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.

Friday, June 19, 2015

Researchers find a copolymer scaffold potentially useful in brain repair after brain injury

When is someone in charge going to take responsibility for pushing stuff like this out to stroke hospitals or create clinical trials to prove this out?  Well shit, we have NO ONE in charge, so this will never occur, our stroke associations will not do this, so survivors are once again screwed.
We have no stroke leaders, get used to it.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=153710&CultureCode=en
After 8 weeks new neurons, glia and blood vessels were found surrounding the scaffold and also inside of the synthetic structure based on a ethyl acrylate (EA) and hydroxyl ethyl acrylate (HEA). This regenerative process did not occur in areas where the scaffold was not present, nor in non-implanted control animals. Professors at the CEU Cardenal Herrera University in Valencia have collaborated in this sudy with researchers from the Universitat Politècnica de València, Universidad Complutense and Hospital Clínico San Carlos, in Madrid.
Professors from the Faculty of Health Sciences of the CEU Cardenal Herrera University (CEU-UCH), in Valencia, José Miguel Soria López and María Ángeles García Esparza, have taken part in a new study in order to evaluate, in vivo, the biocompatibility and cell hosting ability of a copolymer channelled scaffold, after an experimental brain injury. This biomaterial, based on ethyl acrylate (EA) and hydroxyl ethyl acrylate (HEA), was implanted after focal brain damage in rats, allowing cell migration, survival and cell colonization by neurons, glial cells, and endothelial cells, which formed vessel-like neostructures, within the scaffold.
The professors collaborated with researchers from Universitat Politècnica de València, Universidad Complutense and Hospital Clínico San Carlos, in Madrid. The results have been published in Neuroscience Letters.
According to Professor Soria, head of the Research Group on neuro-protection and neuro-repair of the central nervous system, at CEU-UCH, the scaffolds made of this acrylate copolymer were implanted in the site of a previous cryolesion in the brain of Wistar rats: “We evaluated the tissue response to the implanted materials after 8 weeks and we observed that they provoked a minimal scar response by the host tissue and, also, permitted the invasion of neurons and glia inside them.” As Professor Soria adds, “this reparative process did not occur in areas where the scaffold was not present, nor in non-implanted control animals.”
In this study, “our findings indicate that this copolymer may constitute an artificial protective niche for the neural cells produced after injury and migrating from subventricular zone (SVZ) to the site of the lesion. In the absence of it, the area with the lesion is irremediably lost. This fact may be of interest for future clinical applications in the regeneration of injured brain,” says Professor Soria.
Professor García Esparza, member of this research group at CEU-UCH, adds: “This copolymer channelled scaffold proves to offer a suitable environment producing a cellular network potentially useful in brain repair after brain injury. In our group it is of greatest importance to identify types of synthetic materials, as a supporting vehicle or scaffold for the cell population to assist neural regeneration processes and new angiogenesis, after local brain injury."
http://www.ncbi.nlm.nih.gov/pubmed/25980992


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