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stringlengths 17
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19,563,529 | Does the phospholipase A ( 2 ) inhibitor methyl indoxam suppress diet-induced obesity and glucose intolerance in mice? | {
"contexts": [
"Previous results have shown that mice lacking in the group 1B phospholipase A(2) (Pla2g1b) are resistant to obesity and diabetes induced by feeding a diabetogenic high-fat/high-carbohydrate diet. This study examined the potential of using the Pla2g1b inhibitor methyl indoxam as therapy to suppress diet-induced obesity and diabetes.",
"Male C57BL/6 mice were fed the diabetogenic diet with or without methyl indoxam supplementation. Body weight gain, fasting plasma glucose levels, glucose tolerance and postprandial lysophospholipid absorption were compared.",
"Wild-type C57BL/6 mice fed the diabetogenic diet without Pla2g1b inhibitor showed 31 and 69% body weight gain after 4 and 10 weeks respectively. These animals also showed elevated plasma glucose levels and were glucose intolerant. In contrast, C57BL/6 mice fed the diabetogenic diet with 90 mg.kg(-1) of methyl indoxam gained only 5% body weight after 10 weeks. These animals were also euglycaemic and displayed normal glucose excursion rates in glucose tolerance test. Methyl indoxam suppression of diet-induced body weight gain and glucose intolerance was correlated with the inhibition of Pla2g1b-mediated postprandial lysophospholipid absorption."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Anti-Obesity Agents",
"Bile",
"Biphenyl Compounds",
"Caco-2 Cells",
"Dietary Carbohydrates",
"Dietary Fats",
"Eating",
"Glucose Intolerance",
"Group IB Phospholipases A2",
"Humans",
"Hydrolysis",
"Hypoglycemic Agents",
"Indoles",
"Lysophospholipids",
"Male",
"Mice",
"Mice, Inbred C57BL",
"Mice, Knockout",
"Obesity",
"Postprandial Period",
"Recombinant Proteins",
"Weight Gain"
]
} | These results show that oral supplementation of a diabetogenic diet with the Pla2g1b inhibitor methyl indoxam effectively suppresses diet-induced obesity and diabetes in mice. This suggests that Pla2g1b inhibition may be a potentially effective oral therapeutic option for treatment of obesity and diabetes. | yes | [
{
"from": "human",
"value": "Question: Does the phospholipase A ( 2 ) inhibitor methyl indoxam suppress diet-induced obesity and glucose intolerance in mice?\nContext: {'contexts': ['Previous results have shown that mice lacking in the group 1B phospholipase A(2) (Pla2g1b) are resistant to obesity and diabetes induced by feeding a diabetogenic high-fat/high-carbohydrate diet. This study examined the potential of using the Pla2g1b inhibitor methyl indoxam as therapy to suppress diet-induced obesity and diabetes.', 'Male C57BL/6 mice were fed the diabetogenic diet with or without methyl indoxam supplementation. Body weight gain, fasting plasma glucose levels, glucose tolerance and postprandial lysophospholipid absorption were compared.', 'Wild-type C57BL/6 mice fed the diabetogenic diet without Pla2g1b inhibitor showed 31 and 69% body weight gain after 4 and 10 weeks respectively. These animals also showed elevated plasma glucose levels and were glucose intolerant. In contrast, C57BL/6 mice fed the diabetogenic diet with 90 mg.kg(-1) of methyl indoxam gained only 5% body weight after 10 weeks. These animals were also euglycaemic and displayed normal glucose excursion rates in glucose tolerance test. Methyl indoxam suppression of diet-induced body weight gain and glucose intolerance was correlated with the inhibition of Pla2g1b-mediated postprandial lysophospholipid absorption.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Anti-Obesity Agents', 'Bile', 'Biphenyl Compounds', 'Caco-2 Cells', 'Dietary Carbohydrates', 'Dietary Fats', 'Eating', 'Glucose Intolerance', 'Group IB Phospholipases A2', 'Humans', 'Hydrolysis', 'Hypoglycemic Agents', 'Indoles', 'Lysophospholipids', 'Male', 'Mice', 'Mice, Inbred C57BL', 'Mice, Knockout', 'Obesity', 'Postprandial Period', 'Recombinant Proteins', 'Weight Gain']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
19,567,520 | Do physiological thyroid hormone levels regulate numerous skeletal muscle transcripts? | {
"contexts": [
"Skeletal muscle is an important target tissue for thyroid hormone (TH). It is currently unknown which genes are regulated by physiological TH levels.",
"We examined the effects of l-thyroxine on human skeletal muscle transcriptome.",
"Microarray analysis of transcript levels was performed using skeletal muscle biopsies from patients under euthyroid and hypothyroid conditions.",
"The study was conducted in a university hospital laboratory.",
"We studied skeletal muscle obtained from 10 thyroidectomized patients with differentiated thyroid carcinoma on and after 4 wk off L-thyroxine replacement.",
"Gene expression changes were measured using microarrays. Results were analyzed using dedicated statistical methods.",
"We detected 607 differentially expressed genes on L-thyroxine treatment, of which approximately 60% were positively and approximately 40% were negatively regulated. Representative genes were validated by quantitative PCR. Genes involved in energy and fuel metabolism were overrepresented among the up-regulated genes, of which a large number were newly associated with thyroid state. L-thyroxine therapy induced a large down-regulation of the primary transcripts of the noncoding microRNA pair miR-206/miR-133b."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"METHODS",
"METHODS",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Female",
"Gene Expression Regulation",
"Glucose Transporter Type 5",
"Hormone Replacement Therapy",
"Humans",
"Male",
"MicroRNAs",
"Middle Aged",
"Muscle, Skeletal",
"Oligonucleotide Array Sequence Analysis",
"Thyroxine"
]
} | We demonstrated that physiological levels of TH regulate a myriad of genes in human skeletal muscle. The identification of novel putatively TH-responsive genes may provide the molecular basis of clinical effects in subjects with different TH status. The observation that TH regulates microRNAs reveals a new layer of complexity by which TH influences cellular processes. | yes | [
{
"from": "human",
"value": "Question: Do physiological thyroid hormone levels regulate numerous skeletal muscle transcripts?\nContext: {'contexts': ['Skeletal muscle is an important target tissue for thyroid hormone (TH). It is currently unknown which genes are regulated by physiological TH levels.', 'We examined the effects of l-thyroxine on human skeletal muscle transcriptome.', 'Microarray analysis of transcript levels was performed using skeletal muscle biopsies from patients under euthyroid and hypothyroid conditions.', 'The study was conducted in a university hospital laboratory.', 'We studied skeletal muscle obtained from 10 thyroidectomized patients with differentiated thyroid carcinoma on and after 4 wk off L-thyroxine replacement.', 'Gene expression changes were measured using microarrays. Results were analyzed using dedicated statistical methods.', 'We detected 607 differentially expressed genes on L-thyroxine treatment, of which approximately 60% were positively and approximately 40% were negatively regulated. Representative genes were validated by quantitative PCR. Genes involved in energy and fuel metabolism were overrepresented among the up-regulated genes, of which a large number were newly associated with thyroid state. L-thyroxine therapy induced a large down-regulation of the primary transcripts of the noncoding microRNA pair miR-206/miR-133b.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'METHODS', 'METHODS', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Female', 'Gene Expression Regulation', 'Glucose Transporter Type 5', 'Hormone Replacement Therapy', 'Humans', 'Male', 'MicroRNAs', 'Middle Aged', 'Muscle, Skeletal', 'Oligonucleotide Array Sequence Analysis', 'Thyroxine']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
19,565,381 | Does evaluation of a new device to prevent fall in persons with Parkinson 's disease? | {
"contexts": [
"To compare walking characteristics of individuals with Parkinson's disease (PD) using a new walking aid, the WalkAbout, with usual walking.",
"Fifteen subjects with PD were recruited. Subjects walked in their usual fashion and then walked again in the WalkAbout. Gait parameters, 5-min walk, and oxygen consumption were recorded.",
"Stride lengths were shorter when using the WalkAbout. On an average, the distance walked in 5 min and the oxygen uptake was not different when walking with the WalkAbout compared with the usual walk. Eight subjects (responders) walked further with the WalkAbout compared to their usual walk (164.90 +/- 55.72 m vs. 140.82 +/- 55.94 m). Seven subjects (non-responders) walked a shorter distance while using the WalkAbout compared to their usual walk (241.79 +/- 73.06 m vs. 281.24 +/- 82.83 m). Compared to non-responders, responders were older, had more severe disability, and were more likely to use an assistive device for walking. Responders walked more slowly, had a shorter stride length, and walked shorter distances in 5 min than non-responders."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Accidental Falls",
"Aged",
"Aged, 80 and over",
"Female",
"Gait",
"Humans",
"Male",
"Middle Aged",
"Oxygen Consumption",
"Parkinson Disease",
"Walkers",
"Walking"
]
} | The WalkAbout may help persons with PD who have more severe disability to walk farther. These data could be beneficial in selecting a helpful walking aid for persons with PD. | yes | [
{
"from": "human",
"value": "Question: Does evaluation of a new device to prevent fall in persons with Parkinson 's disease?\nContext: {'contexts': [\"To compare walking characteristics of individuals with Parkinson's disease (PD) using a new walking aid, the WalkAbout, with usual walking.\", 'Fifteen subjects with PD were recruited. Subjects walked in their usual fashion and then walked again in the WalkAbout. Gait parameters, 5-min walk, and oxygen consumption were recorded.', 'Stride lengths were shorter when using the WalkAbout. On an average, the distance walked in 5 min and the oxygen uptake was not different when walking with the WalkAbout compared with the usual walk. Eight subjects (responders) walked further with the WalkAbout compared to their usual walk (164.90 +/- 55.72 m vs. 140.82 +/- 55.94 m). Seven subjects (non-responders) walked a shorter distance while using the WalkAbout compared to their usual walk (241.79 +/- 73.06 m vs. 281.24 +/- 82.83 m). Compared to non-responders, responders were older, had more severe disability, and were more likely to use an assistive device for walking. Responders walked more slowly, had a shorter stride length, and walked shorter distances in 5 min than non-responders.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Accidental Falls', 'Aged', 'Aged, 80 and over', 'Female', 'Gait', 'Humans', 'Male', 'Middle Aged', 'Oxygen Consumption', 'Parkinson Disease', 'Walkers', 'Walking']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
19,561,827 | Does higher inpatient medical surgical bed occupancy extend admitted patients ' stay? | {
"contexts": [
"Determine the effect that increased medical surgical (med/surg) bed occupancy has on the time interval from admission order to arrival in the bed for the patients admitted from the emergency department (ED).",
"This retrospective observational study compares the total hospital bed occupancy rate and the medical surgical inpatient bed occupancy rate to daily averages for the time interval from admission order (patient posting for admission) to the patient's arrival in the inpatient bed. Medical surgical inpatient bed occupancy of 92% was chosen because beyond that rate we observed more frequent extended daily transfer times. The data is from a single large tertiary care institute with 590 beds and an annual ED census of 80,000.",
"Group 1 includes 38 days with (med/surg) inpatient bed occupancy rate of less than 92%, with an average ED daily wait of 2.5 hrs (95% confidence interval 2.23-2.96) for transfer from the ED to the appropriate hospital bed. Group 2 includes 68 days with med/surg census greater than 92% with an average ED daily wait of 4.1 hours (95% confidence interval 3.7-4.5). Minimum daily average for the two groups was 1.2 hrs and 1.3 hrs, respectively. The maximum average was 5.6 hrs for group 1 and 8.6 hrs for group 2. Comparison of group 1 to 2 for wait time to hospital bed yielded p <0.01. Total reported hospital occupied capacity shows a correlation coefficient of 0.16 to transfer time interval, which indicates a weak relationship between total occupancy and transfer time into the hospital. Med/surg occupancy, the beds typically used by ED patients, has a 0.62 correlation coefficient for a moderately strong relationship."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": []
} | Med/surg bed occupancy has a better correlation to extended transfer times, and occupancy over 92% at 5 AM in our institution corresponds to an increased frequency of extended transfer times from the ED. The process of ED evaluation, hospital admission, and subsequent transfer into the hospital are all complex processes. This study begins to demonstrate one variable, med/surg occupancy, as one of the intervals that can be followed to evaluate the process of ED admission and hospital flow. | yes | [
{
"from": "human",
"value": "Question: Does higher inpatient medical surgical bed occupancy extend admitted patients ' stay?\nContext: {'contexts': ['Determine the effect that increased medical surgical (med/surg) bed occupancy has on the time interval from admission order to arrival in the bed for the patients admitted from the emergency department (ED).', \"This retrospective observational study compares the total hospital bed occupancy rate and the medical surgical inpatient bed occupancy rate to daily averages for the time interval from admission order (patient posting for admission) to the patient's arrival in the inpatient bed. Medical surgical inpatient bed occupancy of 92% was chosen because beyond that rate we observed more frequent extended daily transfer times. The data is from a single large tertiary care institute with 590 beds and an annual ED census of 80,000.\", 'Group 1 includes 38 days with (med/surg) inpatient bed occupancy rate of less than 92%, with an average ED daily wait of 2.5 hrs (95% confidence interval 2.23-2.96) for transfer from the ED to the appropriate hospital bed. Group 2 includes 68 days with med/surg census greater than 92% with an average ED daily wait of 4.1 hours (95% confidence interval 3.7-4.5). Minimum daily average for the two groups was 1.2 hrs and 1.3 hrs, respectively. The maximum average was 5.6 hrs for group 1 and 8.6 hrs for group 2. Comparison of group 1 to 2 for wait time to hospital bed yielded p <0.01. Total reported hospital occupied capacity shows a correlation coefficient of 0.16 to transfer time interval, which indicates a weak relationship between total occupancy and transfer time into the hospital. Med/surg occupancy, the beds typically used by ED patients, has a 0.62 correlation coefficient for a moderately strong relationship.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
19,561,828 | Is routine laboratory testing to evaluate for medical illness in psychiatric patients in the emergency department largely unrevealing? | {
"contexts": [
"This is a prospective study of psychiatric patients presenting to the emergency department (ED) to determine the value of routine laboratory studies used to attempt to exclude concomitant medical illness.",
"Physical exams and laboratory tests were performed on 375 psychiatric patients presenting for \"medical clearance\" in the ED. Upon completion of these tests, the percentage and impact of abnormal physical exams and laboratory results were assessed.",
"Fifty-six of 375 patients (14.9%) had a non-substance-induced laboratory abnormality. Forty-two of these 56 patients (75.0%) also had abnormal history or physical exam findings indicating laboratory screening. Ten had normal history and physical exams with insignificant laboratory abnormalities. The four (1.1% [95% CI 0.3-2.7%]) remaining patients with normal history and physical exams had abnormal urinalyses which did not affect final disposition or contribute to altered behavior."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": []
} | Patients presenting to the ED with psychiatric chief complaints, benign histories and normal physical exams have a low likelihood of clinically significant laboratory findings. | yes | [
{
"from": "human",
"value": "Question: Is routine laboratory testing to evaluate for medical illness in psychiatric patients in the emergency department largely unrevealing?\nContext: {'contexts': ['This is a prospective study of psychiatric patients presenting to the emergency department (ED) to determine the value of routine laboratory studies used to attempt to exclude concomitant medical illness.', 'Physical exams and laboratory tests were performed on 375 psychiatric patients presenting for \"medical clearance\" in the ED. Upon completion of these tests, the percentage and impact of abnormal physical exams and laboratory results were assessed.', 'Fifty-six of 375 patients (14.9%) had a non-substance-induced laboratory abnormality. Forty-two of these 56 patients (75.0%) also had abnormal history or physical exam findings indicating laboratory screening. Ten had normal history and physical exams with insignificant laboratory abnormalities. The four (1.1% [95% CI 0.3-2.7%]) remaining patients with normal history and physical exams had abnormal urinalyses which did not affect final disposition or contribute to altered behavior.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
19,542,178 | Is copper-induced regression of cardiomyocyte hypertrophy associated with enhanced vascular endothelial growth factor receptor-1 signalling pathway? | {
"contexts": [
"Vascular endothelial growth factor (VEGF) has been well documented to stimulate cell proliferation and differentiation; however, we have observed that copper (Cu)-induced regression of heart hypertrophy was VEGF-dependent. The present study was undertaken to test the hypothesis that Cu causes alterations in the distribution of VEGF receptors (VEGFRs) in hypertrophic cardiomyocytes so that it switches the signalling pathway from stimulation of cell growth to reversal of cell hypertrophy.",
"Primary cultures of neonatal rat cardiomyocytes were exposed to phenylephrine (PE) at a final concentration of 100 microM in cultures for 48 h to induce cell hypertrophy. The hypertrophic cardiomyocytes were exposed to copper sulfate at a final concentration of 5 microM in cultures for 24 h with a concomitant presence of PE. Flow cytometry, gene silencing, and ELISA procedures were used to analyse the changes in VEGFRs and their relationship with regression of cardiomyocyte hypertrophy. Cu did not change the concentration of VEGF in culture media, but increased the ratio of VEGFR-1 to VEGFR-2 two-fold. Gene silencing of VEGFR-2, in the absence of Cu addition, reversed PE-induced cardiomyocyte hypertrophy, which was suppressed by an anti-VEGF antibody. Gene silencing of VEGFR-1 blocked Cu-induced regression of cell hypertrophy and decreased the activity of cGMP-dependent protein kinase-1 (PKG-1). A PKG-1 antagonist, Rp-8-pCPT-cGMPS, blocked both Cu- and VEGFR-2 gene silencing-induced regression of cardiomyocyte hypertrophy."
],
"labels": [
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Animals",
"Cardiomegaly",
"Cells, Cultured",
"Copper",
"Cyclic GMP-Dependent Protein Kinase Type I",
"Cyclic GMP-Dependent Protein Kinases",
"Myocytes, Cardiac",
"Phenylephrine",
"Rats",
"Rats, Sprague-Dawley",
"Signal Transduction",
"Vascular Endothelial Growth Factor Receptor-1",
"Vascular Endothelial Growth Factor Receptor-2"
]
} | Enhanced VEGFR-1 signalling is involved in Cu regression of cardiomyocyte hypertrophy, and the PKG-1 pathway is likely associated with VEGFR-1. | yes | [
{
"from": "human",
"value": "Question: Is copper-induced regression of cardiomyocyte hypertrophy associated with enhanced vascular endothelial growth factor receptor-1 signalling pathway?\nContext: {'contexts': ['Vascular endothelial growth factor (VEGF) has been well documented to stimulate cell proliferation and differentiation; however, we have observed that copper (Cu)-induced regression of heart hypertrophy was VEGF-dependent. The present study was undertaken to test the hypothesis that Cu causes alterations in the distribution of VEGF receptors (VEGFRs) in hypertrophic cardiomyocytes so that it switches the signalling pathway from stimulation of cell growth to reversal of cell hypertrophy.', 'Primary cultures of neonatal rat cardiomyocytes were exposed to phenylephrine (PE) at a final concentration of 100 microM in cultures for 48 h to induce cell hypertrophy. The hypertrophic cardiomyocytes were exposed to copper sulfate at a final concentration of 5 microM in cultures for 24 h with a concomitant presence of PE. Flow cytometry, gene silencing, and ELISA procedures were used to analyse the changes in VEGFRs and their relationship with regression of cardiomyocyte hypertrophy. Cu did not change the concentration of VEGF in culture media, but increased the ratio of VEGFR-1 to VEGFR-2 two-fold. Gene silencing of VEGFR-2, in the absence of Cu addition, reversed PE-induced cardiomyocyte hypertrophy, which was suppressed by an anti-VEGF antibody. Gene silencing of VEGFR-1 blocked Cu-induced regression of cell hypertrophy and decreased the activity of cGMP-dependent protein kinase-1 (PKG-1). A PKG-1 antagonist, Rp-8-pCPT-cGMPS, blocked both Cu- and VEGFR-2 gene silencing-induced regression of cardiomyocyte hypertrophy.'], 'labels': ['OBJECTIVE', 'RESULTS'], 'meshes': ['Animals', 'Cardiomegaly', 'Cells, Cultured', 'Copper', 'Cyclic GMP-Dependent Protein Kinase Type I', 'Cyclic GMP-Dependent Protein Kinases', 'Myocytes, Cardiac', 'Phenylephrine', 'Rats', 'Rats, Sprague-Dawley', 'Signal Transduction', 'Vascular Endothelial Growth Factor Receptor-1', 'Vascular Endothelial Growth Factor Receptor-2']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
19,543,984 | Does myocardial electrical activity affect myocardial electrical impedance measurements? | {
"contexts": [
"Myocardial electrical impedance (MEI) has shown to be an effective indicator of myocardial ischemia. We have previously developed a novel monitor for measuring MEI in near-real time. The object of this study was to test whether drug-induced changes in the frequency of the periodic myocardial electrical activity, as measured by the heart rate (HR), affect MEI measurements made with our monitor.",
"Thirty dogs were randomly assigned to one of three study groups (placebo, isoproterenol or esmolol) and then anesthetized with sodium thiamylal, intubated, ventilated, given isoflurane, and had venous, arterial, and pulmonary artery catheters placed. Median sternotomy was performed to facilitate myocardial exposure and to allow the left anterior descending (LAD) coronary artery to be isolated. Following baseline measurements, saline (control), isoproterenol or esmolol was administered and the LAD coronary artery was occluded in a timed sequence in order to study the effects of heart rate changes and demonstrate induced myocardial ischemia on MEI.",
"Isoproterenol raised the HR and esmolol lowered the HR without affecting our MEI measurements. Myocardial electrical impedance increased during LAD coronary artery occlusion in all groups, as previously shown."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Coronary Circulation",
"Coronary Vessels",
"Dogs",
"Electric Impedance",
"Electrochemistry",
"Electrophysiology",
"Heart",
"Heart Rate",
"Isoproterenol",
"Myocardial Ischemia",
"Myocardium",
"Placebos",
"Propanolamines",
"Time Factors"
]
} | These results demonstrate that our MEI monitor is unaffected by the frequency of the periodic myocardial electrical activity that generates the HR. | no | [
{
"from": "human",
"value": "Question: Does myocardial electrical activity affect myocardial electrical impedance measurements?\nContext: {'contexts': ['Myocardial electrical impedance (MEI) has shown to be an effective indicator of myocardial ischemia. We have previously developed a novel monitor for measuring MEI in near-real time. The object of this study was to test whether drug-induced changes in the frequency of the periodic myocardial electrical activity, as measured by the heart rate (HR), affect MEI measurements made with our monitor.', 'Thirty dogs were randomly assigned to one of three study groups (placebo, isoproterenol or esmolol) and then anesthetized with sodium thiamylal, intubated, ventilated, given isoflurane, and had venous, arterial, and pulmonary artery catheters placed. Median sternotomy was performed to facilitate myocardial exposure and to allow the left anterior descending (LAD) coronary artery to be isolated. Following baseline measurements, saline (control), isoproterenol or esmolol was administered and the LAD coronary artery was occluded in a timed sequence in order to study the effects of heart rate changes and demonstrate induced myocardial ischemia on MEI.', 'Isoproterenol raised the HR and esmolol lowered the HR without affecting our MEI measurements. Myocardial electrical impedance increased during LAD coronary artery occlusion in all groups, as previously shown.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Coronary Circulation', 'Coronary Vessels', 'Dogs', 'Electric Impedance', 'Electrochemistry', 'Electrophysiology', 'Heart', 'Heart Rate', 'Isoproterenol', 'Myocardial Ischemia', 'Myocardium', 'Placebos', 'Propanolamines', 'Time Factors']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
19,540,515 | Is blood pressure elevated in children with primary snoring? | {
"contexts": [
"To compare ambulatory blood pressure (ABP) in nonoverweight, prepubertal children with and without primary snoring (PS), and to investigate whether PS is a part of the dose-response relationship between sleep-disordered breathing (SDB) and BP in children.",
"This was a cross-sectional community-based study involving 190 children age 6 to 13 years. Each participant underwent an overnight sleep study and ABP monitoring after completing a validated sleep symptoms questionnaire. Individual systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial BP were calculated for wake and sleep periods. Subjects were hypertensive if mean SBP or DBP was > 95th percentile (relative to sex and height) of reference.",
"A total of 56 nonsnoring controls, 46 children with PS, 62 children with an apnea-hypopnea index (AHI) of 1 to 3, and 26 children with an AHI > 3 were identified. The daytime and nighttime BP increased across the severity spectrum of SDB. The dose-response trends for the proportion of subjects with nighttime systolic and diastolic hypertension also were significant. Nighttime DBP was significantly higher in the children with PS compared with controls after adjusting for age, sex, and body mass index."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Age Factors",
"Blood Pressure",
"Body Mass Index",
"Case-Control Studies",
"Child",
"Comorbidity",
"Cross-Sectional Studies",
"Female",
"Humans",
"Hypertension",
"Male",
"Polysomnography",
"Severity of Illness Index",
"Sex Factors",
"Sleep Apnea Syndromes",
"Snoring",
"Surveys and Questionnaires"
]
} | PS was demonstrated to be an aspect of the dose-response relationship between SDB and BP in children and should not be considered completely benign. | yes | [
{
"from": "human",
"value": "Question: Is blood pressure elevated in children with primary snoring?\nContext: {'contexts': ['To compare ambulatory blood pressure (ABP) in nonoverweight, prepubertal children with and without primary snoring (PS), and to investigate whether PS is a part of the dose-response relationship between sleep-disordered breathing (SDB) and BP in children.', 'This was a cross-sectional community-based study involving 190 children age 6 to 13 years. Each participant underwent an overnight sleep study and ABP monitoring after completing a validated sleep symptoms questionnaire. Individual systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial BP were calculated for wake and sleep periods. Subjects were hypertensive if mean SBP or DBP was > 95th percentile (relative to sex and height) of reference.', 'A total of 56 nonsnoring controls, 46 children with PS, 62 children with an apnea-hypopnea index (AHI) of 1 to 3, and 26 children with an AHI > 3 were identified. The daytime and nighttime BP increased across the severity spectrum of SDB. The dose-response trends for the proportion of subjects with nighttime systolic and diastolic hypertension also were significant. Nighttime DBP was significantly higher in the children with PS compared with controls after adjusting for age, sex, and body mass index.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Age Factors', 'Blood Pressure', 'Body Mass Index', 'Case-Control Studies', 'Child', 'Comorbidity', 'Cross-Sectional Studies', 'Female', 'Humans', 'Hypertension', 'Male', 'Polysomnography', 'Severity of Illness Index', 'Sex Factors', 'Sleep Apnea Syndromes', 'Snoring', 'Surveys and Questionnaires']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
19,545,209 | Does adult male circumcision reduce the risk of incident Neisseria gonorrhoeae , Chlamydia trachomatis , or Trichomonas vaginalis infection : results from a randomized , controlled trial in Kenya? | {
"contexts": [
"We examined the effect of male circumcision on the acquisition of 3 nonulcerative sexually transmitted infections (STIs).",
"We evaluated the incidence of STI among men aged 18-24 years enrolled in a randomized trial of circumcision to prevent human immunodeficiency virus (HIV) infection in Kisumu, Kenya. The outcome was first incident nonulcerative STI during 2 years of follow-up. STIs examined were laboratory-detected Neisseria gonorrhoeae, Chlamydia trachomatis, and Trichomonas vaginalis infection.",
"There were 342 incident infections among 2655 men followed up. The incidences of infection due to N. gonorrhoeae, C. trachomatis, and T. vaginalis were 3.48, 4.55, and 1.32 cases per 100 person-years, respectively. The combined incidence of N. gonorrhoeae and C. trachomatis infection was 7.26 cases per 100 person-years (95% confidence interval, 6.49-8.13 cases per 100 person-years). The incidences of these STIs, individually or combined, did not differ by circumcision status as a time-dependent variable or a fixed variable based on assignment. Risks for incident STIs in multivariate analysis included an STI at enrollment, multiple sex partners within <30 days, and sexual intercourse during menses in the previous 6 months; condom use was protective."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Animals",
"Chlamydia Infections",
"Chlamydia trachomatis",
"Circumcision, Male",
"Gonorrhea",
"Humans",
"Incidence",
"Kenya",
"Male",
"Neisseria gonorrhoeae",
"Proportional Hazards Models",
"Risk Factors",
"Trichomonas Infections",
"Trichomonas vaginalis",
"Young Adult"
]
} | Circumcision of men in this population did not reduce their risk of acquiring these nonulcerative STIs. Improved STI control will require more-effective STI management, including partner treatment and behavioral risk reduction counseling. | no | [
{
"from": "human",
"value": "Question: Does adult male circumcision reduce the risk of incident Neisseria gonorrhoeae , Chlamydia trachomatis , or Trichomonas vaginalis infection : results from a randomized , controlled trial in Kenya?\nContext: {'contexts': ['We examined the effect of male circumcision on the acquisition of 3 nonulcerative sexually transmitted infections (STIs).', 'We evaluated the incidence of STI among men aged 18-24 years enrolled in a randomized trial of circumcision to prevent human immunodeficiency virus (HIV) infection in Kisumu, Kenya. The outcome was first incident nonulcerative STI during 2 years of follow-up. STIs examined were laboratory-detected Neisseria gonorrhoeae, Chlamydia trachomatis, and Trichomonas vaginalis infection.', 'There were 342 incident infections among 2655 men followed up. The incidences of infection due to N. gonorrhoeae, C. trachomatis, and T. vaginalis were 3.48, 4.55, and 1.32 cases per 100 person-years, respectively. The combined incidence of N. gonorrhoeae and C. trachomatis infection was 7.26 cases per 100 person-years (95% confidence interval, 6.49-8.13 cases per 100 person-years). The incidences of these STIs, individually or combined, did not differ by circumcision status as a time-dependent variable or a fixed variable based on assignment. Risks for incident STIs in multivariate analysis included an STI at enrollment, multiple sex partners within <30 days, and sexual intercourse during menses in the previous 6 months; condom use was protective.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Animals', 'Chlamydia Infections', 'Chlamydia trachomatis', 'Circumcision, Male', 'Gonorrhea', 'Humans', 'Incidence', 'Kenya', 'Male', 'Neisseria gonorrhoeae', 'Proportional Hazards Models', 'Risk Factors', 'Trichomonas Infections', 'Trichomonas vaginalis', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
19,561,339 | Is cardiomyopathy associated with structural remodelling of heart valve extracellular matrix? | {
"contexts": [
"To increase the supply, many countries harvest allograft valves from explanted hearts of transplant recipients with ischaemic (ICM) or dilated cardiomyopathy (DCM). This study determines the structural integrity of valves from cardiomyopathic hearts.",
"Extracellular matrix (ECM) was examined in human valves obtained from normal, ICM, and DCM hearts. To confirm if ECM changes were directly related to the cardiomyopathy, we developed a porcine model of chronic ICM. Histology and immunohistostaining, as well as non-invasive multiphoton and second harmonic generation (SHG) imaging revealed marked disruption of ECM structures in human valves from ICM and DCM hearts. The ECM was unaffected in valves from normal and acute ICM pigs, whereas chronic ICM specimens showed ECM alterations similar to those seen in ICM and DCM patients. Proteins and proteinases implicated in ECM remodelling, including Tenascin C, TGFbeta1, Cathepsin B, MMP2, were upregulated in human ICM and DCM, and porcine chronic ICM specimens."
],
"labels": [
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Aged",
"Animals",
"Cardiomyopathies",
"Chronic Disease",
"Extracellular Matrix",
"Female",
"Gelatinases",
"Heart Valves",
"Humans",
"Male",
"Microscopy, Fluorescence, Multiphoton",
"Middle Aged",
"Myocardial Infarction",
"Swine"
]
} | Valves from cardiomyopathic hearts showed significant ECM deterioration with a disrupted collagen and elastic fibre network. It will be important to determine the impact of this ECM damage on valve durability and calcification in vivo if allografts are to be used from these donors. | yes | [
{
"from": "human",
"value": "Question: Is cardiomyopathy associated with structural remodelling of heart valve extracellular matrix?\nContext: {'contexts': ['To increase the supply, many countries harvest allograft valves from explanted hearts of transplant recipients with ischaemic (ICM) or dilated cardiomyopathy (DCM). This study determines the structural integrity of valves from cardiomyopathic hearts.', 'Extracellular matrix (ECM) was examined in human valves obtained from normal, ICM, and DCM hearts. To confirm if ECM changes were directly related to the cardiomyopathy, we developed a porcine model of chronic ICM. Histology and immunohistostaining, as well as non-invasive multiphoton and second harmonic generation (SHG) imaging revealed marked disruption of ECM structures in human valves from ICM and DCM hearts. The ECM was unaffected in valves from normal and acute ICM pigs, whereas chronic ICM specimens showed ECM alterations similar to those seen in ICM and DCM patients. Proteins and proteinases implicated in ECM remodelling, including Tenascin C, TGFbeta1, Cathepsin B, MMP2, were upregulated in human ICM and DCM, and porcine chronic ICM specimens.'], 'labels': ['OBJECTIVE', 'RESULTS'], 'meshes': ['Aged', 'Animals', 'Cardiomyopathies', 'Chronic Disease', 'Extracellular Matrix', 'Female', 'Gelatinases', 'Heart Valves', 'Humans', 'Male', 'Microscopy, Fluorescence, Multiphoton', 'Middle Aged', 'Myocardial Infarction', 'Swine']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
19,553,877 | Does recent evidence support emotion-regulation interventions for improving health in at-risk and clinical populations? | {
"contexts": [
"The regulation of strong emotions has important implications for health, particularly among individuals with chronic illness. We focus this brief review on effective psychosocial interventions that emphasize and teach skills to improve emotion regulation in the context of health-related outcomes.",
"Recent work in the area of emotion-regulation interventions has tested the effects of emotion-regulation family therapy, group-based emotion-regulation psychotherapy, expressive writing, and school-based prevention programs. Emotion-regulation psychotherapy for families shows some benefits for both patients and their family members. Group emotion-regulation interventions and expressive writing result in physical and psychosocial improvement for patients with medical or psychiatric illness. School-based programs show improved emotion knowledge, emotion regulation, and emotional competence, relative to standard academic curricula and existing prevention programs."
],
"labels": [
"OBJECTIVE",
"RESULTS"
],
"meshes": []
} | Evidence generally supports the use of a variety of emotion-regulation interventions to improve health and well being in at-risk and clinical populations, although factors related to treatment response warrant additional research. | yes | [
{
"from": "human",
"value": "Question: Does recent evidence support emotion-regulation interventions for improving health in at-risk and clinical populations?\nContext: {'contexts': ['The regulation of strong emotions has important implications for health, particularly among individuals with chronic illness. We focus this brief review on effective psychosocial interventions that emphasize and teach skills to improve emotion regulation in the context of health-related outcomes.', 'Recent work in the area of emotion-regulation interventions has tested the effects of emotion-regulation family therapy, group-based emotion-regulation psychotherapy, expressive writing, and school-based prevention programs. Emotion-regulation psychotherapy for families shows some benefits for both patients and their family members. Group emotion-regulation interventions and expressive writing result in physical and psychosocial improvement for patients with medical or psychiatric illness. School-based programs show improved emotion knowledge, emotion regulation, and emotional competence, relative to standard academic curricula and existing prevention programs.'], 'labels': ['OBJECTIVE', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
19,567,417 | Is release of developmental constraints on tetrad shape confirmed in inaperturate pollen of Potamogeton? | {
"contexts": [
"Microsporogenesis in monocots is often characterized by successive cytokinesis with centrifugal cell plate formation. Pollen grains in monocots are predominantly monosulcate, but variation occurs, including the lack of apertures. The aperture pattern can be determined by microsporogenesis features such as the tetrad shape and the last sites of callose deposition among the microspores. Potamogeton belongs to the early divergent Potamogetonaceae and possesses inaperturate pollen, a type of pollen for which it has been suggested that there is a release of the constraint on tetrad shape. This study aimed to investigate the microsporogenesis and the ultrastructure of pollen wall in species of Potamogeton in order to better understand the relationship between microsporogenesis features and the inaperturate condition.",
"The microsporogenesis was investigated using both light and epifluorescence microscopy. The ultrastructure of the pollen grain was studied using transmission electron microscopy.",
"The cytokinesis is successive and formation of the intersporal callose wall is achieved by centrifugal cell plates, as a one-step process. The microspore tetrads were tetragonal, decussate, T-shaped and linear, except in P. pusillus, which showed less variation. This species also showed a callose ring in the microsporocyte, and some rhomboidal tetrads. In the mature pollen, the thickening observed in a broad area of the intine was here interpreted as an artefact."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Microscopy, Electron, Transmission",
"Pollen",
"Potamogetonaceae"
]
} | The data support the view that there is a correlation between the inaperturate pollen production and the release of constraint on tetrad shape. However, in P. pusillus the tetrad shape may be constrained by a callose ring. It is also suggested that the lack of apertures in the pollen of Potamogeton may be due to the lack of specific sites on which callose deposition is completed. Moreover, inaperturate pollen of Potamogeton would be better classified as omniaperturate. | yes | [
{
"from": "human",
"value": "Question: Is release of developmental constraints on tetrad shape confirmed in inaperturate pollen of Potamogeton?\nContext: {'contexts': ['Microsporogenesis in monocots is often characterized by successive cytokinesis with centrifugal cell plate formation. Pollen grains in monocots are predominantly monosulcate, but variation occurs, including the lack of apertures. The aperture pattern can be determined by microsporogenesis features such as the tetrad shape and the last sites of callose deposition among the microspores. Potamogeton belongs to the early divergent Potamogetonaceae and possesses inaperturate pollen, a type of pollen for which it has been suggested that there is a release of the constraint on tetrad shape. This study aimed to investigate the microsporogenesis and the ultrastructure of pollen wall in species of Potamogeton in order to better understand the relationship between microsporogenesis features and the inaperturate condition.', 'The microsporogenesis was investigated using both light and epifluorescence microscopy. The ultrastructure of the pollen grain was studied using transmission electron microscopy.', 'The cytokinesis is successive and formation of the intersporal callose wall is achieved by centrifugal cell plates, as a one-step process. The microspore tetrads were tetragonal, decussate, T-shaped and linear, except in P. pusillus, which showed less variation. This species also showed a callose ring in the microsporocyte, and some rhomboidal tetrads. In the mature pollen, the thickening observed in a broad area of the intine was here interpreted as an artefact.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Microscopy, Electron, Transmission', 'Pollen', 'Potamogetonaceae']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
19,568,424 | Does lactate dehydrogenase-elevating virus induce systemic lymphocyte activation via TLR7-dependent IFNalpha responses by plasmacytoid dendritic cells? | {
"contexts": [
"Lactate dehydrogenase-elevating virus (LDV) is a natural infectious agent of mice. Like several other viruses, LDV causes widespread and very rapid but transient activation of both B cells and T cells in lymphoid tissues and the blood. The mechanism of this activation has not been fully described and is the focus of the current studies.",
"A known inducer of early lymphocyte activation is IFNalpha, a cytokine strongly induced by LDV infection. Neutralization of IFNalpha in the plasma from infected mice ablated its ability to activate lymphocytes in vitro. Since the primary source of virus-induced IFNalpha in vivo is often plasmacytoid dendritic cells (pDC's), we depleted these cells prior to LDV infection and tested for lymphocyte activation. Depletion of pDC's in vivo eradicated both the LDV-induced IFNalpha response and lymphocyte activation. A primary receptor in pDC's for single stranded RNA viruses such as LDV is the toll-like receptor 7 (TLR7) pattern recognition receptor. Infection of TLR7-knockout mice revealed that both the IFNalpha response and lymphocyte activation were dependent on TLR7 signaling in vivo. Interestingly, virus levels in both TLR7 knockout mice and pDC-depleted mice were indistinguishable from controls indicating that LDV is largely resistant to the systemic IFNalpha response."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Animals",
"Dendritic Cells",
"Interferon-alpha",
"Lactate dehydrogenase-elevating virus",
"Lymphocyte Activation",
"Mice",
"Mice, Knockout",
"Toll-Like Receptor 7"
]
} | Results indicate that LDV-induced activation of lymphocytes is due to recognition of LDV nucleic acid by TLR7 pattern recognition receptors in pDC's that respond with a lymphocyte-inducing IFNalpha response. | yes | [
{
"from": "human",
"value": "Question: Does lactate dehydrogenase-elevating virus induce systemic lymphocyte activation via TLR7-dependent IFNalpha responses by plasmacytoid dendritic cells?\nContext: {'contexts': ['Lactate dehydrogenase-elevating virus (LDV) is a natural infectious agent of mice. Like several other viruses, LDV causes widespread and very rapid but transient activation of both B cells and T cells in lymphoid tissues and the blood. The mechanism of this activation has not been fully described and is the focus of the current studies.', \"A known inducer of early lymphocyte activation is IFNalpha, a cytokine strongly induced by LDV infection. Neutralization of IFNalpha in the plasma from infected mice ablated its ability to activate lymphocytes in vitro. Since the primary source of virus-induced IFNalpha in vivo is often plasmacytoid dendritic cells (pDC's), we depleted these cells prior to LDV infection and tested for lymphocyte activation. Depletion of pDC's in vivo eradicated both the LDV-induced IFNalpha response and lymphocyte activation. A primary receptor in pDC's for single stranded RNA viruses such as LDV is the toll-like receptor 7 (TLR7) pattern recognition receptor. Infection of TLR7-knockout mice revealed that both the IFNalpha response and lymphocyte activation were dependent on TLR7 signaling in vivo. Interestingly, virus levels in both TLR7 knockout mice and pDC-depleted mice were indistinguishable from controls indicating that LDV is largely resistant to the systemic IFNalpha response.\"], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Animals', 'Dendritic Cells', 'Interferon-alpha', 'Lactate dehydrogenase-elevating virus', 'Lymphocyte Activation', 'Mice', 'Mice, Knockout', 'Toll-Like Receptor 7']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
19,551,889 | Is yes-associated protein an independent prognostic marker in hepatocellular carcinoma? | {
"contexts": [
"Yes-associated protein (YAP), a downstream target of the Hippo signaling pathway, was recently linked to hepatocarcinogenesis in a mouse hepatocellular carcinoma (HCC) model. The objective of the current study was to investigate the clinical significance of YAP in HCC and its prognostic values in predicting survival and tumor recurrence.",
"The authors collected 177 pairs of tumor and adjacent nontumor tissue from HCC patients with definitive clinicopathologic and follow-up data. YAP expression was determined by immunohistochemistry, Western blot analysis, and quantitative polymerase chain reaction. Association of YAP with each clinicopathologic feature was analyzed by Pearson chi-square test, and HCC-specific disease-free survival and overall survival by Kaplan-Meier curves and log-rank test. Multivariate Cox regression analyses of YAP in HCC were also performed.",
"YAP was expressed in the majority of HCC cases (approximately 62%) and mainly accumulated in the tumor nucleus. Overexpression of YAP in HCC was significantly associated with poorer tumor differentiation (Edmonson grade; P = .021) and high serum alpha-fetoprotein (AFP) level (P < .001). Kaplan-Meier and Cox regression data indicated that YAP was an independent predictor for HCC-specific disease-free survival (hazards ratio [HR], 1.653; 95% confidence interval [95% CI], 1.081-2.528 [P = .02]) and overall survival (HR, 2.148; 95% CI, 1.255-3.677 [P = .005])."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Biomarkers, Tumor",
"Carcinoma, Hepatocellular",
"Female",
"Humans",
"Liver Neoplasms",
"Male",
"Middle Aged",
"Nuclear Proteins",
"Prognosis",
"Survival Analysis",
"Transcription Factors"
]
} | YAP is an independent prognostic marker for overall survival and disease-free survival times of HCC patients and clinicopathologically associated with tumor differentiation and serum AFP level. It is a potential therapeutic target for this aggressive malignancy. | yes | [
{
"from": "human",
"value": "Question: Is yes-associated protein an independent prognostic marker in hepatocellular carcinoma?\nContext: {'contexts': ['Yes-associated protein (YAP), a downstream target of the Hippo signaling pathway, was recently linked to hepatocarcinogenesis in a mouse hepatocellular carcinoma (HCC) model. The objective of the current study was to investigate the clinical significance of YAP in HCC and its prognostic values in predicting survival and tumor recurrence.', 'The authors collected 177 pairs of tumor and adjacent nontumor tissue from HCC patients with definitive clinicopathologic and follow-up data. YAP expression was determined by immunohistochemistry, Western blot analysis, and quantitative polymerase chain reaction. Association of YAP with each clinicopathologic feature was analyzed by Pearson chi-square test, and HCC-specific disease-free survival and overall survival by Kaplan-Meier curves and log-rank test. Multivariate Cox regression analyses of YAP in HCC were also performed.', 'YAP was expressed in the majority of HCC cases (approximately 62%) and mainly accumulated in the tumor nucleus. Overexpression of YAP in HCC was significantly associated with poorer tumor differentiation (Edmonson grade; P = .021) and high serum alpha-fetoprotein (AFP) level (P < .001). Kaplan-Meier and Cox regression data indicated that YAP was an independent predictor for HCC-specific disease-free survival (hazards ratio [HR], 1.653; 95% confidence interval [95% CI], 1.081-2.528 [P = .02]) and overall survival (HR, 2.148; 95% CI, 1.255-3.677 [P = .005]).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Biomarkers, Tumor', 'Carcinoma, Hepatocellular', 'Female', 'Humans', 'Liver Neoplasms', 'Male', 'Middle Aged', 'Nuclear Proteins', 'Prognosis', 'Survival Analysis', 'Transcription Factors']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
19,546,267 | Does the Manchester Triage System provide good reliability in an Australian emergency department? | {
"contexts": [
"The Australasian Triage Scale is a simple five-point system of triage that forms the basis of triage in most emergency departments in Australia. The Manchester Triage System (MTS) is an algorithmic aid to the process of triage. It utilises a series of flow charts that lead the triage nurse to a logical choice of triage category also using a five-point scale.",
"To evaluate the inter-rater reliability of the MTS in an Australian emergency department.",
"50 triage scenarios were derived from the notes of 50 consecutive patients who had presented to the emergency department. All available nurses who had been trained to use the MTS were invited to participate in the study. The nurses were asked to assign a triage category to each scenario using the MTS. Weighted kappas were calculated for all pairs of raters.",
"20 nurses participated in the study. The range of kappas was 0.4007 to 0.8018, with a median of 0.6304."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Algorithms",
"Decision Making",
"Emergencies",
"Emergency Nursing",
"Emergency Service, Hospital",
"Humans",
"New South Wales",
"Observer Variation",
"Reproducibility of Results",
"Triage"
]
} | The MTS is a reliable system of triage in the emergency department. | yes | [
{
"from": "human",
"value": "Question: Does the Manchester Triage System provide good reliability in an Australian emergency department?\nContext: {'contexts': ['The Australasian Triage Scale is a simple five-point system of triage that forms the basis of triage in most emergency departments in Australia. The Manchester Triage System (MTS) is an algorithmic aid to the process of triage. It utilises a series of flow charts that lead the triage nurse to a logical choice of triage category also using a five-point scale.', 'To evaluate the inter-rater reliability of the MTS in an Australian emergency department.', '50 triage scenarios were derived from the notes of 50 consecutive patients who had presented to the emergency department. All available nurses who had been trained to use the MTS were invited to participate in the study. The nurses were asked to assign a triage category to each scenario using the MTS. Weighted kappas were calculated for all pairs of raters.', '20 nurses participated in the study. The range of kappas was 0.4007 to 0.8018, with a median of 0.6304.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Algorithms', 'Decision Making', 'Emergencies', 'Emergency Nursing', 'Emergency Service, Hospital', 'Humans', 'New South Wales', 'Observer Variation', 'Reproducibility of Results', 'Triage']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
19,540,403 | Does serial bedside B-type natriuretic peptide strongly predict prognosis in acute coronary syndrome independent of echocardiographic abnormalities? | {
"contexts": [
"Elevated levels of B-type natriuretic peptide (BNP) are associated with adverse clinical outcomes in acute coronary syndrome (ACS), but several questions remain outstanding. Firstly, it has not yet been determined whether an additional BNP sample at 7 weeks post ACS would enhance risk prediction. Secondly, we assessed whether the prognostic potential of BNP in ACS could be explained by echocardiographic abnormalities such as left ventricular hypertrophy (LVH).",
"We measured bedside BNP levels in 443 consecutive patients presenting with ACS and at 7 weeks outpatient follow-up. Main outcome measure was either all-cause mortality, readmission with ACS, or congestive heart failure) at 10 months from presentation.",
"Of the 443 patients, 120 patients presented with ST-elevation myocardial infarction (27%). There were 90 cardiovascular (CV) events at 10 months. Adjusting for age, sex, hypertension, diabetes mellitus, smoking status, renal dysfunction, left ventricular ejection fraction, and echocardiographic LVH elevated near patient BNP levels (>80 pg/mL) were still associated with subsequent CV events when measured on admission (adjusted relative risk [RR] 2.63 [95% CI 1.34-5.19)] and also at 7 weeks post ACS (adjusted RR 4.12 [95% CI 1.58-10.72]). Patients with persistent BNP elevation at 7 weeks were also at an increased risk of CV events compared to those with an initial high BNP which then fell (unadjusted RR 4.04 [95% CI 1.24-13.15])."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Acute Coronary Syndrome",
"Aged",
"Atrial Function, Left",
"Echocardiography",
"Female",
"Follow-Up Studies",
"Heart Failure",
"Humans",
"Hypertrophy, Left Ventricular",
"Kaplan-Meier Estimate",
"Male",
"Middle Aged",
"Myocardial Infarction",
"Natriuretic Peptide, Brain",
"Point-of-Care Systems",
"Predictive Value of Tests",
"Prognosis",
"Reference Values",
"Risk Factors",
"Ventricular Dysfunction, Left"
]
} | In ACS, bedside BNP levels predict CV events at 10 months, independent of many echocardiographic abnormalities including LVH. Furthermore, our study suggests that an additional 7 weeks post ACS BNP enhances risk stratification over and above a one-off high BNP at baseline. | yes | [
{
"from": "human",
"value": "Question: Does serial bedside B-type natriuretic peptide strongly predict prognosis in acute coronary syndrome independent of echocardiographic abnormalities?\nContext: {'contexts': ['Elevated levels of B-type natriuretic peptide (BNP) are associated with adverse clinical outcomes in acute coronary syndrome (ACS), but several questions remain outstanding. Firstly, it has not yet been determined whether an additional BNP sample at 7 weeks post ACS would enhance risk prediction. Secondly, we assessed whether the prognostic potential of BNP in ACS could be explained by echocardiographic abnormalities such as left ventricular hypertrophy (LVH).', 'We measured bedside BNP levels in 443 consecutive patients presenting with ACS and at 7 weeks outpatient follow-up. Main outcome measure was either all-cause mortality, readmission with ACS, or congestive heart failure) at 10 months from presentation.', 'Of the 443 patients, 120 patients presented with ST-elevation myocardial infarction (27%). There were 90 cardiovascular (CV) events at 10 months. Adjusting for age, sex, hypertension, diabetes mellitus, smoking status, renal dysfunction, left ventricular ejection fraction, and echocardiographic LVH elevated near patient BNP levels (>80 pg/mL) were still associated with subsequent CV events when measured on admission (adjusted relative risk [RR] 2.63 [95% CI 1.34-5.19)] and also at 7 weeks post ACS (adjusted RR 4.12 [95% CI 1.58-10.72]). Patients with persistent BNP elevation at 7 weeks were also at an increased risk of CV events compared to those with an initial high BNP which then fell (unadjusted RR 4.04 [95% CI 1.24-13.15]).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Acute Coronary Syndrome', 'Aged', 'Atrial Function, Left', 'Echocardiography', 'Female', 'Follow-Up Studies', 'Heart Failure', 'Humans', 'Hypertrophy, Left Ventricular', 'Kaplan-Meier Estimate', 'Male', 'Middle Aged', 'Myocardial Infarction', 'Natriuretic Peptide, Brain', 'Point-of-Care Systems', 'Predictive Value of Tests', 'Prognosis', 'Reference Values', 'Risk Factors', 'Ventricular Dysfunction, Left']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
19,539,913 | Do both host and graft vessels contribute to revascularization of xenografted human ovarian tissue in a murine model? | {
"contexts": [
"To characterize the human ovarian xenograft revascularization process.",
"Prospective experimental study.",
"Gynecology research unit in a university hospital.",
"Ovarian biopsies were obtained from 12 women aged 22-35 years.",
"Frozen-thawed human ovarian fragments were intraperitoneally grafted into nude mice.",
"Graft perfusion was evaluated by Hoechst 33342 uptake. Murine and human vascularization was analyzed by CD31 and von Willebrand factor double immunostaining.",
"On day 3, some murine neovessels and perfused areas were located at the periphery of the fragments. Nonperfused native human vessels were present in the fragments. From day 5, perfused areas and murine endothelial areas progressively increased. Host angiogenesis initiated ovarian graft reperfusion: murine neovessels penetrated from the periphery and were colocalized with perfused areas. By day 10, the increase in perfusion and murine vascularization was significant. The center of the fragments was perfused and a significant increase was observed in human vasculature."
