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PubmedQA167520
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: It is widely accepted that type 2 amiodarone-induced thyrotoxicosis (AIT) generally occurs in patients with a normal thyroid gland without signs of thyroid autoimmunity. However, it is currently unknown if the presence of anti-thyroglobulin (TgAb) and/or anti-thyroperoxidase antibodies (TPOAb) in AIT patients without other signs of an underlying thyroid disease may impair the response to glucocorticoid therapy. We performed a pilot retrospective cohort study with matched-subject design and an equivalence hypothesis, comparing the response to glucocorticoid therapy between 20 AIT patients with a normal thyroid gland, low radioiodine uptake, undetectable TSH receptor antibodies and positive TgAb and/or TPOAb (Ab+ group), and 40 patients with the same features and absent thyroid antibodies (Ab- group). The mean cure time was 54 ± 68 days in the Ab+ group and 55 ± 49 days in the Ab- group (p = 0.63). The equivalence test revealed an equivalent cure rate after 60, 90 and 180 days (p = 0.67, 0.88 and 0.278, respectively). The occurrence of permanent hypothyroidism was higher in the Ab+ group than in the Ab- group (26.3 vs 5.13 %, p = 0.032).\n Question: Does the presence of anti-thyroglobulin ( TgAb ) and/or anti-thyroperoxidase antibodies ( TPOAb ) exclude the diagnosis of type 2 amiodarone-induced thyrotoxicosis?\n Output: " }, { "role": "assistant", "content": "no" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: It is widely accepted that type 2 amiodarone-induced thyrotoxicosis (AIT) generally occurs in patients with a normal thyroid gland without signs of thyroid autoimmunity. However, it is currently unknown if the presence of anti-thyroglobulin (TgAb) and/or anti-thyroperoxidase antibodies (TPOAb) in AIT patients without other signs of an underlying thyroid disease may impair the response to glucocorticoid therapy. We performed a pilot retrospective cohort study with matched-subject design and an equivalence hypothesis, comparing the response to glucocorticoid therapy between 20 AIT patients with a normal thyroid gland, low radioiodine uptake, undetectable TSH receptor antibodies and positive TgAb and/or TPOAb (Ab+ group), and 40 patients with the same features and absent thyroid antibodies (Ab- group). The mean cure time was 54 ± 68 days in the Ab+ group and 55 ± 49 days in the Ab- group (p = 0.63). The equivalence test revealed an equivalent cure rate after 60, 90 and 180 days (p = 0.67, 0.88 and 0.278, respectively). The occurrence of permanent hypothyroidism was higher in the Ab+ group than in the Ab- group (26.3 vs 5.13 %, p = 0.032). Question: Does the presence of anti-thyroglobulin ( TgAb ) and/or anti-thyroperoxidase antibodies ( TPOAb ) exclude the diagnosis of type 2 amiodarone-induced thyrotoxicosis? Output:
PubmedQA19793
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The aim of this study is to compare the effects of hypercapnic hyperventilation and normocapnic normoventilation on emergence time from propofol and isoflurane anesthesia. In this clinical trial, the differences in emergence time were evaluated in 80 patients undergoing elective abdominal surgery in Alzahra University hospital, Isfahan, Iran, in 2011-2012. Patients were randomly divided into four groups (groups 1-4) receiving isoflurane hypercapnic hyperventilation, isoflurane normocapnic normoventilation, propofol hypercapnic hyperventilation, and propofol normocapnic normoventilation, respectively. Hypercapnia was maintained by adding CO2 to the patient's inspired gas during hyperventilation. The emergence time and the duration of stay in recovery room in the four groups were measured and compared by one-way analysis of variance (ANOVA) and least significant difference tests. The average emergence time in groups 1, 2, 3, and 4 were (11.3 ± 3.2), (15.2 ± 3.8), (9 ± 4.2) and (11.8 ± 5.3) min, respectively. These differences were significant (P = 0.001). In patients receiving propofol hypercapnic hyperventilation, the emergence time was faster than in other groups. There was also a significant difference in duration of stay in recovery room between the groups (P = 0.004). Patients who received isoflurane hypercapnic hyperventilation had a shortest length of stay in the recovery room.\n Question: Does hypercapnic hyperventilation shorten emergence time from Propofol and Isoflurane anesthesia?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The aim of this study is to compare the effects of hypercapnic hyperventilation and normocapnic normoventilation on emergence time from propofol and isoflurane anesthesia. In this clinical trial, the differences in emergence time were evaluated in 80 patients undergoing elective abdominal surgery in Alzahra University hospital, Isfahan, Iran, in 2011-2012. Patients were randomly divided into four groups (groups 1-4) receiving isoflurane hypercapnic hyperventilation, isoflurane normocapnic normoventilation, propofol hypercapnic hyperventilation, and propofol normocapnic normoventilation, respectively. Hypercapnia was maintained by adding CO2 to the patient's inspired gas during hyperventilation. The emergence time and the duration of stay in recovery room in the four groups were measured and compared by one-way analysis of variance (ANOVA) and least significant difference tests. The average emergence time in groups 1, 2, 3, and 4 were (11.3 ± 3.2), (15.2 ± 3.8), (9 ± 4.2) and (11.8 ± 5.3) min, respectively. These differences were significant (P = 0.001). In patients receiving propofol hypercapnic hyperventilation, the emergence time was faster than in other groups. There was also a significant difference in duration of stay in recovery room between the groups (P = 0.004). Patients who received isoflurane hypercapnic hyperventilation had a shortest length of stay in the recovery room. Question: Does hypercapnic hyperventilation shorten emergence time from Propofol and Isoflurane anesthesia? Output:
PubmedQA5701
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To investigate the expression levels of lymphocyte antigen 6 complex, locus E (LY6E) and interferon-induced protein with tetratricopeptide repeats 1 (IFIT1) genes in the peripheral blood mononuclear cells (PBMCs) of patients with systemic lupus erythematosus (SLE), and to evaluate the relations between these gene expression levels and disease activity. The clinical data of 144 SLE patients, 27 non-SLE patients with rheumatic diseases, and 59 normal controls were collected. The SLE patients were further divided into 2 subgroups: active SLE group (n = 87) and non-active SLE group (n = 57) according to SLEDAI scores. Specimens of peripheral blood were drawn; total RNA was extracted and transcribed into cDNA. Sybr green dye based real-time quantitative PCR method was used to compare the expression levels (indicated as-DeltaDeltaCT value) of LY6E and IFIT1 in patients with SLE and those in the controls. (1) The-DeltaDeltaCT value of LY6E expression level of the SLE patients was 5.4760 +/- 1.9806, significantly higher than those of the non-SLE patients (3.4323 +/- 1.7456) and normal controls (4.5198 +/- 1.6359, both P = 0.001). (2) The-DeltaDeltaCT value of LY6E and IFIT1 mRNA expression of the active SLE patients were 6.1960 +/- 1.7729 and 6.4997 +/- 2.6297 respectively, significantly higher than those observed in the inactive SLE patients (4.3770 +/- 1.7764 and 4.1327 +/- 2.6044 respectively, both P = 0.000). The-DeltaDeltaCT values of LY6E and IFIT1 mRNA of the SLE patients were correlated with the SLEDAI scores, and with the numbers of matched criteria used in the diagnosis of SLE (P < 0.001).\n Question: Are [ Interferon-inducible genes lymphocyte antigen 6 complex E and tetratricopeptide repeats 1 correlated with clinical features of patients with systemic lupus erythematosus ]?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To investigate the expression levels of lymphocyte antigen 6 complex, locus E (LY6E) and interferon-induced protein with tetratricopeptide repeats 1 (IFIT1) genes in the peripheral blood mononuclear cells (PBMCs) of patients with systemic lupus erythematosus (SLE), and to evaluate the relations between these gene expression levels and disease activity. The clinical data of 144 SLE patients, 27 non-SLE patients with rheumatic diseases, and 59 normal controls were collected. The SLE patients were further divided into 2 subgroups: active SLE group (n = 87) and non-active SLE group (n = 57) according to SLEDAI scores. Specimens of peripheral blood were drawn; total RNA was extracted and transcribed into cDNA. Sybr green dye based real-time quantitative PCR method was used to compare the expression levels (indicated as-DeltaDeltaCT value) of LY6E and IFIT1 in patients with SLE and those in the controls. (1) The-DeltaDeltaCT value of LY6E expression level of the SLE patients was 5.4760 +/- 1.9806, significantly higher than those of the non-SLE patients (3.4323 +/- 1.7456) and normal controls (4.5198 +/- 1.6359, both P = 0.001). (2) The-DeltaDeltaCT value of LY6E and IFIT1 mRNA expression of the active SLE patients were 6.1960 +/- 1.7729 and 6.4997 +/- 2.6297 respectively, significantly higher than those observed in the inactive SLE patients (4.3770 +/- 1.7764 and 4.1327 +/- 2.6044 respectively, both P = 0.000). The-DeltaDeltaCT values of LY6E and IFIT1 mRNA of the SLE patients were correlated with the SLEDAI scores, and with the numbers of matched criteria used in the diagnosis of SLE (P < 0.001). Question: Are [ Interferon-inducible genes lymphocyte antigen 6 complex E and tetratricopeptide repeats 1 correlated with clinical features of patients with systemic lupus erythematosus ]? Output:
PubmedQA93378
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Bicuspid aortic valves (BAVs) are associated with premature valve stenosis, regurgitation, and ascending aortic aneurysms. We compared aortic size in BAV patients with aortic size in control patients with matched valvular lesions (aortic regurgitation, aortic stenosis, or mixed lesions) to determine whether intrinsic aortic abnormalities in BAVs account for aortic dilatation beyond that caused by valvular hemodynamic derangement alone. Diameters of the left ventricular outflow tract, sinus of Valsalva, sinotubular junction, and proximal aorta were measured from transthoracic echocardiograms in 118 consecutive BAV patients. Annular area was measured by planimetry, and BAV eccentricity was expressed as the ratio of the right leaflet area to the total annular area. Seventy-seven control patients with tricuspid aortic valves were matched for sex and for combined severity of regurgitation and stenosis. BAV patients (79 men and 39 women, aged 44.1+/-15.5 years) had varying degrees of regurgitation (84 patients [71%]) and stenosis (48 patients [41%]). Within the bicuspid group, multivariate analysis demonstrated that aortic diameters increased with worsening aortic regurgitation (P:<0.001) and advancing age (P:<0.05) but not with the severity of aortic stenosis. BAV patients had larger aortic diameters than did control patients at all ascending aortic levels measured (P:<0.01), despite advanced age in the control patients.\n Question: Are bicuspid aortic valves associated with aortic dilatation out of proportion to coexistent valvular lesions?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Bicuspid aortic valves (BAVs) are associated with premature valve stenosis, regurgitation, and ascending aortic aneurysms. We compared aortic size in BAV patients with aortic size in control patients with matched valvular lesions (aortic regurgitation, aortic stenosis, or mixed lesions) to determine whether intrinsic aortic abnormalities in BAVs account for aortic dilatation beyond that caused by valvular hemodynamic derangement alone. Diameters of the left ventricular outflow tract, sinus of Valsalva, sinotubular junction, and proximal aorta were measured from transthoracic echocardiograms in 118 consecutive BAV patients. Annular area was measured by planimetry, and BAV eccentricity was expressed as the ratio of the right leaflet area to the total annular area. Seventy-seven control patients with tricuspid aortic valves were matched for sex and for combined severity of regurgitation and stenosis. BAV patients (79 men and 39 women, aged 44.1+/-15.5 years) had varying degrees of regurgitation (84 patients [71%]) and stenosis (48 patients [41%]). Within the bicuspid group, multivariate analysis demonstrated that aortic diameters increased with worsening aortic regurgitation (P:<0.001) and advancing age (P:<0.05) but not with the severity of aortic stenosis. BAV patients had larger aortic diameters than did control patients at all ascending aortic levels measured (P:<0.01), despite advanced age in the control patients. Question: Are bicuspid aortic valves associated with aortic dilatation out of proportion to coexistent valvular lesions? Output:
PubmedQA89911
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Serum total creatine kinase (total CK) level increases in the patients following electrical cardioversion. The same has been observed with CK-MB, an isoenzyme of the total CK with some cardiospecificity. Cardiac troponin I (cTnI), a new specific cardiac biological marker, is highly effective to discriminate myocardial and muscular injuries after noncardiac surgery. To assess cardiac damage after cardioversion, we measured serum cTnI, myoglobin, total CK, CK-MB mass, 1, 2, 3, 4, 8, 12, and 24 h after elective cardioversion of supraventricular tachycardia in 28 patients (eight women, 20 men; mean age, 64 +/- 10 years). Cumulative energy was below 370 J in 17 patients, between 370 and 900 J in eight patients, and 1,020 J in three patients. Serum cTnI was measured using a sandwich immunoenzymologic assay. The detection limit of the assay was 0.35 microgram/L and normal values range from 0.35 to 1.3 micrograms/L. In all but three patients, cTnI remained below 0.35 microgram/L. In these three patients, cTnI ranged between 0.35 and 0.9 microgram/L. There was no correlation between cTnI and the number or the energy of cardioversion. Myoglobin and total CK increased to abnormal concentrations in 11 patients (myoglobin, 630 +/- 190 micrograms/L, and total CK, 2,584 +/- 780 U/L) and reached myocardial infarction-like values in five patients. Modest increases of CK-MB were then also observed. A strong correlation was observed between the total energy of direct current cardioversion and the increase of either myoglobin (r = 0.87; p < 001) or total CK (r = 0.81; p < 001).\n Question: Does cardiac troponin I increase after cardioversion?\n Output: " }, { "role": "assistant", "content": "no" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Serum total creatine kinase (total CK) level increases in the patients following electrical cardioversion. The same has been observed with CK-MB, an isoenzyme of the total CK with some cardiospecificity. Cardiac troponin I (cTnI), a new specific cardiac biological marker, is highly effective to discriminate myocardial and muscular injuries after noncardiac surgery. To assess cardiac damage after cardioversion, we measured serum cTnI, myoglobin, total CK, CK-MB mass, 1, 2, 3, 4, 8, 12, and 24 h after elective cardioversion of supraventricular tachycardia in 28 patients (eight women, 20 men; mean age, 64 +/- 10 years). Cumulative energy was below 370 J in 17 patients, between 370 and 900 J in eight patients, and 1,020 J in three patients. Serum cTnI was measured using a sandwich immunoenzymologic assay. The detection limit of the assay was 0.35 microgram/L and normal values range from 0.35 to 1.3 micrograms/L. In all but three patients, cTnI remained below 0.35 microgram/L. In these three patients, cTnI ranged between 0.35 and 0.9 microgram/L. There was no correlation between cTnI and the number or the energy of cardioversion. Myoglobin and total CK increased to abnormal concentrations in 11 patients (myoglobin, 630 +/- 190 micrograms/L, and total CK, 2,584 +/- 780 U/L) and reached myocardial infarction-like values in five patients. Modest increases of CK-MB were then also observed. A strong correlation was observed between the total energy of direct current cardioversion and the increase of either myoglobin (r = 0.87; p < 001) or total CK (r = 0.81; p < 001). Question: Does cardiac troponin I increase after cardioversion? Output:
PubmedQA67262
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Previous studies have shown that metabolic syndrome (MS) is associated with an increased susceptibility to develop cardiovascular damage (CD). Experimental evidence indicates that inflammation and fibrosis could play a critical role in the development of CD in hypertension. This issue has not been clarified yet in patients with MS. The aim of our study was to investigate the relationship between markers of inflammation and fibrosis with CD in hypertensive patients with and without MS. One hundred twenty-eight essential hypertensive patients were included in the study: 51 with MS and 77 without MS. Clinical, biochemical parameters, 24-h urinary albumin excretion rate (UAER), levels of C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-alpha), transforming growth factor-beta (TGF-beta), and procollagen type 1 carboxy-terminal propeptide (PICP) were measured. All patients underwent an echocardiographic examination with transmitral Doppler and tissue Doppler imaging (TDI). Left ventricular mass indexed by height(2.7) (LVM/h(2.7)) (P < .001), early diastolic peak flow velocity/early myocardial diastolic velocity ratio (E/Em ratio), a TDI index of diastolic function (P < .001), and 24-h UAER (P < .05) were significantly higher in the group with MS, whereas peak myocardial systolic velocity (Sm), a TDI index of systolic function (P < .001), was lower. Serum levels of CRP (P < .001), TNF-alpha (P < .05), TGF-beta (P < .01), and PICP (P < .001) were significantly increased in MS. These markers were significantly related to higher LVMI(2.7), higher E/Em ratio, and increased 24-h UAER and a lower Sm in the whole population, with a further significant enhancement in MS.\n Question: Are markers of inflammation and fibrosis related to cardiovascular damage in hypertensive patients with metabolic syndrome?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Previous studies have shown that metabolic syndrome (MS) is associated with an increased susceptibility to develop cardiovascular damage (CD). Experimental evidence indicates that inflammation and fibrosis could play a critical role in the development of CD in hypertension. This issue has not been clarified yet in patients with MS. The aim of our study was to investigate the relationship between markers of inflammation and fibrosis with CD in hypertensive patients with and without MS. One hundred twenty-eight essential hypertensive patients were included in the study: 51 with MS and 77 without MS. Clinical, biochemical parameters, 24-h urinary albumin excretion rate (UAER), levels of C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-alpha), transforming growth factor-beta (TGF-beta), and procollagen type 1 carboxy-terminal propeptide (PICP) were measured. All patients underwent an echocardiographic examination with transmitral Doppler and tissue Doppler imaging (TDI). Left ventricular mass indexed by height(2.7) (LVM/h(2.7)) (P < .001), early diastolic peak flow velocity/early myocardial diastolic velocity ratio (E/Em ratio), a TDI index of diastolic function (P < .001), and 24-h UAER (P < .05) were significantly higher in the group with MS, whereas peak myocardial systolic velocity (Sm), a TDI index of systolic function (P < .001), was lower. Serum levels of CRP (P < .001), TNF-alpha (P < .05), TGF-beta (P < .01), and PICP (P < .001) were significantly increased in MS. These markers were significantly related to higher LVMI(2.7), higher E/Em ratio, and increased 24-h UAER and a lower Sm in the whole population, with a further significant enhancement in MS. Question: Are markers of inflammation and fibrosis related to cardiovascular damage in hypertensive patients with metabolic syndrome? Output:
PubmedQA6686
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Microparticles are membrane vesicles shed by cells upon activation and apoptosis. Agonists capable of inducing microparticle generation include cytokines, bacterial products, P-selectin, histamine. Cigarette smoke extract has also been recognized as an agonist involved in microparticle generation with an apoptosis-dependent mechanism. We investigated the possibility that cigarette smoke extract induces the rapid generation of proinflammatory microparticles by human mononuclear cells with a calcium-dependent mechanism. Human mononuclear cells were exposed to cigarette smoke extract. [Ca(2+)]i mobilization was assessed with the fluorescent probe Fluo-4 NW. Microparticles were quantified with a prothrombinase assay and by flow cytometry. Normal human bronchial epithelial cells and A549 alveolar cells were incubated with cigarette smoke extract-induced microparticles and the generation of ICAM-1, IL-8, and MCP-1 was assessed by ELISA. Exposure to cigarette smoke extract induced a rapid increase in [Ca(2+)]i mobilization. Microparticle generation was also increased. EGTA, verapamil and the calmodulin inhibitor, W-7, inhibited microparticle generation. Incubation of lung epithelial cells with cigarette smoke extract-induced microparticles increased the expression of proinflammatory mediators.\n Question: Is rapid shedding of proinflammatory microparticles by human mononuclear cells exposed to cigarette smoke dependent on Ca2+ mobilization?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Microparticles are membrane vesicles shed by cells upon activation and apoptosis. Agonists capable of inducing microparticle generation include cytokines, bacterial products, P-selectin, histamine. Cigarette smoke extract has also been recognized as an agonist involved in microparticle generation with an apoptosis-dependent mechanism. We investigated the possibility that cigarette smoke extract induces the rapid generation of proinflammatory microparticles by human mononuclear cells with a calcium-dependent mechanism. Human mononuclear cells were exposed to cigarette smoke extract. [Ca(2+)]i mobilization was assessed with the fluorescent probe Fluo-4 NW. Microparticles were quantified with a prothrombinase assay and by flow cytometry. Normal human bronchial epithelial cells and A549 alveolar cells were incubated with cigarette smoke extract-induced microparticles and the generation of ICAM-1, IL-8, and MCP-1 was assessed by ELISA. Exposure to cigarette smoke extract induced a rapid increase in [Ca(2+)]i mobilization. Microparticle generation was also increased. EGTA, verapamil and the calmodulin inhibitor, W-7, inhibited microparticle generation. Incubation of lung epithelial cells with cigarette smoke extract-induced microparticles increased the expression of proinflammatory mediators. Question: Is rapid shedding of proinflammatory microparticles by human mononuclear cells exposed to cigarette smoke dependent on Ca2+ mobilization? Output:
PubmedQA188802
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To evaluate the effects of diazoxide on ischemia/reperfusion (I/R)-injured hepatocytes and further elucidate its underlying mechanisms. Male Sprague-Dawley rats were randomized (8 for donor and recipient per group) into five groups: I/R group (4 h of liver cold ischemia followed by 6 h of reperfusion); heme oxygenase-1 (HO-1) small interfering RNA (siRNA) group (injection of siRNA via donor portal vein 48 h prior to harvest); diazoxide (DZ) group (injection of DZ via donor portal vein 10 min prior to harvest); HO-1 siRNA + DZ group; and siRNA control group. Blood and liver samples were collected at 6 h after reperfusion. The mRNA expressions and protein levels of HO-1 were determined by reverse transcription polymerase chain reaction and Western blotting, and tissue morphology was examined by light and transmission electron microscopy. Serum transaminases level and cytokines concentration were also measured. We observed that a significant reduction of HO-1 mRNA and protein levels in HO-1 siRNA and HO-1 siRNA + DZ group when compared with I/R group, while the increases were prominent in the DZ group. Light and transmission electron microscopy indicated severe disruption of tissue with lobular distortion and mitochondrial cristae damage in the HO-1 siRNA and HO-1 siRNA + DZ groups compared with DZ group. Serum alanine aminotransferase, aspartate transaminase, tumor necrosis factor-α and interleukin-6 levels increased in the HO-1 siRNA and HO-1 siRNA + DZ groups, and decreased in the DZ group.\n Question: Does diazoxide attenuate ischemia/reperfusion injury via upregulation of heme oxygenase-1 after liver transplantation in rats?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To evaluate the effects of diazoxide on ischemia/reperfusion (I/R)-injured hepatocytes and further elucidate its underlying mechanisms. Male Sprague-Dawley rats were randomized (8 for donor and recipient per group) into five groups: I/R group (4 h of liver cold ischemia followed by 6 h of reperfusion); heme oxygenase-1 (HO-1) small interfering RNA (siRNA) group (injection of siRNA via donor portal vein 48 h prior to harvest); diazoxide (DZ) group (injection of DZ via donor portal vein 10 min prior to harvest); HO-1 siRNA + DZ group; and siRNA control group. Blood and liver samples were collected at 6 h after reperfusion. The mRNA expressions and protein levels of HO-1 were determined by reverse transcription polymerase chain reaction and Western blotting, and tissue morphology was examined by light and transmission electron microscopy. Serum transaminases level and cytokines concentration were also measured. We observed that a significant reduction of HO-1 mRNA and protein levels in HO-1 siRNA and HO-1 siRNA + DZ group when compared with I/R group, while the increases were prominent in the DZ group. Light and transmission electron microscopy indicated severe disruption of tissue with lobular distortion and mitochondrial cristae damage in the HO-1 siRNA and HO-1 siRNA + DZ groups compared with DZ group. Serum alanine aminotransferase, aspartate transaminase, tumor necrosis factor-α and interleukin-6 levels increased in the HO-1 siRNA and HO-1 siRNA + DZ groups, and decreased in the DZ group. Question: Does diazoxide attenuate ischemia/reperfusion injury via upregulation of heme oxygenase-1 after liver transplantation in rats? Output:
PubmedQA95436
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The Cephalic Index, an anthropometric measure of head shape, was reported to be different between individuals with and without signs of past or concurrent otitis media (OM). In this study, we compared the Cephalic Index and other measures of head shape among groups of children aged 36-48 months with a documented history of chronic OM with effusion (COME), recurrent acute OM (RAOM) and CONTROLS (few to no OM episodes) to test that hypothesis. In 41 CONTROL, 36 COME and 42 RAOM children, Maximum Head Width, Maximum Head Length and Head Circumference were measured and the Cephalic Index (Head Width/Head Length×100) was calculated. The four measures were compared among the three groups using a General Linear Model that included group, sex and race as factors and age as a covariate. There were no differences among groups in the Cephalic Index or Head Length. Head Width was significantly smaller in the RAOM when compared to the CONTROL group and Head Circumference was significantly smaller in the RAOM and COME groups when compared to the CONTROL group. For all measures, the distribution of values showed significant overlap among groups.\n Question: Is the Cephalic Index different among groups of children aged 36-48 months with chronic otitis media with effusion , recurrent acute otitis media and controls?\n Output: " }, { "role": "assistant", "content": "no" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The Cephalic Index, an anthropometric measure of head shape, was reported to be different between individuals with and without signs of past or concurrent otitis media (OM). In this study, we compared the Cephalic Index and other measures of head shape among groups of children aged 36-48 months with a documented history of chronic OM with effusion (COME), recurrent acute OM (RAOM) and CONTROLS (few to no OM episodes) to test that hypothesis. In 41 CONTROL, 36 COME and 42 RAOM children, Maximum Head Width, Maximum Head Length and Head Circumference were measured and the Cephalic Index (Head Width/Head Length×100) was calculated. The four measures were compared among the three groups using a General Linear Model that included group, sex and race as factors and age as a covariate. There were no differences among groups in the Cephalic Index or Head Length. Head Width was significantly smaller in the RAOM when compared to the CONTROL group and Head Circumference was significantly smaller in the RAOM and COME groups when compared to the CONTROL group. For all measures, the distribution of values showed significant overlap among groups. Question: Is the Cephalic Index different among groups of children aged 36-48 months with chronic otitis media with effusion , recurrent acute otitis media and controls? Output:
PubmedQA33760
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Phospholipid transfer protein (PLTP) is a multifunctional, extracellular lipid transport protein that plays a major role in lipoprotein metabolism and atherosclerosis. Recent in vivo studies suggested that unlike systemic PLTP, macrophage-derived PLTP would be antiatherogenic. The present study aimed at characterizing the atheroprotective properties of macrophage-derived PLTP. Peritoneal macrophages were isolated from PLTP-deficient and wild-type mice and their biochemical characteristics were compared. It is shown that macrophages isolated from PLTP-deficient mice have increased basal cholesterol content and accumulate more cholesterol in the presence of LDL compared with wild-type cells. Cholesterol parameters in macrophages of PLTP-deficient mice were normalized by dietary alpha-tocopherol supplementation.\n Question: Is cholesterol accumulation increased in macrophages of phospholipid transfer protein-deficient mice : normalization by dietary alpha-tocopherol supplementation?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Phospholipid transfer protein (PLTP) is a multifunctional, extracellular lipid transport protein that plays a major role in lipoprotein metabolism and atherosclerosis. Recent in vivo studies suggested that unlike systemic PLTP, macrophage-derived PLTP would be antiatherogenic. The present study aimed at characterizing the atheroprotective properties of macrophage-derived PLTP. Peritoneal macrophages were isolated from PLTP-deficient and wild-type mice and their biochemical characteristics were compared. It is shown that macrophages isolated from PLTP-deficient mice have increased basal cholesterol content and accumulate more cholesterol in the presence of LDL compared with wild-type cells. Cholesterol parameters in macrophages of PLTP-deficient mice were normalized by dietary alpha-tocopherol supplementation. Question: Is cholesterol accumulation increased in macrophages of phospholipid transfer protein-deficient mice : normalization by dietary alpha-tocopherol supplementation? Output:
PubmedQA28232
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Chronic thromboembolic pulmonary hypertension (CTEPH) is characterized by occlusion of pulmonary arteries by organized chronic thrombi. Persistent hypoxemia and residual pulmonary hypertension (PH) following successful pulmonary endarterectomy (PEA) are clinically important problems; however, the underlying mechanisms remain unclear. We have previously reported that residual PH is closely related to severe pulmonary vascular remodeling and hypothesize that this arteriopathy might also be involved in impaired gas exchange. The purpose of this study was to evaluate the association between hypoxemia and pulmonary arteriopathy after PEA. Between December 2011 and November 2014, 23 CTEPH patients underwent PEA and lung biopsy. The extent of pulmonary arteriopathy was quantified pathologically in lung biopsy specimens. We then analyzed the relationship between the severity of pulmonary arteriopathy and gas exchange after PEA. We observed that the severity of pulmonary arteriopathy was negatively correlated with postoperative and follow-up PaO2 (postoperative PaO2: r = -0.73, p = 0.0004; follow-up PaO2: r = -0.66, p = 0.001), but not with preoperative PaO2 (r = -0.373, p = 0.08). Multivariate analysis revealed that the obstruction ratio and patient age were determinants of PaO2 one month after PEA (R2 = 0.651, p = 0.00009). Furthermore, the obstruction ratio and improvement of pulmonary vascular resistance were determinants of PaO2 at follow-up (R2 = 0.545, p = 0.0002). Severe pulmonary arteriopathy might increase the alveolar-arterial oxygen difference and impair diffusion capacity, resulting in hypoxemia following PEA.\n Question: Does severe Pulmonary Arteriopathy be Associated with Persistent Hypoxemia after Pulmonary Endarterectomy in Chronic Thromboembolic Pulmonary Hypertension?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Chronic thromboembolic pulmonary hypertension (CTEPH) is characterized by occlusion of pulmonary arteries by organized chronic thrombi. Persistent hypoxemia and residual pulmonary hypertension (PH) following successful pulmonary endarterectomy (PEA) are clinically important problems; however, the underlying mechanisms remain unclear. We have previously reported that residual PH is closely related to severe pulmonary vascular remodeling and hypothesize that this arteriopathy might also be involved in impaired gas exchange. The purpose of this study was to evaluate the association between hypoxemia and pulmonary arteriopathy after PEA. Between December 2011 and November 2014, 23 CTEPH patients underwent PEA and lung biopsy. The extent of pulmonary arteriopathy was quantified pathologically in lung biopsy specimens. We then analyzed the relationship between the severity of pulmonary arteriopathy and gas exchange after PEA. We observed that the severity of pulmonary arteriopathy was negatively correlated with postoperative and follow-up PaO2 (postoperative PaO2: r = -0.73, p = 0.0004; follow-up PaO2: r = -0.66, p = 0.001), but not with preoperative PaO2 (r = -0.373, p = 0.08). Multivariate analysis revealed that the obstruction ratio and patient age were determinants of PaO2 one month after PEA (R2 = 0.651, p = 0.00009). Furthermore, the obstruction ratio and improvement of pulmonary vascular resistance were determinants of PaO2 at follow-up (R2 = 0.545, p = 0.0002). Severe pulmonary arteriopathy might increase the alveolar-arterial oxygen difference and impair diffusion capacity, resulting in hypoxemia following PEA. Question: Does severe Pulmonary Arteriopathy be Associated with Persistent Hypoxemia after Pulmonary Endarterectomy in Chronic Thromboembolic Pulmonary Hypertension? Output:
PubmedQA134111
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Generally Rh-negative patients need to be transfused with Rh-negative red blood cells. For pregnant women carrying Rh-positive fetus, the antenatal anti-D detection and Rh immunoglobulin prophylaxis are required worldwide. In East Asia, a RhD variant, termed \"Asia type\" DEL, was found in approximately 30% of apparent Rh-negative individuals. The antigenic and molecular properties of the DEL were previously defined. Few data discuss whether DEL could be immunized by D antigen clinically although DEL was reported arousing alloimmunization to true Rh-negative patients. To determine whether the DEL variant can be immunized to the D antigen, we retrospectively evaluated 104 Rh-negative pregnancies with allo-anti-D antibodies, and we also tracked 199 consecutive apparent Rh-negative pregnant women, with a history of gestations or parturitions but not subject to anti-D gamma-globulin prophylaxis, for evidence of allo-anti-D. The DEL variant was first excluded by ccee phenotypes and then identified through PCR analysis or sequencing. In the retrospective study, we expected to find 30 DEL variants, yet none of the anti-D alloimmunized women were DEL-positive. And in the second group, none of 44 DEL-positive women versus 38 of 155 (24.5%) true Rh-negative women (those excluding DEL) formed allo-anti-D.\n Question: Is antenatal Rh prophylaxis unnecessary for `` Asia type '' DEL women?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Generally Rh-negative patients need to be transfused with Rh-negative red blood cells. For pregnant women carrying Rh-positive fetus, the antenatal anti-D detection and Rh immunoglobulin prophylaxis are required worldwide. In East Asia, a RhD variant, termed "Asia type" DEL, was found in approximately 30% of apparent Rh-negative individuals. The antigenic and molecular properties of the DEL were previously defined. Few data discuss whether DEL could be immunized by D antigen clinically although DEL was reported arousing alloimmunization to true Rh-negative patients. To determine whether the DEL variant can be immunized to the D antigen, we retrospectively evaluated 104 Rh-negative pregnancies with allo-anti-D antibodies, and we also tracked 199 consecutive apparent Rh-negative pregnant women, with a history of gestations or parturitions but not subject to anti-D gamma-globulin prophylaxis, for evidence of allo-anti-D. The DEL variant was first excluded by ccee phenotypes and then identified through PCR analysis or sequencing. In the retrospective study, we expected to find 30 DEL variants, yet none of the anti-D alloimmunized women were DEL-positive. And in the second group, none of 44 DEL-positive women versus 38 of 155 (24.5%) true Rh-negative women (those excluding DEL) formed allo-anti-D. Question: Is antenatal Rh prophylaxis unnecessary for `` Asia type '' DEL women? Output:
PubmedQA19437
