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.

Saturday, February 15, 2020

Targeted Myosin-2 Inhibition Improves Brain Regeneration After Stroke by Relaxing Hypoxia-Induced Vasoconstriction in Capillaries

So this seems to solve 1 of 5 neuronal cascade of death issues.  What the fuck is your hospital doing to solve the other 4? What research are they initiating? Or supporting?

Capillaries that don't open due to pericytes

The 5 causes of the neuronal cascade of death in the first week.

 

Targeted Myosin-2 Inhibition Improves Brain Regeneration After Stroke by Relaxing Hypoxia-Induced Vasoconstriction in Capillaries





    Smooth muscle myosin-2 (SMM) is the key regulator of capillary blood flow in the brain tissue. Pre-capillary contractile pericytes (smooth muscle cells, SMCs) block the entrance of brain capillaries in answer to hypoxia during ischemic stroke. One of the major obstacles in stroke therapies is that SMCs remain permanently contracted even after removing the blood clot from large arteries, which hinders healthy blood reperfusion of the infarcted brain regions. Thus, SMM could be an optimal target to improve brain regeneration after clinical interventions. Therefore, we developed an intra-arterial catheter mediated targeted administration of SMM inhibitors into the ischemic brain regions and tested their effects on cerebral blood flow (CBF) after transient middle cerebral artery occlusion (tMCAO) on rats. SPECT and MRI analyses confirmed that different types of SMM inhibitors (e.g. MPH-222) could drastically improve CBF in the ischemic brain areas. We also corroborated this vasodilatation effect on ex vivo human arterioles, where SMM inhibitors could fully relax contracted vessels even in the presence of upstream vasonstrictor signals. Moreover, MPH-222 could also induce neurite outgrowth in different types of neurons through its effect on the non-muscle myosin-2 (NM2) isoforms. These results suggest that targeted, non-selective myosin-2 inhibition is a conceptually new therapeutic way in stroke interventions, which could be combined with current blood clot removing methods (thrombectomy and thrombolysis).




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