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 493 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.My back ground story is here:http://oc1dean.blogspot.com/2010/11/my-background-story_8.html

Sunday, March 22, 2015

Cortical neurogenesis in adult rats after ischemic brain injury: most new neurons fail to mature

Well shit, I was planning on using this to help my recovery. Whom do we have to contact to get this added to the stroke strategy and get human research done on this? Or will this fall thru the cracks like every other interesting stroke research because we have craptastic stroke associations?
http://www.nrronline.org/article.asp?issn=1673-5374;year=2015;volume=10;issue=2;spage=277;epage=285;aulast=Li


1 Department of Neurosurgery, the Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China
2 Department of Neurosurgery, the First Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China

Date of Acceptance13-Oct-2014
Date of Web Publication18-Mar-2015
Correspondence Address:
Ying-bin Li
Department of Neurosurgery, the Second Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province
China
Login to access the Email id

DOI: 10.4103/1673-5374.152383
Get Permissions
  Abstract 
The present study examines the hypothesis that endogenous neural progenitor cells isolated from the neocortex of ischemic brain can differentiate into neurons or glial cells and contribute to neural regeneration. We performed middle cerebral artery occlusion to establish a model of cerebral ischemia/reperfusion injury in adult rats. Immunohistochemical staining of the cortex 1, 3, 7, 14 or 28 days after injury revealed that neural progenitor cells double-positive for nestin and sox-2 appeared in the injured cortex 1 and 3 days post-injury, and were also positive for glial fibrillary acidic protein. New neurons were labeled using bromodeoxyuridine and different stages of maturity were identified using doublecortin, microtubule-associated protein 2 and neuronal nuclei antigen immunohistochemistry. Immature new neurons coexpressing doublecortin and bromodeoxyuridine were observed in the cortex at 3 and 7 days post-injury, and semi-mature and mature new neurons double-positive for microtubule-associated protein 2 and bromodeoxyuridine were found at 14 days post-injury. A few mature new neurons coexpressing neuronal nuclei antigen and bromodeoxyuridine were observed in the injured cortex 28 days post-injury. Glial fibrillary acidic protein/bromodeoxyuridine double-positive astrocytes were also found in the injured cortex. Our findings suggest that neural progenitor cells are present in the damaged cortex of adult rats with cerebral ischemic brain injury, and that they differentiate into astrocytes and immature neurons, but most neurons fail to reach the mature stage.

No comments:

Post a Comment