Objective To investigate the mechanisms of oxygen free radical/JNK signaling pathway on neuronal autophagy after subarachnoid hemorrhage(SAH) in rats.Methods 160 male Sprague-Dawley rats were randomly divided into four groups: sham group, SAH model group, low dose Edaravone group and high dose Edaravone group.The SAH model was established by autologous blood injection into cisterna magna twice, while the rats in the sham group were injected with isotonic saline(0.3mL/time).The high dose of edaravone group and low dose of edaravone group were given 5mg/kg or 10mg/kg of edaravone, respectively, once daily with tail intravenous injection after the models were established.The morphological changes of hippocampus neural cells were detected by light microscope.The malondialdehyde (MDA) level in brain tissue was determined with thiobarbituric acid.The changes of phosphorylated JNK and autophagic biomarkers (Beclin-1 and LC3-II)were detected by immunohistochemical method.The expressions of JNK mRNA,Beclin-1 mRNA and LC3 mRNA in hippocampus was detected by Real time-quantitative PCR.Results The necrotic nerve cells were seen in the hippocampus of SAH group in terms of nuclear dissolution, nuclear fragmentation or nuclear disappearance.Compared with Sham group, the level of MDA and the number of dead neurons, the expression of JNK mRNA, Beclin-1 mRNA and LC3-Ⅱ mRNA were increased in the SAH group (P<0.05).The survival rate of nerve cells in the SAH group was lower than that in the sham group.The immunoreactivity of phosphorylated JNK 、Beclin-1 and LC3-Ⅱ in the SAH group was enhanced than that in the sham group.However the damage of the morphological structure of nerve cells was relatively decreased in both doses groups.Compared with SAH group, the level of MDA and the expression of JNK mRNA in low dose Edaravone group and high dose Edaravone group were decreased.The expression of Beclin-1 mRNA and LC-3 mRNA was higher (P<0.05).Furthermore, the survival rates of nerve cells in both dosesgroups were higher than that in the SAH group (P<0.05).Meanwhile, the immunoreactivity of phosphorylated JNK in both doses groups was weakened than that in the SAH group.The mRNA expression of Beclin-1 and LC3-Ⅱ was increased(P<0.05).Conclusion Oxygen free radical played an important role in process of neuronloss by activating the JNK signaling pathway to regulate Beclin-1 and LC3-Ⅱ expression.

Objective To explore the methods for diagnosis and treatment of malignant meningioma.Methods The clinical data of twenty-nine patients with malignant meningioma were retrospectively analyzed.Results Among the 29 patients,15 underwent Simpson Ⅰ resection,8 underwent Simpson Ⅱ resection and 6 had Simpson Ⅲ resection.Among these patients,Twenty-five cases were successfully followed up for 20-100 months.There are 11 cases who occurred relapse (44％),of whom 2 received Simpson Ⅰ resection,3 received Simpson Ⅱ resection and all the 6 cases receiving Simpson Ⅲ cases.Conclusion Head CT and MRI examination is helpful to diagnose malignant meningioma.The treatment mainly involved surgical resection combined with radiation and chemotherapy,with high postoperative recurrence rate and short survival time depending on the differentiation of the tumor.

Objective: To investigate the effects of cadmium exposure on cardiovascular system of occupational workers. Methods: Cross-sectional study was applied to 992 workers in a nickel-cadmium battery plant in November, 2011, of which 749 were cadmium exposed workers and 243 were controls without cadmium and other expose. Urinary cadmium、electrocardiogram (ECG) and blood pressure were examined simultaneously among 992 workers. The risk factors of ECG abnormality rate and hypertension rate were analyzed by Logistic regression. Results: The level of urinary cadmium in cadmium exposed workers was significantly higher than controls (8.89±4.00 vs 1.34±1.18 μg/g creatinine, P<0.01) . Urinary cadmium level in women was significantly higher than men in both exposure and control group (P<0.05) . According to the group of working years, Urinary cadmium level raised with the increase of working years (F=28.272, P<0.001) . The ECG abnormality rate and hypertension rate of cadmium exposed workers were higher than that of control group, the differences were all statistically significant (P<0.01) . The abnormal rate of ECG and the hypertension rate increased with the prolonging of working years and demonstrated dose-response relationship. With the increase of urinary cadmium level, the abnormal rate of ECG and hypertension rate raised (OR=1.11, P<0.01) and (OR=1.15, P<0.01) respectively. Conclusion Occupational cadmium exposure increased the abnormal rate of ECG and blood pressure and therefore damaged cardiovascular system of workers. This study provided base data for protecting health of cadmium exposed workers.