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PubmedQA118845
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: [\"Orbital fibroblast proliferation and hyaluronic acid (HA) release are responsible for some of the clinical features of Graves' ophthalmopathy (GO). Thus, inhibition of these processes may be a possible therapeutic approach to this syndrome. Enalapril, a widely used antihypertensive drug, was found to have some inhibitory actions on fibroblast proliferation in cheloid scars in vivo, based on which we investigated its effects in primary cultures of orbital fibroblasts from GO patients and control subjects.\", 'Primary cultures of GO and control fibroblasts were treated with enalapril or with a control compound (lisinopril). Cell proliferation assays, lactate dehydrogenase release assays (as a measure of cell necrosis), apoptosis assays, and measurement of HA in the cell media were performed.', 'Enalapril significantly reduced cell proliferation in both GO and control fibroblasts. Because enalapril did not affect cell necrosis and apoptosis, we concluded that its effects on proliferation reflected an inhibition of cell growth and/or a delay in cell cycle. Enalapril significantly reduced HA concentrations in the media from both GO and control fibroblasts.'] Does enalapril reduce proliferation and hyaluronic acid release in orbital fibroblasts?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ["Orbital fibroblast proliferation and hyaluronic acid (HA) release are responsible for some of the clinical features of Graves' ophthalmopathy (GO). Thus, inhibition of these processes may be a possible therapeutic approach to this syndrome. Enalapril, a widely used antihypertensive drug, was found to have some inhibitory actions on fibroblast proliferation in cheloid scars in vivo, based on which we investigated its effects in primary cultures of orbital fibroblasts from GO patients and control subjects.", 'Primary cultures of GO and control fibroblasts were treated with enalapril or with a control compound (lisinopril). Cell proliferation assays, lactate dehydrogenase release assays (as a measure of cell necrosis), apoptosis assays, and measurement of HA in the cell media were performed.', 'Enalapril significantly reduced cell proliferation in both GO and control fibroblasts. Because enalapril did not affect cell necrosis and apoptosis, we concluded that its effects on proliferation reflected an inhibition of cell growth and/or a delay in cell cycle. Enalapril significantly reduced HA concentrations in the media from both GO and control fibroblasts.'] Does enalapril reduce proliferation and hyaluronic acid release in orbital fibroblasts? OUTPUT:
PubmedQA108390
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['The contribution of lactase to isoflavone bioavailability has not been clarified. We evaluated the association between lactase activity and the bioavailability of isoflavone glucosides in Japanese adults.', 'Twenty-six Japanese adult participants completed a study that included tests of breath hydrogen after a lactose load, orocecal transit time, and isoflavone glucoside absorption. Lactose malabsorbers were defined as those with an increase in breath hydrogen level (DeltaH(2)) of more than 20 ppm after a load of lactose (20 g). Participants ingested 200 ml soymilk, and serum isoflavones were analyzed until 480 min.', 'Serum daidzein and genistein levels increased rapidly until 60 min, then slowly increased. The increases of serum isoflavones in the early phase, but not the later phase, were suppressed in lactose malabsorbers. DeltaH(2 max) after a load of lactose inversely correlated with serum daidzein levels at 30 min. The percentage of equol producers tended to be greater among lactose malabsorbers (P=0.067).'] Do low activities of intestinal lactase suppress the early phase absorption of soy isoflavones in Japanese adults?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['The contribution of lactase to isoflavone bioavailability has not been clarified. We evaluated the association between lactase activity and the bioavailability of isoflavone glucosides in Japanese adults.', 'Twenty-six Japanese adult participants completed a study that included tests of breath hydrogen after a lactose load, orocecal transit time, and isoflavone glucoside absorption. Lactose malabsorbers were defined as those with an increase in breath hydrogen level (DeltaH(2)) of more than 20 ppm after a load of lactose (20 g). Participants ingested 200 ml soymilk, and serum isoflavones were analyzed until 480 min.', 'Serum daidzein and genistein levels increased rapidly until 60 min, then slowly increased. The increases of serum isoflavones in the early phase, but not the later phase, were suppressed in lactose malabsorbers. DeltaH(2 max) after a load of lactose inversely correlated with serum daidzein levels at 30 min. The percentage of equol producers tended to be greater among lactose malabsorbers (P=0.067).'] Do low activities of intestinal lactase suppress the early phase absorption of soy isoflavones in Japanese adults? OUTPUT:
PubmedQA97421
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: [\"Introduction and aims: The most recent hypothesis postulated that early restoration of euthyroid state in patients with Graves' disease changes the course of the disease and leads to better disease control. Therefore, we analyzed the efficacy of methimazole therapy and the course of disease in patients with restored euthyroidism and in patients with active disease on first control visit.\", 'We included 63 patients with total T4 level >190 nmol/L or T3 >7 nmol/L and diffuse goiter with no previous episodes of hyperthyroidism. All patients received initially high doses of methimazole (60-80 mg) followed by a rapid dose reduction.', 'Ten percent of patients were excluded from the study due to side effects. Two different groups emerged after 5 weeks of treatment with same dose of methimazole: group 1 with active disease (48%) and group 2 with restored euthyroidism. Further controls on 12th, 24th and 68th weeks of treatment showed no difference in remission rates, number of iatrogenic hypothyroid episodes, and number of exacerbations between the two groups, regardless of methimazole dose. There was no association between age, gender, thyroid hormone levels, and remission and exacerbation rates.'] Is remission of Graves ' disease related to early restoration of euthyroidism with high-dose methimazole therapy?\nOUTPUT:\n" }, { "from": "agent", "value": "no" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ["Introduction and aims: The most recent hypothesis postulated that early restoration of euthyroid state in patients with Graves' disease changes the course of the disease and leads to better disease control. Therefore, we analyzed the efficacy of methimazole therapy and the course of disease in patients with restored euthyroidism and in patients with active disease on first control visit.", 'We included 63 patients with total T4 level >190 nmol/L or T3 >7 nmol/L and diffuse goiter with no previous episodes of hyperthyroidism. All patients received initially high doses of methimazole (60-80 mg) followed by a rapid dose reduction.', 'Ten percent of patients were excluded from the study due to side effects. Two different groups emerged after 5 weeks of treatment with same dose of methimazole: group 1 with active disease (48%) and group 2 with restored euthyroidism. Further controls on 12th, 24th and 68th weeks of treatment showed no difference in remission rates, number of iatrogenic hypothyroid episodes, and number of exacerbations between the two groups, regardless of methimazole dose. There was no association between age, gender, thyroid hormone levels, and remission and exacerbation rates.'] Is remission of Graves ' disease related to early restoration of euthyroidism with high-dose methimazole therapy? OUTPUT:
PubmedQA148274
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Deuterium oxide (D2O), or heavy water, affects a variety of biological activities different from those of water. The authors examined the antitumoral effect of D2O on brain neoplasms and demonstrated D2O-mediated cytotoxicity by using a Rous sarcoma virus-induced murine malignant astrocytoma cell line, RSVM. The mechanism of the observed cytotoxicity may involve D2O-induced apoptosis and cell-cycle modulation.', 'The authors performed an assay with methylthiazol tetrazolium bromide and a trypan blue dye exclusion test to confirm in vitro D2O-mediated cytotoxicity for RSVM cells. At D2O concentrations of 10 to 50%, the cytotoxic effect was dose and time dependent. Flow cytometry analysis revealed programmed cell death (apoptosis) and the accumulation of RSVM cells during the G2/M phase. By applying the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling method, fluorescein isothiocyanate-annexin V and propidium iodide double staining, and caspase-family protease activity analysis, the authors demonstrated both DNA fragmentation and enhancement of caspase activity after a 48-hour treatment with D2O, thus indicating that D2O induces apoptosis in RSVM cells. Apoptotic DNA fragmentation was completely abolished by the caspase inhibitor Z-VAD-FMK (benzyloxycarbonil-Val-Ala-Aps-fluoromethylketone). The findings indicate that the caspase activation pathway may be involved in D2Oinduced apoptosis.'] Does experimental validation of deuterium oxide-mediated antitumoral activity as it relate to apoptosis in murine malignant astrocytoma cells?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Deuterium oxide (D2O), or heavy water, affects a variety of biological activities different from those of water. The authors examined the antitumoral effect of D2O on brain neoplasms and demonstrated D2O-mediated cytotoxicity by using a Rous sarcoma virus-induced murine malignant astrocytoma cell line, RSVM. The mechanism of the observed cytotoxicity may involve D2O-induced apoptosis and cell-cycle modulation.', 'The authors performed an assay with methylthiazol tetrazolium bromide and a trypan blue dye exclusion test to confirm in vitro D2O-mediated cytotoxicity for RSVM cells. At D2O concentrations of 10 to 50%, the cytotoxic effect was dose and time dependent. Flow cytometry analysis revealed programmed cell death (apoptosis) and the accumulation of RSVM cells during the G2/M phase. By applying the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling method, fluorescein isothiocyanate-annexin V and propidium iodide double staining, and caspase-family protease activity analysis, the authors demonstrated both DNA fragmentation and enhancement of caspase activity after a 48-hour treatment with D2O, thus indicating that D2O induces apoptosis in RSVM cells. Apoptotic DNA fragmentation was completely abolished by the caspase inhibitor Z-VAD-FMK (benzyloxycarbonil-Val-Ala-Aps-fluoromethylketone). The findings indicate that the caspase activation pathway may be involved in D2Oinduced apoptosis.'] Does experimental validation of deuterium oxide-mediated antitumoral activity as it relate to apoptosis in murine malignant astrocytoma cells? OUTPUT:
PubmedQA155874
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Posttraumatic stress disorder (PTSD) is a common and debilitating mental disorder that occurs following exposure to a traumatic event. However, most individuals do not develop PTSD following even a severe trauma, leading to a search for new variables, such as genetic and other molecular variation, associated with vulnerability and resilience in the face of trauma exposure.', 'We examined whether serotonin transporter (SLC6A4) promoter genotype and methylation status modified the association between number of traumatic events experienced and PTSD in a subset of 100 individuals from the Detroit Neighborhood Health Study.', 'Number of traumatic events was strongly associated with risk of PTSD. Neither SLC6A4 genotype nor methylation status was associated with PTSD in main effects models. However, SLC6A4 methylation levels modified the effect of the number of traumatic events on PTSD after controlling for SLC6A4 genotype. Persons with more traumatic events were at increased risk for PTSD, but only at lower methylation levels. At higher methylation levels, individuals with more traumatic events were protected from this disorder. This interaction was observed whether the outcome was PTSD diagnosis, symptom severity, or number of symptoms.'] Does sLC6A4 methylation modify the effect of the number of traumatic events on risk for posttraumatic stress disorder?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Posttraumatic stress disorder (PTSD) is a common and debilitating mental disorder that occurs following exposure to a traumatic event. However, most individuals do not develop PTSD following even a severe trauma, leading to a search for new variables, such as genetic and other molecular variation, associated with vulnerability and resilience in the face of trauma exposure.', 'We examined whether serotonin transporter (SLC6A4) promoter genotype and methylation status modified the association between number of traumatic events experienced and PTSD in a subset of 100 individuals from the Detroit Neighborhood Health Study.', 'Number of traumatic events was strongly associated with risk of PTSD. Neither SLC6A4 genotype nor methylation status was associated with PTSD in main effects models. However, SLC6A4 methylation levels modified the effect of the number of traumatic events on PTSD after controlling for SLC6A4 genotype. Persons with more traumatic events were at increased risk for PTSD, but only at lower methylation levels. At higher methylation levels, individuals with more traumatic events were protected from this disorder. This interaction was observed whether the outcome was PTSD diagnosis, symptom severity, or number of symptoms.'] Does sLC6A4 methylation modify the effect of the number of traumatic events on risk for posttraumatic stress disorder? OUTPUT:
PubmedQA124802
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['The implications of measuring and rewarding performance for patients with multiple chronic conditions have not been explored empirically.', \"To examine whether the number of chronic conditions was associated with patient's receipt of recommended preventive care.\", 'We evaluated the association between the likelihood of receiving recommended preventive care and the number of chronic conditions in the diabetic population by analyzing the 2003 Medical Expenditure Panel Survey using logistic regression. Demographic characteristics and the number of chronic conditions were compared using chi(2) tests.', 'Hemoglobin A1C test and diabetic eye exam.', 'In 2003, approximately 14.2 million non-institutionalized Americans had diabetes and 23% of them had five or more chronic conditions besides diabetes. Those patients were 67% (p < 0.05) and 50% (p < 0.001) more likely to receive hemoglobin A1C test and eye exams compared with diabetic patients with no additional chronic conditions. After adjusting for the number of office-based physician visits, a larger number of chronic conditions did not significantly affect the likelihood of receiving recommended care. Diabetic patients with more chronic conditions had more frequent office-based physician visits (p < 0.0001), and patients with 11 or more annual office-based physician visits were 43% (p < 0.05) and 40% (p < 0.01) more likely to receive hemoglobin A1C test and eye exam, respectively, compared with diabetic patients who had less than two office-based physician visits.'] Do patients with multiple chronic conditions receive lower quality of preventive care?\nOUTPUT:\n" }, { "from": "agent", "value": "no" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['The implications of measuring and rewarding performance for patients with multiple chronic conditions have not been explored empirically.', "To examine whether the number of chronic conditions was associated with patient's receipt of recommended preventive care.", 'We evaluated the association between the likelihood of receiving recommended preventive care and the number of chronic conditions in the diabetic population by analyzing the 2003 Medical Expenditure Panel Survey using logistic regression. Demographic characteristics and the number of chronic conditions were compared using chi(2) tests.', 'Hemoglobin A1C test and diabetic eye exam.', 'In 2003, approximately 14.2 million non-institutionalized Americans had diabetes and 23% of them had five or more chronic conditions besides diabetes. Those patients were 67% (p < 0.05) and 50% (p < 0.001) more likely to receive hemoglobin A1C test and eye exams compared with diabetic patients with no additional chronic conditions. After adjusting for the number of office-based physician visits, a larger number of chronic conditions did not significantly affect the likelihood of receiving recommended care. Diabetic patients with more chronic conditions had more frequent office-based physician visits (p < 0.0001), and patients with 11 or more annual office-based physician visits were 43% (p < 0.05) and 40% (p < 0.01) more likely to receive hemoglobin A1C test and eye exam, respectively, compared with diabetic patients who had less than two office-based physician visits.'] Do patients with multiple chronic conditions receive lower quality of preventive care? OUTPUT:
PubmedQA185535
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Critically ill patients often demonstrate extremely unusual volumes of distribution (Vd) and half-lives (t1/2) of drugs. Imipenem is a widely used antibiotic in critically ill patients.', 'We performed high-performance liquid chromatography analysis of imipenem in samples from 50 critically ill patients treated with either 500 or 1,000 mg.', 'Peak imipenem levels varied from 1.56 microg/mL to 58.8 microg/mL. Trough levels varied between 0.0 microg/mL and 15.62 microg/mL. Only 54% of patients maintained a trough level greater than 4 microg/mL. Both the Vd and the t1/2 of imipenem were much greater than observed in other patient populations.'] Are imipenem levels predictable in the critically ill patient?\nOUTPUT:\n" }, { "from": "agent", "value": "no" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Critically ill patients often demonstrate extremely unusual volumes of distribution (Vd) and half-lives (t1/2) of drugs. Imipenem is a widely used antibiotic in critically ill patients.', 'We performed high-performance liquid chromatography analysis of imipenem in samples from 50 critically ill patients treated with either 500 or 1,000 mg.', 'Peak imipenem levels varied from 1.56 microg/mL to 58.8 microg/mL. Trough levels varied between 0.0 microg/mL and 15.62 microg/mL. Only 54% of patients maintained a trough level greater than 4 microg/mL. Both the Vd and the t1/2 of imipenem were much greater than observed in other patient populations.'] Are imipenem levels predictable in the critically ill patient? OUTPUT:
PubmedQA160662
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['The authors investigated the effect of remifentanil administration on resting electroencephalography functional connectivity and its relationship to cognitive function and analgesia in healthy volunteers.', 'Twenty-one healthy male adult subjects were enrolled in this placebo-controlled double-blind cross-over study. For each subject, 2.5 min of multichannel electroencephalography recording, a cognitive test of sustained attention (continuous reaction time), and experimental pain scores to bone-pressure and heat stimuli were collected before and after infusion of remifentanil or placebo. A coherence matrix was calculated from the electroencephalogram, and three graph-theoretical measures (characteristic path-length, mean clustering coefficient, and relative small-worldness) were extracted to characterize the overall cortical network properties.', 'Compared to placebo, most graph-theoretical measures were significantly altered by remifentanil at the alpha and low beta range (8 to 18 Hz; all P < 0.001). Taken together, these alterations were characterized by an increase in the characteristic path-length (alpha 17% and low beta range 24%) and corresponding decrements in mean clustering coefficient (low beta range -25%) and relative small-worldness (alpha -17% and low beta range -42%). Changes in characteristic path-lengths after remifentanil infusion were correlated to the continuous reaction time index (r = -0.57; P = 0.009), while no significant correlations between graph-theoretical measures and experimental pain tests were seen.'] Is disruption of cortical connectivity during remifentanil administration associated with cognitive impairment but not with analgesia?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['The authors investigated the effect of remifentanil administration on resting electroencephalography functional connectivity and its relationship to cognitive function and analgesia in healthy volunteers.', 'Twenty-one healthy male adult subjects were enrolled in this placebo-controlled double-blind cross-over study. For each subject, 2.5 min of multichannel electroencephalography recording, a cognitive test of sustained attention (continuous reaction time), and experimental pain scores to bone-pressure and heat stimuli were collected before and after infusion of remifentanil or placebo. A coherence matrix was calculated from the electroencephalogram, and three graph-theoretical measures (characteristic path-length, mean clustering coefficient, and relative small-worldness) were extracted to characterize the overall cortical network properties.', 'Compared to placebo, most graph-theoretical measures were significantly altered by remifentanil at the alpha and low beta range (8 to 18 Hz; all P < 0.001). Taken together, these alterations were characterized by an increase in the characteristic path-length (alpha 17% and low beta range 24%) and corresponding decrements in mean clustering coefficient (low beta range -25%) and relative small-worldness (alpha -17% and low beta range -42%). Changes in characteristic path-lengths after remifentanil infusion were correlated to the continuous reaction time index (r = -0.57; P = 0.009), while no significant correlations between graph-theoretical measures and experimental pain tests were seen.'] Is disruption of cortical connectivity during remifentanil administration associated with cognitive impairment but not with analgesia? OUTPUT:
PubmedQA67381
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['The aim of this study was to examine the relationship between tissue factor (TF), vascular endothelial growth factor (VEGF) and the onset of angiogenesis in the adenoma-carcinoma sequence (ACS), the stepwise process encompassing colorectal cancer (CRC) disease progression.', '210 surgical specimens comprising the ACS were immunohistochemically stained for endothelial cells (CD31), VEGF and TF. Angiogenesis quantified using Chalkley grid analysis (microvascular density; MVD), and VEGF/TF expression were semiquantitatively graded and correlated with standard prognostic indicators including 5 year follow-up. VEGF and TF were measured by ELISA in tumour specimens and normal mucosa from an additional 90 CRC patients.', \"There was a significant increase in MVD across the ACS (p < 0.0005) with significant correlations with Dukes' stage (p = 0.01) and lymph node involvement (p = 0.02). The greatest increase in MVD was related to the onset of dysplasia, with an associated significant increase in VEGF expression (p < 0.0005). There was a significant relationship between VEGF and TF expression in the initial phase of the ACS (k = 0.44, p < 0.005), although no correlation between VEGF or TF, and MVD, tumour size, Dukes' classification, lymph node involvement or survival was found.\"] Does the angiogenic switch occur at the adenoma stage of the adenoma carcinoma sequence in colorectal cancer?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['The aim of this study was to examine the relationship between tissue factor (TF), vascular endothelial growth factor (VEGF) and the onset of angiogenesis in the adenoma-carcinoma sequence (ACS), the stepwise process encompassing colorectal cancer (CRC) disease progression.', '210 surgical specimens comprising the ACS were immunohistochemically stained for endothelial cells (CD31), VEGF and TF. Angiogenesis quantified using Chalkley grid analysis (microvascular density; MVD), and VEGF/TF expression were semiquantitatively graded and correlated with standard prognostic indicators including 5 year follow-up. VEGF and TF were measured by ELISA in tumour specimens and normal mucosa from an additional 90 CRC patients.', "There was a significant increase in MVD across the ACS (p < 0.0005) with significant correlations with Dukes' stage (p = 0.01) and lymph node involvement (p = 0.02). The greatest increase in MVD was related to the onset of dysplasia, with an associated significant increase in VEGF expression (p < 0.0005). There was a significant relationship between VEGF and TF expression in the initial phase of the ACS (k = 0.44, p < 0.005), although no correlation between VEGF or TF, and MVD, tumour size, Dukes' classification, lymph node involvement or survival was found."] Does the angiogenic switch occur at the adenoma stage of the adenoma carcinoma sequence in colorectal cancer? OUTPUT:
PubmedQA148732
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['We evaluated the role of the renal vascular system and the Rho-A/Rho-kinase pathway in the maintenance of the pressor effects of vasopressin in endotoxemic rats.', 'In vitro and in vivo animal study.', 'University research laboratory.', 'Male Wistar rats (200-300 g).', 'Rats received either saline or lipopolysaccharide (10 mg/kg, intraperitoneal) 6 or 24 hours before the experiments. The effects of vasopressin on isolated aortic rings, cardiac function, mean arterial pressure, and both the renal vascular perfusion pressure of perfused kidneys in vitro and renal blood flow in situ were evaluated. The role of Rho-kinase in the renal and systemic effects of vasopressin was investigated through administration of the selective inhibitor Y-27632 and Western blot analysis.', 'The effect of vasopressin on mean arterial pressure was unaltered and that on renal vascular perfusion pressure enhanced in endotoxemic rats at both 6 and 24 hours after lipopolysaccharide, despite reduced contractile responses in aortic rings and the lack of effect on cardiac function. Vasopressin (3, 10, and 30 pmol/kg, IV) produced increased reduction in renal blood flow in endotoxemic rats. In perfused kidneys from lipopolysaccharide groups, administration of Y-27632 reverted the hyperreactivity to vasopressin. Treatment with Y-27632 partially inhibited the effects of vasopressin on mean arterial pressure and significantly reduced the effects of vasopressin on renal blood flow in control but not in endotoxemic rats. Although the protein levels of Rho-A and Rho-kinase I and II had not been impaired, the levels of phosphorylated myosin phosphatase-targeting subunit 1, the regulatory subunit of myosin phosphatase that is inhibited by Rho-kinase, were increased in both the renal cortex and the renal medulla of endotoxemic rats.'] Is increased activation of the Rho-A/Rho-kinase pathway in the renal vascular system responsible for the enhanced reactivity to exogenous vasopressin in endotoxemic rats?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['We evaluated the role of the renal vascular system and the Rho-A/Rho-kinase pathway in the maintenance of the pressor effects of vasopressin in endotoxemic rats.', 'In vitro and in vivo animal study.', 'University research laboratory.', 'Male Wistar rats (200-300 g).', 'Rats received either saline or lipopolysaccharide (10 mg/kg, intraperitoneal) 6 or 24 hours before the experiments. The effects of vasopressin on isolated aortic rings, cardiac function, mean arterial pressure, and both the renal vascular perfusion pressure of perfused kidneys in vitro and renal blood flow in situ were evaluated. The role of Rho-kinase in the renal and systemic effects of vasopressin was investigated through administration of the selective inhibitor Y-27632 and Western blot analysis.', 'The effect of vasopressin on mean arterial pressure was unaltered and that on renal vascular perfusion pressure enhanced in endotoxemic rats at both 6 and 24 hours after lipopolysaccharide, despite reduced contractile responses in aortic rings and the lack of effect on cardiac function. Vasopressin (3, 10, and 30 pmol/kg, IV) produced increased reduction in renal blood flow in endotoxemic rats. In perfused kidneys from lipopolysaccharide groups, administration of Y-27632 reverted the hyperreactivity to vasopressin. Treatment with Y-27632 partially inhibited the effects of vasopressin on mean arterial pressure and significantly reduced the effects of vasopressin on renal blood flow in control but not in endotoxemic rats. Although the protein levels of Rho-A and Rho-kinase I and II had not been impaired, the levels of phosphorylated myosin phosphatase-targeting subunit 1, the regulatory subunit of myosin phosphatase that is inhibited by Rho-kinase, were increased in both the renal cortex and the renal medulla of endotoxemic rats.'] Is increased activation of the Rho-A/Rho-kinase pathway in the renal vascular system responsible for the enhanced reactivity to exogenous vasopressin in endotoxemic rats? OUTPUT:
PubmedQA119075
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['To evaluate the usefulness of intratesticular and subcutaneous lidocaine in alleviating the intraoperative nociceptive response to castration, measured by pulse rate (PR) and mean arterial pressure (MAP), and to test the applicability of heart rate variability (HRV) analysis in assessing this response.', 'Randomized, controlled, observer-blinded experimental trial.', 'Thirty-nine healthy male cats admitted for castration.', 'One group received general anaesthesia and served as control group (GA), while the treatment group (LA) additionally received local anaesthesia (lidocaine 2 mg kg(-1)) intratesticularly and subcutaneously. PR and MAP were recorded at anaesthesia baseline (T0), treatment (T1), incision left testicle (T2), traction on spermatic cord (T3), tightening of the autoligature and resection of the cord (T4), incision on the right side (T5), traction on spermatic cord (T6), and tightening of the autoligature and resection of cord (T7). HRV analysis was divided into three 5-minute intervals: baseline (H0), treatment (H1), and surgery (H2).', 'There were significant increases in PR and MAP for both groups during surgery from T3 onwards; however, the increase in the treatment group (LA) was significantly lower than for the control group (GA). For HRV analysis, significant differences were found between groups in the following parameters during surgery: TP (total power), VLF (very low frequency), SDNN (standard deviation of NN intervals [= the interval between two consecutive R-waves in the ECG]), and TI (triangular index), which were lower in the LA group. Mean NN was significantly lower in the GA group, whereas LF (low frequency) and LFn (low frequency, normalized value) were lower in the LA group. HF (high frequency) and HFn (high frequency, normalized value) decreased significantly from H1 to H2 in both groups.'] Does intratesticular and subcutaneous lidocaine alter the intraoperative haemodynamic responses and heart rate variability in male cats undergoing castration?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['To evaluate the usefulness of intratesticular and subcutaneous lidocaine in alleviating the intraoperative nociceptive response to castration, measured by pulse rate (PR) and mean arterial pressure (MAP), and to test the applicability of heart rate variability (HRV) analysis in assessing this response.', 'Randomized, controlled, observer-blinded experimental trial.', 'Thirty-nine healthy male cats admitted for castration.', 'One group received general anaesthesia and served as control group (GA), while the treatment group (LA) additionally received local anaesthesia (lidocaine 2 mg kg(-1)) intratesticularly and subcutaneously. PR and MAP were recorded at anaesthesia baseline (T0), treatment (T1), incision left testicle (T2), traction on spermatic cord (T3), tightening of the autoligature and resection of the cord (T4), incision on the right side (T5), traction on spermatic cord (T6), and tightening of the autoligature and resection of cord (T7). HRV analysis was divided into three 5-minute intervals: baseline (H0), treatment (H1), and surgery (H2).', 'There were significant increases in PR and MAP for both groups during surgery from T3 onwards; however, the increase in the treatment group (LA) was significantly lower than for the control group (GA). For HRV analysis, significant differences were found between groups in the following parameters during surgery: TP (total power), VLF (very low frequency), SDNN (standard deviation of NN intervals [= the interval between two consecutive R-waves in the ECG]), and TI (triangular index), which were lower in the LA group. Mean NN was significantly lower in the GA group, whereas LF (low frequency) and LFn (low frequency, normalized value) were lower in the LA group. HF (high frequency) and HFn (high frequency, normalized value) decreased significantly from H1 to H2 in both groups.'] Does intratesticular and subcutaneous lidocaine alter the intraoperative haemodynamic responses and heart rate variability in male cats undergoing castration? OUTPUT:
PubmedQA195901
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['The vasoactive inotrope score (VIS) is a sum of the total vasopressor dose at a single point in time.\\xa0Incorporating duration and magnitude of vasopressor requirements during the postcardiac surgical period could improve VIS sensitivity for predicting poor outcome.', 'This is a retrospective review of 244 infants (aged ≤365 days) who underwent cardiopulmonary bypass during congenital cardiac operations from 2002 to\\xa02011. The VIS was calculated hourly for the first 72\\xa0hours. Poor outcome was defined as prolonged mechanical ventilation (≥6 days) or intensive care length of stay (≥12 days). First, the association between the maximum VIS (maxVIS) in the first 48 postoperative hours and poor outcome was confirmed for our study population. Next, postoperative intervals and VIS values that were significantly associated with poor outcome were identified and incorporated into a formula, termed the VISindex, which was compared with the traditional maxVIS.', 'The VISindex demonstrated improved sensitivity for predicting prolonged mechanical ventilation (VISindex: area under the curve [AUC], 0.85; 95% confidence interval [CI], 0.79 to 0.90; maxVIS: AUC, 0.80; 95%\\xa0CI, 0.75 to 0.86) and intensive care unit length of stay (VISindex: AUC, 0.84; 95% CI, 0.79 to 0.89; maxVIS: AUC, 0.77; 95% CI, 0.71 to 0.83) after cardiac operations in infants.'] Does duration and magnitude of vasopressor support predict poor outcome after infant cardiac operations?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['The vasoactive inotrope score (VIS) is a sum of the total vasopressor dose at a single point in time.\xa0Incorporating duration and magnitude of vasopressor requirements during the postcardiac surgical period could improve VIS sensitivity for predicting poor outcome.', 'This is a retrospective review of 244 infants (aged ≤365 days) who underwent cardiopulmonary bypass during congenital cardiac operations from 2002 to\xa02011. The VIS was calculated hourly for the first 72\xa0hours. Poor outcome was defined as prolonged mechanical ventilation (≥6 days) or intensive care length of stay (≥12 days). First, the association between the maximum VIS (maxVIS) in the first 48 postoperative hours and poor outcome was confirmed for our study population. Next, postoperative intervals and VIS values that were significantly associated with poor outcome were identified and incorporated into a formula, termed the VISindex, which was compared with the traditional maxVIS.', 'The VISindex demonstrated improved sensitivity for predicting prolonged mechanical ventilation (VISindex: area under the curve [AUC], 0.85; 95% confidence interval [CI], 0.79 to 0.90; maxVIS: AUC, 0.80; 95%\xa0CI, 0.75 to 0.86) and intensive care unit length of stay (VISindex: AUC, 0.84; 95% CI, 0.79 to 0.89; maxVIS: AUC, 0.77; 95% CI, 0.71 to 0.83) after cardiac operations in infants.'] Does duration and magnitude of vasopressor support predict poor outcome after infant cardiac operations? OUTPUT:
PubmedQA69128
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['The effect of reactive oxygen species (ROS) on insulin action is unclear. This study was carried out to explore the effect of prolonged low grade oxidative stress and vitamin E treatment on cultured rat L6 muscle cells.', 'L6 myotubes were incubated with vitamin E for 18 h and treated with H2O2 generating system for 12 h. Insulin stimulated glucose uptake, total antioxidant capacity and reduced glutathione concentration were measured.', 'There was a marked decrease in insulin stimulated glucose transport in L6 cells exposed to H2O2 generating system. Pretreatment with vitamin E attenuates the effect of H2O2 on insulin action. Treatment with H2O2 caused a significant reduction in the levels of reduced glutathione and total antioxidant capacity, these alterations were reversed by vitamin E pretreatment. Vitamin E per se had no effect on insulin stimulated glucose transport in cells not exposed to oxidative stress.'] Does vitamin E protect the insulin sensitivity and redox balance in rat L6 muscle cells exposed to oxidative stress?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['The effect of reactive oxygen species (ROS) on insulin action is unclear. This study was carried out to explore the effect of prolonged low grade oxidative stress and vitamin E treatment on cultured rat L6 muscle cells.', 'L6 myotubes were incubated with vitamin E for 18 h and treated with H2O2 generating system for 12 h. Insulin stimulated glucose uptake, total antioxidant capacity and reduced glutathione concentration were measured.', 'There was a marked decrease in insulin stimulated glucose transport in L6 cells exposed to H2O2 generating system. Pretreatment with vitamin E attenuates the effect of H2O2 on insulin action. Treatment with H2O2 caused a significant reduction in the levels of reduced glutathione and total antioxidant capacity, these alterations were reversed by vitamin E pretreatment. Vitamin E per se had no effect on insulin stimulated glucose transport in cells not exposed to oxidative stress.'] Does vitamin E protect the insulin sensitivity and redox balance in rat L6 muscle cells exposed to oxidative stress? OUTPUT:
