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.

Thursday, May 28, 2020

Muscle‐specific sirtuin1 gain‐of‐function ameliorates skeletal muscle atrophy in a pre‐clinical mouse model of cerebral ischemic stroke

And since resveratrol stimulates production of SIRT1, a serum that blocks diseases by speeding up the cell's energy production centers known as mitrochondria. Ask your doctor how much red wine you should be drinking to prevent such atrophy. Until we know a better way on this red wine is the obvious choice. I bet your stroke hospital will never serve red wine.

The latest here:

Muscle‐specific sirtuin1 gain‐of‐function ameliorates skeletal muscle atrophy in a pre‐clinical mouse model of cerebral ischemic stroke

First published: 21 May 2020
This article has been accepted for publication and undergone full peer review but has not been through the copyediting, typesetting, pagination and proofreading process, which may lead to differences between this version and the Version of Record. Please cite this article as doi:10.1096/fba.2020‐00017


Abstract

Stroke causes severe long‐term disability in patients due to the induction of skeletal muscle atrophy and weakness, but the molecular mechanisms remain elusive. Using a preclinical mouse model of cerebral ischemic stroke, we show that stroke robustly induced atrophy as well as significantly decreased  gene expression in the PTA (paralytic tibialis anterior) muscle. Muscle‐specific SirT1 gain‐of‐function mice are resistant to stroke‐induced muscle atrophy and this protective effect requires its deacetylase activity. Although SirT1 counteracts the stroke‐induced up‐regulation of atrogin1, MuRF1 and ZNF216 genes, we found a mechanism that regulates the ZNF216 gene transcription in post‐stroke muscle. Stroke increased the expression of the ZNF216 gene in post‐stroke TA muscle by activating PARP‐1, which binds on the ZNF216 promoter. The SirT1 gain‐of‐function or SirT1 activator, resveratrol, reversed the PARP‐1‐mediated up‐regulation of ZNF216 expression at the promoter level, suggesting a contradicted role for SirT1 and PARP‐1 in the regulation of ZNF216 gene. Overall, our study for the first‐time demonstrated that (1) stroke causes muscle atrophy, in part, through the SirT1/PARP‐1/ZNF216 signaling mechanism, (2) SirT1 can block muscle atrophy in response to different types of atrophic signals via different signaling mechanisms, and (3) identified SirT1 as a critical regulator of post‐stroke muscle mass.

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