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Biotech / Medical : GUMM - Eliminate the Common Cold -- Ignore unavailable to you. Want to Upgrade?

To: DanZ who wrote (1048)	10/10/1999 8:32:00 PM
From: out_of_the_loop	Respond to of 5582

The first article, the "sabotage" article, is from Washington U in St Louis and basically describes how the ICAM-1 (which indirectly activates T-cells) production is controlled by genes. The genes that control the production and expression of ICAM are influenced by the adenovirus. To make a long story short, the adenovirus subverts the whole ICAM production sequence by hijacking cellular machinery. This results in a decrease in T-cell activation so viral infections can last longer. Viruses stimulate production of interferon. The adenovirus has a way of making the interferon less effective. How does this have anything to do with Zicam? It is not entirely clear but, most likely has something to do with this: most cellular biochemical reactions have natural stimulators and inhibitors. Very often, the very product that is made by some genes will end up introducing a signal to the cell to stop making it once a threshold amount is reached. IF one believe the mechanism of action of Zicam is to bind the ICAM, somehow it is possible that the production of ICAM is downregulated (inhibited) by the interaction of ICAM and zicam. That is just a hypothesis at this time and nobody should think that anything about this article intimates that zicam has any effect on adenovirus infections. It does not. * The second article is from Silver Platter, a physicians' search service that describes and condenses articles and abstracts for the time-impaired. It describes a study in the British journal "Lancet" (British equivalent to NEJM) that involved supplying people with a history of allergy an altered allergen to see if the body reacted less to it than the usual allergen (dust mite allergen). The presence of ICAM was the marker of an inflammatory response. How does this relate to Zicam? Pretty much the same idea as above. If ICAM is a main inflammatory mediator, then whatever reduces ICAM production will potentially decrease the overall inflammatory response. * The third article is from Sweden. (se). I presume it is from Karolinska Hospital ("hospital in Swedish" is "sjukhuset", literally, sickhouse, thus the "ks" in a ll their e-mail addresses and "ki" in the URL likely stands for Karolinska Institute, the famous research institute associated with the hospital). I studied there in 1990 for a few months since they are famous for my subspecialty. Anyway, this is an interesting description of all the activities that go on in Dr. Scheynius' lab. It lists her graduate students and summarizes her projects. Cut to the chase: she has blocked allergic responses by blocking ICAM-1 and another mediator with monoclonal antibodies. How does this relate to Zicam? If zicam binds the ICAM and somehow causes a decreased production of it, then the inflammatory response and the symptoms associated with it may be decreased. *** Does Zicam prevent adenovirus infections? No. Does Zicam stop development of dust allergens? No. Does Zicam stop the allergy related to yeast? No. * What it may do for all these things is decrease the intensity of the inflammatory reaction by downregulating the expression of ICAM. Is this known now? NO. Can it be proven in time? Probably, yes, but don't expect anyone to even try until the second part of the second zicam studies (described in a previous press release) are done. If they are successful, then they might be tempted to try (my guess). If not, they probably wouldn't (also my guess).