Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Friday, January 17, 2020

A replacement for exercise?

Would this be useful in preventing your muscle atrophy post stroke? I know of no one in the world to ask that exceedingly simple question. All because we have

fucking failures of stroke associations  doing nothing concrete for stroke survivors.

.

A replacement for exercise?

Whether it be a brisk walk around the park or high intensity training at the gym, exercise does a body good. But what if you could harness the benefits of a good workout without ever moving a muscle? Michigan Medicine researchers studying a class of naturally occurring protein called Sestrin have found that it can mimic many of exercise’s effects in flies and mice. The findings could eventually help scientists combat muscle wasting due to aging and other causes.
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“Researchers have previously observed that Sestrin accumulates in muscle following exercise,” said Myungjin Kim, PhD, a research assistant professor in the Department of Molecular & Integrative Physiology. Kim, working with professor Jun Hee Lee, PhD and a team of researchers wanted to know more about the protein’s apparent link to exercise. Their first step was to encourage a bunch of flies to work out.
Taking advantage of Drosophila flies’ normal instinct to climb up and out of a test tube, their collaborators Robert Wessells, PhD and Alyson Sujkowski of Wayne State University in Detroit developed a type of fly treadmill. Using it, the team trained the flies for 3 weeks and compared the running and flying ability of normal flies with that of flies bred to lack the ability to make Sestrin. “Flies can usually run around 4 to 6 hours at this point and the normal flies’ abilities improved over that period,” says Lee. “The flies without Sestrin did not improve with exercise.”
What’s more, when they overexpressed Sestrin in the muscles of normal flies, essentially maxing out their Sestrin levels, they found those flies had abilities above and beyond the trained flies, even without exercise. In fact, flies with overexpressed Sestrin didn’t develop more endurance when exercised.
The beneficial effects of Sestrin include more than just improved endurance. Mice without Sestrin lacked the improved aerobic capacity, improved respiration and fat burning typically associated with exercise.
“We propose that Sestrin can coordinate these biological activities by turning on or off different metabolic pathways,” says Lee. “This kind of combined effect is important for producing exercise’s effects.”
Lee also helped another collaborator, Pura Muñoz-Cánoves, PhD, of Pompeu Fabra University in Spain, to demonstrate that muscle-specific Sestrin can also help prevent atrophy in a muscle that’s immobilized, such as the type that occurs when a limb is in a cast for a long period of time. “This independent study again highlights that Sestrin alone is sufficient to produce many benefits of physical movement and exercise,” says Lee.
Could Sestrin supplements be on the horizon? Not quite, says Lee. “Sestrins are not small molecules, but we are working to find small molecule modulators of Sestrin.”
Additionally, adds Kim, scientists still don’t know how exercise produces Sestrin in the body. “This is very critical for future study and could lead to a treatment for people who cannot exercise.”
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