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.

Tuesday, December 13, 2016

The role of endoglin in post-ischemic revascularization

Do we need to get this past the blood brain barrier to help recovery?  Whom is doing the followup research?
http://link.springer.com/article/10.1007/s10456-016-9535-4
  • Elena Núñez-Gómez
  • Miguel Pericacho
  • Claudia Ollauri-Ibáñez
  • Carmelo Bernabéu
  • José M. López-Novoa
  • Elena Núñez-Gómez
    • 1
    • 2
  • Miguel Pericacho
    • 1
    • 2
  • Claudia Ollauri-Ibáñez
    • 1
    • 2
  • Carmelo Bernabéu
    • 3
    • 4
  • José M. López-Novoa
    • 1
    • 2
  1. 1.Renal and Cardiovascular Research Unit, Department of Physiology and PharmacologyUniversity of SalamancaSalamancaSpain
  2. 2.Biomedical Research Institute of Salamanca (IBSAL)SalamancaSpain
  3. 3.Centro de Investigaciones BiológicasSpanish National Research Council (CIB, CSIC)MadridSpain
  4. 4.Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER)MadridSpain
Review Paper
DOI: 10.1007/s10456-016-9535-4
Cite this article as:
Núñez-Gómez, E., Pericacho, M., Ollauri-Ibáñez, C. et al. Angiogenesis (2016). doi:10.1007/s10456-016-9535-4
  • 15 Downloads

Abstract

Following arterial occlusion, blood vessels respond by forming a new network of functional capillaries (angiogenesis), by reorganizing preexisting capillaries through the recruitment of smooth muscle cells to generate new arteries (arteriogenesis) and by growing and remodeling preexisting collateral arterioles into physiologically relevant arteries (collateral development). All these processes result in the recovery of organ perfusion. The importance of endoglin in post-occlusion reperfusion is sustained by several observations: (1) endoglin expression is increased in vessels showing active angiogenesis/remodeling; (2) genetic endoglin haploinsufficiency in humans causes deficient angiogenesis; and (3) the reduction of endoglin expression by gene disruption or the administration of endoglin-neutralizing antibodies reduces angiogenesis and revascularization. However, the precise role of endoglin in the several processes associated with revascularization has not been completely elucidated and, in some cases, the function ascribed to endoglin by different authors is controversial. The purpose of this review is to organize in a critical way the information available for the role of endoglin in several phenomena (angiogenesis, arteriogenesis and collateral development) associated with post-ischemic revascularization.

No comments:

Post a Comment