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 : VD's Model Portfolio & Discussion Thread -- Ignore unavailable to you. Want to Upgrade?

To: Arthur Radley who wrote (8400)	11/1/2000 10:49:27 PM
From: scaram(o)uche	Respond to of 9719

Exciting work. However,what rights do they have to inosine itself for this use? None? If they have use rights, why are they looking downstream? Tox? BLSI is (IMO), and has always been (IMO), a bait and switch. For some time now, they have focused on good science. If they can keep the B&S game alive, some day they're going to make it. Look at the numbers on this chart, and don't listen to those who tell you that there's no relationship between BLSI and its predecessor.

To: Arthur Radley who wrote (8400)	11/1/2000 10:57:16 PM
From: scaram(o)uche	Respond to of 9719

Cary: Here's the abstract....... J Neurosci 2000 Nov 1;20(21):8031-41 A purine-sensitive pathway regulates multiple genes involved in axon regeneration in goldfish retinal ganglion cells. Petrausch B, Tabibiazar R, Roser T, Jing Y, Goldman D, Stuermer CA, Irwin N, Benowitz LI Laboratories for Neuroscience Research in Neurosurgery, Children's Hospital, Boston, Massachusetts, Department of Biology, University of Konstanz, Konstanz, Germany, Department of Biochemistry, Mental Health Research Institute, University of Michi. [Medline record in process] In lower vertebrates, retinal ganglion cells (RGCs) can regenerate their axons and reestablish functional connections after optic nerve injury. We show here that in goldfish RGCs, the effects of several trophic factors converge on a purine-sensitive signaling mechanism that controls axonal outgrowth and the expression of multiple growth-associated proteins. In culture, goldfish RGCs regenerate their axons in response to two molecules secreted by optic nerve glia, axogenesis factor-1 (AF-1) and AF-2, along with ciliary neurotrophic factor. The purine analog 6-thioguanine (6-TG) blocked outgrowth induced by each of these factors. Previous studies in PC12 cells have shown that the effects of 6-TG on neurite outgrowth may be mediated via inhibition of a 47 kDa protein kinase. Growth factor-induced axogenesis in RGCs was accompanied by many of the molecular changes that characterize regenerative growth in vivo, e.g. , increased expression of GAP-43 and certain cell surface glycoproteins. 6-TG inhibited all of these changes but not those associated with axotomy per se, e.g., induction of jun family transcription factors, nor did it affect cell survival. Additional studies using RGCs from transgenic zebrafish showed that expression of Talpha-1 tubulin is likewise stimulated by AF-1 and blocked by 6-TG. The purine nucleoside inosine had effects opposite to those of 6-TG. Inosine stimulated outgrowth and the characteristic pattern of molecular changes in RGCs and competitively reversed the inhibitory effects of 6-TG. We conclude that axon regeneration and the underlying program of gene expression in goldfish RGCs are mediated via a common, purine-sensitive pathway.

To: Arthur Radley who wrote (8400)	11/1/2000 11:39:30 PM
From: scaram(o)uche	Read Replies (1) \| Respond to of 9719

One other comment..... didn't we already hear about inosine from them, about a year ago? This seems like a very familiar story.