Objective To analyse risk factors for bile leakage after liver resection.Methods Between January 2011 and December 2012,469 patients underwent elective hepatectomy.We prospectively collected and retrospectively analyzed demographic data,pathological variables,and perioperative variables.Univariate analysis screened the related factors of bile leakage after liver resection.Multivariate analysis identified the independent risk factors of postoperative bile leakage.Results 469 patients were included in the analysis.The prevalence of bile leakage was 22.6％ (n =106).Univariate analysis identified the following risk factors as male gender,portal hypertension,steatosis,cirrhosis,ChildPugh grade,ascites,operative time,intraoperative transfusion,intraoperative blood loss,portal triad clamping,microwave solidification,lymphadenectomy,number of tumor,tumor margin,tumor capsular,diameter of tumor,portal vein invasion or portal branch thrombosis,number of abdominal drains.Multivariate analysis identified 4 independent risk factors for postoperative bile leakage:Cirrhosis [OR =13.2 (2.3,76.9),P =0.004],steatosis [OR =73.1 (17.7,301.5),P ＜ 0.001],infusion volume of the surgery day [OR=1.0 (1.0,1.0),P=0.019] and diameter of tumor [OR=1.2 (1.1,1.3),P=0.003].Conclusions Cirrhosis,steatosis,transfusion volume of the surgery day,and tumor size were risk factors for bile leakage after major liver resection.

Cerebrovascular disease is one of the main diseases that threaten human health and life,and the age of onset become younger and younger. Research shows that Toll-like receptors (TLRs) express in brain, have effects on neurons, play an important role in the occurrence and development of cerebral ischemia and secondary cerebral injury.It is clear that TLR2, TLR3, TLR4, TLR7 and TLR9 have influence on occurrence and development of cerebral ischemia. This is crucial for understanding the relationship between immune inflammation and nerve regeneration, and improving clinical treatment.

Objective To explore whether Yes-associated protein(YAP)affects occurrence and progression of liver fibrosis by regulating epithelial-mesenchymal transition(EMT).Methods In a 8-week-old C57BL/6 mouse model of CCl4-induced liver fibrosis,the effect of verteporfin(a YAP inhibitor)intervention was assessed with HE staining and by detecting liver biochemistry and expressions of YAP and EMT-related genes using immunohistochemistry and Western blotting.Transcriptome and proteomic sequencing and informatics analysis were used to investigate the main downstream pathways of YAP in liver fibrosis.Serum levels of YAP,N-cadherin,vimentin and Twist were examined in 60 healthy individuals,60 patients with chronic hepatitis B(CHB),and 60 patients with HBV-related liver cirrhosis.In another 24 C57BL/6 mice,the effects of Twist inhibitor alone or in combination with harmine(a YAP activator)on CCl4-induced liver fibrosis were evaluated by histopathological examination and Western blotting.Results The mouse models of liver fibrosis showed obvious structural damages of the liver lobes with formation of pseudolobules,and verteporfin treatment significantly improved these pathologies and lowered plasma ALT and AST levels of the mice.Transcriptome and proteomic sequencing and informatics analysis suggested that N-cadherin and Twist were differentially expressed in liver fibrosis in close correlation with YAP.Inhibition of YAP obviously downregulated hepatic N-cadherin and Twist protein expressions in the mice with liver fibrosis.In patients with CHB and liver cirrhosis,serum levels of YAP elevated obviously with the severity of liver fibrosis and were significantly correlated with N-cadherin,vimentin and Twist levels.In mice with liver fibrosis,inhibiting Twist effectively improved liver inflammation and fibrosis,while the combined treatment with YAP activator worsened hepatic collagen fiber deposition and increased hepatic YAP and α-SMA expressions.Conclusion EMT is an important pathogenic mechanism of liver fibrosis,and inhibiting YAP can alleviate liver fibrosis by reducing EMT.

Objective To explore whether Yes-associated protein(YAP)affects occurrence and progression of liver fibrosis by regulating epithelial-mesenchymal transition(EMT).Methods In a 8-week-old C57BL/6 mouse model of CCl4-induced liver fibrosis,the effect of verteporfin(a YAP inhibitor)intervention was assessed with HE staining and by detecting liver biochemistry and expressions of YAP and EMT-related genes using immunohistochemistry and Western blotting.Transcriptome and proteomic sequencing and informatics analysis were used to investigate the main downstream pathways of YAP in liver fibrosis.Serum levels of YAP,N-cadherin,vimentin and Twist were examined in 60 healthy individuals,60 patients with chronic hepatitis B(CHB),and 60 patients with HBV-related liver cirrhosis.In another 24 C57BL/6 mice,the effects of Twist inhibitor alone or in combination with harmine(a YAP activator)on CCl4-induced liver fibrosis were evaluated by histopathological examination and Western blotting.Results The mouse models of liver fibrosis showed obvious structural damages of the liver lobes with formation of pseudolobules,and verteporfin treatment significantly improved these pathologies and lowered plasma ALT and AST levels of the mice.Transcriptome and proteomic sequencing and informatics analysis suggested that N-cadherin and Twist were differentially expressed in liver fibrosis in close correlation with YAP.Inhibition of YAP obviously downregulated hepatic N-cadherin and Twist protein expressions in the mice with liver fibrosis.In patients with CHB and liver cirrhosis,serum levels of YAP elevated obviously with the severity of liver fibrosis and were significantly correlated with N-cadherin,vimentin and Twist levels.In mice with liver fibrosis,inhibiting Twist effectively improved liver inflammation and fibrosis,while the combined treatment with YAP activator worsened hepatic collagen fiber deposition and increased hepatic YAP and α-SMA expressions.Conclusion EMT is an important pathogenic mechanism of liver fibrosis,and inhibiting YAP can alleviate liver fibrosis by reducing EMT.

Animals ; Cellular Reprogramming ; genetics ; DNA Transposable Elements ; genetics ; Genetic Vectors ; genetics ; Genome ; genetics ; Humans ; Induced Pluripotent Stem Cells ; cytology ; metabolism ; Mutagenesis