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

From Hairballs to an Understanding of Transendothelial Migration of Monocytes in Atherosclerosis

If hairballs are listed in the full article I'm not paying for it. But ask your doctor for the explanation.
http://atvb.ahajournals.org/content/34/9/1809.extract?etoc
  1. Aldons J. Lusis
+ Author Affiliations
  1. From the Departments of Medicine (M.C., A.J.L.), Microbiology, Immunology and Molecular Genetics, and Human Genetics (A.J.L.), University of California, Los Angeles.
  1. Correspondence to Aldons J. Lusis, PhD, Division of Cardiology, Department of Medicine, A2-237 CHS, University of California, Los Angeles, Los Angeles, CA 90095. E-mail jlusis@mednet.ucla.edu
Key Words:
In the current issue of ATVB, Shang et al provide compelling evidence for the involvement of LIM domain binding 2 (LDB2) in the transendothelial migration of monocytes in atherosclerosis.1 The article is also of interest because of the systems analyses that led to its identification as a strong candidate.
See accompanying article on page 2068
LDB2 was identified earlier as a key driver of atherosclerosis based on studies of gene expression profiles of tissues obtained from patients.2 Using samples from the Stockholm Atherosclerosis Gene Expression (STAGE) study, the authors profiled gene expression of 5 atherosclerosis-relevant tissues from 114 patients undergoing coronary artery bypass grafting. The tissues collected were distal internal mammary artery, wall of the ascending aorta at the aortic root, anterior hepatic edge, skeletal muscle, and visceral fat. A total of 278 gene expression profiles were used in a coupled 2-way clustering analysis3 to identify 60 gene subnetworks in these tissues. Two of the gene clusters, one in atherosclerotic arterial wall (49 genes) and the other in visceral fat (59 genes), segregated the patients according to the extent of atherosclerosis as measured by quantitative coronary angiography. The authors further validated their findings using expression data obtained from carotid lesions isolated from patients undergoing carotid stenosis surgery. Clustering of data identified 8 gene subnetworks in carotid lesions, one of which segregated the patients according to the extent of atherosclerosis as measured by ultrasound-measured intima-media thickness. This cluster significantly overlapped with the 2 previously identified clusters from …


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