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, August 1, 2013

Evidence Stacks Up That Endothelial Insulin Resistance Is a Culprit in Atherosclerosis

What is your doctor doing with this to prevent your next stroke?
http://circres.ahajournals.org/content/113/4/352.extract.html?etoc
Type 2 diabetes mellitus and the metabolic syndrome greatly increase the risk of cardiovascular disease, manifested as myocardial infarction and stroke. Although it is well known that this risk is largely the result of increased atherosclerosis, the cellular and molecular events within the artery wall responsible for the worsening of atherosclerosis associated with type 2 diabetes mellitus and the metabolic syndrome are less clear. These states are frequently associated with several cardiovascular risk factors, including dyslipidemia, hypertension, obesity, hyperglycemia, and systemic insulin resistance, each of which may contribute to atherosclerosis.
Article, see p 418
Insulin resistance in now known to affect the vascular wall itself, in addition to the better-studied insulin target tissues liver, skeletal muscle, and adipose tissue. Vascular endothelial cells, which play critical roles in atherosclerosis by allowing monocytes and other immune cells to enter the atherosclerotic lesion and by producing proatherogenic and antiatherogenic molecules, develop insulin resistance in both humans and mice concomitant with dyslipidemia and systemic insulin resistance.1 Endothelial cells can also contribute to systemic insulin resistance.2
Insulin has important biological effects in endothelial cells that affect atherosclerosis. Activation of the insulin receptor results in tyrosine phosphorylation of insulin receptor substrate 1 and 2 and subsequent activation of phosphoinositide 3-kinase (PI3K) and the serine/threonine protein kinase Akt. Akt has several targets in endothelial cells, one of which is endothelial nitric oxide (NO) synthase (eNOS). Insulin-induced activation of the PI3K-Akt-eNOS pathway causes increased production of NO, vasorelaxation,3 and suppressed expression of vascular cell adhesion … 

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