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本文引用的文献

1
Emergence of tetracycline resistance in Helicobacter pylori: multiple mutational changes in 16S ribosomal DNA and other genetic loci.幽门螺杆菌中四环素耐药性的出现:16S核糖体DNA及其他基因位点的多重突变变化
Antimicrob Agents Chemother. 2002 Dec;46(12):3940-6. doi: 10.1128/AAC.46.12.3940-3946.2002.
2
16S rRNA mutation-mediated tetracycline resistance in Helicobacter pylori.幽门螺杆菌中16S rRNA突变介导的四环素耐药性
Antimicrob Agents Chemother. 2002 Sep;46(9):2996-3000. doi: 10.1128/AAC.46.9.2996-3000.2002.
3
Mutations in the 16S rRNA genes of Helicobacter pylori mediate resistance to tetracycline.幽门螺杆菌16S rRNA基因的突变介导对四环素的耐药性。
J Bacteriol. 2002 Apr;184(8):2131-40. doi: 10.1128/JB.184.8.2131-2140.2002.
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Analysis of metronidazole, clarithromycin and tetracycline resistance of Helicobacter pylori isolates from Korea.韩国幽门螺杆菌分离株对甲硝唑、克拉霉素和四环素的耐药性分析。
J Antimicrob Chemother. 2001 Apr;47(4):459-61. doi: 10.1093/jac/47.4.459.
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How to treat Helicobacter pylori. First-line, second-line, and future therapies.
Gastroenterol Clin North Am. 2000 Dec;29(4):759-73, vii. doi: 10.1016/s0889-8553(05)70145-x.
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Isolation and characterization of tetracycline-resistant clinical isolates of Helicobacter pylori.幽门螺杆菌四环素耐药临床分离株的分离与鉴定
Antimicrob Agents Chemother. 2000 Nov;44(11):3203-5. doi: 10.1128/AAC.44.11.3203-3205.2000.
7
Resistance of helicobacter pylori to metronidazole, tetracycline and amoxycillin.幽门螺杆菌对甲硝唑、四环素和阿莫西林的耐药性。
J Antimicrob Chemother. 2000 Jul;46(1):121-3. doi: 10.1093/jac/46.1.121.
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Challenges to therapy in the future.
Helicobacter. 2000;5 Suppl 1:S23-6; discussion S27-31. doi: 10.1046/j.1523-5378.2000.0050s1023.x.
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Primary and combined resistance to four antimicrobial agents in Helicobacter pylori in Sofia, Bulgaria.保加利亚索非亚幽门螺杆菌对四种抗菌药物的原发性和联合耐药性
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Pretreatment antibiotic resistance in Helicobacter pylori infection: results of three randomized controlled studies.幽门螺杆菌感染的治疗前抗生素耐药性:三项随机对照研究的结果
Helicobacter. 1999 Jun;4(2):106-12. doi: 10.1046/j.1523-5378.1999.99002.x.

16S rRNA基因突变对幽门螺杆菌四环素耐药性的影响。

Effects of 16S rRNA gene mutations on tetracycline resistance in Helicobacter pylori.

作者信息

Gerrits Monique M, Berning Marco, Van Vliet Arnoud H M, Kuipers Ernst J, Kusters Johannes G

机构信息

Department of Gastroenterology and Hepatology, Erasmus MC-University Medical Center Rotterdam, Rotterdam, The Netherlands.

出版信息

Antimicrob Agents Chemother. 2003 Sep;47(9):2984-6. doi: 10.1128/AAC.47.9.2984-2986.2003.

DOI:10.1128/AAC.47.9.2984-2986.2003
PMID:12937008
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC182601/
Abstract

The triple-base-pair 16S rDNA mutation AGA(926-928)-->TTC mediates high-level tetracycline resistance in Helicobacter pylori. In contrast, single- and double-base-pair mutations mediated only low-level tetracycline resistance and decreased growth rates in the presence of tetracycline, explaining the preference for the TTC mutation in tetracycline-resistant H. pylori isolates.

摘要

三联碱基对16S rDNA突变AGA(926 - 928)-->TTC介导幽门螺杆菌对四环素的高水平耐药。相比之下,单碱基对和双碱基对突变仅介导低水平的四环素耐药,并且在四环素存在的情况下会降低生长速率,这解释了四环素耐药幽门螺杆菌分离株中对TTC突变的偏好。