Objective To investigate the clinical distribution and the drug resistance of carbapenemresistant Proteus mirabilis strains isolated from 2009 to 2012 ; and to study carbapenemase genotypes of the isolates.Methods A total of 15 non-repetitive carbapenem-resistant Proteus mirabilis strains were selected from 422 Proteus mirabilis strains isolated from Ningbo First Hospital during January 2009 to December 2012.The minimal inhibitory concentrations (MIC) of 6 antibacterial agents,including imipenem (IPM),meropenem (MEM),ertapenem (ETP),ciprofloxacin (CIP),amikacin (AK) and minocycline (MIN),against 15 isolates were determined by E-test.The modified Hodge test (MHT) was used to detect the carbapenemase production in isolates.The PCR assay was performed to detect drug resistance genes of blaKPC,blaNDM-1,blaGES,blaSME,blaIMI-1/NmcA and blaSHV-38.Plasmids were extracted from the blaKPC-positive strains and then transformed into Escherichia coli J53 strains by electroporation.The transformed and untransformed Escherichia coli J53 strains were tested for MIC values and blaKPC gene by E-test and PCR respectively.Results The resistance rates of the 15 carbapenem-resistant Proteus mirabilis strains to IPM,MEM,ETP,CIP,AK and MIN were 100％,100％,100％,86.7％ (13/15),33.3％ (5/15) and 80％ (12/15),respectively.7 out of 15 strains were Hodge test positive,and 11 strains were blaKPC-2 positive.Results of PCR amplification showed that the transformed Escherichia coli J53 strains,whose MIC values to IPM,MEM,and ETP were increased by 2 to 64 times,were blaKPC-2 gene positive.Conclusion The carbapenem-resistant Proteus mirabilis strains in this study were resistant to many commonly used antibiotics,however,the resistance rates to AK were relatively low.The dominant carbapenemase genotype was blaKPC-2 carried by the plasmid.Attention should be paid to its easily transmissible feature among the strains in clinic.

Objective To explore the difference between T cells in the synovial fluid and peripheral blood in patients with rheumatoid arthritis(RA). Method Samples from 22 patients were studied. The differentiation and activation markers expressed on T cell surface were detected by immunofluorscence using flow cytometer. The specific proliferation of collagen Ⅱ and heat shock protein 70 was analyzed using standard 3H-TdR incorporation method. Restricted V beta usage of these T cell was analyzed by semi-quantitied RT-PCR. Results The majority of the T cell subsets in the synovial fluid were demonstrated to be CD4 and CD8 positive cells in which (40?10)% were CD4 positive and (36?16)% were CD8 T cells respectively. The ratio between CD4 and CD8 was much lower than that found in the PBL of RA patients. The percentage of CD3+/CD25+ T cells was (16?6)%. The specific proliferation of collagen Ⅱ and HSP70 to CD3+/CD25+ T cell was higher than that of CD3+/CD25+ negative T cells. The T cell receptor expressed on the T cells from both peripheral blood and synovial fluid were tested for ?? TCR (70?26)%. However, the T cells in the synovial fluid showed V?14,16 and 17 restriction. Conclusion The data here reported indicates that T cell subsets in the synovial fluid and peripheral blood circulation in patients with rheumatoid arthritis are different. The T cells in the synovial fluid demonstrates more activation and higher reactivation to collagen Ⅱ and HSP70. The TCR of T cells showes V?14,16 and 17 restriction.

OBJECTIVES: Cardiac hypertrophy and fibrosis are major pathological manifestations observed in left ventricular remodeling induced by angiotensin II (AngII). Low-intensity pulsed ultrasound (LIPUS) has been reported to ameliorate cardiac dysfunction and myocardial fibrosis in myocardial infarction (MI) through mechano-transduction and its downstream pathways. In this study, we aimed to investigate whether LIPUS could exert a protective effect by ameliorating AngII-induced cardiac hypertrophy and fibrosis and if so, to further elucidate the underlying molecular mechanisms. METHODS: We used AngII to mimic animal and cell culture models of cardiac hypertrophy and fibrosis. LIPUS irradiation was applied in vivo for 20 min every 2 d from one week before mini-pump implantation to four weeks after mini-pump implantation, and in vitro for 20 min on each of two occasions 6 h apart. Cardiac hypertrophy and fibrosis levels were then evaluated by echocardiographic, histopathological, and molecular biological methods. RESULTS: Our results showed that LIPUS could ameliorate left ventricular remodeling in vivo and cardiac fibrosis in vitro by reducing AngII-induced release of inflammatory cytokines, but the protective effects on cardiac hypertrophy were limited in vitro. Given that LIPUS increased the expression of caveolin-1 in response to mechanical stimulation, we inhibited caveolin-1 activity with pyrazolopyrimidine 2 (pp2) in vivo and in vitro. LIPUS-induced downregulation of inflammation was reversed and the anti-fibrotic effects of LIPUS were absent. CONCLUSIONS These results indicated that LIPUS could ameliorate AngII-induced cardiac fibrosis by alleviating inflammation via a caveolin-1-dependent pathway, providing new insights for the development of novel therapeutic apparatus in clinical practice.