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Biotech / Medical : Biotech Valuation -- Ignore unavailable to you. Want to Upgrade?

To: IRWIN JAMES FRANKEL who wrote (30881)	4/10/2009 1:10:48 PM
From: Ian@SI	1 Recommendation Read Replies (1) \| Respond to of 52153

RE my 23andme comment: ... this is version 1. I suspect that it will evolve into a useful diagnostic tool;... I had intended to say PREVENTION tool. Even today, should one know of a genetic predisposition, it's possible to take preventive steps to minimize the risk. RE negative Vitamin D PR. I don't trust the researcher's motives. He opens by stating that 75% of Americans are deficient; then makes the erroneous statement that partial skin exposure to the sun for 10 minutes 3 days weekly is enough for anyone completely ignoring the fact that for most of the year, most Americans are not at a latitude where sunlight will cause the skin to produce Vit D. There's a multinational task force reviewing the current Vitamin D dosage recommendation and limits. There's a massive body of evidence that it should be raised. This is the most negative view I've ever seen. As such it's an outlier. On the other hand, I'm probably an outlier on the Pro Vit D side. Happy Easter all, Ian

To: IRWIN JAMES FRANKEL who wrote (30881)	4/10/2009 4:26:14 PM
From: Biomaven	1 Recommendation Read Replies (3) \| Respond to of 52153

I'd say that the article Ian posted is from the fringes. This group claims that autoimmune disease is caused by bacterial infection, which is certainly not a mainstream viewpoint. I did read the one article that was linked to, "Vitamin D: the Alternative Hypothesis" and noted the following passage: Double-blind and/or randomized controlled trials (RCTs) - as recently as 15 years ago, erroneously showed women taking combined hormone replacement therapy (HRT) had a lower-than average incidence of coronary heart disease (CHD). This led doctors to propose HRT was protective against CHD. Well unless I am very much mistaken, these early trials were not RCTs - they were observational trials. If these authors can make a mistake (or misrepresentation) like that, then I'm not sure how much credence to give the rest of their claims. But they do make a good point that things are often more complicated than they seem, and the "silver bullets" that seem so attractive are often deceptive. It is certainly possible that high or low levels of Vitamin D might act very differently at different stages of an autoimmune disease. A good example of how biology is even more complicated than it might first appear is a very recent article in Science that showed that NF-kappa B activation (a central driver of inflammation and immune response) responds differently to pulses of TNF-alpha depending on the frequency of the pulse: Science 10 April 2009: Vol. 324. no. 5924, pp. 242 - 246 DOI: 10.1126/science.1164860 Pulsatile Stimulation Determines Timing and Specificity of NF-{kappa}B-Dependent Transcription Louise Ashall,1* Caroline A. Horton,1* David E. Nelson,1* Pawel Paszek,1* Claire V. Harper,1 Kate Sillitoe,1 Sheila Ryan,1 David G. Spiller,1 John F. Unitt,2 David S. Broomhead,3 Douglas B. Kell,4 David A. Rand,5 Violaine Sée,1 Michael R. H. White1{dagger} The nuclear factor {kappa}B (NF-{kappa}B) transcription factor regulates cellular stress responses and the immune response to infection. NF-{kappa}B activation results in oscillations in nuclear NF-{kappa}B abundance. To define the function of these oscillations, we treated cells with repeated short pulses of tumor necrosis factor–{alpha} at various intervals to mimic pulsatile inflammatory signals. At all pulse intervals that were analyzed, we observed synchronous cycles of NF-{kappa}B nuclear translocation. Lower frequency stimulations gave repeated full-amplitude translocations, whereas higher frequency pulses gave reduced translocation, indicating a failure to reset. Deterministic and stochastic mathematical models predicted how negative feedback loops regulate both the resetting of the system and cellular heterogeneity. Altering the stimulation intervals gave different patterns of NF-{kappa}B–dependent gene expression, which supports the idea that oscillation frequency has a functional role.