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 6, 2014

Optimizing human apyrase to treat arterial thrombosis and limit reperfusion injury without increasing bleeding risk

How useful would this be in limiting the reperfusion  damage post tPA usage? What will your doctor and hospital do to change stroke protocols based on this?  ANYTHING AT ALL? Do they ever do anything to help stroke survivors?
http://stm.sciencemag.org/content/6/248/248ra105.abstract
  1. Dana Abendschein1,*
+ Author Affiliations
  1. 1Center for Cardiovascular Research, Department of Internal Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.
  2. 2APT Therapeutics Inc., 4041 Forest Park Avenue, St. Louis, MO 63108, USA.
  3. 3Division of Gastroenterology/Hepatology, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02115, USA.
  4. 4Thrombosis Research Laboratory, Research Service, Veterans Affairs New York Harbor Healthcare System, New York, NY 10010, USA.
  5. 5Division of Hematology and Medical Oncology, Department of Medicine, Weill Cornell Medical College, New York, NY 10021, USA.
  1. *Corresponding author. E-mail: rchen@apt-therapeutics.com (R.C.); dabendsc@DOM.wustl.edu (D.A.)

Abstract

In patients with acute myocardial infarction undergoing reperfusion therapy to restore blood flow through blocked arteries, simultaneous inhibition of platelet P2Y12 receptors with the current standard of care neither completely prevents recurrent thrombosis nor provides satisfactory protection against reperfusion injury. Additionally, these antiplatelet drugs increase the risk of bleeding. To devise a different strategy, we engineered and optimized the apyrase activity of human nucleoside triphosphate diphosphohydrolase-3 (CD39L3) to enhance scavenging of extracellular adenosine diphosphate, a predominant ligand of P2Y12 receptors. The resulting recombinant protein, APT102, exhibited greater than four times higher adenosine diphosphatase activity and a 50 times longer plasma half-life than did native apyrase. Treatment with APT102 before coronary fibrinolysis with intravenous recombinant human tissue-type plasminogen activator in conscious dogs completely prevented thrombotic reocclusion and significantly decreased infarction size by 81% without increasing bleeding time. In contrast, clopidogrel did not prevent coronary reocclusion and increased bleeding time. In a murine model of myocardial reperfusion injury caused by transient coronary artery occlusion, APT102 also decreased infarct size by 51%, whereas clopidogrel was not effective. These preclinical data suggest that APT102 should be tested for its ability to safely and effectively maximize the benefits of myocardial reperfusion therapy in patients with arterial thrombosis.

No comments:

Post a Comment