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

To: hirogen who wrote (2280)	8/29/2013 11:26:53 AM
From: scaram(o)uche	Respond to of 2344

>> otherwise Merck would have designed the trial to exclude sCRT << Of course. ;-) But they also wanted to launch with good geographies and as many centers as possible. >> overstated << They are what they are, from one very large trial. You and others might believe that the result are "overstated" in that they would not repeat in a large trial restricted to cCRT. I would prefer to understand the results that we have, and it is established, 2013, that cCRT and sCRT groups are different creatures. And, no, I don't know squat about the phase II results, thanks for sharing any that you can. I am relatively new to onty. Welcome to S.I.! Rick edit: just going to paste this here.... I'll post ANYTHING that even hints at a potential indication for pet-lipid-A, as Kirkman et al. are bragging about the sucker but not apparently doing anything innovative with it...... J Mol Endocrinol. 2013 Aug 22. [Epub ahead of print] Lipopolysaccharide Inhibits the Expression of Resistin in Adipocytes. Xiang X, An W, Jiang C, Zhao J, Wang X, Sun G, Li Y, Zhang W. Department of Physiology and Pathophysiology, Peking University Health Science Center, China. Resistin is an adipocytokine leading to insulin resistance. Endotoxin/lipopolysaccharide (LPS) has been reported to decrease the expression of resistin mRNA and protein in both lean and db/db obese mice, although the underlying mechanism remains unclear. Several models such as ex vivo culture of adipose tissues, primary rat adipocytes and 3T3-L1 adipocytes were used to further characterize the effect of LPS on the expression of resistin. LPS attenuated both the resistin mRNA and protein in a time- and dose-dependent manner. In the presence of actinomycin D, LPS failed to reduce the half-life of resistin mRNA, suggesting a transcriptional mechanism. The lipid A fraction is crucial for the inhibition of resistin expression induced by LPS. Pharmacological intervention of c-Jun N-terminal kinase (JNK) reversed the inhibitory effect of LPS. LPS down-regulated CCAAT/enhancer-binding protein a (C/EBP-a) and peroxisome proliferator-activated receptor ? (PPAR-?), while activation of C/EBP-a or PPAR-? by either over-expressing these transcriptional factors or by rosiglitazone, an agonist of PPAR-?, blocked the inhibitory effect of LPS on resistin. C/EBP homologous protein (CHOP 10) was up-regulated by LPS, while a CHOP 10 antisense oligonucleotide reversed the decrement of resistin protein induced by LPS. Taken together, these results suggest that LPS inhibits resistin expression through a unique signaling pathway involving TLR4, JNK, CHOP 10, and C/EBP-a/PPAR-?.