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.

Non-Tech : Bill Wexler's Dog Pound -- Ignore unavailable to you. Want to Upgrade?

To: Hank who wrote (1977)	7/12/1999 12:02:00 PM
From: out_of_the_loop	Read Replies (2) \| Respond to of 10293

Hank, I will answer these questions, but after that I am going to have to either be patient for me to get out from under a pile of work or do some dd yourself. While shorters have the ability to do their own dd, patients do not have the luxury of reading their biopsies from last Friday and the weekend. 1.Regarding the mechanism of action of Zicam vs cold-eze, you could make the argument that the mechanisms are the same but that the absorption of zinc from cold-eze is not predictable or precise (i.e., not repeatable among different people). While part of this is a compliance issue, a real objective look would tell you that the mechanism of action of Zicam, being direct and not requiring transport/diffusion/absorption, is truly different. Compare inhaled steroids with systemic steroids. Would a brain injury patient get the same dose as an allergy patient as a connective tiisue disease patient? No, of course not, but one could argue that the mechanism of action is similar in all three patients because of immunomodulation. Nobody would say that an allergy patient should get either the same dose or have it delivered the same way. Zicam is delivered to the cells at the site of infection. Rhinoviruses infect the nasal epithelium; I do not think that is debatable in 1999. 2. Regarding the mechanism of Zicam and different rhinoviruses, the Zicam remedy will work on any rhinovirus that uses this method of entry. The number of serotypes of rhinoviruses is the reason why there is no cold cure and no vaccine. You will have to wait for the study to see what they did in this regard, call or e-mail the company or look at the web site. This may not satisfy you and if that is the basis for your short, go ahead. Read my posts about who these people are, statistical significance of p,0.001, and confirm facts for yourself. 3. However, this is a developing area with the literature also developing. Here is a reference below that talks about zinc and intercellular adhesion molecules - rhinoviruses are mentioned, but You may have to go to the text of the article and the discussion. The abstract does not say exactly what you want me to have it say, but the fact is that the mechanisms are highly plausible and being studied by basic scientists. That is all I have time for now. I have 116 cases waiting but who is counting... Again, I have answered all questions here as honest and thorough as I could; most (read:"all") of these things have been discussed on the Yahoo and SI GUMM threads.. My advice is to either go ahead and short or do your own dd. The same is true regarding your questions about other drug companies, patent protection, etc. If you forget science for a second and think on economic terms, if you want to go short based on what you might consider incomplete data, when it is fact Zicam will be in more than 40,000 stores in the USA within 8-12 weeks, that is entirely your prerogative. Again you may call the company and check the literature yourself regarding the qualifications of the Gel Tech scientists. ***************************** ***************************** Here is the reference: Molecular mechanisms of zinc-dependent leukocyte adhesion involving the urokinase receptor and beta2-integrins. Chavakis T, May AE, Preissner KT, Kanse SM Blood (1999 May 1) 93(9):2976-83 ISSN: 0006-4971 Antigens, CD18 Leukocytes Receptors, Cell Surface Vitronectin Zinc Antibodies, Monoclonal Cations, Divalent Cell Adhesion Chelating Agents Cobalt Copper Fibrinogen Human Kinetics Manganese Nickel Phenanthrolines Plasminogen Activator Inhibitor 1 Support, Non-U.S. Gov't Tetradecanoylphorbol Acetate Urokinase U937 Cells Medline Database Healthstar Database Cancerlit Database Abstract The trace element Zinc (Zn2+) has been implicated as a mediator in host defense, yet the molecular basis for its extracellular functions remains obscure. Here, we demonstrate that Zn2+ can induce the adhesion of myelomonocytic cells to the endothelium, as well as to the provisional matrix proteins vitronectin (VN) and fibrinogen (FBG), which are pivotal steps for the recruitment of leukocytes into inflamed/injured tissue. Physiologic concentrations of Zn2+ increased the urokinase receptor (uPAR)-mediated adhesion of myelomonocytic cells to VN, whereas other divalent cations had smaller effects. Zn2+- induced cell adhesion to VN was abolished by cation chelators such as 1-10-phenanthroline, as well as by plasminogen activator inhibitor-1 (PAI-1) and a monoclonal antibody (MoAb) against uPAR. These characteristics could be recapitulated with a uPAR-transfected cell line emphasizing the specificity of this receptor system for Zn2+- dependent cell adhesion. Like urokinase (uPA), Zn2+ increased the binding of radiolabeled VN to uPAR-expressing cells, as well as the interaction of VN with immobilized uPAR in an isolated system. Moreover, Zn2+ enhanced leukocytic cell adhesion to FBG and endothelial cell monolayers by activating beta2-integrins. Instead of the direct beta2-integrin activation through the divalent cation binding site, Zn2+-induced integrin activation was mediated via uPAR, a crucial regulator of this system. The present study uncovers for the first time Zn2+-mediated cell adhesion mechanisms that may play a crucial role in modulating leukocyte adhesion to vessel wall components. </b.