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stringlengths 17
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stringlengths 1
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|---|---|---|---|---|---|
24,751,756 | Does indoleamine 2,3-dioxygenase inhibition alter the non-coding RNA transcriptome following renal ischemia-reperfusion injury? | {
"contexts": [
"Indoleamine 2,3 dioxygenase (IDO) degrades the essential amino acid tryptophan and has been shown to minimize rejection in animal models of renal transplantation. Ischemia-reperfusion injury (IRI) is unavoidable in renal transplantation and correlates with shorter graft survival times. Despite its favorable effects on rejection, there is evidence that IDO may facilitate renal IRI. Differentiating the negative impact of IDO on IRI from its pro-tolerant effects in allograft rejection is of clinical relevance. In these studies we hypothesized that constitutive IDO activity may influence renal genes associated with recovery from IRI, and that IDO inhibition may unmask these effects.",
"We examined the renal transcriptome in a rat model of IRI with and without IDO inhibition with 1-methyl-d-tryptophan (1-MT), and assessed for alterations in the gene expression signature.",
"These studies demonstrated that during recovery from renal IRI, pre-treatment with 1-MT alleviated alterations in 105 coding sequences associated with IRI, and in turn triggered new changes in 66 non-coding transcripts, the majority of which were represented by small nucleolar RNA."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Acute Kidney Injury",
"Animals",
"Disease Models, Animal",
"Graft Rejection",
"Graft Survival",
"Indoleamine-Pyrrole 2,3,-Dioxygenase",
"Kidney",
"Kidney Transplantation",
"Male",
"RNA, Untranslated",
"Rats",
"Rats, Sprague-Dawley",
"Reperfusion Injury",
"Transcriptome",
"Tryptophan"
]
} | These results suggest a biologic role for non-coding, IDO-dependent genes in regulating the early response to IRI. | yes | [
{
"from": "human",
"value": "Question: Does indoleamine 2,3-dioxygenase inhibition alter the non-coding RNA transcriptome following renal ischemia-reperfusion injury?\nContext: {'contexts': ['Indoleamine 2,3 dioxygenase (IDO) degrades the essential amino acid tryptophan and has been shown to minimize rejection in animal models of renal transplantation. Ischemia-reperfusion injury (IRI) is unavoidable in renal transplantation and correlates with shorter graft survival times. Despite its favorable effects on rejection, there is evidence that IDO may facilitate renal IRI. Differentiating the negative impact of IDO on IRI from its pro-tolerant effects in allograft rejection is of clinical relevance. In these studies we hypothesized that constitutive IDO activity may influence renal genes associated with recovery from IRI, and that IDO inhibition may unmask these effects.', 'We examined the renal transcriptome in a rat model of IRI with and without IDO inhibition with 1-methyl-d-tryptophan (1-MT), and assessed for alterations in the gene expression signature.', 'These studies demonstrated that during recovery from renal IRI, pre-treatment with 1-MT alleviated alterations in 105 coding sequences associated with IRI, and in turn triggered new changes in 66 non-coding transcripts, the majority of which were represented by small nucleolar RNA.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Acute Kidney Injury', 'Animals', 'Disease Models, Animal', 'Graft Rejection', 'Graft Survival', 'Indoleamine-Pyrrole 2,3,-Dioxygenase', 'Kidney', 'Kidney Transplantation', 'Male', 'RNA, Untranslated', 'Rats', 'Rats, Sprague-Dawley', 'Reperfusion Injury', 'Transcriptome', 'Tryptophan']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,747,591 | Does combined elevation of microRNA-196a and microRNA-196b in sera predict unfavorable prognosis in patients with osteosarcomas? | {
"contexts": [
"To investigate whether the aberrant expression of microRNA (miR)-196a and miR-196b can be used as potential prognostic markers of human osteosarcoma.",
"Quantitative real-time reverse transcriptase-polymerase chain reaction (qRT-PCR) analysis was performed to detect the expression levels of miR-196a and miR-196b in osteosarcoma tissues and patients' sera.",
"Expression levels of miR-196a and miR-196b in osteosarcoma tissues were both significantly higher than those in noncancerous bone tissues (both p<0.001), in line with which, the serum levels of the two miRNAs were also markedly upregulated in patients with osteosarcomas compared with healthy controls (both p<0.001). Then, the elevation of serum miR-196a and miR-196b levels both more frequently occurred in osteosarcoma patients with high tumor grade (p=0.008 and 0.01, respectively), positive metastasis (p=0.001 and 0.006, respectively) and recurrence (p=0.001 and 0.006, respectively). Moreover, high serum miR-196a, high serum miR-196b and conjoined expression of miR-196a/miR-196b were all independent prognostic factors for OS (overall survival) and DFS (disease-free survival) of osteosarcoma patients."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Antineoplastic Agents",
"Bone Neoplasms",
"Disease-Free Survival",
"Female",
"Humans",
"Kaplan-Meier Estimate",
"Male",
"MicroRNAs",
"Odds Ratio",
"Osteosarcoma",
"Prognosis",
"Recurrence",
"Up-Regulation"
]
} | Our present data indicate the involvement of miR-196a and miR-196b upregulation in the pathogenesis of osteosarcoma. More importantly, the altered levels of circulating miR-196a and miR-196b might have great potential to serve as novel and non-invasive prognostic factors for this malignancy. | yes | [
{
"from": "human",
"value": "Question: Does combined elevation of microRNA-196a and microRNA-196b in sera predict unfavorable prognosis in patients with osteosarcomas?\nContext: {'contexts': ['To investigate whether the aberrant expression of microRNA (miR)-196a and miR-196b can be used as potential prognostic markers of human osteosarcoma.', \"Quantitative real-time reverse transcriptase-polymerase chain reaction (qRT-PCR) analysis was performed to detect the expression levels of miR-196a and miR-196b in osteosarcoma tissues and patients' sera.\", 'Expression levels of miR-196a and miR-196b in osteosarcoma tissues were both significantly higher than those in noncancerous bone tissues (both p<0.001), in line with which, the serum levels of the two miRNAs were also markedly upregulated in patients with osteosarcomas compared with healthy controls (both p<0.001). Then, the elevation of serum miR-196a and miR-196b levels both more frequently occurred in osteosarcoma patients with high tumor grade (p=0.008 and 0.01, respectively), positive metastasis (p=0.001 and 0.006, respectively) and recurrence (p=0.001 and 0.006, respectively). Moreover, high serum miR-196a, high serum miR-196b and conjoined expression of miR-196a/miR-196b were all independent prognostic factors for OS (overall survival) and DFS (disease-free survival) of osteosarcoma patients.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Antineoplastic Agents', 'Bone Neoplasms', 'Disease-Free Survival', 'Female', 'Humans', 'Kaplan-Meier Estimate', 'Male', 'MicroRNAs', 'Odds Ratio', 'Osteosarcoma', 'Prognosis', 'Recurrence', 'Up-Regulation']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,747,447 | Does benchmarking trauma centers on mortality alone reflect quality of care : implications for pay-for-performance? | {
"contexts": [
"Trauma centers are currently benchmarked on mortality outcomes alone. However, pay-for-performance measures may financially penalize centers based on complications. Our objective was to determine whether the results would be similar to the current standard method of mortality-based benchmarking if trauma centers were profiled on complications.",
"We analyzed data from the National Trauma Data Bank from 2007 to 2010. Patients 16 years or older with blunt or penetrating injuries and an Injury Severity Score (ISS) of 9 or higher were included. Risk-adjusted observed-to-expected (O/E) mortality ratios for each center were generated and used to rank each facility as high, average, or low performing. We similarly ranked facilities on O/E morbidity ratios defined as occurrence of any major complication. Concordance between hospital performance rankings was evaluated using a weighted κ statistic. Correlation between morbidity- and mortality-based O/E ratios was assessed using Pearson coefficients. Sensitivity analyses were performed to mitigate the competing risk of death for the morbidity analyses.",
"A total of 449,743 patients from 248 facilities were analyzed. The unadjusted morbidity and mortality rates were 10.0% and 6.9%, respectively. No correlation was found between morbidity- and mortality-based O/E ratios (r = -0.01). Only 40% of the centers had similar performance rankings for both mortality and morbidity. Of the 31 high performers for mortality, only 11 centers were also high performers for morbidity. A total of 78 centers were ranked as average, and 11 ranked as low performers on both outcomes. Comparison of hospital performance status using mortality and morbidity outcomes demonstrated poor concordance (weighted κ = 0.03, p = 0.22)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Benchmarking",
"Cause of Death",
"Databases, Factual",
"Female",
"Health Care Surveys",
"Hospital Mortality",
"Humans",
"Injury Severity Score",
"Male",
"Middle Aged",
"Quality of Health Care",
"Reimbursement, Incentive",
"Risk Adjustment",
"Sensitivity and Specificity",
"Survival Analysis",
"Trauma Centers",
"United States",
"Wounds and Injuries",
"Wounds, Nonpenetrating",
"Wounds, Penetrating",
"Young Adult"
]
} | Mortality-based external benchmarking does not identify centers with high complication rates. This creates a dichotomy between current trauma center profiling standards and measures used for pay-for-performance. A benchmarking mechanism that reflects all measures of quality is needed. | no | [
{
"from": "human",
"value": "Question: Does benchmarking trauma centers on mortality alone reflect quality of care : implications for pay-for-performance?\nContext: {'contexts': ['Trauma centers are currently benchmarked on mortality outcomes alone. However, pay-for-performance measures may financially penalize centers based on complications. Our objective was to determine whether the results would be similar to the current standard method of mortality-based benchmarking if trauma centers were profiled on complications.', 'We analyzed data from the National Trauma Data Bank from 2007 to 2010. Patients 16 years or older with blunt or penetrating injuries and an Injury Severity Score (ISS) of 9 or higher were included. Risk-adjusted observed-to-expected (O/E) mortality ratios for each center were generated and used to rank each facility as high, average, or low performing. We similarly ranked facilities on O/E morbidity ratios defined as occurrence of any major complication. Concordance between hospital performance rankings was evaluated using a weighted κ statistic. Correlation between morbidity- and mortality-based O/E ratios was assessed using Pearson coefficients. Sensitivity analyses were performed to mitigate the competing risk of death for the morbidity analyses.', 'A total of 449,743 patients from 248 facilities were analyzed. The unadjusted morbidity and mortality rates were 10.0% and 6.9%, respectively. No correlation was found between morbidity- and mortality-based O/E ratios (r = -0.01). Only 40% of the centers had similar performance rankings for both mortality and morbidity. Of the 31 high performers for mortality, only 11 centers were also high performers for morbidity. A total of 78 centers were ranked as average, and 11 ranked as low performers on both outcomes. Comparison of hospital performance status using mortality and morbidity outcomes demonstrated poor concordance (weighted κ = 0.03, p = 0.22).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Benchmarking', 'Cause of Death', 'Databases, Factual', 'Female', 'Health Care Surveys', 'Hospital Mortality', 'Humans', 'Injury Severity Score', 'Male', 'Middle Aged', 'Quality of Health Care', 'Reimbursement, Incentive', 'Risk Adjustment', 'Sensitivity and Specificity', 'Survival Analysis', 'Trauma Centers', 'United States', 'Wounds and Injuries', 'Wounds, Nonpenetrating', 'Wounds, Penetrating', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
24,773,337 | Does a prenatal prediction model for total nucleated cell count increase the efficacy of umbilical cord blood banking? | {
"contexts": [
"The most important factor for the selection of an umbilical cord blood unit (CBU) for hematopoietic stem cell transplantation is the total nucleated cell (TNC) count as a surrogate marker for stem cell content in the CBU. At present, about one in five donors can provide a CBU with a sufficient TNC count for umbilical cord blood (UCB) banking. It is labor-intensive to obtain consent of all eligible donors and optimization of the selection is needed. The purpose of this study was to investigate prenatal clinical predictors for TNC count that would help to identify successful UCB donors already on admission to the delivery unit.",
"This study was a retrospective analysis of 758 cryopreserved CBUs, collected from 2002 to 2006. Maternal and fetal factors analyzed were maternal age, gravidity, parity, weight, height, diabetes, premature rupture of membranes, gestational age, fetal sex, and birthweight. The impact on a high TNC count (<150 × 10(7) vs. ≥ 150 × 10(7)) of the CBU was modeled in a multivariate analysis model.",
"Fetal birthweight was the strongest predictor (p < 0.001) of TNC count of at least 150 × 10(7). With a composite score of parity, gestational week, maternal weight and height, fetal sex, and birthweight, a nomogram was developed that increased banking rates from 22.7% to 31.9% while decreasing the number of banked CBUs from 149 to 79."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Age Factors",
"Birth Weight",
"Blood Banks",
"Blood Donors",
"Cryopreservation",
"Female",
"Fetal Blood",
"Gravidity",
"Humans",
"Leukocyte Count",
"Models, Biological",
"Predictive Value of Tests",
"Pregnancy",
"Sex Factors",
"Stem Cells"
]
} | Our prenatal prediction model increases the efficacy of obtaining informed consent for UCB banking while still allowing relevant numbers of CBUs to be banked. | yes | [
{
"from": "human",
"value": "Question: Does a prenatal prediction model for total nucleated cell count increase the efficacy of umbilical cord blood banking?\nContext: {'contexts': ['The most important factor for the selection of an umbilical cord blood unit (CBU) for hematopoietic stem cell transplantation is the total nucleated cell (TNC) count as a surrogate marker for stem cell content in the CBU. At present, about one in five donors can provide a CBU with a sufficient TNC count for umbilical cord blood (UCB) banking. It is labor-intensive to obtain consent of all eligible donors and optimization of the selection is needed. The purpose of this study was to investigate prenatal clinical predictors for TNC count that would help to identify successful UCB donors already on admission to the delivery unit.', 'This study was a retrospective analysis of 758 cryopreserved CBUs, collected from 2002 to 2006. Maternal and fetal factors analyzed were maternal age, gravidity, parity, weight, height, diabetes, premature rupture of membranes, gestational age, fetal sex, and birthweight. The impact on a high TNC count (<150 × 10(7) vs. ≥ 150 × 10(7)) of the CBU was modeled in a multivariate analysis model.', 'Fetal birthweight was the strongest predictor (p < 0.001) of TNC count of at least 150 × 10(7). With a composite score of parity, gestational week, maternal weight and height, fetal sex, and birthweight, a nomogram was developed that increased banking rates from 22.7% to 31.9% while decreasing the number of banked CBUs from 149 to 79.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Age Factors', 'Birth Weight', 'Blood Banks', 'Blood Donors', 'Cryopreservation', 'Female', 'Fetal Blood', 'Gravidity', 'Humans', 'Leukocyte Count', 'Models, Biological', 'Predictive Value of Tests', 'Pregnancy', 'Sex Factors', 'Stem Cells']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,776,871 | Does assessment of procedural skills using virtual simulation remain a challenge? | {
"contexts": [
"The LAP Mentor is a procedural simulator that provides a stepwise training for laparoscopic cholecystectomy. This study addresses its \"construct\" validity that is present when a simulator is able to discriminate between persons with known differences in performance level on the laparoscopic cholecystectomy in real life.",
"Three groups with different skill levels performed 2 trials of 4 distinct parts of the cholecystectomy procedure (cholecystectomy exercises) and 1 full procedure on the LAP Mentor. Assessment parameters concerning the quantity and the quality of performance were compared between groups using the Kruskal-Wallis and Mann-Whitney U tests.",
"The entire research was performed in the Center for Surgical Technologies, Leuven, Belgium.",
"For study purposes, 5 expert abdominal laparoscopists (>100 laparoscopic cholecystectomies performed), 11 surgical residents (10-30 cholecystectomies performed), and 10 novices (minimal laparoscopic experience) were recruited.",
"With regard to the quantity of performance (time needed and number of movements), the experts showed significantly better results compared with the novices in the cholecystectomy exercises. Only in the full procedure, the results of all the parameters (except speed) were significantly different between the 3 groups, with the best results observed for the experts and worst for the novices. With respect to quality of performance, only the parameter \"accuracy rate of dissection\" in exercise 3 showed significantly better performance by the experts."
],
"labels": [
"OBJECTIVE",
"METHODS",
"METHODS",
"METHODS",
"RESULTS"
],
"meshes": [
"Cholecystectomy, Laparoscopic",
"Clinical Competence",
"Computer Simulation",
"Humans"
]
} | Only the full procedure of the LAP Mentor procedural simulator has enough discriminative power to claim construct validity. However, the lack of quality control, which is indispensible in the evaluation of procedural skills, makes it currently unsuited for the assessment of procedural laparoscopic skills. The role of the simulator in a training context remains to be elucidated. | yes | [
{
"from": "human",
"value": "Question: Does assessment of procedural skills using virtual simulation remain a challenge?\nContext: {'contexts': ['The LAP Mentor is a procedural simulator that provides a stepwise training for laparoscopic cholecystectomy. This study addresses its \"construct\" validity that is present when a simulator is able to discriminate between persons with known differences in performance level on the laparoscopic cholecystectomy in real life.', 'Three groups with different skill levels performed 2 trials of 4 distinct parts of the cholecystectomy procedure (cholecystectomy exercises) and 1 full procedure on the LAP Mentor. Assessment parameters concerning the quantity and the quality of performance were compared between groups using the Kruskal-Wallis and Mann-Whitney U tests.', 'The entire research was performed in the Center for Surgical Technologies, Leuven, Belgium.', 'For study purposes, 5 expert abdominal laparoscopists (>100 laparoscopic cholecystectomies performed), 11 surgical residents (10-30 cholecystectomies performed), and 10 novices (minimal laparoscopic experience) were recruited.', 'With regard to the quantity of performance (time needed and number of movements), the experts showed significantly better results compared with the novices in the cholecystectomy exercises. Only in the full procedure, the results of all the parameters (except speed) were significantly different between the 3 groups, with the best results observed for the experts and worst for the novices. With respect to quality of performance, only the parameter \"accuracy rate of dissection\" in exercise 3 showed significantly better performance by the experts.'], 'labels': ['OBJECTIVE', 'METHODS', 'METHODS', 'METHODS', 'RESULTS'], 'meshes': ['Cholecystectomy, Laparoscopic', 'Clinical Competence', 'Computer Simulation', 'Humans']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,755,250 | Does morus alba L. suppress the development of atopic dermatitis induced by the house dust mite in NC/Nga mice? | {
"contexts": [
"Morus alba, a medicinal plant in Asia, has been used traditionally to treat diabetes mellitus and hypoglycemia. However, the effects of M. alba extract (MAE) on atopic dermatitis have not been verified scientifically. We investigated the effects of MAE on atopic dermatitis through in vitro and in vivo experiments.",
"We evaluated the effects of MAE on the production of nitric oxide (NO) and prostaglandin E2 (PGE2) in RAW 264.7, as well as thymus and activation-regulated chemokine (TARC/CCL17) in HaCaT cells. In an in vivo experiment, atopic dermatitis was induced by topical application of house dust mites for four weeks, and the protective effects of MAE were investigated by measuring the severity of the skin reaction on the back and ears, the plasma levels of immunoglobulin E (IgE) and histamine, and histopathological changes in the skin on the back and ears.",
"MAE suppressed the production of NO and PGE2 in RAW 264.7 cells, as well as TARC in HaCaT cells, in a dose-dependent manner. MAE treatment of NC/Nga mice reduced the severity of dermatitis and the plasma levels of IgE and histamine. MAE also reduced the histological manifestations of atopic dermatitis-like skin lesions such as erosion, hyperplasia of the epidermis and dermis, and inflammatory cell infiltration in the skin on the back and ears."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Chemokine CCL17",
"Dermatitis, Atopic",
"Disease Models, Animal",
"Histamine",
"Humans",
"Immunoglobulin E",
"Male",
"Mice",
"Morus",
"Plant Extracts",
"Pyroglyphidae",
"Skin"
]
} | Our results suggest that MAE has potent inhibitory effects on atopic dermatitis-like lesion and may be a beneficial natural resource for the treatment of atopic dermatitis. | yes | [
{
"from": "human",
"value": "Question: Does morus alba L. suppress the development of atopic dermatitis induced by the house dust mite in NC/Nga mice?\nContext: {'contexts': ['Morus alba, a medicinal plant in Asia, has been used traditionally to treat diabetes mellitus and hypoglycemia. However, the effects of M. alba extract (MAE) on atopic dermatitis have not been verified scientifically. We investigated the effects of MAE on atopic dermatitis through in vitro and in vivo experiments.', 'We evaluated the effects of MAE on the production of nitric oxide (NO) and prostaglandin E2 (PGE2) in RAW 264.7, as well as thymus and activation-regulated chemokine (TARC/CCL17) in HaCaT cells. In an in vivo experiment, atopic dermatitis was induced by topical application of house dust mites for four weeks, and the protective effects of MAE were investigated by measuring the severity of the skin reaction on the back and ears, the plasma levels of immunoglobulin E (IgE) and histamine, and histopathological changes in the skin on the back and ears.', 'MAE suppressed the production of NO and PGE2 in RAW 264.7 cells, as well as TARC in HaCaT cells, in a dose-dependent manner. MAE treatment of NC/Nga mice reduced the severity of dermatitis and the plasma levels of IgE and histamine. MAE also reduced the histological manifestations of atopic dermatitis-like skin lesions such as erosion, hyperplasia of the epidermis and dermis, and inflammatory cell infiltration in the skin on the back and ears.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Chemokine CCL17', 'Dermatitis, Atopic', 'Disease Models, Animal', 'Histamine', 'Humans', 'Immunoglobulin E', 'Male', 'Mice', 'Morus', 'Plant Extracts', 'Pyroglyphidae', 'Skin']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,758,604 | Is nOX2-generated oxidative stress associated with severity of ultrasound liver steatosis in patients with non-alcoholic fatty liver disease? | {
"contexts": [
"Chronic oxidative stress is one of the key mechanisms responsible for disease progression in non-alcoholic fatty liver disease. However, so far, few studies reported increased circulating levels of oxidative stress markers in patients with non-alcoholic fatty liver and no study has been performed with newer markers of systemic oxidative stress. The aim was to assess the relationship between urinary 8-iso-prostaglandin F2α and serum soluble NOX2-derived peptide and the severity of liver steatosis in subjects with non-alcoholic fatty liver.",
"The study was performed in 264 consecutive patients referred for suspected metabolic disease. Steatosis was defined according to Hamaguchi ultrasonographic criteria. Oxidative stress was assessed by urinary 8-iso- prostaglandin F2α and serum soluble NOX2-derived peptide levels.",
"Patients with non-alcoholic fatty liver had higher (p < 0.001) mean values of urinary 8-iso-PGF2α and of serum soluble NOX2-derived peptide, alanine aminotransferase, Cytokeratin-18 and homeostasis model of insulin resistance and lower values of serum adiponectin as compared to those without. Prevalence of metabolic syndrome and of its clinical features was significantly higher in patients with non-alcoholic fatty liver. Same findings were also observed after the exclusion of obese subjects, or subjects with diabetes or with metabolic syndrome and in those not taking statin medication. In addition, the levels of urinary 8-iso-PGF2α were independent predictors of non-alcoholic fatty liver and a strong association of urinary 8-iso-PGF2α and of serum soluble NOX2-derived peptide with the severity of steatosis at ultrasound was also observed."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Biomarkers",
"Case-Control Studies",
"Cohort Studies",
"Diabetes Mellitus",
"Dinoprost",
"Female",
"Humans",
"Linear Models",
"Male",
"Membrane Glycoproteins",
"Metabolic Syndrome",
"Middle Aged",
"NADPH Oxidase 2",
"NADPH Oxidases",
"Non-alcoholic Fatty Liver Disease",
"Obesity",
"Oxidative Stress",
"Severity of Illness Index",
"Ultrasonography"
]
} | We demonstrated increased markers of oxidative stress in subjects with non-alcoholic fatty liver. Urinary 8-iso-PGF2α and serum soluble NOX2-derived peptide levels were independent from obesity, diabetes and metabolic syndrome and increased with the severity of liver steatosis at ultrasound. | yes | [
{
"from": "human",
"value": "Question: Is nOX2-generated oxidative stress associated with severity of ultrasound liver steatosis in patients with non-alcoholic fatty liver disease?\nContext: {'contexts': ['Chronic oxidative stress is one of the key mechanisms responsible for disease progression in non-alcoholic fatty liver disease. However, so far, few studies reported increased circulating levels of oxidative stress markers in patients with non-alcoholic fatty liver and no study has been performed with newer markers of systemic oxidative stress. The aim was to assess the relationship between urinary 8-iso-prostaglandin F2α and serum soluble NOX2-derived peptide and the severity of liver steatosis in subjects with non-alcoholic fatty liver.', 'The study was performed in 264 consecutive patients referred for suspected metabolic disease. Steatosis was defined according to Hamaguchi ultrasonographic criteria. Oxidative stress was assessed by urinary 8-iso- prostaglandin F2α and serum soluble NOX2-derived peptide levels.', 'Patients with non-alcoholic fatty liver had higher (p\\u2009<\\u20090.001) mean values of urinary 8-iso-PGF2α and of serum soluble NOX2-derived peptide, alanine aminotransferase, Cytokeratin-18 and homeostasis model of insulin resistance and lower values of serum adiponectin as compared to those without. Prevalence of metabolic syndrome and of its clinical features was significantly higher in patients with non-alcoholic fatty liver. Same findings were also observed after the exclusion of obese subjects, or subjects with diabetes or with metabolic syndrome and in those not taking statin medication. In addition, the levels of urinary 8-iso-PGF2α were independent predictors of non-alcoholic fatty liver and a strong association of urinary 8-iso-PGF2α and of serum soluble NOX2-derived peptide with the severity of steatosis at ultrasound was also observed.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Biomarkers', 'Case-Control Studies', 'Cohort Studies', 'Diabetes Mellitus', 'Dinoprost', 'Female', 'Humans', 'Linear Models', 'Male', 'Membrane Glycoproteins', 'Metabolic Syndrome', 'Middle Aged', 'NADPH Oxidase 2', 'NADPH Oxidases', 'Non-alcoholic Fatty Liver Disease', 'Obesity', 'Oxidative Stress', 'Severity of Illness Index', 'Ultrasonography']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,769,011 | Is preeclampsia in high risk women characterized by risk group-specific abnormalities in serum biomarkers? | {
"contexts": [
"To determine if early pregnancy serum biomarkers in high-risk women who develop preeclampsia vary according to risk factor.",
"We performed a secondary analysis of the Maternal-Fetal Medicine Units Network randomized controlled trial of low-dose aspirin for the prevention of preeclampsia in high-risk women. Serum biomarker levels at enrollment (before initiation of aspirin or placebo) were compared between women who did and did not develop preeclampsia, both for the group as a whole and within each of 4 high-risk groups (insulin-dependent diabetes, hypertension, multiple gestation, and previous preeclampsia) using a regression model adjusting for gestational age at collection and prepregnancy body mass index.",
"1258 women were included (233 with insulin-dependent diabetes, 387 with chronic hypertension, 315 with a multiple gestation, 323 with previous preeclampsia). Multiple early pregnancy serum biomarkers differed between women who did and did not develop preeclampsia. Each high-risk group had a unique and largely nonoverlapping pattern of biomarker abnormality. Differences between those who did and did not develop preeclampsia were noted in vascular cell adhesion molecule in the diabetes group; human chorionic gonadotropin, soluble tumor necrosis factor receptor-2, tumor necrosis factor-alpha, selectin and angiogenin in the chronic hypertension group; interleukin-6, placental growth factor, soluble fms-like tyrosine kinase plus endoglin to placental growth factor ratio in the multiple gestation group; and angiogenin in the previous preeclampsia group."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Antigens, CD",
"Biomarkers",
"Chorionic Gonadotropin",
"Diabetes Mellitus, Type 1",
"Endoglin",
"Female",
"Humans",
"Hypertension",
"Placenta Growth Factor",
"Pre-Eclampsia",
"Pregnancy",
"Pregnancy Complications, Cardiovascular",
"Pregnancy Proteins",
"Pregnancy in Diabetics",
"Pregnancy, Multiple",
"Progesterone",
"Receptors, Cell Surface",
"Receptors, Tumor Necrosis Factor, Type II",
"Ribonuclease, Pancreatic",
"Risk Assessment",
"Risk Factors",
"Tumor Necrosis Factor-alpha",
"Vascular Endothelial Growth Factor Receptor-1",
"Young Adult"
]
} | Patterns of serum biomarkers vary by high-risk group. These data support the hypothesis that multiple pathogenic pathways lead to the disease recognized clinically as preeclampsia. | yes | [
{
"from": "human",
"value": "Question: Is preeclampsia in high risk women characterized by risk group-specific abnormalities in serum biomarkers?\nContext: {'contexts': ['To determine if early pregnancy serum biomarkers in high-risk women who develop preeclampsia vary according to risk factor.', 'We performed a secondary analysis of the Maternal-Fetal Medicine Units Network randomized controlled trial of low-dose aspirin for the prevention of preeclampsia in high-risk women. Serum biomarker levels at enrollment (before initiation of aspirin or placebo) were compared between women who did and did not develop preeclampsia, both for the group as a whole and within each of 4 high-risk groups (insulin-dependent diabetes, hypertension, multiple gestation, and previous preeclampsia) using a regression model adjusting for gestational age at collection and prepregnancy body mass index.', '1258 women were included (233 with insulin-dependent diabetes, 387 with chronic hypertension, 315 with a multiple gestation, 323 with previous preeclampsia). Multiple early pregnancy serum biomarkers differed between women who did and did not develop preeclampsia. Each high-risk group had a unique and largely nonoverlapping pattern of biomarker abnormality. Differences between those who did and did not develop preeclampsia were noted in vascular cell adhesion molecule in the diabetes group; human chorionic gonadotropin, soluble tumor necrosis factor receptor-2, tumor necrosis factor-alpha, selectin and angiogenin in the chronic hypertension group; interleukin-6, placental growth factor, soluble fms-like tyrosine kinase plus endoglin to placental growth factor ratio in the multiple gestation group; and angiogenin in the previous preeclampsia group.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Antigens, CD', 'Biomarkers', 'Chorionic Gonadotropin', 'Diabetes Mellitus, Type 1', 'Endoglin', 'Female', 'Humans', 'Hypertension', 'Placenta Growth Factor', 'Pre-Eclampsia', 'Pregnancy', 'Pregnancy Complications, Cardiovascular', 'Pregnancy Proteins', 'Pregnancy in Diabetics', 'Pregnancy, Multiple', 'Progesterone', 'Receptors, Cell Surface', 'Receptors, Tumor Necrosis Factor, Type II', 'Ribonuclease, Pancreatic', 'Risk Assessment', 'Risk Factors', 'Tumor Necrosis Factor-alpha', 'Vascular Endothelial Growth Factor Receptor-1', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,771,334 | Are mannose-binding lectin gene , MBL2 , polymorphisms associated with susceptibility to invasive pneumococcal disease in children? | {
"contexts": [
"Most children are transiently colonized with Streptococcus pneumoniae, but very few develop invasive pneumococcal disease (IPD). Host genetic variation of innate immunity may predispose to IPD. We investigated the effect of genetic variation in the mannose-binding lectin gene, MBL2, on susceptibility and disease severity of IPD in previously healthy children aged <5 years.",
"IPD cases were identified through national registries. DNA was obtained from the Danish Neonatal Screening Biobank. Pneumococcal serotypes were determined by Quellung reaction. The associations between MBL2 diplotypes and IPD susceptibility, serotypes, and outcome were investigated using logistic regression analysis.",
"We included 372 cases with meningitis, 907 with bacteremia, and 1263 age- and sex-matched controls; 2372 individuals were successfully genotyped and assigned MBL2 diplotypes. The median age in our combined case series was 13 months. Children with defective diplotypes were not at higher risk for meningitis than children with other diplotypes (odds ratio [OR], 0.85; 95% confidence interval [CI], .56-1.28). Similar results were found for bacteremia (OR, 0.89; 95% CI, .68-1.15) as well as for all cases (OR, 0.87; 95% CI, .70-1.09). There was no association with susceptibility to recurrent IPD (n = 12) for children with defective diplotypes compared with cases with a single episode (OR, 0.53; 95% CI, .07-4.13) and with all controls (OR, 0.46; 95% CI, .06-3.56). There was no association between diplotypes and mortality or between diplotypes and pneumococcal serotypes."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Child, Preschool",
"Denmark",
"Disease Susceptibility",
"Female",
"Genetic Predisposition to Disease",
"Humans",
"Infant",
"Infant, Newborn",
"Male",
"Mannose-Binding Lectin",
"Pneumococcal Infections",
"Polymorphism, Genetic",
"Serogroup",
"Streptococcus pneumoniae"
]
} | Defective MBL2 polymorphisms did not predict increased IPD susceptibility in children born in Northern Europe. | no | [
{
"from": "human",
"value": "Question: Are mannose-binding lectin gene , MBL2 , polymorphisms associated with susceptibility to invasive pneumococcal disease in children?\nContext: {'contexts': ['Most children are transiently colonized with Streptococcus pneumoniae, but very few develop invasive pneumococcal disease (IPD). Host genetic variation of innate immunity may predispose to IPD. We investigated the effect of genetic variation in the mannose-binding lectin gene, MBL2, on susceptibility and disease severity of IPD in previously healthy children aged <5 years.', 'IPD cases were identified through national registries. DNA was obtained from the Danish Neonatal Screening Biobank. Pneumococcal serotypes were determined by Quellung reaction. The associations between MBL2 diplotypes and IPD susceptibility, serotypes, and outcome were investigated using logistic regression analysis.', 'We included 372 cases with meningitis, 907 with bacteremia, and 1263 age- and sex-matched controls; 2372 individuals were successfully genotyped and assigned MBL2 diplotypes. The median age in our combined case series was 13 months. Children with defective diplotypes were not at higher risk for meningitis than children with other diplotypes (odds ratio [OR], 0.85; 95% confidence interval [CI], .56-1.28). Similar results were found for bacteremia (OR, 0.89; 95% CI, .68-1.15) as well as for all cases (OR, 0.87; 95% CI, .70-1.09). There was no association with susceptibility to recurrent IPD (n = 12) for children with defective diplotypes compared with cases with a single episode (OR, 0.53; 95% CI, .07-4.13) and with all controls (OR, 0.46; 95% CI, .06-3.56). There was no association between diplotypes and mortality or between diplotypes and pneumococcal serotypes.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Child, Preschool', 'Denmark', 'Disease Susceptibility', 'Female', 'Genetic Predisposition to Disease', 'Humans', 'Infant', 'Infant, Newborn', 'Male', 'Mannose-Binding Lectin', 'Pneumococcal Infections', 'Polymorphism, Genetic', 'Serogroup', 'Streptococcus pneumoniae']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
24,778,028 | Does mALDI imaging on tissue microarrays identify molecular features associated with renal cell cancer phenotype? | {
"contexts": [
"To identify molecular features associated with clinico-pathological parameters in renal cell cancer.",
"Matrix-assisted laser desorption/ionization (MALDI) mass spectrometry imaging was employed for a kidney cancer tissue microarray containing tissue samples from 789 patients for which clinical follow-up data were available.",
"A comparison of mass spectrometric signals with clinico-pathological features revealed significant differences between papillary and clear cell renal cell cancer. Within the subgroup of clear cell RCC, statistical associations with tumor stage (seven signals, p<0.01 each), Fuhrman grade (seven signals, p<0.0001 each), and presence of lymph node metastases (10 signals, p<0.01 each) were found. In addition, the presence of one signal was significantly linked to shortened patient survival (p=0.0198)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Carcinoma, Renal Cell",
"Female",
"Humans",
"Kidney Neoplasms",
"Male",
"Middle Aged",
"Neoplasm Grading",
"Neoplasm Staging",
"Phenotype",
"Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization",
"Tissue Array Analysis"
]
} | Our data pinpoint towards various molecules with potential relevance in renal cell cancer. They also demonstrate that the combination of the MALDI mass spectrometry imaging and large-scale tissue microarray platforms represents a powerful approach to identify clinically-relevant molecular cancer features. | yes | [
{
"from": "human",
"value": "Question: Does mALDI imaging on tissue microarrays identify molecular features associated with renal cell cancer phenotype?\nContext: {'contexts': ['To identify molecular features associated with clinico-pathological parameters in renal cell cancer.', 'Matrix-assisted laser desorption/ionization (MALDI) mass spectrometry imaging was employed for a kidney cancer tissue microarray containing tissue samples from 789 patients for which clinical follow-up data were available.', 'A comparison of mass spectrometric signals with clinico-pathological features revealed significant differences between papillary and clear cell renal cell cancer. Within the subgroup of clear cell RCC, statistical associations with tumor stage (seven signals, p<0.01 each), Fuhrman grade (seven signals, p<0.0001 each), and presence of lymph node metastases (10 signals, p<0.01 each) were found. In addition, the presence of one signal was significantly linked to shortened patient survival (p=0.0198).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Carcinoma, Renal Cell', 'Female', 'Humans', 'Kidney Neoplasms', 'Male', 'Middle Aged', 'Neoplasm Grading', 'Neoplasm Staging', 'Phenotype', 'Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization', 'Tissue Array Analysis']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,778,024 | Is formyl Peptide receptor 1 expression associated with tumor progression and survival in gastric cancer? | {
"contexts": [
"Formyl peptide receptor 1 (FPR1) as a regulator of innate inflammatory response has been implicated in tumor progression of gliomas. The purpose of the present study was to evaluate the prognostic significance and the ligand-receptor interaction of FPR1 in gastric cancer (GC).",
"FPR1 was immunohistochemically-analyzed in tissue sections originating from 116 GC patients. Reverse transcription-polymerase chain reaction (RT-PCR) was used for the assessment of interaction between FPR1 and the FPR1 ligand annexin A1 (AnxA1) in GC cells.",
"High FPR1 expression was significantly associated with stage IV disease, submucosal invasion, serosal invasion, and clinical outcome of GC. Multivariate analysis showed that high FPR1 expression was an independent risk factor of poor overall survival in GC patients. FPR1 expression increased significantly when AnxA1 overexpression was present in GC cells. A positive feedback regulation of FPR1 was involved in the AnxA1-FPR1 signal transduction."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Aged, 80 and over",
"Biomarkers, Tumor",
"Disease Progression",
"Female",
"Gastrectomy",
"Humans",
"Immunohistochemistry",
"Kaplan-Meier Estimate",
"Male",
"Middle Aged",
"Prognosis",
"Proportional Hazards Models",
"Receptors, Formyl Peptide",
"Reverse Transcriptase Polymerase Chain Reaction",
"Risk Factors",
"Stomach Neoplasms"
]
} | FPR1 expression may be used as a novel indicator to predict outcome in GC patients after gastrectomy. | yes | [
{
"from": "human",
"value": "Question: Is formyl Peptide receptor 1 expression associated with tumor progression and survival in gastric cancer?\nContext: {'contexts': ['Formyl peptide receptor 1 (FPR1) as a regulator of innate inflammatory response has been implicated in tumor progression of gliomas. The purpose of the present study was to evaluate the prognostic significance and the ligand-receptor interaction of FPR1 in gastric cancer (GC).', 'FPR1 was immunohistochemically-analyzed in tissue sections originating from 116 GC patients. Reverse transcription-polymerase chain reaction (RT-PCR) was used for the assessment of interaction between FPR1 and the FPR1 ligand annexin A1 (AnxA1) in GC cells.', 'High FPR1 expression was significantly associated with stage IV disease, submucosal invasion, serosal invasion, and clinical outcome of GC. Multivariate analysis showed that high FPR1 expression was an independent risk factor of poor overall survival in GC patients. FPR1 expression increased significantly when AnxA1 overexpression was present in GC cells. A positive feedback regulation of FPR1 was involved in the AnxA1-FPR1 signal transduction.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Aged, 80 and over', 'Biomarkers, Tumor', 'Disease Progression', 'Female', 'Gastrectomy', 'Humans', 'Immunohistochemistry', 'Kaplan-Meier Estimate', 'Male', 'Middle Aged', 'Prognosis', 'Proportional Hazards Models', 'Receptors, Formyl Peptide', 'Reverse Transcriptase Polymerase Chain Reaction', 'Risk Factors', 'Stomach Neoplasms']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,761,760 | Does smokeless tobacco increase aneuploidy in oral HPV16 E6/E7-transformed keratinocytes in vitro? | {
"contexts": [
"The scope of this work was to study synergism between human papillomavirus (HPV) infection and tobacco in vitro, both known to be independent risk factors for oral cancer.",
"HPV-positive and HPV-negative oral keratinocytes and oral HPV-negative fibroblasts were exposed to smokeless tobacco extract (STE) prepared from the Scandinavian (STE1) and US-type (STE2) snuff. Cell cycle profiles were determined with flow cytometry, and HPV E6/E7 mRNA expression in HPV-positive cells was assayed using RT-qPCR.",
"The exposure of HPV-positive keratinocytes with STE2 increased the number of aneuploid cells from 27% to 80% of which 44% were in S-phase, while none of the diploid cells were in S-phase. The changes after STE1 exposure were less than seen after STE2: from 27% to 31% of which 34% were in S-phase. STE had no effect on HPV16 E6/E7 expression in HPV-positive keratinocytes. In oral spontaneously transformed, HPV-negative keratinocytes, the number of aneuploid cells at G2-M stage increased after STE1 and STE2 exposure from 3% to 9% and 7%, respectively. In HPV-negative oral fibroblasts, the number of cells at G2-M phase increased from 11% to 21% after STE1 and 29% after STE2 exposure."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Aneugens",
"Aneuploidy",
"Cell Division",
"Cell Line",
"Cell Line, Transformed",
"Cell Transformation, Viral",
"Diploidy",
"Fibroblasts",
"G2 Phase",
"Gingiva",
"Human papillomavirus 16",
"Humans",
"Keratinocytes",
"Mouth Mucosa",
"Nicotine",
"Oncogene Proteins, Viral",
"Papillomavirus E7 Proteins",
"Plant Extracts",
"Repressor Proteins",
"S Phase",
"Skin",
"Tetraploidy",
"Tobacco, Smokeless"
]