],
"labels": [
"OBJECTIVE",
"METHODS",
"METHODS",
"METHODS",
"METHODS",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Animals",
"Benzimidazoles",
"Biopsy",
"Cryopreservation",
"Endothelial Cells",
"Female",
"Fluorescent Dyes",
"Humans",
"Immunohistochemistry",
"Mice",
"Mice, Nude",
"Models, Animal",
"Neovascularization, Physiologic",
"Ovary",
"Platelet Endothelial Cell Adhesion Molecule-1",
"Prospective Studies",
"Regional Blood Flow",
"Time Factors",
"Transplantation, Heterologous",
"Young Adult",
"von Willebrand Factor"
]
} | Host and graft vessels contributed sequentially to graft revascularization: murine angiogenesis initiated reperfusion from day 5 and, by day 10, human angiogenesis was shown to participate in graft revascularization. Host and graft angiogenesis are potential targets to reduce the avascular period after grafting. | yes | [
{
"from": "human",
"value": "Question: Do both host and graft vessels contribute to revascularization of xenografted human ovarian tissue in a murine model?\nContext: {'contexts': ['To characterize the human ovarian xenograft revascularization process.', 'Prospective experimental study.', 'Gynecology research unit in a university hospital.', 'Ovarian biopsies were obtained from 12 women aged 22-35 years.', 'Frozen-thawed human ovarian fragments were intraperitoneally grafted into nude mice.', 'Graft perfusion was evaluated by Hoechst 33342 uptake. Murine and human vascularization was analyzed by CD31 and von Willebrand factor double immunostaining.', 'On day 3, some murine neovessels and perfused areas were located at the periphery of the fragments. Nonperfused native human vessels were present in the fragments. From day 5, perfused areas and murine endothelial areas progressively increased. Host angiogenesis initiated ovarian graft reperfusion: murine neovessels penetrated from the periphery and were colocalized with perfused areas. By day 10, the increase in perfusion and murine vascularization was significant. The center of the fragments was perfused and a significant increase was observed in human vasculature.'], 'labels': ['OBJECTIVE', 'METHODS', 'METHODS', 'METHODS', 'METHODS', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Animals', 'Benzimidazoles', 'Biopsy', 'Cryopreservation', 'Endothelial Cells', 'Female', 'Fluorescent Dyes', 'Humans', 'Immunohistochemistry', 'Mice', 'Mice, Nude', 'Models, Animal', 'Neovascularization, Physiologic', 'Ovary', 'Platelet Endothelial Cell Adhesion Molecule-1', 'Prospective Studies', 'Regional Blood Flow', 'Time Factors', 'Transplantation, Heterologous', 'Young Adult', 'von Willebrand Factor']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
19,545,451 | Do combined effects of obesity and type 2 diabetes contribute to increased breast cancer risk in premenopausal women? | {
"contexts": [
"Both obesity and type 2 diabetes are among the risk factors for breast cancer development. Combined effect of these metabolic abnormalities on breast cancer risk however, has not been examined in premenopausal women. We tested this association in type 2 diabetic women, categorized as obese, overweight and normal body weight groups based on BMI.",
"A total of 101 subjects were included in this study. Serum levels of IL-6, TNF-alpha, C reactive protein, leptin, TGF-alpha, adiponectin and insulin were measured by ELISA. Data were logarithmically transformed for variables not normally distributed. Analysis of variance with post-hoc Bonferroni was applied to compare the data between the groups. Simple and partial correlation coefficients between the variables were determined and a stepwise multiple linear regression analysis was performed to determine the relationships between the variables of interest.",
"Significantly increased levels of IL-6, C reactive protein, leptin and significantly decreased levels of adiponectin were found in obese group, while the levels of TNF-alpha and TGF-alpha were unaltered. A positive correlation between waist circumference and IL-6 was found in obese group. Similarly, C reactive protein, waist and hip circumferences were linearly correlated with BMI in obese group. Stepwise multiple linear regression analysis revealed several significant predictors for breast cancer risk."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Breast Neoplasms",
"Cross-Sectional Studies",
"Diabetes Mellitus, Type 2",
"Female",
"Humans",
"Middle Aged",
"Obesity",
"Premenopause",
"Risk Factors"
]
} | Obesity and type 2 diabetes, owing to their effects on adipocytokines and inflammatory mediators, contribute to increased breast cancer risk in premenopausal women. This study emphasizes healthy life style and better management of these metabolic disorders to avoid the pathogenesis of breast cancer and of other chronic diseases. | yes | [
{
"from": "human",
"value": "Question: Do combined effects of obesity and type 2 diabetes contribute to increased breast cancer risk in premenopausal women?\nContext: {'contexts': ['Both obesity and type 2 diabetes are among the risk factors for breast cancer development. Combined effect of these metabolic abnormalities on breast cancer risk however, has not been examined in premenopausal women. We tested this association in type 2 diabetic women, categorized as obese, overweight and normal body weight groups based on BMI.', 'A total of 101 subjects were included in this study. Serum levels of IL-6, TNF-alpha, C reactive protein, leptin, TGF-alpha, adiponectin and insulin were measured by ELISA. Data were logarithmically transformed for variables not normally distributed. Analysis of variance with post-hoc Bonferroni was applied to compare the data between the groups. Simple and partial correlation coefficients between the variables were determined and a stepwise multiple linear regression analysis was performed to determine the relationships between the variables of interest.', 'Significantly increased levels of IL-6, C reactive protein, leptin and significantly decreased levels of adiponectin were found in obese group, while the levels of TNF-alpha and TGF-alpha were unaltered. A positive correlation between waist circumference and IL-6 was found in obese group. Similarly, C reactive protein, waist and hip circumferences were linearly correlated with BMI in obese group. Stepwise multiple linear regression analysis revealed several significant predictors for breast cancer risk.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Breast Neoplasms', 'Cross-Sectional Studies', 'Diabetes Mellitus, Type 2', 'Female', 'Humans', 'Middle Aged', 'Obesity', 'Premenopause', 'Risk Factors']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,543,339 | Is addition of rituximab associated with survival benefit compared with CHOP alone for patients with stage I diffuse large B-cell lymphoma? | {
"contexts": [
"The role of rituximab in combination with CHOP regimen in patients with stage I diffuse large B-cell lymphoma (DLBCL) remains to be defined. We aimed to compare CHOP plus rituximab (R-CHOP) with CHOP alone and determine the value of radiotherapy in these patients.",
"Between 2003 and 2009, 140 untreated patients with stage I DLBCL were retrospectively analyzed in this study.",
"Seventy-eight patients were treated in R-CHOP group and 62 in CHOP group. Ninety-one patients received additional radiotherapy at the end of chemotherapy. The different treatment groups were well-balanced with respect to baseline characteristics. Complete response (CR) rate was 77% both in R-CHOP and CHOP groups (P=0.945). After a median follow-up period of 56 months, patients received R-CHOP regimen had similar 5-year progression-free survival (PFS) (76% vs. 85%; log-rank P=0.215) and 5-year overall survival (OS) (90% vs. 96%; log-rank P=0.175) compared with those with CHOP alone. Patients with radiotherapy had significantly increased 5-year PFS compared with those who had chemotherapy alone (86% vs. 71%; log-rank P=0.005). At multivariate analysis, patients who had CR (P=0.008) and received radiotherapy (P=0.003) were significantly associated with superior PFS."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": []
} | CHOP alone could be as effective as R-CHOP regimen and additional radiotherapy would be necessary for stage I or stage I non-bulky DLBCL patients. | no | [
{
"from": "human",
"value": "Question: Is addition of rituximab associated with survival benefit compared with CHOP alone for patients with stage I diffuse large B-cell lymphoma?\nContext: {'contexts': ['The role of rituximab in combination with CHOP regimen in patients with stage I diffuse large B-cell lymphoma (DLBCL) remains to be defined. We aimed to compare CHOP plus rituximab (R-CHOP) with CHOP alone and determine the value of radiotherapy in these patients.', 'Between 2003 and 2009, 140 untreated patients with stage I DLBCL were retrospectively analyzed in this study.', 'Seventy-eight patients were treated in R-CHOP group and 62 in CHOP group. Ninety-one patients received additional radiotherapy at the end of chemotherapy. The different treatment groups were well-balanced with respect to baseline characteristics. Complete response (CR) rate was 77% both in R-CHOP and CHOP groups (P=0.945). After a median follow-up period of 56 months, patients received R-CHOP regimen had similar 5-year progression-free survival (PFS) (76% vs. 85%; log-rank P=0.215) and 5-year overall survival (OS) (90% vs. 96%; log-rank P=0.175) compared with those with CHOP alone. Patients with radiotherapy had significantly increased 5-year PFS compared with those who had chemotherapy alone (86% vs. 71%; log-rank P=0.005). At multivariate analysis, patients who had CR (P=0.008) and received radiotherapy (P=0.003) were significantly associated with superior PFS.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
26,546,562 | Is higher education associated with a better rheumatoid arthritis outcome concerning for pain and function but not disease activity : results from the EIRA cohort and Swedish rheumatology register? | {
"contexts": [
"Whether low socioeconomic status (SES) is associated with worse rheumatoid arthritis (RA) outcomes in countries with general tax-financed healthcare systems (such as Sweden) remains to be elucidated. Our aim was to investigate the influence of educational background (achieving university/college degree (high) or not (low)) on the outcomes of early RA, in terms of disease activity (DAS28), pain (VAS-pain), and functional impairment (HAQ).",
"We evaluated DMARD-naïve RA patients recruited in the Epidemiological Investigation of RA (EIRA) study with outcomes followed in the Swedish Rheumatology Quality (SRQ) register (N = 3021). Outcomes were categorized in three ways: (1) scores equal to/above median vs. below median; (2) DAS28-based low disease activity, good response, remission; (3) scores decreased over the median vs. less than median. Associations between educational background and outcomes were calculated by modified Poisson regressions, at diagnosis and at each of the three standard (3, 6, 12 months) follow-up visits.",
"Patients with different educational background had similar symptom durations (195 days) and anti-rheumatic therapies at baseline, and comparable treatment patterns during follow-up. Patients with a high education level had significantly less pain and less functional disability at baseline and throughout the whole follow-up period (VAS-pain: baseline: 49 (28-67) vs. 53 (33-71), p <0.0001; 1-year visit: RR = 0.81 (95% CI 0.73-0.90). HAQ: baseline: 0.88 (0.50-1.38) vs. 1.00 (0.63-1.50), p = 0.001; 1-year visit: 0.84 (0.77-0.92)). They also had greater chances to achieve pain remission (VAS-pain ≤20) after one year (1.17 (1.07-1.28)). Adjustments for smoking and BMI altered the results only marginally. Educational background did not influence DAS28-based outcomes."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Activities of Daily Living",
"Adult",
"Aged",
"Antirheumatic Agents",
"Arthritis, Rheumatoid",
"Cohort Studies",
"Educational Status",
"Female",
"Humans",
"Male",
"Middle Aged",
"Outcome Assessment (Health Care)",
"Pain",
"Registries",
"Socioeconomic Factors",
"Sweden",
"Treatment Outcome"
]
} | In Sweden, with tax-financed, generally accessible healthcare system, RA patients with a high education level experienced less pain and less functional disability. Further, these patients achieved pain remission more often during the first year receiving standard care. Importantly, education background affected neither time to referral to rheumatologists, disease activity nor anti-rheumatic treatments. | yes | [
{
"from": "human",
"value": "Question: Is higher education associated with a better rheumatoid arthritis outcome concerning for pain and function but not disease activity : results from the EIRA cohort and Swedish rheumatology register?\nContext: {'contexts': ['Whether low socioeconomic status (SES) is associated with worse rheumatoid arthritis (RA) outcomes in countries with general tax-financed healthcare systems (such as Sweden) remains to be elucidated. Our aim was to investigate the influence of educational background (achieving university/college degree (high) or not (low)) on the outcomes of early RA, in terms of disease activity (DAS28), pain (VAS-pain), and functional impairment (HAQ).', 'We evaluated DMARD-naïve RA patients recruited in the Epidemiological Investigation of RA (EIRA) study with outcomes followed in the Swedish Rheumatology Quality (SRQ) register (N\\u2009=\\u20093021). Outcomes were categorized in three ways: (1) scores equal to/above median vs. below median; (2) DAS28-based low disease activity, good response, remission; (3) scores decreased over the median vs. less than median. Associations between educational background and outcomes were calculated by modified Poisson regressions, at diagnosis and at each of the three standard (3, 6, 12 months) follow-up visits.', 'Patients with different educational background had similar symptom durations (195 days) and anti-rheumatic therapies at baseline, and comparable treatment patterns during follow-up. Patients with a high education level had significantly less pain and less functional disability at baseline and throughout the whole follow-up period (VAS-pain: baseline: 49 (28-67) vs. 53 (33-71), p\\u2009<0.0001; 1-year visit: RR\\u2009=\\u20090.81 (95% CI 0.73-0.90). HAQ: baseline: 0.88 (0.50-1.38) vs. 1.00 (0.63-1.50), p\\u2009=\\u20090.001; 1-year visit: 0.84 (0.77-0.92)). They also had greater chances to achieve pain remission (VAS-pain\\u2009≤20) after one year (1.17 (1.07-1.28)). Adjustments for smoking and BMI altered the results only marginally. Educational background did not influence DAS28-based outcomes.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Activities of Daily Living', 'Adult', 'Aged', 'Antirheumatic Agents', 'Arthritis, Rheumatoid', 'Cohort Studies', 'Educational Status', 'Female', 'Humans', 'Male', 'Middle Aged', 'Outcome Assessment (Health Care)', 'Pain', 'Registries', 'Socioeconomic Factors', 'Sweden', 'Treatment Outcome']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,539,255 | Does eGCG attenuate Uric Acid-Induced Inflammatory and Oxidative Stress Responses by Medicating the NOTCH Pathway? | {
"contexts": [
"The aim of this study is to investigate whether (-)-epigallocatechin-3-gallate (EGCG) can prevent the UA-induced inflammatory effect of human umbilical vein endothelial cells (HUVEC) and the involved mechanisms in vitro.",
"HUVEC were subjected to uric acid (UA) with or without EGCG treatment. RT-PCR and western blots were performed to determine the level of inflammation marker. The antioxidant activity was evaluated by measuring scavenged reactive oxygen species (ROS). Functional studies of the role of Notch-1 in HUVEC lines were performed using RNA interference analyses.",
"UA significantly increased the expressions of IL-6, ICAM-1, TNF-α, and MCP-1 and the production of ROS in HUVEC. Meanwhile, the expression of Notch-1 and its downstream effects significantly increased. Using siRNA, inhibition of Notch-1 signaling significantly impeded the expressions of inflammatory cytokines under UA treatment. Interestingly, EGCG suppressed the expressions of inflammatory cytokines and the generation of ROS. Western blot analysis of Notch-1 showed that EGCG significantly decreased the expressions of inflammatory cytokines through Notch-1 signaling pathways."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Catechin",
"Chemokine CCL2",
"Down-Regulation",
"Human Umbilical Vein Endothelial Cells",
"Humans",
"Intercellular Adhesion Molecule-1",
"Interleukin-6",
"Oxidative Stress",
"RNA Interference",
"RNA, Small Interfering",
"Reactive Oxygen Species",
"Real-Time Polymerase Chain Reaction",
"Receptors, Notch",
"Signal Transduction",
"Tumor Necrosis Factor-alpha",
"Up-Regulation",
"Uric Acid"
]
} | In summary, our findings indicated that Notch-1 plays an important role in the UA-induced inflammatory response, and the downregulation of Notch-1 by EGCG could be an effective approach to decrease inflammation and oxidative stress induced by UA. | yes | [
{
"from": "human",
"value": "Question: Does eGCG attenuate Uric Acid-Induced Inflammatory and Oxidative Stress Responses by Medicating the NOTCH Pathway?\nContext: {'contexts': ['The aim of this study is to investigate whether (-)-epigallocatechin-3-gallate (EGCG) can prevent the UA-induced inflammatory effect of human umbilical vein endothelial cells (HUVEC) and the involved mechanisms in vitro.', 'HUVEC were subjected to uric acid (UA) with or without EGCG treatment. RT-PCR and western blots were performed to determine the level of inflammation marker. The antioxidant activity was evaluated by measuring scavenged reactive oxygen species (ROS). Functional studies of the role of Notch-1 in HUVEC lines were performed using RNA interference analyses.', 'UA significantly increased the expressions of IL-6, ICAM-1, TNF-α, and MCP-1 and the production of ROS in HUVEC. Meanwhile, the expression of Notch-1 and its downstream effects significantly increased. Using siRNA, inhibition of Notch-1 signaling significantly impeded the expressions of inflammatory cytokines under UA treatment. Interestingly, EGCG suppressed the expressions of inflammatory cytokines and the generation of ROS. Western blot analysis of Notch-1 showed that EGCG significantly decreased the expressions of inflammatory cytokines through Notch-1 signaling pathways.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Catechin', 'Chemokine CCL2', 'Down-Regulation', 'Human Umbilical Vein Endothelial Cells', 'Humans', 'Intercellular Adhesion Molecule-1', 'Interleukin-6', 'Oxidative Stress', 'RNA Interference', 'RNA, Small Interfering', 'Reactive Oxygen Species', 'Real-Time Polymerase Chain Reaction', 'Receptors, Notch', 'Signal Transduction', 'Tumor Necrosis Factor-alpha', 'Up-Regulation', 'Uric Acid']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,539,253 | Is dNA-methylation in C1R a prognostic biomarker for acute myeloid leukemia? | {
"contexts": [
"Epigenetic aberrations play a central role in the pathophysiology of acute myeloid leukemia (AML). It has been shown that molecular signatures based on DNA-methylation (DNAm) patterns can be used for classification of the disease. In this study, we followed the hypothesis that DNAm at a single CpG site might support risk stratification in AML.",
"Using DNAm profiles of 194 patients from The Cancer Genome Atlas (TCGA), we identified a CpG site in complement component 1 subcomponent R (C1R) as best suited biomarker: patients with higher methylation at this CpG site (>27 % DNAm) reveal significantly longer overall survival (53 versus 11 months; P < 0.0001). This finding was validated in an independent set of 62 DNAm profiles of cytogenetically normal AML patients (P = 0.009) and with a region-specific pyrosequencing assay in 84 AML samples (P = 0.012). DNAm of C1R correlated with genomic DNAm and gene expression patterns, whereas there was only moderate association with gene expression levels of C1R. These results indicate that DNAm of C1R is a biomarker reflecting chromatin reorganization rather than being of pathophysiological relevance per se. Notably, DNAm of C1R was associated with occurrence of specific genomic mutations that are traditionally used for risk stratification in AML. Furthermore, DNAm of C1R correlates also with overall survival in several other types of cancer, but the prognostic relevance was less pronounced than in AML."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": []
} | Analysis of DNAm at C1R provides a simple, robust, and cost-effective biomarker to further complement risk assessment in AML. | yes | [
{
"from": "human",
"value": "Question: Is dNA-methylation in C1R a prognostic biomarker for acute myeloid leukemia?\nContext: {'contexts': ['Epigenetic aberrations play a central role in the pathophysiology of acute myeloid leukemia (AML). It has been shown that molecular signatures based on DNA-methylation (DNAm) patterns can be used for classification of the disease. In this study, we followed the hypothesis that DNAm at a single CpG site might support risk stratification in AML.', 'Using DNAm profiles of 194 patients from The Cancer Genome Atlas (TCGA), we identified a CpG site in complement component 1 subcomponent R (C1R) as best suited biomarker: patients with higher methylation at this CpG site (>27\\xa0% DNAm) reveal significantly longer overall survival (53 versus 11\\xa0months; P\\u2009<\\u20090.0001). This finding was validated in an independent set of 62 DNAm profiles of cytogenetically normal AML patients (P\\u2009=\\u20090.009) and with a region-specific pyrosequencing assay in 84 AML samples (P\\u2009=\\u20090.012). DNAm of C1R correlated with genomic DNAm and gene expression patterns, whereas there was only moderate association with gene expression levels of C1R. These results indicate that DNAm of C1R is a biomarker reflecting chromatin reorganization rather than being of pathophysiological relevance per se. Notably, DNAm of C1R was associated with occurrence of specific genomic mutations that are traditionally used for risk stratification in AML. Furthermore, DNAm of C1R correlates also with overall survival in several other types of cancer, but the prognostic relevance was less pronounced than in AML.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,553,031 | Is prediction of critical weight loss during radiation treatment in head and neck cancer patients dependent on BMI? | {
"contexts": [
"The aims of the present study were to explore pre-treatment predictors of weight loss during radiation treatment only in head and neck cancer (HNSCC) patients and investigate the weight loss in patients with or without a feeding tube.",
"Retrospectively, weight change during curative radiotherapy was investigated in 476 consecutive HNSCC patients. Independent predictors were identified using multivariate regression analysis with weight loss below or above 5 % as the primary dependent variable.",
"Baseline BMI, tumor site, and stage predicted weight loss above 5 %. The odds of weight loss above 5 % in patients with BMI >25 were 3.00 ± 0.64 times higher compared with patients with BMI <25 (p < 0.0001). Patients with pharyngeal, oral cavity, or supraglottic tumors had 3.12 ± 0.80 times higher odds of weight loss above 5 % compared with glottic cancer patients (p < 0.0001), and the odds were 1.68 ± 0.40 times higher in stage III-IV patients compared with stage I-II patients (p = 0.03). Seperate analyses revealed that tumor site and stage only predicted weight loss in patients with BMI >25 but not in patients with BMI <25. Patients receiving a feeding tube weighed less than patients without (73.8 vs 78.3 kg) and feeding tube reduced, but did not prevent, weight loss which averaged 6.7 ± 4.7 kg (7.4 ± 4.7 %) compared with 4.7 ± 5.9 kg (5.5 ± 6.0 %) in patients without a feeding tube (P < 0.0001)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Body Mass Index",
"Carcinoma, Squamous Cell",
"Denmark",
"Female",
"Head and Neck Neoplasms",
"Humans",
"Male",
"Middle Aged",
"Nutritional Support",
"Odds Ratio",
"Retrospective Studies",
"Risk Assessment",
"Risk Factors",
"Squamous Cell Carcinoma of Head and Neck",
"Weight Loss"
]
} | Pre-treatment BMI, tumor site and stage predicted weight loss above 5 % in HNSCC patients during radiotherapy. BMI should be considered when analyzing weight loss in HNSCC patients receiving curative radiotherapy. | yes | [
{
"from": "human",
"value": "Question: Is prediction of critical weight loss during radiation treatment in head and neck cancer patients dependent on BMI?\nContext: {'contexts': ['The aims of the present study were to explore pre-treatment predictors of weight loss during radiation treatment only in head and neck cancer (HNSCC) patients and investigate the weight loss in patients with or without a feeding tube.', 'Retrospectively, weight change during curative radiotherapy was investigated in 476 consecutive HNSCC patients. Independent predictors were identified using multivariate regression analysis with weight loss below or above 5 % as the primary dependent variable.', 'Baseline BMI, tumor site, and stage predicted weight loss above 5 %. The odds of weight loss above 5 % in patients with BMI >25 were 3.00\\u2009±\\u20090.64 times higher compared with patients with BMI <25 (p\\u2009<\\u20090.0001). Patients with pharyngeal, oral cavity, or supraglottic tumors had 3.12\\u2009±\\u20090.80 times higher odds of weight loss above 5 % compared with glottic cancer patients (p\\u2009<\\u20090.0001), and the odds were 1.68\\u2009±\\u20090.40 times higher in stage III-IV patients compared with stage I-II patients (p\\u2009=\\u20090.03). Seperate analyses revealed that tumor site and stage only predicted weight loss in patients with BMI >25 but not in patients with BMI <25. Patients receiving a feeding tube weighed less than patients without (73.8 vs 78.3 kg) and feeding tube reduced, but did not prevent, weight loss which averaged 6.7\\u2009±\\u20094.7 kg (7.4\\u2009±\\u20094.7 %) compared with 4.7\\u2009±\\u20095.9 kg (5.5\\u2009±\\u20096.0 %) in patients without a feeding tube (P\\u2009<\\u20090.0001).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Body Mass Index', 'Carcinoma, Squamous Cell', 'Denmark', 'Female', 'Head and Neck Neoplasms', 'Humans', 'Male', 'Middle Aged', 'Nutritional Support', 'Odds Ratio', 'Retrospective Studies', 'Risk Assessment', 'Risk Factors', 'Squamous Cell Carcinoma of Head and Neck', 'Weight Loss']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,548,949 | Does pRL-3 promote gastric cancer migration and invasion through a NF-κB-HIF-1α-miR-210 axis? | {
"contexts": [
"Phosphatase of regenerating liver-3 (PRL-3) has been implicated in controlling cancer cell invasiveness. Deregulated expression of PRL-3 is involved in cancer progression and predicts poor overall survival. Recent studies have revealed critical roles for microRNAs in various cellular processes, including tumorigenic development. In this study, we aimed to explore the linkage between PRL-3 and microRNAs in gastric cancer. We found that PRL-3 transcript levels were positively correlated with miR-210 levels in gastric cancer tissues. In gastric cancer cells, PRL-3 upregulated miR-210 expression in a HIF-1α-dependent fashion under normoxia and hypoxia. In addition, PRL-3 activated NF-κB signaling and promoted HIF-1α expression through modulating phosphorylation of p65. NF-κB signaling, HIF-1α, and miR-210 partially contributed to PRL-3-induced migration and invasion. Furthermore, the levels of PRL-3, HIF-1α, and miR-210 transcripts inversely affected the overall survival of gastric cancer patients. Our work identified the existence of a PRL-3-NF-κB-HIF-1α-miR-210 axis, thus providing new insight into the role of PRL-3 in promoting gastric cancer invasiveness."
],
"labels": [
"UNLABELLED"
],
"meshes": [
"Adult",
"Aged",
"Cell Line, Tumor",
"Cell Movement",
"Cluster Analysis",
"Female",
"Gene Expression Profiling",
"Gene Expression Regulation, Neoplastic",
"Humans",
"Hypoxia",
"Hypoxia-Inducible Factor 1, alpha Subunit",
"Kaplan-Meier Estimate",
"Male",
"MicroRNAs",
"Middle Aged",
"NF-kappa B",
"Neoplasm Grading",
"Neoplasm Invasiveness",
"Neoplasm Proteins",
"Neoplasm Staging",
"Prognosis",
"Protein Tyrosine Phosphatases",
"Signal Transduction",
"Stomach Neoplasms"
]
} | PRL-3 regulates microRNA in gastric cancer. PRL-3 elevates hsa-miR-210 by upregulating HIF-1α. PRL-3 activates a NF-κB-HIF-1α-miR-210 axis by enhancing the phosphorylation of p65. PRL-3 promotes cell migration and invasion via the NF-κB-HIF-1α-miR-210 axis. High levels of PRL-3 and miR-210 are related with poor OS in gastric cancer. | yes | [
{
"from": "human",
"value": "Question: Does pRL-3 promote gastric cancer migration and invasion through a NF-κB-HIF-1α-miR-210 axis?\nContext: {'contexts': ['Phosphatase of regenerating liver-3 (PRL-3) has been implicated in controlling cancer cell invasiveness. Deregulated expression of PRL-3 is involved in cancer progression and predicts poor overall survival. Recent studies have revealed critical roles for microRNAs in various cellular processes, including tumorigenic development. In this study, we aimed to explore the linkage between PRL-3 and microRNAs in gastric cancer. We found that PRL-3 transcript levels were positively correlated with miR-210 levels in gastric cancer tissues. In gastric cancer cells, PRL-3 upregulated miR-210 expression in a HIF-1α-dependent fashion under normoxia and hypoxia. In addition, PRL-3 activated NF-κB signaling and promoted HIF-1α expression through modulating phosphorylation of p65. NF-κB signaling, HIF-1α, and miR-210 partially contributed to PRL-3-induced migration and invasion. Furthermore, the levels of PRL-3, HIF-1α, and miR-210 transcripts inversely affected the overall survival of gastric cancer patients. Our work identified the existence of a PRL-3-NF-κB-HIF-1α-miR-210 axis, thus providing new insight into the role of PRL-3 in promoting gastric cancer invasiveness.'], 'labels': ['UNLABELLED'], 'meshes': ['Adult', 'Aged', 'Cell Line, Tumor', 'Cell Movement', 'Cluster Analysis', 'Female', 'Gene Expression Profiling', 'Gene Expression Regulation, Neoplastic', 'Humans', 'Hypoxia', 'Hypoxia-Inducible Factor 1, alpha Subunit', 'Kaplan-Meier Estimate', 'Male', 'MicroRNAs', 'Middle Aged', 'NF-kappa B', 'Neoplasm Grading', 'Neoplasm Invasiveness', 'Neoplasm Proteins', 'Neoplasm Staging', 'Prognosis', 'Protein Tyrosine Phosphatases', 'Signal Transduction', 'Stomach Neoplasms']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,553,695 | Do calcium Signaling Pathway Genes RUNX2 and CACNA1C Are Associated With Calcific Aortic Valve Disease? | {
"contexts": [
"Calcific aortic valve stenosis (AS) is a life-threatening disease with no medical therapy. The genetic architecture of AS remains elusive. This study combines genome-wide association studies, gene expression, and expression quantitative trait loci mapping in human valve tissues to identify susceptibility genes of AS.",
"A meta-analysis was performed combining the results of 2 genome-wide association studies in 474 and 486 cases from Quebec City (Canada) and Paris (France), respectively. Corresponding controls consisted of 2988 and 1864 individuals with European ancestry from the database of genotypes and phenotypes. mRNA expression levels were evaluated in 9 calcified and 8 normal aortic valves by RNA sequencing. The results were integrated with valve expression quantitative trait loci data obtained from 22 AS patients. Twenty-five single-nucleotide polymorphisms had P<5×10(-6) in the genome-wide association studies meta-analysis. The calcium signaling pathway was the top gene set enriched for genes mapped to moderately AS-associated single-nucleotide polymorphisms. Genes in this pathway were found differentially expressed in valves with and without AS. Two single-nucleotide polymorphisms located in RUNX2 (runt-related transcription factor 2), encoding an osteogenic transcription factor, demonstrated some association with AS (genome-wide association studies P=5.33×10(-5)). The mRNA expression levels of RUNX2 were upregulated in calcified valves and associated with eQTL-SNPs. CACNA1C encoding a subunit of a voltage-dependent calcium channel was upregulated in calcified valves. The eQTL-SNP with the most significant association with AS located in CACNA1C was associated with higher expression of the gene."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Aortic Valve",
"Aortic Valve Stenosis",
"Calcinosis",
"Calcium Channels, L-Type",
"Calcium Signaling",
"Case-Control Studies",
"Core Binding Factor Alpha 1 Subunit",
"Databases, Genetic",
"Female",
"Genome-Wide Association Study",
"Humans",
"Male",
"Polymorphism, Single Nucleotide"
]
} | This integrative genomic study confirmed the role of RUNX2 as a potential driver of AS and identified a new AS susceptibility gene, CACNA1C, belonging to the calcium signaling pathway. | yes | [
{
"from": "human",
"value": "Question: Do calcium Signaling Pathway Genes RUNX2 and CACNA1C Are Associated With Calcific Aortic Valve Disease?\nContext: {'contexts': ['Calcific aortic valve stenosis (AS) is a life-threatening disease with no medical therapy. The genetic architecture of AS remains elusive. This study combines genome-wide association studies, gene expression, and expression quantitative trait loci mapping in human valve tissues to identify susceptibility genes of AS.', 'A meta-analysis was performed combining the results of 2 genome-wide association studies in 474 and 486 cases from Quebec City (Canada) and Paris (France), respectively. Corresponding controls consisted of 2988 and 1864 individuals with European ancestry from the database of genotypes and phenotypes. mRNA expression levels were evaluated in 9 calcified and 8 normal aortic valves by RNA sequencing. The results were integrated with valve expression quantitative trait loci data obtained from 22 AS patients. Twenty-five single-nucleotide polymorphisms had P<5×10(-6) in the genome-wide association studies meta-analysis. The calcium signaling pathway was the top gene set enriched for genes mapped to moderately AS-associated single-nucleotide polymorphisms. Genes in this pathway were found differentially expressed in valves with and without AS. Two single-nucleotide polymorphisms located in RUNX2 (runt-related transcription factor 2), encoding an osteogenic transcription factor, demonstrated some association with AS (genome-wide association studies P=5.33×10(-5)). The mRNA expression levels of RUNX2 were upregulated in calcified valves and associated with eQTL-SNPs. CACNA1C encoding a subunit of a voltage-dependent calcium channel was upregulated in calcified valves. The eQTL-SNP with the most significant association with AS located in CACNA1C was associated with higher expression of the gene.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Aortic Valve', 'Aortic Valve Stenosis', 'Calcinosis', 'Calcium Channels, L-Type', 'Calcium Signaling', 'Case-Control Studies', 'Core Binding Factor Alpha 1 Subunit', 'Databases, Genetic', 'Female', 'Genome-Wide Association Study', 'Humans', 'Male', 'Polymorphism, Single Nucleotide']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,549,734 | Does a Dipeptidyl Peptidase-4 Inhibitor but not Incretins suppress Abdominal Aortic Aneurysms in Angiotensin II-Infused Apolipoprotein E-Null Mice? | {
"contexts": [
"The main pathophysiology of abdominal aortic aneurysm (AAA) considerably overlaps with that of atherosclerosis. We reported that incretins [glucagon-like peptide (GLP)-1 and glucose-dependent insulinotropic polypeptide (GIP)] or a dipeptidyl peptidase-4 inhibitor (DPP-4I) suppressed atherosclerosis in apolipoprotein E-null (Apoe－/－) mice. Here we investigated the effects of incretin-related agents on AAA in a mouse model.",
"Apoe－/－ mice maintained on an atherogenic diet were subcutaneously infused with saline, Ang II (2000 ng/kg/min), Ang II, and native GLP-1 (2.16 nmol/kg/day) or Ang II and native GIP (25 nmol/kg/day) for 4 weeks. DPP-4I (MK0626, 6 mg/kg/day) was provided in the diet to the Ang II-infused mice with or without incretin receptor antagonists [(Pro3) GIP and exendin (9-39)].",
"AAA occurred in 70% of the animals receiving Ang II. DPP-4I reduced this rate to 40% and significantly suppressed AAA dilatation, fibrosis, and thrombosis. In contrast, incretins failed to attenuate AAA. Incretin receptor blockers did not reverse the suppressive effects of DPP-4I on AAA. In the aorta, DPP-4I significantly reduced the expression of Interleukin-1β and increased that of tissue inhibitor of metalloproteinase (TIMP)-2. In addition, DPP-4I increased the ratio of TIMP-2 to matrix metalloproteinases-9."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Angiotensin II",
"Animals",
"Aorta",
"Aortic Aneurysm, Abdominal",
"Apolipoproteins E",
"Blood Pressure",
"Dipeptidyl-Peptidase IV Inhibitors",
"Gastric Inhibitory Polypeptide",
"Gene Expression Regulation",
"Glucagon-Like Peptide 1",
"Incretins",
"Inflammation",
"Interleukin-1beta",
"Male",
"Matrix Metalloproteinase 9",
"Mice",
"Mice, Knockout",
"Plaque, Atherosclerotic",
"Tissue Inhibitor of Metalloproteinase-2"
]
} | DPP-4I, MK0626, but not native incretins has protective effects against AAA in Ang II-infused Apoe－/－ mice via suppression of inflammation, proteolysis, and fibrosis in the aortic wall. | yes | [
{
"from": "human",
"value": "Question: Does a Dipeptidyl Peptidase-4 Inhibitor but not Incretins suppress Abdominal Aortic Aneurysms in Angiotensin II-Infused Apolipoprotein E-Null Mice?\nContext: {'contexts': ['The main pathophysiology of abdominal aortic aneurysm (AAA) considerably overlaps with that of atherosclerosis. We reported that incretins [glucagon-like peptide (GLP)-1 and glucose-dependent insulinotropic polypeptide (GIP)] or a dipeptidyl peptidase-4 inhibitor (DPP-4I) suppressed atherosclerosis in apolipoprotein E-null (Apoe－/－) mice. Here we investigated the effects of incretin-related agents on AAA in a mouse model.', 'Apoe－/－ mice maintained on an atherogenic diet were subcutaneously infused with saline, Ang II (2000 ng/kg/min), Ang II, and native GLP-1 (2.16 nmol/kg/day) or Ang II and native GIP (25 nmol/kg/day) for 4 weeks. DPP-4I (MK0626, 6 mg/kg/day) was provided in the diet to the Ang II-infused mice with or without incretin receptor antagonists [(Pro3) GIP and exendin (9-39)].', 'AAA occurred in 70% of the animals receiving Ang II. DPP-4I reduced this rate to 40% and significantly suppressed AAA dilatation, fibrosis, and thrombosis. In contrast, incretins failed to attenuate AAA. Incretin receptor blockers did not reverse the suppressive effects of DPP-4I on AAA. In the aorta, DPP-4I significantly reduced the expression of Interleukin-1β and increased that of tissue inhibitor of metalloproteinase (TIMP)-2. In addition, DPP-4I increased the ratio of TIMP-2 to matrix metalloproteinases-9.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Angiotensin II', 'Animals', 'Aorta', 'Aortic Aneurysm, Abdominal', 'Apolipoproteins E', 'Blood Pressure', 'Dipeptidyl-Peptidase IV Inhibitors', 'Gastric Inhibitory Polypeptide', 'Gene Expression Regulation', 'Glucagon-Like Peptide 1', 'Incretins', 'Inflammation', 'Interleukin-1beta', 'Male', 'Matrix Metalloproteinase 9', 'Mice', 'Mice, Knockout', 'Plaque, Atherosclerotic', 'Tissue Inhibitor of Metalloproteinase-2']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,544,952 | Do lack of Acute Hand Care in the Southwest United States? | {
"contexts": [
"To describe the epidemiology of acute hand injuries and hand infections and to describe the factors associated with the transfer of these patients to a level 1 trauma center. In addition, we sought to understand management before transfer.",
"Retrospective review of patients with hand trauma or hand infection transferred to our level 1 trauma center from May 2009 to August 2011. We also identified hospitals with emergency departments (EDs) in our region and surveyed ED providers in these hospitals with regard to acute hand care.",
"A level 1 trauma center in the United States.",
"Four hundred sixty consecutive transfers for acute hand care.",
"The average patient age was 38. Most were male (84%), uninsured (51%), and from another county (59%). The average distance of transfer was 51 miles, and 80% were transferred by ground ambulance. The most common reasons for transfer were amputations (24%), infections (21%), lacerations (17%), and fractures/dislocations (16%). Of the 345 hospitals with an ED surveyed, 71% never had hand surgery coverage."
