Silicon Investor (SI) -- The First Internet Community

STOCKTALK

We've detected that you're using an ad content blocking browser plug-in or feature. Ads provide a critical source of revenue to the continued operation of Silicon Investor. We ask that you disable ad blocking while on Silicon Investor in the best interests of our community. If you are not using an ad blocker but are still receiving this message, make sure your browser's tracking protection is set to the 'standard' level.

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

To: Tharos who wrote (6781)	7/23/1998 11:34:00 PM
From: aknahow	Read Replies (1) \| Respond to of 17367

Once you prove to my satisfaction that God is improbably not masculine, I will be happy to answer your question.

To: Tharos who wrote (6781)	7/30/1998 8:38:00 AM
From: Robert K.	Read Replies (2) \| Respond to of 17367

I wonder about those "thrombolytic" properties of bpi........................> >>Acute infectious purpura fulminans: pathogenesis and medical management. Darmstadt GL Department of Pediatrics, Children's Hospital and Regional Medical Center, University of Washington School of Medicine, Seattle 98105, USA. gdarms@chmc.org [Medline record in process] Purpura fulminans (PF) is a potentially disabling and life-threatening disorder characterized by acute onset of progressive cutaneous hemorrhage and necrosis, and disseminated intravascular necrosis. Acute infectious PF occurs most commonly in the setting of meningococcemia due to elaboration of endotoxin. Presence of purpura, particularly when generalized, is an important predictor of a poor outcome following meningococcal infection. Histopathologic hallmarks of acute infectious PF are dermal vascular thrombosis and secondary hemorrhagic necrosis, findings which are identical to those of the Shwartzman reaction. Acute infectious PF and the Shwartzman reaction have a common pathogenesis, involving a disturbance in the balance of anticoagulant and procoagulant activities of endothelial cells. This disturbance, which is triggered by endotoxin, appears to be mediated by cytokines, particularly interleukin-12, interferon-gamma, tumor necrosis factor-alpha, and interleukin-1, leading to the consumption of proteins C and S and antithrombin III. State-of-the-art therapeutic interventions based on recent advances in our understanding of the pathogenesis of acute infectious PF are discussed.