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.

Friday, October 2, 2015

PD-L1 Monoclonal Antibody Treats Ischemic Stroke by Controlling Central Nervous System Inflammation

How many decades before this is rolled out to your hospital? NEVER?
http://stroke.ahajournals.org/content/46/10/2926.abstract?sid=59388841-3a8f-40e1-8b7d-319e6d306b95 
 
  1. Halina Offner, DrMed
+ Author Affiliations
  1. From the Neuroimmunology Research, VA Portland Health Care System, OR (S.B., A.L., A.L.D., A.A.V., H.O.); and Departments of Neurology (S.B., A.L., A.L.D., A.A.V., J.A.S., H.O.), Anesthesiology and Perioperative Medicine (Y.C., J.W., J.A.S., H.O.), Molecular Microbiology and Immunology (A.A.V.), and Medical and Molecular Genetics (J.A.S.), Oregon Health and Science University, Portland.
  1. Correspondence to Halina Offner, DrMed, Neuroimmunology Research, R&D-31, VA Portland Health Care System, 3710 SW US Veterans Hospital Rd, Portland, OR 97239. E-mail offnerva@ohsu.edu
  1. * Drs Bodhankar and Chen contributed equally.

Abstract

Background and Purpose—Both pathogenic and regulatory immune processes are involved in the middle cerebral artery occlusion (MCAO) model of experimental stroke, including interactions involving the programmed death 1 (PD-1) receptor and its 2 ligands, PD-L1 and PD-L2. Although PD-1 reduced stroke severity, PD-L1 and PD-L2 appeared to play pathogenic roles, suggesting the use of anti-PD-L monoclonal antibody therapy for MCAO.
Methods—Male C57BL/6 mice were treated with a single dose of anti-PD-L1 monoclonal antibody 4 hours after MCAO and evaluated for clinical, histological and immunologic changes after 96 hours of reperfusion.
Results—Blockade of the PD-L1 checkpoint using a single injection of 200 μg anti-PD-L1 monoclonal antibody given intravenously 4 hours after occlusion significantly reduced MCAO infarct volumes and improved neurological outcomes after 96 hours of reperfusion. Treatment partially reversed splenic atrophy and decreased central nervous system infiltrating immune cells concomitant with enhanced appearance of CD8+ regulatory T cells in the lesioned central nervous system hemisphere.
Conclusions—This study demonstrates for the first time the beneficial therapeutic effects of PD-L1 checkpoint blockade on MCAO, thus validating proposed mechanisms obtained in our previous studies using PD-1- and PD-L-deficient mice. These results provide strong support for the use of available humanized anti-PD-L1 antibodies for treatment of human stroke subjects.

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