Datasets:

YBXL
/

PubmedQA_train

Dataset card Data Studio Files Files and versions Community

Split (3)

train · 211k rows

Subsets and Splits

No community queries yet

The top public SQL queries from the community will appear here once available.

id stringlengths 9 14	conversations listlengths 2 2	text stringlengths 231 5.9k
PubmedQA127003	[ { "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 anatomic resection of Couinaud's segments is one of the key techniques in liver surgery. However, the territories and volumes of the eight segments are not adequately assessed based on portal branching. Three-dimensional (3D) perfusion-based volumetry was performed in 107 normal livers. Based on Couinaud classification, the portal branches were identified and the volumes of each segment were calculated. The relationships between branching patterns of the portal veins and segmental volumes were assessed. In descending order of volume, median volumes of segments VIII, VII, IV, V, III, VI, II and I were recorded. Segment VIII was the largest, accounting for a median of 26.1% (range: 11.1-38.0%) of total liver volume (TLV), whereas segments II and III each represented <10% of TLV. In 69.2% of subjects, the portal branches of segment V diverged from the trunk of the branches of segment VIII. No relationship was found between branching type and segment volume.\n Question: Does three-dimensional volumetry in 107 normal livers reveal clinically relevant inter-segment variation in size?\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 anatomic resection of Couinaud's segments is one of the key techniques in liver surgery. However, the territories and volumes of the eight segments are not adequately assessed based on portal branching. Three-dimensional (3D) perfusion-based volumetry was performed in 107 normal livers. Based on Couinaud classification, the portal branches were identified and the volumes of each segment were calculated. The relationships between branching patterns of the portal veins and segmental volumes were assessed. In descending order of volume, median volumes of segments VIII, VII, IV, V, III, VI, II and I were recorded. Segment VIII was the largest, accounting for a median of 26.1% (range: 11.1-38.0%) of total liver volume (TLV), whereas segments II and III each represented <10% of TLV. In 69.2% of subjects, the portal branches of segment V diverged from the trunk of the branches of segment VIII. No relationship was found between branching type and segment volume. Question: Does three-dimensional volumetry in 107 normal livers reveal clinically relevant inter-segment variation in size? Output:
PubmedQA9628	[ { "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 previously reported that the neurotoxicity of amyloid beta protein (Abeta(1-42), 10 nM) was blocked by an Abeta-derived tripeptide, Abeta(32-34) (Ile-Gly-Leu, IGL), suggesting that IGL may be a lead compound in the design of Abeta antagonists. In the present study, three stable forms of IGL peptide with acetylation of its N-terminal and/or amidation of its C-terminal (acetyl-IGL, IGL-NH(2) and acetyl-IGL-NH(2)) were synthesized and examined for their effects on Abeta-induced neurotoxicity. Phosphatidylinositol 4-kinase type II (PI4KII) activity was measured using recombinant human PI4KIIalpha kinase and cell viability was assessed in primary cultured hippocampal neurons. To test effects in vivo, 1.5 microl of 100 nM Abeta and/or 100 nM acetyl-IGL was injected into the hippocampal CA1 region of right hemisphere in transgenic mice expressing V337M human tau protein. Four weeks later, behavior performance in the Morris water maze was tested and after another 2 weeks, sections of brain were prepared for immunohistochemistry. Among the three modified tripeptides, acetyl-IGL attenuated the Abeta-induced inhibition of PI4KII activity as well as enhancement of glutamate neurotoxicity in primary cultured rat hippocampal neurons. Injection of Abeta into the hippocampus of mice impaired spatial memory and increased the number of degenerating neurons in bilateral hippocampal regions. Co-injection of acetyl-IGL prevented the learning impairment as well as the neuronal degeneration induced by Abeta.\n Question: Does acetyl-Ile-Gly-Leu protect neurons from Abeta ( 1-42 ) induced toxicity in vitro and in V337M human tau-expressing 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: We previously reported that the neurotoxicity of amyloid beta protein (Abeta(1-42), 10 nM) was blocked by an Abeta-derived tripeptide, Abeta(32-34) (Ile-Gly-Leu, IGL), suggesting that IGL may be a lead compound in the design of Abeta antagonists. In the present study, three stable forms of IGL peptide with acetylation of its N-terminal and/or amidation of its C-terminal (acetyl-IGL, IGL-NH(2) and acetyl-IGL-NH(2)) were synthesized and examined for their effects on Abeta-induced neurotoxicity. Phosphatidylinositol 4-kinase type II (PI4KII) activity was measured using recombinant human PI4KIIalpha kinase and cell viability was assessed in primary cultured hippocampal neurons. To test effects in vivo, 1.5 microl of 100 nM Abeta and/or 100 nM acetyl-IGL was injected into the hippocampal CA1 region of right hemisphere in transgenic mice expressing V337M human tau protein. Four weeks later, behavior performance in the Morris water maze was tested and after another 2 weeks, sections of brain were prepared for immunohistochemistry. Among the three modified tripeptides, acetyl-IGL attenuated the Abeta-induced inhibition of PI4KII activity as well as enhancement of glutamate neurotoxicity in primary cultured rat hippocampal neurons. Injection of Abeta into the hippocampus of mice impaired spatial memory and increased the number of degenerating neurons in bilateral hippocampal regions. Co-injection of acetyl-IGL prevented the learning impairment as well as the neuronal degeneration induced by Abeta. Question: Does acetyl-Ile-Gly-Leu protect neurons from Abeta ( 1-42 ) induced toxicity in vitro and in V337M human tau-expressing mice? Output:
PubmedQA76063	[ { "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 density regulates the expression of various antioxidant enzymes in cell culture. The aim of this study was to study the effect of 2,5 bis-[1-aziridinyl]-1,4 benzoquinone (DZQ), an antitumor quinone bioactivated by NQO1, on HeLa and HepG2 cells cultured at various cell densities. Quinone toxicity was determined by a colorimetric growth inhibition assay. NQO1 and catalase activities were measured spectrophotometrically in soluble fractions, and NQO1 polypeptide was quantified by immunostaining with a commercial polyclonal antiserum. As reported previously, NQO1 activity was much higher in confluent HeLa cells than in sparse cells. However, HepG2 cultures showed an opposite pattern in the regulation of this antioxidant enzyme, sparse cell cultures showing higher NQO1 activity similar to that found in confluent HeLa cells. The expression pattern of catalase activity was similar to that of NQO1 in HeLa cells, but this activity was constant and cell density-independent in HepG2. The growth inhibition effect of DZQ, correlated with NQO1 activity within a given cell type, but HepG2 was always much more sensitive to DZQ than HeLa cells, even under conditions where NQO1 activity was high in HeLa but low in HepG2.\n Question: Are cellular density and cell type the key factors in growth inhibition induced by 2,5bis [ 1-aziridinyl ] -1,4 benzoquinone ( DZQ )?\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 density regulates the expression of various antioxidant enzymes in cell culture. The aim of this study was to study the effect of 2,5 bis-[1-aziridinyl]-1,4 benzoquinone (DZQ), an antitumor quinone bioactivated by NQO1, on HeLa and HepG2 cells cultured at various cell densities. Quinone toxicity was determined by a colorimetric growth inhibition assay. NQO1 and catalase activities were measured spectrophotometrically in soluble fractions, and NQO1 polypeptide was quantified by immunostaining with a commercial polyclonal antiserum. As reported previously, NQO1 activity was much higher in confluent HeLa cells than in sparse cells. However, HepG2 cultures showed an opposite pattern in the regulation of this antioxidant enzyme, sparse cell cultures showing higher NQO1 activity similar to that found in confluent HeLa cells. The expression pattern of catalase activity was similar to that of NQO1 in HeLa cells, but this activity was constant and cell density-independent in HepG2. The growth inhibition effect of DZQ, correlated with NQO1 activity within a given cell type, but HepG2 was always much more sensitive to DZQ than HeLa cells, even under conditions where NQO1 activity was high in HeLa but low in HepG2. Question: Are cellular density and cell type the key factors in growth inhibition induced by 2,5bis [ 1-aziridinyl ] -1,4 benzoquinone ( DZQ )? Output:
PubmedQA152904	[ { "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 etiology of sarcoidosis remains unknown, but recently it was reported that human herpesvirus 8 (HHV-8) may be detected in sarcoid tissue in a high proportion of patients. This study was performed to determine whether HHV-8 is implicated in sarcoidosis in Japan. Peripheral blood mononuclear cells (PBMCs) were obtained from 100 patients with sarcoidosis and 100 healthy donors living in central Japan. Additionally, 19 samples of sarcoid tissue, 10 of tuberculous tissue, and 10 of lung cancers were examined. DNA was extracted from PBMC or tissue samples, and a hemi-nested polymerase chain reaction assay was performed for HHV-8 detection. In the PBMC study, the detection rates for HHV-8 in patients with sarcoidosis and in normal donors were 2% and 1%, respectively, the difference not being significant (p>0.99). In the tissue study, HHV-8 was detected in 10.5% of sarcoid and in 15% of nonsarcoid tissues, again not a significant difference (p>0.99).\n Question: Is human herpesvirus 8 associated with sarcoidosis in Japanese 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: The etiology of sarcoidosis remains unknown, but recently it was reported that human herpesvirus 8 (HHV-8) may be detected in sarcoid tissue in a high proportion of patients. This study was performed to determine whether HHV-8 is implicated in sarcoidosis in Japan. Peripheral blood mononuclear cells (PBMCs) were obtained from 100 patients with sarcoidosis and 100 healthy donors living in central Japan. Additionally, 19 samples of sarcoid tissue, 10 of tuberculous tissue, and 10 of lung cancers were examined. DNA was extracted from PBMC or tissue samples, and a hemi-nested polymerase chain reaction assay was performed for HHV-8 detection. In the PBMC study, the detection rates for HHV-8 in patients with sarcoidosis and in normal donors were 2% and 1%, respectively, the difference not being significant (p>0.99). In the tissue study, HHV-8 was detected in 10.5% of sarcoid and in 15% of nonsarcoid tissues, again not a significant difference (p>0.99). Question: Is human herpesvirus 8 associated with sarcoidosis in Japanese patients? Output:
PubmedQA187034	[ { "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: Agomelatine is an agonist of melatonin that is used in the treatment of major depressive disorders. It has also shown an ability to decrease IOP in experiment animals and in normal human subjects. This pilot study addresses for the first time agomelatine effects on the IOP of patients affected by POAG. Ten patients affected by hypertensive POAG treated by multiple hypotensive topical drugs and under further treatment with agomelatine (25 mg day(-1) per os) for psychiatric problems, were enrolled. IOP tonometric values were measured at enrolment and after 15 and 30 days of agomelatine supplementation. Agomelatine given orally showed a significant hypotonising effect, stably decreasing IOP by roughly 30% of the enrolment value after 15 and 30 days of treatment.\n Question: Does oral treatment with the melatonin agonist agomelatine lower the intraocular pressure of glaucoma 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: Agomelatine is an agonist of melatonin that is used in the treatment of major depressive disorders. It has also shown an ability to decrease IOP in experiment animals and in normal human subjects. This pilot study addresses for the first time agomelatine effects on the IOP of patients affected by POAG. Ten patients affected by hypertensive POAG treated by multiple hypotensive topical drugs and under further treatment with agomelatine (25 mg day(-1) per os) for psychiatric problems, were enrolled. IOP tonometric values were measured at enrolment and after 15 and 30 days of agomelatine supplementation. Agomelatine given orally showed a significant hypotonising effect, stably decreasing IOP by roughly 30% of the enrolment value after 15 and 30 days of treatment. Question: Does oral treatment with the melatonin agonist agomelatine lower the intraocular pressure of glaucoma patients? Output:
PubmedQA144229	[ { "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 investigate the association between metabolic syndrome in the non-pregnant state and the development of preeclampsia. We enrolled 212,463 Korean women who had their first delivery between January, 2011 and December, 2012 and had undergone a national health screening examination through the National Health Insurance during the 1-2 years before their first delivery. Women who had hypertension in the non-pregnant state were excluded. The presence of metabolic syndrome was defined using the modified criteria published in National Cholesterol Education Program Adult Treatment Panel III criteria. The prevalence of metabolic syndrome in non-pregnant state was 1.2%. Preeclampsia developed in 3.1% and its prevalence among women with and without metabolic syndrome was 7.3% and 3.0%, respectively. The pre-pregnancy prevalence of metabolic syndrome was higher in women who developed preeclampsia compared to that in those who had a normal pregnancy (1.1% vs. 2.8%; p<0.001). On multivariate regression analysis, women with metabolic syndrome had an increased risk of developing preeclampsia (odds ratio: 1.48; 95% CI: 1.26 to 1.74) compared to that in those without metabolic syndrome, after adjusting for age, family history of hypertension, smoking status, and pre-pregnancy body mass index. The risk of preeclampsia increased with a rise in the number of components of metabolic syndrome.\n Question: Is metabolic syndrome in the non-pregnant state associated with the development of preeclampsia?\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 investigate the association between metabolic syndrome in the non-pregnant state and the development of preeclampsia. We enrolled 212,463 Korean women who had their first delivery between January, 2011 and December, 2012 and had undergone a national health screening examination through the National Health Insurance during the 1-2 years before their first delivery. Women who had hypertension in the non-pregnant state were excluded. The presence of metabolic syndrome was defined using the modified criteria published in National Cholesterol Education Program Adult Treatment Panel III criteria. The prevalence of metabolic syndrome in non-pregnant state was 1.2%. Preeclampsia developed in 3.1% and its prevalence among women with and without metabolic syndrome was 7.3% and 3.0%, respectively. The pre-pregnancy prevalence of metabolic syndrome was higher in women who developed preeclampsia compared to that in those who had a normal pregnancy (1.1% vs. 2.8%; p<0.001). On multivariate regression analysis, women with metabolic syndrome had an increased risk of developing preeclampsia (odds ratio: 1.48; 95% CI: 1.26 to 1.74) compared to that in those without metabolic syndrome, after adjusting for age, family history of hypertension, smoking status, and pre-pregnancy body mass index. The risk of preeclampsia increased with a rise in the number of components of metabolic syndrome. Question: Is metabolic syndrome in the non-pregnant state associated with the development of preeclampsia? Output:
