Thanks for a job well done

W hen President Rolando and I decided to present the idea of a national bowlathon to increase our contribution to the Muscular Dystrophy Association, we had high hopes. Those hopes were met when we raised more than $340,000 during the first bowlathon. Our goal this year is to top that amount and raise at least $500,000. But that will be done only if as many branches as possible turned out last month. I hope to report in the next Postal Record that we exceeded our goal. If you had an event, send in the report from the packet your branch received. If you didn't get the reporting form, please go to NALC's web page and click on " MDA " under the " Community Services " tab to find the reporting form to send to headquarters. We want to make sure your branch gets credit for the work you've done. To give some insight to how your money is used in research endeavors, I have listed just a few of the many projects that are currently ongoing to help find a cure: Two DNA changes needed to cause FSHD symptoms— MDA-supported scientists uncover a previously missing piece of the puzzle posed by facioscapulohumeral muscular dystrophy. Not only does this disease require the presence of a contracted area of DNA on chromosome 4 (a previously recognized factor), but it also requires a " permissive " DNA signal on the same chromosome, which allows toxic proteins to last long enough to cause muscle damage. The study is expected to provide new therapeutic targets. DMD gene repair strategy takes a big step forward—An MDA-supported research group reports that a new generation of molecules can help cells permanently repair errors in the dystrophin gene, fixing the underlying cause of Duchenne muscular dystrophy. In experiments on cells, the new molecules stimulated more than 10 times the DNA repair levels of previous molecules, providing a " proof of concept " for gene repair as a therapy for DMD. Synthetic enzyme approved for late-onset Pompe dis-ease—Lumizyme, an enzyme manufactured by Genzyme Corp., becomes commercially available for the treatment of late-onset acid maltase deficiency (Pompe disease) in individuals 8 and older. MDA-supported basic research played a role in the development of both Lumizyme and Myozyme, Genzyme's enzyme replacement drug for infants and very young children with Pompe. Therapeutic strategy in MTM opens muscle fibers—MDA-supported researchers report a new …