PubmedQA195240
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Cervical cancer (CeCa) is the second most common cancer in women in developing countries, and human papilloma virus (HPV) is the primary etiological factor. Aberrant expression of HOX transcription factors has been observed in several types of cancer. To date, however, no reports exist on the expression of HOXB2 and HOXB13 proteins during neoplastic progression in CeCa and its correlation with HPV infection.', 'Expression of HOXB2 and HOXB13 proteins was assessed in tissue microarrays from normal cervical epithelium, cervical intraepithelial neoplasias grade 1-3, and CeCa. HPV was detected by PCR and sequencing. Expression of HOX-positive cells was determined in each diagnostic group.', 'Percentage of HOXB2- and HOXB13-positive cells gradually increased from means of 10.9% and 16.7%, respectively, in samples from healthy women, to 75.2% and 88.6% in those from CeCa patients. Frequency of HPV infection also increased from 13% in healthy tissue samples to 92.3% in CeCa. Both HOXB2 and HOXB13 proteins were preferentially expressed in HPV+ samples.'] Is increased expression of HOXB2 and HOXB13 proteins associated with HPV infection and cervical cancer progression?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Cervical cancer (CeCa) is the second most common cancer in women in developing countries, and human papilloma virus (HPV) is the primary etiological factor. Aberrant expression of HOX transcription factors has been observed in several types of cancer. To date, however, no reports exist on the expression of HOXB2 and HOXB13 proteins during neoplastic progression in CeCa and its correlation with HPV infection.', 'Expression of HOXB2 and HOXB13 proteins was assessed in tissue microarrays from normal cervical epithelium, cervical intraepithelial neoplasias grade 1-3, and CeCa. HPV was detected by PCR and sequencing. Expression of HOX-positive cells was determined in each diagnostic group.', 'Percentage of HOXB2- and HOXB13-positive cells gradually increased from means of 10.9% and 16.7%, respectively, in samples from healthy women, to 75.2% and 88.6% in those from CeCa patients. Frequency of HPV infection also increased from 13% in healthy tissue samples to 92.3% in CeCa. Both HOXB2 and HOXB13 proteins were preferentially expressed in HPV+ samples.'] Is increased expression of HOXB2 and HOXB13 proteins associated with HPV infection and cervical cancer progression? OUTPUT:
PubmedQA10397
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Does a 12-week exercise program prevent gestational diabetes and improve insulin resistance in healthy pregnant women with normal body mass index (BMI)?', 'Randomised, controlled trial with concealed allocation and blinded outcome assessment.', 'Two University hospitals in Norway.', 'White adult women with a single fetus. High-risk pregnancies or diseases that would interfere with participation were exclusion criteria. Randomisation of 855 participants allocated 429 to the exercise group and 426 to a control group.', 'Both groups received written advice on pelvic floor muscle exercises, diet, and lumbo-pelvic pain. In addition, the intervention group participated in a standardised group exercise program led by a physiotherapist, once a week for 12 weeks, between 20 and 36 weeks gestation. The program included 30-35 minutes low impact aerobics, 20-25 minutes of strength exercises using body weight as resistance and 5-10 minutes of stretching, breathing, and relaxation exercises. They were also encouraged to follow a 45-minute home exercise program at least twice a week. The control group received standard antenatal care and the customary information given by their midwife or general practitioner.', 'The primary outcomes were the prevalence of gestational diabetes, insulin resistance estimated by the homeostasis model assessment method (HOMA-IR), and fasting insulin and oral glucose tolerance tests at baseline and at the end of the training period. Fasting and 2-hour glucose levels were measured in serum by the routine methods. Gestational diabetes was diagnosed as fasting glucose level 2-hour value ≥7.8mmol/L. Secondary outcome measures were weight, BMI, and pregnancy complications and outcomes.', '702 participants completed the study. At the end of the 12-week program, there was no difference in the prevalence of gestational diabetes (25 (7%) of intervention group compared with 18 (6%) of control group), HOMA-IR (-0.15, 95% CI -0.33 to 0.03), or oral glucose tolerance tests at 2 hours (-0.13mmol/L, 95% CI -0.28 to 0.03) between the groups. Fasting insulin was significantly lower in the intervention group by 1.0 international units/mL (95% CI -0.1 to -1.9). The groups did not differ significantly on any of the secondary outcomes. Adherence to the exercise protocol in the intervention group was 55%. A per protocol analysis of 217 women in the intervention group who adhered to the exercise program demonstrated similar results with no difference in prevalence of diabetes.'] Does a 12-week exercise program performed during the second trimester prevent gestational diabetes in healthy pregnant women?\nOUTPUT:\n" }, { "from": "agent", "value": "no" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Does a 12-week exercise program prevent gestational diabetes and improve insulin resistance in healthy pregnant women with normal body mass index (BMI)?', 'Randomised, controlled trial with concealed allocation and blinded outcome assessment.', 'Two University hospitals in Norway.', 'White adult women with a single fetus. High-risk pregnancies or diseases that would interfere with participation were exclusion criteria. Randomisation of 855 participants allocated 429 to the exercise group and 426 to a control group.', 'Both groups received written advice on pelvic floor muscle exercises, diet, and lumbo-pelvic pain. In addition, the intervention group participated in a standardised group exercise program led by a physiotherapist, once a week for 12 weeks, between 20 and 36 weeks gestation. The program included 30-35 minutes low impact aerobics, 20-25 minutes of strength exercises using body weight as resistance and 5-10 minutes of stretching, breathing, and relaxation exercises. They were also encouraged to follow a 45-minute home exercise program at least twice a week. The control group received standard antenatal care and the customary information given by their midwife or general practitioner.', 'The primary outcomes were the prevalence of gestational diabetes, insulin resistance estimated by the homeostasis model assessment method (HOMA-IR), and fasting insulin and oral glucose tolerance tests at baseline and at the end of the training period. Fasting and 2-hour glucose levels were measured in serum by the routine methods. Gestational diabetes was diagnosed as fasting glucose level 2-hour value ≥7.8mmol/L. Secondary outcome measures were weight, BMI, and pregnancy complications and outcomes.', '702 participants completed the study. At the end of the 12-week program, there was no difference in the prevalence of gestational diabetes (25 (7%) of intervention group compared with 18 (6%) of control group), HOMA-IR (-0.15, 95% CI -0.33 to 0.03), or oral glucose tolerance tests at 2 hours (-0.13mmol/L, 95% CI -0.28 to 0.03) between the groups. Fasting insulin was significantly lower in the intervention group by 1.0 international units/mL (95% CI -0.1 to -1.9). The groups did not differ significantly on any of the secondary outcomes. Adherence to the exercise protocol in the intervention group was 55%. A per protocol analysis of 217 women in the intervention group who adhered to the exercise program demonstrated similar results with no difference in prevalence of diabetes.'] Does a 12-week exercise program performed during the second trimester prevent gestational diabetes in healthy pregnant women? OUTPUT:
PubmedQA180454
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Several genetic aberrations with prognostic impact in first-line therapy have been described in patients with acute myeloid leukemia and normal karyotype. However, little is known about the influence of these aberrations on outcome after relapse. This study aimed to identify clinical and molecular risk factors for patients with relapsed acute myeloid leukemia with normal karyotype.', 'We analyzed 94 patients with acute myeloid leukemia and normal karyotype after first relapse for clinical and molecular risk factors for survival. All patients had received first-line treatment and follow-up within two prospective, multicenter trials. Leukemic blasts were analyzed at diagnosis for genetic aberrations in the FLT3, NPM1, CEBPA, WT1, IDH1 and IDH2 genes by polymerase chain reaction and/or direct sequencing.', 'A second complete remission was achieved in 52% of patients who received re-induction therapy. The presence of an FLT3-internal tandem duplication, duration of first complete remission less than 6 months and age above the median of 47 years were associated with a significantly lower rate of second complete remission. The median survival after relapse was 11 months and the 6-year survival rate was 28%. In multivariate analysis, FLT3-internal tandem duplication and age above the median were the only independent negative prognostic factors for survival. The 6-year survival rate of patients with none of these factors was 56%, whereas it was significantly inferior in patients with one or both of these factors (15% and 6%, respectively). This was also true for patients who underwent allogeneic stem cell transplantation after relapse.'] Are fLT3-internal tandem duplication and age the major prognostic factors in patients with relapsed acute myeloid leukemia with normal karyotype?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Several genetic aberrations with prognostic impact in first-line therapy have been described in patients with acute myeloid leukemia and normal karyotype. However, little is known about the influence of these aberrations on outcome after relapse. This study aimed to identify clinical and molecular risk factors for patients with relapsed acute myeloid leukemia with normal karyotype.', 'We analyzed 94 patients with acute myeloid leukemia and normal karyotype after first relapse for clinical and molecular risk factors for survival. All patients had received first-line treatment and follow-up within two prospective, multicenter trials. Leukemic blasts were analyzed at diagnosis for genetic aberrations in the FLT3, NPM1, CEBPA, WT1, IDH1 and IDH2 genes by polymerase chain reaction and/or direct sequencing.', 'A second complete remission was achieved in 52% of patients who received re-induction therapy. The presence of an FLT3-internal tandem duplication, duration of first complete remission less than 6 months and age above the median of 47 years were associated with a significantly lower rate of second complete remission. The median survival after relapse was 11 months and the 6-year survival rate was 28%. In multivariate analysis, FLT3-internal tandem duplication and age above the median were the only independent negative prognostic factors for survival. The 6-year survival rate of patients with none of these factors was 56%, whereas it was significantly inferior in patients with one or both of these factors (15% and 6%, respectively). This was also true for patients who underwent allogeneic stem cell transplantation after relapse.'] Are fLT3-internal tandem duplication and age the major prognostic factors in patients with relapsed acute myeloid leukemia with normal karyotype? OUTPUT:
PubmedQA52249
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['The tumor suppressor p53 is a key prognostic factor in hepatocellular carcinoma (HCC), yet only 35% of grade III tumors exhibit mutation of p53. Several other pathways have been implicated in HCC and, among these, the role of the Notch1/Snail pathway remains unclear. Therefore, we investigated the expression of p53, Notch1, and Snail proteins in HCC with regard to both clinical grade and p53 mutational status. Immunoblotting for p53 revealed that, whereas in many tumors increased p53 was a result of p53 mutation, wildtype p53 (p53WT) expression was also frequently elevated in HCCs. Coordinated evaluation of p53, Notch1, and Snail expression suggests that grade III HCC can be subdivided based on the expression of these three proteins. We found that Notch1 expression in HCC tissues and cell lines is differentially affected by p53WT and mutant p53 (p53Mut). Notch1 expression was correlated with p53 expression in cells expressing p53WT, but was not elevated in p53Mut-expressing cells. Virally mediated expression or silencing of p53WT or p53Mut confirmed that p53WT overexpression causes Notch1 up-regulation in HCC. Surprisingly, the consequence of Notch1 overexpression for the proliferative and invasive capacity of HCC cells depends on both the p53 mutational status and activation of the Snail pathway.'] Does notch1 differentially regulate oncogenesis by wildtype p53 overexpression and p53 mutation in grade III hepatocellular carcinoma?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['The tumor suppressor p53 is a key prognostic factor in hepatocellular carcinoma (HCC), yet only 35% of grade III tumors exhibit mutation of p53. Several other pathways have been implicated in HCC and, among these, the role of the Notch1/Snail pathway remains unclear. Therefore, we investigated the expression of p53, Notch1, and Snail proteins in HCC with regard to both clinical grade and p53 mutational status. Immunoblotting for p53 revealed that, whereas in many tumors increased p53 was a result of p53 mutation, wildtype p53 (p53WT) expression was also frequently elevated in HCCs. Coordinated evaluation of p53, Notch1, and Snail expression suggests that grade III HCC can be subdivided based on the expression of these three proteins. We found that Notch1 expression in HCC tissues and cell lines is differentially affected by p53WT and mutant p53 (p53Mut). Notch1 expression was correlated with p53 expression in cells expressing p53WT, but was not elevated in p53Mut-expressing cells. Virally mediated expression or silencing of p53WT or p53Mut confirmed that p53WT overexpression causes Notch1 up-regulation in HCC. Surprisingly, the consequence of Notch1 overexpression for the proliferative and invasive capacity of HCC cells depends on both the p53 mutational status and activation of the Snail pathway.'] Does notch1 differentially regulate oncogenesis by wildtype p53 overexpression and p53 mutation in grade III hepatocellular carcinoma? OUTPUT:
PubmedQA67862
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Fibroblast growth factor-10 (FGF10) controls survival, proliferation, and differentiation of distal-alveolar epithelial progenitor cells during lung development.', 'To test for the protective and regenerative effect of Fgf10 overexpression in a bleomycin-induced mouse model of pulmonary inflammation and fibrosis.', 'In SP-C-rtTA; tet(O)Fgf10 double-transgenic mice, lung fibrosis was induced in 2-month-old transgenic mice by subcutaneous delivery of bleomycin (BLM), using an osmotic minipump for 1 week. Exogenous Fgf10 expression in the alveolar epithelium was induced for 7 days with doxycycline during the first, second, and third weeks after bleomycin pump implantation, and lungs were examined at 28 days.', 'Fgf10 overexpression during Week 1 (inflammatory phase) resulted in increased survival and attenuated lung fibrosis score and collagen deposition. In these Fgf10-overexpressing mice, an increase in regulatory T cells and a reduction in both transforming growth factor-beta(1) and matrix metalloproteinase-2 activity were observed in bronchoalveolar lavage fluids whereas the number of surfactant protein C (SP-C)-positive, alveolar epithelial type II cells (AEC2) was markedly elevated. Analysis of SP-C and TUNEL (terminal deoxynucleotidyltransferase dUTP nick end labeling) double-positive cells and isolation of AEC2 from lungs overexpressing Fgf10 demonstrated increased AEC2 survival. Expression of Fgf10 during Weeks 2 and 3 (fibrotic phase) showed significant attenuation of the lung fibrosis score and collagen deposition.'] Does overexpression of fibroblast growth factor-10 during both inflammatory and fibrotic phases attenuate bleomycin-induced pulmonary fibrosis in mice?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Fibroblast growth factor-10 (FGF10) controls survival, proliferation, and differentiation of distal-alveolar epithelial progenitor cells during lung development.', 'To test for the protective and regenerative effect of Fgf10 overexpression in a bleomycin-induced mouse model of pulmonary inflammation and fibrosis.', 'In SP-C-rtTA; tet(O)Fgf10 double-transgenic mice, lung fibrosis was induced in 2-month-old transgenic mice by subcutaneous delivery of bleomycin (BLM), using an osmotic minipump for 1 week. Exogenous Fgf10 expression in the alveolar epithelium was induced for 7 days with doxycycline during the first, second, and third weeks after bleomycin pump implantation, and lungs were examined at 28 days.', 'Fgf10 overexpression during Week 1 (inflammatory phase) resulted in increased survival and attenuated lung fibrosis score and collagen deposition. In these Fgf10-overexpressing mice, an increase in regulatory T cells and a reduction in both transforming growth factor-beta(1) and matrix metalloproteinase-2 activity were observed in bronchoalveolar lavage fluids whereas the number of surfactant protein C (SP-C)-positive, alveolar epithelial type II cells (AEC2) was markedly elevated. Analysis of SP-C and TUNEL (terminal deoxynucleotidyltransferase dUTP nick end labeling) double-positive cells and isolation of AEC2 from lungs overexpressing Fgf10 demonstrated increased AEC2 survival. Expression of Fgf10 during Weeks 2 and 3 (fibrotic phase) showed significant attenuation of the lung fibrosis score and collagen deposition.'] Does overexpression of fibroblast growth factor-10 during both inflammatory and fibrotic phases attenuate bleomycin-induced pulmonary fibrosis in mice? OUTPUT:
PubmedQA46122
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Obesity is associated with deterioration in asthma outcomes. Although airways eosinophil accumulation is characteristic of lung allergic diseases, little is known about the influence of obesity on the allergic eosinophil trafficking from bone marrow to lung tissues, and recruitment to airways lumen. Here, we have assessed the effects of diet-induced obesity on allergic eosinophilic inflammation in mice, examining eosinophil trafficking from bone marrow to airways, and production of T(H)1/T(H)2 cytokines.', 'C57BL/6 mice fed for 10 weeks with standard chow or high-fat diet were sensitized and challenged with ovalbumin. At 24-96 h post-ovalbumin challenge, bronchoalveolar lavage (BAL) fluid, lung tissue and bone marrow were examined.', 'The high-fat-fed mice exhibited increased body weight and epididymal fat, glucose intolerance and alterations in lipid profile compared with the lean mice. Obesity markedly elevated serum leptin and lowered adiponectin levels. Ovalbumin challenge in obese mice promoted a markedly higher eosinophil accumulation in bone marrow and connective tissue surrounding the bronchial and bronchiolar segments. Eosinophil number in BAL fluid of obese mice was lower at 24 and 48 h. Levels of interleukin (IL)-5, eotaxin, tumour necrosis factor-alpha and IL-10 in BAL fluid of obese mice were significantly higher than in lean mice.'] Does obesity enhance eosinophilic inflammation in a murine model of allergic asthma?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Obesity is associated with deterioration in asthma outcomes. Although airways eosinophil accumulation is characteristic of lung allergic diseases, little is known about the influence of obesity on the allergic eosinophil trafficking from bone marrow to lung tissues, and recruitment to airways lumen. Here, we have assessed the effects of diet-induced obesity on allergic eosinophilic inflammation in mice, examining eosinophil trafficking from bone marrow to airways, and production of T(H)1/T(H)2 cytokines.', 'C57BL/6 mice fed for 10 weeks with standard chow or high-fat diet were sensitized and challenged with ovalbumin. At 24-96 h post-ovalbumin challenge, bronchoalveolar lavage (BAL) fluid, lung tissue and bone marrow were examined.', 'The high-fat-fed mice exhibited increased body weight and epididymal fat, glucose intolerance and alterations in lipid profile compared with the lean mice. Obesity markedly elevated serum leptin and lowered adiponectin levels. Ovalbumin challenge in obese mice promoted a markedly higher eosinophil accumulation in bone marrow and connective tissue surrounding the bronchial and bronchiolar segments. Eosinophil number in BAL fluid of obese mice was lower at 24 and 48 h. Levels of interleukin (IL)-5, eotaxin, tumour necrosis factor-alpha and IL-10 in BAL fluid of obese mice were significantly higher than in lean mice.'] Does obesity enhance eosinophilic inflammation in a murine model of allergic asthma? OUTPUT:
PubmedQA191003
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Leptin is emerging as a key regulator of bone remodeling. In a population-based study of 1306 postmenopausal Danish women, nonsynonymous LEPR SNPs were associated with risk of adiposity, BMD, and vertebral fracture. Smoking exacerbates this LEPR-associated fracture risk.', 'Nonsynonymous single nucleotide polymorphisms (SNPs) in the human LEPR gene have been associated with adiposity in a number of studies, but there have been no large-scale studies of their implications for BMD and osteoporotic fracture risk in postmenopausal women.', 'We carried out a population-based study of 1430 women. Three well-known nonsynonymous leptin receptor (LEPR) SNPs (Lys109Arg, Gln223Arg, and Lys656Asn) were genotyped for qualitative and quantitative association analysis. Phenotype characteristics of main interest were DXA measures of body fat and lean tissue mass, BMD, and radiographic vertebral fractures.', 'Gln223Arg associated with risk of vertebral fracture (overall OR = 1.76; OR in smokers = 2.31; p = 0.0004), in addition to BMD of the femoral neck and total hip (p = 0.036 and 0.008, respectively). Heterozygote carriers showed lower BMD at both sites. Gln223Arg was also associated with adiposity (p = 0.001 for total fat mass). For adiposity, the at-risk allele was G (resulting in an arginine at position 223).'] Is leptin receptor genotype at Gln223Arg associated with body composition , BMD , and vertebral fracture in postmenopausal Danish women?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Leptin is emerging as a key regulator of bone remodeling. In a population-based study of 1306 postmenopausal Danish women, nonsynonymous LEPR SNPs were associated with risk of adiposity, BMD, and vertebral fracture. Smoking exacerbates this LEPR-associated fracture risk.', 'Nonsynonymous single nucleotide polymorphisms (SNPs) in the human LEPR gene have been associated with adiposity in a number of studies, but there have been no large-scale studies of their implications for BMD and osteoporotic fracture risk in postmenopausal women.', 'We carried out a population-based study of 1430 women. Three well-known nonsynonymous leptin receptor (LEPR) SNPs (Lys109Arg, Gln223Arg, and Lys656Asn) were genotyped for qualitative and quantitative association analysis. Phenotype characteristics of main interest were DXA measures of body fat and lean tissue mass, BMD, and radiographic vertebral fractures.', 'Gln223Arg associated with risk of vertebral fracture (overall OR = 1.76; OR in smokers = 2.31; p = 0.0004), in addition to BMD of the femoral neck and total hip (p = 0.036 and 0.008, respectively). Heterozygote carriers showed lower BMD at both sites. Gln223Arg was also associated with adiposity (p = 0.001 for total fat mass). For adiposity, the at-risk allele was G (resulting in an arginine at position 223).'] Is leptin receptor genotype at Gln223Arg associated with body composition , BMD , and vertebral fracture in postmenopausal Danish women? OUTPUT:
PubmedQA154266
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Our aim was to evaluate the relationship between serum C-reactive protein (CRP) levels and the neurological prognosis and development of vasospasm in patients with aneurysmal subarachnoid hemorrhage (aSAH).', 'Eighty-two adult patients with aSAH diagnoses were prospectively evaluated. Glasgow Coma Scale (GCS) score, Hunt and Hess grade, Fisher grade, cranial CT scans, digital subtraction angiography studies and daily neurological examinations were recorded. Serial serum CRP measurements were obtained daily between admission and the tenth day. Glasgow Outcome Scale (GOS) and the modified Rankin Scale (mRS) were used to assess the prognosis.', 'Serum CRP levels were related to severity of aSAH. Patients with lower GCS scores and higher Hunt and Hess and Fisher grades presented statistically significant higher serum CRP levels. Patients with higher serum CRP levels had a less favorable prognosis.'] Do serum C-reactive protein levels predict neurological outcome after aneurysmal subarachnoid hemorrhage?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Our aim was to evaluate the relationship between serum C-reactive protein (CRP) levels and the neurological prognosis and development of vasospasm in patients with aneurysmal subarachnoid hemorrhage (aSAH).', 'Eighty-two adult patients with aSAH diagnoses were prospectively evaluated. Glasgow Coma Scale (GCS) score, Hunt and Hess grade, Fisher grade, cranial CT scans, digital subtraction angiography studies and daily neurological examinations were recorded. Serial serum CRP measurements were obtained daily between admission and the tenth day. Glasgow Outcome Scale (GOS) and the modified Rankin Scale (mRS) were used to assess the prognosis.', 'Serum CRP levels were related to severity of aSAH. Patients with lower GCS scores and higher Hunt and Hess and Fisher grades presented statistically significant higher serum CRP levels. Patients with higher serum CRP levels had a less favorable prognosis.'] Do serum C-reactive protein levels predict neurological outcome after aneurysmal subarachnoid hemorrhage? OUTPUT:
PubmedQA32444
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Single-nucleotide polymorphisms (SNPs) in toll-like receptors (TLR) 1, 2, and 6 impair cell signaling in response to spirochetal lipoproteins. We investigated whether common SNPs in TLR1, TLR2, or TLR6 were associated with laboratory- or clinically-defined neurosyphilis.', 'Polymorphisms in the genes for TLR1 (a T→G mutation at position 1805), TLR2 (a G→A mutation at position 2258), and TLR6 (a C→T mutation at position 745) were sought in 456 white patients with syphilis. Laboratory-defined neurosyphilis included a reactive cerebrospinal fluid (CSF)-Venereal Disease Research Laboratory (VDRL) test. Clinically-defined neurosyphilis included new vision or hearing loss. Controls had CSF white blood cells of 5/μL or less, nonreactive CSF-Venereal Disease Research Laboratory, and no vision or hearing loss.', 'Overall, 26.2% of patients had laboratory-defined and 36.2% had clinically-defined neurosyphilis. Compared with controls, patients with any of the 3 SNPs were more likely to have laboratory-defined neurosyphilis. Those with TLR2 or TLR6 SNPs were more likely to have clinically-defined neurosyphilis. These associations were independent of serum rapid plasma reagin titer.'] Are toll-like receptor polymorphisms associated with increased neurosyphilis risk?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Single-nucleotide polymorphisms (SNPs) in toll-like receptors (TLR) 1, 2, and 6 impair cell signaling in response to spirochetal lipoproteins. We investigated whether common SNPs in TLR1, TLR2, or TLR6 were associated with laboratory- or clinically-defined neurosyphilis.', 'Polymorphisms in the genes for TLR1 (a T→G mutation at position 1805), TLR2 (a G→A mutation at position 2258), and TLR6 (a C→T mutation at position 745) were sought in 456 white patients with syphilis. Laboratory-defined neurosyphilis included a reactive cerebrospinal fluid (CSF)-Venereal Disease Research Laboratory (VDRL) test. Clinically-defined neurosyphilis included new vision or hearing loss. Controls had CSF white blood cells of 5/μL or less, nonreactive CSF-Venereal Disease Research Laboratory, and no vision or hearing loss.', 'Overall, 26.2% of patients had laboratory-defined and 36.2% had clinically-defined neurosyphilis. Compared with controls, patients with any of the 3 SNPs were more likely to have laboratory-defined neurosyphilis. Those with TLR2 or TLR6 SNPs were more likely to have clinically-defined neurosyphilis. These associations were independent of serum rapid plasma reagin titer.'] Are toll-like receptor polymorphisms associated with increased neurosyphilis risk? OUTPUT:
PubmedQA193382
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['The authors conducted an in vitro investigation of the role of Ca(2+)-dependent signaling in vascular endothelial growth factor (VEGF)-induced angiogenesis in the retina.', \"Bovine retinal endothelial cells (BRECs) were stimulated with VEGF in the presence or absence of 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-acetoxymethyl ester (BAPTA-AM; intracellular Ca(2+) chelator), U73122 (phospholipase C (PLC) inhibitor), xestospongin C (Xe-C), and 2-aminoethoxydiphenyl borate (2APB) (inhibitors of inositol-1,4,5 triphosphate (IP(3)) signaling). Intracellular Ca(2+) concentration ([Ca(2+)](i)) was estimated using fura-2 Ca(2+) microfluorometry, Akt phosphorylation quantified by Western blot analysis, and angiogenic responses assessed using cell migration, proliferation, tubulogenesis, and sprout formation assays. The effects of the Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) inhibitor KN93 were also evaluated on VEGF-induced Akt signaling and angiogenic activity.\", 'Stimulation of BRECs with 25 ng/mL VEGF induced a biphasic increase in [Ca(2+)](i), with an initial transient peak followed by a sustained plateau phase. VEGF-induced [Ca(2+)](i) increases were almost completely abolished by pretreating the cells with BAPTA-AM, U73122, Xe-C, or 2APB. These agents also inhibited VEGF-induced phosphorylation of Akt, cell migration, proliferation, tubulogenesis, and sprouting angiogenesis. KN93 was similarly effective at blocking the VEGF-induced activation of Akt and angiogenic responses.'] Is vEGF-induced retinal angiogenic signaling critically dependent on Ca²⁺ signaling by Ca²⁺/calmodulin-dependent protein kinase II?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['The authors conducted an in vitro investigation of the role of Ca(2+)-dependent signaling in vascular endothelial growth factor (VEGF)-induced angiogenesis in the retina.', "Bovine retinal endothelial cells (BRECs) were stimulated with VEGF in the presence or absence of 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-acetoxymethyl ester (BAPTA-AM; intracellular Ca(2+) chelator), U73122 (phospholipase C (PLC) inhibitor), xestospongin C (Xe-C), and 2-aminoethoxydiphenyl borate (2APB) (inhibitors of inositol-1,4,5 triphosphate (IP(3)) signaling). Intracellular Ca(2+) concentration ([Ca(2+)](i)) was estimated using fura-2 Ca(2+) microfluorometry, Akt phosphorylation quantified by Western blot analysis, and angiogenic responses assessed using cell migration, proliferation, tubulogenesis, and sprout formation assays. The effects of the Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) inhibitor KN93 were also evaluated on VEGF-induced Akt signaling and angiogenic activity.", 'Stimulation of BRECs with 25 ng/mL VEGF induced a biphasic increase in [Ca(2+)](i), with an initial transient peak followed by a sustained plateau phase. VEGF-induced [Ca(2+)](i) increases were almost completely abolished by pretreating the cells with BAPTA-AM, U73122, Xe-C, or 2APB. These agents also inhibited VEGF-induced phosphorylation of Akt, cell migration, proliferation, tubulogenesis, and sprouting angiogenesis. KN93 was similarly effective at blocking the VEGF-induced activation of Akt and angiogenic responses.'] Is vEGF-induced retinal angiogenic signaling critically dependent on Ca²⁺ signaling by Ca²⁺/calmodulin-dependent protein kinase II? OUTPUT:
PubmedQA208836
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['The fenamates, a family of nonsteroidal anti-inflammatory drugs that are derivatives of N-phenylanthranilic acid, are the inhibitors of cyclo-oxygenase. The ionic mechanism of actions of these compounds in osteoblasts is not well understood.', 'The effects of the fenamates on ionic currents were investigated in a human osteoblast-like cell line (MG-63) with the aid of the whole-cell and inside-out configurations of the patch-clamp technique.', 'In MG-63 cells, niflumic acid and meclofenamic acid increased K+ outward currents (IK). The niflumic acid-stimulated IK was reversed by subsequent application of iberiotoxin or paxilline, yet not by that of glibenclamide or apamin. In the inside-out configuration, niflumic acid (30 micromol/L) added to the bath did not modify single-channel conductance but increased the activity of large-conductance Ca2+-activated K+ (BKCa) channels. The EC50 values for niflumic acid- and meclofenamic acid-induced channel activity were 22 and 24 micromol/L, respectively. Niflumic acid (30 micromol/L) and meclofenamic acid (30 micromol/L) shifted the activation curve of BKCa channels to less positive membrane potentials. Membrane stretch potentiated niflumic acid-stimulated channel activity. The rank order of potency for the activation of BKCa channels in these cells was niflumic acid = meclofenamic acid > tolfenamic acid > flufenamic acid > nimesulide. Evans blue and nordihydroguaiaretic acid increased channel activity; however, indomethacin, piroxicam, and NS-398 had no effect on it.'] Do fenamates stimulate BKCa channel osteoblast-like MG-63 cells activity in the human?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['The fenamates, a family of nonsteroidal anti-inflammatory drugs that are derivatives of N-phenylanthranilic acid, are the inhibitors of cyclo-oxygenase. The ionic mechanism of actions of these compounds in osteoblasts is not well understood.', 'The effects of the fenamates on ionic currents were investigated in a human osteoblast-like cell line (MG-63) with the aid of the whole-cell and inside-out configurations of the patch-clamp technique.', 'In MG-63 cells, niflumic acid and meclofenamic acid increased K+ outward currents (IK). The niflumic acid-stimulated IK was reversed by subsequent application of iberiotoxin or paxilline, yet not by that of glibenclamide or apamin. In the inside-out configuration, niflumic acid (30 micromol/L) added to the bath did not modify single-channel conductance but increased the activity of large-conductance Ca2+-activated K+ (BKCa) channels. The EC50 values for niflumic acid- and meclofenamic acid-induced channel activity were 22 and 24 micromol/L, respectively. Niflumic acid (30 micromol/L) and meclofenamic acid (30 micromol/L) shifted the activation curve of BKCa channels to less positive membrane potentials. Membrane stretch potentiated niflumic acid-stimulated channel activity. The rank order of potency for the activation of BKCa channels in these cells was niflumic acid = meclofenamic acid > tolfenamic acid > flufenamic acid > nimesulide. Evans blue and nordihydroguaiaretic acid increased channel activity; however, indomethacin, piroxicam, and NS-398 had no effect on it.'] Do fenamates stimulate BKCa channel osteoblast-like MG-63 cells activity in the human? OUTPUT:
PubmedQA12711
