Objective To evaluate potential clinical risk factors for the development of early-onset myocardial damage following multiple trauma (MT), and to determine whether early-onset myocardial damage was caused by the combined effects of thoracic and systemic injury factors in MT patients.Methods A total of 231 patients with MT over the last 3 years were retrospectively reviewed. With myocardial damage being a dependent variable and other twenty factors being independent variables, univariate and multivariate logistic regressions were applied to investigate the risk factors for early-onset myocardial damage and to identify the association of thoracic and systemic risk factors with early-onset myocardial damage.Results Multivariable logistic regressions showed that acute physiology and chronic health evaluation Ⅱ (APACHE Ⅱ ) score ≥10, injury severity score (ISS) ≥ 25, shock index ≥ 2,coexisting chest trauma, abbreviated injury scale (AIS) of chest≥3, and hypoxia time ≥ 0.5 h were risk factors. The risk of earlyonset myocardial damage following MT obviously increased when thoracic and systemic injury risk factors were coexisting.Conclusion Our results indicated that thoracic injury combined with systemic injury increased the overall risk of early-onset myocardial damage following MT. Prospective validation of these findings in other clinical settings is warranted.

The human atrial muscle cells were investigated by ultrastructural CMPase cytochemistry and atrial natriuretic factor (ANF) immunocytochemistry. The primary lysosomes and ANF were labelled by these techniques, respectively. ANF was localized in the atrial specific granules, these granules were similar in size and 0.20? 0.051?m in diameter, distributed over the entire cytoplasm, preferentially being located in the subsarcolemmal and perinuclear region and forming clusters. Primary lysosomes were various in size, 0.30?0.191?m in diameter, significantly larger than atrial specific granules (P

Objective To investigate the mechanism of the different levels of ciprofloxacin resistance in qnrA-containing transconjugants.Methods E. coli J53AzR as the recipient,4 qnrA-containing transconiugants were constructed by conjugation from 4 qnrA-carrying clinical isolates.MICs of the transconjugants were measured by E test.aac(6')-Ib-cr was detected by PCR,and qnrA mRNA expression level was determined by real-time RT-PCR.The promoter sequences of qnrA were amplified by PCR from qnrA-bearing plasmids and cloned into plasmid pKK232-8,then transformed into HB101.All promoter fragments were sequenced.Resuits The MICs of ciprofloxacin against 4 transconjugants demonstrated a 10-fold difference from 0.094 μg/ml to 1.000 μg/m1.Of 4 qnrA-bearing plasmids in E.coli J53,ciprofloxacin MICs of pHS4 and pHS5 were 0.094 μg/ml and 0.125 μg/ml,respectively;pHS3,which contained the aac(6')-Ib-cr gene as well,MIC was 0.25μg/ml;and pHS5,which had a high expression level of qnrA and the aac(6')-Ib-cr gene,MIC was 1.00μg/ml.The relative expression levels of qnrA mRNA in J53 pHS6 was 32.5,much higher than the other 3 transconjugants(from 1.0 to 2.5).The promoter in plasmid pHS6 was 12-fold stronger than that in the other 3 plasmids.Compared with pHS3,there was 7 bp(GTTAGCA)deletion between the transcription initiation site and the start of qnrA in pHS6.Conclusion Co-existence of qnrA and aac(6')-Ib-cr in a single plasmid and high level of qnrA expression can account for the different levels of ciprofloxacin resistance in transconjugants.

