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The utility of pathway selective estrogen receptor ligands that inhibit nuclear factor-κB transcriptional activity in models of rheumatoid arthritis 英文参考文献.docVIP

The utility of pathway selective estrogen receptor ligands that inhibit nuclear factor-κB transcriptional activity in models of rheumatoid arthritis 英文参考文献.doc

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The utility of pathway selective estrogen receptor ligands that inhibit nuclear factor-κB transcriptional activity in models of rheumatoid arthritis 英文参考文献

Available online /content/7/3/R427 Research article Open Access Vol 7 No 3 The utility of pathway selective estrogen receptor ligands that inhibit nuclear factor-κB transcriptional activity in models of rheumatoid arthritis James C Keith Jr1, Leo M Albert1, Yelena Leathurby1, Max Follettie2, Lili Wang2, Lisa Borges- Marcucci3, Christopher C Chadwick4, Robert J Steffan5 and Douglas C Harnish3 1Cardiovascular and Metabolic Disease Research, Wyeth Research, Cambridge, MA, USA 2Department Biological Technologies, Cambridge, MA, USA 3Cardiovascular and Metabolic Disease Research, Collegeville, PA, USA 4Womens Health Research Institute, Collegeville, PA, USA 5Chemical and Screening Sciences, Collegeville, PA, USA Corresponding author: Douglas C Harnish, harnisd@ Received: 3 Jun 2004 Revisions requested: 29 Jun 2004 Revisions received: 12 Jan 2005 Accepted: 17 Jan 2005 Published: 21 Feb 2005 Arthritis Research Therapy 2005, 7:R427-R438 (DOI 10.1186/ar1692) ? 2005 Keith et al.; licensee BioMed Central Ltd. /content/7/3/R427 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (/licenses/by/ 2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Rheumatoid arthritis (RA) is a chronic inflammatory disease that suppresses the adjuvant induction of three serum acute phase proteins: haptoglobin, α1-acid glycoprotein (α1-AGP), and C- reactive protein (CRP). Gene expression experiments also demonstrate a global suppression of adjuvant-induced gene expression in the spleen, liver, and popliteal lymph nodes. Finally, WAY-169916 was effective in suppressing tumor necrosis factor-α-mediated inflammatory gene expression in fibroblast-like synoviocytes isolated from patients with RA. Together, these data suggest the utility of WAY-169916, and other compounds in its class, in treating RA th

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