Objective To summarize the changing prevalence of carbapenem resistance in Enterobacterales based on the data of CHINET Antimicrobial Resistance Surveillance Program from 2015 to 2021 for improving antimicrobial treatment in clinical practice.Methods Antimicrobial susceptibility testing was performed using a commercial automated susceptibility testing system according to the unified CHINET protocol.The results were interpreted according to the breakpoints of the Clinical & Laboratory Standards Institute(CLSI)M100 31st ed in 2021.Results Over the seven-year period(2015-2021),the overall prevalence of carbapenem-resistant Enterobacterales(CRE)was 9.43％(62 342/661 235).The prevalence of CRE strains in Klebsiella pneumoniae,Citrobacter freundii,and Enterobacter cloacae was 22.38％,9.73％,and 8.47％,respectively.The prevalence of CRE strains in Escherichia coli was 1.99％.A few CRE strains were also identified in Salmonella and Shigella.The CRE strains were mainly isolated from respiratory specimens(44.23±2.80)％,followed by blood(20.88±3.40)％and urine(18.40±3.45)％.Intensive care units(ICUs)were the major source of the CRE strains(27.43±5.20)％.CRE strains were resistant to all the β-lactam antibiotics tested and most non-β-lactam antimicrobial agents.The CRE strains were relatively susceptible to tigecycline and polymyxins with low resistance rates.Conclusions The prevalence of CRE strains was increasing from 2015 to 2021.CRE strains were highly resistant to most of the antibacterial drugs used in clinical practice.Clinicians should prescribe antimicrobial agents rationally.Hospitals should strengthen antibiotic stewardship in key clinical settings such as ICUs,and take effective infection control measures to curb CRE outbreak and epidemic in hospitals.

Objective To summarize the changing prevalence of carbapenem resistance in Enterobacterales based on the data of CHINET Antimicrobial Resistance Surveillance Program from 2015 to 2021 for improving antimicrobial treatment in clinical practice.Methods Antimicrobial susceptibility testing was performed using a commercial automated susceptibility testing system according to the unified CHINET protocol.The results were interpreted according to the breakpoints of the Clinical & Laboratory Standards Institute(CLSI)M100 31st ed in 2021.Results Over the seven-year period(2015-2021),the overall prevalence of carbapenem-resistant Enterobacterales(CRE)was 9.43％(62 342/661 235).The prevalence of CRE strains in Klebsiella pneumoniae,Citrobacter freundii,and Enterobacter cloacae was 22.38％,9.73％,and 8.47％,respectively.The prevalence of CRE strains in Escherichia coli was 1.99％.A few CRE strains were also identified in Salmonella and Shigella.The CRE strains were mainly isolated from respiratory specimens(44.23±2.80)％,followed by blood(20.88±3.40)％and urine(18.40±3.45)％.Intensive care units(ICUs)were the major source of the CRE strains(27.43±5.20)％.CRE strains were resistant to all the β-lactam antibiotics tested and most non-β-lactam antimicrobial agents.The CRE strains were relatively susceptible to tigecycline and polymyxins with low resistance rates.Conclusions The prevalence of CRE strains was increasing from 2015 to 2021.CRE strains were highly resistant to most of the antibacterial drugs used in clinical practice.Clinicians should prescribe antimicrobial agents rationally.Hospitals should strengthen antibiotic stewardship in key clinical settings such as ICUs,and take effective infection control measures to curb CRE outbreak and epidemic in hospitals.