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Comparison of topical ciprofloxacin/dexamethasone otic suspension (CIP/DEX) to ofloxacin otic solution (OFL) for treatment of granulation tissue in children with AOMT. 599 children aged >/=6 months to 12 years with AOMT of up to 3 weeks' duration were enrolled. Patients received either CIP/DEX 4 drops twice daily for 7 days or OFL 5 drops twice daily for 10 days. Granulation tissue severity was graded at clinic visits on days 1, 3, 11, and 18. Granulation tissue was present in 90 of 599 AOMT patients (15.0%) at baseline. CIP/DEX treatment was superior to OFL for reduction of granulation tissue at the day 11 visit (81.3% compared with 56.1%, P = 0.0067) and the day 18 visit (91.7% compared with 73.2%, P = 0.0223). Both topical otic preparations are safe and well tolerated in pediatric patients.\n Question: Is topical ciprofloxacin/dexamethasone otic suspension superior to ofloxacin otic solution in the treatment of granulation tissue in children with acute otitis media with otorrhea through tympanostomy tubes?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Comparison of topical ciprofloxacin/dexamethasone otic suspension (CIP/DEX) to ofloxacin otic solution (OFL) for treatment of granulation tissue in children with AOMT. 599 children aged >/=6 months to 12 years with AOMT of up to 3 weeks' duration were enrolled. Patients received either CIP/DEX 4 drops twice daily for 7 days or OFL 5 drops twice daily for 10 days. Granulation tissue severity was graded at clinic visits on days 1, 3, 11, and 18. Granulation tissue was present in 90 of 599 AOMT patients (15.0%) at baseline. CIP/DEX treatment was superior to OFL for reduction of granulation tissue at the day 11 visit (81.3% compared with 56.1%, P = 0.0067) and the day 18 visit (91.7% compared with 73.2%, P = 0.0223). Both topical otic preparations are safe and well tolerated in pediatric patients. Question: Is topical ciprofloxacin/dexamethasone otic suspension superior to ofloxacin otic solution in the treatment of granulation tissue in children with acute otitis media with otorrhea through tympanostomy tubes? Output:
PubmedQA189743
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To investigate the course of functional status assessed by health assessment questionnaire (HAQ) in rheumatoid arthritis (RA) patients with sustained clinical remission (REM). In recent RA clinical trials, we identified patients with subsequent visits of ≥24 weeks in clinical REM according to the disease activity score using 28-joint counts including C-reactive protein (DAS28) (≤2.6), or simplified disease activity index (SDAI) (≤3.3). Area under the curve (AUC) and mean HAQ scores throughout the time in sustained REM were compared using t test, analyses of variance (ANOVA) and adjusted general linear modeling (GLM) with repeated measures. In Cox regression analyses, the time to regain full physical function was modeled. Sensitivity analyses were performed in patients of sustained SDAI low disease activity (LDA; SDAI ≤11). A total of 610 out of 4364 patients achieved sustained DAS28 REM (14%) and 252 SDAI REM (5.8%). ANOVA testing for linear trend showed significant decrease of mean HAQ from week 0 (start of REM) to week 24, regardless of REM criteria used. AUC of HAQ throughout 24 weeks of REM was higher in DAS28 compared to SDAI REM (p ≤0.01). GLM adjusting for covariates showed significant decrease of monthly HAQ scores from week 0 to 24 (DAS28: 0.276, 0.243, 0.229, 0.222, 0.219, 0.209 to 0.199; p = 0.0001; SDAI: 0.147, 0.142, 0.149, 0.129, 0.123, 0.117 to 0.114; p = 0.029). Similarly, a decrease of HAQ over time was found in patients of sustained SDAI LDA. In DAS28 REM, the chance of regaining full physical function was higher for female (hazard ratio HR [95% confidence interval]: 1.41 [1.13-1.76]) and early RA patients (disease duration ≤2 years: HR 1.29 [1.01-1.65]); in SDAI REM no significant differences were found.\n Question: Does physical function continue to improve when clinical remission is sustained in rheumatoid arthritis patients?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To investigate the course of functional status assessed by health assessment questionnaire (HAQ) in rheumatoid arthritis (RA) patients with sustained clinical remission (REM). In recent RA clinical trials, we identified patients with subsequent visits of ≥24 weeks in clinical REM according to the disease activity score using 28-joint counts including C-reactive protein (DAS28) (≤2.6), or simplified disease activity index (SDAI) (≤3.3). Area under the curve (AUC) and mean HAQ scores throughout the time in sustained REM were compared using t test, analyses of variance (ANOVA) and adjusted general linear modeling (GLM) with repeated measures. In Cox regression analyses, the time to regain full physical function was modeled. Sensitivity analyses were performed in patients of sustained SDAI low disease activity (LDA; SDAI ≤11). A total of 610 out of 4364 patients achieved sustained DAS28 REM (14%) and 252 SDAI REM (5.8%). ANOVA testing for linear trend showed significant decrease of mean HAQ from week 0 (start of REM) to week 24, regardless of REM criteria used. AUC of HAQ throughout 24 weeks of REM was higher in DAS28 compared to SDAI REM (p ≤0.01). GLM adjusting for covariates showed significant decrease of monthly HAQ scores from week 0 to 24 (DAS28: 0.276, 0.243, 0.229, 0.222, 0.219, 0.209 to 0.199; p = 0.0001; SDAI: 0.147, 0.142, 0.149, 0.129, 0.123, 0.117 to 0.114; p = 0.029). Similarly, a decrease of HAQ over time was found in patients of sustained SDAI LDA. In DAS28 REM, the chance of regaining full physical function was higher for female (hazard ratio HR [95% confidence interval]: 1.41 [1.13-1.76]) and early RA patients (disease duration ≤2 years: HR 1.29 [1.01-1.65]); in SDAI REM no significant differences were found. Question: Does physical function continue to improve when clinical remission is sustained in rheumatoid arthritis patients? Output:
PubmedQA126627
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The purpose of the present study was to investigate whether individuals with pervasive developmental disorders (PDD) show differential activation during an emotional activation task compared with age- and sex-matched controls, by measuring changes in the concentration of oxygenated (oxyHb) and deoxygenated (deoxyHb) hemoglobin, using near-infrared spectroscopy (NIRS). Fourteen patients with PDD and 14 age- and sex-matched healthy controls participated in the study. The relative changes of concentrations of oxyHb and deoxyHb were measured on NIRS during an implicit processing task of fearful expression using Japanese standard faces. PDD patients had significantly reduced oxyHb changes in the prefrontal cortex (PFC) compared to healthy controls.\n Question: Does multi-channel near-infrared spectroscopy show reduced activation in the prefrontal cortex during facial expression processing in pervasive developmental disorder?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The purpose of the present study was to investigate whether individuals with pervasive developmental disorders (PDD) show differential activation during an emotional activation task compared with age- and sex-matched controls, by measuring changes in the concentration of oxygenated (oxyHb) and deoxygenated (deoxyHb) hemoglobin, using near-infrared spectroscopy (NIRS). Fourteen patients with PDD and 14 age- and sex-matched healthy controls participated in the study. The relative changes of concentrations of oxyHb and deoxyHb were measured on NIRS during an implicit processing task of fearful expression using Japanese standard faces. PDD patients had significantly reduced oxyHb changes in the prefrontal cortex (PFC) compared to healthy controls. Question: Does multi-channel near-infrared spectroscopy show reduced activation in the prefrontal cortex during facial expression processing in pervasive developmental disorder? Output:
PubmedQA11976
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: ATP exerts diverse effects on various cell types via specific purinergic P2Y receptors. Intracellular signaling cascades are the main routes of communication between P2Y receptors and regulatory targets in the cell. We examined the role of ATP in the modulation of ERK1/2, JNK1/2, and p38 MAP kinases (MAPKs) in human colon cancer Caco-2 cells. Immunoblot analysis showed that ATP induces the phosphorylation of MAPKs in a time- and dose-dependent manner, peaking at 5 min at 10 microM ATP. Moreover, ATPgammaS, UTP, and UDP but not ADP or ADPbetaS increased phosphorylation of MAPKs, indicating the involvement of, at least, P2Y2/P2Y4 and P2Y6 receptor subtypes. RT-PCR studies and PCR product sequencing supported the expression of P2Y2 and P2Y4 receptors in this cell line. Spectrofluorimetric measurements showed that cell stimulation with ATP induced transient elevations in intracellular calcium concentration. In addition, ATP-induced phosphorylation of MAPKs in Caco-2 cells was dependent on Src family tyrosine kinases, calcium influx, and intracellular Ca2+ release and was partially dependent on the cAMP/PKA and PKC pathways and the EGFR.\n Question: Does extracellular ATP activate MAP kinase cascades through a P2Y purinergic receptor in the human intestinal Caco-2 cell line?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: ATP exerts diverse effects on various cell types via specific purinergic P2Y receptors. Intracellular signaling cascades are the main routes of communication between P2Y receptors and regulatory targets in the cell. We examined the role of ATP in the modulation of ERK1/2, JNK1/2, and p38 MAP kinases (MAPKs) in human colon cancer Caco-2 cells. Immunoblot analysis showed that ATP induces the phosphorylation of MAPKs in a time- and dose-dependent manner, peaking at 5 min at 10 microM ATP. Moreover, ATPgammaS, UTP, and UDP but not ADP or ADPbetaS increased phosphorylation of MAPKs, indicating the involvement of, at least, P2Y2/P2Y4 and P2Y6 receptor subtypes. RT-PCR studies and PCR product sequencing supported the expression of P2Y2 and P2Y4 receptors in this cell line. Spectrofluorimetric measurements showed that cell stimulation with ATP induced transient elevations in intracellular calcium concentration. In addition, ATP-induced phosphorylation of MAPKs in Caco-2 cells was dependent on Src family tyrosine kinases, calcium influx, and intracellular Ca2+ release and was partially dependent on the cAMP/PKA and PKC pathways and the EGFR. Question: Does extracellular ATP activate MAP kinase cascades through a P2Y purinergic receptor in the human intestinal Caco-2 cell line? Output:
PubmedQA169452
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Lassa virus and Marburg virus are two causative agents of viral hemorrhagic fever. Their diagnosis is difficult because patients infected with either pathogen present similar nonspecific symptoms early after infection. Current diagnostic tests are based on detecting viral proteins or nucleic acids in the blood, but these cannot be found during the early stages of disease, before the virus starts replicating in the blood. Using the transcriptional response of the host during infection can lead to earlier diagnoses compared to those of traditional methods. In this study, we use RNA sequencing to obtain a high-resolution view of the in vivo transcriptional dynamics of peripheral blood mononuclear cells (PBMCs) throughout both types of infection. We report a subset of host mRNAs, including heat-shock proteins like HSPA1B, immunoglobulins like IGJ, and cell adhesion molecules like SIGLEC1, whose differences in expression are strong enough to distinguish Lassa infection from Marburg infection in non-human primates. We have validated these infection-specific expression differences by using microarrays on a larger set of samples, and by quantifying the expression of individual genes using RT-PCR.\n Question: Do lassa and Marburg viruses elicit distinct host transcriptional responses early after infection?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Lassa virus and Marburg virus are two causative agents of viral hemorrhagic fever. Their diagnosis is difficult because patients infected with either pathogen present similar nonspecific symptoms early after infection. Current diagnostic tests are based on detecting viral proteins or nucleic acids in the blood, but these cannot be found during the early stages of disease, before the virus starts replicating in the blood. Using the transcriptional response of the host during infection can lead to earlier diagnoses compared to those of traditional methods. In this study, we use RNA sequencing to obtain a high-resolution view of the in vivo transcriptional dynamics of peripheral blood mononuclear cells (PBMCs) throughout both types of infection. We report a subset of host mRNAs, including heat-shock proteins like HSPA1B, immunoglobulins like IGJ, and cell adhesion molecules like SIGLEC1, whose differences in expression are strong enough to distinguish Lassa infection from Marburg infection in non-human primates. We have validated these infection-specific expression differences by using microarrays on a larger set of samples, and by quantifying the expression of individual genes using RT-PCR. Question: Do lassa and Marburg viruses elicit distinct host transcriptional responses early after infection? Output:
PubmedQA114930
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The aim of this work was to compare the functional results of secondary Girdlestone hips with the results of total hip replacement (THR) after a Girdlestone situation. 72 patients with THR following a Girdlestone situation and 87 patients with a Girdlestone situation (90 hips) were compared with regard to defined endpoints. THR following a Girdlestone situation provided for significantly higher patient satisfaction (89 % versus 13 %) and hip function (HHS 63 versus 39 points). The groups only marginally differed with regard to the incidence of complications (0.32 versus 0.26 per patient) and the necessity for surgical revision (0.38 versus 0.31 per patient).\n Question: Is [ Reimplantation of the artificial hip joint in girdlestone hips superior to girdlestone arthroplasty by itself ]?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The aim of this work was to compare the functional results of secondary Girdlestone hips with the results of total hip replacement (THR) after a Girdlestone situation. 72 patients with THR following a Girdlestone situation and 87 patients with a Girdlestone situation (90 hips) were compared with regard to defined endpoints. THR following a Girdlestone situation provided for significantly higher patient satisfaction (89 % versus 13 %) and hip function (HHS 63 versus 39 points). The groups only marginally differed with regard to the incidence of complications (0.32 versus 0.26 per patient) and the necessity for surgical revision (0.38 versus 0.31 per patient). Question: Is [ Reimplantation of the artificial hip joint in girdlestone hips superior to girdlestone arthroplasty by itself ]? Output:
PubmedQA104811
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Nerve repair using photochemically bonded human amnion nerve wraps can result in superior outcomes in comparison with standard suture. When applied to nerve grafts, efficacy has been limited by proteolytic degradation of bonded amnion during extended periods of recovery. Chemical cross-linking of amnion before bonding may improve wrap durability and efficacy. Three nerve wraps (amnion, cross-linked amnion, and cross-linked swine intestinal submucosa) and three fixation methods (suture, fibrin glue, and photochemical bonding) were investigated. One hundred ten Lewis rats had 15-mm left sciatic nerve gaps repaired with isografts. Nine groups (n = 10) had isografts secured by one of the aforementioned wrap/fixation combinations. Positive and negative control groups (n = 10) were repaired with graft and suture and no repair, respectively. Outcomes were assessed using sciatic function index, muscle mass retention, and histomorphometry. Statistical analysis was performed using analysis of variance and the post hoc Bonferroni test (p < 0.05). Cross-linking improved amnion durability. Photochemically bonded cross-linked amnion recovered the greatest sciatic function index, although this was not significant in comparison with graft and suture. Photochemically bonded cross-linked amnion recovered significantly greater muscle mass (67.3 ± 4.4 percent versus 60.0 ± 5.2 percent; p = 0.02), fiber diameter, axon diameter, and myelin thickness (6.87 ± 2.23 μm versus 5.47 ± 1.70 μm; 4.51 ± 1.83 μm versus 3.50 ± 1.44 μm; and 2.35 ± 0.64 μm versus 1.96 ± 0.47 μm, respectively) in comparison with graft and suture.\n Question: Does light-Activated Sealing of Nerve Graft Coaptation Sites improve Outcome following Large Gap Peripheral Nerve Injury?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Nerve repair using photochemically bonded human amnion nerve wraps can result in superior outcomes in comparison with standard suture. When applied to nerve grafts, efficacy has been limited by proteolytic degradation of bonded amnion during extended periods of recovery. Chemical cross-linking of amnion before bonding may improve wrap durability and efficacy. Three nerve wraps (amnion, cross-linked amnion, and cross-linked swine intestinal submucosa) and three fixation methods (suture, fibrin glue, and photochemical bonding) were investigated. One hundred ten Lewis rats had 15-mm left sciatic nerve gaps repaired with isografts. Nine groups (n = 10) had isografts secured by one of the aforementioned wrap/fixation combinations. Positive and negative control groups (n = 10) were repaired with graft and suture and no repair, respectively. Outcomes were assessed using sciatic function index, muscle mass retention, and histomorphometry. Statistical analysis was performed using analysis of variance and the post hoc Bonferroni test (p < 0.05). Cross-linking improved amnion durability. Photochemically bonded cross-linked amnion recovered the greatest sciatic function index, although this was not significant in comparison with graft and suture. Photochemically bonded cross-linked amnion recovered significantly greater muscle mass (67.3 ± 4.4 percent versus 60.0 ± 5.2 percent; p = 0.02), fiber diameter, axon diameter, and myelin thickness (6.87 ± 2.23 μm versus 5.47 ± 1.70 μm; 4.51 ± 1.83 μm versus 3.50 ± 1.44 μm; and 2.35 ± 0.64 μm versus 1.96 ± 0.47 μm, respectively) in comparison with graft and suture. Question: Does light-Activated Sealing of Nerve Graft Coaptation Sites improve Outcome following Large Gap Peripheral Nerve Injury? Output:
PubmedQA141372
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Infusion of insulin produces sympathoexcitation, nitric oxide (NO) generation and NO-mediated vasodilation. Because central nervous system NO may inhibit sympathetic outflow, the present study was designed to determine whether NO synthase blockade would enhance insulin-mediated sympathetic activation. We additionally aimed to determine whether augmented sympathoexcitation and reduced NO-mediated vasodilation, during combined NO synthase blockade and hyperinsulinemia, would result in a blood pressure increase. We infused vehicle (Control; n = 7) or insulin (10 mU/min) in anaesthetized rats receiving either no pretreatment (Insulin; n = 7) or after pretreatment with the NO blocker, NG-monomethyl-L-arginine (L-NMMA-insulin; 0.25 mg/kg per min; n = 7), while measuring mean arterial pressure (MAP), heart rate and lumbar sympathetic nerve activity (SNA) during euglycemic clamp. An additional control group received L-NMMA (L-NMMA; n = 7). Insulin rats had large SNA increases (190 +/- 22% from 100% baseline), contrasting with small increases in the Control (136 +/- 10%) and L-NMMA (135 +/- 20%) groups. Unexpectedly, NO blockade abolished insulin-induced SNA increases in the L-NMMA-insulin group (96 +/- 12%). In agreement with the SNA findings, Insulin rats had heart rate increases while no heart rate changes were observed in the L-NMMA-insulin, Control, or L-NMMA groups. In addition, there was an unexpected was a lack of MAP increase in L-NMMA-insulin rats. MAP also did not change in the Control, L-NMMA or Insulin groups.\n Question: Does inhibition of nitric oxide synthesis attenuate insulin-mediated sympathetic activation in rats?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Infusion of insulin produces sympathoexcitation, nitric oxide (NO) generation and NO-mediated vasodilation. Because central nervous system NO may inhibit sympathetic outflow, the present study was designed to determine whether NO synthase blockade would enhance insulin-mediated sympathetic activation. We additionally aimed to determine whether augmented sympathoexcitation and reduced NO-mediated vasodilation, during combined NO synthase blockade and hyperinsulinemia, would result in a blood pressure increase. We infused vehicle (Control; n = 7) or insulin (10 mU/min) in anaesthetized rats receiving either no pretreatment (Insulin; n = 7) or after pretreatment with the NO blocker, NG-monomethyl-L-arginine (L-NMMA-insulin; 0.25 mg/kg per min; n = 7), while measuring mean arterial pressure (MAP), heart rate and lumbar sympathetic nerve activity (SNA) during euglycemic clamp. An additional control group received L-NMMA (L-NMMA; n = 7). Insulin rats had large SNA increases (190 +/- 22% from 100% baseline), contrasting with small increases in the Control (136 +/- 10%) and L-NMMA (135 +/- 20%) groups. Unexpectedly, NO blockade abolished insulin-induced SNA increases in the L-NMMA-insulin group (96 +/- 12%). In agreement with the SNA findings, Insulin rats had heart rate increases while no heart rate changes were observed in the L-NMMA-insulin, Control, or L-NMMA groups. In addition, there was an unexpected was a lack of MAP increase in L-NMMA-insulin rats. MAP also did not change in the Control, L-NMMA or Insulin groups. Question: Does inhibition of nitric oxide synthesis attenuate insulin-mediated sympathetic activation in rats? Output:
PubmedQA194766
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Although there is growing awareness of the beneficial potential of onion intake to lower the risk of cardiovascular disease, there is little information about the effect of onion on ischemic heart injury, one of the most common cardiovascular diseases. This study investigates the effect of the methanol-soluble extract of onion on ischemic injury in heart-derived H9c2 cells in vitro and in rat hearts in vivo. The underlying mechanism is also investigated. To evaluate the effect of onion on ischemia-induced cell death, LDH release and TUNEL-positivity were assessed in H9c2 cells, and the infarct size was measured in a myocardial infarct model. To investigate the mechanism of the cardioprotection by onion, the reactive oxygen species (ROS) level and the mitochondrial membrane potential (DeltaPsi(m)) were measured using an imaging technique; the caspase-3 activity was assayed, and Western blotting was performed to examine cytochrome c release in H9c2 cells. The methanolic extract of onion had a preventive effect on ischemia/hypoxia-induced apoptotic death in H9c2 cells in vitro and in rat heart in vivo. The onion extract (0.05 g/ml) inhibited the elevation of the ROS, mitochondrial membrane depolarization, cytochrome c release and caspase-3 activation during hypoxia in H9c2 cells. In the in vivo rat myocardial infarction model, onion extract (10 g/kg) significantly reduced the infarct size, the apoptotic cell death of the heart and the plasma MDA level.\n Question: Does methanolic extract of onion ( Allium cepa ) attenuate ischemia/hypoxia-induced apoptosis in cardiomyocytes via antioxidant effect?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Although there is growing awareness of the beneficial potential of onion intake to lower the risk of cardiovascular disease, there is little information about the effect of onion on ischemic heart injury, one of the most common cardiovascular diseases. This study investigates the effect of the methanol-soluble extract of onion on ischemic injury in heart-derived H9c2 cells in vitro and in rat hearts in vivo. The underlying mechanism is also investigated. To evaluate the effect of onion on ischemia-induced cell death, LDH release and TUNEL-positivity were assessed in H9c2 cells, and the infarct size was measured in a myocardial infarct model. To investigate the mechanism of the cardioprotection by onion, the reactive oxygen species (ROS) level and the mitochondrial membrane potential (DeltaPsi(m)) were measured using an imaging technique; the caspase-3 activity was assayed, and Western blotting was performed to examine cytochrome c release in H9c2 cells. The methanolic extract of onion had a preventive effect on ischemia/hypoxia-induced apoptotic death in H9c2 cells in vitro and in rat heart in vivo. The onion extract (0.05 g/ml) inhibited the elevation of the ROS, mitochondrial membrane depolarization, cytochrome c release and caspase-3 activation during hypoxia in H9c2 cells. In the in vivo rat myocardial infarction model, onion extract (10 g/kg) significantly reduced the infarct size, the apoptotic cell death of the heart and the plasma MDA level. Question: Does methanolic extract of onion ( Allium cepa ) attenuate ischemia/hypoxia-induced apoptosis in cardiomyocytes via antioxidant effect? Output:
PubmedQA53227
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The objective of this study was to clarify the usefulness of positron emission tomography (PET) using(18)F-fluorodeoxyglucose (FDG) and carbon 11-labeled acetate (AC) for predicting the histologic types and tumor invasiveness of thymoma in a multicenter study. Forty thymomas were examined using both FDG-PET and AC-PET before surgery. The histologic types were type A in 1 thymoma, type AB in 12 thymomas, type B1 in 11 thymomas, type B2 in 7 thymomas, type B3 in 6 thymomas, and type C in 3 thymomas. Tumor invasiveness was assessed by pathologic tumor stage and was identified as stage I in 17 tumors, stage II in 17 tumors, stage III in 4 tumors, and stage IV in 2 tumors. FDG and AC uptake was measured as the maximum standard uptake value (SUV). The FDG-SUV in type C thymomas was significantly higher than that in the other types (A-B3; P = .001 - P = .048). The AC-SUV in type A/AB thymomas was significantly higher than that in the other tumor types (B1-C; P < .001 - P = .002). All 3 type C tumors had an FDG-SUV >or=6.3, and all 13 type A/AB tumors had an FDG-SUV <6.3 and an AC-SUV >or=5.7. All 17 thymomas that had an FDG-SUV <6.3 and an AC-SUV <5.7 were type B1, B2, or B3. Neither the FDG-SUV nor the AC-SUV differed significantly between the stages I/II tumors and stage III/IV tumors.\n Question: Are 18F-fluorodeoxyglucose and 11C-acetate positron emission tomography useful modalities for diagnosing the histologic type of thymoma?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The objective of this study was to clarify the usefulness of positron emission tomography (PET) using(18)F-fluorodeoxyglucose (FDG) and carbon 11-labeled acetate (AC) for predicting the histologic types and tumor invasiveness of thymoma in a multicenter study. Forty thymomas were examined using both FDG-PET and AC-PET before surgery. The histologic types were type A in 1 thymoma, type AB in 12 thymomas, type B1 in 11 thymomas, type B2 in 7 thymomas, type B3 in 6 thymomas, and type C in 3 thymomas. Tumor invasiveness was assessed by pathologic tumor stage and was identified as stage I in 17 tumors, stage II in 17 tumors, stage III in 4 tumors, and stage IV in 2 tumors. FDG and AC uptake was measured as the maximum standard uptake value (SUV). The FDG-SUV in type C thymomas was significantly higher than that in the other types (A-B3; P = .001 - P = .048). The AC-SUV in type A/AB thymomas was significantly higher than that in the other tumor types (B1-C; P < .001 - P = .002). All 3 type C tumors had an FDG-SUV >or=6.3, and all 13 type A/AB tumors had an FDG-SUV <6.3 and an AC-SUV >or=5.7. All 17 thymomas that had an FDG-SUV <6.3 and an AC-SUV <5.7 were type B1, B2, or B3. Neither the FDG-SUV nor the AC-SUV differed significantly between the stages I/II tumors and stage III/IV tumors. Question: Are 18F-fluorodeoxyglucose and 11C-acetate positron emission tomography useful modalities for diagnosing the histologic type of thymoma? Output:
PubmedQA138706
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Continuous ambulatory peritoneal dialysis (CAPD) induces structural changes in the peritoneal membrane such as fibrosis, vasculopathy and angioneogenesis with a reduction in ultrafiltration capacity. Leukotriene (LT) receptor antagonists have been found to be effective to prevent fibrosis in some nonperitoneal tissues. The aim of this study is to investigate the possible beneficial effect of montelukast, a LT receptor antagonist, on peritoneal membrane exposed to hypertonic peritoneal dialysis in uremic rats. Of the 48 male, 5/6 nephrectomized Wistar rats 29 remained alive and were included in the study. These studied rats were divided into 3 groups: Group I (n=7) was the control group, Group II (n=8) was treated with 20 ml hypertonic PDF intraperitoneally daily and Group III was treated with montelukast and similar PDF treatment protocol. The morphological and functional changes in the peritoneal membrane as well as cytokine expression were compared between groups. Submesothelial thickness and the severity of the degree of hyaline vasculapathy were more prominent in group III when compared to group I. There were no significant differences between group II and other groups in terms of submesothelial thickness and the severity of the degree of hyaline vasculapathy. Increased expressions of TGF-β and VEGF in parietal peritoneal membrane were found in group II and group III when compared to group I. The amount of TGF-β and VEGF expression were similar in group II and group III.\n Question: Does cysteinyl 1 receptor antagonist montelukast , prevent peritoneal membrane damage in experimental chronic peritoneal dialysis model in rats?\n Output: " }, { "role": "assistant", "content": "no" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Continuous ambulatory peritoneal dialysis (CAPD) induces structural changes in the peritoneal membrane such as fibrosis, vasculopathy and angioneogenesis with a reduction in ultrafiltration capacity. Leukotriene (LT) receptor antagonists have been found to be effective to prevent fibrosis in some nonperitoneal tissues. The aim of this study is to investigate the possible beneficial effect of montelukast, a LT receptor antagonist, on peritoneal membrane exposed to hypertonic peritoneal dialysis in uremic rats. Of the 48 male, 5/6 nephrectomized Wistar rats 29 remained alive and were included in the study. These studied rats were divided into 3 groups: Group I (n=7) was the control group, Group II (n=8) was treated with 20 ml hypertonic PDF intraperitoneally daily and Group III was treated with montelukast and similar PDF treatment protocol. The morphological and functional changes in the peritoneal membrane as well as cytokine expression were compared between groups. Submesothelial thickness and the severity of the degree of hyaline vasculapathy were more prominent in group III when compared to group I. There were no significant differences between group II and other groups in terms of submesothelial thickness and the severity of the degree of hyaline vasculapathy. Increased expressions of TGF-β and VEGF in parietal peritoneal membrane were found in group II and group III when compared to group I. The amount of TGF-β and VEGF expression were similar in group II and group III. Question: Does cysteinyl 1 receptor antagonist montelukast , prevent peritoneal membrane damage in experimental chronic peritoneal dialysis model in rats? Output:
PubmedQA116646
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To examine whether platelet-released adenosine diphosphate (ADP) would contribute to the stabilization of rabbit platelet aggregation induced by platelet activating factor (PAF). Rabbit platelet aggregation induced by PAF was measured turbimetrically. ADP release from rabbit platelets stimulated by PAF was determined by HPLC. Intracellular Ca2+ was measured using Ca(2+)-sensitive fluorescent indicator Fura 2-AM. PAF > or = 1 nmol.L-1 induced full platelet aggregation, which did not deaggregate over 5 min after aggregation reached peak. Platelet aggregation was deaggregated in a concentration-dependent manner by subsequent addition of ADP scavenger ATP-diphosphohydrolase (apyrase) at 5-100 mg.L-1. PAF 3 nmol.L-1 stimulated release of ADP (29% vs 6% of control), and elicited a rapid rise in intracellular calcium ([Ca2+]i) which peaked at approximately 15 s. Then the [Ca2+]i gradually decayed from 585 +/- 80 nmol.L-1 within 100 s to a low level (364 +/- 82 nmol.L-1). Apyrase 100 mg.L-1, added 2 min after PAF, reduced [Ca2+]i to a lower level (171 +/- 29 nmol.L-1).\n Question: Does platelet-released ADP stabilize PAF-induced rabbit platelet aggregation by stabilizing intracellular calcium?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To examine whether platelet-released adenosine diphosphate (ADP) would contribute to the stabilization of rabbit platelet aggregation induced by platelet activating factor (PAF). Rabbit platelet aggregation induced by PAF was measured turbimetrically. ADP release from rabbit platelets stimulated by PAF was determined by HPLC. Intracellular Ca2+ was measured using Ca(2+)-sensitive fluorescent indicator Fura 2-AM. PAF > or = 1 nmol.L-1 induced full platelet aggregation, which did not deaggregate over 5 min after aggregation reached peak. Platelet aggregation was deaggregated in a concentration-dependent manner by subsequent addition of ADP scavenger ATP-diphosphohydrolase (apyrase) at 5-100 mg.L-1. PAF 3 nmol.L-1 stimulated release of ADP (29% vs 6% of control), and elicited a rapid rise in intracellular calcium ([Ca2+]i) which peaked at approximately 15 s. Then the [Ca2+]i gradually decayed from 585 +/- 80 nmol.L-1 within 100 s to a low level (364 +/- 82 nmol.L-1). Apyrase 100 mg.L-1, added 2 min after PAF, reduced [Ca2+]i to a lower level (171 +/- 29 nmol.L-1). Question: Does platelet-released ADP stabilize PAF-induced rabbit platelet aggregation by stabilizing intracellular calcium? Output:
PubmedQA11716
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Sleep loss has repeatedly been suggested to affect glucose metabolism adversely, raising the question as to the impact of subtle forms of sleep loss. The aim of the study was to assess the effects of a single night of sleep restriction to 4.5 h on endocrine parameters of glucose metabolism. We conducted crossover, balanced experiments including two conditions, i.e. one night of 4.5 h and one night of 7 h of sleep. In 10 healthy men, circulating concentrations of insulin, C-peptide, epinephrine, norepinephrine, GH, ACTH, cortisol, and glucagon were measured after sleep and sleep restriction, respectively, during basal rest and a subsequent stepwise hypoglycemic clamp. Mild sleep restriction induced a robust reduction in basal plasma glucagon levels that persisted throughout the hypoglycemic clamp (P < 0.03). Basal glucose, insulin, and C-peptide levels were unaffected by sleep restriction. Also, basal and hypoglycemia-stimulated concentrations of epinephrine, norepinephrine, and GH were unchanged after sleep restriction. Concentrations of ACTH (P < 0.05) and cortisol (P < 0.001) were reduced after sleep loss during baseline and at the start of hypoglycemia, but reached roughly comparable levels in both conditions at the end of the clamp (ACTH, P > 0.06; cortisol, P > 0.93).\n Question: Does mild sleep restriction acutely reduce plasma glucagon levels in healthy men?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Sleep loss has repeatedly been suggested to affect glucose metabolism adversely, raising the question as to the impact of subtle forms of sleep loss. The aim of the study was to assess the effects of a single night of sleep restriction to 4.5 h on endocrine parameters of glucose metabolism. We conducted crossover, balanced experiments including two conditions, i.e. one night of 4.5 h and one night of 7 h of sleep. In 10 healthy men, circulating concentrations of insulin, C-peptide, epinephrine, norepinephrine, GH, ACTH, cortisol, and glucagon were measured after sleep and sleep restriction, respectively, during basal rest and a subsequent stepwise hypoglycemic clamp. Mild sleep restriction induced a robust reduction in basal plasma glucagon levels that persisted throughout the hypoglycemic clamp (P < 0.03). Basal glucose, insulin, and C-peptide levels were unaffected by sleep restriction. Also, basal and hypoglycemia-stimulated concentrations of epinephrine, norepinephrine, and GH were unchanged after sleep restriction. Concentrations of ACTH (P < 0.05) and cortisol (P < 0.001) were reduced after sleep loss during baseline and at the start of hypoglycemia, but reached roughly comparable levels in both conditions at the end of the clamp (ACTH, P > 0.06; cortisol, P > 0.93). Question: Does mild sleep restriction acutely reduce plasma glucagon levels in healthy men? Output:
PubmedQA201113
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Abnormal expression of CEACAM6 observed on the ileal epithelium in Crohn's disease (CD) patients allows adherent-invasive Escherichia coli (AIEC) to colonize gut mucosa. Since intestinal permeability is significantly increased in CD patients, we aimed at investigating whether and how AIEC alter barrier function. Tissue microarray was performed on ileal biopsies from CD patients in quiescent and active phases. CEABAC10 or wildtype mice were orally challenged with 10(9) bacteria. Intestinal permeability was assessed by measuring 4 kDa dextran-FITC flux in serum, barrier integrity was analyzed using biotin tracer experiment, and claudin-2 protein immunostaining. Bacterial translocation was analyzed in Ussing chambers. Pore-forming tight junction protein claudin-2 is strongly expressed in the ileum of 51% patients in quiescent phase and in 49% of the patients with active CD. Infection of CEABAC10 transgenic mice expressing human CEACAMs with AIEC, but not with nonpathogenic E. coli, led to a significant 3.0-fold increase in intestinal permeability and to disruption of mucosal integrity in a type 1 pili-dependent mechanism. This is consistent with the claudin-2 abnormal expression at the plasma membrane of intestinal epithelial cells observed in AIEC-infected CEABAC10 mice. AIEC bacteria were able to translocate through CEABAC10 intestinal mucosa.\n Question: Do adherent-invasive Escherichia coli induce claudin-2 expression and barrier defect in CEABAC10 mice and Crohn 's disease patients?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Abnormal expression of CEACAM6 observed on the ileal epithelium in Crohn's disease (CD) patients allows adherent-invasive Escherichia coli (AIEC) to colonize gut mucosa. Since intestinal permeability is significantly increased in CD patients, we aimed at investigating whether and how AIEC alter barrier function. Tissue microarray was performed on ileal biopsies from CD patients in quiescent and active phases. CEABAC10 or wildtype mice were orally challenged with 10(9) bacteria. Intestinal permeability was assessed by measuring 4 kDa dextran-FITC flux in serum, barrier integrity was analyzed using biotin tracer experiment, and claudin-2 protein immunostaining. Bacterial translocation was analyzed in Ussing chambers. Pore-forming tight junction protein claudin-2 is strongly expressed in the ileum of 51% patients in quiescent phase and in 49% of the patients with active CD. Infection of CEABAC10 transgenic mice expressing human CEACAMs with AIEC, but not with nonpathogenic E. coli, led to a significant 3.0-fold increase in intestinal permeability and to disruption of mucosal integrity in a type 1 pili-dependent mechanism. This is consistent with the claudin-2 abnormal expression at the plasma membrane of intestinal epithelial cells observed in AIEC-infected CEABAC10 mice. AIEC bacteria were able to translocate through CEABAC10 intestinal mucosa. Question: Do adherent-invasive Escherichia coli induce claudin-2 expression and barrier defect in CEABAC10 mice and Crohn 's disease patients? Output:
PubmedQA8337
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Seventy percent glycolic acid solutions are being commonly used as superficial chemical peeling agents. The pH of these solutions ranges from 0.08 to 2.75. The histologic effects of these various pH solutions on human skin have not been studied. The histologic effects of several commercially available glycolic acid solutions at various pHs were examined. Test areas of seven glycolic acid solutions were applied to facial skin of two patients. The skin was not prepped for a peel prior to the application of the acid. The solution was left in place for 30 minutes, then neutralized. After 48 hours, a 2-mm punch biopsy was performed and examined histologically. The peeling solutions with a pH below 2 demonstrated the potential to induce crusting and necrosis, which was not seen with the partially neutralized solutions with a pH above 2. The higher concentration acids (70%) created more tissue damage than the lower concentration (50%) when comparing solutions with free acid.\n Question: Does a histological comparison of 50 % and 70 % glycolic acid peel using solutions with various pHs?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Seventy percent glycolic acid solutions are being commonly used as superficial chemical peeling agents. The pH of these solutions ranges from 0.08 to 2.75. The histologic effects of these various pH solutions on human skin have not been studied. The histologic effects of several commercially available glycolic acid solutions at various pHs were examined. Test areas of seven glycolic acid solutions were applied to facial skin of two patients. The skin was not prepped for a peel prior to the application of the acid. The solution was left in place for 30 minutes, then neutralized. After 48 hours, a 2-mm punch biopsy was performed and examined histologically. The peeling solutions with a pH below 2 demonstrated the potential to induce crusting and necrosis, which was not seen with the partially neutralized solutions with a pH above 2. The higher concentration acids (70%) created more tissue damage than the lower concentration (50%) when comparing solutions with free acid. Question: Does a histological comparison of 50 % and 70 % glycolic acid peel using solutions with various pHs? Output:
PubmedQA185352
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: This prospective study evaluated whether extraductal catheter probe EUS as an adjunct to endoscopic retrograde cholangiography can detect or rule out choledocholithiasis and other pathologic conditions of the distal common bile duct. A total of 119 patients referred because of suspected choledocholithiasis or other bile flow obstruction for endoscopic retrograde cholangiography and papillotomy were included in this prospective study. Extraductal EUS of the distal common bile duct with a radial-scanning catheter probe was followed immediately by endoscopic retrograde cholangiography and papillotomy by a second examiner who was blinded to the EUS findings. Extraductal EUS and endoscopic retrograde cholangiography findings were compared. Extraductal EUS detected 33/34 bile duct stones and all papillary adenomas (16 patients). In 8/34 patients, stones were missed on cholangiography but were seen after papillotomy and stone extraction. Extraductal EUS missed 10 peripheral lesions, one pancreatic tumor, and two distal bile duct stenoses. Overall, the sensitivity of EDUS was 78% and specificity was 98%.\n Question: Does catheter probe extraductal EUS reliably detect distal common bile duct abnormalities?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: This prospective study evaluated whether extraductal catheter probe EUS as an adjunct to endoscopic retrograde cholangiography can detect or rule out choledocholithiasis and other pathologic conditions of the distal common bile duct. A total of 119 patients referred because of suspected choledocholithiasis or other bile flow obstruction for endoscopic retrograde cholangiography and papillotomy were included in this prospective study. Extraductal EUS of the distal common bile duct with a radial-scanning catheter probe was followed immediately by endoscopic retrograde cholangiography and papillotomy by a second examiner who was blinded to the EUS findings. Extraductal EUS and endoscopic retrograde cholangiography findings were compared. Extraductal EUS detected 33/34 bile duct stones and all papillary adenomas (16 patients). In 8/34 patients, stones were missed on cholangiography but were seen after papillotomy and stone extraction. Extraductal EUS missed 10 peripheral lesions, one pancreatic tumor, and two distal bile duct stenoses. Overall, the sensitivity of EDUS was 78% and specificity was 98%. Question: Does catheter probe extraductal EUS reliably detect distal common bile duct abnormalities? Output:
PubmedQA207155
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Cytochrome P450 (CYP) 2C9 is expressed in the vascular endothelium and metabolizes arachidonic acid to biologically active epoxyeicosatrienoic acids (EETs), which have the crucial role in the modulation of cardiovascular homeostasis. We sought to assess the association between the human CYP2C9 gene and coronary artery disease (CAD) in Xinjiang Han Population of China. 301 CAD patients and 220 control subjects were genotyped for 4 single-nucleotide polymorphisms (SNPs) of the human CYP2C9 gene (rs4086116, rs2475376, rs1057910, and rs1934967) by a Real-Time PCR instrument. The datas were assessed for 3 groups: total, men, and women via diplotype-based case-control study. For women, the distribution of genotypes, dominant model and alleles of SNP2 (rs2475376) showed significant difference between the CAD patients and control participants (p = 0.033, P = 0.010 and p = 0.038, respectively). The significant difference of the dominant model (CC vs CT + TT) was retained after adjustment for covariates in women (OR: 2.427, 95% confidence interval [CI]: 1.305-4.510, p = 0.005). The haplotype (C-T-A-C) and the diplotypes (CTAC/CTAC) in CYP2C9 gene were lower in CAD patients than in control subjects (p* = 0.0016, and p* = 0.036 respectively). The haplotype (C-C-A-T) was higher in the CAD patients than in the control subjects in women (p* = 0.016).\n Question: Is diplotypes of CYP2C9 gene associated with coronary artery disease in the Xinjiang Han population for women in China?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Cytochrome P450 (CYP) 2C9 is expressed in the vascular endothelium and metabolizes arachidonic acid to biologically active epoxyeicosatrienoic acids (EETs), which have the crucial role in the modulation of cardiovascular homeostasis. We sought to assess the association between the human CYP2C9 gene and coronary artery disease (CAD) in Xinjiang Han Population of China. 301 CAD patients and 220 control subjects were genotyped for 4 single-nucleotide polymorphisms (SNPs) of the human CYP2C9 gene (rs4086116, rs2475376, rs1057910, and rs1934967) by a Real-Time PCR instrument. The datas were assessed for 3 groups: total, men, and women via diplotype-based case-control study. For women, the distribution of genotypes, dominant model and alleles of SNP2 (rs2475376) showed significant difference between the CAD patients and control participants (p = 0.033, P = 0.010 and p = 0.038, respectively). The significant difference of the dominant model (CC vs CT + TT) was retained after adjustment for covariates in women (OR: 2.427, 95% confidence interval [CI]: 1.305-4.510, p = 0.005). The haplotype (C-T-A-C) and the diplotypes (CTAC/CTAC) in CYP2C9 gene were lower in CAD patients than in control subjects (p* = 0.0016, and p* = 0.036 respectively). The haplotype (C-C-A-T) was higher in the CAD patients than in the control subjects in women (p* = 0.016). Question: Is diplotypes of CYP2C9 gene associated with coronary artery disease in the Xinjiang Han population for women in China? Output:
PubmedQA82224
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Endothelial dysfunction is the basic and original sign of atherogenesis. Some evidences show that C-reactive protein (CRP) and perivascular adipose tissue (PVAT) play a pivotal role in atherosclerosis. However, the effects of CRP on atherosclerosis and the related mechanisms require elucidation. The levels of basic total cholesterol, low-density lipoprotein cholesterol, triglyceride, CRP, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), nitric oxide (NO) and endothelin-1 (ET-1) were respectively measured in rabbits, endothelium-dependent vasorelaxation function was also evaluated. Animals were randomly divided into two groups: PVAT(-) and PVAT(+) group (removing or keeping pericarotid adipose tissue (PCAT)). Both of the two groups were exposed to a high-fat diet for six-week, and then sustained CRP treatment was performed for a week, at this time point all the above parameters were remeasured. In addition, mRNA and protein expression of TNF-α, IL-6, and macrophage chemoattractant protein-1 (MCP-1) were respectively evaluated by Polymerase Chain Reaction and immunoblotting in PCAT and cultured adipocytes treated by CRP. High-fat diet greatly increased the serum lipids and inflammatory markers, induced endothelial dysfunction and imbalance between NO and ET-1, increased mRNA and protein expression of TNF-α, IL-6, MCP-1 and enhanced macrophage infiltration of PCAT. CRP treatment could further promote macrophage infiltration of PVAT, induce the imbalance between NO and ET-1, aggravate endothelial dysfunction especially in PVAT(+) arteries, and could also enhance the above-mentioned mRNA and protein expression in PCAT and cultured adipocytes.\n Question: Does c-reactive protein promote vascular endothelial dysfunction partly via activating adipose tissue inflammation in hyperlipidemic rabbits?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Endothelial dysfunction is the basic and original sign of atherogenesis. Some evidences show that C-reactive protein (CRP) and perivascular adipose tissue (PVAT) play a pivotal role in atherosclerosis. However, the effects of CRP on atherosclerosis and the related mechanisms require elucidation. The levels of basic total cholesterol, low-density lipoprotein cholesterol, triglyceride, CRP, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), nitric oxide (NO) and endothelin-1 (ET-1) were respectively measured in rabbits, endothelium-dependent vasorelaxation function was also evaluated. Animals were randomly divided into two groups: PVAT(-) and PVAT(+) group (removing or keeping pericarotid adipose tissue (PCAT)). Both of the two groups were exposed to a high-fat diet for six-week, and then sustained CRP treatment was performed for a week, at this time point all the above parameters were remeasured. In addition, mRNA and protein expression of TNF-α, IL-6, and macrophage chemoattractant protein-1 (MCP-1) were respectively evaluated by Polymerase Chain Reaction and immunoblotting in PCAT and cultured adipocytes treated by CRP. High-fat diet greatly increased the serum lipids and inflammatory markers, induced endothelial dysfunction and imbalance between NO and ET-1, increased mRNA and protein expression of TNF-α, IL-6, MCP-1 and enhanced macrophage infiltration of PCAT. CRP treatment could further promote macrophage infiltration of PVAT, induce the imbalance between NO and ET-1, aggravate endothelial dysfunction especially in PVAT(+) arteries, and could also enhance the above-mentioned mRNA and protein expression in PCAT and cultured adipocytes. Question: Does c-reactive protein promote vascular endothelial dysfunction partly via activating adipose tissue inflammation in hyperlipidemic rabbits? Output:
PubmedQA47760
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The accurate intraoperative localization of malignant nodes can pose a challenge to the surgical oncologist. Positron emission tomography (PET) scanning has significantly increased our ability to detect suspicious lesions. We investigated the ability of a novel, handheld tool to evaluate suspicious nodes intraoperatively and to correlate its findings with those seen on preoperative PET scan. Ten nude rats were inoculated with a lymphogenic mesothelioma tumor line and followed weekly with PET scan studies. When suspicious lymph nodes were found, animals were dissected and the intraoperative amount of tissue radiation was analyzed as \"tumor-to-background ratio\" (TBR) using the PET probes. The intraoperative probe was used to guide dissections and select high-risk nodes based on their specific radiotracer uptake. A total of 52 nodes were harvested; eight of these were suspicious on preoperative PET scan studies. Using a TBR of 2.5, the intraoperative probes were able to localize all suspicious nodes previously seen on PET scan. Both gamma (sensitivity: 100%; specificity: 86%; positive predictive value (PPV): 57%; negative predictive value (NPV): 100%) and beta (sensitivity: 88%; specificity: 91%; PPV: 64%; NPV: 98%) probes showed an excellent area under the curve (AUC) in the receiver operating characteristic analysis (ROC). Both probes had an AUC of 0.95 for localizing suspicious nodes on PET scan. Furthermore, the AUC for detecting malignancy for the gamma probe was 0.90 (95% confidence interval (CI), 0.83-0.99), and for the beta probe it was 0.97 (95% CI, 0.94-1.0), suggesting a better performance of the beta probe for detecting malignancy.\n Question: Do novel handheld PET probes provide intraoperative localization of PET-avid lymph nodes?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The accurate intraoperative localization of malignant nodes can pose a challenge to the surgical oncologist. Positron emission tomography (PET) scanning has significantly increased our ability to detect suspicious lesions. We investigated the ability of a novel, handheld tool to evaluate suspicious nodes intraoperatively and to correlate its findings with those seen on preoperative PET scan. Ten nude rats were inoculated with a lymphogenic mesothelioma tumor line and followed weekly with PET scan studies. When suspicious lymph nodes were found, animals were dissected and the intraoperative amount of tissue radiation was analyzed as "tumor-to-background ratio" (TBR) using the PET probes. The intraoperative probe was used to guide dissections and select high-risk nodes based on their specific radiotracer uptake. A total of 52 nodes were harvested; eight of these were suspicious on preoperative PET scan studies. Using a TBR of 2.5, the intraoperative probes were able to localize all suspicious nodes previously seen on PET scan. Both gamma (sensitivity: 100%; specificity: 86%; positive predictive value (PPV): 57%; negative predictive value (NPV): 100%) and beta (sensitivity: 88%; specificity: 91%; PPV: 64%; NPV: 98%) probes showed an excellent area under the curve (AUC) in the receiver operating characteristic analysis (ROC). Both probes had an AUC of 0.95 for localizing suspicious nodes on PET scan. Furthermore, the AUC for detecting malignancy for the gamma probe was 0.90 (95% confidence interval (CI), 0.83-0.99), and for the beta probe it was 0.97 (95% CI, 0.94-1.0), suggesting a better performance of the beta probe for detecting malignancy. Question: Do novel handheld PET probes provide intraoperative localization of PET-avid lymph nodes? Output:
PubmedQA98352
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Ki-67 is a cell proliferation protein associated with aggressive clear cell renal cell carcinoma (ccRCC). A recent report suggests that Ki-67 may represent a surrogate marker for coagulative tumor necrosis. Thus, the goal was to directly test whether Ki-67 and necrosis convey similar or distinct information for the prognostic assessment of ccRCC. Tumor specimens from 741 consecutively treated patients who underwent surgery for ccRCC between 1990 and 1999 were evaluated. Tumor specimens were assessed for various clinicopathologic features, including levels of tumor cell Ki-67 expression. Associations of these features with death from RCC were evaluated using Cox proportional hazards regression models. At last follow-up, 396 patients had died, including 238 who died from ccRCC at a median of 2.1 years after surgery. Although tumor cell Ki-67 expression and coagulative tumor necrosis were highly correlated, the prognostic information conveyed by these 2 markers failed to overlap. For the subset of patients with necrotic tumors, high levels of Ki-67 more than doubled the risk of death from RCC (risk ratio, 2.18; 95% confidence interval [CI], 1.52-3.11; P < .001). For patients with tumors lacking necrosis, high levels of Ki-67 expression were similarly correlated with an increased risk of death from RCC (risk ratio, 2.50; 95% CI, 1.66-3.77; P < .001).\n Question: Are ki-67 and coagulative tumor necrosis independent predictors of poor outcome for patients with clear cell renal cell carcinoma and not surrogates for each other?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Ki-67 is a cell proliferation protein associated with aggressive clear cell renal cell carcinoma (ccRCC). A recent report suggests that Ki-67 may represent a surrogate marker for coagulative tumor necrosis. Thus, the goal was to directly test whether Ki-67 and necrosis convey similar or distinct information for the prognostic assessment of ccRCC. Tumor specimens from 741 consecutively treated patients who underwent surgery for ccRCC between 1990 and 1999 were evaluated. Tumor specimens were assessed for various clinicopathologic features, including levels of tumor cell Ki-67 expression. Associations of these features with death from RCC were evaluated using Cox proportional hazards regression models. At last follow-up, 396 patients had died, including 238 who died from ccRCC at a median of 2.1 years after surgery. Although tumor cell Ki-67 expression and coagulative tumor necrosis were highly correlated, the prognostic information conveyed by these 2 markers failed to overlap. For the subset of patients with necrotic tumors, high levels of Ki-67 more than doubled the risk of death from RCC (risk ratio, 2.18; 95% confidence interval [CI], 1.52-3.11; P < .001). For patients with tumors lacking necrosis, high levels of Ki-67 expression were similarly correlated with an increased risk of death from RCC (risk ratio, 2.50; 95% CI, 1.66-3.77; P < .001). Question: Are ki-67 and coagulative tumor necrosis independent predictors of poor outcome for patients with clear cell renal cell carcinoma and not surrogates for each other? Output:
PubmedQA152123
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To study the effect of drugs that increase intracellular cyclic adenosine monophosphate on the ability of rat retinal pigment epithelial cells to phagocytize rod outer segments (ROS). Cultured rat retinal pigment epithelial cells were treated with cholera toxin, forskolin, isoproterenol, or isobutylmethylxanthine and the phagocytosis of ROS by such treated cells was compared to that of control specimens. All of the drugs examined inhibited the ingestion, but not the binding of ROS by cultured retinal pigment epithelial cells. Cell viability was not compromised by the drug treatment because they rapidly recovered their ability to ingest ROS when the drug was removed. Dose-response curves for the inhibition of ROS phagocytosis by forskolin and isoproterenol demonstrated that this process is exquisitely sensitive to these agonists, with an IC50 for these drugs of 33 nmol/l. The results showed no measurable quantitative correlation between cyclic adenosine monophosphate levels and the inhibition of ROS phagocytosis.\n Question: Is the phagocytosis of rod outer segments inhibited by drugs linked to cyclic adenosine monophosphate production?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To study the effect of drugs that increase intracellular cyclic adenosine monophosphate on the ability of rat retinal pigment epithelial cells to phagocytize rod outer segments (ROS). Cultured rat retinal pigment epithelial cells were treated with cholera toxin, forskolin, isoproterenol, or isobutylmethylxanthine and the phagocytosis of ROS by such treated cells was compared to that of control specimens. All of the drugs examined inhibited the ingestion, but not the binding of ROS by cultured retinal pigment epithelial cells. Cell viability was not compromised by the drug treatment because they rapidly recovered their ability to ingest ROS when the drug was removed. Dose-response curves for the inhibition of ROS phagocytosis by forskolin and isoproterenol demonstrated that this process is exquisitely sensitive to these agonists, with an IC50 for these drugs of 33 nmol/l. The results showed no measurable quantitative correlation between cyclic adenosine monophosphate levels and the inhibition of ROS phagocytosis. Question: Is the phagocytosis of rod outer segments inhibited by drugs linked to cyclic adenosine monophosphate production? Output:
PubmedQA135138
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Little is known about how parental migration status may be associated with children's diets. We examined whether the intake of selected foods by six-year-old children differed according to their parents' migration status, taking education level into account. This study used pooled baseline data from two clustered randomised controlled trials of A Healthy School Start, conducted in municipalities of low-to-medium socio-economic status in Stockholm County, Sweden. The children's intake of selected healthy and unhealthy foods was reported by parents using the Eating and Physical Activity Questionnaire, and the children's height and weight were measured. Parental education and country of birth were self-reported. Data were available for 520 children. Low parental education was associated with significantly higher intakes of fruit, higher intakes of several unhealthy foods and lower intakes of vegetables. Children of parents born outside the Nordic region had higher intakes of all unhealthy foods as well as fruit and vegetables, even when adjusted for education. A negative association between high education and overweight was only seen in children of Nordic-born parents.\n Question: Does the intake of selected foods by six-year-old Swedish children differ according to parental education and migration status?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Little is known about how parental migration status may be associated with children's diets. We examined whether the intake of selected foods by six-year-old children differed according to their parents' migration status, taking education level into account. This study used pooled baseline data from two clustered randomised controlled trials of A Healthy School Start, conducted in municipalities of low-to-medium socio-economic status in Stockholm County, Sweden. The children's intake of selected healthy and unhealthy foods was reported by parents using the Eating and Physical Activity Questionnaire, and the children's height and weight were measured. Parental education and country of birth were self-reported. Data were available for 520 children. Low parental education was associated with significantly higher intakes of fruit, higher intakes of several unhealthy foods and lower intakes of vegetables. Children of parents born outside the Nordic region had higher intakes of all unhealthy foods as well as fruit and vegetables, even when adjusted for education. A negative association between high education and overweight was only seen in children of Nordic-born parents. Question: Does the intake of selected foods by six-year-old Swedish children differ according to parental education and migration status? Output:
PubmedQA80679
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Systemic inflammation before surgery, as evidenced by the Glasgow prognostic score (GPS), predicts postoperative complications and cancer-specific survival in various types of cancer. The aim of this study was to evaluate the significance GPS in hepatic resection for hepatocellular carcinoma (HCC). Sixty-six patients who underwent elective hepatic resections for HCC were include in the study. Patients were classified into three groups: GPS 0 [C-reactive protein (CRP)≤1.0 mg/dl and serum albumin ≥3.5 g/dl, n = 54], GPS 1 [CRP >1.0 mg/dl or serum albumin <3.5 g/dl, n = 11], and GPS 2 [CRP>1.0 mg/dl and serum albumin <3.5 g/dl, n = 1]. We retrospectively examined the association between GPS (0 or 1) and perioperative clinical variables and outcome. In univariate analysis, GPS 0 patients had significantly better preoperative the retention rate of indocyanine green at 15 minutes (ICGR15) (p=0.0418), Child-Pugh classification (p = 0.0075) and model for end-stage liver disease score (p = 0.0007) than did GPS 1 patients. In multivariate analysis, blood loss and GPS 1 were independent risk factors for pulmonary complications (p = 0.0118 for blood loss, p = 0.0143 for GPS 1), red blood cell concentration transfusion (p = 0.0036 for blood loss, p = 0.0117 for GPS 1) and flesh frozen plasma transfusion (p = 0.0020 for blood loss, p = 0.0044 for GPS 1). Albumin product transfusion, duration of operation (p = 0.0478), blood loss (p = 0.0420) and GPS 1 (p = 0.0111) were independent risk factors. Disease-free and overall survival of GPS 0 and GPS 1 patients were comparable.\n Question: Is glasgow prognostic score related to blood transfusion requirements and post-operative complications in hepatic resection for hepatocellular carcinoma?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Systemic inflammation before surgery, as evidenced by the Glasgow prognostic score (GPS), predicts postoperative complications and cancer-specific survival in various types of cancer. The aim of this study was to evaluate the significance GPS in hepatic resection for hepatocellular carcinoma (HCC). Sixty-six patients who underwent elective hepatic resections for HCC were include in the study. Patients were classified into three groups: GPS 0 [C-reactive protein (CRP)≤1.0 mg/dl and serum albumin ≥3.5 g/dl, n = 54], GPS 1 [CRP >1.0 mg/dl or serum albumin <3.5 g/dl, n = 11], and GPS 2 [CRP>1.0 mg/dl and serum albumin <3.5 g/dl, n = 1]. We retrospectively examined the association between GPS (0 or 1) and perioperative clinical variables and outcome. In univariate analysis, GPS 0 patients had significantly better preoperative the retention rate of indocyanine green at 15 minutes (ICGR15) (p=0.0418), Child-Pugh classification (p = 0.0075) and model for end-stage liver disease score (p = 0.0007) than did GPS 1 patients. In multivariate analysis, blood loss and GPS 1 were independent risk factors for pulmonary complications (p = 0.0118 for blood loss, p = 0.0143 for GPS 1), red blood cell concentration transfusion (p = 0.0036 for blood loss, p = 0.0117 for GPS 1) and flesh frozen plasma transfusion (p = 0.0020 for blood loss, p = 0.0044 for GPS 1). Albumin product transfusion, duration of operation (p = 0.0478), blood loss (p = 0.0420) and GPS 1 (p = 0.0111) were independent risk factors. Disease-free and overall survival of GPS 0 and GPS 1 patients were comparable. Question: Is glasgow prognostic score related to blood transfusion requirements and post-operative complications in hepatic resection for hepatocellular carcinoma? Output:
PubmedQA117761
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The plasma membrane Ca2+-ATPase (PMCA) is the principal means by which sensory neurons expel Ca2+ and thereby regulate the concentration of cytoplasmic Ca2+ and the processes controlled by this critical second messenger. We have previously found that painful nerve injury decreases resting cytoplasmic Ca2+ levels and activity-induced cytoplasmic Ca2+ accumulation in axotomized sensory neurons. Here we examine the contribution of PMCA after nerve injury in a rat model of neuropathic pain. PMCA function was isolated in dissociated sensory neurons by blocking intracellular Ca2+ sequestration with thapsigargin, and cytoplasmic Ca2+ concentration was recorded with Fura-2 fluorometry. Compared to control neurons, the rate at which depolarization-induced Ca2+ transients resolved was increased in axotomized neurons after spinal nerve ligation, indicating accelerated PMCA function. Electrophysiological recordings showed that blockade of PMCA by vanadate prolonged the action potential afterhyperpolarization, and also decreased the rate at which neurons could fire repetitively.\n Question: Does painful nerve injury increase plasma membrane Ca2+-ATPase activity in axotomized sensory neurons?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The plasma membrane Ca2+-ATPase (PMCA) is the principal means by which sensory neurons expel Ca2+ and thereby regulate the concentration of cytoplasmic Ca2+ and the processes controlled by this critical second messenger. We have previously found that painful nerve injury decreases resting cytoplasmic Ca2+ levels and activity-induced cytoplasmic Ca2+ accumulation in axotomized sensory neurons. Here we examine the contribution of PMCA after nerve injury in a rat model of neuropathic pain. PMCA function was isolated in dissociated sensory neurons by blocking intracellular Ca2+ sequestration with thapsigargin, and cytoplasmic Ca2+ concentration was recorded with Fura-2 fluorometry. Compared to control neurons, the rate at which depolarization-induced Ca2+ transients resolved was increased in axotomized neurons after spinal nerve ligation, indicating accelerated PMCA function. Electrophysiological recordings showed that blockade of PMCA by vanadate prolonged the action potential afterhyperpolarization, and also decreased the rate at which neurons could fire repetitively. Question: Does painful nerve injury increase plasma membrane Ca2+-ATPase activity in axotomized sensory neurons? Output:
PubmedQA114483
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To determine whether the initiation or titration of irbesartan alters the pharmacodynamics and/or pharmacokinetics of warfarin in a clinically significant manner, thereby requiring additional monitoring of the anticoagulant effect of warfarin. Daily doses of warfarin were administered to 16 healthy males for 21 days (10 mg on day 1 and 2.5-10 mg on days 2-21). Irbesartan (300 mg/day) or placebo was concomitantly administered on days 15-21. The pharmacodynamic parameters prothrombin time (PT) and prothrombin time ratio (PTR) were evaluated throughout the study. Plasma and urine samples were collected before and up to 24 h after administration on days 14, 15 and 21 for the determination of the maximum concentration (C(max)), time to reach C(max)(t(max)), the area under the concentration-time curve (AUC) of S-warfarin and the cumulative urinary excretion of warfarin and its metabolites. Pre-dose plasma samples were also collected to determine the C(min) of S-warfarin (days 12, 13, 14 and 21) and irbesartan (days 19, 20 and 21). Analysis of PTR data revealed no significant difference between the group mean PTR values at day 22 and those at day 15 (P=0.699). S-warfarin concentrations in plasma and urine, as well as the urinary concentrations of the metabolites of warfarin, were not affected by concomitant single- or multiple-dose administration of irbesartan. Plasma C(min) concentrations of S-warfarin and irbesartan were also not affected.\n Question: Does irbesartan affect the steady-state pharmacodynamics and pharmacokinetics of warfarin?\n Output: " }, { "role": "assistant", "content": "no" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To determine whether the initiation or titration of irbesartan alters the pharmacodynamics and/or pharmacokinetics of warfarin in a clinically significant manner, thereby requiring additional monitoring of the anticoagulant effect of warfarin. Daily doses of warfarin were administered to 16 healthy males for 21 days (10 mg on day 1 and 2.5-10 mg on days 2-21). Irbesartan (300 mg/day) or placebo was concomitantly administered on days 15-21. The pharmacodynamic parameters prothrombin time (PT) and prothrombin time ratio (PTR) were evaluated throughout the study. Plasma and urine samples were collected before and up to 24 h after administration on days 14, 15 and 21 for the determination of the maximum concentration (C(max)), time to reach C(max)(t(max)), the area under the concentration-time curve (AUC) of S-warfarin and the cumulative urinary excretion of warfarin and its metabolites. Pre-dose plasma samples were also collected to determine the C(min) of S-warfarin (days 12, 13, 14 and 21) and irbesartan (days 19, 20 and 21). Analysis of PTR data revealed no significant difference between the group mean PTR values at day 22 and those at day 15 (P=0.699). S-warfarin concentrations in plasma and urine, as well as the urinary concentrations of the metabolites of warfarin, were not affected by concomitant single- or multiple-dose administration of irbesartan. Plasma C(min) concentrations of S-warfarin and irbesartan were also not affected. Question: Does irbesartan affect the steady-state pharmacodynamics and pharmacokinetics of warfarin? Output:
PubmedQA203956
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Patient-perceived noise from prostheses after total hip arthroplasty (THA) does occur, yet questions remain including the overall frequency of this finding, demographic and prosthesis-related factors, and the association of noise generation with patient-reported outcomes. The purposes of this study were (1) to determine the frequency with which patients report noise coming from the hip after THA; (2) to identify patient and prosthesis-related factors associated with noise generation; and (3) to ascertain if noise generation is associated with pain or functional impairment after THA. A five-center study was designed to quantify the degree of residual symptoms and functional deficits in patients undergoing THA. Three centers were academic practices, whereas two centers were private practices that provided training programs for orthopaedic residents and fellows. Each contributing surgeon was fellowship-trained and specialized in joint replacement. Inclusion criteria for this study were (1) men between 18 and 60 years old and women between 18 and 55 years old; (2) patients requiring primary hip surgery as a result of noninflammatory arthritis such as osteoarthritis, traumatic arthritis, or avascular necrosis; (3) a UCLA activity score of 6 or more before they were limited by pain; and (4) patients who had undergone a primary THA within 1 to 4 years before the start of the study and had a minimum of 1 year of clinical followup. Attempts were made to contact all identified patients meeting these inclusion criteria. Data were collected by an independent, third-party survey center blinded to the implant design and bearing surface used who administered questionnaires about residual symptoms, function, and pre- and postoperative activity levels using previously published survey instruments. Patients were specifically queried regarding perceived noise from their THA. We retrospectively identified 1242 eligible patients. Of the 1242 patients, 105 were found to have exclusions during the screening section of the questionnaire: postoperative infection (six THAs), fracture (two), dislocation (seven), or revision (17); limited activity level because of an operation on the opposite hip (34); and premorbid UCLA score of less than 6 (39). In addition, 128 individuals refused to participate, 156 were never available, 108 were not found as a result of a bad address/phone number, 48 were contacted but did not complete the interview, nine had died, and six had a language barrier. This left 682 of the 1137 eligible patients with completed surveys (60% response rate). The mean age was 50 ± 8 years at the time of surgery with 63% being men, and they were contacted at a mean of 3 ± 1 years postoperatively. Bearing surfaces (femoral head-acetabular liner) included 210 (31%) metal-on-metal, 144 (21%) ceramic-on-ceramic, 142 (21%) ceramic-on-polyethylene, 141 (21%) cobalt-chromium-on-polyethylene, and 44 (6%) oxidized zirconium-on-polyethylene. Differences in baseline demographic variables were accounted for using multiple logistic regression statistical analyses. Pearson's correlation coefficients were used to determine the association of noise generation with residual symptoms. Overall, 9% (61 of 682; 95% confidence interval [CI], 7-11) of young patients undergoing primary THA reported noise generation. Females (12% [30 of 251 patients]) were noted to have an increased likelihood of reporting noise versus males (7% [30 of 431 patients]; odds ratio, 1.8; 95% CI, 1.1-3.1; p = 0.03). After controlling for potential confounding variables including female sex and length of followup, patients receiving a ceramic-on-ceramic or metal-on-metal bearing surface (14% [50 of 355]) reported an increased frequency of grinding, popping, and clicking in the 30 days before survey administration versus those receiving a polyethylene liner with a ceramic, oxidized zirconium, or cobalt-chromium femoral head (3% [10 of 327 patients]; odds ratio, 5.6; 95% CI, 2.7-11.5; p < 0.001). Noise generation was associated with increased pain (r = 0.23, p < 0.001) and stiffness (r = 0.22, p < 0.001) after THA.\n Question: Do hard-on-Hard Bearings Are Associated With Increased Noise Generation in Young Patients Undergoing Hip Arthroplasty?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Patient-perceived noise from prostheses after total hip arthroplasty (THA) does occur, yet questions remain including the overall frequency of this finding, demographic and prosthesis-related factors, and the association of noise generation with patient-reported outcomes. The purposes of this study were (1) to determine the frequency with which patients report noise coming from the hip after THA; (2) to identify patient and prosthesis-related factors associated with noise generation; and (3) to ascertain if noise generation is associated with pain or functional impairment after THA. A five-center study was designed to quantify the degree of residual symptoms and functional deficits in patients undergoing THA. Three centers were academic practices, whereas two centers were private practices that provided training programs for orthopaedic residents and fellows. Each contributing surgeon was fellowship-trained and specialized in joint replacement. Inclusion criteria for this study were (1) men between 18 and 60 years old and women between 18 and 55 years old; (2) patients requiring primary hip surgery as a result of noninflammatory arthritis such as osteoarthritis, traumatic arthritis, or avascular necrosis; (3) a UCLA activity score of 6 or more before they were limited by pain; and (4) patients who had undergone a primary THA within 1 to 4 years before the start of the study and had a minimum of 1 year of clinical followup. Attempts were made to contact all identified patients meeting these inclusion criteria. Data were collected by an independent, third-party survey center blinded to the implant design and bearing surface used who administered questionnaires about residual symptoms, function, and pre- and postoperative activity levels using previously published survey instruments. Patients were specifically queried regarding perceived noise from their THA. We retrospectively identified 1242 eligible patients. Of the 1242 patients, 105 were found to have exclusions during the screening section of the questionnaire: postoperative infection (six THAs), fracture (two), dislocation (seven), or revision (17); limited activity level because of an operation on the opposite hip (34); and premorbid UCLA score of less than 6 (39). In addition, 128 individuals refused to participate, 156 were never available, 108 were not found as a result of a bad address/phone number, 48 were contacted but did not complete the interview, nine had died, and six had a language barrier. This left 682 of the 1137 eligible patients with completed surveys (60% response rate). The mean age was 50 ± 8 years at the time of surgery with 63% being men, and they were contacted at a mean of 3 ± 1 years postoperatively. Bearing surfaces (femoral head-acetabular liner) included 210 (31%) metal-on-metal, 144 (21%) ceramic-on-ceramic, 142 (21%) ceramic-on-polyethylene, 141 (21%) cobalt-chromium-on-polyethylene, and 44 (6%) oxidized zirconium-on-polyethylene. Differences in baseline demographic variables were accounted for using multiple logistic regression statistical analyses. Pearson's correlation coefficients were used to determine the association of noise generation with residual symptoms. Overall, 9% (61 of 682; 95% confidence interval [CI], 7-11) of young patients undergoing primary THA reported noise generation. Females (12% [30 of 251 patients]) were noted to have an increased likelihood of reporting noise versus males (7% [30 of 431 patients]; odds ratio, 1.8; 95% CI, 1.1-3.1; p = 0.03). After controlling for potential confounding variables including female sex and length of followup, patients receiving a ceramic-on-ceramic or metal-on-metal bearing surface (14% [50 of 355]) reported an increased frequency of grinding, popping, and clicking in the 30 days before survey administration versus those receiving a polyethylene liner with a ceramic, oxidized zirconium, or cobalt-chromium femoral head (3% [10 of 327 patients]; odds ratio, 5.6; 95% CI, 2.7-11.5; p < 0.001). Noise generation was associated with increased pain (r = 0.23, p < 0.001) and stiffness (r = 0.22, p < 0.001) after THA. Question: Do hard-on-Hard Bearings Are Associated With Increased Noise Generation in Young Patients Undergoing Hip Arthroplasty? Output:
PubmedQA161428
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To determine the dose response of human recombinant basic fibroblast growth factor (bFGF) on mitogenic activity, and the supplementary role of serum in cultured bovine and human corneal endothelial cells (BCECs, HCECs). To investigate the effect of bFGF on endothelial wound healing of human corneas in vitro. In cell culture, DNA synthesis was assessed by 3H-thymidine incorporation. Wound healing was studied using paired human corneas after mechanical damaging of the endothelium. One cornea was treated with bFGF, and the mate served as control. Wound closure was determined after staining with trypan blue. Endothelial cell density (ECD) was assessed in the closed wound area after alizarin red staining. DNA synthesis was assessed using 3H-thymidine autoradiography. In cell culture, bFGF induced a dose-dependent mitogenic response on BCECs and HCECs. Addition of serum to the culture medium shifted the dose-response curve to considerably lower bFGF concentrations. In organ culture, the time of complete wound closure shortened only marginally (0.5 day) after bFGF treatment (P < 0.01). In the closed wound center, ECD was significantly higher in 1 ng/ml bFGF-treated corneas (686 +/- 134 cells/mm2) than in controls (554 +/- 117 cells/mm2), an increase of +25%. Doses of 0.1 and 10 ng/ml also were effective, but less so than with 1 ng/ml (+11% and +15%, respectively), whereas a dose of 100 ng/ml even had a negative effect (-11%). DNA synthesis was marginally enhanced in bFGF-treated (1 ng/ml) corneas.\n Question: Does basic fibroblast growth factor stimulate corneal endothelial cell growth and endothelial wound healing of human corneas?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To determine the dose response of human recombinant basic fibroblast growth factor (bFGF) on mitogenic activity, and the supplementary role of serum in cultured bovine and human corneal endothelial cells (BCECs, HCECs). To investigate the effect of bFGF on endothelial wound healing of human corneas in vitro. In cell culture, DNA synthesis was assessed by 3H-thymidine incorporation. Wound healing was studied using paired human corneas after mechanical damaging of the endothelium. One cornea was treated with bFGF, and the mate served as control. Wound closure was determined after staining with trypan blue. Endothelial cell density (ECD) was assessed in the closed wound area after alizarin red staining. DNA synthesis was assessed using 3H-thymidine autoradiography. In cell culture, bFGF induced a dose-dependent mitogenic response on BCECs and HCECs. Addition of serum to the culture medium shifted the dose-response curve to considerably lower bFGF concentrations. In organ culture, the time of complete wound closure shortened only marginally (0.5 day) after bFGF treatment (P < 0.01). In the closed wound center, ECD was significantly higher in 1 ng/ml bFGF-treated corneas (686 +/- 134 cells/mm2) than in controls (554 +/- 117 cells/mm2), an increase of +25%. Doses of 0.1 and 10 ng/ml also were effective, but less so than with 1 ng/ml (+11% and +15%, respectively), whereas a dose of 100 ng/ml even had a negative effect (-11%). DNA synthesis was marginally enhanced in bFGF-treated (1 ng/ml) corneas. Question: Does basic fibroblast growth factor stimulate corneal endothelial cell growth and endothelial wound healing of human corneas? Output:
PubmedQA179772
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Using longitudinal data from the NICHD Study of Early Child Care and Youth Development, we examined behavior problems and social and academic outcomes from ages 9 through 12 in children classified into five trajectories of physical aggression, on the basis of maternal ratings obtained from 24 months through 9 years (N = 1195). Outcome data were obtained from teacher reports, observations of children's behavior, and children's self-reports. Children on the high-stable aggression trajectory (3% of sample) showed the most severe adjustment problems, including poorer social skills, higher levels of externalizing problems, and more self-reported peer problems; those on the moderate-stable aggression trajectory (15%) showed poor regulation and inattention. Although children with moderate levels of early aggression that decreased sharply by school entry (12%) appeared well adjusted at follow-up, those who showed a low level of stable aggression (25%) evidenced some unanticipated social and behavior problems. Children in the contrast group (45%) were consistently very low in aggression from toddlerhood onward.\n Question: Do trajectories of aggression from toddlerhood to age 9 predict academic and social functioning through age 12?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Using longitudinal data from the NICHD Study of Early Child Care and Youth Development, we examined behavior problems and social and academic outcomes from ages 9 through 12 in children classified into five trajectories of physical aggression, on the basis of maternal ratings obtained from 24 months through 9 years (N = 1195). Outcome data were obtained from teacher reports, observations of children's behavior, and children's self-reports. Children on the high-stable aggression trajectory (3% of sample) showed the most severe adjustment problems, including poorer social skills, higher levels of externalizing problems, and more self-reported peer problems; those on the moderate-stable aggression trajectory (15%) showed poor regulation and inattention. Although children with moderate levels of early aggression that decreased sharply by school entry (12%) appeared well adjusted at follow-up, those who showed a low level of stable aggression (25%) evidenced some unanticipated social and behavior problems. Children in the contrast group (45%) were consistently very low in aggression from toddlerhood onward. Question: Do trajectories of aggression from toddlerhood to age 9 predict academic and social functioning through age 12? Output:
PubmedQA75435
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Rapid bedside triage (RBT), rather than traditional waiting room triage (WRT), is becoming a \"best practice\" in managing emergency department (ED) patient flow, yet little is known about the impact of this process on other aspects of patient care. This study was designed to compare overall adherence to an existing nurse-driven ED pain protocol after changing from a WRT to an RBT process. On November 1, 2011, the triage process at our institution changed from a traditional WRT system to an in-department RBT allowing for comparison of the 2 groups. A retrospective chart review assessing compliance with the department's pain protocol was performed on all patients presenting to the ED during October and November 2011, representing the immediate time periods before and after the implementation of the change in triage process. Patients younger than 19 years, with complaint of isolated extremity pain or injury, were included in this analysis. Compliance was defined as patients having a pain score assessed and pain medication given for scores of 4 or more within 30 minutes of arrival. In total, 546 patients were identified for inclusion in the study; 306 received traditional WRT, and 240 received RBT. Compliance with the pain protocol was seen in 54.6% of patients receiving WRT versus 57.5% receiving RBT (P = 0.50).\n Question: Does rapid bedside triage affect the delivery of pain medication for extremity pain in the pediatric emergency department?\n Output: " }, { "role": "assistant", "content": "no" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Rapid bedside triage (RBT), rather than traditional waiting room triage (WRT), is becoming a "best practice" in managing emergency department (ED) patient flow, yet little is known about the impact of this process on other aspects of patient care. This study was designed to compare overall adherence to an existing nurse-driven ED pain protocol after changing from a WRT to an RBT process. On November 1, 2011, the triage process at our institution changed from a traditional WRT system to an in-department RBT allowing for comparison of the 2 groups. A retrospective chart review assessing compliance with the department's pain protocol was performed on all patients presenting to the ED during October and November 2011, representing the immediate time periods before and after the implementation of the change in triage process. Patients younger than 19 years, with complaint of isolated extremity pain or injury, were included in this analysis. Compliance was defined as patients having a pain score assessed and pain medication given for scores of 4 or more within 30 minutes of arrival. In total, 546 patients were identified for inclusion in the study; 306 received traditional WRT, and 240 received RBT. Compliance with the pain protocol was seen in 54.6% of patients receiving WRT versus 57.5% receiving RBT (P = 0.50). Question: Does rapid bedside triage affect the delivery of pain medication for extremity pain in the pediatric emergency department? Output:
PubmedQA140734
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Steatosis is common in patients with hepatitis C virus (HCV) infection. Its influence on disease progression is only partially understood. The aim of this study was to evaluate the impact of steatosis on fibrosis progression over time in relation to HCV genotype. We retrospectively analyzed 98 patients who underwent dual liver biopsies prior to antiviral treatment. The median follow-up time was 5.8 years. Biopsy specimens were assessed for necroinflammatory activity, fibrosis and steatosis. The prevalence and grade of steatosis were strongly associated with HCV genotype 3, independent of sex, age, body mass index and alcohol consumption. Progressive fibrosis was more prevalent in patients whose initial biopsy showed steatosis, an effect seen mainly in genotype 3 infected patients. Low-grade steatosis was observed in overweight patients, but high-grade steatosis was associated with genotype 3, independent of body mass index.\n Question: Does steatosis accelerate fibrosis development over time in hepatitis C virus genotype 3 infected patients?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Steatosis is common in patients with hepatitis C virus (HCV) infection. Its influence on disease progression is only partially understood. The aim of this study was to evaluate the impact of steatosis on fibrosis progression over time in relation to HCV genotype. We retrospectively analyzed 98 patients who underwent dual liver biopsies prior to antiviral treatment. The median follow-up time was 5.8 years. Biopsy specimens were assessed for necroinflammatory activity, fibrosis and steatosis. The prevalence and grade of steatosis were strongly associated with HCV genotype 3, independent of sex, age, body mass index and alcohol consumption. Progressive fibrosis was more prevalent in patients whose initial biopsy showed steatosis, an effect seen mainly in genotype 3 infected patients. Low-grade steatosis was observed in overweight patients, but high-grade steatosis was associated with genotype 3, independent of body mass index. Question: Does steatosis accelerate fibrosis development over time in hepatitis C virus genotype 3 infected patients? Output:
PubmedQA24410
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: β1,6-N-acetylglucosaminyltransferase V (MGAT5), which is required for the biosynthesis of β1,6GlcNAc-branched N-linked glycans attached to cell surface and secreted glycoproteins, accounts for oncogenic growth signal transduction during the development and progression of various malignancies. Our present study aimed to evaluate the impact of MGAT5 expression on recurrence and survival of patients with clear-cell renal cell carcinoma (ccRCC) following surgery. We retrospectively enrolled 265 patients (196 in the training cohort and 69 in the validation cohort) with ccRCC undergoing nephrectomy at a single institution. Clinicopathologic features, overall survival (OS) and recurrence-free survival (RFS) were recorded. MGAT5 intensities were assessed by immunohistochemistry in specimens of patients. Kaplan-Meier method was applied to compare survival curves. Cox regression models were used to analyze the impact of prognostic factors on OS and RFS. Concordance index (C-index) was calculated to assess predictive accuracy. In both cohorts, MGAT5 expression positively correlated with metastatic and advanced TNM stage. High MGAT5 expression indicated poor survival (P < 0.001 in training set and P < 0.001 in validation set) and early recurrence (P < 0.001 in training set and P = 0.004 in validation set) of patients with ccRCC. After multivariate Cox regression analysis, MGAT5 expression was identified as an independent adverse prognostic factor for survival and recurrence. The predictive accuracy of TNM, UISS and SSIGN prognostic models was improved when MGAT5 expression was added.\n Question: Does β1,6-N-acetylglucosaminyltransferase V predict recurrence and survival of patients with clear-cell renal cell carcinoma after surgical resection?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: β1,6-N-acetylglucosaminyltransferase V (MGAT5), which is required for the biosynthesis of β1,6GlcNAc-branched N-linked glycans attached to cell surface and secreted glycoproteins, accounts for oncogenic growth signal transduction during the development and progression of various malignancies. Our present study aimed to evaluate the impact of MGAT5 expression on recurrence and survival of patients with clear-cell renal cell carcinoma (ccRCC) following surgery. We retrospectively enrolled 265 patients (196 in the training cohort and 69 in the validation cohort) with ccRCC undergoing nephrectomy at a single institution. Clinicopathologic features, overall survival (OS) and recurrence-free survival (RFS) were recorded. MGAT5 intensities were assessed by immunohistochemistry in specimens of patients. Kaplan-Meier method was applied to compare survival curves. Cox regression models were used to analyze the impact of prognostic factors on OS and RFS. Concordance index (C-index) was calculated to assess predictive accuracy. In both cohorts, MGAT5 expression positively correlated with metastatic and advanced TNM stage. High MGAT5 expression indicated poor survival (P < 0.001 in training set and P < 0.001 in validation set) and early recurrence (P < 0.001 in training set and P = 0.004 in validation set) of patients with ccRCC. After multivariate Cox regression analysis, MGAT5 expression was identified as an independent adverse prognostic factor for survival and recurrence. The predictive accuracy of TNM, UISS and SSIGN prognostic models was improved when MGAT5 expression was added. Question: Does β1,6-N-acetylglucosaminyltransferase V predict recurrence and survival of patients with clear-cell renal cell carcinoma after surgical resection? Output:
PubmedQA130335
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To ascertain the neural network mediating reading using intraoperative electrostimulation. A cortical and axonal intraoperative electrical mapping of reading processes was achieved in seven patients who underwent awake surgery for a left occipitotemporal glioma. We performed resection cavity overlapping and superimposition with a diffusion tensor imaging-based white matter atlas. We assessed the relationship between the location of resection cavities and the occurrence of reading impairments of regular, irregular, and pseudowords. Intraoperative stimulation of the left posterior inferior temporal cortex (ITCp) elicited reading disturbances. Subcortical stimulation at the anterior portion of the visual word form area (VWFA) induced addressed phonology (irregular words reading) disturbances. Subcortical stimulation of the connection between VWFA and the posterior segment of the arcuate fascicle (AFp) induced both addressed and assembled phonology (irregular and pseudowords reading) disturbances. Postoperative assessment showed that resection of the posterior portion of the inferior longitudinal fascicle (ILFp), connecting the visual cortex to VWFA, induced long-term and global reading impairment. Resection of the terminations of left AFp in the ITCp-induced irregular and pseudowords reading disturbances with no impairment of regular words reading. Resection of the anterior portion of ILF did not induce reading impairment.\n Question: Does new insights into the neural network mediating reading process provided by cortico-subcortical electrical mapping?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To ascertain the neural network mediating reading using intraoperative electrostimulation. A cortical and axonal intraoperative electrical mapping of reading processes was achieved in seven patients who underwent awake surgery for a left occipitotemporal glioma. We performed resection cavity overlapping and superimposition with a diffusion tensor imaging-based white matter atlas. We assessed the relationship between the location of resection cavities and the occurrence of reading impairments of regular, irregular, and pseudowords. Intraoperative stimulation of the left posterior inferior temporal cortex (ITCp) elicited reading disturbances. Subcortical stimulation at the anterior portion of the visual word form area (VWFA) induced addressed phonology (irregular words reading) disturbances. Subcortical stimulation of the connection between VWFA and the posterior segment of the arcuate fascicle (AFp) induced both addressed and assembled phonology (irregular and pseudowords reading) disturbances. Postoperative assessment showed that resection of the posterior portion of the inferior longitudinal fascicle (ILFp), connecting the visual cortex to VWFA, induced long-term and global reading impairment. Resection of the terminations of left AFp in the ITCp-induced irregular and pseudowords reading disturbances with no impairment of regular words reading. Resection of the anterior portion of ILF did not induce reading impairment. Question: Does new insights into the neural network mediating reading process provided by cortico-subcortical electrical mapping? Output:
PubmedQA50092
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To assess the accuracy of estimating birth weight among twins with discordancy (intra-pair difference in actual birth weight of more than 25%) and to determine the relative accuracy of an intra-pair difference in abdominal circumference (delta AC) of 20 mm or more or in estimated fetal weight (delta EFW) of 25% or more for the identification of discordant growth in twins. Over a 6-year period, we identified all non-anomalous twin pairs with gestational ages greater than 23 weeks and sonographic examinations within 3 weeks of birth. Ultrasonographic biometry of both twins included AC, head circumference, and femur length; these indices were used to estimate fetal weight by Hadlock's formula. Likelihood ratios, receiver-operating characteristic curves, and prediction limits were applied to assess the accuracy of the two diagnostic methods to predict an abnormal outcome. A total of 242 twin pairs were studied. The mean gestational age among the 21 twins with abnormal growth (30.6 +/- 4.6 weeks) was significantly less than among the 221 twins with normal growth (33.2 +/- 4.0 weeks) (P < .005). The biometric measurements of fetal parts, sonographic estimate of fetal weight, and actual birth weight for both fetuses were significantly less for discordant twin pairs (P < .05). The accuracy of predicting birth weight, as determined by mean error and percentage of the estimate within 10% of the actual weight, was similar between the groups. Receiver-operating characteristic curves showed that both diagnostic tests yielded areas under the two curves not significantly different from the area under the nondiagnostic line (P > .05). Most important, prediction limit calculations indicated that a 90% certainty that the actual birth weight discordance was at least 25% was achievable only if delta AC was 172 mm or greater or delta EFW was 112% or more.\n Question: Does sonographic examination predict twin growth discordance accurately?\n Output: " }, { "role": "assistant", "content": "no" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To assess the accuracy of estimating birth weight among twins with discordancy (intra-pair difference in actual birth weight of more than 25%) and to determine the relative accuracy of an intra-pair difference in abdominal circumference (delta AC) of 20 mm or more or in estimated fetal weight (delta EFW) of 25% or more for the identification of discordant growth in twins. Over a 6-year period, we identified all non-anomalous twin pairs with gestational ages greater than 23 weeks and sonographic examinations within 3 weeks of birth. Ultrasonographic biometry of both twins included AC, head circumference, and femur length; these indices were used to estimate fetal weight by Hadlock's formula. Likelihood ratios, receiver-operating characteristic curves, and prediction limits were applied to assess the accuracy of the two diagnostic methods to predict an abnormal outcome. A total of 242 twin pairs were studied. The mean gestational age among the 21 twins with abnormal growth (30.6 +/- 4.6 weeks) was significantly less than among the 221 twins with normal growth (33.2 +/- 4.0 weeks) (P < .005). The biometric measurements of fetal parts, sonographic estimate of fetal weight, and actual birth weight for both fetuses were significantly less for discordant twin pairs (P < .05). The accuracy of predicting birth weight, as determined by mean error and percentage of the estimate within 10% of the actual weight, was similar between the groups. Receiver-operating characteristic curves showed that both diagnostic tests yielded areas under the two curves not significantly different from the area under the nondiagnostic line (P > .05). Most important, prediction limit calculations indicated that a 90% certainty that the actual birth weight discordance was at least 25% was achievable only if delta AC was 172 mm or greater or delta EFW was 112% or more. Question: Does sonographic examination predict twin growth discordance accurately? Output:
PubmedQA145518
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Cell-cell adhesion is a major factor in integrity of epithelia which is frequently disturbed in cancer leading to local invasion and distant metastasis. To define expression and function of activated leukocyte cell adhesion molecule (ALCAM, CD166) in pancreatic cancer and in pancreatic neuroendocrine tumors (PNET), microarray analyses, RT-PCR, immunohistochemistry, RNAi, adhesion, migration, invasion, and chemoresistance assays were used. We demonstrate that expression of ALCAM is altered and its serum levels are increased in pancreatic ductal adenocarcinoma (PDAC). ALCAM was expressed on the membranes of islet cells in the normal pancreas whereas normal pancreatic ducts were ALCAM-negative. In PDAC, ALCAM expression was generally rare though in some tumors, membranous, or cytoplasmic ALCAM was found. PNET were mostly ALCAM-positive with a cytoplasmic staining pattern which was in contrast to the membrane expression observed in non-transformed islet cells. In vitro, ALCAM silencing using RNAi had no effects on growth or invasion of pancreatic cancer cells but reduced cell adhesion and induced chemoresistance. In neuroendocrine tumor cell lines, silencing of ALCAM decreased cell growth.\n Question: Is aLCAM associated with chemoresistance and tumor cell adhesion in pancreatic cancer?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Cell-cell adhesion is a major factor in integrity of epithelia which is frequently disturbed in cancer leading to local invasion and distant metastasis. To define expression and function of activated leukocyte cell adhesion molecule (ALCAM, CD166) in pancreatic cancer and in pancreatic neuroendocrine tumors (PNET), microarray analyses, RT-PCR, immunohistochemistry, RNAi, adhesion, migration, invasion, and chemoresistance assays were used. We demonstrate that expression of ALCAM is altered and its serum levels are increased in pancreatic ductal adenocarcinoma (PDAC). ALCAM was expressed on the membranes of islet cells in the normal pancreas whereas normal pancreatic ducts were ALCAM-negative. In PDAC, ALCAM expression was generally rare though in some tumors, membranous, or cytoplasmic ALCAM was found. PNET were mostly ALCAM-positive with a cytoplasmic staining pattern which was in contrast to the membrane expression observed in non-transformed islet cells. In vitro, ALCAM silencing using RNAi had no effects on growth or invasion of pancreatic cancer cells but reduced cell adhesion and induced chemoresistance. In neuroendocrine tumor cell lines, silencing of ALCAM decreased cell growth. Question: Is aLCAM associated with chemoresistance and tumor cell adhesion in pancreatic cancer? Output:
PubmedQA133785
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: IL-9 is a pleiotropic cytokine that has multiple effects on structural as well as numerous hematopoietic cells, which are central to the pathogenesis of asthma. The contribution of IL-9 to asthma pathogenesis has thus far been unclear, due to conflicting reports in the literature. These earlier studies focused on the role of IL-9 in acute inflammatory models; here we have investigated the effects of IL-9 blockade during chronic allergic inflammation. Mice were exposed to either prolonged ovalbumin or house dust mite allergen challenge to induce chronic inflammation and airway remodeling. We found that IL-9 governs allergen-induced mast cell (MC) numbers in the lung and has pronounced effects on chronic allergic inflammation. Anti-IL-9 antibody-treated mice were protected from airway remodeling with a concomitant reduction in mature MC numbers and activation, in addition to decreased expression of the profibrotic mediators transforming growth factor-β1, vascular endothelial growth factor, and fibroblast growth factor-2 in the lung. Airway remodeling was associated with impaired lung function in the peripheral airways and this was reversed by IL-9 neutralization. In human asthmatic lung tissue, we identified MCs as the main IL-9 receptor expressing population and found them to be sources of vascular endothelial growth factor and fibroblast growth factor-2.\n Question: Does iL-9 govern allergen-induced mast cell numbers in the lung and chronic remodeling of the airways?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: IL-9 is a pleiotropic cytokine that has multiple effects on structural as well as numerous hematopoietic cells, which are central to the pathogenesis of asthma. The contribution of IL-9 to asthma pathogenesis has thus far been unclear, due to conflicting reports in the literature. These earlier studies focused on the role of IL-9 in acute inflammatory models; here we have investigated the effects of IL-9 blockade during chronic allergic inflammation. Mice were exposed to either prolonged ovalbumin or house dust mite allergen challenge to induce chronic inflammation and airway remodeling. We found that IL-9 governs allergen-induced mast cell (MC) numbers in the lung and has pronounced effects on chronic allergic inflammation. Anti-IL-9 antibody-treated mice were protected from airway remodeling with a concomitant reduction in mature MC numbers and activation, in addition to decreased expression of the profibrotic mediators transforming growth factor-β1, vascular endothelial growth factor, and fibroblast growth factor-2 in the lung. Airway remodeling was associated with impaired lung function in the peripheral airways and this was reversed by IL-9 neutralization. In human asthmatic lung tissue, we identified MCs as the main IL-9 receptor expressing population and found them to be sources of vascular endothelial growth factor and fibroblast growth factor-2. Question: Does iL-9 govern allergen-induced mast cell numbers in the lung and chronic remodeling of the airways? Output:
PubmedQA110753
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The coronary sinus (CS) including the great cardiac vein is an important anatomic structure that is considered a landmark for the mitral annulus (MA) and also a target for catheter ablation. This study evaluated the anatomical relationship between the CS and its surrounding structures visualized by multi-detector computed tomography (MDCT). We performed MDCT on 42 patients, and the ranges of the coronary arteries (CAs) and esophagus that ran closest (<5 mm) to the CS were examined. In addition, the distances between the CS and the MA and left ventricle and left atrium were compared with the amplitudes of the local atrial and ventricular electrograms in the CS at the most lateral point (3 o'clock) and the inferior point (6 o'clock) in the CS. The distal portion of the right CA ran near the antero-inferior side of the CS ostium in 92% of the patients. The esophagus and the left circumflex CA proximity to the CS ran from 15 to 41 mm and from 53 to 104 mm from the ostium in all patients. At the 3 o'clock and 6 o'clock position of the MA, the distance between the center of the CS and MA was 12 and 13 mm, respectively, and showed negative correlation with the ratio of atrial and ventricular electrograms.\n Question: Are extracardiac structures frequently present within close proximity to the left atrium : Relevance to catheter ablation?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The coronary sinus (CS) including the great cardiac vein is an important anatomic structure that is considered a landmark for the mitral annulus (MA) and also a target for catheter ablation. This study evaluated the anatomical relationship between the CS and its surrounding structures visualized by multi-detector computed tomography (MDCT). We performed MDCT on 42 patients, and the ranges of the coronary arteries (CAs) and esophagus that ran closest (<5 mm) to the CS were examined. In addition, the distances between the CS and the MA and left ventricle and left atrium were compared with the amplitudes of the local atrial and ventricular electrograms in the CS at the most lateral point (3 o'clock) and the inferior point (6 o'clock) in the CS. The distal portion of the right CA ran near the antero-inferior side of the CS ostium in 92% of the patients. The esophagus and the left circumflex CA proximity to the CS ran from 15 to 41 mm and from 53 to 104 mm from the ostium in all patients. At the 3 o'clock and 6 o'clock position of the MA, the distance between the center of the CS and MA was 12 and 13 mm, respectively, and showed negative correlation with the ratio of atrial and ventricular electrograms. Question: Are extracardiac structures frequently present within close proximity to the left atrium : Relevance to catheter ablation? Output:
PubmedQA27268
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Graves' disease (GD) is caused by thyrotropin (TSH) receptor antibodies (TSHRAbs) that bind to TSHR and activate thyrocytes. The measurement of TSHRAbs therefore has been used to assist in the diagnosis and management of GD. In this study, we evaluated the clinical significance of a newly developed bioreporter assay for the detection of TSHRAbs (Thyretain). The Thyretain bioreporter assay utilizes a chimeric receptor (Mc4), in which residues 262-335 of TSHR are replaced with a rat lutropin-choriogonadtropin receptor segment. This bioreporter is designed to specifically detect stimulating TSHRAbs (Mc4-TSHRAbs). The Mc4-TSHRAb level of sera obtained from 110 normal healthy controls, 103, 99, and 50 patients with untreated GD, painless Hashimoto's thyroiditis (PT), and subacute thyroiditis (SAT) were 27.3% +/- 11.3%, 327.8% +/- 105.9%, 48.9% +/- 48.5%, and 24.9% +/- 13.4%, respectively. Compared with the Mc4-TSHRAb levels of patients with PT and SAT, and normal healthy controls, the Mc4-TSHRAb levels of untreated GD patients were significantly higher (p < 0.01). The sensitivity and specificity of the Thyretain bioreporter assay for GD and PT were 95.1% and 96.0%, respectively, at the optimal cut-off value of 128%. Measurement of TSHRAbs with a bioassay that uses porcine thyroid cells (TSH-stimulating antibody [TSAb]) showed a positive correlation (r = 0.472, p < 0.001) with the Thyretain assay for untreated GD, and strong positive correlation (r = 0.821, p < 0.001) for the entire untreated GD, PT, and SAT population. The positive rate of Mc4-TSHRAbs for GD was significantly higher than that of TSAb (95.1% vs. 89.3%, p < 0.05) and the negative rate of PT by Mc4-TSHRAbs was also significantly higher than that of TSAb (96.0% vs. 86.9%, p < 0.01). As a result, Mc4-TSHRAbs showed statistically better (p < 0.01) diagnostic accuracy in differentiating GD from PT than TSAb.\n Question: Is a novel bioreporter assay for thyrotropin receptor antibodies using a chimeric thyrotropin receptor ( mc4 ) more useful in differentiation of Graves ' disease from painless thyroiditis than conventional thyrotropin-stimulating antibody assay using porcine thyroid cells?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Graves' disease (GD) is caused by thyrotropin (TSH) receptor antibodies (TSHRAbs) that bind to TSHR and activate thyrocytes. The measurement of TSHRAbs therefore has been used to assist in the diagnosis and management of GD. In this study, we evaluated the clinical significance of a newly developed bioreporter assay for the detection of TSHRAbs (Thyretain). The Thyretain bioreporter assay utilizes a chimeric receptor (Mc4), in which residues 262-335 of TSHR are replaced with a rat lutropin-choriogonadtropin receptor segment. This bioreporter is designed to specifically detect stimulating TSHRAbs (Mc4-TSHRAbs). The Mc4-TSHRAb level of sera obtained from 110 normal healthy controls, 103, 99, and 50 patients with untreated GD, painless Hashimoto's thyroiditis (PT), and subacute thyroiditis (SAT) were 27.3% +/- 11.3%, 327.8% +/- 105.9%, 48.9% +/- 48.5%, and 24.9% +/- 13.4%, respectively. Compared with the Mc4-TSHRAb levels of patients with PT and SAT, and normal healthy controls, the Mc4-TSHRAb levels of untreated GD patients were significantly higher (p < 0.01). The sensitivity and specificity of the Thyretain bioreporter assay for GD and PT were 95.1% and 96.0%, respectively, at the optimal cut-off value of 128%. Measurement of TSHRAbs with a bioassay that uses porcine thyroid cells (TSH-stimulating antibody [TSAb]) showed a positive correlation (r = 0.472, p < 0.001) with the Thyretain assay for untreated GD, and strong positive correlation (r = 0.821, p < 0.001) for the entire untreated GD, PT, and SAT population. The positive rate of Mc4-TSHRAbs for GD was significantly higher than that of TSAb (95.1% vs. 89.3%, p < 0.05) and the negative rate of PT by Mc4-TSHRAbs was also significantly higher than that of TSAb (96.0% vs. 86.9%, p < 0.01). As a result, Mc4-TSHRAbs showed statistically better (p < 0.01) diagnostic accuracy in differentiating GD from PT than TSAb. Question: Is a novel bioreporter assay for thyrotropin receptor antibodies using a chimeric thyrotropin receptor ( mc4 ) more useful in differentiation of Graves ' disease from painless thyroiditis than conventional thyrotropin-stimulating antibody assay using porcine thyroid cells? Output:
PubmedQA40806
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The antiatherogenic effect of conjugated linoleic acid (CLA) has been demonstrated in animal models. Although there are plenty of In this study, we assessed the impact of CLA supplementation on the levels of atherosclerosis markers - high-sensitivity C-reactive protein (hs-CRP) and asymmetrical dimethylarginine (ADMA). Seventy-four adult female subjects with body mass index ≥25 kg/m No significant differences were found in hs-CRP and ADMA levels before and after nutritional intervention between both groups. The changes in hs-CRP and ADMA concentration values (Δhs-CRP; ΔADMA median [interquartile range]) did not differ between subjects from the placebo (-0.1 [-0.8 to 0.3]; -0.02 [-0.12 to 0.14]) and CLA (0.2 [-0.7 to 0.9]; 0.04 [-0.14 to 0.13]) groups. The incidence of reduction of hs-CRP or ADMA concentration was not different in subjects of the CLA group compared to those of the placebo group (41.9% vs. 50%, relative risk [RR]=0.8387, 95% confidence interval [CI]=0.4887-1.4493, \n Question: Does twelve-week-conjugated linoleic acid supplementation have no effects on the selected markers of atherosclerosis in obese and overweight women?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The antiatherogenic effect of conjugated linoleic acid (CLA) has been demonstrated in animal models. Although there are plenty of In this study, we assessed the impact of CLA supplementation on the levels of atherosclerosis markers - high-sensitivity C-reactive protein (hs-CRP) and asymmetrical dimethylarginine (ADMA). Seventy-four adult female subjects with body mass index ≥25 kg/m No significant differences were found in hs-CRP and ADMA levels before and after nutritional intervention between both groups. The changes in hs-CRP and ADMA concentration values (Δhs-CRP; ΔADMA median [interquartile range]) did not differ between subjects from the placebo (-0.1 [-0.8 to 0.3]; -0.02 [-0.12 to 0.14]) and CLA (0.2 [-0.7 to 0.9]; 0.04 [-0.14 to 0.13]) groups. The incidence of reduction of hs-CRP or ADMA concentration was not different in subjects of the CLA group compared to those of the placebo group (41.9% vs. 50%, relative risk [RR]=0.8387, 95% confidence interval [CI]=0.4887-1.4493, Question: Does twelve-week-conjugated linoleic acid supplementation have no effects on the selected markers of atherosclerosis in obese and overweight women? Output:
PubmedQA15237
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Evidence does not support an association between systemic corticosteroid use and the development of peptic ulcer disease (PUD) and prophylactic anti-ulcer therapy is not routinely indicated. The aim was to find out the opinion of physicians in the Czech Republic on corticosteroid-induced ulcers. A questionnaire-based study targeting 360 physicians of different specialties (100 from Gastroenterology, 100 from General Practice, 80 from Pneumology/Immunology, and 80 from Neurology/Neurosurgery). Eighty-two percent of the physicians considered corticosteroids ulcerogenic, 7.5% of the responders considered them ulcerogenic only in patients with a family history of PUD, and 10.3% of the physicians considered corticosteroids non-ulcerogenic. Seventy-five percent of the responders would administer concomitant antisecretory treatment. Sixty-seven percent of the physicians thought that PUD was a frequent complication of corticosteroid therapy. If the ulcerogenic potential of ibuprofen, diclofenac, and prednisone was a subject of the physicians' judgment, a majority (40.5%) considered prednisone to be the most ulcerogenic substance. Thirty percent of gastroenterologists (vs. 1.9% of others; p < 0.001) did not consider corticosteroids to be ulcerogenic; 27.4% (vs. 4.3%; p < 0.01) would not administer an antisecretory prophylaxis routinely.\n Question: Are `` A surviving myth '' -- corticosteroids still considered ulcerogenic by a majority of physicians?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Evidence does not support an association between systemic corticosteroid use and the development of peptic ulcer disease (PUD) and prophylactic anti-ulcer therapy is not routinely indicated. The aim was to find out the opinion of physicians in the Czech Republic on corticosteroid-induced ulcers. A questionnaire-based study targeting 360 physicians of different specialties (100 from Gastroenterology, 100 from General Practice, 80 from Pneumology/Immunology, and 80 from Neurology/Neurosurgery). Eighty-two percent of the physicians considered corticosteroids ulcerogenic, 7.5% of the responders considered them ulcerogenic only in patients with a family history of PUD, and 10.3% of the physicians considered corticosteroids non-ulcerogenic. Seventy-five percent of the responders would administer concomitant antisecretory treatment. Sixty-seven percent of the physicians thought that PUD was a frequent complication of corticosteroid therapy. If the ulcerogenic potential of ibuprofen, diclofenac, and prednisone was a subject of the physicians' judgment, a majority (40.5%) considered prednisone to be the most ulcerogenic substance. Thirty percent of gastroenterologists (vs. 1.9% of others; p < 0.001) did not consider corticosteroids to be ulcerogenic; 27.4% (vs. 4.3%; p < 0.01) would not administer an antisecretory prophylaxis routinely. Question: Are `` A surviving myth '' -- corticosteroids still considered ulcerogenic by a majority of physicians? Output:
PubmedQA157343
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To plan preventive intervention after myocardial infarction (MI) the disease prevalence and the age and time from acute event of the index population should be known. We identified all the living patients with MI coded diagnosis in the database of the Italian College of General Practitioners (Health Search Database-HSD). The years from the first acute MI were also determined. 3588 subjects with MI diagnosis were identified (2698 males and 888 females, for 2 gender not recorded). Based on the distribution of our population and on that reported by the Italian Institute of Statistics, stratified by gender and age (segments of 10 years), the estimated number of subjects with MI in Italy (age-standardized rates x 10000) was 309284 for men and 102343 for women.\n Question: Does the database of Italian general practitioners allow a reliable determination of the prevalence of myocardial infarction?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To plan preventive intervention after myocardial infarction (MI) the disease prevalence and the age and time from acute event of the index population should be known. We identified all the living patients with MI coded diagnosis in the database of the Italian College of General Practitioners (Health Search Database-HSD). The years from the first acute MI were also determined. 3588 subjects with MI diagnosis were identified (2698 males and 888 females, for 2 gender not recorded). Based on the distribution of our population and on that reported by the Italian Institute of Statistics, stratified by gender and age (segments of 10 years), the estimated number of subjects with MI in Italy (age-standardized rates x 10000) was 309284 for men and 102343 for women. Question: Does the database of Italian general practitioners allow a reliable determination of the prevalence of myocardial infarction? Output:
PubmedQA153019
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The synucleins (alpha, beta, and gamma) are a family of small cytoplasmic proteins that are expressed predominantly in neurons. alpha synuclein has attracted considerable attention due to its involvement in neurodegenerative diseases. Abnormal expression of gamma synuclein has recently been reported in some breast tumors. In this study, the authors examined a panel of breast and ovarian carcinomas for expression of alpha, beta, and gamma synucleins. Normal breast and ovary tissue samples, tissue from ovaries of women at high risk of ovarian carcinoma, and tissue from breast and ovarian carcinomas were screened by immunohistochemistry and Western blot analysis for synuclein expression. Synucleins were not detectable by Western blot analysis in normal breast tissue. Eighty-two percent (14 of 17) of Stage III/IV breast ductal carcinomas expressed beta synuclein, gamma synuclein, or both simultaneously. Expression of alpha synuclein was not detected in breast carcinomas by Western blot analysis. Synuclein (alpha, beta, and gamma) expression was not detectable by immunohistochemistry in normal ovarian epithelium. Eighty-seven percent (39 of 45) of ovarian carcinomas were found to express at least 1 type of synuclein, and 42% (19 of 45) expressed all 3 synucleins (alpha, beta, and gamma) simultaneously. Highly punctate gamma synuclein expression was also observed in 20% of preneoplastic lesions of the ovary, including epithelial inclusion cysts, hyperplastic epithelium, and papillary structures, suggesting that gamma synuclein up-regulation may occur early in the development of some ovarian tumors.\n Question: Are synucleins expressed in the majority of breast and ovarian carcinomas and in preneoplastic lesions of the ovary?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The synucleins (alpha, beta, and gamma) are a family of small cytoplasmic proteins that are expressed predominantly in neurons. alpha synuclein has attracted considerable attention due to its involvement in neurodegenerative diseases. Abnormal expression of gamma synuclein has recently been reported in some breast tumors. In this study, the authors examined a panel of breast and ovarian carcinomas for expression of alpha, beta, and gamma synucleins. Normal breast and ovary tissue samples, tissue from ovaries of women at high risk of ovarian carcinoma, and tissue from breast and ovarian carcinomas were screened by immunohistochemistry and Western blot analysis for synuclein expression. Synucleins were not detectable by Western blot analysis in normal breast tissue. Eighty-two percent (14 of 17) of Stage III/IV breast ductal carcinomas expressed beta synuclein, gamma synuclein, or both simultaneously. Expression of alpha synuclein was not detected in breast carcinomas by Western blot analysis. Synuclein (alpha, beta, and gamma) expression was not detectable by immunohistochemistry in normal ovarian epithelium. Eighty-seven percent (39 of 45) of ovarian carcinomas were found to express at least 1 type of synuclein, and 42% (19 of 45) expressed all 3 synucleins (alpha, beta, and gamma) simultaneously. Highly punctate gamma synuclein expression was also observed in 20% of preneoplastic lesions of the ovary, including epithelial inclusion cysts, hyperplastic epithelium, and papillary structures, suggesting that gamma synuclein up-regulation may occur early in the development of some ovarian tumors. Question: Are synucleins expressed in the majority of breast and ovarian carcinomas and in preneoplastic lesions of the ovary? Output:
PubmedQA63450
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Zinc (Zn) is related to insulin synthesis, storage, and secretion. This study demonstrates the effects of Zn supplementation in donor rats on the outcomes of islet transplantation. Donor rats received 3 different regimens of dietary Zn supplementation for 2 weeks before undergoing pancreas donation: a standard diet containing Zn at 50 ppm (control), 1 ppm (low-Zn group) or 1000 ppm (high-Zn group), respectively. Diabetic recipient rats underwent islet transplantation, and the blood glucose levels and insulin secretion were monitored for 7 days after transplantation. The serum and pancreatic Zn levels at the time of donation were significantly lower in the low-Zn group (48.8 ± 25.5 µg/dL and 11.3 ± 1.9 µg/g) and higher in the high-Zn group (147.3 ± 17.6 µg/dL and 18.7 ± 2.2 µg/g) when compared with those observed in the controls (118.7 ± 7.9 µg/dL and 14.6 ± 2.0 µg/g) (P < 0.05). The blood glucose levels became re-elevated 2 days after transplantation in rats receiving islet grafts from the controls and the low-Zn groups. In contrast, in the rats that received islets from the high-Zn groups, these were maintained within a reference range (P < 0.01).\n Question: Does dietary zinc supplementation to the donor improve insulin secretion after islet transplantation in chemically induced diabetic rats?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Zinc (Zn) is related to insulin synthesis, storage, and secretion. This study demonstrates the effects of Zn supplementation in donor rats on the outcomes of islet transplantation. Donor rats received 3 different regimens of dietary Zn supplementation for 2 weeks before undergoing pancreas donation: a standard diet containing Zn at 50 ppm (control), 1 ppm (low-Zn group) or 1000 ppm (high-Zn group), respectively. Diabetic recipient rats underwent islet transplantation, and the blood glucose levels and insulin secretion were monitored for 7 days after transplantation. The serum and pancreatic Zn levels at the time of donation were significantly lower in the low-Zn group (48.8 ± 25.5 µg/dL and 11.3 ± 1.9 µg/g) and higher in the high-Zn group (147.3 ± 17.6 µg/dL and 18.7 ± 2.2 µg/g) when compared with those observed in the controls (118.7 ± 7.9 µg/dL and 14.6 ± 2.0 µg/g) (P < 0.05). The blood glucose levels became re-elevated 2 days after transplantation in rats receiving islet grafts from the controls and the low-Zn groups. In contrast, in the rats that received islets from the high-Zn groups, these were maintained within a reference range (P < 0.01). Question: Does dietary zinc supplementation to the donor improve insulin secretion after islet transplantation in chemically induced diabetic rats? Output:
PubmedQA32758
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To determine why athletes decide not to seek medical attention during a game or practice when they believe they have suffered a concussion. A retrospective survey. University Sport Medicine Clinic. A total of 469 male and female university athletes from several varsity team sports were participated in the study. Athletes were surveyed about the previous 12 months to identify specific reasons why those athletes who believed they had suffered a concussion during a game or practice decided not to seek attention at that time, how often these reasons occurred, and how important these reasons were in the decision process. Ninety-two of the 469 athletes (19.6%) believed they had suffered a concussion within the previous 12 months while playing their respective sport, and 72 of these 92 athletes (78.3%) did not seek medical attention during the game or practice at least once during that time. Sports in which athletes were more likely to not reveal their concussion symptoms were football and ice hockey. The reason \"Did not feel the concussion was serious/severe and felt you could still continue to play with little danger to yourself,\" was listed most commonly (55/92) as a cause for not seeking medical attention for a presumed concussion.\n Question: Choose why university athletes to reveal their concussion symptoms during a practice or game?\n Output: " }, { "role": "assistant", "content": "no" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To determine why athletes decide not to seek medical attention during a game or practice when they believe they have suffered a concussion. A retrospective survey. University Sport Medicine Clinic. A total of 469 male and female university athletes from several varsity team sports were participated in the study. Athletes were surveyed about the previous 12 months to identify specific reasons why those athletes who believed they had suffered a concussion during a game or practice decided not to seek attention at that time, how often these reasons occurred, and how important these reasons were in the decision process. Ninety-two of the 469 athletes (19.6%) believed they had suffered a concussion within the previous 12 months while playing their respective sport, and 72 of these 92 athletes (78.3%) did not seek medical attention during the game or practice at least once during that time. Sports in which athletes were more likely to not reveal their concussion symptoms were football and ice hockey. The reason "Did not feel the concussion was serious/severe and felt you could still continue to play with little danger to yourself," was listed most commonly (55/92) as a cause for not seeking medical attention for a presumed concussion. Question: Choose why university athletes to reveal their concussion symptoms during a practice or game? Output:
PubmedQA45478
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Mice with single gene deficiency of thrombin-activatable fibrinolysis inhibitor (TAFI) or plasminogen activator inhibitor-1 (PAI-1) have an enhanced fibrinolytic capacity. To unravel the function and relevance of both antifibrinolytic proteins through the generation and characterization of mice with combined TAFI and PAI-1 gene deficiency. Mating of TAFI knockout (KO) mice with PAI-1 KO mice resulted in the production of TAFI/PAI-1 double-KO mice that were viable, were fertile, and developed normally. In a tail vein bleeding model, the bleeding time and hemoglobin content of the TAFI/PAI-1 double-KO mice did not deviate significantly from those of the single-KO mice or of the wild-type (WT) counterparts. Interestingly, in ex vivo rotational thromboelastometry measurements with whole blood samples, TAFI KO mice and TAFI/PAI-1 double-KO mice were more sensitive to fibrinolytic activation with tissue-type plasminogen activator than WT or PAI-1 KO mice. This enhanced fibrinolytic capacity was confirmed in vivo in a mouse thromboembolism model, as shown by decreased fibrin deposition in the lungs of TAFI KO mice and TAFI/PAI-1 double-KO mice as compared with WT or PAI-1 KO mice.\n Question: Is the hyperfibrinolytic state of mice with combined thrombin-activatable fibrinolysis inhibitor ( TAFI ) and plasminogen activator inhibitor-1 gene deficiency critically dependent on TAFI deficiency?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Mice with single gene deficiency of thrombin-activatable fibrinolysis inhibitor (TAFI) or plasminogen activator inhibitor-1 (PAI-1) have an enhanced fibrinolytic capacity. To unravel the function and relevance of both antifibrinolytic proteins through the generation and characterization of mice with combined TAFI and PAI-1 gene deficiency. Mating of TAFI knockout (KO) mice with PAI-1 KO mice resulted in the production of TAFI/PAI-1 double-KO mice that were viable, were fertile, and developed normally. In a tail vein bleeding model, the bleeding time and hemoglobin content of the TAFI/PAI-1 double-KO mice did not deviate significantly from those of the single-KO mice or of the wild-type (WT) counterparts. Interestingly, in ex vivo rotational thromboelastometry measurements with whole blood samples, TAFI KO mice and TAFI/PAI-1 double-KO mice were more sensitive to fibrinolytic activation with tissue-type plasminogen activator than WT or PAI-1 KO mice. This enhanced fibrinolytic capacity was confirmed in vivo in a mouse thromboembolism model, as shown by decreased fibrin deposition in the lungs of TAFI KO mice and TAFI/PAI-1 double-KO mice as compared with WT or PAI-1 KO mice. Question: Is the hyperfibrinolytic state of mice with combined thrombin-activatable fibrinolysis inhibitor ( TAFI ) and plasminogen activator inhibitor-1 gene deficiency critically dependent on TAFI deficiency? Output:
PubmedQA132128
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Dexamethasone decreases chemotherapy-induced emesis when added to antiemetic regimens. This study was designed to compare the effectiveness of granisetron and dexamethasone with granisetron alone in the prevention of post-operative vomiting after strabismus repair, tonsillectomy with or without adenoidectomy in children. In a randomized, double-blind study, 60 healthy children, 4-10 yr of age, received either granisetron 40 micrograms.kg-1 and saline (Group S) or granisetron 40 micrograms.kg-1 and dexamethasone 4 mg (Group D) iv immediately after the induction of anaesthesia. All subjects received anaesthetics consisting of sevoflurane and nitrous oxide in oxygen Postoperative pain was treated with acetaminophen pr or pentazocine iv. Postoperatively, during the first 24 hr after anaesthesia, the frequencies of retching and vomiting, and the incidence of adverse events were recorded by nursing staff. There were no differences between the treatment groups with regard to demographics, surgical procedure, anaesthetic administered or analgesics used for postoperative pain. The frequency of the symptoms was 27% and 7% in Groups S and D, respectively (P < 0.05). The incidence of adverse events was comparable in the two groups.\n Question: Do granistron and dexamethasone provide more improved prevention of postoperative emesis than granisetron alone in children?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Dexamethasone decreases chemotherapy-induced emesis when added to antiemetic regimens. This study was designed to compare the effectiveness of granisetron and dexamethasone with granisetron alone in the prevention of post-operative vomiting after strabismus repair, tonsillectomy with or without adenoidectomy in children. In a randomized, double-blind study, 60 healthy children, 4-10 yr of age, received either granisetron 40 micrograms.kg-1 and saline (Group S) or granisetron 40 micrograms.kg-1 and dexamethasone 4 mg (Group D) iv immediately after the induction of anaesthesia. All subjects received anaesthetics consisting of sevoflurane and nitrous oxide in oxygen Postoperative pain was treated with acetaminophen pr or pentazocine iv. Postoperatively, during the first 24 hr after anaesthesia, the frequencies of retching and vomiting, and the incidence of adverse events were recorded by nursing staff. There were no differences between the treatment groups with regard to demographics, surgical procedure, anaesthetic administered or analgesics used for postoperative pain. The frequency of the symptoms was 27% and 7% in Groups S and D, respectively (P < 0.05). The incidence of adverse events was comparable in the two groups. Question: Do granistron and dexamethasone provide more improved prevention of postoperative emesis than granisetron alone in children? Output:
PubmedQA208505
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To compare the incidence of hepatitis B virus (HBV)-associated membranous nephropathy (HBVMN) before and after universal HBV vaccination and to identify factors underlying the change. This study included 471 hospitalized children with nephrotic syndrome (NS) and 488 long-term follow-up hepatitis B surface antigen (HBsAg)-carrier children. Horizontal transmission (negative maternal HBsAg status) of HBVMN and HBV was assessed, and the incidence of HBVMN was compared before and after initiation of the universal HBV vaccination program started in 1984. The frequency of HBVMN in children with NS was 11.6% between 1974 and 1984, 4.5% between 1984 and 1994, 2.1% between 1994 and 2004, and 0% between 2004 and 2009. Similarly, the number of HBsAg-seropositive children with NS (mainly via horizontal infection) decreased after universal vaccination. The prevaccination frequency of HBV horizontal transmission in chronic HBsAg carriers from the general population was 36.5% compared with 5% in the postvaccination period. The incidence of HBVMN in these carriers revealed a parallel decline.\n Question: Does universal hepatitis B vaccination reduce childhood hepatitis B virus-associated membranous nephropathy?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To compare the incidence of hepatitis B virus (HBV)-associated membranous nephropathy (HBVMN) before and after universal HBV vaccination and to identify factors underlying the change. This study included 471 hospitalized children with nephrotic syndrome (NS) and 488 long-term follow-up hepatitis B surface antigen (HBsAg)-carrier children. Horizontal transmission (negative maternal HBsAg status) of HBVMN and HBV was assessed, and the incidence of HBVMN was compared before and after initiation of the universal HBV vaccination program started in 1984. The frequency of HBVMN in children with NS was 11.6% between 1974 and 1984, 4.5% between 1984 and 1994, 2.1% between 1994 and 2004, and 0% between 2004 and 2009. Similarly, the number of HBsAg-seropositive children with NS (mainly via horizontal infection) decreased after universal vaccination. The prevaccination frequency of HBV horizontal transmission in chronic HBsAg carriers from the general population was 36.5% compared with 5% in the postvaccination period. The incidence of HBVMN in these carriers revealed a parallel decline. Question: Does universal hepatitis B vaccination reduce childhood hepatitis B virus-associated membranous nephropathy? Output:
PubmedQA172089
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: In several studies, secondary structures of ribosomal genes have been used to improve the quality of phylogenetic reconstructions. An extensive evaluation of the benefits of secondary structure, however, is lacking. This is the first study to counter this deficiency. We inspected the accuracy and robustness of phylogenetics with individual secondary structures by simulation experiments for artificial tree topologies with up to 18 taxa and for divergency levels in the range of typical phylogenetic studies. We chose the internal transcribed spacer 2 of the ribosomal cistron as an exemplary marker region. Simulation integrated the coevolution process of sequences with secondary structures. Additionally, the phylogenetic power of marker size duplication was investigated and compared with sequence and sequence-structure reconstruction methods. The results clearly show that accuracy and robustness of Neighbor Joining trees are largely improved by structural information in contrast to sequence only data, whereas a doubled marker size only accounts for robustness.\n Question: Does including RNA secondary structures improve accuracy and robustness in reconstruction of phylogenetic trees?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: In several studies, secondary structures of ribosomal genes have been used to improve the quality of phylogenetic reconstructions. An extensive evaluation of the benefits of secondary structure, however, is lacking. This is the first study to counter this deficiency. We inspected the accuracy and robustness of phylogenetics with individual secondary structures by simulation experiments for artificial tree topologies with up to 18 taxa and for divergency levels in the range of typical phylogenetic studies. We chose the internal transcribed spacer 2 of the ribosomal cistron as an exemplary marker region. Simulation integrated the coevolution process of sequences with secondary structures. Additionally, the phylogenetic power of marker size duplication was investigated and compared with sequence and sequence-structure reconstruction methods. The results clearly show that accuracy and robustness of Neighbor Joining trees are largely improved by structural information in contrast to sequence only data, whereas a doubled marker size only accounts for robustness. Question: Does including RNA secondary structures improve accuracy and robustness in reconstruction of phylogenetic trees? Output:
PubmedQA45767
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Extracellular matrix accumulation, epithelial-to-mesenchymal transition, tubular atrophy and loss of peritubular capillary network are hallmarks of tubulointerstitial injury in progressive renal diseases. In this study, we analyzed endostatin expression in kidneys subjected to unilateral ureteral obstruction (UUO). Collagen XVIII mRNA expression was evaluated by real-time polymerase chain reaction (PCR). Endostatin and CD31 protein levels were analyzed by Western blot and immunohistochemistry. In vitro quantification of collagen XVIII and fibrosis-related genes in HK2 cells was performed by real-time PCR. UUO significantly increased collagen XVIII mRNA expression and released a 30-kDa endostatin fragment. Immunohistochemistry revealed endostatin expression increased in injured tissue, mainly on tubular cells. Of interest, expression of CD31 was significantly reduced by UUO. Endostatin administration in vitro did not modify the expression of genes related to fibrosis development. However, in vitro TGF-beta1 administration induced expression of collagen XVIII/endostatin mRNA in human tubular cells.\n Question: Is endostatin , an antiangiogenic protein , expressed in the unilateral ureteral obstruction mice model?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Extracellular matrix accumulation, epithelial-to-mesenchymal transition, tubular atrophy and loss of peritubular capillary network are hallmarks of tubulointerstitial injury in progressive renal diseases. In this study, we analyzed endostatin expression in kidneys subjected to unilateral ureteral obstruction (UUO). Collagen XVIII mRNA expression was evaluated by real-time polymerase chain reaction (PCR). Endostatin and CD31 protein levels were analyzed by Western blot and immunohistochemistry. In vitro quantification of collagen XVIII and fibrosis-related genes in HK2 cells was performed by real-time PCR. UUO significantly increased collagen XVIII mRNA expression and released a 30-kDa endostatin fragment. Immunohistochemistry revealed endostatin expression increased in injured tissue, mainly on tubular cells. Of interest, expression of CD31 was significantly reduced by UUO. Endostatin administration in vitro did not modify the expression of genes related to fibrosis development. However, in vitro TGF-beta1 administration induced expression of collagen XVIII/endostatin mRNA in human tubular cells. Question: Is endostatin , an antiangiogenic protein , expressed in the unilateral ureteral obstruction mice model? Output:
PubmedQA29907
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To investigate the significance of changes in intercellular adhesion molecule-1 (ICAM-1) expression on keratinocytes(KCs) during wound healing of second degree burn. With immunohistochemistry technique, the ICAM-1 expression in second degree burn wounds in patients were investigated at four different postburn periods. The normal skins from 6 burn patients (BNG), the normal skins from 8 healthy volunteers (HVG) and the scar tissues (SG) from 8 patients served as controls. There was poor expression of ICAM-1 on basal cells in normal skins of healthy volunteers, while the expression of ICAM-1 enhanced in normal skins of burn patients. On basal cells in second degree burn wounds, the expression of ICAM-1 slightly increased in the first week postburn, obviously enhanced in the second week, and in the third or fourth week, the expression continued to keep strong. In addition, the ICAM-1 in KCs showed polar distribution, and the expression of ICAM-1 markedly enhanced on the multilayer KCs in neogenetic epithelium and the positive cells arranged columnarly.\n Question: Do [ The expression of ICAM-1 on the keratinocytes in second degree human burn skin ]?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To investigate the significance of changes in intercellular adhesion molecule-1 (ICAM-1) expression on keratinocytes(KCs) during wound healing of second degree burn. With immunohistochemistry technique, the ICAM-1 expression in second degree burn wounds in patients were investigated at four different postburn periods. The normal skins from 6 burn patients (BNG), the normal skins from 8 healthy volunteers (HVG) and the scar tissues (SG) from 8 patients served as controls. There was poor expression of ICAM-1 on basal cells in normal skins of healthy volunteers, while the expression of ICAM-1 enhanced in normal skins of burn patients. On basal cells in second degree burn wounds, the expression of ICAM-1 slightly increased in the first week postburn, obviously enhanced in the second week, and in the third or fourth week, the expression continued to keep strong. In addition, the ICAM-1 in KCs showed polar distribution, and the expression of ICAM-1 markedly enhanced on the multilayer KCs in neogenetic epithelium and the positive cells arranged columnarly. Question: Do [ The expression of ICAM-1 on the keratinocytes in second degree human burn skin ]? Output:
PubmedQA164915
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To compare the effects on insulin sensitivity, body composition and glycaemic control of the recommended standard weight-maintaining diabetes diet and an isocaloric low-fat diabetes diet during two, 3-month periods in patients with Type 1 diabetes. Thirteen Type 1 patients were included, of whom 10 completed the cross-over study. Ten non-diabetic, matched control subjects were also examined. Body composition was estimated by dual-energy X-ray absorptiometry (DXA) whole-body scanning, diet intake was monitored by 7-day dietary record and insulin sensitivity was measured by the insulin clamp technique at baseline and after each of the diet intervention periods. On an isocaloric low-fat diet, Type 1 diabetic patients significantly reduced the proportion of fat in the total daily energy intake by 12.1% (or -3.6% of total energy) as compared with a conventional diabetes diet (P = 0.039). The daily protein and carbohydrate intake increased (+4.4% of total energy intake, P = 0.0049 and +2.5%, P = 0.34, respectively), while alcohol intake decreased (-3.2% of total energy intake, P = 0.02). There was a significant improvement in insulin sensitivity on the isocaloric, low-fat diet compared with the standard diabetes diet [7.06 +/- 2.16 mg/kg/min (mean +/- sd) vs. 5.52 +/- 2.35 mg/kg/min (P = 0.03)]. However, insulin sensitivity remained 33% lower than in the control subjects (P = 0.021). No significant changes occurred in body weight or body composition. Glycated haemoglobin rose during both diet intervention periods (P = 0.18), with no difference between the two diets.\n Question: Does a low-fat diet improve peripheral insulin sensitivity in patients with Type 1 diabetes?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To compare the effects on insulin sensitivity, body composition and glycaemic control of the recommended standard weight-maintaining diabetes diet and an isocaloric low-fat diabetes diet during two, 3-month periods in patients with Type 1 diabetes. Thirteen Type 1 patients were included, of whom 10 completed the cross-over study. Ten non-diabetic, matched control subjects were also examined. Body composition was estimated by dual-energy X-ray absorptiometry (DXA) whole-body scanning, diet intake was monitored by 7-day dietary record and insulin sensitivity was measured by the insulin clamp technique at baseline and after each of the diet intervention periods. On an isocaloric low-fat diet, Type 1 diabetic patients significantly reduced the proportion of fat in the total daily energy intake by 12.1% (or -3.6% of total energy) as compared with a conventional diabetes diet (P = 0.039). The daily protein and carbohydrate intake increased (+4.4% of total energy intake, P = 0.0049 and +2.5%, P = 0.34, respectively), while alcohol intake decreased (-3.2% of total energy intake, P = 0.02). There was a significant improvement in insulin sensitivity on the isocaloric, low-fat diet compared with the standard diabetes diet [7.06 +/- 2.16 mg/kg/min (mean +/- sd) vs. 5.52 +/- 2.35 mg/kg/min (P = 0.03)]. However, insulin sensitivity remained 33% lower than in the control subjects (P = 0.021). No significant changes occurred in body weight or body composition. Glycated haemoglobin rose during both diet intervention periods (P = 0.18), with no difference between the two diets. Question: Does a low-fat diet improve peripheral insulin sensitivity in patients with Type 1 diabetes? Output:
PubmedQA210426
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The usefulness of brain-natriuretic-peptide (BNP) and N-terminal-pro-brain-natriuretic-peptide (NT-proBNP) for monitoring of chronic heart failure (CHF) patients has been questioned because of high levels of unexplained variation. Week-to-week total variance (CV(T)), unexplained variation (CV(I)), reference change values (RCV), index of individualities (IOI) and number of samples (N) with week-to-week intervals needed to estimate the underlying homeostatic set point (+/-15%) for BNP and NT-proBNP were calculated in pre-specified stable CHF patients. We measured plasma concentrations of BNP and NT-proBNP, clinical and laboratory variables in 20 CHF patients with a 7-days interval. Only patients considered to be in steady state were included. The CV(I) was 15% (BNP) and 8% (NT-proBNP). CV(T) was 16% (BNP) and 8% (NT-proBNP) and RCV was 43% (BNP) and 23% (NT-proBNP). IOI was 0.14 for BNP and 0.03 for NT-proBNP and N was 1 for BNP and 1 for NT-proBNP.\n Question: Is unexplained week-to-week variation in BNP and NT-proBNP low in chronic heart failure patients during steady state?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The usefulness of brain-natriuretic-peptide (BNP) and N-terminal-pro-brain-natriuretic-peptide (NT-proBNP) for monitoring of chronic heart failure (CHF) patients has been questioned because of high levels of unexplained variation. Week-to-week total variance (CV(T)), unexplained variation (CV(I)), reference change values (RCV), index of individualities (IOI) and number of samples (N) with week-to-week intervals needed to estimate the underlying homeostatic set point (+/-15%) for BNP and NT-proBNP were calculated in pre-specified stable CHF patients. We measured plasma concentrations of BNP and NT-proBNP, clinical and laboratory variables in 20 CHF patients with a 7-days interval. Only patients considered to be in steady state were included. The CV(I) was 15% (BNP) and 8% (NT-proBNP). CV(T) was 16% (BNP) and 8% (NT-proBNP) and RCV was 43% (BNP) and 23% (NT-proBNP). IOI was 0.14 for BNP and 0.03 for NT-proBNP and N was 1 for BNP and 1 for NT-proBNP. Question: Is unexplained week-to-week variation in BNP and NT-proBNP low in chronic heart failure patients during steady state? Output:
PubmedQA95189
