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, July 18, 2016

PDK1 Determines Collagen-Dependent Platelet Ca2+ Signaling and Is Critical to Development of Ischemic Stroke In Vivo

Ask your doctor what the hell this means for your recovery.
http://atvb.ahajournals.org/content/early/2016/06/23/ATVBAHA.115.307105.abstract
  1. Oliver Borst
+ Author Affiliations
  1. From the Department of Cardiology and Cardiovascular Medicine (P.M., B.W.-A., S.G., D.R., D.E., T.G., M.G., O.B.), Department of Physiology (B.W.-A., F.L.), Department of Evolutionary Biology of Invertebrates, Institute for Evolution and Ecology (M.M.), Department of Dermatology (M.S.), and Department of Clinical Pharmacology (M.S.), University of Tübingen, Tübingen, Germany; Department of Neurology, University of Würzburg, Würzburg, Germany (E.G., C.K.); Institute for Immunology and Transfusion Medicine, University of Greifswald, Greifswald, Germany (G.H., A.G.); and Dr Margarete Fischer-Bosch Institute of Clinical Pharmacology, Stuttgart and University of Tübingen, Tübingen, Germany (S.W., E.S., M.S.).
  1. Correspondence to Oliver Borst, MD, Department of Cardiology and Cardiovascular Medicine, University of Tuebingen, Otfried Mueller-Str.10, 72076 Tuebingen, Germany. E-mail oliver.borst@med.uni-tuebingen.de; or Meinrad Gawaz, MD, Department of Cardiology and Cardiovascular Medicine, University of Tuebingen, Otfried Mueller-Str.10, 72076 Tuebingen, Germany. E-mail meinrad.gawaz@med.uni-tuebingen.de

Abstract

Objective—Activation of platelets by subendothelial collagen results in an increase of cytosolic Ca2+ concentration ([Ca2+]i) and is followed by platelet activation and thrombus formation that may lead to vascular occlusion. The present study determined the role of phosphoinositide-dependent protein kinase 1 (PDK1) in collagen-dependent platelet Ca2+ signaling and ischemic stroke in vivo.
Approach and Results—Platelet activation with collagen receptor glycoprotein VI agonists collagen-related peptide or convulxin resulted in a significant increase in PDK1 activity independent of second-wave signaling. PDK1 deficiency was associated with reduced platelet phospholipase Cγ2–dependent inositol-1,4,5-trisphosphate production and intracellular [Ca2+]i in response to stimulation with collagen-related peptide or convulxin. The defective increase of [Ca2+]i resulted in a substantial defect in activation-dependent platelet secretion and aggregation on collagen-related peptide stimulation. Furthermore, Rac1 activation and spreading, adhesion to collagen, and thrombus formation under high arterial shear rates were significantly diminished in PDK1-deficient platelets. Mice with PDK1-deficient platelets were protected against arterial thrombotic occlusion after FeCl3-induced mesenteric arterioles injury and ischemic stroke in vivo. These mice had significantly reduced brain infarct volumes, with a significantly increased survival of 7 days after transient middle cerebral artery occlusion without increase of intracerebral hemorrhage. Tail bleeding time was prolonged in pdk1−/− mice, reflecting an important role of PDK1 in primary hemostasis.
Conclusions—PDK1 is required for Ca2+-dependent platelet activation on stimulation of collagen receptor glycoprotein VI, arterial thrombotic occlusion, and ischemic stroke in vivo.

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