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: [\"This study sought to determine whether elevated concentrations of interleukin-6 in the cervical and vaginal secretions of patients between 24 and 36 weeks' gestation predicted subsequent preterm delivery and/or identified those preterm deliveries associated with maternal infectious morbidity.\", \"A cohort study was undertaken with cervical and vaginal samples collected from 161 consenting patients seen at 3- to 4-week intervals between 24 and 36 weeks. Levels of interleukin-6 were measured by immunoassay. Demographic, obstetric, neonatal, and laboratory data were analyzed by Fisher's exact test, Student t test, or Wilcoxon rank sum test, linear and multiple logistic regression, and receiver-operator characteristic curve analysis.\", \"There were 4.2-fold and 3.4-fold increases in maximal cervical and vaginal interleukin-6 concentrations, respectively, among patients with preterm deliveries versus term deliveries. The receiver-operator characteristics curve analysis indicated that a single cervical interleukin-6 value > 250 pg/ml of sample buffer, present between 24 and 36 weeks' gestation, optimally identified patients with subsequent preterm deliveries versus term deliveries (sensitivity 50.0%, 95% confidence interval 33.2% to 66.8%; specificity 85.0%, 95% confidence interval 78.8% to 91.2%; positive predictive value 47.2%, 95% confidence interval 30.9% to 63.5%; negative predictive value 86.4%, 95% confidence interval 80.4% to 92.4%). The optimal vaginal interleukin-6 cutoff value (> 125 pg/ml) proved less sensitive (45.5%, 95% confidence interval 28.5% to 62.4%) but equally specific (86.6%, 95% confidence interval 80.7% to 92.5%). Multiple logistic regression indicated that a cervical interleukin-6 level > 250 pg/ml was an independent predictor of preterm delivery (adjusted odds ratio 4.8, 95% confidence interval 1.7 to 14.3). Cervical interleukin-6 levels did not correlate with cervical change or gestational age at sampling. Among patients delivered preterm there were no differences in the mean white blood cell count on admission or the prevalence of vaginal pathogens, alkaline vaginal pH, chorioamnionitis, or endometritis among patients with cervical interleukin-6 values > 150 or < or = 250 pg/ml.\"] Are increased interleukin-6 concentrations in cervical secretions associated with preterm delivery?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ["This study sought to determine whether elevated concentrations of interleukin-6 in the cervical and vaginal secretions of patients between 24 and 36 weeks' gestation predicted subsequent preterm delivery and/or identified those preterm deliveries associated with maternal infectious morbidity.", "A cohort study was undertaken with cervical and vaginal samples collected from 161 consenting patients seen at 3- to 4-week intervals between 24 and 36 weeks. Levels of interleukin-6 were measured by immunoassay. Demographic, obstetric, neonatal, and laboratory data were analyzed by Fisher's exact test, Student t test, or Wilcoxon rank sum test, linear and multiple logistic regression, and receiver-operator characteristic curve analysis.", "There were 4.2-fold and 3.4-fold increases in maximal cervical and vaginal interleukin-6 concentrations, respectively, among patients with preterm deliveries versus term deliveries. The receiver-operator characteristics curve analysis indicated that a single cervical interleukin-6 value > 250 pg/ml of sample buffer, present between 24 and 36 weeks' gestation, optimally identified patients with subsequent preterm deliveries versus term deliveries (sensitivity 50.0%, 95% confidence interval 33.2% to 66.8%; specificity 85.0%, 95% confidence interval 78.8% to 91.2%; positive predictive value 47.2%, 95% confidence interval 30.9% to 63.5%; negative predictive value 86.4%, 95% confidence interval 80.4% to 92.4%). The optimal vaginal interleukin-6 cutoff value (> 125 pg/ml) proved less sensitive (45.5%, 95% confidence interval 28.5% to 62.4%) but equally specific (86.6%, 95% confidence interval 80.7% to 92.5%). Multiple logistic regression indicated that a cervical interleukin-6 level > 250 pg/ml was an independent predictor of preterm delivery (adjusted odds ratio 4.8, 95% confidence interval 1.7 to 14.3). Cervical interleukin-6 levels did not correlate with cervical change or gestational age at sampling. Among patients delivered preterm there were no differences in the mean white blood cell count on admission or the prevalence of vaginal pathogens, alkaline vaginal pH, chorioamnionitis, or endometritis among patients with cervical interleukin-6 values > 150 or < or = 250 pg/ml."] Are increased interleukin-6 concentrations in cervical secretions associated with preterm delivery? OUTPUT:
PubmedQA142775
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['The present study investigates whether there is an association between trait impulsivity in the normal population and inhibitory motor control as assessed by the stop task.', 'Low- and high-impulsive participants (as assessed by the I7 questionnaire; both groups n = 31) performed the stop task. Differences in performance were analyzed by an independent samples t-test. Furthermore, a short meta-analysis was performed on this study and three previous studies with a similar aim.', 'The low- and high-impulsive groups did not differ on the speed to stop the response (SSRT). However, the meta-analysis revealed that high-impulsives are marginally slower in stopping than low-impulsives (effect size = -0.26, p= 0.06).'] Are differences between low and high trait impulsivity associated with differences in inhibitory motor control?\nOUTPUT:\n" }, { "from": "agent", "value": "no" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['The present study investigates whether there is an association between trait impulsivity in the normal population and inhibitory motor control as assessed by the stop task.', 'Low- and high-impulsive participants (as assessed by the I7 questionnaire; both groups n = 31) performed the stop task. Differences in performance were analyzed by an independent samples t-test. Furthermore, a short meta-analysis was performed on this study and three previous studies with a similar aim.', 'The low- and high-impulsive groups did not differ on the speed to stop the response (SSRT). However, the meta-analysis revealed that high-impulsives are marginally slower in stopping than low-impulsives (effect size = -0.26, p= 0.06).'] Are differences between low and high trait impulsivity associated with differences in inhibitory motor control? OUTPUT:
PubmedQA44140
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['The bioavailability of β-carotene, the main dietary provitamin A carotenoid, varies among individuals. It is not known whether this variability can affect long-term β-carotene, and hence vitamin A, status.', 'We hypothesized that variations in genes involved in β-carotene absorption and postprandial metabolism could at least partially explain the high interindividual variability in β-carotene bioavailability. Thus, the main objectives of this study were to identify associated single-nucleotide polymorphisms (SNPs), and to estimate whether populations with different allele frequencies at these SNPs could have different abilities to absorb provitamin A carotenoids.', 'In this single-group design, 33 healthy, nonobese adult men were genotyped with the use of whole-genome microarrays. After an overnight fast, they consumed a test meal containing 100 g tomato puree providing 0.4 mg β-carotene. The postprandial plasma chylomicron β-carotene concentration was then measured at regular time intervals over 8 h. Partial least squares (PLS) regression was used to identify the best combination of SNPs in or near candidate genes (54 genes representing 2172 SNPs) that was associated with the postprandial chylomicron β-carotene response (incremental β-carotene area-under-the-curve concentration over 8 h in chylomicrons).', 'The postprandial chylomicron β-carotene response was highly variable (CV = 105%) and was positively correlated with the fasting plasma β-carotene concentration (r = 0.78; P < 0.0001). A significant (P = 6.54 × 10(-3)) multivalidated PLS regression model, which included 25 SNPs in 12 genes, explained 69% of the variance in the postprandial chylomicron β-carotene response, i.e., β-carotene bioavailability.'] Does a Combination of Single-Nucleotide Polymorphisms be Associated with Interindividual Variability in Dietary β-Carotene Bioavailability in Healthy Men?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['The bioavailability of β-carotene, the main dietary provitamin A carotenoid, varies among individuals. It is not known whether this variability can affect long-term β-carotene, and hence vitamin A, status.', 'We hypothesized that variations in genes involved in β-carotene absorption and postprandial metabolism could at least partially explain the high interindividual variability in β-carotene bioavailability. Thus, the main objectives of this study were to identify associated single-nucleotide polymorphisms (SNPs), and to estimate whether populations with different allele frequencies at these SNPs could have different abilities to absorb provitamin A carotenoids.', 'In this single-group design, 33 healthy, nonobese adult men were genotyped with the use of whole-genome microarrays. After an overnight fast, they consumed a test meal containing 100 g tomato puree providing 0.4 mg β-carotene. The postprandial plasma chylomicron β-carotene concentration was then measured at regular time intervals over 8 h. Partial least squares (PLS) regression was used to identify the best combination of SNPs in or near candidate genes (54 genes representing 2172 SNPs) that was associated with the postprandial chylomicron β-carotene response (incremental β-carotene area-under-the-curve concentration over 8 h in chylomicrons).', 'The postprandial chylomicron β-carotene response was highly variable (CV = 105%) and was positively correlated with the fasting plasma β-carotene concentration (r = 0.78; P < 0.0001). A significant (P = 6.54 × 10(-3)) multivalidated PLS regression model, which included 25 SNPs in 12 genes, explained 69% of the variance in the postprandial chylomicron β-carotene response, i.e., β-carotene bioavailability.'] Does a Combination of Single-Nucleotide Polymorphisms be Associated with Interindividual Variability in Dietary β-Carotene Bioavailability in Healthy Men? OUTPUT:
PubmedQA21532
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Mitochondrial ATP-sensitive potassium channels have been proposed to be myoprotective. The relevance and specificity of this mechanism in cardiac surgery was unknown. The purpose of this study was to examine the effects of the mitochondrial potassium ATP-sensitive channel opener diazoxide on regional and global myocardial protection using a model of acute myocardial infarction.', 'Pigs (n=19) were placed on total cardiopulmonary bypass and then subjected to 30 min normothermic regional ischemia by snaring the left anterior descending coronary artery (LAD). The aorta was then crossclamped and cold blood Deaconess Surgical Associates cardioplegia (DSA; n=6) or DSA containing 50 microM diazoxide (DZX; n=6) was delivered via the aortic root and the hearts subjected to 30 min hypothermic global ischemia. The crossclamp and snare were removed and the hearts reperfused for 120 min.', 'No significant differences in preload recruitable stroke work relationship, Tau, proximal, distal or proximal/distal coronary flow, regional or global segmental shortening, systolic bulging or post-systolic shortening were observed within or between DSA and DZX hearts during reperfusion. Infarct was present only in the region of LAD occlusion in both DSA and DZX hearts. Infarct size (% of area at risk) was 33.6+/-2.9% in DSA and was 16.8+/-2.4% in DZX hearts (P<0.01 versus DSA). Apoptosis as estimated by TUNEL positive nuclei was 120.3+/-48.8 in DSA and was significantly decreased to 21.4+/-5.3 in DZX hearts. Myocardial infarct was located centrally within the area at risk in both DSA and DZX hearts but was significantly increased at borderline zones within the area at risk in DSA hearts.'] Does selective opening of mitochondrial ATP-sensitive potassium channels during surgically induced myocardial ischemia decrease necrosis and apoptosis?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Mitochondrial ATP-sensitive potassium channels have been proposed to be myoprotective. The relevance and specificity of this mechanism in cardiac surgery was unknown. The purpose of this study was to examine the effects of the mitochondrial potassium ATP-sensitive channel opener diazoxide on regional and global myocardial protection using a model of acute myocardial infarction.', 'Pigs (n=19) were placed on total cardiopulmonary bypass and then subjected to 30 min normothermic regional ischemia by snaring the left anterior descending coronary artery (LAD). The aorta was then crossclamped and cold blood Deaconess Surgical Associates cardioplegia (DSA; n=6) or DSA containing 50 microM diazoxide (DZX; n=6) was delivered via the aortic root and the hearts subjected to 30 min hypothermic global ischemia. The crossclamp and snare were removed and the hearts reperfused for 120 min.', 'No significant differences in preload recruitable stroke work relationship, Tau, proximal, distal or proximal/distal coronary flow, regional or global segmental shortening, systolic bulging or post-systolic shortening were observed within or between DSA and DZX hearts during reperfusion. Infarct was present only in the region of LAD occlusion in both DSA and DZX hearts. Infarct size (% of area at risk) was 33.6+/-2.9% in DSA and was 16.8+/-2.4% in DZX hearts (P<0.01 versus DSA). Apoptosis as estimated by TUNEL positive nuclei was 120.3+/-48.8 in DSA and was significantly decreased to 21.4+/-5.3 in DZX hearts. Myocardial infarct was located centrally within the area at risk in both DSA and DZX hearts but was significantly increased at borderline zones within the area at risk in DSA hearts.'] Does selective opening of mitochondrial ATP-sensitive potassium channels during surgically induced myocardial ischemia decrease necrosis and apoptosis? OUTPUT:
PubmedQA114771
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Resistance of cancer cells against anticancer agents is caused partly by multidrug resistance-associated protein 1 (MRP1). The exact mechanism of MRP1-involved multidrug resistance has not yet been clarified, although glutathione (GSH) is likely to have a role for the resistance to occur. N-acetylcysteine (NAC) is a pro-glutathione drug. DL-buthionine (S,R)-sulfoximine (BSO) inhibits GSH synthesis. The aim of our study was to investigate the effect of NAC and BSO on MRP1-mediated doxorubicin resistance in human embryonic kidney (HEK293) and its MRP1-transfected 293MRP cells.', 'Human embryonic kidney cells were transfected with a plasmid encoding the whole MRP1 gene. Both cells were incubated with doxorubicin in the presence or absence of NAC and/or BSO. The viability of both cells was determined under different incubation conditions. Glutathione, glutathione S-transferase (GST) and glutathione peroxidase (GPx) levels were measured in the cell extracts obtained from both cells incubated with different drugs.', 'N-acetylcysteine increased the resistance of both cells against doxorubicin. DL-buthionine (S,R)-sulfoximine decreased NAC-enhanced MRP1-mediated doxorubicin resistance, indicating that induction of MRP1-mediated doxorubicin resistance depends on GSH synthesis. Doxorubicin decreased the cellular GSH concentration and increased GPx activity. Glutathione S-transferase activity was decreased by NAC.'] Does n-acetylcysteine enhance multidrug resistance-associated protein 1 mediated doxorubicin resistance?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Resistance of cancer cells against anticancer agents is caused partly by multidrug resistance-associated protein 1 (MRP1). The exact mechanism of MRP1-involved multidrug resistance has not yet been clarified, although glutathione (GSH) is likely to have a role for the resistance to occur. N-acetylcysteine (NAC) is a pro-glutathione drug. DL-buthionine (S,R)-sulfoximine (BSO) inhibits GSH synthesis. The aim of our study was to investigate the effect of NAC and BSO on MRP1-mediated doxorubicin resistance in human embryonic kidney (HEK293) and its MRP1-transfected 293MRP cells.', 'Human embryonic kidney cells were transfected with a plasmid encoding the whole MRP1 gene. Both cells were incubated with doxorubicin in the presence or absence of NAC and/or BSO. The viability of both cells was determined under different incubation conditions. Glutathione, glutathione S-transferase (GST) and glutathione peroxidase (GPx) levels were measured in the cell extracts obtained from both cells incubated with different drugs.', 'N-acetylcysteine increased the resistance of both cells against doxorubicin. DL-buthionine (S,R)-sulfoximine decreased NAC-enhanced MRP1-mediated doxorubicin resistance, indicating that induction of MRP1-mediated doxorubicin resistance depends on GSH synthesis. Doxorubicin decreased the cellular GSH concentration and increased GPx activity. Glutathione S-transferase activity was decreased by NAC.'] Does n-acetylcysteine enhance multidrug resistance-associated protein 1 mediated doxorubicin resistance? OUTPUT:
PubmedQA101047
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['We tested the hypothesis that perinatal oxytocin, given to pregnant women to induce labor, is related to offspring bipolar disorder (BP) and worse childhood cognitive performance among offspring. We also tested the association between childhood cognition and later BP.', 'A population-based birth cohort derived from the Child Health and Development Study (CHDS) which included nearly all pregnant women receiving obstetric care from the Kaiser Permanente Medical Care Plan, Northern California Region (KPNC) between 1959 and 1966. Prospectively obtained medical and offspring cognitive performance were used. Potential cases with BP from the cohort were identified by database linkages. This protocol identified 94 cases who were matched 1:8 to controls.', 'Perinatal oxytocin was associated with a 2.4 times increased odds of later BP. Oxytocin was also associated with decreased performance on the Raven Matrices, but not on the Peabody Picture Vocabulary Test (PPVT). Childhood cognition was not associated with later BP.'] Does perinatal oxytocin increase the risk of offspring bipolar disorder and childhood cognitive impairment?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['We tested the hypothesis that perinatal oxytocin, given to pregnant women to induce labor, is related to offspring bipolar disorder (BP) and worse childhood cognitive performance among offspring. We also tested the association between childhood cognition and later BP.', 'A population-based birth cohort derived from the Child Health and Development Study (CHDS) which included nearly all pregnant women receiving obstetric care from the Kaiser Permanente Medical Care Plan, Northern California Region (KPNC) between 1959 and 1966. Prospectively obtained medical and offspring cognitive performance were used. Potential cases with BP from the cohort were identified by database linkages. This protocol identified 94 cases who were matched 1:8 to controls.', 'Perinatal oxytocin was associated with a 2.4 times increased odds of later BP. Oxytocin was also associated with decreased performance on the Raven Matrices, but not on the Peabody Picture Vocabulary Test (PPVT). Childhood cognition was not associated with later BP.'] Does perinatal oxytocin increase the risk of offspring bipolar disorder and childhood cognitive impairment? OUTPUT:
PubmedQA47215
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Injurious non-microbial factors released from the stressed gut during shocked states contribute to the development of acute lung injury (ALI) and multiple organ dysfunction syndrome (MODS). Since Toll-like receptors (TLR) act as sensors of tissue injury as well as microbial invasion and TLR4 signaling occurs in both sepsis and noninfectious models of ischemia/reperfusion (I/R) injury, we hypothesized that factors in the intestinal mesenteric lymph after trauma hemorrhagic shock (T/HS) mediate gut-induced lung injury via TLR4 activation.', \"The concept that factors in T/HS lymph exiting the gut recreates ALI is evidenced by our findings that the infusion of porcine lymph, collected from animals subjected to global T/HS injury, into naïve wildtype (WT) mice induced lung injury. Using C3H/HeJ mice that harbor a TLR4 mutation, we found that TLR4 activation was necessary for the development of T/HS porcine lymph-induced lung injury as determined by Evan's blue dye (EBD) lung permeability and myeloperoxidase (MPO) levels as well as the induction of the injurious pulmonary iNOS response. TRIF and Myd88 deficiency fully and partially attenuated T/HS lymph-induced increases in lung permeability respectively. Additional studies in TLR2 deficient mice showed that TLR2 activation was not involved in the pathology of T/HS lymph-induced lung injury. Lastly, the lymph samples were devoid of bacteria, endotoxin and bacterial DNA and passage of lymph through an endotoxin removal column did not abrogate the ability of T/HS lymph to cause lung injury in naïve mice.\"] Does trauma hemorrhagic shock-induced lung injury involve a gut-lymph-induced TLR4 pathway in mice?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Injurious non-microbial factors released from the stressed gut during shocked states contribute to the development of acute lung injury (ALI) and multiple organ dysfunction syndrome (MODS). Since Toll-like receptors (TLR) act as sensors of tissue injury as well as microbial invasion and TLR4 signaling occurs in both sepsis and noninfectious models of ischemia/reperfusion (I/R) injury, we hypothesized that factors in the intestinal mesenteric lymph after trauma hemorrhagic shock (T/HS) mediate gut-induced lung injury via TLR4 activation.', "The concept that factors in T/HS lymph exiting the gut recreates ALI is evidenced by our findings that the infusion of porcine lymph, collected from animals subjected to global T/HS injury, into naïve wildtype (WT) mice induced lung injury. Using C3H/HeJ mice that harbor a TLR4 mutation, we found that TLR4 activation was necessary for the development of T/HS porcine lymph-induced lung injury as determined by Evan's blue dye (EBD) lung permeability and myeloperoxidase (MPO) levels as well as the induction of the injurious pulmonary iNOS response. TRIF and Myd88 deficiency fully and partially attenuated T/HS lymph-induced increases in lung permeability respectively. Additional studies in TLR2 deficient mice showed that TLR2 activation was not involved in the pathology of T/HS lymph-induced lung injury. Lastly, the lymph samples were devoid of bacteria, endotoxin and bacterial DNA and passage of lymph through an endotoxin removal column did not abrogate the ability of T/HS lymph to cause lung injury in naïve mice."] Does trauma hemorrhagic shock-induced lung injury involve a gut-lymph-induced TLR4 pathway in mice? OUTPUT:
PubmedQA92085
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: [\"Growth hormone (GH) has been shown to alleviate symptoms in patients with Crohn's disease. Chloride secretion is important in driving intestinal fluid secretion. We examined whether GH inhibits chloride secretion induced by carbachol (CCh, a calcium-dependent pathway), and the downstream effectors responsible.\", 'T(84) cells were pretreated with GH at various concentrations followed by CCh (100 micromol/L). Chloride secretion was assessed as changes in short circuit current ( triangle up I(sc)) in Ussing chambers. Tyrphostins AG1478 (an epidermal growth factor receptor [EGFr] inhibitor) and AG490 (a Janus kinase 2 [JAK2] inhibitor), SB203580 (a p38 inhibitor), and PD98059 (a MEK1 inhibitor) were used.', 'GH inhibited CCh-induced chloride secretion at up to 10 nmol/L, but higher concentrations were less effective. GH caused tyrosine phosphorylation of JAK2 and EGFr. AG490 suppressed activation of JAK2 and EGFr in response to GH. AG1478 prevented GH activation of EGFr and reversed its inhibitory effect on chloride secretion. GH also induced activation of both p38 and ERK1/2. AG490 reversed GH-induced tyrosine phosphorylation of both ERK1/2 and p38, but AG1478 reversed that of ERK1/2 only. PD98059, but not SB203580, reversed the inhibitory effect of GH on chloride secretion.'] Does growth hormone reduce chloride secretion in human colonic epithelial cells via EGF receptor and extracellular regulated kinase?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ["Growth hormone (GH) has been shown to alleviate symptoms in patients with Crohn's disease. Chloride secretion is important in driving intestinal fluid secretion. We examined whether GH inhibits chloride secretion induced by carbachol (CCh, a calcium-dependent pathway), and the downstream effectors responsible.", 'T(84) cells were pretreated with GH at various concentrations followed by CCh (100 micromol/L). Chloride secretion was assessed as changes in short circuit current ( triangle up I(sc)) in Ussing chambers. Tyrphostins AG1478 (an epidermal growth factor receptor [EGFr] inhibitor) and AG490 (a Janus kinase 2 [JAK2] inhibitor), SB203580 (a p38 inhibitor), and PD98059 (a MEK1 inhibitor) were used.', 'GH inhibited CCh-induced chloride secretion at up to 10 nmol/L, but higher concentrations were less effective. GH caused tyrosine phosphorylation of JAK2 and EGFr. AG490 suppressed activation of JAK2 and EGFr in response to GH. AG1478 prevented GH activation of EGFr and reversed its inhibitory effect on chloride secretion. GH also induced activation of both p38 and ERK1/2. AG490 reversed GH-induced tyrosine phosphorylation of both ERK1/2 and p38, but AG1478 reversed that of ERK1/2 only. PD98059, but not SB203580, reversed the inhibitory effect of GH on chloride secretion.'] Does growth hormone reduce chloride secretion in human colonic epithelial cells via EGF receptor and extracellular regulated kinase? OUTPUT:
PubmedQA137869
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Studies have required large numbers of patients to associate regression of left ventricular (LV) mass with a decrease in brachial cuff blood pressure (BP) in the treatment of hypertension. Hence, we prospectively examined potential superiority of pulse wave analysis over conventional BP measurement in predicting treatment-induced LV mass reduction.', 'Forty-six untreated patients (mean age, 56 +/- 7 years) with hypertension received standard medical treatment based on international guidelines. Echocardiography and measurements of various LV load indices were made before and after 1 year of treatment.', 'Antihypertensive treatment significantly (P < .05) reduced LV load, manifest by a decrease in measured brachial BP, estimated aortic BP, carotid-femoral pulse wave velocity (PWV(cf)), aortic augmentation index (AI(a)), aortic augmented pressure (AugP), and radial augmentation index (AI(r)). These changes were accompanied by significant reduction in LV mass index (LVMI) and improvements in systolic ejection fraction and diastolic early-to-atrial ratio of transmitral flow velocities. The treatment-induced LVMI change was not correlated with changes in brachial BP or PWV(cf), but was closely correlated with factors influenced by wave reflection - changes in AI(a), AI(r), AugP, and aorta-to-arm pulse pressure amplification. On multivariate analysis, AI(a) change was the strongest determinant of LVMI change, independent of brachial BP and PWV(cf) changes (beta = 0.51, P < .001). Estimated subject numbers required for predicting a significant LVMI reduction were far less when wave reflection-related factors were used rather than conventional bracial BP.'] Are indices of pulse wave analysis better predictors of left ventricular mass reduction than cuff pressure?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Studies have required large numbers of patients to associate regression of left ventricular (LV) mass with a decrease in brachial cuff blood pressure (BP) in the treatment of hypertension. Hence, we prospectively examined potential superiority of pulse wave analysis over conventional BP measurement in predicting treatment-induced LV mass reduction.', 'Forty-six untreated patients (mean age, 56 +/- 7 years) with hypertension received standard medical treatment based on international guidelines. Echocardiography and measurements of various LV load indices were made before and after 1 year of treatment.', 'Antihypertensive treatment significantly (P < .05) reduced LV load, manifest by a decrease in measured brachial BP, estimated aortic BP, carotid-femoral pulse wave velocity (PWV(cf)), aortic augmentation index (AI(a)), aortic augmented pressure (AugP), and radial augmentation index (AI(r)). These changes were accompanied by significant reduction in LV mass index (LVMI) and improvements in systolic ejection fraction and diastolic early-to-atrial ratio of transmitral flow velocities. The treatment-induced LVMI change was not correlated with changes in brachial BP or PWV(cf), but was closely correlated with factors influenced by wave reflection - changes in AI(a), AI(r), AugP, and aorta-to-arm pulse pressure amplification. On multivariate analysis, AI(a) change was the strongest determinant of LVMI change, independent of brachial BP and PWV(cf) changes (beta = 0.51, P < .001). Estimated subject numbers required for predicting a significant LVMI reduction were far less when wave reflection-related factors were used rather than conventional bracial BP.'] Are indices of pulse wave analysis better predictors of left ventricular mass reduction than cuff pressure? OUTPUT:
PubmedQA107759
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['The neighborhoods in which children live, play, and eat provide an environmental context that may influence obesity risk and ameliorate or exacerbate health disparities. The current study examines whether neighborhood characteristics predict obesity in a prospective cohort of girls.', \"Participants were 174 girls (aged 8-10 years at baseline), a subset from the Cohort Study of Young Girls' Nutrition, Environment, and Transitions. Trained observers completed street audits within a 0.25-mile radius around each girl's residence. Four scales (food and service retail, recreation, walkability, and physical disorder) were created from 40 observed neighborhood features. BMI was calculated from clinically measured height and weight. Obesity was defined as BMI-for-age ≥ 95%. Logistic regression models using generalized estimating equations were used to examine neighborhood influences on obesity risk over 4 years of follow-up, controlling for race/ethnicity, pubertal status, and baseline BMI. Fully adjusted models also controlled for household income, parent education, and a census tract measure of neighborhood socioeconomic status.\", 'A 1-SD increase on the food and service retail scale was associated with a 2.27 (95% confidence interval, 1.42 to 3.61; P < .001) increased odds of being obese. A 1-SD increase in physical disorder was associated with a 2.41 (95% confidence interval, 1.31 to 4.44; P = .005) increased odds of being obese. Other neighborhood scales were not associated with risk for obesity.'] Does neighborhood influence on girls ' obesity risk across the transition to adolescence?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['The neighborhoods in which children live, play, and eat provide an environmental context that may influence obesity risk and ameliorate or exacerbate health disparities. The current study examines whether neighborhood characteristics predict obesity in a prospective cohort of girls.', "Participants were 174 girls (aged 8-10 years at baseline), a subset from the Cohort Study of Young Girls' Nutrition, Environment, and Transitions. Trained observers completed street audits within a 0.25-mile radius around each girl's residence. Four scales (food and service retail, recreation, walkability, and physical disorder) were created from 40 observed neighborhood features. BMI was calculated from clinically measured height and weight. Obesity was defined as BMI-for-age ≥ 95%. Logistic regression models using generalized estimating equations were used to examine neighborhood influences on obesity risk over 4 years of follow-up, controlling for race/ethnicity, pubertal status, and baseline BMI. Fully adjusted models also controlled for household income, parent education, and a census tract measure of neighborhood socioeconomic status.", 'A 1-SD increase on the food and service retail scale was associated with a 2.27 (95% confidence interval, 1.42 to 3.61; P < .001) increased odds of being obese. A 1-SD increase in physical disorder was associated with a 2.41 (95% confidence interval, 1.31 to 4.44; P = .005) increased odds of being obese. Other neighborhood scales were not associated with risk for obesity.'] Does neighborhood influence on girls ' obesity risk across the transition to adolescence? OUTPUT:
PubmedQA207873
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['To compare the clinical and biologic features at diagnosis between sporadic and familial clinically localized prostate cancer (CaP), and to compare the prognosis of familial with that of sporadic cases after radical prostatectomy in southwestern Europe.', \"Eighty-five sporadic (one case of CaP) and 37 familial (two or more CaP cases in the family) patients with clinically localized CaP undergoing radical prostatectomy were compared regarding preoperative (mean age, clinical status, mean prostate-specific antigen level, and mean Gleason score at diagnosis) and postoperative (pT, pN, and pathologic Gleason score) parameters using the Student t test, Fisher's exact test, and the chi-square test. The biochemical relapse-free survival for each group was compared using the Kaplan-Meier method and the log-rank test.\", 'The mean follow-up was about 51.8 months (range 1 to 156) in the sporadic group and 35 months (range 1 to 96) in the familial group. No specific preoperative and postoperative clinical or biologic feature was associated with familial CaP. Biochemical relapse occurred in 40.5% (15 of 37) of cases when the proband had a positive family history of CaP versus 32.9% (28 of 85) in the sporadic cases (P = 0.42). Biochemical relapse-free survival curves did not display any difference (P = 0.46) between familial and sporadic CaP.'] Do familial prostate cancer cases before and after radical prostatectomy show any aggressiveness compared with sporadic cases?\nOUTPUT:\n" }, { "from": "agent", "value": "no" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['To compare the clinical and biologic features at diagnosis between sporadic and familial clinically localized prostate cancer (CaP), and to compare the prognosis of familial with that of sporadic cases after radical prostatectomy in southwestern Europe.', "Eighty-five sporadic (one case of CaP) and 37 familial (two or more CaP cases in the family) patients with clinically localized CaP undergoing radical prostatectomy were compared regarding preoperative (mean age, clinical status, mean prostate-specific antigen level, and mean Gleason score at diagnosis) and postoperative (pT, pN, and pathologic Gleason score) parameters using the Student t test, Fisher's exact test, and the chi-square test. The biochemical relapse-free survival for each group was compared using the Kaplan-Meier method and the log-rank test.", 'The mean follow-up was about 51.8 months (range 1 to 156) in the sporadic group and 35 months (range 1 to 96) in the familial group. No specific preoperative and postoperative clinical or biologic feature was associated with familial CaP. Biochemical relapse occurred in 40.5% (15 of 37) of cases when the proband had a positive family history of CaP versus 32.9% (28 of 85) in the sporadic cases (P = 0.42). Biochemical relapse-free survival curves did not display any difference (P = 0.46) between familial and sporadic CaP.'] Do familial prostate cancer cases before and after radical prostatectomy show any aggressiveness compared with sporadic cases? OUTPUT:
PubmedQA134187
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: [\"Anti-tumor necrosis factor (TNF)α antibodies are effective in treating patients with Crohn's disease whereas soluble TNFα receptors have not shown clinical efficacy; the mechanism that underlies these different effects is not clear. We examined the immunosuppressive effects of different anti-TNFα reagents on activated T cells.\", \"We studied the effects of anti-TNFα antibodies infliximab and adalimumab, the soluble TNFα receptor etanercept, the pegylated F(ab') fragment certolizumab, and certolizumab-immunoglobulin (Ig)G on primary activated T cells. T cells were grown in isolation or in a mixed lymphocyte reaction (MLR). Proliferation was measured by (3)H thymidine incorporation and apoptosis was examined using Annexin V labeling and a colorimetric assay for activated caspase-3. Macrophage phenotypes were assayed by flow cytometry and cytokine secretion.\", \"Infliximab and adalimumab reduced T-cell proliferation in an MLR whereas etanercept and certolizumab did not; this effect was lost after Fc receptors were blocked. The infliximab F(ab')2 fragment did not inhibit proliferation whereas certolizumab-IgG did inhibit proliferation. In the MLR, the antibodies against TNF induced formation of a new population of macrophages in an Fc region-dependent manner; these macrophages had an immunosuppressive phenotype because they inhibit proliferation of activated T cells, produce anti-inflammatory cytokines, and express the regulatory macrophage marker CD206.\"] Do anti-tumor necrosis factor-α antibodies induce regulatory macrophages in an Fc region-dependent manner?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ["Anti-tumor necrosis factor (TNF)α antibodies are effective in treating patients with Crohn's disease whereas soluble TNFα receptors have not shown clinical efficacy; the mechanism that underlies these different effects is not clear. We examined the immunosuppressive effects of different anti-TNFα reagents on activated T cells.", "We studied the effects of anti-TNFα antibodies infliximab and adalimumab, the soluble TNFα receptor etanercept, the pegylated F(ab') fragment certolizumab, and certolizumab-immunoglobulin (Ig)G on primary activated T cells. T cells were grown in isolation or in a mixed lymphocyte reaction (MLR). Proliferation was measured by (3)H thymidine incorporation and apoptosis was examined using Annexin V labeling and a colorimetric assay for activated caspase-3. Macrophage phenotypes were assayed by flow cytometry and cytokine secretion.", "Infliximab and adalimumab reduced T-cell proliferation in an MLR whereas etanercept and certolizumab did not; this effect was lost after Fc receptors were blocked. The infliximab F(ab')2 fragment did not inhibit proliferation whereas certolizumab-IgG did inhibit proliferation. In the MLR, the antibodies against TNF induced formation of a new population of macrophages in an Fc region-dependent manner; these macrophages had an immunosuppressive phenotype because they inhibit proliferation of activated T cells, produce anti-inflammatory cytokines, and express the regulatory macrophage marker CD206."] Do anti-tumor necrosis factor-α antibodies induce regulatory macrophages in an Fc region-dependent manner? OUTPUT:
PubmedQA112680
