Abstract: A group of degenerative inherited diseases which cause muscle weakness and loss of muscle tissue is called Muscular dystrophy. There are many types of muscular dystrophy. Duchenne muscular dystrophy is fetal genetic mutation in 1 of every 3500 boys.This mutation can be diagnosed during child bearing( pregnancy) with the help of genetic studies. The patients of muscular dystrophy cannot produce protein called "Dystrophin" which keeps muscles strong. Boys feel problem in walking by 8 years of age. By their 19 they were on wheel chairs, and onward muscle function is so retarded that they die. If there is family history genetic counseling is advised. Objective: The main objective of this research was to improve the conditions of patients.Tivorsan Pharmaceuticals licensed rights from Brown University for the protein, biglycan, hope to prove potential therapy via clinical trials. Biglycan is a human protein,mainly found in tendons and bones.Biglycan in the presence of protein utrophin restore muscle strengthening. Setting or Place: Brown University in Rhode Island,United States. Design: This experiment was performed on mice who have similar genetic mutation as that of boys with muscular dystrophy. In experiments given in the paper, Fallon's team found that when they administered biglycan to the bloodstream, utrophin went into the cellular membranes of muscular cells. Utrophin protein help in building of cells and their strengthening. Participants: A group of Mice. Results: Mice treated with biglycan retain their muscular functions 50% more than untreated mice. The next big step is to test these results in humans. Latest Medical Researches: If you found this research interesting, you may want to read through other interesting researches such as; Comments10/25/2011 16:38
I know a product that can really help with these types of diseases
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10/26/2011 05:45
I had no idea that muscular dystrophy could eventually lead to death. Is this from the dystrophy of the cardiac tissue? Also, has there been any luck with a synthetic protein to replace the absent Dystrophin?
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