pubid
int32 113k
27.9M
| question
stringlengths 17
664
| context
dict | long_answer
stringlengths 1
3.34k
| final_decision
stringclasses 2
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listlengths 2
2
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|---|---|---|---|---|---|
26,850,090 |
Do patients with perianal Crohn 's disease have poor disease outcomes after primary bowel resection?
|
{
"contexts": [
"The presence of perianal disease in Crohn's disease patients is one of the factors of postoperative recurrence. The aim of this study is to evaluate long-term prognosis of perianal Crohn's disease patients in Asian.",
"Patients with Crohn's disease who had undergone surgical bowel resection were divided into two groups according to the presence of perianal lesion. We monitored the occurrences of abdominal and/or perianal reoperation and readmission due to disease flare-up.",
"The 132 patients included in the study were divided into 2 groups, those with perianal disease (45 patients, 34.1%) and those without perianal disease (87 patients, 65.9%). Patients with perianal disease was younger in age (33.8 years versus 39.8 years, p = 0.015) and had been diagnosed as CD at a younger age (21.9 years versus 28.6 years, p = 0.005) than patients without perianal disease. Patients with perianal disease showed more extra-intestinal manifestation than patients without perianal disease (8 versus 3, p = 0.008). Reoperation was required in 46 (44.8%) patients during the follow-up period. The presence of perianal disease independently increased the risk of reoperation [hazard ratio (HR), 3.112; confidence interval (CI), 1.707-5.675]. Furthermore, patients with perianal disease had increasing risks of abdominal reoperation (HR 1.978; 95% CI, 1.034-3.784)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Abscess",
"Adult",
"Asian Continental Ancestry Group",
"Chi-Square Distribution",
"Crohn Disease",
"Digestive System Surgical Procedures",
"Disease Progression",
"Drainage",
"Female",
"Fissure in Ano",
"Hospitals, University",
"Humans",
"Kaplan-Meier Estimate",
"Male",
"Middle Aged",
"Multivariate Analysis",
"Patient Readmission",
"Proportional Hazards Models",
"Rectal Fistula",
"Recurrence",
"Reoperation",
"Risk Factors",
"Seoul",
"Time Factors",
"Treatment Outcome",
"Young Adult"
]
}
|
Patients with Crohn's disease and perianal lesions had a higher risk of reoperation. Considering these findings, physicians should consider aggressive and early top down therapy for patients with perianal Crohn's disease.
|
yes
|
[
{
"from": "human",
"value": "Question: Do patients with perianal Crohn 's disease have poor disease outcomes after primary bowel resection?\nContext: {'contexts': [\"The presence of perianal disease in Crohn's disease patients is one of the factors of postoperative recurrence. The aim of this study is to evaluate long-term prognosis of perianal Crohn's disease patients in Asian.\", \"Patients with Crohn's disease who had undergone surgical bowel resection were divided into two groups according to the presence of perianal lesion. We monitored the occurrences of abdominal and/or perianal reoperation and readmission due to disease flare-up.\", 'The 132 patients included in the study were divided into 2 groups, those with perianal disease (45 patients, 34.1%) and those without perianal disease (87 patients, 65.9%). Patients with perianal disease was younger in age (33.8 years versus 39.8 years, p = 0.015) and had been diagnosed as CD at a younger age (21.9 years versus 28.6 years, p = 0.005) than patients without perianal disease. Patients with perianal disease showed more extra-intestinal manifestation than patients without perianal disease (8 versus 3, p = 0.008). Reoperation was required in 46 (44.8%) patients during the follow-up period. The presence of perianal disease independently increased the risk of reoperation [hazard ratio (HR), 3.112; confidence interval (CI), 1.707-5.675]. Furthermore, patients with perianal disease had increasing risks of abdominal reoperation (HR 1.978; 95% CI, 1.034-3.784).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Abscess', 'Adult', 'Asian Continental Ancestry Group', 'Chi-Square Distribution', 'Crohn Disease', 'Digestive System Surgical Procedures', 'Disease Progression', 'Drainage', 'Female', 'Fissure in Ano', 'Hospitals, University', 'Humans', 'Kaplan-Meier Estimate', 'Male', 'Middle Aged', 'Multivariate Analysis', 'Patient Readmission', 'Proportional Hazards Models', 'Rectal Fistula', 'Recurrence', 'Reoperation', 'Risk Factors', 'Seoul', 'Time Factors', 'Treatment Outcome', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,872,462 |
Is effector function of CTLs increased by irradiated colorectal tumor cells that modulate OX-40L and 4-1BBL and is reversed following dual blockade?
|
{
"contexts": [
"Sub-lethal doses of ionizing radiation (IR) can alter the phenotype of target tissue by modulating genes that influence effector T cell activity. Previous studies indicate that cancer cells respond to radiation by up-regulating surface expression of death receptors, cell adhesion molecules and tumor-associated antigens (TAA). However, there is limited information available regarding how T cells themselves are altered following these interactions with irradiated tumor cells.",
"Here, several human colorectal tumor cell lines were exposed to radiation (0-10 Gy) in vitro and changes in the expression of molecules costimulatory to effector T cells (4-1BBL, OX-40L, CD70, ICOSL) were examined by flow cytometry. T cell effector function was assessed to determine if changes in these proteins were directly related to the changes in T cell function.",
"We found OX-40L and 4-1BBL to be the most consistently upregulated proteins on the surface of colorectal tumor cells post-IR while ICOSL and CD70 remained largely unaltered. Expression of these gene products correlated with enhanced killing of irradiated human colorectal tumor cells by TAA-specific T-cells. Importantly, blocking of both OX-40L and 4-1BBL reversed radiation-enhanced T-cell killing of human tumor targets as well as T-cell survival and activation."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"4-1BB Ligand",
"CD27 Ligand",
"Carcinoembryonic Antigen",
"Cell Death",
"Cell Line, Tumor",
"Cell Survival",
"Colorectal Neoplasms",
"Humans",
"Inducible T-Cell Co-Stimulator Ligand",
"Lymphocyte Activation",
"Mucins",
"OX40 Ligand",
"Radiation, Ionizing",
"T-Lymphocytes, Cytotoxic"
]
}
|
Overall, results of this study suggest that, beyond simply rendering tumor cells more sensitive to immune attack, radiation can be used to specifically modulate expression of genes that directly stimulate effector T cell activity.
|
yes
|
[
{
"from": "human",
"value": "Question: Is effector function of CTLs increased by irradiated colorectal tumor cells that modulate OX-40L and 4-1BBL and is reversed following dual blockade?\nContext: {'contexts': ['Sub-lethal doses of ionizing radiation (IR) can alter the phenotype of target tissue by modulating genes that influence effector T cell activity. Previous studies indicate that cancer cells respond to radiation by up-regulating surface expression of death receptors, cell adhesion molecules and tumor-associated antigens (TAA). However, there is limited information available regarding how T cells themselves are altered following these interactions with irradiated tumor cells.', 'Here, several human colorectal tumor cell lines were exposed to radiation (0-10\\xa0Gy) in vitro and changes in the expression of molecules costimulatory to effector T cells (4-1BBL, OX-40L, CD70, ICOSL) were examined by flow cytometry. T cell effector function was assessed to determine if changes in these proteins were directly related to the changes in T cell function.', 'We found OX-40L and 4-1BBL to be the most consistently upregulated proteins on the surface of colorectal tumor cells post-IR while ICOSL and CD70 remained largely unaltered. Expression of these gene products correlated with enhanced killing of irradiated human colorectal tumor cells by TAA-specific T-cells. Importantly, blocking of both OX-40L and 4-1BBL reversed radiation-enhanced T-cell killing of human tumor targets as well as T-cell survival and activation.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['4-1BB Ligand', 'CD27 Ligand', 'Carcinoembryonic Antigen', 'Cell Death', 'Cell Line, Tumor', 'Cell Survival', 'Colorectal Neoplasms', 'Humans', 'Inducible T-Cell Co-Stimulator Ligand', 'Lymphocyte Activation', 'Mucins', 'OX40 Ligand', 'Radiation, Ionizing', 'T-Lymphocytes, Cytotoxic']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,856,904 |
Are responses in Rat Core Auditory Cortex Preserved during Sleep Spindle Oscillations?
|
{
"contexts": [
"Sleep is defined as a reversible state of reduction in sensory responsiveness and immobility. A long-standing hypothesis suggests that a high arousal threshold during non-rapid eye movement (NREM) sleep is mediated by sleep spindle oscillations, impairing thalamocortical transmission of incoming sensory stimuli. Here we set out to test this idea directly by examining sensory-evoked neuronal spiking activity during natural sleep.",
"We compared neuronal (n = 269) and multiunit activity (MUA), as well as local field potentials (LFP) in rat core auditory cortex (A1) during NREM sleep, comparing responses to sounds depending on the presence or absence of sleep spindles.",
"We found that sleep spindles robustly modulated the timing of neuronal discharges in A1. However, responses to sounds were nearly identical for all measured signals including isolated neurons, MUA, and LFPs (all differences < 10%). Furthermore, in 10% of trials, auditory stimulation led to an early termination of the sleep spindle oscillation around 150-250 msec following stimulus onset. Finally, active ON states and inactive OFF periods during slow waves in NREM sleep affected the auditory response in opposite ways, depending on stimulus intensity."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Acoustic Stimulation",
"Animals",
"Arousal",
"Auditory Cortex",
"Electroencephalography",
"Evoked Potentials",
"Male",
"Neurons",
"Rats",
"Rats, Inbred WKY",
"Sleep"
]
}
|
Responses in core auditory cortex are well preserved regardless of sleep spindles recorded in that area, suggesting that thalamocortical sensory relay remains functional during sleep spindles, and that sensory disconnection in sleep is mediated by other mechanisms.
|
yes
|
[
{
"from": "human",
"value": "Question: Are responses in Rat Core Auditory Cortex Preserved during Sleep Spindle Oscillations?\nContext: {'contexts': ['Sleep is defined as a reversible state of reduction in sensory responsiveness and immobility. A long-standing hypothesis suggests that a high arousal threshold during non-rapid eye movement (NREM) sleep is mediated by sleep spindle oscillations, impairing thalamocortical transmission of incoming sensory stimuli. Here we set out to test this idea directly by examining sensory-evoked neuronal spiking activity during natural sleep.', 'We compared neuronal (n = 269) and multiunit activity (MUA), as well as local field potentials (LFP) in rat core auditory cortex (A1) during NREM sleep, comparing responses to sounds depending on the presence or absence of sleep spindles.', 'We found that sleep spindles robustly modulated the timing of neuronal discharges in A1. However, responses to sounds were nearly identical for all measured signals including isolated neurons, MUA, and LFPs (all differences < 10%). Furthermore, in 10% of trials, auditory stimulation led to an early termination of the sleep spindle oscillation around 150-250 msec following stimulus onset. Finally, active ON states and inactive OFF periods during slow waves in NREM sleep affected the auditory response in opposite ways, depending on stimulus intensity.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Acoustic Stimulation', 'Animals', 'Arousal', 'Auditory Cortex', 'Electroencephalography', 'Evoked Potentials', 'Male', 'Neurons', 'Rats', 'Rats, Inbred WKY', 'Sleep']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,856,905 |
Are the Benefits of Targeted Memory Reactivation for Consolidation in Sleep Contingent on Memory Accuracy and Direct Cue-Memory Associations?
|
{
"contexts": [
"To investigate how the effects of targeted memory reactivation (TMR) are influenced by memory accuracy prior to sleep and the presence or absence of direct cue-memory associations.",
"30 participants associated each of 50 pictures with an unrelated word and then with a screen location in two separate tasks. During picture-location training, each picture was also presented with a semantically related sound. The sounds were therefore directly associated with the picture locations but indirectly associated with the words. During a subsequent nap, half of the sounds were replayed in slow wave sleep (SWS). The effect of TMR on memory for the picture locations (direct cue-memory associations) and picture-word pairs (indirect cue-memory associations) was then examined.",
"TMR reduced overall memory decay for recall of picture locations. Further analyses revealed a benefit of TMR for picture locations recalled with a low degree of accuracy prior to sleep, but not those recalled with a high degree of accuracy. The benefit of TMR for low accuracy memories was predicted by time spent in SWS. There was no benefit of TMR for memory of the picture-word pairs, irrespective of memory accuracy prior to sleep."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Acoustic Stimulation",
"Adolescent",
"Adult",
"Cues",
"Female",
"Humans",
"Male",
"Memory Consolidation",
"Mental Recall",
"Photic Stimulation",
"Semantics",
"Sleep",
"Sound",
"Young Adult"
]
}
|
TMR provides the greatest benefit to memories recalled with a low degree of accuracy prior to sleep. The memory benefits of TMR may also be contingent on direct cue-memory associations.
|
yes
|
[
{
"from": "human",
"value": "Question: Are the Benefits of Targeted Memory Reactivation for Consolidation in Sleep Contingent on Memory Accuracy and Direct Cue-Memory Associations?\nContext: {'contexts': ['To investigate how the effects of targeted memory reactivation (TMR) are influenced by memory accuracy prior to sleep and the presence or absence of direct cue-memory associations.', '30 participants associated each of 50 pictures with an unrelated word and then with a screen location in two separate tasks. During picture-location training, each picture was also presented with a semantically related sound. The sounds were therefore directly associated with the picture locations but indirectly associated with the words. During a subsequent nap, half of the sounds were replayed in slow wave sleep (SWS). The effect of TMR on memory for the picture locations (direct cue-memory associations) and picture-word pairs (indirect cue-memory associations) was then examined.', 'TMR reduced overall memory decay for recall of picture locations. Further analyses revealed a benefit of TMR for picture locations recalled with a low degree of accuracy prior to sleep, but not those recalled with a high degree of accuracy. The benefit of TMR for low accuracy memories was predicted by time spent in SWS. There was no benefit of TMR for memory of the picture-word pairs, irrespective of memory accuracy prior to sleep.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Acoustic Stimulation', 'Adolescent', 'Adult', 'Cues', 'Female', 'Humans', 'Male', 'Memory Consolidation', 'Mental Recall', 'Photic Stimulation', 'Semantics', 'Sleep', 'Sound', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,872,788 |
Does intratumoral heterogeneity of ( 18 ) F-FDG uptake predict survival in patients with pancreatic ductal adenocarcinoma?
|
{
"contexts": [
"To assess whether intratumoral heterogeneity measured by (18)F-FDG PET texture analysis has potential as a prognostic imaging biomarker in patients with pancreatic ductal adenocarcinoma (PDAC).",
"We evaluated a cohort of 137 patients with newly diagnosed PDAC who underwent pretreatment (18)F-FDG PET/CT from January 2008 to December 2010. First-order (histogram indices) and higher-order (grey-level run length, difference, size zone matrices) textural features of primary tumours were extracted by PET texture analysis. Conventional PET parameters including metabolic tumour volume (MTV), total lesion glycolysis (TLG), and standardized uptake value (SUV) were also measured. To assess and compare the predictive performance of imaging biomarkers, time-dependent receiver operating characteristic (ROC) curves for censored survival data and areas under the ROC curve (AUC) at 2 years after diagnosis were used. Associations between imaging biomarkers and overall survival were assessed using Cox proportional hazards regression models.",
"The best imaging biomarker for overall survival prediction was first-order entropy (AUC = 0.720), followed by TLG (AUC = 0.697), MTV (AUC = 0.692), and maximum SUV (AUC = 0.625). After adjusting for age, sex, clinical stage, tumour size and serum CA19-9 level, multivariable Cox analysis demonstrated that higher entropy (hazard ratio, HR, 5.59; P = 0.028) was independently associated with worse survival, whereas TLG (HR 0.98; P = 0.875) was not an independent prognostic factor."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Aged, 80 and over",
"Biological Transport",
"Carcinoma, Pancreatic Ductal",
"Female",
"Fluorodeoxyglucose F18",
"Glycolysis",
"Humans",
"Male",
"Middle Aged",
"Positron Emission Tomography Computed Tomography",
"Prognosis",
"Retrospective Studies",
"Survival Analysis",
"Tumor Burden"
]
}
|
Intratumoral heterogeneity of (18)F-FDG uptake measured by PET texture analysis is an independent predictor of survival along with tumour stage and serum CA19-9 level in patients with PDAC. In addition, first-order entropy as a measure of intratumoral metabolic heterogeneity is a better quantitative imaging biomarker of prognosis than conventional PET parameters.
|
yes
|
[
{
"from": "human",
"value": "Question: Does intratumoral heterogeneity of ( 18 ) F-FDG uptake predict survival in patients with pancreatic ductal adenocarcinoma?\nContext: {'contexts': ['To assess whether intratumoral heterogeneity measured by (18)F-FDG PET texture analysis has potential as a prognostic imaging biomarker in patients with pancreatic ductal adenocarcinoma (PDAC).', 'We evaluated a cohort of 137 patients with newly diagnosed PDAC who underwent pretreatment (18)F-FDG PET/CT from January 2008 to December 2010. First-order (histogram indices) and higher-order (grey-level run length, difference, size zone matrices) textural features of primary tumours were extracted by PET texture analysis. Conventional PET parameters including metabolic tumour volume (MTV), total lesion glycolysis (TLG), and standardized uptake value (SUV) were also measured. To assess and compare the predictive performance of imaging biomarkers, time-dependent receiver operating characteristic (ROC) curves for censored survival data and areas under the ROC curve (AUC) at 2\\xa0years after diagnosis were used. Associations between imaging biomarkers and overall survival were assessed using Cox proportional hazards regression models.', 'The best imaging biomarker for overall survival prediction was first-order entropy (AUC\\u2009=\\u20090.720), followed by TLG (AUC\\u2009=\\u20090.697), MTV (AUC\\u2009=\\u20090.692), and maximum SUV (AUC\\u2009=\\u20090.625). After adjusting for age, sex, clinical stage, tumour size and serum CA19-9 level, multivariable Cox analysis demonstrated that higher entropy (hazard ratio, HR, 5.59; P\\u2009=\\u20090.028) was independently associated with worse survival, whereas TLG (HR 0.98; P\\u2009=\\u20090.875) was not an independent prognostic factor.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Aged, 80 and over', 'Biological Transport', 'Carcinoma, Pancreatic Ductal', 'Female', 'Fluorodeoxyglucose F18', 'Glycolysis', 'Humans', 'Male', 'Middle Aged', 'Positron Emission Tomography Computed Tomography', 'Prognosis', 'Retrospective Studies', 'Survival Analysis', 'Tumor Burden']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,849,999 |
Does anodal Cerebellar Direct Current Stimulation reduce Facilitation of Propriospinal Neurons in Healthy Humans?
|
{
"contexts": [
"Coordinated muscle synergies in the human upper limb are controlled, in part, by a neural distribution network located in the cervical spinal cord, known as the cervical propriospinal system. Studies in the cat and non-human primate indicate the cerebellum is indirectly connected to this system via output pathways to the brainstem. Therefore, the cerebellum may indirectly modulate excitability of putative propriospinal neurons (PNs) in humans during upper limb coordination tasks.",
"This study aimed to test whether anodal direct current stimulation (DCS) of the cerebellum modulates PNs and upper limb coordination in healthy adults. The hypothesis was that cerebellar anodal DCS would reduce descending facilitation of PNs and improve upper limb coordination.",
"Transcranial magnetic stimulation (TMS), paired with peripheral nerve stimulation, probed activity in facilitatory and inhibitory descending projections to PNs following an established protocol. Coordination was tested using a pursuit rotor task performed by the non-dominant (ipsilateral) hand. Anodal and sham DCS were delivered over the cerebellum ipsilateral to the non-dominant hand in separate experimental sessions. Anodal DCS was applied to a control site lateral to the vertex in a third session. Twelve right-handed healthy adults participated.",
"Pairing TMS with sub-threshold peripheral nerve stimulation facilitated motor evoked potentials at intensities just above threshold in accordance with the protocol. Anodal cerebellar DCS reduced facilitation without influencing inhibition, but the reduction in facilitation was not associated with performance of the pursuit rotor task."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Cerebellum",
"Electrodes",
"Evoked Potentials, Motor",
"Female",
"Hand",
"Humans",
"Male",
"Middle Aged",
"Motor Cortex",
"Nerve Net",
"Neurons",
"Proprioception",
"Spinal Cord",
"Transcranial Direct Current Stimulation",
"Transcranial Magnetic Stimulation",
"Upper Extremity",
"Young Adult"
]
}
|
The results of this study indicate dissociated indirect control over cervical PNs by the cerebellum in humans. Anodal DCS of the cerebellum reduced excitability in the facilitatory descending pathway with no effect on the inhibitory pathway to cervical PNs. The reduction in PN excitability is likely secondary to modulation of primary motor cortex or brainstem nuclei, and identifies a neuroanatomical pathway for the cerebellum to assist in coordination of upper limb muscle synergies in humans.
|
yes
|
[
{
"from": "human",
"value": "Question: Does anodal Cerebellar Direct Current Stimulation reduce Facilitation of Propriospinal Neurons in Healthy Humans?\nContext: {'contexts': ['Coordinated muscle synergies in the human upper limb are controlled, in part, by a neural distribution network located in the cervical spinal cord, known as the cervical propriospinal system. Studies in the cat and non-human primate indicate the cerebellum is indirectly connected to this system via output pathways to the brainstem. Therefore, the cerebellum may indirectly modulate excitability of putative propriospinal neurons (PNs) in humans during upper limb coordination tasks.', 'This study aimed to test whether anodal direct current stimulation (DCS) of the cerebellum modulates PNs and upper limb coordination in healthy adults. The hypothesis was that cerebellar anodal DCS would reduce descending facilitation of PNs and improve upper limb coordination.', 'Transcranial magnetic stimulation (TMS), paired with peripheral nerve stimulation, probed activity in facilitatory and inhibitory descending projections to PNs following an established protocol. Coordination was tested using a pursuit rotor task performed by the non-dominant (ipsilateral) hand. Anodal and sham DCS were delivered over the cerebellum ipsilateral to the non-dominant hand in separate experimental sessions. Anodal DCS was applied to a control site lateral to the vertex in a third session. Twelve right-handed healthy adults participated.', 'Pairing TMS with sub-threshold peripheral nerve stimulation facilitated motor evoked potentials at intensities just above threshold in accordance with the protocol. Anodal cerebellar DCS reduced facilitation without influencing inhibition, but the reduction in facilitation was not associated with performance of the pursuit rotor task.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Cerebellum', 'Electrodes', 'Evoked Potentials, Motor', 'Female', 'Hand', 'Humans', 'Male', 'Middle Aged', 'Motor Cortex', 'Nerve Net', 'Neurons', 'Proprioception', 'Spinal Cord', 'Transcranial Direct Current Stimulation', 'Transcranial Magnetic Stimulation', 'Upper Extremity', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,849,998 |
Is intracortical Inhibition Assessed with Paired-Pulse Transcranial Magnetic Stimulation Modulated during Shortening and Lengthening Contractions in Young and Old Adults?
|
{
"contexts": [
"The modulation of intracortical inhibition is thought to be impaired in older adults, which may contribute to their reduced fine motor control, particularly during lengthening muscle contractions.",
"To quantify the magnitude of intracortical inhibition and movement performance during postural, shortening and lengthening contractions of a hand muscle in young and old adults.",
"In 18 young (23.2 ± 4.2) and 16 old (70.6 ± 6.5) subjects, paired-pulse transcranial magnetic stimulation (TMS) was used to assess short-interval intracortical inhibition (SICI) and long-interval intracortical inhibition (LICI) during a movement task involving the first dorsal interosseous muscle. The task required a constant load (50 g) to be slowly lifted and lowered using the index finger while single- or paired-pulse TMS was delivered during the shortening or lengthening contraction.",
"Relative to postural contractions, SICI during shortening contractions was reduced by 29% in young subjects (P < 0.0001) and 43% in old subjects (P < 0.0001), whereas SICI during lengthening contractions was reduced by 11% in young subjects (P = 0.0004) and 33% in old subjects (P < 0.0001). Furthermore, SICI was significantly less in older adults during lengthening contractions (P-values < 0.01). For LICI, inhibition was not influenced by contraction type in old subjects, but was increased by 11% during shortening contractions (P < 0.0001) and by 9% during lengthening contractions in young subjects (P = 0.0008). In addition, old subjects showed significantly less LICI than young subjects in each movement phase (both P-values < 0.05)."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Aging",
"Female",
"Fingers",
"Humans",
"Male",
"Motor Cortex",
"Movement",
"Muscle Contraction",
"Muscle, Skeletal",
"Neural Inhibition",
"Transcranial Magnetic Stimulation",
"Young Adult",
"gamma-Aminobutyric Acid"
]
}
|
Shortening and lengthening contractions with a constant load are associated with a modulation of GABAergic inhibition that is altered by healthy ageing.
|
yes
|
[
{
"from": "human",
"value": "Question: Is intracortical Inhibition Assessed with Paired-Pulse Transcranial Magnetic Stimulation Modulated during Shortening and Lengthening Contractions in Young and Old Adults?\nContext: {'contexts': ['The modulation of intracortical inhibition is thought to be impaired in older adults, which may contribute to their reduced fine motor control, particularly during lengthening muscle contractions.', 'To quantify the magnitude of intracortical inhibition and movement performance during postural, shortening and lengthening contractions of a hand muscle in young and old adults.', 'In 18 young (23.2 ± 4.2) and 16 old (70.6 ± 6.5) subjects, paired-pulse transcranial magnetic stimulation (TMS) was used to assess short-interval intracortical inhibition (SICI) and long-interval intracortical inhibition (LICI) during a movement task involving the first dorsal interosseous muscle. The task required a constant load (50 g) to be slowly lifted and lowered using the index finger while single- or paired-pulse TMS was delivered during the shortening or lengthening contraction.', 'Relative to postural contractions, SICI during shortening contractions was reduced by 29% in young subjects (P < 0.0001) and 43% in old subjects (P < 0.0001), whereas SICI during lengthening contractions was reduced by 11% in young subjects (P = 0.0004) and 33% in old subjects (P < 0.0001). Furthermore, SICI was significantly less in older adults during lengthening contractions (P-values < 0.01). For LICI, inhibition was not influenced by contraction type in old subjects, but was increased by 11% during shortening contractions (P < 0.0001) and by 9% during lengthening contractions in young subjects (P = 0.0008). In addition, old subjects showed significantly less LICI than young subjects in each movement phase (both P-values < 0.05).'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Aging', 'Female', 'Fingers', 'Humans', 'Male', 'Motor Cortex', 'Movement', 'Muscle Contraction', 'Muscle, Skeletal', 'Neural Inhibition', 'Transcranial Magnetic Stimulation', 'Young Adult', 'gamma-Aminobutyric Acid']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,874,433 |
Does the use of pilocarpine eye drop for estimating the time since death?
|
{
"contexts": [
"The objective of this study was to estimate the time since death using pilocarpine eye drops.",
"In this study, 100 postmortem cases with known time of death were included. In each case, the left pupil was measured in millimeter units using a vernier caliper, and pilocarpine eye drops were applied. The pupil was measured again 10 min later, and statistical analysis was used to analyze the correlation between the time since death and the change in the pupil.",
"The longest duration since death that the pupils showed reaction to pilocarpine was 15 h. The correlation between the change in the pupil and the postmortem interval was found (Spearman's rho, r = -0.304, p = 0.002), and the change in the pupil may be used to predict the postmortem interval by the following regression equation: postmortem interval (PMI) = 8.310-3.702 (Diff) ± 0.735 (PMI was postmortem interval in hours and Diff was the difference in the size of the pupil after administering pilocarpine in millimeter units)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Aged, 80 and over",
"Female",
"Forensic Pathology",
"Humans",
"Male",
"Middle Aged",
"Miotics",
"Ophthalmic Solutions",
"Pilocarpine",
"Postmortem Changes",
"Pupil",
"Regression Analysis",
"Young Adult"
]
}
|
The present study showed that pilocarpine eye drops can be used to estimate the time since death.
|
yes
|
[
{
"from": "human",
"value": "Question: Does the use of pilocarpine eye drop for estimating the time since death?\nContext: {'contexts': ['The objective of this study was to estimate the time since death using pilocarpine eye drops.', 'In this study, 100 postmortem cases with known time of death were included. In each case, the left pupil was measured in millimeter units using a vernier caliper, and pilocarpine eye drops were applied. The pupil was measured again 10 min later, and statistical analysis was used to analyze the correlation between the time since death and the change in the pupil.', \"The longest duration since death that the pupils showed reaction to pilocarpine was 15 h. The correlation between the change in the pupil and the postmortem interval was found (Spearman's rho, r = -0.304, p = 0.002), and the change in the pupil may be used to predict the postmortem interval by the following regression equation: postmortem interval (PMI) = 8.310-3.702 (Diff) ± 0.735 (PMI was postmortem interval in hours and Diff was the difference in the size of the pupil after administering pilocarpine in millimeter units).\"], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Aged, 80 and over', 'Female', 'Forensic Pathology', 'Humans', 'Male', 'Middle Aged', 'Miotics', 'Ophthalmic Solutions', 'Pilocarpine', 'Postmortem Changes', 'Pupil', 'Regression Analysis', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,869,772 |
Do patterns of analgesic adherence predict health care utilization among outpatients with cancer pain?
|
{
"contexts": [
"Studies in chronic noncancer pain settings have found that opioid use increases health care utilization. Despite the key role of analgesics, specifically opioids, in the setting of cancer pain, there is no literature to our knowledge about the relationship between adherence to prescribed around-the-clock (ATC) analgesics and acute health care utilization (hospitalization) among patients with cancer pain.",
"To identify adherence patterns over time for cancer patients taking ATC analgesics for pain, cluster these patterns into adherence types, combine the types into an adherence risk factor for hospitalization, identify other risk factors for hospitalization, and identify risk factors for inconsistent analgesic adherence.",
"Data from a 3-month prospective observational study of patients diagnosed with solid tumors or multiple myeloma, having cancer-related pain, and having at least one prescription of oral ATC analgesics were collected. Adherence data were collected electronically using the medication event-monitoring system. Analyses were conducted using adaptive modeling methods based on heuristic search through alternative models controlled by likelihood cross-validation scores.",
"Six adherence types were identified and combined into the risk factor for hospitalization of inconsistent versus consistent adherence over time. Twenty other individually significant risk factors for hospitalization were identified, but inconsistent analgesic adherence was the strongest of these predictors (ie, generating the largest likelihood cross-validation score). These risk factors were adaptively combined into a model for hospitalization based on six pairwise interaction risk factors with exceptional discrimination (ie, area under the receiver-operating-characteristic curve of 0.91). Patients had from zero to five of these risk factors, with an odds ratio of 5.44 (95% confidence interval 3.09-9.58) for hospitalization, with a unit increase in the number of such risk factors."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": []
}
|
Inconsistent adherence to prescribed ATC analgesics, specifically the interaction of strong opioids and inconsistent adherence, is a strong risk factor for hospitalization among cancer outpatients with pain.
|
yes
|
[
{
"from": "human",
"value": "Question: Do patterns of analgesic adherence predict health care utilization among outpatients with cancer pain?\nContext: {'contexts': ['Studies in chronic noncancer pain settings have found that opioid use increases health care utilization. Despite the key role of analgesics, specifically opioids, in the setting of cancer pain, there is no literature to our knowledge about the relationship between adherence to prescribed around-the-clock (ATC) analgesics and acute health care utilization (hospitalization) among patients with cancer pain.', 'To identify adherence patterns over time for cancer patients taking ATC analgesics for pain, cluster these patterns into adherence types, combine the types into an adherence risk factor for hospitalization, identify other risk factors for hospitalization, and identify risk factors for inconsistent analgesic adherence.', 'Data from a 3-month prospective observational study of patients diagnosed with solid tumors or multiple myeloma, having cancer-related pain, and having at least one prescription of oral ATC analgesics were collected. Adherence data were collected electronically using the medication event-monitoring system. Analyses were conducted using adaptive modeling methods based on heuristic search through alternative models controlled by likelihood cross-validation scores.', 'Six adherence types were identified and combined into the risk factor for hospitalization of inconsistent versus consistent adherence over time. Twenty other individually significant risk factors for hospitalization were identified, but inconsistent analgesic adherence was the strongest of these predictors (ie, generating the largest likelihood cross-validation score). These risk factors were adaptively combined into a model for hospitalization based on six pairwise interaction risk factors with exceptional discrimination (ie, area under the receiver-operating-characteristic curve of 0.91). Patients had from zero to five of these risk factors, with an odds ratio of 5.44 (95% confidence interval 3.09-9.58) for hospitalization, with a unit increase in the number of such risk factors.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,875,746 |
Is reduction of CRKL expression in patients with partial DiGeorge syndrome associated with impairment of T-cell functions?
|
{
"contexts": [
"Partial DiGeorge syndrome (pDGS) is caused by deletion of the 22q11.2 region. Within this region lies CrK-like (CRKL), a gene encoding an adapter protein belonging to the Crk family that is involved in the signaling cascade of IL-2, stromal cell-derived factor 1α, and type I interferon. Although recurrent infections can be observed in patients with deletion of chromosome 22 syndrome, the immune pathogenesis of this condition is yet not fully understood.",
"We aimed to investigate the role of CRKL in T-cell functional responses in patients affected with pDGS.",
"Protein expression levels and phosphorylation of CRKL were evaluated in patients with pDGS. T-cell functional assays in vitro and gene-silencing experiments were also performed.",
"CRKL protein expression, as well as its phosphorylation, were reduced in all patients with pDGS, especially on IL-2 stimulation. Moreover, T cells presented impaired proliferation and reduced IL-2 production on anti-CD3/CD28 stimulation and decreased c-Fos expression. Finally, CRKL silencing in Jurkat T cells resulted in impaired T-cell proliferation and reduced c-Fos expression."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adaptor Proteins, Signal Transducing",
"Adolescent",
"Adult",
"Biomarkers",
"Case-Control Studies",
"Cell Line",
"Child",
"Child, Preschool",
"Cytokines",
"DiGeorge Syndrome",
"Gene Expression Regulation",
"Gene Silencing",
"Humans",
"Immunoglobulin Isotypes",
"Infant",
"Lymphocyte Activation",
"Lymphocyte Subsets",
"Middle Aged",
"Nuclear Proteins",
"Phenotype",
"Phosphorylation",
"RNA Interference",
"STAT5 Transcription Factor",
"T-Lymphocytes",
"Young Adult"
]
}
|
The impaired T-cell proliferation and reduction of CRKL, phosphorylated CRKL, and c-Fos levels suggest a possible role of CRKL in functional deficiencies of T cells in patients with pDGS.
|
yes
|
[
{
"from": "human",
"value": "Question: Is reduction of CRKL expression in patients with partial DiGeorge syndrome associated with impairment of T-cell functions?\nContext: {'contexts': ['Partial DiGeorge syndrome (pDGS) is caused by deletion of the 22q11.2 region. Within this region lies CrK-like (CRKL), a gene encoding an adapter protein belonging to the Crk family that is involved in the signaling cascade of IL-2, stromal cell-derived factor 1α, and type I interferon. Although recurrent infections can be observed in patients with deletion of chromosome 22 syndrome, the immune pathogenesis of this condition is yet not fully understood.', 'We aimed to investigate the role of CRKL in T-cell functional responses in patients affected with pDGS.', 'Protein expression levels and phosphorylation of CRKL were evaluated in patients with pDGS. T-cell functional assays in\\xa0vitro and gene-silencing experiments were also performed.', 'CRKL protein expression, as well as its phosphorylation, were reduced in all patients with pDGS, especially on IL-2 stimulation. Moreover, T\\xa0cells presented impaired proliferation and reduced IL-2 production on anti-CD3/CD28 stimulation and decreased c-Fos expression. Finally, CRKL silencing in Jurkat T\\xa0cells resulted in impaired T-cell proliferation and reduced c-Fos expression.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adaptor Proteins, Signal Transducing', 'Adolescent', 'Adult', 'Biomarkers', 'Case-Control Studies', 'Cell Line', 'Child', 'Child, Preschool', 'Cytokines', 'DiGeorge Syndrome', 'Gene Expression Regulation', 'Gene Silencing', 'Humans', 'Immunoglobulin Isotypes', 'Infant', 'Lymphocyte Activation', 'Lymphocyte Subsets', 'Middle Aged', 'Nuclear Proteins', 'Phenotype', 'Phosphorylation', 'RNA Interference', 'STAT5 Transcription Factor', 'T-Lymphocytes', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,859,683 |
Does next-generation sequencing reveal somatic mutations that confer exceptional response to everolimus?
|
{
"contexts": [
"Given the modest responses to everolimus, a mTOR inhibitor, in multiple tumor types, there is a pressing need to identify predictive biomarkers for this drug. Using targeted ultra-deep sequencing, we aimed to explore genomic alterations that confer extreme sensitivity to everolimus.",
"We collected formalin-fixed paraffin-embedded tumor/normal pairs from 39 patients (22 with exceptional clinical benefit, 17 with no clinical benefit) who were treated with everolimus across various tumor types (13 gastric cancers, 15 renal cell carcinomas, 2 thyroid cancers, 2 head and neck cancer, and 7 sarcomas). Ion AmpliSeqTM Comprehensive Cancer Panel was used to identify alterations across all exons of 409 target genes. Tumors were sequenced to a median coverage of 552x. Cancer genomes are characterized by 219 somatic single-nucleotide variants (181 missense, 9 nonsense, 7 splice-site) and 22 frameshift insertions/deletions, with a median of 2.1 mutations per Mb (0 to 12.4 mutations per Mb). Overall, genomic alterations with activating effect on mTOR signaling were identified in 10 of 22 (45%) patients with clinical benefit and these include MTOR, TSC1, TSC2, NF1, PIK3CA and PIK3CG mutations. Recurrently mutated genes in chromatin remodeling genes (BAP1; n = 2, 12%) and receptor tyrosine kinase signaling (FGFR4; n = 2, 12%) were noted only in patients without clinical benefit."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Adenocarcinoma",
"Adult",
"Aged",
"Aged, 80 and over",
"Antineoplastic Agents",
"Carcinoma, Renal Cell",
"Class I Phosphatidylinositol 3-Kinases",
"Class Ib Phosphatidylinositol 3-Kinase",
"Drug Resistance, Neoplasm",
"Everolimus",
"Female",
"Head and Neck Neoplasms",
"High-Throughput Nucleotide Sequencing",
"Humans",
"Kidney Neoplasms",
"Lacrimal Apparatus",
"Male",
"Middle Aged",
"Mutation",
"Neurofibromin 1",
"Phosphatidylinositol 3-Kinases",
"Polymorphism, Single Nucleotide",
"Sarcoma",
"Stomach Neoplasms",
"TOR Serine-Threonine Kinases",
"Thyroid Neoplasms",
"Tuberous Sclerosis Complex 1 Protein",
"Tuberous Sclerosis Complex 2 Protein",
"Tumor Suppressor Protein p53",
"Tumor Suppressor Proteins",
"Young Adult"
]
}
|
Regardless of different cancer types, mTOR-pathway-activating mutations confer sensitivity to everolimus. Targeted sequencing of mTOR pathway genes facilitates identification of potential candidates for mTOR inhibitors.
|
yes
|
[
{
"from": "human",
"value": "Question: Does next-generation sequencing reveal somatic mutations that confer exceptional response to everolimus?\nContext: {'contexts': ['Given the modest responses to everolimus, a mTOR inhibitor, in multiple tumor types, there is a pressing need to identify predictive biomarkers for this drug. Using targeted ultra-deep sequencing, we aimed to explore genomic alterations that confer extreme sensitivity to everolimus.', 'We collected formalin-fixed paraffin-embedded tumor/normal pairs from 39 patients (22 with exceptional clinical benefit, 17 with no clinical benefit) who were treated with everolimus across various tumor types (13 gastric cancers, 15 renal cell carcinomas, 2 thyroid cancers, 2 head and neck cancer, and 7 sarcomas). Ion AmpliSeqTM Comprehensive Cancer Panel was used to identify alterations across all exons of 409 target genes. Tumors were sequenced to a median coverage of 552x. Cancer genomes are characterized by 219 somatic single-nucleotide variants (181 missense, 9 nonsense, 7 splice-site) and 22 frameshift insertions/deletions, with a median of 2.1 mutations per Mb (0 to 12.4 mutations per Mb). Overall, genomic alterations with activating effect on mTOR signaling were identified in 10 of 22 (45%) patients with clinical benefit and these include MTOR, TSC1, TSC2, NF1, PIK3CA and PIK3CG mutations. Recurrently mutated genes in chromatin remodeling genes (BAP1; n = 2, 12%) and receptor tyrosine kinase signaling (FGFR4; n = 2, 12%) were noted only in patients without clinical benefit.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Adenocarcinoma', 'Adult', 'Aged', 'Aged, 80 and over', 'Antineoplastic Agents', 'Carcinoma, Renal Cell', 'Class I Phosphatidylinositol 3-Kinases', 'Class Ib Phosphatidylinositol 3-Kinase', 'Drug Resistance, Neoplasm', 'Everolimus', 'Female', 'Head and Neck Neoplasms', 'High-Throughput Nucleotide Sequencing', 'Humans', 'Kidney Neoplasms', 'Lacrimal Apparatus', 'Male', 'Middle Aged', 'Mutation', 'Neurofibromin 1', 'Phosphatidylinositol 3-Kinases', 'Polymorphism, Single Nucleotide', 'Sarcoma', 'Stomach Neoplasms', 'TOR Serine-Threonine Kinases', 'Thyroid Neoplasms', 'Tuberous Sclerosis Complex 1 Protein', 'Tuberous Sclerosis Complex 2 Protein', 'Tumor Suppressor Protein p53', 'Tumor Suppressor Proteins', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,875,609 |
Is zinc finger protein A20 involved in the antipsoriatic effect of calcipotriol?
|
{
"contexts": [
"Calcipotriol ameliorates psoriasis through inducing keratinocyte apoptosis and inhibiting nuclear factor kappa B (NF-κB) activation, while zinc finger protein A20 exhibits an anti-apoptotic effect on various types of cells.",
"To understand the potential role of A20 in calcipotriol function.",
"The A20 levels were evaluated in the psoriatic skins from both human patients and K14-vascular endothelial growth factor (VEGF) transgenic mice that received or did not receive topical calcipotriol treatment. The in vitro effect of calcipotriol on A20 expression and the downstream NF-κB pathway was studied using a model of human foreskin keratinocytes (HFKs) that were stimulated with psoriatic cytokines [M5, a cocktail of interleukin (IL)-1a, IL-17A, IL-22, Oncostatin M and tumour necrosis factor-α, each at 10 ng mL(-1) ].",
"A20 expression was enhanced in both psoriatic tissues and keratinocytes when compared with controls, but decreased on calcipotriol treatment. The transfection of A20 small interfering RNA (siRNA) improved cell differentiation, and inhibited psoriatic inflammation in a HFK model. Moreover, the nuclear expression of NF-κB p65 decreased on A20 downregulation in psoriatic tissues and keratinocytes. Interestingly, calcipotriol enhanced the binding of A20 to ring finger protein 114 (RNF114) and A20-binding inhibitor of NF-κB-1 (ABIN-1) in HFKs, two negative regulators of the NF-κB pathway."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Administration, Cutaneous",
"Animals",
"Apoptosis",
"Calcitriol",
"Cell Differentiation",
"Cells, Cultured",
"Cytokines",
"Dermatitis",
"Dermatologic Agents",
"Down-Regulation",
"Female",
"Humans",
"Keratinocytes",
"Mice, Transgenic",
"NF-kappa B",
"Protein Binding",
"Psoriasis",
"RNA, Small Interfering",
"Signal Transduction",
"Skin",
"Transfection",
"Tumor Necrosis Factor alpha-Induced Protein 3"
]
}
|
Calcipotriol exhibits its antipsoriatic function through suppressing A20 expression and stabilizing negative regulators of the NF-κB pathway.
|
yes
|
[
{
"from": "human",
"value": "Question: Is zinc finger protein A20 involved in the antipsoriatic effect of calcipotriol?\nContext: {'contexts': ['Calcipotriol ameliorates psoriasis through inducing keratinocyte apoptosis and inhibiting nuclear factor kappa B (NF-κB) activation, while zinc finger protein A20 exhibits an anti-apoptotic effect on various types of cells.', 'To understand the potential role of A20 in calcipotriol function.', 'The A20 levels were evaluated in the psoriatic skins from both human patients and K14-vascular endothelial growth factor (VEGF) transgenic mice that received or did not receive topical calcipotriol treatment. The in vitro effect of calcipotriol on A20 expression and the downstream NF-κB pathway was studied using a model of human foreskin keratinocytes (HFKs) that were stimulated with psoriatic cytokines [M5, a cocktail of interleukin (IL)-1a, IL-17A, IL-22, Oncostatin M and tumour necrosis factor-α, each at 10 ng mL(-1) ].', 'A20 expression was enhanced in both psoriatic tissues and keratinocytes when compared with controls, but decreased on calcipotriol treatment. The transfection of A20 small interfering RNA (siRNA) improved cell differentiation, and inhibited psoriatic inflammation in a HFK model. Moreover, the nuclear expression of NF-κB p65 decreased on A20 downregulation in psoriatic tissues and keratinocytes. Interestingly, calcipotriol enhanced the binding of A20 to ring finger protein 114 (RNF114) and A20-binding inhibitor of NF-κB-1 (ABIN-1) in HFKs, two negative regulators of the NF-κB pathway.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Administration, Cutaneous', 'Animals', 'Apoptosis', 'Calcitriol', 'Cell Differentiation', 'Cells, Cultured', 'Cytokines', 'Dermatitis', 'Dermatologic Agents', 'Down-Regulation', 'Female', 'Humans', 'Keratinocytes', 'Mice, Transgenic', 'NF-kappa B', 'Protein Binding', 'Psoriasis', 'RNA, Small Interfering', 'Signal Transduction', 'Skin', 'Transfection', 'Tumor Necrosis Factor alpha-Induced Protein 3']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,877,088 |
Do globally distributed Xyleborus species reveal recurrent intercontinental dispersal in a landscape of ancient worldwide distributions?
|
{
"contexts": [
"Invasive species can have devastating effects on native ecosystems and therefore impose a significant threat to human welfare. The introduction rate of invasive species has accelerated dramatically in recent times due to human activity (anthropogenic effects), with a steadily growing pool of widespread tramp species. We present an in-depth analysis of four pantropical species of Xyleborus ambrosia beetles (Xyleborus volvulus, Xyleborus perforans, Xyleborus ferrugineus, and Xyleborus affinis) with similar ecology (fungus cultivation in dead wood), reproductive biology (permanent inbreeding) and genetic system (haplodiploidy). The unique combination of reproductive traits and broad host plant usage pre-adapts these beetles for colonizing of new areas.",
"We found that all four species were broadly distributed long before human-assisted dispersal became common, and that the impact of anthropogenic effects varied among the species. For X. volvulus, X. perforans, and X. affinis there was evidence of ancient establishment in numerous regions, but also of abundant recent introductions into previously colonized areas. For X. ferrugineus, we found clear biogeographical structuring of old clades, but little evidence for recent successful introductions."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Animal Distribution",
"Animals",
"Coleoptera",
"Ecosystem",
"Female",
"Genetic Variation",
"Introduced Species",
"Phylogeography",
"Weevils"
]
}
|
Our results indicate that current human-aided transoceanic dispersal has strongly affected the genetic makeup of three of the species in this study. However, current biogeographical patterns of all four species are equally, if not more strongly, influenced by ancient establishment on different continents.
|
yes
|
[
{
"from": "human",
"value": "Question: Do globally distributed Xyleborus species reveal recurrent intercontinental dispersal in a landscape of ancient worldwide distributions?\nContext: {'contexts': ['Invasive species can have devastating effects on native ecosystems and therefore impose a significant threat to human welfare. The introduction rate of invasive species has accelerated dramatically in recent times due to human activity (anthropogenic effects), with a steadily growing pool of widespread tramp species. We present an in-depth analysis of four pantropical species of Xyleborus ambrosia beetles (Xyleborus volvulus, Xyleborus perforans, Xyleborus ferrugineus, and Xyleborus affinis) with similar ecology (fungus cultivation in dead wood), reproductive biology (permanent inbreeding) and genetic system (haplodiploidy). The unique combination of reproductive traits and broad host plant usage pre-adapts these beetles for colonizing of new areas.', 'We found that all four species were broadly distributed long before human-assisted dispersal became common, and that the impact of anthropogenic effects varied among the species. For X. volvulus, X. perforans, and X. affinis there was evidence of ancient establishment in numerous regions, but also of abundant recent introductions into previously colonized areas. For X. ferrugineus, we found clear biogeographical structuring of old clades, but little evidence for recent successful introductions.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Animal Distribution', 'Animals', 'Coleoptera', 'Ecosystem', 'Female', 'Genetic Variation', 'Introduced Species', 'Phylogeography', 'Weevils']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,872,061 |
Are cerebrospinal fluid chitinase-3-like 2 and chitotriosidase potential prognostic biomarkers in early multiple sclerosis?
|
{
"contexts": [
"The role of chitinases and chitinase-like proteins in multiple sclerosis (MS) is currently unknown; however, cerebrospinal fluid (CSF) levels of chitinase 3-like 1 (CHI3L1) predict prognosis in early MS. Whether this applies to other chitinases and chitinase-like proteins is yet to be established. Our objective was to investigate the potential of chitinase 3-like 2 (CHI3L2) and chitotriosidase as prognostic biomarkers in optic neuritis (ON) as the first demyelinating episode and to evaluate the ability of CHI3L2 to predict long-term MS risk and disability.",
"In a prospective cohort of 73 patients with ON as a first demyelinating episode and 26 age-matched healthy controls levels of CHI3L2 and chitotriosidase in CSF were explored by enzyme-linked immunosorbent assay. Associations with magnetic resonance imaging white matter lesions, CSF oligoclonal bands, immunoglobulin G index and leukocyte count were investigated. Long-term MS risk and disability (Expanded Disability Status Scale, Multiple Sclerosis Functional Composite components) were examined in a retrospective cohort of 78 patients with ON as the first demyelinating episode (mean follow-up 14 years). The predictive ability of CHI3L2 was compared with CHI3L1.",
"Cerebrospinal fluid levels of CHI3L2 and chitotriosidase were significantly elevated in patients with ON and were associated with MS risk measures. CHI3L2 levels predicted MS development after ON (hazard ratio 1.95, P = 0.00039, Cox regression) and cognitive impairment by the Paced Auditory Serial Addition Test (P = 0.0357, linear regression) at follow-up. In a multivariate analysis of MS risk, CHI3L2 performed better than CHI3L1."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Biomarkers",
"Brain",
"Chitinases",
"Disabled Persons",
"Female",
"Hexosaminidases",
"Humans",
"Magnetic Resonance Imaging",
"Male",
"Middle Aged",
"Multiple Sclerosis",
"Optic Neuritis",
"Prognosis",
"Prospective Studies",
"Retrospective Studies",
"Young Adult"
]
}
|
CHI3L2 and chitotriosidase are promising biomarkers in patients with a first demyelinating episode. Our findings thus support a role for these proteins as biomarkers in early MS.
|
yes
|
[
{
"from": "human",
"value": "Question: Are cerebrospinal fluid chitinase-3-like 2 and chitotriosidase potential prognostic biomarkers in early multiple sclerosis?\nContext: {'contexts': ['The role of chitinases and chitinase-like proteins in multiple sclerosis (MS) is currently unknown; however, cerebrospinal fluid (CSF) levels of chitinase 3-like 1 (CHI3L1) predict prognosis in early MS. Whether this applies to other chitinases and chitinase-like proteins is yet to be established. Our objective was to investigate the potential of chitinase 3-like 2 (CHI3L2) and chitotriosidase as prognostic biomarkers in optic neuritis (ON) as the first demyelinating episode and to evaluate the ability of CHI3L2 to predict long-term MS risk and disability.', 'In a prospective cohort of 73 patients with ON as a first demyelinating episode and 26 age-matched healthy controls levels of CHI3L2 and chitotriosidase in CSF were explored by enzyme-linked immunosorbent assay. Associations with magnetic resonance imaging white matter lesions, CSF oligoclonal bands, immunoglobulin G index and leukocyte count were investigated. Long-term MS risk and disability (Expanded Disability Status Scale, Multiple Sclerosis Functional Composite components) were examined in a retrospective cohort of 78 patients with ON as the first demyelinating episode (mean follow-up 14 years). The predictive ability of CHI3L2 was compared with CHI3L1.', 'Cerebrospinal fluid levels of CHI3L2 and chitotriosidase were significantly elevated in patients with ON and were associated with MS risk measures. CHI3L2 levels predicted MS development after ON (hazard ratio 1.95, P = 0.00039, Cox regression) and cognitive impairment by the Paced Auditory Serial Addition Test (P = 0.0357, linear regression) at follow-up. In a multivariate analysis of MS risk, CHI3L2 performed better than CHI3L1.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Biomarkers', 'Brain', 'Chitinases', 'Disabled Persons', 'Female', 'Hexosaminidases', 'Humans', 'Magnetic Resonance Imaging', 'Male', 'Middle Aged', 'Multiple Sclerosis', 'Optic Neuritis', 'Prognosis', 'Prospective Studies', 'Retrospective Studies', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,863,400 |
Does artesunate protect Against the Organ Injury and Dysfunction Induced by Severe Hemorrhage and Resuscitation?
|
{
"contexts": [
"To evaluate the effects of artesunate on organ injury and dysfunction associated with hemorrhagic shock (HS) in the rat.",
"HS is still a common cause of death in severely injured patients and is characterized by impairment of organ perfusion, systemic inflammatory response, and multiple organ failure. There is no specific therapy that reduces organ injury/dysfunction. Artesunate exhibits pharmacological actions beyond its antimalarial activity, such as anticancer, antiviral, and anti-inflammatory effects.",
"Rats were submitted to HS. Mean arterial pressure was reduced to 30 mm Hg for 90 minutes, followed by resuscitation. Rats were randomly treated with artesunate (2.4 or 4.8 mg/kg i.v.) or vehicle upon resuscitation. Four hours later, parameters of organ injury and dysfunction were assessed.",
"Artesunate attenuated the multiple organ injury and dysfunction caused by HS. Pathway analysis of RNA sequencing provided good evidence to support an effect of artesunate on the Akt-survival pathway, leading to downregulation of interleukin-1 receptor-associated kinase 1. Using Western blot analysis, we confirmed that treatment of HS rats with artesunate enhanced the phosphorylation (activation) of Protein kinase B (Akt) and endothelial nitric oxide synthase and the phosphorylation (inhibition) of glycogen synthase kinase-3β (GSK-3β). Moreover, artesunate attenuated the HS-induced activation of nuclear factor kappa B and reduced the expression of proinflammatory proteins (inducible nitric oxide synthase, tumor necrosis factor-α, and interleukin 6)."
],
"labels": [
"OBJECTIVE",
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": []
}
|
Artesunate attenuated the organ injury/dysfunction associated with HS by a mechanism that involves the activation of the Akt-endothelial nitric oxide synthase survival pathway, and the inhibition of glycogen synthase kinase-3β and nuclear factor kappa B. A phase II clinical trial evaluating the effects of good manufacturing practice-artesunate in patients with trauma and severe hemorrhage is planned.This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives 4.0 License, where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially. http://creativecommons.org/licenses/by-nc-nd/4.0.
|
yes
|
[
{
"from": "human",
"value": "Question: Does artesunate protect Against the Organ Injury and Dysfunction Induced by Severe Hemorrhage and Resuscitation?\nContext: {'contexts': ['To evaluate the effects of artesunate on organ injury and dysfunction associated with hemorrhagic shock (HS) in the rat.', 'HS is still a common cause of death in severely injured patients and is characterized by impairment of organ perfusion, systemic inflammatory response, and multiple organ failure. There is no specific therapy that reduces organ injury/dysfunction. Artesunate exhibits pharmacological actions beyond its antimalarial activity, such as anticancer, antiviral, and anti-inflammatory effects.', 'Rats were submitted to HS. Mean arterial pressure was reduced to 30\\u200amm Hg for 90\\u200aminutes, followed by resuscitation. Rats were randomly treated with artesunate (2.4 or 4.8\\u200amg/kg i.v.) or vehicle upon resuscitation. Four hours later, parameters of organ injury and dysfunction were assessed.', 'Artesunate attenuated the multiple organ injury and dysfunction caused by HS. Pathway analysis of RNA sequencing provided good evidence to support an effect of artesunate on the Akt-survival pathway, leading to downregulation of interleukin-1 receptor-associated kinase 1. Using Western blot analysis, we confirmed that treatment of HS rats with artesunate enhanced the phosphorylation (activation) of Protein kinase B (Akt) and endothelial nitric oxide synthase and the phosphorylation (inhibition) of glycogen synthase kinase-3β (GSK-3β). Moreover, artesunate attenuated the HS-induced activation of nuclear factor kappa B and reduced the expression of proinflammatory proteins (inducible nitric oxide synthase, tumor necrosis factor-α, and interleukin 6).'], 'labels': ['OBJECTIVE', 'BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,858,687 |
Do iGF-Binding Proteins in Type-1 Diabetes Are More Severely Altered in the Presence of Complications?
|
{
"contexts": [
"Reduced levels of free and total insulin-like growth factor 1 (IGF-I) have been observed in type-1 diabetes (T1D) patients. The bioavailability of IGF-I from the circulation to the target cells is controlled by multifunctional IGF-binding proteins (IGFBPs). The aim of this study was to profile serum IGFBPs in T1D and its complications.",
"We measured the IGFBP levels in 3662 patient serum samples from our ongoing Phenome and Genome of Diabetes Autoimmunity (PAGODA) study. IGFBP levels of four different groups of T1D patients (with 0, 1, 2, and ≥3 complications) were compared with healthy controls.",
"Three serum IGFBPs (IGFBP-1, -2, and -6) are significantly higher in T1D patients, and these alterations are greater in the presence of diabetic complications. IGFBP-3 is lower in patients with diabetic complications. Analyses using quintiles revealed that risk of T1D complications increases with increasing concentrations of IGFBP-2 (fifth quintile ORs: 18-60, p < 10(-26)), IGFBP-1 (fifth quintile ORs: 8-20, p < 10(-15)), and IGFBP-6 (fifth quintile ORs: 3-148, p < 10(-3)). IGFBP-3 has a negative association with T1D complications (fifth quintile ORs: 0.12-0.25, p < 10(-5))."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": []
}
|
We found that elevated serum levels of IGFBP-1, -2, and -6 were associated with T1D, and its complications and IGFBP-3 level was found to be decreased in T1D with complications. Given the known role of these IGFBPs, the overall impact of these alterations suggests a negative effect on IGF signaling.
|
yes
|
[
{
"from": "human",
"value": "Question: Do iGF-Binding Proteins in Type-1 Diabetes Are More Severely Altered in the Presence of Complications?\nContext: {'contexts': ['Reduced levels of free and total insulin-like growth factor 1 (IGF-I) have been observed in type-1 diabetes (T1D) patients. The bioavailability of IGF-I from the circulation to the target cells is controlled by multifunctional IGF-binding proteins (IGFBPs). The aim of this study was to profile serum IGFBPs in T1D and its complications.', 'We measured the IGFBP levels in 3662 patient serum samples from our ongoing Phenome and Genome of Diabetes Autoimmunity (PAGODA) study. IGFBP levels of four different groups of T1D patients (with 0, 1, 2, and ≥3 complications) were compared with healthy controls.', 'Three serum IGFBPs (IGFBP-1, -2, and -6) are significantly higher in T1D patients, and these alterations are greater in the presence of diabetic complications. IGFBP-3 is lower in patients with diabetic complications. Analyses using quintiles revealed that risk of T1D complications increases with increasing concentrations of IGFBP-2 (fifth quintile ORs: 18-60, p\\u2009<\\u200910(-26)), IGFBP-1 (fifth quintile ORs: 8-20, p\\u2009<\\u200910(-15)), and IGFBP-6 (fifth quintile ORs: 3-148, p\\u2009<\\u200910(-3)). IGFBP-3 has a negative association with T1D complications (fifth quintile ORs: 0.12-0.25, p\\u2009<\\u200910(-5)).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,879,229 |
Does endothelial Mineralocorticoid Receptor mediate Diet-Induced Aortic Stiffness in Females?
|
{
"contexts": [
"Enhanced activation of the mineralocorticoid receptors (MRs) in cardiovascular tissues increases oxidative stress, maladaptive immune responses, and inflammation with associated functional vascular abnormalities. We previously demonstrated that consumption of a Western diet (WD) for 16 weeks results in aortic stiffening, and that these abnormalities were prevented by systemic MR blockade in female mice. However, the cell-specific role of endothelial cell MR (ECMR) in these maladaptive vascular effects has not been explored.",
"We hypothesized that specific deletion of the ECMR would prevent WD-induced increases in endothelial sodium channel activation, reductions in bioavailable nitric oxide, increased vascular remodeling, and associated increases in vascular stiffness in females.",
"Four-week-old female ECMR knockout and wild-type mice were fed either mouse chow or WD for 16 weeks. WD feeding resulted in aortic stiffness and endothelial dysfunction as determined in vivo by pulse wave velocity and ex vivo by atomic force microscopy, and wire and pressure myography. The WD-induced aortic stiffness was associated with enhanced endothelial sodium channel activation, attenuated endothelial nitric oxide synthase activation, increased oxidative stress, a proinflammatory immune response and fibrosis. Conversely, cell-specific ECMR deficiency prevented WD-induced aortic fibrosis and stiffness in conjunction with reductions in endothelial sodium channel activation, oxidative stress and macrophage proinflammatory polarization, restoration of endothelial nitric oxide synthase activation."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Animals",
"Aorta",
"Diet, Western",
"Endothelium, Vascular",
"Female",
"Mice",
"Mice, Knockout",
"Receptors, Mineralocorticoid",
"Vascular Stiffness"
]
}
|
Increased ECMR signaling associated with consumption of a WD plays a key role in endothelial sodium channel activation, reduced nitric oxide production, oxidative stress, and inflammation that lead to aortic remodeling and stiffness in female mice.
|
yes
|
[
{
"from": "human",
"value": "Question: Does endothelial Mineralocorticoid Receptor mediate Diet-Induced Aortic Stiffness in Females?\nContext: {'contexts': ['Enhanced activation of the mineralocorticoid receptors (MRs) in cardiovascular tissues increases oxidative stress, maladaptive immune responses, and inflammation with associated functional vascular abnormalities. We previously demonstrated that consumption of a Western diet (WD) for 16 weeks results in aortic stiffening, and that these abnormalities were prevented by systemic MR blockade in female mice. However, the cell-specific role of endothelial cell MR (ECMR) in these maladaptive vascular effects has not been explored.', 'We hypothesized that specific deletion of the ECMR would prevent WD-induced increases in endothelial sodium channel activation, reductions in bioavailable nitric oxide, increased vascular remodeling, and associated increases in vascular stiffness in females.', 'Four-week-old female ECMR knockout and wild-type mice were fed either mouse chow or WD for 16 weeks. WD feeding resulted in aortic stiffness and endothelial dysfunction as determined in vivo by pulse wave velocity and ex vivo by atomic force microscopy, and wire and pressure myography. The WD-induced aortic stiffness was associated with enhanced endothelial sodium channel activation, attenuated endothelial nitric oxide synthase activation, increased oxidative stress, a proinflammatory immune response and fibrosis. Conversely, cell-specific ECMR deficiency prevented WD-induced aortic fibrosis and stiffness in conjunction with reductions in endothelial sodium channel activation, oxidative stress and macrophage proinflammatory polarization, restoration of endothelial nitric oxide synthase activation.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'RESULTS'], 'meshes': ['Animals', 'Aorta', 'Diet, Western', 'Endothelium, Vascular', 'Female', 'Mice', 'Mice, Knockout', 'Receptors, Mineralocorticoid', 'Vascular Stiffness']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,865,131 |
Does dexmedetomidine post-treatment induce neuroprotection via activation of extracellular signal-regulated kinase in rats with subarachnoid haemorrhage?
|
{
"contexts": [
"Dexmedetomidine, a sedative agent, provides neuroprotection when administered during or before brain ischaemia. This study was designed to determine whether dexmedetomidine post-treatment induces neuroprotection against subarachnoid haemorrhage (SAH) and the mechanisms for this effect.",
"Subarachnoid haemorrhage was induced by endovascular perforation to the junction of the right middle and anterior cerebral arteries in adult rats. Dexmedetomidine was applied immediately or 2 h after onset of SAH. Neurological outcome was evaluated 2 days after SAH. Right frontal cortex area 1 was harvested 24 h after SAH for western blotting.",
"Subarachnoid haemorrhage reduced neurological scores and increased brain oedema and blood-brain barrier permeability. These effects were attenuated by dexmedetomidine post-treatment. Neuroprotection by dexmedetomidine was abolished by PD98095, an inhibitor of extracellular signal-regulated kinase (ERK) activation. Phospho-ERK, the activated form of ERK, was increased by dexmedetomidine; this activation was inhibited by PD98095."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Analgesics, Non-Narcotic",
"Animals",
"Blood-Brain Barrier",
"Blotting, Western",
"Dexmedetomidine",
"Disease Models, Animal",
"Extracellular Signal-Regulated MAP Kinases",
"Male",
"Neuroprotection",
"Neuroprotective Agents",
"Rats",
"Rats, Sprague-Dawley",
"Subarachnoid Hemorrhage"
]
}
|
Dexmedetomidine post-treatment provides neuroprotection against SAH. This effect appears to be mediated by ERK.
|
yes
|
[
{
"from": "human",
"value": "Question: Does dexmedetomidine post-treatment induce neuroprotection via activation of extracellular signal-regulated kinase in rats with subarachnoid haemorrhage?\nContext: {'contexts': ['Dexmedetomidine, a sedative agent, provides neuroprotection when administered during or before brain ischaemia. This study was designed to determine whether dexmedetomidine post-treatment induces neuroprotection against subarachnoid haemorrhage (SAH) and the mechanisms for this effect.', 'Subarachnoid haemorrhage was induced by endovascular perforation to the junction of the right middle and anterior cerebral arteries in adult rats. Dexmedetomidine was applied immediately or 2 h after onset of SAH. Neurological outcome was evaluated 2 days after SAH. Right frontal cortex area 1 was harvested 24 h after SAH for western blotting.', 'Subarachnoid haemorrhage reduced neurological scores and increased brain oedema and blood-brain barrier permeability. These effects were attenuated by dexmedetomidine post-treatment. Neuroprotection by dexmedetomidine was abolished by PD98095, an inhibitor of extracellular signal-regulated kinase (ERK) activation. Phospho-ERK, the activated form of ERK, was increased by dexmedetomidine; this activation was inhibited by PD98095.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Analgesics, Non-Narcotic', 'Animals', 'Blood-Brain Barrier', 'Blotting, Western', 'Dexmedetomidine', 'Disease Models, Animal', 'Extracellular Signal-Regulated MAP Kinases', 'Male', 'Neuroprotection', 'Neuroprotective Agents', 'Rats', 'Rats, Sprague-Dawley', 'Subarachnoid Hemorrhage']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,864,664 |
Is stress urinary incontinence highly prevalent in recreationally active women attending gyms or exercise classes?
|
{
"contexts": [
"The purpose of this study was to determine the prevalence of stress urinary incontinence (SUI) in recreationally active women attending gyms or exercise classes.",
"Data were collected on the frequency and severity of incontinence and the prevalence of SUI risk factors; screening for PFM dysfunction in a fitness appraisal; symptom modification strategies; knowledge of pelvic floor muscle (PFM) exercises and the Pelvic Floor First (PFF) initiative. Three hundred and sixty-one women aged 18-83 who attended exercise classes or gyms in Western Australia were surveyed.",
"Nearly half (49.3 %) of participants reported SUI, the majority of whom slight or moderate leakage. Ninety-six per cent reported at least one SUI risk factor, with the mean being 2.7 (SD = 1.4). Almost all women surveyed had heard of PFM exercises (97.2 %), but only 15.2 % of participants were screened for PFM dysfunction in a fitness appraisal. Forty-three per cent reported that a fitness instructor cued PFM activation during a workout. Less than 1 in 10 (9.7 %) of the women surveyed had heard about the PFF initiative."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Aged",
"Aged, 80 and over",
"Exercise",
"Exercise Test",
"Female",
"Humans",
"Middle Aged",
"Pelvic Floor",
"Prevalence",
"Recreation",
"Risk Factors",
"Surveys and Questionnaires",
"Urinary Incontinence, Stress",
"Western Australia",
"Young Adult"
]
}
|
Urinary incontinence is common in women attending gyms or exercise classes, but is rarely screened for. More education is required to encourage fitness leaders to screen exercise participants and to provide PFM-'friendly" modifications.
|
yes
|
[
{
"from": "human",
"value": "Question: Is stress urinary incontinence highly prevalent in recreationally active women attending gyms or exercise classes?\nContext: {'contexts': ['The purpose of this study was to determine the prevalence of stress urinary incontinence (SUI) in recreationally active women attending gyms or exercise classes.', 'Data were collected on the frequency and severity of incontinence and the prevalence of SUI risk factors; screening for PFM dysfunction in a fitness appraisal; symptom modification strategies; knowledge of pelvic floor muscle (PFM) exercises and the Pelvic Floor First (PFF) initiative. Three hundred and sixty-one women aged 18-83 who attended exercise classes or gyms in Western Australia were surveyed.', 'Nearly half (49.3\\xa0%) of participants reported SUI, the majority of whom slight or moderate leakage. Ninety-six per cent reported at least one SUI risk factor, with the mean being 2.7 (SD\\u2009=\\u20091.4). Almost all women surveyed had heard of PFM exercises (97.2\\xa0%), but only 15.2\\xa0% of participants were screened for PFM dysfunction in a fitness appraisal. Forty-three per cent reported that a fitness instructor cued PFM activation during a workout. Less than 1 in 10 (9.7\\xa0%) of the women surveyed had heard about the PFF initiative.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Aged', 'Aged, 80 and over', 'Exercise', 'Exercise Test', 'Female', 'Humans', 'Middle Aged', 'Pelvic Floor', 'Prevalence', 'Recreation', 'Risk Factors', 'Surveys and Questionnaires', 'Urinary Incontinence, Stress', 'Western Australia', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,857,418 |
Does comparative transcriptome profiling of the injured zebrafish and mouse hearts identify miRNA-dependent repair pathways?
|
{
"contexts": [
"The adult mammalian heart has poor regenerative capacity. In contrast, the zebrafish heart retains a robust capacity for regeneration into adulthood. These distinct responses are consequences of a differential utilization of evolutionary-conserved gene regulatory networks in the damaged heart. To systematically identify miRNA-dependent networks controlling cardiac repair following injury, we performed comparative gene and miRNA profiling of the cardiac transcriptome in adult mice and zebrafish.",
"Using an integrated approach, we show that 45 miRNA-dependent networks, involved in critical biological pathways, are differentially modulated in the injured zebrafish vs. mouse hearts. We study, more particularly, the miR-26a-dependent response. Therefore, miR-26a is down-regulated in the fish heart after injury, whereas its expression remains constant in the mouse heart. Targets of miR-26a involve activators of the cell cycle and Ezh2, a component of the polycomb repressive complex 2 (PRC2). Importantly, PRC2 exerts repressive functions on negative regulators of the cell cycle. In cultured neonatal cardiomyocytes, inhibition of miR-26a stimulates, therefore, cardiomyocyte proliferation. Accordingly, miR-26a knockdown prolongs the proliferative window of cardiomyocytes in the post-natal mouse heart."
],
"labels": [
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Animals",
"Cell Cycle",
"Cell Proliferation",
"Gene Expression Profiling",
"Gene Regulatory Networks",
"Mice, Inbred C57BL",
"MicroRNAs",
"Myocytes, Cardiac",
"Regeneration",
"Wound Healing",
"Zebrafish"
]
}
|
This novel strategy identifies a series of miRNAs and associated pathways, in particular miR-26a, which represent attractive therapeutic targets for inducing repair in the injured heart.
|
yes
|
[
{
"from": "human",
"value": "Question: Does comparative transcriptome profiling of the injured zebrafish and mouse hearts identify miRNA-dependent repair pathways?\nContext: {'contexts': ['The adult mammalian heart has poor regenerative capacity. In contrast, the zebrafish heart retains a robust capacity for regeneration into adulthood. These distinct responses are consequences of a differential utilization of evolutionary-conserved gene regulatory networks in the damaged heart. To systematically identify miRNA-dependent networks controlling cardiac repair following injury, we performed comparative gene and miRNA profiling of the cardiac transcriptome in adult mice and zebrafish.', 'Using an integrated approach, we show that 45 miRNA-dependent networks, involved in critical biological pathways, are differentially modulated in the injured zebrafish vs. mouse hearts. We study, more particularly, the miR-26a-dependent response. Therefore, miR-26a is down-regulated in the fish heart after injury, whereas its expression remains constant in the mouse heart. Targets of miR-26a involve activators of the cell cycle and Ezh2, a component of the polycomb repressive complex 2 (PRC2). Importantly, PRC2 exerts repressive functions on negative regulators of the cell cycle. In cultured neonatal cardiomyocytes, inhibition of miR-26a stimulates, therefore, cardiomyocyte proliferation. Accordingly, miR-26a knockdown prolongs the proliferative window of cardiomyocytes in the post-natal mouse heart.'], 'labels': ['OBJECTIVE', 'RESULTS'], 'meshes': ['Animals', 'Cell Cycle', 'Cell Proliferation', 'Gene Expression Profiling', 'Gene Regulatory Networks', 'Mice, Inbred C57BL', 'MicroRNAs', 'Myocytes, Cardiac', 'Regeneration', 'Wound Healing', 'Zebrafish']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,865,074 |
Does c-reactive protein increase with gestational age during pregnancy among Chinese women?
|
{
"contexts": [
"To examine the concentration of C-reactive protein (CRP) in relation to gestational weeks during pregnancy among Chinese women.",
"From a randomized control trial of prenatal supplementation with folic acid, iron-folic acid, and multiple micronutrients in China, we examined 834 pregnant women with CRP measured initially between 5 and 20 weeks and at follow-up between 28 and 32 weeks gestation. We calculated and plotted CRP geometric means by gestational weeks. The same analysis was repeated for women who had normal pregnancies (624 women) by excluding women with stillbirth, preterm, small for gestational age, body mass index <18.5 kg/m(2) or >30 kg/m(2) at enrollment, and hypertension or anemia during pregnancy.",
"We observed a significant positive trend between log-transformed CRP and gestational age from 5 to 20 weeks and from 28 to 32 weeks both in the full sample and in the subset of women who had normal pregnancies. CRP geometric mean was 0.81 mg/l at 5-7 weeks of gestation, 2.85 mg/l at 19-20 weeks of gestation, and 3.89 mg/l at 32 weeks of gestation. A similar increasing trend in the CRP median or percentage of elevated CRP were also observed."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"C-Reactive Protein",
"China",
"Dietary Supplements",
"Female",
"Folic Acid",
"Gestational Age",
"Humans",
"Iron",
"Micronutrients",
"Pregnancy",
"Young Adult"
]
}
|
We concluded that CRP increased with gestational age among healthy Chinese women who delivered healthy infants. Am. J. Hum. Biol. 28:574-579, 2016. © 2016 Wiley Periodicals, Inc.
|
yes
|
[
{
"from": "human",
"value": "Question: Does c-reactive protein increase with gestational age during pregnancy among Chinese women?\nContext: {'contexts': ['To examine the concentration of C-reactive protein (CRP) in relation to gestational weeks during pregnancy among Chinese women.', 'From a randomized control trial of prenatal supplementation with folic acid, iron-folic acid, and multiple micronutrients in China, we examined 834 pregnant women with CRP measured initially between 5 and 20 weeks and at follow-up between 28 and 32 weeks gestation. We calculated and plotted CRP geometric means by gestational weeks. The same analysis was repeated for women who had normal pregnancies (624 women) by excluding women with stillbirth, preterm, small for gestational age, body mass index <18.5 kg/m(2) or >30 kg/m(2) at enrollment, and hypertension or anemia during pregnancy.', 'We observed a significant positive trend between log-transformed CRP and gestational age from 5 to 20 weeks and from 28 to 32 weeks both in the full sample and in the subset of women who had normal pregnancies. CRP geometric mean was 0.81 mg/l at 5-7 weeks of gestation, 2.85 mg/l at 19-20 weeks of gestation, and 3.89 mg/l at 32 weeks of gestation. A similar increasing trend in the CRP median or percentage of elevated CRP were also observed.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'C-Reactive Protein', 'China', 'Dietary Supplements', 'Female', 'Folic Acid', 'Gestational Age', 'Humans', 'Iron', 'Micronutrients', 'Pregnancy', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,865,506 |
Are pectic polysaccharides attacked by hydroxyl radicals in ripening fruit : evidence from a fluorescent fingerprinting method?
|
{
"contexts": [
"Many fruits soften during ripening, which is important commercially and in rendering the fruit attractive to seed-dispersing animals. Cell-wall polysaccharide hydrolases may contribute to softening, but sometimes appear to be absent. An alternative hypothesis is that hydroxyl radicals ((•)OH) non-enzymically cleave wall polysaccharides. We evaluated this hypothesis by using a new fluorescent labelling procedure to 'fingerprint' (•)OH-attacked polysaccharides.",
"We tagged fruit polysaccharides with 2-(isopropylamino)-acridone (pAMAC) groups to detect (a) any mid-chain glycosulose residues formed in vivo during (•)OH action and (b) the conventional reducing termini. The pAMAC-labelled pectins were digested with Driselase, and the products resolved by high-voltage electrophoresis and high-pressure liquid chromatography.",
"Strawberry, pear, mango, banana, apple, avocado, Arbutus unedo, plum and nectarine pectins all yielded several pAMAC-labelled products. GalA-pAMAC (monomeric galacturonate, labelled with pAMAC at carbon-1) was produced in all species, usually increasing during fruit softening. The six true fruits also gave pAMAC·UA-GalA disaccharides (where pAMAC·UA is an unspecified uronate, labelled at a position other than carbon-1), with yields increasing during softening. Among false fruits, apple and strawberry gave little pAMAC·UA-GalA; pear produced it transiently."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Chromatography, High Pressure Liquid",
"Dimerization",
"Electrophoresis",
"Fluorescent Dyes",
"Fruit",
"Fungal Proteins",
"Glycoside Hydrolases",
"Hydroxyl Radical",
"Pectins",
"Plants",
"Polysaccharides",
"Staining and Labeling"
]
}
|
GalA-pAMAC arises from pectic reducing termini, formed by any of three proposed chain-cleaving agents ((•)OH, endopolygalacturonase and pectate lyase), any of which could cause its ripening-related increase. In contrast, pAMAC·UA-GalA conjugates are diagnostic of mid-chain oxidation of pectins by (•)OH. The evidence shows that (•)OH radicals do indeed attack fruit cell wall polysaccharides non-enzymically during softening in vivo. This applies much more prominently to drupes and berries (true fruits) than to false fruits (swollen receptacles). (•)OH radical attack on polysaccharides is thus predominantly a feature of ovary-wall tissue.
|
yes
|
[
{
"from": "human",
"value": "Question: Are pectic polysaccharides attacked by hydroxyl radicals in ripening fruit : evidence from a fluorescent fingerprinting method?\nContext: {'contexts': [\"Many fruits soften during ripening, which is important commercially and in rendering the fruit attractive to seed-dispersing animals. Cell-wall polysaccharide hydrolases may contribute to softening, but sometimes appear to be absent. An alternative hypothesis is that hydroxyl radicals ((•)OH) non-enzymically cleave wall polysaccharides. We evaluated this hypothesis by using a new fluorescent labelling procedure to 'fingerprint' (•)OH-attacked polysaccharides.\", 'We tagged fruit polysaccharides with 2-(isopropylamino)-acridone (pAMAC) groups to detect (a) any mid-chain glycosulose residues formed in vivo during (•)OH action and (b) the conventional reducing termini. The pAMAC-labelled pectins were digested with Driselase, and the products resolved by high-voltage electrophoresis and high-pressure liquid chromatography.', 'Strawberry, pear, mango, banana, apple, avocado, Arbutus unedo, plum and nectarine pectins all yielded several pAMAC-labelled products. GalA-pAMAC (monomeric galacturonate, labelled with pAMAC at carbon-1) was produced in all species, usually increasing during fruit softening. The six true fruits also gave pAMAC·UA-GalA disaccharides (where pAMAC·UA is an unspecified uronate, labelled at a position other than carbon-1), with yields increasing during softening. Among false fruits, apple and strawberry gave little pAMAC·UA-GalA; pear produced it transiently.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Chromatography, High Pressure Liquid', 'Dimerization', 'Electrophoresis', 'Fluorescent Dyes', 'Fruit', 'Fungal Proteins', 'Glycoside Hydrolases', 'Hydroxyl Radical', 'Pectins', 'Plants', 'Polysaccharides', 'Staining and Labeling']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,859,658 |
Does metformin Treatment Affect Testicular Size in Offspring Born to Mothers with Gestational Diabetes?
|
{
"contexts": [
"Studies in rodents suggest that metformin treatment during pregnancy may have harmful effects on testicular development in offspring. Our aim was to determine whether metformin treatment of gestational diabetes mellitus (GDM) affects testicular size in male offspring.",
"We compared the testicular size in prepubertal boys born to mothers who participated in a randomized controlled trial (RCT) comparing metformin with insulin in the treatment of GDM. Twenty-five (42.4% of invited) and 27 (52.9% of invited) boys whose mothers had been treated with metformin or insulin, respectively, participated in the study. Testicular size was measured by a ruler, an orchidometer, and by ultrasonography at the age of 33 to 85 months.",
"The mean age of the boys was 60 months at the time of examination, and did not differ between the metformin and insulin group (p = 0.88). There was no difference in testicular size between the boys in the two groups (p always ≥ 0.40), and there were no significant differences in height, weight, BMI, BMI z-score, or waist-to-hip ratio (WHR) between the boys in the groups."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Child",
"Child, Preschool",
"Diabetes, Gestational",
"Female",
"Humans",
"Hypoglycemic Agents",
"Insulin",
"Male",
"Metformin",
"Organ Size",
"Pregnancy",
"Prenatal Exposure Delayed Effects",
"Testis",
"Ultrasonography"
]
}
|
Prepubertal testicular size did not differ between offspring born to metformin-treated mothers and those born to insulin-treated mothers.
|
no
|
[
{
"from": "human",
"value": "Question: Does metformin Treatment Affect Testicular Size in Offspring Born to Mothers with Gestational Diabetes?\nContext: {'contexts': ['Studies in rodents suggest that metformin treatment during pregnancy may have harmful effects on testicular development in offspring. Our aim was to determine whether metformin treatment of gestational diabetes mellitus (GDM) affects testicular size in male offspring.', 'We compared the testicular size in prepubertal boys born to mothers who participated in a randomized controlled trial (RCT) comparing metformin with insulin in the treatment of GDM. Twenty-five (42.4% of invited) and 27 (52.9% of invited) boys whose mothers had been treated with metformin or insulin, respectively, participated in the study. Testicular size was measured by a ruler, an orchidometer, and by ultrasonography at the age of 33 to 85 months.', 'The mean age of the boys was 60 months at the time of examination, and did not differ between the metformin and insulin group (p = 0.88). There was no difference in testicular size between the boys in the two groups (p always ≥ 0.40), and there were no significant differences in height, weight, BMI, BMI z-score, or waist-to-hip ratio (WHR) between the boys in the groups.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Child', 'Child, Preschool', 'Diabetes, Gestational', 'Female', 'Humans', 'Hypoglycemic Agents', 'Insulin', 'Male', 'Metformin', 'Organ Size', 'Pregnancy', 'Prenatal Exposure Delayed Effects', 'Testis', 'Ultrasonography']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
] |
26,874,906 |
Does interval aerobic training combined with strength-endurance exercise improve metabolic markers beyond caloric restriction in Zucker rats?
|
{
"contexts": [
"To investigate the effects of interval aerobic training combined with strength-endurance exercise (IASE) and caloric restriction (CR) on body composition, glycaemic and lipid profile and inflammatory markers.",
"Thirty-two Zucker diabetic fatty rats were randomised into 4 groups (sedentary + CR; sedentary + adlibitum; IASE + CR; and IASE + adlibitum). Training groups conducted an IASE programme in the same session, 5 days/week for 2 months. Body weight, fat and muscle mass and body water were measured using a body composition analyser. Plasma total, LDL and HDL cholesterol, phospholipids, triglycerides, insulin, adiponectin, tumour necrosis factor alpha, interleukin 1 and 10 were measured. Blood fasting and postprandial glucose were assessed. Body weight was lower in the CR compared to the adlibitum groups (p < 0.001). Fat mass was lower in the CR compared to the adlibitum (p < 0.05) and in the IASE compared to the sedentary groups (p < 0.001), but IASE increased lean mass (p < 0.001). Triglycerides were lower in the CR compared to the adlibitum groups (p < 0.001) whereas total and LDL-cholesterol and fasting glucose were reduced only in the IASE groups (all, p < 0.001). Phospholipids decreased in the CR compared to the adlibitum (p < 0.05) and the IASE compared to the sedentary groups (p < 0.001). The area under the curve after oral glucose tolerance test, insulin and homoeostatic model assessment were lower in the IASE and the CR compared to the sedentary and adlibitum groups, respectively (all, p < 0.001). Adiponectin was lower in the CR groups (p < 0.001)."
],
"labels": [
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Animal Nutritional Physiological Phenomena",
"Animals",
"Biomarkers",
"Blood Glucose",
"Caloric Restriction",
"Disease Models, Animal",
"Exercise Therapy",
"Inflammation Mediators",
"Lipids",
"Male",
"Metabolic Syndrome",
"Muscle Strength",
"Muscle, Skeletal",
"Nutritional Status",
"Obesity",
"Physical Endurance",
"Rats, Zucker",
"Resistance Training",
"Time Factors",
"Weight Loss"
]
}
|
Overall, IASE as well as CR were both useful interventions, especially when combined. However, IASE showed greater improvements on body composition, inflammatory and glycaemic profile than CR did.
|
yes
|
[
{
"from": "human",
"value": "Question: Does interval aerobic training combined with strength-endurance exercise improve metabolic markers beyond caloric restriction in Zucker rats?\nContext: {'contexts': ['To investigate the effects of interval aerobic training combined with strength-endurance exercise (IASE) and caloric restriction (CR) on body composition, glycaemic and lipid profile and inflammatory markers.', 'Thirty-two Zucker diabetic fatty rats were randomised into 4 groups (sedentary\\xa0+\\xa0CR; sedentary\\xa0+\\xa0adlibitum; IASE\\xa0+\\xa0CR; and IASE\\xa0+\\xa0adlibitum). Training groups conducted an IASE programme in the same session, 5 days/week for 2 months. Body weight, fat and muscle mass and body water were measured using a body composition analyser. Plasma total, LDL and HDL cholesterol, phospholipids, triglycerides, insulin, adiponectin, tumour necrosis factor alpha, interleukin 1 and 10 were measured. Blood fasting and postprandial glucose were assessed. Body weight was lower in the CR compared to the adlibitum groups (p\\xa0<\\xa00.001). Fat mass was lower in the CR compared to the adlibitum (p\\xa0<\\xa00.05) and in the IASE compared to the sedentary groups (p\\xa0<\\xa00.001), but IASE increased lean mass (p\\xa0<\\xa00.001). Triglycerides were lower in the CR compared to the adlibitum groups (p\\xa0<\\xa00.001) whereas total and LDL-cholesterol and fasting glucose were reduced only in the IASE groups (all, p\\xa0<\\xa00.001). Phospholipids decreased in the CR compared to the adlibitum (p\\xa0<\\xa00.05) and the IASE compared to the sedentary groups (p\\xa0<\\xa00.001). The area under the curve after oral glucose tolerance test, insulin and homoeostatic model assessment were lower in the IASE and the CR compared to the sedentary and adlibitum groups, respectively (all, p\\xa0<\\xa00.001). Adiponectin was lower in the CR groups (p\\xa0<\\xa00.001).'], 'labels': ['OBJECTIVE', 'RESULTS'], 'meshes': ['Animal Nutritional Physiological Phenomena', 'Animals', 'Biomarkers', 'Blood Glucose', 'Caloric Restriction', 'Disease Models, Animal', 'Exercise Therapy', 'Inflammation Mediators', 'Lipids', 'Male', 'Metabolic Syndrome', 'Muscle Strength', 'Muscle, Skeletal', 'Nutritional Status', 'Obesity', 'Physical Endurance', 'Rats, Zucker', 'Resistance Training', 'Time Factors', 'Weight Loss']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,879,446 |
Is high melphalan exposure associated with improved overall survival in myeloma patients receiving high dose melphalan and autologous transplantation?
|
{
"contexts": [
"High dose melphalan (HDM) and autologous stem cell transplantation (ASCT) retains a central role in the treatment of myeloma. The aim of this study was to determine whether HDM exposure (area under the concentration vs. time curve, AUC), is significantly associated with transplant outcomes.",
"Melphalan concentrations were measured in six to 11 plasma samples collected after HDM (median 192 mg m(-) (2) ) to determine melphalan AUC for a total of 114 patients. Binary logistic regression was used to assess whether melphalan AUC was associated with severe (≥ grade 3) oral mucositis. Multivariate Cox regression was used to assess whether melphalan AUC was significantly associated with time to progression, progression-free survival and overall survival (OS).",
"Melphalan AUC ranged from 4.9 to 24.6 mg l(-1) h, median 12.84 mg l(-1) h. Melphalan AUC above the median was a risk factor for severe mucositis (HR 1.21, 95% CI 1.06, 1.38, P = 0.004) but was also associated with significantly improved overall survival (OS) (HR 0.40, 95% CI 0.20, 0.81, P = 0.001), with an estimated median survival of 8.50 years vs. 5.38 years for high vs. low AUC groups. Multivariate analysis did not identify melphalan AUC as being significantly associated with time to progression or progression-free survival."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Antineoplastic Agents, Alkylating",
"Area Under Curve",
"Combined Modality Therapy",
"Disease-Free Survival",
"Female",
"Half-Life",
"Humans",
"Logistic Models",
"Male",
"Melphalan",
"Middle Aged",
"Multiple Myeloma",
"Multivariate Analysis",
"Prospective Studies",
"Risk Factors",
"Stem Cell Transplantation",
"Survival Rate",
"Transplantation, Autologous",
"Treatment Outcome"
]
}
|
This large scale pharmacodynamic analysis of HDM demonstrates that high melphalan exposure is associated with improved survival, with an acceptable increase in transplant toxicity. These results suggest studies targeting a higher AUC are warranted in patients undergoing HDM and ASCT for myeloma.
|
yes
|
[
{
"from": "human",
"value": "Question: Is high melphalan exposure associated with improved overall survival in myeloma patients receiving high dose melphalan and autologous transplantation?\nContext: {'contexts': ['High dose melphalan (HDM) and autologous stem cell transplantation (ASCT) retains a central role in the treatment of myeloma. The aim of this study was to determine whether HDM exposure (area under the concentration vs. time curve, AUC), is significantly associated with transplant outcomes.', 'Melphalan concentrations were measured in six to 11 plasma samples collected after HDM (median 192\\xa0mg\\xa0m(-) (2) ) to determine melphalan AUC for a total of 114 patients. Binary logistic regression was used to assess whether melphalan AUC was associated with severe (≥ grade 3) oral mucositis. Multivariate Cox regression was used to assess whether melphalan AUC was significantly associated with time to progression, progression-free survival and overall survival (OS).', 'Melphalan AUC ranged from 4.9 to 24.6\\xa0mg\\xa0l(-1) \\xa0h, median 12.84\\xa0mg\\xa0l(-1) h. Melphalan AUC above the median was a risk factor for severe mucositis (HR 1.21, 95% CI 1.06, 1.38, P\\xa0=\\xa00.004) but was also associated with significantly improved overall survival (OS) (HR 0.40, 95% CI 0.20, 0.81, P\\xa0=\\xa00.001), with an estimated median survival of 8.50\\xa0years vs. 5.38\\xa0years for high vs. low AUC groups. Multivariate analysis did not identify melphalan AUC as being significantly associated with time to progression or progression-free survival.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Antineoplastic Agents, Alkylating', 'Area Under Curve', 'Combined Modality Therapy', 'Disease-Free Survival', 'Female', 'Half-Life', 'Humans', 'Logistic Models', 'Male', 'Melphalan', 'Middle Aged', 'Multiple Myeloma', 'Multivariate Analysis', 'Prospective Studies', 'Risk Factors', 'Stem Cell Transplantation', 'Survival Rate', 'Transplantation, Autologous', 'Treatment Outcome']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,853,697 |
Does a cumulative genetic risk score predict progression in Parkinson 's disease?
|
{
"contexts": [
"The contribution of genetic variability to clinical heterogeneity in Parkinson's disease is insufficiently understood. We aimed to investigate the effect of cumulative genetic risk on clinical outcomes.",
"In a single-center study of 336 patients we genotyped 19 independent susceptibility variants identified in genome-wide association studies of Parkinson's disease. We tested for association between a cumulative genetic risk score and 3 outcome measures: survival, time until progression to Hoehn and Yahr stage 3, and Unified Parkinson's Disease Rating Scale motor score severity.",
"Genetic risk score was significantly associated with time from diagnosis to Hoehn and Yahr stage 3 in a Cox regression model (P = 0.010). We observed no clear association for the other outcomes."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": []
}
|
We present results linking cumulative genetic risk to a motor outcome in Parkinson's disease. Our findings provide a valuable starting point for future large-scale efforts to map the genetic determinants of phenotypic variability.
|
yes
|
[
{
"from": "human",
"value": "Question: Does a cumulative genetic risk score predict progression in Parkinson 's disease?\nContext: {'contexts': [\"The contribution of genetic variability to clinical heterogeneity in Parkinson's disease is insufficiently understood. We aimed to investigate the effect of cumulative genetic risk on clinical outcomes.\", \"In a single-center study of 336 patients we genotyped 19 independent susceptibility variants identified in genome-wide association studies of Parkinson's disease. We tested for association between a cumulative genetic risk score and 3 outcome measures: survival, time until progression to Hoehn and Yahr stage 3, and Unified Parkinson's Disease Rating Scale motor score severity.\", 'Genetic risk score was significantly associated with time from diagnosis to Hoehn and Yahr stage 3 in a Cox regression model (P = 0.010). We observed no clear association for the other outcomes.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,850,874 |
Does interpersonal Violence be Associated With Increased Severity of Geriatric Facial Trauma?
|
{
"contexts": [
"The geriatric population is rapidly increasing in number with increased demand on health care resources including those spent on the treatment of maxillofacial trauma. The purpose of this analysis was to investigate the independent and cumulative associations between potential risk factors (age, gender, mechanism of injury, drug use, and alcohol use) for and the severity of geriatric facial trauma.",
"This was a cross-sectional analysis of secondary data of geriatric (individuals aged ≥65 years) facial trauma using the Allegheny General Hospital Trauma Registry database. Data were collected for diagnosis codes that reflected facial trauma (International Classification of Diseases, Ninth Revision codes 802.0 to 802.9, 800.1 to 801.9, and 803.0 to 804.9) and specific mechanisms of injury (E810 to E819, motor vehicle traffic accidents; E880 to E888, accidental falls; and E960 to E969, injury purposely inflicted by other persons). The Facial Injury Severity Scale (FISS) is a validated measurement that was used to determine the severity of the facial trauma and calculated through analysis of the abstracted data obtained from the trauma registry and patient records. Pearson correlations, 2-way independent t test, 1-way analysis of variance, and multiple linear regression were used to test hypotheses for independent and cumulative associations between the risk factors for and the severity of geriatric facial trauma. Statistical significance was set at the P < .05 level.",
"The sample was composed of 229 patients with a mean age of 72.3 ± 4.5 years. A statistically significant association between mechanism of injury and the severity of geriatric facial trauma (P = .019) was found. Specifically, interpersonal violence (assault) was associated with the greatest facial trauma severity (FISS score, 4.2) when compared with motor vehicle collisions (FISS score, 2.2; P = .011) and falls (FISS score, 2.4; P = .016)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Accidental Falls",
"Accidents, Traffic",
"Aged",
"Aged, 80 and over",
"Cross-Sectional Studies",
"Facial Injuries",
"Female",
"Humans",
"Injury Severity Score",
"Male",
"Registries",
"Retrospective Studies",
"Violence"
]
}
|
Interpersonal violence (assault) is associated with increased severity of geriatric facial trauma compared with other risk factors.
|
yes
|
[
{
"from": "human",
"value": "Question: Does interpersonal Violence be Associated With Increased Severity of Geriatric Facial Trauma?\nContext: {'contexts': ['The geriatric population is rapidly increasing in number with increased demand on health care resources including those spent on the treatment of maxillofacial trauma. The purpose of this analysis was to investigate the independent and cumulative associations between potential risk factors (age, gender, mechanism of injury, drug use, and alcohol use) for and the severity of geriatric facial trauma.', 'This was a cross-sectional analysis of secondary data of geriatric (individuals aged ≥65\\xa0years) facial trauma using the Allegheny General Hospital Trauma Registry database. Data were collected for diagnosis codes that reflected facial trauma (International Classification of Diseases, Ninth Revision codes 802.0 to 802.9, 800.1 to 801.9, and 803.0 to 804.9) and specific mechanisms of injury (E810 to E819, motor vehicle traffic accidents; E880 to E888, accidental falls; and E960 to E969, injury purposely inflicted by other persons). The Facial Injury Severity Scale (FISS) is a validated measurement that was used to determine the severity of the facial trauma and calculated through analysis of the abstracted data obtained from the trauma registry and patient records. Pearson correlations, 2-way independent t test, 1-way analysis of variance, and multiple linear regression were used to test hypotheses for independent and cumulative associations between the risk factors for and the severity of geriatric facial trauma. Statistical significance was set at the P < .05 level.', 'The sample was composed of 229 patients with a mean age of 72.3 ± 4.5\\xa0years. A statistically significant association between mechanism of injury and the severity of geriatric facial trauma (P\\xa0= .019) was found. Specifically, interpersonal violence (assault) was associated with the greatest facial trauma severity (FISS score, 4.2) when compared with motor vehicle collisions (FISS score, 2.2; P\\xa0= .011) and falls (FISS score, 2.4; P\\xa0= .016).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Accidental Falls', 'Accidents, Traffic', 'Aged', 'Aged, 80 and over', 'Cross-Sectional Studies', 'Facial Injuries', 'Female', 'Humans', 'Injury Severity Score', 'Male', 'Registries', 'Retrospective Studies', 'Violence']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,866,578 |
Do patients with colorectal cancer associated with Lynch syndrome and MLH1 promoter hypermethylation have similar prognoses?
|
{
"contexts": [
"Mismatch repair-deficient (dMMR) colorectal cancer (CRC) is caused by Lynch syndrome (LS) in 3% and sporadic inactivation of MLH1 by hypermethylation (MLH1-hm) in 12% of cases. It is not clear whether outcomes between LS-associated and MLH1-hm CRC differ. The objective of this study was to explore differences in clinical factors and outcomes in these two groups.",
"Patients with dMMR CRC identified by immunohistochemistry staining and treated at a single institution from 1998 to 2012 were included. MLH1-hm was established with BRAF mutational analysis or hypermethylation testing. Patients' charts were accessed for information on pathology, germ-line MMR mutation testing, and clinical course.",
"A total of 143 patients had CRC associated with LS (37 patients, 26%) or MLH1-hm (106 patients, 74%). Patients with LS were younger, more often male, presented more often with stage III disease, and had more metachronous disease than patients with MLH1-hm tumors. There was no difference in cancer-specific survival (CSS) between the groups; overall survival was longer in patients with LS, but this difference was minimal after adjusting for age and stage at diagnosis."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Colorectal Neoplasms",
"Colorectal Neoplasms, Hereditary Nonpolyposis",
"DNA Methylation",
"DNA Mismatch Repair",
"Disease-Free Survival",
"Female",
"Germ-Line Mutation",
"Humans",
"Male",
"Middle Aged",
"MutL Protein Homolog 1",
"Prognosis",
"Promoter Regions, Genetic",
"Proto-Oncogene Proteins B-raf"
]
}
|
CSS did not differ in LS-associated CRC compared with MLH1-hm CRC, suggesting that they carry a similar prognosis.Genet Med 18 9, 863-868.
|
yes
|
[
{
"from": "human",
"value": "Question: Do patients with colorectal cancer associated with Lynch syndrome and MLH1 promoter hypermethylation have similar prognoses?\nContext: {'contexts': ['Mismatch repair-deficient (dMMR) colorectal cancer (CRC) is caused by Lynch syndrome (LS) in 3% and sporadic inactivation of MLH1 by hypermethylation (MLH1-hm) in 12% of cases. It is not clear whether outcomes between LS-associated and MLH1-hm CRC differ. The objective of this study was to explore differences in clinical factors and outcomes in these two groups.', \"Patients with dMMR CRC identified by immunohistochemistry staining and treated at a single institution from 1998 to 2012 were included. MLH1-hm was established with BRAF mutational analysis or hypermethylation testing. Patients' charts were accessed for information on pathology, germ-line MMR mutation testing, and clinical course.\", 'A total of 143 patients had CRC associated with LS (37 patients, 26%) or MLH1-hm (106 patients, 74%). Patients with LS were younger, more often male, presented more often with stage III disease, and had more metachronous disease than patients with MLH1-hm tumors. There was no difference in cancer-specific survival (CSS) between the groups; overall survival was longer in patients with LS, but this difference was minimal after adjusting for age and stage at diagnosis.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Colorectal Neoplasms', 'Colorectal Neoplasms, Hereditary Nonpolyposis', 'DNA Methylation', 'DNA Mismatch Repair', 'Disease-Free Survival', 'Female', 'Germ-Line Mutation', 'Humans', 'Male', 'Middle Aged', 'MutL Protein Homolog 1', 'Prognosis', 'Promoter Regions, Genetic', 'Proto-Oncogene Proteins B-raf']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,853,903 |
Are igE and FcεRI highly expressed on innate cells in psoriasis?
|
{
"contexts": [
"Although elevated serum IgE levels have been reported in psoriasis, the role of IgE in psoriasis still needs to be clarified.",
"To analyse serum total IgE levels in addition to the presence and distribution of IgE and FcεRI in psoriatic lesions, and to investigate alteration of IgE and FcεRI after successful systemic treatment.",
"Total serum IgE levels were determined using enzyme-linked immunosorbent assay. The expression and localization of IgE and FcεRI was investigated using immunohistochemistry and double immunofluorescence.",
"Elevated total serum IgE levels were found in 39% of patients with psoriasis. The levels of total serum IgE were significantly higher in male patients compared with female patients. Furthermore, total serum IgE levels decreased after successful systemic treatment. A positive correlation between IgE+ and FcεRI+ cells and a significant increase of these cells was found in psoriatic lesions when compared with normal skin. Interestingly, IgE+ and FcεRI+ cells decreased significantly after successful therapy with ustekinumab. IgE and FcεRI were coexpressed on mast cells, epidermal Langerhans cells, dermal dendritic cells, macrophages and a small number of neutrophils."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Aged",
"Aged, 80 and over",
"Child",
"Dendritic Cells",
"Female",
"Humans",
"Immunity, Innate",
"Immunoglobulin E",
"Male",
"Middle Aged",
"Psoriasis",
"Receptors, IgE",
"Skin",
"Young Adult"
]
}
|
IgE might participate in the development of psoriasis by activating FcεRI-bearing cells.
|
yes
|
[
{
"from": "human",
"value": "Question: Are igE and FcεRI highly expressed on innate cells in psoriasis?\nContext: {'contexts': ['Although elevated serum IgE levels have been reported in psoriasis, the role of IgE in psoriasis still needs to be clarified.', 'To analyse serum total IgE levels in addition to the presence and distribution of IgE and FcεRI in psoriatic lesions, and to investigate alteration of IgE and FcεRI after successful systemic treatment.', 'Total serum IgE levels were determined using enzyme-linked immunosorbent assay. The expression and localization of IgE and FcεRI was investigated using immunohistochemistry and double immunofluorescence.', 'Elevated total serum IgE levels were found in 39% of patients with psoriasis. The levels of total serum IgE were significantly higher in male patients compared with female patients. Furthermore, total serum IgE levels decreased after successful systemic treatment. A positive correlation between IgE+ and FcεRI+ cells and a significant increase of these cells was found in psoriatic lesions when compared with normal skin. Interestingly, IgE+ and FcεRI+ cells decreased significantly after successful therapy with ustekinumab. IgE and FcεRI were coexpressed on mast cells, epidermal Langerhans cells, dermal dendritic cells, macrophages and a small number of neutrophils.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Aged', 'Aged, 80 and over', 'Child', 'Dendritic Cells', 'Female', 'Humans', 'Immunity, Innate', 'Immunoglobulin E', 'Male', 'Middle Aged', 'Psoriasis', 'Receptors, IgE', 'Skin', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,858,639 |
Does thromboxane A2 Receptor Stimulation enhance Microglial Interleukin-1β and NO Biosynthesis Mediated by the Activation of ERK Pathway?
|
{
"contexts": [
"Thromboxane A2 (TXA2) receptors (TP) interact with the ligand TXA2 to induce platelet aggregation and regulate hemostasis. Recently TP-mediated signaling has been suggested to function in multiple cell types in the brain. In this report, we aim to study the expression and physiological role of TP in microglia, in particular after brain ischemia.",
"Ischemic brain sections were analyzed for TP expression. Microglial cell line and primary microglia were cultured, or neuronal cell line co-culture system was used to determine the TP mediated signaling in inflammation and microglia activation.",
"We found that the TP level was significantly increased in ipsilateral mouse brain tissue at 24 h after ischemia-reperfusion, which was also found to partly co-localize with CD11b, a marker for microglial and infiltrated monocyte/macrophage, in peri-infarct area. Immunofluorescence staining of primary microglia and microglial cell line BV2 revealed the predominant membrane distribution of TP. Conditioned culture media from TP agonist U46619-treated BV2 cells decreased neuronal SH-SY5Y cell viability and induced apoptotic morphological changes. Furthermore, U46619 enhanced IL-1β, IL-6, and iNOS mRNA expression as well as IL-1β and NO releases in BV2 cells or primary microglia. Such stimulation could be attenuated by TP antagonist SQ29548 or MEK inhibitor U0126. The dose- and time-dependent extracellular-signal-regulated kinase (ERK) phosphorylation induced by U46619 further demonstrated ERK signaling-mediated microglia activation by TP agonist."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": []
}
|
This study has shown a novel role of TP in microglia activation via the ERK signaling pathway, which provides insights for the management of neuroinflammation in diseases like cerebral infarction.
|
yes
|
[
{
"from": "human",
"value": "Question: Does thromboxane A2 Receptor Stimulation enhance Microglial Interleukin-1β and NO Biosynthesis Mediated by the Activation of ERK Pathway?\nContext: {'contexts': ['Thromboxane A2 (TXA2) receptors (TP) interact with the ligand TXA2 to induce platelet aggregation and regulate hemostasis. Recently TP-mediated signaling has been suggested to function in multiple cell types in the brain. In this report, we aim to study the expression and physiological role of TP in microglia, in particular after brain ischemia.', 'Ischemic brain sections were analyzed for TP expression. Microglial cell line and primary microglia were cultured, or neuronal cell line co-culture system was used to determine the TP mediated signaling in inflammation and microglia activation.', 'We found that the TP level was significantly increased in ipsilateral mouse brain tissue at 24 h after ischemia-reperfusion, which was also found to partly co-localize with CD11b, a marker for microglial and infiltrated monocyte/macrophage, in peri-infarct area. Immunofluorescence staining of primary microglia and microglial cell line BV2 revealed the predominant membrane distribution of TP. Conditioned culture media from TP agonist U46619-treated BV2 cells decreased neuronal SH-SY5Y cell viability and induced apoptotic morphological changes. Furthermore, U46619 enhanced IL-1β, IL-6, and iNOS mRNA expression as well as IL-1β and NO releases in BV2 cells or primary microglia. Such stimulation could be attenuated by TP antagonist SQ29548 or MEK inhibitor U0126. The dose- and time-dependent extracellular-signal-regulated kinase (ERK) phosphorylation induced by U46619 further demonstrated ERK signaling-mediated microglia activation by TP agonist.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,869,043 |
Do bone marrow-derived mesenchymal stromal cells differ in their attachment to fibronectin-derived peptides from term placenta-derived mesenchymal stromal cells?
|
{
"contexts": [
"Human mesenchymal stromal cells (MSCs) can be isolated from different sources including bone marrow and term placenta. These two populations display distinct patterns of proliferation and differentiation in vitro. Since proliferation and differentiation of cells are modulated by cell-matrix interactions, we investigated the attachment of MSCs to a set of peptide-coated surfaces and explored their interactions with peptides in suspension.",
"Human MSCs were isolated from bone marrow and term placenta and expanded. Binding of MSCs to peptides was investigated by a cell-attachment spot assay, by blocking experiments and flow cytometry. The integrin expression pattern was explored by a transcript array and corroborated by quantitative reverse transcription polymerase chain reaction and flow cytometry.",
"Expanded placenta-derived MSCs (pMSCs) attached well to surfaces coated with fibronectin-derived peptides P7, P15, and P17, whereas bone marrow-derived MSCs (bmMSCs) attached to P7, but barely to P15 and P17. The binding of bmMSCs and pMSCs to the peptides was mediated by β1 integrins. In suspension, expanded bmMSCs barely bind to P7, P13, P15, and less to P14 and P17. Ex vivo, bmMSCs failed to bind P7, but displayed a weak interaction with P13, P14, and P15. In suspension, expanded pMSCs displayed binding to many peptides, including P4, P7, P13, P14, P15, and P17. The differences observed in binding of bmMSCs and pMSCs to the peptides were associated with significant differences in expression of integrin α2-, α4-, and α6-chains."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Bone Marrow Cells",
"Cell Adhesion",
"Cells, Cultured",
"Culture Media",
"Female",
"Fibronectins",
"Humans",
"Male",
"Mesenchymal Stem Cells",
"Organ Specificity",
"Peptide Fragments",
"Placenta",
"Pregnancy"
]
}
|
Human bmMSCs and pMSCs show distinct patterns of attachment to defined peptides and maintain differences in expression of integrins in vitro. Interactions of ex vivo bmMSCs with a given peptide yield different staining patterns compared to expanded bmMSCs in suspension. Attachment of expanded MSCs to peptides on surfaces is different from interactions of expanded MSCs with peptides in suspension. Studies designed to investigate the interactions of human MSCs with peptide-augmented scaffolds or peptides in suspension must therefore regard these differences in cell-peptide interactions.
|
yes
|
[
{
"from": "human",
"value": "Question: Do bone marrow-derived mesenchymal stromal cells differ in their attachment to fibronectin-derived peptides from term placenta-derived mesenchymal stromal cells?\nContext: {'contexts': ['Human mesenchymal stromal cells (MSCs) can be isolated from different sources including bone marrow and term placenta. These two populations display distinct patterns of proliferation and differentiation in vitro. Since proliferation and differentiation of cells are modulated by cell-matrix interactions, we investigated the attachment of MSCs to a set of peptide-coated surfaces and explored their interactions with peptides in suspension.', 'Human MSCs were isolated from bone marrow and term placenta and expanded. Binding of MSCs to peptides was investigated by a cell-attachment spot assay, by blocking experiments and flow cytometry. The integrin expression pattern was explored by a transcript array and corroborated by quantitative reverse transcription polymerase chain reaction and flow cytometry.', 'Expanded placenta-derived MSCs (pMSCs) attached well to surfaces coated with fibronectin-derived peptides P7, P15, and P17, whereas bone marrow-derived MSCs (bmMSCs) attached to P7, but barely to P15 and P17. The binding of bmMSCs and pMSCs to the peptides was mediated by β1 integrins. In suspension, expanded bmMSCs barely bind to P7, P13, P15, and less to P14 and P17. Ex vivo, bmMSCs failed to bind P7, but displayed a weak interaction with P13, P14, and P15. In suspension, expanded pMSCs displayed binding to many peptides, including P4, P7, P13, P14, P15, and P17. The differences observed in binding of bmMSCs and pMSCs to the peptides were associated with significant differences in expression of integrin α2-, α4-, and α6-chains.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Bone Marrow Cells', 'Cell Adhesion', 'Cells, Cultured', 'Culture Media', 'Female', 'Fibronectins', 'Humans', 'Male', 'Mesenchymal Stem Cells', 'Organ Specificity', 'Peptide Fragments', 'Placenta', 'Pregnancy']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,857,235 |
Does ex vivo virotherapy with myxoma virus impair hematopoietic stem and progenitor cells?
|
{
"contexts": [
"Relapsing disease is a major challenge after hematopoietic cell transplantation for hematological malignancies. Myxoma virus (MYXV) is an oncolytic virus that can target and eliminate contaminating cancer cells from auto-transplant grafts. The aims of this study were to examine the impact of MYXV on normal hematopoietic stem and progenitor cells and define the optimal treatment conditions for ex vivo virotherapy.",
"Bone marrow (BM) and mobilized peripheral blood stem cells (mPBSCs) from patients with hematologic malignancies were treated with MYXV at various time, temperature and incubation media conditions. Treated BM cells from healthy normal donors were evaluated using flow cytometry for MYXV infection, long-term culture-initiating cell (LTC-IC) assay and colony-forming cell (CFC) assay.",
"MYXV initiated infection in up to 45% of antigen-presenting monocytes, B cells and natural killer cells; however, these infections were uniformly aborted in >95% of all cells. Fresh graft sources showed higher levels of MYXV infection initiation than cryopreserved specimens, but in all cases less than 10% of CD34(+) cells could be infected after ex vivo MYXV treatment. MYXV did not impair LTC-IC colony numbers compared with mock treatment. CFC colony types and numbers were also not impaired by MYXV treatment. MYXV incubation time, temperature or culture media did not significantly change the percentage of infected cells, LTC-IC colony formation or CFC colony formation."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Antigens, CD34",
"Autografts",
"Bone Marrow",
"Bone Marrow Cells",
"Cell Culture Techniques",
"Cell Separation",
"Cells, Cultured",
"Female",
"Hematologic Neoplasms",
"Hematopoietic Stem Cell Transplantation",
"Hematopoietic Stem Cells",
"Humans",
"Male",
"Myxoma virus",
"Neoplasm Recurrence, Local",
"Oncolytic Virotherapy",
"Transplantation Conditioning"
]
}
|
Human hematopoietic cells are non-permissive for MYXV. Human hematopoietic stem and progenitor cells were not infected and thus unaffected by MYXV ex vivo treatment.
|
no
|
[
{
"from": "human",
"value": "Question: Does ex vivo virotherapy with myxoma virus impair hematopoietic stem and progenitor cells?\nContext: {'contexts': ['Relapsing disease is a major challenge after hematopoietic cell transplantation for hematological malignancies. Myxoma virus (MYXV) is an oncolytic virus that can target and eliminate contaminating cancer cells from auto-transplant grafts. The aims of this study were to examine the impact of MYXV on normal hematopoietic stem and progenitor cells and define the optimal treatment conditions for ex vivo virotherapy.', 'Bone marrow (BM) and mobilized peripheral blood stem cells (mPBSCs) from patients with hematologic malignancies were treated with MYXV at various time, temperature and incubation media conditions. Treated BM cells from healthy normal donors were evaluated using flow cytometry for MYXV infection, long-term culture-initiating cell (LTC-IC) assay and colony-forming cell (CFC) assay.', 'MYXV initiated infection in up to 45% of antigen-presenting monocytes, B cells and natural killer cells; however, these infections were uniformly aborted in >95% of all cells. Fresh graft sources showed higher levels of MYXV infection initiation than cryopreserved specimens, but in all cases less than 10% of CD34(+) cells could be infected after ex vivo MYXV treatment. MYXV did not impair LTC-IC colony numbers compared with mock treatment. CFC colony types and numbers were also not impaired by MYXV treatment. MYXV incubation time, temperature or culture media did not significantly change the percentage of infected cells, LTC-IC colony formation or CFC colony formation.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Antigens, CD34', 'Autografts', 'Bone Marrow', 'Bone Marrow Cells', 'Cell Culture Techniques', 'Cell Separation', 'Cells, Cultured', 'Female', 'Hematologic Neoplasms', 'Hematopoietic Stem Cell Transplantation', 'Hematopoietic Stem Cells', 'Humans', 'Male', 'Myxoma virus', 'Neoplasm Recurrence, Local', 'Oncolytic Virotherapy', 'Transplantation Conditioning']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
] |
26,857,234 |
Do endothelial progenitor cells promote efficient ex vivo expansion of cord blood-derived hematopoietic stem/progenitor cells?
|
{
"contexts": [
"Cord blood (CB) hematopoietic stem cell transplantation has often been limited by the scarcity of stem cells. Therefore, the number of CB hematopoietic stem/progenitor cells (HSPCs) should be increased while maintaining the stem cell characteristics.",
"We designed an ex vivo culture system using endothelial progenitor cells (EPCs) as stroma to determine the capacity of expanding CB-HSPCs in a defined medium, the effect on engraftment of the expanded cells in a mouse model and the underlying mechanism.",
"After 7 days of culture, compared with those cultured with cytokines alone (3.25 ± 0.59), CD34+ cells under contact and non-contact co-culture with EPCs were expanded by 5.38 ± 0.61 (P = 0.003) and 4.06 ± 0.43 (P = 0.025)-fold, respectively. Direct cell-to-cell contact co-culture with EPCs resulted in more primitive CD34+ CD38- cells than stroma-free culture (156.17 ± 21.32 versus 79.12 ± 19.77-fold; P = 0.010). Comparable engraftment of day 7 co-cultured HSPCs with respect to HSPCs at day 0 in nonobese diabetic-severe combined immunodeficiency disease (NOD/SCID) mice was measured as a percentage of chimerism (13.3% ± 11.0% versus 16.0% ± 14.3%; P = 0.750). EPCs highly expressed interleukin 6 (IL6) and angiopoietin 1 (ANGPT1), the hematopoietic- related cytokines. A higher transcriptional level of WNT5A genes in EPCs and co-cultured HSPCs suggests that the activation of Wnt signaling pathway may play a role in HSPCs' expansion ex vivo."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Antigens, CD34",
"Cell Culture Techniques",
"Cell Proliferation",
"Cells, Cultured",
"Coculture Techniques",
"Cord Blood Stem Cell Transplantation",
"Endothelial Progenitor Cells",
"Female",
"Fetal Blood",
"Hematopoietic Stem Cell Transplantation",
"Hematopoietic Stem Cells",
"Human Umbilical Vein Endothelial Cells",
"Humans",
"Infant, Newborn",
"Mice",
"Mice, Inbred NOD",
"Mice, SCID",
"Pregnancy"
]
}
|
These data demonstrated that EPCs improve the CD34+ population but do not compromise the repopulating efficacy of the amplified HSPCs, possibly via cytokine secretion and Wnt signaling pathway activation.
|
yes
|
[
{
"from": "human",
"value": "Question: Do endothelial progenitor cells promote efficient ex vivo expansion of cord blood-derived hematopoietic stem/progenitor cells?\nContext: {'contexts': ['Cord blood (CB) hematopoietic stem cell transplantation has often been limited by the scarcity of stem cells. Therefore, the number of CB hematopoietic stem/progenitor cells (HSPCs) should be increased while maintaining the stem cell characteristics.', 'We designed an ex vivo culture system using endothelial progenitor cells (EPCs) as stroma to determine the capacity of expanding CB-HSPCs in a defined medium, the effect on engraftment of the expanded cells in a mouse model and the underlying mechanism.', \"After 7 days of culture, compared with those cultured with cytokines alone (3.25 ± 0.59), CD34+ cells under contact and non-contact co-culture with EPCs were expanded by 5.38 ± 0.61 (P = 0.003) and 4.06 ± 0.43 (P = 0.025)-fold, respectively. Direct cell-to-cell contact co-culture with EPCs resulted in more primitive CD34+ CD38- cells than stroma-free culture (156.17 ± 21.32 versus 79.12 ± 19.77-fold; P = 0.010). Comparable engraftment of day 7 co-cultured HSPCs with respect to HSPCs at day 0 in nonobese diabetic-severe combined immunodeficiency disease (NOD/SCID) mice was measured as a percentage of chimerism (13.3% ± 11.0% versus 16.0% ± 14.3%; P = 0.750). EPCs highly expressed interleukin 6 (IL6) and angiopoietin 1 (ANGPT1), the hematopoietic- related cytokines. A higher transcriptional level of WNT5A genes in EPCs and co-cultured HSPCs suggests that the activation of Wnt signaling pathway may play a role in HSPCs' expansion ex vivo.\"], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Antigens, CD34', 'Cell Culture Techniques', 'Cell Proliferation', 'Cells, Cultured', 'Coculture Techniques', 'Cord Blood Stem Cell Transplantation', 'Endothelial Progenitor Cells', 'Female', 'Fetal Blood', 'Hematopoietic Stem Cell Transplantation', 'Hematopoietic Stem Cells', 'Human Umbilical Vein Endothelial Cells', 'Humans', 'Infant, Newborn', 'Mice', 'Mice, Inbred NOD', 'Mice, SCID', 'Pregnancy']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,857,230 |
Does hepatocyte growth factor enhance the inflammation-alleviating effect of umbilical cord-derived mesenchymal stromal cells in a bronchiolitis obliterans model?
|
{
"contexts": [
"Specific and effective therapy for prevention or reversal of bronchiolitis obliterans (BO) is lacking. In this study, we evaluated the therapeutic effect of hepatocyte growth factor (HGF) gene modified mesenchymal stromal cells (MSCs) on BO.",
"A mouse model of experimental BO was established by subcutaneously transplanting the tracheas from C57BL/6 mice into Balb/C recipients, which were then administered saline, Ad-HGF-modified human umbilical cord-MSCs (MSCs-HGF) or Ad-Null-modified MSCs (MSCs-Null). The therapeutic effects of MSCs-Null and MSCs-HGF were evaluated by using fluorescence-activated cell sorting (FACS) for lymphocyte immunophenotype of spleen, enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (rt-PCR) for cytokine expression, and histopathological analysis for the transplanted trachea.",
"The histopathologic recovery of allograft tracheas was improved significantly after MSCs-Null and MSCs-HGF treatment and the beneficial effects were particularly observed in MSCs-HGF-treated mice. Furthermore, the allo-transplantation-induced immunophenotype disorders of the spleen, including regulatory T (Treg), T helper (Th)1, Th2 and Th17, were attenuated in both cell-treated groups. MSCs-HGF treatment reduced expression and secretion of inflammation cytokines interferon-gamma (IFN-γ), and increased expression of anti-inflammatory cytokine interleukin (IL)-4 and IL-10. It also decreased the expression level of the profibrosis factor transforming growth factor (TGF)-β."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Bronchiolitis Obliterans",
"Cells, Cultured",
"Disease Models, Animal",
"Female",
"Genetic Therapy",
"Hepatocyte Growth Factor",
"Humans",
"Immunomodulation",
"Inflammation",
"Male",
"Mesenchymal Stem Cell Transplantation",
"Mesenchymal Stem Cells",
"Mice",
"Mice, Inbred BALB C",
"Mice, Inbred C57BL",
"T-Lymphocytes, Regulatory",
"Umbilical Cord"
]
}
|
Treatment of BO with HGF gene modified MSCs results in reduction of local inflammation and promotion in recovery of allograft trachea histopathology. These findings might provide an effective therapeutic strategy for BO.
|
yes
|
[
{
"from": "human",
"value": "Question: Does hepatocyte growth factor enhance the inflammation-alleviating effect of umbilical cord-derived mesenchymal stromal cells in a bronchiolitis obliterans model?\nContext: {'contexts': ['Specific and effective therapy for prevention or reversal of bronchiolitis obliterans (BO) is lacking. In this study, we evaluated the therapeutic effect of hepatocyte growth factor (HGF) gene modified mesenchymal stromal cells (MSCs) on BO.', 'A mouse model of experimental BO was established by subcutaneously transplanting the tracheas from C57BL/6 mice into Balb/C recipients, which were then administered saline, Ad-HGF-modified human umbilical cord-MSCs (MSCs-HGF) or Ad-Null-modified MSCs (MSCs-Null). The therapeutic effects of MSCs-Null and MSCs-HGF were evaluated by using fluorescence-activated cell sorting (FACS) for lymphocyte immunophenotype of spleen, enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (rt-PCR) for cytokine expression, and histopathological analysis for the transplanted trachea.', 'The histopathologic recovery of allograft tracheas was improved significantly after MSCs-Null and MSCs-HGF treatment and the beneficial effects were particularly observed in MSCs-HGF-treated mice. Furthermore, the allo-transplantation-induced immunophenotype disorders of the spleen, including regulatory T (Treg), T helper (Th)1, Th2 and Th17, were attenuated in both cell-treated groups. MSCs-HGF treatment reduced expression and secretion of inflammation cytokines interferon-gamma (IFN-γ), and increased expression of anti-inflammatory cytokine interleukin (IL)-4 and IL-10. It also decreased the expression level of the profibrosis factor transforming growth factor (TGF)-β.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Bronchiolitis Obliterans', 'Cells, Cultured', 'Disease Models, Animal', 'Female', 'Genetic Therapy', 'Hepatocyte Growth Factor', 'Humans', 'Immunomodulation', 'Inflammation', 'Male', 'Mesenchymal Stem Cell Transplantation', 'Mesenchymal Stem Cells', 'Mice', 'Mice, Inbred BALB C', 'Mice, Inbred C57BL', 'T-Lymphocytes, Regulatory', 'Umbilical Cord']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,853,425 |
Is heterozygosity of stromelysin-1 ( rs3025058 ) promoter polymorphism associated with gastric cancer?
|
{
"contexts": [
"Gastric cancer (GC) is the third most common cancer in India and is mediated by multiple genetic, epigenetic and environmental risk factors. A single nucleotide polymorphism rs3025058 at -1171 of the stromelysin-1 (matrix metalloproteinase [MMP]-3) promoter is resulting due to insertion/deletion of adenine thought to have an impact on increasing the risk for tumor formation.",
"This study is aimed to understand the role of stromelysin-1 rs3025058 (-1171, 5A/6A) promoter polymorphism in the etiology of GC in Indian population.",
"Genomic DNA was isolated from blood samples of the GC patients and controls. The genotyping of stromelysin-1 rs3025058 (-1171, 5A/6A) promoter polymorphism was carried out by amplification refractory mutation system-polymerase chain reaction method followed by agarose gel electrophoresis.",
"The frequency of 5A/5A, 5A/6A, and 6A/6A genotypes in GC patients were 7.69%, 76.92%, and 15.38%, while in controls were 5.31%, 86.73%, and 7.96%, respectively. There was a significant difference in the distribution of 5A/6A genotype in patients compared to the controls (P < 0.05)."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Genetic Association Studies",
"Genetic Predisposition to Disease",
"Genotype",
"Heterozygote",
"Humans",
"India",
"Matrix Metalloproteinase 3",
"Middle Aged",
"Promoter Regions, Genetic",
"Risk Factors",
"Stomach Neoplasms"
]
}
|
This study showed an increased frequency of heterozygotes for stromelysin-1 rs3025058 and thought to be involved in the etiology of GC.
|
yes
|
[
{
"from": "human",
"value": "Question: Is heterozygosity of stromelysin-1 ( rs3025058 ) promoter polymorphism associated with gastric cancer?\nContext: {'contexts': ['Gastric cancer (GC) is the third most common cancer in India and is mediated by multiple genetic, epigenetic and environmental risk factors. A single nucleotide polymorphism rs3025058 at -1171 of the stromelysin-1 (matrix metalloproteinase [MMP]-3) promoter is resulting due to insertion/deletion of adenine thought to have an impact on increasing the risk for tumor formation.', 'This study is aimed to understand the role of stromelysin-1 rs3025058 (-1171, 5A/6A) promoter polymorphism in the etiology of GC in Indian population.', 'Genomic DNA was isolated from blood samples of the GC patients and controls. The genotyping of stromelysin-1 rs3025058 (-1171, 5A/6A) promoter polymorphism was carried out by amplification refractory mutation system-polymerase chain reaction method followed by agarose gel electrophoresis.', 'The frequency of 5A/5A, 5A/6A, and 6A/6A genotypes in GC patients were 7.69%, 76.92%, and 15.38%, while in controls were 5.31%, 86.73%, and 7.96%, respectively. There was a significant difference in the distribution of 5A/6A genotype in patients compared to the controls (P < 0.05).'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Genetic Association Studies', 'Genetic Predisposition to Disease', 'Genotype', 'Heterozygote', 'Humans', 'India', 'Matrix Metalloproteinase 3', 'Middle Aged', 'Promoter Regions, Genetic', 'Risk Factors', 'Stomach Neoplasms']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,855,781 |
Does ruxolitinib improve symptoms and quality of life in a patient with systemic mastocytosis?
|
{
"contexts": [
"Systemic mastocytosis is a clonal myeloproliferative neoplasm associated with constitutional symptoms from mast cell mediated chemical and cytokine release. According to the literature, Ruxolitinib, a JAK1/JAK2 inhibitor, has been shown to reduce symptoms related to proinflammatory cytokine release in other myeloproliferative neoplasms.",
"Here we present a case using Ruxolitinib for disabling constitutional symptoms despite complete bone marrow response in a patient with aggressive systemic mastocytosis. Assessment tools used to monitor symptoms in previously published Ruxolitinib trials were adopted to track symptom improvement and quality of life."
],
"labels": [
"BACKGROUND",
"METHODS"
],
"meshes": []
}
|
Ruxolitinib significantly improved symptoms and quality of life in our patient with systemic mastocytosis.
|
yes
|
[
{
"from": "human",
"value": "Question: Does ruxolitinib improve symptoms and quality of life in a patient with systemic mastocytosis?\nContext: {'contexts': ['Systemic mastocytosis is a clonal myeloproliferative neoplasm associated with constitutional symptoms from mast cell mediated chemical and cytokine release. According to the literature, Ruxolitinib, a JAK1/JAK2 inhibitor, has been shown to reduce symptoms related to proinflammatory cytokine release in other myeloproliferative neoplasms.', 'Here we present a case using Ruxolitinib for disabling constitutional symptoms despite complete bone marrow response in a patient with aggressive systemic mastocytosis. Assessment tools used to monitor symptoms in previously published Ruxolitinib trials were adopted to track symptom improvement and quality of life.'], 'labels': ['BACKGROUND', 'METHODS'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,849,256 |
Does single and Combined Exposure to Zinc- and Copper-Containing Welding Fumes lead to Asymptomatic Systemic Inflammation?
|
{
"contexts": [
"Recently, it has been shown that exposure to welding fumes containing both zinc and copper leads to asymptomatic systemic inflammation in humans as shown by an increase of blood C-reactive protein. In the present study, it was investigated which metal is responsible for this effect.",
"Fifteen healthy male subjects were exposed under controlled conditions to welding fumes containing either zinc, or copper, or copper and zinc.",
"For each exposure blood C-reactive protein increased."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Air Pollutants, Occupational",
"Asymptomatic Diseases",
"Biomarkers",
"C-Reactive Protein",
"Copper",
"Cross-Over Studies",
"Healthy Volunteers",
"Humans",
"Inflammation",
"Male",
"Occupational Diseases",
"Occupational Exposure",
"Welding",
"Zinc"
]
}
|
Copper- and zinc-containing welding fumes are able to induce systemic inflammation.
|
yes
|
[
{
"from": "human",
"value": "Question: Does single and Combined Exposure to Zinc- and Copper-Containing Welding Fumes lead to Asymptomatic Systemic Inflammation?\nContext: {'contexts': ['Recently, it has been shown that exposure to welding fumes containing both zinc and copper leads to asymptomatic systemic inflammation in humans as shown by an increase of blood C-reactive protein. In the present study, it was investigated which metal is responsible for this effect.', 'Fifteen healthy male subjects were exposed under controlled conditions to welding fumes containing either zinc, or copper, or copper and zinc.', 'For each exposure blood C-reactive protein increased.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Air Pollutants, Occupational', 'Asymptomatic Diseases', 'Biomarkers', 'C-Reactive Protein', 'Copper', 'Cross-Over Studies', 'Healthy Volunteers', 'Humans', 'Inflammation', 'Male', 'Occupational Diseases', 'Occupational Exposure', 'Welding', 'Zinc']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,873,536 |
Does continuing Medical Education improve Gastroenterologists ' Compliance with Inflammatory Bowel Disease Quality Measures?
|
{
"contexts": [
"Low rates of compliance with quality measures for inflammatory bowel disease (IBD) have been reported for US gastroenterologists.",
"We assessed the influence of quality improvement (QI) education on compliance with physician quality reporting system (PQRS) measures for IBD and measures related to National Quality Strategy (NQS) priorities.",
"Forty community-based gastroenterologists participated in the QI study; 20 were assigned to educational intervention and control groups, respectively. At baseline, randomly selected charts of patients with moderate-to-severe ulcerative colitis were retrospectively reviewed for the gastroenterologists' performance of 8 PQRS IBD measures and 4 NQS-related measures. The intervention group participated in a series of accredited continuing medical education (CME) activities focusing on QI. Follow-up chart reviews were conducted 6 months after the CME activities. Independent t tests were conducted to compare between-group differences in baseline-to-follow-up rates of documented compliance with each measure.",
"The analysis included 299 baseline charts and 300 follow-up charts. The intervention group had significantly greater magnitudes of improvement than the control group for the following measures: assessment of IBD type, location, and activity (+14 %, p = 0.009); influenza vaccination (+13 %, p = 0.025); pneumococcal vaccination (+20 %, p = 0.003); testing for latent tuberculosis before anti-TNF-α therapy (+10 %, p = 0.028); assessment of hepatitis B virus status before anti-TNF-α therapy (+9 %, p = 0.010); assessment of side effects (+17 %, p = 0.048), and counseling patients about cancer risks (+13 %, p = 0.013)."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Education, Medical, Continuing",
"Female",
"Gastroenterology",
"Guideline Adherence",
"Humans",
"Inflammatory Bowel Diseases",
"Male",
"Medical Audit",
"Quality Improvement",
"Retrospective Studies"
]
}
|
QI-focused CME improves community-based gastroenterologists' compliance with IBD quality measures and measures aligned with NQS priorities.
|
yes
|
[
{
"from": "human",
"value": "Question: Does continuing Medical Education improve Gastroenterologists ' Compliance with Inflammatory Bowel Disease Quality Measures?\nContext: {'contexts': ['Low rates of compliance with quality measures for inflammatory bowel disease (IBD) have been reported for US gastroenterologists.', 'We assessed the influence of quality improvement (QI) education on compliance with physician quality reporting system (PQRS) measures for IBD and measures related to National Quality Strategy (NQS) priorities.', \"Forty community-based gastroenterologists participated in the QI study; 20 were assigned to educational intervention and control groups, respectively. At baseline, randomly selected charts of patients with moderate-to-severe ulcerative colitis were retrospectively reviewed for the gastroenterologists' performance of 8 PQRS IBD measures and 4 NQS-related measures. The intervention group participated in a series of accredited continuing medical education (CME) activities focusing on QI. Follow-up chart reviews were conducted 6\\xa0months after the CME activities. Independent t tests were conducted to compare between-group differences in baseline-to-follow-up rates of documented compliance with each measure.\", 'The analysis included 299 baseline charts and 300 follow-up charts. The intervention group had significantly greater magnitudes of improvement than the control group for the following measures: assessment of IBD type, location, and activity (+14\\xa0%, p\\xa0=\\xa00.009); influenza vaccination (+13\\xa0%, p\\xa0=\\xa00.025); pneumococcal vaccination (+20\\xa0%, p\\xa0=\\xa00.003); testing for latent tuberculosis before anti-TNF-α therapy (+10\\xa0%, p\\xa0=\\xa00.028); assessment of hepatitis B virus status before anti-TNF-α therapy (+9\\xa0%, p\\xa0=\\xa00.010); assessment of side effects (+17\\xa0%, p\\xa0=\\xa00.048), and counseling patients about cancer risks (+13\\xa0%, p\\xa0=\\xa00.013).'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Education, Medical, Continuing', 'Female', 'Gastroenterology', 'Guideline Adherence', 'Humans', 'Inflammatory Bowel Diseases', 'Male', 'Medical Audit', 'Quality Improvement', 'Retrospective Studies']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,866,603 |
Does circulating Hepcidin-25 be Reduced by Endogenous Estrogen in Humans?
|
{
"contexts": [
"Hepcidin reduces iron absorption by binding to the intestinal iron transporter ferroportin, thereby causing its degradation. Although short-term administration of testosterone or growth hormone (GH) has been reported to decrease circulating hepcidin levels, little is known about how hepcidin is influenced in human endocrine conditions associated with anemia.",
"We used a sensitive and specific dual-monoclonal antibody sandwich immunoassay to measure hepcidin-25 in patients (a) during initiation of in vitro fertilization when endogenous estrogens were elevated vs. suppressed, (b) with GH deficiency before and after 12 months substitution treatment, (c) with hyperthyroidism before and after normalization, and (d) with hyperprolactinemia before and after six months of treatment with a dopamine agonist.",
"In response to a marked stimulation of endogenous estrogen production, median hepcidin levels decreased from 4.85 to 1.43 ng/mL (p < 0.01). Hyperthyroidism, hyperprolactinemia, or GH substitution to GH-deficient patients did not influence serum hepcidin-25 levels."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Aged",
"Anemia",
"C-Reactive Protein",
"Dopamine Agonists",
"Estrogens",
"Female",
"Ferritins",
"Fertilization in Vitro",
"Hepcidins",
"Human Growth Hormone",
"Humans",
"Hyperprolactinemia",
"Hyperthyroidism",
"Immunoassay",
"Iron",
"Male",
"Middle Aged",
"Prolactinoma",
"Transferrin",
"Young Adult"
]
}
|
In humans, gonadotropin-stimulated endogenous estrogen markedly decreases circulating hepcidin-25 levels. No clear and stable correlation between iron biomarkers and hepcidin-25 was seen before or after treatment of hyperthyroidism, hyperprolactinemia or growth hormone deficiency.
|
yes
|
[
{
"from": "human",
"value": "Question: Does circulating Hepcidin-25 be Reduced by Endogenous Estrogen in Humans?\nContext: {'contexts': ['Hepcidin reduces iron absorption by binding to the intestinal iron transporter ferroportin, thereby causing its degradation. Although short-term administration of testosterone or growth hormone (GH) has been reported to decrease circulating hepcidin levels, little is known about how hepcidin is influenced in human endocrine conditions associated with anemia.', 'We used a sensitive and specific dual-monoclonal antibody sandwich immunoassay to measure hepcidin-25 in patients (a) during initiation of in vitro fertilization when endogenous estrogens were elevated vs. suppressed, (b) with GH deficiency before and after 12 months substitution treatment, (c) with hyperthyroidism before and after normalization, and (d) with hyperprolactinemia before and after six months of treatment with a dopamine agonist.', 'In response to a marked stimulation of endogenous estrogen production, median hepcidin levels decreased from 4.85 to 1.43 ng/mL (p < 0.01). Hyperthyroidism, hyperprolactinemia, or GH substitution to GH-deficient patients did not influence serum hepcidin-25 levels.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Aged', 'Anemia', 'C-Reactive Protein', 'Dopamine Agonists', 'Estrogens', 'Female', 'Ferritins', 'Fertilization in Vitro', 'Hepcidins', 'Human Growth Hormone', 'Humans', 'Hyperprolactinemia', 'Hyperthyroidism', 'Immunoassay', 'Iron', 'Male', 'Middle Aged', 'Prolactinoma', 'Transferrin', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,876,342 |
Does community-Based Multidisciplinary Computed Tomography Screening Program improve Lung Cancer Survival?
|
{
"contexts": [
"Lung cancer is the most common cause of cancer deaths in the United States. Overall survival is less than 20%, with the majority of patients presenting with advanced disease. The National Lung Screening Trial, performed mainly in academic medical centers, showed that cancer mortality can be reduced with computed tomography (CT) screening compared with chest radiography in high-risk patients. To determine whether this survival advantage can be duplicated in a community-based multidisciplinary thoracic oncology program, we initiated a CT scan screening program for lung cancer within an established health care system.",
"In 2008, we launched a lung cancer CT screening program within the WellStar Health System (WHS) consisting of five hospitals, three health parks, 140 outpatient medical offices, and 12 imaging centers that provide care in a five-county area of approximately 1.4 million people in Metro-Atlanta. Screening criteria incorporated were the International Early Lung Cancer Action Program (2008 to 2010) and National Comprehensive Cancer Network guidelines (2011 to 2013) for moderate- and high-risk patients.",
"A total of 1,267 persons underwent CT lung cancer screening in WHS from 2008 through 2013; 53% were men, 87% were 50 years of age or older, and 83% were current or former smokers. Noncalcified indeterminate pulmonary nodules were found in 518 patients (41%). Thirty-six patients (2.8%) underwent a diagnostic procedure for positive findings on their CT scan; 30 proved to have cancer, 28 (2.2%) primary lung cancer and 2 metastatic cancer, and 6 had benign disease. Fourteen patients (50%) had their lung cancer discovered on their initial CT scan, 11 on subsequent scans associated with indeterminate pulmonary nodules growth and 3 patients who had a new indeterminate pulmonary nodules. Only 15 (54%) of these 28 patients would have qualified as a National Lung Screening Trial high-risk patient; 75% had stage I or II disease. Overall 5-year survival was 64% and 5-year cancer specific survival was 71% in the screened patients, whereas nonscreened lung cancer patients during that time in WHS had an overall survival of only 19% (p < 0.001)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Early Detection of Cancer",
"Female",
"Humans",
"Lung Neoplasms",
"Male",
"Mass Screening",
"Middle Aged",
"Tomography, X-Ray Computed"
]
}
|
A community-based multidisciplinary lung cancer screening program can improve survival of patients with lung cancer outside of a large multicenter study. This survival advantage was caused by a significant stage shift to earlier disease. Lung cancer CT screening may also benefit patients not meeting the National Lung Screening Trial criteria who are at moderate or high risk for lung cancer.
|
yes
|
[
{
"from": "human",
"value": "Question: Does community-Based Multidisciplinary Computed Tomography Screening Program improve Lung Cancer Survival?\nContext: {'contexts': ['Lung cancer is the most common cause of cancer deaths in the United States. Overall survival is less than 20%, with the majority of patients presenting with advanced disease. The National Lung Screening Trial, performed mainly in academic medical centers, showed that cancer mortality can be reduced with computed tomography (CT) screening compared with chest radiography in high-risk patients. To determine whether this survival advantage can be duplicated in a community-based multidisciplinary thoracic oncology program, we initiated a CT scan screening program for lung cancer within an established health care system.', 'In 2008, we launched a lung cancer CT screening program within the WellStar Health System (WHS) consisting of five hospitals, three health parks, 140 outpatient medical offices, and 12 imaging centers that provide care in a five-county area of approximately 1.4 million people in Metro-Atlanta. Screening criteria incorporated were the International Early Lung Cancer Action Program (2008 to 2010) and National Comprehensive Cancer Network guidelines (2011 to 2013) for moderate- and high-risk patients.', 'A total of 1,267 persons underwent CT lung cancer screening in WHS from 2008 through 2013; 53% were men, 87% were 50 years of age or older, and 83% were current or former smokers. Noncalcified indeterminate pulmonary nodules were found in 518 patients (41%). Thirty-six patients (2.8%) underwent a diagnostic procedure for positive findings on their CT scan; 30 proved to have cancer, 28 (2.2%) primary lung cancer and 2 metastatic cancer, and 6 had benign disease. Fourteen patients (50%) had their lung cancer discovered on their initial CT scan, 11 on subsequent scans associated with indeterminate pulmonary nodules growth and 3 patients who had a new indeterminate pulmonary nodules. Only 15 (54%) of these 28 patients would have qualified as a National Lung Screening Trial high-risk patient; 75% had stage I or II disease. Overall 5-year survival was 64% and 5-year cancer specific survival was 71% in the screened patients, whereas nonscreened lung cancer patients during that time in WHS had an overall survival of only 19% (p < 0.001).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Early Detection of Cancer', 'Female', 'Humans', 'Lung Neoplasms', 'Male', 'Mass Screening', 'Middle Aged', 'Tomography, X-Ray Computed']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,861,863 |
Are mitochondrial and oxidative stress genes differentially expressed in neutrophils of sJIA patients treated with tocilizumab : a pilot microarray study?
|
{
"contexts": [
"Various pathways involved in the pathogenesis of sJIA have been identified through gene expression profiling in peripheral blood mononuclear cells (PBMC), but not in neutrophils. Since neutrophils are important in tissue damage during inflammation, and are elevated as part of the acute phase response, we hypothesised that neutrophil pathways could also be important in the pathogenesis of sJIA. We therefore studied the gene profile in both PBMC and neutrophils of sJIA patients treated with tocilizumab.",
"We studied the transcriptomes of peripheral blood mononuclear cells (PBMC) and neutrophils from eight paired samples obtained from 4 sJIA patients taken before and after treatment, selected on the basis that they achieved ACR90 responses within 12 weeks of therapy initiation with tocilizumab. RNA was extracted and gene expression profiling was performed using Affymetrix GeneChip Human Genome U133 Plus 2.0 microarray platform. A longitudinal analysis using paired t-test (p < 0.05 and FC ≥ 1.5) was applied to identify differentially expressed genes (DEGs) between the two time points followed by ingenuity pathway analysis. Gene Set Enrichment Analysis (GSEA) and quantitative real-time PCR were then performed to verify the microarray results.",
"Gene ontology analysis in neutrophils revealed that response to tocilizumab significantly altered genes regulating mitochondrial dysfunction and oxidative stress (p = 4.6E-05). This was independently verified with GSEA, by identifying a set of oxidative genes whose expression correlated with response to tocilizumab. In PBMC, treatment of sJIA with tocilizumab appeared to affect genes in Oncostatin M signalling and B cell pathways."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Antibodies, Monoclonal, Humanized",
"Arthritis, Juvenile",
"Child",
"Child, Preschool",
"Cytokines",
"Female",
"Gene Expression Regulation",
"Humans",
"Male",
"Microarray Analysis",
"Neutrophils",
"Oxidative Stress",
"Pilot Projects",
"RNA",
"Real-Time Polymerase Chain Reaction"
]
}
|
For the first time we demonstrate that neutrophils from sJIA patients responding to tocilizumab showed significantly different changes in gene expression. These data could highlight the importance of mitochondrial genes that modulate oxidative stress in the pathogenesis of sJIA.
|
yes
|
[
{
"from": "human",
"value": "Question: Are mitochondrial and oxidative stress genes differentially expressed in neutrophils of sJIA patients treated with tocilizumab : a pilot microarray study?\nContext: {'contexts': ['Various pathways involved in the pathogenesis of sJIA have been identified through gene expression profiling in peripheral blood mononuclear cells (PBMC), but not in neutrophils. Since neutrophils are important in tissue damage during inflammation, and are elevated as part of the acute phase response, we hypothesised that neutrophil pathways could also be important in the pathogenesis of sJIA. We therefore studied the gene profile in both PBMC and neutrophils of sJIA patients treated with tocilizumab.', 'We studied the transcriptomes of peripheral blood mononuclear cells (PBMC) and neutrophils from eight paired samples obtained from 4 sJIA patients taken before and after treatment, selected on the basis that they achieved ACR90 responses within 12 weeks of therapy initiation with tocilizumab. RNA was extracted and gene expression profiling was performed using Affymetrix GeneChip Human Genome U133 Plus 2.0 microarray platform. A longitudinal analysis using paired t-test (p\\u2009<\\u20090.05 and FC\\u2009≥\\u20091.5) was applied to identify differentially expressed genes (DEGs) between the two time points followed by ingenuity pathway analysis. Gene Set Enrichment Analysis (GSEA) and quantitative real-time PCR were then performed to verify the microarray results.', 'Gene ontology analysis in neutrophils revealed that response to tocilizumab significantly altered genes regulating mitochondrial dysfunction and oxidative stress (p\\u2009=\\u20094.6E-05). This was independently verified with GSEA, by identifying a set of oxidative genes whose expression correlated with response to tocilizumab. In PBMC, treatment of sJIA with tocilizumab appeared to affect genes in Oncostatin M signalling and B cell pathways.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Antibodies, Monoclonal, Humanized', 'Arthritis, Juvenile', 'Child', 'Child, Preschool', 'Cytokines', 'Female', 'Gene Expression Regulation', 'Humans', 'Male', 'Microarray Analysis', 'Neutrophils', 'Oxidative Stress', 'Pilot Projects', 'RNA', 'Real-Time Polymerase Chain Reaction']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,871,639 |
Does gALNT14 genotype effectively predict the therapeutic response in unresectable hepatocellular carcinoma treated with transcatheter arterial chemoembolization?
|
{
"contexts": [
"Transcatheter arterial chemoembolization is currently the standard treatment in hepatocellular carcinoma patients with Barcelona Clinic Liver Cancer stage B. Genomic variants of GALNT14 were recently identified as effective predictors for chemotherapy responses in Barcelona Clinic Liver Cancer stage C patients.",
"We investigated the prognosis predictive value of GALNT14 genotypes in 327 hepatocelluar carcinoma patients treated by transcatheter arterial chemoembolization.",
"Cox proportional hazards model analysis showed that the genotype 'TT' was associated with shorter time-to-response (multivariate p < 0.001), time-to-complete-response (p = 0.004) and longer time-to-tumor progression (p < 0.001), compared with the genotype 'non-TT'. In patients with albumin <3.5 g/dl, genotype 'TT' was associated with longer overall survival (p = 0.027). Finally, genotype 'TT' correlated with higher cancer-to-noncancer ratios of GALNT14 protein levels, lower cancer-to-noncancer ratios of antiapoptotic cFLIP-S, and a clustered glycosylation pattern in the extracellular domain of death receptor 5."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Antibiotics, Antineoplastic",
"CASP8 and FADD-Like Apoptosis Regulating Protein",
"Carcinoma, Hepatocellular",
"Chemoembolization, Therapeutic",
"Doxorubicin",
"Female",
"Genotype",
"Glycosylation",
"Humans",
"Infusions, Intra-Arterial",
"Liver",
"Liver Neoplasms",
"Male",
"Middle Aged",
"N-Acetylgalactosaminyltransferases",
"Polymorphism, Single Nucleotide",
"Retrospective Studies",
"Tumor Microenvironment"
]
}
|
GALNT14 genotypes were significantly associated with clinical outcomes of transcatheter arterial chemoembolization. The differential status of extrinsic apoptotic signaling between cancerous and non-cancerous tissues might underlie the clinical association.
|
yes
|
[
{
"from": "human",
"value": "Question: Does gALNT14 genotype effectively predict the therapeutic response in unresectable hepatocellular carcinoma treated with transcatheter arterial chemoembolization?\nContext: {'contexts': ['Transcatheter arterial chemoembolization is currently the standard treatment in hepatocellular carcinoma patients with Barcelona Clinic Liver Cancer stage B. Genomic variants of GALNT14 were recently identified as effective predictors for chemotherapy responses in Barcelona Clinic Liver Cancer stage C patients.', 'We investigated the prognosis predictive value of GALNT14 genotypes in 327 hepatocelluar carcinoma patients treated by transcatheter arterial chemoembolization.', \"Cox proportional hazards model analysis showed that the genotype 'TT' was associated with shorter time-to-response (multivariate p < 0.001), time-to-complete-response (p = 0.004) and longer time-to-tumor progression (p < 0.001), compared with the genotype 'non-TT'. In patients with albumin <3.5 g/dl, genotype 'TT' was associated with longer overall survival (p = 0.027). Finally, genotype 'TT' correlated with higher cancer-to-noncancer ratios of GALNT14 protein levels, lower cancer-to-noncancer ratios of antiapoptotic cFLIP-S, and a clustered glycosylation pattern in the extracellular domain of death receptor 5.\"], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Antibiotics, Antineoplastic', 'CASP8 and FADD-Like Apoptosis Regulating Protein', 'Carcinoma, Hepatocellular', 'Chemoembolization, Therapeutic', 'Doxorubicin', 'Female', 'Genotype', 'Glycosylation', 'Humans', 'Infusions, Intra-Arterial', 'Liver', 'Liver Neoplasms', 'Male', 'Middle Aged', 'N-Acetylgalactosaminyltransferases', 'Polymorphism, Single Nucleotide', 'Retrospective Studies', 'Tumor Microenvironment']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,861,372 |
Is flood-Exposure Associated with Higher Prevalence of Child Undernutrition in Rural Eastern India?
|
{
"contexts": [
"Child undernutrition and flooding are highly prevalent public health issues in Asia, yet epidemiological studies investigating this association are lacking.",
"To investigate to what extent floods exacerbate poor nutritional status in children and identify most vulnerable groups, we conducted a population-based survey of children aged 6-59 months inhabiting flooded and non-flooded communities of the Jagatsinghpur district, Odisha (India), one year after large floods in 2008. Anthropometric measurements on 879 children and child, parental and household level variables were collected through face-to-face interviews in September 2009. The association between flooding and the prevalence of wasting, stunting and underweight was examined using weighted multivariate logistic regression for children inhabiting communities exposed solely to floods in 2008 and those communities repeatedly flooded (2006 and 2008) controlling for parental education and other relevant variables. We examined the influence of age on this association. Propensity score matching was conducted to test the robustness of our findings.",
"The prevalence of wasting among children flooded in 2006 and 2008 was 51.6%, 41.4% in those flooded only in 2008, and 21.2% in children inhabiting non-flooded communities. Adjusting by confounders, the increased prevalence relative to non-flooded children in the exposed groups were 2.30 (adjusted prevalence ratio (aPR); 95% CI: 1.86, 2.85) and 1.94 (95% CI: 1.43, 2.63), respectively. Among repeatedly flooded communities, cases of severe wasting in children were 3.37 times more prevalent than for children inhabiting in those non-flooded (95% CI: 2.34, 4.86) and nearly twice more prevalent relative to those flooded only once. Those children younger than one year during previous floods in 2006 showed the largest difference in prevalence of wasting compared to their non-flooded counterparts (aPR: 4.01; 95% CI: 1.51, 10.63). RESULTS were robust to alternative adjusted models and in propensity score matching analyses. For similar analyses, no significant associations were found for child stunting, and more moderate effects were observed in the case of child underweight."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Child Nutrition Disorders",
"Child, Preschool",
"Female",
"Floods",
"Humans",
"India",
"Infant",
"Logistic Models",
"Male",
"Malnutrition",
"Nutritional Status",
"Prevalence",
"Risk Assessment",
"Rural Population",
"Thinness"
]
}
|
Particularly in low-resource or subsistence-farming rural settings, long-lasting nutritional response in the aftermath of floods should be seriously considered to counteract the long-term nutritional effects on children, particularly infants, and include their mothers on whom they are dependent. The systematic monitoring of nutritional status in these groups might help to tailor efficient responses in each particular context.
|
yes
|
[
{
"from": "human",
"value": "Question: Is flood-Exposure Associated with Higher Prevalence of Child Undernutrition in Rural Eastern India?\nContext: {'contexts': ['Child undernutrition and flooding are highly prevalent public health issues in Asia, yet epidemiological studies investigating this association are lacking.', 'To investigate to what extent floods exacerbate poor nutritional status in children and identify most vulnerable groups, we conducted a population-based survey of children aged 6-59 months inhabiting flooded and non-flooded communities of the Jagatsinghpur district, Odisha (India), one year after large floods in 2008. Anthropometric measurements on 879 children and child, parental and household level variables were collected through face-to-face interviews in September 2009. The association between flooding and the prevalence of wasting, stunting and underweight was examined using weighted multivariate logistic regression for children inhabiting communities exposed solely to floods in 2008 and those communities repeatedly flooded (2006 and 2008) controlling for parental education and other relevant variables. We examined the influence of age on this association. Propensity score matching was conducted to test the robustness of our findings.', 'The prevalence of wasting among children flooded in 2006 and 2008 was 51.6%, 41.4% in those flooded only in 2008, and 21.2% in children inhabiting non-flooded communities. Adjusting by confounders, the increased prevalence relative to non-flooded children in the exposed groups were 2.30 (adjusted prevalence ratio (aPR); 95% CI: 1.86, 2.85) and 1.94 (95% CI: 1.43, 2.63), respectively. Among repeatedly flooded communities, cases of severe wasting in children were 3.37 times more prevalent than for children inhabiting in those non-flooded (95% CI: 2.34, 4.86) and nearly twice more prevalent relative to those flooded only once. Those children younger than one year during previous floods in 2006 showed the largest difference in prevalence of wasting compared to their non-flooded counterparts (aPR: 4.01; 95% CI: 1.51, 10.63). RESULTS were robust to alternative adjusted models and in propensity score matching analyses. For similar analyses, no significant associations were found for child stunting, and more moderate effects were observed in the case of child underweight.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Child Nutrition Disorders', 'Child, Preschool', 'Female', 'Floods', 'Humans', 'India', 'Infant', 'Logistic Models', 'Male', 'Malnutrition', 'Nutritional Status', 'Prevalence', 'Risk Assessment', 'Rural Population', 'Thinness']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,878,873 |
Does miR-193b promote autophagy and non-apoptotic cell death in oesophageal cancer cells?
|
{
"contexts": [
"Successful treatment of oesophageal cancer is hampered by recurrent drug resistant disease. We have previously demonstrated the importance of apoptosis and autophagy for the recovery of oesophageal cancer cells following drug treatment. When apoptosis (with autophagy) is induced, these cells are chemosensitive and will not recover following chemotherapy treatment. In contrast, when cancer cells exhibit only autophagy and limited Type II cell death, they are chemoresistant and recover following drug withdrawal.",
"MicroRNA (miRNA) expression profiling of an oesophageal cancer cell line panel was used to identify miRNAs that were important in the regulation of apoptosis and autophagy. The effects of miRNA overexpression on cell death mechanisms and recovery were assessed in the chemoresistant (autophagy inducing) KYSE450 oesophageal cancer cells.",
"MiR-193b was the most differentially expressed miRNA between the chemosensitive and chemoresistant cell lines with higher expression in chemosensitive apoptosis inducing cell lines. Colony formation assays showed that overexpression of miR-193b significantly impedes the ability of KYSE450 cells to recover following 5-fluorouracil (5-FU) treatment. The critical mRNA targets of miR-193b are unknown but target prediction and siRNA data analysis suggest that it may mediate some of its effects through stathmin 1 regulation. Apoptosis was not involved in the enhanced cytotoxicity. Overexpression of miR-193b in these cells induced autophagic flux and non-apoptotic cell death."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Antineoplastic Agents",
"Apoptosis",
"Autophagy",
"Cell Line, Tumor",
"Cell Survival",
"Drug Resistance, Neoplasm",
"Esophageal Neoplasms",
"Fluorouracil",
"Humans",
"MicroRNAs"
]
}
|
These results highlight the importance of miR-193b in determining oesophageal cancer cell viability and demonstrate an enhancement of chemotoxicity that is independent of apoptosis induction.
|
yes
|
[
{
"from": "human",
"value": "Question: Does miR-193b promote autophagy and non-apoptotic cell death in oesophageal cancer cells?\nContext: {'contexts': ['Successful treatment of oesophageal cancer is hampered by recurrent drug resistant disease. We have previously demonstrated the importance of apoptosis and autophagy for the recovery of oesophageal cancer cells following drug treatment. When apoptosis (with autophagy) is induced, these cells are chemosensitive and will not recover following chemotherapy treatment. In contrast, when cancer cells exhibit only autophagy and limited Type II cell death, they are chemoresistant and recover following drug withdrawal.', 'MicroRNA (miRNA) expression profiling of an oesophageal cancer cell line panel was used to identify miRNAs that were important in the regulation of apoptosis and autophagy. The effects of miRNA overexpression on cell death mechanisms and recovery were assessed in the chemoresistant (autophagy inducing) KYSE450 oesophageal cancer cells.', 'MiR-193b was the most differentially expressed miRNA between the chemosensitive and chemoresistant cell lines with higher expression in chemosensitive apoptosis inducing cell lines. Colony formation assays showed that overexpression of miR-193b significantly impedes the ability of KYSE450 cells to recover following 5-fluorouracil (5-FU) treatment. The critical mRNA targets of miR-193b are unknown but target prediction and siRNA data analysis suggest that it may mediate some of its effects through stathmin 1 regulation. Apoptosis was not involved in the enhanced cytotoxicity. Overexpression of miR-193b in these cells induced autophagic flux and non-apoptotic cell death.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Antineoplastic Agents', 'Apoptosis', 'Autophagy', 'Cell Line, Tumor', 'Cell Survival', 'Drug Resistance, Neoplasm', 'Esophageal Neoplasms', 'Fluorouracil', 'Humans', 'MicroRNAs']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,850,198 |
Does immune status predict high-risk HPV in anal condyloma?
|
{
"contexts": [
"More than 90% of anal condyloma is attributed to nonhigh risk strains of human papillomavirus (HPV), thus patients with anal condyloma do not necessarily undergo HPV serotyping unless they are immunocompromised (IC). We hypothesized that IC patients with anal condyloma have a higher risk of high-risk HPV and dysplasia than nonimmunocompromised (NIC) patients.",
"We performed a retrospective chart review of patients who underwent surgical treatment by a single surgeon for anal condyloma from 1/2000 to 1/2012. HPV serotyping was performed on all patient samples. We compared incidence of high-risk HPV and dysplasia in condyloma specimens from IC and NIC patients.",
"High-risk HPV was identified in 14 specimens with serotypes 16, 18, 31, 33, 51, 52, and 67. Twenty-two cases (18.3%) had dysplasia. Invasive carcinoma was identified in one IC patient. The prevalence of dysplasia or high-risk HPV was not significantly different between IC and NIC groups. High-risk HPV was a significant independent predictor of dysplasia (odds ratio [OR] = 5.2; 95% CI = 1.24-21.62). Immune status, however, was not a significant predictor of high-risk HPV (OR = 1.11; 95% CI = 0.16-5.12) nor dysplasia (OR = 0.27; 95% CI = 0.037-1.17)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Aged",
"Anus Neoplasms",
"Condylomata Acuminata",
"Female",
"Humans",
"Immunocompromised Host",
"Male",
"Middle Aged",
"Papillomaviridae",
"Precancerous Conditions",
"Retrospective Studies",
"Young Adult"
]
}
|
IC patients did not have a significantly higher prevalence or risk of high-risk HPV or dysplasia in our study. HPV typing of all condylomata, regardless of immune status, should be considered as it may help predict risk of neoplastic transformation or identify NIC patients with an increased risk of developing anal intraepithelial neoplasia.
|
no
|
[
{
"from": "human",
"value": "Question: Does immune status predict high-risk HPV in anal condyloma?\nContext: {'contexts': ['More than 90% of anal condyloma is attributed to nonhigh risk strains of human papillomavirus (HPV), thus patients with anal condyloma do not necessarily undergo HPV serotyping unless they are immunocompromised (IC). We hypothesized that IC patients with anal condyloma have a higher risk of high-risk HPV and dysplasia than nonimmunocompromised (NIC) patients.', 'We performed a retrospective chart review of patients who underwent surgical treatment by a single surgeon for anal condyloma from 1/2000 to 1/2012. HPV serotyping was performed on all patient samples. We compared incidence of high-risk HPV and dysplasia in condyloma specimens from IC and NIC patients.', 'High-risk HPV was identified in 14 specimens with serotypes 16, 18, 31, 33, 51, 52, and 67. Twenty-two cases (18.3%) had dysplasia. Invasive carcinoma was identified in one IC patient. The prevalence of dysplasia or high-risk HPV was not significantly different between IC and NIC groups. High-risk HPV was a significant independent predictor of dysplasia (odds ratio [OR] = 5.2; 95% CI = 1.24-21.62). Immune status, however, was not a significant predictor of high-risk HPV (OR = 1.11; 95% CI = 0.16-5.12) nor dysplasia (OR = 0.27; 95% CI = 0.037-1.17).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Aged', 'Anus Neoplasms', 'Condylomata Acuminata', 'Female', 'Humans', 'Immunocompromised Host', 'Male', 'Middle Aged', 'Papillomaviridae', 'Precancerous Conditions', 'Retrospective Studies', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
] |
26,876,155 |
Does lovastatin protect keratinocytes from DNA damage-related pro-apoptotic stress responses stimulated by anticancer therapeutics?
|
{
"contexts": [
"Oral mucositis (OM) is a relevant adverse effect of anticancer therapy involving ionizing radiation (IR) and doxorubicin (Doxo). Because DNA damage of keratinocytes is causative for the pathogenesis of OM, we aim to identify pharmacological measures for geno- and cytoprotection of keratinocytes.",
"We investigated the influence of the lipid-lowering drug lovastatin on cell death, proliferation and DNA damage response (DDR) mechanisms of human keratinocytes following treatment with IR and Doxo.",
"Lovastatin protected keratinocytes from the cytotoxic and genotoxic effects of IR and Doxo as shown by a diminished induction of apoptosis as well as a reduced formation and slightly improved repair of DNA damage following Doxo and IR treatment, respectively. Lovastatin selectively blocked the activation of Chk1 and ATR kinases following treatment with IR, Doxo and the ribonucleotide reductase inhibitor hydroxyurea, indicating that the statin antagonizes ATR/Chk1-regulated replicative stress responses. Part of the cytoprotective activity of lovastatin seems to rest on a delayed entry of lovastatin treated cells into S-phase. Yet, because the statin also protected non-proliferating keratinocytes from IR- and Doxo-induced cytotoxicity, cell cycle independent protective mechanisms are involved, too."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Antibiotics, Antineoplastic",
"Apoptosis",
"Ataxia Telangiectasia Mutated Proteins",
"Blotting, Western",
"Cell Cycle",
"Cell Survival",
"Cells, Cultured",
"Checkpoint Kinase 1",
"DNA Damage",
"Dose-Response Relationship, Drug",
"Dose-Response Relationship, Radiation",
"Doxorubicin",
"Enzyme Activation",
"Histones",
"Humans",
"Hydroxymethylglutaryl-CoA Reductase Inhibitors",
"Keratinocytes",
"Lovastatin",
"Protein Kinases",
"Radiation, Ionizing",
"Time Factors"
]
}
|
Lovastatin attenuates pro-toxic DNA damage-related responses of keratinocytes stimulated by OM-inducing anticancer therapeutics. The data encourage forthcoming in vivo and clinical studies addressing the usefulness of statins in the prevention of OM.
|
yes
|
[
{
"from": "human",
"value": "Question: Does lovastatin protect keratinocytes from DNA damage-related pro-apoptotic stress responses stimulated by anticancer therapeutics?\nContext: {'contexts': ['Oral mucositis (OM) is a relevant adverse effect of anticancer therapy involving ionizing radiation (IR) and doxorubicin (Doxo). Because DNA damage of keratinocytes is causative for the pathogenesis of OM, we aim to identify pharmacological measures for geno- and cytoprotection of keratinocytes.', 'We investigated the influence of the lipid-lowering drug lovastatin on cell death, proliferation and DNA damage response (DDR) mechanisms of human keratinocytes following treatment with IR and Doxo.', 'Lovastatin protected keratinocytes from the cytotoxic and genotoxic effects of IR and Doxo as shown by a diminished induction of apoptosis as well as a reduced formation and slightly improved repair of DNA damage following Doxo and IR treatment, respectively. Lovastatin selectively blocked the activation of Chk1 and ATR kinases following treatment with IR, Doxo and the ribonucleotide reductase inhibitor hydroxyurea, indicating that the statin antagonizes ATR/Chk1-regulated replicative stress responses. Part of the cytoprotective activity of lovastatin seems to rest on a delayed entry of lovastatin treated cells into S-phase. Yet, because the statin also protected non-proliferating keratinocytes from IR- and Doxo-induced cytotoxicity, cell cycle independent protective mechanisms are involved, too.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Antibiotics, Antineoplastic', 'Apoptosis', 'Ataxia Telangiectasia Mutated Proteins', 'Blotting, Western', 'Cell Cycle', 'Cell Survival', 'Cells, Cultured', 'Checkpoint Kinase 1', 'DNA Damage', 'Dose-Response Relationship, Drug', 'Dose-Response Relationship, Radiation', 'Doxorubicin', 'Enzyme Activation', 'Histones', 'Humans', 'Hydroxymethylglutaryl-CoA Reductase Inhibitors', 'Keratinocytes', 'Lovastatin', 'Protein Kinases', 'Radiation, Ionizing', 'Time Factors']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,872,252 |
Does gremlin-1 C-Terminus regulate Function of Macrophage Migration Inhibitory Factor ( MIF )?
|
{
"contexts": [
"The counterbalance of macrophage migration inhibitory factor (MIF) and Gremlin-1 is a useful tool to predict the acuity of coronary artery disease (CAD) and plaque stability. Gremlin1 is an endogenous antagonist of MIF and therefore influences plaque vulnerability. This study was designed to elucidate the mechanistic basis determining the biophysical binding of Gremlin-1 to MIF.",
"An in silico model suggested that several charged C-terminal amino acids are crucial in mediating Gremlin-1/MIF-binding. We produced several single amino acid exchange mutants of Gremlin-1 by site-directed mutagenesis. These Gremlin-1 mutants were tested for their ability to reduce MIF effects on monocytes.",
"We observed that the critical element of the Gremlin-1 molecule for regulating MIF-induced chemotactic activity lies at the C-terminal region. A single amino acid exchange of an arginine to an alanine residue is sufficient to abolish the antagonistic effect of Gremlin-1 on MIF. Therefore, the Gremlin-1 mutant R172A failed to reduce MIF-induced monocyte differentiation into macrophages."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Amino Acid Sequence",
"Cell Differentiation",
"Cell Movement",
"Cells, Cultured",
"Chemotaxis",
"Humans",
"Intercellular Signaling Peptides and Proteins",
"Intramolecular Oxidoreductases",
"Macrophage Migration-Inhibitory Factors",
"Macrophages",
"Models, Molecular",
"Monocytes",
"Mutagenesis, Site-Directed",
"Point Mutation",
"Protein Binding",
"Protein Conformation"
]
}
|
Gremlin-1 C-terminus is essential for antagonizing MIF effects. Our results could offer a novel strategy utilizing Gremlin-1 to target pro-inflammatory effects of MIF in various diseases.
|
yes
|
[
{
"from": "human",
"value": "Question: Does gremlin-1 C-Terminus regulate Function of Macrophage Migration Inhibitory Factor ( MIF )?\nContext: {'contexts': ['The counterbalance of macrophage migration inhibitory factor (MIF) and Gremlin-1 is a useful tool to predict the acuity of coronary artery disease (CAD) and plaque stability. Gremlin1 is an endogenous antagonist of MIF and therefore influences plaque vulnerability. This study was designed to elucidate the mechanistic basis determining the biophysical binding of Gremlin-1 to MIF.', 'An in silico model suggested that several charged C-terminal amino acids are crucial in mediating Gremlin-1/MIF-binding. We produced several single amino acid exchange mutants of Gremlin-1 by site-directed mutagenesis. These Gremlin-1 mutants were tested for their ability to reduce MIF effects on monocytes.', 'We observed that the critical element of the Gremlin-1 molecule for regulating MIF-induced chemotactic activity lies at the C-terminal region. A single amino acid exchange of an arginine to an alanine residue is sufficient to abolish the antagonistic effect of Gremlin-1 on MIF. Therefore, the Gremlin-1 mutant R172A failed to reduce MIF-induced monocyte differentiation into macrophages.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Amino Acid Sequence', 'Cell Differentiation', 'Cell Movement', 'Cells, Cultured', 'Chemotaxis', 'Humans', 'Intercellular Signaling Peptides and Proteins', 'Intramolecular Oxidoreductases', 'Macrophage Migration-Inhibitory Factors', 'Macrophages', 'Models, Molecular', 'Monocytes', 'Mutagenesis, Site-Directed', 'Point Mutation', 'Protein Binding', 'Protein Conformation']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,855,429 |
Do estrogenic Compounds Have Divergent Effects on Human Endothelial Progenitor Cell Migration according to Sex of the Donor?
|
{
"contexts": [
"Endothelial progenitor cells (EPCs) are key elements in vascular homeostasis. Their function is regulated by estrogens and estrogen receptors (ERs), but the effect of estrogenic compounds such as bisphenol A (BPA; an agonist of ER-β and agonist and antagonist of ER-α) and (R,R)-5,11-diethyl-5,6,11,12-tetrahydro-2,8-chrysenediol (THC; an agonist of ER-α and antagonist of ER-β) on human EPCs is unknown. We analyzed whether BPA and THC influence the migration of human EPCs, an essential process in endothelial regeneration, in both male and female EPCs.",
"EPCs isolated from healthy adult men and women were assayed for ER expression by Western blotting and chemotaxis assay.",
"Male and female EPCs similarly expressed ERs and did not differ in basal migration. Interestingly, 17-β-estradiol (10(-9) and 10(-10) M) significantly inhibited migration in female EPCs but not in males. Moreover, both 10(-5) M THC and 10(-8) M BPA blocked migration in female EPCs, allowing us to hypothesize that the effect is mediated by ER-α."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adolescent",
"Adult",
"Cells, Cultured",
"Chemotaxis",
"Dose-Response Relationship, Drug",
"Endothelial Progenitor Cells",
"Estrogen Receptor alpha",
"Estrogen Receptor beta",
"Estrogens",
"Female",
"Humans",
"Male",
"Sex Factors",
"Signal Transduction",
"Young Adult"
]
}
|
Estrogenic compounds have a sex divergent effect which could help in understanding differences in the pathophysiology of endothelial function observed between men and women.
|
yes
|
[
{
"from": "human",
"value": "Question: Do estrogenic Compounds Have Divergent Effects on Human Endothelial Progenitor Cell Migration according to Sex of the Donor?\nContext: {'contexts': ['Endothelial progenitor cells (EPCs) are key elements in vascular homeostasis. Their function is regulated by estrogens and estrogen receptors (ERs), but the effect of estrogenic compounds such as bisphenol A (BPA; an agonist of ER-β and agonist and antagonist of ER-α) and (R,R)-5,11-diethyl-5,6,11,12-tetrahydro-2,8-chrysenediol (THC; an agonist of ER-α and antagonist of ER-β) on human EPCs is unknown. We analyzed whether BPA and THC influence the migration of human EPCs, an essential process in endothelial regeneration, in both male and female EPCs.', 'EPCs isolated from healthy adult men and women were assayed for ER expression by Western blotting and chemotaxis assay.', 'Male and female EPCs similarly expressed ERs and did not differ in basal migration. Interestingly, 17-β-estradiol (10(-9) and 10(-10) M) significantly inhibited migration in female EPCs but not in males. Moreover, both 10(-5) M THC and 10(-8) M BPA blocked migration in female EPCs, allowing us to hypothesize that the effect is mediated by ER-α.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adolescent', 'Adult', 'Cells, Cultured', 'Chemotaxis', 'Dose-Response Relationship, Drug', 'Endothelial Progenitor Cells', 'Estrogen Receptor alpha', 'Estrogen Receptor beta', 'Estrogens', 'Female', 'Humans', 'Male', 'Sex Factors', 'Signal Transduction', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,859,892 |
Does lipoicmethylenedioxyphenol reduce Experimental Atherosclerosis through Activation of Nrf2 Signaling?
|
{
"contexts": [
"Oxidative stress is implicated in the pathogenesis of atherosclerosis, and Nrf2 is the transcriptional factor central in cellular antioxidant responses. In the present study, we investigate the effect of a dihydrolipoic acid derivative lipoicmethylenedioxyphenol (LMDP) on the progression of atherosclerosis and test whether its effect on atherosclerosis is mediated by Nrf2.",
"Both magnetic resonance imaging (MRI) scanning and en face analysis reveal that 14 weeks of treatment with LMDP markedly reduced atherosclerotic burden in a rabbit balloon vascular injury model. Myograph analyses show decreased aortic contractile response to phenylephrine and increased aortic response to acetylcholine and insulin in LMDP-treated animals, suggesting that LMDP inhibits atherosclerosis through improving vascular function. A role of Nrf2 signaling in mediating the amelioration of vascular function by LMDP was supported by increased Nrf2 translocation into nuclear and increased expression of Nrf2 target genes. Furthermore, chemotaxis analysis with Boydem chamber shows that leukocytes isolated from LMDP-treated rabbits had reduced chemotaxis, and knock-down of Nrf2 significantly reduced the effect of LMDP on the chemotaxis of mouse macrophages."
],
"labels": [
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Animals",
"Atherosclerosis",
"Blood Vessels",
"Chemotaxis, Leukocyte",
"Disease Models, Animal",
"Disease Progression",
"Male",
"Mice",
"NF-E2-Related Factor 2",
"Oxidative Stress",
"Phenol",
"Rabbits",
"Signal Transduction",
"Thioctic Acid"
]
}
|
Our results support that LMDP has an anti-atherosclerotic effect likely through activation of Nrf2 signaling and subsequent inhibition of macrophage chemotaxis.
|
yes
|
[
{
"from": "human",
"value": "Question: Does lipoicmethylenedioxyphenol reduce Experimental Atherosclerosis through Activation of Nrf2 Signaling?\nContext: {'contexts': ['Oxidative stress is implicated in the pathogenesis of atherosclerosis, and Nrf2 is the transcriptional factor central in cellular antioxidant responses. In the present study, we investigate the effect of a dihydrolipoic acid derivative lipoicmethylenedioxyphenol (LMDP) on the progression of atherosclerosis and test whether its effect on atherosclerosis is mediated by Nrf2.', 'Both magnetic resonance imaging (MRI) scanning and en face analysis reveal that 14 weeks of treatment with LMDP markedly reduced atherosclerotic burden in a rabbit balloon vascular injury model. Myograph analyses show decreased aortic contractile response to phenylephrine and increased aortic response to acetylcholine and insulin in LMDP-treated animals, suggesting that LMDP inhibits atherosclerosis through improving vascular function. A role of Nrf2 signaling in mediating the amelioration of vascular function by LMDP was supported by increased Nrf2 translocation into nuclear and increased expression of Nrf2 target genes. Furthermore, chemotaxis analysis with Boydem chamber shows that leukocytes isolated from LMDP-treated rabbits had reduced chemotaxis, and knock-down of Nrf2 significantly reduced the effect of LMDP on the chemotaxis of mouse macrophages.'], 'labels': ['OBJECTIVE', 'RESULTS'], 'meshes': ['Animals', 'Atherosclerosis', 'Blood Vessels', 'Chemotaxis, Leukocyte', 'Disease Models, Animal', 'Disease Progression', 'Male', 'Mice', 'NF-E2-Related Factor 2', 'Oxidative Stress', 'Phenol', 'Rabbits', 'Signal Transduction', 'Thioctic Acid']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,860,117 |
Does a novel missense mutation in ATRX uncovered in a Yemeni family lead to alpha-thalassemia/mental retardation syndrome without alpha-thalassemia?
|
{
"contexts": [
"Intellectual disability (ID) features in numerous heritable medical conditions that result from ATRX mutations. Alpha-thalassemia mental retardation syndrome (ATR-X syndrome) is the most notable manifestation of ATRX dysfunction. In addition to ID, genitourinary and craniofacial abnormalities are regularly observed with or without alpha-thalassemia.",
"The study sought to characterize two cases of ATR-X in a Yemeni family clinically and molecularly.",
"PCR amplification and Sanger sequencing were used to study the ATRX gene in a Yemeni family. Also, methylation-sensitive PCR was used to perform X-inactivation studies. CADD, SNAP2 and PolyPhen-2 helped to predict the functional consequences of the variant.",
"Molecular testing revealed a novel hemizygous missense mutation (c.5666T>G) in the ATRX gene in the two Yemeni brothers. This mutation was found in a heterozygous state in the mother, with the chromosome harboring the mutated allele being under strongly skewed X-inactivation."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Alleles",
"Heterozygote",
"Humans",
"Infant",
"Intellectual Disability",
"Male",
"Mental Retardation, X-Linked",
"Mutation, Missense",
"alpha-Thalassemia"
]
}
|
The mutated gene is predicted to have a disrupted SNF-2 domain at a conserved residue; p.Leu1889Trp, which is deemed functionally damaging. This report offers, for the first time, full clinical and molecular characterization of a novel ATRX variant in an Arab family.
|
yes
|
[
{
"from": "human",
"value": "Question: Does a novel missense mutation in ATRX uncovered in a Yemeni family lead to alpha-thalassemia/mental retardation syndrome without alpha-thalassemia?\nContext: {'contexts': ['Intellectual disability (ID) features in numerous heritable medical conditions that result from ATRX mutations. Alpha-thalassemia mental retardation syndrome (ATR-X syndrome) is the most notable manifestation of ATRX dysfunction. In addition to ID, genitourinary and craniofacial abnormalities are regularly observed with or without alpha-thalassemia.', 'The study sought to characterize two cases of ATR-X in a Yemeni family clinically and molecularly.', 'PCR amplification and Sanger sequencing were used to study the ATRX gene in a Yemeni family. Also, methylation-sensitive PCR was used to perform X-inactivation studies. CADD, SNAP2 and PolyPhen-2 helped to predict the functional consequences of the variant.', 'Molecular testing revealed a novel hemizygous missense mutation (c.5666T>G) in the ATRX gene in the two Yemeni brothers. This mutation was found in a heterozygous state in the mother, with the chromosome harboring the mutated allele being under strongly skewed X-inactivation.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Alleles', 'Heterozygote', 'Humans', 'Infant', 'Intellectual Disability', 'Male', 'Mental Retardation, X-Linked', 'Mutation, Missense', 'alpha-Thalassemia']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,873,055 |
Is primary and booster vaccination with an inactivated poliovirus vaccine ( IPV ) immunogenic and well-tolerated in infants and toddlers in China?
|
{
"contexts": [
"Replacing live-attenuated oral poliovirus vaccines (OPV) with inactivated poliovirus vaccines (IPV) is part of the global strategy to eradicate poliomyelitis. China was declared polio-free in 2000 but continues to record cases of vaccine-associated-poliomyelitis and vaccine-derived-poliovirus outbreaks. Two pilot safety studies and two larger immunogenicity trials evaluated the non-inferiority of IPV (Poliorix™, GSK Vaccines, Belgium) versus OPV in infants and booster vaccination in toddlers primed with either IPV or OPV in China.",
"In pilot safety studies, 25 infants received 3-dose IPV primary vaccination (Study A, www.clinicaltrial.gov NCT00937404) and 25 received an IPV booster after priming with three OPV doses (Study B, NCT01021293). In the randomised, controlled immunogenicity and safety trial (Study C, NCT00920439), infants received 3-dose primary vaccination with IPV (N=541) or OPV (N=535) at 2,3,4 months of age, and a booster IPV dose at 18-24 months (N=470, Study D, NCT01323647: extension of study C). Blood samples were collected before and one month post-dose-3 and booster. Reactogenicity was assessed using diary cards. Serious adverse events (SAEs) were captured throughout each study.",
"Study A and B showed that IPV priming and IPV boosting (after OPV) was safe. Study C: One month post-dose-3, all IPV and ≥ 98.3% OPV recipients had seroprotective antibody titres towards each poliovirus type. The immune response elicited by IPV was non-inferior to Chinese OPV. Seroprotective antibody titres persisted in ≥ 94.7% IPV and ≥ 96.1% OPV recipients at 18-24 months (Study D). IPV had a clinically acceptable safety profile in all studies. Grade 3 local and systemic reactions were uncommon. No SAEs were related to IPV administration."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Antibodies, Viral",
"Child, Preschool",
"Female",
"Humans",
"Immunization Schedule",
"Immunization, Secondary",
"Infant",
"Male",
"Pilot Projects",
"Poliomyelitis",
"Poliovirus Vaccine, Inactivated",
"Poliovirus Vaccine, Oral"
]
}
|
Trivalent IPV is non-inferior to OPV in terms of seroprotection (in the Chinese vaccination schedule) in infant and toddlers, with a clinically acceptable safety profile.
|
yes
|
[
{
"from": "human",
"value": "Question: Is primary and booster vaccination with an inactivated poliovirus vaccine ( IPV ) immunogenic and well-tolerated in infants and toddlers in China?\nContext: {'contexts': ['Replacing live-attenuated oral poliovirus vaccines (OPV) with inactivated poliovirus vaccines (IPV) is part of the global strategy to eradicate poliomyelitis. China was declared polio-free in 2000 but continues to record cases of vaccine-associated-poliomyelitis and vaccine-derived-poliovirus outbreaks. Two pilot safety studies and two larger immunogenicity trials evaluated the non-inferiority of IPV (Poliorix™, GSK Vaccines, Belgium) versus OPV in infants and booster vaccination in toddlers primed with either IPV or OPV in China.', 'In pilot safety studies, 25 infants received 3-dose IPV primary vaccination (Study A, www.clinicaltrial.gov NCT00937404) and 25 received an IPV booster after priming with three OPV doses (Study B, NCT01021293). In the randomised, controlled immunogenicity and safety trial (Study C, NCT00920439), infants received 3-dose primary vaccination with IPV (N=541) or OPV (N=535) at 2,3,4 months of age, and a booster IPV dose at 18-24 months (N=470, Study D, NCT01323647: extension of study C). Blood samples were collected before and one month post-dose-3 and booster. Reactogenicity was assessed using diary cards. Serious adverse events (SAEs) were captured throughout each study.', 'Study A and B showed that IPV priming and IPV boosting (after OPV) was safe. Study C: One month post-dose-3, all IPV and ≥ 98.3% OPV recipients had seroprotective antibody titres towards each poliovirus type. The immune response elicited by IPV was non-inferior to Chinese OPV. Seroprotective antibody titres persisted in ≥ 94.7% IPV and ≥ 96.1% OPV recipients at 18-24 months (Study D). IPV had a clinically acceptable safety profile in all studies. Grade 3 local and systemic reactions were uncommon. No SAEs were related to IPV administration.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Antibodies, Viral', 'Child, Preschool', 'Female', 'Humans', 'Immunization Schedule', 'Immunization, Secondary', 'Infant', 'Male', 'Pilot Projects', 'Poliomyelitis', 'Poliovirus Vaccine, Inactivated', 'Poliovirus Vaccine, Oral']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,868,728 |
Do african American Patients with Chronic Rhinosinusitis Have a Distinct Phenotype of Polyposis Associated with Increased Asthma Hospitalization?
|
{
"contexts": [
"Chronic rhinosinusitis (CRS) is a common inflammatory disease of the upper airways that is often categorized into subtypes including \"with\" and \"without\" nasal polyps. However, the influence of multiple important epidemiologic factors, including race, on CRS has not been investigated.",
"The present study assessed various phenotypic characteristics of CRS in patients, living in the United States, with different racial backgrounds.",
"We performed a large retrospective cohort study of patients with CRS treated at a large urban tertiary care referral center in Chicago.",
"African American (AA) patients with CRS living in Chicago were more likely to report hyposmia as a symptom of CRS. Furthermore, AA patients with CRS who failed medical therapy and required surgical intervention had a significantly higher frequency of nasal polyposis and aspirin-exacerbated respiratory disease, and a higher disease severity index on computed tomography imaging than did white patients with CRS. The increased polyposis in AAs was associated with increased hospitalization for asthma. There were no differences in the prevalence of atopy, asthma, atopic dermatitis, food allergy, duration of disease, or number of surgeries between different races."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"African Americans",
"Aged",
"Aspirin",
"Asthma",
"Chronic Disease",
"Female",
"Hospitalization",
"Humans",
"Illinois",
"Male",
"Middle Aged",
"Nasal Polyps",
"Phenotype",
"Retrospective Studies",
"Rhinitis",
"Severity of Illness Index",
"Sinusitis",
"Tertiary Care Centers"
]
}
|
AAs with refractory CRS are at increased risk for nasal polyposis, smell loss, aspirin-exacerbated respiratory disease, and a greater severity of disease based on imaging, resulting in increased health care utilization.
|
yes
|
[
{
"from": "human",
"value": "Question: Do african American Patients with Chronic Rhinosinusitis Have a Distinct Phenotype of Polyposis Associated with Increased Asthma Hospitalization?\nContext: {'contexts': ['Chronic rhinosinusitis (CRS) is a common inflammatory disease of the upper airways that is often categorized into subtypes including \"with\" and \"without\" nasal polyps. However, the influence of multiple important epidemiologic factors, including race, on CRS has not been investigated.', 'The present study assessed various phenotypic characteristics of CRS in patients, living in the United States, with different racial backgrounds.', 'We performed a large retrospective cohort study of patients with CRS treated at a large urban tertiary care referral center in Chicago.', 'African American (AA) patients with CRS living in Chicago were more likely to report hyposmia as a symptom of CRS. Furthermore, AA patients with CRS who failed medical therapy and required surgical intervention had a significantly higher frequency of nasal polyposis and aspirin-exacerbated respiratory disease, and a higher disease severity index on computed tomography imaging than did white patients with CRS. The increased polyposis in AAs was associated with increased hospitalization for asthma. There were no differences in the prevalence of atopy, asthma, atopic dermatitis, food allergy, duration of disease, or number of surgeries between different races.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'African Americans', 'Aged', 'Aspirin', 'Asthma', 'Chronic Disease', 'Female', 'Hospitalization', 'Humans', 'Illinois', 'Male', 'Middle Aged', 'Nasal Polyps', 'Phenotype', 'Retrospective Studies', 'Rhinitis', 'Severity of Illness Index', 'Sinusitis', 'Tertiary Care Centers']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,860,538 |
Does autophagy upregulation promote macrophages to escape mesoporous silica nanoparticle ( MSN ) -induced NF-κB-dependent inflammation?
|
{
"contexts": [
"Our previous studies (Int J Nanomed 10:22, 2015) have indicated that a single large dose of mesoporous silica nanoparticles (MSNs) can induce severe and selective nephrotoxicity, which is closely related to inflammation mediated by the NF-κB pathway. However, the effect of MSNs on other organs and the interactions of nanomaterials with biological systems remain rudimentary.",
"This study aimed to clarify the biological behaviour and influence of MSNs on macrophages.",
"The mice received a single intraperitoneal injection of a suspension of 150, 300 of 600 mg/kg MSNs, and RAW 264.7 cells were treated with MSNs at various concentrations and times. Cell viability was determined by MTT assay and LDH release assay. The NF-κB pathway and the target proinflammatory cytokines IL-1β and TNF-α were determined by western blotting or ELISA. Autophagy is considered as an emerging mechanism of nanomaterials. So the autophagic ultrastructural analysis, the determination of Beclin-1 and LC3 expression, and the calculation of LC3II dots were employed to verify autophagy activation. In addition, RNA interference, autophagy agonist and inhibitor were used to explore the role of autophagy in inflammation.",
"The results indicated that MSNs are internalized into macrophages and induce cytotoxicity in a dose- and time-dependent manner. The NF-κB pathway, IL-1β and TNF-α were induced and released by MSNs. The levels of Beclin-1 and LC3II dots were obviously up-regulated by MSNs, which indicated that autophagy was induced in the MSN-treated cells. Moreover, the enhanced autophagy can attenuate the inflammation mediated by the NF-κB pathway, whereas the inhibition of autophagy can contribute to inflammation."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Autophagy",
"Cell Line",
"Cell Survival",
"Female",
"Inflammation",
"Interleukin-1beta",
"Liver",
"Macrophages",
"Mice, Inbred BALB C",
"Microscopy, Electron, Transmission",
"NF-kappa B",
"Nanoparticles",
"Porosity",
"Silicon Dioxide",
"Tumor Necrosis Factor-alpha",
"Up-Regulation"
]
}
|
In summary, our results suggest that autophagy may be a possible protective factor in inflammation induced by MSNs in macrophages.
|
yes
|
[
{
"from": "human",
"value": "Question: Does autophagy upregulation promote macrophages to escape mesoporous silica nanoparticle ( MSN ) -induced NF-κB-dependent inflammation?\nContext: {'contexts': ['Our previous studies (Int J Nanomed 10:22, 2015) have indicated that a single large dose of mesoporous silica nanoparticles (MSNs) can induce severe and selective nephrotoxicity, which is closely related to inflammation mediated by the NF-κB pathway. However, the effect of MSNs on other organs and the interactions of nanomaterials with biological systems remain rudimentary.', 'This study aimed to clarify the biological behaviour and influence of MSNs on macrophages.', 'The mice received a single intraperitoneal injection of a suspension of 150, 300 of 600 mg/kg MSNs, and RAW 264.7 cells were treated with MSNs at various concentrations and times. Cell viability was determined by MTT assay and LDH release assay. The NF-κB pathway and the target proinflammatory cytokines IL-1β and TNF-α were determined by western blotting or ELISA. Autophagy is considered as an emerging mechanism of nanomaterials. So the autophagic ultrastructural analysis, the determination of Beclin-1 and LC3 expression, and the calculation of LC3II dots were employed to verify autophagy activation. In addition, RNA interference, autophagy agonist and inhibitor were used to explore the role of autophagy in inflammation.', 'The results indicated that MSNs are internalized into macrophages and induce cytotoxicity in a dose- and time-dependent manner. The NF-κB pathway, IL-1β and TNF-α were induced and released by MSNs. The levels of Beclin-1 and LC3II dots were obviously up-regulated by MSNs, which indicated that autophagy was induced in the MSN-treated cells. Moreover, the enhanced autophagy can attenuate the inflammation mediated by the NF-κB pathway, whereas the inhibition of autophagy can contribute to inflammation.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Autophagy', 'Cell Line', 'Cell Survival', 'Female', 'Inflammation', 'Interleukin-1beta', 'Liver', 'Macrophages', 'Mice, Inbred BALB C', 'Microscopy, Electron, Transmission', 'NF-kappa B', 'Nanoparticles', 'Porosity', 'Silicon Dioxide', 'Tumor Necrosis Factor-alpha', 'Up-Regulation']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,862,900 |
Does whole Rye Consumption improve Blood and Liver n-3 Fatty Acid Profile and Gut Microbiota Composition in Rats?
|
{
"contexts": [
"Whole rye (WR) consumption seems to be associated with beneficial health effects. Although rye fiber and polyphenols are thought to be bioactive, the mechanisms behind the health effects of WR have yet to be fully identified. This study in rats was designed to investigate whether WR can influence the metabolism of n-3 and n-6 long-chain fatty acids (LCFA) and gut microbiota composition.",
"For 12 weeks, rats were fed a diet containing either 50% WR or 50% refined rye (RR). The WR diet provided more fiber (+21%) and polyphenols (+29%) than the RR diet. Fat intake was the same in both diets and particularly involved similar amounts of essential (18-carbon) n-3 and n-6 LCFAs.",
"The WR diet significantly increased the 24-hour urinary excretion of polyphenol metabolites-including enterolactone-compared with the RR diet. The WR rats had significantly more n-3 LCFA-in particular, eicosapentanoic (EPA) and docosahexanoic (DHA) acids-in their plasma and liver. Compared with the RR diet, the WR diet brought significant changes in gut microbiota composition, with increased diversity in the feces (Shannon and Simpson indices), decreased Firmicutes/Bacteroidetes ratio and decreased proportions of uncultured Clostridiales cluster IA and Clostridium cluster IV in the feces. In contrast, no difference was found between groups with regards to cecum microbiota. The WR rats had lower concentrations of total short-chain fatty acids (SCFA) in cecum and feces (p<0.05). Finally, acetate was lower (p<0.001) in the cecum of WR rats while butyrate was lower (p<0.05) in the feces of WR rats."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Body Weight",
"Cecum",
"Diet",
"Docosahexaenoic Acids",
"Eicosapentaenoic Acid",
"Fatty Acids, Omega-3",
"Fatty Acids, Omega-6",
"Feces",
"Feeding Behavior",
"Gastrointestinal Microbiome",
"Intestines",
"Liver",
"Male",
"Mass Spectrometry",
"Oligonucleotide Array Sequence Analysis",
"Polyphenols",
"Rats",
"Rats, Wistar",
"Secale"
]
}
|
This study shows for the first time that WR consumption results in major biological modifications-increased plasma and liver n-3 EPA and DHA levels and improved gut microbiota profile, notably with increased diversity-known to provide health benefits. Unexpectedly, WR decreased SCFA levels in both cecum and feces. More studies are needed to understand the interactions between whole rye (fiber and polyphenols) and gut microbiota and also the mechanisms of action responsible for stimulating n-3 fatty acid metabolism.
|
yes
|
[
{
"from": "human",
"value": "Question: Does whole Rye Consumption improve Blood and Liver n-3 Fatty Acid Profile and Gut Microbiota Composition in Rats?\nContext: {'contexts': ['Whole rye (WR) consumption seems to be associated with beneficial health effects. Although rye fiber and polyphenols are thought to be bioactive, the mechanisms behind the health effects of WR have yet to be fully identified. This study in rats was designed to investigate whether WR can influence the metabolism of n-3 and n-6 long-chain fatty acids (LCFA) and gut microbiota composition.', 'For 12 weeks, rats were fed a diet containing either 50% WR or 50% refined rye (RR). The WR diet provided more fiber (+21%) and polyphenols (+29%) than the RR diet. Fat intake was the same in both diets and particularly involved similar amounts of essential (18-carbon) n-3 and n-6 LCFAs.', 'The WR diet significantly increased the 24-hour urinary excretion of polyphenol metabolites-including enterolactone-compared with the RR diet. The WR rats had significantly more n-3 LCFA-in particular, eicosapentanoic (EPA) and docosahexanoic (DHA) acids-in their plasma and liver. Compared with the RR diet, the WR diet brought significant changes in gut microbiota composition, with increased diversity in the feces (Shannon and Simpson indices), decreased Firmicutes/Bacteroidetes ratio and decreased proportions of uncultured Clostridiales cluster IA and Clostridium cluster IV in the feces. In contrast, no difference was found between groups with regards to cecum microbiota. The WR rats had lower concentrations of total short-chain fatty acids (SCFA) in cecum and feces (p<0.05). Finally, acetate was lower (p<0.001) in the cecum of WR rats while butyrate was lower (p<0.05) in the feces of WR rats.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Body Weight', 'Cecum', 'Diet', 'Docosahexaenoic Acids', 'Eicosapentaenoic Acid', 'Fatty Acids, Omega-3', 'Fatty Acids, Omega-6', 'Feces', 'Feeding Behavior', 'Gastrointestinal Microbiome', 'Intestines', 'Liver', 'Male', 'Mass Spectrometry', 'Oligonucleotide Array Sequence Analysis', 'Polyphenols', 'Rats', 'Rats, Wistar', 'Secale']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,864,436 |
Does decoration of intramyocellular lipid droplets with PLIN5 modulate fasting-induced insulin resistance and lipotoxicity in humans?
|
{
"contexts": [
"In contrast to insulin-resistant individuals, insulin-sensitive athletes possess high intramyocellular lipid content (IMCL), good mitochondrial function and high perilipin 5 (PLIN5) levels, suggesting a role for PLIN5 in benign IMCL storage. We hypothesised a role for PLIN5 in modulating fasting-mediated insulin resistance.",
"Twelve men were fasted for 60 h, before and after which muscle biopsies were taken and stained for lipid droplets (LDs), PLIN5 and laminin. Confocal microscopy images were analysed for LD size, number, PLIN5 association and subcellular distribution.",
"Fasting elevated IMCL content 2.8-fold and reduced insulin sensitivity (by 55%). Individuals with the most prominent increase in IMCL showed the least reduction in insulin sensitivity (r = 0.657; p = 0.028) and mitochondrial function (r = 0.896; p = 0.006). During fasting, PLIN5 gene expression or PLIN5 protein content in muscle homogenates was unaffected, microscopy analyses revealed that the fraction of PLIN5 associated with LDs (PLIN5+) increased significantly (+26%) upon fasting, suggesting PLIN5 redistribution. The significant increase in LD number (+23%) and size (+23%) upon fasting was entirely accounted for by PLIN5+ LDs, not by LDs devoid of PLIN5. Also the association between IMCL storage capacity and insulin resistance and mitochondrial dysfunction was only apparent for PLIN5+ LDs."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Blotting, Western",
"Fasting",
"Humans",
"Insulin Resistance",
"Laminin",
"Lipid Droplets",
"Male",
"Perilipin-5",
"Real-Time Polymerase Chain Reaction",
"Young Adult"
]
}
|
Fasting results in subcellular redistribution of PLIN5 and promotes the capacity to store excess fat in larger and more numerous PLIN5-decorated LDs. This associates with blunting of fasting-induced insulin resistance and mitochondrial dysfunction, suggesting a role for PLIN5 in the modulation of fasting-mediated lipotoxicity.
|
yes
|
[
{
"from": "human",
"value": "Question: Does decoration of intramyocellular lipid droplets with PLIN5 modulate fasting-induced insulin resistance and lipotoxicity in humans?\nContext: {'contexts': ['In contrast to insulin-resistant individuals, insulin-sensitive athletes possess high intramyocellular lipid content (IMCL), good mitochondrial function and high perilipin 5 (PLIN5) levels, suggesting a role for PLIN5 in benign IMCL storage. We hypothesised a role for PLIN5 in modulating fasting-mediated insulin resistance.', 'Twelve men were fasted for 60\\xa0h, before and after which muscle biopsies were taken and stained for lipid droplets (LDs), PLIN5 and laminin. Confocal microscopy images were analysed for LD size, number, PLIN5 association and subcellular distribution.', 'Fasting elevated IMCL content 2.8-fold and reduced insulin sensitivity (by 55%). Individuals with the most prominent increase in IMCL showed the least reduction in insulin sensitivity (r\\u2009=\\u20090.657; p\\u2009=\\u20090.028) and mitochondrial function (r\\u2009=\\u20090.896; p\\u2009=\\u20090.006). During fasting, PLIN5 gene expression or PLIN5 protein content in muscle homogenates was unaffected, microscopy analyses revealed that the fraction of PLIN5 associated with LDs (PLIN5+) increased significantly (+26%) upon fasting, suggesting PLIN5 redistribution. The significant increase in LD number (+23%) and size (+23%) upon fasting was entirely accounted for by PLIN5+ LDs, not by LDs devoid of PLIN5. Also the association between IMCL storage capacity and insulin resistance and mitochondrial dysfunction was only apparent for PLIN5+ LDs.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Blotting, Western', 'Fasting', 'Humans', 'Insulin Resistance', 'Laminin', 'Lipid Droplets', 'Male', 'Perilipin-5', 'Real-Time Polymerase Chain Reaction', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,861,149 |
Are the best objective response of target lesions and the incidence of treatment-related hypertension associated with the survival of patients with metastatic renal cell carcinoma treated with sunitinib : a Japanese retrospective study?
|
{
"contexts": [
"The aim of this study is to investigate the prognostic relevance of the best objective response of metastatic target lesions during sunitinib treatment in patients with metastatic renal cell carcinoma.",
"Radiographic analysis of the best objective response according to the Response Evaluation Criteria in Solid Tumors was assessed in 50 patients. Clinicopathological characteristics including the Heng risk classification and sunitinib-related adverse reactions were compared among four patient subgroups [complete response or partial response (CR/PR), stable disease (SD), progressive disease (PD), and those without treatment evaluation (NE)]. Kaplan-Meier and Cox proportional regression analyses of progression-free survival and overall survival were performed to identify prognostic variables.",
"The best objective response was CR/PR in 12 (24 %) patients, SD in 22 (44 %), PD in 6 (12 %), and NE in 10 (20 %). The incidence of hypertension and hypothyroidism was associated with a better objective response. Progression-free survival was 15.0, 9.2, 6.8, and 2.2 months in the CR/PR, SD, PD, and NE groups, respectively (P = 0.0004, log-rank test), while the corresponding median overall survival was 59.7, 24.2, 17.1, and 18.1 months, respectively (P = 0.007). Multivariate analysis revealed that hazard ratios for risk of death of the SD, PD, and NE groups were 4.51 (P = 0.06), 7.93 (P = 0.02), and 4.88 (P = 0.04), respectively, as compared to the CR/PR group."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Carcinoma, Renal Cell",
"Demography",
"Disease-Free Survival",
"Female",
"Humans",
"Hypertension",
"Incidence",
"Indoles",
"Japan",
"Kaplan-Meier Estimate",
"Male",
"Middle Aged",
"Multivariate Analysis",
"Proportional Hazards Models",
"Pyrroles",
"Retrospective Studies",
"Sunitinib",
"Treatment Outcome"
]
}
|
Our findings suggested that the best objective response of target lesions was a prognostic marker for both progression-free survival and overall survival in sunitinib treatment. Furthermore, the incidence of sunitinib-induced hypertension was associated with a longer progression-free survival.
|
yes
|
[
{
"from": "human",
"value": "Question: Are the best objective response of target lesions and the incidence of treatment-related hypertension associated with the survival of patients with metastatic renal cell carcinoma treated with sunitinib : a Japanese retrospective study?\nContext: {'contexts': ['The aim of this study is to investigate the prognostic relevance of the best objective response of metastatic target lesions during sunitinib treatment in patients with metastatic renal cell carcinoma.', 'Radiographic analysis of the best objective response according to the Response Evaluation Criteria in Solid Tumors was assessed in 50 patients. Clinicopathological characteristics including the Heng risk classification and sunitinib-related adverse reactions were compared among four patient subgroups [complete response or partial response (CR/PR), stable disease (SD), progressive disease (PD), and those without treatment evaluation (NE)]. Kaplan-Meier and Cox proportional regression analyses of progression-free survival and overall survival were performed to identify prognostic variables.', 'The best objective response was CR/PR in 12 (24\\xa0%) patients, SD in 22 (44\\xa0%), PD in 6 (12\\xa0%), and NE in 10\\xa0(20\\xa0%). The incidence of hypertension and hypothyroidism was associated with a better objective response. Progression-free survival was 15.0, 9.2, 6.8, and 2.2\\xa0months in the CR/PR, SD, PD, and NE groups, respectively (P\\xa0=\\xa00.0004, log-rank test), while the corresponding median overall survival was 59.7, 24.2, 17.1, and 18.1\\xa0months, respectively (P\\xa0=\\xa00.007). Multivariate analysis revealed that hazard ratios for risk of death of the SD, PD, and NE groups were 4.51 (P\\xa0=\\xa00.06), 7.93 (P\\xa0=\\xa00.02), and 4.88 (P\\xa0=\\xa00.04), respectively, as compared to the CR/PR group.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Carcinoma, Renal Cell', 'Demography', 'Disease-Free Survival', 'Female', 'Humans', 'Hypertension', 'Incidence', 'Indoles', 'Japan', 'Kaplan-Meier Estimate', 'Male', 'Middle Aged', 'Multivariate Analysis', 'Proportional Hazards Models', 'Pyrroles', 'Retrospective Studies', 'Sunitinib', 'Treatment Outcome']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,861,891 |
Does mGluR2/3 agonist LY379268 rescue NMDA and GABAA receptor level deficits induced in a two-hit mouse model of schizophrenia?
|
{
"contexts": [
"An imbalance of excitatory and inhibitory neurotransmission underlies the glutamate hypothesis of schizophrenia. Agonists of group II metabotropic glutamate receptors, mGluR2/3, have been proposed as novel therapeutic agents to correct this imbalance. However, the influence of mGluR2/3 activity on excitatory and inhibitory neurotransmitter receptors has not been explored.",
"We aimed to investigate the ability of a novel mGluR2/3 agonist, LY379268, to modulate the availability of the excitatory N-methyl-D-aspartate receptor (NMDA-R) and the inhibitory gamma-aminobutyrate-A receptor (GABAA-R), in a two-hit mouse model of schizophrenia.",
"Wild type (WT) and heterozygous neuregulin 1 transmembrane domain mutant mice (NRG1 HET) were treated daily with phencyclidine (10 mg/kg ip) or saline for 14 days. After a 14-day washout, an acute dose of the mGluR2/3 agonist LY379268 (3 mg/kg), olanzapine (antipsychotic drug comparison, 1.5 mg/kg), or saline was administered. NMDA-R and GABAA-R binding densities were examined by receptor autoradiography in several schizophrenia-relevant brain regions.",
"In both WT and NRG1 HET mice, phencyclidine treatment significantly reduced NMDA-R and GABAA-R binding density in the prefrontal cortex, hippocampus, and nucleus accumbens. Acute treatment with LY379268 restored NMDA-R and GABAA-R levels in the two-hit mouse model comparable to olanzapine."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Amino Acids",
"Animals",
"Antipsychotic Agents",
"Benzodiazepines",
"Bridged Bicyclo Compounds, Heterocyclic",
"Disease Models, Animal",
"Male",
"Mice",
"Mice, Inbred C57BL",
"Mice, Knockout",
"Nucleus Accumbens",
"Olanzapine",
"Phencyclidine",
"Prefrontal Cortex",
"Protein Binding",
"Receptors, GABA-A",
"Receptors, Metabotropic Glutamate",
"Receptors, N-Methyl-D-Aspartate",
"Schizophrenia"
]
}
|
We demonstrate that the mGluR2/3 agonist LY379268 restores excitatory and inhibitory deficits with similar efficiency as olanzapine in our two-hit schizophrenia mouse model. This study significantly contributes to our understanding of the mechanisms underlying the therapeutic effects of LY379268 and supports the use of agents aimed at mGluR2/3.
|
yes
|
[
{
"from": "human",
"value": "Question: Does mGluR2/3 agonist LY379268 rescue NMDA and GABAA receptor level deficits induced in a two-hit mouse model of schizophrenia?\nContext: {'contexts': ['An imbalance of excitatory and inhibitory neurotransmission underlies the glutamate hypothesis of schizophrenia. Agonists of group II metabotropic glutamate receptors, mGluR2/3, have been proposed as novel therapeutic agents to correct this imbalance. However, the influence of mGluR2/3 activity on excitatory and inhibitory neurotransmitter receptors has not been explored.', 'We aimed to investigate the ability of a novel mGluR2/3 agonist, LY379268, to modulate the availability of the excitatory N-methyl-D-aspartate receptor (NMDA-R) and the inhibitory gamma-aminobutyrate-A receptor (GABAA-R), in a two-hit mouse model of schizophrenia.', 'Wild type (WT) and heterozygous neuregulin 1 transmembrane domain mutant mice (NRG1 HET) were treated daily with phencyclidine (10 mg/kg ip) or saline for 14 days. After a 14-day washout, an acute dose of the mGluR2/3 agonist LY379268 (3 mg/kg), olanzapine (antipsychotic drug comparison, 1.5 mg/kg), or saline was administered. NMDA-R and GABAA-R binding densities were examined by receptor autoradiography in several schizophrenia-relevant brain regions.', 'In both WT and NRG1 HET mice, phencyclidine treatment significantly reduced NMDA-R and GABAA-R binding density in the prefrontal cortex, hippocampus, and nucleus accumbens. Acute treatment with LY379268 restored NMDA-R and GABAA-R levels in the two-hit mouse model comparable to olanzapine.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Amino Acids', 'Animals', 'Antipsychotic Agents', 'Benzodiazepines', 'Bridged Bicyclo Compounds, Heterocyclic', 'Disease Models, Animal', 'Male', 'Mice', 'Mice, Inbred C57BL', 'Mice, Knockout', 'Nucleus Accumbens', 'Olanzapine', 'Phencyclidine', 'Prefrontal Cortex', 'Protein Binding', 'Receptors, GABA-A', 'Receptors, Metabotropic Glutamate', 'Receptors, N-Methyl-D-Aspartate', 'Schizophrenia']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,867,567 |
Are hOX transcription factors potential targets and markers in malignant mesothelioma?
|
{
"contexts": [
"The HOX genes are a family of homeodomain-containing transcription factors that determine cellular identity during development and which are dys-regulated in some cancers. In this study we examined the expression and oncogenic function of HOX genes in mesothelioma, a cancer arising from the pleura or peritoneum which is associated with exposure to asbestos.",
"We tested the sensitivity of the mesothelioma-derived lines MSTO-211H, NCI-H28, NCI-H2052, and NCI-H226 to HXR9, a peptide antagonist of HOX protein binding to its PBX co-factor. Apoptosis was measured using a FACS-based assay with Annexin, and HOX gene expression profiles were established using RT-QPCR on RNA extracted from cell lines and primary mesotheliomas. The in vivo efficacy of HXR9 was tested in a mouse MSTO-211H flank tumor xenograft model.",
"We show that HOX genes are significantly dysregulated in malignant mesothelioma. Targeting HOX genes with HXR9 caused apoptotic cell death in all of the mesothelioma-derived cell lines, and prevented the growth of mesothelioma tumors in a mouse xenograft model. Furthermore, the sensitivity of these lines to HXR9 correlated with the relative expression of HOX genes that have either an oncogenic or tumor suppressive function in cancer. The analysis of HOX expression in primary mesothelioma tumors indicated that these cells could also be sensitive to the disruption of HOX activity by HXR9, and that the expression of HOXB4 is strongly associated with overall survival."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Apoptosis",
"Cell Line, Tumor",
"DNA-Binding Proteins",
"Gene Expression Regulation, Neoplastic",
"Homeodomain Proteins",
"Humans",
"Lung Neoplasms",
"Mesothelioma",
"Mice",
"Peptides",
"Pre-B-Cell Leukemia Transcription Factor 1",
"Proto-Oncogene Proteins",
"Transcription Factors",
"Xenograft Model Antitumor Assays"
]
}
|
HOX genes are a potential therapeutic target in mesothelioma, and HOXB4 expression correlates with overall survival.
|
yes
|
[
{
"from": "human",
"value": "Question: Are hOX transcription factors potential targets and markers in malignant mesothelioma?\nContext: {'contexts': ['The HOX genes are a family of homeodomain-containing transcription factors that determine cellular identity during development and which are dys-regulated in some cancers. In this study we examined the expression and oncogenic function of HOX genes in mesothelioma, a cancer arising from the pleura or peritoneum which is associated with exposure to asbestos.', 'We tested the sensitivity of the mesothelioma-derived lines MSTO-211H, NCI-H28, NCI-H2052, and NCI-H226 to HXR9, a peptide antagonist of HOX protein binding to its PBX co-factor. Apoptosis was measured using a FACS-based assay with Annexin, and HOX gene expression profiles were established using RT-QPCR on RNA extracted from cell lines and primary mesotheliomas. The in vivo efficacy of HXR9 was tested in a mouse MSTO-211H flank tumor xenograft model.', 'We show that HOX genes are significantly dysregulated in malignant mesothelioma. Targeting HOX genes with HXR9 caused apoptotic cell death in all of the mesothelioma-derived cell lines, and prevented the growth of mesothelioma tumors in a mouse xenograft model. Furthermore, the sensitivity of these lines to HXR9 correlated with the relative expression of HOX genes that have either an oncogenic or tumor suppressive function in cancer. The analysis of HOX expression in primary mesothelioma tumors indicated that these cells could also be sensitive to the disruption of HOX activity by HXR9, and that the expression of HOXB4 is strongly associated with overall survival.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Apoptosis', 'Cell Line, Tumor', 'DNA-Binding Proteins', 'Gene Expression Regulation, Neoplastic', 'Homeodomain Proteins', 'Humans', 'Lung Neoplasms', 'Mesothelioma', 'Mice', 'Peptides', 'Pre-B-Cell Leukemia Transcription Factor 1', 'Proto-Oncogene Proteins', 'Transcription Factors', 'Xenograft Model Antitumor Assays']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,876,630 |
Does use of population-referenced total activity count percentiles to assess and classify physical activity of population groups?
|
{
"contexts": [
"Population-referenced total activity counts per day (TAC/d) percentiles provide public health practitioners a standardized measure of physical activity (PA) volume obtained from an accelerometer that can be compared across populations. The purpose of this study was to describe the application of TAC/d population-referenced percentiles to characterize the PA levels of population groups relative to US estimates.",
"A total of 679 adults participating in the 2011 NYC Physical Activity Transit survey wore an ActiGraph accelerometer on their hip for seven consecutive days. Accelerometer-derived TAC/d was classified into age- and gender-specific quartiles of US population-referenced TAC/d to compare differences in the distributions by borough (N=5).",
"Males in Brooklyn, Manhattan, and Staten Island had significantly greater TAC/d than US males. Females in Brooklyn and Queens had significantly greater levels of TAC/d compared to US females. The proportion of males in each population-referenced TAC/d quartile varied significantly by borough (χ(2)(12)=2.63, p=0.002), with disproportionately more men in Manhattan and the Bronx found to be in the highest and lowest US population-referenced TAC/d quartiles, respectively. For females, there was no significant difference in US population-reference TAC/d quartile by borough (χ(2)(12)=1.09, p=0.36)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Accelerometry",
"Energy Metabolism",
"Exercise",
"Humans",
"Male",
"New York City",
"Surveys and Questionnaires",
"United States"
]
}
|
These results demonstrate the utility of population-referenced TAC/d percentiles in public health monitoring and surveillance. These findings also provide insights into the PA levels of NYC residents relative to the broader US population, which can be used to guide health promotion efforts.
|
yes
|
[
{
"from": "human",
"value": "Question: Does use of population-referenced total activity count percentiles to assess and classify physical activity of population groups?\nContext: {'contexts': ['Population-referenced total activity counts per day (TAC/d) percentiles provide public health practitioners a standardized measure of physical activity (PA) volume obtained from an accelerometer that can be compared across populations. The purpose of this study was to describe the application of TAC/d population-referenced percentiles to characterize the PA levels of population groups relative to US estimates.', 'A total of 679 adults participating in the 2011 NYC Physical Activity Transit survey wore an ActiGraph accelerometer on their hip for seven consecutive days. Accelerometer-derived TAC/d was classified into age- and gender-specific quartiles of US population-referenced TAC/d to compare differences in the distributions by borough (N=5).', 'Males in Brooklyn, Manhattan, and Staten Island had significantly greater TAC/d than US males. Females in Brooklyn and Queens had significantly greater levels of TAC/d compared to US females. The proportion of males in each population-referenced TAC/d quartile varied significantly by borough (χ(2)(12)=2.63, p=0.002), with disproportionately more men in Manhattan and the Bronx found to be in the highest and lowest US population-referenced TAC/d quartiles, respectively. For females, there was no significant difference in US population-reference TAC/d quartile by borough (χ(2)(12)=1.09, p=0.36).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Accelerometry', 'Energy Metabolism', 'Exercise', 'Humans', 'Male', 'New York City', 'Surveys and Questionnaires', 'United States']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,873,714 |
Do mRI features have a role in pre-surgical planning of colloid cyst removal?
|
{
"contexts": [
"Endoscopic resection is becoming a well-established treatment option for patients with colloid cysts of the third ventricle. A disadvantage of this approach is the decreased ability to resect cysts in their entirety. Correlations between magnetic resonance imaging (MRI) features and cyst content could potentially help surgeons decide on the extent of resection and approach. We attempted to identify a correlation between patients' MRI imaging patterns and difficult cyst removal, post-operative adverse outcomes and the need for cerebrospinal fluid (CSF) diversion, in order to detect markers that may affect pre-surgical planning.",
"A retrospective examination of all patients' records that underwent a colloid cyst excision attempt at our institution between 2001 and 2014, and which had a minimum 1-year follow-up was compiled.",
"Of the 25 patients fulfilling the criteria, we found cysts with a low T2 signal, specifically when combined with high T1 signal, to be significantly correlated with piecemeal, difficult removals. Correlation was also found between high T2 signal cysts and pre-operative hydrocephalus. Among patients that had pre-existing hydrocephalus, those that required a piecemeal removal possessed a strong trend towards a need for subsequent shunting."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Colloid Cysts",
"Female",
"Humans",
"Magnetic Resonance Imaging",
"Male",
"Middle Aged",
"Neuroendoscopy",
"Neurosurgical Procedures",
"Third Ventricle"
]
}
|
We found specific MRI features suggestive of difficult cyst excision. In a subgroup of patients with pre-operative hydrocephalus and imaging features suggestive of difficult removal, significantly higher rates of shunting were observed. We therefore recommend an open approach in cases of low T2, high T1 signal cysts with a diameter of over 15 mm, or CSF shunting in poor surgical candidates. Smaller cysts, with a low T1 signal, a high T2 signal and pre-operative hydrocephalus, constitute a subgroup in which we recommend endoscopic intervention as the procedure of choice.
|
yes
|
[
{
"from": "human",
"value": "Question: Do mRI features have a role in pre-surgical planning of colloid cyst removal?\nContext: {'contexts': [\"Endoscopic resection is becoming a well-established treatment option for patients with colloid cysts of the third ventricle. A disadvantage of this approach is the decreased ability to resect cysts in their entirety. Correlations between magnetic resonance imaging (MRI) features and cyst content could potentially help surgeons decide on the extent of resection and approach. We attempted to identify a correlation between patients' MRI imaging patterns and difficult cyst removal, post-operative adverse outcomes and the need for cerebrospinal fluid (CSF) diversion, in order to detect markers that may affect pre-surgical planning.\", \"A retrospective examination of all patients' records that underwent a colloid cyst excision attempt at our institution between 2001 and 2014, and which had a minimum 1-year follow-up was compiled.\", 'Of the 25 patients fulfilling the criteria, we found cysts with a low T2 signal, specifically when combined with high T1 signal, to be significantly correlated with piecemeal, difficult removals. Correlation was also found between high T2 signal cysts and pre-operative hydrocephalus. Among patients that had pre-existing hydrocephalus, those that required a piecemeal removal possessed a strong trend towards a need for subsequent shunting.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Colloid Cysts', 'Female', 'Humans', 'Magnetic Resonance Imaging', 'Male', 'Middle Aged', 'Neuroendoscopy', 'Neurosurgical Procedures', 'Third Ventricle']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,874,740 |
Does multimodality imaging demonstrate trafficking of liposomes preferentially to ischemic myocardium?
|
{
"contexts": [
"Nanoparticles may serve as a promising means to deliver novel therapeutics to the myocardium following myocardial infarction. We sought to determine whether lipid-based liposomal nanoparticles can be shown through different imaging modalities to specifically target injured myocardium following intravenous injection in an ischemia-reperfusion murine myocardial infarction model.",
"Mice underwent ischemia-reperfusion surgery and then either received tail-vein injection with gadolinium- and fluorescent-labeled liposomes or no injection (control). The hearts were harvested 24h later and underwent T1 and T2-weighted ex vivo imaging using a 7 Tesla Bruker magnet. The hearts were then sectioned for immunohistochemistry and optical fluorescent imaging.",
"The mean size of the liposomes was 100nm. T1-weighted signal intensity was significantly increased in the ischemic vs. the non-ischemic myocardium for mice that received liposomes compared with control. Optical imaging demonstrated significant fluorescence within the infarct area for the liposome group compared with control (163±31% vs. 13±14%, p=0.001) and fluorescent microscopy confirmed the presence of liposomes within the ischemic myocardium."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Albumins",
"Animals",
"Contrast Media",
"Disease Models, Animal",
"Fluorescent Dyes",
"Gadolinium DTPA",
"Immunohistochemistry",
"Injections, Intravenous",
"Liposomes",
"Magnetic Resonance Imaging",
"Male",
"Mice",
"Microscopy, Fluorescence",
"Myocardial Infarction",
"Myocardial Reperfusion Injury",
"Myocardium",
"Nanoparticles",
"Optical Imaging",
"Particle Size",
"Phosphatidylethanolamines",
"Tissue Distribution"
]
}
|
Liposomes traffic to the heart and preferentially home to regions of myocardial injury, enabling improved diagnosis of myocardial injury and could serve as a vehicle for drug delivery.
|
yes
|
[
{
"from": "human",
"value": "Question: Does multimodality imaging demonstrate trafficking of liposomes preferentially to ischemic myocardium?\nContext: {'contexts': ['Nanoparticles may serve as a promising means to deliver novel therapeutics to the myocardium following myocardial infarction. We sought to determine whether lipid-based liposomal nanoparticles can be shown through different imaging modalities to specifically target injured myocardium following intravenous injection in an ischemia-reperfusion murine myocardial infarction model.', 'Mice underwent ischemia-reperfusion surgery and then either received tail-vein injection with gadolinium- and fluorescent-labeled liposomes or no injection (control). The hearts were harvested 24h later and underwent T1 and T2-weighted ex vivo imaging using a 7 Tesla Bruker magnet. The hearts were then sectioned for immunohistochemistry and optical fluorescent imaging.', 'The mean size of the liposomes was 100nm. T1-weighted signal intensity was significantly increased in the ischemic vs. the non-ischemic myocardium for mice that received liposomes compared with control. Optical imaging demonstrated significant fluorescence within the infarct area for the liposome group compared with control (163±31% vs. 13±14%, p=0.001) and fluorescent microscopy confirmed the presence of liposomes within the ischemic myocardium.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Albumins', 'Animals', 'Contrast Media', 'Disease Models, Animal', 'Fluorescent Dyes', 'Gadolinium DTPA', 'Immunohistochemistry', 'Injections, Intravenous', 'Liposomes', 'Magnetic Resonance Imaging', 'Male', 'Mice', 'Microscopy, Fluorescence', 'Myocardial Infarction', 'Myocardial Reperfusion Injury', 'Myocardium', 'Nanoparticles', 'Optical Imaging', 'Particle Size', 'Phosphatidylethanolamines', 'Tissue Distribution']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,854,628 |
Does endophilin A2 protect H2O2-induced apoptosis by blockade of Bax translocation in rat basilar artery smooth muscle cells?
|
{
"contexts": [
"Apoptosis plays a central role in maintaining the normal cell number and tissue homeostasis. Endophilins are a family of evolutionarily conserved proteins that have the critical role in endocytosis. Here, we determined whether endophilin A2 (EndoII) contributes to hydrogen peroxide (H2O2)-induced apoptosis in rat basilar artery smooth muscle cells (BASMCs) and the underlying mechanisms.",
"By using small interference RNA (siRNA) and EndoII overexpression strategy, we found that EndoII siRNA knockdown reduced cell viability and promoted H2O2-induced cell apoptosis, evidenced by loss of mitochondrial membrane potential, release of cytochrome c, and activation of caspase-9, 3 and poly (ADP-ribose) polymerase (PARP). In contrast, EndoII overexpression showed opposite effects and inhibited H2O2-induced BASMCs apoptosis. Further studies revealed that there was a direct interaction between EndoII and Bax. Upon H2O2-induced apoptosis, the association of EndoII with Bax were significantly decreased, while the interaction of Bax/tBid were increased, accompanied by a translocation of Bax from cytosol to mitochondria. Knockdown of EndoII did not affect the expression of Bax, but further promoted the binding of Bax with tBid and favored the accumulation of Bax to mitochondria as well as Bax activation; whereas EndoII overexpression produced the opposite effects. In addition, EndoII siRNA aggravated, but EndoII overexpression alleviated, the reduction of Bcl-2 expression in H2O2-treated cells."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Acyltransferases",
"Animals",
"Apoptosis",
"Basilar Artery",
"Gene Expression Regulation",
"Humans",
"Hydrogen Peroxide",
"Membrane Potential, Mitochondrial",
"Mitochondria",
"Myocytes, Smooth Muscle",
"RNA, Small Interfering",
"Rats",
"bcl-2-Associated X Protein"
]
}
|
These data suggested a role of EndoII in protecting BASMCs apoptosis induced by H2O2, possibly by inhibiting the addressing of Bax to mitochondria. Targeting on EndoII may be a new strategy to treat apoptosis-associated diseases.
|
yes
|
[
{
"from": "human",
"value": "Question: Does endophilin A2 protect H2O2-induced apoptosis by blockade of Bax translocation in rat basilar artery smooth muscle cells?\nContext: {'contexts': ['Apoptosis plays a central role in maintaining the normal cell number and tissue homeostasis. Endophilins are a family of evolutionarily conserved proteins that have the critical role in endocytosis. Here, we determined whether endophilin A2 (EndoII) contributes to hydrogen peroxide (H2O2)-induced apoptosis in rat basilar artery smooth muscle cells (BASMCs) and the underlying mechanisms.', 'By using small interference RNA (siRNA) and EndoII overexpression strategy, we found that EndoII siRNA knockdown reduced cell viability and promoted H2O2-induced cell apoptosis, evidenced by loss of mitochondrial membrane potential, release of cytochrome c, and activation of caspase-9, 3 and poly (ADP-ribose) polymerase (PARP). In contrast, EndoII overexpression showed opposite effects and inhibited H2O2-induced BASMCs apoptosis. Further studies revealed that there was a direct interaction between EndoII and Bax. Upon H2O2-induced apoptosis, the association of EndoII with Bax were significantly decreased, while the interaction of Bax/tBid were increased, accompanied by a translocation of Bax from cytosol to mitochondria. Knockdown of EndoII did not affect the expression of Bax, but further promoted the binding of Bax with tBid and favored the accumulation of Bax to mitochondria as well as Bax activation; whereas EndoII overexpression produced the opposite effects. In addition, EndoII siRNA aggravated, but EndoII overexpression alleviated, the reduction of Bcl-2 expression in H2O2-treated cells.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Acyltransferases', 'Animals', 'Apoptosis', 'Basilar Artery', 'Gene Expression Regulation', 'Humans', 'Hydrogen Peroxide', 'Membrane Potential, Mitochondrial', 'Mitochondria', 'Myocytes, Smooth Muscle', 'RNA, Small Interfering', 'Rats', 'bcl-2-Associated X Protein']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,869,921 |
Is motor Performance Impaired Following Vestibular Stimulation in Ageing Mice?
|
{
"contexts": [
"Balance and maintaining postural equilibrium are important during stationary and dynamic movements to prevent falls, particularly in older adults. While our sense of balance is influenced by vestibular, proprioceptive, and visual information, this study focuses primarily on the vestibular component and its age-related effects on balance. C57Bl/6J mice of ages 1, 5-6, 8-9 and 27-28 months were tested using a combination of standard (such as grip strength and rotarod) and newly-developed behavioral tests (including balance beam and walking trajectory tests with a vestibular stimulus). In the current study, we confirm a decline in fore-limb grip strength and gross motor coordination as age increases. We also show that a vestibular stimulus of low frequency (2-3 Hz) and duration can lead to age-dependent changes in balance beam performance, which was evident by increases in latency to begin walking on the beam as well as the number of times hind-feet slip (FS) from the beam. Furthermore, aged mice (27-28 months) that received continuous access to a running wheel for 4 weeks did not improve when retested. Mice of ages 1, 10, 13 and 27-28 months were also tested for changes in walking trajectory as a result of the vestibular stimulus. While no linear relationship was observed between the changes in trajectory and age, 1-month-old mice were considerably less affected than mice of ages 10, 13 and 27-28 months."
],
"labels": [
"UNLABELLED"
],
"meshes": []
}
|
this study confirms there are age-related declines in grip strength and gross motor coordination. We also demonstrate age-dependent changes to finer motor abilities as a result of a low frequency and duration vestibular stimulus. These changes showed that while the ability to perform the balance beam task remained intact across all ages tested, behavioral changes in task performance were observed.
|
yes
|
[
{
"from": "human",
"value": "Question: Is motor Performance Impaired Following Vestibular Stimulation in Ageing Mice?\nContext: {'contexts': ['Balance and maintaining postural equilibrium are important during stationary and dynamic movements to prevent falls, particularly in older adults. While our sense of balance is influenced by vestibular, proprioceptive, and visual information, this study focuses primarily on the vestibular component and its age-related effects on balance. C57Bl/6J mice of ages 1, 5-6, 8-9 and 27-28 months were tested using a combination of standard (such as grip strength and rotarod) and newly-developed behavioral tests (including balance beam and walking trajectory tests with a vestibular stimulus). In the current study, we confirm a decline in fore-limb grip strength and gross motor coordination as age increases. We also show that a vestibular stimulus of low frequency (2-3 Hz) and duration can lead to age-dependent changes in balance beam performance, which was evident by increases in latency to begin walking on the beam as well as the number of times hind-feet slip (FS) from the beam. Furthermore, aged mice (27-28 months) that received continuous access to a running wheel for 4 weeks did not improve when retested. Mice of ages 1, 10, 13 and 27-28 months were also tested for changes in walking trajectory as a result of the vestibular stimulus. While no linear relationship was observed between the changes in trajectory and age, 1-month-old mice were considerably less affected than mice of ages 10, 13 and 27-28 months.'], 'labels': ['UNLABELLED'], 'meshes': []}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,848,932 |
Are maternal Dietary Patterns Associated with Lower Levels of Cardiometabolic Markers during Pregnancy?
|
{
"contexts": [
"Elevated levels of cardiometabolic markers are characteristic of normal pregnancy, however, insulin resistance and increased glucose, triglyceride, and cholesterol levels can adversely influence maternal and child health. Diet is a modifiable behaviour that could have significant impact on maternal cardiometabolic levels during pregnancy. We investigated the association between dietary patterns and cardiometabolic markers (glucose, insulin, insulin resistance (HOMA-IR), triglycerides, and cholesterol) during pregnancy.",
"Data from the Pregnancy, Infection, and Nutrition prospective cohort study (2000-05) was used (n = 513). Diet was assessed using a food frequency questionnaire. Dietary patterns were derived using latent class analysis (LCA) and the Dietary Approaches to Stop Hypertension (DASH) diet. Linear regression was used to examine the dietary patterns-cardiometabolic markers association during pregnancy.",
"Three dietary patterns evolved from the LCA characterised by high intakes of: (1) hamburgers, hot dogs, bacon, French fries, fried chicken, white bread, and soft drinks; (2) some vegetables, fruit juice, refined grains, mixed dishes, processed meat, and empty calorie foods; and (3) fruits, vegetables, whole grains, low-fat dairy, breakfast bars, and water. After adjustment for potential confounders including prepregnancy body mass index, a diet consistent with Latent Class 3 was negatively associated with maternal insulin (μU/mL: β = -0.12; 95% CI -0.23, -0.01) and HOMA-IR (β = -0.13; 95% CI -0.25, -0.00). Additionally, DASH scores within Tertile 3 (higher dietary quality) were also negatively associated with maternal triglycerides (mg/dL)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Biomarkers",
"Blood Glucose",
"Body Mass Index",
"Diet",
"Feeding Behavior",
"Female",
"Humans",
"Insulin Resistance",
"Maternal Nutritional Physiological Phenomena",
"North Carolina",
"Nutrition Assessment",
"Nutrition Surveys",
"Pregnancy",
"Pregnancy Complications, Cardiovascular",
"Pregnant Women",
"Prospective Studies",
"Risk Factors",
"Triglycerides"
]
}
|
The study findings suggest an association between maternal dietary patterns and several cardiometabolic markers during pregnancy.
|
yes
|
[
{
"from": "human",
"value": "Question: Are maternal Dietary Patterns Associated with Lower Levels of Cardiometabolic Markers during Pregnancy?\nContext: {'contexts': ['Elevated levels of cardiometabolic markers are characteristic of normal pregnancy, however, insulin resistance and increased glucose, triglyceride, and cholesterol levels can adversely influence maternal and child health. Diet is a modifiable behaviour that could have significant impact on maternal cardiometabolic levels during pregnancy. We investigated the association between dietary patterns and cardiometabolic markers (glucose, insulin, insulin resistance (HOMA-IR), triglycerides, and cholesterol) during pregnancy.', 'Data from the Pregnancy, Infection, and Nutrition prospective cohort study (2000-05) was used (n = 513). Diet was assessed using a food frequency questionnaire. Dietary patterns were derived using latent class analysis (LCA) and the Dietary Approaches to Stop Hypertension (DASH) diet. Linear regression was used to examine the dietary patterns-cardiometabolic markers association during pregnancy.', 'Three dietary patterns evolved from the LCA characterised by high intakes of: (1) hamburgers, hot dogs, bacon, French fries, fried chicken, white bread, and soft drinks; (2) some vegetables, fruit juice, refined grains, mixed dishes, processed meat, and empty calorie foods; and (3) fruits, vegetables, whole grains, low-fat dairy, breakfast bars, and water. After adjustment for potential confounders including prepregnancy body mass index, a diet consistent with Latent Class 3 was negatively associated with maternal insulin (μU/mL: β = -0.12; 95% CI -0.23, -0.01) and HOMA-IR (β = -0.13; 95% CI -0.25, -0.00). Additionally, DASH scores within Tertile 3 (higher dietary quality) were also negatively associated with maternal triglycerides (mg/dL).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Biomarkers', 'Blood Glucose', 'Body Mass Index', 'Diet', 'Feeding Behavior', 'Female', 'Humans', 'Insulin Resistance', 'Maternal Nutritional Physiological Phenomena', 'North Carolina', 'Nutrition Assessment', 'Nutrition Surveys', 'Pregnancy', 'Pregnancy Complications, Cardiovascular', 'Pregnant Women', 'Prospective Studies', 'Risk Factors', 'Triglycerides']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,859,826 |
Do high Plasma Concentrations of Zidovudine ( AZT ) Parallel Intracellular Concentrations of AZT-Triphosphates in Infants During Prevention of Mother-to-Child HIV-1 Transmission?
|
{
"contexts": [
"Zidovudine (AZT) is mainly used to prevent mother-to-child HIV-1 transmission (PMTCT). Despite serious concerns on AZT-associated toxicity, there is little information on pharmacokinetics of intracellular AZT metabolites in infants.",
"We conducted a prospective study in 31 HIV-uninfected infants who received AZT for PMTCT. Blood samples were obtained from 14 infants on postdelivery days (PDD) 1, 7, 14, and 28 and from 17 infants at 0 and 4 hours after dosing on PDD-1. Plasma AZT concentrations (pAZT) and intracellular concentrations of AZT-monophosphate (icAZT-MP), diphosphate (icAZT-DP), and triphosphate (icAZT-TP) were determined.",
"Plasma AZT and icAZT-MP concentrations were 2713 nmol/L and 79 fmol/10 cells in PDD-1, but decreased to 1437 nmol/L and 31 fmol/10 cells by PDD-28 (P = 0.02 and P = 0.07 for all PDDs, respectively), whereas those of icAZT-DP and icAZT-TP remained low throughout the sampling period (P = 0.29 and P = 0.61 for all PDDs, respectively) There were no differences in icAZT-TP between infants of the 2 mg/kg 4 times a day dose and 4 mg/kg twice daily dose (P = 0.25), whereas pAZT and icAZT-MP levels were higher in the latter (P < 0.01 and <0.01, respectively). The pAZT and icAZT-MP significantly increased from 0 to 4 hours after dosing (P < 0.001 and <0.001, respectively), whereas icAZT-DP, icAZT-TP levels were not changed (P = 0.41 and 0.33, respectively)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Anti-HIV Agents",
"Chromatography, High Pressure Liquid",
"Dideoxynucleotides",
"Female",
"HIV Infections",
"HIV-1",
"Humans",
"Infant, Newborn",
"Infectious Disease Transmission, Vertical",
"Longitudinal Studies",
"Male",
"Mothers",
"Pregnancy",
"Pregnancy Complications, Infectious",
"Prospective Studies",
"Thymine Nucleotides",
"Treatment Outcome",
"Young Adult",
"Zidovudine"
]
}
|
The level of icAZT-TP did not change with age, time, or a single dose despite the wide range of pAZT concentration. A safer dosage needs to be determined because high pAZT levels do not parallel those of icAZT-TP.
|
no
|
[
{
"from": "human",
"value": "Question: Do high Plasma Concentrations of Zidovudine ( AZT ) Parallel Intracellular Concentrations of AZT-Triphosphates in Infants During Prevention of Mother-to-Child HIV-1 Transmission?\nContext: {'contexts': ['Zidovudine (AZT) is mainly used to prevent mother-to-child HIV-1 transmission (PMTCT). Despite serious concerns on AZT-associated toxicity, there is little information on pharmacokinetics of intracellular AZT metabolites in infants.', 'We conducted a prospective study in 31 HIV-uninfected infants who received AZT for PMTCT. Blood samples were obtained from 14 infants on postdelivery days (PDD) 1, 7, 14, and 28 and from 17 infants at 0 and 4 hours after dosing on PDD-1. Plasma AZT concentrations (pAZT) and intracellular concentrations of AZT-monophosphate (icAZT-MP), diphosphate (icAZT-DP), and triphosphate (icAZT-TP) were determined.', 'Plasma AZT and icAZT-MP concentrations were 2713 nmol/L and 79 fmol/10 cells in PDD-1, but decreased to 1437 nmol/L and 31 fmol/10 cells by PDD-28 (P = 0.02 and P = 0.07 for all PDDs, respectively), whereas those of icAZT-DP and icAZT-TP remained low throughout the sampling period (P = 0.29 and P = 0.61 for all PDDs, respectively) There were no differences in icAZT-TP between infants of the 2 mg/kg 4 times a day dose and 4 mg/kg twice daily dose (P = 0.25), whereas pAZT and icAZT-MP levels were higher in the latter (P < 0.01 and <0.01, respectively). The pAZT and icAZT-MP significantly increased from 0 to 4 hours after dosing (P < 0.001 and <0.001, respectively), whereas icAZT-DP, icAZT-TP levels were not changed (P = 0.41 and 0.33, respectively).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Anti-HIV Agents', 'Chromatography, High Pressure Liquid', 'Dideoxynucleotides', 'Female', 'HIV Infections', 'HIV-1', 'Humans', 'Infant, Newborn', 'Infectious Disease Transmission, Vertical', 'Longitudinal Studies', 'Male', 'Mothers', 'Pregnancy', 'Pregnancy Complications, Infectious', 'Prospective Studies', 'Thymine Nucleotides', 'Treatment Outcome', 'Young Adult', 'Zidovudine']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
] |
26,853,309 |
Does minocycline Effectively protect the Rabbit 's Spinal Cord From Aortic Occlusion-Related Ischemia?
|
{
"contexts": [
"To identify the minocycline anti-inflammatory and antiapoptotic mechanisms through which it is believed to exert spinal cord protection during aortic occlusion in the rabbit model.",
"An animal model of aortic occlusion-related spinal cord ischemia. Randomized study with a control group and pre-ischemia and post-ischemia escalating doses of minocycline to high-dose minocycline in the presence of either hyperglycemia, a pro-apoptotic maneuver, or wortmannin, a specific phosphatidylinositol 3-kinase antagonist.",
"Tertiary medical center and school of medicine laboratory.",
"Laboratory animals-rabbits.",
"Balloon obstruction of infrarenal aorta introduced via femoral artery incision.",
"Severe hindlimb paralysis (mean Tarlov score 0.36±0.81 out of 3) was observed in all the control group animals (9 of 11 with paraplegia and 2 of 11 with paraparesis) compared with 11 of 12 neurologically intact animals (mean Tarlov score 2.58±0.90 [p = 0.001 compared with control]) in the high-dose minocycline group. This protective effect was observed partially during a state of hyperglycemia and was completely abrogated by wortmannin. Minocycline administration resulted in higher neurologic scores (p = 0.003) and a shift to viable neurons and more apoptotic-stained nuclei resulting from reduced necrosis (p = 0.001)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"METHODS",
"METHODS",
"METHODS",
"RESULTS"
],
"meshes": [
"Androstadienes",
"Animals",
"Anti-Inflammatory Agents",
"Aorta, Thoracic",
"Apoptosis",
"Balloon Occlusion",
"Dose-Response Relationship, Drug",
"Femoral Artery",
"Hindlimb",
"Male",
"Minocycline",
"Neurons",
"Paralysis",
"Rabbits",
"Spinal Cord Ischemia",
"Wortmannin"
]
}
|
In a rabbit model of infrarenal aortic occlusion, minocycline effectively reduced paraplegia by increasing the number of viable neurons in a dose-dependent manner. Its action was completely abrogated by inhibiting the phosphatidylinositol 3-kinase pathway and was inhibited partially by the pro-apoptotic hyperglycemia maneuver, indicating that the activation of cell salvage pathways and mitochondrial sites are possible targets of minocycline action in an ischemic spinal cord.
|
yes
|
[
{
"from": "human",
"value": "Question: Does minocycline Effectively protect the Rabbit 's Spinal Cord From Aortic Occlusion-Related Ischemia?\nContext: {'contexts': ['To identify the minocycline anti-inflammatory and antiapoptotic mechanisms through which it is believed to exert spinal cord protection during aortic occlusion in the rabbit model.', 'An animal model of aortic occlusion-related spinal cord ischemia. Randomized study with a control group and pre-ischemia and post-ischemia escalating doses of minocycline to high-dose minocycline in the presence of either hyperglycemia, a pro-apoptotic maneuver, or wortmannin, a specific phosphatidylinositol 3-kinase antagonist.', 'Tertiary medical center and school of medicine laboratory.', 'Laboratory animals-rabbits.', 'Balloon obstruction of infrarenal aorta introduced via femoral artery incision.', 'Severe hindlimb paralysis (mean Tarlov score 0.36±0.81 out of 3) was observed in all the control group animals (9 of 11 with paraplegia and 2 of 11 with paraparesis) compared with 11 of 12 neurologically intact animals (mean Tarlov score 2.58±0.90 [p = 0.001 compared with control]) in the high-dose minocycline group. This protective effect was observed partially during a state of hyperglycemia and was completely abrogated by wortmannin. Minocycline administration resulted in higher neurologic scores (p = 0.003) and a shift to viable neurons and more apoptotic-stained nuclei resulting from reduced necrosis (p = 0.001).'], 'labels': ['OBJECTIVE', 'METHODS', 'METHODS', 'METHODS', 'METHODS', 'RESULTS'], 'meshes': ['Androstadienes', 'Animals', 'Anti-Inflammatory Agents', 'Aorta, Thoracic', 'Apoptosis', 'Balloon Occlusion', 'Dose-Response Relationship, Drug', 'Femoral Artery', 'Hindlimb', 'Male', 'Minocycline', 'Neurons', 'Paralysis', 'Rabbits', 'Spinal Cord Ischemia', 'Wortmannin']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,865,394 |
Do nitric oxide-induced autophagy and the activation of AMPK pathway protect against apoptosis in human dental pulp cells?
|
{
"contexts": [
"To investigate the role of nitric oxide (NO)-induced autophagy in human dental pulp cells (HDPCs) and the involvement of AMP-activated protein kinase (AMPK) pathway.",
"The MTT assay was used to determine the cytotoxic effect of the NO donor sodium nitroprusside (SNP) in HDPCs. Apoptosis was detected by means of the terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay, and apoptosis- or autophagy-related signal molecules were observed by Western blot analysis. Acidic autophagolysosomal vacuoles were stained with acridine orange to detect autophagy in the presence of 3-methyladenine (3MA) used to inhibit autophagy. To explore the mechanism underlying autophagy and its protective role against apoptosis, compound C, the chemical AMPK inhibitor, was used. Statistical analysis was performed using Student's t-test or analysis of variance (ANOVA) followed by the Student-Newman-Keuls test (p<0.05).",
"SNP decreased viability of the HDPCs in a dose- and time-dependent manner. Exposing the HDPCs to SNP increased the levels of p62 and LC3-II, the typical markers of autophagy, and increased the number of acidic autophagolysosomal vacuoles, indicating the appearance of autophagy as detected by acridine orange staining (p<0.05). Pretreatment with 3MA decreased cell viability but increased cleaved poly (ADP-ribose) polymerase (PARP) and caspase-3, apoptosis indicators, in the SNP-treated HDPCs (p<0.05). SNP activated AMPK/ULK signaling, while the inhibition of AMPK by compound C enhanced apoptotic cell death induced by SNP in the HDPCs (p<0.05)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"AMP-Activated Protein Kinases",
"Apoptosis",
"Autophagy",
"Cells, Cultured",
"Dental Pulp",
"Humans",
"Nitric Oxide",
"TOR Serine-Threonine Kinases"
]
}
|
NO induced autophagy with AMPK activation, which plays a role in the survival of HDPCs against NO-induced apoptosis. This article is protected by copyright. All rights reserved.
|
yes
|
[
{
"from": "human",
"value": "Question: Do nitric oxide-induced autophagy and the activation of AMPK pathway protect against apoptosis in human dental pulp cells?\nContext: {'contexts': ['To investigate the role of nitric oxide (NO)-induced autophagy in human dental pulp cells (HDPCs) and the involvement of AMP-activated protein kinase (AMPK) pathway.', \"The MTT assay was used to determine the cytotoxic effect of the NO donor sodium nitroprusside (SNP) in HDPCs. Apoptosis was detected by means of the terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay, and apoptosis- or autophagy-related signal molecules were observed by Western blot analysis. Acidic autophagolysosomal vacuoles were stained with acridine orange to detect autophagy in the presence of 3-methyladenine (3MA) used to inhibit autophagy. To explore the mechanism underlying autophagy and its protective role against apoptosis, compound C, the chemical AMPK inhibitor, was used. Statistical analysis was performed using Student's t-test or analysis of variance (ANOVA) followed by the Student-Newman-Keuls test (p<0.05).\", 'SNP decreased viability of the HDPCs in a dose- and time-dependent manner. Exposing the HDPCs to SNP increased the levels of p62 and LC3-II, the typical markers of autophagy, and increased the number of acidic autophagolysosomal vacuoles, indicating the appearance of autophagy as detected by acridine orange staining (p<0.05). Pretreatment with 3MA decreased cell viability but increased cleaved poly (ADP-ribose) polymerase (PARP) and caspase-3, apoptosis indicators, in the SNP-treated HDPCs (p<0.05). SNP activated AMPK/ULK signaling, while the inhibition of AMPK by compound C enhanced apoptotic cell death induced by SNP in the HDPCs (p<0.05).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['AMP-Activated Protein Kinases', 'Apoptosis', 'Autophagy', 'Cells, Cultured', 'Dental Pulp', 'Humans', 'Nitric Oxide', 'TOR Serine-Threonine Kinases']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,873,514 |
Does glycerol Monolaurate inhibit Lipase Production by Clinical Ocular Isolates Without Affecting Bacterial Cell Viability?
|
{
"contexts": [
"We sought to determine the relative lipase production of a range of ocular bacterial isolates and to assess the efficacy of glycerol monolaurate (GML) in inhibiting this lipase production in high lipase-producing bacteria without affecting bacterial cell growth.",
"Staphylococcus aureus,Staphylococcus epidermidis,Propionibacterium acnes, and Corynebacterium spp. were inoculated at a density of 10(6)/mL in varying concentrations of GML up to 25 μg/mL for 24 hours at 37 °C with constant shaking. Bacterial suspensions were centrifuged, bacterial cell density was determined, and production of bacterial lipase was quantified using a commercial lipase assay kit.",
"Staphylococcus spp. produced high levels of lipase activity compared with P. acnes and Corynebacterium spp. GML inhibited lipase production by Staphylococcal spp. in a dose-dependent manner, with S. epidermidis lipase production consistently more sensitive to GML than S. aureus. Glycerol monolaurate showed significant (P < 0.05) lipase inhibition above concentrations of 15 μg/mL in S. aureus and was not cytotoxic up to 25 μg/mL. For S. epidermidis, GML showed significant (P < 0.05) lipase inhibition above 7.5 μg/mL."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Cell Survival",
"Colorimetry",
"Eye Infections, Bacterial",
"Humans",
"Laurates",
"Lipase",
"Microbial Sensitivity Tests",
"Monoglycerides",
"Staphylococcal Infections",
"Staphylococcus aureus",
"Surface-Active Agents"
]
}
|
Lipase activity varied between species and between strains. Staphylococcal spp. produced higher lipase activity compared with P. acnes and Corynebacterium spp. Glycerol monolaurate inhibited lipase production by S. aureus and S. epidermidis at concentrations that did not adversely affect bacterial cell growth. GML can be used to inhibit ocular bacterial lipase production without proving detrimental to commensal bacteria viability.
|
yes
|
[
{
"from": "human",
"value": "Question: Does glycerol Monolaurate inhibit Lipase Production by Clinical Ocular Isolates Without Affecting Bacterial Cell Viability?\nContext: {'contexts': ['We sought to determine the relative lipase production of a range of ocular bacterial isolates and to assess the efficacy of glycerol monolaurate (GML) in inhibiting this lipase production in high lipase-producing bacteria without affecting bacterial cell growth.', 'Staphylococcus aureus,Staphylococcus epidermidis,Propionibacterium acnes, and Corynebacterium spp. were inoculated at a density of 10(6)/mL in varying concentrations of GML up to 25 μg/mL for 24 hours at 37 °C with constant shaking. Bacterial suspensions were centrifuged, bacterial cell density was determined, and production of bacterial lipase was quantified using a commercial lipase assay kit.', 'Staphylococcus spp. produced high levels of lipase activity compared with P. acnes and Corynebacterium spp. GML inhibited lipase production by Staphylococcal spp. in a dose-dependent manner, with S. epidermidis lipase production consistently more sensitive to GML than S. aureus. Glycerol monolaurate showed significant (P < 0.05) lipase inhibition above concentrations of 15 μg/mL in S. aureus and was not cytotoxic up to 25 μg/mL. For S. epidermidis, GML showed significant (P < 0.05) lipase inhibition above 7.5 μg/mL.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Cell Survival', 'Colorimetry', 'Eye Infections, Bacterial', 'Humans', 'Laurates', 'Lipase', 'Microbial Sensitivity Tests', 'Monoglycerides', 'Staphylococcal Infections', 'Staphylococcus aureus', 'Surface-Active Agents']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,854,086 |
Is bAP1 overexpressed in black compared with white patients with Mx-M1 clear cell renal cell carcinoma : A report from the cancer genome atlas?
|
{
"contexts": [
"Incidence of renal cell carcinoma (RCC) is higher in Black patients with disease-specific and overall survival being lower compared with White patients even though renal tumors among Black patients are more likely to be localized. These disparities have been attributed to higher rates of obesity and hypertension, lower rates of nephrectomy, and a lack of access to quality health care. With scant genomic evidence to account for these disparities, the present study sought to compare BAP1 expression between Black and White patients with clear cell RCC (ccRCC); a gene that inhibits tumor progression when overexpressed and results in poor clinical outcomes when silenced.",
"The cancer genome atlas dataset was used to identify 58 (9.9%) Black and 529 (90.9%) White patients with ccRCC with an initial pathologic diagnosis from 1998 to 2013. BAP1 expression was compared using a Mann-Whitney U test. The association between BAP1 expression and pathologic stage, American Joint Committee on Cancer (AJCC) stage, and Fuhrman grade was assessed for the overall cohort and stratified by race. The association between BAP1 expression and overall survival was assessed using Cox proportion hazards models adjusting for Fuhrman grade, pathologic stage, and the presence of pathologic metastases for the overall cohort and stratified by race.",
"The level of BAP1 expression was significantly higher in Black vs. White patients with ccRCC (10.5 vs. 10.3; P<.001). For the overall cohort, increasing BAP1 expression was associated with decreasing pathologic stage (β =-0.25, P = .004) and decreasing AJCC stage (β =-0.029, P = .006). For Black patients, increasing BAP1 expression was associated with decreasing AJCC stage (β =-0.79, P = .016), decreasing Fuhrman grade (β =-0.55, P = .011), and a decreased risk of pathologic metastases (odds ratio [OR] = 0.83, P = .038). For White patients, increasing BAP1 expression was associated with decreasing pathologic stage (β =-0.20, P = .026)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"African Continental Ancestry Group",
"Aged",
"Carcinoma, Renal Cell",
"European Continental Ancestry Group",
"Female",
"Humans",
"Kidney Neoplasms",
"Male",
"Middle Aged",
"Neoplasm Staging",
"Nephrectomy",
"Prognosis",
"Tumor Suppressor Proteins",
"Ubiquitin Thiolesterase"
]
}
|
BAP1 is significantly overexpressed in Black compared with White patients and is associated with favorable stage. BAP1 overexpression portends distinct pathologic outcomes in Black and White patients demonstrating the need for racial stratification and adequate Black patient sampling in BAP1 biomarker studies.
|
yes
|
[
{
"from": "human",
"value": "Question: Is bAP1 overexpressed in black compared with white patients with Mx-M1 clear cell renal cell carcinoma : A report from the cancer genome atlas?\nContext: {'contexts': ['Incidence of renal cell carcinoma (RCC) is higher in Black patients with disease-specific and overall survival being lower compared with White patients even though renal tumors among Black patients are more likely to be localized. These disparities have been attributed to higher rates of obesity and hypertension, lower rates of nephrectomy, and a lack of access to quality health care. With scant genomic evidence to account for these disparities, the present study sought to compare BAP1 expression between Black and White patients with clear cell RCC (ccRCC); a gene that inhibits tumor progression when overexpressed and results in poor clinical outcomes when silenced.', 'The cancer genome atlas dataset was used to identify 58 (9.9%) Black and 529 (90.9%) White patients with ccRCC with an initial pathologic diagnosis from 1998 to 2013. BAP1 expression was compared using a Mann-Whitney U test. The association between BAP1 expression and pathologic stage, American Joint Committee on Cancer (AJCC) stage, and Fuhrman grade was assessed for the overall cohort and stratified by race. The association between BAP1 expression and overall survival was assessed using Cox proportion hazards models adjusting for Fuhrman grade, pathologic stage, and the presence of pathologic metastases for the overall cohort and stratified by race.', 'The level of BAP1 expression was significantly higher in Black vs. White patients with ccRCC (10.5 vs. 10.3; P<.001). For the overall cohort, increasing BAP1 expression was associated with decreasing pathologic stage (β =-0.25, P = .004) and decreasing AJCC stage (β =-0.029, P = .006). For Black patients, increasing BAP1 expression was associated with decreasing AJCC stage (β =-0.79, P = .016), decreasing Fuhrman grade (β =-0.55, P = .011), and a decreased risk of pathologic metastases (odds ratio [OR] = 0.83, P = .038). For White patients, increasing BAP1 expression was associated with decreasing pathologic stage (β =-0.20, P = .026).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['African Continental Ancestry Group', 'Aged', 'Carcinoma, Renal Cell', 'European Continental Ancestry Group', 'Female', 'Humans', 'Kidney Neoplasms', 'Male', 'Middle Aged', 'Neoplasm Staging', 'Nephrectomy', 'Prognosis', 'Tumor Suppressor Proteins', 'Ubiquitin Thiolesterase']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,879,192 |
Is lymph node hypoplasia associated with adverse outcomes in node-negative colon cancer using advanced lymph node dissection methods?
|
{
"contexts": [
"Lymph node size as a prognostic parameter has not been investigated well in the past. Recent data, however, have indicated that this parameter could be even more important than the lymph node count.",
"Based on the results of earlier studies, we analyzed the lymph node size and number of node-negative colon cancer patients with regard to survival. Data from 115 node-negative cases of colon cancer were analyzed. Lymph nodes with diameters ≤5 mm were defined as small, and all other lymph nodes were classified as intermediate/large in size and labeled LN5. All of the cases were categorized according to the number of LN5s. The LN5 very low (LN5vl) group included cases with less than two LN5s. All of the other cases were assigned to the LN5 low/high (LN5l/h) group.",
"The overall survival analysis revealed significantly worse outcomes for the LN5vl group, with a mean survival of 34 months compared to the LN5l/h group, with a mean survival of 40 months (P = 0.022). After adjusting for the pT1/2 and pT3/4 stages, we still found a significant outcome difference (P = 0.012). Multivariate analysis identified LN5vl and T-stage as being independently correlated with the outcome. The vast majority of LN5vl cases (91 %) were located in the left colon. The location itself, however, was not prognostic (P = 0.478)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aged",
"Aged, 80 and over",
"Cohort Studies",
"Colonic Neoplasms",
"Female",
"Humans",
"Lymph Node Excision",
"Lymph Nodes",
"Male",
"Methylene Blue",
"Middle Aged",
"Neoplasm Invasiveness",
"Reproducibility of Results",
"Survival Analysis",
"Survival Rate"
]
}
|
LN5 count, as a marker of immune response, could be shown as being prognostic in node-negative colon cancer. Patients with low LN5 counts showed poor outcomes. These patients could perhaps profit from adjuvant chemotherapy.
|
yes
|
[
{
"from": "human",
"value": "Question: Is lymph node hypoplasia associated with adverse outcomes in node-negative colon cancer using advanced lymph node dissection methods?\nContext: {'contexts': ['Lymph node size as a prognostic parameter has not been investigated well in the past. Recent data, however, have indicated that this parameter could be even more important than the lymph node count.', 'Based on the results of earlier studies, we analyzed the lymph node size and number of node-negative colon cancer patients with regard to survival. Data from 115 node-negative cases of colon cancer were analyzed. Lymph nodes with diameters ≤5 mm were defined as small, and all other lymph nodes were classified as intermediate/large in size and labeled LN5. All of the cases were categorized according to the number of LN5s. The LN5 very low (LN5vl) group included cases with less than two LN5s. All of the other cases were assigned to the LN5 low/high (LN5l/h) group.', 'The overall survival analysis revealed significantly worse outcomes for the LN5vl group, with a mean survival of 34 months compared to the LN5l/h group, with a mean survival of 40 months (P\\u2009=\\u20090.022). After adjusting for the pT1/2 and pT3/4 stages, we still found a significant outcome difference (P\\u2009=\\u20090.012). Multivariate analysis identified LN5vl and T-stage as being independently correlated with the outcome. The vast majority of LN5vl cases (91 %) were located in the left colon. The location itself, however, was not prognostic (P\\u2009=\\u20090.478).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aged', 'Aged, 80 and over', 'Cohort Studies', 'Colonic Neoplasms', 'Female', 'Humans', 'Lymph Node Excision', 'Lymph Nodes', 'Male', 'Methylene Blue', 'Middle Aged', 'Neoplasm Invasiveness', 'Reproducibility of Results', 'Survival Analysis', 'Survival Rate']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,863,419 |
Does low Cardiac Output lead Hepatic Fibrosis in Right Heart Failure Model Rats?
|
{
"contexts": [
"Hepatic fibrosis progresses with right heart failure, and becomes cardiac cirrhosis in a severe case. Although its causal factor still remains unclear. Here we evaluated the progression of hepatic fibrosis using a pulmonary artery banding (PAB)-induced right heart failure model and investigated whether cardiac output (CO) is responsible for the progression of hepatic fibrosis.",
"Five-week-old Sprague-Dawley rats divided into the PAB and sham-operated control groups. After 4 weeks from operation, we measured CO by echocardiography, and hepatic fibrosis ratio by pathological examination using a color analyzer. In the PAB group, CO was significantly lower by 48% than that in the control group (78.2±27.6 and 150.1±31.2 ml/min, P<0.01). Hepatic fibrosis ratio and serum hyaluronic acid, an index of hepatic fibrosis, were significantly increased in the PAB group than those in the control group (7.8±1.7 and 1.0±0.2%, P<0.01, 76.2±27.5 and 32.7±7.5 ng/ml, P<0.01). Notably, the degree of hepatic fibrosis significantly correlated a decrease in CO. Immunohistological analysis revealed that hepatic stellate cells were markedly activated in hypoxic areas, and HIF-1α positive hepatic cells were increased in the PAB group. Furthermore, by real-time PCR analyses, transcripts of profibrotic and fibrotic factors (TGF-β1, CTGF, procollargen I, procollargen III, MMP 2, MMP 9, TIMP 1, TIMP 2) were significantly increased in the PAB group. In addition, western blot analyses revealed that the protein level of HIF-1α was significantly increased in the PAB group than that in the control group (2.31±0.84 and 1.0±0.18 arbitrary units, P<0.05)."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Animals",
"Cardiac Output, Low",
"Cell Hypoxia",
"Disease Models, Animal",
"Gene Expression",
"Heart Failure",
"Hyaluronic Acid",
"Hypoxia-Inducible Factor 1, alpha Subunit",
"Liver",
"Liver Cirrhosis",
"Male",
"Myofibroblasts",
"Rats, Sprague-Dawley"
]
}
|
Our study demonstrated that low CO and tissue hypoxia were responsible for hepatic fibrosis in right failure heart model rats.
|
yes
|
[
{
"from": "human",
"value": "Question: Does low Cardiac Output lead Hepatic Fibrosis in Right Heart Failure Model Rats?\nContext: {'contexts': ['Hepatic fibrosis progresses with right heart failure, and becomes cardiac cirrhosis in a severe case. Although its causal factor still remains unclear. Here we evaluated the progression of hepatic fibrosis using a pulmonary artery banding (PAB)-induced right heart failure model and investigated whether cardiac output (CO) is responsible for the progression of hepatic fibrosis.', 'Five-week-old Sprague-Dawley rats divided into the PAB and sham-operated control groups. After 4 weeks from operation, we measured CO by echocardiography, and hepatic fibrosis ratio by pathological examination using a color analyzer. In the PAB group, CO was significantly lower by 48% than that in the control group (78.2±27.6 and 150.1±31.2 ml/min, P<0.01). Hepatic fibrosis ratio and serum hyaluronic acid, an index of hepatic fibrosis, were significantly increased in the PAB group than those in the control group (7.8±1.7 and 1.0±0.2%, P<0.01, 76.2±27.5 and 32.7±7.5 ng/ml, P<0.01). Notably, the degree of hepatic fibrosis significantly correlated a decrease in CO. Immunohistological analysis revealed that hepatic stellate cells were markedly activated in hypoxic areas, and HIF-1α positive hepatic cells were increased in the PAB group. Furthermore, by real-time PCR analyses, transcripts of profibrotic and fibrotic factors (TGF-β1, CTGF, procollargen I, procollargen III, MMP 2, MMP 9, TIMP 1, TIMP 2) were significantly increased in the PAB group. In addition, western blot analyses revealed that the protein level of HIF-1α was significantly increased in the PAB group than that in the control group (2.31±0.84 and 1.0±0.18 arbitrary units, P<0.05).'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Animals', 'Cardiac Output, Low', 'Cell Hypoxia', 'Disease Models, Animal', 'Gene Expression', 'Heart Failure', 'Hyaluronic Acid', 'Hypoxia-Inducible Factor 1, alpha Subunit', 'Liver', 'Liver Cirrhosis', 'Male', 'Myofibroblasts', 'Rats, Sprague-Dawley']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,850,884 |
Does cyclic stretch enhance apoptosis in human lumbar ligamentum flavum cells via the induction of reactive oxygen species generation?
|
{
"contexts": [
"The lumbar ligamentum flavum (LF) is an important part of the spine to maintain the stability of the spine. In this study we aimed to examine whether mechanical force by cyclic stretch could induce apoptosis in human LF cells and investigate the underlying mechanism.",
"LF cells were isolated from six young patients undergoing spinal surgery and then cultured in vitro. LF cells were subjected to cyclic stretch and the poptosis was detected by flow cytometry. The level of intracellular reactive oxygen species (ROS) and caspase-9 activity were measured.",
"Cyclic stretch at a frequency of 0.5 Hz with 20% elongation induced the apoptosis of human LF cells in vitro, and this was correlated with increased ROS generation and activation of caspase-9."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Apoptosis",
"Caspase 9",
"Cells, Cultured",
"Humans",
"Ligamentum Flavum",
"Reactive Oxygen Species",
"Stress, Mechanical"
]
}
|
Our study suggests that cyclic stretch-induced apoptosis in human LF cells may be mediated by ROS generation and the activation of caspase-9.
|
yes
|
[
{
"from": "human",
"value": "Question: Does cyclic stretch enhance apoptosis in human lumbar ligamentum flavum cells via the induction of reactive oxygen species generation?\nContext: {'contexts': ['The lumbar ligamentum flavum (LF) is an important part of the spine to maintain the stability of the spine. In this study we aimed to examine whether mechanical force by cyclic stretch could induce apoptosis in human LF cells and investigate the underlying mechanism.', 'LF cells were isolated from six young patients undergoing spinal surgery and then cultured in vitro. LF cells were subjected to cyclic stretch and the poptosis was detected by flow cytometry. The level of intracellular reactive oxygen species (ROS) and caspase-9 activity were measured.', 'Cyclic stretch at a frequency of 0.5\\u2005Hz with 20% elongation induced the apoptosis of human LF cells in vitro, and this was correlated with increased ROS generation and activation of caspase-9.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Apoptosis', 'Caspase 9', 'Cells, Cultured', 'Humans', 'Ligamentum Flavum', 'Reactive Oxygen Species', 'Stress, Mechanical']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,861,730 |
Are clinical and radiological outcomes of lumbar posterior subtraction osteotomies correlated to pelvic incidence and FBI index : Prospective series of 63 cases?
|
{
"contexts": [
"Pedicle subtraction osteotomy (PSO) is one of the surgical options for treating alignment disorders of the fused spine (due to post-surgical fusion or related to arthritis). It enables satisfactory sagittal realignment and improved function due to economic sagittal balance. The aim of this study was to analyze clinical and radiological results of PSO after a minimum follow-up of 2 years and demonstrate the benefit of sub-group analysis as a function of pelvic incidence (PI).",
"A descriptive prospective single center study of 63 patients presenting with spinal global malalignment who underwent correction by PSO. Function was assessed by the Oswestry disability index (ODI), a visual analog scale of lumbar pain (VAS) and a SF-36 questionnaire. Radiographic analyses of pre- and post-operative pelvic-spinal parameters were performed on X-rays obtained by EOS(®) imaging after 3D modeling. Global analysis and analysis of sub-groups as a function of pelvic incidence were performed and the full balance integrated index (FBI) was calculated.",
"this series showed a marked clinical improvement and significant progress of functional scores. Global post-operative radiological analysis showed a significant improvement in all pelvic and spinal parameters. The mean correction obtained after PSO was 31.7° ± 8.4°, hence global improvement of lumbar lordosis of 22°. The sagittal vertical angle (SVA) decreased from +9 cm before surgery to +4.3 cm after surgery. Sub-group analysis demonstrated greater improvement in pelvic tilt, sacral slope and spinal parameters of patients with a small or moderate pelvic incidence; all had an FBI index <10°. Most of the pelvic and spinal parameters of patients with a large pelvic incidence were insufficiently corrected and they had an FBI index >10°"
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Humans",
"Low Back Pain",
"Lumbar Vertebrae",
"Osteotomy",
"Pelvis",
"Posture",
"Prospective Studies",
"Spinal Diseases"
]
}
|
PSO is a surgical procedure enabling correction of multiplane rigid spinal deformities that require major sagittal correction. It was seen to be highly effective in patients with a small or moderate pelvic incidence (PI <60°) but was sometimes less effective in patients with large pelvic incidence due to insufficient lordosis correction. Clinical results were highly correlated with the value of the FBI index.
|
yes
|
[
{
"from": "human",
"value": "Question: Are clinical and radiological outcomes of lumbar posterior subtraction osteotomies correlated to pelvic incidence and FBI index : Prospective series of 63 cases?\nContext: {'contexts': ['Pedicle subtraction osteotomy (PSO) is one of the surgical options for treating alignment disorders of the fused spine (due to post-surgical fusion or related to arthritis). It enables satisfactory sagittal realignment and improved function due to economic sagittal balance. The aim of this study was to analyze clinical and radiological results of PSO after a minimum follow-up of 2\\xa0years and demonstrate the benefit of sub-group analysis as a function of pelvic incidence (PI).', 'A descriptive prospective single center study of 63 patients presenting with spinal global malalignment who underwent correction by PSO. Function was assessed by the Oswestry disability index (ODI), a visual analog scale of lumbar pain (VAS) and a SF-36 questionnaire. Radiographic analyses of pre- and post-operative pelvic-spinal parameters were performed on X-rays obtained by EOS(®) imaging after 3D modeling. Global analysis and analysis of sub-groups as a function of pelvic incidence were performed and the full balance integrated index (FBI) was calculated.', 'this series showed a marked clinical improvement and significant progress of functional scores. Global post-operative radiological analysis showed a significant improvement in all pelvic and spinal parameters. The mean correction obtained after PSO was 31.7°\\xa0±\\xa08.4°, hence global improvement of lumbar lordosis of 22°. The sagittal vertical angle (SVA) decreased from +9\\xa0cm before surgery to +4.3\\xa0cm after surgery. Sub-group analysis demonstrated greater improvement in pelvic tilt, sacral slope and spinal parameters of patients with a small or moderate pelvic incidence; all had an FBI index\\xa0<10°. Most of the pelvic and spinal parameters of patients with a large pelvic incidence were insufficiently corrected and they had an FBI index\\xa0>10°'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Humans', 'Low Back Pain', 'Lumbar Vertebrae', 'Osteotomy', 'Pelvis', 'Posture', 'Prospective Studies', 'Spinal Diseases']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,861,734 |
Does human lung-derived mesenchymal stem cell-conditioned medium exert in vitro antitumor effects in malignant pleural mesothelioma cell lines?
|
{
"contexts": [
"The soluble factors secreted by mesenchymal stem cells are thought to either support or inhibit tumor growth. Herein, we investigated whether the human lung-derived mesenchymal stem cell-conditioned medium (hlMSC-CM) exerts antitumor activity in malignant pleural mesothelioma cell lines H28, H2052 and Meso4.",
"hlMSC-CM was collected from the human lung-derived mesenchymal stem cells. Inhibition of tumor cell growth was based on the reduction of cell viability and inhibition of cell proliferation using the XTT and BrdU assays, respectively. Elimination of tumor spheroids was assessed by the anchorage-independent sphere formation assay. The cytokine profile of hlMSC-CM was determined by a chemiluminescence-based cytokine array.",
"Our data showed that hlMSC-CM contains a broad range of soluble factors which include: cytokines, chemokines, hormones, growth and angiogenic factors, matrix metalloproteinases, metalloproteinase inhibitors and cell-cell mediator proteins. The 48- and 72-hour hlMSC-CM treatments of H28, H2052 and Meso4 cell lines elicited significant decreases in cell viability and inhibited cell proliferation. The 72-hour hlMSC-CM incubation of H28 cells completely eliminated the drug-resistant sphere-forming cells, which is more potent than twice the half maximal inhibitory concentration of cisplatin."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Antineoplastic Agents",
"Cell Line, Tumor",
"Cell Proliferation",
"Cell Survival",
"Culture Media, Conditioned",
"Drug Screening Assays, Antitumor",
"Humans",
"Inhibitory Concentration 50",
"Lung",
"Lung Neoplasms",
"Mesenchymal Stem Cells",
"Mesothelioma",
"Pleural Neoplasms"
]
}
|
Our findings indicate that the cell-free hlMSC-CM confers in vitro antitumor activities via soluble factors in the tested mesothelioma cells and, hence, may serve as a therapeutic tool to augment the current treatment strategies in malignant pleural mesothelioma.
|
yes
|
[
{
"from": "human",
"value": "Question: Does human lung-derived mesenchymal stem cell-conditioned medium exert in vitro antitumor effects in malignant pleural mesothelioma cell lines?\nContext: {'contexts': ['The soluble factors secreted by mesenchymal stem cells are thought to either support or inhibit tumor growth. Herein, we investigated whether the human lung-derived mesenchymal stem cell-conditioned medium (hlMSC-CM) exerts antitumor activity in malignant pleural mesothelioma cell lines H28, H2052 and Meso4.', 'hlMSC-CM was collected from the human lung-derived mesenchymal stem cells. Inhibition of tumor cell growth was based on the reduction of cell viability and inhibition of cell proliferation using the XTT and BrdU assays, respectively. Elimination of tumor spheroids was assessed by the anchorage-independent sphere formation assay. The cytokine profile of hlMSC-CM was determined by a chemiluminescence-based cytokine array.', 'Our data showed that hlMSC-CM contains a broad range of soluble factors which include: cytokines, chemokines, hormones, growth and angiogenic factors, matrix metalloproteinases, metalloproteinase inhibitors and cell-cell mediator proteins. The 48- and 72-hour hlMSC-CM treatments of H28, H2052 and Meso4 cell lines elicited significant decreases in cell viability and inhibited cell proliferation. The 72-hour hlMSC-CM incubation of H28 cells completely eliminated the drug-resistant sphere-forming cells, which is more potent than twice the half maximal inhibitory concentration of cisplatin.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Antineoplastic Agents', 'Cell Line, Tumor', 'Cell Proliferation', 'Cell Survival', 'Culture Media, Conditioned', 'Drug Screening Assays, Antitumor', 'Humans', 'Inhibitory Concentration 50', 'Lung', 'Lung Neoplasms', 'Mesenchymal Stem Cells', 'Mesothelioma', 'Pleural Neoplasms']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,858,119 |
Is the Plasmodium falciparum chloroquine resistance transporter associated with the ex vivo P. falciparum African parasite response to pyronaridine?
|
{
"contexts": [
"The pyronaridine-artesunate combination is one of the most recent oral artemisinin-based therapeutic combinations (ACTs) recommended for the treatment of uncomplicated P. falciparum malaria. The emergence of P. falciparum resistance to artemisinin has recently developed in Southeast Asia. Little data are available on the association between pyronaridine susceptibility and polymorphisms in genes involved in antimalarial drug resistance. The objective of the present study was to investigate the association between ex vivo responses to pyronaridine and the K76T mutation in the pfcrt gene in P. falciparum isolates.",
"The assessment of ex vivo susceptibility to pyronaridine was performed on 296 P. falciparum isolates using a standard 42-h 3H-hypoxanthine uptake inhibition method. The K76T mutation was also investigated.",
"The pyronaridine IC50 (inhibitory concentration 50 %) ranged from 0.55 to 80.0 nM. Ex vivo responses to pyronaridine were significantly associated with the K76T mutation (p-value = 0.020). The reduced susceptibility to pyronaridine, defined as IC50 > 60 nM, was significantly associated with the K76T mutation (p-value = 0.004). Using a Bayesian mixture modelling approach, the pyronaridine IC50 were classified into three components: component A (IC50 median 15.9 nM), component B (IC50 median 34.2 nM) and component C (IC50 median 63.3 nM). The K76T mutation was represented in 46.3% of the isolates in component A, 47.2% of the isolates in component B and 73.3% of the isolates in component C (p-value = 0.021)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Antimalarials",
"Inhibitory Concentration 50",
"Membrane Transport Proteins",
"Mutant Proteins",
"Naphthyridines",
"Parasitic Sensitivity Tests",
"Plasmodium falciparum",
"Protozoan Proteins"
]
}
|
These results showed the ex vivo reduced susceptibility to pyronaridine, i.e., IC50 > 60 nM, associated with the K76T mutation.
|
yes
|
[
{
"from": "human",
"value": "Question: Is the Plasmodium falciparum chloroquine resistance transporter associated with the ex vivo P. falciparum African parasite response to pyronaridine?\nContext: {'contexts': ['The pyronaridine-artesunate combination is one of the most recent oral artemisinin-based therapeutic combinations (ACTs) recommended for the treatment of uncomplicated P. falciparum malaria. The emergence of P. falciparum resistance to artemisinin has recently developed in Southeast Asia. Little data are available on the association between pyronaridine susceptibility and polymorphisms in genes involved in antimalarial drug resistance. The objective of the present study was to investigate the association between ex vivo responses to pyronaridine and the K76T mutation in the pfcrt gene in P. falciparum isolates.', 'The assessment of ex vivo susceptibility to pyronaridine was performed on 296 P. falciparum isolates using a standard 42-h 3H-hypoxanthine uptake inhibition method. The K76T mutation was also investigated.', 'The pyronaridine IC50 (inhibitory concentration 50 %) ranged from 0.55 to 80.0 nM. Ex vivo responses to pyronaridine were significantly associated with the K76T mutation (p-value\\u2009=\\u20090.020). The reduced susceptibility to pyronaridine, defined as IC50\\u2009>\\u200960 nM, was significantly associated with the K76T mutation (p-value\\u2009=\\u20090.004). Using a Bayesian mixture modelling approach, the pyronaridine IC50 were classified into three components: component A (IC50 median 15.9 nM), component B (IC50 median 34.2 nM) and component C (IC50 median 63.3 nM). The K76T mutation was represented in 46.3% of the isolates in component A, 47.2% of the isolates in component B and 73.3% of the isolates in component C (p-value\\u2009=\\u20090.021).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Antimalarials', 'Inhibitory Concentration 50', 'Membrane Transport Proteins', 'Mutant Proteins', 'Naphthyridines', 'Parasitic Sensitivity Tests', 'Plasmodium falciparum', 'Protozoan Proteins']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,857,213 |
Is global longitudinal strain associated with heart failure outcomes in hypertrophic cardiomyopathy?
|
{
"contexts": [
"We hypothesised that abnormal global longitudinal strain (GLS) would predict outcome in hypertrophic cardiomyopathy (HCM) better than current echocardiographic measures.",
"Retrospective analysis of risk markers in relation to outcomes in 472 patients with HCM at a single tertiary institution (2006-2012). Exclusion criteria were left ventricular (LV) hypertrophy of other origin, patients in atrial fibrillation, lost to follow-up and insufficient image quality to perform strain analysis. Standardised echocardiogram recordings were reviewed and standard variables and LV GLS were measured. The primary end-point included all cardiac deaths, appropriate defibrillator shocks and heart failure (HF) admissions. The secondary end-point was death by HF and admissions related to HF.",
"Mean age was 50.0±15.0 years; 322 (68%) were men. At a median of 4.3 years (IQR 0.1-7.8) follow-up, 21 (4.4%) patients experienced cardiovascular death: 6 (1.3%) died from HF, 13 (2.7%) had sudden cardiac death and 2 (0.4%) died secondary to stroke. Four (0.8%) patients experienced appropriate defibrillator shock, and 13 (2.7%) were admitted for HF. On multivariate Fine-Gray proportional hazard analyses, GLS was significantly associated with the primary end-point (HR=0.90, 95% CI 0.83 to 0.98, p=0.018) independently of age, maximal provoked LV outflow-tract gradient and LV end-systolic volume. Moreover, GLS was particularly associated with the secondary end-point (HR=0.82, 95% CI 0.75 to 0.90, p<0.0001) independently of age, previous atrial fibrillation, New York Heart Association (NYHA) class III-IV, LV end-systolic volume, E/E', and outflow-tract gradient. Survival curves confirmed that GLS was associated with HF events (GLS <15.6%, p=0.0035)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Cardiomyopathy, Hypertrophic",
"Cause of Death",
"Echocardiography, Doppler, Color",
"Echocardiography, Doppler, Pulsed",
"Female",
"Heart Failure",
"Hospitalization",
"Humans",
"Kaplan-Meier Estimate",
"London",
"Male",
"Middle Aged",
"Myocardial Contraction",
"Predictive Value of Tests",
"Prognosis",
"Retrospective Studies",
"Risk Factors",
"Stress, Mechanical",
"Time Factors",
"Ventricular Dysfunction, Left",
"Ventricular Function, Left"
]
}
|
In patients with HCM, reduced GLS is an independent factor associated with poor cardiac outcomes, and particularly HF outcomes.
|
yes
|
[
{
"from": "human",
"value": "Question: Is global longitudinal strain associated with heart failure outcomes in hypertrophic cardiomyopathy?\nContext: {'contexts': ['We hypothesised that abnormal global longitudinal strain (GLS) would predict outcome in hypertrophic cardiomyopathy (HCM) better than current echocardiographic measures.', 'Retrospective analysis of risk markers in relation to outcomes in 472 patients with HCM at a single tertiary institution (2006-2012). Exclusion criteria were left ventricular (LV) hypertrophy of other origin, patients in atrial fibrillation, lost to follow-up and insufficient image quality to perform strain analysis. Standardised echocardiogram recordings were reviewed and standard variables and LV GLS were measured. The primary end-point included all cardiac deaths, appropriate defibrillator shocks and heart failure (HF) admissions. The secondary end-point was death by HF and admissions related to HF.', \"Mean age was 50.0±15.0\\u2005years; 322 (68%) were men. At a median of 4.3\\u2005years (IQR 0.1-7.8) follow-up, 21 (4.4%) patients experienced cardiovascular death: 6 (1.3%) died from HF, 13 (2.7%) had sudden cardiac death and 2 (0.4%) died secondary to stroke. Four (0.8%) patients experienced appropriate defibrillator shock, and 13 (2.7%) were admitted for HF. On multivariate Fine-Gray proportional hazard analyses, GLS was significantly associated with the primary end-point (HR=0.90, 95% CI 0.83 to 0.98, p=0.018) independently of age, maximal provoked LV outflow-tract gradient and LV end-systolic volume. Moreover, GLS was particularly associated with the secondary end-point (HR=0.82, 95% CI 0.75 to 0.90, p<0.0001) independently of age, previous atrial fibrillation, New York Heart Association (NYHA) class III-IV, LV end-systolic volume, E/E', and outflow-tract gradient. Survival curves confirmed that GLS was associated with HF events (GLS <15.6%, p=0.0035).\"], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Cardiomyopathy, Hypertrophic', 'Cause of Death', 'Echocardiography, Doppler, Color', 'Echocardiography, Doppler, Pulsed', 'Female', 'Heart Failure', 'Hospitalization', 'Humans', 'Kaplan-Meier Estimate', 'London', 'Male', 'Middle Aged', 'Myocardial Contraction', 'Predictive Value of Tests', 'Prognosis', 'Retrospective Studies', 'Risk Factors', 'Stress, Mechanical', 'Time Factors', 'Ventricular Dysfunction, Left', 'Ventricular Function, Left']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,860,076 |
Do an order set and checklist improve physician transfusion ordering practices to mitigate the risk of transfusion-associated circulatory overload?
|
{
"contexts": [
"There are few studies of quality interventions to mitigate the risk of transfusion-associated circulatory overload (TACO). Our aim was to reduce TACO risk in patients admitted to internal medicine at our hospital, by addressing gaps in transfusion practice.",
"A 3-month baseline audit of red blood cell (RBC) transfusion orders was conducted. An intervention consisting of a transfusion order set and physician checklist was developed and implemented based on identified gaps, followed by a 3-month post-intervention audit. Compliance with appropriateness criteria for RBC transfusion was ascertained, along with documentation of transfusion rate, diuretic usage and consent.",
"A total of 97 transfusion orders from 68 inpatients and 95 orders from 62 inpatients were audited in the baseline and post-intervention groups, respectively. Compliance with appropriateness criteria was similar pre- and post-intervention (87 versus 85%, P = 0·81). Specification of transfusion rate improved (84 versus 98%, P < 0·01), and diuretics were appropriately ordered more frequently for patients with TACO risk factors (37 versus 64%, P < 0·01). Timing of diuretics shifted from between or post-transfusion to pre-transfusion (35 versus 86%, P < 0·01), without increases in hypokalemia or acute kidney injury. No case of TACO was observed during the study. Documentation of specific risks discussed during consent discussion improved (4 versus 23%, P < 0·01)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Checklist",
"Erythrocyte Transfusion",
"Female",
"Humans",
"Male",
"Middle Aged"
]
}
|
A checklist and order set are tools that can improve the quality of transfusion orders by increasing the judicious use of pre-transfusion diuretics and augmenting the specification of transfusion rate. These interventions could be adapted to electronic order formats to improve transfusion safety.
|
yes
|
[
{
"from": "human",
"value": "Question: Do an order set and checklist improve physician transfusion ordering practices to mitigate the risk of transfusion-associated circulatory overload?\nContext: {'contexts': ['There are few studies of quality interventions to mitigate the risk of transfusion-associated circulatory overload (TACO). Our aim was to reduce TACO risk in patients admitted to internal medicine at our hospital, by addressing gaps in transfusion practice.', 'A 3-month baseline audit of red blood cell (RBC) transfusion orders was conducted. An intervention consisting of a transfusion order set and physician checklist was developed and implemented based on identified gaps, followed by a 3-month post-intervention audit. Compliance with appropriateness criteria for RBC transfusion was ascertained, along with documentation of transfusion rate, diuretic usage and consent.', 'A total of 97 transfusion orders from 68 inpatients and 95 orders from 62 inpatients were audited in the baseline and post-intervention groups, respectively. Compliance with appropriateness criteria was similar pre- and post-intervention (87 versus 85%, P = 0·81). Specification of transfusion rate improved (84 versus 98%, P < 0·01), and diuretics were appropriately ordered more frequently for patients with TACO risk factors (37 versus 64%, P < 0·01). Timing of diuretics shifted from between or post-transfusion to pre-transfusion (35 versus 86%, P < 0·01), without increases in hypokalemia or acute kidney injury. No case of TACO was observed during the study. Documentation of specific risks discussed during consent discussion improved (4 versus 23%, P < 0·01).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Checklist', 'Erythrocyte Transfusion', 'Female', 'Humans', 'Male', 'Middle Aged']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,852,107 |
Is volumetric breast density essential for predicting cosmetic outcome at the late stage after breast-conserving surgery?
|
{
"contexts": [
"The critical issue related to breast-conserving therapy (BCT) is that cosmetic outcomes deteriorate with long-term follow-up. There is little research for breast density as a predictor of cosmetic outcomes at the late stage after BCT. To improve the long-term quality of life after BCT of breast cancer patients, the correlation of volumetric breast density (VBD) and cosmetic outcome at the late stage after BCT was evaluated.",
"Breast volume, fibroglandular tissue volume, adipose tissue volume, and VBD were calculated on mammography using image analysis software (Volpara(®)) in 151 patients with BCT. Furthermore, the correlation of breast density and the change of breast volume over time was analyzed on mammography in 99 patients who were followed-up long-term after BCT.",
"On multivariate analysis, VBD was a predictor of cosmetic outcome after BCT with percent breast volume excised (PBVE). Decreased adipose tissue volume and increased fibrosis were more common in patients with VBD < 15%. Furthermore, remnant breast volume continued to decrease over time in low breast density patients during long-term follow-up. 93% of patients with VBD ≥ 15% and PBVE < 10% had a better cosmetic outcome, while 60% of patients with VBD < 15% and PBVE ≥ 10% had a worse cosmetic outcome after BCT."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Breast Neoplasms",
"Female",
"Follow-Up Studies",
"Humans",
"Mammography",
"Mastectomy, Segmental",
"Middle Aged",
"Organ Size",
"Postoperative Period",
"Prognosis",
"Quality of Life",
"ROC Curve",
"Retrospective Studies",
"Time Factors"
]
}
|
While PBVE was involved in cosmetic outcome at the early stage after BCT, VBD was associated with cosmetic outcome at the late stage after BCT. Thus, a combination of VBD and PBVE could predict cosmetic outcome after BCT and contribute to the selection for the appropriate BCT.
|
yes
|
[
{
"from": "human",
"value": "Question: Is volumetric breast density essential for predicting cosmetic outcome at the late stage after breast-conserving surgery?\nContext: {'contexts': ['The critical issue related to breast-conserving therapy (BCT) is that cosmetic outcomes deteriorate with long-term follow-up. There is little research for breast density as a predictor of cosmetic outcomes at the late stage after BCT. To improve the long-term quality of life after BCT of breast cancer patients, the correlation of volumetric breast density (VBD) and cosmetic outcome at the late stage after BCT was evaluated.', 'Breast volume, fibroglandular tissue volume, adipose tissue volume, and VBD were calculated on mammography using image analysis software (Volpara(®)) in 151 patients with BCT. Furthermore, the correlation of breast density and the change of breast volume over time was analyzed on mammography in 99 patients who were followed-up long-term after BCT.', 'On multivariate analysis, VBD was a predictor of cosmetic outcome after BCT with percent breast volume excised (PBVE). Decreased adipose tissue volume and increased fibrosis were more common in patients with VBD < 15%. Furthermore, remnant breast volume continued to decrease over time in low breast density patients during long-term follow-up. 93% of patients with VBD ≥ 15% and PBVE < 10% had a better cosmetic outcome, while 60% of patients with VBD < 15% and PBVE ≥ 10% had a worse cosmetic outcome after BCT.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Breast Neoplasms', 'Female', 'Follow-Up Studies', 'Humans', 'Mammography', 'Mastectomy, Segmental', 'Middle Aged', 'Organ Size', 'Postoperative Period', 'Prognosis', 'Quality of Life', 'ROC Curve', 'Retrospective Studies', 'Time Factors']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,867,127 |
Does cartilage Derived from Bone Marrow Mesenchymal Stem Cells express Lubricin In Vitro and In Vivo?
|
{
"contexts": [
"Lubricin expression in the superficial cartilage will be a crucial factor in the success of cartilage regeneration. Mesenchymal stem cells (MSCs) are an attractive cell source and the use of aggregates of MSCs has some advantages in terms of chondrogenic potential and efficiency of cell adhesion. Lubricin expression in transplanted MSCs has not been fully elucidated so far. Our goals were to determine (1) whether cartilage pellets of human MSCs expressed lubricin in vitro chondrogenesis, (2) whether aggregates of human MSCs promoted lubricin expression, and (3) whether aggregates of MSCs expressed lubricin in the superficial cartilage after transplantation into osteochondral defects in rats.",
"For in vitro analysis, human bone marrow (BM) MSCs were differentiated into cartilage by pellet culture, and also aggregated using the hanging drop technique. For an animal study, aggregates of BM MSCs derived from GFP transgenic rats were transplanted to the osteochondral defect in the trochlear groove of wild type rat knee joints. Lubricin expression was mainly evaluated in differentiated and regenerated cartilages.",
"In in vitro analysis, lubricin was detected in the superficial zone of the pellets and conditioned medium. mRNA expression of Proteoglycan4 (Prg4), which encodes lubricin, in pellets was significantly higher than that of undifferentiated MSCs. Aggregates showed different morphological features between the superficial and deep zone, and the Prg4 mRNA expression increased after aggregate formation. Lubricin was also found in the aggregate. In a rat study, articular cartilage regeneration was significantly better in the MSC group than in the control group as shown by macroscopical and histological analysis. The transmission electron microscope showed that morphology of the superficial cartilage in the MSC group was closer to that of the intact cartilage than in the control group. GFP positive cells remained in the repaired tissue and expressed lubricin in the superficial cartilage."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Bone Marrow Cells",
"Cartilage",
"Cell Differentiation",
"Cells, Cultured",
"Chondrogenesis",
"Female",
"Gene Expression Regulation",
"Glycoproteins",
"Green Fluorescent Proteins",
"Humans",
"Knee Joint",
"Mesenchymal Stem Cell Transplantation",
"Mesenchymal Stem Cells",
"Microscopy, Electron, Transmission",
"Proteoglycans",
"RNA, Messenger",
"Rats",
"Rats, Transgenic",
"Regeneration",
"X-Ray Microtomography"
]
}
|
Cartilage derived from MSCs expressed lubricin protein both in vitro and in vivo. Aggregation promoted lubricin expression of MSCs in vitro and transplantation of aggregates of MSCs regenerated cartilage including the superficial zone in a rat osteochondral defect model. Our results indicate that aggregated MSCs could be clinically relevant for therapeutic approaches to articular cartilage regeneration with an appropriate superficial zone in the future.
|
yes
|
[
{
"from": "human",
"value": "Question: Does cartilage Derived from Bone Marrow Mesenchymal Stem Cells express Lubricin In Vitro and In Vivo?\nContext: {'contexts': ['Lubricin expression in the superficial cartilage will be a crucial factor in the success of cartilage regeneration. Mesenchymal stem cells (MSCs) are an attractive cell source and the use of aggregates of MSCs has some advantages in terms of chondrogenic potential and efficiency of cell adhesion. Lubricin expression in transplanted MSCs has not been fully elucidated so far. Our goals were to determine (1) whether cartilage pellets of human MSCs expressed lubricin in vitro chondrogenesis, (2) whether aggregates of human MSCs promoted lubricin expression, and (3) whether aggregates of MSCs expressed lubricin in the superficial cartilage after transplantation into osteochondral defects in rats.', 'For in vitro analysis, human bone marrow (BM) MSCs were differentiated into cartilage by pellet culture, and also aggregated using the hanging drop technique. For an animal study, aggregates of BM MSCs derived from GFP transgenic rats were transplanted to the osteochondral defect in the trochlear groove of wild type rat knee joints. Lubricin expression was mainly evaluated in differentiated and regenerated cartilages.', 'In in vitro analysis, lubricin was detected in the superficial zone of the pellets and conditioned medium. mRNA expression of Proteoglycan4 (Prg4), which encodes lubricin, in pellets was significantly higher than that of undifferentiated MSCs. Aggregates showed different morphological features between the superficial and deep zone, and the Prg4 mRNA expression increased after aggregate formation. Lubricin was also found in the aggregate. In a rat study, articular cartilage regeneration was significantly better in the MSC group than in the control group as shown by macroscopical and histological analysis. The transmission electron microscope showed that morphology of the superficial cartilage in the MSC group was closer to that of the intact cartilage than in the control group. GFP positive cells remained in the repaired tissue and expressed lubricin in the superficial cartilage.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Bone Marrow Cells', 'Cartilage', 'Cell Differentiation', 'Cells, Cultured', 'Chondrogenesis', 'Female', 'Gene Expression Regulation', 'Glycoproteins', 'Green Fluorescent Proteins', 'Humans', 'Knee Joint', 'Mesenchymal Stem Cell Transplantation', 'Mesenchymal Stem Cells', 'Microscopy, Electron, Transmission', 'Proteoglycans', 'RNA, Messenger', 'Rats', 'Rats, Transgenic', 'Regeneration', 'X-Ray Microtomography']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,853,910 |
Does timing for dose-down of 5-ASA depend on mucosal status with ulcerative colitis?
|
{
"contexts": [
"Although aminosalicylic acid (ASA) preparations have been used as first-line drugs for the treatment of ulcerative colitis (UC), no consistent view has been established regarding the ASA dose during the remission-maintenance phase of the disease. In this study, we examined whether the ASA dose should be reduced during the remission-maintenance phase.",
"This study included 203 patients in the remission-maintenance phase of UC. The Mayo endoscopic subscore (MES) was used to evaluate mucosa. Comparison and analysis were performed between patients whose ASA dose had been unchanged and whose dose had been reduced, between patients with endoscopic healing (EH) group and those without endoscopic healing (WEH) group, and between patients with an MES of 0 and 1.",
"Comparison between the unchanged-ASA and reduced-ASA groups revealed that the remission-maintenance rate was higher in the unchanged-ASA group (p < 0.001). Next, the remission-maintenance rate was higher in the EH/unchanged-ASA group than in the EH/reduced-ASA group (p = 0.042). Comparison between the MES 0 and 1 groups revealed that the remission-maintenance rate was higher in the MES 0 group (p = 0.007). In addition, no significant difference in remission-maintenance rates was observed between the MES 0/unchanged-ASA group and the MES 0/reduced-ASA group (p = 0.108)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Aminosalicylic Acid",
"Colitis, Ulcerative",
"Endoscopy, Gastrointestinal",
"Female",
"Humans",
"Intestinal Mucosa",
"Male",
"Middle Aged",
"Remission Induction"
]
}
|
When the same ASA dose is maintained regardless of the presence or absence of EH, remission is more likely to be maintained. If the ASA dose must be reduced, dose reduction is more advantageous after an MES of 0 is achieved.
|
yes
|
[
{
"from": "human",
"value": "Question: Does timing for dose-down of 5-ASA depend on mucosal status with ulcerative colitis?\nContext: {'contexts': ['Although aminosalicylic acid (ASA) preparations have been used as first-line drugs for the treatment of ulcerative colitis (UC), no consistent view has been established regarding the ASA dose during the remission-maintenance phase of the disease. In this study, we examined whether the ASA dose should be reduced during the remission-maintenance phase.', 'This study included 203 patients in the remission-maintenance phase of UC. The Mayo endoscopic subscore (MES) was used to evaluate mucosa. Comparison and analysis were performed between patients whose ASA dose had been unchanged and whose dose had been reduced, between patients with endoscopic healing (EH) group and those without endoscopic healing (WEH) group, and between patients with an MES of 0 and 1.', 'Comparison between the unchanged-ASA and reduced-ASA groups revealed that the remission-maintenance rate was higher in the unchanged-ASA group (p\\u2009<\\u20090.001). Next, the remission-maintenance rate was higher in the EH/unchanged-ASA group than in the EH/reduced-ASA group (p\\u2009=\\u20090.042). Comparison between the MES 0 and 1 groups revealed that the remission-maintenance rate was higher in the MES 0 group (p\\u2009=\\u20090.007). In addition, no significant difference in remission-maintenance rates was observed between the MES 0/unchanged-ASA group and the MES 0/reduced-ASA group (p\\u2009=\\u20090.108).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Aminosalicylic Acid', 'Colitis, Ulcerative', 'Endoscopy, Gastrointestinal', 'Female', 'Humans', 'Intestinal Mucosa', 'Male', 'Middle Aged', 'Remission Induction']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,849,828 |
Is identification of β-glucosidase 1 as a biomarker and its high expression in hepatocellular carcinoma associated with resistance to chemotherapy drugs?
|
{
"contexts": [
"Long-term prognosis of hepatocellular carcinoma (HCC) patients is challenging, and novel biomarkers are needed to predict patient risk and serve as potential therapeutic target.",
"We found β-glucosidase 1 is significantly overexpressed and activated in primary HCC tissue and multiple HCC cell lines. β-Glucosidase 1 expression is associated with predicting prognosis of HCC patients under chemotherapy. Silencing β-glucosidase 1 inhibits growth and survival of HCC cells, with preferential inhibitory effects on high β-glucosidase 1-expressing cells. Combination of chemo drug with β-glucosidase 1 inhibitor sensitized HCC cells to chemotherapy."
],
"labels": [
"OBJECTIVE",
"RESULTS"
],
"meshes": [
"Apoptosis",
"Biomarkers, Tumor",
"Carcinoma, Hepatocellular",
"Cell Proliferation",
"Drug Resistance, Neoplasm",
"Enzyme Inhibitors",
"Female",
"Gene Expression Regulation, Neoplastic",
"Hep G2 Cells",
"Humans",
"Liver Neoplasms",
"Male",
"Molecular Targeted Therapy",
"beta-Glucosidase"
]
}
|
Our data support β-glucosidase 1 as a HCC biomarker due to its prognosis significance.
|
yes
|
[
{
"from": "human",
"value": "Question: Is identification of β-glucosidase 1 as a biomarker and its high expression in hepatocellular carcinoma associated with resistance to chemotherapy drugs?\nContext: {'contexts': ['Long-term prognosis of hepatocellular carcinoma (HCC) patients is challenging, and novel biomarkers are needed to predict patient risk and serve as potential therapeutic target.', 'We found β-glucosidase 1 is significantly overexpressed and activated in primary HCC tissue and multiple HCC cell lines. β-Glucosidase 1 expression is associated with predicting prognosis of HCC patients under chemotherapy. Silencing β-glucosidase 1 inhibits growth and survival of HCC cells, with preferential inhibitory effects on high β-glucosidase 1-expressing cells. Combination of chemo drug with β-glucosidase 1 inhibitor sensitized HCC cells to chemotherapy.'], 'labels': ['OBJECTIVE', 'RESULTS'], 'meshes': ['Apoptosis', 'Biomarkers, Tumor', 'Carcinoma, Hepatocellular', 'Cell Proliferation', 'Drug Resistance, Neoplasm', 'Enzyme Inhibitors', 'Female', 'Gene Expression Regulation, Neoplastic', 'Hep G2 Cells', 'Humans', 'Liver Neoplasms', 'Male', 'Molecular Targeted Therapy', 'beta-Glucosidase']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,871,734 |
Is combining ECT with pharmacological treatment of depressed inpatients in a naturalistic study associated with serum BDNF level increase?
|
{
"contexts": [
"BDNF blood levels are reduced in MDD. They can be increased with pharmacologic treatment and ECT, but it is not clear whether the combination of treatments promotes an additional increase. The present study aims to evaluate whether combined treatment promotes an increase in BDNF, restoring the level to that of non-depressed controls.",
"Ninety-nine adult inpatients were invited to participate in this naturalistic prospective cohort study between May 2011 and April 2013. Diagnosis was made by MINI, and the symptoms were evaluated at admission and at discharge by HDRS-17. Those inpatients with a diagnosis of depression were included and divided into two groups: those who underwent combined ECT and medication (31 subjects) and those who used only pharmacotherapy (68 subjects). Serum BDNF was measured in blood samples collected at admission and discharge. One hundred healthy blood donors without any psychiatric diagnosis were included as a control group.",
"There were no significant differences in serum BDNF levels between the combined and pharmacological groups at admission and at discharge, and no significant variation in BDNF occurred in any group during the treatment. There were no interactions between time and treatment groups nor significant time effects or treatment group effects for BDNF in the Generalized Estimating Equation Model (GEE). The control group had significantly higher serum BDNF levels in comparison with each of the treatment groups at admission and discharge (p = 0.00)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Antidepressive Agents",
"Brain-Derived Neurotrophic Factor",
"Cohort Studies",
"Depression",
"Electrocardiography",
"Electroconvulsive Therapy",
"Female",
"Humans",
"Inpatients",
"Male",
"Middle Aged",
"Psychiatric Status Rating Scales",
"Statistics, Nonparametric"
]
}
|
Combination of ECT with pharmacological treatment did not result in increased serum BDNF levels and did not restore levels to that of controls.
|
no
|
[
{
"from": "human",
"value": "Question: Is combining ECT with pharmacological treatment of depressed inpatients in a naturalistic study associated with serum BDNF level increase?\nContext: {'contexts': ['BDNF blood levels are reduced in MDD. They can be increased with pharmacologic treatment and ECT, but it is not clear whether the combination of treatments promotes an additional increase. The present study aims to evaluate whether combined treatment promotes an increase in BDNF, restoring the level to that of non-depressed controls.', 'Ninety-nine adult inpatients were invited to participate in this naturalistic prospective cohort study between May 2011 and April 2013. Diagnosis was made by MINI, and the symptoms were evaluated at admission and at discharge by HDRS-17. Those inpatients with a diagnosis of depression were included and divided into two groups: those who underwent combined ECT and medication (31 subjects) and those who used only pharmacotherapy (68 subjects). Serum BDNF was measured in blood samples collected at admission and discharge. One hundred healthy blood donors without any psychiatric diagnosis were included as a control group.', 'There were no significant differences in serum BDNF levels between the combined and pharmacological groups at admission and at discharge, and no significant variation in BDNF occurred in any group during the treatment. There were no interactions between time and treatment groups nor significant time effects or treatment group effects for BDNF in the Generalized Estimating Equation Model (GEE). The control group had significantly higher serum BDNF levels in comparison with each of the treatment groups at admission and discharge (p = 0.00).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Antidepressive Agents', 'Brain-Derived Neurotrophic Factor', 'Cohort Studies', 'Depression', 'Electrocardiography', 'Electroconvulsive Therapy', 'Female', 'Humans', 'Inpatients', 'Male', 'Middle Aged', 'Psychiatric Status Rating Scales', 'Statistics, Nonparametric']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
] |
26,871,730 |
Does electrical pharyngeal stimulation increase substance P level in saliva?
|
{
"contexts": [
"Substance P (SP) is a neuropeptide known to enhance the swallow response. It likely acts as a neurotransmitter in the pharyngeal mucosa in response to local stimuli. It has been proposed that dysphagia after stroke may be related to reduced levels of SP, which therefore constitutes a therapeutic target. In the present pilot study, we evaluated whether electrical pharyngeal stimulation (EPS), a neuromodulation device to enhance cortical reorganization for the restoration of swallowing function after brain injury, is able to increase SP in saliva or serum.",
"In a randomized crossover study design, 20 healthy volunteers were treated with 10 min of real (0.2-ms pulses, 5 Hz, 280 V, stimulation intensity (mA) individually adjusted to tolerance level) or sham EPS on two separate sessions. Stimulation was delivered via a pair of bipolar ring electrodes mounted on an intraluminal catheter positioned in the pharynx. Blood and saliva samples were taken prior to, during, and up to 1 h after EPS and analyzed for their SP concentration by ELISA.",
"Following real EPS but not sham stimulation, SP levels in saliva increased immediately and significantly about 28% (p < 0.01) compared to baseline. Serum levels remained unchanged."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Cross-Over Studies",
"Electric Stimulation",
"Female",
"Humans",
"Male",
"Pharynx",
"Pilot Projects",
"Saliva",
"Substance P",
"Young Adult"
]
}
|
Electrical pharyngeal stimulation is able to induce pharyngeal SP release in healthy subjects.
|
yes
|
[
{
"from": "human",
"value": "Question: Does electrical pharyngeal stimulation increase substance P level in saliva?\nContext: {'contexts': ['Substance P (SP) is a neuropeptide known to enhance the swallow response. It likely acts as a neurotransmitter in the pharyngeal mucosa in response to local stimuli. It has been proposed that dysphagia after stroke may be related to reduced levels of SP, which therefore constitutes a therapeutic target. In the present pilot study, we evaluated whether electrical pharyngeal stimulation (EPS), a neuromodulation device to enhance cortical reorganization for the restoration of swallowing function after brain injury, is able to increase SP in saliva or serum.', 'In a randomized crossover study design, 20 healthy volunteers were treated with 10 min of real (0.2-ms pulses, 5 Hz, 280 V, stimulation intensity (mA) individually adjusted to tolerance level) or sham EPS on two separate sessions. Stimulation was delivered via a pair of bipolar ring electrodes mounted on an intraluminal catheter positioned in the pharynx. Blood and saliva samples were taken prior to, during, and up to 1 h after EPS and analyzed for their SP concentration by ELISA.', 'Following real EPS but not sham stimulation, SP levels in saliva increased immediately and significantly about 28% (p < 0.01) compared to baseline. Serum levels remained unchanged.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Cross-Over Studies', 'Electric Stimulation', 'Female', 'Humans', 'Male', 'Pharynx', 'Pilot Projects', 'Saliva', 'Substance P', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,856,812 |
Does astaxanthin ameliorate prenatal LPS-exposed behavioral deficits and oxidative stress in adult offspring?
|
{
"contexts": [
"Prenatal maternal lipopolysaccharide (LPS) exposure leads to behavioral deficits such as depression, anxiety, and schizophrenia in the adult lives. LPS-exposure resulted in the production of cytokines and oxidative damage. On the contrary, astaxanthin is a carotenoid compound, showed neuroprotective properties via its antioxidant capacity. This study examines the effect of astaxanthin on the prenatal maternal LPS-induced postnatal behavioral deficit in mice.",
"We found that prenatal LPS-exposed mice showed extensive immobile phase in the tail suspension test, higher frequent head dipping in the hole-board test and greater hypolocomotion in the open field test. All these values were statistically significant (p < 0.05). In addition, a marked elevation of the level of lipid peroxidation, advanced protein oxidation product, nitric oxide, while a pronounced depletion of antioxidant enzymes (superoxide dismutase, catalase and glutathione) were observed in the adult offspring mice that were prenatally exposed to LPS. To the contrary, 6-weeks long treatment with astaxanthin significantly improved all behavioral deficits (p < 0.05) and diminished prenatal LPS-induced oxidative stress markers in the brain and liver."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Animals",
"Antioxidants",
"Anxiety",
"Behavior, Animal",
"Depression",
"Female",
"Lipopolysaccharides",
"Male",
"Maternal Exposure",
"Mice",
"Motor Activity",
"Oxidative Stress",
"Pregnancy",
"Prenatal Exposure Delayed Effects",
"Xanthophylls"
]
}
|
Taken together, these results suggest that prenatal maternal LPS-exposure leads to behavioral deficits in the adults, while astaxanthin ameliorates the behavioral deficits presumably via its antioxidant property.
|
yes
|
[
{
"from": "human",
"value": "Question: Does astaxanthin ameliorate prenatal LPS-exposed behavioral deficits and oxidative stress in adult offspring?\nContext: {'contexts': ['Prenatal maternal lipopolysaccharide (LPS) exposure leads to behavioral deficits such as depression, anxiety, and schizophrenia in the adult lives. LPS-exposure resulted in the production of cytokines and oxidative damage. On the contrary, astaxanthin is a carotenoid compound, showed neuroprotective properties via its antioxidant capacity. This study examines the effect of astaxanthin on the prenatal maternal LPS-induced postnatal behavioral deficit in mice.', 'We found that prenatal LPS-exposed mice showed extensive immobile phase in the tail suspension test, higher frequent head dipping in the hole-board test and greater hypolocomotion in the open field test. All these values were statistically significant (p\\xa0<\\xa00.05). In addition, a marked elevation of the level of lipid peroxidation, advanced protein oxidation product, nitric oxide, while a pronounced depletion of antioxidant enzymes (superoxide dismutase, catalase and glutathione) were observed in the adult offspring mice that were prenatally exposed to LPS. To the contrary, 6-weeks long treatment with astaxanthin significantly improved all behavioral deficits (p\\xa0<\\xa00.05) and diminished prenatal LPS-induced oxidative stress markers in the brain and liver.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Animals', 'Antioxidants', 'Anxiety', 'Behavior, Animal', 'Depression', 'Female', 'Lipopolysaccharides', 'Male', 'Maternal Exposure', 'Mice', 'Motor Activity', 'Oxidative Stress', 'Pregnancy', 'Prenatal Exposure Delayed Effects', 'Xanthophylls']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,856,814 |
Does the dual S1PR1/S1PR5 drug BAF312 ( Siponimod ) attenuate demyelination in organotypic slice cultures?
|
{
"contexts": [
"BAF312 (Siponimod) is a dual agonist at the sphingosine-1 phosphate receptors, S1PR1 and S1PR5. This drug is currently undergoing clinical trials for the treatment of secondary progressive multiple sclerosis (MS). Here, we investigated the effects of BAF312 on isolated astrocyte and microglia cultures as well as in slice culture models of demyelination.",
"Mouse and human astrocytes were treated with S1PR modulators and changes in the levels of pERK, pAkt, and calcium signalling as well as S1PR1 internalization and cytokine levels was investigated using Western blotting, immunochemistry, ELISA and confocal microscopy. Organotypic slice cultures were prepared from the cerebellum of 10-day-old mice and treated with lysophosphatidylcholine (LPC), psychosine and/or S1PR modulators, and changes in myelination states were measured by fluorescence of myelin basic protein and neurofilament H.",
"BAF312 treatment of human and mouse astrocytes activated pERK, pAKT and Ca(2+) signalling as well as inducing S1PR1 internalization. Notably, activation of S1PR1 increased pERK and pAKT in mouse astrocytes while both S1PR1 and S1PR3 equally increased pERK and pAKT in human astrocytes, suggesting that the coupling of S1PR1 and S1PR3 to pERK and pAKT differ in mouse and human astrocytes. We also observed that BAF312 moderately attenuated lipopolysaccharide (LPS)- or TNFα/IL17-induced levels of IL6 in both astrocyte and microglia cell cultures. In organotypic slice cultures, BAF312 reduced LPC-induced levels of IL6 and attenuated LPC-mediated demyelination. We have shown previously that the toxic lipid metabolite psychosine induces demyelination in organotypic slice cultures, without altering the levels of cytokines, such as IL6. Importantly, psychosine-induced demyelination was also attenuated by BAF312."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Animals, Newborn",
"Anti-Inflammatory Agents",
"Astrocytes",
"Azetidines",
"Benzyl Compounds",
"Calcium Signaling",
"Cerebellum",
"Demyelinating Diseases",
"Humans",
"Immunosuppressive Agents",
"In Vitro Techniques",
"Indans",
"Interleukin-6",
"Lysophosphatidylcholines",
"Mice",
"Myelin Basic Protein",
"Organ Culture Techniques",
"Oxadiazoles",
"Protein Transport",
"Receptors, Lysosphingolipid",
"Thiophenes",
"Time Factors",
"beta-Alanine",
"eIF-2 Kinase"
]
}
|
Overall, this study suggests that BAF312 can modulate glial cell function and attenuate demyelination, highlighting this drug as a further potential therapy in demyelinating disorders, beyond MS.
|
yes
|
[
{
"from": "human",
"value": "Question: Does the dual S1PR1/S1PR5 drug BAF312 ( Siponimod ) attenuate demyelination in organotypic slice cultures?\nContext: {'contexts': ['BAF312 (Siponimod) is a dual agonist at the sphingosine-1 phosphate receptors, S1PR1 and S1PR5. This drug is currently undergoing clinical trials for the treatment of secondary progressive multiple sclerosis (MS). Here, we investigated the effects of BAF312 on isolated astrocyte and microglia cultures as well as in slice culture models of demyelination.', 'Mouse and human astrocytes were treated with S1PR modulators and changes in the levels of pERK, pAkt, and calcium signalling as well as S1PR1 internalization and cytokine levels was investigated using Western blotting, immunochemistry, ELISA and confocal microscopy. Organotypic slice cultures were prepared from the cerebellum of 10-day-old mice and treated with lysophosphatidylcholine (LPC), psychosine and/or S1PR modulators, and changes in myelination states were measured by fluorescence of myelin basic protein and neurofilament H.', 'BAF312 treatment of human and mouse astrocytes activated pERK, pAKT and Ca(2+) signalling as well as inducing S1PR1 internalization. Notably, activation of S1PR1 increased pERK and pAKT in mouse astrocytes while both S1PR1 and S1PR3 equally increased pERK and pAKT in human astrocytes, suggesting that the coupling of S1PR1 and S1PR3 to pERK and pAKT differ in mouse and human astrocytes. We also observed that BAF312 moderately attenuated lipopolysaccharide (LPS)- or TNFα/IL17-induced levels of IL6 in both astrocyte and microglia cell cultures. In organotypic slice cultures, BAF312 reduced LPC-induced levels of IL6 and attenuated LPC-mediated demyelination. We have shown previously that the toxic lipid metabolite psychosine induces demyelination in organotypic slice cultures, without altering the levels of cytokines, such as IL6. Importantly, psychosine-induced demyelination was also attenuated by BAF312.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Animals, Newborn', 'Anti-Inflammatory Agents', 'Astrocytes', 'Azetidines', 'Benzyl Compounds', 'Calcium Signaling', 'Cerebellum', 'Demyelinating Diseases', 'Humans', 'Immunosuppressive Agents', 'In Vitro Techniques', 'Indans', 'Interleukin-6', 'Lysophosphatidylcholines', 'Mice', 'Myelin Basic Protein', 'Organ Culture Techniques', 'Oxadiazoles', 'Protein Transport', 'Receptors, Lysosphingolipid', 'Thiophenes', 'Time Factors', 'beta-Alanine', 'eIF-2 Kinase']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,852,397 |
Does a Pre-Hospital Patient Education Program improve Outcomes of Bariatric Surgery?
|
{
"contexts": [
"We designed an assessment and education program which was delivered to patients prior to first outpatient appointment for bariatric surgery. We hypothesised that this program would streamline care and would lead to improved weight loss following bariatric surgery.",
"The program incorporates a structured general practitioners (GP) review, a patient information evening and an on-line learning package. It was introduced in September 2012. Patient flow through the program was recorded. Outcomes of the new program were compared with contemporaneously treated patients who did not undertake the pre-hospital program.",
"All 636 patients on the waiting list for first appointment at the Alfred Health bariatric surgery clinic were invited to participate. There were 400 patients ultimately removed from the waiting list for first appointment. Of the remaining 236 patients, 229 consented to participate in the new program. The mean BMI was 47.8 ± 9.2. The fail to attend first appointment rate dropped from 12 to 2.1 %. At 12 months post-bariatric surgery, patients who undertook the new program (n = 82) had a mean excess weight loss (EWL) of 41.1 ± 20.3 % where as those treated on the standard pathway (n = 61) had a mean EWL 32 ± 18.0 % (p = 0.012)."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Bariatric Surgery",
"Female",
"Humans",
"Male",
"Middle Aged",
"Obesity, Morbid",
"Patient Education as Topic",
"Preoperative Period",
"Quality Improvement",
"Weight Loss"
]
}
|
The introduction of a pre-hospital education program has led to an improvement in attendance rates and early weight loss post-bariatric surgery.
|
yes
|
[
{
"from": "human",
"value": "Question: Does a Pre-Hospital Patient Education Program improve Outcomes of Bariatric Surgery?\nContext: {'contexts': ['We designed an assessment and education program which was delivered to patients prior to first outpatient appointment for bariatric surgery. We hypothesised that this program would streamline care and would lead to improved weight loss following bariatric surgery.', 'The program incorporates a structured general practitioners (GP) review, a patient information evening and an on-line learning package. It was introduced in September 2012. Patient flow through the program was recorded. Outcomes of the new program were compared with contemporaneously treated patients who did not undertake the pre-hospital program.', 'All 636 patients on the waiting list for first appointment at the Alfred Health bariatric surgery clinic were invited to participate. There were 400 patients ultimately removed from the waiting list for first appointment. Of the remaining 236 patients, 229 consented to participate in the new program. The mean BMI was 47.8\\u2009±\\u20099.2. The fail to attend first appointment rate dropped from 12 to 2.1\\xa0%. At 12\\xa0months post-bariatric surgery, patients who undertook the new program (n\\u2009=\\u200982) had a mean excess weight loss (EWL) of 41.1\\u2009±\\u200920.3\\xa0% where as those treated on the standard pathway (n\\u2009=\\u200961) had a mean EWL 32\\u2009±\\u200918.0\\xa0% (p\\u2009=\\u20090.012).'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Bariatric Surgery', 'Female', 'Humans', 'Male', 'Middle Aged', 'Obesity, Morbid', 'Patient Education as Topic', 'Preoperative Period', 'Quality Improvement', 'Weight Loss']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,852,395 |
Is duration of extracorporeal membrane oxygenation a poor predictor of hospital survival?
|
{
"contexts": [
"Venovenous extracorporeal membrane oxygenation (ECMO) is increasingly used in patients with respiratory failure. In patients without the option of lung transplantation, prognostication is challenging. We hypothesized that duration of ECMO therapy is inversely correlated with the chance of recovery and therefore hospital survival.",
"A single-center retrospective register analysis was performed. All bridge-to-recovery venovenous ECMO patients without option for lung transplantation treated between October 2010 and September 2015 were included.",
"A total of 175 patients (mean age, 51.61 ± 2.11 years) were detected. Medium time on ECMO was 9.26 ± 1.91 days. Time on ECMO was not significantly shorter in survivors compared to nonsurvivors (8.23 ± 2.04 and 10.15 ± 3.07, respectively; P = .327). Rate of hospital survival and time on ECMO did not correlate (P = .103). The predictive value of ECMO duration on hospital survival was 0.503 in a receiver operating characteristic analysis."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Extracorporeal Membrane Oxygenation",
"Female",
"Hospital Mortality",
"Humans",
"Male",
"Middle Aged",
"Predictive Value of Tests",
"Prospective Studies",
"ROC Curve",
"Respiratory Insufficiency",
"Retrospective Studies",
"Survival Analysis",
"Time Factors"
]
}
|
According to our registry data, duration of ECMO therapy by itself could not predict hospital survival. Prospective studies are needed to confirm this finding.
|
yes
|
[
{
"from": "human",
"value": "Question: Is duration of extracorporeal membrane oxygenation a poor predictor of hospital survival?\nContext: {'contexts': ['Venovenous extracorporeal membrane oxygenation (ECMO) is increasingly used in patients with respiratory failure. In patients without the option of lung transplantation, prognostication is challenging. We hypothesized that duration of ECMO therapy is inversely correlated with the chance of recovery and therefore hospital survival.', 'A single-center retrospective register analysis was performed. All bridge-to-recovery venovenous ECMO patients without option for lung transplantation treated between October 2010 and September 2015 were included.', 'A total of 175 patients (mean age, 51.61 ± 2.11 years) were detected. Medium time on ECMO was 9.26 ± 1.91 days. Time on ECMO was not significantly shorter in survivors compared to nonsurvivors (8.23 ± 2.04 and 10.15 ± 3.07, respectively; P = .327). Rate of hospital survival and time on ECMO did not correlate (P = .103). The predictive value of ECMO duration on hospital survival was 0.503 in a receiver operating characteristic analysis.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Extracorporeal Membrane Oxygenation', 'Female', 'Hospital Mortality', 'Humans', 'Male', 'Middle Aged', 'Predictive Value of Tests', 'Prospective Studies', 'ROC Curve', 'Respiratory Insufficiency', 'Retrospective Studies', 'Survival Analysis', 'Time Factors']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,852,394 |
Are high prolactin levels associated with more delirium in septic patients?
|
{
"contexts": [
"We investigated whether high prolactin levels were associated with delirium in septic patients because neuropsychiatric disorders are frequently associated with hyperprolactinemia.",
"Prolactin levels were measured daily for 4 days in 101 patients with sepsis. Delirium was assessed using the Richmond Agitation Sedation Scale and the Confusion Assessment Method in the ICU.",
"Delirium developed in 79 patients (78%) and was more common in patients older than 65 years. Prolactin levels were higher in patients with delirium than in those without over the 4 days of observation (P = .032). In patients with delirium, higher prolactin levels were associated with a lower incidence of nosocomial infection (P = .006). Multivariable logistic regression showed that the Sequential Organ Failure Assessment score at intensive care unit admission (odds ratio, 1.24; 95% confidence interval, 1.04-1.48; P = .002) and the combined effect of prolactin levels with age (odds ratio, 1.018; 95% confidence interval, 1.01-1.031; P = .006) were associated with the development of delirium."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"APACHE",
"Age Factors",
"Aged",
"Aged, 80 and over",
"Biomarkers",
"Case-Control Studies",
"Critical Care",
"Cross Infection",
"Delirium",
"Female",
"Humans",
"Hyperprolactinemia",
"Intensive Care Units",
"Male",
"Middle Aged",
"Odds Ratio",
"Prolactin",
"Prospective Studies",
"Psychometrics",
"Psychomotor Agitation",
"Risk Factors",
"Sepsis"
]
}
|
High prolactin levels may be a risk factor for delirium in septic patients.
|
yes
|
[
{
"from": "human",
"value": "Question: Are high prolactin levels associated with more delirium in septic patients?\nContext: {'contexts': ['We investigated whether high prolactin levels were associated with delirium in septic patients because neuropsychiatric disorders are frequently associated with hyperprolactinemia.', 'Prolactin levels were measured daily for 4 days in 101 patients with sepsis. Delirium was assessed using the Richmond Agitation Sedation Scale and the Confusion Assessment Method in the ICU.', 'Delirium developed in 79 patients (78%) and was more common in patients older than 65 years. Prolactin levels were higher in patients with delirium than in those without over the 4 days of observation (P = .032). In patients with delirium, higher prolactin levels were associated with a lower incidence of nosocomial infection (P = .006). Multivariable logistic regression showed that the Sequential Organ Failure Assessment score at intensive care unit admission (odds ratio, 1.24; 95% confidence interval, 1.04-1.48; P = .002) and the combined effect of prolactin levels with age (odds ratio, 1.018; 95% confidence interval, 1.01-1.031; P = .006) were associated with the development of delirium.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['APACHE', 'Age Factors', 'Aged', 'Aged, 80 and over', 'Biomarkers', 'Case-Control Studies', 'Critical Care', 'Cross Infection', 'Delirium', 'Female', 'Humans', 'Hyperprolactinemia', 'Intensive Care Units', 'Male', 'Middle Aged', 'Odds Ratio', 'Prolactin', 'Prospective Studies', 'Psychometrics', 'Psychomotor Agitation', 'Risk Factors', 'Sepsis']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,868,512 |
Is low carotid artery wall shear stress independently associated with brain white-matter hyperintensities and cognitive impairment in older patients?