} | The effect of STE varied in the cell lines studied. STE2 increased significantly the proportion of aneuploid cells in HPV-positive oral keratinocytes, but not HPV16 E6/E7 expression. This indicates that tobacco products may enhance the effects of HPV 16 and the risk of DNA aneuploidy increasing risk to malignant transformation. | yes | [
{
"from": "human",
"value": "Question: Does smokeless tobacco increase aneuploidy in oral HPV16 E6/E7-transformed keratinocytes in vitro?\nContext: {'contexts': ['The scope of this work was to study synergism between human papillomavirus (HPV) infection and tobacco in vitro, both known to be independent risk factors for oral cancer.', 'HPV-positive and HPV-negative oral keratinocytes and oral HPV-negative fibroblasts were exposed to smokeless tobacco extract (STE) prepared from the Scandinavian (STE1) and US-type (STE2) snuff. Cell cycle profiles were determined with flow cytometry, and HPV E6/E7 mRNA expression in HPV-positive cells was assayed using RT-qPCR.', 'The exposure of HPV-positive keratinocytes with STE2 increased the number of aneuploid cells from 27% to 80% of which 44% were in S-phase, while none of the diploid cells were in S-phase. The changes after STE1 exposure were less than seen after STE2: from 27% to 31% of which 34% were in S-phase. STE had no effect on HPV16 E6/E7 expression in HPV-positive keratinocytes. In oral spontaneously transformed, HPV-negative keratinocytes, the number of aneuploid cells at G2-M stage increased after STE1 and STE2 exposure from 3% to 9% and 7%, respectively. In HPV-negative oral fibroblasts, the number of cells at G2-M phase increased from 11% to 21% after STE1 and 29% after STE2 exposure.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Aneugens', 'Aneuploidy', 'Cell Division', 'Cell Line', 'Cell Line, Transformed', 'Cell Transformation, Viral', 'Diploidy', 'Fibroblasts', 'G2 Phase', 'Gingiva', 'Human papillomavirus 16', 'Humans', 'Keratinocytes', 'Mouth Mucosa', 'Nicotine', 'Oncogene Proteins, Viral', 'Papillomavirus E7 Proteins', 'Plant Extracts', 'Repressor Proteins', 'S Phase', 'Skin', 'Tetraploidy', 'Tobacco, Smokeless']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,749,562 | Does eGR1 support the osteogenic differentiation of dental stem cells? | {
"contexts": [
"To evaluate whether and how the transcription factor early growth response gene 1 (EGR1) affects the osteogenic differentiation of dental stem cells.",
"Dental stem cells from apical papilla (SCAPs) and from the dental follicle (DFCs) were transfected with EGR1-specific siRNA or EGR-1 expression plasmid. Gene regulation was verified at protein level by Western blotting. The expression of the transcription factors distal-less homeobox 3 (DLX3), alkaline phosphatase (ALP) and bone morphogenetic protein 2 (BMP2), which are all regulators and markers of the osteogenic differentiation in dental stem cells, was determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). To investigate mineralization, SCAP long-term cultures were stained with alizarin red after EGR1 over-expression.",
"EGR1 was induced in SCAPs during osteogenic differentiation. DLX3 and bone morphogenetic protein 2 (BMP2) were up-regulated after EGR1 over-expression and down-regulated after EGR1 depletion. The expression of ALP was also down-regulated after EGR1 depletion. The over-expression of EGR1 in SCAPs promoted mineralization after osteogenic differentiation."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Alkaline Phosphatase",
"Blotting, Western",
"Bone Morphogenetic Protein 2",
"Cell Differentiation",
"Dental Sac",
"Early Growth Response Protein 1",
"Flow Cytometry",
"Homeodomain Proteins",
"Humans",
"Molar, Third",
"Osteogenesis",
"Reverse Transcriptase Polymerase Chain Reaction",
"Staining and Labeling",
"Stem Cells",
"Transcription Factors",
"Transfection"
]
} | EGR1 supported the osteogenic differentiation of dental stem cells by potentially regulating the expression of DLX3 and BMP2. | yes | [
{
"from": "human",
"value": "Question: Does eGR1 support the osteogenic differentiation of dental stem cells?\nContext: {'contexts': ['To evaluate whether and how the transcription factor early growth response gene 1 (EGR1) affects the osteogenic differentiation of dental stem cells.', 'Dental stem cells from apical papilla (SCAPs) and from the dental follicle (DFCs) were transfected with EGR1-specific siRNA or EGR-1 expression plasmid. Gene regulation was verified at protein level by Western blotting. The expression of the transcription factors distal-less homeobox 3 (DLX3), alkaline phosphatase (ALP) and bone morphogenetic protein 2 (BMP2), which are all regulators and markers of the osteogenic differentiation in dental stem cells, was determined by quantitative reverse transcription-polymerase chain reaction (qRT-PCR). To investigate mineralization, SCAP long-term cultures were stained with alizarin red after EGR1 over-expression.', 'EGR1 was induced in SCAPs during osteogenic differentiation. DLX3 and bone morphogenetic protein 2 (BMP2) were up-regulated after EGR1 over-expression and down-regulated after EGR1 depletion. The expression of ALP was also down-regulated after EGR1 depletion. The over-expression of EGR1 in SCAPs promoted mineralization after osteogenic differentiation.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Alkaline Phosphatase', 'Blotting, Western', 'Bone Morphogenetic Protein 2', 'Cell Differentiation', 'Dental Sac', 'Early Growth Response Protein 1', 'Flow Cytometry', 'Homeodomain Proteins', 'Humans', 'Molar, Third', 'Osteogenesis', 'Reverse Transcriptase Polymerase Chain Reaction', 'Staining and Labeling', 'Stem Cells', 'Transcription Factors', 'Transfection']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,761,217 | Does metronomic oral paclitaxel show anti-tumor effects in an orthotopic mouse model of ovarian cancer? | {
"contexts": [
"The purpose of this study was to compare the in vivo anti-tumor efficacy of a mucoadhesive, lipid-based, oral paclitaxel formulation (DHP107) with traditional, intraperitoneal (IP) paclitaxel using an orthotopic mouse model of chemotherapy-sensitive SKOV3ip1 ovarian cancer.",
"To determine the optimal therapeutic dose of oral paclitaxel, DHP107 was administered per os to female athymic nude mice at 0, 25, or 50 mg/kg twice per week. Control mice received 100 µL saline once per week. IP injections of paclitaxel at 5 mg/kg once per week were used for comparison. To evaluate the potential therapeutic effect of metronomic DHP107 chemotherapy, mice received DHP107 50 mg/kg once per week per os, which was compared with 25 mg/kg twice per week and with vehicle-treated controls.",
"Low-dose DHP107 (25 mg/kg) twice per week was as effective as IP paclitaxel (5 mg/kg once a week) but high-dose DHP107 (50 mg/kg once per week) was less effective at inhibiting tumor growth in an orthotopic mouse model (88%, 82%, and 36% decrease in tumor weight, respectively). Mice that received 25 mg/kg DHP107 twice per week or 50 mg/kg DHP107 once per week per os had a significant decrease in tumor weight compared with vehicle-treated controls (p<0.01, both doses)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": []
} | Metronomic oral chemotherapy with DHP107 showed anti-tumor efficacy in vivo similar to IP paclitaxel in an orthotopic mouse model. | yes | [
{
"from": "human",
"value": "Question: Does metronomic oral paclitaxel show anti-tumor effects in an orthotopic mouse model of ovarian cancer?\nContext: {'contexts': ['The purpose of this study was to compare the in vivo anti-tumor efficacy of a mucoadhesive, lipid-based, oral paclitaxel formulation (DHP107) with traditional, intraperitoneal (IP) paclitaxel using an orthotopic mouse model of chemotherapy-sensitive SKOV3ip1 ovarian cancer.', 'To determine the optimal therapeutic dose of oral paclitaxel, DHP107 was administered per os to female athymic nude mice at 0, 25, or 50 mg/kg twice per week. Control mice received 100 µL saline once per week. IP injections of paclitaxel at 5 mg/kg once per week were used for comparison. To evaluate the potential therapeutic effect of metronomic DHP107 chemotherapy, mice received DHP107 50 mg/kg once per week per os, which was compared with 25 mg/kg twice per week and with vehicle-treated controls.', 'Low-dose DHP107 (25 mg/kg) twice per week was as effective as IP paclitaxel (5 mg/kg once a week) but high-dose DHP107 (50 mg/kg once per week) was less effective at inhibiting tumor growth in an orthotopic mouse model (88%, 82%, and 36% decrease in tumor weight, respectively). Mice that received 25 mg/kg DHP107 twice per week or 50 mg/kg DHP107 once per week per os had a significant decrease in tumor weight compared with vehicle-treated controls (p<0.01, both doses).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,757,142 | Does activation of spinal NF-κB/p65 contribute to peripheral inflammation and hyperalgesia in rat adjuvant-induced arthritis? | {
"contexts": [
"It is known that noxious stimuli from inflamed tissue may increase the excitability of spinal dorsal horn neurons (a process known as central sensitization), which can signal back and contribute to peripheral inflammation. However, the underlying mechanisms have yet to be fully defined. A number of recent studies have indicated that spinal NF-κB/p65 is involved in central sensitization, as well as pain-related behavior. Thus, the aim of this study was to determine whether NF-κB/p65 can facilitate a peripheral inflammatory response in rat adjuvant-induced arthritis (AIA).",
"Lentiviral vectors encoding short hairpin RNAs that target NF-κB/p65 (LV-shNF-κB/p65) were constructed for gene silencing. The spines of rats with AIA were injected with LV-shNF-κB/p65 on day 3 or day 10 after treatment with Freund's complete adjuvant (CFA). During an observation period of 20 days, pain-related behavior, paw swelling, and joint histopathologic changes were evaluated. Moreover, the expression levels of spinal tumor necrosis factor α (TNFα), interleukin-1β (IL-1β), and cyclooxygenase 2 (COX-2) were assessed on day 14 after CFA treatment.",
"The presence of peripheral inflammation in rats with AIA induced an increase in NF-κB/p65 expression in the spinal cord, mainly in the dorsal horn neurons and astrocytes. Delivery of LV-shNF-κB/p65 to the spinal cord knocked down the expression of NF-κB/p65 and significantly attenuated hyperalgesia, paw edema, and joint destruction. In addition, spinal delivery of LV-shNF-κB/p65 reduced the overexpression of spinal TNFα, IL-1β, and COX-2."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Arthritis, Experimental",
"Cyclooxygenase 2",
"Hyperalgesia",
"Inflammation",
"Interleukin-1beta",
"Male",
"NF-kappa B",
"Rats",
"Spinal Cord",
"Tumor Necrosis Factor-alpha"
]
} | These findings indicate that spinal NF-κB/p65 plays an important role in the initiation and development of both peripheral inflammation and hyperalgesia. Thus, inhibition of spinal NF-κB/p65 expression may provide a potential treatment to manage painful inflammatory disorders. | yes | [
{
"from": "human",
"value": "Question: Does activation of spinal NF-κB/p65 contribute to peripheral inflammation and hyperalgesia in rat adjuvant-induced arthritis?\nContext: {'contexts': ['It is known that noxious stimuli from inflamed tissue may increase the excitability of spinal dorsal horn neurons (a process known as central sensitization), which can signal back and contribute to peripheral inflammation. However, the underlying mechanisms have yet to be fully defined. A number of recent studies have indicated that spinal NF-κB/p65 is involved in central sensitization, as well as pain-related behavior. Thus, the aim of this study was to determine whether NF-κB/p65 can facilitate a peripheral inflammatory response in rat adjuvant-induced arthritis (AIA).', \"Lentiviral vectors encoding short hairpin RNAs that target NF-κB/p65 (LV-shNF-κB/p65) were constructed for gene silencing. The spines of rats with AIA were injected with LV-shNF-κB/p65 on day 3 or day 10 after treatment with Freund's complete adjuvant (CFA). During an observation period of 20 days, pain-related behavior, paw swelling, and joint histopathologic changes were evaluated. Moreover, the expression levels of spinal tumor necrosis factor α (TNFα), interleukin-1β (IL-1β), and cyclooxygenase 2 (COX-2) were assessed on day 14 after CFA treatment.\", 'The presence of peripheral inflammation in rats with AIA induced an increase in NF-κB/p65 expression in the spinal cord, mainly in the dorsal horn neurons and astrocytes. Delivery of LV-shNF-κB/p65 to the spinal cord knocked down the expression of NF-κB/p65 and significantly attenuated hyperalgesia, paw edema, and joint destruction. In addition, spinal delivery of LV-shNF-κB/p65 reduced the overexpression of spinal TNFα, IL-1β, and COX-2.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Arthritis, Experimental', 'Cyclooxygenase 2', 'Hyperalgesia', 'Inflammation', 'Interleukin-1beta', 'Male', 'NF-kappa B', 'Rats', 'Spinal Cord', 'Tumor Necrosis Factor-alpha']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,757,143 | Is endogenous myeloperoxidase a mediator of joint inflammation and damage in experimental arthritis? | {
"contexts": [
"Myeloperoxidase (MPO) is implicated as a local mediator of tissue damage when released extracellularly in many chronic inflammatory diseases. The purpose of this study was to explore the role of endogenous MPO in experimental rheumatoid arthritis (RA).",
"K/BxN serum-transfer arthritis was induced in C57BL/6 wild-type (WT) and MPO knockout (MPO(-/-) ) mice, and disease development was assessed. MPO activity was measured in joint tissues from mice with or without K/BxN arthritis. Collagen-induced arthritis (CIA) was induced in WT and MPO(-/-) mice, and disease development and immune responses were examined. MPO expression was assessed in synovial biopsy samples from patients with active RA, and the effect of MPO on synovial fibroblasts was tested in vitro.",
"MPO was up-regulated in the joints of mice with K/BxN arthritis, and MPO deficiency attenuated the severity of the disease without affecting circulating cytokine levels. In CIA, MPO(-/-) mice had enhanced CD4+ T cell responses and reduced frequency of regulatory T cells in the lymph nodes and spleen, as well as augmented interleukin-17A and diminished interferon-γ secretion by collagen-stimulated splenocytes, without an effect on circulating anticollagen antibody levels. Despite enhanced adaptive immunity in secondary lymphoid organs, CIA development was attenuated in MPO(-/-) mice. Intracellular and extracellular MPO was detected in the synovium of patients with active RA, and human MPO enhanced the proliferation and decreased the apoptosis of synovial fibroblasts in vitro."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Arthritis, Experimental",
"Arthritis, Rheumatoid",
"Disease Progression",
"Inflammation",
"Joints",
"Male",
"Mice",
"Mice, Inbred C57BL",
"Mice, Knockout",
"Peroxidase",
"Synovial Membrane"
]
} | MPO contributes to the development of arthritis despite suppressing adaptive immunity in secondary lymphoid organs. This suggests distinct effects of local MPO on arthritogenic effector responses. | yes | [
{
"from": "human",
"value": "Question: Is endogenous myeloperoxidase a mediator of joint inflammation and damage in experimental arthritis?\nContext: {'contexts': ['Myeloperoxidase (MPO) is implicated as a local mediator of tissue damage when released extracellularly in many chronic inflammatory diseases. The purpose of this study was to explore the role of endogenous MPO in experimental rheumatoid arthritis (RA).', 'K/BxN serum-transfer arthritis was induced in C57BL/6 wild-type (WT) and MPO knockout (MPO(-/-) ) mice, and disease development was assessed. MPO activity was measured in joint tissues from mice with or without K/BxN arthritis. Collagen-induced arthritis (CIA) was induced in WT and MPO(-/-) mice, and disease development and immune responses were examined. MPO expression was assessed in synovial biopsy samples from patients with active RA, and the effect of MPO on synovial fibroblasts was tested in vitro.', 'MPO was up-regulated in the joints of mice with K/BxN arthritis, and MPO deficiency attenuated the severity of the disease without affecting circulating cytokine levels. In CIA, MPO(-/-) mice had enhanced CD4+ T cell responses and reduced frequency of regulatory T cells in the lymph nodes and spleen, as well as augmented interleukin-17A and diminished interferon-γ secretion by collagen-stimulated splenocytes, without an effect on circulating anticollagen antibody levels. Despite enhanced adaptive immunity in secondary lymphoid organs, CIA development was attenuated in MPO(-/-) mice. Intracellular and extracellular MPO was detected in the synovium of patients with active RA, and human MPO enhanced the proliferation and decreased the apoptosis of synovial fibroblasts in vitro.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Arthritis, Experimental', 'Arthritis, Rheumatoid', 'Disease Progression', 'Inflammation', 'Joints', 'Male', 'Mice', 'Mice, Inbred C57BL', 'Mice, Knockout', 'Peroxidase', 'Synovial Membrane']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,757,140 | Does rebamipide suppress collagen-induced arthritis through reciprocal regulation of th17/treg cell differentiation and heme oxygenase 1 induction? | {
"contexts": [
"Rebamipide, a gastroprotective agent, has the ability to scavenge reactive oxygen radicals. Increased oxidative stress is implicated in the pathogenesis of rheumatoid arthritis (RA). We undertook this study to investigate the impact of rebamipide on the development of arthritis and the pathophysiologic mechanisms by which rebamipide attenuates arthritis severity in a murine model of RA.",
"Collagen-induced arthritis (CIA) was induced in DBA/1J mice. Anti-type II collagen antibody titers and interleukin-17 (IL-17) levels were determined using enzyme-linked immunosorbent assay. The expression of transcription factors was analyzed by immunostaining and Western blotting. Frequencies of IL-17-producing CD4+ T cells (Th17 cells) and CD4+CD25+FoxP3+ Treg cells were analyzed by flow cytometry.",
"Rebamipide reduced the clinical arthritis score and severity of histologic inflammation and cartilage destruction in a dose-dependent manner. The joints isolated from rebamipide-treated mice with CIA showed decreased expression of nitrotyrosine, an oxidative stress marker. Rebamipide-treated mice showed lower circulating levels of type II collagen-specific IgG, IgG1, and IgG2a. Whereas the number of Th17 cells in spleens was decreased in rebamipide-treated mice with CIA, a significant increase in the number of Treg cells in spleens was observed. In vitro, rebamipide inhibited Th17 cell differentiation through STAT-3/retinoic acid receptor-related orphan nuclear receptor γt and reciprocally induced Treg cell differentiation through FoxP3. Rebamipide increased Nrf2 nuclear activities in murine CD4+ T cells and LBRM-33 murine T lymphoma cells. Heme oxygenase 1 (HO-1) expression in the spleens was markedly increased in rebamipide-treated mice."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Alanine",
"Animals",
"Antirheumatic Agents",
"Arthritis, Experimental",
"Autoantibodies",
"Cell Differentiation",
"Cytokines",
"Heme Oxygenase-1",
"Male",
"Mice",
"Mice, Inbred DBA",
"Quinolones",
"T-Lymphocytes, Regulatory",
"Th17 Cells"
]
} | The inhibitory effects of rebamipide on joint inflammation are associated with recovery from an imbalance between Th17 cells and Treg cells and with activation of an Nrf2/HO-1 antioxidant pathway. | yes | [
{
"from": "human",
"value": "Question: Does rebamipide suppress collagen-induced arthritis through reciprocal regulation of th17/treg cell differentiation and heme oxygenase 1 induction?\nContext: {'contexts': ['Rebamipide, a gastroprotective agent, has the ability to scavenge reactive oxygen radicals. Increased oxidative stress is implicated in the pathogenesis of rheumatoid arthritis (RA). We undertook this study to investigate the impact of rebamipide on the development of arthritis and the pathophysiologic mechanisms by which rebamipide attenuates arthritis severity in a murine model of RA.', 'Collagen-induced arthritis (CIA) was induced in DBA/1J mice. Anti-type II collagen antibody titers and interleukin-17 (IL-17) levels were determined using enzyme-linked immunosorbent assay. The expression of transcription factors was analyzed by immunostaining and Western blotting. Frequencies of IL-17-producing CD4+ T cells (Th17 cells) and CD4+CD25+FoxP3+ Treg cells were analyzed by flow cytometry.', 'Rebamipide reduced the clinical arthritis score and severity of histologic inflammation and cartilage destruction in a dose-dependent manner. The joints isolated from rebamipide-treated mice with CIA showed decreased expression of nitrotyrosine, an oxidative stress marker. Rebamipide-treated mice showed lower circulating levels of type II collagen-specific IgG, IgG1, and IgG2a. Whereas the number of Th17 cells in spleens was decreased in rebamipide-treated mice with CIA, a significant increase in the number of Treg cells in spleens was observed. In vitro, rebamipide inhibited Th17 cell differentiation through STAT-3/retinoic acid receptor-related orphan nuclear receptor γt and reciprocally induced Treg cell differentiation through FoxP3. Rebamipide increased Nrf2 nuclear activities in murine CD4+ T cells and LBRM-33 murine T lymphoma cells. Heme oxygenase 1 (HO-1) expression in the spleens was markedly increased in rebamipide-treated mice.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Alanine', 'Animals', 'Antirheumatic Agents', 'Arthritis, Experimental', 'Autoantibodies', 'Cell Differentiation', 'Cytokines', 'Heme Oxygenase-1', 'Male', 'Mice', 'Mice, Inbred DBA', 'Quinolones', 'T-Lymphocytes, Regulatory', 'Th17 Cells']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,757,148 | Does long noncoding RNA related to cartilage injury promote chondrocyte extracellular matrix degradation in osteoarthritis? | {
"contexts": [
"Long noncoding RNAs (lncRNAs) play crucial regulatory roles in diverse biologic processes, but knowledge of lncRNAs in osteoarthritis (OA) is limited. The aim of this study was to identify lncRNA expression in articular cartilage and to explore the function of cartilage injury-related lncRNAs (lncRNA-CIR) in OA.",
"To identify lncRNAs specifically expressed in OA cartilage, we compared the expression of lncRNAs in OA cartilage with that in normal cartilage using microarray and quantitative polymerase chain reaction (qPCR) analyses. In OA cartilage, lncRNA-CIR was specifically, differentially, and highly expressed. The function of lncRNA-CIR was determined by silencing and overexpression in vitro. Extracellular matrix (ECM)-related molecules were detected by qPCR, Western blot, and immunofluorescence analyses.",
"Up to 152 lncRNAs were found to be differentially expressed (>8-fold) in OA and normal cartilage (82 lncRNAs more highly expressed and 70 less highly expressed in OA cartilage than in normal cartilage). A specific differentially expressed lncRNA-CIR was selected according to the results of the higher expression in OA cartilage and OA chondrocytes. The expression of lncRNA-CIR increased in chondrocytes with in vitro treatment with interleukin-1β and tumor necrosis factor α. Silencing of lncRNA-CIR by small interfering RNA promoted the formation of collagen and aggrecan and reduced the expression of matrix-degrading enzymes, such as MMP13 and ADAMTS5. The expression of collagen and aggrecan was reduced, whereas the expression of matrix-degrading enzymes was increased, after overexpression of lncRNA-CIR."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Cartilage, Articular",
"Chondrocytes",
"Extracellular Matrix",
"Female",
"Gene Expression Regulation",
"Humans",
"Interleukin-1beta",
"Male",
"Middle Aged",
"Osteoarthritis, Knee",
"RNA, Long Noncoding",
"Tumor Necrosis Factor-alpha"
]
} | The results indicate that lncRNA-CIR contributes to ECM degradation and plays a key role in the pathogenesis of OA. We propose that lncRNA-CIR could be used as a potential target in OA therapy. | yes | [
{
"from": "human",
"value": "Question: Does long noncoding RNA related to cartilage injury promote chondrocyte extracellular matrix degradation in osteoarthritis?\nContext: {'contexts': ['Long noncoding RNAs (lncRNAs) play crucial regulatory roles in diverse biologic processes, but knowledge of lncRNAs in osteoarthritis (OA) is limited. The aim of this study was to identify lncRNA expression in articular cartilage and to explore the function of cartilage injury-related lncRNAs (lncRNA-CIR) in OA.', 'To identify lncRNAs specifically expressed in OA cartilage, we compared the expression of lncRNAs in OA cartilage with that in normal cartilage using microarray and quantitative polymerase chain reaction (qPCR) analyses. In OA cartilage, lncRNA-CIR was specifically, differentially, and highly expressed. The function of lncRNA-CIR was determined by silencing and overexpression in vitro. Extracellular matrix (ECM)-related molecules were detected by qPCR, Western blot, and immunofluorescence analyses.', 'Up to 152 lncRNAs were found to be differentially expressed (>8-fold) in OA and normal cartilage (82 lncRNAs more highly expressed and 70 less highly expressed in OA cartilage than in normal cartilage). A specific differentially expressed lncRNA-CIR was selected according to the results of the higher expression in OA cartilage and OA chondrocytes. The expression of lncRNA-CIR increased in chondrocytes with in vitro treatment with interleukin-1β and tumor necrosis factor α. Silencing of lncRNA-CIR by small interfering RNA promoted the formation of collagen and aggrecan and reduced the expression of matrix-degrading enzymes, such as MMP13 and ADAMTS5. The expression of collagen and aggrecan was reduced, whereas the expression of matrix-degrading enzymes was increased, after overexpression of lncRNA-CIR.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Cartilage, Articular', 'Chondrocytes', 'Extracellular Matrix', 'Female', 'Gene Expression Regulation', 'Humans', 'Interleukin-1beta', 'Male', 'Middle Aged', 'Osteoarthritis, Knee', 'RNA, Long Noncoding', 'Tumor Necrosis Factor-alpha']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,750,691 | Does hIV Tat protein affect circadian rhythmicity by interfering with the circadian system? | {
"contexts": [
"Sleep disorders are common in patients with HIV/AIDS, and can lead to poor quality of life. Although many studies have investigated the aetiology of these disorders, it is still unclear whether impaired sleep quality is associated with HIV itself, social problems, or side effects of antiretroviral therapy (ART). Moreover, despite its known neurological associations, little is known about the role of the trans-activator of transcription (Tat) protein in sleep disorders in patients with HIV/AIDS. The purpose of this study was to test the hypothesis that the sleep quality of patients with HIV/AIDS affected by an altered circadian rhythm correlates with cerebrospinal HIV Tat protein concentration.",
"Ninety-six patients with HIV/AIDS between 20 and 69 years old completed the Pittsburgh Sleep Quality Index. Their circadian rhythm parameters of blood pressure, Tat concentration in cerebrospinal fluid, melatonin concentration, CD4 cell count and HIV RNA viral load in serum were measured.",
"The circadian amplitude of systolic blood pressure and the score for sleep quality (Pittsburgh Sleep Quality Index) were negatively correlated with HIV Tat protein concentration, while the melatonin value was positively correlated with Tat protein concentration."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Biomarkers",
"Blood Pressure",
"Circadian Rhythm",
"Female",
"HIV Infections",
"Heart Rate",
"Humans",
"Male",
"Melatonin",
"Pineal Gland",
"Quality of Life",
"Sleep Wake Disorders",
"Viral Load",
"tat Gene Products, Human Immunodeficiency Virus"
]
} | The HIV Tat protein affects circadian rhythmicity by interfering with the circadian system in patients with HIV/AIDS and further increases the melatonin excretion value. A Tat protein-related high melatonin value may counteract HIV-related poor sleep quality during the progression of HIV infection. This study provides the first clinical evidence offering an explanation for why sleep quality did not show an association with progression of HIV infection in previous studies. | yes | [
{
"from": "human",
"value": "Question: Does hIV Tat protein affect circadian rhythmicity by interfering with the circadian system?\nContext: {'contexts': ['Sleep disorders are common in patients with HIV/AIDS, and can lead to poor quality of life. Although many studies have investigated the aetiology of these disorders, it is still unclear whether impaired sleep quality is associated with HIV itself, social problems, or side effects of antiretroviral therapy (ART). Moreover, despite its known neurological associations, little is known about the role of the trans-activator of transcription (Tat) protein in sleep disorders in patients with HIV/AIDS. The purpose of this study was to test the hypothesis that the sleep quality of patients with HIV/AIDS affected by an altered circadian rhythm correlates with cerebrospinal HIV Tat protein concentration.', 'Ninety-six patients with HIV/AIDS between 20 and 69 years old completed the Pittsburgh Sleep Quality Index. Their circadian rhythm parameters of blood pressure, Tat concentration in cerebrospinal fluid, melatonin concentration, CD4 cell count and HIV RNA viral load in serum were measured.', 'The circadian amplitude of systolic blood pressure and the score for sleep quality (Pittsburgh Sleep Quality Index) were negatively correlated with HIV Tat protein concentration, while the melatonin value was positively correlated with Tat protein concentration.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Biomarkers', 'Blood Pressure', 'Circadian Rhythm', 'Female', 'HIV Infections', 'Heart Rate', 'Humans', 'Male', 'Melatonin', 'Pineal Gland', 'Quality of Life', 'Sleep Wake Disorders', 'Viral Load', 'tat Gene Products, Human Immunodeficiency Virus']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,762,453 | Does provider awareness alone improve transition readiness skills in adolescent patients with inflammatory bowel disease? | {
"contexts": [
"Adolescent patients with chronic health conditions must gradually assume responsibility for their health. Self-management skills are needed for a successful transfer from adolescent to adult health care, but the development of these skills could be resource intensive. Pediatric providers are already instrumental in teaching patients about their health and may improve these skills. The aim of the study was to evaluate whether informal education of pediatric providers regarding transition improves inflammatory bowel disease (IBD) patient self-management skills.",
"Consecutive patients with IBD older than 10 years who presented to the outpatient setting were administered a survey regarding self-management behaviors in 2008 and 2011. During this time, several conferences on transition were presented to the providers.",
"In 2008, 294 patients completed the survey (82%) compared with 121 patients (89%) in 2011. The patient groups were comparable with respect to sex (boys 50% vs 42%), mean age (16.7 vs 16.2 years), and type of IBD (Crohn 68% vs 66%). The 13- to 15-year-olds reported calling in refills (11%, 8%, respectively), scheduling clinic appointment (0, 1%), preparing questions (13%, 5%), and taking the main role in talking during clinic visits (15%, 24%). The 16- to 18-year-olds reported calling in refills (13%, 27%), scheduling clinic appointments (9%, 6%), preparing questions (9%, 16%), and taking the main role in talking in clinic visits (36%, 45%). Responsibility for behaviors gradually increases with age, but did not differ significantly between 2008 and 2011."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Awareness",
"Child",
"Data Collection",
"Female",
"Health Behavior",
"Health Knowledge, Attitudes, Practice",
"Health Personnel",
"Humans",
"Inflammatory Bowel Diseases",
"Male",
"Patient Education as Topic",
"Pediatrics",
"Self Care",
"Young Adult"
]
} | Increasing awareness around transition readiness for pediatric providers had an insignificant effect on the self-management skills of patients with IBD. A more formal or structured approach is likely required to improve transition skills in adolescent patients. | no | [
{
"from": "human",
"value": "Question: Does provider awareness alone improve transition readiness skills in adolescent patients with inflammatory bowel disease?\nContext: {'contexts': ['Adolescent patients with chronic health conditions must gradually assume responsibility for their health. Self-management skills are needed for a successful transfer from adolescent to adult health care, but the development of these skills could be resource intensive. Pediatric providers are already instrumental in teaching patients about their health and may improve these skills. The aim of the study was to evaluate whether informal education of pediatric providers regarding transition improves inflammatory bowel disease (IBD) patient self-management skills.', 'Consecutive patients with IBD older than 10 years who presented to the outpatient setting were administered a survey regarding self-management behaviors in 2008 and 2011. During this time, several conferences on transition were presented to the providers.', 'In 2008, 294 patients completed the survey (82%) compared with 121 patients (89%) in 2011. The patient groups were comparable with respect to sex (boys 50% vs 42%), mean age (16.7 vs 16.2 years), and type of IBD (Crohn 68% vs 66%). The 13- to 15-year-olds reported calling in refills (11%, 8%, respectively), scheduling clinic appointment (0, 1%), preparing questions (13%, 5%), and taking the main role in talking during clinic visits (15%, 24%). The 16- to 18-year-olds reported calling in refills (13%, 27%), scheduling clinic appointments (9%, 6%), preparing questions (9%, 16%), and taking the main role in talking in clinic visits (36%, 45%). Responsibility for behaviors gradually increases with age, but did not differ significantly between 2008 and 2011.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Awareness', 'Child', 'Data Collection', 'Female', 'Health Behavior', 'Health Knowledge, Attitudes, Practice', 'Health Personnel', 'Humans', 'Inflammatory Bowel Diseases', 'Male', 'Patient Education as Topic', 'Pediatrics', 'Self Care', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
24,748,758 | Do the effectiveness of four methods for stain removal from direct resin-based composite restorative materials? | {
"contexts": [
"Few studies investigated the best method for removing stains from different types of resin-based composite restorations and compared them to the more recently introduced nanocomposites. This study compared the effect of four methods for stain removal from composite resins; finishing with Sof-lex disks, using pumice and brush, bleaching with 10% carbamide peroxide and 38% hydrogen peroxide.",
"Twenty disk specimens were prepared. Specimens were immersed in a staining solution for 3 weeks. The stained surfaces of five specimens from each RBC material were treated with one of the treatment procedures. Colorimetric measurements were taken using spectrophotometer prior to and after staining, and then repeated after surface treatments. Color difference values were calculated.",
"One-way ANOVA indicated significant differences in color change of the three composite resin materials following staining. Filtek Z250 showed the least susceptibility to discoloration followed by Renamel, Filtek Supreme was the material most prone to discoloration. Two-way ANOVA and Tukey's Post Hoc showed that all stain removing procedures except polishing with pumice, were able to return Filtek Z250 to clinically acceptable color difference. While bleaching with 38% carbamide peroxide was not effective with Renamel. Only pumice and 10% carbamide peroxide were able to return Renamel to clinically acceptable color difference."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": []
} | Compositions of resin-based composite resins play an important role in their susceptibility to stain and their amenability to stain removal procedures. Home bleaching showed good results for the three materials, while office bleach was the least effective. | yes | [
{
"from": "human",
"value": "Question: Do the effectiveness of four methods for stain removal from direct resin-based composite restorative materials?\nContext: {'contexts': ['Few studies investigated the best method for removing stains from different types of resin-based composite restorations and compared them to the more recently introduced nanocomposites. This study compared the effect of four methods for stain removal from composite resins; finishing with Sof-lex disks, using pumice and brush, bleaching with 10% carbamide peroxide and 38% hydrogen peroxide.', 'Twenty disk specimens were prepared. Specimens were immersed in a staining solution for 3\\xa0weeks. The stained surfaces of five specimens from each RBC material were treated with one of the treatment procedures. Colorimetric measurements were taken using spectrophotometer prior to and after staining, and then repeated after surface treatments. Color difference values were calculated.', \"One-way ANOVA indicated significant differences in color change of the three composite resin materials following staining. Filtek Z250 showed the least susceptibility to discoloration followed by Renamel, Filtek Supreme was the material most prone to discoloration. Two-way ANOVA and Tukey's Post Hoc showed that all stain removing procedures except polishing with pumice, were able to return Filtek Z250 to clinically acceptable color difference. While bleaching with 38% carbamide peroxide was not effective with Renamel. Only pumice and 10% carbamide peroxide were able to return Renamel to clinically acceptable color difference.\"], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,761,970 | Is time-domain T-wave alternans strongly associated with a history of ventricular fibrillation in patients with Brugada syndrome? | {
"contexts": [
"T-wave alternans (TWA) is an indicator of vulnerability to ventricular arrhythmias and is useful for predicting sudden cardiac death (SCD) in patients with various structural heart diseases. We evaluated whether high levels of time-domain TWA on ambulatory ECG (AECG) are associated with a history of ventricular fibrillation (VF) in Brugada syndrome (BrS) patients.",
"We examined the associations among VF history, family history of SCD, spontaneous type 1 electrocardiogram (ECG), late potentials, VF induction by programmed electrical stimulation, and TWA in 45 BrS patients (44 males; mean age, 45 ± 15 years). TWA analyzed from 24-h AECG recordings using the modified moving average method was positive in 13 of 43 patients (30%). Patients with a history of VF had a significantly higher incidence of a positive TWA test (82% vs. 13%; P < 0.001) and spontaneous type 1 ECG (92% vs. 38%; P = 0.007) than those without VF history. Multivariate analysis indicated that positive TWA (OR 7.217; 95% CI 2.503-35.504; P = 0.002) and spontaneous type 1 ECG (OR 5.530; 95% CI 1.651-34.337; P = 0.020) were closely associated with VF history. Spontaneous type 1 ECG had high sensitivity (92%) but low specificity (63%). Positive TWA was a reliable marker with high sensitivity and specificity (82% and 88%, respectively)."
],
"labels": [
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Brugada Syndrome",
"Electrocardiography, Ambulatory",
"Female",
"Humans",
"Male",
"Middle Aged",
"Retrospective Studies",
"Ventricular Fibrillation"
]
} | Elevated time-domain TWA on AECG confirms arrhythmia risk in symptomatic BrS patients without the need for provocative stimuli. | yes | [
{
"from": "human",
"value": "Question: Is time-domain T-wave alternans strongly associated with a history of ventricular fibrillation in patients with Brugada syndrome?\nContext: {'contexts': ['T-wave alternans (TWA) is an indicator of vulnerability to ventricular arrhythmias and is useful for predicting sudden cardiac death (SCD) in patients with various structural heart diseases. We evaluated whether high levels of time-domain TWA on ambulatory ECG (AECG) are associated with a history of ventricular fibrillation (VF) in Brugada syndrome (BrS) patients.', 'We examined the associations among VF history, family history of SCD, spontaneous type 1 electrocardiogram (ECG), late potentials, VF induction by programmed electrical stimulation, and TWA in 45 BrS patients (44 males; mean age, 45 ± 15 years). TWA analyzed from 24-h AECG recordings using the modified moving average method was positive in 13 of 43 patients (30%). Patients with a history of VF had a significantly higher incidence of a positive TWA test (82% vs. 13%; P < 0.001) and spontaneous type 1 ECG (92% vs. 38%; P = 0.007) than those without VF history. Multivariate analysis indicated that positive TWA (OR 7.217; 95% CI 2.503-35.504; P = 0.002) and spontaneous type 1 ECG (OR 5.530; 95% CI 1.651-34.337; P = 0.020) were closely associated with VF history. Spontaneous type 1 ECG had high sensitivity (92%) but low specificity (63%). Positive TWA was a reliable marker with high sensitivity and specificity (82% and 88%, respectively).'], 'labels': ['OBJECTIVE', 'RESULTS'], 'meshes': ['Brugada Syndrome', 'Electrocardiography, Ambulatory', 'Female', 'Humans', 'Male', 'Middle Aged', 'Retrospective Studies', 'Ventricular Fibrillation']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,777,651 | Does analytical function for beta and gamma absorbed fractions of iodine-131 in spherical and ellipsoidal volumes? | {
"contexts": [
"The beta and gamma absorbed fractions in organs and tissues are the important key factors of radionuclide internal dosimetry based on Medical Internal Radiation Dose (MIRD) approach.",
"The aim of this study is to find suitable analytical functions for beta and gamma absorbed fractions in spherical and ellipsoidal volumes with a uniform distribution of iodine-131 radionuclide.",
"MCNPX code has been used to calculate the energy absorption from beta and gamma rays of iodine-131 uniformly distributed inside different ellipsoids and spheres, and then the absorbed fractions have been evaluated.",
"We have found the fit parameters of a suitable analytical function for the beta absorbed fraction, depending on a generalized radius for ellipsoid based on the radius of sphere, and a linear fit function for the gamma absorbed fraction."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Beta Particles",
"Computer Simulation",
"Gamma Rays",
"Humans",
"Iodine Radioisotopes",
"Male",
"Monte Carlo Method",
"Phantoms, Imaging",
"Prostate",
"Radiation Dosage",
"Radiometry",
"Radionuclide Imaging",
"Radiopharmaceuticals",
"Thyroid Gland",
"Tissue Distribution"
]
} | The analytical functions that we obtained from fitting process in Monte Carlo data can be used for obtaining the absorbed fractions of iodine-131 beta and gamma rays for any volume of the thyroid lobe. Moreover, our results for the spheres are in good agreement with the results of MIRD and other scientific literatures. | yes | [
{
"from": "human",
"value": "Question: Does analytical function for beta and gamma absorbed fractions of iodine-131 in spherical and ellipsoidal volumes?\nContext: {'contexts': ['The beta and gamma absorbed fractions in organs and tissues are the important key factors of radionuclide internal dosimetry based on Medical Internal Radiation Dose (MIRD) approach.', 'The aim of this study is to find suitable analytical functions for beta and gamma absorbed fractions in spherical and ellipsoidal volumes with a uniform distribution of iodine-131 radionuclide.', 'MCNPX code has been used to calculate the energy absorption from beta and gamma rays of iodine-131 uniformly distributed inside different ellipsoids and spheres, and then the absorbed fractions have been evaluated.', 'We have found the fit parameters of a suitable analytical function for the beta absorbed fraction, depending on a generalized radius for ellipsoid based on the radius of sphere, and a linear fit function for the gamma absorbed fraction.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Beta Particles', 'Computer Simulation', 'Gamma Rays', 'Humans', 'Iodine Radioisotopes', 'Male', 'Monte Carlo Method', 'Phantoms, Imaging', 'Prostate', 'Radiation Dosage', 'Radiometry', 'Radionuclide Imaging', 'Radiopharmaceuticals', 'Thyroid Gland', 'Tissue Distribution']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,770,870 | Do base excision repair defects invoke hypersensitivity to PARP inhibition? | {
"contexts": [
"PARP-1 is important for the recognition of both endogenous and exogenous DNA damage, and binds to DNA strand breaks including intermediates of base excision repair (BER). Once DNA-bound, PARP-1 becomes catalytically activated synthesizing PAR polymers onto itself and other repair factors (PARylation). As a result, BER repair proteins such as XRCC1 and DNA polymerase β (pol β) are more efficiently and rapidly recruited to sites of DNA damage. In the presence of an inhibitor of PARP activity (PARPi), PARP-1 binds to sites of DNA damage, but PARylation is prevented. BER enzyme recruitment is hindered, but binding of PARP-1 to DNA is stabilized, impeding DNA repair and leading to double-strand DNA breaks (DSB). Deficiencies in pol β(-/-) and Xrcc1(-/-) cells resulted in hypersensitivity to the PARP inhibitor 4-AN and reexpression of pol β or XRCC1, in these contexts, reversed the 4-AN hypersensitivity phenotype. BER deficiencies also showed evidence of replication defects that lead to DSB-induced apoptosis upon PARPi treatment. Finally, the clinically relevant PARP inhibitors olaparib and veliparib also exhibited hypersensitivity in both pol β(-/-) and Xrcc1(-/-) BER-deficient cells. These results reveal heightened sensitivity to PARPi as a function of BER deficiency."
],
"labels": [
"UNLABELLED"
],
"meshes": [
"Animals",
"Cell Line",
"DNA",
"DNA Breaks, Double-Stranded",
"DNA Damage",
"DNA Repair",
"DNA-Binding Proteins",
"Enzyme Inhibitors",
"Mice",
"Poly(ADP-ribose) Polymerase Inhibitors",
"Poly(ADP-ribose) Polymerases",
"X-ray Repair Cross Complementing Protein 1"
]
} | BER deficiency represents a new therapeutic opportunity to enhance PARPi efficacy. | yes | [
{
"from": "human",
"value": "Question: Do base excision repair defects invoke hypersensitivity to PARP inhibition?\nContext: {'contexts': ['PARP-1 is important for the recognition of both endogenous and exogenous DNA damage, and binds to DNA strand breaks including intermediates of base excision repair (BER). Once DNA-bound, PARP-1 becomes catalytically activated synthesizing PAR polymers onto itself and other repair factors (PARylation). As a result, BER repair proteins such as XRCC1 and DNA polymerase β (pol β) are more efficiently and rapidly recruited to sites of DNA damage. In the presence of an inhibitor of PARP activity (PARPi), PARP-1 binds to sites of DNA damage, but PARylation is prevented. BER enzyme recruitment is hindered, but binding of PARP-1 to DNA is stabilized, impeding DNA repair and leading to double-strand DNA breaks (DSB). Deficiencies in pol β(-/-) and Xrcc1(-/-) cells resulted in hypersensitivity to the PARP inhibitor 4-AN and reexpression of pol β or XRCC1, in these contexts, reversed the 4-AN hypersensitivity phenotype. BER deficiencies also showed evidence of replication defects that lead to DSB-induced apoptosis upon PARPi treatment. Finally, the clinically relevant PARP inhibitors olaparib and veliparib also exhibited hypersensitivity in both pol β(-/-) and Xrcc1(-/-) BER-deficient cells. These results reveal heightened sensitivity to PARPi as a function of BER deficiency.'], 'labels': ['UNLABELLED'], 'meshes': ['Animals', 'Cell Line', 'DNA', 'DNA Breaks, Double-Stranded', 'DNA Damage', 'DNA Repair', 'DNA-Binding Proteins', 'Enzyme Inhibitors', 'Mice', 'Poly(ADP-ribose) Polymerase Inhibitors', 'Poly(ADP-ribose) Polymerases', 'X-ray Repair Cross Complementing Protein 1']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,766,450 | Are subnormal levels of vitamin D associated with acute wheeze in young children? | {
"contexts": [
"This study evaluated risk factors for acute wheeze in preschool children and investigated whether subnormal levels of vitamin D were associated with increased risk for acute wheeze, atopy or viral/bacterial respiratory infections.",
"We recruited 130 children with acute wheeze, aged 6 months to 4 years, from paediatric emergency departments in Stockholm, Sweden, and 101 age-matched controls with no history of wheeze or sensitisation to airborne allergens. Parents answered standardised questionnaires, and blood samples were analysed for specific IgE to airborne and food allergens and levels of 25 hydroxyvitamin D (25(OH)D). Nasopharyngeal virus samples were collected during the emergency department visit in the group of children with wheeze, and a subset were also tested for bacteria.",
"Vitamin D insufficiency (25(OH)D < 75 nmol/L (30 ng/mL)) was associated with an odds ratio of 2.7 (95% confidence interval 1.1-6.2) for acute wheeze. However, no association was found between vitamin D insufficiency and atopy, presence of virus or bacteria or recurrent infections. Children older than 24 months were particularly at risk of subnormal vitamin D levels, irrespective of wheezing history."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Case-Control Studies",
"Child, Preschool",
"Female",
"Humans",
"Infant",
"Life Style",
"Logistic Models",
"Male",
"Recurrence",
"Respiratory Hypersensitivity",
"Respiratory Sounds",
"Respiratory Tract Infections",
"Vitamin D"
]
} | Our findings support the hypothesis that subnormal levels of vitamin D are associated with acute wheeze in young children. | yes | [
{
"from": "human",
"value": "Question: Are subnormal levels of vitamin D associated with acute wheeze in young children?\nContext: {'contexts': ['This study evaluated risk factors for acute wheeze in preschool children and investigated whether subnormal levels of vitamin D were associated with increased risk for acute wheeze, atopy or viral/bacterial respiratory infections.', 'We recruited 130 children with acute wheeze, aged 6\\xa0months to 4\\xa0years, from paediatric emergency departments in Stockholm, Sweden, and 101 age-matched controls with no history of wheeze or sensitisation to airborne allergens. Parents answered standardised questionnaires, and blood samples were analysed for specific IgE to airborne and food allergens and levels of 25 hydroxyvitamin D (25(OH)D). Nasopharyngeal virus samples were collected during the emergency department visit in the group of children with wheeze, and a subset were also tested for bacteria.', 'Vitamin D insufficiency (25(OH)D\\xa0<\\xa075\\xa0nmol/L (30\\xa0ng/mL)) was associated with an odds ratio of 2.7 (95% confidence interval 1.1-6.2) for acute wheeze. However, no association was found between vitamin D insufficiency and atopy, presence of virus or bacteria or recurrent infections. Children older than 24\\xa0months were particularly at risk of subnormal vitamin D levels, irrespective of wheezing history.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Case-Control Studies', 'Child, Preschool', 'Female', 'Humans', 'Infant', 'Life Style', 'Logistic Models', 'Male', 'Recurrence', 'Respiratory Hypersensitivity', 'Respiratory Sounds', 'Respiratory Tract Infections', 'Vitamin D']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,746,942 | Is the systemic exposure to inhaled beclometasone/formoterol pMDI with valved holding chamber independent of age and body size? | {
"contexts": [
"Asthma guidelines recommend prescription of inhaled corticosteroids at a reduced dosage in children compared to older patients in order to minimize the systemic exposure and risk of unwanted side effects. In children, pressurized metered dose inhalers (pMDI) are recommended in combination with a valved holding chamber (VHC) to overcome the problem of coordinating inhalation with actuation. However, the influence of age and body size on the systemic exposure of drugs to be administered via a pMDI with VHC is still not fully elucidated. Therefore, we aimed to compare the systemic exposure to the active ingredients of a fixed combination of beclometasone-dipropionate/formoterol-fumarate administered via pMDI with VHC in children, adolescents and adults.",
"The pharmacokinetics of formoterol and beclometasone-17-monopropionate (active metabolite of beclometasone-dipropionate) was evaluated over 8 h from three studies, each performed in a different age and body size group. Children (7-11 years, n = 20), adolescents (12-17 years, n = 29) and adults (≥18 years, n = 24) received a single dose of beclometasone/formoterol (children: 200 μg/24 μg, adolescents and adults: 400 μg/24 μg) via pMDI with AeroChamber Plus™.",
"The systemic exposure in children in comparison to adolescents was equivalent for formoterol while it was halved for beclometasone-17-monopropionate in accordance with the halved dose of beclometasone administered in children (90% CIs within 0.8-1.25 for formoterol and 0.4-0.625 for beclometasone-17-monopropionate). The systemic exposure to beclometasone-17-monopropionate and formoterol was equivalent between adolescents and adults."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Administration, Inhalation",
"Adolescent",
"Adult",
"Age Factors",
"Aged",
"Anti-Asthmatic Agents",
"Asthma",
"Beclomethasone",
"Child",
"Dose-Response Relationship, Drug",
"Drug Combinations",
"Ethanolamines",
"Female",
"Formoterol Fumarate",
"Humans",
"Male",
"Metered Dose Inhalers",
"Middle Aged",
"Young Adult"
]
} | The systemic exposure to the active ingredients of a fixed dose combination of beclometasone/formoterol administered via pMDI with AeroChamber Plus™ correlates with the nominal dose independently of patient age and body size. Thus, dose reduction in relation to age when using a pMDI with VHC may be unnecessary for reducing the systemic exposure in children. | yes | [
{
"from": "human",
"value": "Question: Is the systemic exposure to inhaled beclometasone/formoterol pMDI with valved holding chamber independent of age and body size?\nContext: {'contexts': ['Asthma guidelines recommend prescription of inhaled corticosteroids at a reduced dosage in children compared to older patients in order to minimize the systemic exposure and risk of unwanted side effects. In children, pressurized metered dose inhalers (pMDI) are recommended in combination with a valved holding chamber (VHC) to overcome the problem of coordinating inhalation with actuation. However, the influence of age and body size on the systemic exposure of drugs to be administered via a pMDI with VHC is still not fully elucidated. Therefore, we aimed to compare the systemic exposure to the active ingredients of a fixed combination of beclometasone-dipropionate/formoterol-fumarate administered via pMDI with VHC in children, adolescents and adults.', 'The pharmacokinetics of formoterol and beclometasone-17-monopropionate (active metabolite of beclometasone-dipropionate) was evaluated over 8\\xa0h from three studies, each performed in a different age and body size group. Children (7-11 years, n\\xa0=\\xa020), adolescents (12-17 years, n\\xa0=\\xa029) and adults (≥18 years, n\\xa0=\\xa024) received a single dose of beclometasone/formoterol (children: 200\\xa0μg/24\\xa0μg, adolescents and adults: 400\\xa0μg/24\\xa0μg) via pMDI with AeroChamber Plus™.', 'The systemic exposure in children in comparison to adolescents was equivalent for formoterol while it was halved for beclometasone-17-monopropionate in accordance with the halved dose of beclometasone administered in children (90% CIs within 0.8-1.25 for formoterol and 0.4-0.625 for beclometasone-17-monopropionate). The systemic exposure to beclometasone-17-monopropionate and formoterol was equivalent between adolescents and adults.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Administration, Inhalation', 'Adolescent', 'Adult', 'Age Factors', 'Aged', 'Anti-Asthmatic Agents', 'Asthma', 'Beclomethasone', 'Child', 'Dose-Response Relationship, Drug', 'Drug Combinations', 'Ethanolamines', 'Female', 'Formoterol Fumarate', 'Humans', 'Male', 'Metered Dose Inhalers', 'Middle Aged', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,763,207 | Is active Transportation to and on Campus Associated With Objectively Measured Fitness Outcomes Among College Students? | {
"contexts": [
"Active transportation (AT) has been associated with positive health outcomes, yet limited research has addressed this with college students, a population at-risk for inactivity. The purpose of this study was to examine the relationship between AT behavior and objectively measured fitness outcomes.",
"A volunteer, convenience sample (n = 299) of college students from a large northeastern university completed a survey about their AT habits to and on campus and psychosocial constructs related to AT and participated in a laboratory-based fitness assessment (cardiovascular endurance, muscular strength and endurance, flexibility, body composition).Off-campus students were dichotomized as nonactive (0-1 AT trips/day) or active travelers (> 1 AT trips/day) to campus; t-tests compared nonactive and active travelers for psychosocial and fitness variables.",
"Students were 56.3% male, 79.2% non-Hispanic White, and primarily living off-campus (87%). Most students (n = 177, 59.2%) reported active travel between classes. Off-campus students were primarily active travelers (76.1%). Active travelers to campus had greater cardiovascular fitness (P = .005), were more flexible (P = .006) and had lower systolic blood pressure (P = .05) compared with nonactive travelers."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Automobile Driving",
"Bicycling",
"Body Composition",
"Cardiovascular Physiological Phenomena",
"Cardiovascular System",
"Data Collection",
"Female",
"Health Behavior",
"Humans",
"Male",
"Motor Vehicles",
"Physical Fitness",
"Students",
"Universities",
"Walking",
"Young Adult"
]
} | This study documents a relationship between AT behavior and objectively measured fitness among college students and provides a rationale for targeting this behavior as a method for improving health outcomes. | yes | [
{
"from": "human",
"value": "Question: Is active Transportation to and on Campus Associated With Objectively Measured Fitness Outcomes Among College Students?\nContext: {'contexts': ['Active transportation (AT) has been associated with positive health outcomes, yet limited research has addressed this with college students, a population at-risk for inactivity. The purpose of this study was to examine the relationship between AT behavior and objectively measured fitness outcomes.', 'A volunteer, convenience sample (n = 299) of college students from a large northeastern university completed a survey about their AT habits to and on campus and psychosocial constructs related to AT and participated in a laboratory-based fitness assessment (cardiovascular endurance, muscular strength and endurance, flexibility, body composition).Off-campus students were dichotomized as nonactive (0-1 AT trips/day) or active travelers (> 1 AT trips/day) to campus; t-tests compared nonactive and active travelers for psychosocial and fitness variables.', 'Students were 56.3% male, 79.2% non-Hispanic White, and primarily living off-campus (87%). Most students (n = 177, 59.2%) reported active travel between classes. Off-campus students were primarily active travelers (76.1%). Active travelers to campus had greater cardiovascular fitness (P = .005), were more flexible (P = .006) and had lower systolic blood pressure (P = .05) compared with nonactive travelers.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Automobile Driving', 'Bicycling', 'Body Composition', 'Cardiovascular Physiological Phenomena', 'Cardiovascular System', 'Data Collection', 'Female', 'Health Behavior', 'Humans', 'Male', 'Motor Vehicles', 'Physical Fitness', 'Students', 'Universities', 'Walking', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,773,920 | Do pseudomonas aeruginosa clinical and environmental isolates constitute a single population with high phenotypic diversity? | {
"contexts": [
"Pseudomonas aeruginosa is an opportunistic pathogen with a high incidence of hospital infections that represents a threat to immune compromised patients. Genomic studies have shown that, in contrast to other pathogenic bacteria, clinical and environmental isolates do not show particular genomic differences. In addition, genetic variability of all the P. aeruginosa strains whose genomes have been sequenced is extremely low. This low genomic variability might be explained if clinical strains constitute a subpopulation of this bacterial species present in environments that are close to human populations, which preferentially produce virulence associated traits.",
"In this work, we sequenced the genomes and performed phenotypic descriptions for four non-human P. aeruginosa isolates collected from a plant, the ocean, a water-spring, and from dolphin stomach. We show that the four strains are phenotypically diverse and that this is not reflected in genomic variability, since their genomes are almost identical. Furthermore, we performed a detailed comparative genomic analysis of the four strains studied in this work with the thirteen previously reported P. aeruginosa genomes by means of describing their core and pan-genomes."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Genome, Bacterial",
"Molecular Sequence Data",
"Phenotype",
"Pseudomonas aeruginosa",
"Virulence"
]
} | Contrary to what has been described for other bacteria we have found that the P. aeruginosa core genome is constituted by a high proportion of genes and that its pan-genome is thus relatively small. Considering the high degree of genomic conservation between isolates of P. aeruginosa from diverse environments, including human tissues, some implications for the treatment of infections are discussed. This work also represents a methodological contribution for the genomic study of P. aeruginosa, since we provide a database of the comparison of all the proteins encoded by the seventeen strains analyzed. | yes | [
{
"from": "human",
"value": "Question: Do pseudomonas aeruginosa clinical and environmental isolates constitute a single population with high phenotypic diversity?\nContext: {'contexts': ['Pseudomonas aeruginosa is an opportunistic pathogen with a high incidence of hospital infections that represents a threat to immune compromised patients. Genomic studies have shown that, in contrast to other pathogenic bacteria, clinical and environmental isolates do not show particular genomic differences. In addition, genetic variability of all the P. aeruginosa strains whose genomes have been sequenced is extremely low. This low genomic variability might be explained if clinical strains constitute a subpopulation of this bacterial species present in environments that are close to human populations, which preferentially produce virulence associated traits.', 'In this work, we sequenced the genomes and performed phenotypic descriptions for four non-human P. aeruginosa isolates collected from a plant, the ocean, a water-spring, and from dolphin stomach. We show that the four strains are phenotypically diverse and that this is not reflected in genomic variability, since their genomes are almost identical. Furthermore, we performed a detailed comparative genomic analysis of the four strains studied in this work with the thirteen previously reported P. aeruginosa genomes by means of describing their core and pan-genomes.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Genome, Bacterial', 'Molecular Sequence Data', 'Phenotype', 'Pseudomonas aeruginosa', 'Virulence']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,764,060 | Are gene-rich large deletions overrepresented in POAG patients of Indian and Caucasian origins? | {
"contexts": [
"Large copy number variations (CNV) can contribute to increased burden for neurodegenerative diseases. In this study, we analyzed the genome-wide burden of large CNVs > 100 kb in primary open angle glaucoma (POAG), a neurodegenerative disease of the eye that is the largest cause of irreversible blindness.",
"Genome-wide analysis of CNVs > 100 kb were analyzed in a total of 1720 individuals, including an Indian cohort (347 POAG cases and 345 controls) and a Caucasian cohort (624 cases and 404 controls). All the CNV data were obtained from experiments performed on Illumina 660W-Quad (infinium) arrays.",
"We observed that for both the populations CNVs > 1 Mb was significantly enriched for gene-rich regions unique to the POAG cases (P < 10(-11)). In the Indian cohort CNVs > 1 Mb (39 calls) in patients influenced 125 genes while in controls 31 such CNVs influenced only 5 genes with no overlap. In both cohorts we observed 1.9-fold gene enrichment in patients for deletions compared to duplications, while such a bias was not observed in controls (0.3-fold). Overall duplications > 1 Mb were more than deletions (Del/Dup = 0.82) confirming that the enrichment of gene-rich deletions in patients was associated with the disease. Of the 39 CNVs > 1 Mb from Indian patients, 28 (72%) also were implicated in other neurodegenerative disorders, like autism, schizophrenia, sensorineural hearing loss, and so forth. We found one large duplication encompassing CNTN4 gene in Indian and Caucasian POAG patients that was absent in the controls."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Contactins",
"DNA",
"DNA Copy Number Variations",
"Ethnic Groups",
"European Continental Ancestry Group",
"Female",
"Gene Deletion",
"Gene Duplication",
"Genetic Variation",
"Genome-Wide Association Study",
"Genotype",
"Glaucoma, Open-Angle",
"Humans",
"India",
"Male",
"Middle Aged"
]
} | To our knowledge, our study is the first report on large CNV bias for gene-rich regions in glaucomatous neurodegeneration, implicating its impact across populations of contrasting ethnicities. We identified CNTN4 as a novel candidate gene for POAG. | yes | [
{
"from": "human",
"value": "Question: Are gene-rich large deletions overrepresented in POAG patients of Indian and Caucasian origins?\nContext: {'contexts': ['Large copy number variations (CNV) can contribute to increased burden for neurodegenerative diseases. In this study, we analyzed the genome-wide burden of large CNVs > 100 kb in primary open angle glaucoma (POAG), a neurodegenerative disease of the eye that is the largest cause of irreversible blindness.', 'Genome-wide analysis of CNVs > 100 kb were analyzed in a total of 1720 individuals, including an Indian cohort (347 POAG cases and 345 controls) and a Caucasian cohort (624 cases and 404 controls). All the CNV data were obtained from experiments performed on Illumina 660W-Quad (infinium) arrays.', 'We observed that for both the populations CNVs > 1 Mb was significantly enriched for gene-rich regions unique to the POAG cases (P < 10(-11)). In the Indian cohort CNVs > 1 Mb (39 calls) in patients influenced 125 genes while in controls 31 such CNVs influenced only 5 genes with no overlap. In both cohorts we observed 1.9-fold gene enrichment in patients for deletions compared to duplications, while such a bias was not observed in controls (0.3-fold). Overall duplications > 1 Mb were more than deletions (Del/Dup = 0.82) confirming that the enrichment of gene-rich deletions in patients was associated with the disease. Of the 39 CNVs > 1 Mb from Indian patients, 28 (72%) also were implicated in other neurodegenerative disorders, like autism, schizophrenia, sensorineural hearing loss, and so forth. We found one large duplication encompassing CNTN4 gene in Indian and Caucasian POAG patients that was absent in the controls.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Contactins', 'DNA', 'DNA Copy Number Variations', 'Ethnic Groups', 'European Continental Ancestry Group', 'Female', 'Gene Deletion', 'Gene Duplication', 'Genetic Variation', 'Genome-Wide Association Study', 'Genotype', 'Glaucoma, Open-Angle', 'Humans', 'India', 'Male', 'Middle Aged']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,767,520 | Do ulcerative and nonulcerative forms of bladder pain syndrome/interstitial cystitis differ in symptom intensity or response to onabotulinum toxin A? | {
"contexts": [
"To determine whether intratrigonal Onabotulinum toxin A (OnabotA) injection produces a different symptomatic outcome and duration of effect on ulcerative (Ulc) and nonulcerative (NUlc) bladder pain syndrome/interstitial cystitis (BPS/IC) patients and to compare the urinary levels of neurotrophines (NGF, BDNF, and GDNF) in response to OnabotA.",
"Ten Ulc and 14 NUlc bladder pain syndrome/interstitial cystitis patients were included in this study. OnabotA (100 U) was injected in 10 trigonal sites, each receiving 10 U in 1 mL of saline. Outcome measures included pain visual analog scale (0-10), a 3-day voiding chart, O'Leary-Sant Score (OSS), and quality of life (QoL) from International Prostate Symptoms Score assessed before treatment, 1 month after injection, and every 3 months afterwards. Urinary NGF, BDNF, and GDNF were accessed using ELISA, at same time points. Treatment duration was determined at the time patients requested another injection.",
"Patients had a mean age of 40 ± 12 years in the Ulc and 47 ± 13 years in the NUlc group (ns). Mean values at baseline of pain intensity, frequency, nocturia, OSS, QoL, and urinary NGF, BDNF, GDNF were identical in the 2 groups. Patients with the Ulc phenotype had a longer duration of symptoms (28.8 ± 11 vs 19.2 ± 8 months, P = .018). Both groups responded equally to OnabotA, with significant improvements in pain intensity, frequency, nocturia, OSS, QoL, and urinary NGF, BDNF, GDNF. The effect lasted for 9 ± 2.8 (Ulc) and 10.5 ± 2 (NUlc) months."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Botulinum Toxins, Type A",
"Cystitis, Interstitial",
"Female",
"Humans",
"Middle Aged",
"Pain Measurement",
"Severity of Illness Index",
"Symptom Assessment",
"Ulcer"
]
} | In this cohort, Ulc and NUlc patients had similar symptoms at baseline and comparable clinical response to intratrigonal OnabotA. These findings suggest that pain may not be directly related with ulcers themselves. | no | [
{
"from": "human",
"value": "Question: Do ulcerative and nonulcerative forms of bladder pain syndrome/interstitial cystitis differ in symptom intensity or response to onabotulinum toxin A?\nContext: {'contexts': ['To determine whether intratrigonal Onabotulinum toxin A (OnabotA) injection produces a different symptomatic outcome and duration of effect on ulcerative (Ulc) and nonulcerative (NUlc) bladder pain syndrome/interstitial cystitis (BPS/IC) patients and to compare the urinary levels of neurotrophines (NGF, BDNF, and GDNF) in response to OnabotA.', \"Ten Ulc and 14 NUlc bladder pain syndrome/interstitial cystitis patients were included in this study. OnabotA (100 U) was injected in 10 trigonal sites, each receiving 10 U in 1 mL of saline. Outcome measures included pain visual analog scale (0-10), a 3-day voiding chart, O'Leary-Sant Score (OSS), and quality of life (QoL) from International Prostate Symptoms Score assessed before treatment, 1 month after injection, and every 3 months afterwards. Urinary NGF, BDNF, and GDNF were accessed using ELISA, at same time points. Treatment duration was determined at the time patients requested another injection.\", 'Patients had a mean age of 40 ± 12 years in the Ulc and 47 ± 13 years in the NUlc group (ns). Mean values at baseline of pain intensity, frequency, nocturia, OSS, QoL, and urinary NGF, BDNF, GDNF were identical in the 2 groups. Patients with the Ulc phenotype had a longer duration of symptoms (28.8 ± 11 vs 19.2 ± 8 months, P = .018). Both groups responded equally to OnabotA, with significant improvements in pain intensity, frequency, nocturia, OSS, QoL, and urinary NGF, BDNF, GDNF. The effect lasted for 9 ± 2.8 (Ulc) and 10.5 ± 2 (NUlc) months.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Botulinum Toxins, Type A', 'Cystitis, Interstitial', 'Female', 'Humans', 'Middle Aged', 'Pain Measurement', 'Severity of Illness Index', 'Symptom Assessment', 'Ulcer']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
24,761,388 | Does factor V Leiden have a role in cryptogenic ischemic stroke among Iranian young adults? | {
"contexts": [
"Different risk factors have been suggested for ischemic stroke in young adults. In a group of these patients despite of extensive diagnostic work-up, the primary cause remains unknown. Coagulation tendency is accounted as a possible cause in these patients. Previous studies on factor V Leiden (FVL) as the main cause of inherited thrombophilia for clarifying the role of FVL in stroke have resulted in controversial findings. The current study investigates the role of this factor in ischemic stroke among Iranians.",
"This case-control study was performed between September 2007 and December 2008 in Isfahan, Iran. The case group comprised of 22 patients of which 15 were males and 7 were females with age range of ≤50 years, diagnosed as ischemic stroke without classic risk factors and the control group consisted of 54 healthy young adults. After filling consent form, venous blood samples were obtained and sent to the laboratory for genetic examination.",
"No FVL mutation was found in the case group. There was one carrier of the mutation as heterozygous in the control group (relative frequency = 1.85%)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": []
} | Based on our study, FVL might not be considered as an independent risk factor for ischemic stroke in Iranian individuals who are not suffering from other risk factors of ischemic stroke. | no | [
{
"from": "human",
"value": "Question: Does factor V Leiden have a role in cryptogenic ischemic stroke among Iranian young adults?\nContext: {'contexts': ['Different risk factors have been suggested for ischemic stroke in young adults. In a group of these patients despite of extensive diagnostic work-up, the primary cause remains unknown. Coagulation tendency is accounted as a possible cause in these patients. Previous studies on factor V Leiden (FVL) as the main cause of inherited thrombophilia for clarifying the role of FVL in stroke have resulted in controversial findings. The current study investigates the role of this factor in ischemic stroke among Iranians.', 'This case-control study was performed between September 2007 and December 2008 in Isfahan, Iran. The case group comprised of 22 patients of which 15 were males and 7 were females with age range of ≤50 years, diagnosed as ischemic stroke without classic risk factors and the control group consisted of 54 healthy young adults. After filling consent form, venous blood samples were obtained and sent to the laboratory for genetic examination.', 'No FVL mutation was found in the case group. There was one carrier of the mutation as heterozygous in the control group (relative frequency = 1.85%).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
24,772,124 | Does qT dispersion increase with low glomerular filtration rate in patients with coronary artery disease? | {
"contexts": [
"We aimed to evaluate the relationship between estimated glomerular filtration rate (eGFR) and QT dispersion (QTd) in patients with coronary artery disease (CAD).",
"Sixty patients(mean age 62.72 ± 12.48 years) included 46 male, (mean age 60.89 ± 12.70 years)and 14 female (mean age 68.71± 9.86 years) were enrolled in this study. Patients were divided into 2 groups according to their eGFR using the 6 variable MDRD equation. Group 1 consisted of patients with estimated eGFR<60 ml/min/1.73m(2) and Group 2 consisted of patients witheGFR ≥ 60 ml/min/1.73m(2).",
"Baseline patient characteristics were homogeneous in both groups except for age, gender and smoking.Also, the extent of CAD was similar in both groups (p > 0.05) QTd values were found higher in group 1 than those of group 2 (57.23 ± 40.65 ms vs. 31.23 ± 14.47 ms, p = 0.002). After adjustment for age, gender and smoking using one-way ANCOVA test, statistically significant difference in QTd still existedbetween the groups (p=0.038)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": []
} | QTd tends to be higher in patients with poor renal function independent of severity of angiographical CAD. QTd may be a potentially useful non-invasive test in the management of patients with poor renal function, especially those with CAD. | yes | [
{
"from": "human",
"value": "Question: Does qT dispersion increase with low glomerular filtration rate in patients with coronary artery disease?\nContext: {'contexts': ['We aimed to evaluate the relationship between estimated glomerular filtration rate (eGFR) and QT dispersion (QTd) in patients with coronary artery disease (CAD).', 'Sixty patients(mean age 62.72 ± 12.48 years) included 46 male, (mean age 60.89 ± 12.70 years)and 14 female (mean age 68.71± 9.86 years) were enrolled in this study. Patients were divided into 2 groups according to their eGFR using the 6 variable MDRD equation. Group 1 consisted of patients with estimated eGFR<60 ml/min/1.73m(2) and Group 2 consisted of patients witheGFR ≥ 60 ml/min/1.73m(2).', 'Baseline patient characteristics were homogeneous in both groups except for age, gender and smoking.Also, the extent of CAD was similar in both groups (p > 0.05) QTd values were found higher in group 1 than those of group 2 (57.23 ± 40.65 ms vs. 31.23 ± 14.47 ms, p = 0.002). After adjustment for age, gender and smoking using one-way ANCOVA test, statistically significant difference in QTd still existedbetween the groups (p=0.038).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,751,108 | Does rNA sequencing identify novel markers of non-small cell lung cancer? | {
"contexts": [
"The development of reliable gene expression profiling technology increasingly impacts our understanding of lung cancer biology. Here, we used RNA sequencing (RNA-Seq) to compare the transcriptomes of non-small cell lung cancer (NSCLC) and normal lung tissues and to investigate expression in lung cancer tissues.",
"We enrolled 88 male patients (mean age, 61.2 years) with NSCLC. RNA-Seq was performed on 88 pairs of NSCLC tumor tissue and non-tumor tissue from 54 patients with adenocarcinoma and 34 patients with squamous cell carcinoma. Immunohistochemistry was performed to validate differential candidate gene expression in a different NSCLC group.",
"RNA-Seq produced 25.41 × 10(6) (± 8.90 × 10(6)) reads in NSCLC tissues and 24.70×10(6) (± 4.70 × 10(6)) reads in normal lung tissues [mean (± standard deviation)]. Among the genes expressed in both tissues, 335 were upregulated and 728 were downregulated ≥ 2-fold (p < 0.001). Four upregulated genes - CBX3, GJB2, CRABP2, and DSP - not previously reported in lung cancer were studied further. Their altered expression was verified by immunohistochemistry in a different set of NSCLC tissues (n = 154). CBX3 was positive in 90.3% (139 cases) of the samples; GJB2, in 22.7% (35 cases); CRABP2, in 72.1% (111 cases); and DSP, in 17.5% (27 cases). The positive rate of CRABP2 was higher in adenocarcinoma than squamous cell carcinoma (p < 0.01)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Biomarkers, Tumor",
"Carcinoma, Non-Small-Cell Lung",
"Chromosomal Proteins, Non-Histone",
"Connexins",
"High-Throughput Nucleotide Sequencing",
"Humans",
"Immunohistochemistry",
"Lung Neoplasms",
"Male",
"Middle Aged",
"Real-Time Polymerase Chain Reaction",
"Receptors, Retinoic Acid",
"Sequence Analysis, RNA",
"Tissue Array Analysis",
"Transcriptome",
"Up-Regulation"
]
} | CBX3 and CRABP2 expression was markedly increased in lung cancer tissues and especially CRABP2 may be promising candidate genes in lung adenocarcinoma. | yes | [
{
"from": "human",
"value": "Question: Does rNA sequencing identify novel markers of non-small cell lung cancer?\nContext: {'contexts': ['The development of reliable gene expression profiling technology increasingly impacts our understanding of lung cancer biology. Here, we used RNA sequencing (RNA-Seq) to compare the transcriptomes of non-small cell lung cancer (NSCLC) and normal lung tissues and to investigate expression in lung cancer tissues.', 'We enrolled 88 male patients (mean age, 61.2 years) with NSCLC. RNA-Seq was performed on 88 pairs of NSCLC tumor tissue and non-tumor tissue from 54 patients with adenocarcinoma and 34 patients with squamous cell carcinoma. Immunohistochemistry was performed to validate differential candidate gene expression in a different NSCLC group.', 'RNA-Seq produced 25.41 × 10(6) (± 8.90 × 10(6)) reads in NSCLC tissues and 24.70×10(6) (± 4.70 × 10(6)) reads in normal lung tissues [mean (± standard deviation)]. Among the genes expressed in both tissues, 335 were upregulated and 728 were downregulated ≥ 2-fold (p < 0.001). Four upregulated genes - CBX3, GJB2, CRABP2, and DSP - not previously reported in lung cancer were studied further. Their altered expression was verified by immunohistochemistry in a different set of NSCLC tissues (n = 154). CBX3 was positive in 90.3% (139 cases) of the samples; GJB2, in 22.7% (35 cases); CRABP2, in 72.1% (111 cases); and DSP, in 17.5% (27 cases). The positive rate of CRABP2 was higher in adenocarcinoma than squamous cell carcinoma (p < 0.01).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Biomarkers, Tumor', 'Carcinoma, Non-Small-Cell Lung', 'Chromosomal Proteins, Non-Histone', 'Connexins', 'High-Throughput Nucleotide Sequencing', 'Humans', 'Immunohistochemistry', 'Lung Neoplasms', 'Male', 'Middle Aged', 'Real-Time Polymerase Chain Reaction', 'Receptors, Retinoic Acid', 'Sequence Analysis, RNA', 'Tissue Array Analysis', 'Transcriptome', 'Up-Regulation']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,747,056 | Is hepatic encephalopathy associated with slowed and delayed stimulus-associated somatosensory alpha activity? | {
"contexts": [
"Hepatic encephalopathy (HE) is associated with motor symptoms and attentional deficits, which are related to pathologically slowed oscillatory brain activity. Here, potential alterations of oscillatory activity in the somatosensory system were investigated.",
"21 patients with liver cirrhosis and varying HE severity and 7 control subjects received electrical stimulation of the right median nerve while brain activity was recorded using magnetoencephalography (MEG). Oscillatory activity within the contralateral primary somatosensory cortex (S1) and its stimulus-induced modulation were analyzed as a function of disease severity.",
"Median nerve stimuli evoked an early broadband power increase followed by suppression and then rebound of S1 alpha and beta activity. Increasing HE severity as quantified by the critical flicker frequency (CFF) was associated with a slowing of the alpha peak frequency and a delay of the alpha rebound."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Alpha Rhythm",
"Electric Stimulation",
"Evoked Potentials, Somatosensory",
"Female",
"Hepatic Encephalopathy",
"Humans",
"Magnetoencephalography",
"Male",
"Median Nerve",
"Middle Aged",
"Time Factors"
]
} | The present results provide the first evidence for a slowing of oscillatory activity in the somatosensory system in HE in combination with a previously unknown deficit of S1 in adjusting activation levels back to baseline. | yes | [
{
"from": "human",
"value": "Question: Is hepatic encephalopathy associated with slowed and delayed stimulus-associated somatosensory alpha activity?\nContext: {'contexts': ['Hepatic encephalopathy (HE) is associated with motor symptoms and attentional deficits, which are related to pathologically slowed oscillatory brain activity. Here, potential alterations of oscillatory activity in the somatosensory system were investigated.', '21 patients with liver cirrhosis and varying HE severity and 7 control subjects received electrical stimulation of the right median nerve while brain activity was recorded using magnetoencephalography (MEG). Oscillatory activity within the contralateral primary somatosensory cortex (S1) and its stimulus-induced modulation were analyzed as a function of disease severity.', 'Median nerve stimuli evoked an early broadband power increase followed by suppression and then rebound of S1 alpha and beta activity. Increasing HE severity as quantified by the critical flicker frequency (CFF) was associated with a slowing of the alpha peak frequency and a delay of the alpha rebound.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Alpha Rhythm', 'Electric Stimulation', 'Evoked Potentials, Somatosensory', 'Female', 'Hepatic Encephalopathy', 'Humans', 'Magnetoencephalography', 'Male', 'Median Nerve', 'Middle Aged', 'Time Factors']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,766,279 | Does sulfhydration of p66Shc at cysteine59 mediate the antioxidant effect of hydrogen sulfide? | {
"contexts": [
"Mitochondrion is considered as the major source of intracellular reactive oxygen species (ROS). H2S has been reported to be an antioxidant, but its mechanism remains largely elusive. P66Shc is an upstream activator of mitochondrial redox signaling. The aim of this study was to explore whether the antioxidant effect of H2S is mediated by p66Shc.",
"Application of exogenous H2S with its donor, NaHS, or overexpression of its generating enzyme, cystathionine β-synthase, induced sulfhydration of p66Shc, but inhibited its phosphorylation caused by H2O2/D-galactose in SH-SY5Y cells or in the mice cortex. H2S also decreased mitochondrial ROS production and protected neuronal cells against stress-induced senescence. PKCβII and PP2A are the two key proteins to regulate p66Shc phosphorylation. Although H2S failed to affect the activities of these two proteins, it disrupted their association. Cysteine-59 resides in proximity to serine-36, the phosphorylation site of p66Shc. The C59S mutant attenuated the above-described biological function of H2S.",
"We revealed a novel mechanism for the antioxidant effect of H2S and its role in oxidative stress-related diseases."
],
"labels": [
"OBJECTIVE",
"RESULTS",
"METHODS"
],
"meshes": [
"Animals",
"Antioxidants",
"Cell Line",
"Cysteine",
"Humans",
"Hydrogen Sulfide",
"Mice",
"Mitochondria",
"Neurons",
"Oxidative Stress",
"Reactive Oxygen Species",
"Shc Signaling Adaptor Proteins",
"Signal Transduction",
"Src Homology 2 Domain-Containing, Transforming Protein 1"
]
} | H2S inhibits mitochondrial ROS production via the sulfhydration of Cys-59 residue, which in turn, prevents the phosphorylation of p66Shc. | yes | [
{
"from": "human",
"value": "Question: Does sulfhydration of p66Shc at cysteine59 mediate the antioxidant effect of hydrogen sulfide?\nContext: {'contexts': ['Mitochondrion is considered as the major source of intracellular reactive oxygen species (ROS). H2S has been reported to be an antioxidant, but its mechanism remains largely elusive. P66Shc is an upstream activator of mitochondrial redox signaling. The aim of this study was to explore whether the antioxidant effect of H2S is mediated by p66Shc.', 'Application of exogenous H2S with its donor, NaHS, or overexpression of its generating enzyme, cystathionine β-synthase, induced sulfhydration of p66Shc, but inhibited its phosphorylation caused by H2O2/D-galactose in SH-SY5Y cells or in the mice cortex. H2S also decreased mitochondrial ROS production and protected neuronal cells against stress-induced senescence. PKCβII and PP2A are the two key proteins to regulate p66Shc phosphorylation. Although H2S failed to affect the activities of these two proteins, it disrupted their association. Cysteine-59 resides in proximity to serine-36, the phosphorylation site of p66Shc. The C59S mutant attenuated the above-described biological function of H2S.', 'We revealed a novel mechanism for the antioxidant effect of H2S and its role in oxidative stress-related diseases.'], 'labels': ['OBJECTIVE', 'RESULTS', 'METHODS'], 'meshes': ['Animals', 'Antioxidants', 'Cell Line', 'Cysteine', 'Humans', 'Hydrogen Sulfide', 'Mice', 'Mitochondria', 'Neurons', 'Oxidative Stress', 'Reactive Oxygen Species', 'Shc Signaling Adaptor Proteins', 'Signal Transduction', 'Src Homology 2 Domain-Containing, Transforming Protein 1']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,753,182 | Is hER-2 expression prognostic in osteosarcoma ; a Children 's Oncology Group prospective biology study? | {
"contexts": [
"Since the initial reports of human epidermal growth factor receptor 2 (HER-2) expression as being prognostic in osteosarcoma, numerous small studies varying in the interpretation of the immunohistochemical (IHC) staining patterns have produced conflicting results. The Children's Oncology Group therefore embarked on a prospective biology study in a larger sample of patients to define in osteosarcoma the prognostic value of HER-2 expression using the methodology employed in the initial North American study describing an association between HER-2 expression and outcome.",
"The analytic patient population was comprised of 149 patients with newly diagnosed osteosarcoma, 135 with localized disease and 14 with metastatic disease, all of whom had follow up clinical data. Paraffin embedded material from the diagnostic biopsy was stained with CB11 antibody and scored by two independent observers. Correlation of HER-2 IHC score and demographic variables was analyzed using a Fisher's exact test and correlation with survival using a Kaplan-Meier analysis.",
"No association was found with HER-2 status and any of the demographic variables tested including the presence or absence of metastatic disease at diagnosis. No association was found between HER-2 status and either event free survival or overall survival in the patients with localized disease."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Biomarkers, Tumor",
"Bone Neoplasms",
"Child",
"Child, Preschool",
"Female",
"Follow-Up Studies",
"Humans",
"Immunoenzyme Techniques",
"Infant",
"Male",
"Neoplasm Metastasis",
"Osteosarcoma",
"Prognosis",
"Prospective Studies",
"Receptor, ErbB-2",
"Survival Rate",
"Young Adult"
]
} | HER-2 expression is not prognostic in osteosarcoma in the context of this large prospective study. HER-2 expression cannot be used as a basis for stratification of therapy. Identification of potential prognostic factors should occur in the context of large multi-institutional biology studies. | no | [
{
"from": "human",
"value": "Question: Is hER-2 expression prognostic in osteosarcoma ; a Children 's Oncology Group prospective biology study?\nContext: {'contexts': [\"Since the initial reports of human epidermal growth factor receptor 2 (HER-2) expression as being prognostic in osteosarcoma, numerous small studies varying in the interpretation of the immunohistochemical (IHC) staining patterns have produced conflicting results. The Children's Oncology Group therefore embarked on a prospective biology study in a larger sample of patients to define in osteosarcoma the prognostic value of HER-2 expression using the methodology employed in the initial North American study describing an association between HER-2 expression and outcome.\", \"The analytic patient population was comprised of 149 patients with newly diagnosed osteosarcoma, 135 with localized disease and 14 with metastatic disease, all of whom had follow up clinical data. Paraffin embedded material from the diagnostic biopsy was stained with CB11 antibody and scored by two independent observers. Correlation of HER-2 IHC score and demographic variables was analyzed using a Fisher's exact test and correlation with survival using a Kaplan-Meier analysis.\", 'No association was found with HER-2 status and any of the demographic variables tested including the presence or absence of metastatic disease at diagnosis. No association was found between HER-2 status and either event free survival or overall survival in the patients with localized disease.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Biomarkers, Tumor', 'Bone Neoplasms', 'Child', 'Child, Preschool', 'Female', 'Follow-Up Studies', 'Humans', 'Immunoenzyme Techniques', 'Infant', 'Male', 'Neoplasm Metastasis', 'Osteosarcoma', 'Prognosis', 'Prospective Studies', 'Receptor, ErbB-2', 'Survival Rate', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
24,766,737 | Does shaoYao decoction ameliorate colitis-associated colorectal cancer by downregulating proinflammatory cytokines and promoting epithelial-mesenchymal transition? | {
"contexts": [
"Shaoyao decoction (SYD) is a traditional Chinese medicine prescription formulated by Liu Wan-Su, a master of traditional Chinese medicine in Jin-Yuan Dynasty. SYD is effective in treating ulcerative colitis. Paeonol, a component of SYD, inhibits colorectal cancer (CRC) cell proliferation and induces CRC cell apoptosis. In this study, azoxymethane (AOM)/dextran sodium sulfate (DSS)-induced colitis-associated CRC (caCRC) model and CRC cell lines were used to examine the effects of SYD on CRC in vivo and in vitro.",
"A translational medicine strategy based on phytomics quality control was adopted. Liquid chromatography was employed for the chemical characterization and chemical fingerprinting of SYD. Protein expression and macrophage existence were determined by immunohistochemistry and western blot. Serum cytokines were quantified by Luminex assay.",
"AOM/DSS-induced caCRC phenotypically resembled human caCRC. SYD significantly increased the survival rate of the mice, ameliorated the general well-being of the mice, and reduced the incidence and multiplicity of colonic neoplasms. SYD inhibited epithelial-mesenchymal transition (EMT), as indicated by upregulated epithelia cadherin and downregulated neuronal cadherin, fibronectin, vimentin, and transcription factor Snail. SYD reduced the expression levels of serum interleukin 1β, interleukin-6, tumor necrosis factor α, tumor-associated macrophages, and p65. These results showed that SYD can attenuate proinflammatory cytokines and inhibit EMT."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Acetophenones",
"Animals",
"Blotting, Western",
"Colitis",
"Colorectal Neoplasms",
"Cytokines",
"Down-Regulation",
"Drugs, Chinese Herbal",
"Epithelial-Mesenchymal Transition",
"Inflammation Mediators",
"Male",
"Mice",
"Mice, Inbred C57BL"
]
} | SYD ameliorates caCRC by suppressing inflammation and inhibiting EMT. SYD might be an alternative therapy for caCRC. | yes | [
{
"from": "human",
"value": "Question: Does shaoYao decoction ameliorate colitis-associated colorectal cancer by downregulating proinflammatory cytokines and promoting epithelial-mesenchymal transition?\nContext: {'contexts': ['Shaoyao decoction (SYD) is a traditional Chinese medicine prescription formulated by Liu Wan-Su, a master of traditional Chinese medicine in Jin-Yuan Dynasty. SYD is effective in treating ulcerative colitis. Paeonol, a component of SYD, inhibits colorectal cancer (CRC) cell proliferation and induces CRC cell apoptosis. In this study, azoxymethane (AOM)/dextran sodium sulfate (DSS)-induced colitis-associated CRC (caCRC) model and CRC cell lines were used to examine the effects of SYD on CRC in vivo and in vitro.', 'A translational medicine strategy based on phytomics quality control was adopted. Liquid chromatography was employed for the chemical characterization and chemical fingerprinting of SYD. Protein expression and macrophage existence were determined by immunohistochemistry and western blot. Serum cytokines were quantified by Luminex assay.', 'AOM/DSS-induced caCRC phenotypically resembled human caCRC. SYD significantly increased the survival rate of the mice, ameliorated the general well-being of the mice, and reduced the incidence and multiplicity of colonic neoplasms. SYD inhibited epithelial-mesenchymal transition (EMT), as indicated by upregulated epithelia cadherin and downregulated neuronal cadherin, fibronectin, vimentin, and transcription factor Snail. SYD reduced the expression levels of serum interleukin 1β, interleukin-6, tumor necrosis factor α, tumor-associated macrophages, and p65. These results showed that SYD can attenuate proinflammatory cytokines and inhibit EMT.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Acetophenones', 'Animals', 'Blotting, Western', 'Colitis', 'Colorectal Neoplasms', 'Cytokines', 'Down-Regulation', 'Drugs, Chinese Herbal', 'Epithelial-Mesenchymal Transition', 'Inflammation Mediators', 'Male', 'Mice', 'Mice, Inbred C57BL']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,768,206 | Does gestational diabetes mellitus alter apoptotic and inflammatory gene expression of trophobasts from human term placenta? | {
"contexts": [
"Increased placental growth secondary to reduced apoptosis may contribute to the development of macrosomia in GDM pregnancies. We hypothesize that reduced apoptosis in GDM placentas is caused by dysregulation of apoptosis related genes from death receptors or mitochondrial pathway or both to enhance placental growth in GDM pregnancies.",
"Newborn and placental weights from women with no pregnancy complications (controls; N=5), or with GDM (N=5) were recorded. Placental villi from both groups were either fixed for TUNEL assay, or snap frozen for gene expression analysis by apoptosis PCR microarrays and qPCR.",
"Maternal, placental and newborn weights were significantly higher in the GDM group vs. Controls. Apoptotic index of placentas from the GDM group was markedly lower than the Controls. At a significant threshold of 1.5, seven genes (BCL10, BIRC6, BIRC7, CASP5, CASP8P2, CFLAR, and FAS) were down regulated, and 13 genes (BCL2, BCL2L1, BCL2L11, CASP4, DAPK1, IκBκE, MCL1, NFκBIZ, NOD1, PEA15, TNF, TNFRSF25, and XIAP) were unregulated in the GDM placentas. qPCR confirmed the consistency of the PCR microarray. Using Western blotting we found significantly decreased placental pro-apoptotic FAS receptor and FAS ligand (FASL), and increased mitochondrial anti-apoptotic BCL2 post GDM insult. Notably, caspase-3, which plays a central role in the execution-phase of apoptosis, and its substrate poly (ADP-ribose) polymerase (PARP) were significantly down regulated in GDM placentas, as compared to non-diabetic Control placentas."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Apoptosis",
"Apoptosis Regulatory Proteins",
"Birth Weight",
"Diabetes, Gestational",
"Female",
"Fetal Macrosomia",
"Gene Expression Profiling",
"Gene Expression Regulation, Developmental",
"Humans",
"Inflammation Mediators",
"Models, Biological",
"Oligonucleotide Array Sequence Analysis",
"Placenta",
"Placentation",
"Pregnancy",
"RNA, Messenger",
"Real-Time Polymerase Chain Reaction",
"Reverse Transcriptase Polymerase Chain Reaction",
"Term Birth"
]
} | Maternal GDM results in heavier placentas with aberrant placental apoptotic and inflammatory gene expression that may account, at least partially, for macrosomia in newborns. | yes | [
{
"from": "human",
"value": "Question: Does gestational diabetes mellitus alter apoptotic and inflammatory gene expression of trophobasts from human term placenta?\nContext: {'contexts': ['Increased placental growth secondary to reduced apoptosis may contribute to the development of macrosomia in GDM pregnancies. We hypothesize that reduced apoptosis in GDM placentas is caused by dysregulation of apoptosis related genes from death receptors or mitochondrial pathway or both to enhance placental growth in GDM pregnancies.', 'Newborn and placental weights from women with no pregnancy complications (controls; N=5), or with GDM (N=5) were recorded. Placental villi from both groups were either fixed for TUNEL assay, or snap frozen for gene expression analysis by apoptosis PCR microarrays and qPCR.', 'Maternal, placental and newborn weights were significantly higher in the GDM group vs. Controls. Apoptotic index of placentas from the GDM group was markedly lower than the Controls. At a significant threshold of 1.5, seven genes (BCL10, BIRC6, BIRC7, CASP5, CASP8P2, CFLAR, and FAS) were down regulated, and 13 genes (BCL2, BCL2L1, BCL2L11, CASP4, DAPK1, IκBκE, MCL1, NFκBIZ, NOD1, PEA15, TNF, TNFRSF25, and XIAP) were unregulated in the GDM placentas. qPCR confirmed the consistency of the PCR microarray. Using Western blotting we found significantly decreased placental pro-apoptotic FAS receptor and FAS ligand (FASL), and increased mitochondrial anti-apoptotic BCL2 post GDM insult. Notably, caspase-3, which plays a central role in the execution-phase of apoptosis, and its substrate poly (ADP-ribose) polymerase (PARP) were significantly down regulated in GDM placentas, as compared to non-diabetic Control placentas.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Apoptosis', 'Apoptosis Regulatory Proteins', 'Birth Weight', 'Diabetes, Gestational', 'Female', 'Fetal Macrosomia', 'Gene Expression Profiling', 'Gene Expression Regulation, Developmental', 'Humans', 'Inflammation Mediators', 'Models, Biological', 'Oligonucleotide Array Sequence Analysis', 'Placenta', 'Placentation', 'Pregnancy', 'RNA, Messenger', 'Real-Time Polymerase Chain Reaction', 'Reverse Transcriptase Polymerase Chain Reaction', 'Term Birth']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,766,300 | Are antihelminthic benzimidazoles novel HIF activators that prevent oxidative neuronal death via binding to tubulin? | {
"contexts": [
"Pharmacological activation of the adaptive response to hypoxia is a therapeutic strategy of growing interest for neurological conditions, including stroke, Huntington's disease, and Parkinson's disease. We screened a drug library with known safety in humans using a hippocampal neuroblast line expressing a reporter of hypoxia-inducible factor (HIF)-dependent transcription.",
"Our screen identified more than 40 compounds with the ability to induce hypoxia response element-driven luciferase activity as well or better than deferoxamine, a canonical activator of hypoxic adaptation. Among the chemical entities identified, the antihelminthic benzimidazoles represented one pharmacophore that appeared multiple times in our screen. Secondary assays confirmed that antihelminthics stabilized the transcriptional activator HIF-1α and induced expression of a known HIF target gene, p21(cip1/waf1), in post-mitotic cortical neurons. The on-target effect of these agents in stimulating hypoxic signaling was binding to free tubulin. Moreover, antihelminthic benzimidazoles also abrogated oxidative stress-induced death in vitro, and this on-target effect also involves binding to free tubulin."
],
"labels": [
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Animals",
"Anthelmintics",
"Benzimidazoles",
"Blotting, Western",
"Cell Line",
"Cell Survival",
"Cyclin-Dependent Kinase Inhibitor p21",
"Hippocampus",
"Humans",
"Hypoxia-Inducible Factor 1, alpha Subunit",
"Immunohistochemistry",
"Mebendazole",
"Mice",
"Neurons",
"Tubulin"
]
} | These studies demonstrate that tubulin-binding drugs can activate a component of the hypoxic adaptive response, specifically the stabilization of HIF-1α and its downstream targets. Tubulin-binding drugs, including antihelminthic benzimidazoles, also abrogate oxidative neuronal death in primary neurons. Given their safety in humans and known ability to penetrate into the central nervous system, antihelminthic benzimidazoles may be considered viable candidates for treating diseases associated with oxidative neuronal death, including stroke. | yes | [
{
"from": "human",
"value": "Question: Are antihelminthic benzimidazoles novel HIF activators that prevent oxidative neuronal death via binding to tubulin?\nContext: {'contexts': [\"Pharmacological activation of the adaptive response to hypoxia is a therapeutic strategy of growing interest for neurological conditions, including stroke, Huntington's disease, and Parkinson's disease. We screened a drug library with known safety in humans using a hippocampal neuroblast line expressing a reporter of hypoxia-inducible factor (HIF)-dependent transcription.\", 'Our screen identified more than 40 compounds with the ability to induce hypoxia response element-driven luciferase activity as well or better than deferoxamine, a canonical activator of hypoxic adaptation. Among the chemical entities identified, the antihelminthic benzimidazoles represented one pharmacophore that appeared multiple times in our screen. Secondary assays confirmed that antihelminthics stabilized the transcriptional activator HIF-1α and induced expression of a known HIF target gene, p21(cip1/waf1), in post-mitotic cortical neurons. The on-target effect of these agents in stimulating hypoxic signaling was binding to free tubulin. Moreover, antihelminthic benzimidazoles also abrogated oxidative stress-induced death in vitro, and this on-target effect also involves binding to free tubulin.'], 'labels': ['OBJECTIVE', 'RESULTS'], 'meshes': ['Animals', 'Anthelmintics', 'Benzimidazoles', 'Blotting, Western', 'Cell Line', 'Cell Survival', 'Cyclin-Dependent Kinase Inhibitor p21', 'Hippocampus', 'Humans', 'Hypoxia-Inducible Factor 1, alpha Subunit', 'Immunohistochemistry', 'Mebendazole', 'Mice', 'Neurons', 'Tubulin']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,755,295 | Does microRNA-181a promote tumor growth and liver metastasis in colorectal cancer by targeting the tumor suppressor WIF-1? | {
"contexts": [
"Given the emerging role of microRNA in tumor disease progression, we investigated the association between microRNA expression, liver metastasis and prognosis of colorectal cancer.",
"Colorectal cancer tissues from patients with or without liver metastases were profiled to identify differentially expressed microRNA. Expression profile was further assessed using quantitative reverse transcription PCR and in situ hybridization. Correlation between miR-181a expression, the most differentially expressed microRNA, between patients with and without liver metastasis, and its downstream target genes were investigated using qRT-PCR. Luciferase reporter assay was conducted to establish functional association between miR-181a and its target genes. Manipulation of miR-181a expression and its consequences in tumor growth and metastasis were demonstrated in various in vitro and in vivo models.",
"miR-181a was revealed being the most elevated in CRC with liver metastases. miR-181a expression correlated with advanced stage, distant metastasis, and served as an independent prognostic factor of poor overall survival. Stable transfection of CRC cell lines with miR-181a promoted cell motility and invasion, as well as tumor growth and liver metastasis,while silencing its expression resulted in reduced migration and invasion. Additionally, we identified WIF-1 as direct and functional targets of miR-181a. Ectopic expression of miR-181a suppressed the epithelial markers E-cadherin and β-catenin, while enhanced the mesenchymal markers vimentin."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adaptor Proteins, Signal Transducing",
"Adenocarcinoma",
"Aged",
"Biomarkers",
"Cadherins",
"Cell Proliferation",
"Colorectal Neoplasms",
"Epigenesis, Genetic",
"Epithelial-Mesenchymal Transition",
"Female",
"Gene Expression Profiling",
"Gene Expression Regulation, Neoplastic",
"Humans",
"Liver Neoplasms",
"Male",
"MicroRNAs",
"Middle Aged",
"Neoplasm Invasiveness",
"Prognosis",
"RNA, Small Interfering",
"Repressor Proteins",
"Signal Transduction",
"Survival Analysis",
"Tumor Cells, Cultured",
"Vimentin",
"beta Catenin"
]
} | Our data demonstrate that miR-181a expression is associated with CRC liver metastasis and survival. miR-181a has strong tumor-promoting effects through inhibiting the expression of WIF-1, and its potential role in promoting epithelial-mesenchymal transition. | yes | [
{
"from": "human",
"value": "Question: Does microRNA-181a promote tumor growth and liver metastasis in colorectal cancer by targeting the tumor suppressor WIF-1?\nContext: {'contexts': ['Given the emerging role of microRNA in tumor disease progression, we investigated the association between microRNA expression, liver metastasis and prognosis of colorectal cancer.', 'Colorectal cancer tissues from patients with or without liver metastases were profiled to identify differentially expressed microRNA. Expression profile was further assessed using quantitative reverse transcription PCR and in situ hybridization. Correlation between miR-181a expression, the most differentially expressed microRNA, between patients with and without liver metastasis, and its downstream target genes were investigated using qRT-PCR. Luciferase reporter assay was conducted to establish functional association between miR-181a and its target genes. Manipulation of miR-181a expression and its consequences in tumor growth and metastasis were demonstrated in various in vitro and in vivo models.', 'miR-181a was revealed being the most elevated in CRC with liver metastases. miR-181a expression correlated with advanced stage, distant metastasis, and served as an independent prognostic factor of poor overall survival. Stable transfection of CRC cell lines with miR-181a promoted cell motility and invasion, as well as tumor growth and liver metastasis,while silencing its expression resulted in reduced migration and invasion. Additionally, we identified WIF-1 as direct and functional targets of miR-181a. Ectopic expression of miR-181a suppressed the epithelial markers E-cadherin and β-catenin, while enhanced the mesenchymal markers vimentin.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adaptor Proteins, Signal Transducing', 'Adenocarcinoma', 'Aged', 'Biomarkers', 'Cadherins', 'Cell Proliferation', 'Colorectal Neoplasms', 'Epigenesis, Genetic', 'Epithelial-Mesenchymal Transition', 'Female', 'Gene Expression Profiling', 'Gene Expression Regulation, Neoplastic', 'Humans', 'Liver Neoplasms', 'Male', 'MicroRNAs', 'Middle Aged', 'Neoplasm Invasiveness', 'Prognosis', 'RNA, Small Interfering', 'Repressor Proteins', 'Signal Transduction', 'Survival Analysis', 'Tumor Cells, Cultured', 'Vimentin', 'beta Catenin']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,749,728 | Does inhibition during early adolescence predict alcohol and marijuana use by late adolescence? | {
"contexts": [
"Adolescent substance use has been associated with poorer neuropsychological functioning, but it is unclear if deficits predate or follow the onset of use. The goal of this prospective study was to understand how neuropsychological functioning during early adolescence could predict substance use by late adolescence.",
"At baseline, participants were 175 substance-use-naïve healthy 12- to 14-year-olds (41% female) recruited from local schools. Participants completed extensive interviews and neuropsychological tests. Each year, participants' substance use was assessed. By late adolescence (ages 17 to 18), 105 participants transitioned into substance use and 75 remained substance-naïve. Hierarchical linear regressions examined how baseline cognitive performance predicted subsequent substance use, controlling for common substance use risk factors (i.e., family history, externalizing behaviors, gender, pubertal development, and age).",
"Poorer baseline performance on tests of cognitive inhibition-interference predicted higher follow-up peak drinks on an occasion (β = -.15; p < .001), more days of drinking (β = -.15; p < .001), and more marijuana use days (β = -.17; p < .001) by ages 17 to 18, above and beyond covariates. Performances on short-term memory, sustained attention, verbal learning and memory, visuospatial functioning, and spatial planning did not predict subsequent substance involvement (ps > .05)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Age Factors",
"Alcohol Drinking",
"Child",
"Executive Function",
"Female",
"Humans",
"Male",
"Marijuana Smoking",
"Neuropsychological Tests",
"Prospective Studies",
"Psychology, Adolescent"
]
} | Compromised inhibitory functioning during early adolescence prior to the onset of substance use was related to more frequent and intense alcohol and marijuana use by late adolescence. Inhibition performance could help identify teens at risk for initiating heavy substance use during adolescence, and potentially could be modified to improve outcome. | yes | [
{
"from": "human",
"value": "Question: Does inhibition during early adolescence predict alcohol and marijuana use by late adolescence?\nContext: {'contexts': ['Adolescent substance use has been associated with poorer neuropsychological functioning, but it is unclear if deficits predate or follow the onset of use. The goal of this prospective study was to understand how neuropsychological functioning during early adolescence could predict substance use by late adolescence.', \"At baseline, participants were 175 substance-use-naïve healthy 12- to 14-year-olds (41% female) recruited from local schools. Participants completed extensive interviews and neuropsychological tests. Each year, participants' substance use was assessed. By late adolescence (ages 17 to 18), 105 participants transitioned into substance use and 75 remained substance-naïve. Hierarchical linear regressions examined how baseline cognitive performance predicted subsequent substance use, controlling for common substance use risk factors (i.e., family history, externalizing behaviors, gender, pubertal development, and age).\", 'Poorer baseline performance on tests of cognitive inhibition-interference predicted higher follow-up peak drinks on an occasion (β = -.15; p < .001), more days of drinking (β = -.15; p < .001), and more marijuana use days (β = -.17; p < .001) by ages 17 to 18, above and beyond covariates. Performances on short-term memory, sustained attention, verbal learning and memory, visuospatial functioning, and spatial planning did not predict subsequent substance involvement (ps > .05).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Age Factors', 'Alcohol Drinking', 'Child', 'Executive Function', 'Female', 'Humans', 'Male', 'Marijuana Smoking', 'Neuropsychological Tests', 'Prospective Studies', 'Psychology, Adolescent']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,753,748 | Does miRNA-26b inhibit cellular proliferation by targeting CDK8 in breast cancer? | {
"contexts": [
"MicroRNA-26b (miR-26b) has been reported to be down-regulated in a wide range of malignant tumors, However, the mechanism by which miR-26b is implicated in breast cancer tumorigenesis is incompletely understood. This study was undertaken to evaluate the expression pattern of miR-26b and characterize its biological role in human breast cancer.",
"Reverse transcription-polymerase chain reaction (RT-PCR) was used to quantify the expression levels of miR-26b in breast cancer and adjacent non-cancerous breast tissues. MTT, colony formation assay and cell cycle assay were carried out to characterize the miR-26b function. Finally, to validate the target gene of miR-26b, luciferase reporter assay was employed, followed by RT-PCR and Western blot confirmation.",
"Here, we found that miR-26b expression was relatively downregulated in breast cancer specimens (P<0.01). Overexpression of miR-26b dramatically suppressed cell proliferation, colony formation and induced G0/G1 cell cycle arrest of MDA-MB-231 and Mcf-7 cells. Luciferase assays revealed that miR-26b directly targeted the 3'UTR of CDK8. Overexpression of miR-26b led to the downregulation of CDK8 and β-catenin expression. Similarly, CDK8 knockdown by siRNA suppressed cell growth and subsequent β-catenin expression."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": []
} | These findings suggest that miR-26b exerts a tumor suppressive role in breast cancer and the miR-26b-mediated growth inhibition is achieved through suppression of a new target gene CDK8. | yes | [
{
"from": "human",
"value": "Question: Does miRNA-26b inhibit cellular proliferation by targeting CDK8 in breast cancer?\nContext: {'contexts': ['MicroRNA-26b (miR-26b) has been reported to be down-regulated in a wide range of malignant tumors, However, the mechanism by which miR-26b is implicated in breast cancer tumorigenesis is incompletely understood. This study was undertaken to evaluate the expression pattern of miR-26b and characterize its biological role in human breast cancer.', 'Reverse transcription-polymerase chain reaction (RT-PCR) was used to quantify the expression levels of miR-26b in breast cancer and adjacent non-cancerous breast tissues. MTT, colony formation assay and cell cycle assay were carried out to characterize the miR-26b function. Finally, to validate the target gene of miR-26b, luciferase reporter assay was employed, followed by RT-PCR and Western blot confirmation.', \"Here, we found that miR-26b expression was relatively downregulated in breast cancer specimens (P<0.01). Overexpression of miR-26b dramatically suppressed cell proliferation, colony formation and induced G0/G1 cell cycle arrest of MDA-MB-231 and Mcf-7 cells. Luciferase assays revealed that miR-26b directly targeted the 3'UTR of CDK8. Overexpression of miR-26b led to the downregulation of CDK8 and β-catenin expression. Similarly, CDK8 knockdown by siRNA suppressed cell growth and subsequent β-catenin expression.\"], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,753,749 | Are activation of circulated immune cells and inflammatory immune adherence involved in the whole process of acute venous thrombosis? | {
"contexts": [
"To investigate localization and distribution of integrin subunit β1, β2 and β3 and morphological changes of ligand-recepter binding in thrombi of acute pulmonary embolism (PE) patients and explore activation of circulated immune cells, inflammatory immune adherence and coagulation response in acute venous thrombosis.",
"Thrombi were collected from patients with acute PE. Immunohistochemistry was done to detect the expression and distribution of integrin β1, β2 and β3 in cells within thrombi, and ligands of integrin subunit β1, β2 and β3 were also determined by immunohistochemistry within the thrombi.",
"1) Acute venous thrombi were red thrombi composed of skeletons and filamentous mesh containing large amounts of red blood cells and white blood cells; 2) Integrin subunit β1, β2 and β3 were expressed on lymphocytes, neutrophils and platelets; 3) No expression of integrin β1 ligands: Laminin, Fibronectin, Collagen I or Collagen-II on lymphocytes; integrin β2 ligands including ICAM, factor X and iC3b are distributed on neutrophils, and ligand fibrinogen bound to neutrophils; integrin β3 was expressed on platelets which form the skeleton of thrombi and bound to fibrinogen to construct mesh structure; 4) Factor Xa was expressed on the filamentous mesh; 5) Filamentous mesh was fully filled with red blood cell dominant blood cells."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": []
} | Acute venous thrombosis is an activation process of circulated lymphocytes, neutrophils and platelets mainly, and a whole process including integrin subunit β2 and β3 binding with their ligands. Activation of immune cells, inflammatory immune adherence and coagulation response are involved in the acute venous thrombosis. | yes | [
{
"from": "human",
"value": "Question: Are activation of circulated immune cells and inflammatory immune adherence involved in the whole process of acute venous thrombosis?\nContext: {'contexts': ['To investigate localization and distribution of integrin subunit β1, β2 and β3 and morphological changes of ligand-recepter binding in thrombi of acute pulmonary embolism (PE) patients and explore activation of circulated immune cells, inflammatory immune adherence and coagulation response in acute venous thrombosis.', 'Thrombi were collected from patients with acute PE. Immunohistochemistry was done to detect the expression and distribution of integrin β1, β2 and β3 in cells within thrombi, and ligands of integrin subunit β1, β2 and β3 were also determined by immunohistochemistry within the thrombi.', '1) Acute venous thrombi were red thrombi composed of skeletons and filamentous mesh containing large amounts of red blood cells and white blood cells; 2) Integrin subunit β1, β2 and β3 were expressed on lymphocytes, neutrophils and platelets; 3) No expression of integrin β1 ligands: Laminin, Fibronectin, Collagen I or Collagen-II on lymphocytes; integrin β2 ligands including ICAM, factor X and iC3b are distributed on neutrophils, and ligand fibrinogen bound to neutrophils; integrin β3 was expressed on platelets which form the skeleton of thrombi and bound to fibrinogen to construct mesh structure; 4) Factor Xa was expressed on the filamentous mesh; 5) Filamentous mesh was fully filled with red blood cell dominant blood cells.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,755,130 | Does flurbiprofen improve dysfunction of T-lymphocyte subsets and natural killer cells in cancer patients receiving post-operative morphine analgesia? | {
"contexts": [
"Acute pain can lead to immune dysfunction, which can be partly ameliorated by successful pain management. Opioids, which are widely used for analgesia, can result in the deterioration of immune function. This study aimed to investigate the influence of morphine with or without flurbiprofen as post-operative analgesics on the immune systems of patients undergoing gastric cancer surgery.",
"60 patients undergoing gastric cancer surgery were equally randomized into two groups. They received post-operative patient-controlled intravenous (IV) analgesia using morphine either with or without flurbiprofen. Visual analogue scale (VAS) scores, Bruggemann comfort scale (BCS) scores, morphine consumption, time of first flatus, incidence of nausea/vomiting, and T-lymphocyte subsets (CD3⁺, CD4⁺, and CD8⁺) and natural killer cells (CD3⁻CD16⁺CD56⁺) were evaluated.",
"No significant difference was observed in the VAS scores, BCS scores, and nausea/vomiting incidence between groups. Less morphine was consumed and the time of first flatus was earlier in patients receiving morphine with flurbiprofen than morphine alone. The expression of CD3⁺, CD4⁺, CD4⁺/CD8⁺, and CD3⁻CD16⁺CD56⁺ decreased at 2 hours after incision and, except for CD3⁻CD16⁺CD56⁺, returned to baseline at 120 hours after surgery. Moreover, the expression of CD3⁻CD16⁺CD56⁺ at 2 hours after incision and the expression of CD3⁺, CD4⁺, CD4⁺/CD8⁺, and CD3⁻CD16⁺CD56⁺ at 24 hours after surgery were higher in patients receiving morphine with flurbiprofen than morphine alone."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Analgesia, Patient-Controlled",
"Analgesics, Opioid",
"Anti-Inflammatory Agents, Non-Steroidal",
"Double-Blind Method",
"Female",
"Flurbiprofen",
"Humans",
"Killer Cells, Natural",
"Male",
"Middle Aged",
"Morphine",
"Pain Measurement",
"Pain, Postoperative",
"Stomach Neoplasms",
"T-Lymphocyte Subsets"
]
} | The combination of morphine and flurbiprofen ameliorates the immune depression in Tlymphocyte subsets and natural killer cells and provides a similar analgesic efficacy to morphine alone in patients undergoing gastric cancer surgery. | yes | [
{
"from": "human",
"value": "Question: Does flurbiprofen improve dysfunction of T-lymphocyte subsets and natural killer cells in cancer patients receiving post-operative morphine analgesia?\nContext: {'contexts': ['Acute pain can lead to immune dysfunction, which can be partly ameliorated by successful pain management. Opioids, which are widely used for analgesia, can result in the deterioration of immune function. This study aimed to investigate the influence of morphine with or without flurbiprofen as post-operative analgesics on the immune systems of patients undergoing gastric cancer surgery.', '60 patients undergoing gastric cancer surgery were equally randomized into two groups. They received post-operative patient-controlled intravenous (IV) analgesia using morphine either with or without flurbiprofen. Visual analogue scale (VAS) scores, Bruggemann comfort scale (BCS) scores, morphine consumption, time of first flatus, incidence of nausea/vomiting, and T-lymphocyte subsets (CD3⁺, CD4⁺, and CD8⁺) and natural killer cells (CD3⁻CD16⁺CD56⁺) were evaluated.', 'No significant difference was observed in the VAS scores, BCS scores, and nausea/vomiting incidence between groups. Less morphine was consumed and the time of first flatus was earlier in patients receiving morphine with flurbiprofen than morphine alone. The expression of CD3⁺, CD4⁺, CD4⁺/CD8⁺, and CD3⁻CD16⁺CD56⁺ decreased at 2 hours after incision and, except for CD3⁻CD16⁺CD56⁺, returned to baseline at 120 hours after surgery. Moreover, the expression of CD3⁻CD16⁺CD56⁺ at 2 hours after incision and the expression of CD3⁺, CD4⁺, CD4⁺/CD8⁺, and CD3⁻CD16⁺CD56⁺ at 24 hours after surgery were higher in patients receiving morphine with flurbiprofen than morphine alone.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Analgesia, Patient-Controlled', 'Analgesics, Opioid', 'Anti-Inflammatory Agents, Non-Steroidal', 'Double-Blind Method', 'Female', 'Flurbiprofen', 'Humans', 'Killer Cells, Natural', 'Male', 'Middle Aged', 'Morphine', 'Pain Measurement', 'Pain, Postoperative', 'Stomach Neoplasms', 'T-Lymphocyte Subsets']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,755,071 | Are human adipocytes highly sensitive to intermittent hypoxia induced NF-kappaB activity and subsequent inflammatory gene expression? | {
"contexts": [
"Intermittent hypoxia (IH)-induced activation of pro-inflammatory pathways is a major contributing factor to the cardiovascular pathophysiology associated with obstructive sleep apnea (OSA). Obesity is commonly associated with OSA although it remains unknown whether adipose tissue is a major source of inflammatory mediators in response to IH. The aim of this study was to test the hypothesis that IH leads to augmented inflammatory responses in human adipocytes when compared to cells of non-adipocyte lineages.",
"Human primary subcutaneous and visceral adipocytes, human primary microvascular pulmonary endothelial cells (HUMEC-L) and human primary small airway epithelial cells (SAEC) were exposed to 0, 6 or 12 cycles of IH or stimulated with tumor necrosis factor (TNF)-α. IH led to a robust increase in NF-κB DNA-binding activity in adipocytes compared with normoxic controls regardless of whether the source of adipocytes was visceral or subcutaneous. Notably, the NF-κB response of adipocytes to both IH and TNF-α was significantly greater than that in HUMEC-L and SAEC. Western blotting confirmed enhanced nuclear translocation of p65 in adipocytes in response to IH, accompanied by phosphorylation of I-κB. Parallel to p65 activation, we observed a significant increase in secretion of the adipokines interleukin (IL)-8, IL-6 and TNF-α with IH in adipocytes accompanied by significant upregulation of mRNA expression. PCR-array suggested profound influence of IH on pro-inflammatory gene expression in adipocytes."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Active Transport, Cell Nucleus",
"Adipocytes, White",
"Adipokines",
"Cardiovascular Diseases",
"Cell Hypoxia",
"Cells, Cultured",
"DNA",
"Gene Expression Regulation",
"Humans",
"I-kappa B Proteins",
"Inflammation Mediators",
"Interleukin-6",
"Interleukin-8",
"Phosphorylation",
"RNA, Messenger",
"Sleep Apnea, Obstructive",
"Transcription Factor RelA",
"Tumor Necrosis Factor-alpha"
]
} | Human adipocytes demonstrate strong sensitivity to inflammatory gene expression in response to acute IH and hence, adipose tissue may be a key source of inflammatory mediators in OSA. | yes | [
{
"from": "human",
"value": "Question: Are human adipocytes highly sensitive to intermittent hypoxia induced NF-kappaB activity and subsequent inflammatory gene expression?\nContext: {'contexts': ['Intermittent hypoxia (IH)-induced activation of pro-inflammatory pathways is a major contributing factor to the cardiovascular pathophysiology associated with obstructive sleep apnea (OSA). Obesity is commonly associated with OSA although it remains unknown whether adipose tissue is a major source of inflammatory mediators in response to IH. The aim of this study was to test the hypothesis that IH leads to augmented inflammatory responses in human adipocytes when compared to cells of non-adipocyte lineages.', 'Human primary subcutaneous and visceral adipocytes, human primary microvascular pulmonary endothelial cells (HUMEC-L) and human primary small airway epithelial cells (SAEC) were exposed to 0, 6 or 12 cycles of IH or stimulated with tumor necrosis factor (TNF)-α. IH led to a robust increase in NF-κB DNA-binding activity in adipocytes compared with normoxic controls regardless of whether the source of adipocytes was visceral or subcutaneous. Notably, the NF-κB response of adipocytes to both IH and TNF-α was significantly greater than that in HUMEC-L and SAEC. Western blotting confirmed enhanced nuclear translocation of p65 in adipocytes in response to IH, accompanied by phosphorylation of I-κB. Parallel to p65 activation, we observed a significant increase in secretion of the adipokines interleukin (IL)-8, IL-6 and TNF-α with IH in adipocytes accompanied by significant upregulation of mRNA expression. PCR-array suggested profound influence of IH on pro-inflammatory gene expression in adipocytes.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Active Transport, Cell Nucleus', 'Adipocytes, White', 'Adipokines', 'Cardiovascular Diseases', 'Cell Hypoxia', 'Cells, Cultured', 'DNA', 'Gene Expression Regulation', 'Humans', 'I-kappa B Proteins', 'Inflammation Mediators', 'Interleukin-6', 'Interleukin-8', 'Phosphorylation', 'RNA, Messenger', 'Sleep Apnea, Obstructive', 'Transcription Factor RelA', 'Tumor Necrosis Factor-alpha']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,749,241 | Does increasing functional variability in the preparatory phase of the takeoff improve elite springboard diving performance? | {
"contexts": [
"Previous research demonstrating that specific performance outcome goals can be achieved in different ways is functionally significant for springboard divers whose performance environment can vary extensively. This body of work raises questions about the traditional approach of balking (terminating the takeoff) by elite divers aiming to perform only identical, invariant movement patterns during practice.",
"A 12-week training program (2 times per day; 6.5 hr per day) was implemented with 4 elite female springboard divers to encourage them to adapt movement patterns under variable takeoff conditions and complete intended dives, rather than balk.",
"Intraindividual analyses revealed small increases in variability in the board-work component of each diver's pretraining and posttraining program reverse-dive takeoffs. No topological differences were observed between movement patterns of dives completed pretraining and posttraining. Differences were noted in the amount of movement variability under different training conditions (evidenced by higher normalized root mean square error indexes posttraining). An increase in the number of completed dives (from 78.91%-86.84% to 95.59%-99.29%) and a decrease in the frequency of balked takeoffs (from 13.16%-19.41% to 0.63%-4.41%) showed that the elite athletes were able to adapt their behaviors during the training program. These findings coincided with greater consistency in the divers' performance during practice as scored by qualified judges."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Athletic Performance",
"Biomechanical Phenomena",
"Diving",
"Female",
"Humans",
"Physical Conditioning, Human",
"Young Adult"
]
} | Results suggested that on completion of training, athletes were capable of successfully adapting their movement patterns under more varied takeoff conditions to achieve greater consistency and stability of performance outcomes. | yes | [
{
"from": "human",
"value": "Question: Does increasing functional variability in the preparatory phase of the takeoff improve elite springboard diving performance?\nContext: {'contexts': ['Previous research demonstrating that specific performance outcome goals can be achieved in different ways is functionally significant for springboard divers whose performance environment can vary extensively. This body of work raises questions about the traditional approach of balking (terminating the takeoff) by elite divers aiming to perform only identical, invariant movement patterns during practice.', 'A 12-week training program (2 times per day; 6.5 hr per day) was implemented with 4 elite female springboard divers to encourage them to adapt movement patterns under variable takeoff conditions and complete intended dives, rather than balk.', \"Intraindividual analyses revealed small increases in variability in the board-work component of each diver's pretraining and posttraining program reverse-dive takeoffs. No topological differences were observed between movement patterns of dives completed pretraining and posttraining. Differences were noted in the amount of movement variability under different training conditions (evidenced by higher normalized root mean square error indexes posttraining). An increase in the number of completed dives (from 78.91%-86.84% to 95.59%-99.29%) and a decrease in the frequency of balked takeoffs (from 13.16%-19.41% to 0.63%-4.41%) showed that the elite athletes were able to adapt their behaviors during the training program. These findings coincided with greater consistency in the divers' performance during practice as scored by qualified judges.\"], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Athletic Performance', 'Biomechanical Phenomena', 'Diving', 'Female', 'Humans', 'Physical Conditioning, Human', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,754,509 | Are anticytomegalovirus antibody titres associated with caregiving burden in younger caregivers? | {
"contexts": [
"This analysis examines whether or not younger caregivers, parents of children with developmental disabilities, differed from controls in terms of cytomegalovirus (CMV) seropositivity and CMV-specific antibody titre. Secondly, it examined whether any particular socio-demographics, health behaviours, or psychological/caregiving variables were associated with a higher CMV antibody titre among caregivers.",
"Young caregivers and age- and sex-matched controls were compared with respect to their reported health behaviour and psychosocial status as well as latent virus control.",
"One hundred and seventeen parents of children with developmental disabilities and 52 control parents completed standard measures of health behaviours, socio-demographics, perceived stress, depression and anxiety, caregiver burden, child problem behaviours. They also provided a blood sample assayed for the presence of CMV-specific antibody.",
"Caregivers were no more likely to be CMV positive than controls and did not have higher antibody titres against CMV. In addition, there was no association between CMV antibody titre in seropositive caregivers and any of the psychological/caregiving variables. However, higher CMV antibody titres were significantly associated with a higher BMI, lower exercise levels, smoking, and lower fruit and vegetable and fat intake among seropositive caregivers."
],
"labels": [
"OBJECTIVE",
"METHODS",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Antibodies, Viral",
"Anxiety",
"Caregivers",
"Cost of Illness",
"Cytomegalovirus Infections",
"Depression",
"Female",
"Health Behavior",
"Humans",
"Male",
"Parents",
"Socioeconomic Factors",
"Stress, Psychological",
"Surveys and Questionnaires"
]
} | These data suggest that in the absence of immunosenescence, the chronic stress of caregiving is not sufficient to compromise the immune response to persistent CMV infection. However, an indirect mechanism to poorer health in caregivers might be via adoption of disadvantageous health behaviours in response to stress. Statement of contribution What is already known on this subject? Older caregivers of spouses with dementia show a poorer immune response against latent viruses when compared to age- and sex-matched controls. Younger parental caregivers of children with developmental disabilities show a poorer antibody response to vaccination. What does this study add? The study showed no association between caregiving stress and CMV antibody titre in young caregivers. There were higher CMV antibody titres in the caregivers who engage in unhealthy behaviours. | no | [
{
"from": "human",
"value": "Question: Are anticytomegalovirus antibody titres associated with caregiving burden in younger caregivers?\nContext: {'contexts': ['This analysis examines whether or not younger caregivers, parents of children with developmental disabilities, differed from controls in terms of cytomegalovirus (CMV) seropositivity and CMV-specific antibody titre. Secondly, it examined whether any particular socio-demographics, health behaviours, or psychological/caregiving variables were associated with a higher CMV antibody titre among caregivers.', 'Young caregivers and age- and sex-matched controls were compared with respect to their reported health behaviour and psychosocial status as well as latent virus control.', 'One hundred and seventeen parents of children with developmental disabilities and 52 control parents completed standard measures of health behaviours, socio-demographics, perceived stress, depression and anxiety, caregiver burden, child problem behaviours. They also provided a blood sample assayed for the presence of CMV-specific antibody.', 'Caregivers were no more likely to be CMV positive than controls and did not have higher antibody titres against CMV. In addition, there was no association between CMV antibody titre in seropositive caregivers and any of the psychological/caregiving variables. However, higher CMV antibody titres were significantly associated with a higher BMI, lower exercise levels, smoking, and lower fruit and vegetable and fat intake among seropositive caregivers.'], 'labels': ['OBJECTIVE', 'METHODS', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Antibodies, Viral', 'Anxiety', 'Caregivers', 'Cost of Illness', 'Cytomegalovirus Infections', 'Depression', 'Female', 'Health Behavior', 'Humans', 'Male', 'Parents', 'Socioeconomic Factors', 'Stress, Psychological', 'Surveys and Questionnaires']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
24,749,793 | Is maternal sleep duration and complaints of vital exhaustion during pregnancy associated with placental abruption? | {
"contexts": [
"Sleep disorders are associated with cardiovascular complications and preterm delivery (PTD). Insufficient sleep results in metabolic alterations and increased inflammation, both known to contribute to placental abruption (abruption), a determinant of PTD. We examined associations of abruption with sleep duration and complaints of vital exhaustion.",
"The study included 164 abruption cases and 160 controls in a multicenter study in Peru. Data on habitual sleep duration and vital exhaustion during the first 6 months of pregnancy were elicited during interviews conducted following delivery. Women were categorized according to short, normal and long sleep duration (≤6, 7-8 and ≥9 h); and frequency of feeling exhausted. Odds ratios (OR) and 95% confidence intervals (CI) were calculated.",
"Short and long sleep durations were associated with increased odds of abruption. The ORs of abruption in relation to short (≤6 h) and long (≥9 h) sleep duration were 2.0 (95% CI 1.1-3.7) and 2.1 (95% CI 1.1-4.1), compared with normal sleep duration (7-8 h). Complaints of vital exhaustion were also associated with abruption (OR = 2.37; 95% CI 1.46-3.85), and were independent of sleep duration."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Abruptio Placentae",
"Adult",
"Case-Control Studies",
"Female",
"Humans",
"Odds Ratio",
"Pregnancy",
"Pregnancy Complications",
"Risk Factors",
"Sleep",
"Sleep Wake Disorders",
"Stress, Psychological",
"Young Adult"
]
} | We extend the existing literature and support the thesis that maternal sleep habits and disorders should be assessed among pregnant women. | yes | [
{
"from": "human",
"value": "Question: Is maternal sleep duration and complaints of vital exhaustion during pregnancy associated with placental abruption?\nContext: {'contexts': ['Sleep disorders are associated with cardiovascular complications and preterm delivery (PTD). Insufficient sleep results in metabolic alterations and increased inflammation, both known to contribute to placental abruption (abruption), a determinant of PTD. We examined associations of abruption with sleep duration and complaints of vital exhaustion.', 'The study included 164 abruption cases and 160 controls in a multicenter study in Peru. Data on habitual sleep duration and vital exhaustion during the first 6 months of pregnancy were elicited during interviews conducted following delivery. Women were categorized according to short, normal and long sleep duration (≤6, 7-8 and ≥9\\u2009h); and frequency of feeling exhausted. Odds ratios (OR) and 95% confidence intervals (CI) were calculated.', 'Short and long sleep durations were associated with increased odds of abruption. The ORs of abruption in relation to short (≤6\\u2009h) and long (≥9\\u2009h) sleep duration were 2.0 (95% CI 1.1-3.7) and 2.1 (95% CI 1.1-4.1), compared with normal sleep duration (7-8\\u2009h). Complaints of vital exhaustion were also associated with abruption (OR\\u2009=\\u20092.37; 95% CI 1.46-3.85), and were independent of sleep duration.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Abruptio Placentae', 'Adult', 'Case-Control Studies', 'Female', 'Humans', 'Odds Ratio', 'Pregnancy', 'Pregnancy Complications', 'Risk Factors', 'Sleep', 'Sleep Wake Disorders', 'Stress, Psychological', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,749,794 | Is the passage of meconium alone a sign of correctly positioned anus? | {
"contexts": [
"The aim of this study is to determine the consequences of delayed presentation of anorectal malformations and emphasize the causes of delayed diagnosis of these malformations.",
"We retrospectively reviewed 54 neonatal patients with a diagnosis of anorectal malformations. Group 1 consisted of 35 patients diagnosed within the first 48 h of life and Group 2 included 19 patients diagnosed after 48 h of life.",
"Obstructive symptoms at the time of diagnosis, overall complications and the mean postoperative hospitalization period in Group 2 were markedly higher than that of Group 1. A comprehensive neonatal examination within the first 48 h of life was performed in 32 (91.4%) patients in Group 1 and 5 (26.3%) of the patients in Group 2 (p < 0.001)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Anal Canal",
"Anorectal Malformations",
"Anus, Imperforate",
"Delayed Diagnosis",
"Female",
"Humans",
"Infant, Newborn",
"Male",
"Meconium",
"Physical Examination",
"Rectum",
"Reflex",
"Retrospective Studies"
]
} | The passage of meconium is not the only sign of correctly positioned anus. A careful physical examination and awareness of this anomaly are of great importance in making a timely diagnosis of anorectal malformations. | no | [
{
"from": "human",
"value": "Question: Is the passage of meconium alone a sign of correctly positioned anus?\nContext: {'contexts': ['The aim of this study is to determine the consequences of delayed presentation of anorectal malformations and emphasize the causes of delayed diagnosis of these malformations.', 'We retrospectively reviewed 54 neonatal patients with a diagnosis of anorectal malformations. Group 1 consisted of 35 patients diagnosed within the first 48\\u2009h of life and Group 2 included 19 patients diagnosed after 48\\u2009h of life.', 'Obstructive symptoms at the time of diagnosis, overall complications and the mean postoperative hospitalization period in Group 2 were markedly higher than that of Group 1. A comprehensive neonatal examination within the first 48\\u2009h of life was performed in 32 (91.4%) patients in Group 1 and 5 (26.3%) of the patients in Group 2 (p\\u2009<\\u20090.001).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Anal Canal', 'Anorectal Malformations', 'Anus, Imperforate', 'Delayed Diagnosis', 'Female', 'Humans', 'Infant, Newborn', 'Male', 'Meconium', 'Physical Examination', 'Rectum', 'Reflex', 'Retrospective Studies']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
24,769,132 | Is endocan useful biomarker of survival and severity in sepsis? | {
"contexts": [
"Coagulation abnormalities which occur as a consequence of endothelial changes are recognized as diagnostic criteria for sepsis, but significance of these changes in the outcome prognosis and prediction of the course of sepsis is still not accurately defined.",
"60 patients who fulfilled the criteria for diagnosis of sepsis were included in our study. Patients were categorized in two groups according to sepsis severity and organ failure and MODS development was assessed in the first 48 h from ICU admission. Prothrombin time (PT), activated partial thromboplastin time (aPTT) and endothelial cell specific molecule-1(endocan) levels, as well as procalcitonin (PCT) and C-reactive protein (CRP) were determined within the first 24h of the onset of the disease. Predictive APACHE II (Acute Physiology and Chronic Health Evaluation II) and SOFA (Sequential Organ Failure Assessment) scores were calculated on the day of ICU admission. Data were used to determine an association between day 1 biomarker levels, organ dysfunction score values and the development of organ failure, multiple organ dysfunction syndrome (MODS), and mortality during 28 days. These connections were determined by plotting of receiver operating characteristic (ROC) curves. Differences between groups were assessed by Mann-Whitney U test. Categorical variables were compared using chi-square test.",
"Concentration of endocan was significantly higher in the group of patients with sepsis induced organ failure, MODS development and in the group of non- survivors in contrast to group with less severe form of the disease, without multiorgan failure, and in contrast to group of survivors (p<0.05). Values of areas under the ROC curves showed that endocan levels had good discriminative power for more severe course of sepsis, MODS development and possible discriminative power for mortality prediction (AUC: 0.81, 0.67, 0.71 retrospectively), better than PCT for fatality (AUC:053) and better than APACHE II (AUC:0.55) and SOFA (AUC: 0.57) scores for organ failure."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"APACHE",
"Adult",
"Aged",
"Aged, 80 and over",
"Area Under Curve",
"Biomarkers",
"C-Reactive Protein",
"Calcitonin",
"Calcitonin Gene-Related Peptide",
"Chi-Square Distribution",
"Female",
"Humans",
"Male",
"Middle Aged",
"Multiple Organ Failure",
"Neoplasm Proteins",
"Organ Dysfunction Scores",
"Partial Thromboplastin Time",
"Predictive Value of Tests",
"Prognosis",
"Protein Precursors",
"Proteoglycans",
"Prothrombin Time",
"ROC Curve",
"Retrospective Studies",
"Sepsis",
"Severity of Illness Index",
"Up-Regulation"
]
} | Results of our study show that endocan can be used as strong and significant predictor of sepsis severity and outcome, perhaps even better than SOFA and APACHE II scores. | yes | [
{
"from": "human",
"value": "Question: Is endocan useful biomarker of survival and severity in sepsis?\nContext: {'contexts': ['Coagulation abnormalities which occur as a consequence of endothelial changes are recognized as diagnostic criteria for sepsis, but significance of these changes in the outcome prognosis and prediction of the course of sepsis is still not accurately defined.', '60 patients who fulfilled the criteria for diagnosis of sepsis were included in our study. Patients were categorized in two groups according to sepsis severity and organ failure and MODS development was assessed in the first 48 h from ICU admission. Prothrombin time (PT), activated partial thromboplastin time (aPTT) and endothelial cell specific molecule-1(endocan) levels, as well as procalcitonin (PCT) and C-reactive protein (CRP) were determined within the first 24h of the onset of the disease. Predictive APACHE II (Acute Physiology and Chronic Health Evaluation II) and SOFA (Sequential Organ Failure Assessment) scores were calculated on the day of ICU admission. Data were used to determine an association between day 1 biomarker levels, organ dysfunction score values and the development of organ failure, multiple organ dysfunction syndrome (MODS), and mortality during 28 days. These connections were determined by plotting of receiver operating characteristic (ROC) curves. Differences between groups were assessed by Mann-Whitney U test. Categorical variables were compared using chi-square test.', 'Concentration of endocan was significantly higher in the group of patients with sepsis induced organ failure, MODS development and in the group of non- survivors in contrast to group with less severe form of the disease, without multiorgan failure, and in contrast to group of survivors (p<0.05). Values of areas under the ROC curves showed that endocan levels had good discriminative power for more severe course of sepsis, MODS development and possible discriminative power for mortality prediction (AUC: 0.81, 0.67, 0.71 retrospectively), better than PCT for fatality (AUC:053) and better than APACHE II (AUC:0.55) and SOFA (AUC: 0.57) scores for organ failure.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['APACHE', 'Adult', 'Aged', 'Aged, 80 and over', 'Area Under Curve', 'Biomarkers', 'C-Reactive Protein', 'Calcitonin', 'Calcitonin Gene-Related Peptide', 'Chi-Square Distribution', 'Female', 'Humans', 'Male', 'Middle Aged', 'Multiple Organ Failure', 'Neoplasm Proteins', 'Organ Dysfunction Scores', 'Partial Thromboplastin Time', 'Predictive Value of Tests', 'Prognosis', 'Protein Precursors', 'Proteoglycans', 'Prothrombin Time', 'ROC Curve', 'Retrospective Studies', 'Sepsis', 'Severity of Illness Index', 'Up-Regulation']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,752,868 | Does hepatocyte nuclear factor 4α-nuclear factor-κB feedback circuit modulate liver cancer progression? | {
"contexts": [
"Hepatocyte nuclear factor 4α (HNF4α) is a liver enriched transcription factor and is indispensable for liver development. However, the role of HNF4α in hepatocellular carcinoma (HCC) progression remains to be elucidated. We report that reduced HNF4α expression correlated well with the aggressive clinicopathological characteristics of HCC and predicted poor prognosis of patients. HNF4α levels were even lower in metastatic HCCs, and ectopic HNF4α expression suppressed the metastasis of hepatoma cells both in vitro and in vivo. Forced HNF4α expression attenuated the expression and nuclear translocation of RelA (p65) and impaired NF-κB activation through an IKK-independent mechanism. Blockage of RelA robustly attenuated the suppressive effect of HNF4α on hepatoma cell metastasis. MicroRNA (miR)-7 and miR-124 were transcriptionally up-regulated by HNF4α, which repressed RelA expression by way of interaction with RelA-3' untranslated region (UTR). In addition, nuclear factor kappa B (NF-κB) up-regulated the expression of miR-21 in hepatoma cells, resulting in decreased HNF4α levels through down-regulating HNF4α-3'UTR activity."