PubmedQA191275	[ { "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: Lung carcinomas show frequent inactivation of the p53 tumor suppressor, which regulates an apoptotic pathway. The objective of the current study was to assess how the p53 apoptotic pathway is altered in nonsmall cell lung carcinoma (NSCLC), especially in tumors without p53 alterations. p53, its upstream regulators (p14(ARF) and HDM2), and downstream effectors of the apoptotic pathway (BAX and BCL2) were studied in 118 NSCLC specimens. p53 was analyzed by single-stranded conformation polymorphism analysis covering exons 2-11 and by immunohistochemistry (IHC). p14(ARF) was analyzed by methylation-specific polymerase chain reaction and IHC. HDM2 was analyzed using Southern blot analysis and IHC. BAX and BCL2 were analyzed by IHC. Two other upstream regulators that regulate the stability of HDM2, PTEN and HAUSP, also were studied. Of 118 NSCLC specimens that were analyzed, p53 alterations were detected in 74 tumors (63%), p14(ARF) inactivation was detected in 53 tumors (45%), and overexpression of HDM2 was found in 31 tumors (26%), including 6 tumors with gene amplification. Although p53 inactivation and HDM2 overexpression were detected simultaneously, HDM2 gene amplification was observed only in tumor specimens without p53 mutations. IHC revealed PTEN down-regulation in 22 of 88 tumors (25%). HAUSP Northern blot analysis demonstrated several-fold differences in gene expression that did not correlate with p53 alterations. Of 118 NSCLC specimens, expression of BAX and BCL2 expression were detected in 46 tumors (39%) and 17 tumors (14%), respectively. Finally, ASPP1 and ASPP2, molecules involved in mediating the transcription function of p53, were not found to be aberrantly expressed when tested by Northern blot analysis.\n Question: Are p53 apoptotic pathway molecules frequently and simultaneously altered in nonsmall cell lung 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: Lung carcinomas show frequent inactivation of the p53 tumor suppressor, which regulates an apoptotic pathway. The objective of the current study was to assess how the p53 apoptotic pathway is altered in nonsmall cell lung carcinoma (NSCLC), especially in tumors without p53 alterations. p53, its upstream regulators (p14(ARF) and HDM2), and downstream effectors of the apoptotic pathway (BAX and BCL2) were studied in 118 NSCLC specimens. p53 was analyzed by single-stranded conformation polymorphism analysis covering exons 2-11 and by immunohistochemistry (IHC). p14(ARF) was analyzed by methylation-specific polymerase chain reaction and IHC. HDM2 was analyzed using Southern blot analysis and IHC. BAX and BCL2 were analyzed by IHC. Two other upstream regulators that regulate the stability of HDM2, PTEN and HAUSP, also were studied. Of 118 NSCLC specimens that were analyzed, p53 alterations were detected in 74 tumors (63%), p14(ARF) inactivation was detected in 53 tumors (45%), and overexpression of HDM2 was found in 31 tumors (26%), including 6 tumors with gene amplification. Although p53 inactivation and HDM2 overexpression were detected simultaneously, HDM2 gene amplification was observed only in tumor specimens without p53 mutations. IHC revealed PTEN down-regulation in 22 of 88 tumors (25%). HAUSP Northern blot analysis demonstrated several-fold differences in gene expression that did not correlate with p53 alterations. Of 118 NSCLC specimens, expression of BAX and BCL2 expression were detected in 46 tumors (39%) and 17 tumors (14%), respectively. Finally, ASPP1 and ASPP2, molecules involved in mediating the transcription function of p53, were not found to be aberrantly expressed when tested by Northern blot analysis. Question: Are p53 apoptotic pathway molecules frequently and simultaneously altered in nonsmall cell lung carcinoma? Output:
PubmedQA132510	[ { "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: Primary human trophoblasts were previously shown to be resistant to viral infection, and able to confer this resistance to nontrophoblast cells. Can trophoblasts protect nontrophoblastic cells from infection by viruses or other intracellular pathogens that are implicated in perinatal infection? Isolated primary term human trophoblasts were cultured for 48-72 hours. Diverse nonplacental human cell lines (U2OS, human foreskin fibroblast, TZM-bl, MeWo, and Caco-2) were preexposed to either trophoblast conditioned medium, nonconditioned medium, or miR-517-3p for 24 hours. Cells were infected with several viral and nonviral pathogens known to be associated with perinatal infections. Cellular infection was defined and quantified by plaque assays, luciferase assays, microscopy, and/or colonization assays. Differences in infection were assessed by Student t test or analysis of variance with Bonferroni correction. Infection by rubella and other togaviruses, human immunodeficiency virus-1, and varicella zoster was attenuated in cells preexposed to trophoblast-conditioned medium (P < .05), and a partial effect by the chromosome 19 microRNA miR-517-3p on specific pathogens. The conditioned medium had no effect on infection by Toxoplasma gondii or Listeria monocytogenes.\n Question: Do human trophoblasts confer resistance to viruses implicated in perinatal 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: Primary human trophoblasts were previously shown to be resistant to viral infection, and able to confer this resistance to nontrophoblast cells. Can trophoblasts protect nontrophoblastic cells from infection by viruses or other intracellular pathogens that are implicated in perinatal infection? Isolated primary term human trophoblasts were cultured for 48-72 hours. Diverse nonplacental human cell lines (U2OS, human foreskin fibroblast, TZM-bl, MeWo, and Caco-2) were preexposed to either trophoblast conditioned medium, nonconditioned medium, or miR-517-3p for 24 hours. Cells were infected with several viral and nonviral pathogens known to be associated with perinatal infections. Cellular infection was defined and quantified by plaque assays, luciferase assays, microscopy, and/or colonization assays. Differences in infection were assessed by Student t test or analysis of variance with Bonferroni correction. Infection by rubella and other togaviruses, human immunodeficiency virus-1, and varicella zoster was attenuated in cells preexposed to trophoblast-conditioned medium (P < .05), and a partial effect by the chromosome 19 microRNA miR-517-3p on specific pathogens. The conditioned medium had no effect on infection by Toxoplasma gondii or Listeria monocytogenes. Question: Do human trophoblasts confer resistance to viruses implicated in perinatal infection? Output:
PubmedQA190546	[ { "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 study was to determine whether fetal echocardiographic findings are predictive of prognosis in recipient fetuses with twin-twin transfusion syndrome (TTTS). A cohort of 30 pregnancies with TTTS between 1990 and 2001 was included. Diagnosis and staging of TTTS were made according to the Quintero system. Fetal echocardiographic findings of cardiomegaly, right ventricular hypertrophy, and tricuspid regurgitation were evaluated for relationship with fetal death. Power analysis revealed an approximately 80% power to detect a 2-fold increased risk of fetal death, with alpha = .05. Logistic regression was used to determine the relationship between echocardiographic findings and death. Most pregnancies were Quintero stage 1, n = 13 (43%), and ranged in severity to Quintero stage 5, n = 4 (13%). Cardiac findings in the recipient fetus that were assessed for a relationship with death included cardiomegaly at the initial appearance of TTTS or at the most severe evaluation findings, right ventricular hypertrophy at initial appearance or at the most severe evaluation findings, or tricuspid regurgitation at initial appearance or at the most severe evaluation findings. Fetal or neonatal death in the recipient twin was not related to the presence of cardiac findings (odds ratio, 0.77; 95% confidence interval, 0.16-3.74).\n Question: Are fetal echocardiographic findings predictive of death in twin-twin transfusion syndrome?\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 purpose of this study was to determine whether fetal echocardiographic findings are predictive of prognosis in recipient fetuses with twin-twin transfusion syndrome (TTTS). A cohort of 30 pregnancies with TTTS between 1990 and 2001 was included. Diagnosis and staging of TTTS were made according to the Quintero system. Fetal echocardiographic findings of cardiomegaly, right ventricular hypertrophy, and tricuspid regurgitation were evaluated for relationship with fetal death. Power analysis revealed an approximately 80% power to detect a 2-fold increased risk of fetal death, with alpha = .05. Logistic regression was used to determine the relationship between echocardiographic findings and death. Most pregnancies were Quintero stage 1, n = 13 (43%), and ranged in severity to Quintero stage 5, n = 4 (13%). Cardiac findings in the recipient fetus that were assessed for a relationship with death included cardiomegaly at the initial appearance of TTTS or at the most severe evaluation findings, right ventricular hypertrophy at initial appearance or at the most severe evaluation findings, or tricuspid regurgitation at initial appearance or at the most severe evaluation findings. Fetal or neonatal death in the recipient twin was not related to the presence of cardiac findings (odds ratio, 0.77; 95% confidence interval, 0.16-3.74). Question: Are fetal echocardiographic findings predictive of death in twin-twin transfusion syndrome? Output:
PubmedQA58691	[ { "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 sought to determine whether L -arginine polymer treatment of vein grafts enhances vascular production of nitric oxide and inhibits the development of neointimal hyperplasia. External jugular veins of New Zealand White rabbits (n = 42) were harvested; treated intraluminally for 15 minutes with phosphate-buffered saline solution or L -arginine polymer 5, 7, or 9 at either 10 or 100 micromol/L; and then grafted into the contralateral carotid artery. Rabbits were killed after 28 days, and 5-microm sections of vessels were stained with hematoxylin and scored for intima/media ratio by using computerized morphometric analysis. Separate veins were treated in a similar fashion with biotinylated polymers and phosphate-buffered saline solution to assess for translocation efficiencies. Finally, vein segments pretreated with either phosphate-buffered saline solution or L -arginine polymers were cultured in Dulbecco's modified Eagle's medium containing lipopolysaccharide (100 microg/mL) and interferon gamma (200 U/mL) for 48 hours before measuring nitric oxide levels by means of the Griess reaction. Biotinylated L -arginine polymers demonstrated a dose- and length-dependent uptake into intimal and medial cells of treated vessels. Nitric oxide levels were significantly higher in vein segments treated with 100 micromol/L of L -arginine polymer 9 compared with control segments. Finally, the intima/media ratio also reflected both length- and concentration-dependent inhibition of neointimal hyperplasia.intima/media ratio PBS R5 R7 R9 10 micromol/L 0.909 +/- 0.072 0.920 +/- 0.073 0.861 +/- 0.138 0.710 +/- 0.122 100 micromol/L 0.924 +/- 0.061 0.581 +/- 0.089* 0.529 +/- 0.093* PBS, Phosphate-buffered saline solution; R, L -arginine polymer. *P <.001 versus phosphate-buffered saline solution and L -arginine polymer 5 controls (Bonferroni-corrected value).\n Question: Do l-arginine polymers inhibit the development of vein graft neointimal hyperplasia?\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 sought to determine whether L -arginine polymer treatment of vein grafts enhances vascular production of nitric oxide and inhibits the development of neointimal hyperplasia. External jugular veins of New Zealand White rabbits (n = 42) were harvested; treated intraluminally for 15 minutes with phosphate-buffered saline solution or L -arginine polymer 5, 7, or 9 at either 10 or 100 micromol/L; and then grafted into the contralateral carotid artery. Rabbits were killed after 28 days, and 5-microm sections of vessels were stained with hematoxylin and scored for intima/media ratio by using computerized morphometric analysis. Separate veins were treated in a similar fashion with biotinylated polymers and phosphate-buffered saline solution to assess for translocation efficiencies. Finally, vein segments pretreated with either phosphate-buffered saline solution or L -arginine polymers were cultured in Dulbecco's modified Eagle's medium containing lipopolysaccharide (100 microg/mL) and interferon gamma (200 U/mL) for 48 hours before measuring nitric oxide levels by means of the Griess reaction. Biotinylated L -arginine polymers demonstrated a dose- and length-dependent uptake into intimal and medial cells of treated vessels. Nitric oxide levels were significantly higher in vein segments treated with 100 micromol/L of L -arginine polymer 9 compared with control segments. Finally, the intima/media ratio also reflected both length- and concentration-dependent inhibition of neointimal hyperplasia.intima/media ratio PBS R5 R7 R9 10 micromol/L 0.909 +/- 0.072 0.920 +/- 0.073 0.861 +/- 0.138 0.710 +/- 0.122 100 micromol/L 0.924 +/- 0.061 0.581 +/- 0.089* 0.529 +/- 0.093* PBS, Phosphate-buffered saline solution; R, L -arginine polymer. *P <.001 versus phosphate-buffered saline solution and L -arginine polymer 5 controls (Bonferroni-corrected value). Question: Do l-arginine polymers inhibit the development of vein graft neointimal hyperplasia? Output:
PubmedQA181463	[ { "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: Ponicidin is recently reported to have anti-tumour effects on a large variety of cancers. The present study was undertaken to investigate the anti-proliferation effects of ponicidin on hepatocellular carcinoma cells and its mechanism. Two hepatocellular carcinoma cell lines, QGY-7701 and HepG-2 cells, were used. Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Cell apoptosis was assessed by flow cytometry and deoxyribonucleic acid fragmentation analysis. Cell morphology was observed by Hoechst 33258 staining. Reverse transcriptase-polymerase chain reaction and Western blot analysis were used to detect Survivin as well as Bax and Bcl-2 expressions. Ponicidin could inhibit the growth of QGY-7701 and HepG-2 cells significantly by induction of apoptosis. Marked morphological changes of apoptosis were observed clearly. Both Survivin and Bcl-2 expressions were down-regulated remarkably while Bax expression up-regulated when apoptosis occurred.\n Question: Does ponicidin inhibit cell growth on hepatocellular carcinoma cells by induction of apoptosis?\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: Ponicidin is recently reported to have anti-tumour effects on a large variety of cancers. The present study was undertaken to investigate the anti-proliferation effects of ponicidin on hepatocellular carcinoma cells and its mechanism. Two hepatocellular carcinoma cell lines, QGY-7701 and HepG-2 cells, were used. Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Cell apoptosis was assessed by flow cytometry and deoxyribonucleic acid fragmentation analysis. Cell morphology was observed by Hoechst 33258 staining. Reverse transcriptase-polymerase chain reaction and Western blot analysis were used to detect Survivin as well as Bax and Bcl-2 expressions. Ponicidin could inhibit the growth of QGY-7701 and HepG-2 cells significantly by induction of apoptosis. Marked morphological changes of apoptosis were observed clearly. Both Survivin and Bcl-2 expressions were down-regulated remarkably while Bax expression up-regulated when apoptosis occurred. Question: Does ponicidin inhibit cell growth on hepatocellular carcinoma cells by induction of apoptosis? Output:
