Objective To explore the expressions of adiponectin and adiponectin receptor 2 (AdipoR2) in the liver of patients with hepatitis B virus (HBV)-related liver failure and their clinical implications in the pathogenesis of liver failure.Methods The healthy controls (HC),patients with chronic hepatitis B (CHB) and patients with HBV-related liver failure (HBV-LF) were enrolled in the study.Each group had 20 participants.The liver tissues from 11 CHB patients who were diagnosed by liver biopsy,6 patients with HBV-LF and 6 liver donors during liver transplantation were collected.Histological specimens were observed by hematoxylin-eosin staining and Masson trichrome staining under microscope.The mRNA and protein expressions of adiponectin and AdipoR2 in the liver were measured by semi-quantitative reverse transcription and polymerase chain reaction (SqRT-PCR) and immunohistochemical staining,respectively.The level of serum adiponectin was detected by enzymelinked immunsorbent assay.Serum biochemical parameters and HBV DNA levels were also measured.The pairwise comparison between groups was done by Student-Newman-Keuls and mann whitney U test.The relationship between two variables was analyzed using Spearman correlation.Results The level of serum adiponectin in HBV-LF group [(0.86 ± 0.15) ng/mL] was higher than those in HC [(0.59±0.15) ng/mL] and CHB groups [(0.62±0.13) ng/mL,Z=3.963,Z=3.774,both P＜0.01)],but showing no difference between CHB and HC groups (P＞0.05).The expressions of adiponectin and AdipoR2 mRNA in the liver were significantly higher in HBV-LF group (0.251 ±0.028 and 0.223 ± 0.021,respectively) than those in HC (0.091 ± 0.018 and 0.072 ± 0.020,respectively) and CHB (0.121±0.019 and 0.097±0.017,respectively) groups (q=18.428,17.069,19.807,18.673,respectively; all P＜0.01).Also,the expressions of adiponectin and AdipoR2 mRNA in CHB group were significantly higher than those in HC group (q=3.895,3.860,both P＜0.05).The expressions of adiponectin and AdipoR2 proteins in the liver were significantly higher in HBV-LF group (8.482±0.772 and 7.654±0.272,respectively) than those in HC (4.045± 0.815 and 2.804±0.623,respectively) and CHB (5.545±0.613 and 4.775±0.458,respectively) groups (q=15.327,11.542; Z=2.802,3.266; respectively; all P＜0.01).Also,the expressions of adiponectin,AdipoR2 proteins in CHB group were significantly higher than those in HC group (q=5.894,Z=3.266,both P＜0.01).In HBV-LF group,serum adiponectin levels as well as the expressions of adiponectin mRNA and protein in the liver were negatively correlated with serum albumin (r=-0.815,-0.886,-0.943; P＜0.01 or P＜0.05),but positively correlated with serum alanine aminotransferase (r=0.701,0.886,0.943; P＜0.01 or P＜0.05).The expression of AdipoR2 mRNA in the liver was negatively correlated with serum albumin (r=-0.943,P＜0.01),but positively correlated with serum aspartate aminotransferase (r=0.829,P＜0.05).Conclusions The expressions of adiponectin and AdipoR2 are up-regulated during HBV infection,especially in patients with HBV-LF,which might reflect the degree of necroinflammation in the liver.

Objective To investigate the effects of antioxidant on the fish oil cream and to enhance its stabil-ity.Methods The fish oil cream containing different antioxidant such as vitamin C,vitamin E,EDTA -2Na were prepared.The content of vitamin A with 6 months acceleration test and 12 months after long -term test were deter-mined by HPLC.Results Antioxidants had significant effect on the vitamin A content in fish oil cream,the sequence that antioxidants enhance the stability of the fish oil cream was as follows:VE +Na2 S2 O5 >VC +Na2 S2 O5 >VE +ED-TA -2Na >VC +EDTA -2Na >VE ﹥ Na2 S2 O5 >VC >EDTA -2Na.Conclusion The fish oil cream with antioxi-dant have favorable stability,composite antioxidant is better than single antioxidant.

OBJECTIVE To evaluate the spectrum of imipenem-resistant Pseudomnas aeruginosa and the production of metallo-?-lactamase.METHODS The clinical strains of P.aeruginosa were collected from Jan to Dec 2007.The results of antimicrobial susceptibility tests and detection of metallo-?-lactamase were analyzed.Antimicrobial susceptibility tests were performed by K-B methods;the production of metallo-?-lactamase was tested by CAZ-EDTA synergy method.RESULTS Sixty strains were isolated,imipenem-sensitive and resistant strains were 40(66.7%) and 20(33.3%),respectively,and 7 strains with metallo-?-lactamase were detected.Among imipenem-resistant strains,at least 90.0% strains were resistant to meropenem,gentamicin,tobramycin,ciprofloxacin and SMZ-TMP;at least 80.0% strains were resistant to piperacillin and piperacillin/tazobactam;50.0% strains were resistant to ceftazidime and cefepime;polymyxin E was less resistant than others.Twenty strains were resistant to at least 3 antimicrobial agents,which was obviously higher than 27.5% of imipenem-resistant strains.CONCLUSIONS The resistance rate of imipenem-resistant P.aeruginosa is higher than imipenem-sensitive ones.The production of metallo-?-lactamase is one of the mechanisms of P.aeruginosa resistance to imipenem and shou1d be detected carefully,which could help us medicate reasonably in clinic and avoid using medicine which could induce and strengthen the resistance.

ObjectiveTo investigate the effects and molecular mechanism of simvastatin in liver fibrosis model of non-alcoholic fatty liver disease (NAFLD) in vivo and hepatic stellate cell in vitro.MethodsFirstly,the rat liver fibrosis model of NAFLD was established by high-fat diet administration and intervened with simvastatin.The expression of endothelial nitric oxide synthase (eNOS),inducible nitric oxide synthase (iNOS) and Collagen Ⅰ at mRNA and protein level were detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot.Secondly,quiescent phenotype of LX-2 cell line was induced by promoting adipocyte differentiation medium in vitro,and then the quiescent phenotype of LX-2 cell were treated with transforming growth factor β1(TGF-β1),Nitroso-L-arginine methyl ester (L-NAME) which was NOS inhibitor,simvastatin,TGFβ1 with simvastatin,and L-NAME with simvastatin separately.The changes of eNOS,iNOS,αsmooth muscle actin (α-SMA) and Collagen Ⅰexpressions at mRNA and protein level were determined by RT-PCR and Western blot.ResultsAs modeling time extended,the expressions of eNOS in rat's liver tissue of model group at mRNA and protein level decreased gradually,however the expression of iNOS and Collagen Ⅰ at mRNA and protein level increased gradually,compared with normal control group and the differences were statistically significant (P ＜0.05 and 0.01).By 24weeks,the expressions of eNOS in rat's liver tissue of simvastatin group at mRNA and protein level were increased,the expression of iNOS at mRNA and protein level were decreased and the expression of Collagen Ⅰ at mRNA and protein level were decreased (all P ＜0.05).The expression of eNOS in rat's liver tissue of model group negatively correlated with the expression of Collagen Ⅰ at mRNA and protein level (all P ＜0.01).The expression of iNOS positively correlated with that of Collagen Ⅰ at mRNA and protein level (all P ＜0.01).In LX-2 cell culture,L-NAME inhibited the activation of LX-2,reduced eNOS and iNOS expression and increased α-SMA and CollagenⅠexpression,consistent with the role of TGF-β1.Simvastatin could directly increase the eNOS expression both in quiescent and activated LX-2 cells,decrease iNOS expression,maintain quiescent phenotype and inhibit its activation.ConclusionsSimvastatin ameliorated the genesis and progression of liver fibrosis by increasing eNOS expression in LX-2 cells and reducing iNOS,α-SMA and Collagen Ⅰ expression.

Objective To investigate the clinical characteristics,surgical treatment and outcome for patients with duodenal stromal tumor.Methods Data of 40 patients with stromal tumor of duodenum were reviewed retrospectively.Results All patients received resection including local resection in 14 cases,segmental resection of the duodenum in 17 cases,and pancreaticoduodenectomy in 9 cases.38 cases were followed-up,and two were lost.The median follow-up was 59 months (range 3-240 mos).The 1,3,and 5-year overall survival rates were 92％,76％ and 68％,respectively.No recurrence was found in very-low-risk tumor (n =1) and low-risk turmors (n =4).The 1,3,and 5-year overall survival rates for intermediate-risk tumors were 95％,80％ and 70％,respectively;and those were 69 ％,31％,and 0 for high-risk tumors,respectively.14 of 33 cases (42％) suffered from recurrence after radical resection for intermediate or high-risk tumors.33 postoperative cases received treatment with Imatinib (Glivec) for more than one year,and one case developed recurrence at 2.5 years after operation.4 patients with synchronous liver metastasis received palliative resection and Imatinib,and two survived more than 1 year.Conclusion Surgery is the first choice for duodenal stromal tumor,and Imatinib should be administered for high-risk disease after surgery.