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.

Wednesday, July 20, 2016

Double agent: Anti-tumor drug already in human trials may combat atherosclerosis

Better than these?


Israeli study uses gold particles to ‘seek and destroy’ artery blockages

Or this?

Shear-Activated Nanoparticle Aggregates Combined With Temporary Endovascular Bypass to Treat Large Vessel Occlusion

A nanoparticle does double duty, imaging and treating atherosclerosis

Remove the plaque.
Do you want the lawnmower?
http://www.articlecity.com/videos/health/Lawnmower-For-Clogged-Arteries-175286465.php
Or Drano? I would be worried about this, sloughing off chunks
http://www.ivanhoe.com/channels/p_channelstory.cfm?storyid=26404
 

  But we will never know because we have NO leaders to ask these simple questions of and NO way to update our missing stroke strategy. 

The latest here:

 Double agent: Anti-tumor drug already in human trials may combat atherosclerosis

Here’s an attention-getting twofer for you: A signal tumor cells display on their surfaces to protect themselves from being devoured by the immune system also plays a role in enabling atherosclerosis, the process underlying heart attacks and strokes.
An injectable drug that can block this so-called “don’t eat me” signal is already being tested in clinical trials in cancer patients, so safety data obtained from those trials can be used to advance the drug’s evaluation for combating cardiovascular disease, the world’s biggest killer.
In a study published in Nature, Stanford cardiologist and vascular surgeon Nick Leeper, MD, and his colleagues found that the “don’t eat me” signal – actually a cell-surface protein scientists call CD47 – is oddly abundant in atherosclerotic plaques. These are composites of fatty substances and dead and dying cells that accumulate at various places inside most people’s arteries and eventually restrict blood flow or, if they rupture, hive off clots that can clog these vessels, suddenly cutting off blood supply to the heart, brain or other organ.
While writing a news release on the study, I asked Leeper to give me some background. He did:
Even a perfectly healthy body turns over more than 100 billion cells a day, every day… One of the several jobs performed by immune cells called macrophages — from the Greek words for ‘big eater’— is to come and gobble up those dead and dying cells, which might otherwise begin releasing substances that can foster inflammation.
Many cells in the body feature CD47 on their surfaces to tell the immune system, “Hey! I’m alive, going strong,  and part of this person’s healthy tissue.” That keeps macrophages from attacking them.
But in the late 1990s and early 2000s, Stanford developmental biologist and stem-cell reseacher Irv Weissman, MD, and his colleagues identified CD47 as being overrepresented on tumor cells, which helps them evade destruction by macrophages. Weissman’s group went on to show that blocking CD47 with monoclonal antibodies that bind to and obstruct the protein on tumor cells restores macrophages’ ability to devour those cells. Phase-1 clinical safety trials of CD47-blocking antibodies in patients with solid tumors and blood cancers are now underway.
In the new Nature study, Leeper’s team found that these same antibodies can prevent and even reverse the buildup of atherosclerotic plaque in several strains of laboratory mice that are particularly predisposed to develop cardiovascular disease.
If what’s worked so well in mice winds up working in people, the rare example of a single agent (the anti-CD47 antibodies) that can effectively treat both cancer and atherosclerosis in one shot, as it were (making it, of course, a “double agent”), could someday become a reality. What’s especially tantalizing is that this drug would fight cardiovascular disease by targeting not mere risk factors, such as high cholesterol or high blood pressure, but the actual atherosclerotic plaques directly responsible for the disorder.


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