PubmedQA197137	[ { "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: CX3C chemokine receptor 1 (CX3CR1), a receptor for CX3CL1, mediates migration of inflammatory cells. Psoriasis is a common skin disorder that causes skin inflammation. The role of CX3CL1 and CX3CR1 in psoriasis remains unclear. To elucidate the role of CX3CL1 and CX3CR1 in psoriasis, we assessed imiquimod-induced psoriasis-like dermatitis in CX3CR1-deficient mice. We evaluated skin inflammation by assessing erythema, scaling, and ear thickness in CX3CR1(-/-) mice and wild-type (WT) mice. Furthermore, we measured cytokine production by quantitative reverse transcription-PCR. We investigated infiltrating cells in skin by immunohistochemistry and flow cytometry. After confirming phenotypical differences in macrophages between WT and CX3CR1(-/-) mice, we analyzed expression levels of IL-1β, IL-6, and TNF-α in peritoneal macrophages with or without stimulation of CX3CL1. We finally transferred peritoneal macrophages into the ear before IMQ application. Skin inflammation assessed by erythema, scaling, and epidermal thickness was significantly reduced in CX3CR1(-/-) mice compared with wild-type (WT) mice, accompanied by decreases in cytokine production for IL-12, IL-23, IL-17A, IL-22, IL-1β, IL-6, TNF-α, and IL-36. On day 6, increase in ear thickness from the baseline of CX3CR1(-/-) mice was one third of that of WT mice. Skin macrophages of CX3CR1(-/-) mice contained increased levels of CCR2 and decreased levels of MCP-1 compared with those from WT mice. Spontaneous expression levels of IL-1β, IL-6, and TNF-α in peritoneal macrophages of naïve CX3CR1(-/-) mice were significantly lower than those of WT mice. Furthermore, stimulation of WT macrophages with CX3CL1 decreased expression of these cytokines, suggesting that altered macrophage populations, but not loss of interaction between CX3CL1 and CX3CR1 signaling, caused differences in cytokine expression and skin inflammation. Moreover, transfer of macrophages from WT mice normalized IMQ-induced psoriasis-like inflammation in CX3CR1(-/-) mice, suggesting that macrophages contributed to the decreased inflammation resulted from CX3CR1 deficiency.\n Question: Does cX3CR1 deficiency attenuate imiquimod-induced psoriasis-like skin inflammation with decreased M1 macrophages?\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: CX3C chemokine receptor 1 (CX3CR1), a receptor for CX3CL1, mediates migration of inflammatory cells. Psoriasis is a common skin disorder that causes skin inflammation. The role of CX3CL1 and CX3CR1 in psoriasis remains unclear. To elucidate the role of CX3CL1 and CX3CR1 in psoriasis, we assessed imiquimod-induced psoriasis-like dermatitis in CX3CR1-deficient mice. We evaluated skin inflammation by assessing erythema, scaling, and ear thickness in CX3CR1(-/-) mice and wild-type (WT) mice. Furthermore, we measured cytokine production by quantitative reverse transcription-PCR. We investigated infiltrating cells in skin by immunohistochemistry and flow cytometry. After confirming phenotypical differences in macrophages between WT and CX3CR1(-/-) mice, we analyzed expression levels of IL-1β, IL-6, and TNF-α in peritoneal macrophages with or without stimulation of CX3CL1. We finally transferred peritoneal macrophages into the ear before IMQ application. Skin inflammation assessed by erythema, scaling, and epidermal thickness was significantly reduced in CX3CR1(-/-) mice compared with wild-type (WT) mice, accompanied by decreases in cytokine production for IL-12, IL-23, IL-17A, IL-22, IL-1β, IL-6, TNF-α, and IL-36. On day 6, increase in ear thickness from the baseline of CX3CR1(-/-) mice was one third of that of WT mice. Skin macrophages of CX3CR1(-/-) mice contained increased levels of CCR2 and decreased levels of MCP-1 compared with those from WT mice. Spontaneous expression levels of IL-1β, IL-6, and TNF-α in peritoneal macrophages of naïve CX3CR1(-/-) mice were significantly lower than those of WT mice. Furthermore, stimulation of WT macrophages with CX3CL1 decreased expression of these cytokines, suggesting that altered macrophage populations, but not loss of interaction between CX3CL1 and CX3CR1 signaling, caused differences in cytokine expression and skin inflammation. Moreover, transfer of macrophages from WT mice normalized IMQ-induced psoriasis-like inflammation in CX3CR1(-/-) mice, suggesting that macrophages contributed to the decreased inflammation resulted from CX3CR1 deficiency. Question: Does cX3CR1 deficiency attenuate imiquimod-induced psoriasis-like skin inflammation with decreased M1 macrophages? Output:
PubmedQA28483	[ { "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: Mesothelin is an emerging marker for cancer diagnosis and target-based therapy, yet relatively little is known about the clinical significance of mesothelin expression in tumors. In this study, we correlate mesothelin immunoreactivity to clinicopathologic features in ovarian serous carcinoma. Mesothelin expression levels were compared among 81 publicly available serial analysis of gene expression (SAGE) libraries of various carcinoma and normal tissue types. Immunohistochemistry using a well-characterized mesothelin monoclonal antibody (5B2) was done to evaluate mesothelin expression in 167 high-grade and 31 low-grade ovarian serous carcinomas. Immunohistochemistry staining scores were correlated with patient survival, tumor site, tumor grade, in vitro drug resistance, and differentiation status of tumor cells. SAGE analysis showed that mesothelin was overexpressed in 50% of ovarian and pancreatic carcinomas but rarely in other cancer types, including liver, colon, kidney, prostate, and breast. Mesothelin immunoreactivity (>5% of tumor cells) was present in 55% of ovarian serous carcinomas with no difference in expression between high-grade and low-grade serous tumors (P = 0.82). Based on Kaplan-Meier analysis, we found that a diffuse mesothelin staining (>50% of tumor cells) in primary high-grade ovarian carcinomas correlated significantly with prolonged survival in patients who had advanced-stage disease and had received optimal debulking surgery followed by chemotherapy (P = 0.023). Mesothelin expression did not correlate significantly with patient age, tumor site, in vitro drug resistance, or tumor differentiation status (P > 0.10).\n Question: Does diffuse mesothelin expression correlate with prolonged patient survival in ovarian serous 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: Mesothelin is an emerging marker for cancer diagnosis and target-based therapy, yet relatively little is known about the clinical significance of mesothelin expression in tumors. In this study, we correlate mesothelin immunoreactivity to clinicopathologic features in ovarian serous carcinoma. Mesothelin expression levels were compared among 81 publicly available serial analysis of gene expression (SAGE) libraries of various carcinoma and normal tissue types. Immunohistochemistry using a well-characterized mesothelin monoclonal antibody (5B2) was done to evaluate mesothelin expression in 167 high-grade and 31 low-grade ovarian serous carcinomas. Immunohistochemistry staining scores were correlated with patient survival, tumor site, tumor grade, in vitro drug resistance, and differentiation status of tumor cells. SAGE analysis showed that mesothelin was overexpressed in 50% of ovarian and pancreatic carcinomas but rarely in other cancer types, including liver, colon, kidney, prostate, and breast. Mesothelin immunoreactivity (>5% of tumor cells) was present in 55% of ovarian serous carcinomas with no difference in expression between high-grade and low-grade serous tumors (P = 0.82). Based on Kaplan-Meier analysis, we found that a diffuse mesothelin staining (>50% of tumor cells) in primary high-grade ovarian carcinomas correlated significantly with prolonged survival in patients who had advanced-stage disease and had received optimal debulking surgery followed by chemotherapy (P = 0.023). Mesothelin expression did not correlate significantly with patient age, tumor site, in vitro drug resistance, or tumor differentiation status (P > 0.10). Question: Does diffuse mesothelin expression correlate with prolonged patient survival in ovarian serous carcinoma? Output:
PubmedQA30402	[ { "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 genus Orbivirus includes several species that infect livestock - including Bluetongue virus (BTV) and African horse sickness virus (AHSV). These viruses have linear dsRNA genomes divided into ten segments, all of which have previously been assumed to be monocistronic. Bioinformatic evidence is presented for a short overlapping coding sequence (CDS) in the Orbivirus genome segment 9, overlapping the VP6 cistron in the +1 reading frame. In BTV, a 77-79 codon AUG-initiated open reading frame (hereafter ORFX) is present in all 48 segment 9 sequences analysed. The pattern of base variations across the 48-sequence alignment indicates that ORFX is subject to functional constraints at the amino acid level (even when the constraints due to coding in the overlapping VP6 reading frame are taken into account; MLOGD software). In fact the translated ORFX shows greater amino acid conservation than the overlapping region of VP6. The ORFX AUG codon has a strong Kozak context in all 48 sequences. Each has only one or two upstream AUG codons, always in the VP6 reading frame, and (with a single exception) always with weak or medium Kozak context. Thus, in BTV, ORFX may be translated via leaky scanning. A long (83-169 codon) ORF is present in a corresponding location and reading frame in all other Orbivirus species analysed except Saint Croix River virus (SCRV; the most divergent). Again, the pattern of base variations across sequence alignments indicates multiple coding in the VP6 and ORFX reading frames.\n Question: Does bioinformatic analysis suggest that the Orbivirus VP6 cistron encodes an overlapping gene?\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 genus Orbivirus includes several species that infect livestock - including Bluetongue virus (BTV) and African horse sickness virus (AHSV). These viruses have linear dsRNA genomes divided into ten segments, all of which have previously been assumed to be monocistronic. Bioinformatic evidence is presented for a short overlapping coding sequence (CDS) in the Orbivirus genome segment 9, overlapping the VP6 cistron in the +1 reading frame. In BTV, a 77-79 codon AUG-initiated open reading frame (hereafter ORFX) is present in all 48 segment 9 sequences analysed. The pattern of base variations across the 48-sequence alignment indicates that ORFX is subject to functional constraints at the amino acid level (even when the constraints due to coding in the overlapping VP6 reading frame are taken into account; MLOGD software). In fact the translated ORFX shows greater amino acid conservation than the overlapping region of VP6. The ORFX AUG codon has a strong Kozak context in all 48 sequences. Each has only one or two upstream AUG codons, always in the VP6 reading frame, and (with a single exception) always with weak or medium Kozak context. Thus, in BTV, ORFX may be translated via leaky scanning. A long (83-169 codon) ORF is present in a corresponding location and reading frame in all other Orbivirus species analysed except Saint Croix River virus (SCRV; the most divergent). Again, the pattern of base variations across sequence alignments indicates multiple coding in the VP6 and ORFX reading frames. Question: Does bioinformatic analysis suggest that the Orbivirus VP6 cistron encodes an overlapping gene? Output:
PubmedQA137979	[ { "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 study examines the effectiveness of Calibrated Peer Review (CPR), a Web-based writing development program, to teach and assess medical students' patient note-writing skills in a standardized fashion. At the end of the clerkship year, 67 medical students were divided into three groups, introduced to CPR, and instructed in patient note-writing. Students then wrote notes for three clinical cases, presented in different order to each group. After training on faculty-calibrated standards, students evaluated their peers' notes and their own notes. Trained faculty, blinded to author, order, and group, also graded student notes. Faculty gave lower scores than students, but both groups found students' scores improved significantly from the first to the third note written.\n Question: Do improved patient notes from medical students during web-based teaching using faculty-calibrated peer review and self-assessment?\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 study examines the effectiveness of Calibrated Peer Review (CPR), a Web-based writing development program, to teach and assess medical students' patient note-writing skills in a standardized fashion. At the end of the clerkship year, 67 medical students were divided into three groups, introduced to CPR, and instructed in patient note-writing. Students then wrote notes for three clinical cases, presented in different order to each group. After training on faculty-calibrated standards, students evaluated their peers' notes and their own notes. Trained faculty, blinded to author, order, and group, also graded student notes. Faculty gave lower scores than students, but both groups found students' scores improved significantly from the first to the third note written. Question: Do improved patient notes from medical students during web-based teaching using faculty-calibrated peer review and self-assessment? Output:
PubmedQA45007	[ { "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: Normal birth weight variation affects schizophrenia risk and cognitive performance in schizophrenia patients and healthy controls. Brain cortical anatomy is altered in psychotic disorders and in low birth weight subjects, but if birth weight variation relates to cortical morphology across the psychosis spectrum is not known. Magnetic Resonance Imaging brain scans and clinical-, neurocognitive-, and medical birth registry data were collected from 359 adults including patients with a DSM-IV diagnosis of schizophrenia (n = 90, mean age 29.4±10.2 [95% CI], 62% male), bipolar disorder (n = 79, age 29.4±11.8, 39% male) or other psychosis (n = 40, age 26.3±10.0, 56% male), and healthy controls (n = 140, age 30.8±12.0,53% male). We explored the relationship between whole-range birth weight variation and cortical surface area and thickness and their possible associations to cognitive performance. Across all groups, lower birth weight was associated with smaller total surface area (t = 3.87, P = .0001), within specific regions of the temporal, parietal, and frontal cortex bilaterally. There were no associations between birth weight and cortical thickness, and no diagnosis by birth weight interaction effects on cortical thickness or surface area. Smaller cortical area (t = 2.50, P = .013) and lower birth weight (t = 2.53, P = .012) were significantly related to poorer working memory performance in all diagnostic groups except schizophrenia.\n Question: Is normal birth weight variation related to cortical morphology across the psychosis spectrum?\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: Normal birth weight variation affects schizophrenia risk and cognitive performance in schizophrenia patients and healthy controls. Brain cortical anatomy is altered in psychotic disorders and in low birth weight subjects, but if birth weight variation relates to cortical morphology across the psychosis spectrum is not known. Magnetic Resonance Imaging brain scans and clinical-, neurocognitive-, and medical birth registry data were collected from 359 adults including patients with a DSM-IV diagnosis of schizophrenia (n = 90, mean age 29.4±10.2 [95% CI], 62% male), bipolar disorder (n = 79, age 29.4±11.8, 39% male) or other psychosis (n = 40, age 26.3±10.0, 56% male), and healthy controls (n = 140, age 30.8±12.0,53% male). We explored the relationship between whole-range birth weight variation and cortical surface area and thickness and their possible associations to cognitive performance. Across all groups, lower birth weight was associated with smaller total surface area (t = 3.87, P = .0001), within specific regions of the temporal, parietal, and frontal cortex bilaterally. There were no associations between birth weight and cortical thickness, and no diagnosis by birth weight interaction effects on cortical thickness or surface area. Smaller cortical area (t = 2.50, P = .013) and lower birth weight (t = 2.53, P = .012) were significantly related to poorer working memory performance in all diagnostic groups except schizophrenia. Question: Is normal birth weight variation related to cortical morphology across the psychosis spectrum? Output:
