Cell Receptor Identified As Target For Anti-inflammatory Immune ... Science Daily (press release) - Nov 29, 2008 ... effects of a common anti-inflammatory drug, intravenous immunoglobulin (IVIG). The finding opens up new possibilities for developing drugs to suppress ...
Smart drug implant has batteries included New Scientist (subscription), UK - ... Australia, made use of this to make a biobattery from a magnesium alloy anode and a conducting polymer cathode that carried an anti-inflammatory drug. ...
Mayo Clinic Seeks New Therapies for Alcoholic Hepatitis MarketWatch - Etanercept is approved for treatment of inflammatory arthritis and is under investigation for effectiveness in treating other inflammatory conditions. ...
MicroRNA Blocker Prevented Heart Failure In Mice Medical News Today, UK - They also targeted miR-21 and prevented heart failure in laboratory mice by using a new experimental drug called antisense oligonucleotide (an anti- miR-21 ...
Drugs you can't have Stuff.co.nz, New Zealand - Nov 30, 2008 Anti-retrovirals for HIV/Aids: Eamonn Smythe, director of positive health at the Aids Foundation, says five years ago New Zealand was six HIV drugs behind ...
Learn about the World Ophthalmic Pharmaceutical Drugs Market MarketWatch - Nov 25, 2008 ... Clinical Efficacy of Steroids II-22 Topical Corticosteroid Drugs II-22 Tapering of Steroid Intake II-23 Non-Steroids Anti Inflammatory Drugs (NSAID) ...
James LeFanu: Doctor's Diary Telegraph.co.uk, United Kingdom - ... and heart attacks, or the closely related non-steroidal anti-inflammatory drugs such as ibuprofen for the relief of aches and pains of arthritis. ...
Cyberchondriacs may be getting bad advice CalorieLab Calorie Counter News, NV - Nov 30, 2008 For example, the page on the anti-inflammatory drug Arthrotec failed to mention it can cause miscarriages, and the HIV drug Prezista shouldn?t be taken with ...
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Recent News and Articles on the Keywords: new + 739 + web Related to the article below (Last Update: 8/7/2008)
Signups and Tryouts Asbury Park Press, NJ - Telephone Fred Liguori at (732) 739-6493, e-mail nando739@verizon.net or visit the Web at www.hazletsoccer.org for additional information. ...
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AT THE COLLEGES ; Bryant University RedOrbit, TX - Aug 3, 2008 For more information, call (401) 739-5000 or visit the Web at www.neit.edu. Appointed: Douglas Sherman, of Cranston, has been appointed associate provost ...
NOTHIN' BUT NET: Favre chatter nonstop on new Web site North County Times, CA - Jul 19, 2008 Contact Bair at (760) 739-6642 or sbair@nctimes.com if you think the former UCLA quarterback should come out of retirement, too. We'll start a Web site.
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Internap Reports Second Quarter 2008 Financial Results StreetInsider.com (subscription), MI - Aug 5, 2008 This information is also available on our Web site under the Investor Services heading. Internap's first quarter 2008 conference call will be held today at ...INAP
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Selective inhibitors of mPGES-1, a new class of anti-inflammatory drugs that might lessen chance of COX-2 cardiovascular events
Researchers at the University of Pennsylvania School of Medicine have clarified the mechanism by which drugs like Celebrex and Vioxx cause heart problems, in multiple animal models.
The findings offer the prospect of a new generation of anti-inflammatory drugs that bypass this issue.
Ever since the association of selective inhibitors of COX-2 – Vioxx ( Rofecoxib ), Bextra ( Valdecoxib ), and Celebrex ( Celecoxib ) - with an increased incidence of heart attack and stroke, there has been intense interest in understanding the mechanism involved. Clarification of this issue offers the prospect of conserving the clinical benefit of these drugs for patients with arthritis, while managing the risk.
Almost 10 years ago, FitzGerald noticed that both Celebrex and Vioxx depressed in healthy individuals a protective fat called prostacyclin, while leaving unaltered a harmful one called thromboxane. This led him to predict that drugs in this class might confer a cardiovascular risk before either reached the US market.
In the study, published in the Journal of Clinical Investigation, the researchers used multiple genetically manipulated mice - including mice that mimicked the impact of either COX-2 inhibitors or low-dose aspirin and compared them with treating healthy mice with COX-2 inhibitors.
They found that genetic disruption of COX-2; inhibition of the enzyme by different inhibitors; and disruption of effects of prostacyclin by removing its receptor all had the same effect - a predisposition to clotting and an elevation of blood pressure.
The researchers also addressed the likely benefit of adding Aspirin to diminish this effect of the inhibitors. Surprisingly, this appeared to reduce not only the clotting response, but also the rise in blood pressure caused by COX-2 inhibitors.
A surprising finding came when the researchers turned to a drug target that might substitute for COX-2 - an enzyme called microsomal prostaglandin E synthase ( mPGES )-1.
Other studies had shown previously that deletion of this enzyme seemed as effective as treatment with NSAIDs in models of pain and inflammation.
FitzGerald and his colleagues showed that deletion of mPGES-1, in contrast to deletion or inhibition of COX-2, did not predispose the animals to thrombosis or elevate blood pressure.
Source: University of Pennsylvania School of Medicine, 2006
