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Extending The Life Of An Appetite-Suppressing Peptide
The peptide alpha-MSH works in a region of the brain known as the hypothalamus to suppress appetite. A team of researchers, at Yale University School of Medicine, New Haven, and the University of California Davis, has provided new insight into the way in which levels of the active form of alpha-MSH are regulated in mice. Specifically, genetic and biochemical analysis performed by the team, led by Sabrina Diano and Craig Warden, indicated that the protein PRCP is expressed in the hypothalamus and breaks down the active form of alpha-MSH, generating a slightly smaller peptide that does not suppress food intake. Importantly, administration of PRCP inhibitors to both normal and obese mice reduced their food intake. Further, mice lacking PRCP had increased levels of the active form of alpha-MSH in the hypothalamus and were leaner and shorter than normal mice; they also did not get obese when fed a high-fat diet. The authors suggest that these data are the first step in identifying PRCP as a candidate drug target for the treatment of obesity and obesity-related disorders. Although Richard Palmiter, at the University of Washington, Seattle, also raises this intriguing possibility, he cautions that any drug would need to penetrate the brain.
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Individuals At Risk For Developing Colon Cancer Identified By Researchers
A new study identifies a group of individuals at increased risk for developing colon cancer and holds the promise for developing new tailored cancer treatments. The study in this week"s issue of the Proceedings of the National Academy of Sciences (PNAS) is by Sanford Markowitz, M.D., Ph.D., the Markowitz-Ingalls Professor of Cancer Genetics at Case Western Reserve University School of Medicine and oncologist at the Ireland Cancer Center of University Hospitals Case Medical Center, and colleagues.
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At American Diabetes Association Meeting, 2 Preclinical Abstracts Published By Versartis
Versartis, Inc., a new company developing novel biologics with enhanced properties for patients with metabolic diseases, published abstracts for preclinical data on its two product candidates, VRS-859 (exenatide-rPEG) and VRS-808 (glucagon-rPEG), at the American Diabetes Association Scientific Sessions annual meeting in New Orleans.
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Acceleron To Present ACE-031 Preclinical Study Results As Treatment For Loss Of Muscle Mass And Function

Acceleron Pharma, Inc., a biopharmaceutical company developing novel therapeutics that modulate the growth of cells and tissues including red blood cells, bone, and muscle, today announced it will provide three oral presentations on data from its ACE-031 program at the Endocrine Society"s 91st Annual Meeting to be held in Washington, DC from June 10-13, 2009. The presentations will provide results from preclinical studies highlighting the effects of its lead investigational product for treating diseases involving the loss of muscle mass and function. "Treatment with a Form of Soluble Activin Receptor Type IIB Ameliorates the Effects of Estrogen Deficiency on Lean, Adipose and Bone Tissues" Date: Wednesday, June 10, 2009 Session Time: 11:15 am Room: 154AB, Walter E. Washington Convention Center "Treatment with a Soluble Activin Receptor Type IIB Prevents Androgen-Deprivation-Induced Effects on Muscle, Bone and Fat" Date: Friday, June 12, 2009 Session Time: 11:15 am Room: 144C, Walter E. Washington Convention Center "Age-Related Lean Tissue Loss and Adipose Tissue Gain Is Attenuated by Treatment with a Form of Soluble Activin Receptor Type IIB" Date: Saturday, June 13, 2009 Session Time: 1:15 pm Room: 143C, Walter E. Washington Convention Center "These three presentations continue the ongoing stream of exciting preclinical data demonstrating the therapeutic effects of Acceleron"s ACE-031 program across a wide array of disease models," said Jasbir Seehra, Ph.D., Chief Scientific Officer at Acceleron. "There is enormous clinical potential of this molecule to treat patients suffering from a range of conditions such as neuromuscular diseases, cancer cachexia, metabolic diseases and age-related muscle loss. We are completing a Phase 1 study in healthy volunteers and look forward to announcing these results later this year." Muscle is increasingly recognized as central to many biological processes and plays a major role in human health. The loss of muscle mass and strength is ultimately directly related to the cause of death in neuromuscular diseases such as muscular dystrophy and amyotrophic lateral sclerosis. Severe muscle loss in cancer leads to serious complications and a poor prognosis. Muscle loss is a natural consequence of aging, similar to bone loss, resulting in decreased muscle strength (frailty), reduced mobility and an increased risk of a fall and broken bones. In metabolic diseases, an imbalance of diet, energy utilization and skeletal muscle leads to poor metabolic function. By increasing muscle mass there is a corresponding decrease in fat mass and improvements in metabolic function. About ACE-031 ACE-031, a soluble molecule based on the activin receptor type IIB (ActRIIB), is a biologic therapeutic that inhibits signaling through the ActRIIB receptor. By blocking signaling though ActRIIB, ACE-031 increases muscle mass and strength. In numerous and varied animal models of disease, ACE-031 significantly increased muscle mass and muscle strength. ACE-031 has shown encouraging preclinical results in animal models of age-related muscle loss, neuromuscular disease, cancer treatment-related muscle loss and metabolic diseases. ACE-031 is currently being studied in a Phase 1 clinical trial. Acceleron


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