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Cardiac Research At Colorado State University Shows Diseased Heart Valves In Dogs Produce Serotonin
A significant part of the question of what causes mitral valve disease in dogs, giving scientists and medical experts clues into new possible ways to treat or prevent the disease, may have been solved by a Colorado State University veterinarian. The discovery refutes the current believe that mitral valve disease, the top heart disease in dogs, is inevitable as a part of aging in pets.

FDA Advisory Committee Votes In Favor Of Zyprexa For Two Adolescent Indications
The U.S. Food and Drug Administration (FDA) Psychopharmacologic Drugs Advisory Committee (PDAC) voted that Zyprexa(R) (olanzapine), an atypical antipsychotic, is effective and acceptably safe for the acute treatment of schizophrenia or manic or mixed episodes associated with bipolar I disorder in adolescents aged 13-17 years old. The panel supported the FDA and Lilly"s position that if Zyprexa is approved for the two indications, prescribers should consider other treatment options first for adolescent patients.
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Pirfenidone May Help Lung Function In IPF Patients According To Large Clinical Trial
A large, well-controlled, multi-national clinical trial program has demonstrated the effectiveness and safety of what may become the first FDA-approved medicine for idiopathic pulmonary fibrosis, or IPF.
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Crohn's Disease: Case Western Reserve Researchers Identify Links Between Inflammatory Disease Genes

Researchers from Case Western Reserve University School of Medicine identified a novel link between ITCH, a gene known to regulate inflammation in the body and NOD2, a gene which causes the majority of genetic Crohn"s Disease diagnoses. ITCH, when malfunctioning, causes widespread inflammatory diseases, including inflammatory bowel disease, gastritis, uncontrolled skin inflammation, and pulmonary pneumonitis. Derek Abbott, M.D., Ph.D., and his team of researchers found that ITCH also influences NOD2-induced inflammation. These findings, published in the August 11th issue of Current Biology, suggest a common pathophysiology exists between multiple inflammatory diseases. The unexpected finding of the interaction between these genes offers the possibility of a new drug target, which would be effective in treating Crohn"s disease - a chronic disorder causing inflammation of the gastrointestinal tract. Autoimmune and inflammatory diseases are striking an increasing portion of the population. They result from an overstimulation of the immune system by the infectious and environmental agents individuals face daily. Unfortunately, despite their increasing prevalence in the Western world and morbidity among younger patients, the pathophysiology of these enigmatic diseases is poorly understood and for this reason, treatment for these diseases is less-than-ideal. This finding links two key signaling pathways to the pathophysiology of diseases associated with ITCH and NOD2 and opens new avenues of pharmacologic pursuit to target these diseases. With an eye towards clinical applications, Dr. Abbott and his colleagues" next step is to determine if currently used pharmacologic agents can be useful in this model of inflammatory disease. They will do so using small molecule drug screening to identify potential drugs that target ITCH. Of those diagnosed with Crohn"s disease, 30 percent have the NOD2 mutation in their genes. For these individuals, this discovery opens up the possibility of individually-tailored treatments with better efficacy toward a particular patient"s disease. "This research is an excellent example of how scientific investments benefit the public with measureable gains. In this case, it led to unexpected insights and opened new fields of endeavor for pharmacological manipulation in this serious chronic disease," says Derek Abbott, M.D., Ph.D., assistant professor of pathology, Case Western Reserve University School of Medicine. "This sort of study will help uncover the pathologic mechanism of disease and ultimately lead to more rational and carefully measured treatment." Jessica Studeny Case Western Reserve University


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