Objective To investigate the types,antimicrobial resistance,and disinfectant resistance of pathogens isolated from hospital environmental inanimate surfaces and hands of health care workers (HCWs).Methods Pathogens isolated from hospital environmental inanimate surfaces and hands of HCWs in intensive care units and general wards in 16 hospitals in Beijing were performed bacterial identification,antimicrobial susceptibility testing,and disinfectant re-sistance testing. The carriage of antimicrobial resistance genes and disinfectant genes in pathogens were also detec-ted.Results A total of 979 specimens were collected from inanimate surfaces and hands of HCWs in 16 hospitals,75 (7.66% )pathogenic strains were isolated,78.67% of which were gram-negative bacilli. The top 3 pathogens were Pseud-omonasaeruginosa (P.aeruginosa,n= 24),Enterobactercloacae (E. cloacae,n= 14),and Klebsiella pneumoniae (K. pneumoniae,n= 4 ). One P. aeruginosa strain was resistant to aztreonam,gentamycin,tobramycin,ciprofloxacin,and levofloxacin;One E. cloacae strain was resistant to piperacillin,7 strains were resistant to nitrofurantoin;4 K. pneumoni-ae strains were all resistant to piperacillin,2 were resistant to cephalosporins,and 1 was resistant meropenem. P. aerugi-nosahad7drug-resistantgenes,positiverateofmirwas100.00% ;E.cloacaehad4drug-resistantgenes,positiveratesof tem 1and shv were both 100.00% ;K. pneumoniae had 5 drug-resistant genes,positive rates of shv and mir were both 100.00% . The resistant rates of P. aeruginosa and E. cloacae to chlorhexidine gluconate were 4.17% and 57.14% re-spectively,to trichloroisocyanuric acid were both 50.00% ,positive rates of drug-resistant genes (qacE△1-sul 1)were 79. 17% and 57.14% respectively;K. pneumoniae had no resistance to two kinds of disinfectant,dug-resistance gene was not found.Conclusion Multiple common pathogens which can cause healthcare-associated infection exist in hospital environ-mental inanimate surfaces and hands of HCWs,which are dominated by gram-negative bacilli,pathogens had resistance to antimicrobial agents and disinfectant in different degrees.

Chronic high-salt diet-associated renal injury is a key risk factor for the development of hypertension. However, the mechanism by which salt triggers kidney damage is poorly understood. Our study investigated how high salt (HS) intake triggers early renal injury by considering the ‘gut-kidney axis’. We fed mice 2% NaCl in drinking water continuously for 8 weeks to induce early renal injury. We found that the ‘quantitative’ and ‘qualitative’ levels of the intestinal microflora were significantly altered after chronic HS feeding, which indicated the occurrence of enteric dysbiosis. In addition, intestinal immunological gene expression was impaired in mice with HS intake. Gut permeability elevation and enteric bacterial translocation into the kidney were detected after chronic HS feeding. Gut bacteria depletion by non-absorbable antibiotic administration restored HS loading-induced gut leakiness, renal injury and systolic blood pressure elevation. The fecal microbiota from mice fed chronic HS could independently cause gut leakiness and renal injury. Our current work provides a novel insight into the mechanism of HS-induced renal injury by investigating the role of the intestine with enteric bacteria and gut permeability and clearly illustrates that chronic HS loading elicited renal injury and dysfunction that was dependent on the intestine.
Animals ; Bacteria ; Bacterial Translocation ; Blood Pressure ; Drinking Water ; Dysbiosis ; Enterobacteriaceae ; Gastrointestinal Microbiome ; Gene Expression ; Hypertension ; Intestines ; Kidney ; Mice* ; Microbiota ; Permeability ; Risk Factors

Objective: To investigate the effect of Δ40p53, an alternative spliced isoform of p53 lacking the N-ter minus, on the pro-apoptotic function of p53. Methods: The wild-type p53 was ectopically expressed in HCT116-p53^-/- (endogenous Δ40p53 expression), HCT116-p53^{+ /+} (wild-type p53) and H1299 (p53-null) cells by adenoviral delivery, while Δ40p53 plasmid were transfected into these cells to overexpress Δ40p53. The levels of Δ40p53 and p53 mRNA were detected by reverse transcription-polymerase chain reaction (RT-PCR) and quantitative PCR. The expression of related proteins was deter mined by Western blotting. The interaction of p53 and Δ40p53 was observed by co-immunoprecipitation assay. Calcein-AM/propidium iodide (PI) staining and flow cytometry were used to detect the apoptotic rate of tested cells in each group. Results: HCT116-p53^-/- cells expressed endogenous Δ40p53 isoform. Neither transcription nor protein expression of wild-type p53 was interfered by the increased expression of Δ40p53. Full length p53 and Δ40p53 could bind to each other. Calcein-AM/PI staining showed that the apoptotic rates of H1299-Control, HCT116-p53^-/- -Control, H1299+ p53, HCT116-p53^-/-+ p53, H1299+ oxaliplatin (Oxa), HCT116-p53^-/-+ Oxa, H1299+ p53+ Oxa and HCT116-p53^-/-+ p53+ Oxa groups were (2.50±0.47)%, (2.40±0.32)%, (5.20±0.58)%, (4.10±0.18)%, (22.40±1.73)%, (19.30±1.11)%, (29.90±1.15)% and (39.30±2.26)%, respectively. It was statistically significant between H1299+ p53+ Oxa and HCT116-p53^-/-+ p53+ Oxa groups (t=3.721, P=0.0205). Moreover, the apoptotic rates of H1299-Control, H1299+ Δ40p53, H1299+ p53, H1299+ p53+ Δ40p53, H1299+ Oxa, H1299+ Δ40p53+ Oxa, H1299+ p53+ Oxa and H1299+ p53+ Δ40p53+ Oxa groups were (2.60±0.35)%, (2.20±0.17)%, (4.80±0.49)%, (4.90±1.10)%, (20.30±1.10)%, (19.60±1.45)%, (27.90±1.39)%, (35.20±1.43)%, respectively. Furthermore, flow cytometry assay showed that the apoptotic rates of above cells were (2.70±0.32)%, (2.20±0.24)%, (4.60±0.48)%, (3.90±0.67)%, (19.30±1.11)%, (17.70±0.66)%, (28.30±2.76)% and (37.50±1.51)%, respectively. H1299+ p53+ Δ40p53+ Oxa cells showed higher cell apoptosis than H1299+ p53+ Oxa cells (t=2.930, P=0.042). Conclusion Δ40p53 isoform can bind to full-length p53, and enhance its pro-apoptotic function in tumor cells.