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PROTECT-1 Phase II/III Induction-Stage Results For ChemoCentryx's Traficet-EN(TM) Presented In Oral Session At DDW 2009 Conference
ChemoCentryx, Inc., announced that Phase II/III clinical data from the company"s PROTECT-1 (the Prospective Randomized Oral Therapy Evaluation in Crohn"s disease Trial) of Traficet-EN(TM) (CCX282-B) in patients with moderate-to-severe Crohn"s disease demonstrated evidence of clinical efficacy in the reduction of disease severity, as defined by a decrease from baseline in the Crohn"s Disease Activity Index (CDAI) score of at least 70 points over the course of 12 weeks; the more stringent criterion of at least a 100 point decrease in the CDAI score was also met by week 12. In addition, Traficet-EN treatment resulted in colonoscopic evidence of improvement. These data, reported from the Induction Stage of the ongoing PROTECT-1 trial, were presented at Digestive Disease Week (DDW) 2009 in Chicago, IL, by Satish Keshav, M.D., Ph.D., Department of Gastroenterology, John Radcliffe Hospital, Oxford University, in an oral session today.

Health Care Costs For Small Businesses Considered
"Health care costs are killing small businesses. Their insurance premiums are rising dramatically and unpredictably," NPR reports. "Jody Hall, who owns Seattle"s Cupcake Royale, now pays as much in health insurance for her employees as she does in rent for four choice Seattle storefronts. A majority of working Americans are employed by small businesses, but according to the Kaiser Family Foundation, only 6 in 10 small businesses provide health care. What"s more, the National Federation of Independent Business reports that small companies pay substantially more in premiums than large firms do. Hall, for example, has just three or four insurers to choose from, and she says they won"t negotiate on price."
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New Control System Of The Body Discovered - Important Modulator Of Immune Cell Entry Into The Brain - Perhaps New Target For The Therapy
Researchers in Berlin, Germany have ameliorated inflammation of the brain in mice caused by immune cells. A receptor they discovered on the surface of T cells in the central nervous system (CNS) plays the key role. The researchers showed that this bradykinin receptor 1 (B1) controls the infiltration of immune cells into the CNS. When they activated B1 in mice with encephalitis, they were able to slow down the crossing of the immune cells through the blood-brain-barrier into the CNS. As a result, the inflammation markedly decreased. The work by Dr. Ulf Schulze-Topphoff, Prof. Orhan Aktas, and Professor Frauke Zipp (Cecilie Vogt-Clinic, Charité - Universitätsmedizin Berlin, Max DelbrÃøck Center for Molecular Medicine (MDC) Berlin-Buch and NeuroCure Research Center) together with researchers in Canada and the USA may unveil a new target for the treatment of chronic inflammatory diseases such as multiple sclerosis (MS) (Nature Medicine, doi 10.1038/nm.1980)*.
Sexual Health

TB -- Hiding In Plain Sight

Current research suggests that Mycobacterium tuberculosis can evade the immune response. The related report by Rahman et al, "Compartmentalization of immune responses in human tuberculosis: few CD8+ effector T cells but elevated levels of FoxP3+ regulatory T cells in the granulomatous lesions," appears in the June 2009 issue of The American Journal of Pathology. More than two million people worldwide die from tuberculosis infection every year. Due in part to inappropriate antibiotic usage, there are a rising number (0.5 million in 2007) of cases of multidrug-resistant (MDR-TB) and extensively drug-resistant (XDR-TB) tuberculosis. New therapies are needed to treat these dangerous infections. Immune responses to tuberculosis rarely result in complete eradication of the infection. Instead, TB-infected immune cells promote the generation of chronic inflammation and the formation of granulomas, which are areas where the bacteria are contained but not destroyed. A group led by Dr. Susanna Grundstrom Brighenti at the Karolinska Institutet in Stockholm, Sweden therefore examined the immune response in patients infected with tuberculosis. This is the first study describing the immunoregulatory mechanism associated with the development of clinical disease at the site of infection in human TB. They found that while the immune cells responsible for killing the tuberculosis bacteria surrounded the granuloma, these cells had low levels of the molecules necessary to kill the TB. Instead, granulomas had high numbers of regulatory immune cells. These regulatory cells suppress the immune response, resulting in the survival of the tuberculosis bacteria and perhaps contributing to persistent long-term infection. This study by Rahman et al "provide[s] evidence that the adaptive immune response in establishment of clinical TB [is] skewed towards a suppressive or regulatory phenotype that may inhibit proper immune activation and down-regulate the host response at the local site of infection. Compartmentalization of the immune response in human TB could be part of the reason why infection is never completely eradicated but instead develops into a chronic disease." In future studies, Dr. Grundstrom Brighenti and colleagues plan to "pursue new strategies developed to enhance cell-mediated immune responses that are known to provide protective immunity in patients with TB. Such an approach may involve targeting of certain subpopulations of immune cells with anti-inflammatory or immunoregulatory properties." This work was supported by grants from the Swedish Society for Medical Research (SSMF), the Swedish Foundation for Strategic Research (SSF), Sida/SAREC, the Swedish Research Council (VR), the Swedish Heart and Lung Foundation (HLF) and the National Board of Health and Wealth fare. Rahman S, Gudetta B, Fink J, Granath A, Ashenafi S, Aseffa A, Derbew M, Svensson M, Andersson J, Grundstrom Brighenti: Compartmentalization of immune responses in human tuberculosis: few CD8+ effector T cells but elevated levels of FoxP3+ regulatory T cells in the granulomatous lesions. Am J Pathol 2009 174: 2211-2224 Angela Colmone American Journal of Pathology


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