ABSTRACT
Objective To understand the antimicrobial resistance of common clinical pathogens to antimicrobial disks containing different ratios of cefoperazone/sulbactam,so as to provide basis for rational application of cefoper-azone/sulbactam in clinic.Methods 1 141 pathogens isolated from clinical specimens in a hospital in the first half year of 2014 were collected,disk diffusion method was adopted to detect antimicrobial activity of two kinds of cef-operazone/sulbactam disks (70/35 μg and 75/75 μg).Results Of 1 141 pathogenic strains,675 (59.16%)were En-terobacteriaceae,447 (39.18%)were non-fermentative bacteria,and 19 (1 .66%)were other gram-negative bacilli. Resistance rates of pathogens to 70/35μg and 75/75 μg cefoperazone/sulbactam antimicrobial disks were as follows:extended-spectrumβ-lactamases(ESBLs)-producing Escherichia coli (n=221)were 7.69% and 2.26% respective-ly,ESBLs-producing Klebsiella pneumoniae (n=92)10.87% and 3.26% respectively,imipenem-resistant Acineto-bacter baumannii (IRAB,n=295)54.92% and 11 .19%respectively;there were significant differences in antimicrobial activity between two ratios of antimicrobial disks(P 0.05).Conclusion Antimicrobial activity of two different ratios of cefoperazone/sulbactam antimicrobial disks to ESBLs-producing Enterobacteriaceae and IRAB is different,attention should be paid to ratios of cefoperazone/sulbactam during the treatment ,so as to achieve the desired therapeutic effect.
ABSTRACT
<p><b>BACKGROUND</b>Endothelin-1 (ET-1) is a potent mitogen involved in tumor cell growth and angiogenesis. The aim of this study is to explore the effect of ET-1 on the proliferation of human lung adenocarcinoma cells SPC-A1.</p><p><b>METHODS</b>Cell number was measured by MTT [3-(4,5-dimethylthiazol-2-yl)-2, 5-diphenyl-tetrazolium bromide] assay. Cell cycle was detected by flow cytometry.</p><p><b>RESULTS</b>ET-1 (1×10⁻¹⁵ -1×10⁻⁸ mol/L) enhanced SPC-A1 cell growth in a dose-dependent manner in vitro, with the greatest effect beginning at 1×10⁻¹¹ mol/L. Effect of ET-1 (1×10⁻¹⁰ mol/L) on the proliferation of SPC-A1 cells was completely blocked by BQ123 (1×10⁻⁷ mol/L), a highly selective endothelin receptor A (ETA) antagonist (P < 0.05), not by BQ788 (1×10⁻⁷ mol/L), a highly selective endothelin receptor B (ETB) antagonist. BQ123 could significantly reduce the basal growth of SPC-A1 cells (P < 0.05), but BQ788 had no such effect. Proliferation induced by ET-1 (1×10⁻¹⁰ mol/L) could also be blocked by the addition of either ethylene diamine tetraacetic acid (EDTA, 0.4mmol/L) or nifedipine (1μmol/L). ET-1 had no significant effect on SPC-A1 cell cycle.</p><p><b>CONCLUSIONS</b>ET-1 enhances SPC-A1 cell proliferation by the activation of ETA receptor. Ca(2+) influx from voltage dependent calcium-channel contributes to this process.</p>