ABSTRACT
Objective To investigate the mechanism and epidemiological characteristics of carbap-enem-resistant Proteus mirabilis ( PM) strains deficient in swarming motility. Methods PM strains were isolated from Hangzhou General Hospital of CAPF ( Chinese People′s Armed Police Forces) during January 2013 to December 2014. Bacterial motility and flagella of the PM strains were observed through semi-solid agar culture and flagella staining. Pulsed-field gel electrophoresis ( PFGE) was performed for homology anal-ysis. Antimicrobial susceptibility test and phenotypic confirmatory test were also carried out. PCR analysis and DNA sequencing were performed to confirm the genotype of resistant genes. Plasmid electroporation and S1-PFGE in combination with Southern blot hybridization were used to determine the location of the carbap-enem-resistant genes. Genetic structure of the blaKPC-2 gene was obtained by PCR mapping. Results A total of 42 PM isolates deficient in swarming motility were screened out and the resistance rates to imipenem and meropenem were 57. 1% and 52. 4%, respectively. PCR analysis and DNA sequencing confirmed that 24 carbapenem-resistant PM isolates deficient in swarming motility carried blaKPC-2 gene and belonged to three clones as indicated by the results of PFGE. Southern blot hybridization indicated that the blaKPC-2 gene was located on plasmids varying in size (26 kb, 55 kb and 139 kb). In addition, some of the strains harbored several resistant genes, such as blaTEM-1 , blaCTX-M-65 and rmtB. The genetic structures of strains carrying blaKPC-2 gene were ISKpn8, blaKPC-2 and ISKpn6-like from upstream to downstream. Conclusion Compared with the PM strains with swarming motility, the carbapenem-resistance rate was significantly higher in these PM strains deficient in swarming motility. Carbapenemases KPC-2 played an important role in the carbapen-em-resistant PM strains deficient in swarming motility. There was a cloning spread trend for carbapenem-re-sistant PM strains in our hospital. Clinicians should pay more attention to the risk of spreading.
ABSTRACT
Objective To explore the effects of ginsenoside Rg3 on the expression of P27 in human erythrol-eukemia cell line K562 and cell proliferation. Methods Human erythroleukemia cell line K562 cells were cultured to exponential phase, then K562 cells were treated with different concentrations of Rg3 (6.25, 12.5, 25, 50, and 100 μg/mL) as Rg3 group, and cells treated without Rg3 (0 μg/mL) were take as control group. After 3 days, K562 cells were observed by Wright-Giemsa staining with microscopy , the proliferation of K562 cells were examined by tetrazolium salt (MTT) assay, and the expression of P27 mRNA were detected by fluorescent quantitative RT-PCR assay. Results MTT assay showed that after treatment with Rg3,the inhibition rate (IR) of proliferation of cells in Rg3 groups were increased gradually , and the differences were significant compared with the control group (P < 0.05). The results of fluorescent quantitative RT-PCR showed the levels of P27 mRNA expression in 25,50 and 100 μg/mL Rg3 groups were significant higher than that of control group (P < 0.05). Conclusion The ginsenoside Rg3 can inhibit the proliferation of K562 cells by inducing the expression of P27.
ABSTRACT
0.05).CONCLUSIONS G1896A Variation principally distributes in HBeAg(-) group that expressed low level HBV DNA.A1762T Variation and HBeAg(+) haven′t obvious correlation.YMDD variation principally distributes in HBeAg(+) group that expressed high lever HBV DNA.YMDD variation initiates acute damage of liver cell.The variation of G1896A or A1762T may contribute to progressive damage of chronic liver disease.