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Patients with frontal lobe epilepsy (FLE) commonly demonstrate motor impairments, suggesting that frontal lobe seizures affect motor function. However, the underlying mechanisms of these deficits are not known, nor has any study systematically examined motor organization in these patients. We therefore examined cortical motor organization in a group of adult patients with FLE, using task-based fMRI.', 'Eleven right FLE patients, six left FLE patients, and ten control subjects underwent task-based fMRI. Two tasks were performed using the right and left hands separately, and both hands together. The first task was a finger-tapping task and the second task was a more complex coordination task. Functional MR data were compared between patient groups and controls. A laterality index of brain activation was also calculated between the epileptic and healthy hemisphere to determine hemispheric dominance during task performance to explore its relationship with a variety of patient-specific epilepsy factors.', 'Overall, right FLE patients demonstrated decreased BOLD activity in the epileptic hemisphere and increased BOLD activity in the healthy hemisphere compared to controls (p<0.05). The comparison of left FLE patients to controls provided less conclusive differences, possibly due to the low number of left FLE patients studied. Laterality indices of the coordination task were positively correlated to the number of months since the last seizure in both patient groups (right FLE: rs=0.779, left FLE: rs=0.943). Patients that had experienced a recent seizure relied more on the sensorimotor cortex of the healthy hemisphere during task performance, compared to those that were relatively seizure free (p<0.05).'] Does recent seizure activity alter motor organization in frontal lobe epilepsy as revealed by task-based fMRI?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Patients with frontal lobe epilepsy (FLE) commonly demonstrate motor impairments, suggesting that frontal lobe seizures affect motor function. However, the underlying mechanisms of these deficits are not known, nor has any study systematically examined motor organization in these patients. We therefore examined cortical motor organization in a group of adult patients with FLE, using task-based fMRI.', 'Eleven right FLE patients, six left FLE patients, and ten control subjects underwent task-based fMRI. Two tasks were performed using the right and left hands separately, and both hands together. The first task was a finger-tapping task and the second task was a more complex coordination task. Functional MR data were compared between patient groups and controls. A laterality index of brain activation was also calculated between the epileptic and healthy hemisphere to determine hemispheric dominance during task performance to explore its relationship with a variety of patient-specific epilepsy factors.', 'Overall, right FLE patients demonstrated decreased BOLD activity in the epileptic hemisphere and increased BOLD activity in the healthy hemisphere compared to controls (p<0.05). The comparison of left FLE patients to controls provided less conclusive differences, possibly due to the low number of left FLE patients studied. Laterality indices of the coordination task were positively correlated to the number of months since the last seizure in both patient groups (right FLE: rs=0.779, left FLE: rs=0.943). Patients that had experienced a recent seizure relied more on the sensorimotor cortex of the healthy hemisphere during task performance, compared to those that were relatively seizure free (p<0.05).'] Does recent seizure activity alter motor organization in frontal lobe epilepsy as revealed by task-based fMRI? OUTPUT:
PubmedQA21534
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['The glomerular filtration rate (GFR) can be predicted from plasma creatinine, age, gender, and body weight, using the formula of Cockcroft and Gault. Cimetidine improved the accuracy of GFR prediction in renal disease and also in diabetes mellitus type 2, due to inhibition of tubular creatinine secretion. We compared the accuracy and precision of GFR prediction from the Cockcroft-Gault formula without cimetidine (CG), with cimetidine (CGcim) and from the creatinine clearance without cimetidine in renal transplant recipients.', 'CG and CGcim were calculated from plasma creatinine before and after 2400 mg of oral cimetidine during the 24 hr preceding the GFR measurement. The endogenous creatinine clearance was measured in 24 outpatients from a 24-hr urine collection (Ccr24) before cimetidine. GFR was measured as the urinary clearance of continuously infused 125I-iothalamate. Creatinine was determined with an automated enzymatic assay in plasma and with an alkaline picrate assay in urine.', 'GFR was 47.8+/-16.8 ml/min/1.73 m2 (mean+/-SD), Ccr24 was 71.8+/-23.1 ml/min/1.73 m2, CG was 62.2+/-15.2 ml/min/1.73 m2, and CGcim was 52.8+/-14.9 ml/min/1.73 m2. Ccr24 overestimated GFR in every patient by an average of 23.8 ml/min/1.73 m2 and CG by an average of 14.3 ml/min/1.73 m2, whereas CGcim overestimated GFR significantly less by an average 4.9 ml/min/1.73 m2 (P<0.001). The precision of CGcim was significantly better than that of Ccr24: the SD of the difference from GFR was 9.0 ml/min/1.73 m2 for CGcim and 14.5 ml/min/1.73 m2 for Ccr24 (P<0.05).'] Does cimetidine improve prediction of the glomerular filtration rate by the Cockcroft-Gault formula in renal transplant recipients?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['The glomerular filtration rate (GFR) can be predicted from plasma creatinine, age, gender, and body weight, using the formula of Cockcroft and Gault. Cimetidine improved the accuracy of GFR prediction in renal disease and also in diabetes mellitus type 2, due to inhibition of tubular creatinine secretion. We compared the accuracy and precision of GFR prediction from the Cockcroft-Gault formula without cimetidine (CG), with cimetidine (CGcim) and from the creatinine clearance without cimetidine in renal transplant recipients.', 'CG and CGcim were calculated from plasma creatinine before and after 2400 mg of oral cimetidine during the 24 hr preceding the GFR measurement. The endogenous creatinine clearance was measured in 24 outpatients from a 24-hr urine collection (Ccr24) before cimetidine. GFR was measured as the urinary clearance of continuously infused 125I-iothalamate. Creatinine was determined with an automated enzymatic assay in plasma and with an alkaline picrate assay in urine.', 'GFR was 47.8+/-16.8 ml/min/1.73 m2 (mean+/-SD), Ccr24 was 71.8+/-23.1 ml/min/1.73 m2, CG was 62.2+/-15.2 ml/min/1.73 m2, and CGcim was 52.8+/-14.9 ml/min/1.73 m2. Ccr24 overestimated GFR in every patient by an average of 23.8 ml/min/1.73 m2 and CG by an average of 14.3 ml/min/1.73 m2, whereas CGcim overestimated GFR significantly less by an average 4.9 ml/min/1.73 m2 (P<0.001). The precision of CGcim was significantly better than that of Ccr24: the SD of the difference from GFR was 9.0 ml/min/1.73 m2 for CGcim and 14.5 ml/min/1.73 m2 for Ccr24 (P<0.05).'] Does cimetidine improve prediction of the glomerular filtration rate by the Cockcroft-Gault formula in renal transplant recipients? OUTPUT:
PubmedQA106946
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Allergy to peanuts results in severe anaphylactic responses in affected individuals, and has dramatic effects on society and public policy. Despite the health impacts of peanut-induced anaphylaxis (PIA), relatively little is known about immune mechanisms underlying the disease. Using a mouse model of PIA, we evaluated mice with deletions in four distinct immune molecules (IL7Rα, L-selectin, CD34, CD103), for perturbed responses.', 'PIA was induced by intragastric sensitization with peanut antigen and cholera toxin adjuvant, followed by intraperitoneal challenge with crude peanut extract (CPE). Disease outcome was assessed by monitoring body temperature, clinical symptoms, and serum histamine levels. Resistant mice were evaluated for total and antigen specific serum IgE, as well as susceptibility to passive systemic anaphylaxis.', 'PIA responses were dramatically reduced in IL7Rα-/- and L-selectin-/- mice, despite normal peanut-specific IgE production and susceptibility to passive systemic anaphylaxis. In contrast, CD34-/- and CD103-/- mice exhibited robust PIA responses, indistinguishable from wild type controls.'] Are iL-7Rα and L-selectin , but not CD103 or CD34 , required for murine peanut-induced anaphylaxis?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Allergy to peanuts results in severe anaphylactic responses in affected individuals, and has dramatic effects on society and public policy. Despite the health impacts of peanut-induced anaphylaxis (PIA), relatively little is known about immune mechanisms underlying the disease. Using a mouse model of PIA, we evaluated mice with deletions in four distinct immune molecules (IL7Rα, L-selectin, CD34, CD103), for perturbed responses.', 'PIA was induced by intragastric sensitization with peanut antigen and cholera toxin adjuvant, followed by intraperitoneal challenge with crude peanut extract (CPE). Disease outcome was assessed by monitoring body temperature, clinical symptoms, and serum histamine levels. Resistant mice were evaluated for total and antigen specific serum IgE, as well as susceptibility to passive systemic anaphylaxis.', 'PIA responses were dramatically reduced in IL7Rα-/- and L-selectin-/- mice, despite normal peanut-specific IgE production and susceptibility to passive systemic anaphylaxis. In contrast, CD34-/- and CD103-/- mice exhibited robust PIA responses, indistinguishable from wild type controls.'] Are iL-7Rα and L-selectin , but not CD103 or CD34 , required for murine peanut-induced anaphylaxis? OUTPUT:
PubmedQA96195
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Black tattoos may involve risk of cancer owing to polycyclic aromatic hydrocarbons including benzo(a)pyrene (BaP) in inks. Ultraviolet radiation (UVR) induces skin cancer. The combination of UVR and black tattoo may\\xa0therefore potentially be very problematic, but has not been previously studied.', \"Immunocompetent C3.Cg/TifBomTac mice (n\\xa0=\\xa099) were tattooed on the back with Starbrite Tribal Black(™) . This ink has a high content of the carcinogen BaP. Half of the mice were irradiated with three standard erythema doses UVR thrice weekly. Time to induction of first, second and third squamous cell carcinoma (SCC) was measured. Controls were 'tattooed' without ink.\", 'All irradiated mice developed SCCs while no malignant tumours were found in the nonirradiated group. In the tattooed and irradiated group, the development of the first, second and third SCC was significantly delayed in comparison with the irradiated controls without black tattoos (212, 232, 247\\xa0days vs. 163, 183, 191\\xa0days, P\\xa0<\\xa00.001).'] Do black tattoos protect against UVR-induced skin cancer in mice?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Black tattoos may involve risk of cancer owing to polycyclic aromatic hydrocarbons including benzo(a)pyrene (BaP) in inks. Ultraviolet radiation (UVR) induces skin cancer. The combination of UVR and black tattoo may\xa0therefore potentially be very problematic, but has not been previously studied.', "Immunocompetent C3.Cg/TifBomTac mice (n\xa0=\xa099) were tattooed on the back with Starbrite Tribal Black(™) . This ink has a high content of the carcinogen BaP. Half of the mice were irradiated with three standard erythema doses UVR thrice weekly. Time to induction of first, second and third squamous cell carcinoma (SCC) was measured. Controls were 'tattooed' without ink.", 'All irradiated mice developed SCCs while no malignant tumours were found in the nonirradiated group. In the tattooed and irradiated group, the development of the first, second and third SCC was significantly delayed in comparison with the irradiated controls without black tattoos (212, 232, 247\xa0days vs. 163, 183, 191\xa0days, P\xa0<\xa00.001).'] Do black tattoos protect against UVR-induced skin cancer in mice? OUTPUT:
PubmedQA96311
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Proinflammatory cytokines like tumor necrosis factor-alpha and oxidative stress induce apoptotic cell death in endothelial cells (ECs). Systemic inflammation and increased oxidative stress in congestive heart failure (CHF) coincide with enhanced EC apoptosis and the development of endothelial dysfunction. Therefore, we investigated the effects of antioxidative vitamin C therapy on EC apoptosis in CHF patients.', 'Vitamin C dose dependently suppressed the induction of EC apoptosis by tumor necrosis factor-alpha and angiotensin II in vitro as assessed by DNA fragmentation, DAPI nuclear staining, and MTT viability assay. The antiapoptotic effect of vitamin C was associated with reduced cytochrome C release from mitochondria and the inhibition of caspase-9 activity. To assess EC protection by vitamin C in CHF patients, we prospectively randomized CHF patients in a double-blind trial to vitamin C treatment versus placebo. Vitamin C administration to CHF patients markedly reduced plasma levels of circulating apoptotic microparticles to 32+/-8% of baseline levels, whereas placebo had no effect (87+/-14%, P<0.005). In addition, vitamin C administration suppressed the proapoptotic activity on EC of the serum of CHF patients (P<0.001).'] Does vitamin C inhibit endothelial cell apoptosis in congestive heart failure?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Proinflammatory cytokines like tumor necrosis factor-alpha and oxidative stress induce apoptotic cell death in endothelial cells (ECs). Systemic inflammation and increased oxidative stress in congestive heart failure (CHF) coincide with enhanced EC apoptosis and the development of endothelial dysfunction. Therefore, we investigated the effects of antioxidative vitamin C therapy on EC apoptosis in CHF patients.', 'Vitamin C dose dependently suppressed the induction of EC apoptosis by tumor necrosis factor-alpha and angiotensin II in vitro as assessed by DNA fragmentation, DAPI nuclear staining, and MTT viability assay. The antiapoptotic effect of vitamin C was associated with reduced cytochrome C release from mitochondria and the inhibition of caspase-9 activity. To assess EC protection by vitamin C in CHF patients, we prospectively randomized CHF patients in a double-blind trial to vitamin C treatment versus placebo. Vitamin C administration to CHF patients markedly reduced plasma levels of circulating apoptotic microparticles to 32+/-8% of baseline levels, whereas placebo had no effect (87+/-14%, P<0.005). In addition, vitamin C administration suppressed the proapoptotic activity on EC of the serum of CHF patients (P<0.001).'] Does vitamin C inhibit endothelial cell apoptosis in congestive heart failure? OUTPUT:
PubmedQA177572
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Resistin is a cysteine rich protein, mainly expressed and secreted by circulating human mononuclear cells. While several factors responsible for transcription of mouse resistin gene have been identified, not much is known about the factors responsible for the differential expression of human resistin.', 'We show that the minimal promoter of human resistin lies within approximately 80 bp sequence upstream of the transcriptional start site (-240) whereas binding sites for cRel, CCAAT enhancer binding protein alpha (C/EBP-alpha), activating transcription factor 2 (ATF-2) and activator protein 1 (AP-1) transcription factors, important for induced expression, are present within sequences up to -619. Specificity Protein 1(Sp1) binding site (-276 to -295) is also present and an interaction of Sp1 with peroxisome proliferator activating receptor gamma (PPARgamma) is necessary for constitutive expression in U937 cells. Indeed co-immunoprecipitation assay demonstrated a direct physical interaction of Sp1 with PPARgamma in whole cell extracts of U937 cells. Phorbol myristate acetate (PMA) upregulated the expression of resistin mRNA in U937 cells by increasing the recruitment of Sp1, ATF-2 and PPARgamma on the resistin gene promoter. Furthermore, PMA stimulation of U937 cells resulted in the disruption of Sp1 and PPARgamma interaction. Chromatin immunoprecipitation (ChIP) assay confirmed the recruitment of transcription factors phospho ATF-2, Sp1, Sp3, PPARgamma, chromatin modifier histone deacetylase 1 (HDAC1) and the acetylated form of histone H3 but not cRel, C/EBP-alpha and phospho c-Jun during resistin gene transcription.'] Does transcription of human resistin gene involve an interaction of Sp1 with peroxisome proliferator-activating receptor gamma ( PPARgamma )?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Resistin is a cysteine rich protein, mainly expressed and secreted by circulating human mononuclear cells. While several factors responsible for transcription of mouse resistin gene have been identified, not much is known about the factors responsible for the differential expression of human resistin.', 'We show that the minimal promoter of human resistin lies within approximately 80 bp sequence upstream of the transcriptional start site (-240) whereas binding sites for cRel, CCAAT enhancer binding protein alpha (C/EBP-alpha), activating transcription factor 2 (ATF-2) and activator protein 1 (AP-1) transcription factors, important for induced expression, are present within sequences up to -619. Specificity Protein 1(Sp1) binding site (-276 to -295) is also present and an interaction of Sp1 with peroxisome proliferator activating receptor gamma (PPARgamma) is necessary for constitutive expression in U937 cells. Indeed co-immunoprecipitation assay demonstrated a direct physical interaction of Sp1 with PPARgamma in whole cell extracts of U937 cells. Phorbol myristate acetate (PMA) upregulated the expression of resistin mRNA in U937 cells by increasing the recruitment of Sp1, ATF-2 and PPARgamma on the resistin gene promoter. Furthermore, PMA stimulation of U937 cells resulted in the disruption of Sp1 and PPARgamma interaction. Chromatin immunoprecipitation (ChIP) assay confirmed the recruitment of transcription factors phospho ATF-2, Sp1, Sp3, PPARgamma, chromatin modifier histone deacetylase 1 (HDAC1) and the acetylated form of histone H3 but not cRel, C/EBP-alpha and phospho c-Jun during resistin gene transcription.'] Does transcription of human resistin gene involve an interaction of Sp1 with peroxisome proliferator-activating receptor gamma ( PPARgamma )? OUTPUT:
PubmedQA146461
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['We have previously shown that Elatoside C reduces cardiomyocyte apoptosis during ischaemia/reperfusion (I/R). Here, we investigated whether Elatoside C improves heart function in isolated rat hearts subjected to I/R and elucidated the potential mechanisms involved in Elatoside C-induced protection.', 'Isolated rat hearts were subjected to global ischaemia followed by reperfusion in the absence or presence of Elatoside C. We found that Elatoside C significantly attenuated cardiac dysfunction and depressed oxidative stress induced by I/R. Consistently, Elatoside C prevented I/R-induced mitochondrial dysfunction, which was evident by the inhibition of mitochondrial ROS production, mitochondrial permeability transition pore (mPTP) opening, cytochrome c release from the mitochondria and Bax translocation. Moreover, Elatoside C improved abnormal calcium handling during I/R, including increasing sarcoplasmic reticulum Ca(2+) ATPase (SERCA2) activity, alleviating [Ca(2+)]ER depletion, and reducing the expression levels of ER stress protein markers. All of these protective effects of Elatoside C were partially abolished by the PI3K/Akt inhibitor LY294002, ERK1/2 inhibitor PD98059, and JAK2/STAT3 inhibitor AG490. Further assessment in isolated cardiomyocytes showed that Elatoside C maintained the Ca(2+) transients and cell shortening against I/R.'] Does elatoside C protect the heart from ischaemia/reperfusion injury through the modulation of oxidative stress and intracellular Ca²⁺ homeostasis?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['We have previously shown that Elatoside C reduces cardiomyocyte apoptosis during ischaemia/reperfusion (I/R). Here, we investigated whether Elatoside C improves heart function in isolated rat hearts subjected to I/R and elucidated the potential mechanisms involved in Elatoside C-induced protection.', 'Isolated rat hearts were subjected to global ischaemia followed by reperfusion in the absence or presence of Elatoside C. We found that Elatoside C significantly attenuated cardiac dysfunction and depressed oxidative stress induced by I/R. Consistently, Elatoside C prevented I/R-induced mitochondrial dysfunction, which was evident by the inhibition of mitochondrial ROS production, mitochondrial permeability transition pore (mPTP) opening, cytochrome c release from the mitochondria and Bax translocation. Moreover, Elatoside C improved abnormal calcium handling during I/R, including increasing sarcoplasmic reticulum Ca(2+) ATPase (SERCA2) activity, alleviating [Ca(2+)]ER depletion, and reducing the expression levels of ER stress protein markers. All of these protective effects of Elatoside C were partially abolished by the PI3K/Akt inhibitor LY294002, ERK1/2 inhibitor PD98059, and JAK2/STAT3 inhibitor AG490. Further assessment in isolated cardiomyocytes showed that Elatoside C maintained the Ca(2+) transients and cell shortening against I/R.'] Does elatoside C protect the heart from ischaemia/reperfusion injury through the modulation of oxidative stress and intracellular Ca²⁺ homeostasis? OUTPUT:
PubmedQA210060
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['A study was undertaken to characterize the plasticity of AMPA receptor (AMPAR)-mediated neurotransmission in the hippocampus during status epilepticus (SE).', 'SE was induced by pilocarpine, and animals were studied 10 minutes (refractory SE) or 60 minutes (late SE) after the onset of the first grade 5 seizures. AMPAR-mediated currents were recorded from CA1 pyramidal neurons and dentate granule cells (DGCs) by voltage clamp technique. The surface expression of GluA2 subunit on hippocampal membranes was determined using a biotinylation assay. GluA2 internalization and changes in intracellular calcium ([Ca](i)) levels were studied in hippocampal cultures using immunocytochemical and live-imaging techniques. AMPAR antagonist treatment of SE was evaluated by video and electroencephalography.', 'AMPAR-mediated currents recorded from CA1 neurons from refractory and late SE animals were inwardly rectifying, and philanthotoxin-sensitive; similar changes were observed in recordings obtained from DGCs from refractory SE animals. GluA2 subunit surface expression was reduced in the hippocampus during refractory and late SE. In cultured hippocampal pyramidal neurons, recurrent bursting diminished surface expression of the GluA2 subunit and enhanced its internalization rate. Recurrent bursting-induced increase in [Ca](i) levels was reduced by selective inhibition of GluA2-lacking AMPARs. GYKI-52466 terminated diazepam-refractory SE.'] Are calcium-permeable AMPA receptors expressed in a rodent model of status epilepticus?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['A study was undertaken to characterize the plasticity of AMPA receptor (AMPAR)-mediated neurotransmission in the hippocampus during status epilepticus (SE).', 'SE was induced by pilocarpine, and animals were studied 10 minutes (refractory SE) or 60 minutes (late SE) after the onset of the first grade 5 seizures. AMPAR-mediated currents were recorded from CA1 pyramidal neurons and dentate granule cells (DGCs) by voltage clamp technique. The surface expression of GluA2 subunit on hippocampal membranes was determined using a biotinylation assay. GluA2 internalization and changes in intracellular calcium ([Ca](i)) levels were studied in hippocampal cultures using immunocytochemical and live-imaging techniques. AMPAR antagonist treatment of SE was evaluated by video and electroencephalography.', 'AMPAR-mediated currents recorded from CA1 neurons from refractory and late SE animals were inwardly rectifying, and philanthotoxin-sensitive; similar changes were observed in recordings obtained from DGCs from refractory SE animals. GluA2 subunit surface expression was reduced in the hippocampus during refractory and late SE. In cultured hippocampal pyramidal neurons, recurrent bursting diminished surface expression of the GluA2 subunit and enhanced its internalization rate. Recurrent bursting-induced increase in [Ca](i) levels was reduced by selective inhibition of GluA2-lacking AMPARs. GYKI-52466 terminated diazepam-refractory SE.'] Are calcium-permeable AMPA receptors expressed in a rodent model of status epilepticus? OUTPUT:
PubmedQA23091
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Maternal history of asthma or atopy is among the most consistently reported risk factors for asthma and atopy in children, yet the molecular basis for this observation remains unclear. Mitochondria are inherited exclusively through the maternal line, raising the possibility that sequence variation in the mitochondrial genome contributes to the pathogenesis of asthma and atopy.', 'We set out to determine whether common European mitochondrial haplogroups are associated with asthma-related atopic phenotypes.', 'We studied 654 self-reported white children age 5 to 12 years with mild to moderate asthma participating in the Childhood Asthma Management Program. Eight haplogroup-tagging polymorphisms were genotyped with TaqMan probe hybridization assays, and mitochondrial haplogroup tests of association with asthma-related and atopy-related phenotypes were performed with haplo.stats.', 'We found significant evidence of mitochondrial haplogroup association with total serum IgE levels (global significance, P = .04), with carriers of European haplogroup U (frequency 11%) having higher total serum IgE levels (median level, 684 IU/L) compared with noncarriers (389 IU/L; P = .001). Haplogroup U carriers also had trends of greater skin prick test reactivity (P = .03) and higher frequency of atopic dermatitis (P = .07), although global haplogroup tests for these later 2 phenotypes were not significant at an alpha level of 0.05.'] Is a common mitochondrial haplogroup associated with elevated total serum IgE levels?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Maternal history of asthma or atopy is among the most consistently reported risk factors for asthma and atopy in children, yet the molecular basis for this observation remains unclear. Mitochondria are inherited exclusively through the maternal line, raising the possibility that sequence variation in the mitochondrial genome contributes to the pathogenesis of asthma and atopy.', 'We set out to determine whether common European mitochondrial haplogroups are associated with asthma-related atopic phenotypes.', 'We studied 654 self-reported white children age 5 to 12 years with mild to moderate asthma participating in the Childhood Asthma Management Program. Eight haplogroup-tagging polymorphisms were genotyped with TaqMan probe hybridization assays, and mitochondrial haplogroup tests of association with asthma-related and atopy-related phenotypes were performed with haplo.stats.', 'We found significant evidence of mitochondrial haplogroup association with total serum IgE levels (global significance, P = .04), with carriers of European haplogroup U (frequency 11%) having higher total serum IgE levels (median level, 684 IU/L) compared with noncarriers (389 IU/L; P = .001). Haplogroup U carriers also had trends of greater skin prick test reactivity (P = .03) and higher frequency of atopic dermatitis (P = .07), although global haplogroup tests for these later 2 phenotypes were not significant at an alpha level of 0.05.'] Is a common mitochondrial haplogroup associated with elevated total serum IgE levels? OUTPUT:
PubmedQA162639
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Over the past 60 years, cytotoxic chemotherapy has targeted the cancer cell. Despite this, there have been few cancer cures. A new approach to cancer therapy is to target the multicellular biological entity of the tumor microenvironment.', 'Lenalidomide, an immunomodulatory drug, sunitinib, a tyrosine kinase inhibitor, and low-dose metronomic cyclophosphamide, were tested alone and in combination for their abilities to inhibit endothelial cell tube formation, rat aortic ring outgrowth, tumor growth, and metastatic development in mice. In addition, ectopic tumor lysates were evaluated for the presence of proangiogenic proteins.', \"The three agents alone were shown to significantly inhibit endothelial cells' ability to form tubes and significantly inhibit the multicellular microenvironment in the rat aortic ring assay (P < 0.01 and P < 0.001). This effect was also significantly augmented when the agents were combined. Furthermore, the three-drug combination was able halt the progression of tumor growth almost completely in xenograft models of ocular melanoma, colon cancer, pancreatic cancer, and cutaneous melanoma. These agents significantly decrease the number of proliferating cells in tumors, significantly increase the number of cells undergoing active cell death in tumors, and significantly decrease the number of blood vessels in treated tumors (P < 0.05). Combination therapy shows a decrease in the compensatory up-regulation of proangiogenic proteins after treatment when compared with single-agent therapy.\"] Do combining agents that target the tumor microenvironment improves the efficacy of anticancer therapy?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Over the past 60 years, cytotoxic chemotherapy has targeted the cancer cell. Despite this, there have been few cancer cures. A new approach to cancer therapy is to target the multicellular biological entity of the tumor microenvironment.', 'Lenalidomide, an immunomodulatory drug, sunitinib, a tyrosine kinase inhibitor, and low-dose metronomic cyclophosphamide, were tested alone and in combination for their abilities to inhibit endothelial cell tube formation, rat aortic ring outgrowth, tumor growth, and metastatic development in mice. In addition, ectopic tumor lysates were evaluated for the presence of proangiogenic proteins.', "The three agents alone were shown to significantly inhibit endothelial cells' ability to form tubes and significantly inhibit the multicellular microenvironment in the rat aortic ring assay (P < 0.01 and P < 0.001). This effect was also significantly augmented when the agents were combined. Furthermore, the three-drug combination was able halt the progression of tumor growth almost completely in xenograft models of ocular melanoma, colon cancer, pancreatic cancer, and cutaneous melanoma. These agents significantly decrease the number of proliferating cells in tumors, significantly increase the number of cells undergoing active cell death in tumors, and significantly decrease the number of blood vessels in treated tumors (P < 0.05). Combination therapy shows a decrease in the compensatory up-regulation of proangiogenic proteins after treatment when compared with single-agent therapy."] Do combining agents that target the tumor microenvironment improves the efficacy of anticancer therapy? OUTPUT:
PubmedQA21527
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Hypoxia can induce tissue injury, including apoptosis of endothelial cells. However, little is known about the effects of hypoxia on endothelial cell function. We assessed the effects of hypoxia inducible factor (HIF)-1alpha on the functional characteristics of endothelial cells, particularly on cell cycle regulators, by cationic liposome-mediated transfection of HIF-1alpha-expression vector into the cells.', 'Transfection of the HIF-1alpha gene in endothelial cells resulted in (a) reduced proliferation and detachment of the cells; (b) up-regulation of intracellular p21waf1/cip1 and down-regulation of bcl-2; (c) reduced activities of cyclin-dependent kinase (CDK)-4 and CDK-6; (d) cell cycle arrest at G0/G1 phase; and (e) apoptosis of the cells.'] Does hypoxia-inducible factor-1alpha induce cell cycle arrest of endothelial cells?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Hypoxia can induce tissue injury, including apoptosis of endothelial cells. However, little is known about the effects of hypoxia on endothelial cell function. We assessed the effects of hypoxia inducible factor (HIF)-1alpha on the functional characteristics of endothelial cells, particularly on cell cycle regulators, by cationic liposome-mediated transfection of HIF-1alpha-expression vector into the cells.', 'Transfection of the HIF-1alpha gene in endothelial cells resulted in (a) reduced proliferation and detachment of the cells; (b) up-regulation of intracellular p21waf1/cip1 and down-regulation of bcl-2; (c) reduced activities of cyclin-dependent kinase (CDK)-4 and CDK-6; (d) cell cycle arrest at G0/G1 phase; and (e) apoptosis of the cells.'] Does hypoxia-inducible factor-1alpha induce cell cycle arrest of endothelial cells? OUTPUT:
PubmedQA174321
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Inflammation and pulmonary injury caused by mechanical ventilation is a complex process in which long pentraxin 3 (PTX3) is suggested to play an important role. The effect of mechanical stretch on PTX3 mRNA and protein expression in human alveolar epithelial cells (A549) was investigated.', 'Immortalized A549 cells were exposed to tightly controlled and physiologically relevant cyclic mechanical stretch. A549 cells grown on collagen I BioFlex plates were exposed to square cyclic stretch at 0.3 Hz using the Flexercell system with 6% or 20% elongation of cells. In another group, cells were pretreated with small interfering RNA directed against PTX3 before stretch. After stretching, conditioned media and cells were collected and analyzed by Western blotting. Real-time PCR of cDNA generated from the stretched cells was performed. Apoptosis and viability of the cells following treatment were assessed using standard procedures.', 'Mechanical cyclic stretch of 20% elongation led to increased PTX3 gene expression, increased release of PTX3 protein, and induced apoptosis and necrosis in A549 cells. Expression of PTX3 highly correlated with the severity of apoptosis. However, the results suggest that PTX3 expression was significantly reduced by pretreatment of the A549 cells with small interfering RNA of PTX3.'] Does mechanical stretch induce pentraxin 3 release by alveolar epithelial cells in vitro?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Inflammation and pulmonary injury caused by mechanical ventilation is a complex process in which long pentraxin 3 (PTX3) is suggested to play an important role. The effect of mechanical stretch on PTX3 mRNA and protein expression in human alveolar epithelial cells (A549) was investigated.', 'Immortalized A549 cells were exposed to tightly controlled and physiologically relevant cyclic mechanical stretch. A549 cells grown on collagen I BioFlex plates were exposed to square cyclic stretch at 0.3 Hz using the Flexercell system with 6% or 20% elongation of cells. In another group, cells were pretreated with small interfering RNA directed against PTX3 before stretch. After stretching, conditioned media and cells were collected and analyzed by Western blotting. Real-time PCR of cDNA generated from the stretched cells was performed. Apoptosis and viability of the cells following treatment were assessed using standard procedures.', 'Mechanical cyclic stretch of 20% elongation led to increased PTX3 gene expression, increased release of PTX3 protein, and induced apoptosis and necrosis in A549 cells. Expression of PTX3 highly correlated with the severity of apoptosis. However, the results suggest that PTX3 expression was significantly reduced by pretreatment of the A549 cells with small interfering RNA of PTX3.'] Does mechanical stretch induce pentraxin 3 release by alveolar epithelial cells in vitro? OUTPUT:
PubmedQA78948
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Glycerol represents an important metabolite for the control of lipid accumulation and hepatic gluconeogenesis. We investigated whether hepatic expression and functionality of aquaporin-9 (AQP9), a channel mediating glycerol influx into hepatocytes, is impaired in non-alcoholic fatty liver disease (NAFLD) and steatohepatitis (NASH) in the context of insulin resistance.', 'Liver biopsies were obtained from 66 morbid obese patients undergoing bariatric surgery (66% women, mean body mass index (BMI) 46.1±1.0\\u2009kg\\u2009m(-2)) with available liver echography and pathology analysis of the biopsies in this cross-sectional study. Subjects were classified according to normoglycemia (NG), impaired glucose tolerance (IGT) or type 2 diabetes (T2D). Hepatic expression of AQP9 was analyzed by real-time PCR, western blotting and immunohistochemistry, while glycerol permeability (P(gly)) was measured by stopped-flow light scattering.', 'AQP9 was the most abundantly (P<0.0001) expressed aquaglyceroporin in human liver (AQP9>>>AQP3>AQP7>AQP10). Obese patients with T2D showed increased plasma glycerol as well as lower P(gly) and hepatic AQP9 expression. The prevalence of NAFLD and NASH in T2D patients was 100 and 65%, respectively. Interestingly, AQP9 expression was decreased in patients with NAFLD and NASH as compared with those without hepatosteatosis, in direct relation to the degree of steatosis and lobular inflammation, being further reduced in insulin-resistant individuals. The association of AQP9 with insulin sensitivity was independent of BMI and age. Consistent with these data, fasting insulin and C-reactive protein contributed independently to 33.1% of the hepatic AQP9 mRNA expression variance after controlling for the effects of age and BMI.'] Are reduced hepatic aquaporin-9 and glycerol permeability related to insulin resistance in non-alcoholic fatty liver disease?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Glycerol represents an important metabolite for the control of lipid accumulation and hepatic gluconeogenesis. We investigated whether hepatic expression and functionality of aquaporin-9 (AQP9), a channel mediating glycerol influx into hepatocytes, is impaired in non-alcoholic fatty liver disease (NAFLD) and steatohepatitis (NASH) in the context of insulin resistance.', 'Liver biopsies were obtained from 66 morbid obese patients undergoing bariatric surgery (66% women, mean body mass index (BMI) 46.1±1.0\u2009kg\u2009m(-2)) with available liver echography and pathology analysis of the biopsies in this cross-sectional study. Subjects were classified according to normoglycemia (NG), impaired glucose tolerance (IGT) or type 2 diabetes (T2D). Hepatic expression of AQP9 was analyzed by real-time PCR, western blotting and immunohistochemistry, while glycerol permeability (P(gly)) was measured by stopped-flow light scattering.', 'AQP9 was the most abundantly (P<0.0001) expressed aquaglyceroporin in human liver (AQP9>>>AQP3>AQP7>AQP10). Obese patients with T2D showed increased plasma glycerol as well as lower P(gly) and hepatic AQP9 expression. The prevalence of NAFLD and NASH in T2D patients was 100 and 65%, respectively. Interestingly, AQP9 expression was decreased in patients with NAFLD and NASH as compared with those without hepatosteatosis, in direct relation to the degree of steatosis and lobular inflammation, being further reduced in insulin-resistant individuals. The association of AQP9 with insulin sensitivity was independent of BMI and age. Consistent with these data, fasting insulin and C-reactive protein contributed independently to 33.1% of the hepatic AQP9 mRNA expression variance after controlling for the effects of age and BMI.'] Are reduced hepatic aquaporin-9 and glycerol permeability related to insulin resistance in non-alcoholic fatty liver disease? OUTPUT:
PubmedQA194970
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['The goal of this study was to determine if brain lesion volume was correlated with dietary glycemic index and glycemic load in elderly individuals.', 'This cross-sectional study was performed at an academic medical center as part of a clinical study of late-life depression.', 'Subjects (n=137) were age 60 or over, and were participating as non-depressed comparison subjects.', 'Food intake was assessed using the Block 1998 food frequency questionnaire. Glycemic index and glycemic load measures were derived from reported food intake. Brain lesion volumes were calculated from magnetic resonance imaging (MRI).', 'No significant associations were found between glycemic index or glycemic load, and brain lesion volume.'] Are glycemic index and glycemic load associated with brain lesions in the elderly?\nOUTPUT:\n" }, { "from": "agent", "value": "no" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['The goal of this study was to determine if brain lesion volume was correlated with dietary glycemic index and glycemic load in elderly individuals.', 'This cross-sectional study was performed at an academic medical center as part of a clinical study of late-life depression.', 'Subjects (n=137) were age 60 or over, and were participating as non-depressed comparison subjects.', 'Food intake was assessed using the Block 1998 food frequency questionnaire. Glycemic index and glycemic load measures were derived from reported food intake. Brain lesion volumes were calculated from magnetic resonance imaging (MRI).', 'No significant associations were found between glycemic index or glycemic load, and brain lesion volume.'] Are glycemic index and glycemic load associated with brain lesions in the elderly? OUTPUT:
PubmedQA155069
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['To evaluate the mechanism of interleukin-1 (IL-1) in tumorigenesis.', 'The miRNA expression was profiled with the Exiqon miRCURY(TM) LNA Array System. And the miRecords algorithm and luciferase reporter assays were employed for identifying the targets of miR-425. Cell proliferation assay was performed with CCK8. Cell apoptosis assay was performed with flow cytometry.', 'IL-1β induced the up-regulation of miR-425, a negative expression regulator of phosphatase and tensin homolog (PTEN). An increase in miR-425 depended upon IL-1β-induced NF-kappaB activation.Repression of PTEN by miR-425 promoted gastric cancer cell proliferation.'] Does [ MiR-425 up-regulation induced by interleukin-1β promote the proliferation of gastric cancer cell AGS ]?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['To evaluate the mechanism of interleukin-1 (IL-1) in tumorigenesis.', 'The miRNA expression was profiled with the Exiqon miRCURY(TM) LNA Array System. And the miRecords algorithm and luciferase reporter assays were employed for identifying the targets of miR-425. Cell proliferation assay was performed with CCK8. Cell apoptosis assay was performed with flow cytometry.', 'IL-1β induced the up-regulation of miR-425, a negative expression regulator of phosphatase and tensin homolog (PTEN). An increase in miR-425 depended upon IL-1β-induced NF-kappaB activation.Repression of PTEN by miR-425 promoted gastric cancer cell proliferation.'] Does [ MiR-425 up-regulation induced by interleukin-1β promote the proliferation of gastric cancer cell AGS ]? OUTPUT:
PubmedQA136546
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Left ventricular noncompaction of the myocardium (LVNC) has been recognized as a cardiomyopathy with a genetic etiology. Mutations in genes encoding sarcomere proteins were shown to be associated with LVNC. We evaluated the potential clinical impact of genetic analysis of sarcomere genes in patients with LVNC.', 'We identified 5 mutations in cardiac myosin-binding protein C (MYBPC3) and 2 mutations in α-tropomyosin (TPM1) in a cohort of unrelated adult probands with isolated LVNC. The mutations in MYBPC3 and TPM1 and in 6 other previously reported sarcomere genes in this cohort resulted in a total of 18 (29%) heterozygous mutations in 63 probands. β-myosin heavy chain (MYH7) was the most prevalent disease gene and accounts for 13% of cases, followed by MYBPC3 (8%). Comparing sarcomere mutation-positive and mutation-negative LVNC probands showed no significant differences in terms of average age, myocardial function, and presence of heart failure or tachyarrhythmias at initial presentation or at follow-up. Familial disease was found in 16 probands of whom 8 were sarcomere mutation positive. Nonpenetrance was detected in 2 of 8 mutation-positive families with LVNC.'] Do sarcomere gene mutations in isolated left ventricular noncompaction cardiomyopathy predict clinical phenotype?\nOUTPUT:\n" }, { "from": "agent", "value": "no" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Left ventricular noncompaction of the myocardium (LVNC) has been recognized as a cardiomyopathy with a genetic etiology. Mutations in genes encoding sarcomere proteins were shown to be associated with LVNC. We evaluated the potential clinical impact of genetic analysis of sarcomere genes in patients with LVNC.', 'We identified 5 mutations in cardiac myosin-binding protein C (MYBPC3) and 2 mutations in α-tropomyosin (TPM1) in a cohort of unrelated adult probands with isolated LVNC. The mutations in MYBPC3 and TPM1 and in 6 other previously reported sarcomere genes in this cohort resulted in a total of 18 (29%) heterozygous mutations in 63 probands. β-myosin heavy chain (MYH7) was the most prevalent disease gene and accounts for 13% of cases, followed by MYBPC3 (8%). Comparing sarcomere mutation-positive and mutation-negative LVNC probands showed no significant differences in terms of average age, myocardial function, and presence of heart failure or tachyarrhythmias at initial presentation or at follow-up. Familial disease was found in 16 probands of whom 8 were sarcomere mutation positive. Nonpenetrance was detected in 2 of 8 mutation-positive families with LVNC.'] Do sarcomere gene mutations in isolated left ventricular noncompaction cardiomyopathy predict clinical phenotype? OUTPUT:
PubmedQA28538
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Cnidarian-dinoflagellate intracellular symbioses are one of the most important mutualisms in the marine environment. They form the trophic and structural foundation of coral reef ecosystems, and have played a key role in the evolutionary radiation and biodiversity of cnidarian species. Despite the prevalence of these symbioses, we still know very little about the molecular modulators that initiate, regulate, and maintain the interaction between these two different biological entities. In this study, we conducted a comparative host anemone transcriptome analysis using a cDNA microarray platform to identify genes involved in cnidarian-algal symbiosis.', 'We detected statistically significant differences in host gene expression profiles between sea anemones (Anthopleura elegantissima) in a symbiotic and non-symbiotic state. The group of genes, whose expression is altered, is diverse, suggesting that the molecular regulation of the symbiosis is governed by changes in multiple cellular processes. In the context of cnidarian-dinoflagellate symbioses, we discuss pivotal host gene expression changes involved in lipid metabolism, cell adhesion, cell proliferation, apoptosis, and oxidative stress.'] Does transcriptome analysis of a cnidarian-dinoflagellate mutualism reveal complex modulation of host gene expression?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Cnidarian-dinoflagellate intracellular symbioses are one of the most important mutualisms in the marine environment. They form the trophic and structural foundation of coral reef ecosystems, and have played a key role in the evolutionary radiation and biodiversity of cnidarian species. Despite the prevalence of these symbioses, we still know very little about the molecular modulators that initiate, regulate, and maintain the interaction between these two different biological entities. In this study, we conducted a comparative host anemone transcriptome analysis using a cDNA microarray platform to identify genes involved in cnidarian-algal symbiosis.', 'We detected statistically significant differences in host gene expression profiles between sea anemones (Anthopleura elegantissima) in a symbiotic and non-symbiotic state. The group of genes, whose expression is altered, is diverse, suggesting that the molecular regulation of the symbiosis is governed by changes in multiple cellular processes. In the context of cnidarian-dinoflagellate symbioses, we discuss pivotal host gene expression changes involved in lipid metabolism, cell adhesion, cell proliferation, apoptosis, and oxidative stress.'] Does transcriptome analysis of a cnidarian-dinoflagellate mutualism reveal complex modulation of host gene expression? OUTPUT:
PubmedQA115399
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['We sought to determine torso injury rates and sensitivities associated with fluid-positive abdominal ultrasound, metabolic acidosis (increased base deficit and lactate), and impaired pulmonary physiology (decreased spirometric volume and PaO2/FiO2).', 'Level I trauma center prospective pilot and post-pilot study (2000-2001) of stable patients. Increased base deficit was < 0.0 in ethanol-negative and < or = -3.0 in ethanol-positive patients. Increased lactate was > 2.5 mmol/L in ethanol-negative and > or = 3.0 mmol/L in ethanol-positive patients. Decreased PaO2/FiO2 was < 350 and decreased spirometric volume was < 1.8 L.', 'Of 215 patients, 66 (30.7%) had a torso injury (abdominal/pelvic injury n = 35 and/or thoracic injury n = 43). Glasgow Coma Scale score was 14.8 +/- 0.5 (13-15). Torso injury rates and sensitivities were: abdominal ultrasound negative and normal base deficit, lactate, PaO2/FiO2, and spirometric volume--0.0% & 0.0%; normal base deficit and normal spirometric volume--4.2% & 4.5%; chest/abdominal soft tissue injury--37.8% & 47.0%; increased lactate--39.7% & 47.0%; increased base deficit--41.3% & 75.8%; increased base deficit and/or decreased spirometric volume--43.8% & 95.5%; decreased PaO2/FiO2--48.9% & 33.3%; positive abdominal ultrasound--62.5% & 7.6%; decreased spirometric volume--73.4% & 71.2%; increased base deficit and decreased spirometric volume--82.9% & 51.5%.'] Do emergency department spirometric volume and base deficit delineate risk for torso injury in stable patients?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['We sought to determine torso injury rates and sensitivities associated with fluid-positive abdominal ultrasound, metabolic acidosis (increased base deficit and lactate), and impaired pulmonary physiology (decreased spirometric volume and PaO2/FiO2).', 'Level I trauma center prospective pilot and post-pilot study (2000-2001) of stable patients. Increased base deficit was < 0.0 in ethanol-negative and < or = -3.0 in ethanol-positive patients. Increased lactate was > 2.5 mmol/L in ethanol-negative and > or = 3.0 mmol/L in ethanol-positive patients. Decreased PaO2/FiO2 was < 350 and decreased spirometric volume was < 1.8 L.', 'Of 215 patients, 66 (30.7%) had a torso injury (abdominal/pelvic injury n = 35 and/or thoracic injury n = 43). Glasgow Coma Scale score was 14.8 +/- 0.5 (13-15). Torso injury rates and sensitivities were: abdominal ultrasound negative and normal base deficit, lactate, PaO2/FiO2, and spirometric volume--0.0% & 0.0%; normal base deficit and normal spirometric volume--4.2% & 4.5%; chest/abdominal soft tissue injury--37.8% & 47.0%; increased lactate--39.7% & 47.0%; increased base deficit--41.3% & 75.8%; increased base deficit and/or decreased spirometric volume--43.8% & 95.5%; decreased PaO2/FiO2--48.9% & 33.3%; positive abdominal ultrasound--62.5% & 7.6%; decreased spirometric volume--73.4% & 71.2%; increased base deficit and decreased spirometric volume--82.9% & 51.5%.'] Do emergency department spirometric volume and base deficit delineate risk for torso injury in stable patients? OUTPUT:
PubmedQA169123
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Although fragmented QRS complex (frag-QRS) reflecting intra-ventricular conduction delay has been shown to be a prognostic marker for cardiac events, few data exist regarding the impact of frag-QRS on cardiac events in hypertrophic cardiomyopathy (HCM).', \"Ninety-four HCM patients (56 male; mean age, 58 ± 17 years) were retrospectively investigated. Frag-QRS was defined as the presence of various RsR' patterns in at least 2 contiguous ECG leads. Major arrhythmic events (MAE) were defined as sudden cardiac death, and combined sustained ventricular tachycardia/ventricular fibrillation. New-onset atrial fibrillation (AF) was diagnosed based on ECG during provisional or routine medical examination. Heart failure (HF) with hospitalization was defined as hospital admission due to subjective or objective symptoms. Frag-QRS was detected in 31 patients (33%).TNNI3 was the most frequent disease-causing gene. Median follow-up was 4.6 years. The 4-year cumulative survival rates of cardiac death, MAE, new-onset AF and HF with hospitalization were 97.6%, 94.6%, 87.5% and 89.3%, respectively. On multivariate analysis, frag-QRS was significantly associated with HF with hospitalization (adjusted hazard ratios [95% confidence intervals]: 5.4 [1.2-36], P=0.03). Moreover, HF-free survival was significantly lower in the frag-QRS (+) group compared to the frag-QRS (-) group (79.0% vs. 95.1%, P=0.03).\"] Does fragmented QRS predict heart failure progression in patients with hypertrophic cardiomyopathy?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Although fragmented QRS complex (frag-QRS) reflecting intra-ventricular conduction delay has been shown to be a prognostic marker for cardiac events, few data exist regarding the impact of frag-QRS on cardiac events in hypertrophic cardiomyopathy (HCM).', "Ninety-four HCM patients (56 male; mean age, 58 ± 17 years) were retrospectively investigated. Frag-QRS was defined as the presence of various RsR' patterns in at least 2 contiguous ECG leads. Major arrhythmic events (MAE) were defined as sudden cardiac death, and combined sustained ventricular tachycardia/ventricular fibrillation. New-onset atrial fibrillation (AF) was diagnosed based on ECG during provisional or routine medical examination. Heart failure (HF) with hospitalization was defined as hospital admission due to subjective or objective symptoms. Frag-QRS was detected in 31 patients (33%).TNNI3 was the most frequent disease-causing gene. Median follow-up was 4.6 years. The 4-year cumulative survival rates of cardiac death, MAE, new-onset AF and HF with hospitalization were 97.6%, 94.6%, 87.5% and 89.3%, respectively. On multivariate analysis, frag-QRS was significantly associated with HF with hospitalization (adjusted hazard ratios [95% confidence intervals]: 5.4 [1.2-36], P=0.03). Moreover, HF-free survival was significantly lower in the frag-QRS (+) group compared to the frag-QRS (-) group (79.0% vs. 95.1%, P=0.03)."] Does fragmented QRS predict heart failure progression in patients with hypertrophic cardiomyopathy? OUTPUT:
PubmedQA130973
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Almost all Helicobacter pylori infected person develop gastritis and severe gastritis is supposed to be the denominator of peptic ulcer diseases, which may lead to gastric cancer. However, it is still an enigma why few strains are associated with ulcer formation, while others are not related with any disease outcome. Although a number of putative virulence factors have been reported for H. pylori, there are contradictory results regarding their connotation with diseases. Recently, there has been a significant attention in strain-specific genes outside the cag pathogenicity island, especially genes within plasticity regions. Studies demonstrated that certain genes in this region may play important roles in the pathogenesis of H. pylori-associated diseases. The aim of this study was to assess the role of selected genes (jhp0940, jhp0945, jhp0947 and jhp0949) in the plasticity region in relation to risk of H. pylori-related diseases in Indian population.', 'A total of 113 H. pylori strains isolated from duodenal ulcer (DU) (n\\xa0=\\xa061) and non-ulcer dyspepsia (NUD) subjects (n\\xa0=\\xa052) were screened by PCR and Dot-Blot to determine the presence of these genes. The comparative study of IL-8 production and apoptosis were also done by co-culturing the AGS cells with H. pylori strains of different genotype.', 'PCR and Dot-Blot results indicated that the prevalence rates of jhp0940, jhp0945, jhp0947 and jhp0949 in the H. pylori strains were 9.8, 47.5, 50.8, 40.9 % and 17.3, 28.8, 26.9, 19.2\\xa0% isolated from DU and NUD, respectively. IL-8 production and apoptotic cell death were significantly higher in H. pylori strains containing jhp0945, jhp0947 and jhp0949 than the strains lacking those genes. Results indicated that the prevalence of jhp0945, jhp0947 and jhp0949 are associated with increased risk of severe diseases in India.'] Are helicobacter pylori plasticity region genes associated with the gastroduodenal diseases manifestation in India?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Almost all Helicobacter pylori infected person develop gastritis and severe gastritis is supposed to be the denominator of peptic ulcer diseases, which may lead to gastric cancer. However, it is still an enigma why few strains are associated with ulcer formation, while others are not related with any disease outcome. Although a number of putative virulence factors have been reported for H. pylori, there are contradictory results regarding their connotation with diseases. Recently, there has been a significant attention in strain-specific genes outside the cag pathogenicity island, especially genes within plasticity regions. Studies demonstrated that certain genes in this region may play important roles in the pathogenesis of H. pylori-associated diseases. The aim of this study was to assess the role of selected genes (jhp0940, jhp0945, jhp0947 and jhp0949) in the plasticity region in relation to risk of H. pylori-related diseases in Indian population.', 'A total of 113 H. pylori strains isolated from duodenal ulcer (DU) (n\xa0=\xa061) and non-ulcer dyspepsia (NUD) subjects (n\xa0=\xa052) were screened by PCR and Dot-Blot to determine the presence of these genes. The comparative study of IL-8 production and apoptosis were also done by co-culturing the AGS cells with H. pylori strains of different genotype.', 'PCR and Dot-Blot results indicated that the prevalence rates of jhp0940, jhp0945, jhp0947 and jhp0949 in the H. pylori strains were 9.8, 47.5, 50.8, 40.9 % and 17.3, 28.8, 26.9, 19.2\xa0% isolated from DU and NUD, respectively. IL-8 production and apoptotic cell death were significantly higher in H. pylori strains containing jhp0945, jhp0947 and jhp0949 than the strains lacking those genes. Results indicated that the prevalence of jhp0945, jhp0947 and jhp0949 are associated with increased risk of severe diseases in India.'] Are helicobacter pylori plasticity region genes associated with the gastroduodenal diseases manifestation in India? OUTPUT:
PubmedQA75036
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Left ventricular abnormalities contribute to cardiovascular disease in patients with chronic kidney disease and may be detected by measurement of B-type natriuretic peptide in serum.', 'In a prospective cohort study of predialysis patients, patients who were on dialysis, and kidney transplant recipients, serum was collected and assayed for both B-type natriuretic peptide and its N-terminal fragment. Median levels were compared using nonparametric tests, and predictors of B-type natriuretic peptide were determined by linear regression. Survival analysis and Cox regression were performed to examine the association of levels of B-type natriuretic peptide with cardiovascular events and death.', 'Levels of B-type natriuretic peptide were highest in patients who were on dialysis. Patients who were receiving dialysis and had known cardiovascular disease, were not on the waiting list for kidney transplantation, or had left ventricular systolic dysfunction on echocardiography had significantly higher levels of B-type natriuretic peptide than patients without these characteristics. Glomerular filtration rate was an important predictor of B-type natriuretic peptide levels for patients who were not on dialysis (predialysis and renal transplant recipients). Left ventricular systolic dysfunction predicted B-type natriuretic peptide levels in patients who were on dialysis. Both forms of B-type natriuretic peptide were associated with a two- to three-fold increased risk for death in patients who were on dialysis.'] Do b-type natriuretic peptides strongly predict mortality in patients who are treated with long-term dialysis?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Left ventricular abnormalities contribute to cardiovascular disease in patients with chronic kidney disease and may be detected by measurement of B-type natriuretic peptide in serum.', 'In a prospective cohort study of predialysis patients, patients who were on dialysis, and kidney transplant recipients, serum was collected and assayed for both B-type natriuretic peptide and its N-terminal fragment. Median levels were compared using nonparametric tests, and predictors of B-type natriuretic peptide were determined by linear regression. Survival analysis and Cox regression were performed to examine the association of levels of B-type natriuretic peptide with cardiovascular events and death.', 'Levels of B-type natriuretic peptide were highest in patients who were on dialysis. Patients who were receiving dialysis and had known cardiovascular disease, were not on the waiting list for kidney transplantation, or had left ventricular systolic dysfunction on echocardiography had significantly higher levels of B-type natriuretic peptide than patients without these characteristics. Glomerular filtration rate was an important predictor of B-type natriuretic peptide levels for patients who were not on dialysis (predialysis and renal transplant recipients). Left ventricular systolic dysfunction predicted B-type natriuretic peptide levels in patients who were on dialysis. Both forms of B-type natriuretic peptide were associated with a two- to three-fold increased risk for death in patients who were on dialysis.'] Do b-type natriuretic peptides strongly predict mortality in patients who are treated with long-term dialysis? OUTPUT:
PubmedQA114294
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Cholecystokinin, a satiety hormone, acts on cholecystokinin A receptor on vagal afferent neurons that project to the nucleus tractus solitarius, resulting in inhibition of feeding. Cholecystokinin is known to be released by electroacupuncture stimulation at certain body sites which elicits profound psychophysiological responses. Our previous study has revealed the involvement of cholecystokinin and cholecystokinin A receptor in the electroacupuncture stimulation-induced modulation of feeding. The aim of the present study was to examine whether electroacupuncture stimulation at the acupuncture point ST36 (Joksamni) activates the nucleus tractus solitarius neurons and whether such effect is mediated by cholecystokinin A receptor.', 'Using an immunofluorescent analysis of Fos, a neuronal activation marker, we compared the Fos immunoreactivity of the nucleus tractus solitarius among three groups of Sprague-Dawley rats: (1) control (48 hour fasting + saline pre-treatment + no electroacupuncture stimulation); (2) SalEA (48 hour fasting + saline pre-treatment + ST36 electroacupuncture stimulation); (3) LorEA (48 hour fasting + pre-treatment of cholecystokinin A receptor antagonist, lorglumide + ST36 electroacupuncture stimulation).', 'ST36 electroacupuncture stimulation significantly reduced 30 minute food intake (p<0.05, SalEA versus control) and increased Fos expression in the nucleus tractus solitarius (p<0.01, SalEA versus control). The effects of electroacupuncture on food intake and Fos were blocked by a lorglumide pre-treatment (p>0.05, LorEA versus control).'] Does electroacupuncture induce Fos expression in the nucleus tractus solitarius via cholecystokinin A receptor signaling in rats?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Cholecystokinin, a satiety hormone, acts on cholecystokinin A receptor on vagal afferent neurons that project to the nucleus tractus solitarius, resulting in inhibition of feeding. Cholecystokinin is known to be released by electroacupuncture stimulation at certain body sites which elicits profound psychophysiological responses. Our previous study has revealed the involvement of cholecystokinin and cholecystokinin A receptor in the electroacupuncture stimulation-induced modulation of feeding. The aim of the present study was to examine whether electroacupuncture stimulation at the acupuncture point ST36 (Joksamni) activates the nucleus tractus solitarius neurons and whether such effect is mediated by cholecystokinin A receptor.', 'Using an immunofluorescent analysis of Fos, a neuronal activation marker, we compared the Fos immunoreactivity of the nucleus tractus solitarius among three groups of Sprague-Dawley rats: (1) control (48 hour fasting + saline pre-treatment + no electroacupuncture stimulation); (2) SalEA (48 hour fasting + saline pre-treatment + ST36 electroacupuncture stimulation); (3) LorEA (48 hour fasting + pre-treatment of cholecystokinin A receptor antagonist, lorglumide + ST36 electroacupuncture stimulation).', 'ST36 electroacupuncture stimulation significantly reduced 30 minute food intake (p<0.05, SalEA versus control) and increased Fos expression in the nucleus tractus solitarius (p<0.01, SalEA versus control). The effects of electroacupuncture on food intake and Fos were blocked by a lorglumide pre-treatment (p>0.05, LorEA versus control).'] Does electroacupuncture induce Fos expression in the nucleus tractus solitarius via cholecystokinin A receptor signaling in rats? OUTPUT:
PubmedQA53980
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['To determine whether Yaktrax Walker (YW), a nonmedical gait-stabilizing device, prevents outdoor falls and injurious falls in fall-prone older people during the winter.', 'Prospective, randomized, interventional trial.', 'Community-based, northern United States, winter, outdoors.', 'Ambulatory, community-dwelling, fall-prone people aged 65 and older.', 'Participants were randomized to wear YW or their usual winter footwear (UWF) outdoors during the winter of 2003/2004.', 'The number of indoor and outdoor slips, falls, and injurious falls was recorded daily in a fall diary. Winter footwear satisfaction survey was completed after study completion.', 'One hundred nine subjects completed 10,724 diary days. Mean age was 74.2. There were 93 indoor slips, 13 indoor falls, 714 outdoor slips, and 62 outdoor falls. The tendency for both groups to slip/fall indoors was comparable. The relative risk (RR) of outdoor slip for YW was 0.50 (P<.04) for all diary days and 0.61 (P=.14) when only days walked on snow and ice was the exposure variable. The RR of outdoor fall for YW was 0.42 (P<.03) when only days walked on snow and ice was the exposure variable. RR of injurious falls per day walked on snow and ice for YW was 0.13 (P<.02). Twelve of 19 outdoor falls occurred when YW subjects were not wearing their assigned device. No serious injury or fracture occurred in either group. The number needed to treat for the YW to prevent one nonserious injurious fall in one winter was six.'] Does a simple gait-stabilizing device reduce outdoor falls and nonserious injurious falls in fall-prone older people during the winter?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['To determine whether Yaktrax Walker (YW), a nonmedical gait-stabilizing device, prevents outdoor falls and injurious falls in fall-prone older people during the winter.', 'Prospective, randomized, interventional trial.', 'Community-based, northern United States, winter, outdoors.', 'Ambulatory, community-dwelling, fall-prone people aged 65 and older.', 'Participants were randomized to wear YW or their usual winter footwear (UWF) outdoors during the winter of 2003/2004.', 'The number of indoor and outdoor slips, falls, and injurious falls was recorded daily in a fall diary. Winter footwear satisfaction survey was completed after study completion.', 'One hundred nine subjects completed 10,724 diary days. Mean age was 74.2. There were 93 indoor slips, 13 indoor falls, 714 outdoor slips, and 62 outdoor falls. The tendency for both groups to slip/fall indoors was comparable. The relative risk (RR) of outdoor slip for YW was 0.50 (P<.04) for all diary days and 0.61 (P=.14) when only days walked on snow and ice was the exposure variable. The RR of outdoor fall for YW was 0.42 (P<.03) when only days walked on snow and ice was the exposure variable. RR of injurious falls per day walked on snow and ice for YW was 0.13 (P<.02). Twelve of 19 outdoor falls occurred when YW subjects were not wearing their assigned device. No serious injury or fracture occurred in either group. The number needed to treat for the YW to prevent one nonserious injurious fall in one winter was six.'] Does a simple gait-stabilizing device reduce outdoor falls and nonserious injurious falls in fall-prone older people during the winter? OUTPUT:
PubmedQA27007
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Distinct sets of corticosteroid-unresponsive genes modulate disease severity in asthma.', 'To identify corticosteroid-unresponsive genes that provide new insights into disease pathogenesis and asthma therapeutics.', 'Experimental murine asthma was induced by nasal administration of house dust mite for 5 days per week. Dexamethasone and apolipoprotein E (apo E) mimetic peptides were administered via osmotic minipumps.', 'Genome-wide expression profiling of the lung transcriptome in a house dust mite-induced model of murine asthma identified increases in apo E mRNA levels that persisted despite corticosteroid treatment. House dust mite-challenged apo E⁻(/)⁻ mice displayed enhanced airway hyperreactivity and goblet cell hyperplasia, which could be rescued by administration of an apo E(130-149) mimetic peptide. Administration of the apo E(130-149) mimetic peptide to house dust mite-challenged apo E⁻(/)⁻ mice also inhibited eosinophilic airway inflammation, IgE production, and the expression of Th2 and Th17 cytokines. House dust mite-challenged low-density lipoprotein receptor (LDLR) knockout mice displayed a similar phenotype as apo E⁻(/)⁻ mice with enhanced airway hyperreactivity, goblet cell hyperplasia, and mucin gene expression, but could not be rescued by the apo E(130-149) mimetic peptide, consistent with a LDLR-dependent mechanism.'] Does apolipoprotein E negatively regulate house dust mite-induced asthma via a low-density lipoprotein receptor-mediated pathway?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Distinct sets of corticosteroid-unresponsive genes modulate disease severity in asthma.', 'To identify corticosteroid-unresponsive genes that provide new insights into disease pathogenesis and asthma therapeutics.', 'Experimental murine asthma was induced by nasal administration of house dust mite for 5 days per week. Dexamethasone and apolipoprotein E (apo E) mimetic peptides were administered via osmotic minipumps.', 'Genome-wide expression profiling of the lung transcriptome in a house dust mite-induced model of murine asthma identified increases in apo E mRNA levels that persisted despite corticosteroid treatment. House dust mite-challenged apo E⁻(/)⁻ mice displayed enhanced airway hyperreactivity and goblet cell hyperplasia, which could be rescued by administration of an apo E(130-149) mimetic peptide. Administration of the apo E(130-149) mimetic peptide to house dust mite-challenged apo E⁻(/)⁻ mice also inhibited eosinophilic airway inflammation, IgE production, and the expression of Th2 and Th17 cytokines. House dust mite-challenged low-density lipoprotein receptor (LDLR) knockout mice displayed a similar phenotype as apo E⁻(/)⁻ mice with enhanced airway hyperreactivity, goblet cell hyperplasia, and mucin gene expression, but could not be rescued by the apo E(130-149) mimetic peptide, consistent with a LDLR-dependent mechanism.'] Does apolipoprotein E negatively regulate house dust mite-induced asthma via a low-density lipoprotein receptor-mediated pathway? OUTPUT:
PubmedQA200133
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['High serum triglyceride (TG) levels is an established risk factor for coronary heart disease (CHD). Fat is stored in the form of TGs in human adipose tissue. We hypothesized that gene co-expression networks in human adipose tissue may be correlated with serum TG levels and help reveal novel genes involved in TG regulation.', \"Gene co-expression networks were constructed from two Finnish and one Mexican study sample using the blockwiseModules R function in Weighted Gene Co-expression Network Analysis (WGCNA). Overlap between TG-associated networks from each of the three study samples were calculated using a Fisher's Exact test. Gene ontology was used to determine known pathways enriched in each TG-associated network.\", 'We measured gene expression in adipose samples from two Finnish and one Mexican study sample. In each study sample, we observed a gene co-expression network that was significantly associated with serum TG levels. The TG modules observed in Finns and Mexicans significantly overlapped and shared 34 genes. Seven of the 34 genes (ARHGAP30, CCR1, CXCL16, FERMT3, HCST, RNASET2, SELPG) were identified as the key hub genes of all three TG modules. Furthermore, two of the 34 genes (ARHGAP9, LST1) reside in previous TG GWAS regions, suggesting them as the regional candidates underlying the GWAS signals.'] Do adipose co-expression networks across Finns and Mexicans identify novel triglyceride-associated genes?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['High serum triglyceride (TG) levels is an established risk factor for coronary heart disease (CHD). Fat is stored in the form of TGs in human adipose tissue. We hypothesized that gene co-expression networks in human adipose tissue may be correlated with serum TG levels and help reveal novel genes involved in TG regulation.', "Gene co-expression networks were constructed from two Finnish and one Mexican study sample using the blockwiseModules R function in Weighted Gene Co-expression Network Analysis (WGCNA). Overlap between TG-associated networks from each of the three study samples were calculated using a Fisher's Exact test. Gene ontology was used to determine known pathways enriched in each TG-associated network.", 'We measured gene expression in adipose samples from two Finnish and one Mexican study sample. In each study sample, we observed a gene co-expression network that was significantly associated with serum TG levels. The TG modules observed in Finns and Mexicans significantly overlapped and shared 34 genes. Seven of the 34 genes (ARHGAP30, CCR1, CXCL16, FERMT3, HCST, RNASET2, SELPG) were identified as the key hub genes of all three TG modules. Furthermore, two of the 34 genes (ARHGAP9, LST1) reside in previous TG GWAS regions, suggesting them as the regional candidates underlying the GWAS signals.'] Do adipose co-expression networks across Finns and Mexicans identify novel triglyceride-associated genes? OUTPUT:
PubmedQA209712
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Investigation of the environmental influences on human behavioral phenotypes is important for our understanding of the causation of psychiatric disorders. However, there are complexities associated with the assessment of environmental influences on behavior.', 'We conducted a series of analyses using a prospective, longitudinal study of a nationally representative birth cohort from Finland (the Northern Finland 1966 Birth Cohort). Participants included a total of 3,761 male and female cohort members who were living in Finland at the age of 16 years and who had complete temperament scores. Our initial analyses (Wessman et al., in press) provide evidence in support of four stable and robust temperament clusters. Using these temperament clusters, as well as independent temperament dimensions for comparison, we conducted a data-driven analysis to assess the influence of a broad set of life course measures, assessed pre-natally, in infancy, and during adolescence, on adult temperament.', \"Measures of early environment, neurobehavioral development, and adolescent behavior significantly predict adult temperament, classified by both cluster membership and temperament dimensions. Specifically, our results suggest that a relatively consistent set of life course measures are associated with adult temperament profiles, including maternal education, characteristics of the family's location and residence, adolescent academic performance, and adolescent smoking.\"] Do early environment and neurobehavioral development predict adult temperament clusters?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Investigation of the environmental influences on human behavioral phenotypes is important for our understanding of the causation of psychiatric disorders. However, there are complexities associated with the assessment of environmental influences on behavior.', 'We conducted a series of analyses using a prospective, longitudinal study of a nationally representative birth cohort from Finland (the Northern Finland 1966 Birth Cohort). Participants included a total of 3,761 male and female cohort members who were living in Finland at the age of 16 years and who had complete temperament scores. Our initial analyses (Wessman et al., in press) provide evidence in support of four stable and robust temperament clusters. Using these temperament clusters, as well as independent temperament dimensions for comparison, we conducted a data-driven analysis to assess the influence of a broad set of life course measures, assessed pre-natally, in infancy, and during adolescence, on adult temperament.', "Measures of early environment, neurobehavioral development, and adolescent behavior significantly predict adult temperament, classified by both cluster membership and temperament dimensions. Specifically, our results suggest that a relatively consistent set of life course measures are associated with adult temperament profiles, including maternal education, characteristics of the family's location and residence, adolescent academic performance, and adolescent smoking."] Do early environment and neurobehavioral development predict adult temperament clusters? OUTPUT:
