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, June 10, 2014

Effects of a Pomegranate Fruit Extract rich in punicalagin on oxidation-sensitive genes and eNOS activity at sites of perturbed shear stress and atherogenesis

So maybe pomegranate and watermelon juice could naturally reduce your plaque. What does your doctor think?
http://cardiovascres.oxfordjournals.org/content/73/2/414.short
The following line from the full text;
Regular pomegranate juice administered to hypertensive patients caused
a significant drop in blood pressure [26], a reduction in carotid plaque development [27] 

The abstract here:

  1. Claudio Napolia,b,*
+ Author Affiliations
  1. aDepartment of General Pathology, School of Medicine, University of Naples, 80134 Italy
  2. bExcellence Research Center of Cardiovascular Diseases, II University of Naples, Italy
  3. cDivision of Anesthesiology University of California, Los Angeles, CA 90095, United States
  4. dDivision of Hypertension, Mayo Clinic Foundation, Rochester, MN 55095, United States
  5. eDepartment of Human Pathology, School of Medicine, University of Naples, 80134 Italy
  6. fDivision of Molecular and Medical Pharmacology, University of California, Los Angeles, CA 90095, United States
  1. *Corresponding author. Department of General Pathology, School of Medicine, University of Naples, 80134 Italy. Email address: claunap@tin.it
  • Received April 14, 2006.
  • Revision received August 19, 2006.
  • Accepted August 25, 2006.

Abstract

Background: Atherosclerosis is enhanced in arterial segments exposed to disturbed flow. Perturbed shear stress increases the expression of oxidation-sensitive responsive genes (such as ELK-1 and p-CREB). Polyphenolic antioxidants contained in the juice derived from the pomegranate contribute to the reduction of oxidative stress and atherogenesis during disturbed shear stress.
Aim of the study: To evaluate the effects of intervention with the Pomegranate Fruit Extract (PFE) rich in polyphones (punicalagin, which is a potent antioxidant) on ELK-1, p-CREB, and endothelial nitric oxide synthase (eNOS) expression induced by high shear stress in vitro and in vivo.
Results: At the doses used in the study, both the PFE and the regular pomegranate juice concentrate reduced the activation of ELK-1 and p-CREB and increased eNOS expression (which was decreased by perturbed shear stress) in cultured human endothelial cells and in atherosclerosis-prone areas of hypercholesterolemic mice. PFE and pomegranate juice increased cyclic GMP levels while there was no significant effect of both compounds on the conversion of l-arginine to l-citrulline. Administration of these compounds to hypercholesterolemic mice significantly reduced the progression of atherosclerosis and isoprostane levels and increased nitrates. This protective effect was relevant with PFE. Vasomotor reactivity was improved and EC25 values in response to Ach and NONOate were significantly increased in treated mice in comparison to controls.
Conclusion: This study indicates that the proatherogenic effects induced by perturbed shear stress can be also reversed by chronic administration of PFE.

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