Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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.
My back ground story is here:

Monday, May 29, 2017

Caspase-independent cell death cascade

In case you want to hire your own researcher to solve for this problem, because your children and grandchildren won't have a solution to this under current stroke leadership.
Figure 1: Caspase-independent cell death cascade. Ischaemia causes calcium influx through multiple channels including, N-methyl-D-aspartate (NMDA) receptor, acid sensing ion channel (ASIC), and TRPM7, which leads to increased neuronal nitric oxide synthase (nNOS), and generation of peroxynitrite (ONOO−) from nitric oxide (NO) and superoxide (O2−), damaging DNA. O2− is generated from NMDA receptor activation of nicotinamide adenine dinucleotide phosphate oxidase. The DNA repair enzyme poly-ADP-ribose polymerase-1 (PARP-1) is activated utilizing cellular nicotinamide adenine dinucleotide (NAD+) forming poly-ADP-ribose (PAR) polymers, which cause nuclear translocation of apoptosis inducing factor (AIF) further damaging DNA. Cell death occurs from AIF-mediated DNA degradation and NAD+ depletion causing energy failure. What plays the role of executioner?

No comments:

Post a Comment