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

To: Cacaito who wrote (7357)	9/28/1998 8:34:00 AM
From: Robert S.	Respond to of 17367

Cacaito, while I believe BPI has the potential to be of some use, I possess doubts as to this potential being realized, especially to the degree that some on this board suggest. General idea: some antibiotics kill the bacteria and release the endotoxins, others do not. The author is not sure what is better, if endotoxins are not release then some defense mechanisms are not started, but if they are a lot of inflammation comes by. BPI goes further, it helps in the killing, it helps regulate the immune defense response, and it regulates it with little if any inflammatory damage, plus other positive actions, like decreasing problems with intravascular coagulation and/or bleeding disorders. It appears BPI does play a role in the immune defense response, but the significance of this role is difficult to quantify and qualify without studying living beings that possess no BPI. Also, is it not true that the inflammation process inherently provides a strong defense versus gram-negative bacteria? In such cases, BPI seemingly would assume a relatively minor role.

To: Cacaito who wrote (7357)	9/28/1998 10:58:00 AM
From: Arthur Radley	Respond to of 17367

Not the Holy Grail but as close as you can get #reply-5857752

To: Cacaito who wrote (7357)	10/31/1998 4:23:00 PM
From: Robert S.	Read Replies (2) \| Respond to of 17367

Cacaito, the press release from Xoma on 10/30/98 contained the following excerpt: >>Endotoxin (lipopolysaccharide or LPS) is a structural component of gram-negative bacteria that can induce an overwhelming systemic inflammatory response. In patients exposed to bacterial endotoxins this reaction can cause complications that in severe cases can result in shock, organ failure and death. LBP, a key initiator of the inflammatory response, is secreted by the liver in direct response to exposure to bacterial endotoxin.<< The Holzheimer study addressed the conflicting evidence pertaining to the role of endotoxin in sepsis and you minimized this research as being a review and not original (Holzhiemer has been publishing since the 80's). The original article below appeared in the peer-reviewed journal The Lancet and the abstract also illustrates that the role of endotoxins in sepsis is indeed perplexing: Lancet 1993 May 1;341(8853):1133-5 Reappraisal of the role of endotoxin in the sepsis syndrome. Hurley JC Division of Infectious Diseases, Children's Hospital and Medical Center, Seattle, Washington 98105. There is strong evidence to implicate endotoxin released from gram negative bacteria in the pathogenesis of the sepsis syndrome and related conditions, but equally compelling data bring the role of endotoxin into doubt. Reappraisal of endotoxin and its release from gram negative bacteria suggests that it is not directly responsible for the complications of sepsis syndrome. Rather, release of endotoxin is a marker for the transition of gram negative organisms to cell-wall-deficient forms (L-forms) that may persist undetected despite antibiotic therapy directed against the parental form. This transition has two consequences in compromised patients: L-forms cause organ failure, and they serve as a sanctuary from which cell-wall-intact revertants may arise. Comments: Comment in: Lancet 1993 Jun 26;341(8861):1662