tailieunhanh - Báo cáo y học: "New approaches to combating antimicrobial drug resistance"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Minireview cung cấp cho các bạn kiến thức về ngành y đề tài: New approaches to combating antimicrobial drug resistance. | Minireview New approaches to combating antimicrobial drug resistance Matthew B Avison Address Department of Cellular and Molecular Medicine Bristol Centre for Antimicrobial Research and Evaluation University of Bristol School of Medical Sciences University Walk Bristol BS8 1TD UK. E-mail Published 23 December 2005 Genome Biology 2005 6 243 doi gb-2005-6-l3-243 The electronic version of this article is the complete one and can be found online at http 2005 6 13 243 2005 BioMed Central Ltd Abstract Recent work shows that the inhibition of the SOS stress response in Escherichia coli reduces the development of resistance to the antibiotics ciprofloxacin and rifampicin. This finding may help in the battle against the rise of resistance to antimicrobial drugs. Bacterial resistance to antimicrobial drugs is currently receiving much publicity and political attention. The cost to health services around the world is counted in billions of dollars an increase in morbidity and mortality are the costs to those infected. The problem is getting worse and treatment options for combating bacteria resistant to multiple drugs are narrowing. Unless something is done we may well return to the horrors of the pre-antibiotic era. In a recent article Cirz and colleagues 1 report the interesting finding that the rate of resistance to some drugs in Escherichia coli can be greatly reduced by interfering with a bacterial stress response. This article sets the work by Cirz et al. 1 in the general context of antimicrobial drug resistance and discusses whether this new finding could be helpful in the battle against the rise of drug-resistant bacteria. Are mutation-busting drugs the answer to the problem of drug resistance Resistance to antimicrobials occurs in four main ways Figure 1 . The first possible mechanism is the mutation of the drug s target a classic example of this is the mutation of gyrA encoding the essential DNA gyrase A subunit

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