PubmedQA167990
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['To investigate the effect of a new infant formula supplemented with a low level (0.24 g/100 mL) of galacto-oligosaccharide (GOS) on intestinal micro-flora (Bifidobacteria, Lactobacilli and E. coli) and fermentation characteristics in term infants, compared with human milk and a standard infant formula without GOS.', 'Term infants (n = 371) were approached in this study in three hospitals of China. All infants started breast-feeding. Those who changed to formula-feeding within 4 wk after birth were randomly assigned to one of the two formula groups. Growth and stool characteristics, and side effects that occurred in recruited infants were recorded in a 3-mo follow-up period. Fecal samples were collected from a subpopulation of recruited infants for analysis of intestinal bacteria (culture technique), acetic acid (gas chromatography) and pH (indicator strip).', 'After 3 mo, the intestinal Bifidobacteria, Lactobacilli, acetic acid and stool frequency were significantly increased, and fecal pH was decreased in infants fed with the GOS-formula or human milk, compared with those fed with the formula without GOS. No significant differences were observed between the GOS formula and human milk groups. Supplementation with GOS did not influence the incidence of crying, regurgitation and vomiting.'] Does low level of galacto-oligosaccharide in infant formula stimulate growth of intestinal Bifidobacteria and Lactobacilli?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['To investigate the effect of a new infant formula supplemented with a low level (0.24 g/100 mL) of galacto-oligosaccharide (GOS) on intestinal micro-flora (Bifidobacteria, Lactobacilli and E. coli) and fermentation characteristics in term infants, compared with human milk and a standard infant formula without GOS.', 'Term infants (n = 371) were approached in this study in three hospitals of China. All infants started breast-feeding. Those who changed to formula-feeding within 4 wk after birth were randomly assigned to one of the two formula groups. Growth and stool characteristics, and side effects that occurred in recruited infants were recorded in a 3-mo follow-up period. Fecal samples were collected from a subpopulation of recruited infants for analysis of intestinal bacteria (culture technique), acetic acid (gas chromatography) and pH (indicator strip).', 'After 3 mo, the intestinal Bifidobacteria, Lactobacilli, acetic acid and stool frequency were significantly increased, and fecal pH was decreased in infants fed with the GOS-formula or human milk, compared with those fed with the formula without GOS. No significant differences were observed between the GOS formula and human milk groups. Supplementation with GOS did not influence the incidence of crying, regurgitation and vomiting.'] Does low level of galacto-oligosaccharide in infant formula stimulate growth of intestinal Bifidobacteria and Lactobacilli? OUTPUT:
PubmedQA193064
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['The frequency of benign stenosis in ulcerative colitis (UC) is low, reported as being 3.2-11.2%, with fibrosis in the submucosa or deeper pointed out as one of the causes. The aim of the present study was to assess stenosis in UC cases using immunostaining and to analyze differences between stenotic and nonstenotic cases, focusing on basic-fibroblast growth factor (b-FGF) expression and myofibroblasts.', 'Totals of 9 stenotic and 17 nonstenotic UC cases were histopathologically examined and immunohistochemically stained for b-FGF, α-smooth muscle actin (α-SMA), CD34, CD68 and IL-6. To identify b-FGF-positive cells, double immunostaining for b-FGF and myeloperoxidase or CD68 was performed.', 'In addition to submucosal fibrosis, a significant increase of b-FGF-positive inflammatory cells and myofibroblasts was observed in stenotic portions. Most b-FGF-positive cells were also positive for myeloperoxidase, and a correlation between b-FGF-positive and total neutrophil counts was found.'] Do submucosal fibrosis and basic-fibroblast growth factor-positive neutrophils correlate with colonic stenosis in cases of ulcerative colitis?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['The frequency of benign stenosis in ulcerative colitis (UC) is low, reported as being 3.2-11.2%, with fibrosis in the submucosa or deeper pointed out as one of the causes. The aim of the present study was to assess stenosis in UC cases using immunostaining and to analyze differences between stenotic and nonstenotic cases, focusing on basic-fibroblast growth factor (b-FGF) expression and myofibroblasts.', 'Totals of 9 stenotic and 17 nonstenotic UC cases were histopathologically examined and immunohistochemically stained for b-FGF, α-smooth muscle actin (α-SMA), CD34, CD68 and IL-6. To identify b-FGF-positive cells, double immunostaining for b-FGF and myeloperoxidase or CD68 was performed.', 'In addition to submucosal fibrosis, a significant increase of b-FGF-positive inflammatory cells and myofibroblasts was observed in stenotic portions. Most b-FGF-positive cells were also positive for myeloperoxidase, and a correlation between b-FGF-positive and total neutrophil counts was found.'] Do submucosal fibrosis and basic-fibroblast growth factor-positive neutrophils correlate with colonic stenosis in cases of ulcerative colitis? OUTPUT:
PubmedQA114639
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['The purpose of this study was to determine the incidence and origin of T-wave changes after ablation of an accessory atrioventricular connection (AC), which could either be a sign of damage to the coronary circulation or a result of persistent abnormal repolarization secondary to previously abnormal ventricular activation (\"cardiac memory\").', 'Ninety of 107 consecutive patients (33 women and 57 men, mean age 36 +/- 5 years) undergoing successful catheter ablation of an AC were studied. Patients with bundle branch block or more than 1 AC were excluded. Sixty-four patients had manifest preexcitation (group 1) and 26 had a concealed AC (group 2). Immediately after loss of preexcitation, 38 (59%) patients with a manifest AC showed T-wave abnormalities. In contrast, none of the patients with a concealed AC had T-wave abnormalities after ablation (P <.05). The T-wave changes (1) did not correlate with the number or duration of energy applications or with markers of tissue injury; (2) correlated with the location of the AC and the degree of preexcitation, respectively; and (3) completely resolved over a period of weeks to months. None of the patients had recurrence of preexcitation or tachycardia during a mean follow-up of 16 +/- 7 months.'] Are persistent T-wave changes after radiofrequency catheter ablation of an accessory connection ( Wolff-parkinson-white syndrome ) caused by `` cardiac memory ''?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['The purpose of this study was to determine the incidence and origin of T-wave changes after ablation of an accessory atrioventricular connection (AC), which could either be a sign of damage to the coronary circulation or a result of persistent abnormal repolarization secondary to previously abnormal ventricular activation ("cardiac memory").', 'Ninety of 107 consecutive patients (33 women and 57 men, mean age 36 +/- 5 years) undergoing successful catheter ablation of an AC were studied. Patients with bundle branch block or more than 1 AC were excluded. Sixty-four patients had manifest preexcitation (group 1) and 26 had a concealed AC (group 2). Immediately after loss of preexcitation, 38 (59%) patients with a manifest AC showed T-wave abnormalities. In contrast, none of the patients with a concealed AC had T-wave abnormalities after ablation (P <.05). The T-wave changes (1) did not correlate with the number or duration of energy applications or with markers of tissue injury; (2) correlated with the location of the AC and the degree of preexcitation, respectively; and (3) completely resolved over a period of weeks to months. None of the patients had recurrence of preexcitation or tachycardia during a mean follow-up of 16 +/- 7 months.'] Are persistent T-wave changes after radiofrequency catheter ablation of an accessory connection ( Wolff-parkinson-white syndrome ) caused by `` cardiac memory ''? OUTPUT:
PubmedQA117678
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Observational studies have shown that glycated haemoglobin (HbA(1c)) is related to mortality, but the shape of the association is less clear. Furthermore, disease duration and medication may modify this association. This observational study explored the association between HbA(1c) measured in stored erythrocytes and mortality. Secondly, it was assessed whether disease duration and medication use influenced the estimates or were independently associated with mortality.', 'Within the European Prospective Investigation into Cancer and Nutrition a cohort was analysed of 4,345 individuals with a confirmed diagnosis of diabetes at enrolment. HbA(1c) was measured in blood samples stored up to 19 years. Multivariable Cox proportional hazard regression models for all-cause mortality investigated HbA(1c) in quartiles as well as per 1% increment, diabetes medication in seven categories of insulin and oral hypoglycaemic agents, and disease duration in quartiles.', 'After a median follow-up of 9.3 years, 460 participants died. Higher HbA(1c) was associated with higher mortality: Hazard Ratio for 1%-increase was 1.11 (95% CI 1.06, 1.17). This association was linear (P-nonlinearity = 0.15) and persistent across categories of medication use, disease duration, and co-morbidities. Compared with metformin, other medication types were not associated with mortality. Longer disease duration was associated with mortality, but not after adjustment for HbA(1c) and medication.'] Is hbA1c measured in stored erythrocytes positively linearly associated with mortality in individuals with diabetes mellitus?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Observational studies have shown that glycated haemoglobin (HbA(1c)) is related to mortality, but the shape of the association is less clear. Furthermore, disease duration and medication may modify this association. This observational study explored the association between HbA(1c) measured in stored erythrocytes and mortality. Secondly, it was assessed whether disease duration and medication use influenced the estimates or were independently associated with mortality.', 'Within the European Prospective Investigation into Cancer and Nutrition a cohort was analysed of 4,345 individuals with a confirmed diagnosis of diabetes at enrolment. HbA(1c) was measured in blood samples stored up to 19 years. Multivariable Cox proportional hazard regression models for all-cause mortality investigated HbA(1c) in quartiles as well as per 1% increment, diabetes medication in seven categories of insulin and oral hypoglycaemic agents, and disease duration in quartiles.', 'After a median follow-up of 9.3 years, 460 participants died. Higher HbA(1c) was associated with higher mortality: Hazard Ratio for 1%-increase was 1.11 (95% CI 1.06, 1.17). This association was linear (P-nonlinearity = 0.15) and persistent across categories of medication use, disease duration, and co-morbidities. Compared with metformin, other medication types were not associated with mortality. Longer disease duration was associated with mortality, but not after adjustment for HbA(1c) and medication.'] Is hbA1c measured in stored erythrocytes positively linearly associated with mortality in individuals with diabetes mellitus? OUTPUT:
PubmedQA28897
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Large granular lymphocyte leukemia (LGL) is a clonal lymphoproliferative disease of CD8+ T cells expressing the CD57 activation marker. It is, however, unknown whether the CD57+ population represents the LGL clone or not. We previously demonstrated that the clone can be found in both CD8+CD57+ and CD8+CD57- cells, indicating that the LGL clone also resides in the CD57- fraction.', 'Here, we quantified the extent of the clonal CD8 expansion in LGL using T-cell receptor Vbeta (TCRBV)-specific monoclonal antibodies, and determined whether the CD4 population also contained skews. Furthermore, dominant TCRBV populations were assessed for clonal status using T-cell receptor-gamma (TCRG) PCR on genomic DNA.', 'We show that the dominant TCRBV in LGL contains CD57+ and CD57- cells. Molecular analysis of CD8+CD57+ and CD8+CD57- subfractions of the dominant TCRBV by TCRG PCR demonstrates that indeed both fractions are clonal, and that the clone is absent from the dominant TCRBV-negative population. Furthermore, we show that CD57 overexpression is not restricted to the LGL clone, but a general phenomenon in CD8 cells of LGL patients.'] Is t-cell large granular lymphocyte leukemia characterized by massive TCRBV-restricted clonal CD8 expansion and a generalized overexpression of the effector cell marker CD57?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Large granular lymphocyte leukemia (LGL) is a clonal lymphoproliferative disease of CD8+ T cells expressing the CD57 activation marker. It is, however, unknown whether the CD57+ population represents the LGL clone or not. We previously demonstrated that the clone can be found in both CD8+CD57+ and CD8+CD57- cells, indicating that the LGL clone also resides in the CD57- fraction.', 'Here, we quantified the extent of the clonal CD8 expansion in LGL using T-cell receptor Vbeta (TCRBV)-specific monoclonal antibodies, and determined whether the CD4 population also contained skews. Furthermore, dominant TCRBV populations were assessed for clonal status using T-cell receptor-gamma (TCRG) PCR on genomic DNA.', 'We show that the dominant TCRBV in LGL contains CD57+ and CD57- cells. Molecular analysis of CD8+CD57+ and CD8+CD57- subfractions of the dominant TCRBV by TCRG PCR demonstrates that indeed both fractions are clonal, and that the clone is absent from the dominant TCRBV-negative population. Furthermore, we show that CD57 overexpression is not restricted to the LGL clone, but a general phenomenon in CD8 cells of LGL patients.'] Is t-cell large granular lymphocyte leukemia characterized by massive TCRBV-restricted clonal CD8 expansion and a generalized overexpression of the effector cell marker CD57? OUTPUT:
PubmedQA110945
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['The glycoprotein erythropoietin (EPO) has been shown to be protective in models of neuronal disease and reduced apoptosis of retinal ganglion cells (RGC) after transection of the optic nerve and in glaucoma. In this study we assessed in vivo the properties of EPO on survival of RGC after ischemia and optic nerve compression, as well as on postischemic visual function. Furthermore, the safety of intravitreal injection was assessed.', 'In all experiments, EPO was administered intravitreally in male Brown Norway rats. Ocular ischemia was induced by elevating the intraocular pressure for 55 min. The calibrated optic nerve compression was performed for 10 s. RGC were marked stereotactically and quantified by fluorescence microscopy. The retinal function was quantified by electroretinography (ERG) and the whole visual pathway by visual evoked potential (VEP).', 'EPO (2 and 20 units per eye, n=9-21) increased the survival of RGC after ischemia by 21+/-21% and 127+/-31% (mean +/- SEM) and after optic nerve compression by 28+/-12% and 58+/-13%. With EPO (20 units), postischemic function was increased, in ERG by 71+/-13% (a-wave) and 75+/-19% (b-wave) and in VEP by 264+/-65% (p=0.053). Neither the ERG parameters, nor the VEP, nor the number of RGC differed significantly after intravitreal injection of EPO (5, 50, and 200 units, n=6-7) in healthy eyes.'] Does [ Erythropoietin protect retinal ganglion cells and visual function after ocular ischemia and optic nerve compression ]?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['The glycoprotein erythropoietin (EPO) has been shown to be protective in models of neuronal disease and reduced apoptosis of retinal ganglion cells (RGC) after transection of the optic nerve and in glaucoma. In this study we assessed in vivo the properties of EPO on survival of RGC after ischemia and optic nerve compression, as well as on postischemic visual function. Furthermore, the safety of intravitreal injection was assessed.', 'In all experiments, EPO was administered intravitreally in male Brown Norway rats. Ocular ischemia was induced by elevating the intraocular pressure for 55 min. The calibrated optic nerve compression was performed for 10 s. RGC were marked stereotactically and quantified by fluorescence microscopy. The retinal function was quantified by electroretinography (ERG) and the whole visual pathway by visual evoked potential (VEP).', 'EPO (2 and 20 units per eye, n=9-21) increased the survival of RGC after ischemia by 21+/-21% and 127+/-31% (mean +/- SEM) and after optic nerve compression by 28+/-12% and 58+/-13%. With EPO (20 units), postischemic function was increased, in ERG by 71+/-13% (a-wave) and 75+/-19% (b-wave) and in VEP by 264+/-65% (p=0.053). Neither the ERG parameters, nor the VEP, nor the number of RGC differed significantly after intravitreal injection of EPO (5, 50, and 200 units, n=6-7) in healthy eyes.'] Does [ Erythropoietin protect retinal ganglion cells and visual function after ocular ischemia and optic nerve compression ]? OUTPUT:
PubmedQA194812
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Recent findings indicate that platelets not only regulate thrombosis and hemostasis but may also be involved in proinflammatory activities. Herein, we hypothesized that platelets may play a role in sepsis by activating and priming circulating neutrophils for subsequent recruitment into the lung.', 'Prospective experimental study.', 'University Hospital Research Unit.', 'Male C57BL/6 mice.', 'Lung edema, bronchoalveolar infiltration of neutrophils, levels of myeloperoxidase, expression and function of membrane-activated complex-1 (Mac-1) on neutrophils and the CXC chemokines, macrophage inflammatory protein-2, and cytokine-induced neutrophil chemoattractant were determined after cecal ligation and puncture (CLP). Mice received a platelet-depleting antibody as well as antibodies directed against P-selectin glycoprotein-ligand-1 and Mac-1 before CLP induction.', 'CLP caused significant pulmonary damage characterized by neutrophil infiltration, increased levels of CXC chemokines, and edema formation in the lung. Furthermore, CLP up-regulated Mac-1 expression on neutrophils and increased the number of neutrophils binding platelets in the circulation. Interestingly, depletion of platelets reduced CLP-induced edema and neutrophil recruitment in the bronchoalveolar space by >60%. Furthermore, depletion of platelets reduced Mac-1 expression on neutrophils. On the other hand, inhibition of P-selectin glycoprotein-ligand-1 abolished CLP-induced neutrophil-platelet aggregation but had no effect on neutrophil expression of Mac-1.'] Do platelets support pulmonary recruitment of neutrophils in abdominal sepsis?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Recent findings indicate that platelets not only regulate thrombosis and hemostasis but may also be involved in proinflammatory activities. Herein, we hypothesized that platelets may play a role in sepsis by activating and priming circulating neutrophils for subsequent recruitment into the lung.', 'Prospective experimental study.', 'University Hospital Research Unit.', 'Male C57BL/6 mice.', 'Lung edema, bronchoalveolar infiltration of neutrophils, levels of myeloperoxidase, expression and function of membrane-activated complex-1 (Mac-1) on neutrophils and the CXC chemokines, macrophage inflammatory protein-2, and cytokine-induced neutrophil chemoattractant were determined after cecal ligation and puncture (CLP). Mice received a platelet-depleting antibody as well as antibodies directed against P-selectin glycoprotein-ligand-1 and Mac-1 before CLP induction.', 'CLP caused significant pulmonary damage characterized by neutrophil infiltration, increased levels of CXC chemokines, and edema formation in the lung. Furthermore, CLP up-regulated Mac-1 expression on neutrophils and increased the number of neutrophils binding platelets in the circulation. Interestingly, depletion of platelets reduced CLP-induced edema and neutrophil recruitment in the bronchoalveolar space by >60%. Furthermore, depletion of platelets reduced Mac-1 expression on neutrophils. On the other hand, inhibition of P-selectin glycoprotein-ligand-1 abolished CLP-induced neutrophil-platelet aggregation but had no effect on neutrophil expression of Mac-1.'] Do platelets support pulmonary recruitment of neutrophils in abdominal sepsis? OUTPUT:
PubmedQA199883
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Highly integrated anatomic and functional interactions between the cerebrum and the cerebellum during development have been reported. In our previous study, we conducted a proteome analysis to identify the proteins present in the congenital noncommunicating hydrocephalus in the cerebellum. We found higher expression of high-mobility group box-1 protein (HMGB-1) in hydrocephalic H-Tx rats.', 'We studied the expression pattern of HMGB-1 in the cerebellum.', 'We studied congenital hydrocephalic H-Tx rats aged 1 day and 7 days along with age-matched nonhydrocephalic H-Tx and Sprague-Dawley rats as controls. Gene and protein expressions of HMGB-1 in the cerebellum were assayed by real-time polymerase chain reaction and Western blotting, respectively; furthermore, immunohistochemical analyses were performed by using HMGB-1 (indicator of apoptosis), single-stranded DNA; adhesion factor related to cell migration, HNK-1; and the Purkinje cell-specific antibody, calbindin.', 'Cytoplasmic HMGB-1 expression observed in Purkinje cells in the 1-day-old hydrocephalic group was stronger than that in the nonhydrocephalic and Sprague-Dawley groups. Double fluorescent staining with single-stranded DNA confirmed that Purkinje cells were undergoing apoptosis. HNK-1 expression was lower in the Purkinje cell layer in the 7-day-old rats in the hydrocephalic group, and Purkinje cells were disrupted in comparison with the control groups. Morphological changes in the cerebellum were observed in the 7-day-old rats in the hydrocephalic group in comparison with the control groups.'] Do cerebellar Purkinje cells exhibit increased expression of HMGB-1 and apoptosis in congenital hydrocephalic H-Tx rats?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Highly integrated anatomic and functional interactions between the cerebrum and the cerebellum during development have been reported. In our previous study, we conducted a proteome analysis to identify the proteins present in the congenital noncommunicating hydrocephalus in the cerebellum. We found higher expression of high-mobility group box-1 protein (HMGB-1) in hydrocephalic H-Tx rats.', 'We studied the expression pattern of HMGB-1 in the cerebellum.', 'We studied congenital hydrocephalic H-Tx rats aged 1 day and 7 days along with age-matched nonhydrocephalic H-Tx and Sprague-Dawley rats as controls. Gene and protein expressions of HMGB-1 in the cerebellum were assayed by real-time polymerase chain reaction and Western blotting, respectively; furthermore, immunohistochemical analyses were performed by using HMGB-1 (indicator of apoptosis), single-stranded DNA; adhesion factor related to cell migration, HNK-1; and the Purkinje cell-specific antibody, calbindin.', 'Cytoplasmic HMGB-1 expression observed in Purkinje cells in the 1-day-old hydrocephalic group was stronger than that in the nonhydrocephalic and Sprague-Dawley groups. Double fluorescent staining with single-stranded DNA confirmed that Purkinje cells were undergoing apoptosis. HNK-1 expression was lower in the Purkinje cell layer in the 7-day-old rats in the hydrocephalic group, and Purkinje cells were disrupted in comparison with the control groups. Morphological changes in the cerebellum were observed in the 7-day-old rats in the hydrocephalic group in comparison with the control groups.'] Do cerebellar Purkinje cells exhibit increased expression of HMGB-1 and apoptosis in congenital hydrocephalic H-Tx rats? OUTPUT:
PubmedQA180930
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['The aim of this study was to determine whether chronic intermittent hypoxia (CIH) could affect the secretion of adipokines, such as resistin, leptin, and adiponectin, in non-obese rats and to investigate the potential mechanisms.', 'An established rodent model of CIH was utilized, in which rats were exposed to varying oxygen levels (7-21 %) respectively over a period of 5 weeks. The area under the curve (AUCG) and the insulin resistance index (homeostasis model of assessment for insulin resistance index, HOMA-IR) were calculated. The levels of several secretory factors in the blood were measured by enzyme-linked immunosorbent assay (ELISA). The mRNA levels and protein expression in adipose tissues was measured by reverse transcription-polymerase chain reaction (RT-PCR).', 'Glucose tolerance and the levels of adiponectin in non-obese rats were decreased in the CIH group both in the serum and adipose tissue compared with the controls, while the insulin resistance index and the levels of resistin and leptin were increased. Moreover, the expressions of hypoxia inducible factor-1α and lactate dehydrogenase A were significantly higher in chronic intermittent hypoxia rats than in control rats, suggesting the presence of adipose tissue hypoxia.'] Does chronic intermittent hypoxia lead to insulin resistance and impaired glucose tolerance through dysregulation of adipokines in non-obese rats?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['The aim of this study was to determine whether chronic intermittent hypoxia (CIH) could affect the secretion of adipokines, such as resistin, leptin, and adiponectin, in non-obese rats and to investigate the potential mechanisms.', 'An established rodent model of CIH was utilized, in which rats were exposed to varying oxygen levels (7-21 %) respectively over a period of 5 weeks. The area under the curve (AUCG) and the insulin resistance index (homeostasis model of assessment for insulin resistance index, HOMA-IR) were calculated. The levels of several secretory factors in the blood were measured by enzyme-linked immunosorbent assay (ELISA). The mRNA levels and protein expression in adipose tissues was measured by reverse transcription-polymerase chain reaction (RT-PCR).', 'Glucose tolerance and the levels of adiponectin in non-obese rats were decreased in the CIH group both in the serum and adipose tissue compared with the controls, while the insulin resistance index and the levels of resistin and leptin were increased. Moreover, the expressions of hypoxia inducible factor-1α and lactate dehydrogenase A were significantly higher in chronic intermittent hypoxia rats than in control rats, suggesting the presence of adipose tissue hypoxia.'] Does chronic intermittent hypoxia lead to insulin resistance and impaired glucose tolerance through dysregulation of adipokines in non-obese rats? OUTPUT:
PubmedQA188716
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: [\"in 2007, the National Patient Safety Agency (NPSA) published 'Slips trips and falls in hospital' and 'Using bedrails safely and effectively'.\", 'this observational study aimed to identify changes in local policies in hospitals in England and Wales following these publications.', 'policies in place during 2006 and 2009 were requested from 50 randomly selected acute hospital trusts and their content was categorised by a single reviewer using defined criteria.', 'thirty-seven trusts responded. Trusts with an inpatient falls prevention policy increased from 65 to 100%, the use of unreferenced numerical falls risk assessments reduced from 50 to 19%, and trusts with a bedrail policy increased from 49 to 89%. It was concerning to find that by 2009 advice on clinical checks after a fall was available in only 51% of trusts, and only 46% of trust policies included specific guidance on avoiding bedrail entrapment gaps.'] Does changes in fall prevention policies in hospital in England and Wales?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ["in 2007, the National Patient Safety Agency (NPSA) published 'Slips trips and falls in hospital' and 'Using bedrails safely and effectively'.", 'this observational study aimed to identify changes in local policies in hospitals in England and Wales following these publications.', 'policies in place during 2006 and 2009 were requested from 50 randomly selected acute hospital trusts and their content was categorised by a single reviewer using defined criteria.', 'thirty-seven trusts responded. Trusts with an inpatient falls prevention policy increased from 65 to 100%, the use of unreferenced numerical falls risk assessments reduced from 50 to 19%, and trusts with a bedrail policy increased from 49 to 89%. It was concerning to find that by 2009 advice on clinical checks after a fall was available in only 51% of trusts, and only 46% of trust policies included specific guidance on avoiding bedrail entrapment gaps.'] Does changes in fall prevention policies in hospital in England and Wales? OUTPUT:
PubmedQA98981
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['To establish whether germination of Botrytis cinerea was affected by the symbiosis of Bacillus subtilis L-form bacteria with Chinese cabbage.', 'Germinating seeds of Chinese cabbage were co-cultivated with either L-forms of Bacillus subtilis or 5% (w/v) mannitol by soaking for 3 h. Seeds were then washed in sterile water, sown on a minimal medium and incubated in controlled conditions. L-form symbiosis was detected over a time course by ELISA. Conidial germination of Botrytis cinerea was significantly reduced on cotyledonous leaves of L-form-treated plants compared with controls.'] Does the symbiosis of Bacillus subtilis L-forms with Chinese cabbage seedlings inhibit conidial germination of Botrytis cinerea?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['To establish whether germination of Botrytis cinerea was affected by the symbiosis of Bacillus subtilis L-form bacteria with Chinese cabbage.', 'Germinating seeds of Chinese cabbage were co-cultivated with either L-forms of Bacillus subtilis or 5% (w/v) mannitol by soaking for 3 h. Seeds were then washed in sterile water, sown on a minimal medium and incubated in controlled conditions. L-form symbiosis was detected over a time course by ELISA. Conidial germination of Botrytis cinerea was significantly reduced on cotyledonous leaves of L-form-treated plants compared with controls.'] Does the symbiosis of Bacillus subtilis L-forms with Chinese cabbage seedlings inhibit conidial germination of Botrytis cinerea? OUTPUT:
PubmedQA61587
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Previous studies indicate that an inability to fully extend the elbow after elbow trauma is indicative of fracture. We hypothesized that maintenance of active range of motion (ROM) of the elbow in flexion, extension, pronation, and supination after elbow trauma is very specific for the absence of fracture or effusion, and limitation of ROM is sensitive for fracture or effusion.', 'This was a prospective observational study with convenience sampling of a carefully selected patient population. This would allow certain types of patients to be excluded from the study. Patients with elbow injury receiving radiographs and meeting enrollment criteria were enrolled between June 2006 and March 2007 at 4 emergency departments in the local region. Demographics, active ROM, and presence of point tenderness at the olecranon, epicondyles, and radial head were recorded by enrolling clinicians. All enrolled patients received standard elbow radiographs. Radiographs were reviewed by blinded radiologists for the presence of fracture and effusion. Sensitivity, specificity, and 95% confidence intervals (CIs) of examination findings were calculated.', 'One hundred thirteen patients were enrolled. Limitation of active ROM was 100% (95% CI, 0.93-1.00) sensitive for fracture or effusion. Preservation of active ROM was 97% (95% CI, 0.89-1.00) specific for the absence of fracture. Point tenderness was also highly sensitive but not specific.'] Does preservation of active range of motion after acute elbow trauma predict absence of elbow fracture?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Previous studies indicate that an inability to fully extend the elbow after elbow trauma is indicative of fracture. We hypothesized that maintenance of active range of motion (ROM) of the elbow in flexion, extension, pronation, and supination after elbow trauma is very specific for the absence of fracture or effusion, and limitation of ROM is sensitive for fracture or effusion.', 'This was a prospective observational study with convenience sampling of a carefully selected patient population. This would allow certain types of patients to be excluded from the study. Patients with elbow injury receiving radiographs and meeting enrollment criteria were enrolled between June 2006 and March 2007 at 4 emergency departments in the local region. Demographics, active ROM, and presence of point tenderness at the olecranon, epicondyles, and radial head were recorded by enrolling clinicians. All enrolled patients received standard elbow radiographs. Radiographs were reviewed by blinded radiologists for the presence of fracture and effusion. Sensitivity, specificity, and 95% confidence intervals (CIs) of examination findings were calculated.', 'One hundred thirteen patients were enrolled. Limitation of active ROM was 100% (95% CI, 0.93-1.00) sensitive for fracture or effusion. Preservation of active ROM was 97% (95% CI, 0.89-1.00) specific for the absence of fracture. Point tenderness was also highly sensitive but not specific.'] Does preservation of active range of motion after acute elbow trauma predict absence of elbow fracture? OUTPUT:
PubmedQA86967
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['To investigate the effect of curcumin on tumor growth and angiogenesis of human gliomas and identify the underlying molecular mechanisms.', 'A mouse xenograft glioma model was established by subcutaneously inoculating tumor cell aggregates derived from the U87 cell line. Mice were treated with 0.01ml/g body weight of curcumin or saline. Tumor volume was measured. Microvessel density was assessed by CD34 immunostaining, and angiogenesis by immunohistochemical staining of vascular endothelial growth factor (VEGF), angiopoietin-2 (Ang-2) and thrombospondin 1 (TSP-1).', 'At 28 days after treatment, tumor weights in the curcumin-treated group were much smaller than in the control group (0.23±0.11g vs 0.44±0.15g,p<0.05), resulting in a 45.8% inhibition of tumor growth. Curcumin also markedly inhibited microvessel density. Expression of VEGF and Ang-2 was inhibited by curcumin, whereas TSP-1 expression was up-regulated.'] Does curcumin suppress tumor growth and angiogenesis in human glioma cells through modulation of vascular endothelial growth factor/angiopoietin-2/thrombospondin-1 signaling?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['To investigate the effect of curcumin on tumor growth and angiogenesis of human gliomas and identify the underlying molecular mechanisms.', 'A mouse xenograft glioma model was established by subcutaneously inoculating tumor cell aggregates derived from the U87 cell line. Mice were treated with 0.01ml/g body weight of curcumin or saline. Tumor volume was measured. Microvessel density was assessed by CD34 immunostaining, and angiogenesis by immunohistochemical staining of vascular endothelial growth factor (VEGF), angiopoietin-2 (Ang-2) and thrombospondin 1 (TSP-1).', 'At 28 days after treatment, tumor weights in the curcumin-treated group were much smaller than in the control group (0.23±0.11g vs 0.44±0.15g,p<0.05), resulting in a 45.8% inhibition of tumor growth. Curcumin also markedly inhibited microvessel density. Expression of VEGF and Ang-2 was inhibited by curcumin, whereas TSP-1 expression was up-regulated.'] Does curcumin suppress tumor growth and angiogenesis in human glioma cells through modulation of vascular endothelial growth factor/angiopoietin-2/thrombospondin-1 signaling? OUTPUT:
PubmedQA78358
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['In the present study, MRI has been used to investigate therapeutic intervention with statins in a model of permanent focal cerebral ischemia in rat.', 'Brain ischemia was induced in rats by the permanent occlusion of middle cerebral artery (MCAO) and the brain infarct size followed up in alive animals 2, 24, and 48 hours after MCAO, using the trace of apparent diffusion coefficient [Tr(D)] maps and T2-weighted images. In vehicle-treated rats, the infarct volumes increased by 38.5% and 89% after 24 and 48 hours, respectively, compared with the damage detected at 2 hours after MCAO. Treatment with simvastatin (20 mg/kg) after MCAO prevented the increase in brain infarct volume occurring at 24 hours and induced a 46.6% reduction after 48 hours. This effect was similar to that observed when simvastatin was administered before the induction of focal ischemia. T2W-MRI images confirmed these findings. The neuroprotective effects of simvastatin were paralleled by an increase in endothelial NO synthase immunoreactivity, detectable in the brain of simvastatin-treated rats.'] Does treatment with statins after induction of focal ischemia in rats reduce the extent of brain damage?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['In the present study, MRI has been used to investigate therapeutic intervention with statins in a model of permanent focal cerebral ischemia in rat.', 'Brain ischemia was induced in rats by the permanent occlusion of middle cerebral artery (MCAO) and the brain infarct size followed up in alive animals 2, 24, and 48 hours after MCAO, using the trace of apparent diffusion coefficient [Tr(D)] maps and T2-weighted images. In vehicle-treated rats, the infarct volumes increased by 38.5% and 89% after 24 and 48 hours, respectively, compared with the damage detected at 2 hours after MCAO. Treatment with simvastatin (20 mg/kg) after MCAO prevented the increase in brain infarct volume occurring at 24 hours and induced a 46.6% reduction after 48 hours. This effect was similar to that observed when simvastatin was administered before the induction of focal ischemia. T2W-MRI images confirmed these findings. The neuroprotective effects of simvastatin were paralleled by an increase in endothelial NO synthase immunoreactivity, detectable in the brain of simvastatin-treated rats.'] Does treatment with statins after induction of focal ischemia in rats reduce the extent of brain damage? OUTPUT:
PubmedQA164938
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Death receptors (DRs) induce intracellular signalling upon engagement of their cognate ligands, leading to apoptosis, cell survival or pro-inflammatory responses. In mammals, DR signalling is mediated by the recruitment of several DD (death domain)-containing molecules, such as FADD (Fas-associated DD) and RIP1 (receptor-interacting protein 1).', 'To elucidate the molecular mechanisms of intracellular DR signalling in Xenopus, we have isolated cDNAs encoding xFADD (Xenopus FADD), and xRIP1 and its short isoform xRIP1beta, which is produced by alternative splicing of the xRIP1 gene. These DD-containing proteins interacted with Xenopus DR members xDR-M1 and xDR-M2 through their DDs in co-transfected HEK-293T cells. Overexpression of xFADD activated not only xCaspase 8, but also AP-1 (activator protein 1), which reflects activation of JNK (c-Jun N-terminal kinase) and NF-kappaB (nuclear factor kappaB). A comparative analysis of xRIP1, a kinase-dead mutant of xRIP1 and xRIP1beta indicated that the kinase activity of xRIP1 was required for the activation of AP-1 and NF-kappaB. Interestingly, xFADD and xRIP1 interacted with each other via their DDs, and the expression of a mutant xRIP1 containing only the DD (xRIP1-DD) repressed the xFADD-induced activation of NF-kappaB and AP-1. xFADD and xRIP1 synergistically induced the activation of AP-1 and NF-kappaB, both of which were partially mediated by TRAF2 (tumour-necrosis-factor-receptor-associated factor 2) and TAK1 (transforming-growth-factor-beta-activated kinase 1). We also found that the activation pathways of NF-kappaB induced by xDR-M2 were inhibited by xRIP1-DD.'] Do xenopus death-domain-containing proteins FADD and RIP1 synergistically activate JNK and NF-kappaB?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Death receptors (DRs) induce intracellular signalling upon engagement of their cognate ligands, leading to apoptosis, cell survival or pro-inflammatory responses. In mammals, DR signalling is mediated by the recruitment of several DD (death domain)-containing molecules, such as FADD (Fas-associated DD) and RIP1 (receptor-interacting protein 1).', 'To elucidate the molecular mechanisms of intracellular DR signalling in Xenopus, we have isolated cDNAs encoding xFADD (Xenopus FADD), and xRIP1 and its short isoform xRIP1beta, which is produced by alternative splicing of the xRIP1 gene. These DD-containing proteins interacted with Xenopus DR members xDR-M1 and xDR-M2 through their DDs in co-transfected HEK-293T cells. Overexpression of xFADD activated not only xCaspase 8, but also AP-1 (activator protein 1), which reflects activation of JNK (c-Jun N-terminal kinase) and NF-kappaB (nuclear factor kappaB). A comparative analysis of xRIP1, a kinase-dead mutant of xRIP1 and xRIP1beta indicated that the kinase activity of xRIP1 was required for the activation of AP-1 and NF-kappaB. Interestingly, xFADD and xRIP1 interacted with each other via their DDs, and the expression of a mutant xRIP1 containing only the DD (xRIP1-DD) repressed the xFADD-induced activation of NF-kappaB and AP-1. xFADD and xRIP1 synergistically induced the activation of AP-1 and NF-kappaB, both of which were partially mediated by TRAF2 (tumour-necrosis-factor-receptor-associated factor 2) and TAK1 (transforming-growth-factor-beta-activated kinase 1). We also found that the activation pathways of NF-kappaB induced by xDR-M2 were inhibited by xRIP1-DD.'] Do xenopus death-domain-containing proteins FADD and RIP1 synergistically activate JNK and NF-kappaB? OUTPUT:
PubmedQA135099
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['To study the effects of metabolic syndrome on prostate α-adrenergic contractile function using fructose-fed rats (FR).', 'Age-matched male Wistar rats were divided into two groups: group I, normal control rats; and group II, 9-week FR. Animal body weight, blood pressure and serum metabolic parameters were monitored. The prostate was removed 9 weeks after induction of metabolic syndrome in the FR. The contractile responses of prostatic strips to phenylephrine (10(-7) to 10(-6) M) and KCl (50 mM) were tested. Prostate α1 -adrenoceptor (α1 -AR) protein expression was studied by Western blotting analysis with a polyclonal antiserum.', 'At week 9, the FR showed significant increases in body weight, blood pressure, plasma glucose, insulin and triglyceride levels. The FR prostate weight was significantly higher than that of the controls (610.5 ± 13.2 vs 422.3 ± 7.7 mg, P < 0.05 for n = 8). FR prostate contractile responses to phenylephrine and KCl were both significantly increased. Interestingly, prostate α1 -AR protein expression level was lower in the FR. However, after in vitro 10(-6) M phenylephrine stimulation, FR prostate α1 -AR protein expression was significantly increased.'] Does metabolic Syndrome enhance Prostate Contractility and In Vitro Phenylephrine-induced α1 -Adrenoceptor Protein Expression in the Fructose-fed Rat?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['To study the effects of metabolic syndrome on prostate α-adrenergic contractile function using fructose-fed rats (FR).', 'Age-matched male Wistar rats were divided into two groups: group I, normal control rats; and group II, 9-week FR. Animal body weight, blood pressure and serum metabolic parameters were monitored. The prostate was removed 9 weeks after induction of metabolic syndrome in the FR. The contractile responses of prostatic strips to phenylephrine (10(-7) to 10(-6) M) and KCl (50 mM) were tested. Prostate α1 -adrenoceptor (α1 -AR) protein expression was studied by Western blotting analysis with a polyclonal antiserum.', 'At week 9, the FR showed significant increases in body weight, blood pressure, plasma glucose, insulin and triglyceride levels. The FR prostate weight was significantly higher than that of the controls (610.5 ± 13.2 vs 422.3 ± 7.7 mg, P < 0.05 for n = 8). FR prostate contractile responses to phenylephrine and KCl were both significantly increased. Interestingly, prostate α1 -AR protein expression level was lower in the FR. However, after in vitro 10(-6) M phenylephrine stimulation, FR prostate α1 -AR protein expression was significantly increased.'] Does metabolic Syndrome enhance Prostate Contractility and In Vitro Phenylephrine-induced α1 -Adrenoceptor Protein Expression in the Fructose-fed Rat? OUTPUT:
PubmedQA205192
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['To determine the association between lowest plasma magnesium concentration and brain metabolism, and whether magnetic resonance imaging brain injury patterns moderated the association in hypoxic-ischemic encephalopathy.', 'In 131 early (day-of-life 3) and 65 late (day-of-life 10) scans of term encephalopathic infants born between 2004 and 2012, we examined the association of lowest plasma magnesium (until day-of-life 3) on basal ganglia and white matter peak metabolite ratios on magnetic resonance spectroscopy independent of covariates, stratified by the predominant patterns of injury (normal, basal nuclei/total, watershed, multifocal) using multiple linear regression.', 'Lowest plasma magnesium was associated with lower white matter N-acetyl-aspartate/choline in the multifocal pattern on early scan (regression-coefficient, β: 0.13; 95% CI: 0.04, 0.22) and in the basal nuclei/total pattern on late scan (β: 0.08; 95% CI: 0.02, 0.15), and was negatively associated with basal ganglia lactate/N-acetyl-aspartate (β: -0.16; 95% CI: -0.05, -0.28) and lactate/choline (β: -0.1; 95% CI: -0.03, -0.17) ratio in the basal nuclei/total pattern on late scan independent of hypomagnesaemia correction, cooling and postmenstrual age at scan. Lowest plasma magnesium was not associated with metabolite ratios in other brain injury patterns.'] Is low plasma magnesium associated with impaired brain metabolism in neonates with hypoxic-ischaemic encephalopathy?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['To determine the association between lowest plasma magnesium concentration and brain metabolism, and whether magnetic resonance imaging brain injury patterns moderated the association in hypoxic-ischemic encephalopathy.', 'In 131 early (day-of-life 3) and 65 late (day-of-life 10) scans of term encephalopathic infants born between 2004 and 2012, we examined the association of lowest plasma magnesium (until day-of-life 3) on basal ganglia and white matter peak metabolite ratios on magnetic resonance spectroscopy independent of covariates, stratified by the predominant patterns of injury (normal, basal nuclei/total, watershed, multifocal) using multiple linear regression.', 'Lowest plasma magnesium was associated with lower white matter N-acetyl-aspartate/choline in the multifocal pattern on early scan (regression-coefficient, β: 0.13; 95% CI: 0.04, 0.22) and in the basal nuclei/total pattern on late scan (β: 0.08; 95% CI: 0.02, 0.15), and was negatively associated with basal ganglia lactate/N-acetyl-aspartate (β: -0.16; 95% CI: -0.05, -0.28) and lactate/choline (β: -0.1; 95% CI: -0.03, -0.17) ratio in the basal nuclei/total pattern on late scan independent of hypomagnesaemia correction, cooling and postmenstrual age at scan. Lowest plasma magnesium was not associated with metabolite ratios in other brain injury patterns.'] Is low plasma magnesium associated with impaired brain metabolism in neonates with hypoxic-ischaemic encephalopathy? OUTPUT:
PubmedQA72722
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Epidemiological studies documented associations between single nucleotide polymorphisms (SNPs) in the nucleotide excision repair gene XPD/ERCC2 and cancer risk. Little is known, however, about the underlying mechanisms for these associations. We explored a novel mechanism that could further explain the reported risk-modifying effect of these SNPs on disease susceptibility.', 'Using quantitative real-time polymerase chain reaction, we examined the relationship between three SNPs in the XPD gene (R156R in exon 6, D312N in exon 10 and K751Q in exon 23) and mRNA levels as a potential mechanism by which these SNPs could alter DNA repair capacity and affect disease risk. To further investigate the mechanism(s) by which these SNPs alter mRNA transcription levels, we performed a localized Mfold structure analysis on the mRNA sequence surrounding the studied SNPs.', 'All three SNPs studied, alone and in combination, significantly decreased constitutive XPD mRNA levels (P<0.003) in lymphocytes of healthy subjects. The decrease in mRNA levels was significantly greater in smokers and was exacerbated by smoking duration and intensity. The decrease was more pronounced in older than in younger subjects. The R156R and the K751Q polymorphisms were predicted to alter mRNA secondary structure, indicating that these SNPs potentially affect local folding and mRNA stability.'] Do single nucleotide polymorphisms of the DNA repair gene XPD/ERCC2 alter mRNA expression?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Epidemiological studies documented associations between single nucleotide polymorphisms (SNPs) in the nucleotide excision repair gene XPD/ERCC2 and cancer risk. Little is known, however, about the underlying mechanisms for these associations. We explored a novel mechanism that could further explain the reported risk-modifying effect of these SNPs on disease susceptibility.', 'Using quantitative real-time polymerase chain reaction, we examined the relationship between three SNPs in the XPD gene (R156R in exon 6, D312N in exon 10 and K751Q in exon 23) and mRNA levels as a potential mechanism by which these SNPs could alter DNA repair capacity and affect disease risk. To further investigate the mechanism(s) by which these SNPs alter mRNA transcription levels, we performed a localized Mfold structure analysis on the mRNA sequence surrounding the studied SNPs.', 'All three SNPs studied, alone and in combination, significantly decreased constitutive XPD mRNA levels (P<0.003) in lymphocytes of healthy subjects. The decrease in mRNA levels was significantly greater in smokers and was exacerbated by smoking duration and intensity. The decrease was more pronounced in older than in younger subjects. The R156R and the K751Q polymorphisms were predicted to alter mRNA secondary structure, indicating that these SNPs potentially affect local folding and mRNA stability.'] Do single nucleotide polymorphisms of the DNA repair gene XPD/ERCC2 alter mRNA expression? OUTPUT:
PubmedQA64844
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Previous studies have implicated stoma formation as an independent factor prolonging length of stay (LOS) after colorectal surgery. We examined whether loop ileostomy (LI) formation during an open anterior resection affected LOS within a newly developed enhanced recovery programme (ERP). This involved reorganization of services, including stoma care, to optimize pre- and perioperative patient education, training and expectation, while applying the standard scientific principles of enhanced recovery.', \"Data were collected prospectively on 72 consecutive open anterior resections (33 with LI) to see whether LI affected LOS. Stomas were fashioned at the surgeon's discretion and patients were discharged according to agreed criteria.\", 'Thirty-three of the 72 patients had a covering LI performed. The overall age range was 32-85 years (median 68), with 40 patients being men. LOS for all 72 patients ranged from 3 to 34 days. The median and mean LOS were the same for both groups (median 6 days, mean 8 days). The complication rate was 44% (32/72) with a leak rate of 7% (5/72) and a mortality of 1.4% (1/72). Between the two groups (no ileostomy vs ileostomy), there was no statistically significant difference in complications (41%vs 48%), leakage (8%vs 6%) and readmission rates (12%vs 5%).'] Does ileostomy formation prolong hospital length of stay after open anterior resection when performed within an enhanced recovery programme?\nOUTPUT:\n" }, { "from": "agent", "value": "no" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Previous studies have implicated stoma formation as an independent factor prolonging length of stay (LOS) after colorectal surgery. We examined whether loop ileostomy (LI) formation during an open anterior resection affected LOS within a newly developed enhanced recovery programme (ERP). This involved reorganization of services, including stoma care, to optimize pre- and perioperative patient education, training and expectation, while applying the standard scientific principles of enhanced recovery.', "Data were collected prospectively on 72 consecutive open anterior resections (33 with LI) to see whether LI affected LOS. Stomas were fashioned at the surgeon's discretion and patients were discharged according to agreed criteria.", 'Thirty-three of the 72 patients had a covering LI performed. The overall age range was 32-85 years (median 68), with 40 patients being men. LOS for all 72 patients ranged from 3 to 34 days. The median and mean LOS were the same for both groups (median 6 days, mean 8 days). The complication rate was 44% (32/72) with a leak rate of 7% (5/72) and a mortality of 1.4% (1/72). Between the two groups (no ileostomy vs ileostomy), there was no statistically significant difference in complications (41%vs 48%), leakage (8%vs 6%) and readmission rates (12%vs 5%).'] Does ileostomy formation prolong hospital length of stay after open anterior resection when performed within an enhanced recovery programme? OUTPUT:
PubmedQA60238
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['This study assesses the mechanisms of apoptosis in patients after on-pump coronary artery bypass graft surgery and the potential involvement of the endogenous cardiac peptide urocortin as a cardiomyocyte salvage mechanism. We have previously described the mechanisms of apoptosis after ischemia-reperfusion injury in the rat heart and shown that endogenous urocortin is cardioprotective. Here we extend these findings to the human heart exposed to ischemic-reperfusion injury.', 'Two sequential biopsy specimens were obtained from the right atriums of 24 patients undergoing coronary artery bypass grafting at the start of grafting and 10 minutes after release of the aortic clamp. Apoptosis was identified by means of immunocytochemical colocalization between terminal deoxynucleotidyl transferase-mediated nick end-labeling positivity and active caspase-3. Immunostaining for active caspase-9 and caspase-8 was performed to identify the pathways of apoptosis induction. Urocortin and adenosine triphosphate-dependent potassium channel expression was also assessed by means of immunocytochemistry.', 'Myocyte apoptosis (<0.1% before coronary artery bypass grafting) was increased after coronary artery bypass grafting and reperfusion and was greater in patients with longer periods of cardioplegic arrest (3.3% +/- 0.5% with <55 minutes and 5.1% +/- 0.9% with 85-100 minutes, P <.001). Processing of caspase-9 was always more pronounced than that of caspase-8 (P <.05). Cardioplegic arrest was also associated with increased urocortin expression (up to 29% +/- 3.5% vs <3% in samples obtained before coronary artery bypass grafting, P <.001) but only in nonapoptotic myocytes. These and surrounding viable myocytes also showed increased Kir6.1 adenosine triphosphate-dependent potassium channel expression.'] Does warm blood cardioplegic arrest induce mitochondrial-mediated cardiomyocyte apoptosis associated with increased urocortin expression in viable cells?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['This study assesses the mechanisms of apoptosis in patients after on-pump coronary artery bypass graft surgery and the potential involvement of the endogenous cardiac peptide urocortin as a cardiomyocyte salvage mechanism. We have previously described the mechanisms of apoptosis after ischemia-reperfusion injury in the rat heart and shown that endogenous urocortin is cardioprotective. Here we extend these findings to the human heart exposed to ischemic-reperfusion injury.', 'Two sequential biopsy specimens were obtained from the right atriums of 24 patients undergoing coronary artery bypass grafting at the start of grafting and 10 minutes after release of the aortic clamp. Apoptosis was identified by means of immunocytochemical colocalization between terminal deoxynucleotidyl transferase-mediated nick end-labeling positivity and active caspase-3. Immunostaining for active caspase-9 and caspase-8 was performed to identify the pathways of apoptosis induction. Urocortin and adenosine triphosphate-dependent potassium channel expression was also assessed by means of immunocytochemistry.', 'Myocyte apoptosis (<0.1% before coronary artery bypass grafting) was increased after coronary artery bypass grafting and reperfusion and was greater in patients with longer periods of cardioplegic arrest (3.3% +/- 0.5% with <55 minutes and 5.1% +/- 0.9% with 85-100 minutes, P <.001). Processing of caspase-9 was always more pronounced than that of caspase-8 (P <.05). Cardioplegic arrest was also associated with increased urocortin expression (up to 29% +/- 3.5% vs <3% in samples obtained before coronary artery bypass grafting, P <.001) but only in nonapoptotic myocytes. These and surrounding viable myocytes also showed increased Kir6.1 adenosine triphosphate-dependent potassium channel expression.'] Does warm blood cardioplegic arrest induce mitochondrial-mediated cardiomyocyte apoptosis associated with increased urocortin expression in viable cells? OUTPUT:
PubmedQA135710
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['To establish the role of prostaglandin E2 (PGE2) formed and released by monocytes and monocyte-derived macrophages (MDM) in the reduced toxoplasmastatic activity of these cells.', 'Determination of PGE2 levels in the serum of AIDS patients, the release of PGE2 by monocytes and MDM from AIDS patients, the toxoplasmastatic activity of these cells and the effect of indomethacin, an inhibitor of PGE2 synthesis, on this cell function.', 'Laboratory of Cellular Immunology of the Department of Infectious Diseases, University Hospital, Leiden.', 'Twenty-six AIDS patients. Healthy blood donors served as controls.', 'The concentration of PGE2 in the serum from AIDS patients was significantly higher compared with serum from controls. Non-stimulated monocytes and lipopolysaccharide-stimulated monocytes and MDM from AIDS patients released significantly more PGE2 than corresponding cells from the controls. The proliferation of Toxoplasma gondii in monocytes and MDM from AIDS patients was significantly higher than in the respective cells from controls. Preincubation of these cells with indomethacin resulted in a decreased proliferation of T. gondii in non-activated monocytes and MDM and in interferon-gamma-activated MDM from AIDS patients. Preincubation of monocytes from healthy donors with PGE2 resulted in a dose-dependent increase of Toxoplasma proliferation which confirms that PGE2 can reduce the toxoplasmastatic activity of monocytes.'] Is reduced toxoplasmastatic activity of monocytes and monocyte-derived macrophages from AIDS patients mediated via prostaglandin E2?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['To establish the role of prostaglandin E2 (PGE2) formed and released by monocytes and monocyte-derived macrophages (MDM) in the reduced toxoplasmastatic activity of these cells.', 'Determination of PGE2 levels in the serum of AIDS patients, the release of PGE2 by monocytes and MDM from AIDS patients, the toxoplasmastatic activity of these cells and the effect of indomethacin, an inhibitor of PGE2 synthesis, on this cell function.', 'Laboratory of Cellular Immunology of the Department of Infectious Diseases, University Hospital, Leiden.', 'Twenty-six AIDS patients. Healthy blood donors served as controls.', 'The concentration of PGE2 in the serum from AIDS patients was significantly higher compared with serum from controls. Non-stimulated monocytes and lipopolysaccharide-stimulated monocytes and MDM from AIDS patients released significantly more PGE2 than corresponding cells from the controls. The proliferation of Toxoplasma gondii in monocytes and MDM from AIDS patients was significantly higher than in the respective cells from controls. Preincubation of these cells with indomethacin resulted in a decreased proliferation of T. gondii in non-activated monocytes and MDM and in interferon-gamma-activated MDM from AIDS patients. Preincubation of monocytes from healthy donors with PGE2 resulted in a dose-dependent increase of Toxoplasma proliferation which confirms that PGE2 can reduce the toxoplasmastatic activity of monocytes.'] Is reduced toxoplasmastatic activity of monocytes and monocyte-derived macrophages from AIDS patients mediated via prostaglandin E2? OUTPUT:
PubmedQA62032
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Iatrogenic semicircular canal (SC) transection during mastoidectomy for chronic otitis media often leads to profound hearing loss. AM-111, an apoptosis inhibitor, has been shown to mitigate hearing loss resulting from a variety of inner ear injuries. The goal of this study was to determine if round window application of AM-111 following SC transection in the presence of Pseudomonas aeruginosa otitis media (PA-OM) may reduce the associated hearing loss.', 'Prospective, randomized, controlled study in an animal model.', 'PA-OM was induced bilaterally in 34 guinea pigs. After 3 days, both bullae were opened and the lateral SC of one ear was transected. AM-111 or vehicle was applied topically to the round window of the ear that had undergone SC transection. Hearing was assessed with auditory brainstem responses.', 'The mean change in hearing thresholds was significantly less in transected ears treated with AM-111 than those receiving vehicle alone when testing with clicks (22.1 dB vs. 35.0 dB; P = .019) and at 4kHz (11.3 dB vs. 40.0 dB; P = .021). A similar trend was shown with 16 kHz tone pips (27.7 dB vs. 41.1 dB; P = .119).'] Does aM-111 prevent hearing loss from semicircular canal injury in otitis media?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Iatrogenic semicircular canal (SC) transection during mastoidectomy for chronic otitis media often leads to profound hearing loss. AM-111, an apoptosis inhibitor, has been shown to mitigate hearing loss resulting from a variety of inner ear injuries. The goal of this study was to determine if round window application of AM-111 following SC transection in the presence of Pseudomonas aeruginosa otitis media (PA-OM) may reduce the associated hearing loss.', 'Prospective, randomized, controlled study in an animal model.', 'PA-OM was induced bilaterally in 34 guinea pigs. After 3 days, both bullae were opened and the lateral SC of one ear was transected. AM-111 or vehicle was applied topically to the round window of the ear that had undergone SC transection. Hearing was assessed with auditory brainstem responses.', 'The mean change in hearing thresholds was significantly less in transected ears treated with AM-111 than those receiving vehicle alone when testing with clicks (22.1 dB vs. 35.0 dB; P = .019) and at 4kHz (11.3 dB vs. 40.0 dB; P = .021). A similar trend was shown with 16 kHz tone pips (27.7 dB vs. 41.1 dB; P = .119).'] Does aM-111 prevent hearing loss from semicircular canal injury in otitis media? OUTPUT:
PubmedQA36663
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['This study sought to assess the differences in coronary flow reserve in patients with and without diabetic retinopathy.', 'Microvascular abnormalities throughout the body and impairment of coronary flow reserve have been described in patients with diabetes mellitus. However, the relation between diabetic retinopathy and coronary microvascular disease has not been investigated.', 'The study included 29 patients with diabetes mellitus (18 with and 11 without diabetic retinopathy) and 15 control patients with chest pain and normal coronary arteries. Diabetic retinopathy was nonproliferative in all 18 patients with this disorder (8 had background, 10 preproliferative retinopathy). Five minutes after injection of 3 mg of isosorbide dinitrate, phasic flow velocities were recorded in the proximal segment of the angiographically normal left anterior descending coronary artery at rest and during hyperemia (0.14 mg/kg body weight per min of adenosine infused intravenously) using a 0.014-in. 15-MHz Doppler guide wire. Coronary blood flow was calculated, and coronary flow reserve was obtained from the hyperemic/baseline flow ratio.', 'Coronary blood flow was significantly lower during hyperemia ([mean +/- SD] 107 +/- 23 and 116 +/- 18 vs. 136 +/- 17 ml/min, respectively) and higher at baseline (58 +/- 16 and 45 +/- 12 vs. 37 +/- 10 ml/min, respectively) in diabetic patients with and without retinopathy than in control subjects (p < 0.05 for both diabetic groups). As a result, coronary flow reserve in both groups of diabetic patients was significantly lower than in control patients (1.9 +/- 0.4 and 2.8 +/- 0.3 vs. 3.3 +/- 0.4, respectively, p < 0.01 for both diabetic groups), and its reduction was greater in patients with than without retinopathy (p < 0.01). Furthermore, in patients with diabetic retinopathy, maximal hyperemic coronary flow (102 +/- 11 vs. 114 +/- 16 ml/min, p < 0.05) and flow reserve (1.6 +/- 0.2 vs. 2.3 +/- 0.2, p < 0.01) were significantly lower in those with preproliferative than background retinopathy.'] Does retinopathy identify marked restriction of coronary flow reserve in patients with diabetes mellitus?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['This study sought to assess the differences in coronary flow reserve in patients with and without diabetic retinopathy.', 'Microvascular abnormalities throughout the body and impairment of coronary flow reserve have been described in patients with diabetes mellitus. However, the relation between diabetic retinopathy and coronary microvascular disease has not been investigated.', 'The study included 29 patients with diabetes mellitus (18 with and 11 without diabetic retinopathy) and 15 control patients with chest pain and normal coronary arteries. Diabetic retinopathy was nonproliferative in all 18 patients with this disorder (8 had background, 10 preproliferative retinopathy). Five minutes after injection of 3 mg of isosorbide dinitrate, phasic flow velocities were recorded in the proximal segment of the angiographically normal left anterior descending coronary artery at rest and during hyperemia (0.14 mg/kg body weight per min of adenosine infused intravenously) using a 0.014-in. 15-MHz Doppler guide wire. Coronary blood flow was calculated, and coronary flow reserve was obtained from the hyperemic/baseline flow ratio.', 'Coronary blood flow was significantly lower during hyperemia ([mean +/- SD] 107 +/- 23 and 116 +/- 18 vs. 136 +/- 17 ml/min, respectively) and higher at baseline (58 +/- 16 and 45 +/- 12 vs. 37 +/- 10 ml/min, respectively) in diabetic patients with and without retinopathy than in control subjects (p < 0.05 for both diabetic groups). As a result, coronary flow reserve in both groups of diabetic patients was significantly lower than in control patients (1.9 +/- 0.4 and 2.8 +/- 0.3 vs. 3.3 +/- 0.4, respectively, p < 0.01 for both diabetic groups), and its reduction was greater in patients with than without retinopathy (p < 0.01). Furthermore, in patients with diabetic retinopathy, maximal hyperemic coronary flow (102 +/- 11 vs. 114 +/- 16 ml/min, p < 0.05) and flow reserve (1.6 +/- 0.2 vs. 2.3 +/- 0.2, p < 0.01) were significantly lower in those with preproliferative than background retinopathy.'] Does retinopathy identify marked restriction of coronary flow reserve in patients with diabetes mellitus? OUTPUT:
PubmedQA192698
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['CXCL10, a member of the CXC chemokine family, is known to mediate chemotaxis, apoptosis, angiogenesis, and cell growth. It is also reportedly involved in tumor development and can affect prognosis in several cancers. However, the precise relationship between CXCL10 and the prognosis of patients with esophageal squamous cell carcinoma (ESCC) is not fully understood.', 'We used ESCC tissue microarrays containing samples from 177 patients to test whether the CXCL10 expression status, determined using immunohistochemical analysis, is predictive of prognosis. We also tested whether CXCL10 expression status could serve as a clinically useful marker for evaluating the need for adjuvant chemotherapy after surgery.', 'We found that high CXCL10 expression in clinical samples was an independent prognostic factor and was predictive of a favorable 5-year overall survival and disease-specific survival (p\\xa0=\\xa00.0102 and 0.0332, respectively). Additionally, no significant difference was detected between patients in the CXCL10-high group treated with surgery alone and those treated with surgery followed by adjuvant chemotherapy. In the CXCL10-low group, on the other hand, patients treated with surgery followed by adjuvant chemotherapy had better 5-year overall survival than those treated with surgery alone.'] Is cXCL10 Expression Status Prognostic in Patients with Advanced Thoracic Esophageal Squamous Cell Carcinoma?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['CXCL10, a member of the CXC chemokine family, is known to mediate chemotaxis, apoptosis, angiogenesis, and cell growth. It is also reportedly involved in tumor development and can affect prognosis in several cancers. However, the precise relationship between CXCL10 and the prognosis of patients with esophageal squamous cell carcinoma (ESCC) is not fully understood.', 'We used ESCC tissue microarrays containing samples from 177 patients to test whether the CXCL10 expression status, determined using immunohistochemical analysis, is predictive of prognosis. We also tested whether CXCL10 expression status could serve as a clinically useful marker for evaluating the need for adjuvant chemotherapy after surgery.', 'We found that high CXCL10 expression in clinical samples was an independent prognostic factor and was predictive of a favorable 5-year overall survival and disease-specific survival (p\xa0=\xa00.0102 and 0.0332, respectively). Additionally, no significant difference was detected between patients in the CXCL10-high group treated with surgery alone and those treated with surgery followed by adjuvant chemotherapy. In the CXCL10-low group, on the other hand, patients treated with surgery followed by adjuvant chemotherapy had better 5-year overall survival than those treated with surgery alone.'] Is cXCL10 Expression Status Prognostic in Patients with Advanced Thoracic Esophageal Squamous Cell Carcinoma? OUTPUT:
PubmedQA111256
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: [\"Recently, we reported that liver Label Retaining Cancer Cells (LRCC) can initiate tumors with only 10 cells and are relatively resistant to the targeted drug Sorafenib, a standard of practice in advanced hepatocellular carcinoma (HCC). LRCC are the only cancer stem cells (CSC) isolated alive according to a stem cell fundamental function, asymmetric cell division. Metformin has been reported to preferentially target many other types of CSC of different organs, including liver. It's important to know if LRCC, a novel class of CSC, are relatively resistant to metformin, unlike other types of CSC. As metformin inhibits the Sorafenib-Target-Protein (STP) PI3K, and LRCC are newly described CSC, we undertook this study to test the effects of Metformin on Sorafenib-treated HCC and HCC-derived-LRCC.\", \"We tested various STP levels and phosphorylation status, associated genes' expression, proliferation, viability, toxicity, and apoptosis profiles, before and after treatment with Sorafenib with/without Metformin.\", 'Metformin enhances the effects of Sorafenib on HCC, and significantly decreased viability/proliferation of HCC cells. This insulin-independent effect was associated with inhibition of multiple STPs (PKC, ERK, JNK and AKT). However, Metformin increased the relative proportion of LRCCs. Comparing LRCC vs. non-LRCC, this effect was associated with improved toxicity and apoptosis profiles, down-regulation of cell death genes and up-regulation of cell proliferation and survival genes in LRCC. Concomitantly, Metformin up-regulated pluripotency, Wnt, Notch and SHH pathways genes in LRCC vs. non-LRCC.'] Do liver Label Retaining Cancer Cells Are Relatively Resistant to the Reported Anti-Cancer Stem Cell Drug Metformin?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ["Recently, we reported that liver Label Retaining Cancer Cells (LRCC) can initiate tumors with only 10 cells and are relatively resistant to the targeted drug Sorafenib, a standard of practice in advanced hepatocellular carcinoma (HCC). LRCC are the only cancer stem cells (CSC) isolated alive according to a stem cell fundamental function, asymmetric cell division. Metformin has been reported to preferentially target many other types of CSC of different organs, including liver. It's important to know if LRCC, a novel class of CSC, are relatively resistant to metformin, unlike other types of CSC. As metformin inhibits the Sorafenib-Target-Protein (STP) PI3K, and LRCC are newly described CSC, we undertook this study to test the effects of Metformin on Sorafenib-treated HCC and HCC-derived-LRCC.", "We tested various STP levels and phosphorylation status, associated genes' expression, proliferation, viability, toxicity, and apoptosis profiles, before and after treatment with Sorafenib with/without Metformin.", 'Metformin enhances the effects of Sorafenib on HCC, and significantly decreased viability/proliferation of HCC cells. This insulin-independent effect was associated with inhibition of multiple STPs (PKC, ERK, JNK and AKT). However, Metformin increased the relative proportion of LRCCs. Comparing LRCC vs. non-LRCC, this effect was associated with improved toxicity and apoptosis profiles, down-regulation of cell death genes and up-regulation of cell proliferation and survival genes in LRCC. Concomitantly, Metformin up-regulated pluripotency, Wnt, Notch and SHH pathways genes in LRCC vs. non-LRCC.'] Do liver Label Retaining Cancer Cells Are Relatively Resistant to the Reported Anti-Cancer Stem Cell Drug Metformin? OUTPUT:
PubmedQA157417
