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, October 7, 2011

Coordinating cell cycle with neurogenesis

Quiz your researcher on phosphorylation.
http://www.nature.com/ncb/journal/v13/n10/full/ncb2356.html

During development of the central nervous system, a lengthening of the cell cycle marks the change from maintenance of progenitor cells to differentiation and neurogenesis. However, the molecular mechanism underlying this process was unclear. Ali et al. (Development 138, 42674277; 2011) now demonstrate that this response may be coordinated by multi-site phosphorylation of the transcription factor neurogenin 2 (Ngn2).

Ali et al. found that Ngn2 phosphorylation is dependent on the cell cycle. Nine sites were identified in Ngn2 that could potentially be phosphorylated, and mutation of all nine resulted in a loss of significant phosphorylation, which was found to be dependent on cyclin-dependent kinases (cdks). Expression of this mutant in Xenopus embryos also led to a significant increase in neurogenesis. The authors found that preventing phosphorylation of Ngn2 increased its stability and enhanced its ability to interact with DNA. Interestingly, rather than some of the specific phosphorylation sites being essential or a threshold level of phosphorylation being required, the authors showed that each phosphorylation has an additive effect on the ability of Ngn2 to bind to its promoters. This could allow fine-tuning of the Ngn2 response to the increasing cell length and the inhibition of cdks that accompanies neurogenesis.

Somebody with a lot more money than me can get the rest of the article for $32.

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