],
"labels": [
"OBJECTIVE",
"METHODS",
"METHODS",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Age Distribution",
"Aged",
"Critical Care",
"Emergency Service, Hospital",
"Female",
"Hand Injuries",
"Health Services Accessibility",
"Humans",
"Infection",
"Male",
"Middle Aged",
"Needs Assessment",
"Orthopedic Procedures",
"Patient Transfer",
"Prevalence",
"Risk Factors",
"Sex Distribution",
"Southwestern United States",
"Trauma Centers",
"Travel",
"Young Adult"
]
} | Patients transferred for acute hand care were young and male, and traveled an average 51 miles to get to our center. More than half of these patients were treated and discharged from our ED. This indicates that a majority may have been managed in a clinic setting. Most EDs in our region do not have a hand surgeon available. Most emergency physicians surveyed had received little training in management of acute hand injuries and hand infections. Further research is needed to identify methods to remove barriers to provision of care for patients with hand trauma. | yes | [
{
"from": "human",
"value": "Question: Do lack of Acute Hand Care in the Southwest United States?\nContext: {'contexts': ['To describe the epidemiology of acute hand injuries and hand infections and to describe the factors associated with the transfer of these patients to a level 1 trauma center. In addition, we sought to understand management before transfer.', 'Retrospective review of patients with hand trauma or hand infection transferred to our level 1 trauma center from May 2009 to August 2011. We also identified hospitals with emergency departments (EDs) in our region and surveyed ED providers in these hospitals with regard to acute hand care.', 'A level 1 trauma center in the United States.', 'Four hundred sixty consecutive transfers for acute hand care.', 'The average patient age was 38. Most were male (84%), uninsured (51%), and from another county (59%). The average distance of transfer was 51 miles, and 80% were transferred by ground ambulance. The most common reasons for transfer were amputations (24%), infections (21%), lacerations (17%), and fractures/dislocations (16%). Of the 345 hospitals with an ED surveyed, 71% never had hand surgery coverage.'], 'labels': ['OBJECTIVE', 'METHODS', 'METHODS', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Age Distribution', 'Aged', 'Critical Care', 'Emergency Service, Hospital', 'Female', 'Hand Injuries', 'Health Services Accessibility', 'Humans', 'Infection', 'Male', 'Middle Aged', 'Needs Assessment', 'Orthopedic Procedures', 'Patient Transfer', 'Prevalence', 'Risk Factors', 'Sex Distribution', 'Southwestern United States', 'Trauma Centers', 'Travel', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,554,540 | Is nedd4L expression decreased in ovarian epithelial cancer tissues compared to ovarian non-cancer tissue? | {
"contexts": [
"Recent studies have demonstrated that the neural precursor cell expressed, developmentally downregulated 4-like (Nedd4L) gene plays a role in the progression of various cancers. However, reports describing Nedd4L expression in ovarian cancer tissues are limited.",
"A cohort (n = 117) of archival formalin-fixed, paraffin embedded resected normal ovarian epithelial tissues (n = 10), benign ovarian epithelial tumor tissues (n = 10), serous borderline ovarian epithelial tumor tissues (n = 14), mucous borderline ovarian epithelial tumor tissues (n = 11), and invasive ovarian epithelial cancer tissues (n = 72) were assessed for Nedd4L protein expression using immunohistochemistry.",
"Nedd4L protein expression was significantly decreased in invasive ovarian epithelial cancer tissues compared to non-cancer tissues (P < 0.05). Decreased Nedd4L protein expression correlated with clinical stage, pathological grade, lymph node metastasis and survival (P < 0.05)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Biomarkers, Tumor",
"Carcinoma, Ovarian Epithelial",
"Endosomal Sorting Complexes Required for Transport",
"Female",
"Humans",
"Immunohistochemistry",
"Middle Aged",
"Nedd4 Ubiquitin Protein Ligases",
"Neoplasm Staging",
"Neoplasms, Glandular and Epithelial",
"Ovarian Neoplasms",
"Ovary",
"Prognosis",
"Ubiquitin-Protein Ligases"
]
} | Nedd4L protein expression may be an independent prognostic marker of ovarian cancer development. | yes | [
{
"from": "human",
"value": "Question: Is nedd4L expression decreased in ovarian epithelial cancer tissues compared to ovarian non-cancer tissue?\nContext: {'contexts': ['Recent studies have demonstrated that the neural precursor cell expressed, developmentally downregulated 4-like (Nedd4L) gene plays a role in the progression of various cancers. However, reports describing Nedd4L expression in ovarian cancer tissues are limited.', 'A cohort (n\\u2009=\\u2009117) of archival formalin-fixed, paraffin embedded resected normal ovarian epithelial tissues (n\\u2009=\\u200910), benign ovarian epithelial tumor tissues (n\\u2009=\\u200910), serous borderline ovarian epithelial tumor tissues (n\\u2009=\\u200914), mucous borderline ovarian epithelial tumor tissues (n\\u2009=\\u200911), and invasive ovarian epithelial cancer tissues (n\\u2009=\\u200972) were assessed for Nedd4L protein expression using immunohistochemistry.', 'Nedd4L protein expression was significantly decreased in invasive ovarian epithelial cancer tissues compared to non-cancer tissues (P\\u2009<\\u20090.05). Decreased Nedd4L protein expression correlated with clinical stage, pathological grade, lymph node metastasis and survival (P\\u2009<\\u20090.05).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Biomarkers, Tumor', 'Carcinoma, Ovarian Epithelial', 'Endosomal Sorting Complexes Required for Transport', 'Female', 'Humans', 'Immunohistochemistry', 'Middle Aged', 'Nedd4 Ubiquitin Protein Ligases', 'Neoplasm Staging', 'Neoplasms, Glandular and Epithelial', 'Ovarian Neoplasms', 'Ovary', 'Prognosis', 'Ubiquitin-Protein Ligases']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,529,285 | Is osteopontin a proximal effector of leptin-mediated non-alcoholic steatohepatitis ( NASH ) fibrosis? | {
"contexts": [
"Liver fibrosis develops when hepatic stellate cells (HSC) are activated into collagen-producing myofibroblasts. In non-alcoholic steatohepatitis (NASH), the adipokine leptin is upregulated, and promotes liver fibrosis by directly activating HSC via the hedgehog pathway. We reported that hedgehog-regulated osteopontin (OPN) plays a key role in promoting liver fibrosis. Herein, we evaluated if OPN mediates leptin-profibrogenic effects in NASH.",
"Leptin-deficient (ob/ob) and wild-type (WT) mice were fed control or methionine-choline deficient (MCD) diet. Liver tissues were assessed by Sirius-red, OPN and αSMA IHC, and qRT-PCR for fibrogenic genes. In vitro, HSC with stable OPN (or control) knockdown were treated with recombinant (r)leptin and OPN-neutralizing or sham-aptamers. HSC response to OPN loss was assessed by wound healing assay. OPN-aptamers were also added to precision-cut liver slices (PCLS), and administered to MCD-fed WT (leptin-intact) mice to determine if OPN neutralization abrogated fibrogenesis.",
"MCD-fed WT mice developed NASH-fibrosis, upregulated OPN, and accumulated αSMA+ cells. Conversely, MCD-fed ob/ob mice developed less fibrosis and accumulated fewer αSMA+ and OPN+ cells. In vitro, leptin-treated HSC upregulated OPN, αSMA, collagen 1α1 and TGFβ mRNA by nearly 3-fold, but this effect was blunted by OPN loss. Inhibition of PI3K and transduction of dominant negative-Akt abrogated leptin-mediated OPN induction, while constitutive active-Akt upregulated OPN. Finally, OPN neutralization reduced leptin-mediated fibrogenesis in both PCLS and MCD-fed mice."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": []
} | OPN overexpression in NASH enhances leptin-mediated fibrogenesis via PI3K/Akt. OPN neutralization significantly reduces NASH fibrosis, reinforcing the potential utility of targeting OPN in the treatment of patients with advanced NASH. | yes | [
{
"from": "human",
"value": "Question: Is osteopontin a proximal effector of leptin-mediated non-alcoholic steatohepatitis ( NASH ) fibrosis?\nContext: {'contexts': ['Liver fibrosis develops when hepatic stellate cells (HSC) are activated into collagen-producing myofibroblasts. In non-alcoholic steatohepatitis (NASH), the adipokine leptin is upregulated, and promotes liver fibrosis by directly activating HSC via the hedgehog pathway. We reported that hedgehog-regulated osteopontin (OPN) plays a key role in promoting liver fibrosis. Herein, we evaluated if OPN mediates leptin-profibrogenic effects in NASH.', 'Leptin-deficient (ob/ob) and wild-type (WT) mice were fed control or methionine-choline deficient (MCD) diet. Liver tissues were assessed by Sirius-red, OPN and αSMA IHC, and qRT-PCR for fibrogenic genes. In vitro, HSC with stable OPN (or control) knockdown were treated with recombinant (r)leptin and OPN-neutralizing or sham-aptamers. HSC response to OPN loss was assessed by wound healing assay. OPN-aptamers were also added to precision-cut liver slices (PCLS), and administered to MCD-fed WT (leptin-intact) mice to determine if OPN neutralization abrogated fibrogenesis.', 'MCD-fed WT mice developed NASH-fibrosis, upregulated OPN, and accumulated αSMA+ cells. Conversely, MCD-fed ob/ob mice developed less fibrosis and accumulated fewer αSMA+ and OPN+ cells. In vitro, leptin-treated HSC upregulated OPN, αSMA, collagen 1α1 and TGFβ mRNA by nearly 3-fold, but this effect was blunted by OPN loss. Inhibition of PI3K and transduction of dominant negative-Akt abrogated leptin-mediated OPN induction, while constitutive active-Akt upregulated OPN. Finally, OPN neutralization reduced leptin-mediated fibrogenesis in both PCLS and MCD-fed mice.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,538,215 | Does a20 suppress hepatocellular carcinoma proliferation and metastasis through inhibition of Twist1 expression? | {
"contexts": [
"Aberrant expression of A20 has been reported in several human malignancies including hepatocellular carcinoma (HCC). However, its clinical relevance and potential role in HCC remain unknown.",
"Quantitative PCR, Western blots and immunohistochemistry analyses were used to quantify A20 expression in HCC samples and cell lines. The correlation of A20 expression with clinicopathologic features was analyzed in a cohort containing 143 patients with primary HCC. Kaplan-Meier curves were used to evaluate the association between A20 expression and patient survival. Functional studies were performed to determine the effects of A20 on proliferation and metastasis of HCC cells in vitro and in vivo.",
"Expression of A20 was increased in HCC tissues and cell lines. Increased expression of A20 was negatively correlated with the tumor size, TNM stage, tumor thrombus formation, capsular invasion and serum AFP levels. Patients with higher A20 expression had a prolonged disease-free survival and overall survival than those with lower A20 expression. Forced expression of A20 significantly inhibited the proliferative and invasive properties of HCC cells both in vitro and in vivo, whereas knockdown of A20 expression showed the opposite effects. Further studies revealed that expression of A20 was inversely correlated with Twist1 levels and NF-κB activity in HCC tissues and cell lines. A20-induced suppression of proliferation and migration of HCC cells were mainly mediated through inhibition of Twist1 expression that was regulated at least partly by A20-induced attenuation of NF-κB activity."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Biomarkers, Tumor",
"Carcinoma, Hepatocellular",
"Cell Line, Tumor",
"Cell Movement",
"Cell Proliferation",
"DNA-Binding Proteins",
"Disease-Free Survival",
"Female",
"Gene Expression Regulation, Neoplastic",
"Humans",
"Immunohistochemistry",
"Intracellular Signaling Peptides and Proteins",
"Liver Neoplasms",
"Male",
"Mice",
"Mice, Nude",
"Middle Aged",
"NF-kappa B",
"Neoplasm Invasiveness",
"Nuclear Proteins",
"Tissue Array Analysis",
"Tumor Necrosis Factor alpha-Induced Protein 3",
"Twist-Related Protein 1",
"Xenograft Model Antitumor Assays"
]
} | Our results demonstrate that A20 plays a negative role in the development and progression of HCC probably through inhibiting Twist1 expression. A20 may serve as a novel prognostic biomarker and potential therapeutic target for HCC patients. | yes | [
{
"from": "human",
"value": "Question: Does a20 suppress hepatocellular carcinoma proliferation and metastasis through inhibition of Twist1 expression?\nContext: {'contexts': ['Aberrant expression of A20 has been reported in several human malignancies including hepatocellular carcinoma (HCC). However, its clinical relevance and potential role in HCC remain unknown.', 'Quantitative PCR, Western blots and immunohistochemistry analyses were used to quantify A20 expression in HCC samples and cell lines. The correlation of A20 expression with clinicopathologic features was analyzed in a cohort containing 143 patients with primary HCC. Kaplan-Meier curves were used to evaluate the association between A20 expression and patient survival. Functional studies were performed to determine the effects of A20 on proliferation and metastasis of HCC cells in vitro and in vivo.', 'Expression of A20 was increased in HCC tissues and cell lines. Increased expression of A20 was negatively correlated with the tumor size, TNM stage, tumor thrombus formation, capsular invasion and serum AFP levels. Patients with higher A20 expression had a prolonged disease-free survival and overall survival than those with lower A20 expression. Forced expression of A20 significantly inhibited the proliferative and invasive properties of HCC cells both in vitro and in vivo, whereas knockdown of A20 expression showed the opposite effects. Further studies revealed that expression of A20 was inversely correlated with Twist1 levels and NF-κB activity in HCC tissues and cell lines. A20-induced suppression of proliferation and migration of HCC cells were mainly mediated through inhibition of Twist1 expression that was regulated at least partly by A20-induced attenuation of NF-κB activity.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Biomarkers, Tumor', 'Carcinoma, Hepatocellular', 'Cell Line, Tumor', 'Cell Movement', 'Cell Proliferation', 'DNA-Binding Proteins', 'Disease-Free Survival', 'Female', 'Gene Expression Regulation, Neoplastic', 'Humans', 'Immunohistochemistry', 'Intracellular Signaling Peptides and Proteins', 'Liver Neoplasms', 'Male', 'Mice', 'Mice, Nude', 'Middle Aged', 'NF-kappa B', 'Neoplasm Invasiveness', 'Nuclear Proteins', 'Tissue Array Analysis', 'Tumor Necrosis Factor alpha-Induced Protein 3', 'Twist-Related Protein 1', 'Xenograft Model Antitumor Assays']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,538,583 | Does endothelial β-Catenin Signaling be Required for Maintaining Adult Blood-Brain Barrier Integrity and Central Nervous System Homeostasis? | {
"contexts": [
"The blood-brain barrier (BBB) formed by brain endothelial cells interconnected by tight junctions is essential for the homeostasis of the central nervous system. Although studies have shown the importance of various signaling molecules in BBB formation during development, little is known about the molecular basis regulating the integrity of the adult BBB.",
"Using a mouse model with tamoxifen-inducible endothelial cell-restricted disruption of ctnnb1 (iCKO), we show here that endothelial β-catenin signaling is essential for maintaining BBB integrity and central nervous system homeostasis in adult mice. The iCKO mice developed severe seizures accompanied by neuronal injury, multiple brain petechial hemorrhages, and central nervous system inflammation, and all had postictal death. Disruption of endothelial β-catenin induced BBB breakdown and downregulation of the specific tight junction proteins claudin-1 and -3 in adult brain endothelial cells. The clinical relevance of the data is indicated by the observation of decreased expression of claudin-1 and nuclear β-catenin in brain endothelial cells of hemorrhagic lesions of hemorrhagic stroke patients."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Animals",
"Ataxia",
"Basal Ganglia",
"Blood-Brain Barrier",
"Brain",
"Cerebral Hemorrhage",
"Claudin-1",
"Claudin-3",
"Crosses, Genetic",
"Cytokines",
"Down-Regulation",
"Endothelial Cells",
"Female",
"Gene Expression Regulation",
"Gene Knockdown Techniques",
"Genes, Reporter",
"Homeostasis",
"Humans",
"Hyperesthesia",
"Inflammation",
"Male",
"Mice",
"Mice, Transgenic",
"Middle Aged",
"Organ Specificity",
"RNA Interference",
"Seizures",
"Tight Junctions",
"Transgenes",
"beta Catenin"
]
} | These results demonstrate the prerequisite role of endothelial β-catenin in maintaining the integrity of adult BBB. The results suggest that BBB dysfunction secondary to defective β-catenin transcription activity is a key pathogenic factor in hemorrhagic stroke, seizure activity, and central nervous system inflammation. | yes | [
{
"from": "human",
"value": "Question: Does endothelial β-Catenin Signaling be Required for Maintaining Adult Blood-Brain Barrier Integrity and Central Nervous System Homeostasis?\nContext: {'contexts': ['The blood-brain barrier (BBB) formed by brain endothelial cells interconnected by tight junctions is essential for the homeostasis of the central nervous system. Although studies have shown the importance of various signaling molecules in BBB formation during development, little is known about the molecular basis regulating the integrity of the adult BBB.', 'Using a mouse model with tamoxifen-inducible endothelial cell-restricted disruption of ctnnb1 (iCKO), we show here that endothelial β-catenin signaling is essential for maintaining BBB integrity and central nervous system homeostasis in adult mice. The iCKO mice developed severe seizures accompanied by neuronal injury, multiple brain petechial hemorrhages, and central nervous system inflammation, and all had postictal death. Disruption of endothelial β-catenin induced BBB breakdown and downregulation of the specific tight junction proteins claudin-1 and -3 in adult brain endothelial cells. The clinical relevance of the data is indicated by the observation of decreased expression of claudin-1 and nuclear β-catenin in brain endothelial cells of hemorrhagic lesions of hemorrhagic stroke patients.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Animals', 'Ataxia', 'Basal Ganglia', 'Blood-Brain Barrier', 'Brain', 'Cerebral Hemorrhage', 'Claudin-1', 'Claudin-3', 'Crosses, Genetic', 'Cytokines', 'Down-Regulation', 'Endothelial Cells', 'Female', 'Gene Expression Regulation', 'Gene Knockdown Techniques', 'Genes, Reporter', 'Homeostasis', 'Humans', 'Hyperesthesia', 'Inflammation', 'Male', 'Mice', 'Mice, Transgenic', 'Middle Aged', 'Organ Specificity', 'RNA Interference', 'Seizures', 'Tight Junctions', 'Transgenes', 'beta Catenin']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,527,425 | Is unplanned return to operating room after lower extremity arterial bypass an independent predictor for hospital readmission? | {
"contexts": [
"Hospital readmissions after surgical operations are considered serious complications and have an impact on health care-associated costs. The Centers for Medicare and Medicaid Services strongly encourage identification and ramification of factors associated with hospital readmissions after operations. Despite advances in endovascular surgery, lower extremity arterial bypass remains the \"gold standard\" treatment for severe, symptomatic peripheral arterial disease. The purpose of this study was to retrospectively review the factors associated with hospital readmission after lower extremity bypass surgery.",
"The 2013 lower extremity revascularization-targeted American College of Surgeons National Surgical Quality Improvement Program (NSQIP) database and generalized 2013 general and vascular surgery NSQIP Participant Use Data File were used for this study. Patient, diagnosis, and procedure characteristics of patients undergoing lower extremity bypass surgery were assessed. Multivariate logistic regression analysis was used to determine independent risk factors for hospital readmission within 30 days after surgery.",
"A total of 2646 patients (65% male, 35% female) were identified in the NSQIP database who underwent lower extremity open revascularization during the year 2013. Indications for operations included tissue loss (39%), rest pain (32%), and severe claudication (25%). Preoperative ankle-brachial indices were 0.4 to 0.9 (32%) and <0.4 (16.5%). A total of 425 patients (16%) were readmitted within 30 days of index operation. Risk factors associated with readmission included wound complication (odds ratio [OR], 8.54; 95% confidence interval [CI], 6.68-10.92; P < .001), need for reoperation (OR, 5.95; 95% CI, 4.45-7.97; P < .001), postoperative myocardial infarction (OR, 2.19; 95% CI, 1.25-3.83; P = .006), wound dehiscence (OR, 8.45; 95% CI, 4.54-15.71; P < .001), organ or space surgical site infection (OR, 7.62; 95% CI, 2.89-20.14; P < .001), postoperative pneumonia (OR, 2.66; 95% CI, 1.28-5.52; P = .009), progressive renal insufficiency (OR, 4.12; 95% CI, 1.52-11.11; P = .005), superficial surgical site infection (OR, 7.37; 95% CI, 5.31-10.23; P < .001), urinary tract infection (OR, 2.67; 95% CI, 1.42-5.01; P = .002), and deep wound infection (OR, 14.0; 95% CI, 7.62-24.80; P < .001)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Arteries",
"Databases, Factual",
"Female",
"Humans",
"Logistic Models",
"Lower Extremity",
"Male",
"Middle Aged",
"Multivariate Analysis",
"Odds Ratio",
"Operating Rooms",
"Patient Readmission",
"Postoperative Complications",
"Reoperation",
"Retrospective Studies",
"Risk Assessment",
"Risk Factors",
"Time Factors",
"Treatment Outcome",
"United States",
"Vascular Grafting"
]
} | Readmission after lower extremity bypass surgery is a serious complication. Various factors put a patient at high risk for readmission. Return to the operating room, wound infection, amputation, deep venous thrombosis, and major reintervention on bypass are independent risk factors for hospital readmission. Return to the operating room is associated with a 5.95-fold increase in hospital readmission. | yes | [
{
"from": "human",
"value": "Question: Is unplanned return to operating room after lower extremity arterial bypass an independent predictor for hospital readmission?\nContext: {'contexts': ['Hospital readmissions after surgical operations are considered serious complications and have an impact on health care-associated costs. The Centers for Medicare and Medicaid Services strongly encourage identification and ramification of factors associated with hospital readmissions after operations. Despite advances in endovascular surgery, lower extremity arterial bypass remains the \"gold standard\" treatment for severe, symptomatic peripheral arterial disease. The purpose of this study was to retrospectively review the factors associated with hospital readmission after lower extremity bypass surgery.', 'The 2013 lower extremity revascularization-targeted American College of Surgeons National Surgical Quality Improvement Program (NSQIP) database and generalized 2013 general and vascular surgery NSQIP Participant Use Data File were used for this study. Patient, diagnosis, and procedure characteristics of patients undergoing lower extremity bypass surgery were assessed. Multivariate logistic regression analysis was used to determine independent risk factors for hospital readmission within 30 days after surgery.', 'A total of 2646 patients (65% male, 35% female) were identified in the NSQIP database who underwent lower extremity open revascularization during the year 2013. Indications for operations included tissue loss (39%), rest pain (32%), and severe claudication (25%). Preoperative ankle-brachial indices were 0.4 to 0.9 (32%) and <0.4 (16.5%). A total of 425 patients (16%) were readmitted within 30 days of index operation. Risk factors associated with readmission included wound complication (odds ratio [OR], 8.54; 95% confidence interval [CI], 6.68-10.92; P < .001), need for reoperation (OR, 5.95; 95% CI, 4.45-7.97; P < .001), postoperative myocardial infarction (OR, 2.19; 95% CI, 1.25-3.83; P = .006), wound dehiscence (OR, 8.45; 95% CI, 4.54-15.71; P < .001), organ or space surgical site infection (OR, 7.62; 95% CI, 2.89-20.14; P < .001), postoperative pneumonia (OR, 2.66; 95% CI, 1.28-5.52; P = .009), progressive renal insufficiency (OR, 4.12; 95% CI, 1.52-11.11; P = .005), superficial surgical site infection (OR, 7.37; 95% CI, 5.31-10.23; P < .001), urinary tract infection (OR, 2.67; 95% CI, 1.42-5.01; P = .002), and deep wound infection (OR, 14.0; 95% CI, 7.62-24.80; P < .001).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Arteries', 'Databases, Factual', 'Female', 'Humans', 'Logistic Models', 'Lower Extremity', 'Male', 'Middle Aged', 'Multivariate Analysis', 'Odds Ratio', 'Operating Rooms', 'Patient Readmission', 'Postoperative Complications', 'Reoperation', 'Retrospective Studies', 'Risk Assessment', 'Risk Factors', 'Time Factors', 'Treatment Outcome', 'United States', 'Vascular Grafting']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,527,582 | Does aganglionosis with the absence of hypertrophied nerve fibres predict disease proximal to rectosigmoid colon? | {
"contexts": [
"The gold standard for the diagnosis of Hirschsprung's disease (HSCR) is the pathologic evaluation of a rectal biopsy that demonstrates the absence of ganglion cells and nerve fibre hypertrophy. However, it has been frequently reported that hypertrophic nerves may not be present in some variants like long-segment HSCR, total colonic aganglionosis, premature and very young infants. The aim of this study was to determine this association.",
"We performed a retrospective review of the HSCR database at our tertiary care children's hospital from 2000 to 2013. In order to analyse the relationship between the diameter of the nerve fibres and the level of aganglionosis, we classified the patient sample into two groups-fibres ≤40 and >40 μm. The groups were statistically compared with P < 0.05 being significant.",
"Rectal biopsies of 92 patients confirmed as HSCR with definitive operation performed at the same institution were reviewed. The mean nerve diameter was 50.1 μm (range 20-87.5 μm). Nerve fibre diameter ≤40 μm was predictive of transition zone above the sigmoid colon. A specificity of 77.3 % and a likelihood ratio of 2.03 supported this perception. No correlation was noted between nerve fibre diameter and gestational age at birth, birth weight or age at biopsy."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Biopsy",
"Child",
"Child, Preschool",
"Colon, Sigmoid",
"Female",
"Hirschsprung Disease",
"Humans",
"Hypertrophy",
"Infant",
"Infant, Newborn",
"Male",
"Nerve Fibers",
"Reproducibility of Results",
"Retrospective Studies"
]
} | The absence of nerve fibre hypertrophy in the presence of aganglionosis on rectal biopsy specimens is predictive of long-segment HSCR. | yes | [
{
"from": "human",
"value": "Question: Does aganglionosis with the absence of hypertrophied nerve fibres predict disease proximal to rectosigmoid colon?\nContext: {'contexts': [\"The gold standard for the diagnosis of Hirschsprung's disease (HSCR) is the pathologic evaluation of a rectal biopsy that demonstrates the absence of ganglion cells and nerve fibre hypertrophy. However, it has been frequently reported that hypertrophic nerves may not be present in some variants like long-segment HSCR, total colonic aganglionosis, premature and very young infants. The aim of this study was to determine this association.\", \"We performed a retrospective review of the HSCR database at our tertiary care children's hospital from 2000 to 2013. In order to analyse the relationship between the diameter of the nerve fibres and the level of aganglionosis, we classified the patient sample into two groups-fibres ≤40 and >40\\xa0μm. The groups were statistically compared with P\\xa0<\\xa00.05 being significant.\", 'Rectal biopsies of 92 patients confirmed as HSCR with definitive operation performed at the same institution were reviewed. The mean nerve diameter was 50.1\\xa0μm (range 20-87.5\\xa0μm). Nerve fibre diameter ≤40\\xa0μm was predictive of transition zone above the sigmoid colon. A specificity of 77.3\\xa0% and a likelihood ratio of 2.03 supported this perception. No correlation was noted between nerve fibre diameter and gestational age at birth, birth weight or age at biopsy.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Biopsy', 'Child', 'Child, Preschool', 'Colon, Sigmoid', 'Female', 'Hirschsprung Disease', 'Humans', 'Hypertrophy', 'Infant', 'Infant, Newborn', 'Male', 'Nerve Fibers', 'Reproducibility of Results', 'Retrospective Studies']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,546,017 | Does prevalence and correlate of Hazardous Drinking among Female Sex Workers in 13 Mexican Cities? | {
"contexts": [
"To describe the prevalence and correlates of hazardous drinking among female sex workers (FSWs) at 13 sites throughout Mexico.",
"FSWs (N = 1089) who were enrolled in a brief sexual risk reduction intervention (Mujer Segura) were queried about their sexual risk and substance use practices and their work contexts. Participants were classified as hazardous or non-hazardous drinkers based on the Alcohol Use Disorders test (AUDIT-C). Logistic regression models were used to examine individual, contextual, and community-level factors as correlates of hazardous drinking.",
"Ninety-two percent of participants reported alcohol consumption in the past month. Among drinkers (N = 1001), 83% met AUDIT-C criteria for hazardous drinking. Factors that were independently associated with hazardous drinking included: drug use in the past month (adjusted odds ratio (AOR) = 3.31; 95% CI 1.29-8.45), being a cigarette smoker (AOR = 1.71; 95% CI 1.13-2.58), being a barmaid or dance hostess (AOR = 3.40; 95% CI 1.95-5.91), alcohol use before or during sex with clients (AOR = 7.78; 95% CI 4.84-12.52), and working in a city with a higher marginalization index (AOR = 1.07; 95% CI 1.04-1.11)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Alcohol Drinking",
"Alcohol-Related Disorders",
"Cities",
"Female",
"Humans",
"Logistic Models",
"Mexico",
"Prevalence",
"Sex Workers",
"Smoking",
"Unsafe Sex"
]
} | Findings support the high prioritization by public health authorities of alcohol prevention and treatment programs for FSWs. | yes | [
{
"from": "human",
"value": "Question: Does prevalence and correlate of Hazardous Drinking among Female Sex Workers in 13 Mexican Cities?\nContext: {'contexts': ['To describe the prevalence and correlates of hazardous drinking among female sex workers (FSWs) at 13 sites throughout Mexico.', 'FSWs (N = 1089) who were enrolled in a brief sexual risk reduction intervention (Mujer Segura) were queried about their sexual risk and substance use practices and their work contexts. Participants were classified as hazardous or non-hazardous drinkers based on the Alcohol Use Disorders test (AUDIT-C). Logistic regression models were used to examine individual, contextual, and community-level factors as correlates of hazardous drinking.', 'Ninety-two percent of participants reported alcohol consumption in the past month. Among drinkers (N = 1001), 83% met AUDIT-C criteria for hazardous drinking. Factors that were independently associated with hazardous drinking included: drug use in the past month (adjusted odds ratio (AOR) = 3.31; 95% CI 1.29-8.45), being a cigarette smoker (AOR = 1.71; 95% CI 1.13-2.58), being a barmaid or dance hostess (AOR = 3.40; 95% CI 1.95-5.91), alcohol use before or during sex with clients (AOR = 7.78; 95% CI 4.84-12.52), and working in a city with a higher marginalization index (AOR = 1.07; 95% CI 1.04-1.11).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Alcohol Drinking', 'Alcohol-Related Disorders', 'Cities', 'Female', 'Humans', 'Logistic Models', 'Mexico', 'Prevalence', 'Sex Workers', 'Smoking', 'Unsafe Sex']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,553,843 | Is twin vaginal delivery associated with lower umbilical arterial blood pH of the second twin and less intrapartum blood loss? | {
"contexts": [
"To clarify actual differences in the neonatal as well as maternal outcome between completed twin vaginal delivery and cesarean delivery.",
"We collected the data from women with a twin pregnancy who delivered two live fetuses between 1 January and 31 December 2014 at 20 teaching hospitals (1) (1) PARTICIPANTS: Adachi Hospital, Hyogo Prefectural Amagasaki General Medical Center, Japan Baptist Hospital, Kitano Hospital, Kobe City Medical Center General Hospital, Kosaka Women's Hospital, Kurashiki Central Hospital, Kyoto University Hospital, Mitsubishi Kyoto Hospital, Nagahama Red Cross Hospital, National Hospital Organization Kyoto Medical Center, National Hospital Organization Osaka National Hospital, Osaka Red Cross Hospital, Otsu Municipal Hospital, Otsu Red Cross Hospital, Red Cross Wakayama Medical Center, Saiseikai Noe Hospital, Shizuoka General Hospital, Takamatsu Red Cross Hospital and Tenri Hospital. in Japan. Only the cases that were retrospectively regarded as eligible for planned vaginal delivery were analyzed according to the actual mode of delivery.",
"Umbilical arterial blood pH (UmA-pH) of the second twin was slightly but significantly lower in the vaginal delivery group (7.26 ± 0.009) than in a cesarean delivery group (7.30 ± 0.006). Vaginal delivery was the only independent risk factor for second twin's UmA-pH <7.20. Intrapartum blood loss was significantly larger in the cesarean delivery group (1444 ± 63 g) than in the vaginal delivery group (820 ± 109 g). Cesarean delivery was an independent risk factor for intrapartum blood loss ≥1500 g."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Cesarean Section",
"Delivery, Obstetric",
"Female",
"Fetal Blood",
"Humans",
"Hydrogen-Ion Concentration",
"Infant, Newborn",
"Japan",
"Postpartum Hemorrhage",
"Pregnancy",
"Pregnancy Outcome",
"Pregnancy, Twin",
"Retrospective Studies",
"Risk Factors",
"Twins"
]
} | Twin vaginal deliveries were associated with slightly but significantly lower UmA-pH of the second twin, whereas twin cesarean delivery was associated with significantly larger intrapartum blood loss. Not only the neonatal risk but also the maternal risk should be taken into account when an optimal delivery mode for the twin pregnancy is considered. | yes | [
{
"from": "human",
"value": "Question: Is twin vaginal delivery associated with lower umbilical arterial blood pH of the second twin and less intrapartum blood loss?\nContext: {'contexts': ['To clarify actual differences in the neonatal as well as maternal outcome between completed twin vaginal delivery and cesarean delivery.', \"We collected the data from women with a twin pregnancy who delivered two live fetuses between 1 January and 31 December 2014 at 20 teaching\\u2009hospitals (1) (1) PARTICIPANTS: Adachi Hospital, Hyogo Prefectural Amagasaki General Medical Center, Japan Baptist Hospital, Kitano Hospital, Kobe City Medical Center General Hospital, Kosaka Women's Hospital, Kurashiki Central Hospital, Kyoto University Hospital, Mitsubishi Kyoto Hospital, Nagahama Red Cross Hospital, National Hospital Organization Kyoto Medical Center, National Hospital Organization Osaka National Hospital, Osaka Red Cross Hospital, Otsu Municipal Hospital, Otsu Red Cross Hospital, Red Cross Wakayama Medical Center, Saiseikai Noe Hospital, Shizuoka General Hospital, Takamatsu Red Cross Hospital and Tenri Hospital. in Japan. Only the cases that were retrospectively regarded as eligible for planned vaginal delivery were analyzed according to the actual mode of delivery.\", \"Umbilical arterial blood pH (UmA-pH) of the second twin was slightly but significantly lower in the vaginal delivery group (7.26\\u2009±\\u20090.009) than in a cesarean delivery group (7.30\\u2009±\\u20090.006). Vaginal delivery was the only independent risk factor for second twin's UmA-pH \\u2009<7.20. Intrapartum blood loss was significantly larger in the cesarean delivery group (1444\\u2009±\\u200963\\u2009g) than in the vaginal delivery group (820\\u2009±\\u2009109\\u2009g). Cesarean delivery was an independent risk factor for intrapartum blood loss\\u2009≥1500\\u2009g.\"], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Cesarean Section', 'Delivery, Obstetric', 'Female', 'Fetal Blood', 'Humans', 'Hydrogen-Ion Concentration', 'Infant, Newborn', 'Japan', 'Postpartum Hemorrhage', 'Pregnancy', 'Pregnancy Outcome', 'Pregnancy, Twin', 'Retrospective Studies', 'Risk Factors', 'Twins']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,543,101 | Does microsomal Prostaglandin E Synthase-1-Derived PGE2 inhibit Vascular Smooth Muscle Cell Calcification? | {
"contexts": [
"Chronic administration of selective cyclooxygenase-2 (COX-2) inhibitors leads to an increased risk of adverse cardiovascular events, including myocardial infarction and stroke. Vascular smooth muscle cell (VSMC) calcification, a common complication of chronic kidney disease, is directly related to cardiovascular morbidity and mortality. Here, we tested whether specific COX-2 inhibition affects vascular calcification during chronic renal failure.",
"The COX-2-specific inhibitors NS398 and SC236 significantly increased high-phosphate (Pi)-induced VSMC calcification. Similarly, COX-2(-/-) VSMCs, COX-2(-/-) aortas rings treated with high Pi and adenine diet-induced COX-2(-/-) chronic renal failure mice displayed enhanced calcium deposition. Metabolomic analysis revealed the differential suppression of PGE2 production by COX-1- and COX-2-specific inhibitors in high-Pi-stimulated VSMCs, indicating the involvement of PGE2 during COX-2 inhibition-aggravated vascular calcification. Indeed, exogenous PGE2 reduced alkaline phosphatase activity, osteogenic transdifferentiation, apoptosis, and calcification of VSMCs. In accordance, downregulation of microsomal prostaglandin E synthase (mPGES)-1 in VSMCs, mPGES-1(-/-) aorta with high-Pi stimulation and mPGES-1(-/-) chronic renal failure mice resulted in enhanced vascular mineralization. Further applications of RNAi and specific antagonists for PGE2 receptors indicated EP4 may mediate PGE2-inhibited vascular calcification."
],
"labels": [
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Adenine",
"Animals",
"Aorta, Abdominal",
"Aorta, Thoracic",
"Aortic Diseases",
"Calcitriol",
"Cells, Cultured",
"Cyclooxygenase 2",
"Cyclooxygenase 2 Inhibitors",
"Dinoprostone",
"Disease Models, Animal",
"Humans",
"Intramolecular Oxidoreductases",
"Kidney Failure, Chronic",
"Male",
"Metabolomics",
"Mice, Inbred C57BL",
"Mice, Knockout",
"Muscle, Smooth, Vascular",
"Myocytes, Smooth Muscle",
"Nephrectomy",
"Phosphates",
"Prostaglandin-E Synthases",
"Prostaglandin-Endoperoxide Synthases",
"Rats, Sprague-Dawley",
"Receptors, Prostaglandin E, EP4 Subtype",
"Signal Transduction",
"Time Factors",
"Vascular Calcification"
]
} | Our data revealed the pivotal role of COX-2-mPGES-1-PGE2 axis in vascular calcification. The selective inhibition of COX-2 or mPGES-1 may increase the risk of calcification and subsequent adverse cardiovascular events during chronic renal failure. | yes | [
{
"from": "human",
"value": "Question: Does microsomal Prostaglandin E Synthase-1-Derived PGE2 inhibit Vascular Smooth Muscle Cell Calcification?\nContext: {'contexts': ['Chronic administration of selective cyclooxygenase-2 (COX-2) inhibitors leads to an increased risk of adverse cardiovascular events, including myocardial infarction and stroke. Vascular smooth muscle cell (VSMC) calcification, a common complication of chronic kidney disease, is directly related to cardiovascular morbidity and mortality. Here, we tested whether specific COX-2 inhibition affects vascular calcification during chronic renal failure.', 'The COX-2-specific inhibitors NS398 and SC236 significantly increased high-phosphate (Pi)-induced VSMC calcification. Similarly, COX-2(-/-) VSMCs, COX-2(-/-) aortas rings treated with high Pi and adenine diet-induced COX-2(-/-) chronic renal failure mice displayed enhanced calcium deposition. Metabolomic analysis revealed the differential suppression of PGE2 production by COX-1- and COX-2-specific inhibitors in high-Pi-stimulated VSMCs, indicating the involvement of PGE2 during COX-2 inhibition-aggravated vascular calcification. Indeed, exogenous PGE2 reduced alkaline phosphatase activity, osteogenic transdifferentiation, apoptosis, and calcification of VSMCs. In accordance, downregulation of microsomal prostaglandin E synthase (mPGES)-1 in VSMCs, mPGES-1(-/-) aorta with high-Pi stimulation and mPGES-1(-/-) chronic renal failure mice resulted in enhanced vascular mineralization. Further applications of RNAi and specific antagonists for PGE2 receptors indicated EP4 may mediate PGE2-inhibited vascular calcification.'], 'labels': ['OBJECTIVE', 'RESULTS'], 'meshes': ['Adenine', 'Animals', 'Aorta, Abdominal', 'Aorta, Thoracic', 'Aortic Diseases', 'Calcitriol', 'Cells, Cultured', 'Cyclooxygenase 2', 'Cyclooxygenase 2 Inhibitors', 'Dinoprostone', 'Disease Models, Animal', 'Humans', 'Intramolecular Oxidoreductases', 'Kidney Failure, Chronic', 'Male', 'Metabolomics', 'Mice, Inbred C57BL', 'Mice, Knockout', 'Muscle, Smooth, Vascular', 'Myocytes, Smooth Muscle', 'Nephrectomy', 'Phosphates', 'Prostaglandin-E Synthases', 'Prostaglandin-Endoperoxide Synthases', 'Rats, Sprague-Dawley', 'Receptors, Prostaglandin E, EP4 Subtype', 'Signal Transduction', 'Time Factors', 'Vascular Calcification']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,541,838 | Does [ MicroRNA-33a regulate the invasion of cervical cancer cells via targeting Twist1 ]? | {
"contexts": [
"To examine the expression of Twist1 in cervical cancer and to explore its biological function in the progression of cervical cancer.
",
"The expressions of Twist1 in 32 cervical cancers and matched normal tissues were examined by immunohistochemistry (IHC). Cell invasive ability and the expression of invasion-related genes were determined in RNAi-based Twist1-silencing HeLa cells. The relationship between Twist1 and microRNA-33a (miR-33a) in cervical cancer was studied by Pearson correlation analysis, and the roles of miR-33a in regulation of Twist1 and cell invasiveness were studied.
",
"The positive expression rate of Twist1 was 75.0% (24/32) and 21.9% (7/32) in the cervical cancer and the matched normal tissues, respectively, with significant difference between them (P<0.05). Twist1 shRNA significantly decreased the invasiveness of HeLa cells (P<0.05). Compared with the matched normal tissues, the expression of miR-33a was increased in the cervical cancer tissues, which was negatively correlated with Twist1 (r=-0.661, P<0.05). Overexpression of miR-33a could significantly suppress Twist1 expression as well as cell invasiveness (P<0.05).
"
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Female",
"Gene Expression Regulation, Neoplastic",
"Genes, Tumor Suppressor",
"HeLa Cells",
"Humans",
"MicroRNAs",
"Neoplasm Invasiveness",
"Nuclear Proteins",
"RNA Interference",
"RNA, Small Interfering",
"Twist-Related Protein 1",
"Uterine Cervical Neoplasms"
]
} | Twist1 is critical for the invasiveness of cervical cancer cells; miR-33a, as a tumor suppressor gene, functions as an upstream regulator of Twist1 and is involved in the invasiveness of cervical cancer cell. | yes | [
{
"from": "human",
"value": "Question: Does [ MicroRNA-33a regulate the invasion of cervical cancer cells via targeting Twist1 ]?\nContext: {'contexts': ['To examine the expression of Twist1 in cervical cancer and to explore its biological function in the progression of cervical cancer.\\u2029', 'The expressions of Twist1 in 32 cervical cancers and matched normal tissues were examined by immunohistochemistry (IHC). Cell invasive ability and the expression of invasion-related genes were determined in RNAi-based Twist1-silencing HeLa cells. The relationship between Twist1 and microRNA-33a (miR-33a) in cervical cancer was studied by Pearson correlation analysis, and the roles of miR-33a in regulation of Twist1 and cell invasiveness were studied.\\u2029', 'The positive expression rate of Twist1 was 75.0% (24/32) and 21.9% (7/32) in the cervical cancer and the matched normal tissues, respectively, with significant difference between them (P<0.05). Twist1 shRNA significantly decreased the invasiveness of HeLa cells (P<0.05). Compared with the matched normal tissues, the expression of miR-33a was increased in the cervical cancer tissues, which was negatively correlated with Twist1 (r=-0.661, P<0.05). Overexpression of miR-33a could significantly suppress Twist1 expression as well as cell invasiveness (P<0.05).\\u2029'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Female', 'Gene Expression Regulation, Neoplastic', 'Genes, Tumor Suppressor', 'HeLa Cells', 'Humans', 'MicroRNAs', 'Neoplasm Invasiveness', 'Nuclear Proteins', 'RNA Interference', 'RNA, Small Interfering', 'Twist-Related Protein 1', 'Uterine Cervical Neoplasms']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,541,837 | Does [ MiRNA-381 inhibit the invasion of renal carcinoma and the underlying mechanisms ]? | {
"contexts": [
"To determine the inhibitory effect of miRNA-381 on renal carcinoma invasion and to explore the underlying mechanisms.
",
"After up-regulation of miRNA-381, the inhibitory effect of miR-381 on cell invasion was investigated. We screened the target genes of miRNA-381 in a database (starBase) through combination of five programs including targetscan, picTar, RNA22, PITA and miRanda. Then, the predicted targeting genes were verified by the dual luciferase reporter assay. We also examined the expression of miRNA-381 and its target genes in renal cancer cells and tissues.
",
"Transfection and up-regulation of miRNA-381 resulted in a significant decrease in trans-membrane cell numbers and the ability of renal cell invasion. Bioinformatics analysis showed that CREB binding protein (CBP), β-catenin and lymphoid enhancer binding factor-1 (LEF-1) were the potential targets of miRNA-381. In the luciferase reporter gene system, co-transfection of miRNA-381 with the 3'UTR of wild-type target gene led to a significant decrease in luciferase activity. The expression of miRNA-381 was decreased in various renal cancer cells, and it was particularly lower in highly metastatic cell lines (786-OHM). On the contrary, the expression levels of miRNA-381 target genes (CBP, β-catenin and LEF-1) were significantly increased in cells and tissues.
"
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"3' Untranslated Regions",
"CREB-Binding Protein",
"Carcinoma, Renal Cell",
"Cell Line, Tumor",
"Computational Biology",
"Gene Expression Regulation, Neoplastic",
"Humans",
"Kidney Neoplasms",
"Lymphoid Enhancer-Binding Factor 1",
"MicroRNAs",
"Neoplasm Invasiveness",
"Transfection",
"Up-Regulation",
"beta Catenin"
]
} | MiRNA-381 can inhibit cell invasion in renal cancer by block the function of CBP, β-catenin and LEF-1. | yes | [
{
"from": "human",
"value": "Question: Does [ MiRNA-381 inhibit the invasion of renal carcinoma and the underlying mechanisms ]?\nContext: {'contexts': ['To determine the inhibitory effect of miRNA-381 on renal carcinoma invasion and to explore the underlying mechanisms.\\u2029', 'After up-regulation of miRNA-381, the inhibitory effect of miR-381 on cell invasion was investigated. We screened the target genes of miRNA-381 in a database (starBase) through combination of five programs including targetscan, picTar, RNA22, PITA and miRanda. Then, the predicted targeting genes were verified by the dual luciferase reporter assay. We also examined the expression of miRNA-381 and its target genes in renal cancer cells and tissues.\\u2029', \"Transfection and up-regulation of miRNA-381 resulted in a significant decrease in trans-membrane cell numbers and the ability of renal cell invasion. Bioinformatics analysis showed that CREB binding protein (CBP), β-catenin and lymphoid enhancer binding factor-1 (LEF-1) were the potential targets of miRNA-381. In the luciferase reporter gene system, co-transfection of miRNA-381 with the 3'UTR of wild-type target gene led to a significant decrease in luciferase activity. The expression of miRNA-381 was decreased in various renal cancer cells, and it was particularly lower in highly metastatic cell lines (786-OHM). On the contrary, the expression levels of miRNA-381 target genes (CBP, β-catenin and LEF-1) were significantly increased in cells and tissues.\\u2029\"], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': [\"3' Untranslated Regions\", 'CREB-Binding Protein', 'Carcinoma, Renal Cell', 'Cell Line, Tumor', 'Computational Biology', 'Gene Expression Regulation, Neoplastic', 'Humans', 'Kidney Neoplasms', 'Lymphoid Enhancer-Binding Factor 1', 'MicroRNAs', 'Neoplasm Invasiveness', 'Transfection', 'Up-Regulation', 'beta Catenin']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,526,066 | Does deletion of aquaporin-4 in APP/PS1 mice exacerbate brain Aβ accumulation and memory deficits? | {
"contexts": [
"Preventing or reducing amyloid-beta (Aβ) accumulation in the brain is an important therapeutic strategy for Alzheimer's disease (AD). Recent studies showed that the water channel aquaporin-4 (AQP4) mediates soluble Aβ clearance from the brain parenchyma along the paravascular pathway. However the direct evidence for roles of AQP4 in the pathophysiology of AD remains absent.",
"Here, we reported that the deletion of AQP4 exacerbated cognitive deficits of 12-moth old APP/PS1 mice, with increases in Aβ accumulation, cerebral amyloid angiopathy and loss of synaptic protein and brain-derived neurotrophic factor in the hippocampus and cortex. Furthermore, AQP4 deficiency increased atrophy of astrocytes with significant decreases in interleukin-1 beta and nonsignificant decreases in interleukin-6 and tumor necrosis factor-alpha in hippocampal and cerebral samples."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Alzheimer Disease",
"Amyloid beta-Peptides",
"Animals",
"Aquaporin 4",
"Brain",
"Brain-Derived Neurotrophic Factor",
"Cerebral Amyloid Angiopathy",
"Cognition Disorders",
"Inflammation",
"Memory Disorders",
"Mice, Transgenic"
]
} | These results suggest that AQP4 attenuates Aβ pathogenesis despite its potentially inflammatory side-effects, thus serving as a promising target for treating AD. | yes | [
{
"from": "human",
"value": "Question: Does deletion of aquaporin-4 in APP/PS1 mice exacerbate brain Aβ accumulation and memory deficits?\nContext: {'contexts': [\"Preventing or reducing amyloid-beta (Aβ) accumulation in the brain is an important therapeutic strategy for Alzheimer's disease (AD). Recent studies showed that the water channel aquaporin-4 (AQP4) mediates soluble Aβ clearance from the brain parenchyma along the paravascular pathway. However the direct evidence for roles of AQP4 in the pathophysiology of AD remains absent.\", 'Here, we reported that the deletion of AQP4 exacerbated cognitive deficits of 12-moth old APP/PS1 mice, with increases in Aβ accumulation, cerebral amyloid angiopathy and loss of synaptic protein and brain-derived neurotrophic factor in the hippocampus and cortex. Furthermore, AQP4 deficiency increased atrophy of astrocytes with significant decreases in interleukin-1 beta and nonsignificant decreases in interleukin-6 and tumor necrosis factor-alpha in hippocampal and cerebral samples.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Alzheimer Disease', 'Amyloid beta-Peptides', 'Animals', 'Aquaporin 4', 'Brain', 'Brain-Derived Neurotrophic Factor', 'Cerebral Amyloid Angiopathy', 'Cognition Disorders', 'Inflammation', 'Memory Disorders', 'Mice, Transgenic']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,539,667 | Does umbilical cord gene expression reveal the molecular architecture of the fetal inflammatory response in extremely preterm newborns? | {
"contexts": [
"The fetal inflammatory response (FIR) in placental membranes to an intrauterine infection often precedes premature birth raising neonatal mortality and morbidity. However, the precise molecular events behind FIR still remain largely unknown, and little has been investigated at gene expression level.",
"We collected publicly available microarray expression data profiling umbilical cord (UC) tissue derived from the cohort of extremely low gestational age newborns (ELGANs) and interrogate them for differentially expressed (DE) genes between FIR and non-FIR-affected ELGANs.",
"We found a broad and complex FIR UC gene expression signature, changing up to 19% (3,896/20,155) of all human genes at 1% false discovery rate. Significant changes of a minimum 50% magnitude (1,097/3,896) affect the upregulation of many inflammatory pathways and molecules, such as cytokines, toll-like receptors, and calgranulins. Remarkably, they also include the downregulation of neurodevelopmental pathways and genes, such as Fragile-X mental retardation 1 (FMR1), contactin 1 (CNTN1), and adenomatous polyposis coli (APC)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adenomatous Polyposis Coli Protein",
"Cohort Studies",
"Contactin 1",
"False Positive Reactions",
"Female",
"Fragile X Mental Retardation Protein",
"Gene Expression Profiling",
"Gene Expression Regulation",
"Gestational Age",
"Humans",
"Immune System",
"Infant, Extremely Premature",
"Infant, Newborn",
"Inflammation",
"Male",
"Oligonucleotide Array Sequence Analysis",
"Signal Transduction",
"Umbilical Cord"
]
} | The FIR expression signature in UC tissue contains molecular clues about signaling pathways that trigger FIR, and it is consistent with an acute inflammatory response by fetal innate and adaptive immune systems, which participate in the pathogenesis of neonatal brain damage. | yes | [
{
"from": "human",
"value": "Question: Does umbilical cord gene expression reveal the molecular architecture of the fetal inflammatory response in extremely preterm newborns?\nContext: {'contexts': ['The fetal inflammatory response (FIR) in placental membranes to an intrauterine infection often precedes premature birth raising neonatal mortality and morbidity. However, the precise molecular events behind FIR still remain largely unknown, and little has been investigated at gene expression level.', 'We collected publicly available microarray expression data profiling umbilical cord (UC) tissue derived from the cohort of extremely low gestational age newborns (ELGANs) and interrogate them for differentially expressed (DE) genes between FIR and non-FIR-affected ELGANs.', 'We found a broad and complex FIR UC gene expression signature, changing up to 19% (3,896/20,155) of all human genes at 1% false discovery rate. Significant changes of a minimum 50% magnitude (1,097/3,896) affect the upregulation of many inflammatory pathways and molecules, such as cytokines, toll-like receptors, and calgranulins. Remarkably, they also include the downregulation of neurodevelopmental pathways and genes, such as Fragile-X mental retardation 1 (FMR1), contactin 1 (CNTN1), and adenomatous polyposis coli (APC).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adenomatous Polyposis Coli Protein', 'Cohort Studies', 'Contactin 1', 'False Positive Reactions', 'Female', 'Fragile X Mental Retardation Protein', 'Gene Expression Profiling', 'Gene Expression Regulation', 'Gestational Age', 'Humans', 'Immune System', 'Infant, Extremely Premature', 'Infant, Newborn', 'Inflammation', 'Male', 'Oligonucleotide Array Sequence Analysis', 'Signal Transduction', 'Umbilical Cord']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,540,658 | Does active Maintenance of the Gradient of Refractive Index be Required to Sustain the Optical Properties of the Lens? | {
"contexts": [
"To determine whether the cellular physiology of the lens actively maintains the optical properties of the lens and whether inhibition of lens transport affects overall visual quality.",
"One lens from a pair of bovine lenses was cultured in artificial aqueous humor (AAH), while the other was cultured in either AAH-High-K+ or AAH + 0.1 mM ouabain for 4 hours. Lens pairs or whole enucleated eyes were then imaged in 4.7 Tesla (T) high-field small animal magnet. Lens surface curvatures, T1 measurements of water content, and T2 measurements of water/protein ratios were extracted from cultured lenses, while the geometrical parameters that define the optical pathway were obtained from whole eyes. Gradients of refractive index (GRIN), calculated from T2 measurements, and the extracted geometric parameters were inputted into optical models of the isolated lens and the whole bovine eye.",
"Inhibiting circulating fluxes by inhibiting the Na/K-ATPase with ouabain or depolarization of the lens potential by High K+ caused changes to lens water content, the water/protein ratio (GRIN) and surface geometry that manifested as an increase in optical power and a decrease in negative spherical aberration in cultured lenses. Changes to optical properties of the lens resulted in a myopic shift that impaired vision quality in the optical model of the bovine eye."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Cattle",
"Lens, Crystalline",
"Magnetic Resonance Imaging",
"Models, Biological",
"Refraction, Ocular"
]
} | The cellular physiology of the lens actively maintains its optical properties and inhibiting the Na/K/ATPase induces a myopic shift in vision similar to that observed clinically in patients who go on to develop cataract. | yes | [
{
"from": "human",
"value": "Question: Does active Maintenance of the Gradient of Refractive Index be Required to Sustain the Optical Properties of the Lens?\nContext: {'contexts': ['To determine whether the cellular physiology of the lens actively maintains the optical properties of the lens and whether inhibition of lens transport affects overall visual quality.', 'One lens from a pair of bovine lenses was cultured in artificial aqueous humor (AAH), while the other was cultured in either AAH-High-K+ or AAH + 0.1 mM ouabain for 4 hours. Lens pairs or whole enucleated eyes were then imaged in 4.7 Tesla (T) high-field small animal magnet. Lens surface curvatures, T1 measurements of water content, and T2 measurements of water/protein ratios were extracted from cultured lenses, while the geometrical parameters that define the optical pathway were obtained from whole eyes. Gradients of refractive index (GRIN), calculated from T2 measurements, and the extracted geometric parameters were inputted into optical models of the isolated lens and the whole bovine eye.', 'Inhibiting circulating fluxes by inhibiting the Na/K-ATPase with ouabain or depolarization of the lens potential by High K+ caused changes to lens water content, the water/protein ratio (GRIN) and surface geometry that manifested as an increase in optical power and a decrease in negative spherical aberration in cultured lenses. Changes to optical properties of the lens resulted in a myopic shift that impaired vision quality in the optical model of the bovine eye.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Cattle', 'Lens, Crystalline', 'Magnetic Resonance Imaging', 'Models, Biological', 'Refraction, Ocular']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,534,898 | Are higher levels of procoagulant microparticles in women with recurrent miscarriage associated with antiphospholipid antibodies? | {
"contexts": [
"Are the levels of circulating cell-derived microparticles (cMPs) in patients with recurrent miscarriage (RM) associated with the antiphospholipid syndrome (APS)?"
],
"labels": [
"OBJECTIVE"
],
"meshes": [
"Abortion, Habitual",
"Adult",
"Antibodies, Antiphospholipid",
"Antiphospholipid Syndrome",
"Case-Control Studies",
"Cell-Derived Microparticles",
"Female",
"Humans",
"Pregnancy"
]
} | cMPs in women with RM are not associated with antiphospholipid antibodies (aPLs). | no | [
{
"from": "human",
"value": "Question: Are higher levels of procoagulant microparticles in women with recurrent miscarriage associated with antiphospholipid antibodies?\nContext: {'contexts': ['Are the levels of circulating cell-derived microparticles (cMPs) in patients with recurrent miscarriage (RM) associated with the antiphospholipid syndrome (APS)?'], 'labels': ['OBJECTIVE'], 'meshes': ['Abortion, Habitual', 'Adult', 'Antibodies, Antiphospholipid', 'Antiphospholipid Syndrome', 'Case-Control Studies', 'Cell-Derived Microparticles', 'Female', 'Humans', 'Pregnancy']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
26,545,946 | Is meis2 essential for cranial and cardiac neural crest development? | {
"contexts": [
"TALE-class homeodomain transcription factors Meis and Pbx play important roles in formation of the embryonic brain, eye, heart, cartilage or hematopoiesis. Loss-of-function studies of Pbx1, 2 and 3 and Meis1 documented specific functions in embryogenesis, however, functional studies of Meis2 in mouse are still missing. We have generated a conditional allele of Meis2 in mice and shown that systemic inactivation of the Meis2 gene results in lethality by the embryonic day 14 that is accompanied with hemorrhaging.",
"We show that neural crest cells express Meis2 and Meis2-defficient embryos display defects in tissues that are derived from the neural crest, such as an abnormal heart outflow tract with the persistent truncus arteriosus and abnormal cranial nerves. The importance of Meis2 for neural crest cells is further confirmed by means of conditional inactivation of Meis2 using crest-specific AP2α-IRES-Cre mouse. Conditional mutants display perturbed development of the craniofacial skeleton with severe anomalies in cranial bones and cartilages, heart and cranial nerve abnormalities."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Animals",
"Cartilage",
"Cranial Nerves",
"Forkhead Transcription Factors",
"Heart",
"Heart Defects, Congenital",
"Hemorrhage",
"Homeodomain Proteins",
"Mice",
"Mice, Inbred C57BL",
"Mice, Knockout",
"Neural Crest",
"Repressor Proteins",
"SOX9 Transcription Factor",
"Skull"
]
} | Meis2-null mice are embryonic lethal. Our results reveal a critical role of Meis2 during cranial and cardiac neural crest cells development in mouse. | yes | [
{
"from": "human",
"value": "Question: Is meis2 essential for cranial and cardiac neural crest development?\nContext: {'contexts': ['TALE-class homeodomain transcription factors Meis and Pbx play important roles in formation of the embryonic brain, eye, heart, cartilage or hematopoiesis. Loss-of-function studies of Pbx1, 2 and 3 and Meis1 documented specific functions in embryogenesis, however, functional studies of Meis2 in mouse are still missing. We have generated a conditional allele of Meis2 in mice and shown that systemic inactivation of the Meis2 gene results in lethality by the embryonic day 14 that is accompanied with hemorrhaging.', 'We show that neural crest cells express Meis2 and Meis2-defficient embryos display defects in tissues that are derived from the neural crest, such as an abnormal heart outflow tract with the persistent truncus arteriosus and abnormal cranial nerves. The importance of Meis2 for neural crest cells is further confirmed by means of conditional inactivation of Meis2 using crest-specific AP2α-IRES-Cre mouse. Conditional mutants display perturbed development of the craniofacial skeleton with severe anomalies in cranial bones and cartilages, heart and cranial nerve abnormalities.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Animals', 'Cartilage', 'Cranial Nerves', 'Forkhead Transcription Factors', 'Heart', 'Heart Defects, Congenital', 'Hemorrhage', 'Homeodomain Proteins', 'Mice', 'Mice, Inbred C57BL', 'Mice, Knockout', 'Neural Crest', 'Repressor Proteins', 'SOX9 Transcription Factor', 'Skull']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,542,176 | Does endostatin exert radiosensitizing effect in non-small cell lung cancer cells by inhibiting VEGFR2 expression? | {
"contexts": [
"To determine the effects of endostatin on vascular growth factor receptor 2 (VEGFR2) expression in non-small cell lung cancer (NSCLC) cells and the mechanisms underlying its radiosensitizing effect.",
"VEGFR2 mRNA levels were determined in different NSCLC cell lines using qRT-PCR. RT-PCR and Western blot assays were used to assess the expression of mRNA and proteins. The radiosensitivity of the cells was determined by colony-formation assays; and cell apoptosis and cell cycle distribution were determined by flow cytometry.",
"VEGFR2 mRNA levels differed among the five NSCLC cell lines (P < 0.01), with the highest expression in Calu-1 cells and lowest in A549 cells. Endostatin significantly inhibited the growth of Calu-1 cells (P < 0.01) (IC20 = 296.5 μg/ml), and the expression of VEGFR2 and HIF-1α (P < 0.05). Phosphorylation of protein kinase B (Akt), extracellular signal-regulated kinases 1/2 (ERK1/2), and p38 were significantly lower in endostatin-treated cells than control (P < 0.05). Endostatin enhanced the radiosensitivity of Calu-1 cells to SER = 1.38 and induced apoptosis (P < 0.01) and G2/M blockage (P < 0.01). However, endostatin had limited effects on A549 cells. Compared with Calu-1 cells, there was not significantly effects on cell radiosensitivity (SER = 1.09)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Carcinoma, Non-Small-Cell Lung",
"Cell Death",
"Cell Line, Tumor",
"Down-Regulation",
"Endostatins",
"Gamma Rays",
"Gene Expression Regulation, Neoplastic",
"Humans",
"Lung Neoplasms",
"Radiation Tolerance",
"Radiation-Sensitizing Agents",
"Vascular Endothelial Growth Factor Receptor-2"
]
} | Endostatin induces apoptosis and enhances radiosensitivity of the VEGFR2 high-expressing cell line Calu-1, but it has a limited effect on the VEGFR2 low-expressing cell line A549. | yes | [
{
"from": "human",
"value": "Question: Does endostatin exert radiosensitizing effect in non-small cell lung cancer cells by inhibiting VEGFR2 expression?\nContext: {'contexts': ['To determine the effects of endostatin on vascular growth factor receptor 2 (VEGFR2) expression in non-small cell lung cancer (NSCLC) cells and the mechanisms underlying its radiosensitizing effect.', 'VEGFR2 mRNA levels were determined in different NSCLC cell lines using qRT-PCR. RT-PCR and Western blot assays were used to assess the expression of mRNA and proteins. The radiosensitivity of the cells was determined by colony-formation assays; and cell apoptosis and cell cycle distribution were determined by flow cytometry.', 'VEGFR2 mRNA levels differed among the five NSCLC cell lines (P < 0.01), with the highest expression in Calu-1 cells and lowest in A549 cells. Endostatin significantly inhibited the growth of Calu-1 cells (P < 0.01) (IC20 = 296.5 μg/ml), and the expression of VEGFR2 and HIF-1α (P < 0.05). Phosphorylation of protein kinase B (Akt), extracellular signal-regulated kinases 1/2 (ERK1/2), and p38 were significantly lower in endostatin-treated cells than control (P < 0.05). Endostatin enhanced the radiosensitivity of Calu-1 cells to SER = 1.38 and induced apoptosis (P < 0.01) and G2/M blockage (P < 0.01). However, endostatin had limited effects on A549 cells. Compared with Calu-1 cells, there was not significantly effects on cell radiosensitivity (SER = 1.09).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Carcinoma, Non-Small-Cell Lung', 'Cell Death', 'Cell Line, Tumor', 'Down-Regulation', 'Endostatins', 'Gamma Rays', 'Gene Expression Regulation, Neoplastic', 'Humans', 'Lung Neoplasms', 'Radiation Tolerance', 'Radiation-Sensitizing Agents', 'Vascular Endothelial Growth Factor Receptor-2']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,550,050 | Does software-Based Hybrid Perfusion SPECT/CT provide Diagnostic Accuracy When Other Pulmonary Embolism Imaging Is Indeterminate? | {
"contexts": [
"To investigate the diagnostic performance of perfusion single-photon emission computed tomography/computed tomography (Q-SPECT/CT) in patients suspected to have pulmonary embolism (PE) but with indeterminate computed tomographic pulmonary angiography (CTPA) or planar ventilation/perfusion (V/Q) scans.",
"This retrospective study included two groups of patients. Group I consisted of 49 patients with nondiagnostic CTPA. These 49 patients underwent subsequent V/Q scans. Further Q-SPECTs were obtained in patients with indeterminate planar images and fused with existing CTPA. Group II consisted of 182 non-CTPA patients with indeterminate V/Q scans. These 182 patients underwent further Q-SPECT and separate noncontrast low-dose CT chest. Fusion Q-SPECT/CT scans were obtained through FDA-approved software and interpreted according to published criteria as positive, negative, or indeterminate for PE. Upon retrospective analyses, the final diagnosis was made using composite reference standards including all available clinical and imaging information for at least 6-month follow-up.",
"In group I patients, 1 was positive, 24 were negative, and another 24 (49 %, 24/49) were indeterminate. In the subsequent 24 Q-SPECT/CTPAs, 4 were positive, 19 were negative, and 1 was indeterminate (4.2 %, 1/24). In group II patients, 9 (4.9 %, 9/182) were indeterminate, 33 were positive, and 140 were negative. The combined nondiagnostic rate for Q-SPECT/CT was only 4.9 % (10/206). There was six false-negative and one false-positive Q-SPECT/CT examinations. The sensitivity, specificity, and positive and negative predictive value of Q-SPECT/CT were 85.7 % (36/42), 99.4 % (153/154), 97.3 % (36/37) and 96.2 % (153/159), respectively."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": []
} | Q-SPECT/CT improves the diagnostic rate with promising accuracy in diagnosing PE that yields a satisfactory clinical verdict, especially when the CTPA and planar V/Q scan are indeterminate. | yes | [
{
"from": "human",
"value": "Question: Does software-Based Hybrid Perfusion SPECT/CT provide Diagnostic Accuracy When Other Pulmonary Embolism Imaging Is Indeterminate?\nContext: {'contexts': ['To investigate the diagnostic performance of perfusion single-photon emission computed tomography/computed tomography (Q-SPECT/CT) in patients suspected to have pulmonary embolism (PE) but with indeterminate computed tomographic pulmonary angiography (CTPA) or planar ventilation/perfusion (V/Q) scans.', 'This retrospective study included two groups of patients. Group I consisted of 49 patients with nondiagnostic CTPA. These 49 patients underwent subsequent V/Q scans. Further Q-SPECTs were obtained in patients with indeterminate planar images and fused with existing CTPA. Group II consisted of 182 non-CTPA patients with indeterminate V/Q scans. These 182 patients underwent further Q-SPECT and separate noncontrast low-dose CT chest. Fusion Q-SPECT/CT scans were obtained through FDA-approved software and interpreted according to published criteria as positive, negative, or indeterminate for PE. Upon retrospective analyses, the final diagnosis was made using composite reference standards including all available clinical and imaging information for at least 6-month follow-up.', 'In group I patients, 1 was positive, 24 were negative, and another 24 (49\\xa0%, 24/49) were indeterminate. In the subsequent 24 Q-SPECT/CTPAs, 4 were positive, 19 were negative, and 1 was indeterminate (4.2\\xa0%, 1/24). In group II patients, 9 (4.9\\xa0%, 9/182) were indeterminate, 33 were positive, and 140 were negative. The combined nondiagnostic rate for Q-SPECT/CT was only 4.9\\xa0% (10/206). There was six false-negative and one false-positive Q-SPECT/CT examinations. The sensitivity, specificity, and positive and negative predictive value of Q-SPECT/CT were 85.7\\xa0% (36/42), 99.4\\xa0% (153/154), 97.3\\xa0% (36/37) and 96.2\\xa0% (153/159), respectively.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,530,935 | Does impaired GLP-1 signaling contribute to reduced sensitivity to duodenal nutrients in obesity-prone rats during high-fat feeding? | {
"contexts": [
"Increased consumption of a high-fat (HF) diet is a salient contributor to obesity; however, how diminished satiation signaling contributes to overconsumption and obesity development remains poorly understood.",
"Using obese-prone (OP) and obese-resistant (OR) rats, we tested feeding responses to intragastric liquid meal replacement, prior and after HF feeding. Next, chow- and HF-fed OP and OR rats were tested for sensitivity to intraduodenal glucose, intralipid, and meal replacement loads. To examine the role of glucagon-like peptide-1 (GLP-1) and vagal signaling, animals were treated with exendin-9, GLP-1 receptor antagonist, prior to meal replacement infusion, and Fos-like immunoreactivity (Fos-Li) in the dorsal hindbrain was examined after infusion.",
"OP and OR rats reduced chow intake equally following gastric liquid meal; however, after 2 weeks of HF feeding, intragastric meal replacement reduced food intake less in OP than OR. Similarly, HF feeding, but not chow, diminished the suppressive effects of intraduodenal meal replacement, glucose, and intralipid in OP compared to OR. This effect was associated with lower Fos-Li expression in the dorsal hindbrain of OP rats. Finally, exendin-9 failed to attenuate reduction of food intake by meal replacement in OP rats during HF feeding."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Diet, High-Fat",
"Dietary Fats",
"Disease Susceptibility",
"Duodenum",
"Eating",
"Glucagon-Like Peptide 1",
"Male",
"Obesity",
"Rats",
"Satiation",
"Signal Transduction"
]
} | Susceptibility to obesity coupled with HF feeding results in rapid impairments in nutrient-induced satiation through blunted responses in endogenous GLP-1 and hindbrain vagal afferent signaling. | yes | [
{
"from": "human",
"value": "Question: Does impaired GLP-1 signaling contribute to reduced sensitivity to duodenal nutrients in obesity-prone rats during high-fat feeding?\nContext: {'contexts': ['Increased consumption of a high-fat (HF) diet is a salient contributor to obesity; however, how diminished satiation signaling contributes to overconsumption and obesity development remains poorly understood.', 'Using obese-prone (OP) and obese-resistant (OR) rats, we tested feeding responses to intragastric liquid meal replacement, prior and after HF feeding. Next, chow- and HF-fed OP and OR rats were tested for sensitivity to intraduodenal glucose, intralipid, and meal replacement loads. To examine the role of glucagon-like peptide-1 (GLP-1) and vagal signaling, animals were treated with exendin-9, GLP-1 receptor antagonist, prior to meal replacement infusion, and Fos-like immunoreactivity (Fos-Li) in the dorsal hindbrain was examined after infusion.', 'OP and OR rats reduced chow intake equally following gastric liquid meal; however, after 2 weeks of HF feeding, intragastric meal replacement reduced food intake less in OP than OR. Similarly, HF feeding, but not chow, diminished the suppressive effects of intraduodenal meal replacement, glucose, and intralipid in OP compared to OR. This effect was associated with lower Fos-Li expression in the dorsal hindbrain of OP rats. Finally, exendin-9 failed to attenuate reduction of food intake by meal replacement in OP rats during HF feeding.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Diet, High-Fat', 'Dietary Fats', 'Disease Susceptibility', 'Duodenum', 'Eating', 'Glucagon-Like Peptide 1', 'Male', 'Obesity', 'Rats', 'Satiation', 'Signal Transduction']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,550,269 | Does fasudil alleviate traumatic optic neuropathy by inhibiting Rho signaling pathway? | {
"contexts": [
"The present study is to investigate the pathological changes in rabbits with traumatic optic neuropathy (TON), as well as the effect of fasudil on the lesions.",
"A total of 144 New Zealand rabbits were successfully established as TON models. Twelve hours after surgery, the rabbits in control, dexamethasone, and fasudil groups were administrated with saline, dexamethasone, and fasudil via ear veins, respectively. Then, retinas of the rabbits were obtained at 72 h and on days 7, 14 and 21 after surgery. The pathological changes in retina and optic nerves were observed by hematoxylin and eosin staining and transmission electron microscopy. The expression levels of Rho-associated genes were measured using quantitative real-time polymerase chain reaction.",
"In control group, the axons were swelling, and mitochondria showed vacuolation after optic nerve crush. Mitochondria were swelled slightly in dexamethasone group. By contrast, nerves in fasudil group were repaired. Retinal ganglion cells in control group were reduced significantly due to optic nerve crush. The loss of retinal ganglion cells was alleviated in fasudil group. Quantitative real-time polymerase chain reaction showed that the expression of Rho-associated genes were down-regulated."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": []
} | The present study demonstrates that fasudil inhibits the apoptosis of retinal ganglion cells and ameliorates damages of optic nerves in traumatic optic neuropathy. | yes | [
{
"from": "human",
"value": "Question: Does fasudil alleviate traumatic optic neuropathy by inhibiting Rho signaling pathway?\nContext: {'contexts': ['The present study is to investigate the pathological changes in rabbits with traumatic optic neuropathy (TON), as well as the effect of fasudil on the lesions.', 'A total of 144 New Zealand rabbits were successfully established as TON models. Twelve hours after surgery, the rabbits in control, dexamethasone, and fasudil groups were administrated with saline, dexamethasone, and fasudil via ear veins, respectively. Then, retinas of the rabbits were obtained at 72 h and on days 7, 14 and 21 after surgery. The pathological changes in retina and optic nerves were observed by hematoxylin and eosin staining and transmission electron microscopy. The expression levels of Rho-associated genes were measured using quantitative real-time polymerase chain reaction.', 'In control group, the axons were swelling, and mitochondria showed vacuolation after optic nerve crush. Mitochondria were swelled slightly in dexamethasone group. By contrast, nerves in fasudil group were repaired. Retinal ganglion cells in control group were reduced significantly due to optic nerve crush. The loss of retinal ganglion cells was alleviated in fasudil group. Quantitative real-time polymerase chain reaction showed that the expression of Rho-associated genes were down-regulated.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,542,058 | Does eRRα be a Marker of Tamoxifen Response and Survival in Triple-Negative Breast Cancer? | {
"contexts": [
"Estrogen-related receptor alpha (ERRα) signaling has recently been implicated in breast cancer. We investigated the clinical value of ERRα in randomized cohorts of tamoxifen-treated and adjuvant-untreated patients.",
"Cox proportional hazards regression was used to evaluate the significance of associations between ERRα gene expression levels and patient DMFS in a previously published microarray dataset representing 2,000 breast tumor cases derived from multiple medical centers worldwide. The 912 tumors used for immunostaining were from a tamoxifen-randomized primary breast cancer trial conducted in Stockholm, Sweden, during 1976-1990. Mouse model was used to study the effect of tamoxifen treatment on lung colonization of MDA-MB-231 control cells and MDA-MB-231 cells with stable knockdown of ERRα. The phenotypic effects associated with ERRα modulation were studied using immunoblotting analyses and wound-healing assay.",
"We found that in ER-negative and triple-negative breast cancer (TNBC) adjuvant-untreated patients, ERRα expression indicated worse prognosis and correlated with poor outcome predictors. However, in tamoxifen-treated patients, an improved outcome was observed with high ERRα gene and protein expression. Reduced ERRα expression was oncogenic in the presence of tamoxifen, measured by in vitro proliferation and migration assays and in vivo metastasis studies."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Antineoplastic Agents, Hormonal",
"Biomarkers, Tumor",
"Cell Line, Tumor",
"Female",
"Gene Expression",
"Gene Knockout Techniques",
"Humans",
"Neoplasm Grading",
"Prognosis",
"Protein Transport",
"RNA, Small Interfering",
"Receptors, Estrogen",
"Tamoxifen",
"Treatment Outcome",
"Triple Negative Breast Neoplasms"
]
} | Taken together, these data show that ERRα expression predicts response to tamoxifen treatment, and ERRα could be a biomarker of tamoxifen sensitivity and a prognostic factor in TNBC. | yes | [
{
"from": "human",
"value": "Question: Does eRRα be a Marker of Tamoxifen Response and Survival in Triple-Negative Breast Cancer?\nContext: {'contexts': ['Estrogen-related receptor alpha (ERRα) signaling has recently been implicated in breast cancer. We investigated the clinical value of ERRα in randomized cohorts of tamoxifen-treated and adjuvant-untreated patients.', 'Cox proportional hazards regression was used to evaluate the significance of associations between ERRα gene expression levels and patient DMFS in a previously published microarray dataset representing 2,000 breast tumor cases derived from multiple medical centers worldwide. The 912 tumors used for immunostaining were from a tamoxifen-randomized primary breast cancer trial conducted in Stockholm, Sweden, during 1976-1990. Mouse model was used to study the effect of tamoxifen treatment on lung colonization of MDA-MB-231 control cells and MDA-MB-231 cells with stable knockdown of ERRα. The phenotypic effects associated with ERRα modulation were studied using immunoblotting analyses and wound-healing assay.', 'We found that in ER-negative and triple-negative breast cancer (TNBC) adjuvant-untreated patients, ERRα expression indicated worse prognosis and correlated with poor outcome predictors. However, in tamoxifen-treated patients, an improved outcome was observed with high ERRα gene and protein expression. Reduced ERRα expression was oncogenic in the presence of tamoxifen, measured by in vitro proliferation and migration assays and in vivo metastasis studies.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Antineoplastic Agents, Hormonal', 'Biomarkers, Tumor', 'Cell Line, Tumor', 'Female', 'Gene Expression', 'Gene Knockout Techniques', 'Humans', 'Neoplasm Grading', 'Prognosis', 'Protein Transport', 'RNA, Small Interfering', 'Receptors, Estrogen', 'Tamoxifen', 'Treatment Outcome', 'Triple Negative Breast Neoplasms']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,541,225 | Does microRNA-340 mediate Metabolic Shift in Oral Squamous Cell Carcinoma by Targeting Glucose Transporter-1? | {
"contexts": [
"MicroRNA-340 (miR-340) is deregulated in many human cancers in correlation with tumor progression. Recent studies have found that microRNAs play key roles in energy metabolism. This study explored the contributions of miR-340 to the metabolic shift in oral squamous cell carcinoma (OSCC).",
"MiR-340 expression was measured by real-time polymerase chain reaction. MiR-340 mimics, miR-340 inhibitor, and scramble small interfering RNA were transfected into SAS human tongue SCC cells to observe their effects on cell proliferation, colony formation, lactate secretion, and glucose uptake rate. Moreover, the relation between the level of miR-340 and glucose transporter-1 (Glut1) was investigated.",
"The expression of miR-340 was decreased and thus induced a metabolic switch in oral cancer cells. The decrease in miR-340 increased Glut1 expression, leading to an increase in lactate secretion and glucose uptake rate. The altered metabolism induced by miR-340 resulted in the rapid proliferation of oral cancer cells."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Carcinoma, Squamous Cell",
"Cell Count",
"Cell Line, Tumor",
"Cell Proliferation",
"Cell Survival",
"Epithelial Cells",
"Gene Knockdown Techniques",
"Glucose",
"Glucose Transporter Type 1",
"Glycolysis",
"HEK293 Cells",
"Humans",
"Lactic Acid",
"MicroRNAs",
"Mouth Mucosa",
"Plasmids",
"RNA, Small Interfering",
"Tongue Neoplasms",
"Transfection"
]
} | The findings suggest that miR-340 might act as a molecular switch that contributes to the regulation of glycolysis in OSCC by regulating Glut1 expression. | yes | [
{
"from": "human",
"value": "Question: Does microRNA-340 mediate Metabolic Shift in Oral Squamous Cell Carcinoma by Targeting Glucose Transporter-1?\nContext: {'contexts': ['MicroRNA-340 (miR-340) is deregulated in many human cancers in correlation with tumor progression. Recent studies have found that microRNAs play key roles in energy metabolism. This study explored the contributions of miR-340 to the metabolic shift in oral squamous cell carcinoma (OSCC).', 'MiR-340 expression was measured by real-time polymerase chain reaction. MiR-340 mimics, miR-340 inhibitor, and scramble small interfering RNA were transfected into SAS human tongue SCC cells to observe their effects on cell proliferation, colony formation, lactate secretion, and glucose uptake rate. Moreover, the relation between the level of miR-340 and glucose transporter-1 (Glut1) was investigated.', 'The expression of miR-340 was decreased and thus induced a metabolic switch in oral cancer cells. The decrease in miR-340 increased Glut1 expression, leading to an increase in lactate secretion and glucose uptake rate. The altered metabolism induced by miR-340 resulted in the rapid proliferation of oral cancer cells.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Carcinoma, Squamous Cell', 'Cell Count', 'Cell Line, Tumor', 'Cell Proliferation', 'Cell Survival', 'Epithelial Cells', 'Gene Knockdown Techniques', 'Glucose', 'Glucose Transporter Type 1', 'Glycolysis', 'HEK293 Cells', 'Humans', 'Lactic Acid', 'MicroRNAs', 'Mouth Mucosa', 'Plasmids', 'RNA, Small Interfering', 'Tongue Neoplasms', 'Transfection']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,550,183 | Does estrogen receptor α ( ESR1 ) IVS1-397T > C polymorphism lower risk of fracture? | {
"contexts": [
"Genetic factors are reported to affect fracture incidence. Many groups have explored the correlation of fracture risk with ESR1 IVS1-397T>C. The observed associations, however, are largely inconsistent. This meta-analysis of data from early-released studies was performed in an effort to determine the role of IVS1-397T>C in fracture.",
"Relevant studies were searched through Pubmed, Embase, ScienceDirect, and Wiley Online Library databases. 16 studies meeting all selection criteria were finally identified. We calculated ORs with 95% CIs to assess risk of fracture. Subgroup analyses were performed by subtype, ethnicity and gender.",
"Data on 2916 cases and 19170 controls were analyzed in the meta-analysis. Overall, we found moderately decreased risk in association with IVS1-397 CC genotype (OR = 0.82, 95% CI = 0.73-0.92; OR = 0.84, 95% CI = 0.76-0.94). The decrease persisted in both hip fracture (OR = 0.82, 95% CI = 0.71-0.94; OR = 0.83, 95% CI = 0.73-0.94) and vertebral fracture (OR = 0.67, 95% CI = 0.50-0.91; OR = 0.78, 95% CI = 0.64-0.97; OR = 0.82, 95% CI = 0.68-0.98) when data were stratified by subtype. We also found a significant trend of decreasing risk in relation to the CC genotype in Caucasian, male and female. All fixed-effects meta-analysis results were homogeneous."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": []
} | The meta-analysis demonstrates that risk of fracture seems likely to be decreased due to IVS1-397 CC or CT genotype. | yes | [
{
"from": "human",
"value": "Question: Does estrogen receptor α ( ESR1 ) IVS1-397T > C polymorphism lower risk of fracture?\nContext: {'contexts': ['Genetic factors are reported to affect fracture incidence. Many groups have explored the correlation of fracture risk with ESR1 IVS1-397T>C. The observed associations, however, are largely inconsistent. This meta-analysis of data from early-released studies was performed in an effort to determine the role of IVS1-397T>C in fracture.', 'Relevant studies were searched through Pubmed, Embase, ScienceDirect, and Wiley Online Library databases. 16 studies meeting all selection criteria were finally identified. We calculated ORs with 95% CIs to assess risk of fracture. Subgroup analyses were performed by subtype, ethnicity and gender.', 'Data on 2916 cases and 19170 controls were analyzed in the meta-analysis. Overall, we found moderately decreased risk in association with IVS1-397 CC genotype (OR = 0.82, 95% CI = 0.73-0.92; OR = 0.84, 95% CI = 0.76-0.94). The decrease persisted in both hip fracture (OR = 0.82, 95% CI = 0.71-0.94; OR = 0.83, 95% CI = 0.73-0.94) and vertebral fracture (OR = 0.67, 95% CI = 0.50-0.91; OR = 0.78, 95% CI = 0.64-0.97; OR = 0.82, 95% CI = 0.68-0.98) when data were stratified by subtype. We also found a significant trend of decreasing risk in relation to the CC genotype in Caucasian, male and female. All fixed-effects meta-analysis results were homogeneous.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,545,868 | Is willis-Ekbom disease associated with poor cardiovascular health in adults? | {
"contexts": [
"Willis-Ekbom disease (WED), also called restless legs syndrome (RLS), is a neurologic sensorimotor disease that may be associated with cardiovascular disease. Given high morbidity and mortality rates of cardiovascular disease worldwide, we assessed the relation between WED/RLS and cardiovascular health risks in a native South American population. We prospectively analyzed data from The Atahualpa Project of Ecuadorian adults aged 40 years and older. Physicians interviewed consented persons on the health behavior and health factors of the American Heart Association (AHA) for ideal cardiovascular health in adults and underwent fasting laboratory blood collection and blood pressure evaluation. Certified neurologists conducted face-to-face interviews using the International Restless Legs Syndrome Study Group (IRLSSG) field instrument. Persons testing positive for WED/RLS and age-and sex-matched controls underwent confirmatory physical examinations conducted by a neurologist and a sleep specialist to whom IRLSSG designation was blinded.",
"Of 665 persons, 94 (14 %) tested positive in IRLSSG; 40 (6 %) had a diagnosis of WED/RLS after neurologic examination and interview. Patients with WED/RLS were younger (53.5 vs 59.9 years, P = .001), without significant differences in sex ratios. Among AHA risk factors, only obesity was significantly more prevalent among patients with WED/RLS (42.5 % vs 23.5 %, P = .01). However, after adjustment for confounders, body mass index was not significantly associated with WED/RLS."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Adult",
"Cardiovascular Diseases",
"Ecuador",
"Female",
"Health Status",
"Humans",
"Indians, South American",
"Male",
"Middle Aged",
"Prospective Studies",
"Restless Legs Syndrome"
]
} | In adult Amerindians, although obesity and body mass index were associated with WED/RLS on univariate analyses, the association was not present after adjustment for confounders. No other significant associations were found between WED/RLS and AHA cardiovascular metrics. | no | [
{
"from": "human",
"value": "Question: Is willis-Ekbom disease associated with poor cardiovascular health in adults?\nContext: {'contexts': ['Willis-Ekbom disease (WED), also called restless legs syndrome (RLS), is a neurologic sensorimotor disease that may be associated with cardiovascular disease. Given high morbidity and mortality rates of cardiovascular disease worldwide, we assessed the relation between WED/RLS and cardiovascular health risks in a native South American population. We prospectively analyzed data from The Atahualpa Project of Ecuadorian adults aged 40\\xa0years and older. Physicians interviewed consented persons on the health behavior and health factors of the American Heart Association (AHA) for ideal cardiovascular health in adults and underwent fasting laboratory blood collection and blood pressure evaluation. Certified neurologists conducted face-to-face interviews using the International Restless Legs Syndrome Study Group (IRLSSG) field instrument. Persons testing positive for WED/RLS and age-and sex-matched controls underwent confirmatory physical examinations conducted by a neurologist and a sleep specialist to whom IRLSSG designation was blinded.', 'Of 665 persons, 94 (14\\xa0%) tested positive in IRLSSG; 40 (6\\xa0%) had a diagnosis of WED/RLS after neurologic examination and interview. Patients with WED/RLS were younger (53.5 vs 59.9\\xa0years, P\\u2009=\\u2009.001), without significant differences in sex ratios. Among AHA risk factors, only obesity was significantly more prevalent among patients with WED/RLS (42.5\\xa0% vs 23.5\\xa0%, P\\u2009=\\u2009.01). However, after adjustment for confounders, body mass index was not significantly associated with WED/RLS.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Adult', 'Cardiovascular Diseases', 'Ecuador', 'Female', 'Health Status', 'Humans', 'Indians, South American', 'Male', 'Middle Aged', 'Prospective Studies', 'Restless Legs Syndrome']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
26,535,257 | Is idiopathic Cam Morphology Caused by Subclinical Slipped Capital Femoral Epiphysis : An MRI and CT Study? | {
"contexts": [
"Cam impingement as a known sequelae of slipped capital femoral epiphysis (SCFE) has led to speculation that subclinical SCFEs may be the causative factor in idiopathic cam morphology; alternatively, others have implicated an abnormal extension of the growth plate as a causative factor.",
