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.

Tuesday, January 26, 2016

Endothelin Receptors, Mitochondria and Neurogenesis in Cerebral Ischemia

This would seem to be incredibly important to find out, getting more nitric oxide and increasing blood flow to the brain. I bet nothing will occur because we have NO stroke leadership or stroke strategy. We are completely fucked because we have fucking failures for stroke associations. I weep for your children and grandchildren. Will no one think of the children? Will no one think at all?
http://www.ncbi.nlm.nih.gov/pubmed/26786146 

Abstract

The ET family consists of three isopeptides (ET-1, ET-2 and ET-3) that produce biological actions by acting on two types of receptors (ETA and ETB). Stimulation of ETA receptors produces potent vasoconstrictor effect, while activation of ETB receptors causes vasodilation by releasing nitric oxide (NO) and prostacyclins. In the central nervous system (CNS) ETA receptors are potent constrictors of the cerebral vasculature and appear to contribute in the causation of cerebral ischemia. ETA receptor antagonists have been found to be effective in animal model of cerebral ischemia; however, clinical studies have shown no efficacy.(Well don't give up, figure out why) Mitochondrial functions are critically important for several neural development processes such as neurogenesis, axonal and dendritic growth, and synaptic formation. ET appears to impair mitochondrial functions through activation of ETA receptors. On the other hand, blocking ETB receptors has been shown to trigger apoptotic processes by activating intrinsic mitochondrial pathway. Mitochondria are important for their role in molecular regulation of neurogenesis and angiogenesis. Stimulation of ETB receptors in the adult ischemic brain has been found to promote angiogenesis and neurogenesis mediated through vascular endothelial growth factor (VEGF) and nerve growth factor (NGF). It will be interesting to investigate the effect of ETB receptor stimulation on mitochondrial functions in the CNS following cerebral ischemia. In the CNS stimulation of ETB receptors has a beneficial effect in animal models of stroke. Since angiogenesis and neurogenesis have recently been implicated in cerebral ischemia, the positive effect of stimulating ETB receptors in cerebral ischemia may be mediated through mitochondrial functions.
 

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