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Olesoxime is a small cholesterol-oxime promoting rat embryonic motor neurons survival in the absence of trophic factors. Because olesoxime can substitute for neurotrophic factors in many situations, and to gain further understanding of its mechanism of action, we wondered if it could prevent neuronal death induced by camptothecin (CPT) and compared its effects with those of brain-derived neurotrophic factor (BDNF). E17 rat embryonic cortical neurons were treated with olesoxime, BDNF or vehicle and intoxicated with CPT. Caspase-dependent and caspase-independent death pathways along with pro-survival pathways activation were explored. As previously reported for BDNF, olesoxime dose-dependently delayed CPT-induced cell death. Both compounds acted downstream of p53 activation preventing cytochrome c release and caspases activation. When caspase activation was blocked, both olesoxime and BDNF provided additional neuroprotective effect, potentially through the prevention of apoptosis-inducing factor release from mitochondria. While BDNF activates both the PI3K/Akt and the ERK pathway, olesoxime induced only a late activation of the ERK pathways, which did not seem to play a major role in its neuroprotection against CPT. Rather, our results favour preserved mitochondrial membrane integrity by olesoxime.\n Question: Does olesoxime protect embryonic cortical neurons from camptothecin intoxication by a mechanism distinct from BDNF?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Olesoxime is a small cholesterol-oxime promoting rat embryonic motor neurons survival in the absence of trophic factors. Because olesoxime can substitute for neurotrophic factors in many situations, and to gain further understanding of its mechanism of action, we wondered if it could prevent neuronal death induced by camptothecin (CPT) and compared its effects with those of brain-derived neurotrophic factor (BDNF). E17 rat embryonic cortical neurons were treated with olesoxime, BDNF or vehicle and intoxicated with CPT. Caspase-dependent and caspase-independent death pathways along with pro-survival pathways activation were explored. As previously reported for BDNF, olesoxime dose-dependently delayed CPT-induced cell death. Both compounds acted downstream of p53 activation preventing cytochrome c release and caspases activation. When caspase activation was blocked, both olesoxime and BDNF provided additional neuroprotective effect, potentially through the prevention of apoptosis-inducing factor release from mitochondria. While BDNF activates both the PI3K/Akt and the ERK pathway, olesoxime induced only a late activation of the ERK pathways, which did not seem to play a major role in its neuroprotection against CPT. Rather, our results favour preserved mitochondrial membrane integrity by olesoxime. Question: Does olesoxime protect embryonic cortical neurons from camptothecin intoxication by a mechanism distinct from BDNF? Output:
PubmedQA184252
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The purpose of this paper is to determine whether antimullerian hormone (AMH) levels were associated with BMI in patients with diagnosed infertility, and more specifically, in patients with polycystic ovarian syndrome (PCOS). A retrospective cohort study reviewed all females who presented to the clinical investigators' practice between November 2011 and March 2013. The following data was retrieved from the medical record: (1) AMH level, (2) age, (3) BMI, (4) ethnicity, and (5) if infertile, etiology of infertility. AMH levels were available for 489 women. Of these, 104 were diagnosed with PCOS. Overall, there was no association between BMI and AMH (r -0.04, p > 0.05). On the other hand, in the women with PCOS, there was a significant association between BMI and AMH (r -0.31, p < 0.01).\n Question: Are antimullerian hormone levels inversely associated with body mass index ( BMI ) in women with polycystic ovary syndrome?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The purpose of this paper is to determine whether antimullerian hormone (AMH) levels were associated with BMI in patients with diagnosed infertility, and more specifically, in patients with polycystic ovarian syndrome (PCOS). A retrospective cohort study reviewed all females who presented to the clinical investigators' practice between November 2011 and March 2013. The following data was retrieved from the medical record: (1) AMH level, (2) age, (3) BMI, (4) ethnicity, and (5) if infertile, etiology of infertility. AMH levels were available for 489 women. Of these, 104 were diagnosed with PCOS. Overall, there was no association between BMI and AMH (r -0.04, p > 0.05). On the other hand, in the women with PCOS, there was a significant association between BMI and AMH (r -0.31, p < 0.01). Question: Are antimullerian hormone levels inversely associated with body mass index ( BMI ) in women with polycystic ovary syndrome? Output:
PubmedQA29913
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The human gene FLRG, identified from a B-cell chronic lymphocytic leukemia bearing a t(11;19) translocation, encodes a secreted glycoprotein highly homologous with follistatin. Activin A is a TGF-beta family member involved in the regulation of growth and differentiation of various types of cells, such as those of the hematopoietic system. Its biological activity is antagonized by binding with follistatin. We investigated the binding of FLRG to activin A and the expression pattern of FLRG, follistatin, and activin A during hematopoiesis. The binding of FLRG with activin A was investigated by immunoprecipitation and Far-Western blot analysis. Gene expression was analyzed by reverse transcriptase polymerase chain reaction (RT-PCR) and Northern Blot in purified hematopoietic populations. We demonstrate that FLRG, like follistatin, is able to bind to activin A. In bone marrow stromal cells, both mRNA and protein FLRG levels were found to be dramatically increased by TGF-beta. FLRG and activin A are expressed in the same cells, with a higher level of expression in the myeloid cells compared with the erythroid and megakaryocytic cells. FLRG and follistatin expression were different in the hematopoietic subpopulations tested. Moreover, we observed that FLRG and activin A expression was up-regulated during hematopoiesis.\n Question: Is expression of FLRG , a novel activin A ligand , regulated by TGF-beta and during hematopoiesis [ corrected ]?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The human gene FLRG, identified from a B-cell chronic lymphocytic leukemia bearing a t(11;19) translocation, encodes a secreted glycoprotein highly homologous with follistatin. Activin A is a TGF-beta family member involved in the regulation of growth and differentiation of various types of cells, such as those of the hematopoietic system. Its biological activity is antagonized by binding with follistatin. We investigated the binding of FLRG to activin A and the expression pattern of FLRG, follistatin, and activin A during hematopoiesis. The binding of FLRG with activin A was investigated by immunoprecipitation and Far-Western blot analysis. Gene expression was analyzed by reverse transcriptase polymerase chain reaction (RT-PCR) and Northern Blot in purified hematopoietic populations. We demonstrate that FLRG, like follistatin, is able to bind to activin A. In bone marrow stromal cells, both mRNA and protein FLRG levels were found to be dramatically increased by TGF-beta. FLRG and activin A are expressed in the same cells, with a higher level of expression in the myeloid cells compared with the erythroid and megakaryocytic cells. FLRG and follistatin expression were different in the hematopoietic subpopulations tested. Moreover, we observed that FLRG and activin A expression was up-regulated during hematopoiesis. Question: Is expression of FLRG , a novel activin A ligand , regulated by TGF-beta and during hematopoiesis [ corrected ]? Output:
PubmedQA165652
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Some anaesthetics inhibit bacterial growth, and thus may lead to low rates of positive cultures from bacterial keratitis. Antibacterial properties of lidocaine were compared with those of oxybuprocaine or tetracaine, either in current commercial eye lotions or in extemporaneous solutions. Forty-eight bacterial strains were used to determine the minimum inhibitory and bactericidal concentrations of four commercial eye lotions containing oxybuprocaine or tetracaine, of a non-ophthalmic 1% lidocaine commercial solution and of extemporaneously prepared solutions of oxybuprocaine, tetracaine, lidocaine and benzalkonium. Most strains had their growth inhibited by 0.2% oxybuprocaine or 0.4% tetracaine, which corresponds to a 1/2 dilution of the commercial eye-drops. Bacterial growth was still observed with a 1% lidocaine solution.\n Question: Does non-preserved 1 % lidocaine solution have less antibacterial properties than currently available anaesthetic eye-drops?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Some anaesthetics inhibit bacterial growth, and thus may lead to low rates of positive cultures from bacterial keratitis. Antibacterial properties of lidocaine were compared with those of oxybuprocaine or tetracaine, either in current commercial eye lotions or in extemporaneous solutions. Forty-eight bacterial strains were used to determine the minimum inhibitory and bactericidal concentrations of four commercial eye lotions containing oxybuprocaine or tetracaine, of a non-ophthalmic 1% lidocaine commercial solution and of extemporaneously prepared solutions of oxybuprocaine, tetracaine, lidocaine and benzalkonium. Most strains had their growth inhibited by 0.2% oxybuprocaine or 0.4% tetracaine, which corresponds to a 1/2 dilution of the commercial eye-drops. Bacterial growth was still observed with a 1% lidocaine solution. Question: Does non-preserved 1 % lidocaine solution have less antibacterial properties than currently available anaesthetic eye-drops? Output:
PubmedQA143718
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Advances in bag connection technology have reduced the incidence of peritonitis in CAPD patients but there is little information on the effect of the new peritoneal dialysis fluids. We studied the incidence of CAPD peritonitis for about 3 years in 100 incident patients--50 patients dialysed with lactate-buffered solution, pH 5.5 and containing glucose degradation products (GDP) (lactate group), and 50 patients with pure bicarbonate-buffered solution, pH 7.4 and low GDP (bicarbonate group). Patients in both groups were similar in age, sex, length of time on CAPD, connection technology and handling of dialysis. In the lactate group, 74 episodes of peritonitis were recorded compared with 43 in the bicarbonate group, i.e. one episode per 21 patient-months with the lactate dialysis fluid and one episode per 36 patient-months with the bicarbonate dialysis fluid (OR 0.58, 95% CI 0.37-0.91, P = 0.017). A total of 3369 exchanges per episode of peritonitis were recorded for bicarbonate compared with 2004 exchanges per episode of peritonitis in the lactate group. The majority of organisms isolated in both groups were Gram-positive bacteria, with a predominance of the oropharyngeal and cutaneous endogenous flora. Three episodes of fungal peritonitis occurred in the lactate group and none in the bicarbonate group.\n Question: Does use of pure bicarbonate-buffered peritoneal dialysis fluid reduce the incidence of CAPD peritonitis?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Advances in bag connection technology have reduced the incidence of peritonitis in CAPD patients but there is little information on the effect of the new peritoneal dialysis fluids. We studied the incidence of CAPD peritonitis for about 3 years in 100 incident patients--50 patients dialysed with lactate-buffered solution, pH 5.5 and containing glucose degradation products (GDP) (lactate group), and 50 patients with pure bicarbonate-buffered solution, pH 7.4 and low GDP (bicarbonate group). Patients in both groups were similar in age, sex, length of time on CAPD, connection technology and handling of dialysis. In the lactate group, 74 episodes of peritonitis were recorded compared with 43 in the bicarbonate group, i.e. one episode per 21 patient-months with the lactate dialysis fluid and one episode per 36 patient-months with the bicarbonate dialysis fluid (OR 0.58, 95% CI 0.37-0.91, P = 0.017). A total of 3369 exchanges per episode of peritonitis were recorded for bicarbonate compared with 2004 exchanges per episode of peritonitis in the lactate group. The majority of organisms isolated in both groups were Gram-positive bacteria, with a predominance of the oropharyngeal and cutaneous endogenous flora. Three episodes of fungal peritonitis occurred in the lactate group and none in the bicarbonate group. Question: Does use of pure bicarbonate-buffered peritoneal dialysis fluid reduce the incidence of CAPD peritonitis? Output:
PubmedQA151990
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The aim of this study was to assess the incidence of organ failure in trauma patients treated in an intensive care unit (ICU), and to study the relationship between organ failure and long-term survival and functional status. This is a cohort study of all adult ICU trauma patients admitted to a university hospital during 1998 to 2003. Organ failure was quantified by the Sequential Organ Failure Assessment (SOFA) score. A telephone interview was conducted in 2005 (2 to 7 years after trauma) using the Karnofsky Index to measure functional status, and the Glasgow Outcome Score to measure recovery. Of the 322 patients included, 47% had multiple organ failure (MOF), and 28% had single organ failure. In a Cox regression, MOF increased the overall risk of death 6.0 times. At follow-up, 242 patients (75%) were still alive. Patients with MOF had 3.9 times greater odds for requiring personal assistance in activities of daily living compared to patients without organ failure. Long-term survival and functional status were the same for patients suffering single organ failure and no organ failure. Complete recovery occurred in 52% of survivors, and 87% were able to look after themselves.\n Question: Does multiple organ failure after trauma affect even long-term survival and functional status?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The aim of this study was to assess the incidence of organ failure in trauma patients treated in an intensive care unit (ICU), and to study the relationship between organ failure and long-term survival and functional status. This is a cohort study of all adult ICU trauma patients admitted to a university hospital during 1998 to 2003. Organ failure was quantified by the Sequential Organ Failure Assessment (SOFA) score. A telephone interview was conducted in 2005 (2 to 7 years after trauma) using the Karnofsky Index to measure functional status, and the Glasgow Outcome Score to measure recovery. Of the 322 patients included, 47% had multiple organ failure (MOF), and 28% had single organ failure. In a Cox regression, MOF increased the overall risk of death 6.0 times. At follow-up, 242 patients (75%) were still alive. Patients with MOF had 3.9 times greater odds for requiring personal assistance in activities of daily living compared to patients without organ failure. Long-term survival and functional status were the same for patients suffering single organ failure and no organ failure. Complete recovery occurred in 52% of survivors, and 87% were able to look after themselves. Question: Does multiple organ failure after trauma affect even long-term survival and functional status? Output:
PubmedQA165407
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To determine whether changes in standard and novel risk factors during the Actos Now for Prevention of Diabetes trial explained the slower rate of carotid intima media thickness (CIMT) progression with pioglitazone treatment in persons with prediabetes. CIMT was measured in 382 participants at the beginning and up to 3 additional times during follow-up of the Actos Now for Prevention of Diabetes trial. During an average follow-up of 2.3 years, the mean unadjusted annual rate of CIMT progression was significantly (P=0.01) lower with pioglitazone treatment (4.76×10(-3) mm/year; 95% CI: 2.39×10(-3)-7.14×10(-3) mm/year) compared with placebo (9.69×10(-3) mm/year; 95% CI: 7.24×10(-3)-12.15×10(-3) mm/year). High-density lipoprotein cholesterol, fasting and 2-hour glucose, HbA(1c), fasting insulin, Matsuda insulin sensitivity index, adiponectin, and plasminogen activator inhibitor-1 levels improved significantly with pioglitazone treatment compared with placebo (P<0.001). However, the effect of pioglitazone on CIMT progression was not attenuated by multiple methods of adjustment for traditional, metabolic, and inflammatory risk factors and concomitant medications, and was independent of changes in risk factors during pioglitazone treatment.\n Question: Does pioglitazone slow progression of atherosclerosis in prediabetes independent of changes in cardiovascular risk factors?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To determine whether changes in standard and novel risk factors during the Actos Now for Prevention of Diabetes trial explained the slower rate of carotid intima media thickness (CIMT) progression with pioglitazone treatment in persons with prediabetes. CIMT was measured in 382 participants at the beginning and up to 3 additional times during follow-up of the Actos Now for Prevention of Diabetes trial. During an average follow-up of 2.3 years, the mean unadjusted annual rate of CIMT progression was significantly (P=0.01) lower with pioglitazone treatment (4.76×10(-3) mm/year; 95% CI: 2.39×10(-3)-7.14×10(-3) mm/year) compared with placebo (9.69×10(-3) mm/year; 95% CI: 7.24×10(-3)-12.15×10(-3) mm/year). High-density lipoprotein cholesterol, fasting and 2-hour glucose, HbA(1c), fasting insulin, Matsuda insulin sensitivity index, adiponectin, and plasminogen activator inhibitor-1 levels improved significantly with pioglitazone treatment compared with placebo (P<0.001). However, the effect of pioglitazone on CIMT progression was not attenuated by multiple methods of adjustment for traditional, metabolic, and inflammatory risk factors and concomitant medications, and was independent of changes in risk factors during pioglitazone treatment. Question: Does pioglitazone slow progression of atherosclerosis in prediabetes independent of changes in cardiovascular risk factors? Output:
PubmedQA33548
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Using a massively bowel-resected rat model, our previous study demonstrated that small bowel segment reversal stimulates jejunal hyperplasia but may also increase the possibility of bacterial translocation and the elevation of circulating white blood cells and serum interleukin-6 that may reduce the whole-body anabolism. The aim of this study is to investigate whether oral antibiotics might attenuate the inflammatory responses and might therefore facilitate the beneficial effects of bowel segment reversal. Male Wistar rats (approximately 270 g) underwent a 70% small bowel resection with (REV group) or without (CON group) a 3-cm small bowel segment reversal, or underwent a sham operation (SHAM group). After surgeries, half of the animals in the REV group were given oral clindamycin plus amoxicillin (50 plus 50 mg/kg/d, ANT group) for 3 weeks. Oral antibiotics administration significantly attenuated the decreases in feeding efficiency (g of body weight/100 kcal diet) and increases in the circulation of white blood cells, serum nitric oxide, and interleukin-6 (1-way ANOVA, p < .05), which are associated with bowel segment reversal. In addition, antibiotics significantly increased serum concentrations of insulin-like growth factor-I, significantly decreased the total numbers of bacteria in the intestine, and tended to reduce the extent of jejunal hyperplasia in rats with bowel segment reversal.\n Question: Do oral antibiotics attenuate bowel segment reversal-induced systemic inflammatory response and body weight loss in massively bowel-resected rats?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Using a massively bowel-resected rat model, our previous study demonstrated that small bowel segment reversal stimulates jejunal hyperplasia but may also increase the possibility of bacterial translocation and the elevation of circulating white blood cells and serum interleukin-6 that may reduce the whole-body anabolism. The aim of this study is to investigate whether oral antibiotics might attenuate the inflammatory responses and might therefore facilitate the beneficial effects of bowel segment reversal. Male Wistar rats (approximately 270 g) underwent a 70% small bowel resection with (REV group) or without (CON group) a 3-cm small bowel segment reversal, or underwent a sham operation (SHAM group). After surgeries, half of the animals in the REV group were given oral clindamycin plus amoxicillin (50 plus 50 mg/kg/d, ANT group) for 3 weeks. Oral antibiotics administration significantly attenuated the decreases in feeding efficiency (g of body weight/100 kcal diet) and increases in the circulation of white blood cells, serum nitric oxide, and interleukin-6 (1-way ANOVA, p < .05), which are associated with bowel segment reversal. In addition, antibiotics significantly increased serum concentrations of insulin-like growth factor-I, significantly decreased the total numbers of bacteria in the intestine, and tended to reduce the extent of jejunal hyperplasia in rats with bowel segment reversal. Question: Do oral antibiotics attenuate bowel segment reversal-induced systemic inflammatory response and body weight loss in massively bowel-resected rats? Output:
PubmedQA2785
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Genistein, a soy component, has been shown to have a biphasic proliferative effect in breast cancer cells, inhibiting in vitro cell proliferation at high concentrations (>10 micromol/l), while stimulating cell proliferation at lower concentrations (<10 micromol/l). However, epidemiological studies have shown an inverse correlation between the intake of genistein and the incidence of breast cancer. One of the possible reasons for this discrepancy could be the differing status of the estrogen receptor (ERalpha and/or ERbeta). Genistein selectively binds to ERbeta with strong affinity and thereby could be a potential chemotherapeutic agent against breast cancer of the ERalpha-negative and ERbeta-positive type. Therefore, the objective of the present study was to determine whether the proliferative effects of genistein were caused by its activity as a selective ERbeta agonist or merely as an antiestrogen. This study was carried out in MDA-MB-231 (ERbeta) and T47D (ERalpha and ERbeta) human breast cancer cells. Cell proliferation was determined by the MTT (3-[4,5-dimethyl-2-thiazolyl]-2,5-diphenyl-2H-tetrazolium bromide) assay. The cells were grown in estrogen-starved media and exposed to genistein at different concentrations for 72 h, either in the presence or absence of 17beta-estradiol. A significant decrease in cell proliferation was seen in MDA-MB-231 cells at low concentrations of genistein in the presence of 17beta-estradiol, as compared to genistein alone. In T47D cells, which are known to have a predominance of ERalpha over ERbeta, genistein showed a biphasic cell proliferative response both in the presence and absence of 17beta-estradiol.\n Question: Does genistein in the presence of 17beta-estradiol inhibit proliferation of ERbeta breast cancer cells?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Genistein, a soy component, has been shown to have a biphasic proliferative effect in breast cancer cells, inhibiting in vitro cell proliferation at high concentrations (>10 micromol/l), while stimulating cell proliferation at lower concentrations (<10 micromol/l). However, epidemiological studies have shown an inverse correlation between the intake of genistein and the incidence of breast cancer. One of the possible reasons for this discrepancy could be the differing status of the estrogen receptor (ERalpha and/or ERbeta). Genistein selectively binds to ERbeta with strong affinity and thereby could be a potential chemotherapeutic agent against breast cancer of the ERalpha-negative and ERbeta-positive type. Therefore, the objective of the present study was to determine whether the proliferative effects of genistein were caused by its activity as a selective ERbeta agonist or merely as an antiestrogen. This study was carried out in MDA-MB-231 (ERbeta) and T47D (ERalpha and ERbeta) human breast cancer cells. Cell proliferation was determined by the MTT (3-[4,5-dimethyl-2-thiazolyl]-2,5-diphenyl-2H-tetrazolium bromide) assay. The cells were grown in estrogen-starved media and exposed to genistein at different concentrations for 72 h, either in the presence or absence of 17beta-estradiol. A significant decrease in cell proliferation was seen in MDA-MB-231 cells at low concentrations of genistein in the presence of 17beta-estradiol, as compared to genistein alone. In T47D cells, which are known to have a predominance of ERalpha over ERbeta, genistein showed a biphasic cell proliferative response both in the presence and absence of 17beta-estradiol. Question: Does genistein in the presence of 17beta-estradiol inhibit proliferation of ERbeta breast cancer cells? Output:
PubmedQA123636
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To investigate the impact of AAV-encoding NT4-TAT-His-PR39 fusion gene expression on HIF-1alpha level in ECV304 cultured under hypoxic condition (1%O(2)) and on angiogenesis in hypoxic chick embryo. PR39 cDNA was connected with NT4, TAT, 6 x His cDNA by molecular biology methods. The recombinant AAV vector was obtained by three plasmid co-transfection in 293 cells. Then ECV304 were respectively infected with AAV-NT4-TAT-His-PR39, 6 x His expression and HIF-1alpha level in ECV304 were detected by immunocytochemistry. The chicken embryos were randomized into the AAV-PR39, EV and PBS groups (n = 10 each) subject to hypoxia (5%O(2), n = 15) or normoxia environments (n = 15), the vessel density of the chicken chorioallantoic membrane (CAM) were measured by Image Pro Plus (IPP) software. The expression of 6 x His protein was detected in AAV-PR39 infected ECV304 cells. HIF-1alpha protein activity was significantly increased in AAV-PR39 infected ECV304 underwent hypoxia compared to PBS and non-infected ECV304 groups (P < 0.05). The vessel density of chicken CAM in hypoxia environment but not in normoxia environment was also significantly higher in AAV-PR39 group than in EV group and PBS group (all P < 0.05).\n Question: Does [ Secretory expression of PR39 following adeno-associated viral-encoding fusion gene transfer induce angiogenesis in hypoxia chick embryo ]?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To investigate the impact of AAV-encoding NT4-TAT-His-PR39 fusion gene expression on HIF-1alpha level in ECV304 cultured under hypoxic condition (1%O(2)) and on angiogenesis in hypoxic chick embryo. PR39 cDNA was connected with NT4, TAT, 6 x His cDNA by molecular biology methods. The recombinant AAV vector was obtained by three plasmid co-transfection in 293 cells. Then ECV304 were respectively infected with AAV-NT4-TAT-His-PR39, 6 x His expression and HIF-1alpha level in ECV304 were detected by immunocytochemistry. The chicken embryos were randomized into the AAV-PR39, EV and PBS groups (n = 10 each) subject to hypoxia (5%O(2), n = 15) or normoxia environments (n = 15), the vessel density of the chicken chorioallantoic membrane (CAM) were measured by Image Pro Plus (IPP) software. The expression of 6 x His protein was detected in AAV-PR39 infected ECV304 cells. HIF-1alpha protein activity was significantly increased in AAV-PR39 infected ECV304 underwent hypoxia compared to PBS and non-infected ECV304 groups (P < 0.05). The vessel density of chicken CAM in hypoxia environment but not in normoxia environment was also significantly higher in AAV-PR39 group than in EV group and PBS group (all P < 0.05). Question: Does [ Secretory expression of PR39 following adeno-associated viral-encoding fusion gene transfer induce angiogenesis in hypoxia chick embryo ]? Output:
PubmedQA138638
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The goal was to determine if there was a relation between the introduction of evidence-based radioactive iodine (RAI) treatment guidelines for differentiated thyroid cancer (DTC) at Cedars-Sinai Medical Center (CSMC) and subsequent RAI use. In addition, we compared RAI treatment rates for DTC at CSMC to data from the National Cancer Database (NCDB) to see if the trends in RAI use at CSMC differed from the national trends. RAI data from the CSMC Thyroid Cancer Center were reviewed to determine if RAI treatment was given appropriately. Kaplan-Meier curves were used to estimate disease-free survival for patients who received or did not receive treatment. RAI data from the NCDB were also used to compare how CSMC treatment rates compare nationally. There were 444 CSMC patients identified with DTC between 2009 and 2012. Approximately 95% of the patients had papillary thyroid cancer (n=423) with 65% in the stage I risk group (n=290). Kaplan-Meier curves for stages I-III show that those who did not receive RAI treatment had 100% disease-free survival, which was better than those who had received RAI. However, given that the total population in both stages II and III is quite small, having received RAI ablation was not found to be statistically significant. Stage I patients who received RAI had a significantly increased incidence of recurrent disease. The NCDB RAI rates for all DTC stages in each year have consistently been over 50% with an overall treatment rate of 57%. There were significant differences in the treatment rates between CSMC and NCDB, with a decrease in the use of RAI in low-risk patients with stage I tumors at CSMC following institution of the guidelines.\n Question: Does use of evidence-based guidelines reduce radioactive iodine treatment in patients with low-risk differentiated thyroid cancer?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The goal was to determine if there was a relation between the introduction of evidence-based radioactive iodine (RAI) treatment guidelines for differentiated thyroid cancer (DTC) at Cedars-Sinai Medical Center (CSMC) and subsequent RAI use. In addition, we compared RAI treatment rates for DTC at CSMC to data from the National Cancer Database (NCDB) to see if the trends in RAI use at CSMC differed from the national trends. RAI data from the CSMC Thyroid Cancer Center were reviewed to determine if RAI treatment was given appropriately. Kaplan-Meier curves were used to estimate disease-free survival for patients who received or did not receive treatment. RAI data from the NCDB were also used to compare how CSMC treatment rates compare nationally. There were 444 CSMC patients identified with DTC between 2009 and 2012. Approximately 95% of the patients had papillary thyroid cancer (n=423) with 65% in the stage I risk group (n=290). Kaplan-Meier curves for stages I-III show that those who did not receive RAI treatment had 100% disease-free survival, which was better than those who had received RAI. However, given that the total population in both stages II and III is quite small, having received RAI ablation was not found to be statistically significant. Stage I patients who received RAI had a significantly increased incidence of recurrent disease. The NCDB RAI rates for all DTC stages in each year have consistently been over 50% with an overall treatment rate of 57%. There were significant differences in the treatment rates between CSMC and NCDB, with a decrease in the use of RAI in low-risk patients with stage I tumors at CSMC following institution of the guidelines. Question: Does use of evidence-based guidelines reduce radioactive iodine treatment in patients with low-risk differentiated thyroid cancer? Output:
PubmedQA122566
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: We investigated whether the high-dose administration of tranilast could be used to create an animal model of interstitial cystitis (IC). Then, we used this model to assess the relationship between IC and changes in the vascular permeability of the bladder. Female rats were divided into the following 4 groups: a control group, a tranilast group, a carbazochrome group and a combination (tranilast+carbazochrome) group. Continuous cystometry, bladder distension, and the Evans blue dye extravasation test were performed 4weeks after drug administration. Locomotor activity, the plasma TGF-β1 level, and collagen fibers in the bladder wall were also examined in the control and tranilast groups. The interval between bladder contractions was shorter and the leakage of Evans blue dye into the bladder wall was greater in the tranilast group than in the control group. Glomerulations of the bladder wall after bladder distention and thinning of the collagen fiber layer in the bladder were observed in the tranilast group. Locomotor activity in darkness and the plasma TGF-β1 level were both lower in the tranilast group than in the control group. In the combination group, the leakage of Evans blue dye was greater than in the control group; however, it was less prominent than in the tranilast group.\n Question: Does high-dose tranilast administration to rats create interstitial cystitis-like symptoms with increased vascular permeability?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: We investigated whether the high-dose administration of tranilast could be used to create an animal model of interstitial cystitis (IC). Then, we used this model to assess the relationship between IC and changes in the vascular permeability of the bladder. Female rats were divided into the following 4 groups: a control group, a tranilast group, a carbazochrome group and a combination (tranilast+carbazochrome) group. Continuous cystometry, bladder distension, and the Evans blue dye extravasation test were performed 4weeks after drug administration. Locomotor activity, the plasma TGF-β1 level, and collagen fibers in the bladder wall were also examined in the control and tranilast groups. The interval between bladder contractions was shorter and the leakage of Evans blue dye into the bladder wall was greater in the tranilast group than in the control group. Glomerulations of the bladder wall after bladder distention and thinning of the collagen fiber layer in the bladder were observed in the tranilast group. Locomotor activity in darkness and the plasma TGF-β1 level were both lower in the tranilast group than in the control group. In the combination group, the leakage of Evans blue dye was greater than in the control group; however, it was less prominent than in the tranilast group. Question: Does high-dose tranilast administration to rats create interstitial cystitis-like symptoms with increased vascular permeability? Output:
PubmedQA46582
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Nitric oxide (NO) has been identified as a putative neurotransmitter in choroidal perivascular nerve fibers originating parasympathetically. Although constitutively produced NO has been implicated in the regulation of the choroidal circulation, the specific role of neurally derived NO in choroidal vasodilation has not been determined. This study examined the role of neurally derived NO in the control of the choroidal blood flow (ChBF) in vivo. Resting ChBF and a increase in ChBF elicited by electrical stimulation of the nucleus of Edinger-Westphal (EW) were measured transclerally by laser Doppler flowmetry in anesthetized pigeons before and after administration of a selective inhibitor of neural NO synthase, 7-Nitroindazole (7NI; 50 mg/kg given intraperitoneally); a nonselective NO synthase inhibitor, Ng-nitro-L-arginine methyl ester (L-NAME; 30 mg/kg given intravenously); L-arginine (300 mg/kg given intravenously) followed by 7NI (50 mg/kg given intraperitoneally); or vehicle. The 7NI and L-NAME, but not the vehicle, attenuated the EW-evoked response (maximally by 78% and 83%, respectively), and this effect lasted for at least 1 hour. Pretreatment with L-arginine abolished this effect of 7NI. Resting ChBF was reduced and systemic blood pressure was increased after L-NAME administration, but both were unchanged after 7NI or vehicle were administered.\n Question: Does neural nitric oxide mediate Edinger-Westphal nucleus evoked increase in choroidal blood flow in the pigeon?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Nitric oxide (NO) has been identified as a putative neurotransmitter in choroidal perivascular nerve fibers originating parasympathetically. Although constitutively produced NO has been implicated in the regulation of the choroidal circulation, the specific role of neurally derived NO in choroidal vasodilation has not been determined. This study examined the role of neurally derived NO in the control of the choroidal blood flow (ChBF) in vivo. Resting ChBF and a increase in ChBF elicited by electrical stimulation of the nucleus of Edinger-Westphal (EW) were measured transclerally by laser Doppler flowmetry in anesthetized pigeons before and after administration of a selective inhibitor of neural NO synthase, 7-Nitroindazole (7NI; 50 mg/kg given intraperitoneally); a nonselective NO synthase inhibitor, Ng-nitro-L-arginine methyl ester (L-NAME; 30 mg/kg given intravenously); L-arginine (300 mg/kg given intravenously) followed by 7NI (50 mg/kg given intraperitoneally); or vehicle. The 7NI and L-NAME, but not the vehicle, attenuated the EW-evoked response (maximally by 78% and 83%, respectively), and this effect lasted for at least 1 hour. Pretreatment with L-arginine abolished this effect of 7NI. Resting ChBF was reduced and systemic blood pressure was increased after L-NAME administration, but both were unchanged after 7NI or vehicle were administered. Question: Does neural nitric oxide mediate Edinger-Westphal nucleus evoked increase in choroidal blood flow in the pigeon? Output:
PubmedQA76895