"To investigate the growth plate tilt angle in 4 patient cohorts: normal patients, patients with idiopathic cam morphology (CamIP), patients with cam morphology secondary to known SCFE (CamSCFE), and patients with incidental findings of an asymptomatic cam (Camasymp).",
"Case-control study; Level of evidence, 3.",
"A database of 192 computed tomography scans of abdomens/pelvises of patients (ages, 5-19 years) with no known orthopaedic issues, reformatted to neutral tilt, inclination, and rotation, were utilized for the normal cohort, the Camasymp cohort, and to create an age- and sex-matched control cohort. In addition, a retrospective review of all patients treated for femoroacetabular impingement (FAI) with preoperative advance imaging was conducted, and patients were separated to CamIP and CamSCFE cohorts. The alpha angle and tilt angle were measured on each hip. Statistical analysis was performed.",
"The mean tilt angle among the normal patients was 12.1°, with 1.9% of the variation in tilt angle being explained by age; each additional year of age decreased the tilt angle by 0.27° (P = .008). The tilt angle for the CamSCFE cohort (mean, 44.5°) was found to be significantly greater than both the CamIP cohort (mean, 5.9°; P < .001) and the control cohort (mean, 12.8°; P < .001). The tilt angle for the CamIP cohort was found to be significantly less than the control cohort (P = .003). The alpha angle and tilt angle were positively correlated in the CamIP cohort, but no correlation was found in the other cohorts. The mean tilt angle of the 18 hips in the Camasymp cohort was 13.9° ± 11.5° (range, -12° to 37°), with 12 hips (67%) in the tilt angle range of CamIP cohort and 6 in the tilt angle range of CamSCFE."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"METHODS",
"RESULTS"
],
"meshes": []
} | The proximal femoral growth plate normally has a posterior tilt that becomes more anterior through maturation. Idiopathic cam morphology has a drastically different growth plate tilt angle than cam morphology secondary to SCFE, suggesting that a majority of idiopathic cam morphology is not the result of subclinical SCFEs. | no | [
{
"from": "human",
"value": "Question: Is idiopathic Cam Morphology Caused by Subclinical Slipped Capital Femoral Epiphysis : An MRI and CT Study?\nContext: {'contexts': ['Cam impingement as a known sequelae of slipped capital femoral epiphysis (SCFE) has led to speculation that subclinical SCFEs may be the causative factor in idiopathic cam morphology; alternatively, others have implicated an abnormal extension of the growth plate as a causative factor.', 'To investigate the growth plate tilt angle in 4 patient cohorts: normal patients, patients with idiopathic cam morphology (CamIP), patients with cam morphology secondary to known SCFE (CamSCFE), and patients with incidental findings of an asymptomatic cam (Camasymp).', 'Case-control study; Level of evidence, 3.', 'A database of 192 computed tomography scans of abdomens/pelvises of patients (ages, 5-19 years) with no known orthopaedic issues, reformatted to neutral tilt, inclination, and rotation, were utilized for the normal cohort, the Camasymp cohort, and to create an age- and sex-matched control cohort. In addition, a retrospective review of all patients treated for femoroacetabular impingement (FAI) with preoperative advance imaging was conducted, and patients were separated to CamIP and CamSCFE cohorts. The alpha angle and tilt angle were measured on each hip. Statistical analysis was performed.', 'The mean tilt angle among the normal patients was 12.1°, with 1.9% of the variation in tilt angle being explained by age; each additional year of age decreased the tilt angle by 0.27° (P = .008). The tilt angle for the CamSCFE cohort (mean, 44.5°) was found to be significantly greater than both the CamIP cohort (mean, 5.9°; P < .001) and the control cohort (mean, 12.8°; P < .001). The tilt angle for the CamIP cohort was found to be significantly less than the control cohort (P = .003). The alpha angle and tilt angle were positively correlated in the CamIP cohort, but no correlation was found in the other cohorts. The mean tilt angle of the 18 hips in the Camasymp cohort was 13.9° ± 11.5° (range, -12° to 37°), with 12 hips (67%) in the tilt angle range of CamIP cohort and 6 in the tilt angle range of CamSCFE.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
26,529,096 | Does tNF accelerate Death of Mandibular Condyle Chondrocytes in Rats with Biomechanical Stimulation-Induced Temporomandibular Joint Disease? | {
"contexts": [
"To determine if temporomandibular joint chondrocyte apoptosis is induced in rats with dental biomechanical stimulation and what a role TNF takes.",
"Thirty-two rats were divided into 4 groups (n = 8/group) and exposed to incisor mal-occlusion induced by unilateral anterior crossbite biomechanical stimulation. Two groups were sampled at 2 or 4 weeks. The other two groups were treated with local injections of a TNF inhibitor or PBS into the temporomandibular joints area at 2 weeks and then sampled at 4 weeks. Twenty-four rats either served as unilateral anterior crossbite mock operation controls (n = 8/group) with sampling at 2 or 4 weeks or received a local injection of the TNF inhibitor at 2 weeks with sampling at 4 weeks. Chondrocytes were isolated from the temporomandibular joints of 6 additional rats and treated with TNF in vitro. Joint samples were assessed using Hematoxylin&eosin, Safranin O, TUNEL and immunohistochemistry staining, real-time PCR, fluorogenic activity assays and Western blot analyses. The isolated chondrocytes were also analyzed by flow cytometry.",
"Unilateral anterior crossbite stimulation led to temporomandibular joint cartilage degradation, associated with an increase in TUNEL-positive chondrocytes number, caspase-9 expression levels, and the release of cytochrome c from mitochondria at 2 weeks without changes in TNF and caspase-8 levels until after 4 weeks. TNF stimulated apoptosis of the isolated chondrocytes and up-regulated caspase-8 expression, but did not change caspase-9 expression levels. Local injection of TNF inhibitor down-regulated caspase-8 expression and reduced TUNEL-positive cell number, but did not reverse cartilage thickness reduction, caspase-9 up-regulation or cytochrome c release."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Apoptosis",
"Caspase 8",
"Cells, Cultured",
"Chondrocytes",
"Cytochromes c",
"Down-Regulation",
"Female",
"Gene Expression Regulation, Enzymologic",
"Mandibular Condyle",
"Rats",
"Rats, Sprague-Dawley",
"Temporomandibular Joint Disorders",
"Tumor Necrosis Factor-alpha"
]
} | Unilateral anterior crossbite stimulation induces mitochondrion-mediated apoptosis of articular chondrocytes. TNF accelerated the unilateral anterior crossbite induced chondrocytes apoptosis via death-receptor pathway. However, anti-TNF therapy does not prevent cartilage loss in this model of temporomandibular joint. | yes | [
{
"from": "human",
"value": "Question: Does tNF accelerate Death of Mandibular Condyle Chondrocytes in Rats with Biomechanical Stimulation-Induced Temporomandibular Joint Disease?\nContext: {'contexts': ['To determine if temporomandibular joint chondrocyte apoptosis is induced in rats with dental biomechanical stimulation and what a role TNF takes.', 'Thirty-two rats were divided into 4 groups (n = 8/group) and exposed to incisor mal-occlusion induced by unilateral anterior crossbite biomechanical stimulation. Two groups were sampled at 2 or 4 weeks. The other two groups were treated with local injections of a TNF inhibitor or PBS into the temporomandibular joints area at 2 weeks and then sampled at 4 weeks. Twenty-four rats either served as unilateral anterior crossbite mock operation controls (n = 8/group) with sampling at 2 or 4 weeks or received a local injection of the TNF inhibitor at 2 weeks with sampling at 4 weeks. Chondrocytes were isolated from the temporomandibular joints of 6 additional rats and treated with TNF in vitro. Joint samples were assessed using Hematoxylin&eosin, Safranin O, TUNEL and immunohistochemistry staining, real-time PCR, fluorogenic activity assays and Western blot analyses. The isolated chondrocytes were also analyzed by flow cytometry.', 'Unilateral anterior crossbite stimulation led to temporomandibular joint cartilage degradation, associated with an increase in TUNEL-positive chondrocytes number, caspase-9 expression levels, and the release of cytochrome c from mitochondria at 2 weeks without changes in TNF and caspase-8 levels until after 4 weeks. TNF stimulated apoptosis of the isolated chondrocytes and up-regulated caspase-8 expression, but did not change caspase-9 expression levels. Local injection of TNF inhibitor down-regulated caspase-8 expression and reduced TUNEL-positive cell number, but did not reverse cartilage thickness reduction, caspase-9 up-regulation or cytochrome c release.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Apoptosis', 'Caspase 8', 'Cells, Cultured', 'Chondrocytes', 'Cytochromes c', 'Down-Regulation', 'Female', 'Gene Expression Regulation, Enzymologic', 'Mandibular Condyle', 'Rats', 'Rats, Sprague-Dawley', 'Temporomandibular Joint Disorders', 'Tumor Necrosis Factor-alpha']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,553,007 | Does g-8 indicate overall and quality-adjusted survival in older head and neck cancer patients treated with curative radiochemotherapy? | {
"contexts": [
"Evidence-based guidelines concerning the older head and neck cancer (HNCA) patient are lacking. Accurate patient selection for optimal care management is therefore challenging. We examined if geriatric assessment is indicative of long-term health-related quality of life (HRQOL) and overall survival in this unique population.",
"All HNCA patients, aged ≥65 years, eligible for curative radio(chemo)therapy were evaluated with the Geriatric-8 (G-8) questionnaire and a comprehensive geriatric assessment (CGA). Euroqol-5 dimensions (EQ-5D) and survival were collected until 36 months post treatment start. Repeated measures ANOVA was applied to analyse HRQOL evolution in 'fit' and 'vulnerable' patients, defined by G-8. Kaplan-Meier curves and cox proportional hazard analysis were established for determination of the prognostic value of geriatric assessments. Quality-adjusted survival was calculated in both patient subgroups.",
"One hundred patients were recruited. Seventy-two percent of patients were considered vulnerable according to CGA (≥2 abnormal tests). Fit patients maintained a relatively acceptable long-term HRQOL, whilst vulnerable patients showed significantly lower median health states. The difference remained apparent at 36 months. Vulnerability, as classified by G-8 or CGA, came forward as independent predictor for lower EQ-5D index scores. After consideration of confounders, a significantly lower survival was observed in patients defined vulnerable according to G-8, compared to fit patients. A similar trend was seen based on CGA. Calculation of quality-adjusted survival showed significantly less remaining life months in perfect health in vulnerable patients, compared to fit ones."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Aged, 80 and over",
"Chemoradiotherapy",
"Female",
"Geriatric Assessment",
"Head and Neck Neoplasms",
"Humans",
"Kaplan-Meier Estimate",
"Male",
"Quality of Life",
"Surveys and Questionnaires"
]
} | G-8 is indicative of quality-adjusted survival, and should be considered at time of treatment decisions for the older HNCA patient. | yes | [
{
"from": "human",
"value": "Question: Does g-8 indicate overall and quality-adjusted survival in older head and neck cancer patients treated with curative radiochemotherapy?\nContext: {'contexts': ['Evidence-based guidelines concerning the older head and neck cancer (HNCA) patient are lacking. Accurate patient selection for optimal care management is therefore challenging. We examined if geriatric assessment is indicative of long-term health-related quality of life (HRQOL) and overall survival in this unique population.', \"All HNCA patients, aged ≥65 years, eligible for curative radio(chemo)therapy were evaluated with the Geriatric-8 (G-8) questionnaire and a comprehensive geriatric assessment (CGA). Euroqol-5 dimensions (EQ-5D) and survival were collected until 36 months post treatment start. Repeated measures ANOVA was applied to analyse HRQOL evolution in 'fit' and 'vulnerable' patients, defined by G-8. Kaplan-Meier curves and cox proportional hazard analysis were established for determination of the prognostic value of geriatric assessments. Quality-adjusted survival was calculated in both patient subgroups.\", 'One hundred patients were recruited. Seventy-two percent of patients were considered vulnerable according to CGA (≥2 abnormal tests). Fit patients maintained a relatively acceptable long-term HRQOL, whilst vulnerable patients showed significantly lower median health states. The difference remained apparent at 36 months. Vulnerability, as classified by G-8 or CGA, came forward as independent predictor for lower EQ-5D index scores. After consideration of confounders, a significantly lower survival was observed in patients defined vulnerable according to G-8, compared to fit patients. A similar trend was seen based on CGA. Calculation of quality-adjusted survival showed significantly less remaining life months in perfect health in vulnerable patients, compared to fit ones.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Aged, 80 and over', 'Chemoradiotherapy', 'Female', 'Geriatric Assessment', 'Head and Neck Neoplasms', 'Humans', 'Kaplan-Meier Estimate', 'Male', 'Quality of Life', 'Surveys and Questionnaires']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,546,559 | Does an environmental route of exposure affect the formation of nanoparticle coronas in blood plasma? | {
"contexts": [
"Nanoparticles (NPs) in contact with biological fluids become covered by a tightly bound layer of proteins, the \"protein corona\", and it is largely accepted that this corona gives a new identity to NPs in biological milieu. We here consider the exposing scenario of NPs through an environmental route exemplified by the use of hydrophobins, highly adhesive proteins that are secreted into the environment in large quantities by fungi. HFBII of Trichoderma reesei has been used as a model protein and we have shown strong binding to polystyrene NPs of different sizes and surface groups. Hydrophobin coated NPs are shown to strongly increase the stability and the dispersion when exposed to human plasma compared to pristine ones particles. It is also shown that the presence of hydrophobin on the NPs results in an attenuated protein corona formation, in a different corona composition, and we also show that hydrophobin remained strongly associated to the NPs in competition with plasma proteins. As a conclusion we therefore suggest that the route of exposure of nanoparticles strongly affects their surface properties and their possible physiological behavior."
],
"labels": [
"UNLABELLED"
],
"meshes": [
"Blood Proteins",
"Environmental Exposure",
"Fungal Proteins",
"Humans",
"Nanoparticles",
"Trichoderma"
]
} | This work shows how a self-assembling protein, class II hydrophobin HFBII, with interesting biocompatible coating properties, strongly adsorbs on polystyrene NPs. HFBII is also shown to reduce aggregation of the NPs in human plasma which can increase their bioavailability with potential use in biomedical applications. The results here are also of significance for understanding possible interactions of NPs with living organisms. Hydrophobins are secreted in large quantities into the environment by fungi and this work shows how the biological environment of NPs determines the surface and colloidal properties of the particles by forming a protein corona, and that the history of the particle environment, here simulated with hydrophobin exposure, affects both plasma protein corona formation and dispersion behavior. This work thus simulates how alternative exposure routes affect nanoparticle properties, important in understanding the biological fate of NPs. | yes | [
{
"from": "human",
"value": "Question: Does an environmental route of exposure affect the formation of nanoparticle coronas in blood plasma?\nContext: {'contexts': ['Nanoparticles (NPs) in contact with biological fluids become covered by a tightly bound layer of proteins, the \"protein corona\", and it is largely accepted that this corona gives a new identity to NPs in biological milieu. We here consider the exposing scenario of NPs through an environmental route exemplified by the use of hydrophobins, highly adhesive proteins that are secreted into the environment in large quantities by fungi. HFBII of Trichoderma reesei has been used as a model protein and we have shown strong binding to polystyrene NPs of different sizes and surface groups. Hydrophobin coated NPs are shown to strongly increase the stability and the dispersion when exposed to human plasma compared to pristine ones particles. It is also shown that the presence of hydrophobin on the NPs results in an attenuated protein corona formation, in a different corona composition, and we also show that hydrophobin remained strongly associated to the NPs in competition with plasma proteins. As a conclusion we therefore suggest that the route of exposure of nanoparticles strongly affects their surface properties and their possible physiological behavior.'], 'labels': ['UNLABELLED'], 'meshes': ['Blood Proteins', 'Environmental Exposure', 'Fungal Proteins', 'Humans', 'Nanoparticles', 'Trichoderma']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,553,138 | Does combining carbon ion irradiation and non-homologous end-joining repair inhibitor NU7026 efficiently kill cancer cells? | {
"contexts": [
"Our previous data demonstrated that targeting non-homologous end-joining repair (NHEJR) yields a higher radiosensitivity than targeting homologous recombination repair (HRR) to heavy ions using DNA repair gene knockouts (KO) in mouse embryonic fibroblast (MEF). In this study, we determined if combining the use of an NHEJR inhibitor with carbon (C) ion irradiation was more efficient in killing human cancer cells compared with only targeting a HRR inhibitor.",
"The TP53-null human non-small cell lung cancer cell line H1299 was used for testing the radiosensitizing effect of NHEJR-related DNA-dependent protein kinase (DNA-PK) inhibitor NU7026, HRR-related Rad51 inhibitor B02, or both to C ion irradiation using colony forming assays. The mechanism underlying the inhibitor radiosensitization was determined by flow cytometry after H2AX phosphorylation staining. HRR-related Rad54-KO, NHEJR-related Lig4-KO, and wild-type TP53-KO MEF were also included to confirm the suppressing effect specificity of these inhibitors.",
"NU7026 showed significant sensitizing effect to C ion irradiation in a concentration-dependent manner. In contrast, B02 showed a slight sensitizing effect to C ion irradiation. The addition of NU7026 significantly increased H2AX phosphorylation after C ion and x-ray irradiations in H1299 cells, but not B02. NU7026 had no effect on radiosensitivity to Lig4-KO MEF and B02 had no effect on radiosensitivity to Rad54-KO MEF in both irradiations."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Carcinoma, Non-Small-Cell Lung",
"Cell Line, Tumor",
"Chromones",
"DNA End-Joining Repair",
"Heavy Ion Radiotherapy",
"Humans",
"Lung Neoplasms",
"Morpholines",
"Radiation Tolerance",
"Radiation-Sensitizing Agents"
]
} | These results suggest that inhibitors targeting the NHEJR pathway could significantly enhance radiosensitivity of human cancer cells to C ion irradiation, rather than targeting the HRR pathway. | yes | [
{
"from": "human",
"value": "Question: Does combining carbon ion irradiation and non-homologous end-joining repair inhibitor NU7026 efficiently kill cancer cells?\nContext: {'contexts': ['Our previous data demonstrated that targeting non-homologous end-joining repair (NHEJR) yields a higher radiosensitivity than targeting homologous recombination repair (HRR) to heavy ions using DNA repair gene knockouts (KO) in mouse embryonic fibroblast (MEF). In this study, we determined if combining the use of an NHEJR inhibitor with carbon (C) ion irradiation was more efficient in killing human cancer cells compared with only targeting a HRR inhibitor.', 'The TP53-null human non-small cell lung cancer cell line H1299 was used for testing the radiosensitizing effect of NHEJR-related DNA-dependent protein kinase (DNA-PK) inhibitor NU7026, HRR-related Rad51 inhibitor B02, or both to C ion irradiation using colony forming assays. The mechanism underlying the inhibitor radiosensitization was determined by flow cytometry after H2AX phosphorylation staining. HRR-related Rad54-KO, NHEJR-related Lig4-KO, and wild-type TP53-KO MEF were also included to confirm the suppressing effect specificity of these inhibitors.', 'NU7026 showed significant sensitizing effect to C ion irradiation in a concentration-dependent manner. In contrast, B02 showed a slight sensitizing effect to C ion irradiation. The addition of NU7026 significantly increased H2AX phosphorylation after C ion and x-ray irradiations in H1299 cells, but not B02. NU7026 had no effect on radiosensitivity to Lig4-KO MEF and B02 had no effect on radiosensitivity to Rad54-KO MEF in both irradiations.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Carcinoma, Non-Small-Cell Lung', 'Cell Line, Tumor', 'Chromones', 'DNA End-Joining Repair', 'Heavy Ion Radiotherapy', 'Humans', 'Lung Neoplasms', 'Morpholines', 'Radiation Tolerance', 'Radiation-Sensitizing Agents']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,553,540 | Does microRNA profiling unveil hyperglycaemic memory in the diabetic heart? | {
"contexts": [
"Recent randomized trials suggest that intensive glycaemic control fails to reduce heart failure-related events in patients with diabetes. The molecular cues underlying persistent myocardial damage despite normoglycaemia restoration remain elusive. MicroRNAs (miRNAs), a class of small non-coding RNAs, orchestrate transcriptional programs implicated in adverse cardiac remodelling. The present study investigates whether miRNAs participate to hyperglycaemic memory in the diabetic heart.",
"miRNA landscape was assessed by Mouse miRNome miRNA PCR Arrays in left ventricular specimens collected from 4-month-old streptozotocin-induced diabetic mice, with or without intensive glycaemic control by slow-release insulin implants. A dysregulation of 316 out of 1008 total miRNAs was observed in the diabetic hearts when compared with controls. Of these, 209 were up-regulated and 107 were down-regulated by >2.0-fold. Interestingly enough, the expression of 268 of those miRNAs remained significantly altered in diabetic mice even after subsequent normoglycaemia. Ingenuity pathway analysis revealed that dysregulated miRNAs were implicated in myocardial signalling networks triggering apoptosis (miR-320b, miR-378, miR-34a), fibrosis (miR-125b, miR-150, miR-199a, miR-29b, miR30a), hypertrophic growth (miR-1, miR-150, miR-199a, miR-133a, miR-214, miR-29a, miR-125b, miR-221, miR-212), autophagy (miR-133a, miR-221, miR-212, miR30a), oxidative stress (miR-221, miR-146a, miR-34a, miR-210, miR-19b, miR-125b, miR27a, miR-155), and heart failure (miR-423, miR-499, miR-199a), respectively."
],
"labels": [
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Animals",
"Blood Glucose",
"Diabetes Mellitus, Experimental",
"Diabetic Cardiomyopathies",
"Down-Regulation",
"Hyperglycemia",
"Hypoglycemic Agents",
"Insulin",
"Male",
"Mice, Inbred C57BL",
"MicroRNAs"
]
} | Glycaemic control is not able to rescue hyperglycaemia-induced alterations of miRNA landscape in the diabetic heart. These findings may provide novel insights to understand why diabetic cardiomyopathy progresses despite normalization of blood glucose levels. | yes | [
{
"from": "human",
"value": "Question: Does microRNA profiling unveil hyperglycaemic memory in the diabetic heart?\nContext: {'contexts': ['Recent randomized trials suggest that intensive glycaemic control fails to reduce heart failure-related events in patients with diabetes. The molecular cues underlying persistent myocardial damage despite normoglycaemia restoration remain elusive. MicroRNAs (miRNAs), a class of small non-coding RNAs, orchestrate transcriptional programs implicated in adverse cardiac remodelling. The present study investigates whether miRNAs participate to hyperglycaemic memory in the diabetic heart.', 'miRNA landscape was assessed by Mouse miRNome miRNA PCR Arrays in left ventricular specimens collected from 4-month-old streptozotocin-induced diabetic mice, with or without intensive glycaemic control by slow-release insulin implants. A dysregulation of 316 out of 1008 total miRNAs was observed in the diabetic hearts when compared with controls. Of these, 209 were up-regulated and 107 were down-regulated by >2.0-fold. Interestingly enough, the expression of 268 of those miRNAs remained significantly altered in diabetic mice even after subsequent normoglycaemia. Ingenuity pathway analysis revealed that dysregulated miRNAs were implicated in myocardial signalling networks triggering apoptosis (miR-320b, miR-378, miR-34a), fibrosis (miR-125b, miR-150, miR-199a, miR-29b, miR30a), hypertrophic growth (miR-1, miR-150, miR-199a, miR-133a, miR-214, miR-29a, miR-125b, miR-221, miR-212), autophagy (miR-133a, miR-221, miR-212, miR30a), oxidative stress (miR-221, miR-146a, miR-34a, miR-210, miR-19b, miR-125b, miR27a, miR-155), and heart failure (miR-423, miR-499, miR-199a), respectively.'], 'labels': ['OBJECTIVE', 'RESULTS'], 'meshes': ['Animals', 'Blood Glucose', 'Diabetes Mellitus, Experimental', 'Diabetic Cardiomyopathies', 'Down-Regulation', 'Hyperglycemia', 'Hypoglycemic Agents', 'Insulin', 'Male', 'Mice, Inbred C57BL', 'MicroRNAs']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,537,625 | Does tSG101 Silencing suppress Hepatocellular Carcinoma Cell Growth by Inducing Cell Cycle Arrest and Autophagic Cell Death? | {
"contexts": [
"The tumor susceptibility gene 101 (TSG101) was originally identified as a tumor-suppressor gene that mediates many molecular and biological processes, such as ubiquitination, endosomal trafficking, cell survival, and virus budding, but its role in hepatocellular carcinoma (HCC) is currently unknown.",
"We assessed the expression of TSG101 in HCC and paracancerous tissues using qPCR. Then, we used the TSG101-specific siRNA mix to disrupt the expression of TSG101 to investigate the subsequent effect on human hepatoma-7 (Huh7) cells. Western blot was used to detect the protein expression of TSG101 and other molecules. Cell growth assay was performed using CCK8. Transwell assay was used to investigate the migration and invasion ability of Huh7 cells after transfection with of TSG101 siRNA. Flow cytometry was used to estimate the effect of TSG101 knockdown on cell cycle and apoptosis. Confocal laser scanning microscopy was used to observe the actin filaments change and the formation of autophagy.",
"TSG101 was over-expressed in HCC tissues. TSG101 silence was able to suppress Huh7 cell proliferation, migration, and invasion. Furthermore, silencing of TSG101 could induce cell cycle arrest at G1 phase and inhibit the expression of cyclin A and cyclin D, while up-regulating the expression of CDK2. The mechanism might be induction of autophagic cell death and inactivation of Akt and ERK1/2."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Apoptosis",
"Autophagy",
"Carcinoma, Hepatocellular",
"Cell Cycle Checkpoints",
"Cell Death",
"Cell Line, Tumor",
"Cell Movement",
"Cell Proliferation",
"Cyclin A",
"Cyclin D",
"DNA-Binding Proteins",
"Endosomal Sorting Complexes Required for Transport",
"Flow Cytometry",
"G1 Phase",
"Gene Deletion",
"Gene Silencing",
"Humans",
"Liver Neoplasms",
"Microscopy, Confocal",
"Microscopy, Fluorescence",
"Neoplasm Invasiveness",
"RNA, Small Interfering",
"Transcription Factors"
]
} | TSG101 plays an important role in the development of HCC and may be a target for molecular therapy. | yes | [
{
"from": "human",
"value": "Question: Does tSG101 Silencing suppress Hepatocellular Carcinoma Cell Growth by Inducing Cell Cycle Arrest and Autophagic Cell Death?\nContext: {'contexts': ['The tumor susceptibility gene 101 (TSG101) was originally identified as a tumor-suppressor gene that mediates many molecular and biological processes, such as ubiquitination, endosomal trafficking, cell survival, and virus budding, but its role in hepatocellular carcinoma (HCC) is currently unknown.', 'We assessed the expression of TSG101 in HCC and paracancerous tissues using qPCR. Then, we used the TSG101-specific siRNA mix to disrupt the expression of TSG101 to investigate the subsequent effect on human hepatoma-7 (Huh7) cells. Western blot was used to detect the protein expression of TSG101 and other molecules. Cell growth assay was performed using CCK8. Transwell assay was used to investigate the migration and invasion ability of Huh7 cells after transfection with of TSG101 siRNA. Flow cytometry was used to estimate the effect of TSG101 knockdown on cell cycle and apoptosis. Confocal laser scanning microscopy was used to observe the actin filaments change and the formation of autophagy.', 'TSG101 was over-expressed in HCC tissues. TSG101 silence was able to suppress Huh7 cell proliferation, migration, and invasion. Furthermore, silencing of TSG101 could induce cell cycle arrest at G1 phase and inhibit the expression of cyclin A and cyclin D, while up-regulating the expression of CDK2. The mechanism might be induction of autophagic cell death and inactivation of Akt and ERK1/2.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Apoptosis', 'Autophagy', 'Carcinoma, Hepatocellular', 'Cell Cycle Checkpoints', 'Cell Death', 'Cell Line, Tumor', 'Cell Movement', 'Cell Proliferation', 'Cyclin A', 'Cyclin D', 'DNA-Binding Proteins', 'Endosomal Sorting Complexes Required for Transport', 'Flow Cytometry', 'G1 Phase', 'Gene Deletion', 'Gene Silencing', 'Humans', 'Liver Neoplasms', 'Microscopy, Confocal', 'Microscopy, Fluorescence', 'Neoplasm Invasiveness', 'RNA, Small Interfering', 'Transcription Factors']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,552,568 | Is concomitant lamotrigine use associated with decreased efficacy of the ketogenic diet in childhood refractory epilepsy? | {
"contexts": [
"Anti-epileptic drugs (AEDs) and the ketogenic diet (KD) are often used concomitantly in children with refractory epilepsy. It has been hypothesised that certain AEDs may interfere with KD. The purpose of this study was to elucidate relationships between efficacy of KD and use of specific AEDs.",
"A retrospective study was performed in 71 children with refractory epilepsy starting the KD between 2008 and 2014 in Erasmus University Hospital Sophia Children's Hospital. Efficacy of the KD (defined as 50% seizure reduction) was evaluated after three months of treatment and related to the AEDs used.",
"The KD was successful after three months in 61% of the children (N=71). Efficacy was significantly reduced if children (n=16) used lamotrigine (31%) at diet initiation or in the course of the diet, compared to other antiepileptic drugs (69%) (p=0.006). In comparison to children using other antiepileptic drugs, the percentage of children that had adequate ketosis was significantly reduced in case of lamotrigine use (p=0.049)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Anticonvulsants",
"Child",
"Child, Preschool",
"Combined Modality Therapy",
"Diet, Ketogenic",
"Drug Resistant Epilepsy",
"Female",
"Humans",
"Infant",
"Infant, Newborn",
"Ketosis",
"Lamotrigine",
"Male",
"Retrospective Studies",
"Seizures",
"Treatment Outcome",
"Triazines"
]
} | Lamotrigine treatment during KD is associated with a decreased efficacy of the KD. | yes | [
{
"from": "human",
"value": "Question: Is concomitant lamotrigine use associated with decreased efficacy of the ketogenic diet in childhood refractory epilepsy?\nContext: {'contexts': ['Anti-epileptic drugs (AEDs) and the ketogenic diet (KD) are often used concomitantly in children with refractory epilepsy. It has been hypothesised that certain AEDs may interfere with KD. The purpose of this study was to elucidate relationships between efficacy of KD and use of specific AEDs.', \"A retrospective study was performed in 71 children with refractory epilepsy starting the KD between 2008 and 2014 in Erasmus University Hospital Sophia Children's Hospital. Efficacy of the KD (defined as 50% seizure reduction) was evaluated after three months of treatment and related to the AEDs used.\", 'The KD was successful after three months in 61% of the children (N=71). Efficacy was significantly reduced if children (n=16) used lamotrigine (31%) at diet initiation or in the course of the diet, compared to other antiepileptic drugs (69%) (p=0.006). In comparison to children using other antiepileptic drugs, the percentage of children that had adequate ketosis was significantly reduced in case of lamotrigine use (p=0.049).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Anticonvulsants', 'Child', 'Child, Preschool', 'Combined Modality Therapy', 'Diet, Ketogenic', 'Drug Resistant Epilepsy', 'Female', 'Humans', 'Infant', 'Infant, Newborn', 'Ketosis', 'Lamotrigine', 'Male', 'Retrospective Studies', 'Seizures', 'Treatment Outcome', 'Triazines']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,539,962 | Do macrophages dictate the progression and manifestation of hypertensive heart disease? | {
"contexts": [
"Inflammation has been implicated in the initiation, progression and manifestation of hypertensive heart disease. We sought to determine the role of monocytes/macrophages in hypertension and pressure overload induced left ventricular (LV) remodeling.",
"We used two models of LV hypertrophy (LVH). First, to induce hypertension and LVH, we fed Sabra salt-sensitive rats with a high-salt diet. The number of macrophages increased in the hypertensive hearts, peaking at 10 weeks after a high-salt diet. Surprisingly, macrophage depletion, by IV clodronate (CL) liposomes, inhibited the development of hypertension. Moreover, macrophage depletion reduced LVH by 17% (p<0.05), and reduced cardiac fibrosis by 75%, compared with controls (p=0.001). Second, to determine the role of macrophages in the development and progression of LVH, independent of high-salt diet, we depleted macrophages in mice subjected to transverse aortic constriction and pressure overload. Significantly, macrophage depletion, for 3 weeks, attenuated LVH: a 12% decrease in diastolic and 20% in systolic wall thickness (p<0.05), and a 13% in LV mass (p=0.04), compared with controls. Additionally, macrophage depletion reduced cardiac fibrosis by 80% (p=0.006). Finally, macrophage depletion down-regulated the expression of genes associated with cardiac remodeling and fibrosis: transforming growth factor beta-1 (by 80%) collagen type III alpha-1 (by 71%) and atrial natriuretic factor (by 86%)."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Animals",
"Blood Pressure",
"Disease Models, Animal",
"Disease Progression",
"Hypertrophy, Left Ventricular",
"Macrophages",
"Male",
"Myocardium",
"Rats",
"Rats, Inbred SHR",
"Ventricular Function, Left",
"Ventricular Remodeling"
]
} | Macrophages mediate the development of hypertension, LVH, adverse cardiac remodeling, and fibrosis. Macrophages, therefore, should be considered as a therapeutic target to reduce the adverse consequences of hypertensive heart disease. | yes | [
{
"from": "human",
"value": "Question: Do macrophages dictate the progression and manifestation of hypertensive heart disease?\nContext: {'contexts': ['Inflammation has been implicated in the initiation, progression and manifestation of hypertensive heart disease. We sought to determine the role of monocytes/macrophages in hypertension and pressure overload induced left ventricular (LV) remodeling.', 'We used two models of LV hypertrophy (LVH). First, to induce hypertension and LVH, we fed Sabra salt-sensitive rats with a high-salt diet. The number of macrophages increased in the hypertensive hearts, peaking at 10 weeks after a high-salt diet. Surprisingly, macrophage depletion, by IV clodronate (CL) liposomes, inhibited the development of hypertension. Moreover, macrophage depletion reduced LVH by 17% (p<0.05), and reduced cardiac fibrosis by 75%, compared with controls (p=0.001). Second, to determine the role of macrophages in the development and progression of LVH, independent of high-salt diet, we depleted macrophages in mice subjected to transverse aortic constriction and pressure overload. Significantly, macrophage depletion, for 3 weeks, attenuated LVH: a 12% decrease in diastolic and 20% in systolic wall thickness (p<0.05), and a 13% in LV mass (p=0.04), compared with controls. Additionally, macrophage depletion reduced cardiac fibrosis by 80% (p=0.006). Finally, macrophage depletion down-regulated the expression of genes associated with cardiac remodeling and fibrosis: transforming growth factor beta-1 (by 80%) collagen type III alpha-1 (by 71%) and atrial natriuretic factor (by 86%).'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Animals', 'Blood Pressure', 'Disease Models, Animal', 'Disease Progression', 'Hypertrophy, Left Ventricular', 'Macrophages', 'Male', 'Myocardium', 'Rats', 'Rats, Inbred SHR', 'Ventricular Function, Left', 'Ventricular Remodeling']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,538,206 | Are procedure Delays and Time of Day Associated With Reductions in Quality of Screening Colonoscopies? | {
"contexts": [
"There have been conflicting results from studies to determine whether factors unrelated to endoscopist skill, such as fatigue, affect the quality of screening colonoscopy. We studied the effects of human and system factors on screening colonoscopy withdrawal time and likelihood of detecting an adenoma in a large cohort of patients.",
"We performed a retrospective analysis of operation and quality improvement data in colonoscopies performed at single academic medical center from November 2012 through February 2014. We collected data from the Northwestern Medicine Enterprise Data Warehouse on endoscopy procedure reports, patient demographics, and pathology reports of all patients undergoing endoscopy. We identified all screening colonoscopies during the study period and determined whether an adenoma was identified in each screening colonoscopy procedure. Our study included data from 7004 screening colonoscopies of patients 50-75 years old performed by endoscopists who performed at least 100 screening colonoscopies during the study period (n = 18).",
"Approximately 27% of procedures began on time; the median colonoscope insertion time was 5.9 minutes (interquartile range, 4.0-8.6). In multivariable logistic regression analysis adjusting for covariates and endoscopist-level clustering, adenoma detection was not associated with procedure delay (P = .48), hour of day (P = .40), or performing the second of 2 colonoscopy blocks in 1 day (P = .88). Adenoma detection was associated with insertion time overall (P = .006), but there was no consistent directional relationship across insertion quintiles."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Academic Medical Centers",
"Adenoma",
"Colonic Neoplasms",
"Colonoscopy",
"Fatigue",
"Female",
"Health Services Research",
"Humans",
"Male",
"Mass Screening",
"Middle Aged",
"Retrospective Studies",
"Time Factors"
]
} | Procedure delays and measured factors associated with fatigue, including time of day and multiple procedure blocks, do not reduce the odds of detecting an adenoma. Adenoma detection varies widely among providers, so efforts to improve adenoma detection should focus mainly on optimizing physician skill. | no | [
{
"from": "human",
"value": "Question: Are procedure Delays and Time of Day Associated With Reductions in Quality of Screening Colonoscopies?\nContext: {'contexts': ['There have been conflicting results from studies to determine whether factors unrelated to endoscopist skill, such as fatigue, affect the quality of screening colonoscopy. We studied the effects of human and system factors on screening colonoscopy withdrawal time and likelihood of detecting an adenoma in a large cohort of patients.', 'We performed a retrospective analysis of operation and quality improvement data in colonoscopies performed at single academic medical center from November 2012 through February 2014. We collected data from the Northwestern Medicine Enterprise Data Warehouse on endoscopy procedure reports, patient demographics, and pathology reports of all patients undergoing endoscopy. We identified all screening colonoscopies during the study period and determined whether an adenoma was identified in each screening colonoscopy procedure. Our study included data from 7004 screening colonoscopies of patients 50-75 years old performed by endoscopists who performed at least 100 screening colonoscopies during the study period (n = 18).', 'Approximately 27% of procedures began on time; the median colonoscope insertion time was 5.9 minutes (interquartile range, 4.0-8.6). In multivariable logistic regression analysis adjusting for covariates and endoscopist-level clustering, adenoma detection was not associated with procedure delay (P = .48), hour of day (P = .40), or performing the second of 2 colonoscopy blocks in 1 day (P = .88). Adenoma detection was associated with insertion time overall (P = .006), but there was no consistent directional relationship across insertion quintiles.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Academic Medical Centers', 'Adenoma', 'Colonic Neoplasms', 'Colonoscopy', 'Fatigue', 'Female', 'Health Services Research', 'Humans', 'Male', 'Mass Screening', 'Middle Aged', 'Retrospective Studies', 'Time Factors']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
26,537,746 | Do surgical management of damaged inferior alveolar nerve caused by endodontic overfilling of calcium hydroxide paste? | {
"contexts": [
"To evaluate the neurosensory outcome of management of damaged inferior alveolar nerves caused by endodontic overfilling and to assess the efficacy of delayed surgical intervention.",
"Nine patients who underwent surgical removal of extruded endodontic material were included. All patients were evaluated for neurosensory function using a set of standardized tests. The outcome of surgical intervention was evaluated through patient interview and quantitative statistical analysis.",
"Surgical procedures included foreign body removal, microsurgical external/internal decompression, excision of neuroma followed by nerve repair, and excision of damaged nerve segment with interpositional nerve graft. Seven of the nine patients had significant improvement according to the follow-up neurosensory assessment. Four patients reported significant improvement, three patients reported mild improvement and two patients reported no appreciable improvement in the Visual Analog Scale (VAS). Two patients who reported no appreciable improvement in VAS also did not achieve FSR. In these patients, calcium hydroxide was spread widely along the IAN and a surgical approach was obtained via sagittal spit osteotomy. The mean time to reach FSR was 222.7 (±41.8) days with a range of 106-397 days. In the early repair group who received surgery within 60 days, three out of five patients achieved FSR in a mean time of 198.0 (±76.2) days. The mean time to FSR in all four subjects who received surgical attention over 60 days after injury was 241.3 (±139.8) days with a range of 106-397 days. As all four cases in the late repair group with limited amount of nerve injury achieved FSR, only 3 of 5 early repair cases with wide-spread injury achieved a similar outcome."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Calcium Hydroxide",
"Female",
"Follow-Up Studies",
"Humans",
"Male",
"Mandibular Nerve",
"Middle Aged",
"Paresthesia",
"Radiography, Dental",
"Root Canal Filling Materials",
"Root Canal Obturation",
"Sensory Thresholds",
"Tooth, Nonvital",
"Trigeminal Nerve Injuries",
"Young Adult"
]
} | The results of this case series confirmed the notion that surgical management of the inferior alveolar nerve is effective in the treatment of nerve injuries caused by endodontic extrusion of calcium hydroxide paste. Delayed surgical repair of the inferior alveolar nerve can be indicated and helpful for the neurosensory recovery of damaged IAN, however, the surgical management was less effective in case of widespread nerve injuries. | yes | [
{
"from": "human",
"value": "Question: Do surgical management of damaged inferior alveolar nerve caused by endodontic overfilling of calcium hydroxide paste?\nContext: {'contexts': ['To evaluate the neurosensory outcome of management of damaged inferior alveolar nerves caused by endodontic overfilling and to assess the efficacy of delayed surgical intervention.', 'Nine patients who underwent surgical removal of extruded endodontic material were included. All patients were evaluated for neurosensory function using a set of standardized tests. The outcome of surgical intervention was evaluated through patient interview and quantitative statistical analysis.', 'Surgical procedures included foreign body removal, microsurgical external/internal decompression, excision of neuroma followed by nerve repair, and excision of damaged nerve segment with interpositional nerve graft. Seven of the nine patients had significant improvement according to the follow-up neurosensory assessment. Four patients reported significant improvement, three patients reported mild improvement and two patients reported no appreciable improvement in the Visual Analog Scale (VAS). Two patients who reported no appreciable improvement in VAS also did not achieve FSR. In these patients, calcium hydroxide was spread widely along the IAN and a surgical approach was obtained via sagittal spit osteotomy. The mean time to reach FSR was 222.7 (±41.8)\\xa0days with a range of 106-397\\xa0days. In the early repair group who received surgery within 60\\xa0days, three out of five patients achieved FSR in a mean time of 198.0 (±76.2)\\xa0days. The mean time to FSR in all four subjects who received surgical attention over 60\\xa0days after injury was 241.3 (±139.8)\\xa0days with a range of 106-397\\xa0days. As all four cases in the late repair group with limited amount of nerve injury achieved FSR, only 3 of 5 early repair cases with wide-spread injury achieved a similar outcome.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Calcium Hydroxide', 'Female', 'Follow-Up Studies', 'Humans', 'Male', 'Mandibular Nerve', 'Middle Aged', 'Paresthesia', 'Radiography, Dental', 'Root Canal Filling Materials', 'Root Canal Obturation', 'Sensory Thresholds', 'Tooth, Nonvital', 'Trigeminal Nerve Injuries', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,548,541 | Is standards and guidelines for observational studies : quality in the eye of the beholder? | {
"contexts": [
"Patient care decisions demand high-quality research. To assist those decisions, numerous observational studies are being performed. Are the standards and guidelines to assess observational studies consistent and actionable? What policy considerations should be considered to ensure decision makers can determine if an observational study is of high-quality and valid to inform treatment decisions?",
"Based on a literature review and input from six experts, we compared and contrasted nine standards/guidelines using 23 methodological elements involved in observational studies (e.g., study protocol, data analysis, and so forth).",
"Fourteen elements (61%) were addressed by at least seven standards/guidelines; 12 of these elements disagreed in the approach. Nine elements (39%) were addressed by six or fewer standards/guidelines. Ten elements (43%) were not actionable in at least one standard/guideline that addressed the element."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Evidence-Based Medicine",
"Humans",
"Observational Studies as Topic",
"Research Design"
]
} | The lack of observational study standard/guideline agreement may contribute to variation in study conduct; disparities in what is considered credible research; and ultimately, what evidence is adopted. A common set of agreed on standards/guidelines for conducting observational studies will benefit funders, researchers, journal editors, and decision makers. | yes | [
{
"from": "human",
"value": "Question: Is standards and guidelines for observational studies : quality in the eye of the beholder?\nContext: {'contexts': ['Patient care decisions demand high-quality research. To assist those decisions, numerous observational studies are being performed. Are the standards and guidelines to assess observational studies consistent and actionable? What policy considerations should be considered to ensure decision makers can determine if an observational study is of high-quality and valid to inform treatment decisions?', 'Based on a literature review and input from six experts, we compared and contrasted nine standards/guidelines using 23 methodological elements involved in observational studies (e.g., study protocol, data analysis, and so forth).', 'Fourteen elements (61%) were addressed by at least seven standards/guidelines; 12 of these elements disagreed in the approach. Nine elements (39%) were addressed by six or fewer standards/guidelines. Ten elements (43%) were not actionable in at least one standard/guideline that addressed the element.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Evidence-Based Medicine', 'Humans', 'Observational Studies as Topic', 'Research Design']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,525,359 | Does isorhamnetin protect mice from lipopolysaccharide-induced acute lung injury via the inhibition of inflammatory responses? | {
"contexts": [
"Isorhamnetin (Isor), a 3-O-methylated metabolite of quercetin, has shown antioxidant and anti-proliferative effects in previous studies. In this study, we investigated the anti-inflammatory effect of Isor on LPS-induced acute lung injury (ALI). Accordingly, we evaluated the effect of Isor on cytokine production elevated by LPS (1 μg/ml) in vitro. An in vivo ALI murine model was also established via lipopolysaccharide inhalation (LPS, 20 mg/kg), and the cytokine levels and inflammatory cell count in bronchoalveolar lavage fluid (BALF) were evaluated. The observed lung injury was assessed using histopathologic sections via H&E straining. Furthermore, to investigate whether the anti-inflammatory effect of Isor is associated with NF-κB and MAPKs pathway activation, the phosphorylated levels of ERK, JNK, IκBa and NF-κB(p65) were determined.",
"Isor significantly inhibited LPS-induced TNF-α, IL-1β and IL-6 secretion both in vitro and in vivo. Neutrophil infiltration and edema in an ALI model were substantially alleviated. The histopathological changes induced by LPS were lessened by Isor. Additionally, Isor notably suppressed the phosphorylation of ERK, JNK, IκBa and NF-κB(p65) activated by LPS in vivo."
