Objective: To analyse correlation of bispectral index,spectral edge frequency of electroencephalogram with midazolam-induced sedation. Method: 30ASA grade Ⅰ-Ⅱ adult patients, undergoing elective surgery under regional anesthesia were randomly devided into three groups according to intravenous bolus doses of midazolam,i, e. group Ⅰ:0.05mg?kg~(-1),group Ⅱ:0.1mg?kg~(-1),group Ⅲ:0.2mg?kg~(-1). After an intravenous bolus dose of mida zolam was administered,both bispectral index (BIS), 95% spectral edge freguency (SEF) of electroencephalogram were monitored and their correlation with midazolam induced sedation was analysed. Result: Both BIS and 95% SEF-correlated with midazolam-induced sedation significantly (r= 0.86,0.73, P

Objective To investigate the expression and significance of syntaxin 8 (STX8) in non-small cell lung cancer (NSCLC),and analyze the relationship between STX8 expression and clinicopathological features of NSCLC.Methods Seventy samples of NSCLC and 70 samples of pericancerous tissues were collected for immunohistochemistry staining,and another 10 samples of NSCLC and pericancerous tissues were used for RNA and protein extraction,qRT-PCR was performed to detect the expression of STX8 mRNA,and Western blot assay was adopted to detect the expression of STX8 protein.The relationship between STX8 expression and clinicopathological features of NSCLC was analyzed.Results Results of qRT-PCR showed that the expression of STX8 mRNA was significantly higher in NSCLC tissues than that in the pericancerous tissues (3.962 5±0.487 3 vs.0.538 2±0.097 5,t=21.797,P＜0.01).Immunohistochemistry results showed that the high expression rate of STX8 was significantly higher in NSCLC tissues than that in the pericancerous tissues [71.43％ (50/70) vs.38.57％ (27/70),x2=15.267,P＜0.01].Western blot results showed that the expression of STX8 protein was significantly higher in NSCLC tissues than that in the pericancerous tissues (2.496 1±0.362 5 vs.0.340 2±0.119 1,t=17.876,P＜0.01).The high expression rate of STX8 was significantly different in different histological types of NSCLC (P ＜0.05).The high expression rate of STX8 was higher in squamous cell carcinoma and adenocarcinoma than that in adenosquamous carcinoma,and the high expression rate of STX8 was not observed in large cell carcinoma.There were no significant differences in expressions of STX8 in NSCLC patients with different gender,ages,tumor diameters,TNM stages and with or without lymph node metastasis (P＞0.05).Conclusion A high expression of STX8 in NSCLC tissues may be correlated with the occurrence and development of NSCLC.

Objective To investigate the expression of syntaxin 8(STX8)in glioma and its clinical signif-icance. Methods Specimens of glioma were collected from 57 patients at Beijing Renhe Hospital from May 2013 to December 2015. 57 pieces of glioma tissue were used as a study group ,12 of which were Ⅰ+ Ⅱ(low grade) and the rest 45 were Ⅲ+Ⅳ;normal brain tissues from 15 individuals were used as a control group. Real-time PCR,immunohistochemistry,and Western blot were used to detect expression of STX8. Results As compared with the normal brain tissue ,the mRNA expression of STX8 was significantly increased in glioma tissue ,with a relative expression volume of 1.6855 ± 0.07124 in low grade and 2.8207 ± 0.0692 in high grade tissues,there was significant differences between the two groups;and the difference was also significant as compared with the control group(P < 0.05). The results of immunohistochemistry showed that the expression of STX8 was higher in glioma tissue than in normal tissue. Western Blot showed that the expression of STX8 protein was significantly higher in glioma than in normal tissue(P<0.05);the relative expression volume of STX8 was 2.271 ± 0.1621 in low grade tissue and 4.937 ± 0.1851 in high grade tissue,with a significant difference between the two groups;the difference was also significant as compared with the control group(P<0.05). The correlation analysis showed that higher STX8 expression in glioma was not significantly related to gender,age and pathological types,but there was a significant difference between pathological stages. Conclusion STX8 has abnormal high expression in glioma,which may be closely related with the occurrence and development of glioma.

Objective To study the function and mechanism of receptor-interacting protein kinase 3 (RIPK3)-mediated necroptosis in liver ischemia-reperfusion injury (IRI) in mice.Methods Sixty mice were randomly divided into four groups using Stata statistical software:Wild-type (WT)-sham group,WT-IRI group,HKO (HKO:RIPK3 liver-specific knockout)-sham group and HKO-IRI group.Sham operation was used as a control in which only the hepatic portal blood vessels were freed after laparotomy,and blood flow was not blocked.In the WT-IRI group and the HKO-IRI group,the hepatic portal vein was freed,and the blood supply of left hepatic lobe and the mid-hepatic lobe wer blocked for 90 min,then the blood vessels were opened for 6 h.Blood and liver tissue samples of each group of mice were taken to detect liver function.Inflammatory infiltration and liver injury were detected by immunohistochemistry and hematoxylin and eosin (HE) staining,and autophagyassociated protein LC3-Ⅱ and P62 were detected by Western blotting.The primary hepatocytes of WT mice and HKO mice were extracted and divided into control group and hypoxia-reoxygenation group (HIR group).After attachment of primary hepatocytes,the HIR group was given hypoxia for 6 h and reoxygenated for 4 h.The supernatant was taken for detecting ALT and AST,and the cell extract protein was used to detect LC3-Ⅱ and P62.Results As compared with the control groups,the liver functions of the IRI groups were significantly impaired,and as compared with the WT-IRI group,the liver damage was significantly aggravated in the HKI-IRI group (P ＜ 0.05),and the LC3-Ⅱ protein content was significantly decreased and the P62 protein content was increased.Similarly,after hepatocytes were were given hypoxia and reoxygenated,HKO-derived hepatocytes were more severely damaged than WT-derived hepatocytes.Conclusions Blocking RIPK3-mediated necroptosis of hepatocytes could induce autophagy inhibition,which aggravates hepatic ischemia-reperfusion injury.