1.Survey on the genes conferring plasmid-mediated quinolone resistance and those encoding β-lactamases in Escherichia coli isolates
Fangjun LAN ; Juan WU ; Qingwen HE ; Yingping CAO ; Bin LI
Chinese Journal of Infection and Chemotherapy 2017;17(3):293-297
Objective To examine the prevalence of plasmid mediated quinolone resistance (PMQR) genes and their correlation with the genes encoding β-lactamases in E.coli isolates.Methods A total of 200 levofloxacin-and/or ciprofloxacin-resistant E.coli isolates were collected from Fujian Medical University Union Hospital during the period from July to December 2013.PCR method was used to screen these E.coli isolates for the presence of qnrA,qnrB,qnrC,qnrD,qnrS,aac(6')-Ib-cr,qepA,oqxAB genes,and the blaTEM,blasnv and blacTx-M genes in the PMQR positive strains.Agar dilution method was utilized to measure the antimicrobial susceptibility of PMQR-positive strains.Phylogenetic analysis was conducted by triplex PCR.Enterobacterial repetitive intergenic consensus-polymerase chain reaction (ERIC-PCR) was used to evaluate the genetic similarity between the PMQR-positive isolates.Results Of the 200 clinical isolates of E.coli,58 (29.0%)were PMQR-positive.And qnr,aac(6')-Ib-cr,oqxAB,and qepA genes were positive in 11 (5.5%),41 (20.5%),16 (8.0%),1 (0.5%) strains,respectively.The genes encoding CTX-M-1,CTX-M-9 and TEM type enzymes was positive in 32 (55.2%),17 (29.3%),and 1 (1.7%) of the PMQR-positive strains,respectively.The blasHv gene was not identified in any isolate.PMQR-positive strains were multi-drug resistant.Phylogenetic analysis indicated that 21 (36.2%),17 (29.3%),11 (19.0%),and 9 (15.5%) of the PMQR-positive strains belonged to group A,group D,group B2 and group B 1,respectively.ERIC-PCR suggested the PMQR-positive isolates belonged to 50 different types.Only one strain was non-typeable.Conclusions Most of the PMQR-related genes in E.coli are aac(6')-Ib-cr,qnr,and oqxAB in our hospital,which are highly relevant to β-1actamase genes.PMQR-positive strains may spread by way of non-clonal dissemination in our hospital.
2.Relationship Between BIM Gene Polymorphism and Therapeutic Efficacy in the Retreatment of Advanced Non-small Cell Lung Cancer with Tyrosine Kinase Inhibitor
ZHENG LEI ; LIN BAOCHAI ; SONG ZHENGBO ; XIE FANGJUN ; HONG WEI ; FENG JIANGUO ; SHAO LAN ; ZHANG YINGPING
Chinese Journal of Lung Cancer 2013;(12):632-638
Background and objective BIM gene is a member of the BCL-2 family, is involved in cell death. The aim of this study is to explore the relationship between BIM gene polymorphism and therapeutic efficacy in the retreatment advanced non-small cell lung cancer (NSCLC) with tyrosine kinase inhibitor (EGFR-TKI). Methods In the study, there were 123 patients who were diagnosed with advanced NSCLC in Zhejiang Province Cancer Hospital bewteen January 2009 to October 2012, all of who were received gefitinib and erlotinib therapy after failure to chemotherapy. We detected the genotype of peripheral blood leukocytes of patients with BIM gene polymorphism though polymerase chain reaction (PCR). Statistical analysis was performed by SPSS version 13.0. Results On the disease control rates, BIM gene with no polymorphism type was slightly better trend than polymorphism types in disease control rate DCR (75.5% vs 57.1%, χ2=2.931, P=0.087). Univariate analysis the median PFS, women were longer than men (6.9 months vs 4.5 months, χ2 =7.077, P=0.008). Non-smokers were longer than smokers (8.0 months vs 2.5 months, χ2 =15.277, P<0.001). Adenocarcinoma were longer than others pathological type (7.0 months vs 2.0 months, χ2 =14.978, P<0.001). The median PFS in BIM gene with no polymorphism type were longer than with polymorphism type (6.0 months vs 3.5 months, χ2=7.035, P=0.008). Multi-factor analysis showed that smoking, pathological type, the BIM gene polymorphism were the independent prognostic factors for PFS. Conclusion The patients with the BIM gene no polymorphism have longer the median progression-free time than the polymorphism types in retreatment advanced non-small cell lung cancer patients with tyrosine kinase inhibitor.