],
"labels": [
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Acute Lung Injury",
"Animals",
"Anti-Inflammatory Agents",
"Bronchoalveolar Lavage Fluid",
"Cytokines",
"Lipopolysaccharides",
"Lung",
"MAP Kinase Signaling System",
"Male",
"Mice",
"Mice, Inbred BALB C",
"Mitogen-Activated Protein Kinases",
"NF-kappa B",
"Neutrophil Infiltration",
"Pulmonary Edema",
"Quercetin",
"RAW 264.7 Cells"
]
} | Isor showed efficient protective effects on an LPS-induced ALI model. MAPKs and NF-κB pathways are critical for Isor to perform its protective effects. | yes | [
{
"from": "human",
"value": "Question: Does isorhamnetin protect mice from lipopolysaccharide-induced acute lung injury via the inhibition of inflammatory responses?\nContext: {'contexts': ['Isorhamnetin (Isor), a 3-O-methylated metabolite of quercetin, has shown antioxidant and anti-proliferative effects in previous studies. In this study, we investigated the anti-inflammatory effect of Isor on LPS-induced acute lung injury (ALI). Accordingly, we evaluated the effect of Isor on cytokine production elevated by LPS (1\\xa0μg/ml) in vitro. An in vivo ALI murine model was also established via lipopolysaccharide inhalation (LPS, 20\\xa0mg/kg), and the cytokine levels and inflammatory cell count in bronchoalveolar lavage fluid (BALF) were evaluated. The observed lung injury was assessed using histopathologic sections via H&E straining. Furthermore, to investigate whether the anti-inflammatory effect of Isor is associated with NF-κB and MAPKs pathway activation, the phosphorylated levels of ERK, JNK, IκBa and NF-κB(p65) were determined.', 'Isor significantly inhibited LPS-induced TNF-α, IL-1β and IL-6 secretion both in vitro and in vivo. Neutrophil infiltration and edema in an ALI model were substantially alleviated. The histopathological changes induced by LPS were lessened by Isor. Additionally, Isor notably suppressed the phosphorylation of ERK, JNK, IκBa and NF-κB(p65) activated by LPS in vivo.'], 'labels': ['OBJECTIVE', 'RESULTS'], 'meshes': ['Acute Lung Injury', 'Animals', 'Anti-Inflammatory Agents', 'Bronchoalveolar Lavage Fluid', 'Cytokines', 'Lipopolysaccharides', 'Lung', 'MAP Kinase Signaling System', 'Male', 'Mice', 'Mice, Inbred BALB C', 'Mitogen-Activated Protein Kinases', 'NF-kappa B', 'Neutrophil Infiltration', 'Pulmonary Edema', 'Quercetin', 'RAW 264.7 Cells']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,527,417 | Does the ileal bile acid transporter inhibitor A4250 decrease serum bile acids by interrupting the enterohepatic circulation? | {
"contexts": [
"Reabsorption of bile acids from the intestine by ileal bile acid transporter is pivotal for the enterohepatic circulation of BAs and sterol homoeostasis.",
"To assess tolerability and study, bile acid metabolism in a phase 1 trial with the selective ileal bile acid transporter inhibitor A4250.",
"A randomised double-blind, single-ascending dose (SAD) and multiple-ascending-dose study consisting of five cohorts comprising 40 individuals with a single administration of A4250 (0.1, 0.3, 1, 3, or 10 mg) or placebo and three cohorts comprising 24 individuals with a 1-week administration of A4250 (1 or 3 mg once daily or 1.5 mg twice daily) or placebo. For the multiple-ascending-dose study, bile acids were measured by HPLC-MS in plasma and faeces, and fibroblast growth factor 19 (FGF19) and 7α-hydroxy-4-cholesten-3-one (C4) were measured in plasma.",
"No serious adverse events occurred and all participants finished the trial per protocol. At the end of the multiple-ascending-dose study, plasma total bile acids and FGF19 decreased by 47% and 76%, respectively, at 3 mg/day (P < 0.01), and by 15% and 16%, respectively, at 1.5 mg twice daily (P < 0.05). Plasma C4 and faecal bile acids increased at all dose regimens, by 555%, 664%, 292% and 338%, 421%, 420%, respectively (P < 0.01-0.05). The primary bile acids cholic and chenodeoxycholic acids constituted the majority of faecal bile acids in the A4250-treated groups."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Bile Acids and Salts",
"Carrier Proteins",
"Chenodeoxycholic Acid",
"Cholestenones",
"Double-Blind Method",
"Enterohepatic Circulation",
"Feces",
"Female",
"Fibroblast Growth Factors",
"Humans",
"Ileum",
"Intestinal Mucosa",
"Male",
"Membrane Glycoproteins"
]
} | A4250 is well tolerated. By blocking ileal bile acid transporter in the terminal ileum, it highly efficiently interrupts the enterohepatic circulation of BAs, and should be of benefit to patients with cholestatic liver diseases. Clinical Trial registration EudraCT 2013-001175-21. | yes | [
{
"from": "human",
"value": "Question: Does the ileal bile acid transporter inhibitor A4250 decrease serum bile acids by interrupting the enterohepatic circulation?\nContext: {'contexts': ['Reabsorption of bile acids from the intestine by ileal bile acid transporter is pivotal for the enterohepatic circulation of BAs and sterol homoeostasis.', 'To assess tolerability and study, bile acid metabolism in a phase 1 trial with the selective ileal bile acid transporter inhibitor A4250.', 'A randomised double-blind, single-ascending dose (SAD) and multiple-ascending-dose study consisting of five cohorts comprising 40 individuals with a single administration of A4250 (0.1, 0.3, 1, 3, or 10\\xa0mg) or placebo and three cohorts comprising 24 individuals with a 1-week administration of A4250 (1 or 3\\xa0mg once daily or 1.5\\xa0mg twice daily) or placebo. For the multiple-ascending-dose study, bile acids were measured by HPLC-MS in plasma and faeces, and fibroblast growth factor 19 (FGF19) and 7α-hydroxy-4-cholesten-3-one (C4) were measured in plasma.', 'No serious adverse events occurred and all participants finished the trial per protocol. At the end of the multiple-ascending-dose study, plasma total bile acids and FGF19 decreased by 47% and 76%, respectively, at 3\\xa0mg/day (P\\xa0<\\xa00.01), and by 15% and 16%, respectively, at 1.5\\xa0mg twice daily (P\\xa0<\\xa00.05). Plasma C4 and faecal bile acids increased at all dose regimens, by 555%, 664%, 292% and 338%, 421%, 420%, respectively (P\\xa0<\\xa00.01-0.05). The primary bile acids cholic and chenodeoxycholic acids constituted the majority of faecal bile acids in the A4250-treated groups.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Bile Acids and Salts', 'Carrier Proteins', 'Chenodeoxycholic Acid', 'Cholestenones', 'Double-Blind Method', 'Enterohepatic Circulation', 'Feces', 'Female', 'Fibroblast Growth Factors', 'Humans', 'Ileum', 'Intestinal Mucosa', 'Male', 'Membrane Glycoproteins']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,526,641 | Is narrow band CE-Chirp auditory steady-state response more reliable than the conventional ASSR in predicting the behavioral hearing threshold? | {
"contexts": [
"We evaluated conventional ASSR (Bio-logic MASTER II) and NB CE-Chirp ASSR thresholds as objective hearing measures in both normal and hearing loss subjects.",
"Patients with sensorineural hearing loss and volunteer normal hearing subjects were enrolled. Pure tone thresholds at 0.5, 1, 2 and 4 kHz were compared with the corresponding thresholds measured using Bio-logic MASTER II and the Eclipse ASSR systems. The threshold differences and correlation with pure tone were measured and reliability was evaluated with Cronbach's α. In part I of the study, all subjects were included, in part II of the study, only mild hearing loss and normal hearing subjects were included.",
"In part I, NB CE-Chirp ASSR revealed a significantly smaller difference in threshold than conventional ASSR, a better correlation and better reliability. However, lower frequencies of NB CE-Chirp tended to be less reliable than higher frequencies. In part II, NB CE-Chirp revealed smaller threshold differences than conventional ASSR. Both correlation scores and reliability values were generally lower in the part II results."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Acoustic Stimulation",
"Adult",
"Audiometry, Evoked Response",
"Audiometry, Pure-Tone",
"Auditory Threshold",
"Case-Control Studies",
"Evoked Potentials, Auditory",
"Female",
"Hearing Loss, Sensorineural",
"Humans",
"Male",
"Middle Aged",
"Young Adult"
]
} | NB CE-Chirp ASSR generally revealed more favorable outcomes. However, its reliability was reduced at lower frequencies and in patients with milder hearing loss. | yes | [
{
"from": "human",
"value": "Question: Is narrow band CE-Chirp auditory steady-state response more reliable than the conventional ASSR in predicting the behavioral hearing threshold?\nContext: {'contexts': ['We evaluated conventional ASSR (Bio-logic MASTER II) and NB CE-Chirp ASSR thresholds as objective hearing measures in both normal and hearing loss subjects.', \"Patients with sensorineural hearing loss and volunteer normal hearing subjects were enrolled. Pure tone thresholds at 0.5, 1, 2 and 4 kHz were compared with the corresponding thresholds measured using Bio-logic MASTER II and the Eclipse ASSR systems. The threshold differences and correlation with pure tone were measured and reliability was evaluated with Cronbach's α. In part I of the study, all subjects were included, in part II of the study, only mild hearing loss and normal hearing subjects were included.\", 'In part I, NB CE-Chirp ASSR revealed a significantly smaller difference in threshold than conventional ASSR, a better correlation and better reliability. However, lower frequencies of NB CE-Chirp tended to be less reliable than higher frequencies. In part II, NB CE-Chirp revealed smaller threshold differences than conventional ASSR. Both correlation scores and reliability values were generally lower in the part II results.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Acoustic Stimulation', 'Adult', 'Audiometry, Evoked Response', 'Audiometry, Pure-Tone', 'Auditory Threshold', 'Case-Control Studies', 'Evoked Potentials, Auditory', 'Female', 'Hearing Loss, Sensorineural', 'Humans', 'Male', 'Middle Aged', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,545,015 | Are infectious diseases associated with carotid intima media thickness in adolescence? | {
"contexts": [
"Inflammatory risk factors in childhood, e.g. obesity, impact on carotid artery intima media thickness (CIMT), an early indicator of atherosclerosis. Little is known on potential infectious origins in childhood. We investigated the association between number of reported different childhood infectious diseases and CIMT in adolescence.",
"288 SAPALDIA offspring (8-21years) underwent a clinical examination in 2010-2011: anthropometry, blood pressure, CIMT, blood draw (cardiovascular biomarkers, cotinine). Offspring and parents gave information on individuals' and family health, child's vaccination status, infectious diseases and other early life factors. Life-time prevalence of bronchitis, pneumonia, tonsillitis, otitis, mononucleosis, meningitis, appendicitis, and scarlet fever were investigated, separately, and as cumulative infectious disease score. Multilevel adjusted linear regression analysis on the association between subjects' CIMT average and infectious diseases score was performed, stratifying by sex.",
"Youth (mean age 14.8 yrs; 53% female) reported on average 1.3 of the listed infectious diseases; 22% boys and 15% girls reported ≥3 infectious diseases (p = 0.136). Two-thirds were vaccinated according to recommendations (boys 56%, girls 61.5%, p = 0.567). Sex-stratified analyses yielded significantly increased CIMT in boys with ≥3 infectious diseases vs. none (0.046 mm, 95%CI 0.024; 0.068). In girls, the effect was of same direction but statistically non-significant (0.011 mm, 95%CI -0.015; 0.036)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Age Distribution",
"Age Factors",
"Carotid Arteries",
"Carotid Artery Diseases",
"Carotid Intima-Media Thickness",
"Child",
"Communicable Diseases",
"Comorbidity",
"Cross-Sectional Studies",
"Female",
"Humans",
"Life Style",
"Linear Models",
"Male",
"Multivariate Analysis",
"Predictive Value of Tests",
"Prevalence",
"Protective Factors",
"Risk Assessment",
"Risk Factors",
"Sex Distribution",
"Sex Factors",
"Surveys and Questionnaires",
"Switzerland",
"Time Factors",
"Vaccination",
"Young Adult"
]
} | The SAPALDIA Youth study complements current evidence on infectious origins of atherosclerosis in adults. The larger effects observed in boys may relate to a higher vulnerability of the vasculature and/or to infectious pathogens. Our data are suggestive of an early impact of childhood infectious diseases on vascular health. | yes | [
{
"from": "human",
"value": "Question: Are infectious diseases associated with carotid intima media thickness in adolescence?\nContext: {'contexts': ['Inflammatory risk factors in childhood, e.g. obesity, impact on carotid artery intima media thickness (CIMT), an early indicator of atherosclerosis. Little is known on potential infectious origins in childhood. We investigated the association between number of reported different childhood infectious diseases and CIMT in adolescence.', \"288 SAPALDIA offspring (8-21years) underwent a clinical examination in 2010-2011: anthropometry, blood pressure, CIMT, blood draw (cardiovascular biomarkers, cotinine). Offspring and parents gave information on individuals' and family health, child's vaccination status, infectious diseases and other early life factors. Life-time prevalence of bronchitis, pneumonia, tonsillitis, otitis, mononucleosis, meningitis, appendicitis, and scarlet fever were investigated, separately, and as cumulative infectious disease score. Multilevel adjusted linear regression analysis on the association between subjects' CIMT average and infectious diseases score was performed, stratifying by sex.\", 'Youth (mean age 14.8\\xa0yrs; 53% female) reported on average 1.3 of the listed infectious diseases; 22% boys and 15% girls reported ≥3 infectious diseases (p\\xa0=\\xa00.136). Two-thirds were vaccinated according to recommendations (boys 56%, girls 61.5%, p\\xa0=\\xa00.567). Sex-stratified analyses yielded significantly increased CIMT in boys with ≥3 infectious diseases vs. none (0.046\\xa0mm, 95%CI 0.024; 0.068). In girls, the effect was of same direction but statistically non-significant (0.011\\xa0mm, 95%CI\\xa0-0.015; 0.036).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Age Distribution', 'Age Factors', 'Carotid Arteries', 'Carotid Artery Diseases', 'Carotid Intima-Media Thickness', 'Child', 'Communicable Diseases', 'Comorbidity', 'Cross-Sectional Studies', 'Female', 'Humans', 'Life Style', 'Linear Models', 'Male', 'Multivariate Analysis', 'Predictive Value of Tests', 'Prevalence', 'Protective Factors', 'Risk Assessment', 'Risk Factors', 'Sex Distribution', 'Sex Factors', 'Surveys and Questionnaires', 'Switzerland', 'Time Factors', 'Vaccination', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,545,012 | Do apolipoprotein E-deficient rats develop atherosclerotic plaques in partially ligated carotid arteries? | {
"contexts": [
"The goal of this study was to establish an apolipoprotein E-deficient (ApoE(-/-)) rat model.",
"The ApoE(-/-) rat was created by TALEN-mediated gene targeting in the genetic background of Sprague Dawley rat. Six-to eight-week-old male rats were used in the experiments (n = 10 in each group).",
"After fed with high-cholesterol diet (HCD) for 12 weeks, the ApoE(-/-) rats displayed typical dyslipidemia. In contrast, HCD failed to induce hypercholesterolemia in wild-type rats. However, there was no obvious atherosclerotic lesion in oil red O-stained en face aortas and the aortic root sections in both genetic types of rats. Interestingly, partial ligation caused the formation of plaques consist of lipid and macrophages in carotid arteries from ApoE(-/-) rats, but induced the neointimal hyperplasia in wild-type rats. Additionally, we found that HCD slightly increased the expression of adhesion molecules, while partial ligation dramatically upregulated these molecules."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Apolipoproteins E",
"Carotid Arteries",
"Carotid Artery Diseases",
"Cell Adhesion Molecules",
"Cholesterol, Dietary",
"Diet, High-Fat",
"Disease Models, Animal",
"Genetic Predisposition to Disease",
"Hypercholesterolemia",
"Hyperplasia",
"Inflammation Mediators",
"Ligation",
"Lipids",
"Macrophages",
"Male",
"Neointima",
"Phenotype",
"Plaque, Atherosclerotic",
"Rats, Sprague-Dawley",
"Rats, Transgenic"
]
} | The ApoE(-/-) rat is a novel model for dyslipidemia and could also be used in the research of atherosclerosis. | yes | [
{
"from": "human",
"value": "Question: Do apolipoprotein E-deficient rats develop atherosclerotic plaques in partially ligated carotid arteries?\nContext: {'contexts': ['The goal of this study was to establish an apolipoprotein E-deficient (ApoE(-/-)) rat model.', 'The ApoE(-/-) rat was created by TALEN-mediated gene targeting in the genetic background of Sprague Dawley rat. Six-to eight-week-old male rats were used in the experiments (n\\xa0=\\xa010 in each group).', 'After fed with high-cholesterol diet (HCD) for 12 weeks, the ApoE(-/-) rats displayed typical dyslipidemia. In contrast, HCD failed to induce hypercholesterolemia in wild-type rats. However, there was no obvious atherosclerotic lesion in oil red O-stained en face aortas and the aortic root sections in both genetic types of rats. Interestingly, partial ligation caused the formation of plaques consist of lipid and macrophages in carotid arteries from ApoE(-/-) rats, but induced the neointimal hyperplasia in wild-type rats. Additionally, we found that HCD slightly increased the expression of adhesion molecules, while partial ligation dramatically upregulated these molecules.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Apolipoproteins E', 'Carotid Arteries', 'Carotid Artery Diseases', 'Cell Adhesion Molecules', 'Cholesterol, Dietary', 'Diet, High-Fat', 'Disease Models, Animal', 'Genetic Predisposition to Disease', 'Hypercholesterolemia', 'Hyperplasia', 'Inflammation Mediators', 'Ligation', 'Lipids', 'Macrophages', 'Male', 'Neointima', 'Phenotype', 'Plaque, Atherosclerotic', 'Rats, Sprague-Dawley', 'Rats, Transgenic']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,546,875 | Do dual inhibition of nuclear factor kappa-B and Mdm2 enhance the antitumor effect of radiation therapy for pancreatic cancer? | {
"contexts": [
"Radiation therapy, alone or in combination with chemotherapy, is effective for patients with locally advanced and recurrent pancreatic cancer. Ionizing radiation induces cell cycle arrest and cell apoptosis through enhancement several signals such as p53, p21(Waf1/Cip1), and caspase. However, the therapeutic efficacy is attenuated by radiation-induced activation of NF-κB. Nafamostat mesilate, a synthetic serine protease inhibitor, inhibits NF-κB activation in pancreatic cancer. Therefore, we hypothesized that nafamostat mesilate inhibited radiation-induced activation of NF-κB and improves therapeutic outcome.",
"In combination group, NF-κB activation was significantly inhibited in comparison with that of radiation group. Nafamostat mesilate obviously down-regulated the expression levels of Mdm2 compared with control cells or irradiated cells. Consequently, p53 expression was stabilized inversely in correlation with Mdm2 protein expression level. The expression levels of p53, p21(Waf1/Cip1), cleaved caspase-3 and -8 were the highest in the combination group. Nafamostat mesilate enhanced ionizing radiation-induced cell apoptosis and G2/M cell cycle arrest. In combination group, cell proliferation and tumor growth were significantly slower than those in other groups."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Animals",
"Apoptosis",
"Cell Cycle Checkpoints",
"Cell Line, Tumor",
"Guanidines",
"Humans",
"Male",
"Mice",
"Mice, Inbred BALB C",
"NF-kappa B",
"Pancreatic Neoplasms",
"Proto-Oncogene Proteins c-mdm2",
"Radiation-Sensitizing Agents",
"Serine Proteinase Inhibitors",
"Tumor Suppressor Protein p53"
]
} | Combination therapy of radiation with nafamostat mesilate exerts enhanced anti-tumor effect against human pancreatic cancer. | yes | [
{
"from": "human",
"value": "Question: Do dual inhibition of nuclear factor kappa-B and Mdm2 enhance the antitumor effect of radiation therapy for pancreatic cancer?\nContext: {'contexts': ['Radiation therapy, alone or in combination with chemotherapy, is effective for patients with locally advanced and recurrent pancreatic cancer. Ionizing radiation induces cell cycle arrest and cell apoptosis through enhancement several signals such as p53, p21(Waf1/Cip1), and caspase. However, the therapeutic efficacy is attenuated by radiation-induced activation of NF-κB. Nafamostat mesilate, a synthetic serine protease inhibitor, inhibits NF-κB activation in pancreatic cancer. Therefore, we hypothesized that nafamostat mesilate inhibited radiation-induced activation of NF-κB and improves therapeutic outcome.', 'In combination group, NF-κB activation was significantly inhibited in comparison with that of radiation group. Nafamostat mesilate obviously down-regulated the expression levels of Mdm2 compared with control cells or irradiated cells. Consequently, p53 expression was stabilized inversely in correlation with Mdm2 protein expression level. The expression levels of p53, p21(Waf1/Cip1), cleaved caspase-3 and -8 were the highest in the combination group. Nafamostat mesilate enhanced ionizing radiation-induced cell apoptosis and G2/M cell cycle arrest. In combination group, cell proliferation and tumor growth were significantly slower than those in other groups.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Animals', 'Apoptosis', 'Cell Cycle Checkpoints', 'Cell Line, Tumor', 'Guanidines', 'Humans', 'Male', 'Mice', 'Mice, Inbred BALB C', 'NF-kappa B', 'Pancreatic Neoplasms', 'Proto-Oncogene Proteins c-mdm2', 'Radiation-Sensitizing Agents', 'Serine Proteinase Inhibitors', 'Tumor Suppressor Protein p53']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,528,352 | Does apelin-13 protect the heart against ischemia-reperfusion injury through the RISK-GSK-3β-mPTP pathway? | {
"contexts": [
"Apelin plays an important role in the protection against myocardial ischemia-reperfusion (I/R) injury, while the mechanism still remains unclear. In the current study, we aimed to evaluate the protective effect of apelin-13, and the main mechanism.",
"The in vivo I/R injury model (Sprague-Dawley rat) was established, then infarct size, expression levels of phospho-protein kinase B (p-Akt), phospho-extracellular signal-regulated kinase (p-ERK) and phospho-glycogen synthase kinase-3β (p-GSK-3β) were measured. The fluorescence intensity of tetramethylrhodamine ethyl ester perchlorate (TMRE) of the isolated myocardial cells was determined to evaluate the opening of the mitochondrial permeability transition pore (mPTP) caused by oxidant stress and hypoxia/reoxygenation.",
"For the established I/R injury model, apelin-13 and SB216763 (GSK-3β inhibitor) significantly reduced the infarct size (p < 0.05), which could be abolished by LY294002 (PI3K inhibitor), PD98059 (MEK inhibitor) and atractyloside (mPTP accelerator). The enhanced expression levels of p-Akt, p-ERK and p-GSK-3β caused by apelin-13 (p < 0.05) could be counteracted by LY294002 and PD98059. The reduced fluorescence intensity of TMRE in the H2O2/apelin-13 and H2O2/SB216763 treated groups was significantly lower (p < 0.05), indicating that apelin-13 and SB216763 could reduce the decline in mitochondrial membrane potential caused by oxidant stress, and the fluorescence intensity in the hypoxia/reoxygenation + apelin-13 group was significantly lower (p < 0.05), which suggested that apelin-13 could inhibit the mitochondrial membrane potential changes induced by hypoxia/reoxygenation."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": []
} | The protective mechanism of apelin-13 might be that inactivation of GSK-3β could inhibit the opening of mPTP by activating PI3K/Akt and ERK1/2 involved in the reperfusion injury salvage kinase (RISK) pathway. | yes | [
{
"from": "human",
"value": "Question: Does apelin-13 protect the heart against ischemia-reperfusion injury through the RISK-GSK-3β-mPTP pathway?\nContext: {'contexts': ['Apelin plays an important role in the protection against myocardial ischemia-reperfusion (I/R) injury, while the mechanism still remains unclear. In the current study, we aimed to evaluate the protective effect of apelin-13, and the main mechanism.', 'The in vivo I/R injury model (Sprague-Dawley rat) was established, then infarct size, expression levels of phospho-protein kinase B (p-Akt), phospho-extracellular signal-regulated kinase (p-ERK) and phospho-glycogen synthase kinase-3β (p-GSK-3β) were measured. The fluorescence intensity of tetramethylrhodamine ethyl ester perchlorate (TMRE) of the isolated myocardial cells was determined to evaluate the opening of the mitochondrial permeability transition pore (mPTP) caused by oxidant stress and hypoxia/reoxygenation.', 'For the established I/R injury model, apelin-13 and SB216763 (GSK-3β inhibitor) significantly reduced the infarct size (p < 0.05), which could be abolished by LY294002 (PI3K inhibitor), PD98059 (MEK inhibitor) and atractyloside (mPTP accelerator). The enhanced expression levels of p-Akt, p-ERK and p-GSK-3β caused by apelin-13 (p < 0.05) could be counteracted by LY294002 and PD98059. The reduced fluorescence intensity of TMRE in the H2O2/apelin-13 and H2O2/SB216763 treated groups was significantly lower (p < 0.05), indicating that apelin-13 and SB216763 could reduce the decline in mitochondrial membrane potential caused by oxidant stress, and the fluorescence intensity in the hypoxia/reoxygenation + apelin-13 group was significantly lower (p < 0.05), which suggested that apelin-13 could inhibit the mitochondrial membrane potential changes induced by hypoxia/reoxygenation.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,547,123 | Do simultaneous multi-slice readout-segmented echo planar imaging for accelerated diffusion-weighted imaging of the breast? | {
"contexts": [
"Readout-segmented echo planar imaging (rs-EPI) significantly reduces susceptibility artifacts in diffusion-weighted imaging (DWI) of the breast compared to single-shot EPI but is limited by longer scan times. To compensate for this, we tested a new simultaneous multi-slice (SMS) acquisition for accelerated rs-EPI.",
"After approval by the local ethics committee, eight healthy female volunteers (age, 38.9 ± 13.1 years) underwent breast MRI at 3T. Conventional as well as two-fold (2× SMS) and three-fold (3× SMS) slice-accelerated rs-EPI sequences were acquired at b-values of 50 and 800 s/mm(2). Two independent readers analyzed the apparent diffusion coefficient (ADC) in fibroglandular breast parenchyma. The signal-to-noise ratio (SNR) was estimated based on the subtraction method. ADC and SNR were compared between sequences by using the Friedman test.",
"The acquisition time was 4:21 min for conventional rs-EPI, 2:35 min for 2× SMS rs-EPI and 1:44 min for 3× SMS rs-EPI. ADC values were similar in all sequences (mean values 1.62 × 10(-3)mm(2)/s, p=0.99). Mean SNR was 27.7-29.6, and no significant differences were found among the sequences (p=0.83)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Artifacts",
"Breast",
"Breast Neoplasms",
"Diffusion Magnetic Resonance Imaging",
"Echo-Planar Imaging",
"Female",
"Humans",
"Middle Aged",
"Observer Variation",
"Reproducibility of Results",
"Signal-To-Noise Ratio",
"Subtraction Technique"
]
} | SMS rs-EPI yields similar ADC values and SNR compared to conventional rs-EPI at markedly reduced scan time. Thus, SMS excitation increases the clinical applicability of rs-EPI for DWI of the breast. | yes | [
{
"from": "human",
"value": "Question: Do simultaneous multi-slice readout-segmented echo planar imaging for accelerated diffusion-weighted imaging of the breast?\nContext: {'contexts': ['Readout-segmented echo planar imaging (rs-EPI) significantly reduces susceptibility artifacts in diffusion-weighted imaging (DWI) of the breast compared to single-shot EPI but is limited by longer scan times. To compensate for this, we tested a new simultaneous multi-slice (SMS) acquisition for accelerated rs-EPI.', 'After approval by the local ethics committee, eight healthy female volunteers (age, 38.9 ± 13.1 years) underwent breast MRI at 3T. Conventional as well as two-fold (2× SMS) and three-fold (3× SMS) slice-accelerated rs-EPI sequences were acquired at b-values of 50 and 800 s/mm(2). Two independent readers analyzed the apparent diffusion coefficient (ADC) in fibroglandular breast parenchyma. The signal-to-noise ratio (SNR) was estimated based on the subtraction method. ADC and SNR were compared between sequences by using the Friedman test.', 'The acquisition time was 4:21 min for conventional rs-EPI, 2:35 min for 2× SMS rs-EPI and 1:44 min for 3× SMS rs-EPI. ADC values were similar in all sequences (mean values 1.62 × 10(-3)mm(2)/s, p=0.99). Mean SNR was 27.7-29.6, and no significant differences were found among the sequences (p=0.83).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Artifacts', 'Breast', 'Breast Neoplasms', 'Diffusion Magnetic Resonance Imaging', 'Echo-Planar Imaging', 'Female', 'Humans', 'Middle Aged', 'Observer Variation', 'Reproducibility of Results', 'Signal-To-Noise Ratio', 'Subtraction Technique']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,542,590 | Does minimally Invasive Pancreaticoduodenectomy Improve Use or Time to Initiation of Adjuvant Chemotherapy for Patients With Pancreatic Adenocarcinoma? | {
"contexts": [
"The modifiable variable best proven to improve survival after resection of pancreatic adenocarcinoma is the addition of adjuvant chemotherapy. A theoretical advantage of minimally invasive pancreaticoduodenectomy (MI-PD) is the potential for greater use and earlier initiation of adjuvant therapy, but this benefit remains unproven.",
"The 2010-2012 National Cancer Data Base (NCDB) was queried for patients undergoing pancreaticoduodenectomy for pancreatic adenocarcinoma. Subjects were classified as MI-PD versus open pancreaticoduodenectomy (O-PD). Baseline variables were compared between groups. The independent effect of surgical approach on the use and timing of adjuvant chemotherapy was estimated using multivariable regression analyses.",
"For this study, 7967 subjects were identified: 1191 MI-PD (14.9%) and 6776 O-PD (85.1%) patients. Patients who underwent MI-PD were more likely to have been treated at academic hospitals. Otherwise, the groups had no baseline differences. In both the MI-PD and O-PD groups, approximately 50% of the patients received adjuvant chemotherapy, initiated at a median of 54 versus 55 days postoperatively (p = 0.08). After multivariable adjustment, surgical approach was not independently associated with use (odds ratio 1.00; p = 0.99) or time to initiation of adjuvant chemotherapy (-2.3 days; p = 0.07). Younger age, insured status, lower comorbidity score, higher tumor stage, and the presence of lymph node metastases were independently associated with the use of adjuvant chemotherapy."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adenocarcinoma",
"Aged",
"Antineoplastic Combined Chemotherapy Protocols",
"Chemotherapy, Adjuvant",
"Female",
"Follow-Up Studies",
"Humans",
"Lymphatic Metastasis",
"Male",
"Minimally Invasive Surgical Procedures",
"Neoplasm Staging",
"Pancreatic Neoplasms",
"Pancreaticoduodenectomy",
"Prognosis",
"Retrospective Studies",
"Survival Rate",
"Time-to-Treatment"
]
} | At a national level, MI-PD does not result in greater use or earlier initiation of adjuvant chemotherapy. As surgeons and institutions continue to gain experience with this complex procedure, it will be important to revisit this benchmark as a justification for its increasing use for patients with pancreatic cancer. | no | [
{
"from": "human",
"value": "Question: Does minimally Invasive Pancreaticoduodenectomy Improve Use or Time to Initiation of Adjuvant Chemotherapy for Patients With Pancreatic Adenocarcinoma?\nContext: {'contexts': ['The modifiable variable best proven to improve survival after resection of pancreatic adenocarcinoma is the addition of adjuvant chemotherapy. A theoretical advantage of minimally invasive pancreaticoduodenectomy (MI-PD) is the potential for greater use and earlier initiation of adjuvant therapy, but this benefit remains unproven.', 'The 2010-2012 National Cancer Data Base (NCDB) was queried for patients undergoing pancreaticoduodenectomy for pancreatic adenocarcinoma. Subjects were classified as MI-PD versus open pancreaticoduodenectomy (O-PD). Baseline variables were compared between groups. The independent effect of surgical approach on the use and timing of adjuvant chemotherapy was estimated using multivariable regression analyses.', 'For this study, 7967 subjects were identified: 1191 MI-PD (14.9%) and 6776 O-PD (85.1%) patients. Patients who underwent MI-PD were more likely to have been treated at academic hospitals. Otherwise, the groups had no baseline differences. In both the MI-PD and O-PD groups, approximately 50% of the patients received adjuvant chemotherapy, initiated at a median of 54 versus 55 days postoperatively (p = 0.08). After multivariable adjustment, surgical approach was not independently associated with use (odds ratio 1.00; p = 0.99) or time to initiation of adjuvant chemotherapy (-2.3 days; p = 0.07). Younger age, insured status, lower comorbidity score, higher tumor stage, and the presence of lymph node metastases were independently associated with the use of adjuvant chemotherapy.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adenocarcinoma', 'Aged', 'Antineoplastic Combined Chemotherapy Protocols', 'Chemotherapy, Adjuvant', 'Female', 'Follow-Up Studies', 'Humans', 'Lymphatic Metastasis', 'Male', 'Minimally Invasive Surgical Procedures', 'Neoplasm Staging', 'Pancreatic Neoplasms', 'Pancreaticoduodenectomy', 'Prognosis', 'Retrospective Studies', 'Survival Rate', 'Time-to-Treatment']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
26,550,436 | Does notch-1 promote breast cancer cells proliferation by regulating LncRNA GAS5? | {
"contexts": [
"Notch signaling is indicated as novel therapeutic targets to prevent recurrence of breast cancer. LncRNAs were identified as downstream target of Notch pathway. However, the exact mechanisms involved in Notch signaling, lncRNAs and breast cancer remain to be explained.",
"This original research aimed to determine the prognostic implications of Notch-1 for breast cancer, and explain mechanisms involved in regulation of lnRNA GAS5 by Notch-1, and identify the function of this mechanism on breast cancer.",
"Thirty breast cancer patients were included from The First Affiliated Hospital of Anhui Medical University (China) since January 2006 in this study. The mRNA level by RT-PCR and protein level of Notch-1 by western blot in tumor tissues and adjacent normal tissues were evaluated and 5-year survival analysis was applied to examine the significance of Notch-1. The levels of ten reported lncRNAs were determined by RT-PCR, and subsequently linear analysis was applied to analyze the relationship between these four unique lncRNAs and protein level of Notch-1, which identified the most relevant lncRNA GAS5 with Notch-1 in breast cancer. Subsequently, Notch1-siRNA was applied to influence the expression of Notch-1 in T47D, then the level of RSA5 was measured by RT-PCR, and CCK-8 assay was applied to measure the proliferation of T47D cells.",
"High level of Notch-1 provided a poor prognosis in breast cancer. Interference of Notch-1 significantly suppressed proliferation of T47D cell (P < 0.05), and significantly increased the level of GAS5."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": []
} | Notch-1 promotes breast cancer cells proliferation by regulating LncRNA GAS5. | yes | [
{
"from": "human",
"value": "Question: Does notch-1 promote breast cancer cells proliferation by regulating LncRNA GAS5?\nContext: {'contexts': ['Notch signaling is indicated as novel therapeutic targets to prevent recurrence of breast cancer. LncRNAs were identified as downstream target of Notch pathway. However, the exact mechanisms involved in Notch signaling, lncRNAs and breast cancer remain to be explained.', 'This original research aimed to determine the prognostic implications of Notch-1 for breast cancer, and explain mechanisms involved in regulation of lnRNA GAS5 by Notch-1, and identify the function of this mechanism on breast cancer.', 'Thirty breast cancer patients were included from The First Affiliated Hospital of Anhui Medical University (China) since January 2006 in this study. The mRNA level by RT-PCR and protein level of Notch-1 by western blot in tumor tissues and adjacent normal tissues were evaluated and 5-year survival analysis was applied to examine the significance of Notch-1. The levels of ten reported lncRNAs were determined by RT-PCR, and subsequently linear analysis was applied to analyze the relationship between these four unique lncRNAs and protein level of Notch-1, which identified the most relevant lncRNA GAS5 with Notch-1 in breast cancer. Subsequently, Notch1-siRNA was applied to influence the expression of Notch-1 in T47D, then the level of RSA5 was measured by RT-PCR, and CCK-8 assay was applied to measure the proliferation of T47D cells.', 'High level of Notch-1 provided a poor prognosis in breast cancer. Interference of Notch-1 significantly suppressed proliferation of T47D cell (P < 0.05), and significantly increased the level of GAS5.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,541,281 | Does steroid treatment resolve acute respiratory failure in patient transferred for ECMO? | {
"contexts": [
"Space-consuming mediastinal tumors can create respiratory failure.",
"We are reporting on a case of mediastinal lymphoma, which created respiratory failure in our patient. IV steroid therapy was used in our patient, who presented with end-stage respiratory failure.",
"Conservative management of our patient was possible without the application of ECMO."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Extracorporeal Membrane Oxygenation",
"Female",
"Humans",
"Lymphoma",
"Mediastinal Neoplasms",
"Respiratory Insufficiency",
"Treatment Outcome"
]
} | In the right patient population, IV steroid treatment can avoid further deterioration of end-stage respiratory failure. | yes | [
{
"from": "human",
"value": "Question: Does steroid treatment resolve acute respiratory failure in patient transferred for ECMO?\nContext: {'contexts': ['Space-consuming mediastinal tumors can create respiratory failure.', 'We are reporting on a case of mediastinal lymphoma, which created respiratory failure in our patient. IV steroid therapy was used in our patient, who presented with end-stage respiratory failure.', 'Conservative management of our patient was possible without the application of ECMO.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Extracorporeal Membrane Oxygenation', 'Female', 'Humans', 'Lymphoma', 'Mediastinal Neoplasms', 'Respiratory Insufficiency', 'Treatment Outcome']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,537,554 | Do term neonates with infection and shock display high cortisol precursors despite low levels of normal cortisol? | {
"contexts": [
"Neonatal therapy-resistant septic shock is a common problem in middle and low-income countries. We investigated whether newborn infants with infection and therapy-resistant hypotension showed evidence of abnormal levels of cortisol or cortisol precursors.",
"A total of 60 term or near term neonates with evidence of infection were enrolled after informed consent. Of these, 30 had an infection and refractory shock and 30 had an infection without shock. There were no detectable differences between the groups in the length of gestation, birth weight or gender distribution. Serum was obtained during days four and 14 after birth. Cortisol and cortisol precursor concentrations were analysed using liquid chromatography-tandem mass spectrometry.",
"The cortisol concentrations were low considering the expected responses to stress and they did not differ between the groups. The infants with infection and shock had higher serum dehydroepiandrosterone (DHEA) levels than those without shock (319.0 ± 110.3 μg/dL, versus 22.3 ± 18.3 μg/dL; p < 0.0001) and they also had higher 17-hydroxy-pregnenolone, pregnenolone and progesterone concentrations. There were no detectable differences in the levels of 17-hydroxy-progesterone, 11-deoxy-cortisol, cortisol or cortisone."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Cortisone",
"Dehydroepiandrosterone",
"Humans",
"Hydrocortisone",
"Infant, Newborn",
"Infant, Newborn, Diseases",
"Infection",
"Pregnenolone",
"Progesterone",
"Shock"
]
} | Septic newborn infants with therapy-resistant hypotension had very high DHEA levels, suggesting that 3-beta-hydroxysteroid dehydrogenase activity limited the rate of cortisol synthesis. | yes | [
{
"from": "human",
"value": "Question: Do term neonates with infection and shock display high cortisol precursors despite low levels of normal cortisol?\nContext: {'contexts': ['Neonatal therapy-resistant septic shock is a common problem in middle and low-income countries. We investigated whether newborn infants with infection and therapy-resistant hypotension showed evidence of abnormal levels of cortisol or cortisol precursors.', 'A total of 60 term or near term neonates with evidence of infection were enrolled after informed consent. Of these, 30 had an infection and refractory shock and 30 had an infection without shock. There were no detectable differences between the groups in the length of gestation, birth weight or gender distribution. Serum was obtained during days four and 14 after birth. Cortisol and cortisol precursor concentrations were analysed using liquid chromatography-tandem mass spectrometry.', 'The cortisol concentrations were low considering the expected responses to stress and they did not differ between the groups. The infants with infection and shock had higher serum dehydroepiandrosterone (DHEA) levels than those without shock (319.0 ± 110.3 μg/dL, versus 22.3 ± 18.3 μg/dL; p < 0.0001) and they also had higher 17-hydroxy-pregnenolone, pregnenolone and progesterone concentrations. There were no detectable differences in the levels of 17-hydroxy-progesterone, 11-deoxy-cortisol, cortisol or cortisone.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Cortisone', 'Dehydroepiandrosterone', 'Humans', 'Hydrocortisone', 'Infant, Newborn', 'Infant, Newborn, Diseases', 'Infection', 'Pregnenolone', 'Progesterone', 'Shock']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,536,130 | Does aging be Accompanied by a Blunted Muscle Protein Synthetic Response to Protein Ingestion? | {
"contexts": [
"Progressive loss of skeletal muscle mass with aging (sarcopenia) forms a global health concern. It has been suggested that an impaired capacity to increase muscle protein synthesis rates in response to protein intake is a key contributor to sarcopenia. We assessed whether differences in post-absorptive and/or post-prandial muscle protein synthesis rates exist between large cohorts of healthy young and older men.",
"We performed a cross-sectional, retrospective study comparing in vivo post-absorptive muscle protein synthesis rates determined with stable isotope methodologies between 34 healthy young (22±1 y) and 72 older (75±1 y) men, and post-prandial muscle protein synthesis rates between 35 healthy young (22±1 y) and 40 older (74±1 y) men.",
"Post-absorptive muscle protein synthesis rates did not differ significantly between the young and older group. Post-prandial muscle protein synthesis rates were 16% lower in the older subjects when compared with the young. Muscle protein synthesis rates were >3 fold more responsive to dietary protein ingestion in the young. Irrespective of age, there was a strong negative correlation between post-absorptive muscle protein synthesis rates and the increase in muscle protein synthesis rate following protein ingestion."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Aging",
"Cross-Sectional Studies",
"Dietary Proteins",
"Humans",
"Male",
"Muscle Proteins",
"Postprandial Period",
"Protein Biosynthesis",
"Retrospective Studies",
"Sarcopenia",
"Young Adult"
]
} | Aging is associated with the development of muscle anabolic inflexibility which represents a key physiological mechanism underpinning sarcopenia. | yes | [
{
"from": "human",
"value": "Question: Does aging be Accompanied by a Blunted Muscle Protein Synthetic Response to Protein Ingestion?\nContext: {'contexts': ['Progressive loss of skeletal muscle mass with aging (sarcopenia) forms a global health concern. It has been suggested that an impaired capacity to increase muscle protein synthesis rates in response to protein intake is a key contributor to sarcopenia. We assessed whether differences in post-absorptive and/or post-prandial muscle protein synthesis rates exist between large cohorts of healthy young and older men.', 'We performed a cross-sectional, retrospective study comparing in vivo post-absorptive muscle protein synthesis rates determined with stable isotope methodologies between 34 healthy young (22±1 y) and 72 older (75±1 y) men, and post-prandial muscle protein synthesis rates between 35 healthy young (22±1 y) and 40 older (74±1 y) men.', 'Post-absorptive muscle protein synthesis rates did not differ significantly between the young and older group. Post-prandial muscle protein synthesis rates were 16% lower in the older subjects when compared with the young. Muscle protein synthesis rates were >3 fold more responsive to dietary protein ingestion in the young. Irrespective of age, there was a strong negative correlation between post-absorptive muscle protein synthesis rates and the increase in muscle protein synthesis rate following protein ingestion.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Aging', 'Cross-Sectional Studies', 'Dietary Proteins', 'Humans', 'Male', 'Muscle Proteins', 'Postprandial Period', 'Protein Biosynthesis', 'Retrospective Studies', 'Sarcopenia', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,528,103 | Are polymorphisms of estrogen metabolism-related genes ESR1 , UGT2B17 , and UGT1A1 associated with osteoporosis in surgically menopausal Japanese women? | {
"contexts": [
"Bilateral salpingo-oophorectomy (BSO) is a risk factor for osteoporosis. Previous studies have reported an association between genetic polymorphisms and the risk of developing osteoporosis. However, the relationship between osteoporosis and genetic polymorphisms in Japanese women treated with BSO is not well understood. To improve the quality of life for post-BSO patients, it is important to determine the genetic factors that influence their risk for osteoporosis. The aim of this study was to investigate the association between gene variations of estrogen metabolism-related genes and osteoporosis in surgically menopausal patients, which may improve their quality of life.",
"This study included 203 menopausal women treated with BSO because of gynecologic disorders. One hundred and twenty-six women with artificial (surgical) menopause, who had undergone BSO in the premenopausal period, were compared with 77 women with natural menopause, who had undergone BSO in the postmenopausal period. The women were tested for bone mineral density to diagnose osteoporosis. Polymorphisms of estrogen receptor 1 (ESR1) and UDP-glucuronosyl transferase (UGT) genes UGT2B17 and UGT1A1 were analyzed, and their association with bone mass and osteoporosis was statistically evaluated.",
"No significant association was found between osteoporosis and polymorphisms in ESR1, UGT2B17, or UGT1A1 in both groups, suggesting that BSO might be a more significant physiological factor in influencing bone mass density compared to genetic variations."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": []
} | These results suggest that the ESR1, UGT2B17, and UGT1A1 polymorphisms are not genetic factors affecting osteoporosis in postmenopausal Japanese women. | no | [
{
"from": "human",
"value": "Question: Are polymorphisms of estrogen metabolism-related genes ESR1 , UGT2B17 , and UGT1A1 associated with osteoporosis in surgically menopausal Japanese women?\nContext: {'contexts': ['Bilateral salpingo-oophorectomy (BSO) is a risk factor for osteoporosis. Previous studies have reported an association between genetic polymorphisms and the risk of developing osteoporosis. However, the relationship between osteoporosis and genetic polymorphisms in Japanese women treated with BSO is not well understood. To improve the quality of life for post-BSO patients, it is important to determine the genetic factors that influence their risk for osteoporosis. The aim of this study was to investigate the association between gene variations of estrogen metabolism-related genes and osteoporosis in surgically menopausal patients, which may improve their quality of life.', 'This study included 203 menopausal women treated with BSO because of gynecologic disorders. One hundred and twenty-six women with artificial (surgical) menopause, who had undergone BSO in the premenopausal period, were compared with 77 women with natural menopause, who had undergone BSO in the postmenopausal period. The women were tested for bone mineral density to diagnose osteoporosis. Polymorphisms of estrogen receptor 1 (ESR1) and UDP-glucuronosyl transferase (UGT) genes UGT2B17 and UGT1A1 were analyzed, and their association with bone mass and osteoporosis was statistically evaluated.', 'No significant association was found between osteoporosis and polymorphisms in ESR1, UGT2B17, or UGT1A1 in both groups, suggesting that BSO might be a more significant physiological factor in influencing bone mass density compared to genetic variations.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
26,550,256 | Does up-regulation of serum miR-744 predict poor prognosis in patients with nasopharyngeal carcinoma? | {
"contexts": [
"MiRNAs has been shown to be implicated in the pathogenesis of many human diseases including cancer. Dysregulation of miR-744 is common in a number of cancers, indicating miR-774 might be closely correlated with the tumorigenesis process. However, the role and clinical significance of miR-774 in nasopharyngeal carcinoma (NPC) is poorly known. Thus the aim of this study is to investigate whether there was any clinical value of serum miR-744 in detecting and predicting the prognosis of NPC.",
"Real-time PCR was used to examine the expression level of serum miR-744 in patients with NPC and the healthy volunteers. The changes in serum miR-744 expression level of NPC patients after receiving chemo-radiotherapy were also evaluated. The association between pre-treatment serum miR-744 expression level and NPC clinicopathological parameters was investigated. Finally we employed Kaplan-Meier method and Cox proportional hazards model to evaluate the clinical value of serum miR-744 in predicting the prognosis of NPC.",
"Our study showed the expression level of serum miR-744 was significant higher in patients with NPC in comparison with healthy controls (P<0.01). The serum miR-744 expression level was down-regulated significantly in NPC patients after receiving chemo-radiotherapy (P<0.01). The Pre-treatment Serum miR-744 expression level was correlated with various important NPC clinicopathological parameters including N stage, clinical stage and grade. In addition, NPC patients with higher serum miR-744 expression had poorer 5 year overall survival rate and relapse-free survival rate. What was more, serum miR-744 was showed to be an independent factor for predicting the prognosis of NPC."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": []
} | Serum miR-744 was up-regulated in NPC patients. Higher expression level of serum miR-744 was closely correlated with was associated with poor prognosis in NPC and it might be employed as a potential biomarker for predicting the clinical outcome of NPC patients. | yes | [
{
"from": "human",
"value": "Question: Does up-regulation of serum miR-744 predict poor prognosis in patients with nasopharyngeal carcinoma?\nContext: {'contexts': ['MiRNAs has been shown to be implicated in the pathogenesis of many human diseases including cancer. Dysregulation of miR-744 is common in a number of cancers, indicating miR-774 might be closely correlated with the tumorigenesis process. However, the role and clinical significance of miR-774 in nasopharyngeal carcinoma (NPC) is poorly known. Thus the aim of this study is to investigate whether there was any clinical value of serum miR-744 in detecting and predicting the prognosis of NPC.', 'Real-time PCR was used to examine the expression level of serum miR-744 in patients with NPC and the healthy volunteers. The changes in serum miR-744 expression level of NPC patients after receiving chemo-radiotherapy were also evaluated. The association between pre-treatment serum miR-744 expression level and NPC clinicopathological parameters was investigated. Finally we employed Kaplan-Meier method and Cox proportional hazards model to evaluate the clinical value of serum miR-744 in predicting the prognosis of NPC.', 'Our study showed the expression level of serum miR-744 was significant higher in patients with NPC in comparison with healthy controls (P<0.01). The serum miR-744 expression level was down-regulated significantly in NPC patients after receiving chemo-radiotherapy (P<0.01). The Pre-treatment Serum miR-744 expression level was correlated with various important NPC clinicopathological parameters including N stage, clinical stage and grade. In addition, NPC patients with higher serum miR-744 expression had poorer 5 year overall survival rate and relapse-free survival rate. What was more, serum miR-744 was showed to be an independent factor for predicting the prognosis of NPC.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,551,408 | Does resting-state functional network connectivity in prefrontal regions differ between unmedicated patients with bipolar and major depressive disorders? | {
"contexts": [
"Differentiating bipolar disorder (BD) from major depressive disorder (MDD) often poses a major clinical challenge, and optimal clinical care can be hindered by misdiagnoses. This study investigated the differences between BD and MDD in resting-state functional network connectivity (FNC) using a data-driven image analysis method.",
"In this study, fMRI data were collected from unmedicated subjects including 13 BD, 40 MDD and 33 healthy controls (HC). The FNC was calculated between functional brain networks derived from fMRI using group independent component analysis (ICA). Group comparisons were performed on connectivity strengths and other graph measures of FNC matrices.",
"Statistical tests showed that, compared to MDD, the FNC in BD was characterized by more closely connected and more efficient topological structures as assessed by graph theory. The differences were found at both the whole-brain-level and the functional-network-level in prefrontal networks located in the dorsolateral/ventrolateral prefrontal cortex (DLPFC, VLPFC) and anterior cingulate cortex (ACC). Furthermore, interconnected structures in these networks in both patient groups were negatively associated with symptom severity on depression rating scales."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Bipolar Disorder",
"Brain",
"Case-Control Studies",
"Depressive Disorder, Major",
"Female",
"Functional Neuroimaging",
"Gyrus Cinguli",
"Humans",
"Magnetic Resonance Imaging",
"Male",
"Neural Pathways",
"Prefrontal Cortex"
]
} | As patients were unmedicated, the sample sizes were relatively small, although they were comparable to those in previous fMRI studies comparing BD and MDD. | yes | [
{
"from": "human",
"value": "Question: Does resting-state functional network connectivity in prefrontal regions differ between unmedicated patients with bipolar and major depressive disorders?\nContext: {'contexts': ['Differentiating bipolar disorder (BD) from major depressive disorder (MDD) often poses a major clinical challenge, and optimal clinical care can be hindered by misdiagnoses. This study investigated the differences between BD and MDD in resting-state functional network connectivity (FNC) using a data-driven image analysis method.', 'In this study, fMRI data were collected from unmedicated subjects including 13 BD, 40 MDD and 33 healthy controls (HC). The FNC was calculated between functional brain networks derived from fMRI using group independent component analysis (ICA). Group comparisons were performed on connectivity strengths and other graph measures of FNC matrices.', 'Statistical tests showed that, compared to MDD, the FNC in BD was characterized by more closely connected and more efficient topological structures as assessed by graph theory. The differences were found at both the whole-brain-level and the functional-network-level in prefrontal networks located in the dorsolateral/ventrolateral prefrontal cortex (DLPFC, VLPFC) and anterior cingulate cortex (ACC). Furthermore, interconnected structures in these networks in both patient groups were negatively associated with symptom severity on depression rating scales.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Bipolar Disorder', 'Brain', 'Case-Control Studies', 'Depressive Disorder, Major', 'Female', 'Functional Neuroimaging', 'Gyrus Cinguli', 'Humans', 'Magnetic Resonance Imaging', 'Male', 'Neural Pathways', 'Prefrontal Cortex']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,538,111 | Does 2D cine DENSE with low encoding frequencies accurately quantify cardiac mechanics with improved image characteristics? | {
"contexts": [
"Displacement Encoding with Stimulated Echoes (DENSE) encodes displacement into the phase of the magnetic resonance signal. The encoding frequency (ke) maps the measured phase to tissue displacement while the strength of the encoding gradients affects image quality. 2D cine DENSE studies have used a ke of 0.10 cycles/mm, which is high enough to remove an artifact-generating echo from k-space, provide high sensitivity to tissue displacements, and dephase the blood pool. However, through-plane dephasing can remove the unwanted echo and dephase the blood pool without relying on high ke. Additionally, the high sensitivity comes with the costs of increased phase wrapping and intra-voxel dephasing. We hypothesized that ke below 0.10 cycles/mm can be used to improve image characteristics and provide accurate measures of cardiac mechanics.",
"Spiral cine DENSE images were obtained for 10 healthy subjects and 10 patients with a history of heart disease on a 3 T Siemens Trio. A mid-ventricular short-axis image was acquired with different ke: 0.02, 0.04, 0.06, 0.08, and 0.10 cycles/mm. Peak twist, circumferential strain, and radial strain were compared between acquisitions employing different ke using Bland-Altman analyses and coefficients of variation. The percentage of wrapped pixels in the phase images at end-systole was calculated for each ke. The dephasing of the blood signal and signal to noise ratio (SNR) were also calculated and compared.",
"Negligible differences were seen in strains and twist for all ke between 0.04 and 0.10 cycles/mm. These differences were of the same magnitude as inter-test differences. Specifically, the acquisitions with 0.04 cycles/mm accurately quantified cardiac mechanics and had zero phase wrapping. Compared to 0.10 cycles/mm, the acquisitions with 0.04 cycles/mm had 9 % greater SNR and negligible differences in blood pool dephasing."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Algorithms",
"Artifacts",
"Biomechanical Phenomena",
"Case-Control Studies",
"Female",
"Heart Diseases",
"Humans",
"Image Interpretation, Computer-Assisted",
"Magnetic Resonance Imaging, Cine",
"Male",
"Middle Aged",
"Myocardial Contraction",
"Predictive Value of Tests",
"Reproducibility of Results",
"Signal-To-Noise Ratio",
"Stress, Mechanical",
"Ventricular Function",
"Young Adult"
]
} | For 2D cine DENSE with through-plane dephasing, the encoding frequency can be lowered to 0.04 cycles/mm without compromising the quantification of twist or strain. The amount of wrapping can be reduced with this lower value to greatly simplify the input to unwrapping algorithms. The strain and twist results from studies using different encoding frequencies can be directly compared. | yes | [
{
"from": "human",
"value": "Question: Does 2D cine DENSE with low encoding frequencies accurately quantify cardiac mechanics with improved image characteristics?\nContext: {'contexts': ['Displacement Encoding with Stimulated Echoes (DENSE) encodes displacement into the phase of the magnetic resonance signal. The encoding frequency (ke) maps the measured phase to tissue displacement while the strength of the encoding gradients affects image quality. 2D cine DENSE studies have used a ke of 0.10\\xa0cycles/mm, which is high enough to remove an artifact-generating echo from k-space, provide high sensitivity to tissue displacements, and dephase the blood pool. However, through-plane dephasing can remove the unwanted echo and dephase the blood pool without relying on high ke. Additionally, the high sensitivity comes with the costs of increased phase wrapping and intra-voxel dephasing. We hypothesized that ke below 0.10\\xa0cycles/mm can be used to improve image characteristics and provide accurate measures of cardiac mechanics.', 'Spiral cine DENSE images were obtained for 10 healthy subjects and 10 patients with a history of heart disease on a 3\\xa0T Siemens Trio. A mid-ventricular short-axis image was acquired with different ke: 0.02, 0.04, 0.06, 0.08, and 0.10\\xa0cycles/mm. Peak twist, circumferential strain, and radial strain were compared between acquisitions employing different ke using Bland-Altman analyses and coefficients of variation. The percentage of wrapped pixels in the phase images at end-systole was calculated for each ke. The dephasing of the blood signal and signal to noise ratio (SNR) were also calculated and compared.', 'Negligible differences were seen in strains and twist for all ke between 0.04 and 0.10\\xa0cycles/mm. These differences were of the same magnitude as inter-test differences. Specifically, the acquisitions with 0.04\\xa0cycles/mm accurately quantified cardiac mechanics and had zero phase wrapping. Compared to 0.10\\xa0cycles/mm, the acquisitions with 0.04\\xa0cycles/mm had 9\\xa0% greater SNR and negligible differences in blood pool dephasing.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Algorithms', 'Artifacts', 'Biomechanical Phenomena', 'Case-Control Studies', 'Female', 'Heart Diseases', 'Humans', 'Image Interpretation, Computer-Assisted', 'Magnetic Resonance Imaging, Cine', 'Male', 'Middle Aged', 'Myocardial Contraction', 'Predictive Value of Tests', 'Reproducibility of Results', 'Signal-To-Noise Ratio', 'Stress, Mechanical', 'Ventricular Function', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,538,117 | Does linc00152 promote proliferation in gastric cancer through the EGFR-dependent pathway? | {
"contexts": [
"Linc00152 has been identified highly associated with the tumorigenesis and development of gastric cancer, however, the detailed mechanism of Linc00152 involved still remains unclear.",
"RT-PCR and western blot were used to detect the expression of Linc00152 and EGFR. The CCK8 and EDU assay was employed to measure cell proliferation while xenotransplantation technology was applied in BALB/C nude mice. The interaction between lncRNA and target protein was investigated by RNA pull-down and RNA immunoprecipitation assay.",
"In this study, we first confirmed the upregulation of cytoplasmic expressed Linc00152 in 72 pair tissues of gastric patients. A suppression of cell proliferation and tumor growth was obtained in MGC803 and HGC-27 cells treated with Linc00152 shRNA. RNA pull-down and RIP assay revealed that Linc00152 could directly bind with EGFR which caused an activation of PI3K/AKT signaling."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Cell Line, Tumor",
"Cell Proliferation",
"Cell Transformation, Neoplastic",
"Cytoplasm",
"Disease Models, Animal",
"ErbB Receptors",
"Heterografts",
"Humans",
"Mice",
"Phosphatidylinositol 3-Kinases",
"Proto-Oncogene Proteins c-akt",
"RNA Transport",
"RNA, Long Noncoding",
"Signal Transduction",
"Stomach Neoplasms",
"Tumor Burden"
]
} | We first found that Linc00152 could promote tumor growth through EGFR-mediated PI3K/AKT pathway which may serve as potential targets for therapy in the future. | yes | [
{
"from": "human",
"value": "Question: Does linc00152 promote proliferation in gastric cancer through the EGFR-dependent pathway?\nContext: {'contexts': ['Linc00152 has been identified highly associated with the tumorigenesis and development of gastric cancer, however, the detailed mechanism of Linc00152 involved still remains unclear.', 'RT-PCR and western blot were used to detect the expression of Linc00152 and EGFR. The CCK8 and EDU assay was employed to measure cell proliferation while xenotransplantation technology was applied in BALB/C nude mice. The interaction between lncRNA and target protein was investigated by RNA pull-down and RNA immunoprecipitation assay.', 'In this study, we first confirmed the upregulation of cytoplasmic expressed Linc00152 in 72 pair tissues of gastric patients. A suppression of cell proliferation and tumor growth was obtained in MGC803 and HGC-27 cells treated with Linc00152 shRNA. RNA pull-down and RIP assay revealed that Linc00152 could directly bind with EGFR which caused an activation of PI3K/AKT signaling.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Cell Line, Tumor', 'Cell Proliferation', 'Cell Transformation, Neoplastic', 'Cytoplasm', 'Disease Models, Animal', 'ErbB Receptors', 'Heterografts', 'Humans', 'Mice', 'Phosphatidylinositol 3-Kinases', 'Proto-Oncogene Proteins c-akt', 'RNA Transport', 'RNA, Long Noncoding', 'Signal Transduction', 'Stomach Neoplasms', 'Tumor Burden']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,530,759 | Does novel Manganese-Porphyrin Superoxide Dismutase-Mimetic widen the Therapeutic Margin in a Preclinical Head and Neck Cancer Model? | {
"contexts": [
"To test the effects of a novel Mn porphyrin oxidative stress modifier, Mn(III) meso-tetrakis(N-n-butoxyethylpyridinium-2-yl)porphyrin (MnBuOE), for its radioprotective and radiosensitizing properties in normal tissue versus tumor, respectively.",
"Murine oral mucosa and salivary glands were treated with a range of radiation doses with or without MnBuOE to establish the dose-effect curves for mucositis and xerostomia. Radiation injury was quantified by intravital near-infrared imaging of cathepsin activity, assessment of salivation, and histologic analysis. To evaluate effects of MnBuOE on the tumor radiation response, we administered the drug as an adjuvant to fractionated radiation of FaDu xenografts. Again, a range of radiation therapy (RT) doses was administered to establish the radiation dose-effect curve. The 50% tumor control dose values with or without MnBuOE and dose-modifying factor were determined.",
"MnBuOE protected normal tissue by reducing RT-mediated mucositis, xerostomia, and fibrosis. The dose-modifying factor for protection against xerostomia was 0.77. In contrast, MnBuOE increased tumor local control rates compared with controls. The dose-modifying factor, based on the ratio of 50% tumor control dose values, was 1.3. Immunohistochemistry showed that MnBuOE-treated tumors exhibited a significant influx of M1 tumor-associated macrophages, which provides mechanistic insight into its radiosensitizing effects in tumors."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Dose-Response Relationship, Radiation",
"Drug Evaluation, Preclinical",
"Fibrosis",
"Head and Neck Neoplasms",
"Metalloporphyrins",
"Mice",
"Mice, Inbred C57BL",
"Mice, Nude",
"Mouth Mucosa",
"Organs at Risk",
"Radiation Dosage",
"Radiation Injuries, Experimental",
"Radiation-Protective Agents",
"Radiation-Sensitizing Agents",
"Random Allocation",
"Salivary Glands",
"Stomatitis",
"Xerostomia"
]
} | MnBuOE widens the therapeutic margin by decreasing the dose of radiation required to control tumor, while increasing normal tissue resistance to RT-mediated injury. This is the first study to quantitatively demonstrate the magnitude of a single drug's ability to radioprotect normal tissue while radiosensitizing tumor. | yes | [
{
"from": "human",
"value": "Question: Does novel Manganese-Porphyrin Superoxide Dismutase-Mimetic widen the Therapeutic Margin in a Preclinical Head and Neck Cancer Model?\nContext: {'contexts': ['To test the effects of a novel Mn porphyrin oxidative stress modifier, Mn(III) meso-tetrakis(N-n-butoxyethylpyridinium-2-yl)porphyrin (MnBuOE), for its radioprotective and radiosensitizing properties in normal tissue versus tumor, respectively.', 'Murine oral mucosa and salivary glands were treated with a range of radiation doses with or without MnBuOE to establish the dose-effect curves for mucositis and xerostomia. Radiation injury was quantified by intravital near-infrared imaging of cathepsin activity, assessment of salivation, and histologic analysis. To evaluate effects of MnBuOE on the tumor radiation response, we administered the drug as an adjuvant to fractionated radiation of FaDu xenografts. Again, a range of radiation therapy (RT) doses was administered to establish the radiation dose-effect curve. The 50% tumor control dose values with or without MnBuOE and dose-modifying factor were determined.', 'MnBuOE protected normal tissue by reducing RT-mediated mucositis, xerostomia, and fibrosis. The dose-modifying factor for protection against xerostomia was 0.77. In contrast, MnBuOE increased tumor local control rates compared with controls. The dose-modifying factor, based on the ratio of 50% tumor control dose values, was 1.3. Immunohistochemistry showed that MnBuOE-treated tumors exhibited a significant influx of M1 tumor-associated macrophages, which provides mechanistic insight into its radiosensitizing effects in tumors.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Dose-Response Relationship, Radiation', 'Drug Evaluation, Preclinical', 'Fibrosis', 'Head and Neck Neoplasms', 'Metalloporphyrins', 'Mice', 'Mice, Inbred C57BL', 'Mice, Nude', 'Mouth Mucosa', 'Organs at Risk', 'Radiation Dosage', 'Radiation Injuries, Experimental', 'Radiation-Protective Agents', 'Radiation-Sensitizing Agents', 'Random Allocation', 'Salivary Glands', 'Stomatitis', 'Xerostomia']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,554,234 | Are serum Gamma-Glutamyltransferase and Ferritin Related to Insulin Resistance : A Population-Based Study? | {
"contexts": [
"Recent studies have reported the association of gamma-glutamyltransferase (GGT) or ferritin with metabolic disorders. However, there has been no large population-based study assessing the interrelationship of these two biomarkers and their association with insulin resistance.",
"A population-based cross-sectional study was carried out in the Chinese Liangshan Yi ethnic group. 756 eligible subjects, aged 20 - 74 years, were included. Demographic characteristics, medical history, and lifestyle data were collected through questionnaires. An oral glucose tolerance test was performed. Laboratory tests, including GGT and ferritin measurements, were conducted. Spearman's rank-order correlation and multiple linear regression were used to calculate the correlation of GGT with ferritin and their relationship to the insulin resistance index determined by the homeostasis model assessment (HOMA-IR).",
"A significant correlation between serum GGT and ferritin levels was found (r = 0.393, p < 0.05). GGT was independently correlated with ferritin after adjustment for age, gender, place of residence, education, income, leisure-time physical activity, drinking, smoking, body mass index, systolic pressure, diastolic pressure, hepatitis B surface antigen, anti-hepatitis C virus, aspartate aminotransferase, alanine aminotransferase, total cholesterol, low density lipoprotein-cholesterol, triglyceride, high density lipoprotein-cholesterol, fasting plasma glucose, 2-hour postprandial plasma glucose, uric acid, and urinary albumin to creatinine ratio (p < 0.05). Positive correlations were established between HOMA-IR and GGT (standard β = 0.252) or ferritin (standard β = 0.181) after adjustment for multiple confounders (p < 0.05)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Alcohol Drinking",
"Biomarkers",
"Cross-Sectional Studies",
"Female",
"Ferritins",
"Glucose Tolerance Test",
"Humans",
"Insulin Resistance",
"Male",
"Middle Aged",
"Models, Biological",
"Smoking",
"Socioeconomic Factors",
"Surveys and Questionnaires",
"gamma-Glutamyltransferase"
]
} | Insulin resistance is associated with elevated serum GGT and ferritin. A combined determination of GGT and ferritin might lead to better predictions in patients with insulin resistance. | yes | [
{
"from": "human",
"value": "Question: Are serum Gamma-Glutamyltransferase and Ferritin Related to Insulin Resistance : A Population-Based Study?\nContext: {'contexts': ['Recent studies have reported the association of gamma-glutamyltransferase (GGT) or ferritin with metabolic disorders. However, there has been no large population-based study assessing the interrelationship of these two biomarkers and their association with insulin resistance.', \"A population-based cross-sectional study was carried out in the Chinese Liangshan Yi ethnic group. 756 eligible subjects, aged 20 - 74 years, were included. Demographic characteristics, medical history, and lifestyle data were collected through questionnaires. An oral glucose tolerance test was performed. Laboratory tests, including GGT and ferritin measurements, were conducted. Spearman's rank-order correlation and multiple linear regression were used to calculate the correlation of GGT with ferritin and their relationship to the insulin resistance index determined by the homeostasis model assessment (HOMA-IR).\", 'A significant correlation between serum GGT and ferritin levels was found (r = 0.393, p < 0.05). GGT was independently correlated with ferritin after adjustment for age, gender, place of residence, education, income, leisure-time physical activity, drinking, smoking, body mass index, systolic pressure, diastolic pressure, hepatitis B surface antigen, anti-hepatitis C virus, aspartate aminotransferase, alanine aminotransferase, total cholesterol, low density lipoprotein-cholesterol, triglyceride, high density lipoprotein-cholesterol, fasting plasma glucose, 2-hour postprandial plasma glucose, uric acid, and urinary albumin to creatinine ratio (p < 0.05). Positive correlations were established between HOMA-IR and GGT (standard β = 0.252) or ferritin (standard β = 0.181) after adjustment for multiple confounders (p < 0.05).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Alcohol Drinking', 'Biomarkers', 'Cross-Sectional Studies', 'Female', 'Ferritins', 'Glucose Tolerance Test', 'Humans', 'Insulin Resistance', 'Male', 'Middle Aged', 'Models, Biological', 'Smoking', 'Socioeconomic Factors', 'Surveys and Questionnaires', 'gamma-Glutamyltransferase']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,528,611 | Do [ Experience in the use of high-frequency selective percutaneous rhizotomy in trigeminal neuralgia associated with multiple sclerosis ]? | {
"contexts": [
"the study was aimed at assessment of the efficacy of percutaneous high frequency selective rhizotomy (PHFSR) after failure of conservative treatment of trigeminal neuralgia (TN) in multiple sclerosis (MS).",
"A retrospective analysis of 28 patients with TN associated with MS who underwent percutaneous rhizotomy in the period from 2000 to 2014 was performed. All patients were definitely diagnosed with MS according to the McDonald criteria (version of 2001, 2005, and 2010). The patients were divided by age, gender, and the trigeminal nerve branches involved in the process. The patients' condition was evaluated at different times after surgery.",
"Good outcomes in the form of pain syndrome regression were achieved in 100% of the patients. A disease recurrence was observed in 6 (21%) patients during a follow-up period of 3 months to 14 years. Dysesthesia complications occurred in 4 (14%) patients. There were no deaths and severe complications. The percentage of minor complications was low."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Electrodes",
"Electrosurgery",
"Female",
"Humans",
"Magnetic Resonance Imaging",
"Male",
"Middle Aged",
"Multiple Sclerosis",
"Retrospective Studies",
"Rhizotomy",
"Stereotaxic Techniques",
"Treatment Outcome",
"Trigeminal Neuralgia"
]
} | These data confirm that PHFSR is a safe, repeatable, and effective method of symptomatic neurosurgical treatment of TN associated with MS and may be recommended in the case of failure/intolerance of medication. | yes | [
{
"from": "human",
"value": "Question: Do [ Experience in the use of high-frequency selective percutaneous rhizotomy in trigeminal neuralgia associated with multiple sclerosis ]?\nContext: {'contexts': ['the study was aimed at assessment of the efficacy of percutaneous high frequency selective rhizotomy (PHFSR) after failure of conservative treatment of trigeminal neuralgia (TN) in multiple sclerosis (MS).', \"A retrospective analysis of 28 patients with TN associated with MS who underwent percutaneous rhizotomy in the period from 2000 to 2014 was performed. All patients were definitely diagnosed with MS according to the McDonald criteria (version of 2001, 2005, and 2010). The patients were divided by age, gender, and the trigeminal nerve branches involved in the process. The patients' condition was evaluated at different times after surgery.\", 'Good outcomes in the form of pain syndrome regression were achieved in 100% of the patients. A disease recurrence was observed in 6 (21%) patients during a follow-up period of 3 months to 14 years. Dysesthesia complications occurred in 4 (14%) patients. There were no deaths and severe complications. The percentage of minor complications was low.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Electrodes', 'Electrosurgery', 'Female', 'Humans', 'Magnetic Resonance Imaging', 'Male', 'Middle Aged', 'Multiple Sclerosis', 'Retrospective Studies', 'Rhizotomy', 'Stereotaxic Techniques', 'Treatment Outcome', 'Trigeminal Neuralgia']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,553,199 | Does severe cranial neuropathies caused by fall from heights in children? | {
"contexts": [
"Falls from heights are the most common traumatic event associated with emergency department visits in children. This study investigated the incidence and clinical course of cranial neuropathies caused by falls from heights in children.",
"The computerized records of a tertiary pediatric medical center were searched for all patients admitted to the emergency department in 2004-2014 with a head injury caused by falling from a height. Those with cranial neuropathies involving optic and eye-motility disturbances were identified, and their clinical, imaging, and outcome data were evaluated.",
"Of the estimated 61,968 patients who presented to the emergency department during the study period because of a fall, 18,758 (30.3 %) had head trauma. Only 12 (seven boys, five girls, average age 6.7 years) had a visual disturbance. Eight were diagnosed with traumatic optic neuropathy, one after a 6-month delay, including two with accompanying cranial nerve (CN) III injuries. Five patients had anisocoria or an abnormal pupillary response to light at presentation, one patient had CN VI paralysis and temporary vision loss, and one patient had an isolated CN III injury diagnosed on follow-up. Visual improvement varied among the patients."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Accidental Falls",
"Adolescent",
"Child",
"Child, Preschool",
"Craniocerebral Trauma",
"Emergency Service, Hospital",
"Female",
"Hospitals, Pediatric",
"Humans",
"Incidence",
"Infant",
"Infant, Newborn",
"Israel",
"Male",
"Ocular Motility Disorders",
"Oculomotor Nerve Diseases",
"Optic Nerve Diseases",
"Tomography, X-Ray Computed"
]
} | Cranial neuropathies due to falls from heights are rare in children and are associated with high visual morbidity. Vision or ocular motility impairment, especially monocular vision loss, may be missed during acute intake to the emergency department, and a high index of suspicion is needed. Assessment of the pupillary response to light is essential. | yes | [
{
"from": "human",
"value": "Question: Does severe cranial neuropathies caused by fall from heights in children?\nContext: {'contexts': ['Falls from heights are the most common traumatic event associated with emergency department visits in children. This study investigated the incidence and clinical course of cranial neuropathies caused by falls from heights in children.', 'The computerized records of a tertiary pediatric medical center were searched for all patients admitted to the emergency department in 2004-2014 with a head injury caused by falling from a height. Those with cranial neuropathies involving optic and eye-motility disturbances were identified, and their clinical, imaging, and outcome data were evaluated.', 'Of the estimated 61,968 patients who presented to the emergency department during the study period because of a fall, 18,758 (30.3\\xa0%) had head trauma. Only 12 (seven boys, five girls, average age 6.7\\xa0years) had a visual disturbance. Eight were diagnosed with traumatic optic neuropathy, one after a 6-month delay, including two with accompanying cranial nerve (CN) III injuries. Five patients had anisocoria or an abnormal pupillary response to light at presentation, one patient had CN VI paralysis and temporary vision loss, and one patient had an isolated CN III injury diagnosed on follow-up. Visual improvement varied among the patients.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Accidental Falls', 'Adolescent', 'Child', 'Child, Preschool', 'Craniocerebral Trauma', 'Emergency Service, Hospital', 'Female', 'Hospitals, Pediatric', 'Humans', 'Incidence', 'Infant', 'Infant, Newborn', 'Israel', 'Male', 'Ocular Motility Disorders', 'Oculomotor Nerve Diseases', 'Optic Nerve Diseases', 'Tomography, X-Ray Computed']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,553,192 | Does med14 cooperate with brg1 in the differentiation of skeletogenic neural crest? | {
"contexts": [
"An intricate gene regulatory network drives neural crest migration and differentiation. How epigenetic regulators contribute to this process is just starting to be understood.",
"We found that mutation of med14 or brg1 in zebrafish embryos resulted in a cluster of neural crest cell-related defects. In med14 or brg1 mutants, neural crest cells that form the jaw skeleton were specified normally and migrated to target sites. However, defects in their subsequent terminal differentiation were evident. Transplantation experiments demonstrated that med14 and brg1 are required directly in neural crest cells. Analysis of med14; brg1 double mutant embryos suggested the existence of a strong genetic interaction between members of the Mediator and BAF complexes."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Adaptor Proteins, Signal Transducing",
"Animals",
"Cell Differentiation",
"Cell Movement",
"Cell Proliferation",
"Cells, Cultured",
"Embryo, Nonmammalian",
"Gene Expression Regulation, Developmental",
"Gene Regulatory Networks",
"Jaw",
"Jaw Abnormalities",
"Maxillofacial Development",
"Mediator Complex",
"Neural Crest",
"Osteogenesis",
"Zebrafish",
"Zebrafish Proteins"
]
} | These results suggest a critical role for Mediator and BAF complex function in neural crest development, and may also clarify the nature of defects in some craniofacial abnormalities. | yes | [
{
"from": "human",
"value": "Question: Does med14 cooperate with brg1 in the differentiation of skeletogenic neural crest?\nContext: {'contexts': ['An intricate gene regulatory network drives neural crest migration and differentiation. How epigenetic regulators contribute to this process is just starting to be understood.', 'We found that mutation of med14 or brg1 in zebrafish embryos resulted in a cluster of neural crest cell-related defects. In med14 or brg1 mutants, neural crest cells that form the jaw skeleton were specified normally and migrated to target sites. However, defects in their subsequent terminal differentiation were evident. Transplantation experiments demonstrated that med14 and brg1 are required directly in neural crest cells. Analysis of med14; brg1 double mutant embryos suggested the existence of a strong genetic interaction between members of the Mediator and BAF complexes.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Adaptor Proteins, Signal Transducing', 'Animals', 'Cell Differentiation', 'Cell Movement', 'Cell Proliferation', 'Cells, Cultured', 'Embryo, Nonmammalian', 'Gene Expression Regulation, Developmental', 'Gene Regulatory Networks', 'Jaw', 'Jaw Abnormalities', 'Maxillofacial Development', 'Mediator Complex', 'Neural Crest', 'Osteogenesis', 'Zebrafish', 'Zebrafish Proteins']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,552,246 | Do [ Long-term follow-up study of titanium implant impact on pediatric mandibular growth and development ]? | {
"contexts": [
"To explore the impact of titanium implant on the growth and development of pediatric mandible after suffering from mandibular fracture and undergoing open reduction and internal fixation (ORIF) compared with those that underwent titanium plate removal postoperatively.",
"Fifteen pediatric patients with mandibular fracture who underwent ORIF were included in this study. Eight patients did not undergo titanium implant removal postoperatively, whereas the other seven patients underwent the routine. The postoperative data of the pediatrics were collected for comparative analysis by taking the patients' frontal and lateral photos, recording the inter-incisor distance, and measuring the height of mandibular ramus, length of the mandibular body, and combined length of the mandible in three-dimensional reconstruction image.",
"All patients had acceptable facial contour, mouth opening, and occlusion, without obvious abnormalities. The radiography showed no significant difference between the bilateral mandibular lengths in the two groups of patients (P>0.05)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Bone Plates",
"Dental Implants",
"Dental Occlusion",
"Follow-Up Studies",
"Fracture Fixation, Internal",
"Humans",
"Mandible",
"Mandibular Fractures",
"Prostheses and Implants",
"Time Factors",
"Titanium"
]
} | The titanium plants have no significant impact on the growth and development of pediatric mandible postoperatively; hence, the question on whether the titanium plates should be removed or not may be neglected. The removal operation may lead to secondary trauma; thus, performing titanium plate removal routinely is not recommended. | yes | [
{
"from": "human",
"value": "Question: Do [ Long-term follow-up study of titanium implant impact on pediatric mandibular growth and development ]?\nContext: {'contexts': ['To explore the impact of titanium implant on the growth and development of pediatric mandible after suffering from mandibular fracture and undergoing open reduction and internal fixation (ORIF) compared with those that underwent titanium plate removal postoperatively.', \"Fifteen pediatric patients with mandibular fracture who underwent ORIF were included in this study. Eight patients did not undergo titanium implant removal postoperatively, whereas the other seven patients underwent the routine. The postoperative data of the pediatrics were collected for comparative analysis by taking the patients' frontal and lateral photos, recording the inter-incisor distance, and measuring the height of mandibular ramus, length of the mandibular body, and combined length of the mandible in three-dimensional reconstruction image.\", 'All patients had acceptable facial contour, mouth opening, and occlusion, without obvious abnormalities. The radiography showed no significant difference between the bilateral mandibular lengths in the two groups of patients (P>0.05).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Bone Plates', 'Dental Implants', 'Dental Occlusion', 'Follow-Up Studies', 'Fracture Fixation, Internal', 'Humans', 'Mandible', 'Mandibular Fractures', 'Prostheses and Implants', 'Time Factors', 'Titanium']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,553,587 | Does arjunolic acid protect against DNCB-induced atopic dermatitis-like symptoms in mice by restoring a normal cytokine balance? | {
"contexts": [
"Atopic dermatitis (AD) is a chronically relapsing, pruritic, eczematous skin disorder accompanying allergic inflammation. AD is triggered by oxidative stress and immune imbalance. The effect of oral arjunolic acid (AA) on 2,4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis in mice was investigated.",
"Repeated epicutaneous application of DNCB to the ear and shaved dorsal skin of mice was performed to induce AD-like symptoms and skin lesions: 250mg/kg AA was given orally for three weeks to assess its anti-pruritic effects. Serum levels of tumor necrosis factor (TNF)-α, interleukin (IL)-4, IL-6, IL-10, immunoglobulin (Ig)E and caspase-3 were assessed by ELISA.",
"We found that AA alleviated DNCB-induced AD-like symptoms as quantified by skin lesions, dermatitis score, ear thickness and scratching behavior. Levels of reactive oxygen species in the AA group were significantly inhibited compared with those in the DNCB group. In parallel, AA blocked a DNCB-induced reduction in serum levels of IL-4 and IL-10 associated with an attenuation of DNCB-induced increases in serum TNF-α, IL-6, IgE and caspase-3."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Caspase 3",
"Cytokines",
"Dermatitis, Atopic",
"Dinitrochlorobenzene",
"Disease Models, Animal",
"Immunoglobulin E",
"Inflammation Mediators",
"Leukocyte Count",
"Mice",
"Oxidative Stress",
"Protective Agents",
"Skin",
"Triterpenes"
]
} | The results indicate that AA suppresses DNCB-induced AD in mice via redox balance and immune modulation, and could be a safe clinical treatment for AD. | yes | [
{
"from": "human",
"value": "Question: Does arjunolic acid protect against DNCB-induced atopic dermatitis-like symptoms in mice by restoring a normal cytokine balance?\nContext: {'contexts': ['Atopic dermatitis (AD) is a chronically relapsing, pruritic, eczematous skin disorder accompanying allergic inflammation. AD is triggered by oxidative stress and immune imbalance. The effect of oral arjunolic acid (AA) on 2,4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis in mice was investigated.', 'Repeated epicutaneous application of DNCB to the ear and shaved dorsal skin of mice was performed to induce AD-like symptoms and skin lesions: 250mg/kg AA was given orally for three weeks to assess its anti-pruritic effects. Serum levels of tumor necrosis factor (TNF)-α, interleukin (IL)-4, IL-6, IL-10, immunoglobulin (Ig)E and caspase-3 were assessed by ELISA.', 'We found that AA alleviated DNCB-induced AD-like symptoms as quantified by skin lesions, dermatitis score, ear thickness and scratching behavior. Levels of reactive oxygen species in the AA group were significantly inhibited compared with those in the DNCB group. In parallel, AA blocked a DNCB-induced reduction in serum levels of IL-4 and IL-10 associated with an attenuation of DNCB-induced increases in serum TNF-α, IL-6, IgE and caspase-3.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Caspase 3', 'Cytokines', 'Dermatitis, Atopic', 'Dinitrochlorobenzene', 'Disease Models, Animal', 'Immunoglobulin E', 'Inflammation Mediators', 'Leukocyte Count', 'Mice', 'Oxidative Stress', 'Protective Agents', 'Skin', 'Triterpenes']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,553,017 | Does n2 extenuate experimental ischemic stroke through platelet aggregation inhibition? | {
"contexts": [
"Thromboxane A2 (TXA2) can induce the platelet aggregation and lead to thrombosis. This will cause the low-reflow phenomenon after ischemic stroke and aggravate the damage of brain issues. Therefore, it is potential to develop the drugs inhibiting TXA2 pathway to treat cerebral ischemia.",
"This study aims to prove the protective effect of N2 (4-(2-(1H-imidazol-1-yl) ethoxy)-3-methoxybenzoic acid) on focal cerebral ischemia and reperfusion injury through platelet aggregation inhibition.",
"Middle cerebral artery occlusion/reperfusion (MCAO/R) is used as the animal model. Neurological deficit score, Morris water maze, postural reflex test, Limb-use asymmetry test, infarct volume, and water content were performed to evaluate the protective effect of N2 in MCAO/R rats. 9, 11-dieoxy-11α, 9α-methanoepoxyprostaglandin F2α (U46619) or adenosine diphosphate (ADP) was used as the inducer of platelet aggregation."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS"
],
"meshes": [
"15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid",
"Adenosine Diphosphate",
"Animals",
"Arteriovenous Shunt, Surgical",
"Blood Coagulation",
"Brain",
"Brain Ischemia",
"Edema",
"Enzyme-Linked Immunosorbent Assay",
"Epoprostenol",
"Female",
"Imidazoles",
"Male",
"Maze Learning",
"Platelet Aggregation",
"Rats",
"Rats, Sprague-Dawley",
"Stroke",
"Thrombosis",
"Thromboxane A2",
"Vanillic Acid"
]
} | N2 can improve the motor function, learning and memory ability in MCAO/R rats while reducing the infarct volume. N2 can inhibit TXA2 formation but promote PGI2, and can inhibit platelet aggregation induced by U46619 and ADP. Further, N2 inhibits thrombosis with a minor adverse effect of bleeding than Clopidogrel. In conclusion, N2 can produce the protective effect on MCAO/R brain injury through inhibiting TXA2 formation, platelet aggregation and thrombosis. | yes | [
{
"from": "human",
"value": "Question: Does n2 extenuate experimental ischemic stroke through platelet aggregation inhibition?\nContext: {'contexts': ['Thromboxane A2 (TXA2) can induce the platelet aggregation and lead to thrombosis. This will cause the low-reflow phenomenon after ischemic stroke and aggravate the damage of brain issues. Therefore, it is potential to develop the drugs inhibiting TXA2 pathway to treat cerebral ischemia.', 'This study aims to prove the protective effect of N2 (4-(2-(1H-imidazol-1-yl) ethoxy)-3-methoxybenzoic acid) on focal cerebral ischemia and reperfusion injury through platelet aggregation inhibition.', 'Middle cerebral artery occlusion/reperfusion (MCAO/R) is used as the animal model. Neurological deficit score, Morris water maze, postural reflex test, Limb-use asymmetry test, infarct volume, and water content were performed to evaluate the protective effect of N2 in MCAO/R rats. 9, 11-dieoxy-11α, 9α-methanoepoxyprostaglandin F2α (U46619) or adenosine diphosphate (ADP) was used as the inducer of platelet aggregation.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS'], 'meshes': ['15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid', 'Adenosine Diphosphate', 'Animals', 'Arteriovenous Shunt, Surgical', 'Blood Coagulation', 'Brain', 'Brain Ischemia', 'Edema', 'Enzyme-Linked Immunosorbent Assay', 'Epoprostenol', 'Female', 'Imidazoles', 'Male', 'Maze Learning', 'Platelet Aggregation', 'Rats', 'Rats, Sprague-Dawley', 'Stroke', 'Thrombosis', 'Thromboxane A2', 'Vanillic Acid']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,541,061 | Is the differentially methylated region of MEG8 hypermethylated in patients with Temple syndrome? | {
"contexts": [
"To investigate the DNA-methylation levels in the newly described MEG8 differentially methylated region (DMR) in the imprinted cluster in 14q32 in patients with Temple syndrome.",
"We included three patients with Temple syndrome which were studied by Infinium HumanMethylation450 BeadChips, locus-specific bisulfite-pyrosequencing, methylation-specific-MLPA and microsatellite analyses. The tag-CpG of the MEG8-DMR was investigated using the Infinium HumanMethylation450 BeadChip.",
"In all three patients, the identical pattern of DNA-hypermethylation of the MEG8-DMR was observed along with DNA-hypomethylation of the IG-DMR and MEG3-DMR."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Child",
"Child, Preschool",
"Chromosomes, Human, Pair 14",
"CpG Islands",
"DNA Methylation",
"Developmental Disabilities",
"Epigenesis, Genetic",
"Female",
"Genomic Imprinting",
"High-Throughput Nucleotide Sequencing",
"Humans",
"Male",
"Microsatellite Repeats",
"Polymerase Chain Reaction",
"RNA Isoforms",
"RNA, Long Noncoding",
"Uniparental Disomy"
]
} | Based on the observed MEG8-DMR DNA-hypermethylation and previously published data, we conclude that DNA-methylation of the MEG3- and MEG8-DMR is functionally dependent on the DNA-methylation pattern of the IG-DMR. The observed combination of epimutations is predicted to be associated with bi-allelic MEG3 and MEG8 expression in individuals with Temple syndrome. | yes | [
{
"from": "human",
"value": "Question: Is the differentially methylated region of MEG8 hypermethylated in patients with Temple syndrome?\nContext: {'contexts': ['To investigate the DNA-methylation levels in the newly described MEG8 differentially methylated region (DMR) in the imprinted cluster in 14q32 in patients with Temple syndrome.', 'We included three patients with Temple syndrome which were studied by Infinium HumanMethylation450 BeadChips, locus-specific bisulfite-pyrosequencing, methylation-specific-MLPA and microsatellite analyses. The tag-CpG of the MEG8-DMR was investigated using the Infinium HumanMethylation450 BeadChip.', 'In all three patients, the identical pattern of DNA-hypermethylation of the MEG8-DMR was observed along with DNA-hypomethylation of the IG-DMR and MEG3-DMR.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Child', 'Child, Preschool', 'Chromosomes, Human, Pair 14', 'CpG Islands', 'DNA Methylation', 'Developmental Disabilities', 'Epigenesis, Genetic', 'Female', 'Genomic Imprinting', 'High-Throughput Nucleotide Sequencing', 'Humans', 'Male', 'Microsatellite Repeats', 'Polymerase Chain Reaction', 'RNA Isoforms', 'RNA, Long Noncoding', 'Uniparental Disomy']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,543,036 | Does catalase improve saccharification of lignocellulose by reducing lytic polysaccharide monooxygenase-associated enzyme inactivation? | {
"contexts": [
"Efficient enzymatic saccharification of plant cell wall material is key to industrial processing of agricultural and forestry waste such as straw and wood chips into fuels and chemicals.",
"Saccharification assays were performed on steam-pretreated wheat straw under ambient and O2-deprived environments and in the absence and presence of a lytic polysaccharide monooxygenase (LPMO) and catalase. A kinetic model was used to calculate catalytic rate and first-order inactivation rate constants of the cellulases from reaction progress curves. The addition of a LPMO significantly (P < 0.01, Student's T test) enhanced the rate of glucose release from 2.8 to 6.9 h(-1) under ambient O2 conditions. However, this also significantly (P < 0.01, Student's T test) increased the rate of inactivation of the enzyme mixture, thereby reducing the performance half-life from 65 to 35 h. Decreasing O2 levels or, strikingly, the addition of catalase significantly reduced (P < 0.01, Student's T test) enzyme inactivation and, as a consequence, higher efficiency of the cellulolytic enzyme cocktail was achieved."
],
"labels": [
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Catalase",
"Cellulases",
"Glucose",
"Kinetics",
"Lignin",
"Mixed Function Oxygenases",
"Oxidation-Reduction",
"Plant Stems",
"Triticum"
]
} | Oxidative inactivation of commercial cellulase mixtures is a significant factor influencing the overall saccharification efficiency and the addition of catalase can be used to protect these mixtures from inactivation. | yes | [
{
"from": "human",
"value": "Question: Does catalase improve saccharification of lignocellulose by reducing lytic polysaccharide monooxygenase-associated enzyme inactivation?\nContext: {'contexts': ['Efficient enzymatic saccharification of plant cell wall material is key to industrial processing of agricultural and forestry waste such as straw and wood chips into fuels and chemicals.', \"Saccharification assays were performed on steam-pretreated wheat straw under ambient and O2-deprived environments and in the absence and presence of a lytic polysaccharide monooxygenase (LPMO) and catalase. A kinetic model was used to calculate catalytic rate and first-order inactivation rate constants of the cellulases from reaction progress curves. The addition of a LPMO significantly (P\\xa0<\\xa00.01, Student's T test) enhanced the rate of glucose release from 2.8 to 6.9\\xa0h(-1) under ambient O2 conditions. However, this also significantly (P\\xa0<\\xa00.01, Student's T test) increased the rate of inactivation of the enzyme mixture, thereby reducing the performance half-life from 65 to 35\\xa0h. Decreasing O2 levels or, strikingly, the addition of catalase significantly reduced (P\\xa0<\\xa00.01, Student's T test) enzyme inactivation and, as a consequence, higher efficiency of the cellulolytic enzyme cocktail was achieved.\"], 'labels': ['OBJECTIVE', 'RESULTS'], 'meshes': ['Catalase', 'Cellulases', 'Glucose', 'Kinetics', 'Lignin', 'Mixed Function Oxygenases', 'Oxidation-Reduction', 'Plant Stems', 'Triticum']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,526,322 | Does purpose in life predict allostatic load ten years later? | {
"contexts": [
"Living a purposeful life is associated with better mental and physical health, including longevity. Accumulating evidence shows that these associations might be explained by the association between life purpose and regulation of physiological systems involved in the stress response. The aim of this study was to investigate the prospective associations between life purpose and allostatic load over a 10-year period.",
"Analyses were conducted using data from the Midlife in the United States (MIDUS) survey. Assessment of life purpose, psychological covariates and demographics were obtained at baseline, while biomarkers of allostatic load were assessed at the 10-year follow-up.",
"We found that greater life purpose predicted lower levels of allostatic load at follow-up, even when controlling for other aspects of psychological well-being potentially associated with allostatic load. Further, life purpose was also a strong predictor of individual differences in self-health locus of control-i.e., beliefs about how much influence individuals can exert on their own health-which, in turn, partially mediated the association between purpose and allostatic load. Although life purpose was also negatively linked to other-health locus of control-i.e., the extent to which individuals believe their health is controlled by others/chance-this association did not mediate the impact of life purpose on allostatic load."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Allostasis",
"Biomarkers",
"Female",
"Health Behavior",
"Humans",
"Individuality",
"Internal-External Control",
"Male",
"Middle Aged",
"Mortality",
"Prospective Studies",
"Quality of Life",
"Socioeconomic Factors",
"United States"
]
} | The current study provides the first empirical evidence for the long-term physiological correlates of life purpose and supports the hypothesis that self-health locus of control acts as one proximal psychological mechanism through which life purpose may be linked to positive biological outcomes. | yes | [
{
"from": "human",
"value": "Question: Does purpose in life predict allostatic load ten years later?\nContext: {'contexts': ['Living a purposeful life is associated with better mental and physical health, including longevity. Accumulating evidence shows that these associations might be explained by the association between life purpose and regulation of physiological systems involved in the stress response. The aim of this study was to investigate the prospective associations between life purpose and allostatic load over a 10-year period.', 'Analyses were conducted using data from the Midlife in the United States (MIDUS) survey. Assessment of life purpose, psychological covariates and demographics were obtained at baseline, while biomarkers of allostatic load were assessed at the 10-year follow-up.', 'We found that greater life purpose predicted lower levels of allostatic load at follow-up, even when controlling for other aspects of psychological well-being potentially associated with allostatic load. Further, life purpose was also a strong predictor of individual differences in self-health locus of control-i.e., beliefs about how much influence individuals can exert on their own health-which, in turn, partially mediated the association between purpose and allostatic load. Although life purpose was also negatively linked to other-health locus of control-i.e., the extent to which individuals believe their health is controlled by others/chance-this association did not mediate the impact of life purpose on allostatic load.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Allostasis', 'Biomarkers', 'Female', 'Health Behavior', 'Humans', 'Individuality', 'Internal-External Control', 'Male', 'Middle Aged', 'Mortality', 'Prospective Studies', 'Quality of Life', 'Socioeconomic Factors', 'United States']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,538,066 | Do gene-expression patterns in peripheral blood classify familial breast cancer susceptibility? | {
"contexts": [
"Women with a family history of breast cancer face considerable uncertainty about whether to pursue standard screening, intensive screening, or prophylactic surgery. Accurate and individualized risk-estimation approaches may help these women make more informed decisions. Although highly penetrant genetic variants have been associated with familial breast cancer (FBC) risk, many individuals do not carry these variants, and many carriers never develop breast cancer. Common risk variants have a relatively modest effect on risk and show limited potential for predicting FBC development. As an alternative, we hypothesized that additional genomic data types, such as gene-expression levels, which can reflect genetic and epigenetic variation, could contribute to classifying a person's risk status. Specifically, we aimed to identify common patterns in gene-expression levels across individuals who develop FBC.",
"We profiled peripheral blood mononuclear cells from women with a family history of breast cancer (with or without a germline BRCA1/2 variant) and from controls. We used the support vector machines algorithm to differentiate between patients who developed FBC and those who did not. Our study used two independent datasets, a training set of 124 women from Utah (USA) and an external validation (test) set from Ontario (Canada) of 73 women (197 total). We controlled for expression variation associated with clinical, demographic, and treatment variables as well as lymphocyte markers.",
"Our multigene biomarker provided accurate, individual-level estimates of FBC occurrence for the Utah cohort (AUC = 0.76 [0.67-84]) . Even at their lower confidence bounds, these accuracy estimates meet or exceed estimates from alternative approaches. Our Ontario cohort resulted in similarly high levels of accuracy (AUC = 0.73 [0.59-0.86]), thus providing external validation of our findings. Individuals deemed to have \"high\" risk by our model would have an estimated 2.4 times greater odds of developing familial breast cancer than individuals deemed to have \"low\" risk."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Breast Neoplasms",
"Case-Control Studies",
"Cohort Studies",
"Computational Biology",
"Female",
"Genetic Predisposition to Disease",
"Humans",
"Leukocytes, Mononuclear",
"Middle Aged",
"Mutation",
"Pedigree",
"Support Vector Machine",
"Transcriptome"
]
} | Together, these findings suggest that gene-expression levels in peripheral blood cells reflect genomic variation associated with breast cancer risk and that such data have potential to be used as a non-invasive biomarker for familial breast cancer risk. | yes | [
{
"from": "human",
"value": "Question: Do gene-expression patterns in peripheral blood classify familial breast cancer susceptibility?\nContext: {'contexts': [\"Women with a family history of breast cancer face considerable uncertainty about whether to pursue standard screening, intensive screening, or prophylactic surgery. Accurate and individualized risk-estimation approaches may help these women make more informed decisions. Although highly penetrant genetic variants have been associated with familial breast cancer (FBC) risk, many individuals do not carry these variants, and many carriers never develop breast cancer. Common risk variants have a relatively modest effect on risk and show limited potential for predicting FBC development. As an alternative, we hypothesized that additional genomic data types, such as gene-expression levels, which can reflect genetic and epigenetic variation, could contribute to classifying a person's risk status. Specifically, we aimed to identify common patterns in gene-expression levels across individuals who develop FBC.\", 'We profiled peripheral blood mononuclear cells from women with a family history of breast cancer (with or without a germline BRCA1/2 variant) and from controls. We used the support vector machines algorithm to differentiate between patients who developed FBC and those who did not. Our study used two independent datasets, a training set of 124 women from Utah (USA) and an external validation (test) set from Ontario (Canada) of 73 women (197 total). We controlled for expression variation associated with clinical, demographic, and treatment variables as well as lymphocyte markers.', 'Our multigene biomarker provided accurate, individual-level estimates of FBC occurrence for the Utah cohort (AUC = 0.76 [0.67-84]) . Even at their lower confidence bounds, these accuracy estimates meet or exceed estimates from alternative approaches. Our Ontario cohort resulted in similarly high levels of accuracy (AUC = 0.73 [0.59-0.86]), thus providing external validation of our findings. Individuals deemed to have \"high\" risk by our model would have an estimated 2.4 times greater odds of developing familial breast cancer than individuals deemed to have \"low\" risk.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Breast Neoplasms', 'Case-Control Studies', 'Cohort Studies', 'Computational Biology', 'Female', 'Genetic Predisposition to Disease', 'Humans', 'Leukocytes, Mononuclear', 'Middle Aged', 'Mutation', 'Pedigree', 'Support Vector Machine', 'Transcriptome']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,525,737 | Is previous chronic cerebral infarction predictive for new cerebral ischemia after carotid endarterectomy? | {
"contexts": [
"The purpose of this study was to investigate the relation between preoperative chronic cerebral ischemia and postoperative new cerebral ischemia in patients undergoing carotid endarterectomy (CEA).",
"We reviewed the diffusion weighted magnetic resonance images (DWI) of the 51 patients (37 men, mean age 68.8 ± 8.4 years) undergoing isolated CEA in the preoperative and early postoperative period. The number, anatomic location and the size of new ischemic lesions were recorded.",
"In the preoperative period, 28 (54.9 %) patients were symptomatic. There was chronic cerebral infarction in the preoperative DWI images of 17 patients (33.3 %). In the postoperative period, there was newly developed cerebral ischemia in postoperative DWI images of eight (15.7 %) patients. Six of the eight patients with newly developed cerebral ischemia had chronic cerebral infarction in their preoperative DWI images. The incidence of newly developed cerebral ischemia after CEA in patients with preoperative chronic cerebral ischemia was significantly higher than the incidence in patients without preoperative chronic cerebral ischemia (p = 0.01)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Aged, 80 and over",
"Brain Ischemia",
"Cerebral Infarction",
"Endarterectomy, Carotid",
"Female",
"Humans",
"Male",
"Middle Aged",
"Postoperative Complications",
"Predictive Value of Tests"
]
} | The results of the present study suggest that preoperative chronic cerebral ischemia may aggravate postoperative newly developed cerebral ischemia in patients undergoing CEA. | yes | [
{
"from": "human",
"value": "Question: Is previous chronic cerebral infarction predictive for new cerebral ischemia after carotid endarterectomy?\nContext: {'contexts': ['The purpose of this study was to investigate the relation between preoperative chronic cerebral ischemia and postoperative new cerebral ischemia in patients undergoing carotid endarterectomy (CEA).', 'We reviewed the diffusion weighted magnetic resonance images (DWI) of the 51 patients (37 men, mean age 68.8\\u2009±\\u20098.4 years) undergoing isolated CEA in the preoperative and early postoperative period. The number, anatomic location and the size of new ischemic lesions were recorded.', 'In the preoperative period, 28 (54.9 %) patients were symptomatic. There was chronic cerebral infarction in the preoperative DWI images of 17 patients (33.3 %). In the postoperative period, there was newly developed cerebral ischemia in postoperative DWI images of eight (15.7 %) patients. Six of the eight patients with newly developed cerebral ischemia had chronic cerebral infarction in their preoperative DWI images. The incidence of newly developed cerebral ischemia after CEA in patients with preoperative chronic cerebral ischemia was significantly higher than the incidence in patients without preoperative chronic cerebral ischemia (p\\u2009=\\u20090.01).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Aged, 80 and over', 'Brain Ischemia', 'Cerebral Infarction', 'Endarterectomy, Carotid', 'Female', 'Humans', 'Male', 'Middle Aged', 'Postoperative Complications', 'Predictive Value of Tests']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,545,365 | Does miR-362-5p promote the malignancy of chronic myelocytic leukaemia via down-regulation of GADD45α? | {
"contexts": [
"MicroRNAs (miR, miRNAs) play pivotal roles in numerous physiological and pathophysiological contexts. We investigated whether miR-362-5p act as an oncogene in chronic myeloid leukaemia (CML) and aimed to understand its potential underlying mechanisms.",
"We compared the miR-362-5p expression levels between CML and non-CML cell lines, and between fresh blood samples from CML patients and normal healthy controls using quantitative real-time PCR (qPCR). Cell counting kit-8 (CCK-8) and Annexin V-FITC/PI analyses were used to measure the effects of miR-362-5p on proliferation and apoptosis, and Transwell assays were used to evaluate migration and invasion. A xenograft model was used to examine in vivo tumourigenicity. The potential target of miR-362-5p was confirmed by a luciferase reporter assay, qPCR and western blotting. Involvement of the JNK1/2 and P38 pathways was investigated by western blotting.",
"miR-362-5p was up-regulated in CML cell lines and fresh blood samples from CML patients, and was associated with Growth arrest and DNA damage-inducible (GADD)45α down-regulation. Inhibition of miR-362-5p simultaneously repressed tumour growth and up-regulated GADD45α expression in a xenograft model. Consistently, the knockdown of GADD45α expression partially neutralized the effects of miR-362-5p inhibition. Furthermore study suggested that GADD45α mediated downstream the effects of miR-362-5p, which might indirectly regulates the activation of the JNK1/2 and P38 signalling pathways."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Apoptosis",
"Cell Cycle",
"Cell Cycle Proteins",
"Cell Line, Tumor",
"Cell Movement",
"Cell Proliferation",
"Down-Regulation",
"Female",
"Gene Expression Regulation, Neoplastic",
"HEK293 Cells",
"Humans",
"K562 Cells",
"Leukemia, Myelogenous, Chronic, BCR-ABL Positive",
"Mice",
"Mice, Inbred BALB C",
"Mice, Nude",
"MicroRNAs",
"Nuclear Proteins",
"Real-Time Polymerase Chain Reaction"
]
} | miR-362-5p acts as an oncomiR that down-regulates GADD45α, which consequently activates the JNK1/2 and P38 signalling. This finding provides novel insights into CML leukaemogenesis and may help identify new diagnostic and therapeutic targets. | yes | [
{
"from": "human",
"value": "Question: Does miR-362-5p promote the malignancy of chronic myelocytic leukaemia via down-regulation of GADD45α?\nContext: {'contexts': ['MicroRNAs (miR, miRNAs) play pivotal roles in numerous physiological and pathophysiological contexts. We investigated whether miR-362-5p act as an oncogene in chronic myeloid leukaemia (CML) and aimed to understand its potential underlying mechanisms.', 'We compared the miR-362-5p expression levels between CML and non-CML cell lines, and between fresh blood samples from CML patients and normal healthy controls using quantitative real-time PCR (qPCR). Cell counting kit-8 (CCK-8) and Annexin V-FITC/PI analyses were used to measure the effects of miR-362-5p on proliferation and apoptosis, and Transwell assays were used to evaluate migration and invasion. A xenograft model was used to examine in vivo tumourigenicity. The potential target of miR-362-5p was confirmed by a luciferase reporter assay, qPCR and western blotting. Involvement of the JNK1/2 and P38 pathways was investigated by western blotting.', 'miR-362-5p was up-regulated in CML cell lines and fresh blood samples from CML patients, and was associated with Growth arrest and DNA damage-inducible (GADD)45α down-regulation. Inhibition of miR-362-5p simultaneously repressed tumour growth and up-regulated GADD45α expression in a xenograft model. Consistently, the knockdown of GADD45α expression partially neutralized the effects of miR-362-5p inhibition. Furthermore study suggested that GADD45α mediated downstream the effects of miR-362-5p, which might indirectly regulates the activation of the JNK1/2 and P38 signalling pathways.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Apoptosis', 'Cell Cycle', 'Cell Cycle Proteins', 'Cell Line, Tumor', 'Cell Movement', 'Cell Proliferation', 'Down-Regulation', 'Female', 'Gene Expression Regulation, Neoplastic', 'HEK293 Cells', 'Humans', 'K562 Cells', 'Leukemia, Myelogenous, Chronic, BCR-ABL Positive', 'Mice', 'Mice, Inbred BALB C', 'Mice, Nude', 'MicroRNAs', 'Nuclear Proteins', 'Real-Time Polymerase Chain Reaction']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,554,238 | Is rs219780 SNP of Claudin 14 Gene Related to Clinical Expression in Primary Hyperparathyroidism? | {
"contexts": [
"The CLDN14 gene encodes a protein involved in the regulation of paracellular permeability or ion transport at epithelial tight junctions as in the nephron. The C allele of the rs219780 SNP (single nucleotide polymorphism) of CLDN14 has been associated with renal lithiasis, high levels of parathormone (PTH), and with low bone mineral density (BMD) in healthy women. Our aim is to study the relationship between rs219780 SNP of CLDN14 and renal lithiasis, fractures, and BMD in patients with primary hyperparathyroidism (PHPT).",
"We enrolled 298 Caucasian patients with PHPT and 328 healthy volunteers in a cross-sectional study. We analysed anthropometric data, history of fractures or kidney stones, biochemical parameters including markers for bone remodelling, abdominal ultrasound, and BMD and genotyping for the rs219780 SNP of CLDN14.",
"We did not find any difference in the frequency of fractures or renal lithiasis between the genotype groups in PHPT patients. Moreover, we did not find any relationship between the T or C alleles and BMD or biochemical parameters."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Alleles",
"Biomarkers",
"Bone Density",
"Bone Remodeling",
"Calcium",
"Claudins",
"Cross-Sectional Studies",
"Female",
"Fractures, Spontaneous",
"Gene Frequency",
"Genetic Predisposition to Disease",
"Humans",
"Hypercalcemia",
"Hyperparathyroidism, Primary",
"Male",
"Menopause",
"Middle Aged",
"Nephrolithiasis",
"Osteoporosis",
"Parathyroid Hormone",
"Risk Factors",
"Spain"
]
} | rs219780 SNP of CLDN14 does not appear to be a risk factor for the development of PHPT nor does it seem to influence the clinical expression of PHPT. | no | [
{
"from": "human",
"value": "Question: Is rs219780 SNP of Claudin 14 Gene Related to Clinical Expression in Primary Hyperparathyroidism?\nContext: {'contexts': ['The CLDN14 gene encodes a protein involved in the regulation of paracellular permeability or ion transport at epithelial tight junctions as in the nephron. The C allele of the rs219780 SNP (single nucleotide polymorphism) of CLDN14 has been associated with renal lithiasis, high levels of parathormone (PTH), and with low bone mineral density (BMD) in healthy women. Our aim is to study the relationship between rs219780 SNP of CLDN14 and renal lithiasis, fractures, and BMD in patients with primary hyperparathyroidism (PHPT).', 'We enrolled 298 Caucasian patients with PHPT and 328 healthy volunteers in a cross-sectional study. We analysed anthropometric data, history of fractures or kidney stones, biochemical parameters including markers for bone remodelling, abdominal ultrasound, and BMD and genotyping for the rs219780 SNP of CLDN14.', 'We did not find any difference in the frequency of fractures or renal lithiasis between the genotype groups in PHPT patients. Moreover, we did not find any relationship between the T or C alleles and BMD or biochemical parameters.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Alleles', 'Biomarkers', 'Bone Density', 'Bone Remodeling', 'Calcium', 'Claudins', 'Cross-Sectional Studies', 'Female', 'Fractures, Spontaneous', 'Gene Frequency', 'Genetic Predisposition to Disease', 'Humans', 'Hypercalcemia', 'Hyperparathyroidism, Primary', 'Male', 'Menopause', 'Middle Aged', 'Nephrolithiasis', 'Osteoporosis', 'Parathyroid Hormone', 'Risk Factors', 'Spain']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
26,554,236 | Is a Functional Single-Nucleotide Polymorphism in Pre-microRNA-196a2 Associated with Atrial Fibrillation in Han Chinese? | {
"contexts": [
"MicroRNAs are small, single-stranded, non-protein-coding RNAs of about 22 nucleotides. MicroRNA molecules have been identified to play key roles in a broad range of physiologic and pathologic processes. Polymorphisms in the corresponding sequence space are likely to make a significant contribution to phenotypic variation. A T/C genetic variant (rs11614913) in the pre-miR-196a2 sequence could alter mature miR-196a expression and target mRNA binding. The aim of the present study is to evaluate the relationship between this polymorphism and atrial fibrillation (AF).",
"A total of 123 participants were enrolled, 65 AF patients were confirmed with electrocardiogram (ECG) or dynamic electrocardiography, 58 normal individuals were assigned to the control group. Genotypes of the premiR-196a2 were distinguished using the method of polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay.",
"The distribution of the pre-miR-196a2 genotypes (TT, TC, and CC) was 15.38%, 46.15%, and 38.46% in the AF group and 39.66%, 46.55%, and 13.79% in the controls, respectively (p = 0.0011). Compared with the TT genotype, the C allele carriers (TC+CC genotypes) had a 3.968-fold increased risk of AF (adjusted OR = 3.968, 95% CI = 1.633 - 9.644, p = 0.002). AF patients with the TC+CC genotype had greater left atrial dimension than did patients with the TT genotype (42.10 ± 8.74 vs. 35.13 ± 8.16, p = 0.0224)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Alleles",
"Asian Continental Ancestry Group",
"Atrial Fibrillation",
"Base Sequence",
"China",
"Diabetes Mellitus",
"Electrocardiography",
"Ethnic Groups",
"Female",
"Gene Frequency",
"Genotype",
"Heart Atria",
"Humans",
"Hypertension",
"Male",
"MicroRNAs",
"Middle Aged",
"Molecular Sequence Data",
"Organ Size",
"Polymorphism, Restriction Fragment Length",
"Polymorphism, Single Nucleotide",
"Risk Factors"
]
} | Our data support that the pre-miR-196a2 polymorphism is associated with AF, and the C allele is a risk factor for AF. | yes | [
{
"from": "human",
"value": "Question: Is a Functional Single-Nucleotide Polymorphism in Pre-microRNA-196a2 Associated with Atrial Fibrillation in Han Chinese?\nContext: {'contexts': ['MicroRNAs are small, single-stranded, non-protein-coding RNAs of about 22 nucleotides. MicroRNA molecules have been identified to play key roles in a broad range of physiologic and pathologic processes. Polymorphisms in the corresponding sequence space are likely to make a significant contribution to phenotypic variation. A T/C genetic variant (rs11614913) in the pre-miR-196a2 sequence could alter mature miR-196a expression and target mRNA binding. The aim of the present study is to evaluate the relationship between this polymorphism and atrial fibrillation (AF).', 'A total of 123 participants were enrolled, 65 AF patients were confirmed with electrocardiogram (ECG) or dynamic electrocardiography, 58 normal individuals were assigned to the control group. Genotypes of the premiR-196a2 were distinguished using the method of polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay.', 'The distribution of the pre-miR-196a2 genotypes (TT, TC, and CC) was 15.38%, 46.15%, and 38.46% in the AF group and 39.66%, 46.55%, and 13.79% in the controls, respectively (p = 0.0011). Compared with the TT genotype, the C allele carriers (TC+CC genotypes) had a 3.968-fold increased risk of AF (adjusted OR = 3.968, 95% CI = 1.633 - 9.644, p = 0.002). AF patients with the TC+CC genotype had greater left atrial dimension than did patients with the TT genotype (42.10 ± 8.74 vs. 35.13 ± 8.16, p = 0.0224).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Alleles', 'Asian Continental Ancestry Group', 'Atrial Fibrillation', 'Base Sequence', 'China', 'Diabetes Mellitus', 'Electrocardiography', 'Ethnic Groups', 'Female', 'Gene Frequency', 'Genotype', 'Heart Atria', 'Humans', 'Hypertension', 'Male', 'MicroRNAs', 'Middle Aged', 'Molecular Sequence Data', 'Organ Size', 'Polymorphism, Restriction Fragment Length', 'Polymorphism, Single Nucleotide', 'Risk Factors']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,525,976 | Does first-Trimester Maternal Abdominal Adiposity predict Dysglycemia and Gestational Diabetes Mellitus in Midpregnancy? | {
"contexts": [
"This study assessed the association between first-trimester abdominal adiposity and dysglycemia and gestational diabetes mellitus (GDM) in midpregnancy.",
"In a prospective cohort of 485 women, we measured subcutaneous (SAT), visceral (VAT), and total (TAT) adipose tissue depth, using ultrasound at 11-14 weeks' gestation. Logistic regression analysis assessed the relation between quartiles of SAT, VAT, or TAT depth and the composite outcome of impaired fasting glucose (IFG), impaired glucose tolerance (IGT), or GDM, based on a 75-g oral glucose tolerance test at 24-28 weeks.",
"Adjusting for maternal age, ethnicity, family history of diabetes, and BMI, quartile 4 versus quartile 1 VAT (adjusted odds ratio [aOR] 3.1, 95% CI 1.1-9.5) and TAT (aOR 2.7, 95% CI 1.1-7.8) were significantly associated with the composite outcome, but SAT was not (aOR 1.8, 95% CI 0.70-4.8). The same was seen for GDM alone."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Diabetes, Gestational",
"Female",
"Gestational Age",
"Glucose Intolerance",
"Glucose Tolerance Test",
"Humans",
"Intra-Abdominal Fat",
"Maternal Age",
"Obesity, Abdominal",
"Odds Ratio",
"Predictive Value of Tests",
"Pregnancy",
"Pregnancy Trimester, First",
"Prospective Studies"
]
} | Elevated first-trimester VAT and TAT depth independently predicted the risk of dysglycemia later in pregnancy. | yes | [
{
"from": "human",
"value": "Question: Does first-Trimester Maternal Abdominal Adiposity predict Dysglycemia and Gestational Diabetes Mellitus in Midpregnancy?\nContext: {'contexts': ['This study assessed the association between first-trimester abdominal adiposity and dysglycemia and gestational diabetes mellitus (GDM) in midpregnancy.', \"In a prospective cohort of 485 women, we measured subcutaneous (SAT), visceral (VAT), and total (TAT) adipose tissue depth, using ultrasound at 11-14 weeks' gestation. Logistic regression analysis assessed the relation between quartiles of SAT, VAT, or TAT depth and the composite outcome of impaired fasting glucose (IFG), impaired glucose tolerance (IGT), or GDM, based on a 75-g oral glucose tolerance test at 24-28 weeks.\", 'Adjusting for maternal age, ethnicity, family history of diabetes, and BMI, quartile 4 versus quartile 1 VAT (adjusted odds ratio [aOR] 3.1, 95% CI 1.1-9.5) and TAT (aOR 2.7, 95% CI 1.1-7.8) were significantly associated with the composite outcome, but SAT was not (aOR 1.8, 95% CI 0.70-4.8). The same was seen for GDM alone.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Diabetes, Gestational', 'Female', 'Gestational Age', 'Glucose Intolerance', 'Glucose Tolerance Test', 'Humans', 'Intra-Abdominal Fat', 'Maternal Age', 'Obesity, Abdominal', 'Odds Ratio', 'Predictive Value of Tests', 'Pregnancy', 'Pregnancy Trimester, First', 'Prospective Studies']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,538,301 | Is neurodegeneration in frontotemporal lobar degeneration and motor neurone disease associated with expansions in C9orf72 linked to TDP-43 pathology and not associated with aggregated forms of dipeptide repeat proteins? | {
"contexts": [
"A hexanucleotide expansion in C9orf72 is the major genetic cause of inherited behavioural variant Frontotemporal dementia (bvFTD) and motor neurone disease (MND), although the pathological mechanism(s) underlying disease remains uncertain.",
"Using antibodies to poly-GA, poly-GP, poly-GR, poly-AP and poly-PR proteins, we examined sections of cerebral cortex, hippocampus, thalamus, cerebellum and spinal cord, from 20 patients with bvFTD and/or MND bearing an expansion in C9orf72 for aggregated deposits of dipeptide repeat proteins (DPR).",
"Antibodies to poly-GA, poly-GP and poly-GR detected numerous rounded cytoplasmic inclusions (NCI) within granule cells of hippocampal dentate gyrus and those of the cerebellum, as well as 'star-burst' shaped NCI in pyramidal neurones of CA3/4 region of hippocampus. NCI were uncommon in Purkinje cells, and only very rarely seen in anterior horn cells. Poly-PA antibody detected occasional NCI within CA3/4 neurones alone, whereas poly-PR antibody did not identify any NCI but immunostained the nucleus of anterior horn cells, CA3/4 neurones and Purkinje cells, in patients with or without expansion in C9orf72, as well as in normal controls. Poly-GA antibody generally detected more DPR than poly-GP, which in turn was greater than poly-GR. All patients with bvFTD + MND or MND showed plentiful p62/TDP-43 positive inclusions in remaining anterior horn cells."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"C9orf72 Protein",
"DNA Repeat Expansion",
"DNA-Binding Proteins",
"Dipeptides",
"Female",
"Frontotemporal Lobar Degeneration",
"Humans",
"Immunohistochemistry",
"Inclusion Bodies",
"Male",
"Middle Aged",
"Motor Neuron Disease",
"Nerve Degeneration",
"Neurons",
"Proteins"
]
} | Degeneration and loss of anterior horn cells associated with expansions in C9orf72 occurs in the absence of DPR, and implies that changes involving loss of nuclear staining for and a cytoplasmic aggregation of TDP-43 are more likely to be the cause of this. | yes | [
{
"from": "human",
"value": "Question: Is neurodegeneration in frontotemporal lobar degeneration and motor neurone disease associated with expansions in C9orf72 linked to TDP-43 pathology and not associated with aggregated forms of dipeptide repeat proteins?\nContext: {'contexts': ['A hexanucleotide expansion in C9orf72 is the major genetic cause of inherited behavioural variant Frontotemporal dementia (bvFTD) and motor neurone disease (MND), although the pathological mechanism(s) underlying disease remains uncertain.', 'Using antibodies to poly-GA, poly-GP, poly-GR, poly-AP and poly-PR proteins, we examined sections of cerebral cortex, hippocampus, thalamus, cerebellum and spinal cord, from 20 patients with bvFTD and/or MND bearing an expansion in C9orf72 for aggregated deposits of dipeptide repeat proteins (DPR).', \"Antibodies to poly-GA, poly-GP and poly-GR detected numerous rounded cytoplasmic inclusions (NCI) within granule cells of hippocampal dentate gyrus and those of the cerebellum, as well as 'star-burst' shaped NCI in pyramidal neurones of CA3/4 region of hippocampus. NCI were uncommon in Purkinje cells, and only very rarely seen in anterior horn cells. Poly-PA antibody detected occasional NCI within CA3/4 neurones alone, whereas poly-PR antibody did not identify any NCI but immunostained the nucleus of anterior horn cells, CA3/4 neurones and Purkinje cells, in patients with or without expansion in C9orf72, as well as in normal controls. Poly-GA antibody generally detected more DPR than poly-GP, which in turn was greater than poly-GR. All patients with bvFTD + MND or MND showed plentiful p62/TDP-43 positive inclusions in remaining anterior horn cells.\"], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'C9orf72 Protein', 'DNA Repeat Expansion', 'DNA-Binding Proteins', 'Dipeptides', 'Female', 'Frontotemporal Lobar Degeneration', 'Humans', 'Immunohistochemistry', 'Inclusion Bodies', 'Male', 'Middle Aged', 'Motor Neuron Disease', 'Nerve Degeneration', 'Neurons', 'Proteins']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
26,537,870 | Is lamin A/C deficiency an independent risk factor for cervical cancer? | {
"contexts": [
"In the past, cervical cancer has been linked to Human Papilloma Virus (HPV) infection. Previously, we found that pre-neoplastic breast and ovarian lesions may be associated with lamin A/C deficiency, resulting in abnormal nuclear morphologies and chromosomal instability. Ultimately, these phenomena are thought to lead to cancer. Here, we assessed lamin A/C deficiency as an indicator for the risk to develop cervical cancer.",
"The expression of lamin A/C was assessed by Western blotting in cervical uterine smears (CUS) of 76 adult women from Benin concomitant with nuclear morphology assessment and HPV genotyping using microscopy and PCR-based assays, respectively. In vitro analyses were performed to uncover the mechanism underlying lamin A/C expression alterations observed in vivo. The presence of cervical intra-epithelial neoplasia (CIN) was assessed by colposcopy.",
"Normal lamin A/C expression (group A) was observed in 39% of the CUS, weak lamin A/C expression (group B) was observed in 28% of the CUS and no lamin A/C expression (group C) was observed in 33% of the CUS tested. Infection with oncogenic HPV was found to be significantly higher in group C (36%) than in groups A (17%) and B (14%). Two years after our first assessment, CIN was observed in 20% of the women in group C. The in vitro application of either a histone deacetylase inhibitor (trichostatin) or a protein kinase inhibitor (staurosporine) was found to restore lamin A/C expression in cervical cancer-derived cells."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Blotting, Western",
"Cell Line, Tumor",
"Cell Nucleus",
"Cell Nucleus Shape",
"Cervical Intraepithelial Neoplasia",
"Colposcopy",
"Female",
"Follow-Up Studies",
"Humans",
"Immunohistochemistry",
"Incidence",
"Lamin Type A",
"Middle Aged",
"Papillomavirus Infections",
"Risk Factors",
"Uterine Cervical Neoplasms",
"Vaginal Smears",
"Young Adult"
]
} | Lamin A/C deficiency may serve as an independent risk factor for CIN development and as an indicator for preventive therapy in cervical cancer. | yes | [
{
"from": "human",
"value": "Question: Is lamin A/C deficiency an independent risk factor for cervical cancer?\nContext: {'contexts': ['In the past, cervical cancer has been linked to Human Papilloma Virus (HPV) infection. Previously, we found that pre-neoplastic breast and ovarian lesions may be associated with lamin A/C deficiency, resulting in abnormal nuclear morphologies and chromosomal instability. Ultimately, these phenomena are thought to lead to cancer. Here, we assessed lamin A/C deficiency as an indicator for the risk to develop cervical cancer.', 'The expression of lamin A/C was assessed by Western blotting in cervical uterine smears (CUS) of 76 adult women from Benin concomitant with nuclear morphology assessment and HPV genotyping using microscopy and PCR-based assays, respectively. In vitro analyses were performed to uncover the mechanism underlying lamin A/C expression alterations observed in vivo. The presence of cervical intra-epithelial neoplasia (CIN) was assessed by colposcopy.', 'Normal lamin A/C expression (group A) was observed in 39% of the CUS, weak lamin A/C expression (group B) was observed in 28% of the CUS and no lamin A/C expression (group C) was observed in 33% of the CUS tested. Infection with oncogenic HPV was found to be significantly higher in group C (36%) than in groups A (17%) and B (14%). Two years after our first assessment, CIN was observed in 20% of the women in group C. The in vitro application of either a histone deacetylase inhibitor (trichostatin) or a protein kinase inhibitor (staurosporine) was found to restore lamin A/C expression in cervical cancer-derived cells.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Blotting, Western', 'Cell Line, Tumor', 'Cell Nucleus', 'Cell Nucleus Shape', 'Cervical Intraepithelial Neoplasia', 'Colposcopy', 'Female', 'Follow-Up Studies', 'Humans', 'Immunohistochemistry', 'Incidence', 'Lamin Type A', 'Middle Aged', 'Papillomavirus Infections', 'Risk Factors', 'Uterine Cervical Neoplasms', 'Vaginal Smears', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
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