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Louis J. Magnotti

Researcher at University of Medicine and Dentistry of New Jersey

Publications -  33
Citations -  1900

Louis J. Magnotti is an academic researcher from University of Medicine and Dentistry of New Jersey. The author has contributed to research in topics: Lung injury & Poison control. The author has an hindex of 21, co-authored 33 publications receiving 1749 citations. Previous affiliations of Louis J. Magnotti include University of Tennessee Health Science Center.

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Gut-derived mesenteric lymph but not portal blood increases endothelial cell permeability and promotes lung injury after hemorrhagic shock.

TL;DR: Gut barrier failure after hemorrhagic shock may be involved in the pathogenesis of shock-induced distant organ injury via gut-derived factors carried in the mesenteric lymph rather than the portal circulation.
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Burns, bacterial translocation, gut barrier function, and failure.

TL;DR: The goal of this review will be to provide a perspective on the evolution of the gut hypothesis of systemic inflammation and distant organ dysfunction.
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Temporary Abdominal Closure Techniques: A Prospective Randomized Trial Comparing Polyglactin 910 Mesh and Vacuum-Assisted Closure

TL;DR: MESH and VAC are both useful methods for abdominal coverage, and are equally likely to produce delayed primary closure, and neither method precludes secondary abdominal wall reconstruction.
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Gut-Derived Mesenteric Lymph A Link Between Burn and Lung Injury

TL;DR: The hypothesis that gut-derived factors carried in the mesenteric lymph contribute to burn-induced lung injury and may therefore play a role in postburn respiratory failure is supported and suggests that intestinal bacterial overgrowth primes the host such that when animals are exposed to a second stimulus (such as thermal injury) an exaggerated response occurs.
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Relationship between disruption of the unstirred mucus layer and intestinal restitution in loss of gut barrier function after trauma hemorrhagic shock.

TL;DR: Studies of intestinal permeability documented that T/HS-induced loss of gut barrier function persisted throughout the 3-hour reperfusion period and were associated with injury to the mucus layer as well as the villi.