Effects of microRNA-26b on proliferation and invasion of glioma cells and related mechanisms.

Neuroglioma is the most common primary malignant tumor in neurosurgery. Due to its short survival period and high patient mortality rate, neuroglioma is a major challenge in clinics. Elucidating the pathogenic mechanisms and associated molecular targets of neuroglioma can therefore benefit diagnosis and treatment of glioma. Previous studies have established the role of microRNA (miR)­26b in various tumors, including breast cancer, lymphoma and glioma. Its function and mechanism in neuroglioma, however, remains to be elucidated. In the present study, in vitro cultured U87 glioma cells were randomly divided into miR­26b mimic, miR­26b inhibitor and respective control (NC) groups. MTT assay was performed to detect the effect of miR­26b on cell proliferation, while a cell invasion assay detected its effects on cell invasion. Caspase­3 activity was also quantified to test cell apoptosis, followed by reverse transcription-quantitative polymerase chain reaction and western blotting to detect the variation of Bcl­2 expression under the effect of miR­26b. miR­26b mimics transfection upregulated its expression in U87 cells, which had significantly reduced Bcl­2 mRNA and protein expression levels and higher casapse3 activity, and inhibited cell proliferation and invasion compared with the control group. The transfection of miR­26b inhibitor, in contrast, facilitated U87 cell proliferation and invasion, inhibited caspase­3 activity and elevated Bcl­2 mRNA/protein expression. In conclusion, miR­26 could facilitate apoptosis and inhibit proliferation/invasion of neuroglioma cells via downregulating Bcl­2 expression and potentiating caspase-3 activity.

Role of galectin-3 in plasma as a predictive biomarker of outcome after acute intracerebral hemorrhage.

OBJECTIVE: Inflammation is involved in pathophysiological mechanisms underlying secondary brain injury after intracerebral hemorrhage. Enhanced circulating levels of galectin-3, a proinflammatory cytokine, have close relation to poor prognosis of some inflammatory illnesses. This study was designed to investigate whether plasma galectin-3 levels are related to the inflammation, severity and prognosis following intracerebral hemorrhage. METHODS: In this observational, prospective study, plasma galectin-3 levels of 110 patients and 110 controls were determined. We further assessed the association of galectin-3 levels with inflammation reflected by systemic C-reactive protein levels, severity indicated by hematoma volumes and National Institutes of Health Stroke Scale (NIHSS) scores, and endpoints including 1-week mortality, 6-month mortality, 6-month overall survival and 6-month unfavorable outcome (modified Rankin Scale score>2). RESULTS: Plasma galectin-3 levels of patients were significantly higher than those of controls. Galectin-3 was identified as an independent prognostic predictor for 1-week mortality, 6-month mortality, 6-month overall survival and 6-month unfavorable outcome, as well as had strong relation to C-reactive protein levels, hematoma volumes and NIHSS scores. Compared with NIHSS scores and hematoma volumes, plasma galectin-3 levels had similar areas under receiver operating characteristic curve (AUC). Moreover, galectin-3 levels significantly improved AUCs of NIHSS scores or hematoma volumes alone for prediction of 6-month mortality and 6-month unfavorable outcome. CONCLUSIONS: Elevated plasma galectin-3 levels are strongly associated with the inflammation, severity and poor prognosis after intracerebral hemorrhage, indicating galectin-3, involved in brain inflammation, might have the potential to be a prognostic biomarker for hemorrhagic stroke.

Leptin as a marker for severity and prognosis of aneurysmal subarachnoid hemorrhage.

Leptin has been identified as a plasma marker for outcomes in traumatic brain injury and intracerebral hemorrhage. We further investigated whether leptin might serve as a marker for severity and prognosis in aneurysmal subarachnoid hemorrhage. One hundred and eight consecutive patients and 108 sex and age - matched healthy subjects were recruited. Plasma leptin levels were measured by enzyme-linked immunosorbent assay. Clinical severity was assessed using World Federation of Neurological Surgeons score and Fisher score. Mortality and poor long-term outcome (Glasgow outcome scale scores of 1-3) at 6 months were recorded. Plasma leptin levels on admission were substantially higher in patients than in healthy controls, and were significantly associated with the clinical severity. There was also a significant association between leptin levels and clinical outcomes at 6 months in multivariate logistic regression analysis. Using receiver operating characteristic curves, we calculated areas under the curve for clinical outcomes at 6 months. The predictive performance of leptin was similar to, but did not obviously improve those of World Federation of Neurological Surgeons score and Fisher score. Thus, leptin may indicate clinical severity of the initial bleeding and also have prognostic value for clinical outcomes in aneurysmal subarachnoid hemorrhage and may therefore help in guiding treatment decisions in the setting of aneurysmal subarachnoid hemorrhage.

Increased plasma 8-iso-prostaglandin F2α concentration in severe human traumatic brain injury.

