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, December 26, 2017

Mitochondrial Dysfunction in Ischemic Stroke

A description of the problem but NO solution. Damn, I hate these lazy researchers. Do stroke survivors care about describing their problems? NO!!!. Provide solutions to their problems you blithering idiots. 
https://link.springer.com/chapter/10.1007/978-981-10-5804-2_10
  1. 1.Department of NeurologyShanghai Ninth People’s Hospital, Shanghai Jiao Tong University School of MedicineShanghaiChina
  2. 2.East HospitalTongji University School of MedicineShanghaiChina
Chapter
First Online:
  • 15 Downloads
Part of the Translational Medicine Research book series (TRAMERE)

Abstract

Mitochondrion is the powerhouse of the cell, which is essential for cell survival after cerebral ischemia/reperfusion. Mitochondrion is a sensitive organelle susceptible to brain ischemia/reperfusion injury. Mitochondrial dysfunction is one of the foremost events involved in brain ischemia/reperfusion process and then induces further damage to brain cells. It influences not only the fate of neural cells but also blood-brain barrier permeability after ischemic stroke. The underlying mechanism of mitochondria dysfunction in determining cell survival and cell death involves in many cell signaling pathways including apoptosis, autophagy, and mitochondrial biogenesis. Mitochondria apoptosis pathway was extensively explored in the past. Many apoptosis-related regulator families were involved in mitochondria apoptosis pathway, like Bcl-2 family, caspase family, p53 gene family, and so on. On the other hand, ROS injury, Ca2+ overload, and mPTP opening are also detrimental to mitochondrial function after cerebral ischemia/reperfusion. Recent interests were focused on the important role of mitophagy and mitochondrial biogenesis on cell survival after cerebral ischemia/reperfusion, which are thought to be endogenous protective mechanisms of mitochondrial dysfunction. Therefore, under ischemia/reperfusion conditions, promoting endogenous protective mechanisms and inhibiting exogenous damage mechanisms are both important therapeutic strategies. In summary, mitochondrial dysfunction is not simply the result of ischemia/reperfusion injury but also the cause of cascading damage. So, protecting dysfunctional mitochondria is pivotal to cell survival after ischemic stroke.
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