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Biotech / Medical : CYTR: CytRx Corporation -- Ignore unavailable to you. Want to Upgrade?

To: mopgcw who wrote (12)	6/9/2008 2:40:27 PM
From: scaram(o)uche	Read Replies (1) \| Respond to of 51

Off 19% on the IVPH munch. Just glancing at yahoo with no appreciation or knowledge of real-world issues.... they hold 49% of RXII, trading at a capitalization of $100m (13X book). Know anything about why rxii might trade at that multiple to book? Yahoo lists current cash at cytr as 43m and the intraday capitalization as 73m. Current projects include a phase II shot on ALS goal, but look relatively long-shot worthless? In any event, decided to take my first RNAi shot and just bought a few shares at 0.82. Reverse split coming, looks like, so perhaps a stooooooopid move. Was the predominant buyer of ivph at a dime a few weeks ago, but there were only about 60K shares available.... not enough to cover the losses from shares purchased at north of two bucks. Was also the predominant seller this morning at 0.35, and sold it all. Not much out there on the "chaperone enhancers", not that I can care much. Latest that I've found........ Stroke. 2008 Mar;39(3):1022-4. Epub 2008 Jan 31. Reverse regulation of endothelial cells and myointimal hyperplasia on cell proliferation by a heatshock protein-coinducer after hypoxia. Denes L, Bori Z, Csonka E, Entz L, Nagy Z. BACKGROUND AND PURPOSE: Myointimal hyperplasia (MIH) cells are related to permanent upregulated proliferation as tumor-like cells. The aim of this study is to assess whether treatment of cells after hypoxia by Iroxanadine heat-shock protein (HSP-coinducer) predicts recovery through cell proliferation. METHODS: Vascular smooth muscle cells (VSMC) and brain capillary endothelial cells (HBEC) were isolated from human origin and MIH-cells from early carotid restenosis after surgery. Cell proliferation was quantified by bromuridine (BrdU) incorporation after hypoxia/reoxygenation. HSP72 and cyclin-dependent kinase (CDKN1A) mRNA expression was assessed by reverse transcription-polymerase chain reaction (PCR) and cell cycle distribution by flow cytometry (FACS) analysis. RESULTS: After hypoxia/reoxygenation, the proliferation of MIH-cells increased, whereas endothelial cells decreased (MIH: 0.266+/-0.016 versus 0.336+/-0.024; P<0.05; HBEC: 1.249+/-0.10 versus 0.878+/-0.11; P<0.05). Whereas augmented proliferation of MIH-cells was reduced (40% to 45%) by HSP-coinducer, diminished HBEC proliferation increased (46.2%). Stress-activated-protein-kinase (SAPK)p38-dependent cell cycle redistribution was generated by an increase in HSP72 and CDKN1A mRNA levels in MIH-cells. CONCLUSIONS: The 2 key players of early restenosis (MIH, EC) were oppositely regulated and correspondingly after treatment by HSP-coinducer reverse recovered. Drug candidate may have therapeutic potential in (re)restenosis.