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, February 5, 2013

MFGE8 inhibits inflammasome-induced IL-1β production and limits postischemic cerebral injury

Get your researcher after this to see what human clinical trials can do to limit the neuronal cascade of death.
http://www.jci.org/articles/view/65167?key=9c368b2173b91a4a0e01

Results and Discussion

MFGE8 reduces postischemic cerebral tissue damage and inflammatory response. We first compared Mfge8–/– mice and control WT littermates in a model of focal cerebral ischemia. We found that infarct size was significantly larger in Mfge8–/– mice compared with their controls (Figure 1A), a noteworthy augmentation of 38% which was abrogated by supplementation of Mfge8–/– with recombinant murine MFGE8 (rMFGE8) (Figure 1B). These results clearly indicate that endogenous MFGE8 is required for protection against excessive postischemic cerebral damage. We also found that supplementation of WT mice (Figure 1C) with rMFGE8 induced a significant reduction of infarct volume, in agreement with the recently reported beneficial effect of recombinant human MFGE8 in a model of cerebral injury in rats

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