PubmedQA159343	[ { "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: Deposition of paramagnetic substances in basal ganglia, resulting in increased signals in T1-weighted magnetic resonance images (bright basal ganglia), is frequently seen in liver cirrhosis. The present study describes the prevalence of bright basal ganglia and its clinical significance in patients with long-standing portal vein thrombosis in the absence of liver cirrhosis. Six patients with angiographically proven complete portal vein thrombosis and cavernomatous transformation without signs of acute or chronic liver disease were studied by magnetic resonance imaging of the brain, neuropsychiatric evaluation, psychometric tests, electroencephalography, and determination of arterial ammonia levels and of serum manganese concentrations from peripheral venous blood. Five out of six patients demonstrated increased signal intensity in the basal ganglia. Overt portal-systemic encephalopathy was not noted prior to or at the time of evaluation. Normal EEG results were recorded in all patients. Only one of the six patients had pathological results in at least two out of four psychometric tests. This latter patient had had a large right-sided brain infarction. Arterial ammonia concentrations were normal in four of the six patients; one patient with increased ammonia levels had concomitant renal insufficiency with azotemia. The other four patients had no relevant concomitant diseases. Serum manganese levels were non-significantly increased compared with a control group (p=0.06), but they were significantly correlated to basal ganglia signal intensity (R=0.88; p=0.02).\n Question: Are bright basal ganglia in T1-weighted magnetic resonance images frequent in patients with portal vein thrombosis without liver cirrhosis and not suggestive of hepatic encephalopathy?\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: Deposition of paramagnetic substances in basal ganglia, resulting in increased signals in T1-weighted magnetic resonance images (bright basal ganglia), is frequently seen in liver cirrhosis. The present study describes the prevalence of bright basal ganglia and its clinical significance in patients with long-standing portal vein thrombosis in the absence of liver cirrhosis. Six patients with angiographically proven complete portal vein thrombosis and cavernomatous transformation without signs of acute or chronic liver disease were studied by magnetic resonance imaging of the brain, neuropsychiatric evaluation, psychometric tests, electroencephalography, and determination of arterial ammonia levels and of serum manganese concentrations from peripheral venous blood. Five out of six patients demonstrated increased signal intensity in the basal ganglia. Overt portal-systemic encephalopathy was not noted prior to or at the time of evaluation. Normal EEG results were recorded in all patients. Only one of the six patients had pathological results in at least two out of four psychometric tests. This latter patient had had a large right-sided brain infarction. Arterial ammonia concentrations were normal in four of the six patients; one patient with increased ammonia levels had concomitant renal insufficiency with azotemia. The other four patients had no relevant concomitant diseases. Serum manganese levels were non-significantly increased compared with a control group (p=0.06), but they were significantly correlated to basal ganglia signal intensity (R=0.88; p=0.02). Question: Are bright basal ganglia in T1-weighted magnetic resonance images frequent in patients with portal vein thrombosis without liver cirrhosis and not suggestive of hepatic encephalopathy? Output:
PubmedQA157328	[ { "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: Many patients with localised prostate cancer present with symptoms of benign prostatic hypertrophy (BPH) and require neoadjuvant hormone therapy to shrink the gland before brachytherapy. The impact of this hormone therapy has been evaluated in 667 patients treated with Iodine seed monotherapy. Prospective data from 667 patients treated between 1995 and 2001 by I-125 seeds prostate implant as monotherapy were analysed. The mean age was 63 years (42--77 years). Three hundred and forty-six (51.9%) patients had a short course of neo adjuvant hormone therapy and 321 (49.1%) did not. The prescribed minimum peripheral dose was 145 Gy (TG 43). Patients were followed up to a maximum of 8.2 years and a minimum of 18 months. Statistical analysis was performed to identify factors that would predict PSA relapse-free survival (PSA-RFS) defined by the American Society for Therapeutic Radiology and Oncology (ASTRO). Overall the PSA relapse-free survival is 76.1 and 72.6% for patient cohorts being on pre-treatment hormones and not, respectively (P=0.107). Subdivided into risk groups the low risk group showed 92.5% PSA-RFS with hormones and 75.1% without (P=0.327). The intermediate group 75.7% with hormones and 72.9% without (P=0.148) and for the high-risk group 51.1% with and 51.1% without hormones (P=0.942). Evaluation of post-implant dosimetry in patients with and without hormone therapy showed that the D90 for those who received hormone therapy was 130.8 Gy compared with 145.1 Gy for those who did not (P<0.001). This may be related to the degree of oedema at the time of post-implant dosimetry. The CT to ultrasound prostate volume ratio was 1.17 for patients who received hormone therapy and 0.98 for those who did not (P<0.001). It is suggested that in the interval between stopping hormone therapy and doing post-implant dosimetry there was an increase in prostate volume, which results in a lower D90. Significant correlation was found between D90 and prostate volume on post-implant CT dosimetry with higher D90s for small volume prostates (P<0.001).\n Question: Do the impact of hormone therapy on post-implant dosimetry and outcome following Iodine-125 implant monotherapy for localised prostate 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: Many patients with localised prostate cancer present with symptoms of benign prostatic hypertrophy (BPH) and require neoadjuvant hormone therapy to shrink the gland before brachytherapy. The impact of this hormone therapy has been evaluated in 667 patients treated with Iodine seed monotherapy. Prospective data from 667 patients treated between 1995 and 2001 by I-125 seeds prostate implant as monotherapy were analysed. The mean age was 63 years (42--77 years). Three hundred and forty-six (51.9%) patients had a short course of neo adjuvant hormone therapy and 321 (49.1%) did not. The prescribed minimum peripheral dose was 145 Gy (TG 43). Patients were followed up to a maximum of 8.2 years and a minimum of 18 months. Statistical analysis was performed to identify factors that would predict PSA relapse-free survival (PSA-RFS) defined by the American Society for Therapeutic Radiology and Oncology (ASTRO). Overall the PSA relapse-free survival is 76.1 and 72.6% for patient cohorts being on pre-treatment hormones and not, respectively (P=0.107). Subdivided into risk groups the low risk group showed 92.5% PSA-RFS with hormones and 75.1% without (P=0.327). The intermediate group 75.7% with hormones and 72.9% without (P=0.148) and for the high-risk group 51.1% with and 51.1% without hormones (P=0.942). Evaluation of post-implant dosimetry in patients with and without hormone therapy showed that the D90 for those who received hormone therapy was 130.8 Gy compared with 145.1 Gy for those who did not (P<0.001). This may be related to the degree of oedema at the time of post-implant dosimetry. The CT to ultrasound prostate volume ratio was 1.17 for patients who received hormone therapy and 0.98 for those who did not (P<0.001). It is suggested that in the interval between stopping hormone therapy and doing post-implant dosimetry there was an increase in prostate volume, which results in a lower D90. Significant correlation was found between D90 and prostate volume on post-implant CT dosimetry with higher D90s for small volume prostates (P<0.001). Question: Do the impact of hormone therapy on post-implant dosimetry and outcome following Iodine-125 implant monotherapy for localised prostate cancer? Output:
PubmedQA91378	[ { "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: Circumferential pulmonary vein isolation (PVI) is the cornerstone of the current state-of-the-art management of atrial fibrillation (AF). However, the precise mechanisms behind AF relapses post PVI are still unknown. Since the activity of the autonomous nervous system is crucial in triggering paroxysmal AF, we hypothesized that PVI is associated with changes of cardiac sympathetic activity. Sixteen patients with paroxysmal AF underwent cardiac iodine-123-meta-iodobenzylguanidine (123I-mIBG) planar cardiac imaging and single-photon emission computed tomography with low-dose computed tomography (SPECT/CT) for attenuation correction before and 4 weeks after PVI. The heart-to-mediastinum ratio (H/M ratio), washout rate (WR), regional myocardial uptake, and regional washout were analyzed. The late H/M ratio was unchanged by PVI (pre, 2.9 ± 0.5 vs. post, 2.7 ± 0.6, p = 0.53). Four of the 16 patients (25%) displayed regional deficits before PVI. After PVI, regional deficits were present in ten patients (62.5%) with newly emerging deficits localized in the inferolateral wall. In a 6-month follow-up, four out of the ten patients (40%) with regional 123I-mIBG defects suffered from a recurrence of AF, while only one of the six patients (16.7%) without a regional 123I-mIBG defect experienced a recurrence.\n Question: Is pulmonary vein isolation in patients with paroxysmal atrial fibrillation associated with regional cardiac sympathetic denervation?\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: Circumferential pulmonary vein isolation (PVI) is the cornerstone of the current state-of-the-art management of atrial fibrillation (AF). However, the precise mechanisms behind AF relapses post PVI are still unknown. Since the activity of the autonomous nervous system is crucial in triggering paroxysmal AF, we hypothesized that PVI is associated with changes of cardiac sympathetic activity. Sixteen patients with paroxysmal AF underwent cardiac iodine-123-meta-iodobenzylguanidine (123I-mIBG) planar cardiac imaging and single-photon emission computed tomography with low-dose computed tomography (SPECT/CT) for attenuation correction before and 4 weeks after PVI. The heart-to-mediastinum ratio (H/M ratio), washout rate (WR), regional myocardial uptake, and regional washout were analyzed. The late H/M ratio was unchanged by PVI (pre, 2.9 ± 0.5 vs. post, 2.7 ± 0.6, p = 0.53). Four of the 16 patients (25%) displayed regional deficits before PVI. After PVI, regional deficits were present in ten patients (62.5%) with newly emerging deficits localized in the inferolateral wall. In a 6-month follow-up, four out of the ten patients (40%) with regional 123I-mIBG defects suffered from a recurrence of AF, while only one of the six patients (16.7%) without a regional 123I-mIBG defect experienced a recurrence. Question: Is pulmonary vein isolation in patients with paroxysmal atrial fibrillation associated with regional cardiac sympathetic denervation? Output:
PubmedQA17298	[ { "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 impact of infliximab on the postoperative course of patients with IBD is under debate. The aim of this study was to evaluate the influence of infliximab on perioperative outcomes in patients undergoing elective laparoscopic resection for IBD. This study is a retrospective analysis of a prospectively collected, institutional review board-approved database. SETTING, PATIENTS, INTERVENTIONS: Patients undergoing laparoscopic resection on preoperative infliximab (infliximab group) were compared with patients who did not receive infliximab (noninfliximab group). The short-term and long-term morbidity and mortality rates were assessed. Elective laparoscopic resection for IBD was performed on 518 patients from January 2004 through June 2011; 142 patients were treated with infliximab preoperatively. Both groups had similar demographics, type and severity of IBD, comorbidities, and type of surgery. A significantly higher number of patients in the infliximab group had been on aggressive medical therapy to control symptoms of IBD during the month preceding surgery, including steroids (73.9 vs 58.8%, p = 0.002) and immunosuppressors (32.4 vs 20.5%, p = 0.006). Operative time and blood loss were similar (p = 0.50 and p = 0.34). Intraoperative complication rate was 2.1% in both groups. No significant differences were observed in terms of the conversion rate to laparotomy (6.3% vs 9.3%, p = 0.36), overall 30-day postoperative morbidity (p = 0.93), or mortality (p = 0.61). The rates of anastomotic leak (2.1% vs 1.3%, p = 0.81), infections (12% vs 11.2%, p = 0.92), and thrombotic complications (3.5% vs 5.6%, p = 0.46) were similar. Subgroup analyses confirmed similar rates of overall, infectious, and thrombotic complications regardless of whether patients had ulcerative colitis or Crohn's disease.\n Question: Does preoperative infliximab therapy increase morbidity and mortality after laparoscopic resection for inflammatory bowel disease?\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 impact of infliximab on the postoperative course of patients with IBD is under debate. The aim of this study was to evaluate the influence of infliximab on perioperative outcomes in patients undergoing elective laparoscopic resection for IBD. This study is a retrospective analysis of a prospectively collected, institutional review board-approved database. SETTING, PATIENTS, INTERVENTIONS: Patients undergoing laparoscopic resection on preoperative infliximab (infliximab group) were compared with patients who did not receive infliximab (noninfliximab group). The short-term and long-term morbidity and mortality rates were assessed. Elective laparoscopic resection for IBD was performed on 518 patients from January 2004 through June 2011; 142 patients were treated with infliximab preoperatively. Both groups had similar demographics, type and severity of IBD, comorbidities, and type of surgery. A significantly higher number of patients in the infliximab group had been on aggressive medical therapy to control symptoms of IBD during the month preceding surgery, including steroids (73.9 vs 58.8%, p = 0.002) and immunosuppressors (32.4 vs 20.5%, p = 0.006). Operative time and blood loss were similar (p = 0.50 and p = 0.34). Intraoperative complication rate was 2.1% in both groups. No significant differences were observed in terms of the conversion rate to laparotomy (6.3% vs 9.3%, p = 0.36), overall 30-day postoperative morbidity (p = 0.93), or mortality (p = 0.61). The rates of anastomotic leak (2.1% vs 1.3%, p = 0.81), infections (12% vs 11.2%, p = 0.92), and thrombotic complications (3.5% vs 5.6%, p = 0.46) were similar. Subgroup analyses confirmed similar rates of overall, infectious, and thrombotic complications regardless of whether patients had ulcerative colitis or Crohn's disease. Question: Does preoperative infliximab therapy increase morbidity and mortality after laparoscopic resection for inflammatory bowel disease? Output:
PubmedQA445	[ { "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 failing heart displays increased glycolytic flux that is not matched by a commensurate increase in glucose oxidation. This mismatch induces increased anaplerotic flux and inefficient glucose metabolism. We previously found adult transgenic mouse hearts expressing the fetal troponin I isoform, (ssTnI) to be protected from ischemia by increased glycolysis. In this study, we investigated the metabolic response of adult mouse hearts expressing ssTnI to chronic pressure overload. At 2 to 3 months of age, ssTnI mice or their nontransgenic littermates underwent aortic constriction (TAC). TAC induced a 25% increase in nontransgenic heart size but only a 7% increase in ssTnI hearts (P<0.05). Nontransgenic TAC developed diastolic dysfunction (65% increase in E/A ratio), whereas the E/A ratio actually decreased in ssTnI TAC. Isolated perfused hearts from nontransgenic TAC mice showed reduced cardiac function and reduced creatine phosphate:ATP (16% reduction), but ssTnI TAC hearts maintained cardiac function and energy charge. Contrasting nontransgenic TAC, ssTnI TAC significantly increased glucose oxidation at the expense of palmitate oxidation, preventing the increase in anaplerosis observed in nontransgenic TAC hearts. Elevated glucose oxidation was mediated by a reduction in pyruvate dehydrogenase kinase 4 expression, enabling pyruvate dehydrogenase to compete against anaplerotic enzymes for pyruvate carboxylation.\n Question: Does metabolic efficiency promote protection from pressure overload in hearts expressing slow skeletal troponin I?\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 failing heart displays increased glycolytic flux that is not matched by a commensurate increase in glucose oxidation. This mismatch induces increased anaplerotic flux and inefficient glucose metabolism. We previously found adult transgenic mouse hearts expressing the fetal troponin I isoform, (ssTnI) to be protected from ischemia by increased glycolysis. In this study, we investigated the metabolic response of adult mouse hearts expressing ssTnI to chronic pressure overload. At 2 to 3 months of age, ssTnI mice or their nontransgenic littermates underwent aortic constriction (TAC). TAC induced a 25% increase in nontransgenic heart size but only a 7% increase in ssTnI hearts (P<0.05). Nontransgenic TAC developed diastolic dysfunction (65% increase in E/A ratio), whereas the E/A ratio actually decreased in ssTnI TAC. Isolated perfused hearts from nontransgenic TAC mice showed reduced cardiac function and reduced creatine phosphate:ATP (16% reduction), but ssTnI TAC hearts maintained cardiac function and energy charge. Contrasting nontransgenic TAC, ssTnI TAC significantly increased glucose oxidation at the expense of palmitate oxidation, preventing the increase in anaplerosis observed in nontransgenic TAC hearts. Elevated glucose oxidation was mediated by a reduction in pyruvate dehydrogenase kinase 4 expression, enabling pyruvate dehydrogenase to compete against anaplerotic enzymes for pyruvate carboxylation. Question: Does metabolic efficiency promote protection from pressure overload in hearts expressing slow skeletal troponin I? Output:
PubmedQA76164	[ { "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 kidney transplanted children, it is difficult to obtain blood levels of mycophenolic acid between 2 and 4 microg/mL, when mycophenolate mofetil doses up to 30 mg/kg/d are given two or three times a day. We proposed that using mycophenolic acid, instead of the salt mycophenolate mofetil, may help us to reach target levels. We sought to describe the pharmacokinetics of mycophenolic acid in eight kidney transplanted children over a period of 1.2 +/- 0.8 years. Eight patients (5 boys and 3 girls) aged 7.0 +/- 1.8 years received cadaveric kidney transplantations. Induction with basiliximab was followed by cyclosporine (n = 4) or tacrolimus (n = 4), tapered steroids (withdrawal at 12 months in six cases and maintained at 0.15 mg/kg/d in two cases), and mycophenolate mofetil (25 to 30 mg/kg/d two or three times a day). For 1.0 +/- 0.3 years mycophenolic acid levels were between 0.8 +/- 0.3 microg/mL. When mycophenolic acid sodium tablets were available, all patients were switched to this drug. After the conversion, blood levels obtained at 8 +/- 3 days were 1.5 to 5.0 microg/mL (median, 3.2), which were far closer to the target 2 to 4 microg/mL. No gastrointestinal disorders were observed with the follow-up of 72 +/- 18 days.\n Question: Does mycophenolic Acid reach therapeutic levels whereas mycophenolate mofetil does not?\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 kidney transplanted children, it is difficult to obtain blood levels of mycophenolic acid between 2 and 4 microg/mL, when mycophenolate mofetil doses up to 30 mg/kg/d are given two or three times a day. We proposed that using mycophenolic acid, instead of the salt mycophenolate mofetil, may help us to reach target levels. We sought to describe the pharmacokinetics of mycophenolic acid in eight kidney transplanted children over a period of 1.2 +/- 0.8 years. Eight patients (5 boys and 3 girls) aged 7.0 +/- 1.8 years received cadaveric kidney transplantations. Induction with basiliximab was followed by cyclosporine (n = 4) or tacrolimus (n = 4), tapered steroids (withdrawal at 12 months in six cases and maintained at 0.15 mg/kg/d in two cases), and mycophenolate mofetil (25 to 30 mg/kg/d two or three times a day). For 1.0 +/- 0.3 years mycophenolic acid levels were between 0.8 +/- 0.3 microg/mL. When mycophenolic acid sodium tablets were available, all patients were switched to this drug. After the conversion, blood levels obtained at 8 +/- 3 days were 1.5 to 5.0 microg/mL (median, 3.2), which were far closer to the target 2 to 4 microg/mL. No gastrointestinal disorders were observed with the follow-up of 72 +/- 18 days. Question: Does mycophenolic Acid reach therapeutic levels whereas mycophenolate mofetil does not? Output:
PubmedQA80004	[ { "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: Limited evidence exists about the usefulness of ethanol or acetone application to desiccate caries lesions before resin infiltration. Therefore, this in vitro study aimed to compare the penetration depths (PD) of an infiltrant (DMG, Germany) into natural caries lesions using various pretreatments. Extracted permanent human molars and premolars showing non-cavitated caries lesions were etched (90 s, 15 % HCl gel) and stored in pooled saliva (7 days). Lesions were etched again (30 s, 15 % HCl gel), washed (30 s), air-dried (30 s), and randomly allocated to one of the pretreatments: none (negative control), air-drying (incubator, 37 °C, 24 h; positive control), once ethanol (E1), twice ethanol (E2), once acetone (A1), and twice acetone (A2). Subsequently, the infiltrant was applied for 5 min and light-cured. Ground sections were prepared for analyses of lesion depths (LD) and PD using confocal microscopy. Median LD (Q25/Q75) of all lesions (n = 91) and lesions ≥500 μm (n = 57) were 629 (395/798) and 731 (638/876) μm, respectively. When all lesions were analyzed, no significant differences between various pretreatments could be observed (p > 0.05, Kruskal-Wallis). For lesions ≥500 μm, significantly deeper PP was observed in groups PC, E1, A1, and A2 compared with NC (p < 0.05; Mann-Whitney), but not after adjustment for multiple comparison (p > 0.05).\n Question: Does pretreatment of natural caries lesions affect penetration depth of infiltrants in vitro?\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: Limited evidence exists about the usefulness of ethanol or acetone application to desiccate caries lesions before resin infiltration. Therefore, this in vitro study aimed to compare the penetration depths (PD) of an infiltrant (DMG, Germany) into natural caries lesions using various pretreatments. Extracted permanent human molars and premolars showing non-cavitated caries lesions were etched (90 s, 15 % HCl gel) and stored in pooled saliva (7 days). Lesions were etched again (30 s, 15 % HCl gel), washed (30 s), air-dried (30 s), and randomly allocated to one of the pretreatments: none (negative control), air-drying (incubator, 37 °C, 24 h; positive control), once ethanol (E1), twice ethanol (E2), once acetone (A1), and twice acetone (A2). Subsequently, the infiltrant was applied for 5 min and light-cured. Ground sections were prepared for analyses of lesion depths (LD) and PD using confocal microscopy. Median LD (Q25/Q75) of all lesions (n = 91) and lesions ≥500 μm (n = 57) were 629 (395/798) and 731 (638/876) μm, respectively. When all lesions were analyzed, no significant differences between various pretreatments could be observed (p > 0.05, Kruskal-Wallis). For lesions ≥500 μm, significantly deeper PP was observed in groups PC, E1, A1, and A2 compared with NC (p < 0.05; Mann-Whitney), but not after adjustment for multiple comparison (p > 0.05). Question: Does pretreatment of natural caries lesions affect penetration depth of infiltrants in vitro? Output:
PubmedQA122125	[ { "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 study examined visual and verbal learning in the early phase of recovery for 48 Veterans with alcohol use (AUD) and substance use disorders (SUD, primarily cocaine and opiate abusers). Previous studies have demonstrated visual and verbal learning deficits in AUD, however little is known about the differences between AUD and SUD on these domains. Since the DSM-5 specifically identifies problems with learning in AUD and not in SUD, and problems with visual and verbal learning have been more prevalent in the literature for AUD than SUD, we predicted that people with AUD would be more impaired on measures of visual and verbal learning than people with SUD. Participants were enrolled in a comprehensive rehabilitation program and were assessed within the first 5 weeks of abstinence. Verbal learning was measured using the Hopkins Verbal Learning Test (HVLT) and visual learning was assessed using the Brief Visuospatial Memory Test (BVMT). Results indicated significantly greater decline in verbal learning on the HVLT across the three learning trials for AUD participants but not for SUD participants (F=4.653, df=48, p=0.036). Visual learning was less impaired than verbal learning across learning trials for both diagnostic groups (F=0.197, df=48, p=0.674); there was no significant difference between groups on visual learning (F=0.401, df=14, p=0.538).\n Question: Do visual and verbal learning deficits in Veterans with alcohol and substance use disorders?\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 study examined visual and verbal learning in the early phase of recovery for 48 Veterans with alcohol use (AUD) and substance use disorders (SUD, primarily cocaine and opiate abusers). Previous studies have demonstrated visual and verbal learning deficits in AUD, however little is known about the differences between AUD and SUD on these domains. Since the DSM-5 specifically identifies problems with learning in AUD and not in SUD, and problems with visual and verbal learning have been more prevalent in the literature for AUD than SUD, we predicted that people with AUD would be more impaired on measures of visual and verbal learning than people with SUD. Participants were enrolled in a comprehensive rehabilitation program and were assessed within the first 5 weeks of abstinence. Verbal learning was measured using the Hopkins Verbal Learning Test (HVLT) and visual learning was assessed using the Brief Visuospatial Memory Test (BVMT). Results indicated significantly greater decline in verbal learning on the HVLT across the three learning trials for AUD participants but not for SUD participants (F=4.653, df=48, p=0.036). Visual learning was less impaired than verbal learning across learning trials for both diagnostic groups (F=0.197, df=48, p=0.674); there was no significant difference between groups on visual learning (F=0.401, df=14, p=0.538). Question: Do visual and verbal learning deficits in Veterans with alcohol and substance use disorders? Output:
PubmedQA11568	[ { "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 identify specific transcription factors that are activated in the cartilage tissue of osteoarthritis (OA) patients and are involved in the expression of matrix metalloproteinase 1 (MMP-1). DNase I footprint and electrophoretic mobility shift assays were performed to identify active elements of the MMP1 promoter and the transcription factors that interact with it. The relative abundance of the involved transcription factor in the cartilage was determined by immunohistochemical analysis. The role of serum amyloid A-activating factor 1 (SAF-1) in MMP-1 expression was assessed by transient transfection assay with plasmids containing either a functional or an antisense SAF-1 complementary DNA. A novel promoter element was detected in the human MMP1 gene, and the inflammation-responsive transcription factor SAF-1 was found to interact with it. SAF-1 activity was detected in the chondrocytes of OA cartilage, where most of the cells stained positive for SAF-1. Overexpression of SAF-1 in OA chondrocytes increased the expression of the MMP1 promoter, and interference of endogenous SAF-1 activity by antisense SAF-1 messenger RNA inhibited interleukin-1-mediated MMP1 promoter activity.\n Question: Is induction of matrix metalloproteinase 1 gene expression regulated by inflammation-responsive transcription factor SAF-1 in osteoarthritis?\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 identify specific transcription factors that are activated in the cartilage tissue of osteoarthritis (OA) patients and are involved in the expression of matrix metalloproteinase 1 (MMP-1). DNase I footprint and electrophoretic mobility shift assays were performed to identify active elements of the MMP1 promoter and the transcription factors that interact with it. The relative abundance of the involved transcription factor in the cartilage was determined by immunohistochemical analysis. The role of serum amyloid A-activating factor 1 (SAF-1) in MMP-1 expression was assessed by transient transfection assay with plasmids containing either a functional or an antisense SAF-1 complementary DNA. A novel promoter element was detected in the human MMP1 gene, and the inflammation-responsive transcription factor SAF-1 was found to interact with it. SAF-1 activity was detected in the chondrocytes of OA cartilage, where most of the cells stained positive for SAF-1. Overexpression of SAF-1 in OA chondrocytes increased the expression of the MMP1 promoter, and interference of endogenous SAF-1 activity by antisense SAF-1 messenger RNA inhibited interleukin-1-mediated MMP1 promoter activity. Question: Is induction of matrix metalloproteinase 1 gene expression regulated by inflammation-responsive transcription factor SAF-1 in osteoarthritis? Output:
PubmedQA70037	[ { "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: Valve development is a multistep process involving the activation of the cardiac endothelium, epithelial-mesenchymal transition (EMT) and the progressive alignment and differentiation of distinct mesenchymal cell types. Several pathways such as Notch/delta, Tgf-beta and/or Vegf signaling have been implicated in crucial steps of valvulogenesis. We have previously demonstrated discrete changes in microRNAs expression during cardiogenesis, which are predicted to target Bmp- and Tgf-beta signaling. We now analyzed the expression profile of 20 candidate microRNAs in atrial, ventricular, and atrioventricular canal regions at four different developmental stages. qRT-PCR analyses of microRNAs demonstrated a highly dynamic and distinct expression profiles within the atrial, ventricular, and atrioventricular canal regions of the developing chick heart. miR-23b, miR-199a, and miR-15a displayed increased expression during early AVC development whereas others such as miR-130a and miR-200a display decreased expression levels. Functional analyses of miR-23b, miR-199a, and miR-15a overexpression led to in vitro EMT blockage. Molecular analyses demonstrate that distinct EMT signaling pathways are impaired after microRNA expression, including a large subset of EMT-related genes that are predicted to be targeted by these microRNAs.\n Question: Do miR-23b and miR-199a impair epithelial-to-mesenchymal transition during atrioventricular endocardial cushion formation?\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: Valve development is a multistep process involving the activation of the cardiac endothelium, epithelial-mesenchymal transition (EMT) and the progressive alignment and differentiation of distinct mesenchymal cell types. Several pathways such as Notch/delta, Tgf-beta and/or Vegf signaling have been implicated in crucial steps of valvulogenesis. We have previously demonstrated discrete changes in microRNAs expression during cardiogenesis, which are predicted to target Bmp- and Tgf-beta signaling. We now analyzed the expression profile of 20 candidate microRNAs in atrial, ventricular, and atrioventricular canal regions at four different developmental stages. qRT-PCR analyses of microRNAs demonstrated a highly dynamic and distinct expression profiles within the atrial, ventricular, and atrioventricular canal regions of the developing chick heart. miR-23b, miR-199a, and miR-15a displayed increased expression during early AVC development whereas others such as miR-130a and miR-200a display decreased expression levels. Functional analyses of miR-23b, miR-199a, and miR-15a overexpression led to in vitro EMT blockage. Molecular analyses demonstrate that distinct EMT signaling pathways are impaired after microRNA expression, including a large subset of EMT-related genes that are predicted to be targeted by these microRNAs. Question: Do miR-23b and miR-199a impair epithelial-to-mesenchymal transition during atrioventricular endocardial cushion formation? Output:
PubmedQA63306	[ { "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: A plant investing in reproduction partitions resources between flowering and seed production. Under resource limitation, altered allocations may result in floral trait variations, leading to compromised fecundity. Floral longevity and timing of selfing are often the traits most likely to be affected. The duration of corolla retention determines whether fecundity results from outcrossing or by delayed selfing-mediated reproductive assurance. In this study, the role of pollination schedules and soil water availability on floral longevity and seed production is tested in Collinsia heterophylla (Plantaginaceae). Using three different watering regimes and pollination schedules, effects on floral longevity and seed production were studied in this protandrous, flowering annual. The results reveal that soil water status and pollination together influence floral longevity with low soil water and hand-pollinations early in the floral lifespan reducing longevity. However, early pollinations under excess water did not extend longevity, implying that resource surplus does not lengthen the outcrossing period. The results also indicate that pollen receipt, a reliable cue for fecundity, accelerates flower drop. Early corolla abscission under drought stress could potentially exacerbate sexual conflict in this protandrous, hermaphroditic species by ensuring self-pollen paternity and enabling male control of floral longevity. While pollination schedules did not affect fecundity, water stress reduced per-capita seed numbers. Unmanipulated flowers underwent delayed autonomous selfing, producing very few seeds, suggesting that inbreeding depression may limit benefits of selfing.\n Question: Are floral longevity and autonomous selfing altered by pollination and water availability in Collinsia heterophylla?\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: A plant investing in reproduction partitions resources between flowering and seed production. Under resource limitation, altered allocations may result in floral trait variations, leading to compromised fecundity. Floral longevity and timing of selfing are often the traits most likely to be affected. The duration of corolla retention determines whether fecundity results from outcrossing or by delayed selfing-mediated reproductive assurance. In this study, the role of pollination schedules and soil water availability on floral longevity and seed production is tested in Collinsia heterophylla (Plantaginaceae). Using three different watering regimes and pollination schedules, effects on floral longevity and seed production were studied in this protandrous, flowering annual. The results reveal that soil water status and pollination together influence floral longevity with low soil water and hand-pollinations early in the floral lifespan reducing longevity. However, early pollinations under excess water did not extend longevity, implying that resource surplus does not lengthen the outcrossing period. The results also indicate that pollen receipt, a reliable cue for fecundity, accelerates flower drop. Early corolla abscission under drought stress could potentially exacerbate sexual conflict in this protandrous, hermaphroditic species by ensuring self-pollen paternity and enabling male control of floral longevity. While pollination schedules did not affect fecundity, water stress reduced per-capita seed numbers. Unmanipulated flowers underwent delayed autonomous selfing, producing very few seeds, suggesting that inbreeding depression may limit benefits of selfing. Question: Are floral longevity and autonomous selfing altered by pollination and water availability in Collinsia heterophylla? Output:
PubmedQA126356	[ { "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 Arabidopsis thaliana dgat1 mutant, AS11, has an oil content which is decreased by 30%, and a strongly increased ratio of 18:3/20:1, compared to wild type. Despite lacking a functional DGAT1, AS11 still manages to make 70% of WT seed oil levels. Recently, it was demonstrated that in the absence of DGAT1, PDAT1 was essential for normal seed development, and is a dominant determinant in Arabidopsis TAG biosynthesis. Biochemical, metabolic and gene expression studies combined with genetic crossing of selected Arabidopsis mutants have been carried out to demonstrate the contribution of Arabidopsis PDAT1 and LPCAT2 in the absence of DGAT1 activity. Through microarray and RT-PCR gene expression analyses of AS11 vs. WT mid-developing siliques, we observed consistent trends between the two methods. FAD2 and FAD3 were up-regulated and FAE1 down-regulated, consistent with the AS11 acyl phenotype. PDAT1 expression was up-regulated by ca 65% while PDAT2 expression was up-regulated only 15%, reinforcing the dominant role of PDAT1 in AS11 TAG biosynthesis. The expression of LPCAT2 was up-regulated by 50-75%, while LPCAT1 expression was not significantly affected. In vitro LPCAT activity was enhanced by 75-125% in microsomal protein preparations from mid-developing AS11 seed vs WT. Co-incident homozygous knockout lines of dgat1/lpcat2 exhibited severe penalties on TAG biosynthesis, delayed plant development and seed set, even with a functional PDAT1; the double mutant dgat1/lpcat1 showed only marginally lower oil content than AS11.\n Question: Is triacylglycerol synthesis by PDAT1 in the absence of DGAT1 activity dependent on re-acylation of LPC by LPCAT2?\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 Arabidopsis thaliana dgat1 mutant, AS11, has an oil content which is decreased by 30%, and a strongly increased ratio of 18:3/20:1, compared to wild type. Despite lacking a functional DGAT1, AS11 still manages to make 70% of WT seed oil levels. Recently, it was demonstrated that in the absence of DGAT1, PDAT1 was essential for normal seed development, and is a dominant determinant in Arabidopsis TAG biosynthesis. Biochemical, metabolic and gene expression studies combined with genetic crossing of selected Arabidopsis mutants have been carried out to demonstrate the contribution of Arabidopsis PDAT1 and LPCAT2 in the absence of DGAT1 activity. Through microarray and RT-PCR gene expression analyses of AS11 vs. WT mid-developing siliques, we observed consistent trends between the two methods. FAD2 and FAD3 were up-regulated and FAE1 down-regulated, consistent with the AS11 acyl phenotype. PDAT1 expression was up-regulated by ca 65% while PDAT2 expression was up-regulated only 15%, reinforcing the dominant role of PDAT1 in AS11 TAG biosynthesis. The expression of LPCAT2 was up-regulated by 50-75%, while LPCAT1 expression was not significantly affected. In vitro LPCAT activity was enhanced by 75-125% in microsomal protein preparations from mid-developing AS11 seed vs WT. Co-incident homozygous knockout lines of dgat1/lpcat2 exhibited severe penalties on TAG biosynthesis, delayed plant development and seed set, even with a functional PDAT1; the double mutant dgat1/lpcat1 showed only marginally lower oil content than AS11. Question: Is triacylglycerol synthesis by PDAT1 in the absence of DGAT1 activity dependent on re-acylation of LPC by LPCAT2? Output:
PubmedQA88144	[ { "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: Resolution of the link between micro- and macroevolution calls for comparing both processes on the same deterministic landscape, such as genomic, metabolic or fitness networks. We apply this perspective to the evolution of carotenoid pigmentation that produces spectacular diversity in avian colors and show that basic structural properties of the underlying carotenoid metabolic network are reflected in global patterns of elaboration and diversification in color displays. Birds color themselves by consuming and metabolizing several dietary carotenoids from the environment. Such fundamental dependency on the most upstream external compounds should intrinsically constrain sustained evolutionary elongation of multi-step metabolic pathways needed for color elaboration unless the metabolic network gains robustness - the ability to synthesize the same carotenoid from an additional dietary starting point. We found that gains and losses of metabolic robustness were associated with evolutionary cycles of elaboration and stasis in expressed carotenoids in birds. Lack of metabolic robustness constrained lineage's metabolic explorations to the immediate biochemical vicinity of their ecologically distinct dietary carotenoids, whereas gains of robustness repeatedly resulted in sustained elongation of metabolic pathways on evolutionary time scales and corresponding color elaboration.\n Question: Does tradeoff between robustness and elaboration in carotenoid networks produce cycles of avian color diversification?\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: Resolution of the link between micro- and macroevolution calls for comparing both processes on the same deterministic landscape, such as genomic, metabolic or fitness networks. We apply this perspective to the evolution of carotenoid pigmentation that produces spectacular diversity in avian colors and show that basic structural properties of the underlying carotenoid metabolic network are reflected in global patterns of elaboration and diversification in color displays. Birds color themselves by consuming and metabolizing several dietary carotenoids from the environment. Such fundamental dependency on the most upstream external compounds should intrinsically constrain sustained evolutionary elongation of multi-step metabolic pathways needed for color elaboration unless the metabolic network gains robustness - the ability to synthesize the same carotenoid from an additional dietary starting point. We found that gains and losses of metabolic robustness were associated with evolutionary cycles of elaboration and stasis in expressed carotenoids in birds. Lack of metabolic robustness constrained lineage's metabolic explorations to the immediate biochemical vicinity of their ecologically distinct dietary carotenoids, whereas gains of robustness repeatedly resulted in sustained elongation of metabolic pathways on evolutionary time scales and corresponding color elaboration. Question: Does tradeoff between robustness and elaboration in carotenoid networks produce cycles of avian color diversification? Output:
PubmedQA121761	[ { "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 renal function predicts the development of cardiovascular disease and other arterial vascular events in patients with SLE. An inception cohort of 437 females was studied. Baseline estimated glomerular filtration rate (eGFR) was calculated using serum creatinine and the abbreviated Modification of Diet in Renal Disease Study Group formula. Arterial events including myocardial infarction, angina, transient ischaemic attacks, cerebral vascular accidents and other arterial events were documented at up to 15 years since the first visit. Disease activity was determined using SLEDAI. Patients were classified into those with or without arterial events and further into events that occurred within or after 3 years since the first visit (events <3 years, events ≥3 years). The association between eGFR and risks of arterial events was investigated using the Cox proportional hazards model. There was a total of 58 arterial events of which 51.9% were events ≥ 3 years. Patients with arterial events had a significantly lower baseline eGFR and were significantly older than those without arterial events. Furthermore, baseline eGFR was significantly lower in events <3 years compared with events ≥ 3 years. Baseline eGFR, age and baseline SLEDAI were significantly associated with the risks of arterial events [eGFR: hazard ratio (HR) = 0.986; age: HR = 1.032; SLEDAI: HR = 1.041].\n Question: Does glomerular filtration rate predict arterial events in women 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 determine whether renal function predicts the development of cardiovascular disease and other arterial vascular events in patients with SLE. An inception cohort of 437 females was studied. Baseline estimated glomerular filtration rate (eGFR) was calculated using serum creatinine and the abbreviated Modification of Diet in Renal Disease Study Group formula. Arterial events including myocardial infarction, angina, transient ischaemic attacks, cerebral vascular accidents and other arterial events were documented at up to 15 years since the first visit. Disease activity was determined using SLEDAI. Patients were classified into those with or without arterial events and further into events that occurred within or after 3 years since the first visit (events <3 years, events ≥3 years). The association between eGFR and risks of arterial events was investigated using the Cox proportional hazards model. There was a total of 58 arterial events of which 51.9% were events ≥ 3 years. Patients with arterial events had a significantly lower baseline eGFR and were significantly older than those without arterial events. Furthermore, baseline eGFR was significantly lower in events <3 years compared with events ≥ 3 years. Baseline eGFR, age and baseline SLEDAI were significantly associated with the risks of arterial events [eGFR: hazard ratio (HR) = 0.986; age: HR = 1.032; SLEDAI: HR = 1.041]. Question: Does glomerular filtration rate predict arterial events in women with systemic lupus erythematosus? Output:
PubmedQA186197	[ { "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: Studies have shown the existence of p21 induction in a p53-dependent and -independent pathway. Our previous study indicates that DOX-induced p65 is able to bind the p21 promoter to activate its transactivation in the cells. Over-expression and knock-down experiments were performed in Human Pancreatic Carcinoma (PANC1) cells. Cell cycle and cell death related proteins were assessed by Western Blotting. Cytotoxicity assay was checked by CCK-8 kit. Cell growth was analyzed by flow cytometers. Here we showed that over-expression of p65 decreased the cytotoxic effect of DOX on PANC1 cells, correlating with increased induction of cytoplasmic p21. We observed that pro-caspase-3 physically associated with cytoplasmic p21, which may be contribution to prevent p21 translocation into the nucleus. Our data also suggested that no clear elevation of nuclear p21 by p65 provides a survival advantage by progression cell cycle after treatment of DOX. Likewise, down-regulation of p65 expression enhanced the cytotoxic effect of DOX, due to a significant decrease of mRNA levels of anti-apoptotic genes, such as the cellular inhibitor of apoptosis-1 (c-IAP1), and the long isoform of B cell leukemia/lymphoma-2 (Bcl-2), leading to efficient induction of caspase-3 cleavage in the cells. More, we present evidence that over-expression of p53 or p53/p65 in the PANC1 cells were more sensitive to DOX treatment, correlated with activation of caspase-3 and clear elevation of nuclear p21 level. Our previous data suggested that expression of p21 increases Gefitinib-induced cell death by blocking the cell cycle at the G1 and G2 phases. The present findings here reinforced this idea by showing p21's ability of potentiality of DOX-induced cell death correlated with its inhibition of cell cycle progression after over-expression of p53 or p53/p65.\n Question: Does cytoplasmic p21 induced by p65 prevent doxorubicin-induced cell death in pancreatic carcinoma 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: Studies have shown the existence of p21 induction in a p53-dependent and -independent pathway. Our previous study indicates that DOX-induced p65 is able to bind the p21 promoter to activate its transactivation in the cells. Over-expression and knock-down experiments were performed in Human Pancreatic Carcinoma (PANC1) cells. Cell cycle and cell death related proteins were assessed by Western Blotting. Cytotoxicity assay was checked by CCK-8 kit. Cell growth was analyzed by flow cytometers. Here we showed that over-expression of p65 decreased the cytotoxic effect of DOX on PANC1 cells, correlating with increased induction of cytoplasmic p21. We observed that pro-caspase-3 physically associated with cytoplasmic p21, which may be contribution to prevent p21 translocation into the nucleus. Our data also suggested that no clear elevation of nuclear p21 by p65 provides a survival advantage by progression cell cycle after treatment of DOX. Likewise, down-regulation of p65 expression enhanced the cytotoxic effect of DOX, due to a significant decrease of mRNA levels of anti-apoptotic genes, such as the cellular inhibitor of apoptosis-1 (c-IAP1), and the long isoform of B cell leukemia/lymphoma-2 (Bcl-2), leading to efficient induction of caspase-3 cleavage in the cells. More, we present evidence that over-expression of p53 or p53/p65 in the PANC1 cells were more sensitive to DOX treatment, correlated with activation of caspase-3 and clear elevation of nuclear p21 level. Our previous data suggested that expression of p21 increases Gefitinib-induced cell death by blocking the cell cycle at the G1 and G2 phases. The present findings here reinforced this idea by showing p21's ability of potentiality of DOX-induced cell death correlated with its inhibition of cell cycle progression after over-expression of p53 or p53/p65. Question: Does cytoplasmic p21 induced by p65 prevent doxorubicin-induced cell death in pancreatic carcinoma cell line? Output:
PubmedQA23545	[ { "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: Distinguishing types of lymphocytic scarring alopecia is often difficult because of the overlapping features. Recently, the presence of plasmacytoid dendritic cells (PDCs) in cutaneous lupus erythematosus (LE) was demonstrated and further shown to help distinguish lupus from other dermatoses.1-6 This study aims to determine if the presence and distribution of PDCs can aid in the diagnosis of scarring alopecia. Cases of scarring alopecia due to chronic cutaneous lupus erythematosus (CCLE), lichen planopilaris (LPP) and central centrifugal cicatricial alopecia (CCCA) were examined histopathologically. A total of 45 total biopsies were evaluated and CD123 immunohistochemistry was performed on all samples. The relative percentage of PDCs, the presence of clusters and the distribution of CD123+ cells were noted. PDCs comprised a greater percentage of the infiltrate and were arranged in clusters in cases of CCLE vs. LPP or CCCA. In CCLE, the location of PDCs was perivascular, perifollicular, perieccrine and/or at the follicular junction. In LPP and CCCA, PDCs were mainly arranged as single, interstitial cells.\n Question: Is cD123 immunohistochemistry for plasmacytoid dendritic cells useful in the diagnosis of scarring alopecia?\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: Distinguishing types of lymphocytic scarring alopecia is often difficult because of the overlapping features. Recently, the presence of plasmacytoid dendritic cells (PDCs) in cutaneous lupus erythematosus (LE) was demonstrated and further shown to help distinguish lupus from other dermatoses.1-6 This study aims to determine if the presence and distribution of PDCs can aid in the diagnosis of scarring alopecia. Cases of scarring alopecia due to chronic cutaneous lupus erythematosus (CCLE), lichen planopilaris (LPP) and central centrifugal cicatricial alopecia (CCCA) were examined histopathologically. A total of 45 total biopsies were evaluated and CD123 immunohistochemistry was performed on all samples. The relative percentage of PDCs, the presence of clusters and the distribution of CD123+ cells were noted. PDCs comprised a greater percentage of the infiltrate and were arranged in clusters in cases of CCLE vs. LPP or CCCA. In CCLE, the location of PDCs was perivascular, perifollicular, perieccrine and/or at the follicular junction. In LPP and CCCA, PDCs were mainly arranged as single, interstitial cells. Question: Is cD123 immunohistochemistry for plasmacytoid dendritic cells useful in the diagnosis of scarring alopecia? Output:
PubmedQA29172	[ { "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 our study was to investigate the epidemiology and resulting injuries following falls sustained by infants seated in a variety of seating devices. A retrospective chart review of a cohort of infants less than 12 months old who presented to our institution from 1991 to 2010 after a fall from various seating devices was performed. Two hundred five infants were identified, including 146 patients who were admitted to our institution (1991-2010) and 59 patients who were seen and discharged from the ED (2008-2010). Mean age of admitted infants was younger (3.5 vs. 5.3 months). Two patients (1%) required surgery for a depressed skull fracture. Overall, 18% had an intra-cranial hemorrhage. More patients requiring an admission secondary to their injuries fell from a table or counter (42% vs. 27%).\n Question: Does inappropriate use of infant seating devices increase risks of 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: The purpose of our study was to investigate the epidemiology and resulting injuries following falls sustained by infants seated in a variety of seating devices. A retrospective chart review of a cohort of infants less than 12 months old who presented to our institution from 1991 to 2010 after a fall from various seating devices was performed. Two hundred five infants were identified, including 146 patients who were admitted to our institution (1991-2010) and 59 patients who were seen and discharged from the ED (2008-2010). Mean age of admitted infants was younger (3.5 vs. 5.3 months). Two patients (1%) required surgery for a depressed skull fracture. Overall, 18% had an intra-cranial hemorrhage. More patients requiring an admission secondary to their injuries fell from a table or counter (42% vs. 27%). Question: Does inappropriate use of infant seating devices increase risks of injury? Output:
PubmedQA151730	[ { "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: Laser Doppler flowmetry (LDF) is a noninvasive method to assess pulpal blood-flow (PBF). Osteotomies may have segment-related losses of pulpal sensibility. To determine the effect of segmental Le Fort I osteotomy on tooth-type related PBF values. In 12 volunteers, maxillary incisors, canines, and premolars were investigated bilaterally by LDF to assess local PBF values before and after surgery. Perfusion units (PU) were in 3 sessions, on the day before surgery and at 4 and 56 days after osteotomy. Measurements before surgery were significantly higher than at 4 days after surgery for the canine (P <.01) and for the overall PBF values (P <.01). At 4 days assessment, PBF values of tooth types adjacent to vertical osteotomy cuts showed a significant decrease for the lateral incisors (P <.05), canines, and first premolars (P <.05), with no significant differences between the preoperative and postoperative values for tooth types not adjacent to vertical osteotomy cuts (P <.05).\n Question: Do effect of segmental Le Fort I osteotomy on maxillary tooth type-related pulpal blood-flow characteristics?\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: Laser Doppler flowmetry (LDF) is a noninvasive method to assess pulpal blood-flow (PBF). Osteotomies may have segment-related losses of pulpal sensibility. To determine the effect of segmental Le Fort I osteotomy on tooth-type related PBF values. In 12 volunteers, maxillary incisors, canines, and premolars were investigated bilaterally by LDF to assess local PBF values before and after surgery. Perfusion units (PU) were in 3 sessions, on the day before surgery and at 4 and 56 days after osteotomy. Measurements before surgery were significantly higher than at 4 days after surgery for the canine (P <.01) and for the overall PBF values (P <.01). At 4 days assessment, PBF values of tooth types adjacent to vertical osteotomy cuts showed a significant decrease for the lateral incisors (P <.05), canines, and first premolars (P <.05), with no significant differences between the preoperative and postoperative values for tooth types not adjacent to vertical osteotomy cuts (P <.05). Question: Do effect of segmental Le Fort I osteotomy on maxillary tooth type-related pulpal blood-flow characteristics? Output:
PubmedQA196528	[ { "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: Latent autoimmune diabetes in adults (LADA) is phenotypically a hybrid of type 1 and type 2 diabetes. Genetically LADA is poorly characterised but does share genetic predisposition with type 1 diabetes. We aimed to improve the genetic characterisation of LADA and hypothesised that type 2 diabetes-associated gene variants also predispose to LADA, and that the associations would be strongest in LADA patients with low levels of GAD autoantibodies (GADA). We assessed 41 type 2 diabetes-associated gene variants in Finnish (phase I) and Swedish (phase II) patients with LADA (n = 911) or type 1 diabetes (n = 406), all diagnosed after the age of 35 years, as well as in non-diabetic control individuals 40 years or older (n = 4,002). Variants in the ZMIZ1 (rs12571751, p = 4.1 × 10(-5)) and TCF7L2 (rs7903146, p = 5.8 × 10(-4)) loci were strongly associated with LADA. Variants in the KCNQ1 (rs2237895, p = 0.0012), HHEX (rs1111875, p = 0.0024 in Finns) and MTNR1B (rs10830963, p = 0.0039) loci showed the strongest association in patients with low GADA, supporting the hypothesis that the disease in these patients is more like type 2 diabetes. In contrast, variants in the KLHDC5 (rs10842994, p = 9.5 × 10(-4) in Finns), TP53INP1 (rs896854, p = 0.005), CDKAL1 (rs7756992, p = 7.0 × 10(-4); rs7754840, p = 8.8 × 10(-4)) and PROX1 (rs340874, p = 0.003) loci showed the strongest association in patients with high GADA. For type 1 diabetes, a strong association was seen for MTNR1B (rs10830963, p = 3.2 × 10(-6)) and HNF1A (rs2650000, p = 0.0012).\n Question: Do type 2 diabetes susceptibility gene variants predispose to adult-onset autoimmune 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: Latent autoimmune diabetes in adults (LADA) is phenotypically a hybrid of type 1 and type 2 diabetes. Genetically LADA is poorly characterised but does share genetic predisposition with type 1 diabetes. We aimed to improve the genetic characterisation of LADA and hypothesised that type 2 diabetes-associated gene variants also predispose to LADA, and that the associations would be strongest in LADA patients with low levels of GAD autoantibodies (GADA). We assessed 41 type 2 diabetes-associated gene variants in Finnish (phase I) and Swedish (phase II) patients with LADA (n = 911) or type 1 diabetes (n = 406), all diagnosed after the age of 35 years, as well as in non-diabetic control individuals 40 years or older (n = 4,002). Variants in the ZMIZ1 (rs12571751, p = 4.1 × 10(-5)) and TCF7L2 (rs7903146, p = 5.8 × 10(-4)) loci were strongly associated with LADA. Variants in the KCNQ1 (rs2237895, p = 0.0012), HHEX (rs1111875, p = 0.0024 in Finns) and MTNR1B (rs10830963, p = 0.0039) loci showed the strongest association in patients with low GADA, supporting the hypothesis that the disease in these patients is more like type 2 diabetes. In contrast, variants in the KLHDC5 (rs10842994, p = 9.5 × 10(-4) in Finns), TP53INP1 (rs896854, p = 0.005), CDKAL1 (rs7756992, p = 7.0 × 10(-4); rs7754840, p = 8.8 × 10(-4)) and PROX1 (rs340874, p = 0.003) loci showed the strongest association in patients with high GADA. For type 1 diabetes, a strong association was seen for MTNR1B (rs10830963, p = 3.2 × 10(-6)) and HNF1A (rs2650000, p = 0.0012). Question: Do type 2 diabetes susceptibility gene variants predispose to adult-onset autoimmune diabetes? Output:
PubmedQA160552	[ { "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: Asthma and tobacco exposure is common among pregnant women. We investigated the effect of passive and active smoking on asthma control during pregnancy. Prospective observational design. Patients had their asthma control, based on symptoms, use of medication, spirometry, and exhaled nitric oxide [FENO], assessed every four weeks during 2nd and 3rd trimester of pregnancy; data on tobacco exposure were also collected prospectively. The primary outcome was episodes of uncontrolled and partly controlled asthma during pregnancy (defined according to GINA-guidelines). A total of 500 pregnant women with asthma (mean age 30.8 years, range 17 to 44) were consecutively included, of whom 32 (6.4%), 115 (23.0%) and 353 (70.6%), respectively, were current smokers, ex-smokers and never smokers [NS]. Sixty-five NS (18.4%) reported passive tobacco exposure. NS with passive tobacco exposure had significantly lower FEV1% predicted (p<0.02) and FENO (p = 0.01) compared to NS without passive tobacco exposure. The relative risk [RR] of an episode of uncontrolled asthma during pregnancy was 4.5 (95% CI 2.7-7.5: p<0.001) in current and ex-smokers compared with never smokers, and 2.9 (95% CI 1.4-5.9; p = 0.004) in NS-women with passive tobacco exposure compared with NS-women not reporting passive tobacco exposure. Treatment with inhaled corticosteroids, most likely as a marker of more severe asthma, was also associated with a higher risk (RR 8.1, 95% CI 5.1-13.0; p<0.001) of an episode of uncontrolled asthma.\n Question: Is passive smoking associated with poor asthma control during pregnancy : a prospective study of 500 pregnancies?\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: Asthma and tobacco exposure is common among pregnant women. We investigated the effect of passive and active smoking on asthma control during pregnancy. Prospective observational design. Patients had their asthma control, based on symptoms, use of medication, spirometry, and exhaled nitric oxide [FENO], assessed every four weeks during 2nd and 3rd trimester of pregnancy; data on tobacco exposure were also collected prospectively. The primary outcome was episodes of uncontrolled and partly controlled asthma during pregnancy (defined according to GINA-guidelines). A total of 500 pregnant women with asthma (mean age 30.8 years, range 17 to 44) were consecutively included, of whom 32 (6.4%), 115 (23.0%) and 353 (70.6%), respectively, were current smokers, ex-smokers and never smokers [NS]. Sixty-five NS (18.4%) reported passive tobacco exposure. NS with passive tobacco exposure had significantly lower FEV1% predicted (p<0.02) and FENO (p = 0.01) compared to NS without passive tobacco exposure. The relative risk [RR] of an episode of uncontrolled asthma during pregnancy was 4.5 (95% CI 2.7-7.5: p<0.001) in current and ex-smokers compared with never smokers, and 2.9 (95% CI 1.4-5.9; p = 0.004) in NS-women with passive tobacco exposure compared with NS-women not reporting passive tobacco exposure. Treatment with inhaled corticosteroids, most likely as a marker of more severe asthma, was also associated with a higher risk (RR 8.1, 95% CI 5.1-13.0; p<0.001) of an episode of uncontrolled asthma. Question: Is passive smoking associated with poor asthma control during pregnancy : a prospective study of 500 pregnancies? Output:
PubmedQA148209	[ { "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 recently found that resting muscle sympathetic nerve activity is inversely related to peak oxygen uptake (VO(2) peak) in patients with heart failure, suggesting a peripheral neurogenic limit to exercise in heart failure. No such relationship was observed in healthy controls. To determine whether this observation is specific to sympathetic discharge to skeletal muscle, we tested the null hypothesis that VO(2) peak would not relate to resting cardiac noradrenaline spillover, which is also elevated in heart failure. We measured cardiac noradrenaline spillover at rest by a radiotracer technique and VO(2) peak, during cycle ergometry, by open circuit spirometry in 49 heart failure patients (mean age 54.4+/-1.4 (SE)). There was a significant relationship between age and peak VO(2) (P=0.022). There was no significant relationship between cardiac noradrenaline spillover and either absolute or relative VO(2) peak (P=0.136), with age included in a multiple linear regression model, and none between cardiac noradrenaline spillover and the percent predicted VO2) peak achieved (P=0.34).\n Question: Is peak oxygen uptake determined by cardiac noradrenaline spillover in heart failure?\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: We recently found that resting muscle sympathetic nerve activity is inversely related to peak oxygen uptake (VO(2) peak) in patients with heart failure, suggesting a peripheral neurogenic limit to exercise in heart failure. No such relationship was observed in healthy controls. To determine whether this observation is specific to sympathetic discharge to skeletal muscle, we tested the null hypothesis that VO(2) peak would not relate to resting cardiac noradrenaline spillover, which is also elevated in heart failure. We measured cardiac noradrenaline spillover at rest by a radiotracer technique and VO(2) peak, during cycle ergometry, by open circuit spirometry in 49 heart failure patients (mean age 54.4+/-1.4 (SE)). There was a significant relationship between age and peak VO(2) (P=0.022). There was no significant relationship between cardiac noradrenaline spillover and either absolute or relative VO(2) peak (P=0.136), with age included in a multiple linear regression model, and none between cardiac noradrenaline spillover and the percent predicted VO2) peak achieved (P=0.34). Question: Is peak oxygen uptake determined by cardiac noradrenaline spillover in heart failure? Output:
PubmedQA14277	[ { "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 increase in risk for cardiovascular complications in diabetic women is even greater than that in diabetic men. We found arterial stiffness to be increased in women, but not in men, with Type 1 diabetes mellitus (DM). The aims of the present study were to evaluate whether the changes in arterial distensibility are influenced by diabetes duration and to evaluate any association between autonomic neuropathy and decreased arterial distensibility. Stiffness of the abdominal aorta was measured noninvasively using echo-tracking sonography and parasympathetic function by heart rate variation during deep breathing (E/I ratio) in 40 women (mean age 33 years, range 20-61) and 38 men (mean age 36 years, range 22-56) with Type 1 DM. There was a significant correlation between aortic stiffness and duration of diabetes in women (r = 0.41, P = 0.008), but not in men (r = 0.15, P = 0.35). There was also a significant correlation between aortic stiffness and the E/I ratio in women (r = -0.49, P = 0.002), but not in men (r = -0.14, P = 0.41). When adjusted for diabetes duration, the significant association between the E/I ratio and aortic stiffness remained in diabetic women (r = -0.44, P = 0.008) and was stronger than the association between diabetes duration and aortic stiffness. There were no significant correlations between aortic stiffness and triglycerides or total cholesterol, respectively.\n Question: Is increased aortic stiffness in women with type 1 diabetes mellitus associated with diabetes duration and autonomic nerve function?\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 increase in risk for cardiovascular complications in diabetic women is even greater than that in diabetic men. We found arterial stiffness to be increased in women, but not in men, with Type 1 diabetes mellitus (DM). The aims of the present study were to evaluate whether the changes in arterial distensibility are influenced by diabetes duration and to evaluate any association between autonomic neuropathy and decreased arterial distensibility. Stiffness of the abdominal aorta was measured noninvasively using echo-tracking sonography and parasympathetic function by heart rate variation during deep breathing (E/I ratio) in 40 women (mean age 33 years, range 20-61) and 38 men (mean age 36 years, range 22-56) with Type 1 DM. There was a significant correlation between aortic stiffness and duration of diabetes in women (r = 0.41, P = 0.008), but not in men (r = 0.15, P = 0.35). There was also a significant correlation between aortic stiffness and the E/I ratio in women (r = -0.49, P = 0.002), but not in men (r = -0.14, P = 0.41). When adjusted for diabetes duration, the significant association between the E/I ratio and aortic stiffness remained in diabetic women (r = -0.44, P = 0.008) and was stronger than the association between diabetes duration and aortic stiffness. There were no significant correlations between aortic stiffness and triglycerides or total cholesterol, respectively. Question: Is increased aortic stiffness in women with type 1 diabetes mellitus associated with diabetes duration and autonomic nerve function? Output:
PubmedQA141548	[ { "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: Despite much work over past decades, whether antigen-specific immune reactions occur in rheumatoid arthritis (RA) and to what extent such reactions are directed towards joint-specific autoantigens is still questionable. One strong indicator for antigenic involvement in RA is the fact that certain major histocompatibility complex (MHC) class II genotypes [human leucocyte antigen (HLA)-DR4 and HLA-DR1[ predispose for the development of the disease [1]. In the present report, collagen type II (CII) was studied as a putative autoantigen on the basis of both clinical and experimental data that show an increased frequency of antibodies to CII in RA patients [2-4] and that show that CII can induce experimental arthritis [5]. It is evident from the literature that RA peripheral blood mononuclear cells (PBMCs) respond poorly to antigenic stimulation [6-8], and in particular evidence for a partial tolerization to CII has been presented [9]. The strategy of the present work has accordingly been to reinvestigate T-cell reactivity to CII in RA patients, to relate it to the response to commonly used recall antigens and to analyze interferon (IFN)-gamma responses as an alternative to proliferative responses. To study cellular immune reactivity to CII in patients with RA and in healthy control individuals and to correlate this reactivity to HLA class II genotypes and to the presence of antibodies to CII in serum. Forty-five patients who met the 1987 American college of Rheumatology classification criteria for RA [10] and 25 healthy control individuals of similar age and sex were included. Twenty-six of these patients who had low levels of anti-CII in serum were randomly chosen, whereas 19 patients with high anti-CII levels were identified by enzyme-linked immunosorbent assay (ELISA)-screening of 400 RA sera. Heparinized blood was density gradient separated and PBMCs were cultured at 1 x 10(6)/ml in RPMI-10% fetal calf serum with or without antigenic stimulation: native or denatured CII (100 microgram/ml), killed influenza virus (Vaxigrip, Pasteur Merieux, Lyon, France; diluted 1:1000) or purified protein derivative (PPD; 10 microgram/ml). CII was heat-denatured in 56 degrees C for 30 min. Cell supernatants were collected after 7 days and IFN-gamma contents were analyzed using ELISA. HLA-DR and HLA-DQ genotyping was performed utilizing a polymerase chain reaction-based technique with sequence-specific oligonucleotide probe hybridization. Nonparametric statistical analyses were utilized throughout the study. PBMCs from both RA patients and healthy control individuals responded with IFN-gamma production to the same degree to stimulation with native and denatured CII (Fig. 1a), giving median stimulation indexes with native CII of 4.6 for RA patients and 5.4 for health control individuals, and with denatured CII of 2.9 for RA patients and 2.6 for healthy control individuals. RA patients with elevated levels of anti-CII had a weaker IFN-gamma response to both native and denatured CII that did healthy control individuals (P-).02 and 0.04, respectively). Stimulation with the standard recall antigens PPD and killed influenza virus yielded a median stimulation index with PPD of 10.0 for RA patients and 51.3 for healthy control individuals and with influenza of 12.3 for RA patients and 25.7 for healthy, control individuals. The RA patients displayed markedly lower responsiveness to both PPD and killed influenza virus than did healthy control individuals (Fig. 1b). IFN-gamma responses to all antigens were abrogated when coincubating with antibodies blocking MHC class II. The low response to PPD and killed influenza virus in RA patients relative to that of healthy control individuals reflects a general downregulation of antigen-induced responsiveness of T cells from RA patients [6-8]. That no difference between the RA group and the control group was recorded CII-induced IFN-gamma production therefore indicates that there may be an underlying increased responsiveness to CII in RA patients, which is obscured by the general downregulation of T-cell responsiveness in these patients. In order to address this possibility, we calculated the fraction between individual values for the CII-induced IFN-gamma production and the PPD-induced and killed influenza virus-induced IFN-gamma production and the PPD-induced and killed influenza virus-induced IFN-gamma production, and compared these fractions. A highly significant difference between the RA and health control groups was apparent after stimulation with both native CII and denatured CII when expressing the response as a fraction of that with PPD (Fig. 2a). Similar data were obtained using killed influenza virus-stimulated IFN-gamma values as the denominator (Fig. 2b).When comparing the compensated IFN-gamma response to denatured CII stimulation between RA patients with different HLA genotypes, highly significant differences were evident, with HLA-DRB10401 patients having greater CII responsiveness than patients who lacked this genotype (Fig. 3a). HLA-DQ8 positive patients also displayed a high responsiveness to CII as compared with HLA-DQ8 negative RA patients (Fig. 3b). These associations between the relative T-cell reactivity to denatured CII and HLA class II genotypes were not seen in healthy control individuals. Similar results were achieved using influenza as denominator (P = 0.02 for HLA-DRB10401 and P = 0.01 for HLA-DQ8).\n Question: Is interferon-gamma production in response to in vitro stimulation with collagen type II in rheumatoid arthritis associated with HLA-DRB1 ( * ) 0401 and HLA-DQ8?\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: Despite much work over past decades, whether antigen-specific immune reactions occur in rheumatoid arthritis (RA) and to what extent such reactions are directed towards joint-specific autoantigens is still questionable. One strong indicator for antigenic involvement in RA is the fact that certain major histocompatibility complex (MHC) class II genotypes [human leucocyte antigen (HLA)-DR4 and HLA-DR1[ predispose for the development of the disease [1]. In the present report, collagen type II (CII) was studied as a putative autoantigen on the basis of both clinical and experimental data that show an increased frequency of antibodies to CII in RA patients [2-4] and that show that CII can induce experimental arthritis [5]. It is evident from the literature that RA peripheral blood mononuclear cells (PBMCs) respond poorly to antigenic stimulation [6-8], and in particular evidence for a partial tolerization to CII has been presented [9]. The strategy of the present work has accordingly been to reinvestigate T-cell reactivity to CII in RA patients, to relate it to the response to commonly used recall antigens and to analyze interferon (IFN)-gamma responses as an alternative to proliferative responses. To study cellular immune reactivity to CII in patients with RA and in healthy control individuals and to correlate this reactivity to HLA class II genotypes and to the presence of antibodies to CII in serum. Forty-five patients who met the 1987 American college of Rheumatology classification criteria for RA [10] and 25 healthy control individuals of similar age and sex were included. Twenty-six of these patients who had low levels of anti-CII in serum were randomly chosen, whereas 19 patients with high anti-CII levels were identified by enzyme-linked immunosorbent assay (ELISA)-screening of 400 RA sera. Heparinized blood was density gradient separated and PBMCs were cultured at 1 x 10(6)/ml in RPMI-10% fetal calf serum with or without antigenic stimulation: native or denatured CII (100 microgram/ml), killed influenza virus (Vaxigrip, Pasteur Merieux, Lyon, France; diluted 1:1000) or purified protein derivative (PPD; 10 microgram/ml). CII was heat-denatured in 56 degrees C for 30 min. Cell supernatants were collected after 7 days and IFN-gamma contents were analyzed using ELISA. HLA-DR and HLA-DQ genotyping was performed utilizing a polymerase chain reaction-based technique with sequence-specific oligonucleotide probe hybridization. Nonparametric statistical analyses were utilized throughout the study. PBMCs from both RA patients and healthy control individuals responded with IFN-gamma production to the same degree to stimulation with native and denatured CII (Fig. 1a), giving median stimulation indexes with native CII of 4.6 for RA patients and 5.4 for health control individuals, and with denatured CII of 2.9 for RA patients and 2.6 for healthy control individuals. RA patients with elevated levels of anti-CII had a weaker IFN-gamma response to both native and denatured CII that did healthy control individuals (P-).02 and 0.04, respectively). Stimulation with the standard recall antigens PPD and killed influenza virus yielded a median stimulation index with PPD of 10.0 for RA patients and 51.3 for healthy control individuals and with influenza of 12.3 for RA patients and 25.7 for healthy, control individuals. The RA patients displayed markedly lower responsiveness to both PPD and killed influenza virus than did healthy control individuals (Fig. 1b). IFN-gamma responses to all antigens were abrogated when coincubating with antibodies blocking MHC class II. The low response to PPD and killed influenza virus in RA patients relative to that of healthy control individuals reflects a general downregulation of antigen-induced responsiveness of T cells from RA patients [6-8]. That no difference between the RA group and the control group was recorded CII-induced IFN-gamma production therefore indicates that there may be an underlying increased responsiveness to CII in RA patients, which is obscured by the general downregulation of T-cell responsiveness in these patients. In order to address this possibility, we calculated the fraction between individual values for the CII-induced IFN-gamma production and the PPD-induced and killed influenza virus-induced IFN-gamma production and the PPD-induced and killed influenza virus-induced IFN-gamma production, and compared these fractions. A highly significant difference between the RA and health control groups was apparent after stimulation with both native CII and denatured CII when expressing the response as a fraction of that with PPD (Fig. 2a). Similar data were obtained using killed influenza virus-stimulated IFN-gamma values as the denominator (Fig. 2b).When comparing the compensated IFN-gamma response to denatured CII stimulation between RA patients with different HLA genotypes, highly significant differences were evident, with HLA-DRB10401 patients having greater CII responsiveness than patients who lacked this genotype (Fig. 3a). HLA-DQ8 positive patients also displayed a high responsiveness to CII as compared with HLA-DQ8 negative RA patients (Fig. 3b). These associations between the relative T-cell reactivity to denatured CII and HLA class II genotypes were not seen in healthy control individuals. Similar results were achieved using influenza as denominator (P = 0.02 for HLA-DRB10401 and P = 0.01 for HLA-DQ8). Question: Is interferon-gamma production in response to in vitro stimulation with collagen type II in rheumatoid arthritis associated with HLA-DRB1 ( * ) 0401 and HLA-DQ8? Output:
PubmedQA91660	[ { "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: Data from epidemiological and experimental studies suggest that dietary protein intake may play a role in inhibiting prostate and breast cancer by modulating the IGF/AKT/mTOR pathway. In this study we investigated the effects of diets with different protein content or quality on prostate and breast cancer. To test our hypothesis we assessed the inhibitory effect of protein diet restriction on prostate and breast cancer growth, serum PSA and IGF-1 concentrations, mTOR activity and epigenetic markers, by using human xenograft cancer models. Our results showed a 70% inhibition of tumor growth in the castrate-resistant LuCaP23.1 prostate cancer model and a 56% inhibition in the WHIM16 breast cancer model fed with a 7% protein diet when compared to an isocaloric 21% protein diet. Inhibition of tumor growth correlated, in the LuCaP23.1 model, with decreased serum PSA and IGF-1 levels, down-regulation of mTORC1 activity, decreased cell proliferation as indicated by Ki67 staining, and reduction in epigenetic markers of prostate cancer progression, including the histone methyltransferase EZH2 and the associated histone mark H3K27me3. In addition, we observed that modifications of dietary protein quality, independently of protein quantity, decreased tumor growth. A diet containing 20% plant protein inhibited tumor weight by 37% as compared to a 20% animal dairy protein diet.\n Question: Does dietary protein restriction inhibit tumor growth in human xenograft models?\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: Data from epidemiological and experimental studies suggest that dietary protein intake may play a role in inhibiting prostate and breast cancer by modulating the IGF/AKT/mTOR pathway. In this study we investigated the effects of diets with different protein content or quality on prostate and breast cancer. To test our hypothesis we assessed the inhibitory effect of protein diet restriction on prostate and breast cancer growth, serum PSA and IGF-1 concentrations, mTOR activity and epigenetic markers, by using human xenograft cancer models. Our results showed a 70% inhibition of tumor growth in the castrate-resistant LuCaP23.1 prostate cancer model and a 56% inhibition in the WHIM16 breast cancer model fed with a 7% protein diet when compared to an isocaloric 21% protein diet. Inhibition of tumor growth correlated, in the LuCaP23.1 model, with decreased serum PSA and IGF-1 levels, down-regulation of mTORC1 activity, decreased cell proliferation as indicated by Ki67 staining, and reduction in epigenetic markers of prostate cancer progression, including the histone methyltransferase EZH2 and the associated histone mark H3K27me3. In addition, we observed that modifications of dietary protein quality, independently of protein quantity, decreased tumor growth. A diet containing 20% plant protein inhibited tumor weight by 37% as compared to a 20% animal dairy protein diet. Question: Does dietary protein restriction inhibit tumor growth in human xenograft models? Output: