-7 cells, showed the HDAC6 gene to be late responsive, estrogen induced, and up-regulated. This led us to hypothesize that there was a link between levels of HDAC6 expression and the metastatic potential of breast cancer and also, therefore, the prognosis of these patients. In the present study, the level of HDAC6 mRNA expression was analyzed with quantitative real-time reverse transcription-PCR, in 135 female patients with invasive breast cancer. HDAC6 protein expression was also determined by immunohistochemistry. An association was sought between HDAC6 expression and various clinicopathologic factors. HDAC6 mRNA was expressed at significantly higher levels in breast cancer patients with small tumors measuring less than 2 cm, with low histologic grade, and in estrogen receptor alpha- and progesterone receptor-positive tumors. By contrast, no relationship was found between HDAC6 mRNA expression and any of the other clinicopathologic factors, namely, age, menopausal status, and axillary lymph node involvement. Patients expressing high levels of HDAC6 mRNA and protein had a better prognosis than those expressing low levels, in terms of disease-free survival. However, multivariate analysis failed to show that HDAC6 mRNA and protein are an independent prognostic factors for disease-free survival and overall survival. Furthermore, the patients with high levels of HDAC6 mRNA tended to be more responsive to endocrine treatment than those with low levels. Specific HDAC6 staining was found in the nucleus of some normal epithelial cells and in the cytoplasm of the majority of cancer cells. Although postmenopausal patients showed higher HDAC6 protein expression, there were no relationship between protein expression and any other clinicopathologic factors.\n\nQuestion:\nIs hDAC6 expression correlated with better survival in 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:\nPre-eclampsia (PE) is a complex, multi-systemic condition of pregnancy which greatly impacts maternal and perinatal morbidity and mortality. MicroRNAs (miRs) are differentially expressed in PE and may be important in helping to understand the condition and its pathogenesis. Case-control studies investigating expression of miRs in PE were collected through a systematic literature search. Data was extracted and compared from 58 studies to identify the most promising miRs associated with PE pathogenesis and identify areas of methodology which could account for often conflicting results. Some of the most frequently differentially expressed miRs in PE include miR-210, miR-223 and miR-126/126* which associate strongly with the etiological domains of hypoxia, immunology and angiogenesis. Members of the miR-515 family belonging to the imprinted chromosome 19 miR cluster with putative roles in trophoblast invasion were also found to be differentially expressed. Certain miRs appear to associate with more severe forms of PE such as miR-210 and the immune-related miR-181a and miR-15 families. Patterns of miR expression may help pinpoint key pathways (e.g. IL-6/miR-223/STAT3) and aid in untangling the heterogeneous nature of PE. The detectable presence of many PE-associated miRs in antenatal circulatory samples suggests their usefulness as predictive biomarkers. Further progress in ascertaining the clinical value of miRs and in understanding how they might contribute to pathogenesis is predicated upon resolving current methodological challenges in studies. These include differences in diagnostic criteria, cohort characteristics, sampling technique, RNA isolation and platform-dependent variation in miR profiling.\n\nQuestion:\nDoes systematic Review of Micro-RNA Expression in Pre-Eclampsia identify a Number of Common Pathways Associated with the 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:\nThe link between reproductive life history and incidence of ovarian tumors is well known. Periods of reduced ovulations may confer protection against ovarian cancer. Using phenotypic data available for mouse, a possible association between the ovarian transcriptome, reproductive records and spontaneous ovarian tumor rates was investigated in four mouse inbred strains. NIA15k-DNA microarrays were employed to obtain expression profiles of BalbC, C57BL6, FVB and SWR adult ovaries. Linear regression analysis with multiple-test control (adjusted p ≤ 0.05) resulted in ovarian tumor frequency (OTF) and number of litters (NL) as the top-correlated among five tested phenotypes. Moreover, nearly one-hundred genes were coincident between these two traits and were decomposed in 76 OTF(-) NL(+) and 20 OTF(+) NL(-) genes, where the plus/minus signs indicate the direction of correlation. Enriched functional categories were RNA-binding/mRNA-processing and protein folding in the OTF(-) NL(+) and the OTF(+) NL(-) subsets, respectively. In contrast, no associations were detected between OTF and litter size (LS), the latter a measure of ovulation events in a single estrous cycle.\n\nQuestion:\nAre tumor and reproductive traits linked by RNA metabolism genes in the mouse ovary : a transcriptome-phenotype association 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:\nStress-related glucocorticoid and glutamate release have been implicated in hippocampal atrophy evident in patients with post-traumatic stress disorder (PTSD). Glutamatergic mechanisms activate nitric oxide synthase (NOS), while gamma-amino-butyric acid (GABA) may inhibit both glutamatergic and nitrergic transmission. Animal studies support a role for NOS in stress. We have studied the role of NOS and glucocorticoids, as well as inhibitory and excitatory transmitters, in a putative animal model of PTSD that emphasizes repeated trauma. Hippocampal NOS activity, N-methyl-D-aspartate (NMDA) receptor binding characteristics and GABA levels were studied in Sprague-Dawley rats 21 days after exposure to a stress-restress paradigm, using radiometric analysis, radioligand studies and high-performance liquid chromatography (HPLC) analysis with electrochemical detection, respectively. The NOS isoform involved, and the role of stress-mediated corticosterone release in NOS activation, was verified with the administration of selective iNOS and nNOS inhibitors, aminoguanidine (50 mg/kg/day i.p.) and 7-nitroindazole (12.5 mg/kg/day i.p.), and the steroid synthesis inhibitor, ketoconazole (24 mg/kg/day i.p.), administered for 21 days prior to and during the stress procedure. Stress evoked a sustained increase in NOS activity, but reduced NMDA receptor density and total GABA levels. Aminoguanidine or ketoconazole, but not 7-nitroindazole or saline, blocked stress-induced NOS activation.\n\nQuestion:\nDoes stress-restress evoke sustained iNOS activity and altered GABA levels and NMDA receptors in rat hippocampus?\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:\nLeptin is involved in the regulation of bodyweight and metabolism in man and might also be involved in the pathophysiology of the insulin resistance syndrome, which is associated with the development of cardiovascular diseases. We tested whether leptin is a risk factor for acute myocardial infarction (AMI) in a nested case-referent study. Sixty-two men with first-ever AMI were identified who, prior to AMI, had participated in population-based health surveys in Northern Sweden. Referents were matched for sex, age, date and type of health survey, and geographical region. Blood pressure, body mass index (BMI) and the presence of smoking, diabetes and hypertension were recorded. Total cholesterol, apolipoprotein A-1 (apo A-1), apolipoprotein B (apo B), plasminogen activator inhibitor (PAI-1), insulin, and leptin were analysed in stored samples. Their influences on first-ever AMI were analysed by conditional logistic regression analysis. Men with first-ever AMI had higher BMI, plasma insulin and leptin, and diastolic blood pressure than the referents. Furthermore, they had lower plasma apo A-1 and were more often smokers. Smoking, high leptin, PAI-1 and cholesterol, and low apo A-1 levels were significant risk factors for first-ever AMI in univariate analysis. High leptin (OR 8.97; 95% CI: 1.73-46.5) and cholesterol (OR 5.18; 95% CI: 1.34-20.0) levels remained significant risk factors for AMI in a multivariate model. High apo A-1 was protective (OR = 0.13; 95% CI: 0.03-0.55). The combination of high leptin and low apo A-1 was associated with a particularly pronounced increased risk for AMI.\n\nQuestion:\nIs leptin associated with increased risk of 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:\nVoltage-dependent Na+ currents are important determinants of excitability. We hypothesized that gastric inflammation alters Na+ current properties in primary sensory neurons. The stomach was surgically exposed in rats to inject the retrograde tracer 1.1'-dioctadecyl-3,3,3,'3-tetramethylindocarbocyanine methanesulfonate and saline (control) or 20% acetic acid (ulcer group) into the gastric wall. Nodose or thoracic dorsal root ganglia (DRG) were harvested after 7 days to culture neurons and record Na+ currents using patch clamp techniques. There were no lesions in the control and 3 +/- 1 ulcers in the ulcer group. Na+ currents recovered significantly more rapidly from inactivation in nodose and DRG neurons obtained from animals in the ulcer group compared with controls. This was partially a result of an increase in the relative contribution of the tetrodotoxin-resistant to the peak sodium current. In addition, the recovery kinetics of the tetrodotoxin-sensitive current were faster. In DRG neurons, gastric inflammation shifted the voltage-dependence of activation of the tetrodotoxin-resistant current to more hyperpolarized potentials.\n\nQuestion:\nDo experimental ulcers alter voltage-sensitive sodium currents in rat gastric sensory neurons?\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 action of palmitate on insulin receptor (IR) signaling pathway in rat pancreatic islets. The following proteins were studied: IR substrate-1 and -2 (IRS1 and IRS2), phosphatidylinositol 3-kinase, extracellular signal-regulated protein kinase-1 and -2 (ERK1/2), and signal transducer and activator of transcription 3 (STAT3). Immunoblotting and immunoprecipitation assays were used to evaluate the phosphorylation states of IRS1 and IRS2 (tyrosine [Tyr]), ERK1/2 (threonine 202 [Thr202]/Tyr204), and STAT3 (serine [Ser727]). The exposure of rat pancreatic islets to 0.1-mmol/L palmitate for up to 30 minutes produced a significant increase of Tyr phosphorylation in IRS2 but not in IRS1. The association of phosphatidylinositol 3-kinase with IRS2 was also upregulated by palmitate. Exposure to 5.6-mmol/L glucose caused a gradual decrease in ERK1/2 (Thr202/Tyr204) and STAT3 (serine [Ser727]) phosphorylations after 30-minute incubation. The addition of palmitate (0.1 mmol/L), associated with 5.6-mmol/L glucose, abolished these latter effects of glucose after 15-minute incubation.\n\nQuestion:\nDoes palmitate activate insulin signaling pathway in pancreatic rat islets?\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 the Model End-Stage Liver Disease (MELD) score has been effective in the prediction of mortality in patients awaiting liver transplantation, its predictive value of survival after living donor liver transplantation (LDLT) needs further study. We report our experience with 142 cases of LDLT, analyzing the impact of the MELD score on the graft survival after LDLT. Of 142 grafts, 18 failed during the observation period. One-, 3- and 5-year survival rates were 92%, 87% and 82%, respectively. Cox proportional hazard model revealed that MELD score did not predict graft survival (p=0.43, relative risk = 1.0).\n\nQuestion:\nDoes model for End Stage Liver Disease score predict graft survival after living donor liver transplantation?\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:\nConstitutive activation of signal transducer and activator of transcription 3 at tyrosine residue 705 (p-STAT3 (tyr705)) has been associated with many types of human cancers. However, its potential roles and biological effects in hepatocellular carcinoma (HCC) are not well established. To explore whether an altered p-STAT3 (tyr705) expression is associated with angiogenesis or proliferation and thereby plays a part in HCC development. Paraffin-wax-embedded sections from 69 patients with HCC were collected in this study. Using a semiquantitative immunohistochemical staining method, the expression patterns of p-STAT3 (tyr705) in both HCC lesions and the adjacent non-tumorous liver parenchyma were analysed. The results obtained were further correlated with intratumour microvessel density (MVD), Ki-67 expression, clinicopathological parameters and overall survival. A strong p-STAT3 (tyr705) nuclear staining was observed in 49.3% of HCC lesions, but was reported only in 5.8% of the adjacent non-tumorous liver parenchyma (p<0.001). The expression of p-STAT3 (tyr705) in HCC lesions was significantly and positively correlated with the intratumour MVD (p = 0.002), but not with Ki-67 expression. No significant correlation of p-STAT3 (tyr705) was found in addition to histological grading (p = 0.019). Multivariate Cox regression analysis showed that p-STAT3 (tyr705) expression was a significant predictor of overall survival for HCC (p = 0.036), although the Kaplan-Meier survival curves showed no significant difference between the high and low p-STAT3 (tyr705) expression subgroups.\n\nQuestion:\nIs altered p-STAT3 ( tyr705 ) expression associated with histological grading and intratumour microvessel density in hepatocellular 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 determine whether an active intervention is beneficial for the survival of elderly patients with hepatocellular carcinoma (HCC). The survival of 740 patients who received various treatments for HCC between 1983 and 2011 was compared among different age groups using Cox regression analysis. Therapeutic options were principally selected according to the clinical practice guidelines for HCC from the Japanese Society of Hepatology. The treatment most likely to achieve regional control capability was chosen, as far as possible, in the following order: resection, radiofrequency ablation, percutaneous ethanol injection, transcatheter arterial chemoembolization, transarterial oily chemoembolization, hepatic arterial infusion chemotherapy, systemic chemotherapy including molecular targeting, or best supportive care. Each treatment was used alone, or in combination, with a clinical goal of striking the best balance between functional hepatic reserve and the volume of the targeted area, irrespective of their age. The percent survival to life expectancy was calculated based on a Japanese national population survey. The median ages of the subjects during each 5-year period from 1986 were 61, 64, 67, 68 and 71 years and increased significantly with time (P < 0.0001). The Child-Pugh score was comparable among younger (59 years of age or younger), middle-aged (60-79 years of age), and older (80 years of age or older) groups (P = 0.34), whereas the tumor-node-metastasis stage tended to be more advanced in the younger group (P = 0.060). Advanced disease was significantly more frequent in the younger group compared with the middle-aged group (P = 0.010), whereas there was no difference between the middle-aged and elderly groups (P = 0.75). The median survival times were 2593, 2011, 1643, 1278 and 1195 d for 49 years of age or younger, 50-59 years of age, 60-69 years of age, 70-79 years of age, or 80 years of age or older age groups, respectively, whereas the median percent survival to life expectancy were 13.9%, 21.9%, 24.7%, 25.7% and 37.6% for each group, respectively. The impact of age on actual survival time was significant (P = 0.020) with a hazard ratio of 1.021, suggesting that a 10-year-older patient has a 1.23-fold higher risk for death, and the overall survival was the worst in the oldest group. On the other hand, when the survival benefit was evaluated on the basis of percent survival to life expectancy, age was again found to be a significant explanatory factor (P = 0.022); however, the oldest group showed the best survival among the five different age groups. The youngest group revealed the worst outcomes in this analysis, and the hazard ratio of the oldest against the youngest was 0.35 for death. The survival trends did not differ substantially between the survival time and percent survival to life expectancy, when survival was compared overall or among various therapeutic interventions.\n\nQuestion:\nAre active treatments a rational approach for hepatocellular carcinoma in elderly 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:\nThe goal of this study was to determine the impact of an oral hygiene education programme for caregivers on the oral health of institutionalised elderly and to examine the effect of disability and low muscle strength on programme outcomes. The subjects of this study were geriatric patients (n = 80) from a nursing home. Katz Index for activities of daily living, handgrip strength and mucosal-plaque score (MPS) was evaluated at baseline and 1 year after intervention. The intervention consisted of an educational programme and specific guidelines for caregivers (to perform oral hygiene for dependent elderly and to supervise the independent elderly during oral hygiene practices). Differences on MPS were evaluated using a paired-sample t-test. A stratified analysis was carried out to identify differences in response to the programme according to the Katz Index and handgrip strength of elderly. The MPS was significantly reduced (p = 0.001) at follow-up; however, a separate analysis showed that only the independent elderly (p = 0.002) and those with normal muscle strength (p = 0.006) showed a reduction in MPS during the follow-up examination.\n\nQuestion:\nDoes oral hygiene caregivers ' educational programme improve oral health conditions in institutionalised independent and functional elderly?\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:\nChildren born very preterm are at risk for impaired motor performance ranging from cerebral palsy (CP) to milder abnormalities, such as developmental coordination disorder. White matter abnormalities (WMA) at term have been associated with CP in very preterm children; however, little is known about the impact of WMA on the range of motor impairments. The aim of this study was to assess whether WMA were predictive of all levels of motor impairments in very preterm children. Two hundred and twenty-seven very preterm infants (< 30 wks gestational age or birthweight < 1250 g) had brain magnetic resonance imaging at term-equivalent age to assess for WMA, which were categorized as nil, mild, or moderate to severe. At 5 years of age children were classified as having a moderate to severe motor impairment if they were below the 5th centile or mild to severe motor impairment if their score placed them no higher than the 15th centile on the Movement Assessment Battery for Children (MABC). WMA (nil vs mild and nil vs moderate-severe) were explored as predictors of motor impairment using logistic regression. Analyses were repeated adjusting for the effects of other perinatal variables and excluding children with CP. Of the 193 very preterm children (97 males, 96 females) assessed with the MABC, 53 (27%) were classified as having a moderate to severe motor impairment and 96 (50%) a mild to severe motor impairment. WMA were predictive of motor impairment in very preterm children, with mild versus no WMA increasing the odds of moderate to severe motor impairment by over fivefold (odds ratio [OR] 5.6; 95% confidence interval [CI] 1.9-16.1; p=0.002) and mild to severe impairment by twofold (OR 2.2; 95% CI 1.1-4.2; p=0.02). Compared with no WMA, moderate to severe WMA increased the odds for moderate to severe impairment 19-fold (OR 19.4; 95% CI 5.6-66.7; p<0.001) and for mild to severe motor impairment ninefold (OR 9.4; 95% CI 3.2-28.1; p<0.001). Results remained similar after controlling for several potential confounders and after excluding 14 children who had CP at age 2 years.\n\nQuestion:\nDoes neonatal white matter abnormality predict childhood motor impairment in very preterm children?\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:\nPatients with severe cerebral ischemia may lose autoregulation to increase cerebral blood flow following neural activity. Although the steal phenomenon under conventional cerebral blood flow study has been known as a high-risk factor for stroke, the cerebral oxygen hemodynamics in ischemic patients during functional activation has not been thoroughly investigated. In this study, we present rare cases with intracortical steal phenomenon during motor tasks detected by multichannel functional near-infrared spectroscopy before and after surgery. The relative concentration change of oxygenated, deoxygenated and total hemoglobin in and around the primary sensorimotor cortex during contralateral hand grasping was investigated in 11 patients with severe internal carotid artery stenosis. In 3 patients, the concentration of total hemoglobin around the primary sensorimotor cortex significantly decreased in response to motor stimulation and returned to baseline soon after termination of the motor task. This phenomenon partially disappeared postoperatively in all patients who underwent surgery. The remaining 8 patients showed no signs of total hemoglobin decrease in and around the sensorimotor cortex. In 9 patients, lack of decrease in deoxygenated hemoglobin in the center of the primary motor cortex during the motor task was observed and 3 of them showed significant increase in deoxygenated hemoglobin.\n\nQuestion:\nDo motor-related intracortical steal phenomenon detected by multichannel functional near-infrared spectroscopy imaging?\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:\nProvoked vestibulodynia is a poorly understood disease that affects 8-15% of women in their lifetime. There is significant inflammation and nerve growth in vestibular biopsies from affected women treated by vestibulectomy compared with matched female population controls without vestibulodynia. The triggers leading to this neurogenic inflammation are unknown, but they are likely multifactorial. Our objective was to determine whether vestibulodynia is more common in close and distantly related female relatives of women diagnosed with the disease and those specifically treated by vestibulectomy. Excess familial clustering would support a potential genetic predisposition for vestibulodynia and warrant further studies to isolate risk alleles. Using population-based genealogy linked to University of Utah Hospital CPT coded data, we estimated the relative risk of vestibulectomy in female relatives of affected women. We also compared the average pairwise relatedness of cases to the expected relatedness of the population and identified high-disease-burden pedigrees. A total of 183 potential vestibulectomy probands were identified using CPT codes. The relative risk of vestibulectomy was elevated in first-degree (20 [6.6-47], P < .00001), second-degree (4.5 [0.5-16], P = .07), and third-degree female relatives (3.4 [1.2-8.8], P = .03). Seventy of these 183 CPT-based probands had available clinical history to confirm a diagnosis of moderate to severe vestibulodynia. Notably, this smaller group of confirmed probands (n = 70) revealed a similar familiality in first-degree (54 [17.5-126], P < .00001), second-degree (19.7 [2.4-71], P = .005), and third-degree relatives (12 [3.3-31], P = .0004), despite less statistical power for analysis. Overall, the average pairwise relatedness of affected women was significantly higher than expected (P < .001) and a number of high-disease-burden Utah families were identified.\n\nQuestion:\nDoes familiality analysis of provoked vestibulodynia treated by vestibulectomy support genetic predisposition?\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:\nMagnesium (Mg(2+)) is essential for cellular growth and the maintenance of normal cellular processes. However, little is known about how maternal hypomagnesemia during pregnancy affects fetal growth and development. This study investigated the effects of maternal hypomagnesemia on the late gestation placenta and fetus, and postnatal outcomes until weaning. Female CD1 mice consumed a control (0.2% w/w Mg(2+)), moderately Mg(2+) deficient (MMD; 0.02% w/w Mg(2+)) or severely Mg(2+) deficient (SMD; 0.005% w/w Mg(2+)) diet for 4 weeks prior to mating and throughout pregnancy. Dams were killed at E18.5 for embryonic studies or allowed to litter naturally and the offspring studied up to postnatal day 21. At E18.5, both Mg(2+) deficient diets decreased maternal plasma and bone Mg(2+) but only the SMD diet decreased fetal plasma Mg(2+). Maternal hypomagnesemia led to fetal loss and fetal growth restriction. Maternal Mg(2+) deficiency increased placental glycogen cell area and decreased spongiotrophoblast cell area while upregulating mRNA expression of the MagT1 Mg(2+) transporter in spongiotrophoblast cells. The SMD animals also displayed instances of gross placental abnormalities. After birth, pups in the SMD group had increased early postnatal mortality and failed to thrive. Pups in the MMD group underwent catch-up growth but remained shorter than controls at PN21 and were hypomagnesemic and hypoglycemic.\n\nQuestion:\nDoes maternal hypomagnesemia cause placental abnormalities and fetal and postnatal mortality?\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:\nMaternal glucocorticoid (GC) treatment is widely used to prevent lung immaturity in preterm infants. There is growing evidence that GCs may be detrimental to the Central Nervous System (CNS). We investigated whether antenatal GC administration affects CNS function in a dose-dependent manner by measuring urine concentrations of a well-established brain damage marker, S100B. We conducted a case-control-study in 70 preterm infants (1 GC vs 1 control) whose mothers received a complete GC-course (GC2, n=16), half-course (GC1, n=19), and controls (n=35). At four predetermined time-points, in the first 72 h from birth, we assessed S100B urine concentrations, using a commercially available immunoluminometric assay (Lia-mat Sangtec 100, AB Sangtec Medical, Bromma, Sweden). Data were correlated with primary neonatal outcomes (incidence of respiratory distress syndrome, length of ventilatory support and hospital stay, incidence of intraventricular hemorrhage, adverse 7th day neurological follow-up and neonatal death). S100B in GC2 group at all monitoring time-points was significantly lower (P<0.01) than controls and GC1 group, while no differences (P>0.05) were evident between controls and GC1 group. No significant differences (P>0.05) were shown in primary outcomes between half or complete GC-course treated groups.\n\nQuestion:\nDoes antenatal glucocorticoid treatment affect preterm infants ' S100B urine concentration in a dose-dependent manner?\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:\nTransplant arteriosclerosis is characterized by intraluminal obstructive proliferation occurring in response to immune-mediated arterial wall injury. Cell therapy with vascular progenitor cells have been suggested to repair intimal lesions following endothelial injury. The aim of the current study was to assess the effects of autologous bone marrow cell direct transfer and of Fucan-mobilization bone marrow-derived progenitor cells on intimal thickening in vascular grafts. Aortic allografts were performed in Brown Norway (BN) and Lewis (LEW) rats. Cell therapy was performed by injection of two doses of 10 million LEW bone marrow mononuclear cells to recipient LEW following aortic grafting. Fucan, a low molecular weight sulfated polysaccharide (LMWF) was used to mobilize bone marrow-derived progenitor cells. Five groups of 10 rats included: untreated isografts (BN to BN), untreated allografts, and three allografted groups, respectively, treated by fucan therapy, cell therapy, or cell and fucan therapy. Aorta were studied by morphometric analysis at 30 d. In the absence of treatment, intimal thickening was greater in allograft than in isograft groups (299±50 versus 3.5±1.7 μm, P<0.001). Cell therapy alone, fucan therapy alone, and the combined treatment were shown to prevent intimal thickening in allografts (5.1±1.7, 6.1±2.3, 4.1±2.5, versus 299±50 μm respectively, P<0.001). In the three treated groups, the intimal lining was a single layer of endothelial cells expressing CD34 positive, endothelial nitric oxide synthase (eNOS) positive, and Ox3 specific-recipient monoclonal antibody positive.\n\nQuestion:\nDoes syngeneic bone marrow cell therapy prevent intimal proliferation in allogeneic vascular transplantation?\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:\nMitosis is regulated by MPF (maturation promoting factor), the active form of Cdc2/28-cyclin B complexes. Increasing levels of cyclin B abundance and the loss of inhibitory phosphates from Cdc2/28 drives cells into mitosis, whereas cyclin B destruction inactivates MPF and drives cells out of mitosis. Cells with defective spindles are arrested in mitosis by the spindle-assembly checkpoint, which prevents the destruction of mitotic cyclins and the inactivation of MPF. We have investigated the relationship between the spindle-assembly checkpoint, cyclin destruction, inhibitory phosphorylation of Cdc2/28, and exit from mitosis. The previously characterized budding yeast mad mutants lack the spindle-assembly checkpoint. Spindle depolymerization does not arrest them in mitosis because they cannot stabilize cyclin B. In contrast, a newly isolated mutant in the budding yeast CDC55 gene, which encodes a protein phosphatase 2A (PP2A) regulatory subunit, shows a different checkpoint defect. In the presence of a defective spindle, these cells separate their sister chromatids and leave mitosis without inducing cyclin B destruction. Despite the persistence of B-type cyclins, cdc55 mutant cells inactivate MPF. Two experiments show that this inactivation is due to inhibitory phosphorylation on Cdc28: phosphotyrosine accumulates on Cdc28 in cdc55 delta cells whose spindles have been depolymerized, and a cdc28 mutant that lacks inhibitory phosphorylation sites on Cdc28 allows spindle defects to arrest cdc55 mutants in mitosis with active MPF and unseparated sister chromatids.\n\nQuestion:\nDoes protein phosphatase 2A regulate MPF activity and sister chromatid cohesion in budding yeast?\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:\nPatients with myocardial ischemia after noncardiac surgery have a three- to ninefold increased risk of adverse cardiac events. In this study we tested the hypothesis that altered preoperative heart rate variability (HRV) predicts postoperative prolonged myocardial ischemia (>10 min) in elderly surgical patients. Thirty-two patients, age 60 yr or older, admitted to hospital for surgical repair of a traumatic hip fracture with preoperative night and daytime Holter recordings were included. Holter monitoring was initiated at arrival at hospital and continued until the third postoperative morning. Conventional HRV measures along with analysis of short-term fractal scaling exponent (alpha(1)) of RR intervals were assessed for night (from 2 AM to 5 AM) and day (7 AM to 12 AM) periods in each patient. Preoperative alpha(1) was significantly lower (i.e., increased randomness in HRV) during the nighttime compared with daytime (mean +/- SEM; 0.92 +/- 0.08 versus 1.03 +/- 0.06; P = 0.002) in patients with postoperative myocardial ischemia. Patients without ischemia had no such difference. In stepwise multivariate logistic regression analysis, increased preoperative night-day difference of alpha(1) was the only independent predictor of postoperative prolonged ischemia. The odds ratio for an increase of 0.16 U in night-day difference of alpha(1) (corresponding to interquartile range) was 7.7 (95% confidence interval, 1.9-51.4; P = 0.0018). Breakdown of fractal-like heart rate dynamics is predictive for postoperative prolonged myocardial ischemia in elderly patients having emergency surgery for traumatic hip fracture.\n\nQuestion:\nDoes the breakdown of fractal heart rate dynamics predict prolonged postoperative myocardial ischemia?\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 report a qualitative study which explores registered nurses' views on the issue of time in the workplace. There is a worldwide shortage of healthcare workers, subsequently time as a healthcare resource is both finite and scarce. As a result, increased attention is being paid to the restructuring of nursing work. However, the experience of time passing is a subjective one and there exists little research which, over a prolonged period of time, describes nurses' experiences of working in time-pressurized environments. A narrative inquiry. Five registered nurses were individually interviewed a total of three times over a period of 12 months, amounting to a total of 15 interviews and 30 hours of data. Data were collected and analysed following a narrative enquiry approach during the period 2008-2010. Participants describe how attempts to work more effectively sometimes resulted in unintended negative consequences for patient care and how time pressure encourages collegiality amongst nurses. Furthermore, the registered nurses' account of how they opportunistically create time for communication with patients compels us to re-evaluate the nature of communication during procedural nursing care.\n\nQuestion:\nAre the relationships between communication , care and time intertwined : a narrative inquiry exploring the impact of time on registered nurses ' work?\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 whole-genome association study of 4631 progeny-tested Nordic Red dairy cattle bulls using imputed next-generation sequencing data revealed a major quantitative trait locus (QTL) that affects birth index (BI) on Bos taurus autosome (BTA) 23. We analyzed this QTL to identify which of the component traits of BI are affected and understand its molecular basis. A genome-wide scan of BI in Nordic Red dairy cattle detected major QTL on BTA6, 14 and 23. The strongest associated single nucleotide polymorphism (SNP) on BTA23 was located at 13,313,896 bp with [Formula: see text]. Analyses of component traits showed that the QTL had a large effect on stillbirth. Based on the 10 most strongly associated SNPs with stillbirth, we constructed a haplotype. Among this haplotype's alleles, HAPQTL had a large negative effect on stillbirth. No animals were found to be homozygous for HAPQTL. Analysis of stillbirth records that were categorized by carrier status for HAPQTL of the sire and maternal grandsire suggested that this haplotype had a recessive mode of inheritance. Illumina BovineHD BeadChip genotypes and genotype intensity data indicated a chromosomal deletion between 12.28 and 12.81 Mbp on BTA23. An independent set of Illumina Bovine50k BeadChip genotypes identified a recessive lethal haplotype that spanned the deleted region.\n\nQuestion:\nIs a 0.5-Mbp deletion on bovine chromosome 23 a strong candidate for stillbirth in Nordic Red cattle?\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 researches have shown that myeloperoxidase (MPO) is a potential inflammatory risk factor for coronary heart disease (CHD). In the present study, the possible associations of MPO with acute coronary syndrome (ACS), low density lipoprotein cholesterol (LDL-C) and other risk factors in CHD patients were investigated. Five hundred thirty-six CHD patients [363 ACS and 173 stable angina pectoris (SAP)] and 181 non-CHD patients confirmed by coronary angiography were enrolled in this study. The association study was performed by logistic regression analysis. ACS patients had significantly higher MPO activities than SAP and non-CHD patients (p < 0.001). The area under the receiver operating characteristic (ROC) curve of MPO for diagnosing ACS was 0.84 (95% CI: 0.80-0.88, p < 0.001). The optimal cut-off value (sensitivity; specificity) of MPO was 164.77 ng/mL (79.1% and 82.1%). LDL-C (III versus I tertile, OR: 3.24, 95% CI: 1.67-6.29, p = 0.001) and ACS (yes versus no, OR 2.74, 95% CI: 1.71-4.39, p < 0.001) were significantly associated with elevated serum MPO activities, which had the highest odds ratio in quantitative and qualitative variables, respectively. There were significant increase trends in the prevalence of ACS and high LDL-C levels from I to III MPO tertile, which were 46.4% and 8.9% for I, 68.0% and 31.5% for II, 88.8% and 59.8% for III tertile, respectively (p < 0.001).\n\nQuestion:\nAre elevated serum myeloperoxidase activities significantly associated with the prevalence of ACS and High LDL-C levels in CHD 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:\nNon-alcoholic fatty liver disease (NAFLD) appears to be a new risk factor for the development of coronary artery disease (CAD). Members of a class of non-coding RNAs, termed microRNAs (miRNAs), have been identified as post-transcriptional regulators of cholesterol homoeostasis and can contribute to the development of NAFLD. The aims of this study were to (i) to assess the relationship between NAFLD and sudden cardiac death (SCD) from severe CAD in forensic autopsies and (ii) to quantify several hepatic miRNAs previously associated with lipid metabolism and NAFLD to correlate their expression with the presence of NAFLD, CAD, obesity parameters and postmortem lipid profile. A total of 133 cases of autopsies with SCD and established CAD (patient group, CAD-SCD) and 106 cases of non-CAD sudden death (control group, non-CAD-SD) were included. miRNAs were quantified in frozen liver tissues. Males predominated in both groups. Patients more frequently exhibited NAFLD and necroinflammatory steatohepatitis (NASH) than controls (62% vs 26%, P = 0.001 and 42% vs 26%, P = 0.001 respectively). In both groups, the presence of NAFLD correlated with body mass index and abdominal circumference (P < 0.05). An increase in miR-34a-5p and a decrease in miR-122-5p and -29c-3p in patients with NASH vs controls without NAFLD were observed (P < 0.05). Finally, significant correlations between miR-122-5p and unfavourable lipid profile and also hs-CRP and miR-34a-5p were noted.\n\nQuestion:\nDo deregulated hepatic microRNAs underlie the association between non-alcoholic fatty liver disease and coronary artery 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:\nTo analyze the total grip force and load distribution of the hand with midcarpal fusion (MCF) and total wrist fusion (TWF). Twelve patients with unilateral TWF and 12 patients with unilateral MCF were assessed at an average 64 months (range, 19-100 months) postoperatively. The total grip force and load distribution of both hands were measured by the Manugraphy system using 3 cylinder sizes. The load applied to 7 anatomical areas of the hand during cylinder grip was analyzed, comparing the operated and the nonsurgical hands. For the 100 mm and 150 mm cylinders, a significantly lower total grip force was found in hands operated with either TWF or MCF. For the 200 mm cylinder, there was a significant difference between nonsurgical hands and those with MCF but not between nonsurgical hands and those with TWF. For the 100 mm cylinder, the difference between nonsurgical and operated hands was greater in hands with TWF than those with MCF. For the load distribution of the hand, no differences between the operated and the nonsurgical hand were found for either MCF or TWF.\n\nQuestion:\nDo the Effect of Midcarpal Versus Total Wrist Fusion on the Hand 's Load Distribution During Gripping?\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 evaluate the impact of different prognostic factors that has been suggested to be useful in predicting the survival of patients with multiple myeloma (MM). A longitudinal prospective study was conducted on 24 adult Mexican patients diagnosed with primary MM. The levels of expression of CD38, CD138 and cyclin D1 were analyzed in plasma cells (PCs) from patients and mononuclear cells from healthy donors. Serum levels of lactate dehydrogenase, creatinine, calcium, beta2 microglobulin and interleukin-6 (IL-6) as well as hemoglobin and platelet count were taken into consideration. RESULTS; CD138 and cyclin D1 levels in absolute numbers were significantly overexpressed in malignant PCs. A positive correlation was noted between cyclin D1 and CD38 expression levels in malignant PCs. IL-6 and serum calcium were also positively correlated in MM patients. Cyclin D1 overexpression was not associated with better overall survival (OS). Normal calcium levels were associated with better overall survival (OS). Serum calcium was the only variable correlating with better OS in Cox regression analysis.\n\nQuestion:\nIs serum calcium an independent prognostic factor of overall survival in Mexican patients with multiple myeloma?\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:\nAccording to the ISO, the radiopacity of luting cements should be equal to or greater than that of aluminum. The aim of this in vitro study was to determine the radiopacity of 13 commercially available dental luting cements and compare them with human enamel and dentin. Five classes of luting cements were evaluated: zinc phosphate (Cegal N and Harvard Zinc Phosphate), zinc polycarboxylate (Harvard Polycarboxylate and Hoffmann's Carboxylate), glass ionomers (Ketac Cem Easymix, Ketac Cem Radiopaque, and Fuji I), resin-modified glass ionomer (Rely X Luting), and resin cements (Multilink Automix, Variolink II, Speed CEM, Rely X Unicem Automix, and three shades of Variolink Veneer). Tooth slices served as controls. Five specimens of each material measuring 8 mm in diameter and 1 mm thick were prepared and radiographed alongside tooth slices and an aluminum stepwedge using a Trophy RVG sensor. The radiopacity values were expressed in mm Al and analyzed by the ANOVA and Tukey tests (P < .05). All the cements examined except Variolink Veneer had significantly higher radiopacities than that of dentin. Rely X Unicem Automix, glass ionomer, and resin-modified glass-ionomer cements demonstrated radiopacities that were not significantly different with respect to enamel. Zinc phosphate, zinc polycarboxylate, and three of the resin cements presented radiopacity values that were significantly greater than that of enamel.\n\nQuestion:\nDoes an in vitro radiographic analysis of the density of dental luting cement as measured by CCD-based digital radiography?\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:\nEpidemiological studies show strong associations between kidney dysfunction and risk of ischemic stroke (IS), the mechanisms of which are incompletely understood. We investigated whether these associations may reflect shared heritability because of a common polygenic basis and whether this differed for IS subtypes. Polygenic models were derived using genome-wide association studies meta-analysis results for 3 kidney traits: estimated glomerular filtration rate using serum creatinine (eGFRcrea: n=73 998), eGFR using cystatin C (eGFRcys: n=22 937), and urinary albumin to creatinine ratio (n=31 580). For each, single nucleotide polymorphisms passing 10 P value thresholds were used to form profile scores in 4561 IS cases and 7094 controls from the United Kingdom, Germany, and Australia. Scores were tested for association with IS and its 3 aetiological subtypes: large artery atherosclerosis, cardioembolism, and small vessel disease. Polygenic scores correlating with higher eGFRcrea were associated with reduced risk of large artery atherosclerosis, with 5 scores reaching P<0.05 (peak P=0.004) and all showing the epidemiologically expected direction of effect. A similar pattern was observed for polygenic scores reflecting higher urinary albumin to creatinine ratio, of which 3 associated with large artery atherosclerosis (peak P=0.01) and all showed the expected directional association. One urinary albumin to creatinine ratio-based score also associated with small vessel disease (P=0.03). The global pattern of results was unlikely to have occurred by chance (P=0.02).\n\nQuestion:\nDo polygenic overlap between kidney function and large artery atherosclerotic stroke?\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:\nIntraperitoneal administration of paclitaxel (PTX) can elicit a marked clinical response in peritoneal metastases of gastric cancer. In this study, we retrospectively analyzed the clinical outcome of 17 patients who underwent R0 resection with D2 dissection for advanced gastric cancer with macroscopic serosal exposure and received intraperitoneal PTX as adjuvant therapy. A pathological study revealed that the depth of invasion of the primary tumor was pT4a or pT4b in 10 cases, and that the pN stage was more than pN2 in 8 cases. Genetic analysis of peritoneal lavage fluid was performed in 14 cases, all of which were positive for carcinoembryonic antigen mRNA. In these patients, PTX was intraperitoneally administered at 20-60 mg/m(2) with oral S-1 for 3-36 months after surgery. In a median follow-up period of 66 months, recurrence occurred in the liver and peritoneum in 2 (11.7%) and 1 (5.9%) patients, respectively, and no nodal recurrence was observed. Five-year overall survival and disease-free survival were 88.2 and 82.3%, respectively.\n\nQuestion:\nIs intraperitoneal Paclitaxel useful as adjuvant chemotherapy for advanced gastric cancer with serosal exposure?\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 present study is designed to explore the metastasis-inhibitory effect of physcion 8-O-β-glucopyranoside (PG) in human breast cancer, and the mechanisms underlying its role in tumor metastasis. Both in vitro and in vivo studies were conducted. Cell migration and invasion were analyzed by transwell assay. The translocation of β-catenin from the nucleus to cytoplasm membrane was demonstrated by immunofluorescent staining. The expression of signaling molecules was determined by Western blot or qRT-PCR. The present study showed that PG suppressed the migration, invasion, and EMT of breast cancer cells MDA-MB-231 in a dose-dependent manner. The results also revealed that impairment of the metastatic potential caused by PG was associated with the activation of AMPK and downregulation of both DNMT1 and Sp1. Moreover, the data from the in vivo model also supported the in vitro findings, which showed that inhibition of metastasis by PG was associated with the downregulation of DNMT1 and Sp1 as well as increased level of phosphorylated AMPK.\n\nQuestion:\nDoes physcion 8-O-β-glucopyranoside suppress the metastasis of breast cancer in vitro and in vivo by modulating DNMT1?\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:\nAlcohol-related driving accidents and fatalities occur most frequently at nighttime and at dawn, that is, a mesopic lighting condition in which visual processing depends on both rod and cone photoreceptors. The temporal functions of the rod and cone pathways are critical for driving in this lighting condition. However, how alcohol influences the temporal functions in the rod and cone pathways at mesopic light levels is inconclusive. To address this, this study investigated whether an acute intoxicating dose of alcohol impairs rod- and/or cone-mediated critical fusion frequency (CFF; the lowest frequency of which an intermittent or flickering light stimulus is perceived as steady). In Experiment I, we measured the CFFs for 3 types of visual stimuli (rod stimulus alone, cone stimulus alone, and the mixture of both stimuli types), under 3 illuminant light levels (dim illuminance: 2 Td; low illuminance: 20 Td; and medium illuminance: 80 Td) in moderate-heavy social drinkers before and after they consumed an intoxicating dose of alcohol (0.8 g/kg) compared with a placebo beverage. In Experiment II, we examined whether the illuminance level (dark vs. light) of the visual area surrounding the test stimuli alters alcohol's effect on the temporal processing of rods and cones. The results showed that compared with placebo, alcohol significantly reduced CFFs of all stimulus types at all illuminance levels. Furthermore, alcohol intoxication produced a larger impairment on rod-pathway-mediated CFFs under light versus dark surround.\n\nQuestion:\nDoes alcohol Intoxication impair Mesopic Rod and Cone Temporal Processing in Social Drinkers?\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:\nAutosomal recessive retinitis pigmentosa (arRP) is a genetically heterogeneous disease resulting in progressive loss of photoreceptors that leads to blindness. To date, 36 genes are known to cause arRP, rendering the molecular diagnosis a challenge. The aim of this study was to use homozygosity mapping to identify the causative mutation in a series of inbred families with arRP. arRP patients underwent standard ophthalmic examination, Goldman perimetry, fundus examination, retinal OCT, autofluorescence measurement, and full-field electroretinogram. Fifteen consanguineous families with arRP excluded for USH2A and EYS were genotyped on 250 K SNP arrays. Homozygous regions were listed, and known genes within these regions were PCR sequenced. Familial segregation and mutation analyzes were performed. We found ten mutations, seven of which were novel mutations in eight known genes, including RP1, IMPG2, NR2E3, PDE6A, PDE6B, RLBP1, CNGB1, and C2ORF71, in ten out of 15 families. The patients carrying RP1, C2ORF71, and IMPG2 mutations presented with severe RP, while those with PDE6A, PDE6B, and CNGB1 mutations were less severely affected. The five families without mutations in known genes could be a source of identification of novel genes.\n\nQuestion:\nDoes homozygosity mapping in autosomal recessive retinitis pigmentosa families detect novel mutations?