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Biotech / Medical : XOMA. Bull or Bear? -- Ignore unavailable to you. Want to Upgrade?

To: LarryS who wrote (6407)	6/2/1998 10:20:00 PM
From: aknahow	Respond to of 17367

Larry, lets see, you have a recollection of something you don't remember, but you think I should? Gee, even Yahoo is easier! By summer XOMA thought or wanted to have 40 hospitals as sites for the trials. Don't believe there is anything else expected for Trauma this soon.

To: LarryS who wrote (6407)	6/4/1998 12:13:00 AM
From: aknahow	Respond to of 17367

Larry, this might be what you were asking about. Think it happened in June or November. Or perhaps it's a answer to a question you might have asked in 1995 or will ask in the future. Liver Failure Induces a Systemic Inflammatory Response Prevention by Recombinant N-Terminal Bactericidal/Permeability-Increasing Protein The American Journal of Pathology: Volume 147, Number 05; Pages: 1428-1440; November 1995 Marja A. Boermeester, Alexander P. J. Houdijk, Sybren Meyer, Miguel A. Cuesta, Ben J. Appelmelk, Robert I. C. Wesdorp, C. Erik Hack, Paul A. M. Van Leeuwen c 1995 by the American Society for Investigative Pathology The observed increased susceptibility of patients with fulminant hepatic failure for local and systemic infections has been hypothesized to be due to a failure of the hepatic clearance function and subsequent leaking of endogenous endotoxins into the systemic circulation. However, experimental evidence for such a systemic inflammation during liver failure due to endogenous endotoxemia is lacking. Therefore, we designed a study to clarify whether circulating endotoxins due to liver failure could lead to the development of systemic inflammation. In a rat model for liver failure induced by a two-thirds partial hepatectomy, we evaluated the course of circulating tumor necrosis factor and interleukin-6, changes in blood chemistry and hemodynamics, and histopathological changes in the lungs. Partially hepatectomized animals, but not sham-operated animals, demonstrated cardiac failure, increased levels of creatinin and urea, metabolic acidosis, high plasma levels of tumor necrosis factor and interleukin-6, and an influx of PMNs in the lungs-together indicating the development of a systemic inflammatory response. Continuous infusion of recombinant N-terminal bactericidal/permeability-increasing protein (rBPI23), a well described endotoxin-neutralizing protein, prevented these inflammatory reactions. Ex vivo experiments with rat plasma samples confirmed the presence of circulating endotoxins in partially hepatectomized rats as opposed to those treated with rBPI23. Thus, our results indicate that the early phase of liver failure induces a systemic inflammatory response triggered by circulating endotoxins, which can be prevented by perioperative infusion of rBPI23.