Hi sou,sou wrote: At what cost? I don't mean in gold.
As part of an even more aggressive cancer therapy, Cyclophosphamide at high dose has a long history with an "acceptable" safety record.sou wrote: Cyclophosphamide is a mutagen. How can we know that it won't cause cancer? And how do we know that it will really work? It should! It kills the bad immune system.
That's an incorrect statement in a situation in which correctness is essential. Cyclophosphamide is capable of total ablation, and total ablation is, of course the goal in rebooting and total ablation defines the ENTIRE difference in the situations you mention.sou wrote:Why do immune compromised people with AIDS do suffer relapses? HIV is more potent an immunosuppressor than cyclophosphamide.
Please provide reason to believe that statement is true.sou wrote: Why is there no immune system involvement in 30-40% of MS lesions?
NOTHING is certain in the world of MS but to the majority of people who do believe that MS involves the immune system, MS treatment has always seemed a delicate conundrum regardingsou wrote: Why do relapses tend to happen when the immune system is in a really bad shape?
While rebooting seems to have separated itself greatly from other treatments in showing marked and obvious changes in the course of the disease, there is no getting around the fact that time is the judge and no one, including myself, can truthfully say that rebooting will forever stop the disease process.sou wrote:Steroids relieve from many of the symptoms without affecting the course of the disease at all. How can we know that a cyclophosphamide-indecued MS parenthesis will affect the long term course of the disease?
However, while dystrophin is vital for muscle development, the protein also needs several "helpers" to maintain the muscle tissue. One of these "helper" molecular compounds is nNOS, which produces nitric oxide. This is important for muscles that are in use during high intensity movements, such as exercise.
"When you exercise, not only does the muscle contract, but the blood vessels are constricted," Duan said. "nNOS is important because it produces nitric oxide that relaxes the blood vessels, helping to maintain the muscle with a healthy blood supply. If no blood reaches the muscle cells, they will eventually die. In DMD patients, this means the disease will progress as the muscle cells are replaced by the fibrous, bony or fatty tissue."
Since 1994, researchers have known about the importance of nNOS, but have not been able to determine how to produce nNOS in a dystrophic muscle, or a muscle lacking dystrophin. Many scientists have tried to solve this mystery without success. In his most recent study, published Monday in The Journal of Clinical Investigation, Duan and his team identified the location of genetic material responsible for the production of nNOS.
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