OBJECTIVE To investigate the bacteriologic feature and the spectrum of drug resistance in lung cancer patients who got nosocomial nonfermenters bacteria infection,and to conclude the experience and how to prevent and control the nosocomial infection.METHODS A rectrospective analysis of the composition of the pathogens,the feature of drug resistance and the prognosis of 109 lung cancer inpatients with nosocomial infection was made.RESULTS Nosocomial nonfermenters bacteria infections were most happened in hospital lung cancer patients.Main strains included Pseudomonas aeruginosa 55(49.5%),Acinetobacter baumannii 23(20.7%),and Stenotrophomonas maltophilia 8(7.2%).The sensitive rate of P.aeruginosa to imipenem was 100%,but to Cotrimoxazole,the resistant rate was 100%.The sensitive rate was relatively high to ticarcillin,piperacillin and their compounds.The antimicrobial resistance rate of A.baumannii was higher than P.aeruginosa.Stenotrophomonas were resistant to most antibiotics,and the resistance rate to imipenem was 100.0%.CONCLUSIONS The resistance rate of nosocomial nonfermenters bacteria infection is high.The treatment is difficult and the prognosis is bad.The mortality of multiple infection is high.

OBJECTIVE To evaluate the commonly encountered pathogens and drng resistance of bacteria causing secondary infection in patients with malignant tumors and provide reference for clinical antimicrobial usage.METHODS Statistical analysis was made retrospectively in the classification and antimicrobial susceptibility testing in 1 204 strains of pathogens isolated from clinical samples of hospitalized patients with malignant tumors from Jan 2003 to Oct 2005.RESULTS Among 1 204 strains,Gram-positive strains accounted for 31.1%;Gram-negative ones accounted for 52.8%;and fungi accounted for 16.1%.The principal strains were Candida albicans,Escherichia coli,Staphylococcus aureus,Klebsiella pneumoniae,and Pseudomonas aeruginosa.The most frequent infection sites were in respiratory tract,urinary tract and skin-soft tissue.Multiple drug resistant rate of Gram-positive and Gram-negative strains had a tendency of elevation.CONCLUSIONS To reduce the coming of drug resistant strains,etiologic examination should be done in treatment of infectious diseases and antimicrobial therapy should be decided according to the results of susceptibility.

OBJECTIVEChronic intermittent hypoxia (CIH) animal model was used to mimic the status of obstructive sleep apnea (OSA) in order to investigate the pathological mechanism of CIH-induced cardiac remodeling and observe the protective effect of antioxidants.

METHODSFVB mice (8-10 weeks-old) were randomly divided into control (saline, i.p.) group and CIH group, reduced form of nicotinamide adenine dinucleotide phosphate oxidase inhibitor, apocynin (APO, 3 mg×kg(-1)×d(-1), i.p.) alone or CIH+APO, SOD mimic MnTMPyP (SODM, 5 mg×kg(-1)×d(-1), i.p.) alone or CIH+SODM (n = 5 each). After 4 weeks, cardiac function and structure were determined by echocardiography, cardiac inflammation, apoptosis, cardiac fibrosis and cardiac MDA contents were examined by Western blot and chemical-biological methods, respectively.

RESULTS(1) Heart weight, LVIDd and LVIDs were increased while LVEF and FS were reduced in CIH group compared to control group (all P < 0.05). (2) Myocardial protein expression of ANP and VCAM-1 was significantly upregulated, myocardial MDA content and apoptosis as well as myocardial fibrosis marker CTGF and PAI-1 were increased in CIH group compared to control group (all P < 0.05). (3) Above parameters were similar between APO and CIH+APO as well as SODM and CIH+SODM (all P > 0.05).

CONCLUSIONCIH could induce cardiac remodeling and CIH-induced cardiac inflammation, cardiac oxidative injury, cardiac apoptosis and cardiac fibrosis serve as the pathological mechanisms of CIH-induced cardiac remodeling. The protective effects of the two antioxidants suggest that the main mechanism of CIH-induced cardiac injury is oxidative stress.

Acetophenones ; Animals ; Antioxidants ; physiology ; Apoptosis ; Disease Models, Animal ; Heart ; Hypoxia ; Mice ; Mice, Inbred Strains ; Myocardium ; NADPH Oxidases ; Oxidative Stress ; Plasminogen Activator Inhibitor 1 ; biosynthesis ; Sleep Apnea, Obstructive ; complications ; Vascular Cell Adhesion Molecule-1 ; biosynthesis ; Vascular Remodeling