Deans' stroke musings: What Makes Good Cholesterol Go Bad?

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, February 23, 2012

What Makes Good Cholesterol Go Bad?

And maybe they will eventually find out why cholesterol turns into plaque.
http://www.everydayhealth.com/high-cholesterol/0223/what-makes-good-cholesterol-go-bad.aspx

Researchers have discovered how specific proteins in the blood transform HDL cholesterol (the good kind) into LDL Cholesterol (the bad kind). Here's how it works, plus ways to amp up your good cholesterol levels through diet and exercise.

Blame it on a tiny, banana-shaped protein molecule called CETP, which stands for cholesteryl ester transfer protein.

Research from the U.S. Department of Energy (DOE)’s Lawrence Berkeley National Laboratory (Berkeley Lab) has revealed how CETP turns good cholesterol (high density lipoproteins, or HDL) into bad cholesterol (low density lipoproteins, LDL).

Lipoproteins are substances that carry cholesterol throughout the body. LDLs do so in a way that can clog arteries — blocking blood flow, and potentially causing heart disease or stroke. Hence the “bad” label. HDLs, on the other hand, carry cholesterol out of the bloodstream and into the liver, where it’s excreted. That way, it doesn’t build up in the arteries.

It turns out that CETP molecules transfer cholesterol from those good HDLs to bad LDLs via a tunnel that runs through its center.

The findings, published in the journal Nature Chemical Biology, could lead to more efficient ways of preventing the development of heart disease. “Our model identifies new interfaces of CETP that interact with HDL and LDL and delineates the mechanism by which the transfer of cholesterol takes place,” says Gang Ren, PhD, of Berkeley Lab’s Molecular Foundry, who led the study. “This is an important step toward the rational design of next generation CETP inhibitors for treating cardiovascular disease.”