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, August 13, 2014

A new look at heart disease

Ask your doctor if anything in here will change how they treat your plaque problems.
 http://medicalxpress.com/news/2014-08-heart-disease.html
Scientists at the Interfaculty Institute of Biochemistry (IFIB) have collaborated with colleagues from the Department of Pharmacy and the Department of Dermatology of the University of Tübingen to identify a long-overlooked function of vascular smooth muscle cells in atherosclerosis.

Atherosclerosis, the buildup of plaques in the arteries, leads to myocardial infarction and stroke and is the major cause of death in the Western world. It is a chronic inflammatory disease of the arteries arising from interactions of modified lipoproteins and various cell types including monocyte-derived macrophages from the blood and (SMCs) in the vessel wall. "It is unclear, however, how each particular cell type contributes to the development of an atherosclerotic lesion," says Professor Robert Feil, senior author of the study. "One highly controversial issue is the contribution of vascular SMCs to plaque growth."

The IFIB researchers performed lineage tracing experiments in mice, in which they have genetically labeled mature SMCs in the vessel wall of young mice before the onset of the disease and then monitored their fate in older atherosclerotic animals. "Surprisingly, we found that SMCs in the arterial wall can undergo clonal expansion during disease progression and convert into macrophage-like that have lost the classical SMC marker, α-smooth muscle actin," says Dr. Susanne Feil, the first author of the publication. "It seems that certain atherosclerotic lesions contain even more SMC-derived macrophages than traditional monocyte-derived macrophages."

These findings indicate that previous studies based on immunostaining of plaque cells for smooth muscle and macrophage markers have vastly underestimated the role of SMCs and overestimated the role of monocyte-derived macrophages in atherosclerosis. Robert Feil notes that the results in the mouse model might also translate to humans. "Targeting SMC-to-macrophage transdifferentiation could be a novel therapeutic strategy to treat atherosclerotic heart disease and perhaps many other diseases with a component."

This work was supported by grants from VolkswagenStiftung, Deutsche Forschungsgemeinschaft, fortüne-Programm der Medizinischen Fakultät der Universität Tübingen, and Dr. Karl Kuhn-Stiftung.

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