Objective To investigate thein vitro activity of tigecycline and minocycline against VanM-type vancomycin-resistant Enterococcusfaecium.Methods A total of 45 strains of VanM-type vancomycin-resistantE. faecium were obtained from hospitals in Shanghai between 2006 and 2014. Species and vancomycin resistance genotype were identiifed by PCR and sequencing analysis. Minimal inhibitory concentrations (MICs) of ten antimicrobial agents against these strains were determined.Results All the 45 isolates were VanM-type vancomycin-resistantE. faecium, and resistant to vancomycin (MIC: 128 to >256 mg/L). And 71.1%of the strains were resistant to teicoplanin. Almost all isolates showed resistance to levolfoxacin (100%) and ampicillin (97.8%). About 15.6%, 64.4% and 82.2% of the strains were resistant to minocycline, gentamicin and rifampicin, respectively.Conclusion Tigecycline and minocycline exhibit excellentin vitro activity against these VanM-type vancomycin-resistantE. faecium isolates.

Objective To screen fosfomycin-resistant genes in the clinical isolates of Enterococcus faecium Efm-HS0661 and verify their functions. MethodsAntimicrobial susceptibility and conjugation experiments were carried out to determine if the antimicrobial resistance in clinical strain was transferable.By Solexa high-throughput sequencing,the genes conferring fosfomycin resistance were screened. The function of resistance gene was identified by cloning.ResultsThe clinical isolates of Enterococcus faecium Efm-HS0661 were resistant to glycopeptide antibiotics and fosfomycin, and the fosfomycin resistance was found to be transferred by conjugation. Within the 2414 bp nucleotide sequence obtained by high-throughput sequencing, fosB, a plasmid-mediated fosfomycin resistance gene was found. The fosB gene was 420 bp in length, which shared 99. 8％ amino acid identity with other fosB from Staphylococcus spp. The minimal inhibitory concentration (MIC) of DH5α transformant containing fosB gene against fosfomycin was higher than that of DHSa transformant without fosB gene. ConclusionsThe high-throughput sequencing can be used to screen unknown resistance genes in clinical isolates. The plasmidmediated resistance gene fosB can confer fosfomycin resistance in Enterococcus faecium.

BACKGROUND: Electrical stimulation at different intensity, frequency and time on the human body may produce a variety of pathophysiological reactions. OBJECTIVE: To observe the effects of surface electric-impulse stimulation on heart rhythm and heart rate in mice. METHODS: Thirty Kunming mice were randomly divided into three groups, each group contained 10 mice. Electrical stimulation at different voltage, time and frequency was respectively applied to the three groups. The stimulus power was supplied by BL-420F Data Acquisition & Analysis System. The II lead electrocardiogram was recorded. The systemic reactions and local body changes of mice were observed.

Objective To investigate the antibiotic resistance pattern and molecular epidemiology of carbapenem-resistant Pseudomonas aeruginosa.Methods The antimicrobial susceptibility was measured by agar dilution method for the 104 strains of carbapenem-resistant P.aeruginosa (CRPA) collected from Huashan Hospital.The homology between these strains was evaluated by pulsed field gel electrophoresis (PFGE).Results Of thel04 CRPA strains,85.6％ were resistant to meropenem and 98.1％ to imipenem.These strains also showed various percentages of resistance to amikacin (18.3％),gentamicin (40.4％),ceftazidime (26.9％),cefepime (21.2％),ciprofloxacin (44.2％),levofloxacin (50.0％),piperacillin-tazobactam (19.2％),cefoperazone-sulbactam (26.9％),ticarcillin-clavulanic acid (52.9％),aztreonam (26.9％),and colistin (5.8％).PFGE analysis showed that these strains were divided into 48 types,belonging to 9 clones.Only 3 strains were non-typeable.Clone A was the primary epidemic strain (41.6％,42/101),which was mainly isolated from Neurosurgery,Geriatrics and General Ward.Clone B accounted for 5.9％ (6/101) of the strains.Conclusions Multiple clones of carbapenem resistant Pseudomonas aeruginosa were prevalent in Huashan hospital.Effective infection control approaches should be adopted to prevent the development and the further spreading of antimicrobial resistance.

