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.

Monday, August 22, 2011

Agmatine enhances neurogenesis by increasing ERK1/2 expression

More neurogenesis and a new word to understand - astrogenesis.
http://www.sciencedirect.com/science/article/pii/S0024320511003365

Abstract

Aim


Our study aimed to demonstrate whether agmatine could regulate proliferation and cell fate determination of subventricular zone neural stem cells (SVZ NSCs).

Main methods


SVZ NSCs were grown in the presence of epidermal growth factor (EGF) and basic fibroblast growth factor (bFGF) (20 ng/ml) until 4 days in vitro (DIV) and later the culture medium was replaced without EGF and bFGF until 11 DIV in the absence (EGF/bFGF+/−/Ag) or presence of agmatine (EGF/bFGF+/−/Ag+). Another set SVZ NSCs were maintained with EGF and bFGF until 11 DIV without (EGF/bFGF+/+/Ag) or with agmatine treatment (EGF/bFGF+/+/Ag+). Agmatine's effect on proliferation and cell death (H and PI staining and Caspase-3 immunostaining) was examined at DIV 4 and 11. Agmatine's (100 μM) effect on cell fate determination was confirmed by immunostaining and Western blot at 11 DIV.

Key findings


Agmatine treatment reduced the neurosphere size and total cell count number dose-dependently in all the experimental groups both at DIV 4 and11. Immunoblotting and staining results showed that agmatine increased the Tuj1 and MAP2 and decreased the GFAP with no change in the Oligo2 protein expressions. This neurogenesis effect of agmatine seems to have a relation with ERK1/2 activation and anti-astrogenesis effect is thought to be related with the suppression of BMP 2,4 and SMAD 1,5,8 protein expression.

Significance


This model could be an invaluable tool to study whether agmatine treated SVZ NSC transplantation to the CNS injury could trigger neurogenesis and decrypt the full range of molecular events involved during neurogenesis in vivo as evidenced in vitro.
I like this last line.

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