PEPTIDOGLYCAN ANALYSIS OF VSE AND VRE

VSE 和 VRE 的肽聚糖分析

• 批准号: 8361373
• 负责人: JACOB SCHAEFER
• 金额: $ 1.08万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-01-01 至 2011-12-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8361373
• 关键词: Anabolism; Antibiotics; Binding Sites; Categories; Cell Death; Cell Wall; Enterococcus; Enterococcus faecium; Funding; Glycopeptides; Grant; Hospitals; Human; Incidence; Infection; Mass Spectrum Analysis; National Center for Research Resources; Penicillins; Peptidoglycan; Pharmaceutical Preparations; Principal Investigator; Problem Solving; Research; Research Infrastructure; Resistance; Resort; Resources; Source; United States National Institutes of Health; Vancomycin; biomedical resource; cost; pathogen

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Enterococcus faecium, an opportunistic pathogen, causes a substantial proportion of enterococcal human infections, particularly in hospitals. Due to the intrinsic resistance that enterococci demonstrate towards many categories of antibiotics (e.g., penicillins), the most successful treatment has been glycopeptides. Glycopeptides cause bacterial cell death by perturbing the integrity of the cell wall. The most powerful glycopeptide, the so-called "drug of last resort," is vancomycin. However, the incidence of infections resistant to vancomycin has increased rapidly since 1988. Solving the problem of enterococcal resistance requires an understanding of the biosynthesis and organization of the cell-wall peptidoglycan, a potential binding site of vancomycin.

这个子项目是许多利用资源的研究子项目之一 由NIH/NCRR资助的中心拨款提供。子项目的主要支持 子项目的主要研究者可能是由其他来源提供的， 包括其他NIH来源。 列出的子项目总成本可能 代表子项目使用的中心基础设施的估计数量， 而不是由NCRR赠款提供给子项目或子项目工作人员的直接资金。 屎肠球菌是一种机会致病菌，引起相当大比例的肠球菌人类感染，特别是在医院。 由于肠球菌对许多种类的抗生素表现出内在的耐药性（例如，青霉素类），最成功的治疗是糖肽类。 糖肽通过扰乱细胞壁的完整性引起细菌细胞死亡。 最强大的糖肽，所谓的“最后的药物”，是万古霉素。 然而，自1988年以来，万古霉素耐药感染的发生率迅速增加。 解决肠球菌耐药问题需要了解细胞壁肽聚糖（万古霉素的潜在结合位点）的生物合成和组织。