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 21, 2014

Coenzyme Q10 Increases Cholesterol Efflux and Inhibits Atherosclerosis Through MicroRNAs

What does your doctor have to say about this?
Can coenzyme Q10 reduce the risk of side effects from statins?
 

 

Or is this  atherosclerosis inhibition a better reason for it?
Coenzyme Q10 Increases Cholesterol Efflux and Inhibits Atherosclerosis Through MicroRNAs

  1. Kasey C. Vickers
+ Author Affiliations
  1. From the Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN.
  1. Correspondence to Kasey C. Vickers, PhD, Department of Medicine, Vanderbilt University School of Medicine, 2220 Pierce Ave 312B PRB, Nashville, TN 37232. E-mail kasey.c.vickers@vanderbilt.edu
Key Words:
Atherosclerosis is a progressive inflammatory disease of the artery wall and the underlying basis for cardiovascular disease (CVD), which accounts for ≈32% of all deaths in the United States and is the leading cause of mortality in the world.1 Atherosclerosis is classically defined by the accumulation of lipid and cholesterol deposits within the subendothelial space in the artery wall which leads to chronic inflammation and proinflammatory, cholesterol-laden macrophages which differentiate into resident foam cells in the lesion, ultimately forming an acellular necrotic core.2 To date, the statin drug class has been overwhelmingly successful at reducing circulating total cholesterol levels, namely low-density lipoproteins cholesterol, the number one risk factor for CVD. Although pharmacological intervention with statins has dramatically reduced the number of cardiovascular events, many patients do not tolerate statins and a substantial disease burden remains even in patients who are on statins. Therefore, a great need remains to identify new drug targets and novel approaches to prevent and treat atherosclerosis and CVD. One strategy that has been extensively studied, but remains central to atherosclerosis reduction, is identifying new ways to increase the removal of excess cholesterol from peripheral cells and lesions through the reverse cholesterol transport (RCT) pathway. Briefly, the RCT pathway involves the transport of cholesterol from peripheral tissues (ie, foam cells within atherosclerotic lesions) to the liver by high-density lipoproteins (HDL), where cholesterol is excreted from the body as bile.3 This pathway is mediated by a number of lipid and cholesterol transporters, including the widely …

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