Objective To investigate the values of the APACHE O,APACHE-Ⅲ,Ranson and Balthazar CT(CTSI) scoring systems in predicting prognosis of severe acute pancreatitis.Methods Data were collected prospectively from 321 consecutive patients who were admitted into our hospital from 2005-01-01 to 2011-01-01 with acute pancreatitis (AP).The sensitivity,specificity and accuracy of the APACHE-O,APACHE-Ⅱ,Ranson,Balthazar CT scoring systems at different cut-off levels were calculated.The receiver-operating curves (ROC) for the prediction of severe AP in the early period were calculated using the APACHE-O,APACHE-Ⅱ,Ranson and Balthazar CT scores in different cut-off levels on hospital admission.The area under the curve (AUC) was used to compare the predictive accuracy.Using ROC curves,the values in predicting systemic complications,local complications and morbidities were also compared.Results At a cut-off point of 7,the APACHE O had a sensitivity of 95.4％,a specificity of 76.6％ and an overall accuracy of 79.4％.The Youden's index and the AUC of the APACHE-O score were 0.720 and 0.736,respectively.At a cut-off point of 8,the APACHE-Ⅱ had a sensitivity of 90.4％,a specificity of 81.0％ and an overall accuracy of 842.6％.The Youden's index and the AUC of the APACHE-Ⅱ were 0.714 and 0.699,respectively.At a cut-off point of 3,the Ranson had a sensitivity of 75.0％,a specificity of 78.1％ and an overall accuracy of 77.6％,respectively.The Youden’s index and the AUC of the Ranson were 0.531 and 0.703,respectively.At a cut-off point of 5,the CTSI had a sensitivity of 82.7％,a specificity of 91.4％ and an overall accuracy of 90.0％,respectively.The Youden's index and the AUC of the CTSI were 0.741 and 0.777,respectively.The CTSI system was the best in predicting local complications with a Youden’s index of 0.766,and an AUC of 0.777,respectively. At a cut-off point of 5,the CTSI had a sensitivity of 85.4％,a specificity of 91.2％ and an overall accuracy of 90.3％,respectively.The APACHE-O system was the best in predicting systematic complications with a Youden’s index of 0.789 and an AUC of 0.779,respectively.At a cut -off point of 8,the CTSI had a sensitivity of 91.1 ％,a specificity of 87.8％ and an overall accuracy of 88.2％,respectively.The CTSI system was the best in predicting local complications with a Youden’s index 0.952 and an AUC of 0.847,respectively.At a cut-off point of 8,the CTSI had a sensitivity of 100％,a specificity of 95.2％,and an overall accuracy of 95.3％,respectively.Conclusions The results suggested that the CTSI is the most useful system in predicting local complications and morbidities of severe AP in the early period.The APACHE-O is most useful in predicting systemic complications of severe AP.

Objective To evaluate the surgical approaches for gastric carcinoma accompanied by portal hypertension ( PHT).Methods The clinical data of 22 patients with PHT undergoing operation during 5 years were retrospectively analyzed.The liver function was Child's A in 12 cases, Child's B in 10 cases.Total gastrectomy + pericardial devascularization was performed in 11 cases, distal subtotal gastrectomy in 9 cases, distal subtotal gastrectomy + splenectomy in one, distal subtotal gastrectomy + pericardial devascularization in one.12 cases with Child's A underwent D2 lymph node (LN) dissection and 10 cases with Child's B were treated with D1 LN dissection.Liver biopsy was taken in all patients.Results Postoperative complications developed in 50% and mortality rate was 9%.The rate of liver function deterioration in patients of Child A ungergoing D2 lymph node dissection was 42% , and that of patients with Child B was 70%.The rate of postoperatiave complications in patients with Child A ungergoing D2 lymph node dissection was 25% , while that of patients with Child B was 80%.There was no significant difference in liver function deterioration rate between Child A and Child B (P ＞ 0.05) , but the rate of postoperative complications in Child A is much lower than those in Child B(P ＜ 0.05).The complication rate in patients receiving PHT targeting measures was 77% ,much higher than 11% in those without concurrent treatment of PHT ( P ＜ 0.05 ).Conclusions Individualized surgical approache is crucial for treatment of gastric carcinoma accompanied by PHT.Surgical treatment should be on the basis of liver function and the severity of PHT.