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Anaphylaxis is a life-threatening outcome of immediate-type hypersensitivity to allergen, consecutive to mast cell degranulation by allergen-specific IgE. Regulatory T cells (Treg) can control allergic sensitization and mast cell degranulation, yet their clinical benefit on anaphylactic symptoms is poorly documented. Here we investigated whether Treg action during the effector arm of the allergic response alleviates anaphylaxis. We used a validated model of IgE-mediated passive systemic anaphylaxis, induced by intravenous challenge with DNP-HSA in mice passively sensitized with DNP-specific IgE. Anaphylaxis was monitored by the drop in body temperature as well as plasma histamine and serum mMCP1 levels. The role of Treg was analyzed using MHC class II-deficient (Aβ(°/°)) mice, treatment with anti-CD25 or anti-CD4 mAbs and conditional ablation of Foxp3(+) Treg in DEREG mice. Therapeutic efficacy of Treg was also evaluated by transfer experiments using FoxP3-eGFP knock-in mice. Anaphylaxis did not occur in mast cell-deficient W/W(v) mutant mice and was only moderate and transient in mice deficient for histamine receptor-1. Defects in constitutive Treg, either genetic or induced by antibody or toxin treatment resulted in a more severe and/or sustained hypothermia, associated with a rise in serum mMCP1, but not histamine. Adoptive transfer of Foxp3(+) Treg from either naïve or DNP-sensitized donors similarly alleviated body temperature loss in Treg-deficient DEREG mice.\n Question: Do regulatory CD4+Foxp3+ T cells control the severity of anaphylaxis?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Anaphylaxis is a life-threatening outcome of immediate-type hypersensitivity to allergen, consecutive to mast cell degranulation by allergen-specific IgE. Regulatory T cells (Treg) can control allergic sensitization and mast cell degranulation, yet their clinical benefit on anaphylactic symptoms is poorly documented. Here we investigated whether Treg action during the effector arm of the allergic response alleviates anaphylaxis. We used a validated model of IgE-mediated passive systemic anaphylaxis, induced by intravenous challenge with DNP-HSA in mice passively sensitized with DNP-specific IgE. Anaphylaxis was monitored by the drop in body temperature as well as plasma histamine and serum mMCP1 levels. The role of Treg was analyzed using MHC class II-deficient (Aβ(°/°)) mice, treatment with anti-CD25 or anti-CD4 mAbs and conditional ablation of Foxp3(+) Treg in DEREG mice. Therapeutic efficacy of Treg was also evaluated by transfer experiments using FoxP3-eGFP knock-in mice. Anaphylaxis did not occur in mast cell-deficient W/W(v) mutant mice and was only moderate and transient in mice deficient for histamine receptor-1. Defects in constitutive Treg, either genetic or induced by antibody or toxin treatment resulted in a more severe and/or sustained hypothermia, associated with a rise in serum mMCP1, but not histamine. Adoptive transfer of Foxp3(+) Treg from either naïve or DNP-sensitized donors similarly alleviated body temperature loss in Treg-deficient DEREG mice. Question: Do regulatory CD4+Foxp3+ T cells control the severity of anaphylaxis? Output:
PubmedQA61331
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To explore outflow from the eye and to determine and modulate the influence of lymphatic drainage on corneal graft survival in mice. Tracer experiments were conducted in BALB/c mice using the (99m)Tc colloidal albumin Nanocoll. Count rates were determined in the eyes, submandibular lymph nodes, spleen, liver and blood 24 h after subconjunctival, intracorneal, intracameral (anterior chamber), intravenous and subcutaneous lower-lid or upper-lid injections ( n=6 each). Four groups of BALB/c mice ( n=8) received corneal transplants from C3H mice; two of them were treated ballistically with vector CTLA4+IL-4 onto the leg or the lower lid, one group was untreated and the other control group was treated with an empty minimalistic, immunologically defined, gene expression (MIDGE) vector. Radioactivity was detected in the liver, spleen and ipsilateral submandibular lymph node after intracameral injection as follows: 91.9%, 6.6% and 1.2% respectively. Radioactivity uptake of the ipsilateral submandibular lymph node was also low after intravenous injection (0.1%) but high after intracorneal (33.8%), lower-lid (62.0%) and subconjunctival (71.2%) injection. Vector CTLA4+IL-4 treatment of the lower lid but not of the leg prolonged graft survival ( P=0.004).\n Question: Does ballistic CTLA4 and IL-4 gene transfer into the lower lid prolong orthotopic corneal graft survival in mice?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To explore outflow from the eye and to determine and modulate the influence of lymphatic drainage on corneal graft survival in mice. Tracer experiments were conducted in BALB/c mice using the (99m)Tc colloidal albumin Nanocoll. Count rates were determined in the eyes, submandibular lymph nodes, spleen, liver and blood 24 h after subconjunctival, intracorneal, intracameral (anterior chamber), intravenous and subcutaneous lower-lid or upper-lid injections ( n=6 each). Four groups of BALB/c mice ( n=8) received corneal transplants from C3H mice; two of them were treated ballistically with vector CTLA4+IL-4 onto the leg or the lower lid, one group was untreated and the other control group was treated with an empty minimalistic, immunologically defined, gene expression (MIDGE) vector. Radioactivity was detected in the liver, spleen and ipsilateral submandibular lymph node after intracameral injection as follows: 91.9%, 6.6% and 1.2% respectively. Radioactivity uptake of the ipsilateral submandibular lymph node was also low after intravenous injection (0.1%) but high after intracorneal (33.8%), lower-lid (62.0%) and subconjunctival (71.2%) injection. Vector CTLA4+IL-4 treatment of the lower lid but not of the leg prolonged graft survival ( P=0.004). Question: Does ballistic CTLA4 and IL-4 gene transfer into the lower lid prolong orthotopic corneal graft survival in mice? Output:
PubmedQA64830
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Genomic imprinting of the largest known cluster, the Kcnq1/KCNQ1 domain on mChr7/hChr11, displays significant differences between mouse and man. Of the fourteen transcripts in this cluster, imprinting of six is ubiquitous in mice and humans, however, imprinted expression of the other eight transcripts is only found in the mouse placenta. The human orthologues of the latter eight transcripts are biallelically expressed, at least from the first trimester onwards. However, as early development is less divergent between species, placental specific imprinting may be present in very early gestation in both mice and humans. Human embryonic stem (hES) cells can be differentiated to embryoid bodies and then to trophoblast stem (EB-TS) cells. Using EB-TS cells as a model of post-implantation invading cytotrophoblast, we analysed allelic expression of two telomeric transcripts whose imprinting is placental specific in the mouse, as well as the ncRNA KCNQ1OT1, whose imprinted expression is ubiquitous in early human and mouse development. KCNQ1OT1 expression was monoallelic in all samples but OSBPL5 and NAP1L4 expression was biallelic in EB-TS cells, as well as undifferentiated hES cells and first trimester human fetal placenta. DCN on hChr12, another gene imprinted in the mouse placenta only, was also biallelically expressed in EB-TS cells. The germline maternal methylation imprint at the KvDMR was maintained in both undifferentiated hES cells and EB-TS cells.\n Question: Are telomeric NAP1L4 and OSBPL5 of the KCNQ1 cluster , and the DECORIN gene imprinted in human trophoblast stem cells?\n Output: " }, { "role": "assistant", "content": "no" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Genomic imprinting of the largest known cluster, the Kcnq1/KCNQ1 domain on mChr7/hChr11, displays significant differences between mouse and man. Of the fourteen transcripts in this cluster, imprinting of six is ubiquitous in mice and humans, however, imprinted expression of the other eight transcripts is only found in the mouse placenta. The human orthologues of the latter eight transcripts are biallelically expressed, at least from the first trimester onwards. However, as early development is less divergent between species, placental specific imprinting may be present in very early gestation in both mice and humans. Human embryonic stem (hES) cells can be differentiated to embryoid bodies and then to trophoblast stem (EB-TS) cells. Using EB-TS cells as a model of post-implantation invading cytotrophoblast, we analysed allelic expression of two telomeric transcripts whose imprinting is placental specific in the mouse, as well as the ncRNA KCNQ1OT1, whose imprinted expression is ubiquitous in early human and mouse development. KCNQ1OT1 expression was monoallelic in all samples but OSBPL5 and NAP1L4 expression was biallelic in EB-TS cells, as well as undifferentiated hES cells and first trimester human fetal placenta. DCN on hChr12, another gene imprinted in the mouse placenta only, was also biallelically expressed in EB-TS cells. The germline maternal methylation imprint at the KvDMR was maintained in both undifferentiated hES cells and EB-TS cells. Question: Are telomeric NAP1L4 and OSBPL5 of the KCNQ1 cluster , and the DECORIN gene imprinted in human trophoblast stem cells? Output:
PubmedQA84872
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Fibromyalgia (FM) is characterized by widespread pain and high levels of sleep disturbance, fatigue, and altered cognition. Psychological stress can modulate these features. In this study, we examined the thinking style of rumination in women with FM to assess the effect of rumination on stress levels and other psychological variables in FM. Ninety-eight women with FM completed questionnaires to assess levels of rumination, stress, anxiety, depression, optimism, control, and coping. T-tests and bivariate (Pearson) analysis was performed to assess relationships between rumination and other psychological factors. We found that those with higher levels of rumination had increased the use of negative coping techniques (p<0.001), higher anxiety (p<0.001), depression (p<0.001), and poor sleep levels (p<0.05). Higher rumination correlated with lower optimism (p<0.001) and control (Mastery) (p<0.001). High rumination correlated strongest with stress (p<0.001). Rumination predicted 26% of variance for perceived stress.\n Question: Does rumination modulate stress and other psychological processes in fibromyalgia?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Fibromyalgia (FM) is characterized by widespread pain and high levels of sleep disturbance, fatigue, and altered cognition. Psychological stress can modulate these features. In this study, we examined the thinking style of rumination in women with FM to assess the effect of rumination on stress levels and other psychological variables in FM. Ninety-eight women with FM completed questionnaires to assess levels of rumination, stress, anxiety, depression, optimism, control, and coping. T-tests and bivariate (Pearson) analysis was performed to assess relationships between rumination and other psychological factors. We found that those with higher levels of rumination had increased the use of negative coping techniques (p<0.001), higher anxiety (p<0.001), depression (p<0.001), and poor sleep levels (p<0.05). Higher rumination correlated with lower optimism (p<0.001) and control (Mastery) (p<0.001). High rumination correlated strongest with stress (p<0.001). Rumination predicted 26% of variance for perceived stress. Question: Does rumination modulate stress and other psychological processes in fibromyalgia? Output:
PubmedQA181776
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To study the protective effect of recombinant adenovirus-mediated human cytosolic glutathione peroxidase (hCGPx) gene transfection on vascular endothelial cells ECV304 from oxidative damage. pGEM-T Easy Vector containing hCGPx cDNA and recombinant adenovirus shuttle plasmid pACCMV-pLpA were used to construct the shuttle plasmid pACCMV-hCGPx for cotransfection of 293 cells with pJM17, thereby to obtain the recombinant adenovirus AdCMV-hCGPx. Cultured ECV304 cells were transfected with AdCMV-hCGPx for 24, 48 and 72 h, respectively, with the cells transfected with the empty vector serving as control, and hCGPx gene expression was then examined in the transfected cells. The transfected cell viability and apoptotic cell ratio were evaluated after treatment of the cells with H(2)O(2). The expression ratio of hCGPx gene was significantly higher in the AdCMV-hCGPx-transfected cells than in those with empty vector transfection (P<0.01). The hCGPx gene-transfected cells showed significantly higher viability and significantly lower apoptotic ratio than the control cells following challenge with H(2)O(2)-induced oxidative damage.\n Question: Does [ Recombinant adenovirus-mediated human cytosolic glutathione peroxidase gene transfection protect vascular endothelial cells from oxidative damage ]?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To study the protective effect of recombinant adenovirus-mediated human cytosolic glutathione peroxidase (hCGPx) gene transfection on vascular endothelial cells ECV304 from oxidative damage. pGEM-T Easy Vector containing hCGPx cDNA and recombinant adenovirus shuttle plasmid pACCMV-pLpA were used to construct the shuttle plasmid pACCMV-hCGPx for cotransfection of 293 cells with pJM17, thereby to obtain the recombinant adenovirus AdCMV-hCGPx. Cultured ECV304 cells were transfected with AdCMV-hCGPx for 24, 48 and 72 h, respectively, with the cells transfected with the empty vector serving as control, and hCGPx gene expression was then examined in the transfected cells. The transfected cell viability and apoptotic cell ratio were evaluated after treatment of the cells with H(2)O(2). The expression ratio of hCGPx gene was significantly higher in the AdCMV-hCGPx-transfected cells than in those with empty vector transfection (P<0.01). The hCGPx gene-transfected cells showed significantly higher viability and significantly lower apoptotic ratio than the control cells following challenge with H(2)O(2)-induced oxidative damage. Question: Does [ Recombinant adenovirus-mediated human cytosolic glutathione peroxidase gene transfection protect vascular endothelial cells from oxidative damage ]? Output:
PubmedQA97156
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Assessment of glomerular filtration rate (GFR) by common creatininebasedmethods is potentially inaccurate in patients with cirrhosis. Cirrhoticpatients have several underlying conditions that contribute to falsely low serumcreatinine concentrations, even in the presence of moderate to severe renalimpairment. Therefore creatinine-based methods usually overestimate trueGFR in these patients. Cystatin-C is a low molecular weight protein and anendogenous marker of GFR. We compared the accuracy of plasma cystatin-Cand creatinine in assessing renal function in cirrhotic patients. We serially enrolled cirrhotic patients with stable renal function admitted inour ward if they met the inclusion criteria and consented to participate. Child-Pugh (CP) score was calculated for all patients. GFR was calculated usingserum creatinine, serum cystatin-C, and 99m TC-DTPA clearance with the lastone serving as the gold standard. The area under curve (AUC) on receiveroperatingcharacteristic curves (ROC) were used to assess the diagnostic accuracyof each calculated GFR with that measured by DTPA. Fourty-eight patients were enrolled (32 males, 66.7%). Nine were in class-A,20 in class-B and 19 in class-C of CP. Cystatin-C did not perform well in predictingthe true GFR, while serum creatinine performed relatively accurately atGFR<80ml/min (AUC=0.764, p=0.004). Serum creatinine at a cutoff of 1.4 mg/dl was 20% sensitive & 92% specific and with at a cutoff of 0.9 mg/dl was 77%sensitive & 72% specific for diagnosis of impaired renal function. Cystatin-Ccould not predict GFR effectively even after stratification for CP score, gender,and BMI. Serum creatinine could predict GFR<65ml/min in females (ROCcurve AUC=0.844, p=0.045). In those with BMI>20 kg/m2 a GFR<80 ml/mincould also be predicted by serum creatinine (ROC curve AUC=0.739, p=0.034).It also could predict GFR<80ml/min in patients with CP class A & B (ROC curveAUC=0.795, p=0.01), but not in patients with CP class C.\n Question: Is serum cystatin-C superior to serum creatinine in predicting glomerular filtration rate in cirrhotic patients?\n Output: " }, { "role": "assistant", "content": "no" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Assessment of glomerular filtration rate (GFR) by common creatininebasedmethods is potentially inaccurate in patients with cirrhosis. Cirrhoticpatients have several underlying conditions that contribute to falsely low serumcreatinine concentrations, even in the presence of moderate to severe renalimpairment. Therefore creatinine-based methods usually overestimate trueGFR in these patients. Cystatin-C is a low molecular weight protein and anendogenous marker of GFR. We compared the accuracy of plasma cystatin-Cand creatinine in assessing renal function in cirrhotic patients. We serially enrolled cirrhotic patients with stable renal function admitted inour ward if they met the inclusion criteria and consented to participate. Child-Pugh (CP) score was calculated for all patients. GFR was calculated usingserum creatinine, serum cystatin-C, and 99m TC-DTPA clearance with the lastone serving as the gold standard. The area under curve (AUC) on receiveroperatingcharacteristic curves (ROC) were used to assess the diagnostic accuracyof each calculated GFR with that measured by DTPA. Fourty-eight patients were enrolled (32 males, 66.7%). Nine were in class-A,20 in class-B and 19 in class-C of CP. Cystatin-C did not perform well in predictingthe true GFR, while serum creatinine performed relatively accurately atGFR<80ml/min (AUC=0.764, p=0.004). Serum creatinine at a cutoff of 1.4 mg/dl was 20% sensitive & 92% specific and with at a cutoff of 0.9 mg/dl was 77%sensitive & 72% specific for diagnosis of impaired renal function. Cystatin-Ccould not predict GFR effectively even after stratification for CP score, gender,and BMI. Serum creatinine could predict GFR<65ml/min in females (ROCcurve AUC=0.844, p=0.045). In those with BMI>20 kg/m2 a GFR<80 ml/mincould also be predicted by serum creatinine (ROC curve AUC=0.739, p=0.034).It also could predict GFR<80ml/min in patients with CP class A & B (ROC curveAUC=0.795, p=0.01), but not in patients with CP class C. Question: Is serum cystatin-C superior to serum creatinine in predicting glomerular filtration rate in cirrhotic patients? Output:
PubmedQA106505
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Obesity is associated with insulin resistance of glucose and lipid metabolism. We sought to determine the effects of obesity on the insulin sensitivity of protein metabolism. Whole-body [(13)C]leucine and [(3)H]glucose kinetics were measured in 9 lean and 10 obese women in the postabsorptive state and during a hyperinsulinemic, euglycemic, isoaminoacidemic clamp. In the postabsorptive state, the leucine endogenous rate of appearance (catabolism), normalized for fat-free mass, was 11% greater and the nonoxidative rate of disappearance (synthesis) was 8% greater in the obese than in the lean women, but net balance was 29% more negative (P < 0.05). Clamp amino acid and glucose infusion rates were significantly lower in the obese women than in the lean women (0.65 +/- 0.02 compared with 0.85 +/- 0.04 and 5.7 +/- 0.3 compared with 9.1 +/- 0.5 mg x kg fat-free mass(-1) x min(-1), respectively; P < 0.0001 for both), and their rates correlated positively (r = 0.635, P = 0.005). During hyperinsulinemia, synthesis was stimulated less and net leucine balance was much lower in the obese women than in the lean women (-0.08 +/- 0.06 and 0.30 +/- 0.03 mumol x kg fat-free mass(-1) x min(-1), respectively; P < 0.0001). The percentage change in net leucine balance correlated negatively with all adiposity indexes. Plasma free fatty acids were less suppressed and the respiratory quotient was lower in the obese women than in the lean women.\n Question: Is whole-body protein anabolic response resistant to the action of insulin in obese women?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Obesity is associated with insulin resistance of glucose and lipid metabolism. We sought to determine the effects of obesity on the insulin sensitivity of protein metabolism. Whole-body [(13)C]leucine and [(3)H]glucose kinetics were measured in 9 lean and 10 obese women in the postabsorptive state and during a hyperinsulinemic, euglycemic, isoaminoacidemic clamp. In the postabsorptive state, the leucine endogenous rate of appearance (catabolism), normalized for fat-free mass, was 11% greater and the nonoxidative rate of disappearance (synthesis) was 8% greater in the obese than in the lean women, but net balance was 29% more negative (P < 0.05). Clamp amino acid and glucose infusion rates were significantly lower in the obese women than in the lean women (0.65 +/- 0.02 compared with 0.85 +/- 0.04 and 5.7 +/- 0.3 compared with 9.1 +/- 0.5 mg x kg fat-free mass(-1) x min(-1), respectively; P < 0.0001 for both), and their rates correlated positively (r = 0.635, P = 0.005). During hyperinsulinemia, synthesis was stimulated less and net leucine balance was much lower in the obese women than in the lean women (-0.08 +/- 0.06 and 0.30 +/- 0.03 mumol x kg fat-free mass(-1) x min(-1), respectively; P < 0.0001). The percentage change in net leucine balance correlated negatively with all adiposity indexes. Plasma free fatty acids were less suppressed and the respiratory quotient was lower in the obese women than in the lean women. Question: Is whole-body protein anabolic response resistant to the action of insulin in obese women? Output:
PubmedQA195253
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Schizophrenia is associated with structural brain abnormalities that may be present before disease onset. It remains unclear whether these represent general vulnerability indicators or are associated with the clinical state itself. To investigate this, structural brain scans were acquired at two time points (mean scan interval 1.87 years) in a cohort of individuals at high familial risk of schizophrenia (n = 142) and control subjects (n = 36). Cortical reconstructions were generated using FreeSurfer. The high-risk cohort was subdivided into individuals that remained well during the study, individuals that had transient psychotic symptoms, and individuals that subsequently became ill. Baseline measures and longitudinal change in global estimates of thickness and surface area and lobar values were compared, focusing on overall differences between high-risk individuals and control subjects and then on group differences within the high-risk cohort. Longitudinally, control subjects showed a significantly greater reduction in cortical surface area compared with the high-risk group. Within the high-risk group, differences in surface area at baseline predicted clinical course, with individuals that subsequently became ill having significantly larger surface area than individuals that remained well during the study. For thickness, longitudinal reductions were most prominent in the frontal, cingulate, and occipital lobes in all high-risk individuals compared with control subjects.\n Question: Does cortical Surface Area differentiate Familial High Risk Individuals Who Go on to Develop Schizophrenia?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Schizophrenia is associated with structural brain abnormalities that may be present before disease onset. It remains unclear whether these represent general vulnerability indicators or are associated with the clinical state itself. To investigate this, structural brain scans were acquired at two time points (mean scan interval 1.87 years) in a cohort of individuals at high familial risk of schizophrenia (n = 142) and control subjects (n = 36). Cortical reconstructions were generated using FreeSurfer. The high-risk cohort was subdivided into individuals that remained well during the study, individuals that had transient psychotic symptoms, and individuals that subsequently became ill. Baseline measures and longitudinal change in global estimates of thickness and surface area and lobar values were compared, focusing on overall differences between high-risk individuals and control subjects and then on group differences within the high-risk cohort. Longitudinally, control subjects showed a significantly greater reduction in cortical surface area compared with the high-risk group. Within the high-risk group, differences in surface area at baseline predicted clinical course, with individuals that subsequently became ill having significantly larger surface area than individuals that remained well during the study. For thickness, longitudinal reductions were most prominent in the frontal, cingulate, and occipital lobes in all high-risk individuals compared with control subjects. Question: Does cortical Surface Area differentiate Familial High Risk Individuals Who Go on to Develop Schizophrenia? Output:
PubmedQA125406
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Morphological analyses in and around the epiphyseal cartilage of mice deficient in insulin receptor substrate-1 (IRS-1) showed IRS-1 signaling to be important for skeletal growth by preventing early closure of the epiphyseal cartilage and maintaining the subsequent bone turnover at the primary spongiosa. IRS-1 is an essential molecule for intracellular signaling by IGF-I and insulin, both of which are potent anabolic regulators of cartilage and bone metabolism. To clarify the role of IRS-1 signaling in the skeletal growth, morphological analyses were performed in and around the epiphyseal cartilage of mice deficient in IRS-1 (IRS-1(-/-)), whose limbs and trunk were 20-30% shorter than wildtype (WT) mice. The epiphyseal cartilage and the primary spongiosa at proximal tibias of homozygous IRS-1(-/-) and WT male littermates were compared using histological, immunohistochemical, enzyme cytohistochemical, ultrastructural, and bone histomorphometrical analyses. In and around the WT epiphyseal cartilage, IRS-1 and insulin-like growth factor (IGF)-1 receptors were widely expressed, whereas IRS-2 was weakly localized in bone cells. Chronological observation revealed that height of the proliferative zone and the size of hypertrophic chondrocytes were decreased in WT mice as a function of age, and these decreases were accelerated in the IRS-1 (-/-) cartilage, whose findings at 12 weeks were similar to those of WT at 24 weeks. In the IRS-1(-/-) cartilage, proliferating chondrocytes with positive proliferating cell nuclear antigen (PCNA) or parathyroid hormone (PTH)/PTH-related peptide (PTHrP) receptor immunostaining had almost disappeared by 12 weeks. Contrarily, TUNEL+ apoptotic cells were increased in the hypertrophic zone, at the bottom of which most of the chondrocytes were surrounded by the calcified matrix, suggesting the closure of the cartilage. In the primary spongiosa, bone volume, alkaline phosphatase (ALP)+ osteoblasts, TRACP+ osteoclasts, and the osteopontin-positive cement line were markedly decreased. Bone histomorphometrical parameters for both bone formation and resorption were significantly lower in IRS-1(-/-) mice, indicating the suppression of bone turnover.\n Question: Does deficiency of insulin receptor substrate-1 impair skeletal growth through early closure of epiphyseal cartilage?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Morphological analyses in and around the epiphyseal cartilage of mice deficient in insulin receptor substrate-1 (IRS-1) showed IRS-1 signaling to be important for skeletal growth by preventing early closure of the epiphyseal cartilage and maintaining the subsequent bone turnover at the primary spongiosa. IRS-1 is an essential molecule for intracellular signaling by IGF-I and insulin, both of which are potent anabolic regulators of cartilage and bone metabolism. To clarify the role of IRS-1 signaling in the skeletal growth, morphological analyses were performed in and around the epiphyseal cartilage of mice deficient in IRS-1 (IRS-1(-/-)), whose limbs and trunk were 20-30% shorter than wildtype (WT) mice. The epiphyseal cartilage and the primary spongiosa at proximal tibias of homozygous IRS-1(-/-) and WT male littermates were compared using histological, immunohistochemical, enzyme cytohistochemical, ultrastructural, and bone histomorphometrical analyses. In and around the WT epiphyseal cartilage, IRS-1 and insulin-like growth factor (IGF)-1 receptors were widely expressed, whereas IRS-2 was weakly localized in bone cells. Chronological observation revealed that height of the proliferative zone and the size of hypertrophic chondrocytes were decreased in WT mice as a function of age, and these decreases were accelerated in the IRS-1 (-/-) cartilage, whose findings at 12 weeks were similar to those of WT at 24 weeks. In the IRS-1(-/-) cartilage, proliferating chondrocytes with positive proliferating cell nuclear antigen (PCNA) or parathyroid hormone (PTH)/PTH-related peptide (PTHrP) receptor immunostaining had almost disappeared by 12 weeks. Contrarily, TUNEL+ apoptotic cells were increased in the hypertrophic zone, at the bottom of which most of the chondrocytes were surrounded by the calcified matrix, suggesting the closure of the cartilage. In the primary spongiosa, bone volume, alkaline phosphatase (ALP)+ osteoblasts, TRACP+ osteoclasts, and the osteopontin-positive cement line were markedly decreased. Bone histomorphometrical parameters for both bone formation and resorption were significantly lower in IRS-1(-/-) mice, indicating the suppression of bone turnover. Question: Does deficiency of insulin receptor substrate-1 impair skeletal growth through early closure of epiphyseal cartilage? Output:
PubmedQA88755
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The frequency and importance of microembolization in patients with acute coronary syndromes and during coronary interventions have recently been appreciated. Experimental microembolization induces immediate ischemic dysfunction, which recovers within minutes. Subsequently, progressive contractile dysfunction develops over several hours and is not associated with reduced regional myocardial blood flow (perfusion-contraction mismatch) but rather with a local inflammatory reaction. We have now studied the effect of antiinflammatory glucocorticoid treatment on this progressive contractile dysfunction. Microembolization was induced by injecting microspheres (42-microm diameter) into the left circumflex coronary artery. Anesthetized dogs were followed up for 8 hours and received placebo (n=7) or methylprednisolone 30 mg/kg IV either 30 minutes before (n=7) or 30 minutes after (n=5) microembolization. In addition, chronically instrumented dogs received either placebo (n=4) or methylprednisolone (n=4) 30 minutes after microembolization and were followed up for 1 week. In acute placebo dogs, posterior systolic wall thickening was decreased from 20.0+/-2.1% (mean+/-SEM) at baseline to 5.8+/-0.6% at 8 hours after microembolization. Methylprednisolone prevented the progressive myocardial dysfunction. Increased leukocyte infiltration in the embolized myocardium was prevented only when methylprednisolone was given before microembolization. In chronic placebo dogs, progressive dysfunction recovered from 5.0+/-0.7% at 4 to 6 hours after microembolization back to baseline (19.1+/-1.6%) within 5 days. Again, methylprednisolone prevented the progressive myocardial dysfunction.\n Question: Does glucocorticoid treatment prevent progressive myocardial dysfunction resulting from experimental coronary microembolization?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The frequency and importance of microembolization in patients with acute coronary syndromes and during coronary interventions have recently been appreciated. Experimental microembolization induces immediate ischemic dysfunction, which recovers within minutes. Subsequently, progressive contractile dysfunction develops over several hours and is not associated with reduced regional myocardial blood flow (perfusion-contraction mismatch) but rather with a local inflammatory reaction. We have now studied the effect of antiinflammatory glucocorticoid treatment on this progressive contractile dysfunction. Microembolization was induced by injecting microspheres (42-microm diameter) into the left circumflex coronary artery. Anesthetized dogs were followed up for 8 hours and received placebo (n=7) or methylprednisolone 30 mg/kg IV either 30 minutes before (n=7) or 30 minutes after (n=5) microembolization. In addition, chronically instrumented dogs received either placebo (n=4) or methylprednisolone (n=4) 30 minutes after microembolization and were followed up for 1 week. In acute placebo dogs, posterior systolic wall thickening was decreased from 20.0+/-2.1% (mean+/-SEM) at baseline to 5.8+/-0.6% at 8 hours after microembolization. Methylprednisolone prevented the progressive myocardial dysfunction. Increased leukocyte infiltration in the embolized myocardium was prevented only when methylprednisolone was given before microembolization. In chronic placebo dogs, progressive dysfunction recovered from 5.0+/-0.7% at 4 to 6 hours after microembolization back to baseline (19.1+/-1.6%) within 5 days. Again, methylprednisolone prevented the progressive myocardial dysfunction. Question: Does glucocorticoid treatment prevent progressive myocardial dysfunction resulting from experimental coronary microembolization? Output:
PubmedQA96398
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: In the present study, vastus lateralis de-oxygenation was monitored contemporarily with VO2 changes along a severe constant intensity running exercise, after the 3rd min up to volitional exhaustion. Blood lactate accumulation was also measured before, during and after running. Eleven male amateur soccer players volunteered for the study. Subjects mean age, height, and body weight were 22.9+/-2 yrs, 177.5+/-6.2 cm, 71.7+/-4 kg, respectively. Measurements were carried out during running on a treadmill. Ventilatory and gas exchange parameters were measured at the mouth on a breath-by-breath basis. For blood lactate concentration accumulation measurement, capillary blood samples were taken from the fingertip. The oxygenation of the vastus lateralis muscle were measured by a continuous wave NIRS portable instrument. By means of two pretests the onset of [La]b accumulation and its associated velocity (vOBLA), and the peak of oxygen uptake and its associated velocity (vVO2,peak) were assessed. The test consisted of running on the treadmill up to volitional exhaustion at a constant velocity corresponding to vOBLA plus 50% of the difference between vVO2,peak and vOBLA (v50%Delta). The principal finding of this study was that vastus lateralis de-oxygenation changes measured during running correlate with a) oxygen uptake changes between the 3rd min of exercise and the time corresponding to the subject's volitional exhaustion; b) blood lactate concentration increments measured at the 3rd and the 6th min of exercise and at the time corresponding to the subject's volitional exhaustion.\n Question: Does vO2 slow component correlate with vastus lateralis de-oxygenation and blood lactate accumulation during running?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: In the present study, vastus lateralis de-oxygenation was monitored contemporarily with VO2 changes along a severe constant intensity running exercise, after the 3rd min up to volitional exhaustion. Blood lactate accumulation was also measured before, during and after running. Eleven male amateur soccer players volunteered for the study. Subjects mean age, height, and body weight were 22.9+/-2 yrs, 177.5+/-6.2 cm, 71.7+/-4 kg, respectively. Measurements were carried out during running on a treadmill. Ventilatory and gas exchange parameters were measured at the mouth on a breath-by-breath basis. For blood lactate concentration accumulation measurement, capillary blood samples were taken from the fingertip. The oxygenation of the vastus lateralis muscle were measured by a continuous wave NIRS portable instrument. By means of two pretests the onset of [La]b accumulation and its associated velocity (vOBLA), and the peak of oxygen uptake and its associated velocity (vVO2,peak) were assessed. The test consisted of running on the treadmill up to volitional exhaustion at a constant velocity corresponding to vOBLA plus 50% of the difference between vVO2,peak and vOBLA (v50%Delta). The principal finding of this study was that vastus lateralis de-oxygenation changes measured during running correlate with a) oxygen uptake changes between the 3rd min of exercise and the time corresponding to the subject's volitional exhaustion; b) blood lactate concentration increments measured at the 3rd and the 6th min of exercise and at the time corresponding to the subject's volitional exhaustion. Question: Does vO2 slow component correlate with vastus lateralis de-oxygenation and blood lactate accumulation during running? Output:
PubmedQA203144
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Long-acting bronchodilators are first-line treatment for chronic obstructive pulmonary disease (COPD), and their efficacy on lung function and clinical parameters is recognized. To explore the available evidence about the effects of long acting bronchodilators on Health Related Quality of Life (HRQoL) and Health Status (HS) in clinical research. Randomized controlled trials published till December 2012 evaluating HRQoL/HS in COPD by means of validated questionnaires were analysed. Fifty-one trials on Long acting β2 agonist (LABA) and Long acting Anticholinergic (LAMA) met the inclusion criteria. A total of 37,225 moderate-severe COPD patients testing 6 drugs, 12 different devices and 22 different dosages, with a study duration ranging from 4 weeks to 4 years were studied. A statistical significant HRQoL/HS improvement was reached in 93% of the studies. Nevertheless, the Minimal Important Difference (MID) was reached in 70.6% of the studies considering the difference between baseline and end of the study, and in 50% when comparing active treatment and placebo.\n Question: Do long-acting bronchodilators improve health related quality of life in patients with COPD?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Long-acting bronchodilators are first-line treatment for chronic obstructive pulmonary disease (COPD), and their efficacy on lung function and clinical parameters is recognized. To explore the available evidence about the effects of long acting bronchodilators on Health Related Quality of Life (HRQoL) and Health Status (HS) in clinical research. Randomized controlled trials published till December 2012 evaluating HRQoL/HS in COPD by means of validated questionnaires were analysed. Fifty-one trials on Long acting β2 agonist (LABA) and Long acting Anticholinergic (LAMA) met the inclusion criteria. A total of 37,225 moderate-severe COPD patients testing 6 drugs, 12 different devices and 22 different dosages, with a study duration ranging from 4 weeks to 4 years were studied. A statistical significant HRQoL/HS improvement was reached in 93% of the studies. Nevertheless, the Minimal Important Difference (MID) was reached in 70.6% of the studies considering the difference between baseline and end of the study, and in 50% when comparing active treatment and placebo. Question: Do long-acting bronchodilators improve health related quality of life in patients with COPD? Output:
PubmedQA179635
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Overexpression of the transcriptional regulatory factor activator protein 1 might contribute to T-cell glucocorticoid (GC) refractoriness in GC-resistant asthma. We sought to address the hypothesis that clinically GC-resistant asthma is accompanied by failure of systemic GCs to inhibit phosphorylation of c-jun and c-jun N-terminal kinase (JNK) in bronchial mucosal cells. We performed enumeration of total (CD45+) leukocytes and cells expressing c-fos and total and phosphorylated c-jun and JNK in bronchial biopsy sections from 9 GC-sensitive and 17 GC-resistant asthmatic patients taken before and after oral prednisolone (40 mg/1.72 m(2) body surface area daily for 14 days) using specific antibodies, immunohistochemistry, and image analysis. At baseline, mean total (CD45+) mucosal leukocytes, total cells expressing phosphorylated c-jun and JNK, and mean percentages of cells in which these molecules were phosphorylated were similar in both groups, whereas mean total numbers of c-fos-immunoreactive cells were increased in the GC-resistant asthmatic subjects (P = .04). After prednisolone, the mean total cells expressing phosphorylated c-jun and JNK and the mean percentages of cells in which these molecules were phosphorylated were significantly reduced in the GC-sensitive (P < or = .02) but not the GC-resistant asthmatic subjects. Mean total CD45+ leukocytes and c-fos-immunoreactive cells were not significantly altered in either group.\n Question: Does systemic glucocorticoid reduce bronchial mucosal activation of activator protein 1 components in glucocorticoid-sensitive but not glucocorticoid-resistant asthmatic patients?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Overexpression of the transcriptional regulatory factor activator protein 1 might contribute to T-cell glucocorticoid (GC) refractoriness in GC-resistant asthma. We sought to address the hypothesis that clinically GC-resistant asthma is accompanied by failure of systemic GCs to inhibit phosphorylation of c-jun and c-jun N-terminal kinase (JNK) in bronchial mucosal cells. We performed enumeration of total (CD45+) leukocytes and cells expressing c-fos and total and phosphorylated c-jun and JNK in bronchial biopsy sections from 9 GC-sensitive and 17 GC-resistant asthmatic patients taken before and after oral prednisolone (40 mg/1.72 m(2) body surface area daily for 14 days) using specific antibodies, immunohistochemistry, and image analysis. At baseline, mean total (CD45+) mucosal leukocytes, total cells expressing phosphorylated c-jun and JNK, and mean percentages of cells in which these molecules were phosphorylated were similar in both groups, whereas mean total numbers of c-fos-immunoreactive cells were increased in the GC-resistant asthmatic subjects (P = .04). After prednisolone, the mean total cells expressing phosphorylated c-jun and JNK and the mean percentages of cells in which these molecules were phosphorylated were significantly reduced in the GC-sensitive (P < or = .02) but not the GC-resistant asthmatic subjects. Mean total CD45+ leukocytes and c-fos-immunoreactive cells were not significantly altered in either group. Question: Does systemic glucocorticoid reduce bronchial mucosal activation of activator protein 1 components in glucocorticoid-sensitive but not glucocorticoid-resistant asthmatic patients? Output:
PubmedQA141383
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Proton pump inhibitors taken twice daily before meals (proton pump inhibitor b.d. AC) effectively controls daytime gastric pH; however, nocturnal gastric acid breakthrough (NAB) occurs in more than 75% of patients. Adding an H2-blocker at bedtime decreases NAB in normal subjects. The efficacy of this regimen has not been evaluated in GERD patients. The aim of this study was to assess the effects of proton pump inhibitor b.d., both with and without bedtime H2-blocker on intragastric pH and the occurrence of NAB in GERD patients. Prolonged ambulatory pH studies in GERD patients were reviewed. Group A: 60 patients (mean age 53 years, male 30) taking either omeprazole 20 mg or lansoprazole 30 mg b.d. Group B: 45 patients (mean age 49 years, male 23) on proton pump inhibitor b.d. (omeprazole 20 mg or lansoprazole 30 mg) plus an H2-blocker at bedtime (ranitidine 300 mg, famotidine 40 mg or nizatidine 300 mg). Eleven patients were evaluated during treatment with both regimens (group C). The percentage time of nocturnal and daytime intragastric pH > 4 and per cent of patients with gastric NAB were analysed. In the patients with NAB, its duration and associated oesophageal acid exposure also were analysed. Median percentage time intragastric pH > 4 overnight was 51% in group A, compared to 96% in group B (P < 0.0001). Median percentage daytime pH > 4 was 73% in group A and 79.8% in group B (P=0.14). Median percentage time intragastric pH >p 4 overnight increased from 54.6% without H2RA to 96.5% after adding bedtime H2RA (P=0.0013) in group C patients. NAB occurred in 82% patients in group A and 40% in group B (P < 0.0001). The mean duration of oesophageal acid exposure during NAB was significantly shorter in group B (18 +/- 6 min) than in group A (42 +/- 9 min, P=0.04).\n Question: Do bedtime H2 blockers improve nocturnal gastric acid control in GERD patients on proton pump inhibitors?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Proton pump inhibitors taken twice daily before meals (proton pump inhibitor b.d. AC) effectively controls daytime gastric pH; however, nocturnal gastric acid breakthrough (NAB) occurs in more than 75% of patients. Adding an H2-blocker at bedtime decreases NAB in normal subjects. The efficacy of this regimen has not been evaluated in GERD patients. The aim of this study was to assess the effects of proton pump inhibitor b.d., both with and without bedtime H2-blocker on intragastric pH and the occurrence of NAB in GERD patients. Prolonged ambulatory pH studies in GERD patients were reviewed. Group A: 60 patients (mean age 53 years, male 30) taking either omeprazole 20 mg or lansoprazole 30 mg b.d. Group B: 45 patients (mean age 49 years, male 23) on proton pump inhibitor b.d. (omeprazole 20 mg or lansoprazole 30 mg) plus an H2-blocker at bedtime (ranitidine 300 mg, famotidine 40 mg or nizatidine 300 mg). Eleven patients were evaluated during treatment with both regimens (group C). The percentage time of nocturnal and daytime intragastric pH > 4 and per cent of patients with gastric NAB were analysed. In the patients with NAB, its duration and associated oesophageal acid exposure also were analysed. Median percentage time intragastric pH > 4 overnight was 51% in group A, compared to 96% in group B (P < 0.0001). Median percentage daytime pH > 4 was 73% in group A and 79.8% in group B (P=0.14). Median percentage time intragastric pH >p 4 overnight increased from 54.6% without H2RA to 96.5% after adding bedtime H2RA (P=0.0013) in group C patients. NAB occurred in 82% patients in group A and 40% in group B (P < 0.0001). The mean duration of oesophageal acid exposure during NAB was significantly shorter in group B (18 +/- 6 min) than in group A (42 +/- 9 min, P=0.04). Question: Do bedtime H2 blockers improve nocturnal gastric acid control in GERD patients on proton pump inhibitors? Output:
PubmedQA157079
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The HIV virus is known for its ability to exploit numerous genetic and evolutionary mechanisms to ensure its proliferation, among them, high replication, mutation and recombination rates. Sliding MinPD, a recently introduced computational method 1, was used to investigate the patterns of evolution of serially-sampled HIV-1 sequence data from eight patients with a special focus on the emergence of X4 strains. Unlike other phylogenetic methods, Sliding MinPD combines distance-based inference with a nonparametric bootstrap procedure and automated recombination detection to reconstruct the evolutionary history of longitudinal sequence data. We present serial evolutionary networks as a longitudinal representation of the mutational pathways of a viral population in a within-host environment. The longitudinal representation of the evolutionary networks was complemented with charts of clinical markers to facilitate correlation analysis between pertinent clinical information and the evolutionary relationships. Analysis based on the predicted networks suggests the following:: significantly stronger recombination signals (p = 0.003) for the inferred ancestors of the X4 strains, recombination events between different lineages and recombination events between putative reservoir virus and those from a later population, an early star-like topology observed for four of the patients who died of AIDS. A significantly higher number of recombinants were predicted at sampling points that corresponded to peaks in the viral load levels (p = 0.0042).\n Question: Do serial evolutionary networks of within-patient HIV-1 sequences reveal patterns of evolution of X4 strains?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The HIV virus is known for its ability to exploit numerous genetic and evolutionary mechanisms to ensure its proliferation, among them, high replication, mutation and recombination rates. Sliding MinPD, a recently introduced computational method 1, was used to investigate the patterns of evolution of serially-sampled HIV-1 sequence data from eight patients with a special focus on the emergence of X4 strains. Unlike other phylogenetic methods, Sliding MinPD combines distance-based inference with a nonparametric bootstrap procedure and automated recombination detection to reconstruct the evolutionary history of longitudinal sequence data. We present serial evolutionary networks as a longitudinal representation of the mutational pathways of a viral population in a within-host environment. The longitudinal representation of the evolutionary networks was complemented with charts of clinical markers to facilitate correlation analysis between pertinent clinical information and the evolutionary relationships. Analysis based on the predicted networks suggests the following:: significantly stronger recombination signals (p = 0.003) for the inferred ancestors of the X4 strains, recombination events between different lineages and recombination events between putative reservoir virus and those from a later population, an early star-like topology observed for four of the patients who died of AIDS. A significantly higher number of recombinants were predicted at sampling points that corresponded to peaks in the viral load levels (p = 0.0042). Question: Do serial evolutionary networks of within-patient HIV-1 sequences reveal patterns of evolution of X4 strains? Output:
PubmedQA136843
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The full mechanism of action of isotretinoin [13-cis retinoic acid (13-cis RA)] in treating acne is unknown. 13-cis RA induces key genes in sebocytes that are involved in apoptosis, including Tumor necrosis factor Related Apoptosis Inducing Ligand (TRAIL). In this study, we investigated the role of 13-cis RA-induced TRAIL within SEB-1 sebocytes. Using 13-cis RA and recombinant human TRAIL (rhTRAIL) protein, we assessed induction of TRAIL and apoptosis in SEB-1 sebocytes, normal keratinocytes and patient skin biopsies. Treatment with rhTRAIL protein increased TUNEL-positive staining in SEB-1 sebocytes. TRAIL siRNA significantly decreased the percentage of TUNEL-positive SEB-1 sebocytes in response to 13-cis RA treatment. Furthermore, TRAIL expression increased in the skin of patients with acne after 1 week of isotretinoin therapy compared with baseline. TRAIL expression localized within sebaceous glands. Unlike sebocytes, TRAIL protein expression was not increased in normal human epidermal keratinocytes in response to 13-cis RA, nor did rhTRAIL induce apoptosis in keratinocytes, suggesting that TRAIL is key in the sebocyte-specific apoptotic effects of 13-cis RA.\n Question: Does tRAIL contribute to the apoptotic effect of 13-cis retinoic acid in human sebaceous gland cells?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The full mechanism of action of isotretinoin [13-cis retinoic acid (13-cis RA)] in treating acne is unknown. 13-cis RA induces key genes in sebocytes that are involved in apoptosis, including Tumor necrosis factor Related Apoptosis Inducing Ligand (TRAIL). In this study, we investigated the role of 13-cis RA-induced TRAIL within SEB-1 sebocytes. Using 13-cis RA and recombinant human TRAIL (rhTRAIL) protein, we assessed induction of TRAIL and apoptosis in SEB-1 sebocytes, normal keratinocytes and patient skin biopsies. Treatment with rhTRAIL protein increased TUNEL-positive staining in SEB-1 sebocytes. TRAIL siRNA significantly decreased the percentage of TUNEL-positive SEB-1 sebocytes in response to 13-cis RA treatment. Furthermore, TRAIL expression increased in the skin of patients with acne after 1 week of isotretinoin therapy compared with baseline. TRAIL expression localized within sebaceous glands. Unlike sebocytes, TRAIL protein expression was not increased in normal human epidermal keratinocytes in response to 13-cis RA, nor did rhTRAIL induce apoptosis in keratinocytes, suggesting that TRAIL is key in the sebocyte-specific apoptotic effects of 13-cis RA. Question: Does tRAIL contribute to the apoptotic effect of 13-cis retinoic acid in human sebaceous gland cells? Output:
PubmedQA119189
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Nuts are rich in unsaturated fatty acids as well as other bioactive constituents. The present study investigated the association between nut consumption and the incidence of type 2 diabetes mellitus (T2DM) in a Middle Eastern population. The study was conducted within the framework of the Tehran Lipid and Glucose Study (TLGS), in which 1984 participants (920 men and 1064 women) free of DM, aged≥20 years, were followed from phase III (2005-2008) to phase V (2011-2014). Dietary data were obtained from valid and reliable food-frequency questionnaires at baseline. Using multiple logistic regression, odds ratios (ORs) and 95% confidence intervals (CIs) were calculated, with adjustments for age, gender, BMI, serum cholesterol and triglycerides, smoking and energy intake. Study participants' means±SD of age and of BMI were 40.1±13.1 years and 27.0±4.8kg/m\n Question: Is nut consumption associated with lower incidence of type 2 diabetes : The Tehran Lipid and Glucose Study?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Nuts are rich in unsaturated fatty acids as well as other bioactive constituents. The present study investigated the association between nut consumption and the incidence of type 2 diabetes mellitus (T2DM) in a Middle Eastern population. The study was conducted within the framework of the Tehran Lipid and Glucose Study (TLGS), in which 1984 participants (920 men and 1064 women) free of DM, aged≥20 years, were followed from phase III (2005-2008) to phase V (2011-2014). Dietary data were obtained from valid and reliable food-frequency questionnaires at baseline. Using multiple logistic regression, odds ratios (ORs) and 95% confidence intervals (CIs) were calculated, with adjustments for age, gender, BMI, serum cholesterol and triglycerides, smoking and energy intake. Study participants' means±SD of age and of BMI were 40.1±13.1 years and 27.0±4.8kg/m Question: Is nut consumption associated with lower incidence of type 2 diabetes : The Tehran Lipid and Glucose Study? Output:
PubmedQA20214
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The aim of this study was to examine the association of risk factors including diabetes mellitus (DM) with the age of onset in Japanese pancreatic cancer (PC) patients. We retrospectively reviewed 688 PC patients diagnosed at our institute. We analyzed the association between the age of onset of PC and the following variables: sex, smoking, alcohol, DM, and a family history of cancer especially PC. The mean age of PC diagnosis was 67.6 years. The onset of PC occurred earlier in current smokers (63.6 years old, P < 0.001) compared with past smokers (69.5 years old) and never smokers (68.6 years old). Patients with long-standing DM (>2 years) were older (70.5 years, P < 0.001) when diagnosed with PC than patients with new-onset DM (within 2 years) (66.9 years old) and patients without DM (66.7 years old). In the multivariate analysis, current smokers and a family history of cancer other than PC were associated with earlier onset. Conversely, long-standing DM was associated with later onset.\n Question: Are smoking , family history of cancer , and diabetes mellitus associated with the age of onset of pancreatic cancer in Japanese patients?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The aim of this study was to examine the association of risk factors including diabetes mellitus (DM) with the age of onset in Japanese pancreatic cancer (PC) patients. We retrospectively reviewed 688 PC patients diagnosed at our institute. We analyzed the association between the age of onset of PC and the following variables: sex, smoking, alcohol, DM, and a family history of cancer especially PC. The mean age of PC diagnosis was 67.6 years. The onset of PC occurred earlier in current smokers (63.6 years old, P < 0.001) compared with past smokers (69.5 years old) and never smokers (68.6 years old). Patients with long-standing DM (>2 years) were older (70.5 years, P < 0.001) when diagnosed with PC than patients with new-onset DM (within 2 years) (66.9 years old) and patients without DM (66.7 years old). In the multivariate analysis, current smokers and a family history of cancer other than PC were associated with earlier onset. Conversely, long-standing DM was associated with later onset. Question: Are smoking , family history of cancer , and diabetes mellitus associated with the age of onset of pancreatic cancer in Japanese patients? Output:
PubmedQA34222
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Children with pyelonephritis are at risk for renal damage. We assess the value of clinical signs and urological abnormalities in predicting renal scars in children following pyelonephritis. A total of 64 hospitalized children (29 females and 35 males, median age 2.9 years) underwent ultrasonography and technetium labeled dimercapto-succinic acid (DMSA) scintigraphy imaging within 1 week following the diagnosis of the first pyelonephritis. Voiding cystourethrography was performed 8 weeks after the diagnosis. Followup DMSA scintigraphy was performed in 58 patients after 2 years of followup. Urological abnormalities observed were vesicoureteral reflux (VUR, grade 2 or higher) in 11 patients (19%), nonrefluxing and nonobstructed megaureter in 2 (4%) and pyeloureteral obstruction in 1 (2%). The first DMSA scintigraphy showed parenchymal defects in 48% of patients. VUR did not increase the risk of renal defects. At 2 years after the infection 12 of the 58 patients (21%) had renal scars. Nine of these patients did not have VUR. However, 2 patients with high grade VUR and repeat infections demonstrated deterioration of kidney function during followup. The patients with renal scars were older than those without scars (3.1 vs 0.8 years, p = 0.0291) at the time of infection.\n Question: Are post-pyelonephritic renal scars associated with vesicoureteral reflux in children?\n Output: " }, { "role": "assistant", "content": "no" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Children with pyelonephritis are at risk for renal damage. We assess the value of clinical signs and urological abnormalities in predicting renal scars in children following pyelonephritis. A total of 64 hospitalized children (29 females and 35 males, median age 2.9 years) underwent ultrasonography and technetium labeled dimercapto-succinic acid (DMSA) scintigraphy imaging within 1 week following the diagnosis of the first pyelonephritis. Voiding cystourethrography was performed 8 weeks after the diagnosis. Followup DMSA scintigraphy was performed in 58 patients after 2 years of followup. Urological abnormalities observed were vesicoureteral reflux (VUR, grade 2 or higher) in 11 patients (19%), nonrefluxing and nonobstructed megaureter in 2 (4%) and pyeloureteral obstruction in 1 (2%). The first DMSA scintigraphy showed parenchymal defects in 48% of patients. VUR did not increase the risk of renal defects. At 2 years after the infection 12 of the 58 patients (21%) had renal scars. Nine of these patients did not have VUR. However, 2 patients with high grade VUR and repeat infections demonstrated deterioration of kidney function during followup. The patients with renal scars were older than those without scars (3.1 vs 0.8 years, p = 0.0291) at the time of infection. Question: Are post-pyelonephritic renal scars associated with vesicoureteral reflux in children? Output:
PubmedQA152098
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: Up-regulation of gamma-aminobutyric acidA (GABAA) receptors and decreased GABA uptake in the cerebral cortex of schizophrenics suggest altered GABAergic transmission, which could be caused by primary disturbance of GABA synapses or by decreased production of the transmitter. Decreased production could be due to a shutdown in GABA production or to loss of GABA neurons caused by cell death or their failure to migrate to the cortex during brain development. To discriminate between these possibilities, we quantified levels of messenger RNA (mRNA) for the 67-kd isoform of glutamic acid decarboxylase (GAD), the key enzyme in GABA synthesis, and the number and laminar distribution of GAD mRNA--expressing neurons in the dorsolateral prefrontal cortex (DLPFC) of schizophrenics and matched controls, using in situ hybridization-histochemistry, densitometry, and cell-counting methods. These data were compared with the total number of neurons, the number of small, round or ovoid neurons 8 to 15 microns in diameter, and overall frontal lobe volume. As a control, mRNA levels for type II calcium-calmodulin-dependent protein kinase (CamIIK) were quantified. Schizophrenics showed a pronounced decrease in GAD mRNA levels in neurons of layer I (40%) and layer II (48%) and an overall 30% decrease in layers III to VI. There were also strong overall reductions in GAD mRNA levels. The CamIIK mRNA levels showed no significant differences between samples. No differences were found in the total number of neurons nor in small, round or ovoid neurons, which should include a majority of the GABA cells. Prefrontal gray and white matter volume did not differ significantly between controls and schizophrenics.\n Question: Is gene expression for glutamic acid decarboxylase reduced without loss of neurons in prefrontal cortex of schizophrenics?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: Up-regulation of gamma-aminobutyric acidA (GABAA) receptors and decreased GABA uptake in the cerebral cortex of schizophrenics suggest altered GABAergic transmission, which could be caused by primary disturbance of GABA synapses or by decreased production of the transmitter. Decreased production could be due to a shutdown in GABA production or to loss of GABA neurons caused by cell death or their failure to migrate to the cortex during brain development. To discriminate between these possibilities, we quantified levels of messenger RNA (mRNA) for the 67-kd isoform of glutamic acid decarboxylase (GAD), the key enzyme in GABA synthesis, and the number and laminar distribution of GAD mRNA--expressing neurons in the dorsolateral prefrontal cortex (DLPFC) of schizophrenics and matched controls, using in situ hybridization-histochemistry, densitometry, and cell-counting methods. These data were compared with the total number of neurons, the number of small, round or ovoid neurons 8 to 15 microns in diameter, and overall frontal lobe volume. As a control, mRNA levels for type II calcium-calmodulin-dependent protein kinase (CamIIK) were quantified. Schizophrenics showed a pronounced decrease in GAD mRNA levels in neurons of layer I (40%) and layer II (48%) and an overall 30% decrease in layers III to VI. There were also strong overall reductions in GAD mRNA levels. The CamIIK mRNA levels showed no significant differences between samples. No differences were found in the total number of neurons nor in small, round or ovoid neurons, which should include a majority of the GABA cells. Prefrontal gray and white matter volume did not differ significantly between controls and schizophrenics. Question: Is gene expression for glutamic acid decarboxylase reduced without loss of neurons in prefrontal cortex of schizophrenics? Output:
PubmedQA157276
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: ABL tyrosine kinases control actin remodeling in development and in response to environmental stimuli. These changes affect cell adhesion, cell migration, and cell-cell contact. Little is known, however, about upstream mechanisms regulating ABL protein activation. We report that the RAS effector RIN1 is an activator of ABL tyrosine kinases. RIN1 expression in fibroblasts promotes the formation of membrane spikes; similar effects have been reported for ABL overexpression. RIN1 binds to the ABL SH3 and SH2 domains, and these interactions stimulate ABL2 catalytic activity. This leads to increased phosphorylation of CRK and CRKL, inhibiting these cytoskeletal regulators by promoting intramolecular over intermolecular associations. Activated RAS participates in a stable RAS-RIN1-ABL2 complex and stimulates the tyrosine kinase-activation function of RIN1. Deletion of the RAS binding domain (RBD) strongly stimulated the ABL2 activation function of RIN1, suggesting that RAS activation results from the relief of RIN1 autoinhibition. The ABL binding domain of RIN1 (RIN1-ABD) increased the activity of ABL2 immune complexes and purified RIN1-ABD-stimulated ABL2 kinase activity toward CRK. Mammary epithelial cells (MECs) from Rin1-/- mice showed accelerated cell adhesion and increased motility in comparison to wild-type cells. Knockdown of RIN1 in epithelial-cell lines blocked the induction of CRKL phosphorylation, confirming that RIN1 normally functions as an inhibitor of cell motility.\n Question: Is rIN1 an ABL tyrosine kinase activator and a regulator of epithelial-cell adhesion and migration?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: ABL tyrosine kinases control actin remodeling in development and in response to environmental stimuli. These changes affect cell adhesion, cell migration, and cell-cell contact. Little is known, however, about upstream mechanisms regulating ABL protein activation. We report that the RAS effector RIN1 is an activator of ABL tyrosine kinases. RIN1 expression in fibroblasts promotes the formation of membrane spikes; similar effects have been reported for ABL overexpression. RIN1 binds to the ABL SH3 and SH2 domains, and these interactions stimulate ABL2 catalytic activity. This leads to increased phosphorylation of CRK and CRKL, inhibiting these cytoskeletal regulators by promoting intramolecular over intermolecular associations. Activated RAS participates in a stable RAS-RIN1-ABL2 complex and stimulates the tyrosine kinase-activation function of RIN1. Deletion of the RAS binding domain (RBD) strongly stimulated the ABL2 activation function of RIN1, suggesting that RAS activation results from the relief of RIN1 autoinhibition. The ABL binding domain of RIN1 (RIN1-ABD) increased the activity of ABL2 immune complexes and purified RIN1-ABD-stimulated ABL2 kinase activity toward CRK. Mammary epithelial cells (MECs) from Rin1-/- mice showed accelerated cell adhesion and increased motility in comparison to wild-type cells. Knockdown of RIN1 in epithelial-cell lines blocked the induction of CRKL phosphorylation, confirming that RIN1 normally functions as an inhibitor of cell motility. Question: Is rIN1 an ABL tyrosine kinase activator and a regulator of epithelial-cell adhesion and migration? Output:
PubmedQA8266
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: The C-terminus of the serotonin transporter (SERT) contains binding domains for different proteins and is critical for its functional expression. In endogenous and heterologous expression systems, our proteomic and biochemical analysis demonstrated that an intermediate filament, vimentin, binds to the C-terminus of SERT. It has been reported that 5HT-stimulation of cells leads to disassembly and spatial reorientation of vimentin filaments. We tested the impact of 5HT-stimulation on vimentin-SERT association and found that 5HT-stimulation accelerates the translocation of SERT from the plasma membrane via enhancing the level of association between phosphovimentin and SERT. Furthermore a progressive truncation of the C-terminus of SERT was performed to map the vimentin-SERT association domain. Deletion of up to 20, but not 14 amino acids arrested the transporters at intracellular locations. Although, truncation of the last 14 amino acids, did not alter 5HT uptake rates of transporter but abolished its association with vimentin. To understand the involvement of 5HT in phosphovimentin-SERT association from the plasma membrane, we further investigated the six amino acids between Delta14 and Delta20, i.e., the SITPET sequence of SERT. While the triple mutation on the possible kinase action sites, S(611), T(613), and T(616) arrested the transporter at intracellular locations, replacing the residues with aspartic acid one at a time altered neither the 5HT uptake rates nor the vimentin association of these mutants. However, replacing the three target sites with alanine, either simultaneously or one at a time, had no significant effect on 5HT uptake rates or the vimentin association with transporter.\n Question: Is the cellular distribution of serotonin transporter impeded on serotonin-altered vimentin network?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: The C-terminus of the serotonin transporter (SERT) contains binding domains for different proteins and is critical for its functional expression. In endogenous and heterologous expression systems, our proteomic and biochemical analysis demonstrated that an intermediate filament, vimentin, binds to the C-terminus of SERT. It has been reported that 5HT-stimulation of cells leads to disassembly and spatial reorientation of vimentin filaments. We tested the impact of 5HT-stimulation on vimentin-SERT association and found that 5HT-stimulation accelerates the translocation of SERT from the plasma membrane via enhancing the level of association between phosphovimentin and SERT. Furthermore a progressive truncation of the C-terminus of SERT was performed to map the vimentin-SERT association domain. Deletion of up to 20, but not 14 amino acids arrested the transporters at intracellular locations. Although, truncation of the last 14 amino acids, did not alter 5HT uptake rates of transporter but abolished its association with vimentin. To understand the involvement of 5HT in phosphovimentin-SERT association from the plasma membrane, we further investigated the six amino acids between Delta14 and Delta20, i.e., the SITPET sequence of SERT. While the triple mutation on the possible kinase action sites, S(611), T(613), and T(616) arrested the transporter at intracellular locations, replacing the residues with aspartic acid one at a time altered neither the 5HT uptake rates nor the vimentin association of these mutants. However, replacing the three target sites with alanine, either simultaneously or one at a time, had no significant effect on 5HT uptake rates or the vimentin association with transporter. Question: Is the cellular distribution of serotonin transporter impeded on serotonin-altered vimentin network? Output:
PubmedQA110561
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To analyse the influence of long-term smoking on the hearing threshold of individuals subjected to occupational noise exposure. Prospective observational cohort study. Occupational health examination of noise-exposed employees in the brick manufacturing industry. A study group of long-term smokers (n = 30) and a control group of non-smokers (n = 58) were identified from a population of 227 male noise-exposed employees. Individuals of both groups were employed for 10 years or more at a single brick manufacturing plant. Data on noise exposure, smoking habits, medical and otological history were collected and standard pure tone audiometry was obtained. Exclusion criteria included asymmetrical or conductive hearing loss, uncontrolled systemic illnesses, history of head injury, chronic middle ear pathology or major ear operations. Pure tone audiometry. Both groups had similar mean age and total duration of occupational noise exposure. The median age-corrected hearing thresholds at 3 and 4 kHz in the smokers group were significantly higher (approximately 7dB) than those in the non-smokers group. No statistical difference in the hearing thresholds between both groups was found in any other tested frequency (0.5, 1, 2, 6 and 8 kHz).\n Question: Is noise-induced hearing loss exacerbated by long-term smoking?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To analyse the influence of long-term smoking on the hearing threshold of individuals subjected to occupational noise exposure. Prospective observational cohort study. Occupational health examination of noise-exposed employees in the brick manufacturing industry. A study group of long-term smokers (n = 30) and a control group of non-smokers (n = 58) were identified from a population of 227 male noise-exposed employees. Individuals of both groups were employed for 10 years or more at a single brick manufacturing plant. Data on noise exposure, smoking habits, medical and otological history were collected and standard pure tone audiometry was obtained. Exclusion criteria included asymmetrical or conductive hearing loss, uncontrolled systemic illnesses, history of head injury, chronic middle ear pathology or major ear operations. Pure tone audiometry. Both groups had similar mean age and total duration of occupational noise exposure. The median age-corrected hearing thresholds at 3 and 4 kHz in the smokers group were significantly higher (approximately 7dB) than those in the non-smokers group. No statistical difference in the hearing thresholds between both groups was found in any other tested frequency (0.5, 1, 2, 6 and 8 kHz). Question: Is noise-induced hearing loss exacerbated by long-term smoking? Output:
PubmedQA148670
[ { "role": "user", "content": "TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer.\n INPUT: To use multimodality imaging to explore the relationship of biomarkers of inflammation, T-cell activation and monocyte activation with coronary calcification and subclinical vascular disease in a population of HIV-infected patients on antiretroviral therapy (ART). Cross-sectional. A panel of soluble and cellular biomarkers of inflammation and immune activation was measured in 147 HIV-infected adults on ART with HIV RNA less than 1000 copies/ml and low-density lipoprotein cholesterol (LDL-C) 130  mg/dl or less. We examined the relationship of biomarkers to coronary calcium (CAC) score and multiple ultrasound measures of subclinical vascular disease. Overall, median (interquartile range, IQR) age was 46 (40-53) years; three-quarters of participants were male and two-thirds African-American. Median 10-year Framingham risk score was 6%. Participants with CAC more than 0 were older, less likely to be African-American and had higher current and lower nadir CD4 T-cell counts. Most biomarkers were similar between those with and without CAC; however, soluble CD14 was independently associated with CAC after adjustment for traditional risk factors. Among those with a CAC score of zero, T-cell activation and systemic inflammation correlated with carotid intima-media thickness and brachial hyperemic velocity, respectively. Compared with normal participants and those with CAC only, participants with increasing degrees of subclinical vascular disease had higher levels of sCD14, hs-CRP and fibrinogen (all P<0.05).\n Question: Is soluble CD14 independently associated with coronary calcification and extent of subclinical vascular disease in treated HIV infection?\n Output: " }, { "role": "assistant", "content": "yes" } ]
TASK: Your task is to answer the biomedical question based on the provided input. Only output yes, no, or maybe as answer. INPUT: To use multimodality imaging to explore the relationship of biomarkers of inflammation, T-cell activation and monocyte activation with coronary calcification and subclinical vascular disease in a population of HIV-infected patients on antiretroviral therapy (ART). Cross-sectional. A panel of soluble and cellular biomarkers of inflammation and immune activation was measured in 147 HIV-infected adults on ART with HIV RNA less than 1000 copies/ml and low-density lipoprotein cholesterol (LDL-C) 130  mg/dl or less. We examined the relationship of biomarkers to coronary calcium (CAC) score and multiple ultrasound measures of subclinical vascular disease. Overall, median (interquartile range, IQR) age was 46 (40-53) years; three-quarters of participants were male and two-thirds African-American. Median 10-year Framingham risk score was 6%. Participants with CAC more than 0 were older, less likely to be African-American and had higher current and lower nadir CD4 T-cell counts. Most biomarkers were similar between those with and without CAC; however, soluble CD14 was independently associated with CAC after adjustment for traditional risk factors. Among those with a CAC score of zero, T-cell activation and systemic inflammation correlated with carotid intima-media thickness and brachial hyperemic velocity, respectively. Compared with normal participants and those with CAC only, participants with increasing degrees of subclinical vascular disease had higher levels of sCD14, hs-CRP and fibrinogen (all P<0.05). Question: Is soluble CD14 independently associated with coronary calcification and extent of subclinical vascular disease in treated HIV infection? Output: