Objective To observe the effect of high mobility group box-1 protein (HMGB1) on the expression of intestinal epithelial tight junction protein occludin in murine severe acute pancreatitis (SAP).Methods Rat SAP model was estabilished by retrograde injection of 5 ％ sodium taurocholate into choledochopancreatic duct.Healthy wistar rats were divided randomly (random number) into three groups:control group,SAP group,pyrrolidine dithiocarbamate (PDTC) therapy group.Levels of plasm amylase,lipopolysaccharide (LPS) and D-lactate were determined.The changes of morphological damage of pancreasand intestinal tissues were observed by microscopy.The distribution and expression of occludin protein were observed by SP immunohistochemistry. The mRNA expression of HMGB1 in the intestinal mucosa was detected by reverse-transcription polymerase chain reaction (RT-PCR).The expressions of HMGB1 and occludin were determined by western blotting. One-way analysis of variance was performed with SPSS Windows 13.0 statistical analysis software,and a difference was accepted as significant if P ＜ 0.05.Results In comparison with the other two groups,levels of plasma LPS and D-lactate in SAP group increased markedly at 24 h after operation,which indicated that the penetrability of intestinal mucosal barrier increased (P ＜ 0.05 ). The expression of HMGB1 in the intestinal mucosa of SAP group increased significantly compared with control group (P ＜ 0.05).Whereas,the expression of occludin was significantly lower than control group (P ＜0.05).Compared with SAP group,the expression of HMGB1 was lower and the expression of occludin was higher in PDTC group ( P ＜ 0.05).Conclusions The over-expression of HMGB1 could down regulate the expression of occludin in intestinal tissues of SAP rats,and thus mediate an increase in penetrability of intestinal mucosal barrier.As PDTC inhibited the expression of HMGB1,the expression of occludin protein was up-regulated and the function of intestinal mucosal barrier was improved.

Objective To study the effects of midazolam on expression of vascular endothelial growth factor (VEGF) of gerbils following total cerebral ischemia-reperfusion injury to look for an experimental basis for the rational clinical use of midazolam. Methods Seventy-two male gerbils (Mongolian gerbil) were randomly assigned into three groups (24 each): sham injury group, injury group and midazolam treatment group. Total cerebral ischemia was reproduced by blocking the bilateral carotid arteries for 10 minutes with bulldog clamps. When reperfusion began, with release of the clamps, 5mg/kg of midazolam was intraperitoneally injected to the animals in midazolam group, and 50ml/kg of normal saline was given by the same way in the gerbils in injury group. Then the parameters listed below were observed: positron emission tomography (PET) images at 6h, 1d, 3d and 7d after reperfusion, and the expression of VEGF in cerebral tissue was immunohistochemically assessed. Results No obvious abnormality was found in the cerebral tissue of sham injury group. For the animals in the injury group and midazolam treatment group, the brain reinfusion area enlarged obviously (P

Objective To explore the effects of ethyl pyruvate (EP) on hepatic high mobility group box-1 protein (HMGB1) expression in experimental routine with acute necrotizing pancreatitis (ANT). Method ANP model was induced by retrograde injection of 5 % sodium taurocholate into pancreatic duct. Twenty-four male wistar rats were divided randomly into 3 groups(8 rats in each group): group A (ANT group); group B (ANP rats re-ceived ethyl pyruvate therapy) and group C (control group with sham operation). The concentration of plasma amylase (AMY), A.sr and ALT, and the activity of myeloperoxidase (MPO) in the liver were determined. The ex-pression of HMGB1 mRNA in liver was detected by using reverse transcription polymerase chain reaction (RT-PCR). The changes of morphological damage were observed under microscopy. The expression of HMGB1 in the liver was observed by using SP immunohistochemistry. ANOVA was performed with SPSS 10.0 statistical analysis software and the difference was accepted as significant if the P<0.05, as verified by using Duncan's and Tukey' s post hoc test. Results Compared with gxoup A,levels of plasma AMY,AST and ALT in group B were markedly lower (P<0.05). Compared with group C, MPO in group A was higher significantly (P<0.01).with group A, the pathological changes of pancreas and liver in group B were milder. Compared with group C,the hepatic HMGB1 mRNA expression was markedly higher in group A [(0.28±0.04) vs. (0.73±0.06), P<0.01]. By contrast,the HMGB1 mRNA expression was markedly lower in group B compared with group A [(0.46±0.05) vs. (0.73±0.06), P<0.05]. The HMGB1 protein expression in hepatocytes and Kupffer's cells of rats with ANP was significantly up-regulated compared with control group, but it was reduced significantly in EP treatment group. Conclusions HMGB1 as a late mediator in liver might be involved in the pathogenesis of acute hepatic injury with ANP. EP could down-regulate the hepatic HMGB1 expression together with improvement of liver function in rats with ANP.

