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.

An increased level of reactive oxygen species is a key factor in neuronal apoptosis and epileptic seizures. Irisin reportedly attenuates the apoptosis and injury induced by oxidative stress. Therefore, we evaluated the effects of exogenous irisin in a kainic acid (KA)-induced chronic spontaneous epilepsy rat model. The results indicated that exogenous irisin significantly attenuated the KA-induced neuronal injury, learning and memory defects, and seizures. Irisin treatment also increased the levels of brain-derived neurotrophic factor (BDNF) and uncoupling protein 2 (UCP2), which were initially reduced following KA administration. Furthermore, the specific inhibitor of UCP2 (genipin) was administered to evaluate the possible protective mechanism of irisin. The reduced apoptosis, neurodegeneration, and spontaneous seizures in rats treated with irisin were significantly reversed by genipin administration. Our findings indicated that neuronal injury in KA-induced chronic epilepsy might be related to reduced levels of BDNF and UCP2. Moreover, our results confirmed the inhibition of neuronal injury and epileptic seizures by exogenous irisin. The protective effects of irisin may be mediated through the BDNF-mediated UCP2 level. Our results thus highlight irisin as a valuable therapeutic strategy against neuronal injury and epileptic seizures.
Rats ; Animals ; Kainic Acid/toxicity* ; Brain-Derived Neurotrophic Factor/metabolism* ; Fibronectins/metabolism* ; Hippocampus/metabolism* ; Rats, Sprague-Dawley ; Epilepsy/metabolism* ; Seizures/prevention & control*