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High-molecular-weight polyethylene glycol prevents lethal sepsis due to intestinal Pseudomonas aeruginosa.
Chronic acid water feeding protects mice against lethal gut-derived sepsis due to Pseudomonas aeruginosa.
Depletion of intestinal phosphate after operative injury activates the virulence of P aeruginosa causing lethal gut-derived sepsis.
Structure-function aspects of PstS in multi-drug-resistant Pseudomonas aeruginosa.
Surgical injury and metabolic stress enhance the virulence of the human opportunistic pathogen Pseudomonas aeruginosa.
Prevention of siderophore- mediated gut-derived sepsis due to P. aeruginosa can be achieved without iron provision by maintaining local phosphate abundance: role of pH.
Pseudomonas aeruginosa potentiates the lethal effect of intestinal ischemia-reperfusion injury: the role of in vivo virulence activation.
Host stress and virulence expression in intestinal pathogens: development of therapeutic strategies using mice and C. elegans.
Pseudomonas aeruginosa virulence expression is directly activated by morphine and is capable of causing lethal gut-derived sepsis in mice during chronic morphine administration.
The intestinal environment of surgical injury transforms Pseudomonas aeruginosa into a discrete hypervirulent morphotype capable of causing lethal peritonitis.
Localization of DING proteins on PstS-containing outer-surface appendages of Pseudomonas aeruginosa.
Pseudomonas aeruginosa wound infection involves activation of its iron acquisition system in response to fascial contact.
Agent-based model of epithelial host-pathogen interactions in anastomotic leak.
Enterococcus faecalis exploits the human fibrinolytic system to drive excess collagenolysis: implications in gut healing and identification of druggable targets.