Cell proteins could offer a future drug target against weight gain Two cell proteins that relax the gut and help accommodate a big meal have been recognized by UCL researchers. The proteins could offer another drug target against fat gain, by avoiding the abdomen from expanding. In a paper released in this month’s issue of the Journal of Pharmacology and Experimental Therapeutics, Dr Brian King and Dr Andrea Townsend-Nicholson explored the molecular basis of relaxations of the gut brands . These proteins were recognized in the guinea pig, but are present in the human gut also, and thus provide potential as another target for medications. Further research by the UCL team will concentrate on the individual isoform of the P2Y11 proteins receptor. This expansion is usually controlled by nerves inside the stomach wall and these nerves launch molecules that stimulate the P2Y1 and P2Y11 receptor proteins embedded in muscle mass cells in the gut wall structure. We want to identify drugs that would block the P2Y11 receptor and, consequently, prevent slow relaxation of the stomach. Because of blocking the P2Y11-based mechanism, meal size will be smaller, offering the person a better potential for regulating their diet. At the moment, the most successful way to help obese individuals lose weight is normally gastric banding or stomach stapling, both of which reduce the maximum volume of the stomach. But they are tricky surgical treatments also, not without attendant risks. A pill that could replace this operation, yet have the same impact, might be a useful alternative. , a innovator in regenerative medicine, announced today the publication of a key research in the American Journal of Physiology Renal Physiology by researchers at Tengion. In the study, rodents with chronic kidney disease had been treated with healthful kidney cells to catalyze the regeneration of functional kidney tissue and delay disease progression, as evidenced by expanded survival, improved kidney filtration, and reduced severity of kidney cells pathology. The released data demonstrate that delivery of a selected inhabitants of kidney cells to the kidney significantly extended long-term survival and improved kidney function in rodents with persistent kidney disease during six months of follow-up. Further, the therapeutic effects reported in this study were more pronounced and stronger than have already been previously reported with this animal model. These data provide in-vivo proof-of-idea for a possibly transformational approach to preventing kidney failure, said Steven Nichtberger, M.D., cEO and president of Tengion. We anticipate presenting initial scientific results from these studies in the near future.D., an advisor to Chief and Tengion, Division of Transplantation, Department of Surgery, University of NEW YORK. A treatment approach that may increase kidney tissue and improve function will be a significant advancement in the care of these patients. An interview with Dr Kazazian The scientific community has historically regarded that CKD evolves from an imbalance between tissue damage and the kidney’s ability to restoration and regenerate itself, said Rusty Kelley, Ph.D., Senior Scientist at Tengion and the business lead study author. These preclinical data provide clear evidence that regeneration of functional renal cells can delay progression of CKD. By using the patient’s own kidney cells, procured by a needle biopsy, the business is developing a product candidate that’s implanted into the failing kidney and catalyzes the regeneration of functional kidney tissue. Tengion provides additional information on its item development plans to investors today at the Rodman & Renshaw Healthcare Conference and slides from that presentation will be available on the Company’s website. The paper entitled, A tubular cell-enriched subpopulation of main renal cells enhances survival and augments kidney function in a rodent style of persistent kidney disease, is available on-line at the American Journal of Physiology Renal Physiology website – – and will show up in the November 2010 printing concern.