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.

Monday, December 7, 2015

Scientists redefine arterial wall inflammation, offer cardiovascular disease treatment hope

Maybe we are finally solving the real problem of atherosclerosis and can get away from statins and the stupid focus on cholesterol.
http://medicalxpress.com/news/2015-12-scientists-redefine-arterial-wall-inflammation.html

Researchers from the University of Toronto have found that a specific cell type plays a key role in maintaining healthy arteries after inflammation. It's a discovery that could provide treatment options for cardiovascular disease—one of the leading causes of death in Canada.
 
The researchers found that a specific type of tissue macrophage, a group of that defend against infection, are created and operate separately from other that come from the . Unlike bone marrow macrophages, these cells live in the outer layer of the , can self-replicate and help to heal the vessel after .
"We've discovered that a group of macrophages are created when the embryo is developing, before the bone marrow is functioning," said Clinton Robbins, a professor in the Faculty of Medicine's Departments of Laboratory Medicine and Pathobiology and Immunology. "These macrophages can self-replicate and likely regulate the normal function of our arteries. This is a fundamental biological discovery that could play an important role in many cardiovascular diseases."
The journal Nature Immunology published the results of the study today.
Robbins and his team found that during infection these self-replicating macrophages leave the arterial wall, while macrophages from the bone marrow come in and engulf the bacteria. The team thinks that once inflammation resolves, the self-renewing macrophages return to heal the damaged tissue.
Using a special tagging system, they accurately traced where the macrophages were coming from.
"Previously, we couldn't identify one macrophage from another because we were limited by technology," said Robbins, who is also the Peter Munk Chair of Aortic Disease Research in the Toronto General Research Institute at University Health Network. "Now we can see exactly where they're coming from and where they're going. Our job now is to get a better understanding of what these different macrophage populations are doing."
Next, the researchers will study how these resident macrophages interact with their tissue environment and exactly what role they might play in . By understanding the relationship between the different cell types, they hope to target inflammation caused by infection or atherosclerosis more effectively.
"We know that while bone marrow macrophages remove bacteria, they can also cause atherosclerosis by entering the arterial wall and multiplying," said Rickvinder Besla, graduate student and co-lead author. "In the old model, you might try to shut the bone marrow response down, but this leaves the patient immunosuppressed. Our new model suggests we could possibly reduce inflammation by boosting the activity of these self-replicating macrophages."
Robbins acknowledges that there's still a lot to learn about the complexity of these macrophages and how they interact with their environment and other cells.
"Arteries are more than tubes that shuttle blood around. They create a complex and dynamic network that reacts to inflammation and disease in different ways. We're excited to figure out another piece of this puzzle and how we might target cardiovascular disease in the future."
More information: Sherine Ensan et al. Self-renewing resident arterial macrophages arise from embryonic CX3CR1+ precursors and circulating monocytes immediately after birth, Nature Immunology (2015). DOI: 10.1038/ni.3343

Journal reference: Nature Immunology search and more info website
Provided by: University Health Network

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