Objective To investigate whether apolipoprotein E (APOE) genotype specifically modulates cognition function and cerebral blood flow in patients with amnesic mild cognitive impairment (aMCI) by using pulsed arterial spin labeling (ASL) MR imaging.Methods Eighty-three aMCI subjects and 130 healthy controls (HCs) were recruited through heath screening in community from 2012 to 2014 in our hospital.They all underwent neuropsychological battery assessments,genetic screening and MR imaging.The aMCI subjects included 8 APOE ε2ε3 carriers,46 APOE ε3ε3 carriers and 29 APOE ε3ε4 carriers;however,in HCs,there were 35 APOE ε2ε3 carriers,46 APOE ε3ε3 carriers and 49 APOE ε3ε4/ε4ε4 carriers.Neuropsychological scale was performed in all subjects.ASL data were preprocessed by the ASLtbx toolbox.A voxel-wise two-way ANOVA was performed to examine the main effects of'disease'(MCI) and ‘genotype’ (APOE),and the disease-by-genotype interactions on regional cerebral blood flow (rCBF) maps.Multiple linear regression analysis was performed to examine the relationships between neuropsychological scale scores and rCBF values in brain areas showing significant diagnosis-by-genotype interactions.Results (1) As compared with HCs,the aMCI subjects exhibited significantly higher rCBF values primarily in the left superior and middle frontal gyrus (P＜0.05).APOE ε3ε4/ε4ε4 carriers showed significantly higher rCBF values in the right anterior and posterior cingulate cortex,right ventromedial prefrontal cortex/anterior cingutate than those of A POE ε2ε3 carriers and ε3ε3 carriers,respectively (P＜0.05).Significant disease-by-genotype interactions on rCBF were observed in the left superior frontal gyrus,right ventromedial prefrontal cortex/anterior cingutate and bilateral superior temporal gyrus;as compared with A POE ε2ε3 and A POE ε3ε3 carriers,APOE ε3ε4 carriers had significantly higher rCBF values in the above areas in the aMCI group (P＜0.05).(2) The rCBF values in the right anterior cingulate/medial prefomtal gyrus and superior temporal gyrus of APOE ε3ε4 carriers in aMCI group were negatively correlated with the similarity test scores (r=-0.453,P=0.014;r=-0.497,P=0.006).Conclusions The APOE genotype has disease-specific effects on cerebral perfusion;APOE genotype can specifically regulate cerebral blood perfusion in aMCI subjects.The carriers ofAPOE ε3ε4 genotype in aMCI subjects may maintain their overall cognitive function by increasing lateral ventricle-temporal lobe cerebral blood perfusion.

Proceeding from the requirements of teaching target for postgraduate students,the course of progress in pathophysiology was constructed and administrated.The course objective was defined which combined teaching knowledge with fostering students' ability together,especially the ability to think new ideas and to do scientific research.Aiming at this teaching target,the teaching contents which combined with the direction of scientific research of the department was growing together with scientific development,especially in new knowledge and new technique.Multiple teaching means and several mode of examine were adopted during the process of teaching practice.

OBJECTIVETo investigate the effect of tumor necrosis factor-α (TNF-α) on nutritional status and proteolysis of respiratory muscle in a rat model of chronic obstructive pulmonary disease (COPD).

METHODSNinety healthy male adult Wistar rats were randomly divided into model group (A) and normal control group (B). COPD malnutrition rat models were established by cigarettes smoke and nutrient limitation and divided into normal nutrition COPD group (A(1)), malnutrition COPD group (A(2)), and malnutrition COPD intervention group (A(3)). In group A(3), the rats received intravenous injection of TNF-α mAb (0.1 mg/kg). TNF-α levels in the serum and respiratory muscle homogenates were measured using enzyme-linked immunosorbent assay (ELISA), and plasma levels of glucose, albumin, and triglyceride were measured with an automatic biochemistry analyzer. High-performance liquid chromatography was used to measure the contents of 3-methylhistidine and tyrosine in the respiratory muscle homogenates.

RESULTSThe serum TNF-α level and plasma levels of glucose and triglyceride were significantly higher but the plasma albumin level was significantly lower in group A(2) than in groups B, A(1), and A(3) (P<0.01). The contents of 3-MH and Tyr in the respiratory muscle homogenates were significantly higher in group A(2) than in the other 3 groups (P<0.01, P<0.01). TNF-α in the respiratory muscle showed a strong positive correlation to 3-MH and Tyr.

CONCLUSIONTNF-α is one of the causes of increased proteolysis of the respiratory muscle.

Animals ; Lung ; pathology ; Male ; Nutritional Status ; Proteolysis ; Pulmonary Disease, Chronic Obstructive ; metabolism ; pathology ; Rats ; Respiratory Muscles ; metabolism ; Tobacco Products ; Tumor Necrosis Factor-alpha ; pharmacology