Note: Always consult your doctor before undertaking a weight loss plan.

I have always had problems with my weight. From the time I was 5, I’ve had round, chubby (some would say pinch-able) cheeks — and my cheeks weren’t my only round part.

When I was in high school I started really battling with weight. I decided to diet my senior year and lost 12 pounds. I thought that was the toughest dieting I would ever do, and I thought I was done with it. Wrong!

For eight long years, Terrence Stevens — who goes by the nickname "T-Wheels" — had the dubious distinction of being the only inmate in the New York state prison system with “muscular dystrophy.”

Stevens actually has spinal muscular atrophy (SMA) type 3, but he says no one in prison knew or cared what his true diagnosis was.

Conditions were horrible for inmates with disabilities, says Stevens, 43, who is nonambulatory and has only limited use of his hands.

Editor's note 2/7/11: A link to the Tivorsan Pharmaceuticals website has been added.

Duchenne and Becker muscular dystrophies

MDA has awarded a $1.4 million grant to the biopharmaceutical company Repligen Corp. to help advance the company’s experimental drug for spinal muscular atrophy (SMA) to phase 1 human clinical trials.

The drug, RG3039, has demonstrated potential throughout its early development, and is Repligen's lead therapeutic candidate for treatment of SMA.

MDA has awarded 38 new research grants totaling more than $14 million and covering more than a dozen neuromuscular diseases. 

MDA's Board of Directors met in Los Angeles July 16, where it reviewed and approved the new grants based on recommendations from the MDA Scientific and Medical Advisory Committees. Grants were scored and recommended for approval based on the capabilities of the applicant, the scientific merit of the project, and the proposal's relevance to developing treatments for the disease. The effective start date for all grants was July 1, 2010.

Scientists have found that mice with a disease resembling a mild form of spinal muscular atrophy (SMA) known as SMA type 3 showed more production of a needed protein in their spinal cords and more normal-looking ears and tails after treatment with a gene-modifying molecule that researchers hope could become a treatment for human SMA.

About the new findings

A research group from the University of Sheffield in the United Kingdom has found that mice with a disease mimicking human spinal muscular atrophy (SMA) benefited significantly from intravenous transfer of the gene for the SMN (survival of motor neurons) protein. The mice lived significantly longer than untreated mice of the same type.

A research team at the University of Pennsylvania in Philadelphia has characterized the mechanism responsible for rapid decay of the survival of motor neurons (SMN) protein that is encoded by the human SMN2 gene and which plays a key role in a variety of therapeutic strategies under development for spinal muscular atrophy (SMA). 

Scientists at four U.S. institutions have successfully used gene therapy to treat very young mice with a disease resembling severe spinal muscular atrophy (SMA).  Study results were published online Feb. 28, 2010, in the journal Nature Biotechnology.

 A process called trans-splicing has been shown to increase levels of a needed protein in mice with a disease resembling severe human spinal muscular atrophy (SMA), says a research team at the University of Missouri-Columbia, whose findings were published Jan. 6, 2010, in the Journal of Neuroscience.