OBJECTIVE: To observe the effects of salvianolate on rats with postoperative intestinal adhesion and to explore the prevention mechanism. METHODS: Forty SD male rats with intestinal adhesion were randomly divided into four groups: untreated group, low-dose salvianolate-treated group (12 mg/kg), medium-dose salvianolate-treated group (24 mg/kg) and high-dose salvianolate-treated group (48 mg/kg), with another ten SD male rats as normal control. Intraperitoneal injection of glucose was administered to the rats in the normal control group and the untreated group, and intraperitoneal injection of salvianolate was administered to the rats in the low-, medium- and high-dose salvianolate-treated groups. They were all treated for 8 days and once a day. On the eighth day after surgery the blood samples of each group were collected. Grades of intestinal adhesion were ranked by macroscopic observation. The adhesive tissues between viscera and belly wall were taken for pathological observation. The levels of interleukin-1beta (IL-1beta), interleukin-4 (IL-4) and tumor necrosis factor-alpha (TNF-alpha) were determined by enzyme linked immunosorbent assay. RESULTS: Salvianolate can significantly reduce the extent of postoperative intestinal adhesion, obviously decrease the levels of IL-1beta, TNF-alpha and inhibit the hyperplasy of fibrous connective tissue. However, there was no significant impact on the level of IL-4. CONCLUSION: Salvianolate can reduce the extent of postoperative intestinal adhesion, decrease the expression of IL-1beta and TNF-alpha and inhibit the hyperplasy of fibrous connective tissue. This may be the mechanism of salvianolate in preventing intestinal adhesion.

Objective To determine the genotype of dengue virus (DENV) and its molecular characteristics of E gene from 1 case imported from Bangladesh to Wuhu city.Methods The viral RNA was extracted from patient serum sample,the serotype of DENV was determined by Real-time RT-PCR through screening the universal and serotypes 1/2/3/4 of DENV.The completed sequence of DENV E gene was amplified,the phylogenetic tree of E gene was constructed by MEGA 7.0 software,and the nucleotide and amino acid sequences alignments of E gene were analyzed.Results Patient serum was positive for DENV type 2 nucleic acid.The DENV type 2 belonged to the Cosmopolitan genotype by phylogenetic analysis of the E gene,and it had the highest homology with the isolate D2/Malaysia/1408aTw which was imported from Malaysia to Taiwan in 2014,the homologies of nucleotide and amino acid reached 99.60％ and 99.80％,respectively.Totally 6 nucleotides (42:G→A;141:G→A;490:G→A;516:A→G;954:A→G;1344:C→ T) and 1 amino acid (164:V→I) had changed in E gene.E protein possessed attenuated strain characteristic site E126-E and virulent strain characteristic site E383-385-E-P-G.Conclusions The imported patient is infected with DENV type 2 and the virus is originated from Malaysia.

Background/Aims: Metabolic dysfunction–associated steatotic liver disease (MASLD) is a chronic liver disease characterized by hepatic steatosis. Ubiquitin-specific protease 29 (USP29) plays pivotal roles in hepatic ischemiareperfusion injury and hepatocellular carcinoma, but its role in MASLD remains unexplored. Therefore, the aim of this study was to reveal the effects and underlying mechanisms of USP29 in MASLD progression. Methods: USP29 expression was assessed in liver samples from MASLD patients and mice. The role and molecular mechanism of USP29 in MASLD were assessed in high-fat diet-fed and high-fat/high-cholesterol diet-fed mice and palmitic acid and oleic acid treated hepatocytes. Results: USP29 protein levels were significantly reduced in mice and humans with MASLD. Hepatic steatosis, inflammation and fibrosis were significantly exacerbated by USP29 deletion and relieved by USP29 overexpression. Mechanistically, USP29 significantly activated the expression of genes related to fatty acid β-oxidation (FAO) under metabolic stimulation, directly interacted with long-chain acyl-CoA synthase 5 (ACSL5) and repressed ACSL5 degradation by increasing ACSL5 K48-linked deubiquitination. Moreover, the effect of USP29 on hepatocyte lipid accumulation and MASLD was dependent on ACSL5. Conclusions USP29 functions as a novel negative regulator of MASLD by stabilizing ACSL5 to promote FAO. The activation of the USP29-ACSL5 axis may represent a potential therapeutic strategy for MASLD.

Background/Aims: Metabolic dysfunction–associated steatotic liver disease (MASLD) is a chronic liver disease characterized by hepatic steatosis. Ubiquitin-specific protease 29 (USP29) plays pivotal roles in hepatic ischemiareperfusion injury and hepatocellular carcinoma, but its role in MASLD remains unexplored. Therefore, the aim of this study was to reveal the effects and underlying mechanisms of USP29 in MASLD progression. Methods: USP29 expression was assessed in liver samples from MASLD patients and mice. The role and molecular mechanism of USP29 in MASLD were assessed in high-fat diet-fed and high-fat/high-cholesterol diet-fed mice and palmitic acid and oleic acid treated hepatocytes. Results: USP29 protein levels were significantly reduced in mice and humans with MASLD. Hepatic steatosis, inflammation and fibrosis were significantly exacerbated by USP29 deletion and relieved by USP29 overexpression. Mechanistically, USP29 significantly activated the expression of genes related to fatty acid β-oxidation (FAO) under metabolic stimulation, directly interacted with long-chain acyl-CoA synthase 5 (ACSL5) and repressed ACSL5 degradation by increasing ACSL5 K48-linked deubiquitination. Moreover, the effect of USP29 on hepatocyte lipid accumulation and MASLD was dependent on ACSL5. Conclusions USP29 functions as a novel negative regulator of MASLD by stabilizing ACSL5 to promote FAO. The activation of the USP29-ACSL5 axis may represent a potential therapeutic strategy for MASLD.

Background/Aims: Metabolic dysfunction–associated steatotic liver disease (MASLD) is a chronic liver disease characterized by hepatic steatosis. Ubiquitin-specific protease 29 (USP29) plays pivotal roles in hepatic ischemiareperfusion injury and hepatocellular carcinoma, but its role in MASLD remains unexplored. Therefore, the aim of this study was to reveal the effects and underlying mechanisms of USP29 in MASLD progression. Methods: USP29 expression was assessed in liver samples from MASLD patients and mice. The role and molecular mechanism of USP29 in MASLD were assessed in high-fat diet-fed and high-fat/high-cholesterol diet-fed mice and palmitic acid and oleic acid treated hepatocytes. Results: USP29 protein levels were significantly reduced in mice and humans with MASLD. Hepatic steatosis, inflammation and fibrosis were significantly exacerbated by USP29 deletion and relieved by USP29 overexpression. Mechanistically, USP29 significantly activated the expression of genes related to fatty acid β-oxidation (FAO) under metabolic stimulation, directly interacted with long-chain acyl-CoA synthase 5 (ACSL5) and repressed ACSL5 degradation by increasing ACSL5 K48-linked deubiquitination. Moreover, the effect of USP29 on hepatocyte lipid accumulation and MASLD was dependent on ACSL5. Conclusions USP29 functions as a novel negative regulator of MASLD by stabilizing ACSL5 to promote FAO. The activation of the USP29-ACSL5 axis may represent a potential therapeutic strategy for MASLD.