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, January 27, 2016

A Nuclear Attack on Thrombosis and Inflammation

What is your doctor doing with this to stop your arterial inflammation? ANYTHING AT ALL?
http://atvb.ahajournals.org/content/36/2/221.extract?etoc 
  1. Edward M. Conway
+ Author Affiliations
  1. From the Department of Medicine, Centre for Blood Research, University of British Columbia, Vancouver, Canada.
  1. Correspondence to Edward M. Conway, MD, PhD, Department of Medicine, Centre for Blood Research, 4306-2350 Health Sciences Mall, University of British Columbia, Vancouver BC V6T 1Z3, Canada. E-mail ed.conway@ubc.ca  
Email for your doctor if they have questions on the procedures. There are no excuses for your doctor not applying this for you.
Key Words:
Thrombomodulin is a transmembrane glycoprotein expressed on the lumenal surface of endothelial cells, where it maintains vascular homeostasis via its anti-inflammatory, anticoagulant, and anti-fibrinolytic properties. These effects of thrombomodulin are achieved through dynamic interactions primarily with thrombin, protein C, thrombin activatable fibrinolysis inhibitor, complement components, and the proinflammatory danger signal high mobility group box 1 (HMGB1).1 When bound to thrombomodulin, thrombin loses its procoagulant/proinflammatory properties, while efficiently generating activated protein C and activated thrombin activatable fibrinolysis inhibitor. Activated protein C is a potent anticoagulant, anti-inflammatory and cytoprotective protease. Activated thrombin activatable fibrinolysis inhibitor inhibits fibrinolysis, and inactivates proinflammatory mediators and anaphylatoxins. The lectin-like domain of thrombomodulin also dampens inflammation by blocking HMGB1 and suppressing complement activation. Diminished expression of thrombomodulin is a feature of endothelial cell dysfunction, and it is a driver in the pathogenesis of several disorders, including venous thromboembolic disease, sepsis, disseminated intravascular coagulation (DIC), atherosclerosis, stroke, inflammatory arthritis and colitis, thrombotic microangiopathies, and diabetic nephropathy. To offset the imbalance associated with reduced thrombomodulin, and with the aim of preventing organ damage, systemic administration of recombinant forms of thrombomodulin has shown efficacy in several preclinical models of thrombosis and inflammation, and in humans with DIC and sepsis.2
See accompanying article on page 361
Yang et al3 have taken a different approach to augment endothelial thrombomodulin and limit disease, particularly focusing on thrombosis. Going nuclear, they examined the role of 2 transcription factors, Nur77 and Nor1, members of the family of nuclear orphan NR4A receptors. These …

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