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Senate HELP Committee Approves Bill That Would Allow FDA To Regulate Tobacco
The Senate Health, Education, Labor and Pensions Committee on Wednesday voted 15-8 to approve a bill (S 982) giving FDA authority to regulate tobacco products, the Wall Street Journal reports. Under the bill, FDA could ban certain tobacco products, such as candy-flavored cigarettes, restrict tobacco advertising to black-and-white ads, and prohibit use of the terms "mild" and "low tar" (Yoest/Mundy, Wall Street Journal, 5/21). FDA also could limit the amount of nicotine in tobacco products, as well as enlarge warning labels. To pay for the new regulatory efforts, the bill would require all tobacco companies to pay a fee that would raise nearly $5.4 billion over the first 10 years. Committee members voted down a number of amendments:

Widespead And On The Increase - Vitamin D Deficiency
A new report issued by the International Osteoporosis Foundation (IOF) and published in the scientific journal Osteoporosis International1, shows that populations across the globe are suffering from the impact of low levels of vitamin D. The problem is widespread and on the increase, with potentially severe repercussions for overall health and fracture rates.
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Don't Forget Your Condoms At Birmingham Pride, Says Terrence Higgins Trust
HIV and sexual health charity Terrence Higgins Trust (THT) is joining forces with other local HIV organisations to remind visitors to Birmingham Pride (23 - 24 May) not to put their sexual health at risk by getting carried away with the party mood.
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Important Modulator Of Immune Cell Entry Into The Brain Discovered

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. Commenting on the findings, Helen Yates, Multiple Sclerosis Re Centre Chief Executive said, "This is a very important piece of research. We have long known that the crossing of immune cells into the CNS is a major problem in MS. This work shows that inflammation can be decreased and hopefully will lead to further research into prevention of the inflammatory response completely." 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)*. It has been known for a long time that T cells can attack the body"s own structures and, if they infiltrate the CNS, cause diseases such as multiple sclerosis (MS). The T cells damage the myelin sheath, the material that surrounds and protects the fibers of nerve cells. This damage slows down or blocks messages between the brain and the body, leading to various symptoms of MS such as impaired movements. The molecular analysis of damaged tissue from patients with MS led the researchers to the B1-receptor. The data they evaluated showed that two different pathways known to play a crucial role in the cardiovascular area also seem to play an important role in the CNS: namely, the renin-angiotensin-system, and the kallikrein-kinin-system, the latter of which the researchers in Berlin put their focus on. The B1-receptor is part of the kallikrein-kinin-system. Together with Professor Alexandre Prat from the Université de Montréal, Montréal, Canada, and Professor Lawrence Steinman from Stanford University in Stanford, California, USA, the researchers in Berlin detected the B1-receptor on T cells of MS patients as well as on T cells of mice with encephalitis, an inflammation of the brain. The disease got worse in those mice that lacked B1 on their T cells. Therefore, using a certain substance (Sar-[D-Phe]desArg9-bradykinin), they activated the receptor in mice which had B1 on their T cells. As a result, the entry of T cells into the CNS slowed down and the clinical symptoms of the inflammation markedly decreased. "We have discovered a control mechanism, which reduces inflammation caused by the immune system" neurologist and MDC research group leader Professor Zipp explains. "It remains to be seen if we succeed in developing a new therapy for chronic inflammation in the CNS, such as MS, in the future." Multiple Sclerosis Re Centre


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