\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:\nIncreased carotid artery intima-media thickness (IMT) is a noninvasive marker of systemic arterial disease, associated with atherosclerosis, abnormal arterial mechanics, myocardial infarction, and stroke. In the elderly, clinically elevated IMT is related to diminished attention-executive function. In this context, previous work involving paper-and-pencil measures of cognition has demonstrated that a threshold of pathology (i.e., IMT>or=0.9 mm) is needed before IMT consistently relates to poor neuropsychological test performance. Given the critical role of arterial health in the development of cognitive dysfunction, the goal of this study was to investigate early markers of brain vulnerability by examining subclinical levels of IMT in relation to a sensitive marker of neuronal integrity, cerebral N-acetyl-aspartate/creatine (NAA/Cr) ratio, in midlife. A total of 40 participants aged 50+/-6 years, underwent neuropsychological assessment, proton magnetic resonance spectroscopy ((1)H MRS) examination of occipitoparietal grey matter and B-mode ultrasound of the common carotid artery. IMT was defined as the distance between the luminal-endothelial interface and the junction between the media and the adventitia. The relation between IMT and cerebral metabolite ratios was modeled using a single multivariate multiple regression analysis adjusted for age and current systolic blood pressure. Increased IMT was associated with significantly lower NAA/Cr ratios (IMT beta=-0.62, p=0.001), independent of age and systolic blood pressure (F(3,36)=4.928, p=0.006).\n\nQuestion:\nIs subclinical atherosclerosis related to lower neuronal viability in middle-aged adults : a 1H MRS 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:\nTo identify risk factors for reoperation following surgery for spontaneous pneumothorax. This is a retrospective clinical study conducted on 240 consecutive patients operated on for spontaneous pneumothorax in Lund University Hospital between January 1996 and December 2003. Patient information was gained from medical charts and operation reports. Logistic regression analysis was used to evaluate risk factors. Median follow-up was 54 months. Video-assisted thoracoscopic surgery (VATS) was used in 93% of the patients, where bullectomy with or without pleurodesis/pleurectomy was performed in most cases. Conversion to anterolateral thoracotomy was required in 6 cases (2.3%). Operative mortality (<30 days) was 0.8% (0% after VATS). Altogether 35 patients (13.7%) required a reoperation. Twenty patients were reoperated on within one month from surgery, most often due to prolonged air leakage (n=13, 5.1%) and bleeding (n=6, 2.3%). Fifteen patients (5.8%) were reoperated on because of recurrent pneumothorax, on average 17 months (range 1-39 months) after the primary operation. Significant independent risk factors for reoperation were; young age, operations performed for secondary pneumothorax due to emphysema and recurrent pneumothorax. The risk was also increased in patients where wedge resection was not performed. However, the type of pleurodesis or pleurectomy was not related to increased risk.\n\nQuestion:\nAre reoperations common following VATS for spontaneous pneumothorax : study of risk factors?\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:\nSera of patients with IgA nephropathy (IgAN) contain circulating immune complexes (CIC) composed of galactose-deficient IgA1 complexed with antiglycan antibodies. The role of these CIC in the pathogenesis of IgAN is not known. We studied how proliferation of cultured mesangial cells (MC) is affected by CIC prepared from sera of IgAN patients and healthy control subjects using size-exclusion chromatography. CIC-containing fractions were added to serum-starved MC in culture, and cell proliferation was measured using (3)H-thymidine incorporation. The results were confirmed by staining MC using an antibody against proliferating cell nuclear antigen. The incubation of starved MC with serum fractions with M(r) 800 to 900 kD, rich with galactose-deficient IgA1, stimulated proliferation, while fractions with smaller complexes were inhibitory. Furthermore, CIC-containing larger molecular mass fractions isolated from serum of an IgAN patient collected during an episode of macroscopic hematuria stimulated MC proliferation more than CIC obtained during a subsequent quiescent phase. To examine the role of IgA, we removed IgA1 from serum before fractionation. The resultant IgA1-depleted fractions were devoid of stimulatory IgA-CIC. Sera of IgAN patients were also fractionated after addition of desialylated galactose-deficient polymeric IgA1 to form additional immune complexes. Supplementation with a small quantity of this IgA1 increased cellular proliferation in assays using serum fractions of M(r)>/=800 to 900 kD; uncomplexed IgA1 did not affect MC proliferation significantly. In contrast, supplementation with a larger quantity of this IgA1 inhibited cellular proliferation in assays using serum fractions of M(r) 700 to 800 kD.\n\nQuestion:\nDo igA1-containing immune complexes in IgA nephropathy differentially affect proliferation of mesangial 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:\nBrief reversible ischemic episodes (ischemic preconditioning, IPC) protect the heart against arrhythmias during a subsequent prolonged low-flow ischemia. We have recently shown that this protection involves release of bradykinin, activation of bradykinin B2 receptors followed by opening of sarcolemmal, but not mitochondrial ATP-sensitive K+ channels. The goal of this study was to clarify a trigger and/or mediator role of bradykinin in the antiarrhythmic effects of IPC during low-flow ischemia. Isolated perfused rat hearts underwent 60 minutes of low-flow ischemia induced by reducing perfusion pressure followed by 60 minutes of reperfusion. Preconditioning was induced by 2 x 5 minutes episodes of zero-flow ischemia. In yet other groups, preconditioned or non-preconditioned hearts were treated either with bradykinin (10 nmol/L) or with HOE 140 (bradykinin B2 receptor antagonist, 100 nmol/L). IPC reduced the number of ventricular premature beats, as well as the incidence of ventricular tachycardia and of ventricular fibrillation during low-flow ischemia. In addition, this protection was abolished by HOE 140 given during low-flow ischemia. Pharmacological preconditioning using short bradykinin perfusion instead of IPC did not show antiarrhythmic effects. However, bradykinin administered during low-flow ischemia and reperfusion reduced the number of ventricular premature beats and the incidence of ventricular tachycardia and of ventricular fibrillation during low-flow ischemia.\n\nQuestion:\nIs bradykinin a mediator , but unlikely a trigger , of antiarrhythmic effects of ischemic preconditioning?\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:\nBile acids (BAs) play a crucial role in dietary fat digestion and in the regulation of lipid, glucose, and energy metabolism. Thyroid-stimulating hormone (TSH) is a hormone produced by the anterior pituitary gland that directly regulates several metabolic pathways. However, the impact of TSH on BA homeostasis remains largely unknown. We analyzed serum BA and TSH levels in healthy volunteers under strict control of caloric intake. Thyroidectomized rats were administered thyroxine and injected with different doses of TSH. Tshr(-/-) mice were supplemented with thyroxine, and C57BL/6 mice were injected with Tshr-siRNA via the tail vein. The serum BA levels, BA pool size, and fecal BA excretion rate were measured. The regulation of SREBP-2, HNF-4α, and CYP7A1 by TSH were analyzed using luciferase reporter, RNAi, EMSA, and CHIP assays. A negative correlation was observed between the serum levels of TSH and the serum BA levels in healthy volunteers. TSH administration led to a decrease in BA content and CYP7A1 activity in thyroidectomized rats supplemented with thyroxine. When Tshr was silenced in mice, the BA pool size, fecal BA excretion rate, and serum BA levels all increased. Additionally, we found that HNF-4α acts as a critical molecule through which TSH represses CYP7A1 activity. We further confirmed that the accumulation of mature SREBP-2 protein could impair the capacity of nuclear HNF-4α to bind to the CYP7A1 promoter, a mechanism that appears to mediate the effects of TSH.