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.

Wednesday, January 25, 2012

TRPM 2 and TRPM 7: Expression Patterns in CNS Cells After Oxygen-Glucose Deprivation

We should have graduate students rewrite these while they still think like the rest of humanity. From the 2011 Canadian Stroke Congress.
Page 81 here:
http://www.strokecongress.org/2011/wp-content/uploads/2011/12/CSC_Abstracts.pdf

TRPM7 and TRPM2 have previously been implicated as regulators of stroke-induced neuronal death. Since, other cation channels implicated in regulating stroke-induced cell death are highly enriched in cortical neurons, we sought to determine the expression of TRPM2 and TRPM7 in various CNS regions over perinatal development
and in specific cell types. Expression patterns were examined in age-specific rat brain tissues and cell-specific primary cultures (enriched neuronal, microglial and astrocyte cultures) using TaqMan real-time PCR to measure dynamic changes in mRNA levels and western blot analyses to quantify protein levels. Furthermore, cell-specific
cultures were subjected to oxygen-glucose deprivation (OGD), and TRP mRNA and protein levels were determined.
Our results indicated that TRPM7 and TRPM2 expression decreased as animals aged. TRPM2 was found to be differentially expressed between cell types, present only in microglia but not cortical neurons or astrocytes, whereas, TRPM7 was expressed at similar levels in all cell types. Also, after a 60 minute period of OGD, TRP levels
had increased. Increased TRP expression after OGD supports previous research implicating TRPM2 and TRPM7 in stroke. Our study also suggests an important role for glial TRPM2, which might inform future development of cell-specific pharmacological inhibitors of TRPM channels.

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