[1]逄宇,夏辉,姜广路,等. 中国结核分枝杆菌寡核苷酸基因分型及其耐药性分析.中华检验医学杂志,2011,34(11):1023-1028.[2]Zhao Y, Xu S, Wang L, et al. National survey of drug-resis-tant tuberculosis in China. N Engl J Med,2012,366(23):2161-2170.[3]丁海榕,秦川,占玲俊. 部分抗结核分枝杆菌药物的耐药机理研究进展. 中国防痨杂志, 2013,35(8): 615-620.[4]Louw GE, Warren RM, Gey van Pittius NC, et al. A balancing act: efflux/influx in mycobacterial drug resistance. Antimicrob Agents Chemother, 2009,53(8): 3181-3189.[5]Supply P, Allix C, Lesjean S, et al. Proposal for standardization of optimized mycobacterial interspersed repetitive unit-variable-number tandem repeat typing of Mycobacterium tuberculosis. J Clin Microbiol, 2006,44(12): 4498-4510.[6]王晓平,逄宇,赵晓,等.宁夏回族自治区结核分枝杆菌基因分型及与耐药性关系的研究. 中国防痨杂志, 2013,35(9): 655-659.[7]Leonard B, Coronel J, Siedner M, et al. Inter- and intra-assay reproducibility of microplate Alamar blue assay results for isoniazid, rifampicin, ethambutol, streptomycin, ciprofloxacin, and capreomycin drug susceptibility testing of Mycobacterium tuberculosis. J Clin Microbiol, 2008,46(10): 3526-3529.[8]Gupta AK, Katoch VM, Chauhan DS, et al. Microarray ana-lysis of efflux pump genes in multidrug-resistant Mycobacterium tuberculosis during stress induced by common anti-tuberculous drugs. Microb Drug Resist, 2010,16(1): 21-28.[9]李桂莲, 王撷秀, 谢彤, 等. 药物外排泵基因表达与结核分枝杆菌耐药关系的探讨. 中华检验医学杂志, 2011, 34(7):605-611.[10]Baysarowich J, Koteva K, Hughes DW, et al. Rifamycin antibiotic resistance by ADP-ribosylation: Structure and diversity of Arr. Proc Natl Acad Sci U S A, 2008,105(12): 4886-4891.[11]Surcouf C, Heng S, Pierre-Audigier C, et al. Molecular detection of fluoroquinolone-resistance in multi-drug resistant tuberculosis in Cambodia suggests low association with XDR phenotypes. BMC Infect Dis,2011, (11):255.[12]Von Groll A, Martin A, Jureen P, et al.Fluoroquinolone resistance in Mycobacterium tuberculosis and mutations in gyrA and gyrB. Antimicrob Agents Chemother, 2009,53(10): 4498-4500.[13]Pasca MR, Guglierame P, Arcesi F, et al.Rv2686c-Rv2687c-Rv2688c, an ABC fluoroquinolone efflux pump in Mycobacte-rium tuberculosis. Antimicrob Agents Chemother, 2004,48(8): 3175-3178.[14]Rifat D, Bishai WR, Karakousis PC. Phosphate depletion: a novel trigger for Mycobacterium tuberculosis persistence. J Infectious Diseases, 2009, 200(7): 1126-1135.[15]Sarin J, Aggarwal S, Chaba R, et al. B-subunit of phosphate-specific transporter from Mycobacterium tuberculosis is a thermostable ATPase. J Biol Chem, 2001,276(48): 44590-44597.[16]Banerjee SK, Bhatt K, Misra P,et al. Involvement of a natural transport system in the process of efflux-mediated drug resis-tance in Mycobacterium smegmatis. Mol Gen Genet,2000,262(6):949-956.[17]Bhatt K, Banerjee SK, Chakraborti PK. Evidence that phosphate specific transporter is amplified in a fluoroquinolone resistant Mycobacterium smegmatis. Eur J Biochem,2000,267(13): 4028-4032.[18]Hughes D, Brandis G. Rifampicin resistance: fitness costs and the significance of compensatory evolution. Antibiotics, 2013, 2(2): 206-216.[19]Banerjee SK, Misra P, Bhatt K,et al. Identification of an ABC transporter gene that exhibits mRNA level overexpression in fluoroquinolone-resistant Mycobacterium smegmatis. FEBS Lett,1998,42(1):151-156. |