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Biotech / Medical : Indications -- Psoriasis/Chronic Inflammation -- Ignore unavailable to you. Want to Upgrade?

To: Icebrg who wrote (477)	12/12/2003 12:53:22 PM
From: scaram(o)uche	Read Replies (1) \| Respond to of 631

Message 18022671 Parasites, opportunists. IMO.

To: Icebrg who wrote (477)	1/4/2004 5:45:12 PM
From: Icebrg	Respond to of 631

A new direction for psoriasis research? Journal of Investigative Dermatology paper shows that genetic change in vascular system may contribute to psoriasis susceptibility Portland, Ore., Jan. 3, 2004 – The National Psoriasis Foundation today hailed research that may eventually lead to additional therapies for treating psoriasis, an incurable immune-mediated disease that affects 5 million Americans. In a paper to be published January 3 in the Journal of Investigative Dermatology, Dr. Helen S. Young and colleagues at the University of Manchester, in Manchester, UK, provide the first evidence that there are alterations in a gene involving the development of the vascular system that may contribute to psoriasis susceptibility. "This work offers a new way of thinking about psoriasis, and may open up new approaches to treating the disease," said Gail Zimmerman, president and CEO of the National Psoriasis Foundation. "While therapies focused on the immune system are proving highly beneficial for many psoriasis patients, therapies that target the vascular system might also one day provide relief to those facing this challenging, and often debilitating, disease." It has been previously observed that aspects of the vascular system, or blood vessel network in the skin, are altered in psoriasis. An essential regulator of vascular development produced by skin cells, called VEGF or Vascular Endothelial Growth Factor, is found in high levels in psoriatic skin lesions. In this study, the authors show that certain SNPs, or single nucleotide polymorphisms, of the VEGF gene itself occur with greater frequency in a subset of people with psoriasis. In a commentary appearing alongside the Young et al paper, Michael Detmar, M.D., of the Cutaneous Biology Research Center at Massachusetts General Hospital in Boston writes: "Together with the biological evidence for a pathogenetic role of VEGF in psoriasis, the study by Young et al suggests that VEGF acts as a modifier gene in psoriasis and that therapeutic blockade of the VEGF/VEGF receptor system might represent a novel, pharmacogenomic approach for the future treatment of psoriasis." Psoriasis patients can hope that drugs that block the activity of VEGF – "anti-VEGF" therapies – may one day be used to treat psoriasis, much the same way that anti-VEGF therapies are currently being tested in clinical trials as a cancer treatment. "This important paper by Young and colleagues provides additional insight into the multiple genetic polymorphisms that likely determine the occurrence and severity of psoriasis," said David A. Norris, M.D., chairman of the University of Colorado School of Medicine in Denver and chairman of the Psoriasis Foundation's Scientific Review Committee. "The finding of polymorphisms in the VEGF gene relating to susceptibility to psoriasis reinforces the concept that angiogenesis is an important component of the psoriasis phenotype, and indicates that multiple genes (including those controlling the immune response, keratinocyte proliferation and differentiation, and angiogenesis) might determine susceptibility to psoriasis." The Young et al paper is called "Single Nucleotide Polymorphisms of Vascular Endothelial Growth Factor (VEGF) in Psoriasis of Early Onset." eurekalert.org

To: Icebrg who wrote (477)	5/14/2004 2:50:35 AM
From: Icebrg	Respond to of 631

Oral simvastatin treatment in relapsing-remitting multiple sclerosis Timothy Vollmer, Lyndon Key, Valerie Durkalski, William Tyor, John Corboy, Silva Markovic-Plese, Jana Preiningerova, Marco Rizzo, Inderjit Singh Many drugs have been approved for relapsing forms of multiple sclerosis but are only partly effective, are injected, and are expensive. We aimed to investigate use of of oral simvastatin (80 mg) in 30 individuals with relapsing-remitting multiple sclerosis. The mean number of gadolinium-enhancing lesions at months 4, 5, and 6 of treatment was compared with the mean number of lesions noted on pretreatment brain MRI scans. Number and volume of Gd-enhancing lesions declined by 44%, (p<0·0001) and 41% (p=0·0018), respectively. Treatment was well tolerated. Oral simvastatin might inhibit inflammatory components of multiple sclerosis that lead to neurological disability.