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, June 7, 2016

Bumetanide promotes neural precursor cell regeneration and dendritic development in the hippocampal dentate gyrus in the chronic stage of cerebral ischemia

We will never know if this might help stroke survivors because we have no fucking stroke leaders that followup promising research with human clinical trials. You'll be screwed forever until we destroy the existing stroke leadership.

Bumetanide promotes neural precursor cell regeneration and dendritic development in the hippocampal dentate gyrus in the chronic stage of cerebral ischemia




1 Department of Neurology, First Affiliated Hospital of China Medical University, Shenyang, Liaoning Province; Neuroinfection and Neuroimmunology Center, Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
2 Department of Interventional Neuroradiology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
3 Department of Neurology, First Affiliated Hospital of China Medical University, Shenyang; Department of Neurology, Benxi Central Hospital of China Medical University, Benxi, Liaoning Province, China
4 Department of Neurology, First Affiliated Hospital of China Medical University, Shenyang, Liaoning Province, China
5 Department of Medical Genetics, School of Basic Medicine, Peking University, Beijing, China
6 Neuroinfection and Neuroimmunology Center, Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China

Date of Acceptance25-Feb-2016
Date of Web Publication1-Jun-2016
Correspondence Address:
Chuan-sheng Zhao
Department of Neurology, First Affiliated Hospital of China Medical University, Shenyang, Liaoning Province
China
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Source of Support: None, Conflict of Interest: None
DOI: 10.4103/1673-5374.182700
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  Abstract 
Bumetanide has been shown to lessen cerebral edema and reduce the infarct area in the acute stage of cerebral ischemia. Few studies focus on the effects of bumetanide on neuroprotection and neurogenesis in the chronic stage of cerebral ischemia. We established a rat model of cerebral ischemia by injecting endothelin-1 in the left cortical motor area and left corpus striatum. Seven days later, bumetanide 200 µg/kg/day was injected into the lateral ventricle for 21 consecutive days with a mini-osmotic pump. Results demonstrated that the number of neuroblasts cells and the total length of dendrites increased, escape latency reduced, and the number of platform crossings increased in the rat hippocampal dentate gyrus in the chronic stage of cerebral ischemia. These findings suggest that bumetanide promoted neural precursor cell regeneration, dendritic development and the recovery of cognitive function, and protected brain tissue in the chronic stage of ischemia.
Keywords: nerve regeneration; cerebral ischemia; bumetanide; Na + -K + -2Cl- cotransporter 1; hippocampal dentate gyrus; neurogenesis; neural precursor cells; dendritic development; cognitive function; neural regeneration

How to cite this article:
Xu Ws, Sun X, Song Cg, Mu Xp, Ma Wp, Zhang Xh, Zhao Cs. Bumetanide promotes neural precursor cell regeneration and dendritic development in the hippocampal dentate gyrus in the chronic stage of cerebral ischemia. Neural Regen Res 2016;11:745-51

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