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.

Saturday, October 29, 2022

Neuroprotective Effect of Angiopoietin2 Is Associated with Angiogenesis in Mouse Brain Following Ischemic Stroke

Any research that has neuroprotection working in animals should immediately have research conducted in humans. But it won't since we have NO STROKE LEADERSHIP OR STRATEGY!  It's amazingly obvious to everyone but the stroke medical world.

 Neuroprotective Effect of Angiopoietin2 Is Associated withAngiogenesis in Mouse Brain Following Ischemic Stroke

Citation: Lv, L.-L.; Du, Y.-T.; Chen, X.;
Lei, Y.; Sun, F.-Y. Neuroprotective
Effect of Angiopoietin2 Is Associatedwith Angiogenesis in Mouse BrainFollowing Ischemic Stroke. Brain Sci.2022, 12, 1428. https://doi.org/10.3390/brainsci12111428Academic Editors: Kenneth Fong andKunwei WuReceived: 20 September 2022Accepted: 20 October 2022Published: 24 October 2022Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations.Copyright: © 2022 by the authors.Licensee MDPI, Basel, Switzerland.This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).brainsciencesLing-Ling Lv 1,2,†, Yi-Ting Du 1,2,†, Xiao Chen1,2, Yu Lei 1,2 and Feng-Yan Sun 1,2,*1 Department of Neurobiology and State Key Laboratory of Medical Neurobiology, School of Basic MedicalSciences, Shanghai Medical College, Fudan University, Shanghai 200032, China2Institute for Basic Research on Aging and Medicine of School of Basic Medical Sciences and National ClinicalResearch Center for Aging and Medicine, Huashan Hospital, Hanghai Medical College, Fudan University,Shanghai 200032, China* Correspondence: fysun@shmu.edu.cn These authors contributed equally to this work.

Abstract: 

 Angiogenic factors play an important role in protecting, repairing, and reconstructingvessels after ischemic stroke. In the brains of transient focal cerebral ischemic mice, we observed a reduction in infarct volume after the administration of Angiopoietin 2 (Angpt2), but whether this process is promoted by Angpt2-induced angiogenesis has not been fully elaborated. Therefore, this study explored the angiogenic activities, in reference to CD34 which is a marker of activated ECs and blood vessels, of cultured ECs in vitro and in ischemic damaged cerebral area in mice following Angpt2 administration. Our results demonstrate that Angpt2 administration (100 ng/mL) is neuroprotective by significantly increasing the CD34 expression in in vitro-cultured ECs, reducing the infarct volume and mitigating neuronal loss, as well as enhancing CD34+vascular length andarea. In conclusion, these results indicate that Angpt2 promotes repair and attenuates ischemic injury,and that the mechanism of this is closely associated with angiogenesis in the brain after stroke.

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