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Objective To investigate the variation characteristics of adenovirus type 55 (HAdV-B55) gene on plateaus.Methods Throat swabs were collected from HAdV-B55 infected patients and used for virus isolation in HEp-2 cells.The whole-genome sequence was obtained by PCR and sequencing.HAdV-B55 gene sequence was blast with the previously reported virus.Results HAdV-B55 strains were isolated from throat swabs, which were named LS89/Tibet/2016.The whole-genome sequence was obtained and submitted to GenBank with the accession number of KY002683.No large fragment gene recombination was found between this HAdV-B55 strain and previous strains, and the sequence similarity with QS-DLL strain was 99.9%.Conclusion This study provides more information for the evolution patterns of adenovirus 55 and will contribute to the prevention and control of HAdV-B55 infection in the future.
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Objective To explore the biofilm forming ability and the ability to survive in stress environment of staphylococcus epidermidis strains isolated from catheters .Methods Semiquantitative biofilm assay and bacteria cell counting were performed to explore the biofilm forming ability and the ability to survive in stress environment of staphylococcus epidermidis strains .Results Staphylococcus epidermidis strain of 1457 and 5 clinical strains isolated from catheters had the similar ability of biofilm formation (P>0 .05) ,similar growth ability of planktonic and biofilm cells ,similar attachment ability to polystyrene ,similar ability to survive in an oxidative and ethanol stress environment (P>0 .05) .Conclusion The biofilm forming ability and the ability to survive in stress environment of staphylococcus epidermidis strains isolated from catheters were similar to staphylococcus epidermidis 1457 strain .
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Objective To explore the sensitivity of Enterococcus f aecium and Enterococcus f aecalis isolated from 2011 to 2013 and provide reference for anti-infection therapy .Methods The identification and drug sensitivity test of clinical isolates were carried out by using VITEK2 Compact system .Results The ratio of Enterococcus f aecium to Enterococcus f aecalis isolates was 1 .93 and it was increasing year by year .No vancomycin ,linezolid and tigecycline resistant Enterococcus f aecium and Enterococcus f aecalis i-solates was detected .The rates of Enterococcus f aecium sensitive to quinupristin-dalfopristin and tetracycline were higher than En-terococcus f aecalis(P<0 .05) ,and the rates of Enterococcus f aecium sensitive to nitrofurantoin ,ampicillin ,penicillin G ,moxifloxa-cin ,levofloxacin and ciprofloxacin were lower than that of Enterococcus f aecalis(P<0 .05) .Conclusion The detection rates of En-terococcus was shifting to Enterococcus f aecium ,and the trends became obvious year after year .The drug sensitivity of Enterococcus f aecium and Enterococcus f aecalis is different ,and doctors should choose the proper therapy according to their specific drug resist-ance .At present ,vancomycin ,linezolid and tigecycline are preffered for the treatment against infection caused by Enterococcus f aeci-um and Enterococcus f aecalis .
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Objective To study the resistance and molecular profiles of Staphylococcus aureus strains isolated from the clinical specimens.Methods Antimicrobial susceptibility was tested with 56 strains of Staphylococcus aureus isolated from a hospital from May to November 2011.The mecA and pvl genes were detected.The spa genetic types were analyzed.Results A total of 21 (37.5%)Staphylococcus aureus strains were resistant to methicillin (MRSA)and 35 (62.5%)were sensitive to methicillin (MSSA).Nineteen of the 21 (90.5%)MRSA strains carried mecA gene.Compared with MSSA,MRSA were much less sen-sitive to rifampin,fluoroqunolones,tetracycline and gentamicin (P <0.05).All the MRSA isolates were susceptible to vanco-mycin,linezolid,tigecycline,quinupristin-dalfopristin and nitrofurantoin.Six spa types were identified among the MRSA strains.Type t030 was the most prevalent,accounting for 66.7% (14/21)of all the MRSA strains.MRSA-t030 and MRSA-t002 were resistant to multiple antibiotics.Eighteen spa types were identified among the MSSA strains.Type t189,t377 and t034 were the top three spa types of MSSA,accounting for 14.3%,14.3% and 11.4%,respectively.A new MSSA spa typ-ing strain new1 was isolated from pus.There were five Panton-Valentine leukocidin (PVL)-positive isolates,3 of which was MSSA-t189 type. Conclusions Type t030 is the most prevalent spa type among clinical MRSA strains,which is resistant to many kinds of antibiotics and widely spreads in the hospital setting.There are many different spa types a-mong the MSSA strains.Type t389,t377 and t034 are the top three spa types of MSSA.
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Aim To investigate the effects of tamoxifen on the proliferation and DNA synthesis of cultured human pituitary adenoma cells and make a further investigation of the mechanism of the inhibitory effect of tamoxifen on the proliferation of pituitary adenoma cells. Methods The techniques of MTT colorimetry, 3H-TdR, flow cytometry, PKC activity detection and cAMP/ cGMP levels detection were used to detect or observe the effects of tamoxifen on proliferation, DNA synthesis, cell cycle, PKC activity and cAMP/ cGMP levels of cultured human pituitary adenoma cells, respectively.Results ①Tamoxifen (0.1,1 and 10 ?mol?L -1) inhibited the proliferation and DNA synthesis of cultured human pituitary adenoma cells in a dose-dependent manner.② tamoxifen (1,10 and 20 ?mol?L -1) increased the ratio of G_1 phase of pituitary adenoma cells, and decreased the ratio of S and G_2 phase markedly;②compared with control, PMA, a PKC activator, increased the activity of membrane and total PKC in human pituitary adenoma cells. However, after a 15-min treatment with tamoxifen (10 ?mol?L -1),a significant reduction of the activity of cytoplasm, membrane and total PKC in human pituitary adenoma cells was observed;③tamoxifen (1 and 10 ?mol?L -1) increased the amount of cAMP in the cytoplasm of human pituitary adenoma cells, but had no effect on that of cGMP. Conclusion These data provide an important clue to explore the molecular mechanisms of the inhibitory effect of tamoxifen on the proliferation of pituitary adenoma cells, and suggest that the modulating effect of tamoxifen on the proliferation of pituitary adenoma cells results from interactions of several cellular signaling pathways.