],
"labels": [
"UNLABELLED"
],
"meshes": [
"Adult",
"Aged",
"Aged, 80 and over",
"Animals",
"Carcinoma, Hepatocellular",
"Cells, Cultured",
"China",
"Disease Progression",
"Epithelial-Mesenchymal Transition",
"Feedback, Physiological",
"Female",
"Hepatocyte Nuclear Factor 4",
"Humans",
"Liver Neoplasms",
"Male",
"MicroRNAs",
"Middle Aged",
"NF-kappa B",
"Rats, Wistar",
"Transcription Factor RelA",
"Young Adult"
]
} | Collectively, an HNF4α-NF-κB feedback circuit including miR-124, miR-7, and miR-21 was identified in HCC, and the combination of HNF4α and NF-κB exhibited more powerful predictive efficiency of patient prognosis. These findings broaden the knowledge of hepatic inflammation and cancer initiation/progression, and also provide novel prognostic biomarkers and therapeutic targets for HCC. | yes | [
{
"from": "human",
"value": "Question: Does hepatocyte nuclear factor 4α-nuclear factor-κB feedback circuit modulate liver cancer progression?\nContext: {'contexts': [\"Hepatocyte nuclear factor 4α (HNF4α) is a liver enriched transcription factor and is indispensable for liver development. However, the role of HNF4α in hepatocellular carcinoma (HCC) progression remains to be elucidated. We report that reduced HNF4α expression correlated well with the aggressive clinicopathological characteristics of HCC and predicted poor prognosis of patients. HNF4α levels were even lower in metastatic HCCs, and ectopic HNF4α expression suppressed the metastasis of hepatoma cells both in vitro and in vivo. Forced HNF4α expression attenuated the expression and nuclear translocation of RelA (p65) and impaired NF-κB activation through an IKK-independent mechanism. Blockage of RelA robustly attenuated the suppressive effect of HNF4α on hepatoma cell metastasis. MicroRNA (miR)-7 and miR-124 were transcriptionally up-regulated by HNF4α, which repressed RelA expression by way of interaction with RelA-3' untranslated region (UTR). In addition, nuclear factor kappa B (NF-κB) up-regulated the expression of miR-21 in hepatoma cells, resulting in decreased HNF4α levels through down-regulating HNF4α-3'UTR activity.\"], 'labels': ['UNLABELLED'], 'meshes': ['Adult', 'Aged', 'Aged, 80 and over', 'Animals', 'Carcinoma, Hepatocellular', 'Cells, Cultured', 'China', 'Disease Progression', 'Epithelial-Mesenchymal Transition', 'Feedback, Physiological', 'Female', 'Hepatocyte Nuclear Factor 4', 'Humans', 'Liver Neoplasms', 'Male', 'MicroRNAs', 'Middle Aged', 'NF-kappa B', 'Rats, Wistar', 'Transcription Factor RelA', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,751,748 | Do intraoperative measurement for a new transcutaneous bone conduction hearing implant? | {
"contexts": [
"To investigate the possibility of using a modified reverse transfer function (RTF) measurement intraoperatively during surgery of a new transcutaneous bone conduction hearing implant to evaluate the status of the device.",
"Tests were performed on a cadaver skull (preclinically) and two conductive hearing loss patients implanted with a new transcutaneous bone conduction implant. During intraoperative activation, the RTF was measured using a microphone attached perpendicularly and directly to the skin in the middle section of the forehead.",
"The RTF could be measured for all frequencies from 500 to 6, 000 Hz."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Audiometry",
"Bone Conduction",
"Hearing Aids",
"Hearing Loss, Conductive",
"Humans",
"Prostheses and Implants"
]
} | The usage of an intraoperative RTF measurement may be a good method to verify the mechanical coupling of the bone conduction floating mass transducer and to test the functional integrity of the implant in an objective way. | yes | [
{
"from": "human",
"value": "Question: Do intraoperative measurement for a new transcutaneous bone conduction hearing implant?\nContext: {'contexts': ['To investigate the possibility of using a modified reverse transfer function (RTF) measurement intraoperatively during surgery of a new transcutaneous bone conduction hearing implant to evaluate the status of the device.', 'Tests were performed on a cadaver skull (preclinically) and two conductive hearing loss patients implanted with a new transcutaneous bone conduction implant. During intraoperative activation, the RTF was measured using a microphone attached perpendicularly and directly to the skin in the middle section of the forehead.', 'The RTF could be measured for all frequencies from 500 to 6, 000 Hz.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Audiometry', 'Bone Conduction', 'Hearing Aids', 'Hearing Loss, Conductive', 'Humans', 'Prostheses and Implants']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,752,092 | Does [ Sanhuangyinchi decoction pretreatment ameliorate acute hepatic failure in rats by suppressing antioxidant stress and caspase-3 expression ]? | {
"contexts": [
"To observe the effects of Sanhuangyinchi decoction (SHYCD) pretreatment on acute hepatic failure (AHF) induced by D-galactosamine and lipopolysaccharide (LPS) in rats and explore the possible mechanisms involving antioxidant stress and cell apoptosis-related protein expression.",
"Forty-eight SD rats were randomized equally into control group, AHF model group, high-, medium- and low-dose SHYCD groups, and Bicyclol group. Five days after administration of the corresponding drugs, the rats were challenged with peritoneal D-galactosamine (700 mg/kg) plus LPS (10 ug/kg) injections to induce AHF acute hepatic failure except for those in the control group. At 48 h after the injections, blood samples were collected from the rats to detect the levels of ALT, AST, TBIL, PT, INR and FIB, and pathological changes and superoxide dismutase (SOD) and malondialdehyde (MDA) contents in the liver were examined; immunohistochemistry and western blotting were used to detect caspase-3 protein expression in the liver.",
"The levels of ALT, AST, TBIL, TP and INR in the 3 SHYCD groups and Bicyclol group significantly decreased (P<0.05) while FIB significantly increased in comparison with those in the model group. SHYCD obviously ameliorated the pathological changes, enhanced SOD activity (P<0.05), and decreased MDA levels (P<0.05) and caspase-3 expression (P<0.05) in the liver tissue. SHYCD at the medium dose produced similar effects to Bicyclol (P>0.05) and showed better effects at the high dose than Bicyclol (P<0.05)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Caspase 3",
"Drugs, Chinese Herbal",
"Liver Failure, Acute",
"Male",
"Malondialdehyde",
"Oxidative Stress",
"Phytotherapy",
"Rats",
"Rats, Sprague-Dawley",
"Superoxide Dismutase"
]
} | SHYCD pretreatment can dose-dependently ameliorate AHF in rats possibly by suppressing antioxidant stress and caspase-3 expression to decrease hepatic cell apoptosis. | yes | [
{
"from": "human",
"value": "Question: Does [ Sanhuangyinchi decoction pretreatment ameliorate acute hepatic failure in rats by suppressing antioxidant stress and caspase-3 expression ]?\nContext: {'contexts': ['To observe the effects of Sanhuangyinchi decoction (SHYCD) pretreatment on acute hepatic failure (AHF) induced by D-galactosamine and lipopolysaccharide (LPS) in rats and explore the possible mechanisms involving antioxidant stress and cell apoptosis-related protein expression.', 'Forty-eight SD rats were randomized equally into control group, AHF model group, high-, medium- and low-dose SHYCD groups, and Bicyclol group. Five days after administration of the corresponding drugs, the rats were challenged with peritoneal D-galactosamine (700 mg/kg) plus LPS (10 ug/kg) injections to induce AHF acute hepatic failure except for those in the control group. At 48 h after the injections, blood samples were collected from the rats to detect the levels of ALT, AST, TBIL, PT, INR and FIB, and pathological changes and superoxide dismutase (SOD) and malondialdehyde (MDA) contents in the liver were examined; immunohistochemistry and western blotting were used to detect caspase-3 protein expression in the liver.', 'The levels of ALT, AST, TBIL, TP and INR in the 3 SHYCD groups and Bicyclol group significantly decreased (P<0.05) while FIB significantly increased in comparison with those in the model group. SHYCD obviously ameliorated the pathological changes, enhanced SOD activity (P<0.05), and decreased MDA levels (P<0.05) and caspase-3 expression (P<0.05) in the liver tissue. SHYCD at the medium dose produced similar effects to Bicyclol (P>0.05) and showed better effects at the high dose than Bicyclol (P<0.05).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Caspase 3', 'Drugs, Chinese Herbal', 'Liver Failure, Acute', 'Male', 'Malondialdehyde', 'Oxidative Stress', 'Phytotherapy', 'Rats', 'Rats, Sprague-Dawley', 'Superoxide Dismutase']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,752,094 | Does [ 1,25-dihydroxyvitamin D3 pretreatment inhibit house dust mite-induced thymic stromal lymphopoietin release by human airway epithelial cells ]? | {
"contexts": [
"To investigate the effect of 1,25-dihydroxyvitamin D3 (1,25VD3) on house dust mites (HDM)-induced expression of thymic stromal lymphopoietin (TSLP) in human airway epithelial cells in vitro.",
"Human airway epithelial 16HBE cells were incubated with 200, 400, and 800 U/L in the absence or presence of 1,25VD3 (10(-8) mol/L) for 6 h and 24 h, and TSLP mRNA and protein expressions in the cells were assessed using quantitative PCR and ELISA.",
"16HBE cells incubated with HDM at 200, 400, and 800 U/L showed significantly increased TSLP mRNA and protein expressions (P<0.05). Pretreatment of the cells with 1,25VD3 obviously lowered 400 U/L HDM-induced TSLP expressions (P<0.05), but 1,25VD3 added along with HDM in the cells did not produce significant effects on TSLP expressions (P=0.58)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Bronchi",
"Calcitriol",
"Cell Line",
"Cytokines",
"Epithelial Cells",
"Humans",
"Pyroglyphidae"
]
} | Both 1,25VD3 and HDM can induce TSLP expression and release in 16HBE cells, but pretreatment with 1,25VD3 can decrease HDM-augmented TSLP expression in the cells. | yes | [
{
"from": "human",
"value": "Question: Does [ 1,25-dihydroxyvitamin D3 pretreatment inhibit house dust mite-induced thymic stromal lymphopoietin release by human airway epithelial cells ]?\nContext: {'contexts': ['To investigate the effect of 1,25-dihydroxyvitamin D3 (1,25VD3) on house dust mites (HDM)-induced expression of thymic stromal lymphopoietin (TSLP) in human airway epithelial cells in vitro.', 'Human airway epithelial 16HBE cells were incubated with 200, 400, and 800 U/L in the absence or presence of 1,25VD3 (10(-8) mol/L) for 6 h and 24 h, and TSLP mRNA and protein expressions in the cells were assessed using quantitative PCR and ELISA.', '16HBE cells incubated with HDM at 200, 400, and 800 U/L showed significantly increased TSLP mRNA and protein expressions (P<0.05). Pretreatment of the cells with 1,25VD3 obviously lowered 400 U/L HDM-induced TSLP expressions (P<0.05), but 1,25VD3 added along with HDM in the cells did not produce significant effects on TSLP expressions (P=0.58).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Bronchi', 'Calcitriol', 'Cell Line', 'Cytokines', 'Epithelial Cells', 'Humans', 'Pyroglyphidae']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,752,098 | Does [ SCF/c-Kit signaling promote invasion of T24 cells via PI3K pathway ]? | {
"contexts": [
"To explore the role of SCF/c-Kit signaling in the invasion of bladder cancer T24 cells.",
"Western blotting was used to detect the expression of c-Kit and PI3K pathway activation stimulated by stem cell factor (SCF) in T24 cells. The invasiveness of T24 cells before and after SCF stimulation and Wortmannin (aspecific PI3K inhibitor) treatment was evaluated using Transwell invasion assay (direct and indirect counting methods).",
"T24 cells expressed c-Kit protein and showed obvious Akt phosphorylation after stimulation with SCF (1 ng/ml) for 24 h. Compared to the control group, SCF stimulation (1 ng/ml) caused a greater number of T24 cells to migrate through the polycarbonate film (P<0.01), and this effect was blocked by the application of Wortmannin before the stimulation."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Carcinoma, Transitional Cell",
"Cell Line, Tumor",
"Humans",
"Neoplasm Invasiveness",
"Proto-Oncogene Proteins c-kit",
"Signal Transduction",
"Stem Cell Factor",
"Urinary Bladder Neoplasms"
]
} | SCF/c-Kit signaling promotes the invasiveness of T24 cells, and this effect is mediated by the PI3K pathway. | yes | [
{
"from": "human",
"value": "Question: Does [ SCF/c-Kit signaling promote invasion of T24 cells via PI3K pathway ]?\nContext: {'contexts': ['To explore the role of SCF/c-Kit signaling in the invasion of bladder cancer T24 cells.', 'Western blotting was used to detect the expression of c-Kit and PI3K pathway activation stimulated by stem cell factor (SCF) in T24 cells. The invasiveness of T24 cells before and after SCF stimulation and Wortmannin (aspecific PI3K inhibitor) treatment was evaluated using Transwell invasion assay (direct and indirect counting methods).', 'T24 cells expressed c-Kit protein and showed obvious Akt phosphorylation after stimulation with SCF (1 ng/ml) for 24 h. Compared to the control group, SCF stimulation (1 ng/ml) caused a greater number of T24 cells to migrate through the polycarbonate film (P<0.01), and this effect was blocked by the application of Wortmannin before the stimulation.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Carcinoma, Transitional Cell', 'Cell Line, Tumor', 'Humans', 'Neoplasm Invasiveness', 'Proto-Oncogene Proteins c-kit', 'Signal Transduction', 'Stem Cell Factor', 'Urinary Bladder Neoplasms']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,752,115 | Does [ Serum follicle-stimulating hormone in combination with serum inhibin B evaluate spermatogenesis of azoospermic men ]? | {
"contexts": [
"This study is in an attempt to evaluate the diagnostic significance to predict the spermatogenesis of azoospermic men in examination of serum follicle-stimulating hormone (FSH) combination with serum inhibin B (INHB).",
"Quantitative examination of serum FSH and INHB was performed in 95 case of azoospermic men. According to their classifications of testicular biopsy with histopathological examination, there were 20 patients of Sertoli cell only, 25 of hypospermatogenesis, 18 of spermatogenic maturation arrest (complete or incomplete), and 32 of normal spermatogenesis. The association of serum FSH and INHB levels with histopathological classifications were analyzed by using statistical software.",
"Serum FSH, INHB and INHB/FSH levels of Sertoli cell only differed with statistical significance from hypospermatogenesis, spermatogenic maturation arrest and normal spermatogenesis (P<0.05). FSH, in which there were no statistical significance among the latter three classifications (P>0.05). Serum FSH, INHB and INHB/FSH levels were no relationship with maturation arrest (P>0.05), but were negatively related to the other classifications (P<0.05). INHB level less than 28.55 pg/ml predicted Sertoli cell only in a sensitivity of 97% and a specificity of 85%."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Azoospermia",
"Follicle Stimulating Hormone",
"Humans",
"Infertility, Male",
"Inhibins",
"Male",
"Middle Aged",
"Oligospermia",
"Spermatogenesis",
"Testis",
"Young Adult"
]
} | Serum FSH and INHB levels is ineffective to distinguish the spermatogenic classifications from azoospermic men, but they are available to confirm the disease of Sertoli cell only. The other abnormalities of azoospermic men is also dependent on bioptic histopathology to confirm the subtypes. | yes | [
{
"from": "human",
"value": "Question: Does [ Serum follicle-stimulating hormone in combination with serum inhibin B evaluate spermatogenesis of azoospermic men ]?\nContext: {'contexts': ['This study is in an attempt to evaluate the diagnostic significance to predict the spermatogenesis of azoospermic men in examination of serum follicle-stimulating hormone (FSH) combination with serum inhibin B (INHB).', 'Quantitative examination of serum FSH and INHB was performed in 95 case of azoospermic men. According to their classifications of testicular biopsy with histopathological examination, there were 20 patients of Sertoli cell only, 25 of hypospermatogenesis, 18 of spermatogenic maturation arrest (complete or incomplete), and 32 of normal spermatogenesis. The association of serum FSH and INHB levels with histopathological classifications were analyzed by using statistical software.', 'Serum FSH, INHB and INHB/FSH levels of Sertoli cell only differed with statistical significance from hypospermatogenesis, spermatogenic maturation arrest and normal spermatogenesis (P<0.05). FSH, in which there were no statistical significance among the latter three classifications (P>0.05). Serum FSH, INHB and INHB/FSH levels were no relationship with maturation arrest (P>0.05), but were negatively related to the other classifications (P<0.05). INHB level less than 28.55 pg/ml predicted Sertoli cell only in a sensitivity of 97% and a specificity of 85%.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Azoospermia', 'Follicle Stimulating Hormone', 'Humans', 'Infertility, Male', 'Inhibins', 'Male', 'Middle Aged', 'Oligospermia', 'Spermatogenesis', 'Testis', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,773,080 | Does highly prevalent SERPINB7 founder mutation cause pseudodominant inheritance pattern in Nagashima-type palmoplantar keratosis? | {
"contexts": [
"Nagashima-type palmoplantar keratosis (NPPK) is a distinct autosomal recessive genodermatosis characterized by diffuse transgressive palmoplantar keratoderma (PPK). Very recently, putative loss-of-function mutations in SERPINB7, which encodes a member of the serine protease inhibitor superfamily and is abundantly expressed in the epidermis, have been identified as a cause of NPPK.",
"To confirm further the role of SERPINB7 mutations in the pathogenesis of NPPK.",
"We analysed 10 Japanese families with NPPK using Sanger and/or whole-exome sequencing.",
"We identified one novel and three recurrent null mutations in SERPINB7. In all the families, the NPPK trait was inherited in an autosomal recessive manner; in one of the families, there was pseudodominant inheritance, which had not been described in NPPK."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Aged",
"Child",
"Child, Preschool",
"DNA Mutational Analysis",
"Female",
"Founder Effect",
"Genes, Dominant",
"Heterozygote",
"Homozygote",
"Humans",
"Infant",
"Inheritance Patterns",
"Keratoderma, Palmoplantar",
"Male",
"Middle Aged",
"Pedigree",
"Serpins"
]
} | These data clearly provide further evidence that NPPK is caused by loss-of-function mutations in SERPINB7. | yes | [
{
"from": "human",
"value": "Question: Does highly prevalent SERPINB7 founder mutation cause pseudodominant inheritance pattern in Nagashima-type palmoplantar keratosis?\nContext: {'contexts': ['Nagashima-type palmoplantar keratosis (NPPK) is a distinct autosomal recessive genodermatosis characterized by diffuse transgressive palmoplantar keratoderma (PPK). Very recently, putative loss-of-function mutations in SERPINB7, which encodes a member of the serine protease inhibitor superfamily and is abundantly expressed in the epidermis, have been identified as a cause of NPPK.', 'To confirm further the role of SERPINB7 mutations in the pathogenesis of NPPK.', 'We analysed 10 Japanese families with NPPK using Sanger and/or whole-exome sequencing.', 'We identified one novel and three recurrent null mutations in SERPINB7. In all the families, the NPPK trait was inherited in an autosomal recessive manner; in one of the families, there was pseudodominant inheritance, which had not been described in NPPK.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Aged', 'Child', 'Child, Preschool', 'DNA Mutational Analysis', 'Female', 'Founder Effect', 'Genes, Dominant', 'Heterozygote', 'Homozygote', 'Humans', 'Infant', 'Inheritance Patterns', 'Keratoderma, Palmoplantar', 'Male', 'Middle Aged', 'Pedigree', 'Serpins']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,751,313 | Do augmentative therapies potentiate the antidepressant-like effects of deep brain stimulation in rats? | {
"contexts": [
"Clinical trials have shown promising results with the use of subcallosal cingulate gyrus deep brain stimulation (DBS) for treatment-resistant depression. However, strategies to manage patients who do not respond to this therapy have not been explored in detail. In rats, DBS in the ventromedial prefrontal cortex (vmPFC) induces a significant antidepressant-like response in the forced swim test (FST). We have used this test to investigate potential interactions between DBS and clinically used augmentative regimens.",
"Rats undergoing the FST were treated with vmPFC DBS along with different augmentative drugs, namely buspirone, risperidone and pindolol. Locomotor activity was tested in an open field.",
"DBS induced a significant reduction in immobility scores as compared to saline treated controls. These antidepressant-like effects, however, were not potentiated by the co-administration of buspirone, risperidone or pindolol."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Behavior, Animal",
"Buspirone",
"Deep Brain Stimulation",
"Depression",
"Dopamine Antagonists",
"Gyrus Cinguli",
"Male",
"Pindolol",
"Prefrontal Cortex",
"Rats",
"Rats, Sprague-Dawley",
"Risperidone"
]
} | Despite having good predictive validity, animal models are limited from a translational perspective. | no | [
{
"from": "human",
"value": "Question: Do augmentative therapies potentiate the antidepressant-like effects of deep brain stimulation in rats?\nContext: {'contexts': ['Clinical trials have shown promising results with the use of subcallosal cingulate gyrus deep brain stimulation (DBS) for treatment-resistant depression. However, strategies to manage patients who do not respond to this therapy have not been explored in detail. In rats, DBS in the ventromedial prefrontal cortex (vmPFC) induces a significant antidepressant-like response in the forced swim test (FST). We have used this test to investigate potential interactions between DBS and clinically used augmentative regimens.', 'Rats undergoing the FST were treated with vmPFC DBS along with different augmentative drugs, namely buspirone, risperidone and pindolol. Locomotor activity was tested in an open field.', 'DBS induced a significant reduction in immobility scores as compared to saline treated controls. These antidepressant-like effects, however, were not potentiated by the co-administration of buspirone, risperidone or pindolol.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Behavior, Animal', 'Buspirone', 'Deep Brain Stimulation', 'Depression', 'Dopamine Antagonists', 'Gyrus Cinguli', 'Male', 'Pindolol', 'Prefrontal Cortex', 'Rats', 'Rats, Sprague-Dawley', 'Risperidone']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
24,751,319 | Does both body weight and BMI predict improvement in symptom and functioning for patients with major depressive disorder? | {
"contexts": [
"Obesity has shown a positive association with depression. We aimed to investigate the relationships among body weight, body mass index (BMI=kg/m(2)), change in a depression rating scale, and change in a functional scale with fluoxetine treatment for hospitalized patients with major depressive disorder (MDD).",
"A total of 131 acutely ill inpatients with MDD were enrolled to receive 20mg of fluoxetine daily for 6 weeks. The 17-item Hamilton Depression Rating Scale (HAMD-17) for symptom and the Work and Social Adjustment Scale (WSAS) for functioning were assessed at weeks 0, 1, 2, 3, 4, and 6. Remission was defined as a score of≤7 on the HAMD-17 at endpoint. Body weight, body length, and BMI were measured at baseline. Pearson correlation coefficients (r) were calculated among body weight, BMI, HAMD-17 score change, and WSAS score change.",
"Of the 131 participants, 126 (96.2%) had at least one post-baseline assessment and were included in the analysis. Significant differences in body weight and BMI existed between remitters and nonremitters. There were statistically significant relationships among baseline body weight, baseline BMI, HAMD-17 score change, and WSAS score change at end point."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Antidepressive Agents, Second-Generation",
"Body Mass Index",
"Body Weight",
"Depressive Disorder, Major",
"Double-Blind Method",
"Female",
"Fluoxetine",
"Humans",
"Male",
"Middle Aged",
"Obesity",
"Prognosis"
]
} | This is a short-term trial with relatively small sample size. | yes | [
{
"from": "human",
"value": "Question: Does both body weight and BMI predict improvement in symptom and functioning for patients with major depressive disorder?\nContext: {'contexts': ['Obesity has shown a positive association with depression. We aimed to investigate the relationships among body weight, body mass index (BMI=kg/m(2)), change in a depression rating scale, and change in a functional scale with fluoxetine treatment for hospitalized patients with major depressive disorder (MDD).', 'A total of 131 acutely ill inpatients with MDD were enrolled to receive 20mg of fluoxetine daily for 6 weeks. The 17-item Hamilton Depression Rating Scale (HAMD-17) for symptom and the Work and Social Adjustment Scale (WSAS) for functioning were assessed at weeks 0, 1, 2, 3, 4, and 6. Remission was defined as a score of≤7 on the HAMD-17 at endpoint. Body weight, body length, and BMI were measured at baseline. Pearson correlation coefficients (r) were calculated among body weight, BMI, HAMD-17 score change, and WSAS score change.', 'Of the 131 participants, 126 (96.2%) had at least one post-baseline assessment and were included in the analysis. Significant differences in body weight and BMI existed between remitters and nonremitters. There were statistically significant relationships among baseline body weight, baseline BMI, HAMD-17 score change, and WSAS score change at end point.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Antidepressive Agents, Second-Generation', 'Body Mass Index', 'Body Weight', 'Depressive Disorder, Major', 'Double-Blind Method', 'Female', 'Fluoxetine', 'Humans', 'Male', 'Middle Aged', 'Obesity', 'Prognosis']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,749,506 | Is density and duration of pneumococcal carriage maintained by transforming growth factor β1 and T regulatory cells? | {
"contexts": [
"Nasopharyngeal carriage of Streptococcus pneumoniae is a prerequisite for invasive disease, but the majority of carriage episodes are asymptomatic and self-resolving. Interactions determining the development of carriage versus invasive disease are poorly understood but will influence the effectiveness of vaccines or therapeutics that disrupt nasal colonization.",
"We sought to elucidate immunological mechanisms underlying noninvasive pneumococcal nasopharyngeal carriage.",
"Pneumococcal interactions with human nasopharyngeal and bronchial fibroblasts and epithelial cells were investigated in vitro. A murine model of nasopharyngeal carriage and an experimental human pneumococcal challenge model were used to characterize immune responses in the airways during carriage.",
"We describe the previously unknown immunological basis of noninvasive carriage and highlight mechanisms whose perturbation may lead to invasive disease. We identify the induction of active transforming growth factor (TGF)-β1 by S. pneumoniae in human host cells and highlight the key role for TGF-β1 and T regulatory cells in the establishment and maintenance of nasopharyngeal carriage in mice and humans. We identify the ability of pneumococci to drive TGF-β1 production from nasopharyngeal cells in vivo and show that an immune tolerance profile, characterized by elevated TGF-β1 and high nasopharyngeal T regulatory cell numbers, is crucial for prolonged carriage of pneumococci. Blockade of TGF-β1 signaling prevents prolonged carriage and leads to clearance of pneumococci from the nasopharynx."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Biomarkers",
"Carrier State",
"Humans",
"In Vitro Techniques",
"Mice",
"Nasopharynx",
"Pneumococcal Infections",
"Streptococcus pneumoniae",
"T-Lymphocytes, Regulatory",
"Time Factors",
"Transforming Growth Factor beta1"
]
} | These data explain the mechanisms by which S. pneumoniae colonize the human nasopharynx without inducing damaging host inflammation and provide insight into the role of bacterial and host constituents that allow and maintain carriage. | yes | [
{
"from": "human",
"value": "Question: Is density and duration of pneumococcal carriage maintained by transforming growth factor β1 and T regulatory cells?\nContext: {'contexts': ['Nasopharyngeal carriage of Streptococcus pneumoniae is a prerequisite for invasive disease, but the majority of carriage episodes are asymptomatic and self-resolving. Interactions determining the development of carriage versus invasive disease are poorly understood but will influence the effectiveness of vaccines or therapeutics that disrupt nasal colonization.', 'We sought to elucidate immunological mechanisms underlying noninvasive pneumococcal nasopharyngeal carriage.', 'Pneumococcal interactions with human nasopharyngeal and bronchial fibroblasts and epithelial cells were investigated in vitro. A murine model of nasopharyngeal carriage and an experimental human pneumococcal challenge model were used to characterize immune responses in the airways during carriage.', 'We describe the previously unknown immunological basis of noninvasive carriage and highlight mechanisms whose perturbation may lead to invasive disease. We identify the induction of active transforming growth factor (TGF)-β1 by S. pneumoniae in human host cells and highlight the key role for TGF-β1 and T regulatory cells in the establishment and maintenance of nasopharyngeal carriage in mice and humans. We identify the ability of pneumococci to drive TGF-β1 production from nasopharyngeal cells in vivo and show that an immune tolerance profile, characterized by elevated TGF-β1 and high nasopharyngeal T regulatory cell numbers, is crucial for prolonged carriage of pneumococci. Blockade of TGF-β1 signaling prevents prolonged carriage and leads to clearance of pneumococci from the nasopharynx.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Biomarkers', 'Carrier State', 'Humans', 'In Vitro Techniques', 'Mice', 'Nasopharynx', 'Pneumococcal Infections', 'Streptococcus pneumoniae', 'T-Lymphocytes, Regulatory', 'Time Factors', 'Transforming Growth Factor beta1']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,758,222 | Does chronic stress impair GABAergic control of amygdala through suppressing the tonic GABAA receptor currents? | {
"contexts": [
"Chronic stress is generally known to exacerbate the development of numerous neuropsychiatric diseases such as fear and anxiety disorders, which is at least partially due to the disinhibition of amygdala subsequent to the prolonged stress exposure. GABA receptor A (GABAAR) mediates the primary component of inhibition in brain and its activation produces two forms of inhibition: the phasic and tonic inhibition. While both of them are critically engaged in limiting the activity of amygdala, their roles in the amygdala disinhibition subsequent to chronic stress exposure are largely unknown.",
"We investigated the possible alterations of phasic and tonic GABAAR currents and their roles in the amygdala disinhibition subsequent to chronic stress. We found that both chronic immobilization and unpredictable stress led to long lasting loss of tonic GABAAR currents in the projection neurons of lateral amygdala. By contrast, the phasic GABAAR currents, as measured by the spontaneous inhibitory postsynaptic currents, were virtually unaltered. The loss of tonic inhibition varied with the duration of daily stress and the total days of stress exposure. It was prevented by pretreatment with metyrapone to block corticosterone synthesis or RU 38486, a glucocorticoid receptor antagonist, suggesting the critical involvement of glucocorticoid receptor activation. Moreover, chronic treatment with corticosterone mimicked the effect of chronic stress and reduced the tonic inhibition in lateral amygdala of control mice. The loss of tonic inhibition resulted in the impaired GABAergic gating on neuronal excitability in amygdala, which was prevented by metyrapone pretreatment."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Action Potentials",
"Amygdala",
"Animals",
"Chronic Disease",
"Corticosterone",
"Immobilization",
"Inhibition (Psychology)",
"Inhibitory Postsynaptic Potentials",
"Ion Channel Gating",
"Male",
"Mice",
"Mice, Inbred C57BL",
"Neurons",
"Receptors, GABA-A",
"Receptors, Glucocorticoid",
"Stress, Psychological",
"gamma-Aminobutyric Acid"
]
} | Our study suggests that enduring loss of tonic but not phasic GABAAR currents critically contributes to the prolonged amygdala disinhibition subsequent to chronic stress. We propose that the preferential loss of tonic inhibition may account for the development of stress-related neuropsychiatric diseases. | yes | [
{
"from": "human",
"value": "Question: Does chronic stress impair GABAergic control of amygdala through suppressing the tonic GABAA receptor currents?\nContext: {'contexts': ['Chronic stress is generally known to exacerbate the development of numerous neuropsychiatric diseases such as fear and anxiety disorders, which is at least partially due to the disinhibition of amygdala subsequent to the prolonged stress exposure. GABA receptor A (GABAAR) mediates the primary component of inhibition in brain and its activation produces two forms of inhibition: the phasic and tonic inhibition. While both of them are critically engaged in limiting the activity of amygdala, their roles in the amygdala disinhibition subsequent to chronic stress exposure are largely unknown.', 'We investigated the possible alterations of phasic and tonic GABAAR currents and their roles in the amygdala disinhibition subsequent to chronic stress. We found that both chronic immobilization and unpredictable stress led to long lasting loss of tonic GABAAR currents in the projection neurons of lateral amygdala. By contrast, the phasic GABAAR currents, as measured by the spontaneous inhibitory postsynaptic currents, were virtually unaltered. The loss of tonic inhibition varied with the duration of daily stress and the total days of stress exposure. It was prevented by pretreatment with metyrapone to block corticosterone synthesis or RU 38486, a glucocorticoid receptor antagonist, suggesting the critical involvement of glucocorticoid receptor activation. Moreover, chronic treatment with corticosterone mimicked the effect of chronic stress and reduced the tonic inhibition in lateral amygdala of control mice. The loss of tonic inhibition resulted in the impaired GABAergic gating on neuronal excitability in amygdala, which was prevented by metyrapone pretreatment.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Action Potentials', 'Amygdala', 'Animals', 'Chronic Disease', 'Corticosterone', 'Immobilization', 'Inhibition (Psychology)', 'Inhibitory Postsynaptic Potentials', 'Ion Channel Gating', 'Male', 'Mice', 'Mice, Inbred C57BL', 'Neurons', 'Receptors, GABA-A', 'Receptors, Glucocorticoid', 'Stress, Psychological', 'gamma-Aminobutyric Acid']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,758,223 | Do brainstem infarcts predict REM sleep behavior disorder in acute ischemic stroke? | {
"contexts": [
"Rapid eye movement (REM) sleep behavior disorder (RBD) is a sleep disturbance in which patients enact their dreams while in REM sleep. The behavior is typically violent in association with violent dream content, so serious harm can be done to the patient or the bed partner. The prevalence of RBD is well-known in Parkinson's disease, Lewy body dementia, and multiple systems atrophy. However, its prevalence and causes in stroke remained unclear. The aim of this study was to determine factors influencing the appearance of RBD in a prospective cohort of patients with acute ischemic stroke.",
"A total of 2,024 patients with first-ever or recurrent acute ischemic stroke were admitted to the Acute Stroke Unit at the Prince of Wales Hospital between January 2010 and November 2011; 775 of them received an MRI scan. Within 2 days of admission, a research nurse collected demographic and clinical data and assessed the severity of each stroke using the National Institute of Health Stroke Scale (NIHSS). One hundred and nineteen of the 775 patients meeting study entry criteria formed the study sample. All eligible participants were invited to attend a research clinic 3 months after the onset of the index stroke. In the attendance, a research assistant administered the MMSE and the 13-item RBD questionnaire (RBDQ).",
"Among 119 stroke patients, 10.9% were exhibited RBD, defined as an REM sleep behavior disorder questionnaire score of 19 or above. The proportion of patients with acute brainstem infarct was significantly higher in RBD patients than those without RBD. Compared with patients without RBD, RBD patients were more likely to have brainstem infarcts and had smaller infarct volumes. In a multivariate analysis, in which stroke location and infarct volume were inserted, brainstem infarcts were an independent predictor of RBD (odds ratio = 3.686; P = 0.032)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Brain Stem Infarctions",
"Female",
"Humans",
"Male",
"REM Sleep Behavior Disorder",
"Stroke"
]
} | The results support the notion of a predominant role of brainstem injury in the development of RBD and suggest that patients with brainstem infarcts RBD should be evaluated by a clinical neurologist. | yes | [
{
"from": "human",
"value": "Question: Do brainstem infarcts predict REM sleep behavior disorder in acute ischemic stroke?\nContext: {'contexts': [\"Rapid eye movement (REM) sleep behavior disorder (RBD) is a sleep disturbance in which patients enact their dreams while in REM sleep. The behavior is typically violent in association with violent dream content, so serious harm can be done to the patient or the bed partner. The prevalence of RBD is well-known in Parkinson's disease, Lewy body dementia, and multiple systems atrophy. However, its prevalence and causes in stroke remained unclear. The aim of this study was to determine factors influencing the appearance of RBD in a prospective cohort of patients with acute ischemic stroke.\", 'A total of 2,024 patients with first-ever or recurrent acute ischemic stroke were admitted to the Acute Stroke Unit at the Prince of Wales Hospital between January 2010 and November 2011; 775 of them received an MRI scan. Within 2 days of admission, a research nurse collected demographic and clinical data and assessed the severity of each stroke using the National Institute of Health Stroke Scale (NIHSS). One hundred and nineteen of the 775 patients meeting study entry criteria formed the study sample. All eligible participants were invited to attend a research clinic 3 months after the onset of the index stroke. In the attendance, a research assistant administered the MMSE and the 13-item RBD questionnaire (RBDQ).', 'Among 119 stroke patients, 10.9% were exhibited RBD, defined as an REM sleep behavior disorder questionnaire score of 19 or above. The proportion of patients with acute brainstem infarct was significantly higher in RBD patients than those without RBD. Compared with patients without RBD, RBD patients were more likely to have brainstem infarcts and had smaller infarct volumes. In a multivariate analysis, in which stroke location and infarct volume were inserted, brainstem infarcts were an independent predictor of RBD (odds ratio\\u2009=\\u20093.686; P\\u2009=\\u20090.032).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Brain Stem Infarctions', 'Female', 'Humans', 'Male', 'REM Sleep Behavior Disorder', 'Stroke']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,758,227 | Does severe hypoxia exert parallel and cell-specific regulation of gene expression and alternative splicing in human mesenchymal stem cells? | {
"contexts": [
"The endosteum of the bone marrow provides a specialized hypoxic niche that may serve to preserve the integrity, pluripotency, longevity and stemness of resident mesenchymal stem cells (MSCs). To explore the molecular genetic consequences of such a niche we subjected human (h) MSCs to a pO2 of 4 mmHg and analyzed global gene expression and alternative splicing (AS) by genome-exon microarray and RT-qPCR, and phenotype by western blot and immunostaining.",
"Out of 446 genes differentially regulated by >2.5-fold, down-regulated genes outnumbered up-regulated genes by 243:203. Exon analyses revealed 60 hypoxia-regulated AS events with splice indices (SI) >1.0 from 53 genes and a correlation between high SI and degree of transcript regulation. Parallel analyses of a publicly available AS study on human umbilical vein endothelial cells (HUVECs) showed that there was a strong cell-specific component with only 11 genes commonly regulated in hMSCs and HUVECs and 17 common differentially spliced genes. Only 3 genes were differentially responsive to hypoxia at the gene (>2.0) and AS levels in both cell types. Functional assignments revealed unique profiles of gene expression with complex regulation of differentiation, extracellular matrix, intermediate filament and metabolic marker genes. Antioxidant genes, striated muscle genes and insulin/IGF-1 signaling intermediates were down-regulated. There was a coordinate induction of 9 out of 12 acidic keratins that along with other epithelial and cell adhesion markers implies a partial mesenchymal to epithelial transition."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Alternative Splicing",
"Cell Differentiation",
"Cell Proliferation",
"Gene Expression Regulation",
"Glucose",
"Humans",
"Hypoxia",
"Mesenchymal Stem Cells",
"Oligonucleotide Array Sequence Analysis"
]
} | We conclude that severe hypoxia confers a quiescent phenotype in hMSCs that is reflected by both the transcriptome profile and gene-specific changes of splicosome actions. The results reveal that severe hypoxia imposes markedly different patterns of gene regulation of MSCs compared with more moderate hypoxia. This is the first study to report hypoxia-regulation of AS in stem/progenitor cells and the first molecular genetic characterization of MSC in a hypoxia-induced quiescent immobile state. | yes | [
{
"from": "human",
"value": "Question: Does severe hypoxia exert parallel and cell-specific regulation of gene expression and alternative splicing in human mesenchymal stem cells?\nContext: {'contexts': ['The endosteum of the bone marrow provides a specialized hypoxic niche that may serve to preserve the integrity, pluripotency, longevity and stemness of resident mesenchymal stem cells (MSCs). To explore the molecular genetic consequences of such a niche we subjected human (h) MSCs to a pO2 of 4 mmHg and analyzed global gene expression and alternative splicing (AS) by genome-exon microarray and RT-qPCR, and phenotype by western blot and immunostaining.', 'Out of 446 genes differentially regulated by >2.5-fold, down-regulated genes outnumbered up-regulated genes by 243:203. Exon analyses revealed 60 hypoxia-regulated AS events with splice indices (SI) >1.0 from 53 genes and a correlation between high SI and degree of transcript regulation. Parallel analyses of a publicly available AS study on human umbilical vein endothelial cells (HUVECs) showed that there was a strong cell-specific component with only 11 genes commonly regulated in hMSCs and HUVECs and 17 common differentially spliced genes. Only 3 genes were differentially responsive to hypoxia at the gene (>2.0) and AS levels in both cell types. Functional assignments revealed unique profiles of gene expression with complex regulation of differentiation, extracellular matrix, intermediate filament and metabolic marker genes. Antioxidant genes, striated muscle genes and insulin/IGF-1 signaling intermediates were down-regulated. There was a coordinate induction of 9 out of 12 acidic keratins that along with other epithelial and cell adhesion markers implies a partial mesenchymal to epithelial transition.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Alternative Splicing', 'Cell Differentiation', 'Cell Proliferation', 'Gene Expression Regulation', 'Glucose', 'Humans', 'Hypoxia', 'Mesenchymal Stem Cells', 'Oligonucleotide Array Sequence Analysis']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,750,438 | Does impact of postoperative renal replacement therapy on long-term outcome after cardiac surgery increase with age? | {
"contexts": [
"In the present study, we investigated the survival of patients who received postoperative renal replacement therapy (RRT) after cardiac surgery. We specifically focused on factors predicting long-term outcome in elderly patients.",
"Data of all patients that received unintentional renal replacement therapy following cardiac surgery between 2004 and 2010 were analyzed. Logistic- and Cox regression analyses were performed to detect the predictors of early and late mortality, respectively.",
"During the study period, 11,899 patients underwent cardiac surgery in our center. Post-operative RRT was performed in 138 patients (1.2%). In this group of patients, 30-day mortality included 72 patients (52%) and the total overall mortality included 107 patients (77.5%). Regression analyses revealed that age predicted 30-day mortality (odds ratio = 1.08 [1.03 to 1.12]) as well as late mortality (odds ratio = 1.05 [1.02 to 1.07]."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Acute Kidney Injury",
"Age Factors",
"Aged",
"Cardiac Surgical Procedures",
"Female",
"Humans",
"Logistic Models",
"Male",
"Postoperative Care",
"Postoperative Complications",
"Proportional Hazards Models",
"Renal Replacement Therapy",
"Risk Factors",
"Survival Rate",
"Time Factors",
"Treatment Outcome"
]
} | Patients requiring RRT after cardiac surgery have a poor prognosis with a high mortality. Older age predicted both 30-day and late mortality in these patients. | yes | [
{
"from": "human",
"value": "Question: Does impact of postoperative renal replacement therapy on long-term outcome after cardiac surgery increase with age?\nContext: {'contexts': ['In the present study, we investigated the survival of patients who received postoperative renal replacement therapy (RRT) after cardiac surgery. We specifically focused on factors predicting long-term outcome in elderly patients.', 'Data of all patients that received unintentional renal replacement therapy following cardiac surgery between 2004 and 2010 were analyzed. Logistic- and Cox regression analyses were performed to detect the predictors of early and late mortality, respectively.', 'During the study period, 11,899 patients underwent cardiac surgery in our center. Post-operative RRT was performed in 138 patients (1.2%). In this group of patients, 30-day mortality included 72 patients (52%) and the total overall mortality included 107 patients (77.5%). Regression analyses revealed that age predicted 30-day mortality (odds ratio\\u2009=\\u20091.08 [1.03 to 1.12]) as well as late mortality (odds ratio\\u2009=\\u20091.05 [1.02 to 1.07].'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Acute Kidney Injury', 'Age Factors', 'Aged', 'Cardiac Surgical Procedures', 'Female', 'Humans', 'Logistic Models', 'Male', 'Postoperative Care', 'Postoperative Complications', 'Proportional Hazards Models', 'Renal Replacement Therapy', 'Risk Factors', 'Survival Rate', 'Time Factors', 'Treatment Outcome']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,773,329 | Does collaborative DTM reduce hospitalization and healthcare costs in patients with diabetes treated with polypharmacy? | {
"contexts": [
"To evaluate the effects of a collaborative pharmacy benefits manager (PBM)/ health plan-administered drug therapy management (DTM) program on healthcare utilization and costs in patients with diabetes treated with polypharmacy.",
"Retrospective quasi-experimental design with comparison group.",
"This DTM program was a collaborative effort between the PBM, PerformRx, and the care management departments of Keystone First (KF) and AmeriHealth Caritas Pennsylvania (ACP) care management departments, targeting patients with diabetes using >15 medications. Pharmacists reviewed member profiles and made evidencebased prescriber and patient interventions, working directly with prescribers and indirectly with members, via care managers. Care managers provided additional services not otherwise within the scope of DTM. The study group consisted of 954 DTM participants reviewed by a pharmacist between November 1, 2010, and July 31, 2011. The control group consisted of 810 matched DTM participants not reviewed by a pharmacist.",
"Intervention acceptance rates for KF and ACP were 33% and 26%, respectively. The study group demonstrated lower inpatient admissions and emergency department utilization rates, although only the KF study group inpatient admission rate achieved statistical significance (76.4%; P = .0002). The study groups realized statistically significant total cost savings (pharmacy + medical) compared with their corresponding control groups (47.8% KF, P = .0039; 50.7% ACP, P = .0497) despite non-statistically significant increases in pharmacy costs."
],
"labels": [
"OBJECTIVE",
"METHODS",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Case-Control Studies",
"Cost Savings",
"Diabetes Mellitus",
"Emergency Service, Hospital",
"Female",
"Health Care Costs",
"Hospitalization",
"Humans",
"Male",
"Medication Therapy Management",
"Middle Aged",
"Pennsylvania",
"Pharmacists",
"Polypharmacy",
"Retrospective Studies"
]
} | A collaborative pharmacist-driven DTM program with a care manager-executed patient outreach component results in reduced hospital utilization and significant healthcare cost savings. | yes | [
{
"from": "human",
"value": "Question: Does collaborative DTM reduce hospitalization and healthcare costs in patients with diabetes treated with polypharmacy?\nContext: {'contexts': ['To evaluate the effects of a collaborative pharmacy benefits manager (PBM)/ health plan-administered drug therapy management (DTM) program on healthcare utilization and costs in patients with diabetes treated with polypharmacy.', 'Retrospective quasi-experimental design with comparison group.', 'This DTM program was a collaborative effort between the PBM, PerformRx, and the care management departments of Keystone First (KF) and AmeriHealth Caritas Pennsylvania (ACP) care management departments, targeting patients with diabetes using >15 medications. Pharmacists reviewed member profiles and made evidencebased prescriber and patient interventions, working directly with prescribers and indirectly with members, via care managers. Care managers provided additional services not otherwise within the scope of DTM. The study group consisted of 954 DTM participants reviewed by a pharmacist between November 1, 2010, and July 31, 2011. The control group consisted of 810 matched DTM participants not reviewed by a pharmacist.', 'Intervention acceptance rates for KF and ACP were 33% and 26%, respectively. The study group demonstrated lower inpatient admissions and emergency department utilization rates, although only the KF study group inpatient admission rate achieved statistical significance (76.4%; P = .0002). The study groups realized statistically significant total cost savings (pharmacy + medical) compared with their corresponding control groups (47.8% KF, P = .0039; 50.7% ACP, P = .0497) despite non-statistically significant increases in pharmacy costs.'], 'labels': ['OBJECTIVE', 'METHODS', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Case-Control Studies', 'Cost Savings', 'Diabetes Mellitus', 'Emergency Service, Hospital', 'Female', 'Health Care Costs', 'Hospitalization', 'Humans', 'Male', 'Medication Therapy Management', 'Middle Aged', 'Pennsylvania', 'Pharmacists', 'Polypharmacy', 'Retrospective Studies']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,772,492 | Does tetanus toxin reduce local and descending regulation of the H-reflex? | {
"contexts": [
"Skeletal muscles that are under the influence of tetanus toxin show an exaggerated reflex response to stretch. We examined which changes in the stretch reflex may underlie the exaggerated response.",
"H-reflexes were obtained from the tibialis anterior (TA) and flexor digitorum brevis (FDB) muscles in rats 7 days after intramuscular injection of tetanus toxin into the TA.",
"We found effects of the toxin on the threshold, amplitude, and duration of H-waves from the TA. The toxin inhibited rate-dependent depression in the FDB between the stimulation frequencies of 0.5–50 HZ and when a conditioning magnetic stimulus applied to the brain preceded a test electrical stimulus delivered to the plantar nerve."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Electric Stimulation",
"Female",
"H-Reflex",
"Muscle, Skeletal",
"Rats",
"Rats, Sprague-Dawley",
"Reflex, Stretch",
"Tetanus Toxin"
]
} | Tetanus toxin increased the amplitude of the Hwave and reduced the normal depression of H-wave amplitude that is associated with closely timed stimuli, two phenomena that could contribute to hyperactivity of the stretch reflex. | yes | [
{
"from": "human",
"value": "Question: Does tetanus toxin reduce local and descending regulation of the H-reflex?\nContext: {'contexts': ['Skeletal muscles that are under the influence of tetanus toxin show an exaggerated reflex response to stretch. We examined which changes in the stretch reflex may underlie the exaggerated response.', 'H-reflexes were obtained from the tibialis anterior (TA) and flexor digitorum brevis (FDB) muscles in rats 7 days after intramuscular injection of tetanus toxin into the TA.', 'We found effects of the toxin on the threshold, amplitude, and duration of H-waves from the TA. The toxin inhibited rate-dependent depression in the FDB between the stimulation frequencies of 0.5–50 HZ and when a conditioning magnetic stimulus applied to the brain preceded a test electrical stimulus delivered to the plantar nerve.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Electric Stimulation', 'Female', 'H-Reflex', 'Muscle, Skeletal', 'Rats', 'Rats, Sprague-Dawley', 'Reflex, Stretch', 'Tetanus Toxin']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,755,710 | Is arterial blood pressure closely related to ascites development in compensated HCV-related cirrhosis? | {
"contexts": [
"Arterial blood pressure (BP) is a reliable marker of circulatory dysfunction in cirrhotic patients. There are no prospective studies evaluating the association between different levels of arterial BP and ascites development in compensated cirrhotic patients. Therefore, we evaluated the relationship between arterial BP and ascites development in compensated cirrhotic patients.",
"A total of 402 patients with compensated HCV-related cirrhosis were prospectively followed during 6 years to identify ascites development. At baseline, patients underwent systolic, diastolic and mean arterial pressure (MAP) measurements. Any history of arterial hypertension was also recorded. The occurrence of events such as bleeding, hepatocellular carcinoma, death and liver transplantation prior to ascites development were considered as competing risk events.",
"Over a median of 156 weeks, ascites occurred in 54 patients (13%). At baseline, MAP was significantly lower in patients with ascites development (75.9 mm/Hg [95%CI, 70.3-84.3]) than those without ascites (93.6 mm/Hg [95% CI: 86.6-102.3]). After adjusting for covariates, the 6-year cumulative incidence of ascites was 40% (95%CI, 34%-48%) for patients with MAP<83.32 mm/Hg. In contrast, cumulative incidences of ascites were almost similar among patients with MAP values between 83.32 mm/Hg and 93.32 mm/Hg (7% [95% CI: 4%-12%]), between 93.32 mm/Hg and 100.31 mm/Hg (5% [95% CI: 4%-11%]) or higher than 100.31 mm/Hg (3% [95% CI: 1%-6%]). The MAP was an independent predictor of ascites development."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Arterial Pressure",
"Ascites",
"Female",
"Follow-Up Studies",
"Hepatitis C, Chronic",
"Humans",
"Liver Cirrhosis",
"Male",
"Prospective Studies"
]
} | The MAP is closely related to the development of ascites in compensated HCV-related cirrhosis. The risk of ascites development increases in 4.4 fold for subjects with MAP values <83.32 mm/Hg. | yes | [
{
"from": "human",
"value": "Question: Is arterial blood pressure closely related to ascites development in compensated HCV-related cirrhosis?\nContext: {'contexts': ['Arterial blood pressure (BP) is a reliable marker of circulatory dysfunction in cirrhotic patients. There are no prospective studies evaluating the association between different levels of arterial BP and ascites development in compensated cirrhotic patients. Therefore, we evaluated the relationship between arterial BP and ascites development in compensated cirrhotic patients.', 'A total of 402 patients with compensated HCV-related cirrhosis were prospectively followed during 6 years to identify ascites development. At baseline, patients underwent systolic, diastolic and mean arterial pressure (MAP) measurements. Any history of arterial hypertension was also recorded. The occurrence of events such as bleeding, hepatocellular carcinoma, death and liver transplantation prior to ascites development were considered as competing risk events.', 'Over a median of 156 weeks, ascites occurred in 54 patients (13%). At baseline, MAP was significantly lower in patients with ascites development (75.9 mm/Hg [95%CI, 70.3-84.3]) than those without ascites (93.6 mm/Hg [95% CI: 86.6-102.3]). After adjusting for covariates, the 6-year cumulative incidence of ascites was 40% (95%CI, 34%-48%) for patients with MAP<83.32 mm/Hg. In contrast, cumulative incidences of ascites were almost similar among patients with MAP values between 83.32 mm/Hg and 93.32 mm/Hg (7% [95% CI: 4%-12%]), between 93.32 mm/Hg and 100.31 mm/Hg (5% [95% CI: 4%-11%]) or higher than 100.31 mm/Hg (3% [95% CI: 1%-6%]). The MAP was an independent predictor of ascites development.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Arterial Pressure', 'Ascites', 'Female', 'Follow-Up Studies', 'Hepatitis C, Chronic', 'Humans', 'Liver Cirrhosis', 'Male', 'Prospective Studies']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,755,712 | Is evidence that the lung Adenocarcinoma EML4-ALK fusion gene caused by exposure to secondhand tobacco smoke during childhood? | {
"contexts": [
"The EML4-ALK fusion gene is more frequently found in younger, never smoking patients with lung cancer. Meanwhile, never smokers exposed to secondhand tobacco smoke (SHS) during childhood are diagnosed at a younger age compared with never smoking patients with lung cancer who are not exposed. We, therefore, hypothesized that SHS, which can induce DNA damage, is associated with the EML4-ALK fusion gene.",
"We compared the frequency of the EML4-ALK fusion gene among 197 never smoker patients with lung cancer with and without a history of exposure to SHS during childhood at Mayo Clinic.",
"The EML4-ALK fusion gene was detected in 33% of cases from never smokers with a history of SHS exposure during childhood, whereas 47% of never smoking lung cancer cases without a history of childhood SHS exposure tested positive for the fusion gene."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adenocarcinoma",
"Adult",
"Child",
"Female",
"Humans",
"In Situ Hybridization, Fluorescence",
"Lung Neoplasms",
"Male",
"Oncogene Proteins, Fusion",
"Tobacco Smoke Pollution"
]
} | The EML4-ALK fusion gene is not enriched in tumors from individuals exposed to SHS during childhood. | no | [
{
"from": "human",
"value": "Question: Is evidence that the lung Adenocarcinoma EML4-ALK fusion gene caused by exposure to secondhand tobacco smoke during childhood?\nContext: {'contexts': ['The EML4-ALK fusion gene is more frequently found in younger, never smoking patients with lung cancer. Meanwhile, never smokers exposed to secondhand tobacco smoke (SHS) during childhood are diagnosed at a younger age compared with never smoking patients with lung cancer who are not exposed. We, therefore, hypothesized that SHS, which can induce DNA damage, is associated with the EML4-ALK fusion gene.', 'We compared the frequency of the EML4-ALK fusion gene among 197 never smoker patients with lung cancer with and without a history of exposure to SHS during childhood at Mayo Clinic.', 'The EML4-ALK fusion gene was detected in 33% of cases from never smokers with a history of SHS exposure during childhood, whereas 47% of never smoking lung cancer cases without a history of childhood SHS exposure tested positive for the fusion gene.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adenocarcinoma', 'Adult', 'Child', 'Female', 'Humans', 'In Situ Hybridization, Fluorescence', 'Lung Neoplasms', 'Male', 'Oncogene Proteins, Fusion', 'Tobacco Smoke Pollution']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
24,769,857 | Are genetic variants in microRNA machinery genes associated [ corrected ] with idiopathic recurrent pregnancy loss risk? | {
"contexts": [
"Key molecules involved in microRNA (miRNA) biogenesis, such as DROSHA, XPO5, and DICER, have been identified in trophoblast cells, confirming that the miRNA biogenesis pathway is active in human placenta. In addition, miRNAs regulate uterine gene expression associated with inflammatory responses during the peri-implantation period and participate in maternal-fetal immune tolerance. The purpose of this study was to demonstrate whether genetic polymorphisms in miRNA machinery genes show an association with idiopathic recurrent pregnancy loss (RPL) in Korean women.",
"We performed a case-control study with 238 controls and 338 women who had experienced at least two consecutive pregnancy losses between 1999 and 2010. Genotypes of miRNA machinery genes, including DICER rs3742330, DROSHA rs10719, RAN GTPase (RAN) rs14035, and exportin-5 (XPO5) rs11077 were analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay. The logistic odds ratios (ORs) of RPL were estimated with a 95% confidence interval (CI) in multivariate analysis after maternal age adjustment. Gene-gene interactions among the loci of the four gene polymorphisms were evaluated using the multifactor dimensionality reduction (MDR) method.",
"The RAN rs14035 CC genotype and DICER rs3742330/DROSHA rs10719 GG/TC+CC, rs3742330/RAN rs14035 GG/CC, and DICER rs3742330/XPO5 rs11077 GG/AC+CC combinations were significantly associated with increased RPL risk, whereas the RAN rs14035 CT, DICER rs3742330/RAN rs14035 AA+AG/CT+TT, DROSHA rs10719/RAN rs14035 TC+CC/CT+TT, and RAN rs14035/XPO5 rs11077 CT+TT/AA combinations reduced RPL risk. The A-T-T-C and G-C-T-A allele combinations (DICER/DROSHA/RAN/XPO5) were 20 times more frequent in the RPL group than in the control group."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Abortion, Habitual",
"Adult",
"Case-Control Studies",
"DEAD-box RNA Helicases",
"Epistasis, Genetic",
"Female",
"Gene Frequency",
"Genetic Association Studies",
"Genetic Predisposition to Disease",
"Humans",
"Karyopherins",
"Polymorphism, Single Nucleotide",
"Pregnancy",
"Ribonuclease III",
"Risk",
"Sequence Analysis, DNA",
"Young Adult",
"ran GTP-Binding Protein"
]
} | Our study demonstrates the relationship between RPL development and the polymorphism of the miRNA machinery gene RAN and combined genotype of DROSHA/DICER. | yes | [
{
"from": "human",
"value": "Question: Are genetic variants in microRNA machinery genes associated [ corrected ] with idiopathic recurrent pregnancy loss risk?\nContext: {'contexts': ['Key molecules involved in microRNA (miRNA) biogenesis, such as DROSHA, XPO5, and DICER, have been identified in trophoblast cells, confirming that the miRNA biogenesis pathway is active in human placenta. In addition, miRNAs regulate uterine gene expression associated with inflammatory responses during the peri-implantation period and participate in maternal-fetal immune tolerance. The purpose of this study was to demonstrate whether genetic polymorphisms in miRNA machinery genes show an association with idiopathic recurrent pregnancy loss (RPL) in Korean women.', 'We performed a case-control study with 238 controls and 338 women who had experienced at least two consecutive pregnancy losses between 1999 and 2010. Genotypes of miRNA machinery genes, including DICER rs3742330, DROSHA rs10719, RAN GTPase (RAN) rs14035, and exportin-5 (XPO5) rs11077 were analyzed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay. The logistic odds ratios (ORs) of RPL were estimated with a 95% confidence interval (CI) in multivariate analysis after maternal age adjustment. Gene-gene interactions among the loci of the four gene polymorphisms were evaluated using the multifactor dimensionality reduction (MDR) method.', 'The RAN rs14035 CC genotype and DICER rs3742330/DROSHA rs10719 GG/TC+CC, rs3742330/RAN rs14035 GG/CC, and DICER rs3742330/XPO5 rs11077 GG/AC+CC combinations were significantly associated with increased RPL risk, whereas the RAN rs14035 CT, DICER rs3742330/RAN rs14035 AA+AG/CT+TT, DROSHA rs10719/RAN rs14035 TC+CC/CT+TT, and RAN rs14035/XPO5 rs11077 CT+TT/AA combinations reduced RPL risk. The A-T-T-C and G-C-T-A allele combinations (DICER/DROSHA/RAN/XPO5) were 20 times more frequent in the RPL group than in the control group.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Abortion, Habitual', 'Adult', 'Case-Control Studies', 'DEAD-box RNA Helicases', 'Epistasis, Genetic', 'Female', 'Gene Frequency', 'Genetic Association Studies', 'Genetic Predisposition to Disease', 'Humans', 'Karyopherins', 'Polymorphism, Single Nucleotide', 'Pregnancy', 'Ribonuclease III', 'Risk', 'Sequence Analysis, DNA', 'Young Adult', 'ran GTP-Binding Protein']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,760,181 | Is collagen type III alpha 1 polymorphism ( rs1800255 , COL3A1 2209 G > A ) assessed with high-resolution melting analysis associated with pelvic organ prolapse in the Dutch population? | {
"contexts": [
"The rs1800255, COL3A1 2209 G>A polymorphism in the alpha 1 chain of collagen type III has been associated with an increased risk of pelvic organ prolapse (POP). In one of our previous studies however, polymerase chain reaction-based restriction fragment length polymorphism (PCR-RFLP) misdiagnosed rs1800255, COL3A1 2209 G>A in 6 % of cases. The high-resolution melting (HRM) analysis on the contrary obtained a 100 % accordance for this specific polymorphism and was used in the present study to validate this risk factor for POP.",
"In this case-control study, women with and without symptoms of POP were included and compared. DNA was extracted from blood samples. HRM analysis was used to assess for the presence of the homozygous rs1800255. Groups were compared using the Pearson chi-square, Mann-Whitney, and t tests. The discrepancy between HRM and PCR-RFLP results was investigated using PCR-RFLP results available from our previous study.",
"The study included 354 women: 272 patients with POP and 82 controls; 18 (7 %) cases versus 3 (4 %) controls had a homozygous rs1800255, COL3A1 2209 G>A polymorphism (odds ratio 1.9, 95 % confidence interval 0.5-6.9, compared to the wild type), and thus no association between POP and the homozygous polymorphism could be demonstrated. A discrepancy between HRM and PCR-RFLP results was found in 8 % of the samples."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Case-Control Studies",
"Cohort Studies",
"Collagen Type III",
"Female",
"Humans",
"Middle Aged",
"Netherlands",
"Nucleic Acid Denaturation",
"Pelvic Organ Prolapse",
"Polymerase Chain Reaction",
"Polymorphism, Restriction Fragment Length",
"Polymorphism, Single Nucleotide"
]
} | The previously found statistically significant association between the rs1800255, COL3A1 2209 G>A polymorphism as measured with PCR-RFLP and POP could no longer be demonstrated. This raises concerns regarding the results of other association studies using PCR-RFLP. | no | [
{
"from": "human",
"value": "Question: Is collagen type III alpha 1 polymorphism ( rs1800255 , COL3A1 2209 G > A ) assessed with high-resolution melting analysis associated with pelvic organ prolapse in the Dutch population?\nContext: {'contexts': ['The rs1800255, COL3A1 2209\\xa0G>A polymorphism in the alpha 1 chain of collagen type III has been associated with an increased risk of pelvic organ prolapse (POP). In one of our previous studies however, polymerase chain reaction-based restriction fragment length polymorphism (PCR-RFLP) misdiagnosed rs1800255, COL3A1 2209\\xa0G>A in 6\\xa0% of cases. The high-resolution melting (HRM) analysis on the contrary obtained a 100\\xa0% accordance for this specific polymorphism and was used in the present study to validate this risk factor for POP.', 'In this case-control study, women with and without symptoms of POP were included and compared. DNA was extracted from blood samples. HRM analysis was used to assess for the presence of the homozygous rs1800255. Groups were compared using the Pearson chi-square, Mann-Whitney, and t tests. The discrepancy between HRM and PCR-RFLP results was investigated using PCR-RFLP results available from our previous study.', 'The study included 354 women: 272 patients with POP and 82 controls; 18 (7\\xa0%) cases versus 3 (4\\xa0%) controls had a homozygous rs1800255, COL3A1 2209\\xa0G>A polymorphism (odds ratio 1.9, 95\\xa0% confidence interval 0.5-6.9, compared to the wild type), and thus no association between POP and the homozygous polymorphism could be demonstrated. A discrepancy between HRM and PCR-RFLP results was found in 8\\xa0% of the samples.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Case-Control Studies', 'Cohort Studies', 'Collagen Type III', 'Female', 'Humans', 'Middle Aged', 'Netherlands', 'Nucleic Acid Denaturation', 'Pelvic Organ Prolapse', 'Polymerase Chain Reaction', 'Polymorphism, Restriction Fragment Length', 'Polymorphism, Single Nucleotide']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
24,771,329 | Is severe malarial anemia associated with long-term neurocognitive impairment? | {
"contexts": [
"Cerebral malaria (CM) is associated with long-term neurocognitive impairment in children ≥5 years of age. No prospective studies to date have assessed neurocognitive impairment in children with CM <5 years of age, or in children with severe malarial anemia (SMA), a form of severe malaria estimated to affect as many as 5 million children annually.",
"Children <5 years of age presenting to Mulago Hospital, Kampala, Uganda, with CM (n = 80) or SMA (n = 86) were assessed for overall cognitive ability, attention, and associative memory 1 week after discharge and 6 and 12 months later. The z scores for each domain were computed based on scores of 61 healthy community children (CC), who were also tested at enrollment and 6 and 12 months later. Groups were compared using mixed linear models, adjusted for age, weight for age, and child's education.",
"At 12 months, children with CM had lower adjusted scores than CC in cognitive ability (P < .001), attention (P = .02), and associative memory, (P = .002). Children with SMA had lower scores than CC in cognitive ability (P = .01) but not attention or associative memory. Cognitive ability scores in children with CM and SMA did not differ significantly."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Anemia",
"Child, Preschool",
"Cognition Disorders",
"Female",
"Humans",
"Infant",
"Malaria, Cerebral",
"Male",
"Patient Discharge",
"Prospective Studies",
"Uganda"
]
} | In children <5 years of age, SMA is associated with long-term impairment in cognitive ability, whereas CM is associated with additional impairment in the areas of attention and associative memory. SMA may be a major contributor to long-term neurocognitive impairment in children in sub-Saharan Africa. | yes | [
{
"from": "human",
"value": "Question: Is severe malarial anemia associated with long-term neurocognitive impairment?\nContext: {'contexts': ['Cerebral malaria (CM) is associated with long-term neurocognitive impairment in children ≥5 years of age. No prospective studies to date have assessed neurocognitive impairment in children with CM <5 years of age, or in children with severe malarial anemia (SMA), a form of severe malaria estimated to affect as many as 5 million children annually.', \"Children <5 years of age presenting to Mulago Hospital, Kampala, Uganda, with CM (n = 80) or SMA (n = 86) were assessed for overall cognitive ability, attention, and associative memory 1 week after discharge and 6 and 12 months later. The z scores for each domain were computed based on scores of 61 healthy community children (CC), who were also tested at enrollment and 6 and 12 months later. Groups were compared using mixed linear models, adjusted for age, weight for age, and child's education.\", 'At 12 months, children with CM had lower adjusted scores than CC in cognitive ability (P < .001), attention (P = .02), and associative memory, (P = .002). Children with SMA had lower scores than CC in cognitive ability (P = .01) but not attention or associative memory. Cognitive ability scores in children with CM and SMA did not differ significantly.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Anemia', 'Child, Preschool', 'Cognition Disorders', 'Female', 'Humans', 'Infant', 'Malaria, Cerebral', 'Male', 'Patient Discharge', 'Prospective Studies', 'Uganda']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,759,437 | Do neural responses to exclusion predict susceptibility to social influence? | {
"contexts": [
"Social influence is prominent across the lifespan, but sensitivity to influence is especially high during adolescence and is often associated with increased risk taking. Such risk taking can have dire consequences. For example, in American adolescents, traffic-related crashes are leading causes of nonfatal injury and death. Neural measures may be especially useful in understanding the basic mechanisms of adolescents' vulnerability to peer influence.",
"We examined neural responses to social exclusion as potential predictors of risk taking in the presence of peers in recently licensed adolescent drivers. Risk taking was assessed in a driving simulator session occurring approximately 1 week after the neuroimaging session.",
"Increased activity in neural systems associated with the distress of social exclusion and mentalizing during an exclusion episode predicted increased risk taking in the presence of a peer (controlling for solo risk behavior) during a driving simulator session outside the neuroimaging laboratory 1 week later. These neural measures predicted risky driving behavior above and beyond self-reports of susceptibility to peer pressure and distress during exclusion."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Accident Prevention",
"Accidents, Traffic",
"Adolescent",
"Adolescent Behavior",
"Automobile Driving",
"Female",
"Humans",
"Male",
"Peer Group",
"Risk Assessment",
"Risk-Taking",
"Social Behavior",
"United States",
"Wounds and Injuries"
]
} | These results address the neural bases of social influence and risk taking; contribute to our understanding of social and emotional function in the adolescent brain; and link neural activity in specific, hypothesized, regions to risk-relevant outcomes beyond the neuroimaging laboratory. Results of this investigation are discussed in terms of the mechanisms underlying risk taking in adolescents and the public health implications for adolescent driving. | yes | [
{
"from": "human",
"value": "Question: Do neural responses to exclusion predict susceptibility to social influence?\nContext: {'contexts': [\"Social influence is prominent across the lifespan, but sensitivity to influence is especially high during adolescence and is often associated with increased risk taking. Such risk taking can have dire consequences. For example, in American adolescents, traffic-related crashes are leading causes of nonfatal injury and death. Neural measures may be especially useful in understanding the basic mechanisms of adolescents' vulnerability to peer influence.\", 'We examined neural responses to social exclusion as potential predictors of risk taking in the presence of peers in recently licensed adolescent drivers. Risk taking was assessed in a driving simulator session occurring approximately 1 week after the neuroimaging session.', 'Increased activity in neural systems associated with the distress of social exclusion and mentalizing during an exclusion episode predicted increased risk taking in the presence of a peer (controlling for solo risk behavior) during a driving simulator session outside the neuroimaging laboratory 1 week later. These neural measures predicted risky driving behavior above and beyond self-reports of susceptibility to peer pressure and distress during exclusion.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Accident Prevention', 'Accidents, Traffic', 'Adolescent', 'Adolescent Behavior', 'Automobile Driving', 'Female', 'Humans', 'Male', 'Peer Group', 'Risk Assessment', 'Risk-Taking', 'Social Behavior', 'United States', 'Wounds and Injuries']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,752,070 | Is viral infection uncommon in adult patients with severe hospital-acquired pneumonia? | {
"contexts": [
"Viral pathogens have not generally been regarded as important causes of severe hospital-acquired pneumonia (HAP), except in patients with hematologic malignancy or transplant recipients. We investigated the role and distribution of viruses in adult with severe HAP who required intensive care.",
"From March 2010 to February 2012, adult patients with severe HAP required admission to the intensive care unit (ICU), 28-bed medical ICU in a tertiary care hospital, were prospectively enrolled. Respiratory viruses were detected using multiplex reverse-transcription polymerase chain reaction and/or shell vial culture.",
"A total of 262 patients were enrolled and 107 patients (40.8%) underwent bronchoscopic BAL for etiologic diagnosis. One hundred and fifty-six patients (59.5%) had bacterial infections and 59 patients (22.5%) had viral infections. Viruses were detected in BAL fluid specimens of 37 patients (62.7%, 37/59). The most commonly identified viruses were respiratory syncytial virus and parainfluenza virus (both 27.1%, 16/59), followed by rhinovirus (25.4%, 15/59), and influenza virus (16.9%, 10/59). Twenty-one patients (8.0%, 21/262) had bacterial-viral coinfections and Staphylococcus aureus was the most commonly coexisting bacteria (n = 10). Viral infection in non-immunocompromised patients was not uncommon (11.1%, 16/143), although it was not as frequent as that in immunocompromised patients (36.4%, 43/119). Non-immunocompromised patients were significantly older than immunocompromised patients and had significantly higher rates of underlying chronic obstructive pulmonary disease, tuberculous destroyed lung and chronic kidney disease. The 28 day mortalities of patients with bacterial infections, viral infections and bacterial-viral coinfections were not significantly different (29.5%, 35.6% and 19.0%, respectively; p = 0.321)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Cross Infection",
"Female",
"Hospitalization",
"Hospitals",
"Humans",
"Logistic Models",
"Male",
"Middle Aged",
"Pneumonia",
"Staphylococcus aureus",
"Virus Diseases"
]
} | Viral pathogens are not uncommon in adult patients with severe HAP who required ICU admission. Since viral pathogens may cause severe HAP and could be a potential source of viral transmission, further investigation is required to delineate the role of viral pathogens in severe HAP. | no | [
{
"from": "human",
"value": "Question: Is viral infection uncommon in adult patients with severe hospital-acquired pneumonia?\nContext: {'contexts': ['Viral pathogens have not generally been regarded as important causes of severe hospital-acquired pneumonia (HAP), except in patients with hematologic malignancy or transplant recipients. We investigated the role and distribution of viruses in adult with severe HAP who required intensive care.', 'From March 2010 to February 2012, adult patients with severe HAP required admission to the intensive care unit (ICU), 28-bed medical ICU in a tertiary care hospital, were prospectively enrolled. Respiratory viruses were detected using multiplex reverse-transcription polymerase chain reaction and/or shell vial culture.', 'A total of 262 patients were enrolled and 107 patients (40.8%) underwent bronchoscopic BAL for etiologic diagnosis. One hundred and fifty-six patients (59.5%) had bacterial infections and 59 patients (22.5%) had viral infections. Viruses were detected in BAL fluid specimens of 37 patients (62.7%, 37/59). The most commonly identified viruses were respiratory syncytial virus and parainfluenza virus (both 27.1%, 16/59), followed by rhinovirus (25.4%, 15/59), and influenza virus (16.9%, 10/59). Twenty-one patients (8.0%, 21/262) had bacterial-viral coinfections and Staphylococcus aureus was the most commonly coexisting bacteria (n = 10). Viral infection in non-immunocompromised patients was not uncommon (11.1%, 16/143), although it was not as frequent as that in immunocompromised patients (36.4%, 43/119). Non-immunocompromised patients were significantly older than immunocompromised patients and had significantly higher rates of underlying chronic obstructive pulmonary disease, tuberculous destroyed lung and chronic kidney disease. The 28 day mortalities of patients with bacterial infections, viral infections and bacterial-viral coinfections were not significantly different (29.5%, 35.6% and 19.0%, respectively; p = 0.321).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Cross Infection', 'Female', 'Hospitalization', 'Hospitals', 'Humans', 'Logistic Models', 'Male', 'Middle Aged', 'Pneumonia', 'Staphylococcus aureus', 'Virus Diseases']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
24,764,283 | Is proteinuria testing among patients with diabetes mellitus associated with bladder cancer diagnosis : potential for unmeasured confounding in studies of pioglitazone and bladder cancer? | {
"contexts": [
"The observed association between pioglitazone and bladder cancer could be causal or because of bias in the design of prior studies. We hypothesize that proteinuria testing may lead to detection bias if routine test results for proteinuria lead to a full urinalysis.",
"We reanalyzed patients with diabetes mellitus within Kaiser Permanente Northern California. Logistic and Cox regression adjusted for age, sex, race, and smoking were used to assess the association of proteinuria testing with pioglitazone use, subsequent full urinalysis, and diagnosis with bladder cancer.",
"Patients treated with pioglitazone were more likely than others with diabetes to undergo testing for proteinuria (p < 0.001). The odds of positive tests for proteinuria were higher among pioglitazone-treated patients (OR = 1.41, 95%CI 1.36-1.46). A positive proteinuria test was associated with increased odds of completing a urinalysis in the following 6 months (OR = 1.78, 95%CI 1.73-1.85). Negative and positive proteinuria test results were inversely (hazard ratio (HR) 0.63, 95%CI 0.52-0.75) and positively associated (HR 2.45, 95%CI 2.12-2.82) with bladder cancer risk, respectively. Adjustment for negative and positive proteinuria testing reduced the magnitude of association between pioglitazone and bladder cancer by only 5 to 10% (ever-exposed HR: from 1.06 to 1.01 and >4 years exposure HR: from 1.38 to 1.28)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Aged, 80 and over",
"California",
"Cohort Studies",
"Confounding Factors (Epidemiology)",
"Diabetes Mellitus, Type 2",
"Female",
"Follow-Up Studies",
"Humans",
"Hypoglycemic Agents",
"Male",
"Middle Aged",
"Pioglitazone",
"Proteinuria",
"Thiazolidinediones",
"Urinary Bladder Neoplasms"
]
} | Proteinuria testing may be a confounder in studies of pioglitazone and bladder cancer but does not fully explain the association between pioglitazone and bladder cancer in this cohort. Optimal adjustment for proteinuria testing likely requires knowledge of the test result. | yes | [
{
"from": "human",
"value": "Question: Is proteinuria testing among patients with diabetes mellitus associated with bladder cancer diagnosis : potential for unmeasured confounding in studies of pioglitazone and bladder cancer?\nContext: {'contexts': ['The observed association between pioglitazone and bladder cancer could be causal or because of bias in the design of prior studies. We hypothesize that proteinuria testing may lead to detection bias if routine test results for proteinuria lead to a full urinalysis.', 'We reanalyzed patients with diabetes mellitus within Kaiser Permanente Northern California. Logistic and Cox regression adjusted for age, sex, race, and smoking were used to assess the association of proteinuria testing with pioglitazone use, subsequent full urinalysis, and diagnosis with bladder cancer.', 'Patients treated with pioglitazone were more likely than others with diabetes to undergo testing for proteinuria (p\\u2009<\\u20090.001). The odds of positive tests for proteinuria were higher among pioglitazone-treated patients (OR\\u2009=\\u20091.41, 95%CI 1.36-1.46). A positive proteinuria test was associated with increased odds of completing a urinalysis in the following 6\\u2009months (OR\\u2009=\\u20091.78, 95%CI 1.73-1.85). Negative and positive proteinuria test results were inversely (hazard ratio (HR) 0.63, 95%CI 0.52-0.75) and positively associated (HR 2.45, 95%CI 2.12-2.82) with bladder cancer risk, respectively. Adjustment for negative and positive proteinuria testing reduced the magnitude of association between pioglitazone and bladder cancer by only 5 to 10% (ever-exposed HR: from 1.06 to 1.01 and >4\\u2009years exposure HR: from 1.38 to 1.28).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Aged, 80 and over', 'California', 'Cohort Studies', 'Confounding Factors (Epidemiology)', 'Diabetes Mellitus, Type 2', 'Female', 'Follow-Up Studies', 'Humans', 'Hypoglycemic Agents', 'Male', 'Middle Aged', 'Pioglitazone', 'Proteinuria', 'Thiazolidinediones', 'Urinary Bladder Neoplasms']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,748,941 | Does survey of sonoanatomic distances for lumbar medial branch nerve block in healthy volunteers? | {
"contexts": [
"The precise knowledge of anatomy and the region of transverse process (TP) and superior articular processes (AP) and their distance from the skin are important in blocking and treating lumbar facet syndrome. Evaluation of these anatomic distances from 3rd and 5th lumbar vertebrae in both sides and in different body mass index (BMI) in healthy volunteers might improve knowledge of ultrasound (US) lumbar medial branch nerve blocks (LMBB).",
"Bilateral US in the 3rd and 5th lumbar vertebrae of 64 volunteers carried out and the distance between skin to TP and skin to AP was measured. These distances were compared on both sides and in different BMI groups. The analysis was done using SPSS 11. Analysis of variance was used to compare the means at three vertebral levels (L3-L5) and different BMI groups. P values less than 0.05 were considered statistically significant. The paired t-test was used to compare the mean distance between skin to TP and skin to AP on both sides.",
"The distance between skin to TP and skin to AP of 3rd vertebrae to 5th vertebrae was increased in both right and left sides (P < 0.001) from up to down. The mean distance from skin to TP were greater on the left side compared to the right in all three vertebral levels from L3 to L5 (P values 0.014, 0.024, and 0.006 respectively). The mean distance from skin to TP and the skin to AP was statistically significant in different BMI groups (P < 0.001)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": []
} | We found many anatomic distances which may increase awareness of US guided LMBB. | yes | [
{
"from": "human",
"value": "Question: Does survey of sonoanatomic distances for lumbar medial branch nerve block in healthy volunteers?\nContext: {'contexts': ['The precise knowledge of anatomy and the region of transverse process (TP) and superior articular processes (AP) and their distance from the skin are important in blocking and treating lumbar facet syndrome. Evaluation of these anatomic distances from 3rd and 5th lumbar vertebrae in both sides and in different body mass index (BMI) in healthy volunteers might improve knowledge of ultrasound (US) lumbar medial branch nerve blocks (LMBB).', 'Bilateral US in the 3rd and 5th lumbar vertebrae of 64 volunteers carried out and the distance between skin to TP and skin to AP was measured. These distances were compared on both sides and in different BMI groups. The analysis was done using SPSS 11. Analysis of variance was used to compare the means at three vertebral levels (L3-L5) and different BMI groups. P values less than 0.05 were considered statistically significant. The paired t-test was used to compare the mean distance between skin to TP and skin to AP on both sides.', 'The distance between skin to TP and skin to AP of 3rd vertebrae to 5th vertebrae was increased in both right and left sides (P < 0.001) from up to down. The mean distance from skin to TP were greater on the left side compared to the right in all three vertebral levels from L3 to L5 (P values 0.014, 0.024, and 0.006 respectively). The mean distance from skin to TP and the skin to AP was statistically significant in different BMI groups (P < 0.001).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,761,122 | Does margaritaria discoidea ( Euphorbiaceae ) stem bark extract attenuate allergy and Freund 's adjuvant-induced arthritis in rodents? | {
"contexts": [
"Various parts of Margaritaria discoidea find use in traditional medicine in the treatment of pain and oedema. This study evaluated the anti-allergic, anti-inflammatory and anti-arthritic effects of a 70% (v/v) aqueous ethanol extract of the stem bark of Margaritaria discoidea, MDE in rodents.",
"Systemic anaphylaxis was induced by the injection of compound 48/80 into mice and their survival rate was monitored to evaluate the anti-allergic action of the extract. The effect of MDE assessed on the maximal and total oedema responses in the mouse carrageenan-induced paw oedema was used to evaluate the anti-inflammatory action of the extract while the Freund's adjuvant-induced arthritis model was employed to study the anti-arthritic effects of MDE.",
"MDE dose-dependently increased the time for compound 48/80-induced mortality in mice. MDE suppressed the mean maximal swelling and the total paw swellings induced over 6 h in the carrageenan-induced paw oedema when administered either prophylactically or therapeutically. MDE caused a reduction in serum levels of TNFα and IL-6 and significantly suppressed Freund's adjuvant-induced arthritis."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": []
} | Margaritaria discoidea suppresses allergy and exhibits anti-inflammatory activity in mice. In addition it attenuates Freund's adjuvant-induced arthritis through a reduction in serum levels of TNFα and IL-6 in rats. | yes | [
{
"from": "human",
"value": "Question: Does margaritaria discoidea ( Euphorbiaceae ) stem bark extract attenuate allergy and Freund 's adjuvant-induced arthritis in rodents?\nContext: {'contexts': ['Various parts of Margaritaria discoidea find use in traditional medicine in the treatment of pain and oedema. This study evaluated the anti-allergic, anti-inflammatory and anti-arthritic effects of a 70% (v/v) aqueous ethanol extract of the stem bark of Margaritaria discoidea, MDE in rodents.', \"Systemic anaphylaxis was induced by the injection of compound 48/80 into mice and their survival rate was monitored to evaluate the anti-allergic action of the extract. The effect of MDE assessed on the maximal and total oedema responses in the mouse carrageenan-induced paw oedema was used to evaluate the anti-inflammatory action of the extract while the Freund's adjuvant-induced arthritis model was employed to study the anti-arthritic effects of MDE.\", \"MDE dose-dependently increased the time for compound 48/80-induced mortality in mice. MDE suppressed the mean maximal swelling and the total paw swellings induced over 6 h in the carrageenan-induced paw oedema when administered either prophylactically or therapeutically. MDE caused a reduction in serum levels of TNFα and IL-6 and significantly suppressed Freund's adjuvant-induced arthritis.\"], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,769,314 | Is stromal transforming growth factor-beta 1 crucial for reinforcing the invasive potential of low invasive cancer? | {
"contexts": [
"Tumour cells alter the characteristics of the adjacent stroma to create a supportive microenvironment during cancer progression. In vitro and in vivo experiments were carried out to verify the role of stromal TGF-β1 in reinforcing of the invasive potential in low invasive cancer.",
"Isolated NF or CAF was co-cultured with low invasive HSC-2 cells to evaluate whether stromal TGF-β1 induced PDPN expression by Transwell invasion and influenced tumour growth in orthotopic xenografts.",
"Stimulation by TGF-β1 promoted PDPN expression and Transwell invasion through SMAD signalling as well as activation of Src, P38 mitogen activated protein kinase and extracellular regulated kinase 1/2. PDPN induction was TβRII-dependent. Tumour growth of HSC-2 OSCC in a mouse xenograft was intensified in the tumour CAF microenvironment."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Blotting, Western",
"Carcinoma, Squamous Cell",
"Coculture Techniques",
"Disease Progression",
"Enzyme-Linked Immunosorbent Assay",
"Fibroblasts",
"Heterografts",
"Immunohistochemistry",
"Male",
"Membrane Glycoproteins",
"Mice",
"Mice, Inbred BALB C",
"Mice, Nude",
"Mouth Neoplasms",
"Neoplasm Invasiveness",
"Phenotype",
"Signal Transduction",
"Transforming Growth Factor beta1",
"Tumor Microenvironment"
]
} | Stromal TGF-β1 signalling promoted PDPN expression in cancer cells, thereby enhancing tumour growth and leading to a more invasive phenotype. | yes | [
{
"from": "human",
"value": "Question: Is stromal transforming growth factor-beta 1 crucial for reinforcing the invasive potential of low invasive cancer?\nContext: {'contexts': ['Tumour cells alter the characteristics of the adjacent stroma to create a supportive microenvironment during cancer progression. In vitro and in vivo experiments were carried out to verify the role of stromal TGF-β1 in reinforcing of the invasive potential in low invasive cancer.', 'Isolated NF or CAF was co-cultured with low invasive HSC-2 cells to evaluate whether stromal TGF-β1 induced PDPN expression by Transwell invasion and influenced tumour growth in orthotopic xenografts.', 'Stimulation by TGF-β1 promoted PDPN expression and Transwell invasion through SMAD signalling as well as activation of Src, P38 mitogen activated protein kinase and extracellular regulated kinase 1/2. PDPN induction was TβRII-dependent. Tumour growth of HSC-2 OSCC in a mouse xenograft was intensified in the tumour CAF microenvironment.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Blotting, Western', 'Carcinoma, Squamous Cell', 'Coculture Techniques', 'Disease Progression', 'Enzyme-Linked Immunosorbent Assay', 'Fibroblasts', 'Heterografts', 'Immunohistochemistry', 'Male', 'Membrane Glycoproteins', 'Mice', 'Mice, Inbred BALB C', 'Mice, Nude', 'Mouth Neoplasms', 'Neoplasm Invasiveness', 'Phenotype', 'Signal Transduction', 'Transforming Growth Factor beta1', 'Tumor Microenvironment']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,761,873 | Does eGF reverse multi-drug resistance via the p-ERK pathway in HepG2/ADM and SMMC7721/ADM hepatocellular carcinoma models? | {
"contexts": [
"To investigate signaling pathways for reversal of EGF-mediated multi-drug resistance (MDR) in hepatocellular carcinoma (HCC) models.",
"HCC MDR cell strain HepG2/adriamycin (ADM) and SMMC7721/ADM models were established using a method of exposure to medium with ADM between low and high concentration with gradually increasing concentration. Drug sensitivity and reversal of multi-drug resistance by EGF were determined and the cell cycle distribution and apoptosis were analyzed by flow cytometry. Phosphorylation of ERK1, ERK2, ERK5 and expression of Bim were detected by Western blotting.",
"The results showed that HepG2/ADM and SMMC7721/ADM cells were resistant not only to ADM, but also to multiple anticancer drugs. When used alone, EGF had no anti-tumor activity in HepG2/ADM and SMMC7721/ADM cells in vitro, while it increased the cytotoxicity of ADM. EGF induced cell apoptosis and G0/G1 phase cell cycle arrest in HepG2/ADM And SMMC7721/ADM cells, while enhancing activity of p-ERKs and up-regulated expression of BimEL."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Antibiotics, Antineoplastic",
"Apoptosis",
"Blotting, Western",
"Carcinoma, Hepatocellular",
"Cell Cycle",
"Cell Proliferation",
"Doxorubicin",
"Drug Resistance, Multiple",
"Drug Resistance, Neoplasm",
"Epidermal Growth Factor",
"Flow Cytometry",
"Humans",
"Liver Neoplasms",
"Mitogen-Activated Protein Kinase 1",
"Mitogen-Activated Protein Kinase 3",
"Phosphorylation",
"Tumor Cells, Cultured"
]
} | EGF might enhance the chemosensitivity of HepG2/ADM and SMMC7721/ADM cells via up-regulating p-ERKs and BimEL protein. | yes | [
{
"from": "human",
"value": "Question: Does eGF reverse multi-drug resistance via the p-ERK pathway in HepG2/ADM and SMMC7721/ADM hepatocellular carcinoma models?\nContext: {'contexts': ['To investigate signaling pathways for reversal of EGF-mediated multi-drug resistance (MDR) in hepatocellular carcinoma (HCC) models.', 'HCC MDR cell strain HepG2/adriamycin (ADM) and SMMC7721/ADM models were established using a method of exposure to medium with ADM between low and high concentration with gradually increasing concentration. Drug sensitivity and reversal of multi-drug resistance by EGF were determined and the cell cycle distribution and apoptosis were analyzed by flow cytometry. Phosphorylation of ERK1, ERK2, ERK5 and expression of Bim were detected by Western blotting.', 'The results showed that HepG2/ADM and SMMC7721/ADM cells were resistant not only to ADM, but also to multiple anticancer drugs. When used alone, EGF had no anti-tumor activity in HepG2/ADM and SMMC7721/ADM cells in vitro, while it increased the cytotoxicity of ADM. EGF induced cell apoptosis and G0/G1 phase cell cycle arrest in HepG2/ADM And SMMC7721/ADM cells, while enhancing activity of p-ERKs and up-regulated expression of BimEL.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Antibiotics, Antineoplastic', 'Apoptosis', 'Blotting, Western', 'Carcinoma, Hepatocellular', 'Cell Cycle', 'Cell Proliferation', 'Doxorubicin', 'Drug Resistance, Multiple', 'Drug Resistance, Neoplasm', 'Epidermal Growth Factor', 'Flow Cytometry', 'Humans', 'Liver Neoplasms', 'Mitogen-Activated Protein Kinase 1', 'Mitogen-Activated Protein Kinase 3', 'Phosphorylation', 'Tumor Cells, Cultured']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,778,708 | Does psychiatric staff on the wards share attitudes on aggression? | {
"contexts": [
"The concept of ward culture has been proposed as a reason for the often reported differences in treatment decisions when managing inpatient aggression. We therefore studied whether staff on wards actually shares similar perceptions and attitudes about aggression and whether the specialty of the ward on which the staff members work influences these opinions.",
"The Attitudes Towards Aggression Scale was used to assess attitudes towards aggression in 31 closed psychiatric wards. Altogether 487 staff members working on the study wards were asked to fill in the scale. Respondent's gender, age, educational level, working experience on the current ward, and specialty of this ward (acute, forensic, rehabilitation) served as background variables.",
"Most of the variance found was due to differences between individuals. Belonging to the personnel of a particular ward did not explain much of the variance."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": []
} | Psychiatric staff on the wards does not share attitudes on aggression. As each staff member has his/her own opinion about aggression, training for dealing with aggression or violent incidents should be done, at least partly, on an individual level. We also suggest caution in using the concept of ward culture as an explanation for the use of restrictive measures on psychiatric wards. | no | [
{
"from": "human",
"value": "Question: Does psychiatric staff on the wards share attitudes on aggression?\nContext: {'contexts': ['The concept of ward culture has been proposed as a reason for the often reported differences in treatment decisions when managing inpatient aggression. We therefore studied whether staff on wards actually shares similar perceptions and attitudes about aggression and whether the specialty of the ward on which the staff members work influences these opinions.', \"The Attitudes Towards Aggression Scale was used to assess attitudes towards aggression in 31 closed psychiatric wards. Altogether 487 staff members working on the study wards were asked to fill in the scale. Respondent's gender, age, educational level, working experience on the current ward, and specialty of this ward (acute, forensic, rehabilitation) served as background variables.\", 'Most of the variance found was due to differences between individuals. Belonging to the personnel of a particular ward did not explain much of the variance.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: no"
}
]
|
24,757,138 | Do fcγ receptor III and Fcγ receptor IV on macrophages drive autoimmune valvular carditis in mice? | {
"contexts": [
"Arthritis and valvular carditis coexist in several human rheumatic diseases, including systemic lupus erythematosus, rheumatic fever, and rheumatoid arthritis. T cell receptor-transgenic K/BxN mice develop spontaneous autoantibody-associated arthritis and valvular carditis. The common Fc receptor γ (FcRγ) signaling chain is required for carditis to develop in K/BxN mice. FcRγ pairs with numerous receptors in a variety of cells. The aim of this study was to identify the FcRγ-associated receptors and Fcγ receptor (FcγR)-expressing cells that mediate valvular carditis in this model.",
"We bred K/BxN mice lacking the genes that encode activating Fcγ receptors (FcγRI, FcγRIII, and FcγRIV), and we assessed these mice for valvular carditis. We similarly evaluated complement component C3-deficient K/BxN mice. Immunohistochemistry, bone marrow transplantation, and macrophage depletion were used to define the key FcRγ-expressing cell type.",
"Genetic deficiency of only one of the activating Fcγ receptors did not prevent carditis, whereas deficiency of all 3 activating Fcγ receptors did. Further analysis demonstrated that FcγRIII and FcγRIV were the key drivers of valve inflammation; FcγRI was dispensable. C3 was not required. FcRγ expression by radioresistant cells was critical for valvular carditis to develop, and further analysis indicated that macrophages were the key candidate FcγR-expressing effectors of carditis."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Arthritis, Experimental",
"Arthritis, Rheumatoid",
"Autoantibodies",
"Macrophages",
"Mice",
"Mice, Transgenic",
"Myocarditis",
"Receptors, IgG",
"T-Lymphocytes"
]
} | FcγRIII and FcγRIV act redundantly to promote valvular carditis in K/BxN mice with systemic autoantibody-associated arthritis. Macrophage depletion reduced the severity of valve inflammation. These findings suggest that pathogenic autoantibodies engage Fcγ receptors on macrophages to drive valvular carditis. Our study provides new insight into the pathogenesis of cardiovascular inflammation in the setting of autoantibody-associated chronic inflammatory diseases. | yes | [
{
"from": "human",
"value": "Question: Do fcγ receptor III and Fcγ receptor IV on macrophages drive autoimmune valvular carditis in mice?\nContext: {'contexts': ['Arthritis and valvular carditis coexist in several human rheumatic diseases, including systemic lupus erythematosus, rheumatic fever, and rheumatoid arthritis. T cell receptor-transgenic K/BxN mice develop spontaneous autoantibody-associated arthritis and valvular carditis. The common Fc receptor γ (FcRγ) signaling chain is required for carditis to develop in K/BxN mice. FcRγ pairs with numerous receptors in a variety of cells. The aim of this study was to identify the FcRγ-associated receptors and Fcγ receptor (FcγR)-expressing cells that mediate valvular carditis in this model.', 'We bred K/BxN mice lacking the genes that encode activating Fcγ receptors (FcγRI, FcγRIII, and FcγRIV), and we assessed these mice for valvular carditis. We similarly evaluated complement component C3-deficient K/BxN mice. Immunohistochemistry, bone marrow transplantation, and macrophage depletion were used to define the key FcRγ-expressing cell type.', 'Genetic deficiency of only one of the activating Fcγ receptors did not prevent carditis, whereas deficiency of all 3 activating Fcγ receptors did. Further analysis demonstrated that FcγRIII and FcγRIV were the key drivers of valve inflammation; FcγRI was dispensable. C3 was not required. FcRγ expression by radioresistant cells was critical for valvular carditis to develop, and further analysis indicated that macrophages were the key candidate FcγR-expressing effectors of carditis.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Arthritis, Experimental', 'Arthritis, Rheumatoid', 'Autoantibodies', 'Macrophages', 'Mice', 'Mice, Transgenic', 'Myocarditis', 'Receptors, IgG', 'T-Lymphocytes']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,764,073 | Do aM-PAC `` 6-Clicks '' functional assessment scores predict acute care hospital discharge destination? | {
"contexts": [
"Physical therapists and occupational therapists practicing in acute care hospitals play a crucial role in discharge planning. A standardized assessment of patients' function could be useful for discharge recommendations.",
"The study objective was to determine the accuracy of \"6-Clicks\" basic mobility and daily activity measures for predicting discharge from an acute care hospital to a home or institutional setting.",
"The study was retrospective and observational.",
"\"6-Clicks\" scores obtained at initial visits by physical therapists or occupational therapists and patients' discharge destinations were used to develop and validate receiver operating characteristic curves for predicting discharge destination. Positive predictive values (PPV), negative predictive values (NPV), and likelihood ratios were calculated.",
"Areas under the receiver operating characteristic curves for basic mobility scores were 0.857 (95% confidence interval [CI]=0.852, 0.862) and 0.855 (95% CI=0.850, 0.860) in development and validation samples, respectively. Areas under the curves for daily activity scores were 0.846 (95% CI=0.841, 0.851) and 0.845 (95% CI=0.840, 0.850) in development and validation samples, respectively. Cutoff scores providing the best accuracy for determining discharge destination were 42.9 for basic mobility and 39.4 for daily activity. For basic mobility, the PPV was 0.748 and the NPV was 0.801 in both development and validation samples. For daily activity, the PPVs were 0.787 and 0.784 and the NPVs were 0.748 and 0.746 in development and validation samples, respectively."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"METHODS",
"RESULTS"
],
"meshes": [
"Activities of Daily Living",
"Adolescent",
"Adult",
"Aged",
"Aged, 80 and over",
"Area Under Curve",
"Disability Evaluation",
"Female",
"Humans",
"Male",
"Middle Aged",
"Mobility Limitation",
"Needs Assessment",
"Occupational Therapy",
"Outcome Assessment (Health Care)",
"Patient Discharge",
"Physical Therapy Specialty",
"Predictive Value of Tests",
"Retrospective Studies"
]
} | Limitations included lack of information on the rater reliability of "6-Clicks" instruments, use of surrogate data for some discharge designations, and use of a clinical database for research purposes. | yes | [
{
"from": "human",
"value": "Question: Do aM-PAC `` 6-Clicks '' functional assessment scores predict acute care hospital discharge destination?\nContext: {'contexts': [\"Physical therapists and occupational therapists practicing in acute care hospitals play a crucial role in discharge planning. A standardized assessment of patients' function could be useful for discharge recommendations.\", 'The study objective was to determine the accuracy of \"6-Clicks\" basic mobility and daily activity measures for predicting discharge from an acute care hospital to a home or institutional setting.', 'The study was retrospective and observational.', '\"6-Clicks\" scores obtained at initial visits by physical therapists or occupational therapists and patients\\' discharge destinations were used to develop and validate receiver operating characteristic curves for predicting discharge destination. Positive predictive values (PPV), negative predictive values (NPV), and likelihood ratios were calculated.', 'Areas under the receiver operating characteristic curves for basic mobility scores were 0.857 (95% confidence interval [CI]=0.852, 0.862) and 0.855 (95% CI=0.850, 0.860) in development and validation samples, respectively. Areas under the curves for daily activity scores were 0.846 (95% CI=0.841, 0.851) and 0.845 (95% CI=0.840, 0.850) in development and validation samples, respectively. Cutoff scores providing the best accuracy for determining discharge destination were 42.9 for basic mobility and 39.4 for daily activity. For basic mobility, the PPV was 0.748 and the NPV was 0.801 in both development and validation samples. For daily activity, the PPVs were 0.787 and 0.784 and the NPVs were 0.748 and 0.746 in development and validation samples, respectively.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'METHODS', 'RESULTS'], 'meshes': ['Activities of Daily Living', 'Adolescent', 'Adult', 'Aged', 'Aged, 80 and over', 'Area Under Curve', 'Disability Evaluation', 'Female', 'Humans', 'Male', 'Middle Aged', 'Mobility Limitation', 'Needs Assessment', 'Occupational Therapy', 'Outcome Assessment (Health Care)', 'Patient Discharge', 'Physical Therapy Specialty', 'Predictive Value of Tests', 'Retrospective Studies']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,762,493 | Does proteomic analysis reveal novel proteins associated with progression and differentiation of colorectal carcinoma? | {
"contexts": [
"The objective of this study is to characterize differential proteomic expression among well-differentiation and poor-differentiation colorectal carcinoma tissues and normal mucous epithelium.",
"The study is based on quantitative 2-dimensional gel electrophoresis and analyzed by PDquest.",
"Excluding redundancies due to proteolysis and posttranslational modified isoforms of over 600 protein spots, 11 proteins were revealed as regulated with statistical variance being within the 95th confidence level and were identified by peptide mass fingerprinting in matrix assisted laser desorption/ionization time-of-flight mass spectrometry. Progression-associated proteins belong to the functional complexes of tumorigenesis, proliferation, differentiation, metabolism, and the regulation of major histocompatibility complex processing and other functions. Partial but significant overlap was revealed with previous proteomics and transcriptomics studies in CRC. Among various differentiation stage of CRC tissues, we identified calreticulin precursor, MHC class I antigen (human leukocyte antigen A ), glutathione S-transferase pi1, keratin 8, heat shock protein 27, tubulin beta chain, triosephosphate, fatty acid-binding protein, hemoglobin (deoxy) mutant with val b 1 replaced by met (HBB), and zinc finger protein 312 (FEZF2)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Colorectal Neoplasms",
"Disease Progression",
"Female",
"Humans",
"Intestinal Mucosa",
"Male",
"Middle Aged",
"Neoplasm Grading",
"Protein Interaction Mapping",
"Protein Interaction Maps",
"Proteome",
"Proteomics",
"Reproducibility of Results"
]
} | Their functional networks were analyzed by Ingenuity systems Ingenuity Pathways Analysis and revealed the potential roles as novel biomarkers for progression in various differentiation stages of CRC. | yes | [
{
"from": "human",
"value": "Question: Does proteomic analysis reveal novel proteins associated with progression and differentiation of colorectal carcinoma?\nContext: {'contexts': ['The objective of this study is to characterize differential proteomic expression among well-differentiation and poor-differentiation colorectal carcinoma tissues and normal mucous epithelium.', 'The study is based on quantitative 2-dimensional gel electrophoresis and analyzed by PDquest.', 'Excluding redundancies due to proteolysis and posttranslational modified isoforms of over 600 protein spots, 11 proteins were revealed as regulated with statistical variance being within the 95th confidence level and were identified by peptide mass fingerprinting in matrix assisted laser desorption/ionization time-of-flight mass spectrometry. Progression-associated proteins belong to the functional complexes of tumorigenesis, proliferation, differentiation, metabolism, and the regulation of major histocompatibility complex processing and other functions. Partial but significant overlap was revealed with previous proteomics and transcriptomics studies in CRC. Among various differentiation stage of CRC tissues, we identified calreticulin precursor, MHC class I antigen (human leukocyte antigen A ), glutathione S-transferase pi1, keratin 8, heat shock protein 27, tubulin beta chain, triosephosphate, fatty acid-binding protein, hemoglobin (deoxy) mutant with val b 1 replaced by met (HBB), and zinc finger protein 312 (FEZF2).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Colorectal Neoplasms', 'Disease Progression', 'Female', 'Humans', 'Intestinal Mucosa', 'Male', 'Middle Aged', 'Neoplasm Grading', 'Protein Interaction Mapping', 'Protein Interaction Maps', 'Proteome', 'Proteomics', 'Reproducibility of Results']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,768,874 | Does omentin prevent myocardial ischemic injury through AMP-activated protein kinase- and Akt-dependent mechanisms? | {
"contexts": [
"This study examined the impact of omentin on myocardial injury in a mouse model of ischemia/reperfusion (I/R) and explored its underlying mechanisms.",
"Obesity is a major risk factor for ischemic heart disease. Omentin is a circulating adipokine that is down-regulated by obesity.",
"In patients who underwent successful reperfusion treatment after acute myocardial infarction, cardiac function and perfusion defect were assessed by using scintigraphic images. Mice were subjected to myocardial ischemia followed by reperfusion.",
"This study found that high levels of plasma omentin were associated with improvement of heart damage and function after reperfusion therapy in patients with acute myocardial infarction. Systemic administration of human omentin to mice led to a reduction in myocardial infarct size and apoptosis after I/R, which was accompanied by enhanced phosphorylation of AMP-activated protein kinase (AMPK) and Akt in the ischemic heart. Fat-specific overexpression of human omentin also resulted in reduction of infarct size after I/R. Blockade of AMPK or Akt activity reversed omentin-induced inhibition of myocardial ischemic damage and apoptosis in mice. In cultured cardiomyocytes, omentin suppressed hypoxia/reoxygenation-induced apoptosis, which was blocked by inactivation of AMPK or Akt."
],
"labels": [
"OBJECTIVE",
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"AMP-Activated Protein Kinases",
"Animals",
"Apoptosis",
"Biomarkers",
"Cytokines",
"Disease Models, Animal",
"Female",
"GPI-Linked Proteins",
"Humans",
"Lectins",
"Male",
"Mice",
"Mice, Inbred C57BL",
"Mice, Transgenic",
"Middle Aged",
"Myocardial Reperfusion",
"Myocardial Reperfusion Injury",
"Oncogene Protein v-akt",
"Percutaneous Coronary Intervention",
"Phosphorylation"
]
} | Our data indicate that omentin functions as an adipokine that ameliorates acute ischemic injury in the heart by suppressing myocyte apoptosis through both AMPK- and Akt-dependent mechanisms. | yes | [
{
"from": "human",
"value": "Question: Does omentin prevent myocardial ischemic injury through AMP-activated protein kinase- and Akt-dependent mechanisms?\nContext: {'contexts': ['This study examined the impact of omentin on myocardial injury in a mouse model of ischemia/reperfusion (I/R) and explored its underlying mechanisms.', 'Obesity is a major risk factor for ischemic heart disease. Omentin is a circulating adipokine that is down-regulated by obesity.', 'In patients who underwent successful reperfusion treatment after acute myocardial infarction, cardiac function and perfusion defect were assessed by using scintigraphic images. Mice were subjected to myocardial ischemia followed by reperfusion.', 'This study found that high levels of plasma omentin were associated with improvement of heart damage and function after reperfusion therapy in patients with acute myocardial infarction. Systemic administration of human omentin to mice led to a reduction in myocardial infarct size and apoptosis after I/R, which was accompanied by enhanced phosphorylation of AMP-activated protein kinase (AMPK) and Akt in the ischemic heart. Fat-specific overexpression of human omentin also resulted in reduction of infarct size after I/R. Blockade of AMPK or Akt activity reversed omentin-induced inhibition of myocardial ischemic damage and apoptosis in mice. In cultured cardiomyocytes, omentin suppressed hypoxia/reoxygenation-induced apoptosis, which was blocked by inactivation of AMPK or Akt.'], 'labels': ['OBJECTIVE', 'BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['AMP-Activated Protein Kinases', 'Animals', 'Apoptosis', 'Biomarkers', 'Cytokines', 'Disease Models, Animal', 'Female', 'GPI-Linked Proteins', 'Humans', 'Lectins', 'Male', 'Mice', 'Mice, Inbred C57BL', 'Mice, Transgenic', 'Middle Aged', 'Myocardial Reperfusion', 'Myocardial Reperfusion Injury', 'Oncogene Protein v-akt', 'Percutaneous Coronary Intervention', 'Phosphorylation']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,768,531 | Are hyperglycemia , hypoglycemia , and glycemic complexity associated with worse outcomes after surgery? | {
"contexts": [
"The purpose of this study was to determine if glycemic complexity, along with hypoglycemia and hyperglycemia, was associated with worse outcomes after cardiac surgery.",
"We conducted a retrospective analysis of 970 patients who had insulin infusions designed to keep blood glucose levels between 80 and 110 mg/dL. Glycemic complexity was calculated using jackknifed approximate entropy. Logistic regression was used to adjust for confounders.",
"A total of 495 patients (51%) developed complications, and 32 patients (3.3%) died. Along with older age, comorbidities, and complicated surgeries, any hypoglycemia (glucose<71 mg/dL) and the number of glucose values greater than 140 mg/dL were independent predictors of complications. Increased risk of mortality, after adjusting for other risk factors, was associated with older age, longer perfusion time, receiving intraoperative transfusions, and greater jackknifed approximate entropy of the glucose time series."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Age Factors",
"Aged",
"Blood Glucose",
"Cardiac Surgical Procedures",
"Comorbidity",
"Critical Illness",
"Entropy",
"Female",
"Humans",
"Hyperglycemia",
"Hypoglycemia",
"Hypoglycemic Agents",
"Insulin",
"Logistic Models",
"Male",
"Middle Aged",
"Retrospective Studies",
"Risk Factors",
"Treatment Outcome"
]
} | We found that hypoglycemia (glucose<71 mg/dL) and hyperglycemia (glucose>140 mg/dL) were associated with increased risk of complications, whereas greater complexity of the glucose time series was associated with mortality. | yes | [
{
"from": "human",
"value": "Question: Are hyperglycemia , hypoglycemia , and glycemic complexity associated with worse outcomes after surgery?\nContext: {'contexts': ['The purpose of this study was to determine if glycemic complexity, along with hypoglycemia and hyperglycemia, was associated with worse outcomes after cardiac surgery.', 'We conducted a retrospective analysis of 970 patients who had insulin infusions designed to keep blood glucose levels between 80 and 110 mg/dL. Glycemic complexity was calculated using jackknifed approximate entropy. Logistic regression was used to adjust for confounders.', 'A total of 495 patients (51%) developed complications, and 32 patients (3.3%) died. Along with older age, comorbidities, and complicated surgeries, any hypoglycemia (glucose<71 mg/dL) and the number of glucose values greater than 140 mg/dL were independent predictors of complications. Increased risk of mortality, after adjusting for other risk factors, was associated with older age, longer perfusion time, receiving intraoperative transfusions, and greater jackknifed approximate entropy of the glucose time series.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Age Factors', 'Aged', 'Blood Glucose', 'Cardiac Surgical Procedures', 'Comorbidity', 'Critical Illness', 'Entropy', 'Female', 'Humans', 'Hyperglycemia', 'Hypoglycemia', 'Hypoglycemic Agents', 'Insulin', 'Logistic Models', 'Male', 'Middle Aged', 'Retrospective Studies', 'Risk Factors', 'Treatment Outcome']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,768,533 | Does the Intermountain Risk Score predict mortality in trauma patients? | {
"contexts": [
"Intermountain Risk Score (IMRS) uses the admission complete blood count and basic metabolic profile to predict mortality. Intermountain Risk Score has been validated in medical patients but has not been evaluated in trauma. This study tested whether IMRS is predictive of mortality in a trauma population at a level I trauma center.",
"Admitted trauma patients with complete blood count and basic metabolic profile from October 2005 to December 2011 were evaluated. Thirty-day and 1-year IMRS were calculated using multivariable modeling. Mortality was determined using the medical record and Social Security Administration death data.",
"Three thousand six hundred thirty-seven females and 5901 males were evaluated. Intermountain Risk Score was highly predictive of death at 30 days (c-statistics, c = 0.772 for females; c = 0.783 males) and 1 year (c = 0.778 for females; c = 0.831 males). Cox regression analysis, adjusted for injury severity score, blunt vs penetrating, and length of stay, showed increased mortality risks among patients in the moderate- and high-risk IMRS-defined groups at both 30 days and 1 year, with hazard ratios ranging from 4.96 to 57.88 (all P < .001)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Area Under Curve",
"Female",
"Humans",
"Incidence",
"Injury Severity Score",
"Length of Stay",
"Male",
"Middle Aged",
"Predictive Value of Tests",
"ROC Curve",
"Risk",
"Risk Assessment",
"Sex Factors",
"Trauma Centers",
"United States",
"Wounds, Nonpenetrating",
"Wounds, Penetrating"
]
} | Intermountain Risk Score strongly predicts mortality in trauma patients at this single level I trauma center. The ability to accurately determine a patient's mortality risk at admission makes IMRS a potentially clinically important tool. | yes | [
{
"from": "human",
"value": "Question: Does the Intermountain Risk Score predict mortality in trauma patients?\nContext: {'contexts': ['Intermountain Risk Score (IMRS) uses the admission complete blood count and basic metabolic profile to predict mortality. Intermountain Risk Score has been validated in medical patients but has not been evaluated in trauma. This study tested whether IMRS is predictive of mortality in a trauma population at a level I trauma center.', 'Admitted trauma patients with complete blood count and basic metabolic profile from October 2005 to December 2011 were evaluated. Thirty-day and 1-year IMRS were calculated using multivariable modeling. Mortality was determined using the medical record and Social Security Administration death data.', 'Three thousand six hundred thirty-seven females and 5901 males were evaluated. Intermountain Risk Score was highly predictive of death at 30 days (c-statistics, c = 0.772 for females; c = 0.783 males) and 1 year (c = 0.778 for females; c = 0.831 males). Cox regression analysis, adjusted for injury severity score, blunt vs penetrating, and length of stay, showed increased mortality risks among patients in the moderate- and high-risk IMRS-defined groups at both 30 days and 1 year, with hazard ratios ranging from 4.96 to 57.88 (all P < .001).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Area Under Curve', 'Female', 'Humans', 'Incidence', 'Injury Severity Score', 'Length of Stay', 'Male', 'Middle Aged', 'Predictive Value of Tests', 'ROC Curve', 'Risk', 'Risk Assessment', 'Sex Factors', 'Trauma Centers', 'United States', 'Wounds, Nonpenetrating', 'Wounds, Penetrating']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,770,679 | Is cytoplasmic YAP expression associated with prolonged survival in patients with lung adenocarcinomas and epidermal growth factor receptor tyrosine kinase inhibitor treatment? | {
"contexts": [
"Yes-associated protein (YAP) has been reported to be associated with the prognosis of various cancers and also to affect epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) activity in ovarian cancer cell lines. However, few studies have evaluated YAP protein expression in lung cancer, and the results have lacked consistency.",
"YAP expression was evaluated in a total of 205 curatively resected lung adenocarcinomas and 36 cases of EGFR-mutated TKI-treated patients. Correlations between the expression of YAP and clinicopathologic features, response to EGFR-TKI treatment, and prognostic significance were analyzed.",
"High cytoplasmic YAP expression was positively correlated with the clinicopathologic parameters that have been associated with favorable prognosis. Multivariate analysis revealed that high cytoplasmic YAP expression was an independent prognostic factor in lung adenocarcinomas (progression-free survival: hazard ratio [HR] 0.659; 95 % confidence interval [CI] 0.431-1.010; p = 0.050; overall survival: HR, 0.474; 95 % CI 0.263-0.854; p = 0.013) and EGFR-TKI-treated patients with EGFR mutation (progression-free survival: HR, 0.346; 95 % CI 0.146-0.818; p = 0.016; overall survival: HR, 0.291; 95 % CI 0.125-0.676; p = 0.004)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adaptor Proteins, Signal Transducing",
"Adenocarcinoma",
"Adult",
"Aged",
"Aged, 80 and over",
"Cytoplasm",
"Disease-Free Survival",
"ErbB Receptors",
"Erlotinib Hydrochloride",
"Female",
"Gefitinib",
"Humans",
"Lung",
"Lung Neoplasms",
"Male",
"Middle Aged",
"Mutation",
"Phosphoproteins",
"Pneumonectomy",
"Protein Kinase Inhibitors",
"Quinazolines",
"Response Evaluation Criteria in Solid Tumors",
"Survival Rate",
"Young Adult"
]
} | High cytoplasmic YAP expression predicted a good clinical outcome for patients with lung adenocarcinoma and in EGFR-TKI-treated patients. Therefore, YAP may play a role in EGFR-TKI-treated lung cancer, and YAP targeting may enhance therapeutic effects in combination with other cancer drugs. | yes | [
{
"from": "human",
"value": "Question: Is cytoplasmic YAP expression associated with prolonged survival in patients with lung adenocarcinomas and epidermal growth factor receptor tyrosine kinase inhibitor treatment?\nContext: {'contexts': ['Yes-associated protein (YAP) has been reported to be associated with the prognosis of various cancers and also to affect epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) activity in ovarian cancer cell lines. However, few studies have evaluated YAP protein expression in lung cancer, and the results have lacked consistency.', 'YAP expression was evaluated in a total of 205 curatively resected lung adenocarcinomas and 36 cases of EGFR-mutated TKI-treated patients. Correlations between the expression of YAP and clinicopathologic features, response to EGFR-TKI treatment, and prognostic significance were analyzed.', 'High cytoplasmic YAP expression was positively correlated with the clinicopathologic parameters that have been associated with favorable prognosis. Multivariate analysis revealed that high cytoplasmic YAP expression was an independent prognostic factor in lung adenocarcinomas (progression-free survival: hazard ratio [HR] 0.659; 95 % confidence interval [CI] 0.431-1.010; p = 0.050; overall survival: HR, 0.474; 95 % CI 0.263-0.854; p = 0.013) and EGFR-TKI-treated patients with EGFR mutation (progression-free survival: HR, 0.346; 95 % CI 0.146-0.818; p = 0.016; overall survival: HR, 0.291; 95 % CI 0.125-0.676; p = 0.004).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adaptor Proteins, Signal Transducing', 'Adenocarcinoma', 'Adult', 'Aged', 'Aged, 80 and over', 'Cytoplasm', 'Disease-Free Survival', 'ErbB Receptors', 'Erlotinib Hydrochloride', 'Female', 'Gefitinib', 'Humans', 'Lung', 'Lung Neoplasms', 'Male', 'Middle Aged', 'Mutation', 'Phosphoproteins', 'Pneumonectomy', 'Protein Kinase Inhibitors', 'Quinazolines', 'Response Evaluation Criteria in Solid Tumors', 'Survival Rate', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,773,597 | Does frequency of mealtime insulin bolus predict glycated hemoglobin in youths with type 1 diabetes? | {
"contexts": [
"Within pediatric diabetes management, two electronic measures of adherence exist: frequency of daily blood glucose monitoring (BGM) and the BOLUS score, a measure of frequency of mealtime insulin bolusing. Past research has demonstrated that the BOLUS score is superior to daily BGM in predicting youths' glycated hemoglobin (HbA1c) in a cross-sectional study. We present data comparing the two adherence measures in predicting HbA1c using a prospective, longitudinal design.",
"Blood glucose meter data and insulin pump records were collected from a clinical database of 175 youths with type 1 diabetes (mean age, 11.7 ± 3.6 years at baseline). Youths' HbA1c levels occurring at the download time and at 3, 6, 9, and 12 months post-downloads were also collected. We calculated youths' mean BGM and BOLUS score using a standardized protocol.",
"Intraclass correlations (ICCs) revealed significant absolute equivalence between youths' predicted HbA1c values using BOLUS and BGM scores and future actual HbA1c values up to 12 months post-download. However, the ICCs of BOLUS scores with future HbA1c values were consistently higher than those of the BGM scores. Also, the predictions of the BOLUS scores were significantly more accurate (P ≤ 0.002) than those of the BGM scores based on the root mean squared error of predictions."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adolescent Behavior",
"Blood Glucose",
"Blood Glucose Self-Monitoring",
"Child",
"Cross-Sectional Studies",
"Diabetes Mellitus, Type 1",
"Female",
"Glycated Hemoglobin A",
"Humans",
"Hypoglycemic Agents",
"Insulin",
"Longitudinal Studies",
"Male",
"Meals",
"Medication Adherence",
"Postprandial Period",
"Predictive Value of Tests",
"Prospective Studies",
"Reproducibility of Results"
]
} | In a prospective, longitudinal design, youths' BOLUS scores were superior to youths' daily BGM in predicting future values of HbA1c. Calculating a BOLUS score versus BGM can help researchers and clinicians achieve a better prediction of youths' HbA1c. | yes | [
{
"from": "human",
"value": "Question: Does frequency of mealtime insulin bolus predict glycated hemoglobin in youths with type 1 diabetes?\nContext: {'contexts': [\"Within pediatric diabetes management, two electronic measures of adherence exist: frequency of daily blood glucose monitoring (BGM) and the BOLUS score, a measure of frequency of mealtime insulin bolusing. Past research has demonstrated that the BOLUS score is superior to daily BGM in predicting youths' glycated hemoglobin (HbA1c) in a cross-sectional study. We present data comparing the two adherence measures in predicting HbA1c using a prospective, longitudinal design.\", \"Blood glucose meter data and insulin pump records were collected from a clinical database of 175 youths with type 1 diabetes (mean age, 11.7 ± 3.6 years at baseline). Youths' HbA1c levels occurring at the download time and at 3, 6, 9, and 12 months post-downloads were also collected. We calculated youths' mean BGM and BOLUS score using a standardized protocol.\", \"Intraclass correlations (ICCs) revealed significant absolute equivalence between youths' predicted HbA1c values using BOLUS and BGM scores and future actual HbA1c values up to 12 months post-download. However, the ICCs of BOLUS scores with future HbA1c values were consistently higher than those of the BGM scores. Also, the predictions of the BOLUS scores were significantly more accurate (P ≤ 0.002) than those of the BGM scores based on the root mean squared error of predictions.\"], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adolescent Behavior', 'Blood Glucose', 'Blood Glucose Self-Monitoring', 'Child', 'Cross-Sectional Studies', 'Diabetes Mellitus, Type 1', 'Female', 'Glycated Hemoglobin A', 'Humans', 'Hypoglycemic Agents', 'Insulin', 'Longitudinal Studies', 'Male', 'Meals', 'Medication Adherence', 'Postprandial Period', 'Predictive Value of Tests', 'Prospective Studies', 'Reproducibility of Results']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,752,914 | Is isatis canescens a rich source of glucobrassicin and other health-promoting compounds? | {
"contexts": [
"Glucobrassicin (GBS), a glucosinolate contained in many brassica vegetables, is the precursor of chemopreventive compounds such as indole-3-carbinol. Large amounts of GBS would be needed to perform studies aimed at elucidating its role in the diet. This study was mainly undertaken to evaluate the flower buds of Isatis canescens as a source for GBS purification. In order to investigate the health-promoting potential of this species, glucosinolate, phenol and flavonoid content as well as the whole antioxidant capacity were also determined. Flower bud samples were collected in four localities around Mount Etna in Sicily, Italy, where I. canescens is widespread, as they are locally traditionally eaten.",
"I. canescens flower buds displayed high GBS concentrations, up to 60 µmol g(-1) dry weight. The purification method consisted of two chromatographic steps, which made it possible to obtain GBS with a purity of 92-95%, with a yield of 21 g kg(-1) . The total glucosinolates, phenols, flavonoids and antioxidant activity were considerable, with the southern locality showing the highest concentrations for all the phytochemicals."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Anticarcinogenic Agents",
"Antioxidants",
"Flavonoids",
"Flowers",
"Glucosinolates",
"Health Promotion",
"Indoles",
"Isatis",
"Italy",
"Phenols"
]
} | I. canescens flower buds represent a naturally rich source of GBS, at a level suitable for its purification. Furthermore, flower bud consumption could provide an intake of health-promoting compounds, with possible antioxidant and chemopreventive properties. | yes | [
{
"from": "human",
"value": "Question: Is isatis canescens a rich source of glucobrassicin and other health-promoting compounds?\nContext: {'contexts': ['Glucobrassicin (GBS), a glucosinolate contained in many brassica vegetables, is the precursor of chemopreventive compounds such as indole-3-carbinol. Large amounts of GBS would be needed to perform studies aimed at elucidating its role in the diet. This study was mainly undertaken to evaluate the flower buds of Isatis canescens as a source for GBS purification. In order to investigate the health-promoting potential of this species, glucosinolate, phenol and flavonoid content as well as the whole antioxidant capacity were also determined. Flower bud samples were collected in four localities around Mount Etna in Sicily, Italy, where I. canescens is widespread, as they are locally traditionally eaten.', 'I. canescens flower buds displayed high GBS concentrations, up to 60 µmol g(-1) dry weight. The purification method consisted of two chromatographic steps, which made it possible to obtain GBS with a purity of 92-95%, with a yield of 21 g kg(-1) . The total glucosinolates, phenols, flavonoids and antioxidant activity were considerable, with the southern locality showing the highest concentrations for all the phytochemicals.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Anticarcinogenic Agents', 'Antioxidants', 'Flavonoids', 'Flowers', 'Glucosinolates', 'Health Promotion', 'Indoles', 'Isatis', 'Italy', 'Phenols']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,757,635 | Does comorbidity influence multiple aspects of well-being of patients with ischemic heart disease? | {
"contexts": [
"Comorbidity is prevalent among patients with Ischemic Heart Disease (IHD) and may influence patients' subjective and objective domains of well-being.",
"We aimed to investigate the associations between comorbidity and different measures of well-being (i.e. health related quality of life, psychological distress, sleep quality, and dyadic adjustment) among patients with IHD.",
"In this cross-sectional study, 796 outpatients with documented IHD were enrolled from an outpatient cardiology clinic in 2006. Comorbidity (Ifudu index), quality of life (SF36), psychological distress (Hospital Anxiety Depression Scale; HADS), sleep quality (Pittsburg Sleep Quality Index; PSQI), and dyadic adjustment quality (Revised Dyadic Adjustment Scale; RDAS) were measured. Associations between comorbidity and different measures of well-being were determined.",
"Significant correlations were found between comorbidity score and all measures of well-being. Comorbidity score was correlated with physical quality of life (r = -0.471, P < 0.001), mental quality of life (r = -0.447, P < 0.001), psychological distress (r = 0.344, P < 0.001), sleep quality (r = 0.358, P < 0.001), and dyadic adjustment (r = -0.201, P < 0.001)."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": []
} | This study showed a consistent pattern of associations between somatic comorbidities and multiple aspects of well-being among patients with IHD. Findings may increase cardiologists' interest to identify and treat somatic conditions among IHD patients. | yes | [
{
"from": "human",
"value": "Question: Does comorbidity influence multiple aspects of well-being of patients with ischemic heart disease?\nContext: {'contexts': [\"Comorbidity is prevalent among patients with Ischemic Heart Disease (IHD) and may influence patients' subjective and objective domains of well-being.\", 'We aimed to investigate the associations between comorbidity and different measures of well-being (i.e. health related quality of life, psychological distress, sleep quality, and dyadic adjustment) among patients with IHD.', 'In this cross-sectional study, 796 outpatients with documented IHD were enrolled from an outpatient cardiology clinic in 2006. Comorbidity (Ifudu index), quality of life (SF36), psychological distress (Hospital Anxiety Depression Scale; HADS), sleep quality (Pittsburg Sleep Quality Index; PSQI), and dyadic adjustment quality (Revised Dyadic Adjustment Scale; RDAS) were measured. Associations between comorbidity and different measures of well-being were determined.', 'Significant correlations were found between comorbidity score and all measures of well-being. Comorbidity score was correlated with physical quality of life (r = -0.471, P < 0.001), mental quality of life (r = -0.447, P < 0.001), psychological distress (r = 0.344, P < 0.001), sleep quality (r = 0.358, P < 0.001), and dyadic adjustment (r = -0.201, P < 0.001).'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,774,536 | Is the effect of Rho kinase inhibition on long-term keratinocyte proliferation rapid and conditional? | {
"contexts": [
"We previously demonstrated that the lifespan of primary human keratinocytes could be extended indefinitely by culture in the presence of the Rho kinase (ROCK) inhibitor Y-27632. This technique has proven to be very useful in diverse areas of basic and clinical research.",
"In this follow-up study we determine whether the continual presence of Y-27632 is required for sustained proliferation. We also test whether different ROCK inhibitors can be used for this technique and whether it can also promote indefinite proliferation of animal keratinocytes. We measure keratinocyte gene expression, proliferation, behaviour and lifespan in the presence and absence of Y-27632.",
"We demonstrate that the extension of lifespan observed by culture of keratinocytes in the presence of fibroblast feeders and a ROCK inhibitor is reversible and that cells senesce gradually when the inhibitor is removed from the medium. Conversely, keratinocytes that are close to the end of their replicative life span can be revived by ROCK inhibition. We demonstrate that different inhibitors of ROCK can also efficiently extend the lifespan of human keratinocytes and that ROCK inhibition extends the lifespan of animal keratinocytes derived from mouse and bovine epithelia. Gene expression analysis of human epidermal keratinocytes cells grown in the presence of Y-27632 demonstrates that ROCK inhibition primarily inhibits keratinocyte differentiation. Live-imaging of keratinocytes cultured with ROCK inhibitors show that the effect of ROCK inhibition on cellular proliferation is immediate and ROCK inhibited cells proliferate rapidly without differentiation or stratification."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Amides",
"Animals",
"Cattle",
"Cell Differentiation",
"Cell Proliferation",
"Cells, Cultured",
"Enzyme Inhibitors",
"Humans",
"Keratinocytes",
"Pyridines",
"rho-Associated Kinases"
]
} | ROCK inhibition rapidly and conditionally induces indefinite proliferation of keratinocytes. This method has far-reaching applications for basic research, as well as for regenerative and personalized medicine. | yes | [
{
"from": "human",
"value": "Question: Is the effect of Rho kinase inhibition on long-term keratinocyte proliferation rapid and conditional?\nContext: {'contexts': ['We previously demonstrated that the lifespan of primary human keratinocytes could be extended indefinitely by culture in the presence of the Rho kinase (ROCK) inhibitor Y-27632. This technique has proven to be very useful in diverse areas of basic and clinical research.', 'In this follow-up study we determine whether the continual presence of Y-27632 is required for sustained proliferation. We also test whether different ROCK inhibitors can be used for this technique and whether it can also promote indefinite proliferation of animal keratinocytes. We measure keratinocyte gene expression, proliferation, behaviour and lifespan in the presence and absence of Y-27632.', 'We demonstrate that the extension of lifespan observed by culture of keratinocytes in the presence of fibroblast feeders and a ROCK inhibitor is reversible and that cells senesce gradually when the inhibitor is removed from the medium. Conversely, keratinocytes that are close to the end of their replicative life span can be revived by ROCK inhibition. We demonstrate that different inhibitors of ROCK can also efficiently extend the lifespan of human keratinocytes and that ROCK inhibition extends the lifespan of animal keratinocytes derived from mouse and bovine epithelia. Gene expression analysis of human epidermal keratinocytes cells grown in the presence of Y-27632 demonstrates that ROCK inhibition primarily inhibits keratinocyte differentiation. Live-imaging of keratinocytes cultured with ROCK inhibitors show that the effect of ROCK inhibition on cellular proliferation is immediate and ROCK inhibited cells proliferate rapidly without differentiation or stratification.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Amides', 'Animals', 'Cattle', 'Cell Differentiation', 'Cell Proliferation', 'Cells, Cultured', 'Enzyme Inhibitors', 'Humans', 'Keratinocytes', 'Pyridines', 'rho-Associated Kinases']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,758,567 | Does hypoxia augment the calcium-activated chloride current carried by anoctamin-1 in cardiac vascular endothelial cells of neonatal mice? | {
"contexts": [
"The molecular identity of calcium-activated chloride channels (CaCCs) in vascular endothelial cells remains unknown. This study sought to identify whether anoctamin-1 (Ano1, also known as TMEM16A) functions as a CaCC and whether hypoxia alters the biophysical properties of Ano1 in mouse cardiac vascular endothelial cells (CVECs).",
"Western blot, quantitative real-time PCR, confocal imaging analysis and patch-clamp analysis combined with pharmacological approaches were used to determine whether Ano1 was expressed and functioned as CaCC in CVECs.",
"Ano1 was expressed in CVECs. The biophysical properties of the current generated in the CVECs, including the Ca(2+) and voltage dependence, outward rectification, anion selectivity and the pharmacological profile, are similar to those described for CaCCs. The density of ICl ( C a) detected in CVECs was significantly inhibited by T16Ainh -A01, an Ano1 inhibitor, and a pore-targeting, specific anti-Ano1 antibody, and was markedly decreased in Ano1 gene knockdown CVECs. The density of ICl ( C a) was significantly potentiated in CVECs exposed to hypoxia, and this hypoxia-induced increase in the density of ICl ( C a) was inhibited by T16Ainh -A01 or anti-Ano1 antibody. Hypoxia also increased the current density of ICl ( C a) in Ano1 gene knockdown CVECs."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Animals, Newborn",
"Anoctamin-1",
"Base Sequence",
"Calcium",
"Cell Proliferation",
"Cells, Cultured",
"Chloride Channels",
"Endothelial Cells",
"Gene Silencing",
"Green Fluorescent Proteins",
"Heart Ventricles",
"Hypoxia",
"Mice, Inbred BALB C",
"Molecular Sequence Data",
"Transfection"
]
} | Ano1 formed CaCC in CVECs of neonatal mice. Hypoxia enhances Ano1-mediated ICl ( C a) density via increasing its expression, altering the ratio of its splicing variants, sensitivity to membrane voltage and to Ca(2+) . Ano1 may play a role in the pathophysiological processes during ischaemia in heart, and therefore, Ano1 might be a potential therapeutic target to prevent ischaemic damage. | yes | [
{
"from": "human",
"value": "Question: Does hypoxia augment the calcium-activated chloride current carried by anoctamin-1 in cardiac vascular endothelial cells of neonatal mice?\nContext: {'contexts': ['The molecular identity of calcium-activated chloride channels (CaCCs) in vascular endothelial cells remains unknown. This study sought to identify whether anoctamin-1 (Ano1, also known as TMEM16A) functions as a CaCC and whether hypoxia alters the biophysical properties of Ano1 in mouse cardiac vascular endothelial cells (CVECs).', 'Western blot, quantitative real-time PCR, confocal imaging analysis and patch-clamp analysis combined with pharmacological approaches were used to determine whether Ano1 was expressed and functioned as CaCC in CVECs.', 'Ano1 was expressed in CVECs. The biophysical properties of the current generated in the CVECs, including the Ca(2+) and voltage dependence, outward rectification, anion selectivity and the pharmacological profile, are similar to those described for CaCCs. The density of ICl ( C a) detected in CVECs was significantly inhibited by T16Ainh -A01, an Ano1 inhibitor, and a pore-targeting, specific anti-Ano1 antibody, and was markedly decreased in Ano1 gene knockdown CVECs. The density of ICl ( C a) was significantly potentiated in CVECs exposed to hypoxia, and this hypoxia-induced increase in the density of ICl ( C a) was inhibited by T16Ainh -A01 or anti-Ano1 antibody. Hypoxia also increased the current density of ICl ( C a) in Ano1 gene knockdown CVECs.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Animals, Newborn', 'Anoctamin-1', 'Base Sequence', 'Calcium', 'Cell Proliferation', 'Cells, Cultured', 'Chloride Channels', 'Endothelial Cells', 'Gene Silencing', 'Green Fluorescent Proteins', 'Heart Ventricles', 'Hypoxia', 'Mice, Inbred BALB C', 'Molecular Sequence Data', 'Transfection']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,762,601 | Do matrix metalloproteinase-8 inhibitors mitigate sepsis-induced myocardial injury in rats? | {
"contexts": [
"Sepsis-induced myocardial injury (SIMI) is caused by a variety of mechanisms. The aim of the study is to investigate the effects of metalloproteinase-8 (MMP-8) on SIMI and its mechanisms in rats.",
"Forty male Sprague Dawley rats were randomly divided into four groups: MMP-8 inhibitor (M8I), dexamethasone (DEX), sepsis, and sham groups. The sepsis model was established by cecal ligation and puncture (CLP). Rats in the M8I group immediately received an intraperitoneal injection of M8I (0.1 mg/kg) after CLP. Rats in the DEX group immediately received an intraperitoneal (IP) injection of DEX (2 mg/kg). Rats in the sepsis and sham groups received intraperitoneal injections of normal saline. Rats were sacrificed 12 hours after CLP. Paraffin sections were stained with hematoxylin and eosin to observe the myocardium. The myocardial ultrastructure was observed with transmission electron microscopy. MMP-8, tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) were detected by immunohistochemistry. The expression of MMP-8 was measured by Western blotting. TNF-α and IL-1β levels in serum and myocardial tissue were determined by enzyme-linked immunosorbent assay.",
"Compared with the sham group, the myocardium in the sepsis group was seriously injured. MMP-8, TNF-α and IL-1β expression was higher in the sepsis group than in the sham group. Treatment with M8I or DEX, however, attenuated sepsis induced histopathological changes in the heart, and was associated with significant reductions in serum and myocardial levels of TNF-α and IL-1β (P < 0.05). M8I significantly inhibited MMP-8 expression in myocardial tissue (P < 0.05). In addition, treatment with DEX was not associated with a change in myocardial levels of MMP-8 (P > 0.05)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Dexamethasone",
"Disease Models, Animal",
"Enzyme-Linked Immunosorbent Assay",
"Heart Diseases",
"Interleukin-1beta",
"Male",
"Matrix Metalloproteinase 8",
"Matrix Metalloproteinase Inhibitors",
"Rats",
"Rats, Sprague-Dawley",
"Sepsis",
"Tumor Necrosis Factor-alpha"
]
} | MMP-8 inhibitor attenuated myocardial injury in septic rats, which might be related to reduced expression of TNF-α and IL-1β. | yes | [
{
"from": "human",
"value": "Question: Do matrix metalloproteinase-8 inhibitors mitigate sepsis-induced myocardial injury in rats?\nContext: {'contexts': ['Sepsis-induced myocardial injury (SIMI) is caused by a variety of mechanisms. The aim of the study is to investigate the effects of metalloproteinase-8 (MMP-8) on SIMI and its mechanisms in rats.', 'Forty male Sprague Dawley rats were randomly divided into four groups: MMP-8 inhibitor (M8I), dexamethasone (DEX), sepsis, and sham groups. The sepsis model was established by cecal ligation and puncture (CLP). Rats in the M8I group immediately received an intraperitoneal injection of M8I (0.1 mg/kg) after CLP. Rats in the DEX group immediately received an intraperitoneal (IP) injection of DEX (2 mg/kg). Rats in the sepsis and sham groups received intraperitoneal injections of normal saline. Rats were sacrificed 12 hours after CLP. Paraffin sections were stained with hematoxylin and eosin to observe the myocardium. The myocardial ultrastructure was observed with transmission electron microscopy. MMP-8, tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) were detected by immunohistochemistry. The expression of MMP-8 was measured by Western blotting. TNF-α and IL-1β levels in serum and myocardial tissue were determined by enzyme-linked immunosorbent assay.', 'Compared with the sham group, the myocardium in the sepsis group was seriously injured. MMP-8, TNF-α and IL-1β expression was higher in the sepsis group than in the sham group. Treatment with M8I or DEX, however, attenuated sepsis induced histopathological changes in the heart, and was associated with significant reductions in serum and myocardial levels of TNF-α and IL-1β (P < 0.05). M8I significantly inhibited MMP-8 expression in myocardial tissue (P < 0.05). In addition, treatment with DEX was not associated with a change in myocardial levels of MMP-8 (P > 0.05).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Dexamethasone', 'Disease Models, Animal', 'Enzyme-Linked Immunosorbent Assay', 'Heart Diseases', 'Interleukin-1beta', 'Male', 'Matrix Metalloproteinase 8', 'Matrix Metalloproteinase Inhibitors', 'Rats', 'Rats, Sprague-Dawley', 'Sepsis', 'Tumor Necrosis Factor-alpha']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,762,600 | Does metformin ameliorate insulin resistance in L6 rat skeletal muscle cells through upregulation of SIRT3? | {
"contexts": [
"SIRT3 is an important regulator in cell metabolism, and recent studies have shown that it may be involved in the pharmacological effects of metformin. However, the molecular mechanisms underlying this process are unclear.",
"The effects of SIRT3 on the regulation of oxidative stress and insulin resistance in skeletal muscle were evaluated in vitro. Differentiated L6 skeletal muscle cells were treated with 750 µmol/L palmitic acid to induce insulin resistance. SIRT3 was knocked down and overexpressed in L6 cells. SIRT3, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) p65, c-Jun N-terminal kinase 1 (JNK1), and superoxide dismutase 2 (SOD2) were evaluated by Western blotting.",
"Over expression of SIRT3 increased glucose uptake and decreased ROS production in L6-IR cells as well as in L6 cells. Knock-down of SIRT3 induced increased production of ROS while decreased glucose uptake in both L6 and L6-IR cells, and these effects were reversed by N-acetyl-L-cysteine (NAC). Metformin increased the expression of SIRT3 (1.5-fold) and SOD2 (2-fold) while down regulating NF-κB p65 (1.5-fold) and JNK1 (1.5-fold). Knockdown of SIRT3 (P < 0.05) reversed the metformin-induced decreases in NF-κB p65 and JNK1 and the metformin-induced increase in SOD2 (P < 0.05)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Cell Line",
"Insulin Resistance",
"Metformin",
"Muscle Fibers, Skeletal",
"Oxidative Stress",
"Rats",
"Sirtuin 3",
"Transcription Factor RelA"
]
} | Upregulated SIRT3 is involved in the pharmacological mechanism by which metformin promotes glucose uptake. Additionally, SIRT3 may function as an important regulator of oxidative stress and a new alternative approach for targeting insulin resistance-related diseases. | yes | [
{
"from": "human",
"value": "Question: Does metformin ameliorate insulin resistance in L6 rat skeletal muscle cells through upregulation of SIRT3?\nContext: {'contexts': ['SIRT3 is an important regulator in cell metabolism, and recent studies have shown that it may be involved in the pharmacological effects of metformin. However, the molecular mechanisms underlying this process are unclear.', 'The effects of SIRT3 on the regulation of oxidative stress and insulin resistance in skeletal muscle were evaluated in vitro. Differentiated L6 skeletal muscle cells were treated with 750 µmol/L palmitic acid to induce insulin resistance. SIRT3 was knocked down and overexpressed in L6 cells. SIRT3, nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) p65, c-Jun N-terminal kinase 1 (JNK1), and superoxide dismutase 2 (SOD2) were evaluated by Western blotting.', 'Over expression of SIRT3 increased glucose uptake and decreased ROS production in L6-IR cells as well as in L6 cells. Knock-down of SIRT3 induced increased production of ROS while decreased glucose uptake in both L6 and L6-IR cells, and these effects were reversed by N-acetyl-L-cysteine (NAC). Metformin increased the expression of SIRT3 (1.5-fold) and SOD2 (2-fold) while down regulating NF-κB p65 (1.5-fold) and JNK1 (1.5-fold). Knockdown of SIRT3 (P < 0.05) reversed the metformin-induced decreases in NF-κB p65 and JNK1 and the metformin-induced increase in SOD2 (P < 0.05).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Cell Line', 'Insulin Resistance', 'Metformin', 'Muscle Fibers, Skeletal', 'Oxidative Stress', 'Rats', 'Sirtuin 3', 'Transcription Factor RelA']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,762,604 | Does theanine improve the function of dendritic cells via the downregulation of cyclooxygenase-2 expression? | {
"contexts": [
"Tumor cells can reduce the number of dendritic cells (DCs) in the tumor environment and cause DC dysfunction through autocrine or paracrine pathways. We sought to measure cyclooxygenase-2 (COX-2) expression in bombesin-inhibited DCs treated with theanine in vitro and to explore the protection and activation effects of theanine on DCs.",
"Enzyme-linked immunosorbent assay (ELISA), reverse transcription-polymerase chain reaction (RT-PCR), and Western blotting were used to analyze the effects of theanine on COX-2 expression and interleukin (IL)-12/IL-10 secretion of bombesin-treated DCs.",
"DCs acquired an impaired phenotype as a result of bombesin treatment. Theanine increased the expression of mature DC surface molecules. The number of cell apoptosis with the treatment of bombesin and theanine significantly decreased, accounting for 15.9%, compared with 26.1% of cell apoptosis with bombesin. COX-2 expression in bombesin-treated DCs was inhibited by theanine in a dose-dependent manner. Theanine promoted DC secretion of IL-12. IL-12 levels reached (137.4 ± 4.9) pg/ml with theanine at 200 µmol/L. However, theanine inhibited the secretion of IL-10 in a dose-dependent manner. IL-10 levels were only (58.4 ± 6.9) pg/ml with theanine at 200 µmol/L."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Bombesin",
"Cells, Cultured",
"Cyclooxygenase 2",
"Dendritic Cells",
"Enzyme-Linked Immunosorbent Assay",
"Glutamates",
"Humans",
"Interleukin-10",
"Interleukin-12"
]
} | Theanine inhibits the transcription and translation of COX-2 and regulates the balance of IL-10/IL-12 secretion in bombesin-inhibited DCs, leading to the recovery of a state of activation in DCs. | yes | [
{
"from": "human",
"value": "Question: Does theanine improve the function of dendritic cells via the downregulation of cyclooxygenase-2 expression?\nContext: {'contexts': ['Tumor cells can reduce the number of dendritic cells (DCs) in the tumor environment and cause DC dysfunction through autocrine or paracrine pathways. We sought to measure cyclooxygenase-2 (COX-2) expression in bombesin-inhibited DCs treated with theanine in vitro and to explore the protection and activation effects of theanine on DCs.', 'Enzyme-linked immunosorbent assay (ELISA), reverse transcription-polymerase chain reaction (RT-PCR), and Western blotting were used to analyze the effects of theanine on COX-2 expression and interleukin (IL)-12/IL-10 secretion of bombesin-treated DCs.', 'DCs acquired an impaired phenotype as a result of bombesin treatment. Theanine increased the expression of mature DC surface molecules. The number of cell apoptosis with the treatment of bombesin and theanine significantly decreased, accounting for 15.9%, compared with 26.1% of cell apoptosis with bombesin. COX-2 expression in bombesin-treated DCs was inhibited by theanine in a dose-dependent manner. Theanine promoted DC secretion of IL-12. IL-12 levels reached (137.4 ± 4.9) pg/ml with theanine at 200 µmol/L. However, theanine inhibited the secretion of IL-10 in a dose-dependent manner. IL-10 levels were only (58.4 ± 6.9) pg/ml with theanine at 200 µmol/L.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Bombesin', 'Cells, Cultured', 'Cyclooxygenase 2', 'Dendritic Cells', 'Enzyme-Linked Immunosorbent Assay', 'Glutamates', 'Humans', 'Interleukin-10', 'Interleukin-12']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,767,545 | Does optic nerve crush induce spatial and temporal gene expression patterns in retina and optic nerve of BALB/cJ mice? | {
"contexts": [
"Central nervous system (CNS) trauma and neurodegenerative disorders trigger a cascade of cellular and molecular events resulting in neuronal apoptosis and regenerative failure. The pathogenic mechanisms and gene expression changes associated with these detrimental events can be effectively studied using a rodent optic nerve crush (ONC) model. The purpose of this study was to use a mouse ONC model to: (a) evaluate changes in retina and optic nerve (ON) gene expression, (b) identify neurodegenerative pathogenic pathways and (c) discover potential new therapeutic targets.",
"Only 54% of total neurons survived in the ganglion cell layer (GCL) 28 days post crush. Using Bayesian Estimation of Temporal Regulation (BETR) gene expression analysis, we identified significantly altered expression of 1,723 and 2,110 genes in the retina and ON, respectively. Meta-analysis of altered gene expression (≥1.5, ≤-1.5, p < 0.05) using Partek and DAVID demonstrated 28 up and 20 down-regulated retinal gene clusters and 57 up and 41 down-regulated optic nerve clusters. Regulated gene clusters included regenerative change, synaptic plasticity, axonogenesis, neuron projection, and neuron differentiation. Expression of selected genes (Vsnl1, Syt1, Synpr and Nrn1) from retinal and ON neuronal clusters were quantitatively and qualitatively examined for their relation to axonal neurodegeneration by immunohistochemistry and qRT-PCR."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Animals",
"Apoptosis",
"Disease Models, Animal",
"Gene Expression Regulation",
"Immunohistochemistry",
"Mice",
"Mice, Inbred BALB C",
"Nerve Crush",
"Nerve Degeneration",
"Nerve Regeneration",
"Neurodegenerative Diseases",
"Oligonucleotide Array Sequence Analysis",
"Optic Nerve",
"Real-Time Polymerase Chain Reaction",
"Retina",
"Reverse Transcriptase Polymerase Chain Reaction",
"Transcriptome"
]
} | A number of detrimental gene expression changes occur that contribute to trauma-induced neurodegeneration after injury to ON axons. Nrn1 (synaptic plasticity gene), Synpr and Syt1 (synaptic vesicle fusion genes), and Vsnl1 (neuron differentiation associated gene) were a few of the potentially unique genes identified that were down-regulated spatially and temporally in our rodent ONC model. Bioinformatic meta-analysis identified significant tissue-specific and time-dependent gene clusters associated with regenerative changes, synaptic plasticity, axonogenesis, neuron projection, and neuron differentiation. These ONC induced neuronal loss and regenerative failure associated clusters can be extrapolated to changes occurring in other forms of CNS trauma or in clinical neurodegenerative pathological settings. In conclusion, this study identified potential therapeutic targets to address two key mechanisms of CNS trauma and neurodegeneration: neuronal loss and regenerative failure. | yes | [
{
"from": "human",
"value": "Question: Does optic nerve crush induce spatial and temporal gene expression patterns in retina and optic nerve of BALB/cJ mice?\nContext: {'contexts': ['Central nervous system (CNS) trauma and neurodegenerative disorders trigger a cascade of cellular and molecular events resulting in neuronal apoptosis and regenerative failure. The pathogenic mechanisms and gene expression changes associated with these detrimental events can be effectively studied using a rodent optic nerve crush (ONC) model. The purpose of this study was to use a mouse ONC model to: (a) evaluate changes in retina and optic nerve (ON) gene expression, (b) identify neurodegenerative pathogenic pathways and (c) discover potential new therapeutic targets.', 'Only 54% of total neurons survived in the ganglion cell layer (GCL) 28 days post crush. Using Bayesian Estimation of Temporal Regulation (BETR) gene expression analysis, we identified significantly altered expression of 1,723 and 2,110 genes in the retina and ON, respectively. Meta-analysis of altered gene expression (≥1.5, ≤-1.5, p\\u2009<\\u20090.05) using Partek and DAVID demonstrated 28 up and 20 down-regulated retinal gene clusters and 57 up and 41 down-regulated optic nerve clusters. Regulated gene clusters included regenerative change, synaptic plasticity, axonogenesis, neuron projection, and neuron differentiation. Expression of selected genes (Vsnl1, Syt1, Synpr and Nrn1) from retinal and ON neuronal clusters were quantitatively and qualitatively examined for their relation to axonal neurodegeneration by immunohistochemistry and qRT-PCR.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Animals', 'Apoptosis', 'Disease Models, Animal', 'Gene Expression Regulation', 'Immunohistochemistry', 'Mice', 'Mice, Inbred BALB C', 'Nerve Crush', 'Nerve Degeneration', 'Nerve Regeneration', 'Neurodegenerative Diseases', 'Oligonucleotide Array Sequence Analysis', 'Optic Nerve', 'Real-Time Polymerase Chain Reaction', 'Retina', 'Reverse Transcriptase Polymerase Chain Reaction', 'Transcriptome']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,768,399 | Is cardiopulmonary exercise testing more accurate than ECG-stress testing in diagnosing myocardial ischemia in subjects with chest pain? | {
"contexts": [
"Cardiopulmonary exercise stress testing (CPET) is used to grade the severity of heart failure and to assess its prognosis. However it is unknown whether CPET may improve diagnostic accuracy of standard ECG stress testing to identify or exclude obstructive coronary artery disease (O-CAD) in patients with chest pain.",
"We prospectively studied 1265 consecutive subjects (55 ± 8 years, 156 women) who were evaluated with ECG stress testing (ET) for chest pain. No one had a documented O-CAD. All patients performed an incremental CPET with ECG recordings on an electronically braked cycle ergometer.",
"Of 1265 patients, 73 had a positive CPET and 1192 had a negative CPET. Seventy-three patients with a positive CPET and 71 patients with a negative CPET agreed to undergo nuclear SPECT imaging and coronary angiography. Follow-up lasted 48 ± 7 months. As compared with ET, sensitivity, specificity, PPV and NPV were all improved significantly (ET: 48%, 55%, 33%, 95%; CPET: 88%, 98%, 73%, 99%, respectively, P<0.001). Patients with both peak VO2>91% of predicted VO2 max and absence of VO2-related signs of myocardial ischemia had no evidence of O-CAD in 100% of cases. Cardiac events occurred in 32 patients with a positive CPET and 8 patients with a negative CPET (log rank 18.2, P<0.0001)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Chest Pain",
"Electrocardiography",
"Exercise Test",
"Female",
"Humans",
"Male",
"Middle Aged",
"Myocardial Ischemia",
"Prospective Studies",
"Reproducibility of Results"
]
} | In patients with chest pain, CPET showed a better diagnostic and predictive accuracy than traditional ET to detect/exclude myocardial ischemia. Its use should be encouraged among physicians as a first line diagnostic tool in clinical practice. | yes | [
{
"from": "human",
"value": "Question: Is cardiopulmonary exercise testing more accurate than ECG-stress testing in diagnosing myocardial ischemia in subjects with chest pain?\nContext: {'contexts': ['Cardiopulmonary exercise stress testing (CPET) is used to grade the severity of heart failure and to assess its prognosis. However it is unknown whether CPET may improve diagnostic accuracy of standard ECG stress testing to identify or exclude obstructive coronary artery disease (O-CAD) in patients with chest pain.', 'We prospectively studied 1265 consecutive subjects (55 ± 8 years, 156 women) who were evaluated with ECG stress testing (ET) for chest pain. No one had a documented O-CAD. All patients performed an incremental CPET with ECG recordings on an electronically braked cycle ergometer.', 'Of 1265 patients, 73 had a positive CPET and 1192 had a negative CPET. Seventy-three patients with a positive CPET and 71 patients with a negative CPET agreed to undergo nuclear SPECT imaging and coronary angiography. Follow-up lasted 48 ± 7 months. As compared with ET, sensitivity, specificity, PPV and NPV were all improved significantly (ET: 48%, 55%, 33%, 95%; CPET: 88%, 98%, 73%, 99%, respectively, P<0.001). Patients with both peak VO2>91% of predicted VO2 max and absence of VO2-related signs of myocardial ischemia had no evidence of O-CAD in 100% of cases. Cardiac events occurred in 32 patients with a positive CPET and 8 patients with a negative CPET (log rank 18.2, P<0.0001).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Chest Pain', 'Electrocardiography', 'Exercise Test', 'Female', 'Humans', 'Male', 'Middle Aged', 'Myocardial Ischemia', 'Prospective Studies', 'Reproducibility of Results']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,766,723 | Does long-term reduction of T-cell intracellular antigens lead to increased beta-actin expression? | {
"contexts": [
"The permanent down-regulated expression of T-cell intracellular antigen (TIA) proteins in HeLa cells improves cytoskeleton-mediated functions such as cell proliferation and tumor growth.",
"Making use of human and mouse cells with knocked down/out expression of T-cell intracellular antigen 1 (TIA1) and/or TIA1 related/like (TIAR/TIAL1) proteins and classical RNA (e.g. reverse transcription-quantitative polymerase chain reaction, polysomal profiling analysis using sucrose gradients, immunoblotting, immunoprecipitation, electrophoretic mobility shift assays, ultraviolet light crosslinking and poly (A+) test analysis) and cellular (e.g. immunofluorescence microscopy and quimeric mRNA transfections) biology methods, we have analyzed the regulatory role of TIA proteins in the post-transcriptional modulation of beta-actin (ACTB) mRNA.",
"Our observations show that the acquisition of above cellular capacities is concomitant with increased expression levels of the actin beta subunit (ACTB) protein. Regulating TIA abundance does not modify ACTB mRNA levels, however, an increase of ACTB mRNA translation is observed. This regulatory capacity of TIA proteins is linked to the ACTB mRNA 3'-untranslated region (3'-UTR), where these proteins could function as RNA binding proteins. The expression of GFP from a chimeric reporter containing human ΑCΤΒ 3'-UTR recapitulates the translational control found by the endogenous ACTB mRNA in the absence of TIA proteins. Additionally, murine embryonic fibroblasts (MEF) knocked out for TIA1 rise mouse ACTB protein expression compared to the controls. Once again steady-state levels of mouse ACTB mRNA remained unchanged."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"3' Untranslated Regions",
"Actins",
"Animals",
"Base Sequence",
"Fibroblasts",
"Gene Expression Regulation",
"Genes, Reporter",
"Green Fluorescent Proteins",
"HeLa Cells",
"Humans",
"Mice",
"Molecular Sequence Data",
"Poly(A)-Binding Proteins",
"RNA-Binding Proteins",
"Signal Transduction",
"T-Cell Intracellular Antigen-1"
]
} | Collectively, these results suggest that TIA proteins can function as long-term regulators of the ACTB mRNA metabolism in mouse and human cells. | yes | [
{
"from": "human",
"value": "Question: Does long-term reduction of T-cell intracellular antigens lead to increased beta-actin expression?\nContext: {'contexts': ['The permanent down-regulated expression of T-cell intracellular antigen (TIA) proteins in HeLa cells improves cytoskeleton-mediated functions such as cell proliferation and tumor growth.', 'Making use of human and mouse cells with knocked down/out expression of T-cell intracellular antigen 1 (TIA1) and/or TIA1 related/like (TIAR/TIAL1) proteins and classical RNA (e.g. reverse transcription-quantitative polymerase chain reaction, polysomal profiling analysis using sucrose gradients, immunoblotting, immunoprecipitation, electrophoretic mobility shift assays, ultraviolet light crosslinking and poly (A+) test analysis) and cellular (e.g. immunofluorescence microscopy and quimeric mRNA transfections) biology methods, we have analyzed the regulatory role of TIA proteins in the post-transcriptional modulation of beta-actin (ACTB) mRNA.', \"Our observations show that the acquisition of above cellular capacities is concomitant with increased expression levels of the actin beta subunit (ACTB) protein. Regulating TIA abundance does not modify ACTB mRNA levels, however, an increase of ACTB mRNA translation is observed. This regulatory capacity of TIA proteins is linked to the ACTB mRNA 3'-untranslated region (3'-UTR), where these proteins could function as RNA binding proteins. The expression of GFP from a chimeric reporter containing human ΑCΤΒ 3'-UTR recapitulates the translational control found by the endogenous ACTB mRNA in the absence of TIA proteins. Additionally, murine embryonic fibroblasts (MEF) knocked out for TIA1 rise mouse ACTB protein expression compared to the controls. Once again steady-state levels of mouse ACTB mRNA remained unchanged.\"], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': [\"3' Untranslated Regions\", 'Actins', 'Animals', 'Base Sequence', 'Fibroblasts', 'Gene Expression Regulation', 'Genes, Reporter', 'Green Fluorescent Proteins', 'HeLa Cells', 'Humans', 'Mice', 'Molecular Sequence Data', 'Poly(A)-Binding Proteins', 'RNA-Binding Proteins', 'Signal Transduction', 'T-Cell Intracellular Antigen-1']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,749,853 | Does epigenome-wide DNA methylation assay reveal placental epigenetic markers for noninvasive fetal single-nucleotide polymorphism genotyping in maternal plasma? | {
"contexts": [
"The use of DNA methylation difference between maternal blood cell and fetal (placental) DNA is one of the main areas of interest for the development of fetal epigenetics markers in maternal plasma.",
"We employed a methylation array (HumanMethylation450 array, Illumina, Inc.) to identify novel biomarkers that are specially hypermethylated in placental DNA versus maternal blood cells in a genome-wide basis. Validation by bisulfite genomic sequencing was performed and the priority was given to potential targets that harbor differential methylated CpG sites overlapped with at least two methylation-sensitive restriction enzyme (MSRE) recognizing sites, as well as one polymorphic single-nucleotide polymorphism (SNP), within a short DNA stretch. Three candidate regions of PSMB8, SKI, and CHST11 gene were selected for developing a preliminary polymerase chain reaction assay with MSRE digestion of maternal plasma DNA. SNP genotypes were confirmed by direct sequencing.",
"We identified 2944 and 5218 fetal-specific hypermethylated CpG sites in the first- and third-trimester placenta, respectively, of which 2613 were overlapped, suggesting a consistency of differential methylation during the whole pregnancy. The array results were confirmed by bisulfite genomic sequencing. The preliminary tests in maternal plasma showed that postdigestion hypermathylated versions of these candidate molecules were detectable only in pregnant women. We further revealed that methylated targets in maternal plasma possessed the fetal SNP genotypes."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"CpG Islands",
"DNA Methylation",
"Epigenesis, Genetic",
"Female",
"Fetus",
"Genetic Markers",
"Genetic Testing",
"Genotyping Techniques",
"Humans",
"Oligonucleotide Array Sequence Analysis",
"Placenta",
"Polymorphism, Single Nucleotide",
"Pregnancy",
"Prenatal Diagnosis"
]
} | The present studies systematically identified hypermethylated sites in fetal tissues and preliminarily demonstrated that some of the fetal epigenetic markers that contain informative SNPs have great potential for noninvasive fetal genetic diagnosis. | yes | [
{
"from": "human",
"value": "Question: Does epigenome-wide DNA methylation assay reveal placental epigenetic markers for noninvasive fetal single-nucleotide polymorphism genotyping in maternal plasma?\nContext: {'contexts': ['The use of DNA methylation difference between maternal blood cell and fetal (placental) DNA is one of the main areas of interest for the development of fetal epigenetics markers in maternal plasma.', 'We employed a methylation array (HumanMethylation450 array, Illumina, Inc.) to identify novel biomarkers that are specially hypermethylated in placental DNA versus maternal blood cells in a genome-wide basis. Validation by bisulfite genomic sequencing was performed and the priority was given to potential targets that harbor differential methylated CpG sites overlapped with at least two methylation-sensitive restriction enzyme (MSRE) recognizing sites, as well as one polymorphic single-nucleotide polymorphism (SNP), within a short DNA stretch. Three candidate regions of PSMB8, SKI, and CHST11 gene were selected for developing a preliminary polymerase chain reaction assay with MSRE digestion of maternal plasma DNA. SNP genotypes were confirmed by direct sequencing.', 'We identified 2944 and 5218 fetal-specific hypermethylated CpG sites in the first- and third-trimester placenta, respectively, of which 2613 were overlapped, suggesting a consistency of differential methylation during the whole pregnancy. The array results were confirmed by bisulfite genomic sequencing. The preliminary tests in maternal plasma showed that postdigestion hypermathylated versions of these candidate molecules were detectable only in pregnant women. We further revealed that methylated targets in maternal plasma possessed the fetal SNP genotypes.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['CpG Islands', 'DNA Methylation', 'Epigenesis, Genetic', 'Female', 'Fetus', 'Genetic Markers', 'Genetic Testing', 'Genotyping Techniques', 'Humans', 'Oligonucleotide Array Sequence Analysis', 'Placenta', 'Polymorphism, Single Nucleotide', 'Pregnancy', 'Prenatal Diagnosis']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,755,984 | Does notch pathway target proangiogenic regulator Sox17 to restrict angiogenesis? | {
"contexts": [
"The Notch pathway stabilizes sprouting angiogenesis by favoring stalk cells over tip cells at the vascular front. Because tip and stalk cells have different properties in morphology and function, their transcriptional regulation remains to be distinguished. Transcription factor Sox17 is specifically expressed in endothelial cells, but its expression and role at the vascular front remain largely unknown.",
"To specify the role of Sox17 and its relationship with the Notch pathway in sprouting angiogenesis.",
"Endothelial-specific Sox17 deletion reduces sprouting angiogenesis in mouse embryonic and postnatal vascular development, whereas Sox17 overexpression increases it. Sox17 promotes endothelial migration by destabilizing endothelial junctions and rearranging cytoskeletal structure and upregulates expression of several genes preferentially expressed in tip cells. Interestingly, Sox17 expression is suppressed in stalk cells in which Notch signaling is relatively high. Notch activation by overexpressing Notch intracellular domain reduces Sox17 expression both in primary endothelial cells and in retinal angiogenesis, whereas Notch inhibition by delta-like ligand 4 (Dll4) blockade increases it. The Notch pathway regulates Sox17 expression mainly at the post-transcriptional level. Furthermore, endothelial Sox17 ablation rescues vascular network from excessive tip cell formation and hyperbranching under Notch inhibition in developmental and tumor angiogenesis."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Animals",
"Carcinoma, Lewis Lung",
"Cell Differentiation",
"Cell Movement",
"Cytoskeleton",
"Embryo, Mammalian",
"Embryonic Stem Cells",
"Endothelial Cells",
"Gene Expression Regulation",
"HMGB Proteins",
"Human Umbilical Vein Endothelial Cells",
"Humans",
"Intercellular Junctions",
"Mice",
"Mice, Inbred C57BL",
"Mice, Knockout",
"Mice, Transgenic",
"Morphogenesis",
"Neovascularization, Pathologic",
"Neovascularization, Physiologic",
"Protein Structure, Tertiary",
"RNA, Small Interfering",
"Receptor, Notch1",
"Receptors, Notch",
"Recombinant Fusion Proteins",
"Retinal Vessels",
"SOXF Transcription Factors",
"Signal Transduction",
"Specific Pathogen-Free Organisms",
"Transcription, Genetic"
]
} | Our findings demonstrate that the Notch pathway restricts sprouting angiogenesis by reducing the expression of proangiogenic regulator Sox17. | yes | [
{
"from": "human",
"value": "Question: Does notch pathway target proangiogenic regulator Sox17 to restrict angiogenesis?\nContext: {'contexts': ['The Notch pathway stabilizes sprouting angiogenesis by favoring stalk cells over tip cells at the vascular front. Because tip and stalk cells have different properties in morphology and function, their transcriptional regulation remains to be distinguished. Transcription factor Sox17 is specifically expressed in endothelial cells, but its expression and role at the vascular front remain largely unknown.', 'To specify the role of Sox17 and its relationship with the Notch pathway in sprouting angiogenesis.', 'Endothelial-specific Sox17 deletion reduces sprouting angiogenesis in mouse embryonic and postnatal vascular development, whereas Sox17 overexpression increases it. Sox17 promotes endothelial migration by destabilizing endothelial junctions and rearranging cytoskeletal structure and upregulates expression of several genes preferentially expressed in tip cells. Interestingly, Sox17 expression is suppressed in stalk cells in which Notch signaling is relatively high. Notch activation by overexpressing Notch intracellular domain reduces Sox17 expression both in primary endothelial cells and in retinal angiogenesis, whereas Notch inhibition by delta-like ligand 4 (Dll4) blockade increases it. The Notch pathway regulates Sox17 expression mainly at the post-transcriptional level. Furthermore, endothelial Sox17 ablation rescues vascular network from excessive tip cell formation and hyperbranching under Notch inhibition in developmental and tumor angiogenesis.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'RESULTS'], 'meshes': ['Animals', 'Carcinoma, Lewis Lung', 'Cell Differentiation', 'Cell Movement', 'Cytoskeleton', 'Embryo, Mammalian', 'Embryonic Stem Cells', 'Endothelial Cells', 'Gene Expression Regulation', 'HMGB Proteins', 'Human Umbilical Vein Endothelial Cells', 'Humans', 'Intercellular Junctions', 'Mice', 'Mice, Inbred C57BL', 'Mice, Knockout', 'Mice, Transgenic', 'Morphogenesis', 'Neovascularization, Pathologic', 'Neovascularization, Physiologic', 'Protein Structure, Tertiary', 'RNA, Small Interfering', 'Receptor, Notch1', 'Receptors, Notch', 'Recombinant Fusion Proteins', 'Retinal Vessels', 'SOXF Transcription Factors', 'Signal Transduction', 'Specific Pathogen-Free Organisms', 'Transcription, Genetic']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
24,755,985 | Does hemodynamic disturbed flow induce differential DNA methylation of endothelial Kruppel-Like Factor 4 promoter in vitro and in vivo? | {
"contexts": [
"Hemodynamic disturbed flow (DF) is associated with susceptibility to atherosclerosis. Endothelial Kruppel-Like Factor 4 (KLF4) is an important anti-inflammatory atheroprotective transcription factor that is suppressed in regions of DF.",
"The plasticity of epigenomic KLF4 transcriptional regulation by flow-mediated DNA methylation was investigated in vitro and in arterial tissue.",
"To recapitulate dominant flow characteristics of atheroprotected and atherosusceptible arteries, human aortic endothelial cells were subjected to pulsatile undisturbed flow or oscillatory DF containing a flow-reversing phase. Differential CpG site methylation was measured by methylation-specific polymerase chain reaction, bisulfite pyrosequencing, and restriction enzyme-polymerase chain reaction. The methylation profiles of endothelium from disturbed and undisturbed flow sites of adult swine aortas were also investigated. In vitro, DF increased DNA methylation of CpG islands within the KLF4 promoter that significantly contributed to suppression of KLF4 transcription; the effects were mitigated by DNA methyltransferase (DNMT) inhibitors and knockdown of DNMT3A. Contributory mechanisms included DF-induced increase of DNMT3A protein (1.7-fold), DNMT3A enrichment (11-fold) on the KLF4 promoter, and competitive blocking of a myocyte enhancer factor-2 binding site in the KLF4 promoter near the transcription start site. DF also induced DNMT-sensitive propathological expression of downstream KLF4 transcription targets nitric oxide synthase 3, thrombomodulin, and monocyte chemoattractant protein-1. In support of the in vitro findings, swine aortic endothelium isolated from DF regions expressed significantly lower KLF4 and nitric oxide synthase 3, and bisulfite sequencing of KLF4 promoter identified a hypermethylated myocyte enhancer factor-2 binding site."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Animals",
"Atherosclerosis",
"Blood Circulation",
"Cells, Cultured",
"CpG Islands",
"DNA (Cytosine-5-)-Methyltransferases",
"DNA Methylation",
"Endothelium, Vascular",
"Hemodynamics",
"Humans",
"Kruppel-Like Transcription Factors",
"MEF2 Transcription Factors",
"Nitric Oxide Synthase Type III",
"Promoter Regions, Genetic",
"Swine"
]
} | Hemodynamics influence endothelial KLF4 expression through DNMT enrichment/myocyte enhancer factor-2 inhibition mechanisms of KLF4 promoter CpG methylation with regional consequences for atherosusceptibility. | yes | [
{
"from": "human",
"value": "Question: Does hemodynamic disturbed flow induce differential DNA methylation of endothelial Kruppel-Like Factor 4 promoter in vitro and in vivo?\nContext: {'contexts': ['Hemodynamic disturbed flow (DF) is associated with susceptibility to atherosclerosis. Endothelial Kruppel-Like Factor 4 (KLF4) is an important anti-inflammatory atheroprotective transcription factor that is suppressed in regions of DF.', 'The plasticity of epigenomic KLF4 transcriptional regulation by flow-mediated DNA methylation was investigated in vitro and in arterial tissue.', 'To recapitulate dominant flow characteristics of atheroprotected and atherosusceptible arteries, human aortic endothelial cells were subjected to pulsatile undisturbed flow or oscillatory DF containing a flow-reversing phase. Differential CpG site methylation was measured by methylation-specific polymerase chain reaction, bisulfite pyrosequencing, and restriction enzyme-polymerase chain reaction. The methylation profiles of endothelium from disturbed and undisturbed flow sites of adult swine aortas were also investigated. In vitro, DF increased DNA methylation of CpG islands within the KLF4 promoter that significantly contributed to suppression of KLF4 transcription; the effects were mitigated by DNA methyltransferase (DNMT) inhibitors and knockdown of DNMT3A. Contributory mechanisms included DF-induced increase of DNMT3A protein (1.7-fold), DNMT3A enrichment (11-fold) on the KLF4 promoter, and competitive blocking of a myocyte enhancer factor-2 binding site in the KLF4 promoter near the transcription start site. DF also induced DNMT-sensitive propathological expression of downstream KLF4 transcription targets nitric oxide synthase 3, thrombomodulin, and monocyte chemoattractant protein-1. In support of the in vitro findings, swine aortic endothelium isolated from DF regions expressed significantly lower KLF4 and nitric oxide synthase 3, and bisulfite sequencing of KLF4 promoter identified a hypermethylated myocyte enhancer factor-2 binding site.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'RESULTS'], 'meshes': ['Animals', 'Atherosclerosis', 'Blood Circulation', 'Cells, Cultured', 'CpG Islands', 'DNA (Cytosine-5-)-Methyltransferases', 'DNA Methylation', 'Endothelium, Vascular', 'Hemodynamics', 'Humans', 'Kruppel-Like Transcription Factors', 'MEF2 Transcription Factors', 'Nitric Oxide Synthase Type III', 'Promoter Regions, Genetic', 'Swine']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
]
|
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