ABSTRACT
Objective To investigate antimicrobial resistance and pathogen in hebei antibacterial resistance investigation net in 2012.Methods Antimicrobial susceptibility test was detected by Kirby-Bauer method or broth dilution test.Results were analyzed according to CLSI 2010 breakpoints.WHONET 5.5 software was used to analyze the data.Results A total of 10 504 clinical isolates were collected in 2012,of which gram negative bacilli and gram positive cocci accounted for 76.2%, 23.8%,respectively.The most common pathogen in gram-negative rod was E.coli,K.pneumoniae,P.aeruginosa, A.baumanii and E.cloacae respectively.The most common pathogen in gram-positive cocci was S.aureus,E.facium,E-.faecalis,S.pneumoniae and S.epidermidis.ESBL rate of E.coli and K.pneumoniae was 66.5 and 46.7%.The resistant rate of E.coli,K.pneumoniae,E.cloacae to imipenem was 0.1%,0.5%,8.9% and to meropenem was 0.1%,0.6%,4.2%, respectively.P.aeruginosa was resistant to imipenem and meropenem were 38.9% and 32.3%.A.baumanii was resistant to imipenem and meropenem were 5 6.5% and 5 9.7%.Methicillin-resistant strains accounted for an average of 5 7.5% in S.aureus and 87.3% in coagulase negative staphylococcus.Staphylococcus was still susceptible to minocycline and chloram-phenicol.No staphylococcal strains were found resistant to vancomycin,linezolid.But a few coagulase negative staphylococcal strains were resistant to teicoplanin.Conclusion Surveillance of antimicrobial agents played an important role in controlling hospital infection.
ABSTRACT
Objectives To explore the possible mechanism of all-trans-retinoic acid (ATRA) therapy for pulmonary ar-terial hypertension by observing the effect of ATRA on the expression ofα-smooth muscle actin (α-SMA) in monocrotaline (MCT)-induced rats with pulmonary hypertension. Methods Thirty SD rats were randomly divided into control group, MCT-induced pulmonary hypertension group (model group) and ATRA treatment group (therapeutic group). MCT (60mg/kg) was injected to the rats in the model group and the therapeutic group to induce pulmonary arterial hypertension. And at the same day ATRA [30mg/(kg?d)] was given to rats in the therapeutic group and continually given for 28 days. The mean pulmonary arte-rial pressure and right ventricular hypertrophy index (RVHI), percentage of wall thickness (WT%) and percentage of wall area (WA%) of pulmonary arterioles were evaluated at day 28. The expression ofα-SMA mRNA and protein in the lung tissue were detected by Real-time PCR and Western blot. Results Mean pulmonary arterial pressure, RVHI, WT%and WA%were signiif-cantly higher in the model group than those in the therapeutic group (P0.05). Conclusions ATRA has therapeutic effect on pulmonary hypertension through down-regulation ofα-SMA expression.