Objective To understand the resistance mechanism and clinical feature of linezolid-resistant S.capitis isolated from blood samples.Methods Antimicrobial susceptibility testing was carried out to determine the susceptibility of clinical strains.PCR and sequencing analysis were used to analyze cfr gene and 23S rRNA mutation,which were associated with linezolid resistance.Patterns of pulsed-field gel electrophoresis (PFGE) were analyzed in combination with clinical data to understand the clinical feature of S.capitis strains.Results Five linezolid-resistant S.capitis strains were isolated from blood samples of 3 patients.These strains were resistant not only to linezolid,but also to most of the commonly used antimicrobial agents except glycopeptides,rifampin,and trimethoprim-sulfamethoxazole.Mutation was identified in 23S rRNA genes of all the five strains and cfr gene was found in four of the five strains.PFGE typing showed the same type,which supported the homology of the 5 strains.Three patients had deep vein indwelling catheter and two of them were treated with linezolid.Conclusions Linezolid-resistant S.capitis isolates showed the phenotype of resistance to multiple antimicrobial agents.Linezolid resistance may be mediated by cfr gene and 23S rRNA mutations in S.capitis.Long-term use of deep vein indwelling catheter and linezolid treatment may increase the risk of linezolid-resistant S.capitis infection.

Objective The aim of this study is to evaluate clinical outcomes of patients with acute type A intranural hematoma of the aorta(IMH) received surgical treatment.Methods We analyzed 40 consecutive patients with acute type A aortic IMH in Fuwai hospital.The patients are from 2012.1.1 to 2015.12.31.The average age of patients is(56 ± 11) years.Clinical outcomes and morphological evolution by CT were analyzed for 2 years.Results Most of the patients were treated medically during their initial hospitalization.There were 2 patients died in in-hospital and no 2-year mortality.16 patients (40％) were received acute surgery,24 patients(60％)were received normal surgery.Conclusion Surgical treatment would be a favorable treatment option in type A acute IMH.

Objective To observe whether treatment with cannabidiol (CBD) affect nonalcoholic steatohepatitis (NASH) induced by methionine choline-deficient diet (MCD) in rats and investigate the underlying molecular mechanism. Methods Sixty-three adult male SD rats were randomly divided in to three groups as follows: Control group (rats fed with normal diet), MCD group (rats fed with MCD and MCD+CBD group [rats fed with MCD and treated with cannabidiol, 2mg/(kg.d), i.p.]. Ten weeks later, steatohepatitis and fibrosis were evaluated by hematoxylin-eosin and Masson staining, respectively. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were measured by using an automatic biochemical analyzer and hepatic levels of cholesterol and triacylglycerol were determined with kits. Autophagic flux in livers was evaluated by Western blotting. Results Treatment with cannabidiol reduced ratio of liver/body weightratio (4.2%±0.6% versus 3.1%±0.6%, P<0.05), histological scores (4.7±1.1 versus 2.2±0.5, P<0.05) and fibrosis (1.4%±0.4% versus 0.8%±0.3%, P<0.05) in rat livers, lowered levels of ALT (214.5±54.1U/L versus 92.1±36.0U/L, P<0.05) and AST (175.9±55.2U/L versus 70.8±24.9U/L, P<0.05) in serum, attenuated hepatic fat accumulation (cholesterol, 182.4±42.7mmol/mg protein versus 101.0±33.8mmol/mg protein, P<0.05; triglyceride, 71.4±12.5mmol/mg protein versus 38.7±11.1mmol/mg protein, P<0.05), and down-regulated mRNA expression of Col1A1 (2.9±0.4 versus 1.6±0.3, P<0.05) in livers of rats fed with MCD. Furthermore, cannabidiol led to the LC3 turnover (LC3-Ⅱ/LC3-I, 37.1±10.8 versus 71.2±17.1, P<0.05) and p62 decrease (202.4±40.9 versus 125.8±32.7, P<0.05) in the livers of MCD-fed rats. Conclusion Treatment with cannabidiol could relieve MCD-induced NASH in rats, at least in part, by autophagic flux promotion.