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) exposure prior to chick embryo incubation (GD 0) induces dilated cardiomyopathy, and reduces myocardial hypoxia, vascular endothelial growth factor A (VEGF-A) expression, and coronary vascularization. We investigated whether reduced coronary vascularization 1) occurs in the absence of changes in cardiac morphology and 2) is associated with altered secretion of VEGF-A and/or an antivasculogenic factor.', 'Chicken eggs were treated with control (corn oil) or TCDD (0.075-0.3 pmol of TCDD/gm) on GD 5. In vivo cardiac morphology and artery number were determined on GD 10, while in vitro vascular outgrowth and VEGF-A secretion were determined from cardiac explants on GD 6. Effects of recombinant VEGF-A (rcVEGF-A), soluble flt-1 (sFlt-1) receptor plus rcVEGF-A, and control conditioned media were assessed in TCDD explants, while effects of TCDD-conditioned media was assessed in control explants.', 'TCDD reduced coronary artery number in vivo by 53 +/- 8% and induced a dose-related reduction in tube outgrowth in vitro, but had no effect on cardiac morphology. All TCDD doses reduced explant VEGF-A secretion equally (43 +/- 3%), compared to control. sFlt-1 blocked outgrowth in control cultures and blocked rcVEGF-A-mediated rescue of outgrowth in TCDD explants. Control conditioned media partially rescued outgrowth from TCDD explants, while conditioned media from TCDD explants had no effect on controls.'] Is 2,3,7,8-tetrachlorodibenzo-p-dioxin ( TCDD ) inhibition of coronary vasculogenesis mediated , in part , by reduced responsiveness to endogenous angiogenic stimuli , including vascular endothelial growth factor A ( VEGF-A )?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) exposure prior to chick embryo incubation (GD 0) induces dilated cardiomyopathy, and reduces myocardial hypoxia, vascular endothelial growth factor A (VEGF-A) expression, and coronary vascularization. We investigated whether reduced coronary vascularization 1) occurs in the absence of changes in cardiac morphology and 2) is associated with altered secretion of VEGF-A and/or an antivasculogenic factor.', 'Chicken eggs were treated with control (corn oil) or TCDD (0.075-0.3 pmol of TCDD/gm) on GD 5. In vivo cardiac morphology and artery number were determined on GD 10, while in vitro vascular outgrowth and VEGF-A secretion were determined from cardiac explants on GD 6. Effects of recombinant VEGF-A (rcVEGF-A), soluble flt-1 (sFlt-1) receptor plus rcVEGF-A, and control conditioned media were assessed in TCDD explants, while effects of TCDD-conditioned media was assessed in control explants.', 'TCDD reduced coronary artery number in vivo by 53 +/- 8% and induced a dose-related reduction in tube outgrowth in vitro, but had no effect on cardiac morphology. All TCDD doses reduced explant VEGF-A secretion equally (43 +/- 3%), compared to control. sFlt-1 blocked outgrowth in control cultures and blocked rcVEGF-A-mediated rescue of outgrowth in TCDD explants. Control conditioned media partially rescued outgrowth from TCDD explants, while conditioned media from TCDD explants had no effect on controls.'] Is 2,3,7,8-tetrachlorodibenzo-p-dioxin ( TCDD ) inhibition of coronary vasculogenesis mediated , in part , by reduced responsiveness to endogenous angiogenic stimuli , including vascular endothelial growth factor A ( VEGF-A )? OUTPUT:
PubmedQA184558
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Mouse has served as an excellent model for studying human development and diseases due to its similarity to human. Advances in transgenic and knockout studies in mouse have dramatically strengthened the use of this model and significantly improved our understanding of gene function during development in the past few decades. More recently, global gene expression analyses have revealed novel features in early embryogenesis up to gastrulation stages and have indeed provided molecular evidence supporting the conservation in early development in human and mouse. On the other hand, little information is known about the gene regulatory networks governing the subsequent organogenesis. Importantly, mouse and human development diverges during organogenesis. For instance, the mouse embryo is born around the end of organogenesis while in human the subsequent fetal period of ongoing growth and maturation of most organs spans more than 2/3 of human embryogenesis. While two recent studies reported the gene expression profiles during human organogenesis, no global gene expression analysis had been done for mouse organogenesis.', 'Here we report a detailed analysis of the global gene expression profiles from egg to the end of organogenesis in mouse. Our studies have revealed distinct temporal regulation patterns for genes belonging to different functional (Gene Ontology or GO) categories that support their roles during organogenesis. More importantly, comparative analyses identify both conserved and divergent gene regulation programs in mouse and human organogenesis, with the latter likely responsible for the developmental divergence between the two species, and further suggest a novel developmental strategy during vertebrate evolution.'] Does global expression profiling reveal genetic programs underlying the developmental divergence between mouse and human embryogenesis?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Mouse has served as an excellent model for studying human development and diseases due to its similarity to human. Advances in transgenic and knockout studies in mouse have dramatically strengthened the use of this model and significantly improved our understanding of gene function during development in the past few decades. More recently, global gene expression analyses have revealed novel features in early embryogenesis up to gastrulation stages and have indeed provided molecular evidence supporting the conservation in early development in human and mouse. On the other hand, little information is known about the gene regulatory networks governing the subsequent organogenesis. Importantly, mouse and human development diverges during organogenesis. For instance, the mouse embryo is born around the end of organogenesis while in human the subsequent fetal period of ongoing growth and maturation of most organs spans more than 2/3 of human embryogenesis. While two recent studies reported the gene expression profiles during human organogenesis, no global gene expression analysis had been done for mouse organogenesis.', 'Here we report a detailed analysis of the global gene expression profiles from egg to the end of organogenesis in mouse. Our studies have revealed distinct temporal regulation patterns for genes belonging to different functional (Gene Ontology or GO) categories that support their roles during organogenesis. More importantly, comparative analyses identify both conserved and divergent gene regulation programs in mouse and human organogenesis, with the latter likely responsible for the developmental divergence between the two species, and further suggest a novel developmental strategy during vertebrate evolution.'] Does global expression profiling reveal genetic programs underlying the developmental divergence between mouse and human embryogenesis? OUTPUT:
PubmedQA51665
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Compared with other animal venoms, ant venoms remain little explored. Ants have evolved complex venoms to rapidly immobilize arthropod prey and to protect their colonies from predators and pathogens. Many ants have retained peptide-rich venoms that are similar to those of other arthropod groups.', 'With the goal of conducting a broad and comprehensive survey of ant venom peptide diversity, we investigated the peptide composition of venoms from 82 stinging ant species from nine subfamilies using matrix-assisted laser desorption/ionisation time-of-flight mass spectrometry (MALDI-TOFMS). We also conducted an in-depth investigation of eight venoms using reversed-phase high-performance liquid chromatography (RP-HPLC) separation coupled with offline MALDI-TOFMS.', 'Our results reveal that the peptide compositions of ant venom peptidomes from both poneroid and formicoid ant clades comprise hundreds of small peptides (<4 kDa), while large peptides (>4 kDa) are also present in the venom of formicoids. Chemical reduction revealed the presence of disulfide-linked peptides in most ant subfamilies, including peptides structured by one, two or three disulfide bonds as well as dimeric peptides reticulated by three disulfide bonds.'] Is the complexity and structural diversity of ant venom peptidomes revealed by mass spectrometry profiling?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Compared with other animal venoms, ant venoms remain little explored. Ants have evolved complex venoms to rapidly immobilize arthropod prey and to protect their colonies from predators and pathogens. Many ants have retained peptide-rich venoms that are similar to those of other arthropod groups.', 'With the goal of conducting a broad and comprehensive survey of ant venom peptide diversity, we investigated the peptide composition of venoms from 82 stinging ant species from nine subfamilies using matrix-assisted laser desorption/ionisation time-of-flight mass spectrometry (MALDI-TOFMS). We also conducted an in-depth investigation of eight venoms using reversed-phase high-performance liquid chromatography (RP-HPLC) separation coupled with offline MALDI-TOFMS.', 'Our results reveal that the peptide compositions of ant venom peptidomes from both poneroid and formicoid ant clades comprise hundreds of small peptides (<4 kDa), while large peptides (>4 kDa) are also present in the venom of formicoids. Chemical reduction revealed the presence of disulfide-linked peptides in most ant subfamilies, including peptides structured by one, two or three disulfide bonds as well as dimeric peptides reticulated by three disulfide bonds.'] Is the complexity and structural diversity of ant venom peptidomes revealed by mass spectrometry profiling? OUTPUT:
PubmedQA140991
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Among several clinical factors, nerve or prostatic fascia preservation is associated with an improved continence outcome in several studies.', 'We study the clinical aspects associated with urine continence after prostatectomy, paying special attention to the extent and location of fascia preservation.', 'European Organisation for Research and Treatment of Cancer (EORTC) Quality of Life-Core 30 (QLQ-C30) and Prostate Cancer Module (PR25) questionnaires were used to evaluate quality-of-life (QoL) parameters prior to and at 6 and 12 mo after surgery for 151 men treated with robot-assisted laparoscopic prostatectomy (RALP) for localised prostate cancer. Fascia preservation was scored at 12 locations around the circumference of the prostate. Any involuntary urine loss showed a strong correlation with several domains of the EORTC QLQ-C30 and was therefore chosen as the definition of urine incontinence.', 'Robot-assisted laparoscopic prostatectomy (RALP).', 'Any urine incontinence.'] Is preservation of lateral prostatic fascia associated with urine continence after robotic-assisted prostatectomy?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Among several clinical factors, nerve or prostatic fascia preservation is associated with an improved continence outcome in several studies.', 'We study the clinical aspects associated with urine continence after prostatectomy, paying special attention to the extent and location of fascia preservation.', 'European Organisation for Research and Treatment of Cancer (EORTC) Quality of Life-Core 30 (QLQ-C30) and Prostate Cancer Module (PR25) questionnaires were used to evaluate quality-of-life (QoL) parameters prior to and at 6 and 12 mo after surgery for 151 men treated with robot-assisted laparoscopic prostatectomy (RALP) for localised prostate cancer. Fascia preservation was scored at 12 locations around the circumference of the prostate. Any involuntary urine loss showed a strong correlation with several domains of the EORTC QLQ-C30 and was therefore chosen as the definition of urine incontinence.', 'Robot-assisted laparoscopic prostatectomy (RALP).', 'Any urine incontinence.'] Is preservation of lateral prostatic fascia associated with urine continence after robotic-assisted prostatectomy? OUTPUT:
PubmedQA65593
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Glucose transporter member 1 (GLUT-1) is one of the major facilitated glucose transporters and contributes to the promotion of keratinocyte proliferation in psoriasis and carcinogenic lesions. In this study, we postulate that GLUT-1 is involved in ultraviolet B (UVB)-induced epidermal hyperplasia. The purpose of this study is to investigate the possible role of GLUT-1 in UVB-induced hyperplasia.', 'The effects of UVB on GLUT-1 expression levels were investigated in in vitro and in vivo studies. In addition, the involvement of epidermal growth factor (EGF) and hypoxia inducible factor-1 alpha (HIF-1α), transcriptional factors for GLUT-1, in GLUT-1-related events were investigated.', 'GLUT-1 mRNA and its protein levels were markedly increased by UVB irradiation in HaCaT cells. In in vivo studies, a strong immunofluorescence signal of GLUT-1 was clearly observed around the basal layer of the epidermis, which proliferated excessively by UVB irradiation. In HaCaT cells, EGF mRNA and its protein levels were markedly increased by UVB irradiation, and then the GLUT-1 mRNA level was significantly increased by treatment with EGF. Additionally, the upregulation of GLUT-1 by both UVB irradiation and treatment with EGF was significantly suppressed by transfection with HIF-1α siRNA.'] Is glucose transporter member 1 involved in UVB-induced epidermal hyperplasia by enhancing proliferation in epidermal keratinocytes?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Glucose transporter member 1 (GLUT-1) is one of the major facilitated glucose transporters and contributes to the promotion of keratinocyte proliferation in psoriasis and carcinogenic lesions. In this study, we postulate that GLUT-1 is involved in ultraviolet B (UVB)-induced epidermal hyperplasia. The purpose of this study is to investigate the possible role of GLUT-1 in UVB-induced hyperplasia.', 'The effects of UVB on GLUT-1 expression levels were investigated in in vitro and in vivo studies. In addition, the involvement of epidermal growth factor (EGF) and hypoxia inducible factor-1 alpha (HIF-1α), transcriptional factors for GLUT-1, in GLUT-1-related events were investigated.', 'GLUT-1 mRNA and its protein levels were markedly increased by UVB irradiation in HaCaT cells. In in vivo studies, a strong immunofluorescence signal of GLUT-1 was clearly observed around the basal layer of the epidermis, which proliferated excessively by UVB irradiation. In HaCaT cells, EGF mRNA and its protein levels were markedly increased by UVB irradiation, and then the GLUT-1 mRNA level was significantly increased by treatment with EGF. Additionally, the upregulation of GLUT-1 by both UVB irradiation and treatment with EGF was significantly suppressed by transfection with HIF-1α siRNA.'] Is glucose transporter member 1 involved in UVB-induced epidermal hyperplasia by enhancing proliferation in epidermal keratinocytes? OUTPUT:
PubmedQA195887
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['The relationship between sleep and immune function is not well understood at a functional or molecular level. We therefore used a genetic approach in Drosophila to manipulate sleep and evaluated effects on the ability of flies to fight bacterial infection.', 'Laboratory.', 'Drosophila melanogaster.', 'We used a genetic approach to transiently alter neuronal excitability in the mushroom body, a region in the central brain that is known to regulate sleep. Flies with increased sleep for up to two days prior to a bacterial infection showed increased resistance to the infection and improved survival. These flies also had increased expression levels of a subset of anti-microbial peptide mRNA prior to infection, as well as increased NFκB activity during infection as indicated by in vivo luciferase reporter activity. In contrast, flies that experienced reduced sleep for up to two days prior to infection had no effect on survival or on NFκB activity during infection. However, flies with reduced sleep showed an altered defense mechanism, such that resistance to infection was increased, but at the expense of reduced tolerance. This effect was dependent on environmental condition.'] Does increased sleep promote survival during a bacterial infection in Drosophila?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['The relationship between sleep and immune function is not well understood at a functional or molecular level. We therefore used a genetic approach in Drosophila to manipulate sleep and evaluated effects on the ability of flies to fight bacterial infection.', 'Laboratory.', 'Drosophila melanogaster.', 'We used a genetic approach to transiently alter neuronal excitability in the mushroom body, a region in the central brain that is known to regulate sleep. Flies with increased sleep for up to two days prior to a bacterial infection showed increased resistance to the infection and improved survival. These flies also had increased expression levels of a subset of anti-microbial peptide mRNA prior to infection, as well as increased NFκB activity during infection as indicated by in vivo luciferase reporter activity. In contrast, flies that experienced reduced sleep for up to two days prior to infection had no effect on survival or on NFκB activity during infection. However, flies with reduced sleep showed an altered defense mechanism, such that resistance to infection was increased, but at the expense of reduced tolerance. This effect was dependent on environmental condition.'] Does increased sleep promote survival during a bacterial infection in Drosophila? OUTPUT:
PubmedQA6713
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['IL-17 is the defining cytokine of the Th17, Tc17, and γδ T cell populations that plays a critical role in mediating inflammation and autoimmunity. Psoriasis vulgaris is an inflammatory skin disease mediated by Th1 and Th17 cytokines with relevant contributions of IFN-γ, TNF-α, and IL-17. Despite the pivotal role IL-17 plays in psoriasis, and in contrast to the other key mediators involved in the psoriasis cytokine cascade that are capable of inducing broad effects on keratinocytes, IL-17 was demonstrated to regulate the expression of a limited number of genes in monolayer keratinocytes cultured in vitro.', 'Given the clinical efficacy of anti-IL-17 agents is associated with an impressive reduction in a large set of inflammatory genes, we sought a full-thickness skin model that more closely resemble in vivo epidermal architecture. Using a reconstructed human epidermis (RHE), IL-17 was able to upregulate 419 gene probes and downregulate 216 gene probes. As possible explanation for the increased gene induction in the RHE model is that C/CAAT-enhancer-binding proteins (C/EBP) -β, the transcription factor regulating IL-17-responsive genes, is expressed preferentially in differentiated keratinocytes.'] Does iL-17 induce an expanded range of downstream genes in reconstituted human epidermis model?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['IL-17 is the defining cytokine of the Th17, Tc17, and γδ T cell populations that plays a critical role in mediating inflammation and autoimmunity. Psoriasis vulgaris is an inflammatory skin disease mediated by Th1 and Th17 cytokines with relevant contributions of IFN-γ, TNF-α, and IL-17. Despite the pivotal role IL-17 plays in psoriasis, and in contrast to the other key mediators involved in the psoriasis cytokine cascade that are capable of inducing broad effects on keratinocytes, IL-17 was demonstrated to regulate the expression of a limited number of genes in monolayer keratinocytes cultured in vitro.', 'Given the clinical efficacy of anti-IL-17 agents is associated with an impressive reduction in a large set of inflammatory genes, we sought a full-thickness skin model that more closely resemble in vivo epidermal architecture. Using a reconstructed human epidermis (RHE), IL-17 was able to upregulate 419 gene probes and downregulate 216 gene probes. As possible explanation for the increased gene induction in the RHE model is that C/CAAT-enhancer-binding proteins (C/EBP) -β, the transcription factor regulating IL-17-responsive genes, is expressed preferentially in differentiated keratinocytes.'] Does iL-17 induce an expanded range of downstream genes in reconstituted human epidermis model? OUTPUT:
PubmedQA21835
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Both glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) are gut hormones involved in energy homoeostasis. Obesity, insulin resistance and hyperglycaemia are significant confounders when GLP-1 and PYY secretion is assessed. Thus, we evaluated GLP-1 and PYY response after fat load in morbidly obese patients with different degrees of insulin resistance and glycemic status.', 'We studied 40 morbidly obese subjects (mean age, 40·6 ± 1·3 years; mean BMI, 53·1 ± 1·2 kg/m(2) ) divided into groups according to their glycemic status: normal fasting glucose (NFG) group, impaired fasting glucose (IFG) group and type 2 diabetes mellitus (T2D) group. NFG patients were additionally subclassified, according to the homoeostasis model assessment of insulin resistance (HOMAIR ), into a low insulin-resistance (LIR) group (HOMAIR <3·9) or a high insulin-resistance (HIR) group (HOMAIR ≥3·9).', 'Lipid emulsion was administered orally and measurements made at baseline and 180 min postprandially of levels of GLP-1, PYY, insulin, glucose, free fatty acids, triglycerides and leptin.', 'At the 180-minute postprandial reading, GLP-1 and PYY had increased in LIR-NFG subjects (41·84%, P = 0·01; 35·7%, P = 0·05; respectively), whereas no changes were observed in HIR-NFG, IFG or T2D subjects.'] Is gLP-1 and peptide YY secretory response after fat load impaired by insulin resistance , impaired fasting glucose and type 2 diabetes in morbidly obese subjects?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Both glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) are gut hormones involved in energy homoeostasis. Obesity, insulin resistance and hyperglycaemia are significant confounders when GLP-1 and PYY secretion is assessed. Thus, we evaluated GLP-1 and PYY response after fat load in morbidly obese patients with different degrees of insulin resistance and glycemic status.', 'We studied 40 morbidly obese subjects (mean age, 40·6 ± 1·3 years; mean BMI, 53·1 ± 1·2 kg/m(2) ) divided into groups according to their glycemic status: normal fasting glucose (NFG) group, impaired fasting glucose (IFG) group and type 2 diabetes mellitus (T2D) group. NFG patients were additionally subclassified, according to the homoeostasis model assessment of insulin resistance (HOMAIR ), into a low insulin-resistance (LIR) group (HOMAIR <3·9) or a high insulin-resistance (HIR) group (HOMAIR ≥3·9).', 'Lipid emulsion was administered orally and measurements made at baseline and 180 min postprandially of levels of GLP-1, PYY, insulin, glucose, free fatty acids, triglycerides and leptin.', 'At the 180-minute postprandial reading, GLP-1 and PYY had increased in LIR-NFG subjects (41·84%, P = 0·01; 35·7%, P = 0·05; respectively), whereas no changes were observed in HIR-NFG, IFG or T2D subjects.'] Is gLP-1 and peptide YY secretory response after fat load impaired by insulin resistance , impaired fasting glucose and type 2 diabetes in morbidly obese subjects? OUTPUT:
PubmedQA130394
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['To investigate the effect of nutrient withdrawal on human intestinal epithelial barrier function (EBF). We hypothesized that unfed mucosa results in decreased EBF. This was tested in a series of surgical small intestinal resection specimens.', 'Small bowel specifically excluding inflamed tissue, was obtained from pediatric patients (aged 2 days to 19 years) undergoing intestinal resection. EBF was assessed in Ussing chambers for transepithelial resistance (TER) and passage of fluorescein isothiocyanate (FITC)-dextran (4 kD). Tight junction and adherence junction proteins were imaged with immunofluorescence staining. Expression of Toll-like receptors (TLR) and inflammatory cytokines were measured in loop ileostomy takedowns in a second group of patients.', 'Because TER increased with patient age (P < .01), results were stratified into infant versus teenage groups. Fed bowel had significantly greater TER versus unfed bowel (P < .05) in both age populations. Loss of EBF was also observed by an increase in FITC-dextran permeation in enteral nutrient-deprived segments (P < .05). Immunofluorescence staining showed marked declines in intensity of ZO-1, occludin, E-cadherin, and claudin-4 in unfed intestinal segments, as well as a loss of structural formation of tight junctions. Analysis of cytokine and TLR expression showed significant increases in tumor necrosis factor (TNF)-α and TLR4 in unfed segments of bowel compared with fed segments from the same individual.'] Does enteral nutrient deprivation in patients lead to a loss of intestinal epithelial barrier function?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['To investigate the effect of nutrient withdrawal on human intestinal epithelial barrier function (EBF). We hypothesized that unfed mucosa results in decreased EBF. This was tested in a series of surgical small intestinal resection specimens.', 'Small bowel specifically excluding inflamed tissue, was obtained from pediatric patients (aged 2 days to 19 years) undergoing intestinal resection. EBF was assessed in Ussing chambers for transepithelial resistance (TER) and passage of fluorescein isothiocyanate (FITC)-dextran (4 kD). Tight junction and adherence junction proteins were imaged with immunofluorescence staining. Expression of Toll-like receptors (TLR) and inflammatory cytokines were measured in loop ileostomy takedowns in a second group of patients.', 'Because TER increased with patient age (P < .01), results were stratified into infant versus teenage groups. Fed bowel had significantly greater TER versus unfed bowel (P < .05) in both age populations. Loss of EBF was also observed by an increase in FITC-dextran permeation in enteral nutrient-deprived segments (P < .05). Immunofluorescence staining showed marked declines in intensity of ZO-1, occludin, E-cadherin, and claudin-4 in unfed intestinal segments, as well as a loss of structural formation of tight junctions. Analysis of cytokine and TLR expression showed significant increases in tumor necrosis factor (TNF)-α and TLR4 in unfed segments of bowel compared with fed segments from the same individual.'] Does enteral nutrient deprivation in patients lead to a loss of intestinal epithelial barrier function? OUTPUT:
PubmedQA169615
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Obstructive sleep apnoea (OSA) is a common public health problem. Sleeping position dependency has been related to OSA, and around half of OSA patients suffer from positional OSA where majority of the respiratory events occur in supine position. The consequences of supine dominant OSA have not been thoroughly investigated in long-term follow-up studies. The aim of the study was to retrospectively investigate the effects of supine dominant OSA on morbidity and mortality risk ratios during long-term follow-up and compare the findings with a non-supine OSA group at different OSA severities.', 'Ambulatory polygraphic recordings of 793 patients with median follow-up time of 194.5\\xa0months were retrospectively analysed. The risk ratios of morbidity and mortality of supine dominant OSA and non-supine OSA patients were compared.', 'Supine dominant OSA patients, having majority of the obstruction events occurring in supine position, showed higher mortality and morbidity risk ratios in severe OSA category than the non-supine OSA patients. In severe category, the observed risk ratios were statistically significant.'] Are morbidity and mortality risk ratios elevated in severe supine dominant OSA : a long-term follow-up study?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Obstructive sleep apnoea (OSA) is a common public health problem. Sleeping position dependency has been related to OSA, and around half of OSA patients suffer from positional OSA where majority of the respiratory events occur in supine position. The consequences of supine dominant OSA have not been thoroughly investigated in long-term follow-up studies. The aim of the study was to retrospectively investigate the effects of supine dominant OSA on morbidity and mortality risk ratios during long-term follow-up and compare the findings with a non-supine OSA group at different OSA severities.', 'Ambulatory polygraphic recordings of 793 patients with median follow-up time of 194.5\xa0months were retrospectively analysed. The risk ratios of morbidity and mortality of supine dominant OSA and non-supine OSA patients were compared.', 'Supine dominant OSA patients, having majority of the obstruction events occurring in supine position, showed higher mortality and morbidity risk ratios in severe OSA category than the non-supine OSA patients. In severe category, the observed risk ratios were statistically significant.'] Are morbidity and mortality risk ratios elevated in severe supine dominant OSA : a long-term follow-up study? OUTPUT:
PubmedQA34212
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['To document the effects of the abolition of user fees on utilization of health services in Uganda with emphasis on poor and vulnerable groups.', 'A longitudinal study using quantitative and qualitative methods was carried out in 106 health facilities across the country. Health records were reviewed to determine trends in overall utilization patterns and use among vulnerable groups. A modification of wealth ranking as defined by the Uganda Poverty Participatory Assessment Project was used to categorize households by socio-economic status in order to compare utilization by the poor against that of other socio-economic groups.', 'There was a marked increase in utilization in all population groups that was fluctuating in nature. The increase in utilization varied from 26% in public referral facilities in 2001, rising to 55% in 2002 compared with 2000. The corresponding figures for the lower level facilities were 44% and 77%, respectively. Increase in utilization among the poor was more than for other socio-economic categories. Women utilized health services more than men both before and after cost-sharing. Higher increases in utilization were noted among the over-five age group compared with the under-fives. There were no increases in utilization for preventive and inpatient services. With respect to quality of care, there were fewer drug stock-outs in 2002 compared with 2000 and 2001. There was no deterioration of other indicators such as cleanliness, compound maintenance and staff availability reported.'] Is abolition of cost-sharing pro-poor : evidence from Uganda?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['To document the effects of the abolition of user fees on utilization of health services in Uganda with emphasis on poor and vulnerable groups.', 'A longitudinal study using quantitative and qualitative methods was carried out in 106 health facilities across the country. Health records were reviewed to determine trends in overall utilization patterns and use among vulnerable groups. A modification of wealth ranking as defined by the Uganda Poverty Participatory Assessment Project was used to categorize households by socio-economic status in order to compare utilization by the poor against that of other socio-economic groups.', 'There was a marked increase in utilization in all population groups that was fluctuating in nature. The increase in utilization varied from 26% in public referral facilities in 2001, rising to 55% in 2002 compared with 2000. The corresponding figures for the lower level facilities were 44% and 77%, respectively. Increase in utilization among the poor was more than for other socio-economic categories. Women utilized health services more than men both before and after cost-sharing. Higher increases in utilization were noted among the over-five age group compared with the under-fives. There were no increases in utilization for preventive and inpatient services. With respect to quality of care, there were fewer drug stock-outs in 2002 compared with 2000 and 2001. There was no deterioration of other indicators such as cleanliness, compound maintenance and staff availability reported.'] Is abolition of cost-sharing pro-poor : evidence from Uganda? OUTPUT:
PubmedQA67150
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['In our institution, patients with medullary thyroid carcinoma (MTC) concurrent with nodular goiter (NG) have a nearly 100% survival rate, but the reasons and characteristics are unclear.', 'Eighty patients with MTC who underwent surgery in our center between 1971 and 2011 were reviewed.', 'A total of 21 MTC/NG and 59 MTC only patients were identified. The stage of the two groups had no significant difference (P\\u2009=\\u20090.13). The MTC/NG group had lower preoperative serum calcitonin (CT) levels (914.7\\u2009ng/L vs. 1162.6\\u2009ng/L, P\\u2009=\\u20090.003), lower postoperative serum CT levels (371.4\\u2009ng/L vs. 582.5\\u2009ng/L, P\\u2009<\\u20090.001), lower carcinoembryonic antigen levels (18.3\\u2009ng/ml vs. 130.5\\u2009ng/ml, P\\u2009<\\u20090.001), a lower propensity toward lymph node metastasis (40.0% vs. 66.7%, P\\u2009=\\u20090.07), and a lower proportion of multifocality (19.1% vs. 42.4%, P\\u2009=\\u20090.06), capsular invasion (9.5% vs. 25.4%, P\\u2009=\\u20090.21), and vascular invasion (4.8% vs. 10.1%, P\\u2009=\\u20090.67). The mean tumor diameter of the two groups was similar (20.3\\u2009mm vs. 22.1\\u2009mm, P\\u2009=\\u20090.6). Overall 15-year survival in MTC/NG versus MTC only groups was 100% versus 57.0% (P\\u2009=\\u20090.03).'] Does medullary thyroid carcinoma with nodular goiter carry an excellent prognosis?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['In our institution, patients with medullary thyroid carcinoma (MTC) concurrent with nodular goiter (NG) have a nearly 100% survival rate, but the reasons and characteristics are unclear.', 'Eighty patients with MTC who underwent surgery in our center between 1971 and 2011 were reviewed.', 'A total of 21 MTC/NG and 59 MTC only patients were identified. The stage of the two groups had no significant difference (P\u2009=\u20090.13). The MTC/NG group had lower preoperative serum calcitonin (CT) levels (914.7\u2009ng/L vs. 1162.6\u2009ng/L, P\u2009=\u20090.003), lower postoperative serum CT levels (371.4\u2009ng/L vs. 582.5\u2009ng/L, P\u2009<\u20090.001), lower carcinoembryonic antigen levels (18.3\u2009ng/ml vs. 130.5\u2009ng/ml, P\u2009<\u20090.001), a lower propensity toward lymph node metastasis (40.0% vs. 66.7%, P\u2009=\u20090.07), and a lower proportion of multifocality (19.1% vs. 42.4%, P\u2009=\u20090.06), capsular invasion (9.5% vs. 25.4%, P\u2009=\u20090.21), and vascular invasion (4.8% vs. 10.1%, P\u2009=\u20090.67). The mean tumor diameter of the two groups was similar (20.3\u2009mm vs. 22.1\u2009mm, P\u2009=\u20090.6). Overall 15-year survival in MTC/NG versus MTC only groups was 100% versus 57.0% (P\u2009=\u20090.03).'] Does medullary thyroid carcinoma with nodular goiter carry an excellent prognosis? OUTPUT:
PubmedQA17503
[ { "from": "human", "value": "TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer.\nINPUT: ['Pantropical intercontinental disjunction is a common biogeographical pattern in flowering plants exhibiting a discontinuous distribution primarily in tropical Asia, Africa and the Americas. Only a few plant groups with this pattern have been investigated at the generic level with molecular phylogenetic and biogeographical methods. Paederia (Rubiaceae) is a pantropical genus of 31 species of woody lianas, with the greatest species diversity in continental Asia and Madagascar and only two species from tropical America. The aim of this study was to reconstruct the biogeographical history of Paederia based on phylogenetic analyses to explore how the genus attained its pantropical distribution.', 'Maximum parsimony and Bayesian inference were used for phylogenetic analyses using sequences of five plastid markers (the rbcL gene, rps16 intron, trnT-F region, atpB-rbcL spacer and psbA-trnH spacer). Biogeographical inferences were based on a Bayesian uncorrelated lognormal relaxed molecular clock together with both Bayesian and likelihood ancestral area reconstructions.', 'The data suggest an early diverged Asian lineage sister to the clade of the remaining species consisting of a predominantly Asian sub-clade and a primarily Malagasy sub-clade. Paederia is inferred to have originated in the Oligocene in tropical continental Asia. It then reached Africa in the early to middle Miocene, most probably via long-distance dispersal across the Indian Ocean. The two Neotropical species are inferred to have derived independently in the late Miocene from ancestors of Asia and East Africa, respectively.'] Do post-Boreotropical dispersals explain the pantropical disjunction in Paederia ( Rubiaceae )?\nOUTPUT:\n" }, { "from": "agent", "value": "yes" } ]
TASK: Your task is to answer biomedical questions using the given abstract. Only output yes, no, or maybe as answer. INPUT: ['Pantropical intercontinental disjunction is a common biogeographical pattern in flowering plants exhibiting a discontinuous distribution primarily in tropical Asia, Africa and the Americas. Only a few plant groups with this pattern have been investigated at the generic level with molecular phylogenetic and biogeographical methods. Paederia (Rubiaceae) is a pantropical genus of 31 species of woody lianas, with the greatest species diversity in continental Asia and Madagascar and only two species from tropical America. The aim of this study was to reconstruct the biogeographical history of Paederia based on phylogenetic analyses to explore how the genus attained its pantropical distribution.', 'Maximum parsimony and Bayesian inference were used for phylogenetic analyses using sequences of five plastid markers (the rbcL gene, rps16 intron, trnT-F region, atpB-rbcL spacer and psbA-trnH spacer). Biogeographical inferences were based on a Bayesian uncorrelated lognormal relaxed molecular clock together with both Bayesian and likelihood ancestral area reconstructions.', 'The data suggest an early diverged Asian lineage sister to the clade of the remaining species consisting of a predominantly Asian sub-clade and a primarily Malagasy sub-clade. Paederia is inferred to have originated in the Oligocene in tropical continental Asia. It then reached Africa in the early to middle Miocene, most probably via long-distance dispersal across the Indian Ocean. The two Neotropical species are inferred to have derived independently in the late Miocene from ancestors of Asia and East Africa, respectively.'] Do post-Boreotropical dispersals explain the pantropical disjunction in Paederia ( Rubiaceae )? OUTPUT: