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

To: John Patterson who wrote (6843)	7/30/1998 12:40:00 AM
From: Minos	Read Replies (2) \| Respond to of 17367

Threaders, As a long-time lurker, I want to commend everyone who contributes regularly to this thread for keeping the rest of us informed. Your knowledge of the underlying science behind XOMA is astounding -- much more than I can comprehend -- and your sharing of information is most generous. The science fascinates me even though it is over my head. Nevertheless, what I do understand is that we are approaching a 52 week low, and my small investment is getting smaller and smaller. My question: when, realistically, could we expect to see some meaningful appreciation in the stock price? Patience has never been one of my virtues, but I remain long....for the moment. Help me stay long rather than cutting and running. -Minos

To: John Patterson who wrote (6843)	7/30/1998 7:24:00 AM
From: Robert K.	Respond to of 17367

Sir Robin ,Sir Robin. While this isnt directly related, it does show the complexity of our task. Remember Robin Barkley> Posted that bpi might be promising on his website. He is a author here.(it appears)> > Proinflammatory mediator activity, endogenous antagonists and the systemic inflammatory response in intra-abdominal sepsis. Scottish Sepsis Intervention Group. Wakefield CH, Barclay GR, Fearon KC, Goldie AS, Ross JA, Grant IS, Ramsay G, Howie JC University Department of Surgery, Royal Infirmary, Edinburgh, UK. [Medline record in process] BACKGROUND: Severe intra-abdominal sepsis continues to carry a high mortality rate. The physiological response to sepsis in this condition and its relationship with proinflammatory mediators and their endogenous antagonists require further clarification. METHODS: Fifty-seven patients were stratified by Acute Physiology And Chronic Health Evaluation (APACHE) II score at the time of admission to an intensive care unit (group 1, score of less than 20; group 2, score of 20 or more). Serial measurements of clinical and immunological variables were made. RESULTS: Non-survivors from group 2 had a raised acute physiology score (P = 0.01), a higher peak serum interleukin (IL) 6 concentration (P = 0.03) and a depressed level of endogenous immunoglobulin (Ig) G class antiendotoxin core antibody (P = 0.005). In group 1, although organ failure score increased progressively in non-survivors, physiology score and peak IL-6 level were similar to those in survivors, and endogenous IgG class antiendotoxin core antibody titre rose (P = 0.02). In both groups IL-1 and tumour necrosis factor alpha were detected infrequently, but their natural antagonists were present in much higher concentrations in both survivors and non-survivors. Levels of C-reactive protein were raised in both but were not significantly different between survivors and non-survivors. CONCLUSION: During the development of organ failure and death, the pattern of proinflammatory mediators and their endogenous antagonists can vary markedly and may in part be determined by the extent of the initial physiological disturbance.