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https://www.selleckchem.com/products/vcmmae.html Siderophore-microcins are antimicrobial peptides produced by enterobacteria, especially Escherichia coli and Klebsiella pneumoniae strains. The antibiotic peptide is post-translationally modified by the linkage of a siderophore moiety. Therefore, it can enter and kill phylogenetically related bacteria by a "Trojan Horse" stratagem, by mimicking the iron-siderophore complexes. Consequently, these antimicrobial peptides are key determinants of bacterial competition within the intestinal niche, which is the reservoir for pathogenic E. coli. The most frequent extraintestinal infections caused by E. coli are urinary tract infections. Uropathogenic E. coli (UPEC) can produce many virulence factors, including siderophore-microcins. Siderophore-microcins are chromosomally encoded by small genomic islands that exhibit conserved organization. In UPEC, the siderophore-microcin gene clusters and biosynthetic pathways differ from the "archetypal" models described in fecal strains. The gene cluster is shorter. Thus, active siderophore-microcin production requires proteins from two other genomic islands that also code for virulence factors. This functional and modular synergy confers a strong selective advantage for the domination of the colonic niche, which is the first step toward infection. This optimization of genetic resources might favor the selection of additional virulence factors, which are essential in the subsequent steps of pathogenesis in E. coli infection. By the time an intervention is ready for evaluation in a definitive RCT the context of the evidence base may have evolved. To avoid research waste, it is imperative that intervention design and evaluation is an adaptive process incorporating emerging evidence and novel concepts. The aim of this study is to describe changes that were made to an evidence based intervention at the protocol stage of the definitive RCT to incorporate emerging evidence. The original eviden

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