\n\nQuestion:\nDoes thyroid-stimulating hormone regulate hepatic bile acid homeostasis via SREBP-2/HNF-4α/CYP7A1 axis?\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:\nNon-Fc-binding anti-CD3-specific antibodies represent a promising therapy for preserving C-peptide production in subjects with recent-onset type 1 diabetes. However, the mechanisms by which anti-CD3 exerts its beneficial effect are still poorly understood, and it is questionable whether this therapeutic approach will prove durable with regard to its ability to impart metabolic preservation without additional actions designed to maintain immunological tolerance. We used the NOD mouse model to test whether rapamycin, a compound well-known for its immunomodulatory activity in mice and humans, could increase the therapeutic effectiveness of anti-CD3 treatment in type 1 diabetes. Rapamycin was administered to diabetic NOD mice simultaneously with anti-CD3 or to NOD mice cured by anti-CD3 therapy. The ability of this combined therapy to revert type 1 diabetes and maintain a state of long-term tolerance was monitored and compared with that of anti-CD3 therapy alone. Rapamycin inhibited the ability of anti-CD3 to revert disease without affecting the frequency/phenotype of T-cells. Rapamycin also reinstated diabetes in mice whose disease was previously reversed by anti-CD3. Withdrawal of rapamycin in these latter animals promptly restored a normoglycemic state.\n\nQuestion:\nDoes rapamycin prevent and breaks the anti-CD3-induced tolerance in NOD 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:\nTo assess the association between demographic and lifestyle parameters and perceived severity of the climacteric syndrome in perimenopausal women. A cross-sectional study of 151 healthy women aged 45-55 years who attended the University Medical Center affiliated menopause clinics. The analysis was based on self completion of the Greene climacteric score, consisting of psychological, somatic/physical, sexual and vasomotor subscores. The Greene total score and subscores were the main outcomes of the study. Of all demographic, anthropometric and lifestyle parameters recorded, the correlates with reduced total Greene score were high-order maternity and regular physical exercise. Mothers of 3 or more children reported significantly lower total Greene score (18±12.8 vs. 22.1±8.1) (p=0.01) as well as lower psychological subscore (8.7±6.8 vs. 11.5±5.4) (p=0.01). Regular physical activity was also associated with significantly lower total Greene score (17.0±11.0 vs. 22.6±11.3) (p=0.01) and specifically lower psychological subscore (9.5±6.6 vs. 12.8±7.7) (p=0.03) and sexual subscore (1.1±0.99 vs. 1.61±1.05) (p=0.03). Linear regression models showed that regular exercise was the lifestyle parameter most significantly correlated with a lower total Greene score (p=0.006) independent of menopausal status. Of particular note, regular exercise was significantly correlated with lower psychological (p=0.006) and physical subscores (p=0.06). Moreover, the higher the frequency of exercise (both aerobic and non aerobic), the lower the severity of the climacteric symptoms reported, yet the vasomotor and sexual subscores remained unchanged.\n\nQuestion:\nIs regular exercise the most significant lifestyle parameter associated with the severity of climacteric symptoms : a cross sectional 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:\nTest-retest reliability of an asthma paper diary versus an electronic diary (e-diary) with an integrated peak flow meter was investigated. The equivalence of the two modes was also evaluated. Prospective, randomized crossover study design in adolescents (12-17 years) and adults (≥18 years). Key inclusion criteria were persistent asthma, Asthma Control Test (ACT) scores ≥16, use of inhaled corticosteroid with or without long-acting beta-agonist for ≥12 weeks, nocturnal awakenings <2 times in the past week, and activity limitations <1 per week. Participants were randomized to either paper then e-diary or e-diary then paper, to be completed for 14 days each. Forty-seven participants completed all study visits. Weekly percentage of symptom-free days (SFDs) and rescue-free days (RFDs) were calculated. Intraclass correlation coefficients (ICCs) of Week 1 mean SFD and RFD (test) and Week 2 mean SFD and RFD (retest), respectively, were estimated in three groups defined as stable: (i) minimal changes in asthma symptoms, as measured by the global patient reported symptom change question, (ii) less than 15% change (absolute value) in 1 second FEV(1) at adjacent study visits, and (iii) changes in ACT scores less than three points for each mode. SFD demonstrated acceptable ICC (≥0.70) using all three definitions of asthma stability for both modes.\n\nQuestion:\nIs an electronic diary shown to be more reliable than a paper diary : results from a randomized crossover study in patients with persistent asthma?\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:\nInfection rates for breast surgery are 3 to 15 percent, higher than average for a clean surgical procedure. Preoperative and postoperative antibiotics have lowered infection rates in other surgical groups, yet there is no consensus on postoperative prophylactic antibiotic use in microsurgical breast reconstruction. A retrospective review of consecutive patients who underwent autologous breast reconstruction between 2006 and 2009 was performed. Specific risk factors for autologous reconstruction were reviewed, including medical comorbidities, irradiation, and chemotherapy history. Data were collected on type and duration of prophylactic antibiotics. A prospective cohort of patients who received only 24 hours of postoperative antibiotics was identified. The incidence of surgical-site infections was measured using Centers for Disease Control and Prevention criteria. A total of 256 patients with 360 microvascular breast reconstructions who received both preoperative and postoperative prophylactic antibiotics were analyzed. The overall surgical-site infection rate was 17.2 percent (44 of 256 patients). Surgical-site infection was correlated with increased age, tobacco use, and prior radiation. Duration of postoperative antibiotic use did not differ in those patients who developed surgical-site infections (6.2 versus 7.7 days; p = 0.19). Eighty-two patients (32 percent) received only 24 hours of postoperative antibiotics, while 174 (68 percent) received more than 24 hours of antibiotics for a median duration of 10 days. There was no difference in the overall surgical-site infection rate in those who received more than 24 hours of antibiotics (19.5 versus 15.5 percent; p = 0.47).\n\nQuestion:\nDoes duration of antibiotics after microsurgical breast reconstruction change surgical infection rate?\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 sphincter of Oddi (SO) manometry via the transpapillary route is performed usually for a period of several minutes. To investigate whether there is a considerable variation in the manometric measurements of SO over a longer period of time, we have performed long-term manometry of SO via the transpapillary (n = 5) as well as the percutaneous (n = 7) routes. Transpapillary manometry of SO was carried out by a conventional low-compliant continuously perfused technique. The location of the manometric catheter was maintained at the same level by observing the video monitor. SO manometry and the duodenal migrating motor complex (MMC) was simultaneously measured with a specially designed catheter via the percutaneous route. The mean recording time was 41 min (range 11-72 min). The frequency of phasic contractions of SO varied from 0 to 12/min. Throughout the entire recording period, high-frequency contractions (over 8/min) were noted 14.9% of the time. In the cases of percutaneous transductal SO manometry, the periods of high-frequency contractions coincided with phase III of duodenal MMC. The interval between the first high-frequency contractions and the second was 47 min. The mean duration of high-frequency contractions was 6 min and 42 s. There was no significant change in the amplitude, basal pressure, and contraction sequence among the various periods of frequencies.\n\nQuestion:\nIs frequency of phasic wave contraction variable during long-term sphincter of Oddi manometry?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]