|
{
"contexts": [
"Brain white-matter lesions and cognitive impairment are increasing because of the increasing number of patients aged ≥80 y. Wall shear stress (WSS) plays a pivotal role as a fluid mechanical mediator in vascular reactivity and atherosclerosis. In this study, we investigated the associations among common carotid artery (CCA) WSS, white-matter lesions, and cognitive impairment in patients aged ≥80 y",
"We enrolled 384 patients aged ≥80 y. All subjects had CCA-WSS, brain white-matter hyperintensities (WMH), and Mini-Mental State Examination (MMSE) assessments and were divided into three groups using tertiles of mean and peak CCA-WSS.",
"For groups classified by the tertile of mean CCA-WSS, WMH, and WMH fraction were decreased; the MMSE score increased from low to high in the respective groups. Differences in WMH, WMH fraction, and the MMSE score were significant between any two groups (all adjusted p < 0.001). Groups classified by the tertile of peak CCA-WSS had the same pattern. Mean and peak CCA-WSS were significantly and inversely correlated with WMH (r = -0.575 and -0.570, respectively; p < 0.001) and WMH fraction (r = -0.574 and -0.569, respectively; p < 0.001) but positively correlated with the MMSE score (r = 0.390 and 0.278, respectively; p < 0.001). Multiple linear backward stepwise regression indicated the mean and peak CCA-WSS were significantly and independently associated with WMH, WMH fraction, and the MMSE score (all adjusted p < 0.001)."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Age Factors",
"Aged, 80 and over",
"Blood Flow Velocity",
"Carotid Artery Diseases",
"Carotid Artery, Common",
"Carotid Intima-Media Thickness",
"Cognition",
"Cognition Disorders",
"Cross-Sectional Studies",
"Female",
"Humans",
"Leukoencephalopathies",
"Linear Models",
"Magnetic Resonance Imaging",
"Male",
"Multivariate Analysis",
"Psychiatric Status Rating Scales",
"Regional Blood Flow",
"Risk Factors",
"Stress, Mechanical",
"Ultrasonography, Doppler, Duplex"
]
}
|
Carotid artery WSS was independently associated with brain white-matter lesions and cognitive impairment in patients aged ≥80 y.
|
yes
|
[
{
"from": "human",
"value": "Question: Is low carotid artery wall shear stress independently associated with brain white-matter hyperintensities and cognitive impairment in older patients?\nContext: {'contexts': ['Brain white-matter lesions and cognitive impairment are increasing because of the increasing number of patients aged ≥80 y. Wall shear stress (WSS) plays a pivotal role as a fluid mechanical mediator in vascular reactivity and atherosclerosis. In this study, we investigated the associations among common carotid artery (CCA) WSS, white-matter lesions, and cognitive impairment in patients aged ≥80 y', 'We enrolled 384 patients aged ≥80 y. All subjects had CCA-WSS, brain white-matter hyperintensities (WMH), and Mini-Mental State Examination (MMSE) assessments and were divided into three groups using tertiles of mean and peak CCA-WSS.', 'For groups classified by the tertile of mean CCA-WSS, WMH, and WMH fraction were decreased; the MMSE score increased from low to high in the respective groups. Differences in WMH, WMH fraction, and the MMSE score were significant between any two groups (all adjusted p < 0.001). Groups classified by the tertile of peak CCA-WSS had the same pattern. Mean and peak CCA-WSS were significantly and inversely correlated with WMH (r = -0.575 and -0.570, respectively; p < 0.001) and WMH fraction (r = -0.574 and -0.569, respectively; p < 0.001) but positively correlated with the MMSE score (r = 0.390 and 0.278, respectively; p < 0.001). Multiple linear backward stepwise regression indicated the mean and peak CCA-WSS were significantly and independently associated with WMH, WMH fraction, and the MMSE score (all adjusted p < 0.001).'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Age Factors', 'Aged, 80 and over', 'Blood Flow Velocity', 'Carotid Artery Diseases', 'Carotid Artery, Common', 'Carotid Intima-Media Thickness', 'Cognition', 'Cognition Disorders', 'Cross-Sectional Studies', 'Female', 'Humans', 'Leukoencephalopathies', 'Linear Models', 'Magnetic Resonance Imaging', 'Male', 'Multivariate Analysis', 'Psychiatric Status Rating Scales', 'Regional Blood Flow', 'Risk Factors', 'Stress, Mechanical', 'Ultrasonography, Doppler, Duplex']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,863,634 |
Does large-scale profiling of signalling pathways reveal an asthma specific signature in bronchial smooth muscle cells?
|
{
"contexts": [
"Bronchial smooth muscle (BSM) cells from asthmatic patients maintain in vitro a distinct hyper-reactive (\"primed\") phenotype, characterized by increased release of pro-inflammatory factors and mediators, as well as hyperplasia and/or hypertrophy. This \"primed\" phenotype helps to understand pathogenesis of asthma, as changes in BSM function are essential for manifestation of allergic and inflammatory responses and airway wall remodelling.",
"To identify signalling pathways in cultured primary BSMs of asthma patients and non-asthmatic subjects by genome wide profiling of differentially expressed mRNAs and activated intracellular signalling pathways (ISPs).",
"Transcriptome profiling by cap-analysis-of-gene-expression (CAGE), which permits selection of preferentially capped mRNAs most likely to be translated into proteins, was performed in human BSM cells from asthmatic (n=8) and non-asthmatic (n=6) subjects and OncoFinder tool were then exploited for identification of ISP deregulations.",
"CAGE revealed >600 RNAs differentially expressed in asthma vs control cells (p≤0.005), with asthma samples showing a high degree of similarity among them. Comprehensive ISP activation analysis revealed that among 269 pathways analysed, 145 (p<0.05) or 103 (p<0.01) are differentially active in asthma, with profiles that clearly characterize BSM cells of asthmatic individuals. Notably, we identified 7 clusters of coherently acting pathways functionally related to the disease, with ISPs down-regulated in asthma mostly targeting cell death-promoting pathways and up-regulated ones affecting cell growth and proliferation, inflammatory response, control of smooth muscle contraction and hypoxia-related signalization."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adult",
"Aged",
"Asthma",
"Bronchi",
"Female",
"Gene Expression Profiling",
"Humans",
"Male",
"Middle Aged",
"Myocytes, Smooth Muscle",
"Signal Transduction",
"Transcriptome",
"Young Adult"
]
}
|
These first-time results can now be exploited toward development of novel therapeutic strategies targeting ISP signatures linked to asthma pathophysiology.
|
yes
|
[
{
"from": "human",
"value": "Question: Does large-scale profiling of signalling pathways reveal an asthma specific signature in bronchial smooth muscle cells?\nContext: {'contexts': ['Bronchial smooth muscle (BSM) cells from asthmatic patients maintain in vitro a distinct hyper-reactive (\"primed\") phenotype, characterized by increased release of pro-inflammatory factors and mediators, as well as hyperplasia and/or hypertrophy. This \"primed\" phenotype helps to understand pathogenesis of asthma, as changes in BSM function are essential for manifestation of allergic and inflammatory responses and airway wall remodelling.', 'To identify signalling pathways in cultured primary BSMs of asthma patients and non-asthmatic subjects by genome wide profiling of differentially expressed mRNAs and activated intracellular signalling pathways (ISPs).', 'Transcriptome profiling by cap-analysis-of-gene-expression (CAGE), which permits selection of preferentially capped mRNAs most likely to be translated into proteins, was performed in human BSM cells from asthmatic (n=8) and non-asthmatic (n=6) subjects and OncoFinder tool were then exploited for identification of ISP deregulations.', 'CAGE revealed >600 RNAs differentially expressed in asthma vs control cells (p≤0.005), with asthma samples showing a high degree of similarity among them. Comprehensive ISP activation analysis revealed that among 269 pathways analysed, 145 (p<0.05) or 103 (p<0.01) are differentially active in asthma, with profiles that clearly characterize BSM cells of asthmatic individuals. Notably, we identified 7 clusters of coherently acting pathways functionally related to the disease, with ISPs down-regulated in asthma mostly targeting cell death-promoting pathways and up-regulated ones affecting cell growth and proliferation, inflammatory response, control of smooth muscle contraction and hypoxia-related signalization.'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adult', 'Aged', 'Asthma', 'Bronchi', 'Female', 'Gene Expression Profiling', 'Humans', 'Male', 'Middle Aged', 'Myocytes, Smooth Muscle', 'Signal Transduction', 'Transcriptome', 'Young Adult']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,871,414 |
Do cytotoxic amounts of cisplatin induce either checkpoint adaptation or apoptosis in a concentration-dependent manner in cancer cells?
|
{
"contexts": [
"Checkpoint adaptation (entry into mitosis with damaged DNA) is a process that links arrest at the G2/M cell cycle checkpoint and cell death in cancer cells. It is not known, however, whether cells treated with the genotoxic agent, cisplatin, undergo checkpoint adaptation or if checkpoint adaptation is a major pathway leading to cell death or not. Therefore, we investigated the relationship between treatment with cisplatin and cytotoxicity in cancer cells.",
"Treatment of HT-29 human colorectal adenocarcinoma cells with cisplatin can induce cell death by one of two different mechanisms. Cells treated with a cytotoxic 30 μM amount of cisplatin died after undergoing checkpoint adaptation. Before dying, however, almost all treated cells were positive for histone γH2AX staining and contained high levels of cyclin B1. Rounded cells appeared that were positive for phospho-Ser10 histone H3, with low levels of phospho-Tyr15 cyclin-dependent kinase 1, high levels of cyclin-dependent kinase 1 activity, and checkpoint kinase 1 that was not phosphorylated on Ser345. These cells were in mitosis with damaged DNA. Strikingly, with 30 μM cisplatin, 81% of cells had entered mitosis before dying. By contrast, after treatment with 100 μM cisplatin, nearly all cells died but only 7% of cells had entered mitosis. Instead, these cells died by apoptosis; they were positive for annexin-V staining, contained cleaved caspase 3, cleaved caspase 9 and cleaved PARP and did not contain Mcl-1."
],
"labels": [
"BACKGROUND",
"RESULTS"
],
"meshes": [
"Adenocarcinoma",
"Apoptosis",
"Cisplatin",
"Colorectal Neoplasms",
"Cyclin B1",
"Dose-Response Relationship, Drug",
"G2 Phase Cell Cycle Checkpoints",
"Histones",
"Humans",
"M Phase Cell Cycle Checkpoints",
"Neoplasm Proteins"
]
}
|
Our data demonstrate that cancer cells treated with cisplatin can undergo one of two modes of cell death depending upon concentration used. These findings suggest that checkpoint adaptation is likely a primary pathway in genotoxic cell death at pharmacological concentrations of cisplatin.
|
yes
|
[
{
"from": "human",
"value": "Question: Do cytotoxic amounts of cisplatin induce either checkpoint adaptation or apoptosis in a concentration-dependent manner in cancer cells?\nContext: {'contexts': ['Checkpoint adaptation (entry into mitosis with damaged DNA) is a process that links arrest at the G2/M cell cycle checkpoint and cell death in cancer cells. It is not known, however, whether cells treated with the genotoxic agent, cisplatin, undergo checkpoint adaptation or if checkpoint adaptation is a major pathway leading to cell death or not. Therefore, we investigated the relationship between treatment with cisplatin and cytotoxicity in cancer cells.', 'Treatment of HT-29 human colorectal adenocarcinoma cells with cisplatin can induce cell death by one of two different mechanisms. Cells treated with a cytotoxic 30 μM amount of cisplatin died after undergoing checkpoint adaptation. Before dying, however, almost all treated cells were positive for histone γH2AX staining and contained high levels of cyclin B1. Rounded cells appeared that were positive for phospho-Ser10 histone H3, with low levels of phospho-Tyr15 cyclin-dependent kinase 1, high levels of cyclin-dependent kinase 1 activity, and checkpoint kinase 1 that was not phosphorylated on Ser345. These cells were in mitosis with damaged DNA. Strikingly, with 30 μM cisplatin, 81% of cells had entered mitosis before dying. By contrast, after treatment with 100 μM cisplatin, nearly all cells died but only 7% of cells had entered mitosis. Instead, these cells died by apoptosis; they were positive for annexin-V staining, contained cleaved caspase 3, cleaved caspase 9 and cleaved PARP and did not contain Mcl-1.'], 'labels': ['BACKGROUND', 'RESULTS'], 'meshes': ['Adenocarcinoma', 'Apoptosis', 'Cisplatin', 'Colorectal Neoplasms', 'Cyclin B1', 'Dose-Response Relationship, Drug', 'G2 Phase Cell Cycle Checkpoints', 'Histones', 'Humans', 'M Phase Cell Cycle Checkpoints', 'Neoplasm Proteins']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,860,080 |
Does andrographolide attenuate LPS-stimulated up-regulation of C-C and C-X-C motif chemokines in rodent cortex and primary astrocytes?
|
{
"contexts": [
"Andrographolide is the major bioactive compound isolated from Andrographis paniculata, a native South Asian herb used medicinally for its anti-inflammatory properties. In this study, we aimed to assess andrographolide's potential utility as an anti-neuroinflammatory therapeutic.",
"The effects of andrographolide on lipopolysaccharide (LPS)-induced chemokine up-regulation both in mouse cortex and in cultured primary astrocytes were measured, including cytokine profiling, gene expression, and, in cultured astrocytes, activation of putative signaling regulators.",
"Orally administered andrographolide significantly attenuated mouse cortical chemokine levels from the C-C and C-X-C subfamilies. Similarly, andrographolide abrogated a range of LPS-induced chemokines as well as tumor necrosis factor (TNF)-α in astrocytes. In astrocytes, the inhibitory actions of andrographolide on chemokine and TNF-α up-regulation appeared to be mediated by nuclear factor-κB (NF-κB) or c-Jun N-terminal kinase (JNK) activation."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Analysis of Variance",
"Animals",
"Anti-Inflammatory Agents",
"Astrocytes",
"Cell Survival",
"Cerebral Cortex",
"Chemokines, CXC",
"Diterpenes",
"Dose-Response Relationship, Drug",
"Lipopolysaccharides",
"MAP Kinase Kinase 4",
"Mice",
"NF-kappa B",
"Rats",
"Up-Regulation"
]
}
|
These results suggest that andrographolide may be useful as a therapeutic for neuroinflammatory diseases, especially those characterized by chemokine dysregulation.
|
yes
|
[
{
"from": "human",
"value": "Question: Does andrographolide attenuate LPS-stimulated up-regulation of C-C and C-X-C motif chemokines in rodent cortex and primary astrocytes?\nContext: {'contexts': [\"Andrographolide is the major bioactive compound isolated from Andrographis paniculata, a native South Asian herb used medicinally for its anti-inflammatory properties. In this study, we aimed to assess andrographolide's potential utility as an anti-neuroinflammatory therapeutic.\", 'The effects of andrographolide on lipopolysaccharide (LPS)-induced chemokine up-regulation both in mouse cortex and in cultured primary astrocytes were measured, including cytokine profiling, gene expression, and, in cultured astrocytes, activation of putative signaling regulators.', 'Orally administered andrographolide significantly attenuated mouse cortical chemokine levels from the C-C and C-X-C subfamilies. Similarly, andrographolide abrogated a range of LPS-induced chemokines as well as tumor necrosis factor (TNF)-α in astrocytes. In astrocytes, the inhibitory actions of andrographolide on chemokine and TNF-α up-regulation appeared to be mediated by nuclear factor-κB (NF-κB) or c-Jun N-terminal kinase (JNK) activation.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Analysis of Variance', 'Animals', 'Anti-Inflammatory Agents', 'Astrocytes', 'Cell Survival', 'Cerebral Cortex', 'Chemokines, CXC', 'Diterpenes', 'Dose-Response Relationship, Drug', 'Lipopolysaccharides', 'MAP Kinase Kinase 4', 'Mice', 'NF-kappa B', 'Rats', 'Up-Regulation']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,857,228 |
Does choice of xenogenic-free expansion media significantly influence the myogenic differentiation potential of human bone marrow-derived mesenchymal stromal cells?
|
{
"contexts": [
"Mesenchymal stromal cells (MSCs) have great potential for use in cell-based therapies for restoration of structure and function of many tissue types including smooth muscle.",
"We compared proliferation, immunophenotype, differentiation capability and gene expression of bone marrow-derived MSCs expanded in different media containing human serum, plasma and platelet lysate in combination with commonly used protocols for myogenic, osteogenic, chondrogenic and adipogenic differentiation. Moreover, we developed a xenogenic-free protocol for myogenic differentiation of MSCs.",
"Expansion of MSCs in media complemented with serum, serum + platelet lysate or plasma + platelet lysate were multipotent because they differentiated toward four mesenchymal (myogenic, osteogenic, chondrogenic, adipogenic) lineages. Addition of platelet lysate to expansion media increased the proliferation of MSCs and their expression of CD146. Incubation of MSCs in medium containing human serum or plasma plus 5% human platelet lysate in combination with smooth muscle cell (SMC)-inducing growth factors TGFβ1, PDGF and ascorbic acid induced high expression of ACTA2, TAGLN, CNN1 and/or MYH11 contractile SMC markers. Osteogenic, adipogenic and chondrogenic differentiations served as controls."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adipogenesis",
"Antigens, Heterophile",
"Blood Platelets",
"Bone Marrow Cells",
"Cell Culture Techniques",
"Cell Differentiation",
"Cell- and Tissue-Based Therapy",
"Cells, Cultured",
"Chondrogenesis",
"Culture Media",
"Humans",
"Immunophenotyping",
"Mesenchymal Stem Cells",
"Muscle Development",
"Myocytes, Smooth Muscle"
]
}
|
Our study provides novel data on the myogenic differentiation potential of human MSCs toward the SMC lineage using different xenogenic-free cell culture expansion media in combination with distinct differentiation medium compositions. We show that the choice of expansion medium significantly influences the differentiation potential of human MSCs toward the smooth muscle cell, as well as osteogenic, adipogenic and chondrogenic lineages. These results can aid in designing studies using MSCs for tissue-specific therapeutic applications.
|
yes
|
[
{
"from": "human",
"value": "Question: Does choice of xenogenic-free expansion media significantly influence the myogenic differentiation potential of human bone marrow-derived mesenchymal stromal cells?\nContext: {'contexts': ['Mesenchymal stromal cells (MSCs) have great potential for use in cell-based therapies for restoration of structure and function of many tissue types including smooth muscle.', 'We compared proliferation, immunophenotype, differentiation capability and gene expression of bone marrow-derived MSCs expanded in different media containing human serum, plasma and platelet lysate in combination with commonly used protocols for myogenic, osteogenic, chondrogenic and adipogenic differentiation. Moreover, we developed a xenogenic-free protocol for myogenic differentiation of MSCs.', 'Expansion of MSCs in media complemented with serum, serum + platelet lysate or plasma + platelet lysate were multipotent because they differentiated toward four mesenchymal (myogenic, osteogenic, chondrogenic, adipogenic) lineages. Addition of platelet lysate to expansion media increased the proliferation of MSCs and their expression of CD146. Incubation of MSCs in medium containing human serum or plasma plus 5% human platelet lysate in combination with smooth muscle cell (SMC)-inducing growth factors TGFβ1, PDGF and ascorbic acid induced high expression of ACTA2, TAGLN, CNN1 and/or MYH11 contractile SMC markers. Osteogenic, adipogenic and chondrogenic differentiations served as controls.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adipogenesis', 'Antigens, Heterophile', 'Blood Platelets', 'Bone Marrow Cells', 'Cell Culture Techniques', 'Cell Differentiation', 'Cell- and Tissue-Based Therapy', 'Cells, Cultured', 'Chondrogenesis', 'Culture Media', 'Humans', 'Immunophenotyping', 'Mesenchymal Stem Cells', 'Muscle Development', 'Myocytes, Smooth Muscle']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,857,229 |
Is galectin-1 a local but not systemic immunomodulatory factor in mesenchymal stromal cells?
|
{
"contexts": [
"Mesenchymal stromal cells (MSCs) have powerful immunosuppressive activity. This function of MSCs is attributed to plethora of the expressed immunosuppressive factors, such as galectin-1 (Gal-1), a pleiotropic lectin with robust anti-inflammatory effect. Nevertheless, whether Gal-1 renders or contributes to the immunosuppressive effect of MSCs has not been clearly established. Therefore, this question was the focus of a complex study.",
"MSCs were isolated from bone marrows of wild-type and Gal-1 knockout mice and their in vitro anti-proliferative and apoptosis-inducing effects on activated T cells were examined. The in vivo immunosuppressive activity was tested in murine models of type I diabetes and delayed-type hypersensitivity.",
"Both Gal-1-expressing and -deficient MSCs inhibited T-cell proliferation. Inhibition of T-cell proliferation by MSCs was mediated by nitric oxide but not PD-L1 or Gal-1. In contrast, MSC-derived Gal-1 triggered apoptosis in activated T cells that were directly coupled to MSCs, representing a low proportion of the T-cell population. Furthermore, absence of Gal-1 in MSCs did not affect their in vivo immunosuppressive effect."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Apoptosis",
"Bone Marrow",
"Cell Communication",
"Cell Proliferation",
"Cells, Cultured",
"Galectin 1",
"Immunologic Factors",
"Immunosuppressive Agents",
"Lymphocyte Activation",
"Male",
"Mesenchymal Stem Cells",
"Mice",
"Mice, Inbred C57BL",
"Mice, Knockout",
"T-Lymphocytes"
]
}
|
These results serve as evidence that Gal-1 does not play a role in the systemic immunosuppressive effect of MSCs. However, a local contribution of Gal-1 to modulation of T-cell response by direct cell-to-cell interaction cannot be excluded. Notably, this study serves a good model to understand how the specificity of a pleiotropic protein depends on the type and localization of the producing effector cell and its target.
|
yes
|
[
{
"from": "human",
"value": "Question: Is galectin-1 a local but not systemic immunomodulatory factor in mesenchymal stromal cells?\nContext: {'contexts': ['Mesenchymal stromal cells (MSCs) have powerful immunosuppressive activity. This function of MSCs is attributed to plethora of the expressed immunosuppressive factors, such as galectin-1 (Gal-1), a pleiotropic lectin with robust anti-inflammatory effect. Nevertheless, whether Gal-1 renders or contributes to the immunosuppressive effect of MSCs has not been clearly established. Therefore, this question was the focus of a complex study.', 'MSCs were isolated from bone marrows of wild-type and Gal-1 knockout mice and their in vitro anti-proliferative and apoptosis-inducing effects on activated T cells were examined. The in vivo immunosuppressive activity was tested in murine models of type I diabetes and delayed-type hypersensitivity.', 'Both Gal-1-expressing and -deficient MSCs inhibited T-cell proliferation. Inhibition of T-cell proliferation by MSCs was mediated by nitric oxide but not PD-L1 or Gal-1. In contrast, MSC-derived Gal-1 triggered apoptosis in activated T cells that were directly coupled to MSCs, representing a low proportion of the T-cell population. Furthermore, absence of Gal-1 in MSCs did not affect their in vivo immunosuppressive effect.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Apoptosis', 'Bone Marrow', 'Cell Communication', 'Cell Proliferation', 'Cells, Cultured', 'Galectin 1', 'Immunologic Factors', 'Immunosuppressive Agents', 'Lymphocyte Activation', 'Male', 'Mesenchymal Stem Cells', 'Mice', 'Mice, Inbred C57BL', 'Mice, Knockout', 'T-Lymphocytes']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,874,752 |
Is activation of microglia within paraventricular nucleus of hypothalamus involved in maintenance of established hypertension?
|
{
"contexts": [
"Inflammation within paraventricular nucleus of the hypothalamus (PVN), a key circulatory control center in the hypothalamus, is an important pathology of sympathetic hyperactivity. Brain inflammation is mainly mediated by microglia, innate immune cells in the brain. Activated microglia produce inflammatory cytokines with alteration of their morphology. Increase in inflammatory cytokines synthesis coincides with activation of microglia within PVN of angiotensin II-induced hypertensive model and myocardial infarction-induced heart failure model. Although the increase in inflammatory cytokines and the microglial activation within PVN were also seen in spontaneously hypertensive rats (SHR), the model of essential hypertension, their involvement in blood pressure regulation has still be fully clarified. In the present study, we examined whether activated microglia within PVN were involved in maintenance of established severe hypertension with sympathoexcitation.",
"Minocycline (25mg/kg/day), an inhibitor of microglial activation, or vehicle were orally administered to stroke-prone SHR (SHRSP) and normotensive Wistar-Kyoto (WKY) rats for 2 weeks from 15-weeks-old, the age of established hypertension.",
"Systolic blood pressure was comparable between minocycline treated-SHRSP and vehicle treated-SHRSP, whereas morphological analysis of microglia revealed smaller cell size in minocycline treated-SHRSP than vehicle treated-SHRSP, implying that minocycline deactivated microglia within PVN."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Anti-Bacterial Agents",
"Hypertension",
"Microglia",
"Minocycline",
"Paraventricular Hypothalamic Nucleus",
"Rats, Inbred SHR",
"Rats, Inbred WKY"
]
}
|
Activated microglia with morphological alteration within PVN are not involved in the maintenance of established severe hypertension, and inflammation within PVN could not be the therapeutic target of established hypertension.
|
no
|
[
{
"from": "human",
"value": "Question: Is activation of microglia within paraventricular nucleus of hypothalamus involved in maintenance of established hypertension?\nContext: {'contexts': ['Inflammation within paraventricular nucleus of the hypothalamus (PVN), a key circulatory control center in the hypothalamus, is an important pathology of sympathetic hyperactivity. Brain inflammation is mainly mediated by microglia, innate immune cells in the brain. Activated microglia produce inflammatory cytokines with alteration of their morphology. Increase in inflammatory cytokines synthesis coincides with activation of microglia within PVN of angiotensin II-induced hypertensive model and myocardial infarction-induced heart failure model. Although the increase in inflammatory cytokines and the microglial activation within PVN were also seen in spontaneously hypertensive rats (SHR), the model of essential hypertension, their involvement in blood pressure regulation has still be fully clarified. In the present study, we examined whether activated microglia within PVN were involved in maintenance of established severe hypertension with sympathoexcitation.', 'Minocycline (25mg/kg/day), an inhibitor of microglial activation, or vehicle were orally administered to stroke-prone SHR (SHRSP) and normotensive Wistar-Kyoto (WKY) rats for 2 weeks from 15-weeks-old, the age of established hypertension.', 'Systolic blood pressure was comparable between minocycline treated-SHRSP and vehicle treated-SHRSP, whereas morphological analysis of microglia revealed smaller cell size in minocycline treated-SHRSP than vehicle treated-SHRSP, implying that minocycline deactivated microglia within PVN.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Anti-Bacterial Agents', 'Hypertension', 'Microglia', 'Minocycline', 'Paraventricular Hypothalamic Nucleus', 'Rats, Inbred SHR', 'Rats, Inbred WKY']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
] |
26,868,017 |
Do distinct genomic and epigenomic features demarcate hypomethylated blocks in colon cancer?
|
{
"contexts": [
"Large mega base-pair genomic regions show robust alterations in DNA methylation levels in multiple cancers. A vast majority of these regions are hypomethylated in cancers. These regions are generally enriched for CpG islands, Lamin Associated Domains and Large organized chromatin lysine modification domains, and are associated with stochastic variability in gene expression. Given the size and consistency of hypomethylated blocks (HMB) across cancer types, we hypothesized that the immediate causes of methylation instability are likely to be encoded in the genomic region near HMB boundaries, in terms of specific genomic or epigenomic signatures. However, a detailed characterization of the HMB boundaries has not been reported.",
"Here, we focused on ~13 k HMBs, encompassing approximately half of the genome, identified in colon cancer. We modeled the genomic features of HMB boundaries by Random Forest to identify their salient features, in terms of transcription factor (TF) binding motifs. Additionally we analyzed various epigenomic marks, and chromatin structural features of HMB boundaries relative to the non-HMB genomic regions.",
"We found that the classical promoter epigenomic mark--H3K4me3, is highly enriched at HMB boundaries, as are CTCF bound sites. HMB boundaries harbor distinct combinations of TF motifs. Our Random Forest model based on TF motifs can accurately distinguish boundaries not only from regions inside and outside HMBs, but surprisingly, from active promoters as well. Interestingly, the distinguishing TFs and their interacting proteins are involved in chromatin modification. Finally, HMB boundaries significantly coincide with the boundaries of Topologically Associating Domains of the chromatin."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Cell Line, Tumor",
"Chromatin",
"Colonic Neoplasms",
"CpG Islands",
"DNA Methylation",
"Epigenomics",
"Genome, Human",
"Histones",
"Humans",
"Promoter Regions, Genetic"
]
}
|
Our analyses suggest that the overall architecture of HMBs is guided by pre-existing chromatin architecture, and are associated with aberrant activity of promoter-like sequences at the boundary.
|
yes
|
[
{
"from": "human",
"value": "Question: Do distinct genomic and epigenomic features demarcate hypomethylated blocks in colon cancer?\nContext: {'contexts': ['Large mega base-pair genomic regions show robust alterations in DNA methylation levels in multiple cancers. A vast majority of these regions are hypomethylated in cancers. These regions are generally enriched for CpG islands, Lamin Associated Domains and Large organized chromatin lysine modification domains, and are associated with stochastic variability in gene expression. Given the size and consistency of hypomethylated blocks (HMB) across cancer types, we hypothesized that the immediate causes of methylation instability are likely to be encoded in the genomic region near HMB boundaries, in terms of specific genomic or epigenomic signatures. However, a detailed characterization of the HMB boundaries has not been reported.', 'Here, we focused on ~13 k HMBs, encompassing approximately half of the genome, identified in colon cancer. We modeled the genomic features of HMB boundaries by Random Forest to identify their salient features, in terms of transcription factor (TF) binding motifs. Additionally we analyzed various epigenomic marks, and chromatin structural features of HMB boundaries relative to the non-HMB genomic regions.', 'We found that the classical promoter epigenomic mark--H3K4me3, is highly enriched at HMB boundaries, as are CTCF bound sites. HMB boundaries harbor distinct combinations of TF motifs. Our Random Forest model based on TF motifs can accurately distinguish boundaries not only from regions inside and outside HMBs, but surprisingly, from active promoters as well. Interestingly, the distinguishing TFs and their interacting proteins are involved in chromatin modification. Finally, HMB boundaries significantly coincide with the boundaries of Topologically Associating Domains of the chromatin.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Cell Line, Tumor', 'Chromatin', 'Colonic Neoplasms', 'CpG Islands', 'DNA Methylation', 'Epigenomics', 'Genome, Human', 'Histones', 'Humans', 'Promoter Regions, Genetic']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,861,893 |
Does long-Term Pain Reduction Imply Improved Functional Outcome in Patients Treated With Combined Supraorbital and Occipital Nerve Stimulation for Chronic Migraine?
|
{
"contexts": [
"Dual supraorbital and occipital nerve stimulation (SONS and ONS) have shown promising efficacy in treating primary headaches. However, its functional outcome is not well studied.",
"To present functional outcome studies of combined SONS and ONS for chronic migraine using verified metrics.",
"Consecutive patients with both SONS and ONS assessed with Migraine Disability Assessment (MIDAS) and Beck Depression Index (BDI) both preoperatively and postoperatively were studied. Selected predictor variables included patients with ≥50% improvement of pain, disability status, number of years from diagnosis to implantation, and narcotic use. Functional outcome variables included net improvement of ranked MIDAS and BDI scores. Multivariate analysis of variance was performed to assess the correlation between the outcome and predictor variables.",
"Sixteen patients (12 female; average age 52 years old) were studied. Follow-up ranged from 5 to 80 months (average 44.5; σ = 21.4 months). At most recent follow-up, eight patients had a positive response (≥50% improvement in headache), which was the only predictor of functional outcome (total MIDAS, MIDAS-B, and BDI) (p = 0.021). Of note, improvement in functional outcome was only significant during the perioperative 3-6 months period and not throughout long-term follow-up. Among the predictor variables, a strong inverse correlation was found between disability status and positive response to stimulation (r = -0.582)."
],
"labels": [
"BACKGROUND",
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Chronic Disease",
"Cranial Nerves",
"Electric Stimulation Therapy",
"Female",
"Follow-Up Studies",
"Humans",
"Male",
"Middle Aged",
"Migraine Disorders",
"Mood Disorders",
"Pain Measurement",
"Psychiatric Status Rating Scales",
"Quality of Life",
"Spinal Nerves",
"Treatment Outcome"
]
}
|
There is a paucity of studies in quality of life, productivity, and psychosocial aspects with peripheral nerve stimulation therapy for headache. Patients with a positive response to SONS and ONS also reported overall improvement in their functional status as reflected by MIDAS and BDI in the perioperative period. Unfortunately, this effect waned over the long-term follow-up.
|
no
|
[
{
"from": "human",
"value": "Question: Does long-Term Pain Reduction Imply Improved Functional Outcome in Patients Treated With Combined Supraorbital and Occipital Nerve Stimulation for Chronic Migraine?\nContext: {'contexts': ['Dual supraorbital and occipital nerve stimulation (SONS and ONS) have shown promising efficacy in treating primary headaches. However, its functional outcome is not well studied.', 'To present functional outcome studies of combined SONS and ONS for chronic migraine using verified metrics.', 'Consecutive patients with both SONS and ONS assessed with Migraine Disability Assessment (MIDAS) and Beck Depression Index (BDI) both preoperatively and postoperatively were studied. Selected predictor variables included patients with ≥50% improvement of pain, disability status, number of years from diagnosis to implantation, and narcotic use. Functional outcome variables included net improvement of ranked MIDAS and BDI scores. Multivariate analysis of variance was performed to assess the correlation between the outcome and predictor variables.', 'Sixteen patients (12 female; average age 52 years old) were studied. Follow-up ranged from 5 to 80 months (average 44.5; σ\\u2009=\\u200921.4 months). At most recent follow-up, eight patients had a positive response (≥50% improvement in headache), which was the only predictor of functional outcome (total MIDAS, MIDAS-B, and BDI) (p\\u2009=\\u20090.021). Of note, improvement in functional outcome was only significant during the perioperative 3-6 months period and not throughout long-term follow-up. Among the predictor variables, a strong inverse correlation was found between disability status and positive response to stimulation (r\\u2009=\\u2009-0.582).'], 'labels': ['BACKGROUND', 'OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Chronic Disease', 'Cranial Nerves', 'Electric Stimulation Therapy', 'Female', 'Follow-Up Studies', 'Humans', 'Male', 'Middle Aged', 'Migraine Disorders', 'Mood Disorders', 'Pain Measurement', 'Psychiatric Status Rating Scales', 'Quality of Life', 'Spinal Nerves', 'Treatment Outcome']}"
},
{
"from": "gpt",
"value": "Answer: no"
}
] |
26,851,971 |
Does epigallocatechin Gallate extend the Therapeutic Window of Recombinant Tissue Plasminogen Activator Treatment in Ischemic Rats?
|
{
"contexts": [
"Ischemic stroke is the leading cause of death and disability worldwide. To date, recombinant tissue plasminogen activator (rt-PA) remains the only safe and effective pharmaceutical treatment for brain ischemia, but delayed rt-PA administration leads to hyperperfusion, which severely limits its clinical efficacy.",
"In this study, we investigated the effect of epigallocatechin gallate (EGCG) in extending the therapeutic window of rt-PA using a rat middle cerebral artery occlusion (MCAO) model.",
"Simultaneous treatment of EGCG and rt-PA significantly recovered the neurobehavioral deficit, when administered even 4 hours after MCAO. Pathological examinations on the ischemic brain samples revealed that EGCG significantly alleviated the common side effects of delayed rt-PA treatment, including brain infarction, cerebral edema, and blood-brain barrier disruption. We further found that EGCG exerted its protective functions against delayed rt-PA through upregulation of plasminogen activator inhibitor-1, as well as downregulation of matrix metalloproteinases."
],
"labels": [
"BACKGROUND",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Blood-Brain Barrier",
"Brain Edema",
"Catechin",
"Disease Models, Animal",
"Drug Therapy, Combination",
"Fibrinolytic Agents",
"Gene Expression Regulation",
"Infarction, Middle Cerebral Artery",
"Male",
"Matrix Metalloproteinase 1",
"Matrix Metalloproteinase 9",
"Neuroprotective Agents",
"Permeability",
"Plasminogen Activator Inhibitor 1",
"Rats",
"Rats, Sprague-Dawley",
"Sensory Gating",
"Time Factors",
"Tissue Plasminogen Activator",
"Treatment Outcome"
]
}
|
Our study has demonstrated for the first time in vivo results supporting the potential of EGCG to be coadministered with rt-PA, to extend its therapeutic window in treating acute brain ischemia.
|
yes
|
[
{
"from": "human",
"value": "Question: Does epigallocatechin Gallate extend the Therapeutic Window of Recombinant Tissue Plasminogen Activator Treatment in Ischemic Rats?\nContext: {'contexts': ['Ischemic stroke is the leading cause of death and disability worldwide. To date, recombinant tissue plasminogen activator (rt-PA) remains the only safe and effective pharmaceutical treatment for brain ischemia, but delayed rt-PA administration leads to hyperperfusion, which severely limits its clinical efficacy.', 'In this study, we investigated the effect of epigallocatechin gallate (EGCG) in extending the therapeutic window of rt-PA using a rat middle cerebral artery occlusion (MCAO) model.', 'Simultaneous treatment of EGCG and rt-PA significantly recovered the neurobehavioral deficit, when administered even 4\\u2009hours after MCAO. Pathological examinations on the ischemic brain samples revealed that EGCG significantly alleviated the common side effects of delayed rt-PA treatment, including brain infarction, cerebral edema, and blood-brain barrier disruption. We further found that EGCG exerted its protective functions against delayed rt-PA through upregulation of plasminogen activator inhibitor-1, as well as downregulation of matrix metalloproteinases.'], 'labels': ['BACKGROUND', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Blood-Brain Barrier', 'Brain Edema', 'Catechin', 'Disease Models, Animal', 'Drug Therapy, Combination', 'Fibrinolytic Agents', 'Gene Expression Regulation', 'Infarction, Middle Cerebral Artery', 'Male', 'Matrix Metalloproteinase 1', 'Matrix Metalloproteinase 9', 'Neuroprotective Agents', 'Permeability', 'Plasminogen Activator Inhibitor 1', 'Rats', 'Rats, Sprague-Dawley', 'Sensory Gating', 'Time Factors', 'Tissue Plasminogen Activator', 'Treatment Outcome']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,873,905 |
Does empagliflozin reduce body weight and indices of adipose distribution in patients with type 2 diabetes mellitus?
|
{
"contexts": [
"To determine the effects of empagliflozin on adiposity indices among patients with type 2 diabetes mellitus.",
"Changes in weight, waist circumference, estimated total body fat, index of central obesity and visceral adiposity index were assessed using analysis of covariance and testing of treatment by strata for age, sex and baseline waist circumference in patients with type 2 diabetes mellitus randomized to blinded treatment with empagliflozin versus placebo in clinical trials of 12 weeks (cohort 1) or 24 weeks (cohort 2) duration.",
"This study comprised 3300 patients (cohort 1, N = 823; cohort 2, N = 2477). Empagliflozin reduced weight, waist circumference and adiposity indices versus placebo in both cohorts. Adjusted mean (95% confidence interval) change from baseline in empagliflozin versus placebo was -1.7 kg (-2.1 to -1.4 kg) and -1.9 kg (-2.1 to -1.7 kg) for body weight (p < 0.001); -1.3 cm (-1.8 to -0.7 cm) and -1.3 cm (-1.7 to -1.0 cm) for waist circumference (p < 0.001); -0.2% (-0.7% to 0.3%; p = 0.45) and -0.3% (-0.7% to 0.0%; p = 0.08) for estimated total body fat; -0.007 (-0.011 to -0.004) and -0.008 (-0.010 to -0.006) for index of central obesity (p < 0.001); and -0.3 (-0.5 to 0.0; p = 0.07) and -0.4 (-0.7 to -0.1; p = 0.003) for visceral adiposity index in cohorts 1 and 2, respectively. Adipose reductions were seen across most age, sex and waist circumference subgroups."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Adiposity",
"Adult",
"Aged",
"Benzhydryl Compounds",
"Blood Glucose",
"Body Mass Index",
"Diabetes Mellitus, Type 2",
"Female",
"Glucosides",
"Humans",
"Hypoglycemic Agents",
"Male",
"Metformin",
"Middle Aged",
"Obesity",
"Weight Loss"
]
}
|
Empagliflozin significantly reduced weight and adiposity indices with the potential to improve cardiometabolic risk among patients with type 2 diabetes mellitus.
|
yes
|
[
{
"from": "human",
"value": "Question: Does empagliflozin reduce body weight and indices of adipose distribution in patients with type 2 diabetes mellitus?\nContext: {'contexts': ['To determine the effects of empagliflozin on adiposity indices among patients with type 2 diabetes mellitus.', 'Changes in weight, waist circumference, estimated total body fat, index of central obesity and visceral adiposity index were assessed using analysis of covariance and testing of treatment by strata for age, sex and baseline waist circumference in patients with type 2 diabetes mellitus randomized to blinded treatment with empagliflozin versus placebo in clinical trials of 12 weeks (cohort 1) or 24 weeks (cohort 2) duration.', 'This study comprised 3300 patients (cohort 1, N = 823; cohort 2, N = 2477). Empagliflozin reduced weight, waist circumference and adiposity indices versus placebo in both cohorts. Adjusted mean (95% confidence interval) change from baseline in empagliflozin versus placebo was -1.7 kg (-2.1 to -1.4 kg) and -1.9 kg (-2.1 to -1.7 kg) for body weight (p < 0.001); -1.3 cm (-1.8 to -0.7 cm) and -1.3 cm (-1.7 to -1.0 cm) for waist circumference (p < 0.001); -0.2% (-0.7% to 0.3%; p = 0.45) and -0.3% (-0.7% to 0.0%; p = 0.08) for estimated total body fat; -0.007 (-0.011 to -0.004) and -0.008 (-0.010 to -0.006) for index of central obesity (p < 0.001); and -0.3 (-0.5 to 0.0; p = 0.07) and -0.4 (-0.7 to -0.1; p = 0.003) for visceral adiposity index in cohorts 1 and 2, respectively. Adipose reductions were seen across most age, sex and waist circumference subgroups.'], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Adiposity', 'Adult', 'Aged', 'Benzhydryl Compounds', 'Blood Glucose', 'Body Mass Index', 'Diabetes Mellitus, Type 2', 'Female', 'Glucosides', 'Humans', 'Hypoglycemic Agents', 'Male', 'Metformin', 'Middle Aged', 'Obesity', 'Weight Loss']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
26,853,752 |
Do rNA binding proteins regulate anabolic and catabolic gene expression in chondrocytes?
|
{
"contexts": [
"Regulation of anabolic and catabolic factors is considered essential in maintaining the homoeostasis of healthy articular cartilage. In this study we investigated the influence of RNA binding proteins (RNABPs) in this process.",
"Using small interfering RNA (siRNA), RNABP expression was knocked down in SW1353 chondrosarcoma cells and human articular chondrocytes. Gene expression and messenger RNA (mRNA) decay of anabolic (SOX9, Aggrecan) and catabolic (matrix metalloproteinase (MMP)13) factors were analysed using reverse transcription quantitative polymerase chain reaction (RT-qPCR). RNA-electromobility shift assays (EMSAs) were used to investigate RNABP interactions with the SOX9 mRNA 3' untranslated region (UTR). Immunohistochemical localisation of MMP13 and the RNABP human antigen R (HuR) was performed in E13.5 and E16.5 mouse embryo sections.",
"SOX9 mRNA, mRNA half-life and protein expression were increased with siRNA targeting the RNABP tristetraprolin (TTP) in both HACs and SW1353s. TTP knockdown also stimulated aggrecan mRNA expression but did not affect its stability. RNA-EMSAs demonstrated that adenine uracil (AU)-rich elements in the SOX9 mRNA 3'UTR interacted with chondrocyte proteins with three specific elements interacting with TTP. HuR knockdown significantly increased MMP13 expression and also regulated the expression of a number of known transcriptional repressors of MMP13. HuR was ubiquitously expressed within mouse embryos yet displayed regional down-regulation within developing skeletal structures."
],
"labels": [
"OBJECTIVE",
"METHODS",
"RESULTS"
],
"meshes": [
"Animals",
"Cartilage, Articular",
"Cells, Cultured",
"Chondrocytes",
"Gene Expression",
"Gene Expression Regulation",
"Humans",
"Mice",
"RNA-Binding Proteins"
]
}
|
This study demonstrates for the first time how RNABPs are able to affect the balance of anabolic and catabolic gene expression in human chondrocytes. The post-transcriptional mechanisms controlled by RNABPs present novel avenues of regulation and potential points of intervention for controlling the expression of SOX9 and MMP13 in chondrocytes.
|
yes
|
[
{
"from": "human",
"value": "Question: Do rNA binding proteins regulate anabolic and catabolic gene expression in chondrocytes?\nContext: {'contexts': ['Regulation of anabolic and catabolic factors is considered essential in maintaining the homoeostasis of healthy articular cartilage. In this study we investigated the influence of RNA binding proteins (RNABPs) in this process.', \"Using small interfering RNA (siRNA), RNABP expression was knocked down in SW1353 chondrosarcoma cells and human articular chondrocytes. Gene expression and messenger RNA (mRNA) decay of anabolic (SOX9, Aggrecan) and catabolic (matrix metalloproteinase (MMP)13) factors were analysed using reverse transcription quantitative polymerase chain reaction (RT-qPCR). RNA-electromobility shift assays (EMSAs) were used to investigate RNABP interactions with the SOX9 mRNA 3' untranslated region (UTR). Immunohistochemical localisation of MMP13 and the RNABP human antigen R (HuR) was performed in E13.5 and E16.5 mouse embryo sections.\", \"SOX9 mRNA, mRNA half-life and protein expression were increased with siRNA targeting the RNABP tristetraprolin (TTP) in both HACs and SW1353s. TTP knockdown also stimulated aggrecan mRNA expression but did not affect its stability. RNA-EMSAs demonstrated that adenine uracil (AU)-rich elements in the SOX9 mRNA 3'UTR interacted with chondrocyte proteins with three specific elements interacting with TTP. HuR knockdown significantly increased MMP13 expression and also regulated the expression of a number of known transcriptional repressors of MMP13. HuR was ubiquitously expressed within mouse embryos yet displayed regional down-regulation within developing skeletal structures.\"], 'labels': ['OBJECTIVE', 'METHODS', 'RESULTS'], 'meshes': ['Animals', 'Cartilage, Articular', 'Cells, Cultured', 'Chondrocytes', 'Gene Expression', 'Gene Expression Regulation', 'Humans', 'Mice', 'RNA-Binding Proteins']}"
},
{
"from": "gpt",
"value": "Answer: yes"
}
] |
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