BACKGROUND: 8-Iso-Prostaglandin F2α (8-iso-PGF2α) is considered as a gold standard for measuring oxidative stress in vivo. The present study was undertaken to investigate plasma 8-iso-PGF2α concentrations in severe human traumatic brain injury (TBI) and to analyze its correlation with disease outcome. METHODS: One hundred six healthy subjects and 106 severe TBI patients were recruited. The correlations of plasma 8-iso-PGF2α concentration with 1-year mortality and unfavorable outcome (Glasgow Outcome Scale score of 1-3) were analyzed. RESULTS: Thirty-one patients (29.2%) died and 48 patients (45.3%) had an unfavorable outcome at 1 year after TBI. Patients had significantly higher plasma 8-iso-PGF2α levels compared to healthy controls (572.1±157.5 pg/ml vs. 84.3±18.9 pg/ml, P<0.001). A multivariate analysis selected plasma 8-iso-PGF2α level as an independent predictor for 1-year unfavorable outcome [odds ratio (OR) 1.401, 95% confidence interval (CI) 1.107-2.371, P=0.005] and mortality (OR 1.609, 95% CI 1.113-3.142, P=0.003). A receiver operating characteristic curve analysis showed plasma 8-iso-PGF2α level predicted 1-year unfavorable outcome [area under curve (AUC), 0.871; 95% CI, 0.792-0.928] and mortality (AUC, 0.881; 95% CI, 0.804-0.936) as statistically significantly. The prognostic value of 8-iso-PGF2α was similar to that of Glasgow Coma Scale score for 1-year clinical outcomes (both P>0.05). However, 8-iso-PGF2α did not improve the prognostic value of Glasgow Coma Scale score for 1-year clinical outcomes (both P>0.05). CONCLUSIONS: Plasma 8-iso-PGF2α level is highly associated with 1-year clinical outcomes of TBI.

High concentrations of visfatin in the peripheral blood of patients with acute basal ganglia hemorrhage are associated with poor outcome.

Higher plasma visfatin concentration has been associated with clinical outcomes of traumatic brain injury. No published information exists to date about change in plasma visfatin after intracerebral hemorrhage. This study included one hundred and twenty-eight healthy controls and 128 patients with intracerebral hemorrhage. The unfavorable outcome was defined as modified Rankin Scale score >2 at 6 months. The patients had higher plasma visfatin measurements than control subjects. Plasma visfatin levels were highly correlated with National Institutes of Health Stroke Scale score and plasma C-reactive protein levels in the patients. A multivariate analysis identified plasma visfatin level as an independent predictor for 6-month mortality and unfavorable outcome. According to receiver operating characteristic curve analysis, the predictive value of the plasma visfatin concentration was similar to National Institutes of Health Stroke Scale score. In a combined logistic-regression model, visfatin improved the predictive value of National Institutes of Health Stroke Scale score for 6-month unfavorable outcome. Thus, increased plasma visfatin level is associated with 6-month clinical outcomes after intracerebral hemorrhage.

Prognostic value of copeptin: one-year outcome in patients with traumatic brain injury.

High plasma copeptin level has been associated with one-month mortality after traumatic brain injury. However, not much is known regarding its relation with long-term outcome. Thus, we investigated the ability of copeptin to predict 1-year outcome in patients with traumatic brain injury. One hundred and six healthy controls and 106 patients with acute severe traumatic brain injury were included. Plasma samples were obtained on admission. Its concentration was measured by enzyme-linked immunosorbent assay. Forty-eight patients (45.3%) suffered from unfavorable outcome (Glasgow Outcome Scale score of 1-3) and 31 patients (29.2%) died in 1 year after traumatic brain injury. Upon admission, plasma copeptin level in patients was substantially higher than that in healthy controls. A forward stepwise logistic regression selected plasma copeptin level as an independent predictor for 1-year unfavorable outcome and mortality of patients. A receiver operating characteristic curve analysis showed plasma copeptin level predicted 1-year unfavorable outcome and mortality obviously. The predictive value of the copeptin concentration was thus similar to that of Glasgow Coma Scale score for the prediction of unfavorable outcome and mortality after 1 year. In a combined logistic-regression model, copeptin improved the area under curve of Glasgow Coma Scale score for the prediction of unfavorable outcome and mortality after 1 year, but the differences were not significant. Thus, copeptin level is a useful, complementary tool to predict functional outcome and mortality 1 year after traumatic brain injury.

Comparison of standard large trauma craniotomy with routine craniotormy in treatment of acute subdural hematoma.

OBJECTIVE: To compare the therapeutic effect and indication between standard large trauma craniotomy and routine craniotomy. METHODS: There were 97 patients in the standard large trauma craniotomy group and 110 patients in the routine craniotomy group. The mortality, postoperative ICP (intracranial pressure), ratio of pupil rebound, complication and results of six month follow-up after operation were compared between the two groups. RESULTS: Fifteen patients (15.6%) died in the standard large trauma craniotomy group and 30 (27.7%) in the routine craniotomy group. The postoperative mean ICP was 3.75 kPa+/-1.89 kPa in the standard large trauma craniotomy group and 5.11 kPa+/-1.57 kPa in the routine craniotomy group. The pupil rebound was found in 47 patients (61.0%) in the standard large trauma craniotomy group and in 41 patients (46.1%) in the routine craniotomy group (P<0.01). The rate of complication was lower in the standard large trauma craniotomy group, but no obvious difference in long-term therapeutic effect was found between the two groups. CONCLUSIONS: Standard large trauma craniotomy can attenuate brain hernia and the mortality of the patients with acute subdural hematoma. The incidence of complication can also be decreased. But the long term life quality of the patients can not be improved.