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David G. Hesse

Researcher at NewYork–Presbyterian Hospital

Publications -  16
Citations -  5311

David G. Hesse is an academic researcher from NewYork–Presbyterian Hospital. The author has contributed to research in topics: Tumor necrosis factor alpha & Cytokine. The author has an hindex of 13, co-authored 16 publications receiving 5259 citations. Previous affiliations of David G. Hesse include Cornell University.

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Anti-cachectin/TNF monoclonal antibodies prevent septic shock during lethal bacteraemia

TL;DR: Protection against shock, vital organ dysfunction, persistent stress hormone release and death was conferred by administration of antibodies 2 h before bacterial infusion, indicating that cachectin is a mediator of fatal bacteraemic shock and suggesting that antibodies against Cachectin offer a potential therapy of life-threatening infection.
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Cachectin/tumor necrosis factor induces cachexia, anemia, and inflammation.

TL;DR: Data suggests that the exposure of the normal host to cachectin is capable of inducing a pathophysiological syndrome of cachexia, anemia, and inflammation similar to that observed during inflammatory states or malignancy.
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Antibodies to cachectin/tumor necrosis factor reduce interleukin 1 beta and interleukin 6 appearance during lethal bacteremia.

TL;DR: It is suggested that cachectin/TNF is essential for the initiation or amplification of IL-1 and IL-6 release during lethal gram-negative septic shock syndrome.
Journal Article

Cytokine appearance in human endotoxemia and primate bacteremia.

TL;DR: The results suggest that the transient release of cachectin/TNF, followed by interleukin-1 and interferon-gamma, may participate in the cascade of events noted in overwhelming bacterial invasion.
Journal Article

Cachectin/tumor necrosis factor induces lethal shock and stress hormone responses in the dog

TL;DR: Cachectin appears to occupy a crucial role in physiopathologic responses to infection, and likely participates in the mobilization of host energy stores, intravascular depletion and shock after lethal endotoxemia.