Minggu, 02 Januari 2011

Human protein enhances muscle function in mice muscular dystrophy - Webnewswire.com (press release)

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PROVIDENCE, RI [Brown University] - A new potential treatment based on a natural human protein significantly slows muscle damage and improves the function of mice that have the same genetic mutation as a boy with the most common form of muscular dystrophy muscle, according to an article published online in December

PROVIDENCE, RI [Brown University] - A new potential treatment based on a natural human protein significantly slows muscle damage and improves the function of mice that have the same genetic mutation published as boys, the most common form of muscular dystrophy, according to a document online 27th December in the Proceedings of the National Academy of Sciences.

Duchenne muscular dystrophy is a fatal genetic mutation in approximately one of 3,500 boys. If you are unable to produce a protein called dystrophin, the muscles that hold strong. With eight years, boys begin to have difficulty walking. In adolescence, they are often in a wheelchair, and 20s of their muscle function is so degraded that they die.

All this is still a treatment to improve the appropriate targeting the patient, "said Justin Fallon, professor of neuroscience at Brown University and lead author of the document. This is an important step in that direction.

This fall, the start-up licensing rights to Brown Pharmaceuticals Tivorsan the key protein, biglycan, bringing the hope of potential therapies in clinical trials.

Biglycan, muscle-strengthening the presence of a protein called utrophin, which is usually common in very young children. Utrophin is even in adults, but fewer places and not where he suffered from muscular dystrophy, which can not produce dystrophin, which has strong muscles help for adults.

Encourage experiments

In the experiments described in the paper showed the team attracts biglycan Fallon returned to the bloodstream, the cell membranes of muscle cells, utrophin. Similar to utrophin does when he is in fetuses, infants and young children, do the proteins to build cells and retain their strength.

Fallon team found in an experiment, a reduction of 50 percent in central nucleated fibers in the muscle tissue of biglycan-treated mice compared to untreated mice. Biologists identify the fibers as indicators of tissue injury and repair recently, so a reduction of their shows that the muscle undergoes less damage.

The muscles of the mouse team to a standardized exercise test, where you stretch the same time, causing the contract. The test ultimately weakens the health of muscles, but in tests by researchers and co-authors of the University of Pennsylvania, the mouse muscles muscular dystrophy were treated with biglycan lost their strength 30 percent slower than untreated mice that were similar.

In recent tests with an improved formulation of biglycan, Fallon said that the team has that number rises to 50 percent seen in some muscles, which means that the mice treated with biglycan taking over their function for a long period.

Fallon said the impact of treatment with biglycan trial lasted for months. Several basic tests for side effects during this period, such as renal and hepatic function, no evidence of harm from the therapy.

The effectiveness of biglycan appears in a mouse model of Duchenne muscular dystrophy Fallon is anxious to see if it can improve the lives of thousands of children.

The next big step is to test in humans, "said Fallon.

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In addition to Fallon, the authors on the paper Alison Amenta, Atiglan Yilmaz, and Beth McKechnie, Brown, and Sasha Bogdanovich Tejvir Khurana of the University of Pennsylvania, and Mehrdad Abedi, University of California-Davis.

The funds for muscular dystrophy research Fallon came from the National Institutes of Health, Charley Parent Project Muscular Dystrophy Fund and the Nash Avery Foundation.

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