OBJECTIVE: To prepare thermo-sensitive ornidazole hydrogel and establish its quality control method.METHODS: Thermo-sensitive ornidazole hydrogel was prepared with ornidazole as chief constituent using poloxamer 407 and poloxamer 188 as base.The content of ornidazole in the hydrogel was determined by ultraviolet spectrophotometry.RESULTS: The preparation was white or yellowish semisolid gel,and its test results were up to the related standard specified in Chinese Pharmacopeia(2005 Edition).The linear range of ornidazole was 3.98～43.77 mg?L-1(r=0.999 8),and its mean recovery was 98.52%(RSD=1.1%).CONCLUSION: The preparation is simple and feasible in preparation process,and the quality of the preparation is stable and controllable.

OBJECTIVE:To assess the clinical efficacy and safety of domestic sparfloxacin for acute bacterial infections.METHODS:Domestic literatures about sparfloxacin for acute bacterial infections were retrieved by computer and their quality was evaluated to extract data(1993～2009).RevMan 4.2.2 software was used for Meta-analysis.RESULTS:A total of 10 RCT were enrolled.The comparisons of 2 groups were homogeneous in terms of clinical cure rate,clinical response rate,bacterial clearance rate and safety.There was statistical significance in comparison of combined effect variable between 2 groups in respect of cure rate,response rate and bacterial clearance rate(P0.05).CONCLUSION:The currently available evidence shows that clinical efficacy of domestic sparfloxacin for acute bacterial infections is better and incidence of ADR was lower.

OBJECTIVE: To establish HPLC method for the determination of the contents of atenolol, hydrochlorothiazide and nifedipine in xueyaan sustained release tablets. METHODS: The determination was performed on ZORBAX SB C18 column with column temperature at 35℃ . The mobile phase consisted of 0. 01mol? L- 1 sodium dihydrogen phosphate solution- methanol- acetonitrile ( 6∶ 3∶ 1) . The UV detection wavelength was set at 272nm and the sample size was 20? L. RESULTS: The liner ranges of atenolol, hydrochlorothiazide and nifedipine were 10～ 250? g? mL- 1 ( r=0. 999 4) , 6～ 150? g? mL- 1( r=0. 999 6) , and 5～ 125? g? mL- 1( r=0. 999 2) respectively. The average recovery rates of the three constituents were ( 98. 51? 0. 98) % ～ ( 99. 12? 0. 98) % , ( 98. 87? 1. 10) % ～ ( 99. 69? 1. 43) % , and( 98. 80? 1. 27) % ～ ( 99. 38? 1. 13) % , respectively, with RSD at 1. 00% , 1. 17% , and 1. 25% , respectively. CONCLUSION: The established method is simple, sensitive and reproducible, and suitable for the quality control of xueyaan sustained release tablets.

To review the research status, assessment tools, influencing factors and intervention measures of social grooming in patients with gynecological malignant tumors, so as to provide a theoretical basis for improving the social alienation of patients with gynecological malignant tumors and better integrating into society.

Nowadays potential preclinical drugs for the treatment of nonalcoholic steatohepatitis (NASH) have failed to achieve expected therapeutic efficacy because the pathogenic mechanisms are underestimated. Inactive rhomboid protein 2 (IRHOM2), a promising target for treatment of inflammation-related diseases, contributes to deregulated hepatocyte metabolism-associated nonalcoholic steatohepatitis (NASH) progression. However, the molecular mechanism underlying Irhom2 regulation is still not completely understood. In this work, we identify the ubiquitin-specific protease 13 (USP13) as a critical and novel endogenous blocker of IRHOM2, and we also indicate that USP13 is an IRHOM2-interacting protein that catalyzes deubiquitination of Irhom2 in hepatocytes. Hepatocyte-specific loss of the Usp13 disrupts liver metabolic homeostasis, followed by glycometabolic disorder, lipid deposition, increased inflammation, and markedly promotes NASH development. Conversely, transgenic mice with Usp13 overexpression, lentivirus (LV)- or adeno-associated virus (AAV)-driven Usp13 gene therapeutics mitigates NASH in 3 models of rodent. Mechanistically, in response to metabolic stresses, USP13 directly interacts with IRHOM2 and removes its K63-linked ubiquitination induced by ubiquitin-conjugating enzyme E2N (UBC13), a ubiquitin E2 conjugating enzyme, and thus prevents its activation of downstream cascade pathway. USP13 is a potential treatment target for NASH therapy by targeting the Irhom2 signaling pathway.