Acinetobacter baumannii, a glucose-nonfermentative gram-negative coccobacillus, is an important pathogen isolated in nosocomial infections, and the clinical detection rate has been increasing in recent years. Acinetobacter baumannii attracts widespread attention due to strong viability, broad resistance spectrum and high rate of drug resistance. The resistance mechanisms include the production of β-lactamases, alterations in penicillin-binding proteins, decreased outer membrane permeability and overexpression of active efflux pumps. The mechanisms of Acinetobacter baumannii resistance to β-lactarn antibiotics, especially those of the outer membrane porin and active efflux system are reviewed in this paper.

Objective To analyze the antimicrobial resistance profile and homology of the Acinetobacter baumannii strains isolated from Rushan People's Hospital in a three-year period for better control of hospital infections.Methods A.baumannii strains were isolated from clinical specimens during the period from 2013 to 2015.Homology analysis were conducted by pulsed field gel electrophoresis (PFGE) for 60 randomly selected isolates.Results A total of 567 A.baumannii isolates were isolated,85 isolates in 2013,156 in 2014,and 326 in 2015.These isolates were mainly from Department of Respiratory Diseases (47.4％) and ICU (23.8 ％).Overall,62.1％ of the isolates were from sputum specimens followed by secretions (15.2％).All isolates were sensitive to polymyxin B,but all resistant to sulfamethoxazole and ampicillin.The A.baumannii isolates showed increasing resistance rate to imipenem,meropenem,ceftriaxone,and trimethoprim-sulfamethoxazole over the 3-year period,but decreasing resistance rate to gentamicin.The 60 selected isolates were grouped into 4 types by PFGE.A-type was the main pattern.Conclusions A.baumannii strains were mainly isolated from inpatients with respiratory tract infections.The A.baumannii strains showed serious antimicrobial resistance associated with possible clonal spread in this hospital.

Objective To explore the change of CD4+CD25+Foxp3+ regulatory T (Treg) cells during aging and the relation with lung tumor. Methods The Lewis lung cancer model was set up in C57BL/6 female mice, and the 36 mice were divided into young health group, middle-aged health group, elderly health group, young tumor group, middle-aged tumor group and elderly tumor group. The percentages of CD4+CD25+Foxp3+ Treg in CD4+ T cells in mice spleen cells were measured by flow cytometry, for reflecting the quantity of CD4+CD25+Foxp3+ Treg cells. And the level of Foxp3 mRNA in splenocyte was tested by real-time PCR method. Results The level of CD4+CD25+Foxp3+/CD4+ T cells and the quantity of Foxp3 mRNA were higher in tumor groups than in healthy groups(both P＜0.05 ). Besides, in the healthy groups, there were statistical differences in the level of CD4+CD25+Foxp3+/CD4+ T cells (F=47.70, P=0.000) and the quantity of Foxp3 mRNA among the different months groups. Accumulation of the CD4+CD25+Foxp3+ Treg cells was accompanied with aging, the elderly mice contained a significantly larger population of CD4+CD25+Foxp3+ Treg cells in their spleen when compared with the younger counterparts, and the highest was the elderly tumor group. So it was with the functional gene Foxp3 mRNA (F=6.56, P=0.009). Conclusions The results suggest a close relationship of the change of CD4+CD25+Foxp3+Treg cells with aging and the genesis and development of lung tumor.