[Investigation of molecular epidemiology of methicillin-resistant staphylococcus aureus in department of critical care medicine].

Objective: To investigate the feature of antimicrobial resistance, homology and other molecular epidemiology of methicillin-resistant staphylococcus aureus(MRSA) in Department of Critical Care Medicine(ICU). Methods: From October 2010 to December 2011, 149 strains of MRSA were collected and identified through sputum culture of patients from 10 ICUs of 10 teaching hospitals distributed in 9 chinese central city of China. Susceptibility testing to 18 kinds of antibiotic was performed, the method of pulsed field gel electrophoresis (PFGE) was used to analyze the homology, and the technique of multilocus sequencing typing (MLST) was used to identify the sequence type (ST). Results: Antibiotic susceptibility testing implied that vancomycin, daptomycin and linezolid are 100% sensitive to collected 149 strains of MRSA. Cotrimoxazole resistance rate is about 0-11.1%. Rifampicin resistant rate was less than 25% in 2 hospitals; the resistance rate of gentamicin and moxifloxacin were more than 80% besides of 50% to70% in 3 hospitals; beta lactam resistant rate was 100%. In 149 strains of MRSA, the main types of PFGE were J (28.9%), C (19.5%), G (10.7%), F (8%)types. J, C, G types mainly distributed in the North, while the F type only distributed in the Guiyang region. The MLST type: 8 ST types were determined ultimately. In which, was dominated by ST-239(67 strains, 45%), distributed in the South and North; followed by ST-5 (54 strains, 36.2%), mainly in the Northeast region (χ2=26.42, P<0.01). Conclusions: Vancomycin, daptomycin and linezolid are 100% sensitive drugs to MRSA in ICU; Higher regional homology for MRSA were observed and it is probably that homologic disseminated infection exited in ICU. It is necessary to enhance continuous monitoring and take effective nosocomial infection control action to avoid MRSA homologic outbreak.

Effects of autologous SCF- and G-CSF-mobilized bone marrow stem cells on hypoxia-inducible factor-1 in rats with ischemia-reperfusion renal injury.

To explore the mechanism whereby stem cell factor (SCF) and granulocyte colony-stimulating factor (G-CSF) jointly mobilize bone marrow stem cells (BMSCs) and promote kidney repair, male Sprague-Dawley rats were randomly assigned into 4 groups. In the treatment control group, rats were administered SCF (200 µg·kg(-1)·day(-1)) and G-CSF (50 µg·kg-1·day-1) for 5 days. In the treatment group, RIRI models were established, and 6 h later, SCF (200 µg·kg(-1)·day(-1)) and G-CSF (50 µg·kg(-1)·day(-1)) were administered for 5 days. In the model and treatment groups, tubular epithelial cell degeneration and necrosis were noticed, but the extent of repair in the treatment group was significantly better than in the model group. Five days after the operation, renal tissue CD34+ cells significantly increased in the model and treatment groups compared with the control and treatment control groups. HIF-1α, VEGF, and EPO expression in treatment groups increased significantly compared with the other groups. HIF- 1α, VEGF, EPO expression in the treatment control group increased significantly compared with the control group. Joint use of SCF and G-CSF increased the number of BMSCs in damaged kidney tissue and reduced the degree of renal tissue damage. BMSCs promote increased HIF-1α expression in renal tissue. Increased kidney tissue HIF- 1α and its target gene products VEGF and EPO expression possibly induce SCF and G-CSF to promote acute tubular necrosis repair.