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

To: Robert S. who wrote (7770)	11/19/1998 9:04:00 AM
From: Robert K.	Read Replies (2) \| Respond to of 17367

So you say bpi will have no effect on the other mediators of sepsis! What evidence.>> Read on. decide for yourself. Do you retract or not? > Infect Immun 1994 Sep;62(9):3930-6 Bactericidal/permeability-increasing protein protects vascular endothelial cells from lipopolysaccharide-induced activation and injury. Arditi M, Zhou J, Huang SH, Luckett PM, Marra MN, Kim KS Division of Infectious Diseases, Children's Hospital Los Angeles, University of Southern California School of Medicine 90027. Bactericidal/permeability-increasing protein (BPI), a human neutrophil granule protein, has been shown to bind lipopolysaccharide (LPS) and neutralize LPS-mediated cytokine production in adherent monocytes and the whole-blood system. In this study we investigated the ability of recombinant human BPI (rBPI) to inhibit LPS-induced vascular endothelial cell (EC) injury and activation. rBPI inhibited significantly both rough and smooth LPS-mediated injury for cultured bovine brain microvessel ECs, as measured by lactic dehydrogenase release, and blocked the LPS-induced interleukin-6 (IL-6) release from human umbilical vein ECs in a dose-dependent manner. BPI was able to inhibit LPS-mediated EC injury or activation whether it was added before or at the same time with LPS, but delaying the time of addition of rBPI resulted only in a partial inhibition. BPI also inhibited LPS-induced tumor necrosis factor alpha, IL-1 beta, and IL-6 release from human whole blood. This inhibition of tumor necrosis factor alpha, IL-1 beta, and IL-6 release from whole blood was maximal when BPI was premixed with LPS before addition to blood and was partial when BPI was added simultaneously with LPS, but no inhibition was observed when the addition of rBPI was delayed for 5 min. These findings suggest that rBPI is a potent inhibitor of LPS-mediated responses in ECs and whole blood and underscore the potential use of BPI in treatment or prevention of endotoxic shock. In contrast, the anti-lipid A monoclonal antibodies HA-1A and E5 were ineffective in inhibiting LPS-mediated EC injury and activation as well as LPS-induced cytokine release in whole blood.

To: Robert S. who wrote (7770)	11/19/1998 10:37:00 PM
From: Tharos	Respond to of 17367

>>Regardless of the "proof of concept" thesis, Wall Street does not get excited about therapeutic treatments that target small markets.<< Better said, "Regardless of the 'proof of concept' thesis, Wall Street does not get excited about therapeutic treatments that it perceives to target small markets." Viagra would be an excellent example of valuation re perception, but then Pfizer followed up on a secondary indication and built clinical trials targeted specifically at one indication, which is the sign of bad clinical practice according to your previous posts. >>Comparing the internet stocks with the biotech sector is ludicrous.<< Why?

To: Robert S. who wrote (7770)	11/20/1998 8:10:00 AM
From: Robert K.	Respond to of 17367

The main question, ( in case you forgot) > Your posting to me> >RobertK, you are, of course, entitled to your opinions: "Lets see. Bpi doesnt address the other mediators of sepsis you say. You better check your facts their dude. Major error IMO".(my view) Where is the evidence to support your claims? End Robert S. posting Questions again>> Does bpi affect the other mediators of sepsis? (in your opinion robert S.) Is that different than your previous view? Does that alter your view AT ALL? Curious. (all disclaimers)