OBJECTIVE To investigate the distribution and bacterial resistance of nosocomial infection.METHODS The data of 45 hospitals from Shandong Provincial Nosocomial Surveillance System from Jan 2003 to Dec 2005 were analyzed.RESULTS Of total 5 626 isolates strains from the nosocomial infection cases,G-bacilli,G+ cocci and fungi accounted for 58.27%,25.84% and 15.89%,respectively.The ampicillin-resistant rate of commonly encountered G-bacilli was above 89%.There were 72.98% of E.coli resistant to ciprofloxacin.The rates of resistance of S.aureus and coagulase negative Staphylococcus to penicillin,ampicillin and erythromycin were all above 80%;the lincomycin-resistant rate of S.aureus increased gradually to 86.64%.CONCLUSIONS Drug resistance of the nosocomial infective bacteria is a serous problem.Surveillance of bacterial resistance should be strengthened.

It has been found in recent years that adipose tissue is not only the organ for storing energy, but can also secrete many adipokines including leptin, adiponectin, and resistin. Leptin and adiponectin play important roles in the formation and treatment of non-alcoholic fatty liver disease (NAFLD) due to their important biological functions, which bring a new direction for the clinical treatment of this disease. This article briefly describes the biological functions of leptin and adiponectin and their relationship with NAFLD. It is pointed out that leptin and adiponectin play essential roles in the treatment of NAFLD and may become novel therapeutic targets.

Objective To purify the anti-T cell immunoglobulin mucin ( TIM)-3 monoclonal antibody 4E8 and examine its biological function in vitro. Methods The mouse monoclonal antibody against human TIM-3, clone 4E8, was obtained by standard protocol for monoclonal antibody purification. The cell lines expressing human TIM-3 molecule were obtained by cell transfection technique. We ex-amined the ability of 4E8 binding to human TIM-3 by flow cytometry. The ability of 4E8 blocking the binding of fusion protein TIM-3 Ig-huFc with phosphatidylserine( PtdSer) , the apoptotic cell surface TIM-3 ligand, was also analyzed by flow cytometry. Mixed lympho-cyte reaction ( MLR) and ELISA assays were used to determine the effect of TIM-3 monoclonal antibody ( 4E8) on IFN-γsecretion in CD4+ T cells. Results 4E8 specifically bound to human TIM-3 but could not block the binding of TIM-3 to Ptdser. Compared with the negative control (IFN-γ secretion: 958.3±153.2), 4E8 enhanced the ability of CD4+ T cells to secrete IFN-γ in MLR (4E8 of 10μg/mL group:IFN-γ secretion 2563±150.3 and 4E8 of 3.33 μg/mL group:IFN-γ secretion 1981±211.5) with statistically signifi-cant difference ( P<0.05) . In addition, the combined application of 4E8 with the anti-programmed death-1 ( PD-1) monoclonal anti-body nivolumab showed synergistic effects for increasing IFN-γ secretion in MLR assay ( 4E8 of 10 μg/mL group: IFN-γ secretion 3049±80.5 and 4E8 of 0.33μg/mL group:IFN-γsecretion 1957±321.3) as compared with 4E8 alone (10μg /mL group:IFN-γse-cretion 2563±150.3 and 0.33 μg/mL group:IFN-γ secretion 844±76.2) with statistically significant difference (P<0.05). Conclu-sion We successfully obtained a 4E8 clone of monoclonal antibody to human TIM-3 which may enhance the capacity of IFN-γsecre-tion from CD4+ T cells. The effect of enhancing IFN-γ secretion of CD4+T cells by TIM-3 monoclonal antibody was independent from blocking the binding of TIM-3 with Ptdser.