Objective To evaluate correlation of radial head fracture with forearm interosseous membrane (IOM) injury.Methods Twenty-six patients with radial head fractures were studied prospectively between September 2007 and June 2010.There were 15 men and 11 women,with an average age of 37.6years (range,21-53).According to the Mason classification,there were 7 cases of type Ⅰ,9 cases of type Ⅱ,10 cases of type ⅢL All patients were subjected to forearm X-ray,CT scans and the MR within a week.Clinical and radiographic data of all the patients were collected.Spearman rank correlation statistical analysis was used to analyze the correlation between the radial head fracture and the IOM injury.Results The radial head fractures and IOM injury were directly related.The IOM injury was noted in all type of radial head fracture.The more severity radial head fracture had,the more IOM injury happened.In Mason Ⅰ-Ⅲ fractures,IOM injury was found in 2,4 and 7 cases respectively.The different degree of radial head fracture caused different effects on IOM injury.The severity of radial head fracture was correlated with damage degree of IOM.In Mason type Ⅰ and type Ⅱ fractures,the IOM injury were just partial disruption with distal part of the IOM and did not reach the biomechanically essential central band.In type Ⅲ fractures,central band disruption was found in 3 cases.Conclusion Mason Ⅰ-Ⅲ radial head fractures are associated with forearm IOM injury.There was a positive correlation between radial head fractures and IOM injury.If IOM lesions are suspected,magnetic resonance imaging should be performed,especially Mason Ⅲ fractures.

Objective To explore the effects of ethyl pyruvate (EP) on high mobility group box-1 protein (HMGB1) expression in severe acute pancreatitis (SAP) rats.Methods Ninety male wistar rats were divided randomly into three groups: Group A (SAP group); group B (SAP rats received ethyl pyruvate therapy); group C (control group). Specimens from rats in the three groups were taken at 3, 6, 12, 24 and 48 h after operation respectively. The concentration of plasma amylase and D-lactate the activity of malonyl dialdehyde (MAD) in the intestinal tissue were determined. The changes of morphological damage of intestinal tissue was observed by microscopy. The expression of HMGB1 in intestinal mucosa was observed by SP immunohistochemistry and the activity of HMGB1 was determined by western blot.Results Compared with group A, Ievels of plasma amylase, and D-lactate in group B decreased markedly (P

Objective To evaluate the effect of activating adenosine A2A receptors on myocardial is-chemia-reperfusion ( I∕R) injury in diabetic rats and the relationship with autophagy. Methods Clean-grade healthy male Sprague-Dawley rats, aged 6 weeks, weighing 200-250 g, were studied. The diabetic rat model was established by intraperitoneal injection of 1％ streptozotocin 60 mg∕kg. Forty diabetic rats were divided into 4 groups ( n=10 each ) using a random number table method: sham operation group ( group Sham) , I∕R group ( group I∕R) , I∕R plus adenosine A2A receptor agonist CGS21680 group ( group CGS) , and I∕R plus CGS21680 plus adenosine A2A receptor antagonist ZM241385 group ( group CGS+ZM) . Myocardial I∕R was produced by occlusion of the left anterior descending branch of the coronary artery for 30 min followed by 120-min reperfusion. Adenosine A2A receptor agonist CGS2168010μg∕100g was in-travenously injected at 10 min before reperfusion in group CGS. CGS2168010 ug∕100g and ZM2413850. 2 mg∕kg were intravenously injected sequentially at 10 min before reperfusion in group CGS+ZM. Blood sam-ples were obtained at the end of reperfusion for determination of concentrations of creatine kinase-MB ( CK-MB), lactate dehydrogenase (LDH) and cardiac troponin I (cTnI) in serum (by enzyme-linked immu-nosorbent assay). The animals were sacrificed, and myocardial tissues were obtained for measurement of the percentage of myocardial infarct volume ( by TTC staining) and for determination of the expression of mi-crotubule-associated protein 1 light chain 3 Ⅰ ( LC3Ⅰ) , LC3 Ⅱ, p62 and Beclin-1 ( by Western blot) . LC3 Ⅱ∕LC3 Ⅰ ratio was calculated. Results Compared with group Sham, the serum CK-MB, LDH and cTnI concentrations and percentage of myocardial infarct volume were significantly increased, the expression of p62 and Beclin-1 was up-regulated, and the LC3Ⅱ∕LC3Ⅰratio was increased in group I∕R ( P<0. 05) . Compared with group I∕R, the concentrations of serum CK-MB, LDH and cTnI and percentage of myocardial infarct volume were significantly decreased, the expression of p62 and Beclin-1 was down-regulated, and the ratio of LC3Ⅱ∕LC3Ⅰwas increased in group CGS ( P<0. 05) , and no significant change was found in the pa-rameters mentioned above in group CGS+ZM (P>0. 05). Compared with group CGS, the concentrations of serum CK-MB, LDH and cTnI and percentage of myocardial infarct volume were significantly increased, the expression of p62 and Beclin-1 was down-regulated, and the ratio of LC3Ⅱ∕LC3Ⅰwas decreased in group CGS+ZM ( P<0. 05) . Conclusion Activating adenosine A2A receptors can mitigate myocardial I∕R injury, and the mechanism may be related to enhancing autophagy in diabetic rats.