Publications by authors named "Luyer M"

Objective: To investigate the effects of high-lipid enteral nutrition in a setting of developing inflammation and tissue damage.

Background: An excessive inflammatory response following severe trauma is associated with poor clinical outcome. Currently, therapies directed at attenuation of an ongoing inflammatory cascade are lacking.

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Purpose Of Review: In clinical research, increased permeability has been scrutinized as a potential indicator of the severity of gastrointestinal disease and as a potential cause of the perpetuation of severe inflammatory activity in infectious states. This review discusses old and recent epidemiological and clinical evidence to establish whether increased permeability in sepsis is a sequel or a cause of multiple organ failure. In addition, old and new evidence linking inflammation and permeability in abnormal gastrointestinal anatomy and function to liver abnormalities in susceptible patients will be reviewed.

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Article Synopsis
  • - The study investigates the impact of high-fat enteral nutrition on liver injury in a rat model following hemorrhagic shock.
  • - Rats were either starved or fed low-fat or high-fat diets before exposure to hemorrhagic shock, and various markers of liver damage and stress responses were measured.
  • - Results showed that high-fat diet significantly reduced liver injury and stress protein activation compared to low-fat and starved groups, suggesting potential protective effects of high-fat nutrition, though the underlying mechanism remains unclear.
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Objective: To investigate the role of bacterial DNA in development of an excessive inflammatory response and loss of gut barrier loss following systemic hypotension.

Summary Background Data: Bacterial infection may contribute to development of inflammatory complications following major surgery; however, the pathogenesis is not clear. A common denominator of bacterial infection is bacterial DNA characterized by unmethylated CpG motifs.

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The immune system in vertebrates senses exogenous and endogenous danger signals by way of complex cellular and humoral processes, and responds with an inflammatory reaction to combat putative attacks. A strong protective immunity is imperative to prevent invasion of pathogens; however, equivalent responses to commensal flora and dietary components in the intestine have to be avoided. The autonomic nervous system plays an important role in sensing luminal contents in the gut by way of hard-wired connections and chemical messengers, such as cholecystokinin (CCK).

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Probiotic therapy modulates the composition of the intestinal flora and inhibits the inflammatory response. These properties may be of benefit in the preservation of gut barrier integrity after injury or stress. In this study, we examined the effect of two Lactobacillus strains selected for their pathogen exclusion properties on intestinal barrier integrity following hemorrhagic shock.

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Background/aims: Cholestatic patients are prone to septic complications after major surgery due to an increased susceptibility to endotoxin and hypotension. High-fat enteral nutrition reduces endotoxin after hemorrhagic shock. However, it is unknown whether this nutritional intervention is protective in biliary obstruction.

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Objective: To determine whether potential enhancement of endotoxin neutralization via high-fat enteral nutrition affects endotoxemia and bacterial translocation after hemorrhage.

Summary Background Data: Endotoxin and bacterial translocation due to gut barrier failure are important initiating events in the pathogenesis of sepsis after hemorrhage. Systemic inhibition of endotoxin activity attenuates bacterial translocation and distant organ damage.

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Gram-negative sepsis is a potentially fatal clinical syndrome characterized by a proinflammatory response (tumor necrosis factor-alpha) to bacterial (endo)toxins and gut barrier function loss. Recently, we found that high-fat enteral nutrition protects against late bacterial translocation in a model of hemorrhagic shock in rats. However, the basis for this protection is unknown.

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Estrogen replacement therapy decreases the risk of arterial disease while at the same time increases the risk for venous thrombosis. Whether a common mechanism(s) of coagulation and inflammation contributes to both responses is unclear. This study determined simultaneous effects of estrogen replacement therapy on regulators of the direct (extrinsic) pathway for activation of coagulation, coagulation, and the acute phase response.

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