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.

Showing posts with label neovascularization. Show all posts
Showing posts with label neovascularization. Show all posts

Saturday, May 21, 2022

Optical excitation of organic semiconductors as a highly selective strategy to induce vascular regeneration and tissue repair

How close is your doctor to using this in your recovery?

Optical excitation of organic semiconductors as a highly selective strategy to induce vascular regeneration and tissue repair

https://doi.org/10.1016/j.vph.2022.106998Get rights and content

Abstract

Therapeutic neovascularization represents a promising strategy to rescue the vascular network and restore organ function in cardiovascular disorders (CVDs), including acute myocardial infarction, heart failure, peripheral artery disease, and brain stroke. Endothelial colony forming cells (ECFCs), which are mobilized in circulation upon an ischemic insult, are commonly regarded as the most suitable cellular tool to achieve therapeutic neovascularization. ECFCs can be genetically or pharmacologically manipulated to enhance their vasoreparative potential by boosting specific pro-angiogenic signalling pathways. However, optical stimulation represents the most reliable approach to control cellular activity because of its high selectivity and unprecedented spatio-temporal resolution. Herein, we discuss a novel strategy to drive ECFC angiogenic activity in ischemic tissues by combining geneless optical excitation with photosensitive organic semiconductors. We describe how photoexcitation of the conducting polymer poly(3-hexylthiophene-2,5-diyl), also known as P3HT, stimulates extracellular Ca2+ entry through Transient Receptor Potential Vanilloid 1 (TRPV1) channels upon the production of hydrogen peroxide (H2O2) in the cleft between the nanomaterial and the cell membrane. H2O2-induced TRPV1-dependent Ca2+ entry stimulates ECFC proliferation and tube formation, thereby providing the proof-of-concept that photoexcitation of organic semiconductors may offer a reliable strategy to stimulate ECFCs-dependent neovascularization in CVDs.

 

Sunday, June 9, 2013

Physical activity improves long-term stroke outcome via endothelial nitric oxide synthase-dependent augmentation of neovascularization and cerebral blood flow.

And only from 2006, so what have your doctors been doing for the last 7 years? Amy has already told us how to create nitric oxide by ourselves by chanting. No self-prescription, you know how dangerous chanting is without a prescription from your doctor. You might start flying like those TM practitioners.
http://www.ncbi.nlm.nih.gov/pubmed/17038638

Abstract

Physical activity upregulates endothelial nitric oxide synthase (eNOS), improves endothelium function, and protects from vascular disease. Here, we tested whether voluntary running would enhance neovascularization and long-term recovery following mild brain ischemia. Wild-type mice were exposed to 30 minutes of middle-cerebral artery occlusion (MCAo) and reperfusion. Continuous voluntary running on wheels conferred long-term upregulation of eNOS in the vasculature and of endothelial progenitor cells (EPCs) in the spleen and bone marrow (BM). This was associated with higher numbers of circulating EPCs in the blood and enhanced neovascularization. Moreover, engraftment of TIE2/LacZ-positive BM-derived cells was increased in the ischemic brain. Four weeks after the insult, trained animals showed higher numbers of newly generated cells in vascular sites, increased density of perfused microvessels and sustained augmentation of cerebral blood flow within the ischemic striatum. Moreover, running conferred tissue sparing and improved functional outcome at 4 weeks. The protective effects of running on angiogenesis and outcome were completely abolished when animals were treated with a NOS inhibitor or the antiangiogenic compound endostatin after brain ischemia, and in animals lacking eNOS expression. Voluntary physical activity improves long-term stroke outcome by eNOS-dependent mechanisms related to improved angiogenesis and cerebral blood flow

Friday, May 31, 2013

POLYMERIC MATERIALS FOR NEOVASCULARIZATION

You will need to ask your doctor the difference between angiogenesis and neovascularization. A great dissertation.
https://www.ideals.illinois.edu/bitstream/handle/2142/44267/Ross_Devolder.pdf?sequence=1
Only 122 pages for your doctor.
Revascularization therapies have emerged as a promising strategy to treat various acute and
chronic wounds, cardiovascular diseases, and tissue defects
.
It is common to either administer proangiogenic growth factors, such as vascular endothelial growth factor (VEGF) or transplant cells that
endogenously express multiple proangiogenic factors.
Additionally, these strategies utilize a wide variety
of polymeric systems, including hydrogels and biodegradable plastics, to deliver proangiogenic factors in a sophisticated manner to maintain a sustained proangiogenic environment.
Despite some impressive results in rebuilding vascular networks, it is still
a challenging task to engineer mature and functional neovessels in
target tissues, because of the increasing complexities involved with neovascularization
applications
.
To resolve these challenges, this work aims to design a wide variety of proangiogenic biomaterial systems with tunable properties used for neovascularization therapies.
This thesis describes the design of several biomaterial systems used for the delivery of proangiogenic factors in neovascularization therapies, including: an electrospun/e
lectrosprayed biodegradable plastic patch used for directional blood vessel growth (Chapter 2), an alginate-
g
-
pyrrolehydrogel system that biochemically stimulates cellular endogenous proangiogenic factor expression (Chapter 3), an enzyme catalyzed alginate
-
g
-
pyrrole hydrogel system for VEGF delivery (Chapter 4), an
enzyme activated alginate
-
g
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pyrrole hydrogel system with systematically controllable electrical and
mechanical properties (Chapter 5), and an alginate
-
g
-
pyrrole hydrogel that enables the decoupled control
of electrical conductivity and mechanical rigidity and is use to electrically stimulate cellular endogenous proangiogenic factor expression (Chapter 6). Overall, the
biomaterial systems developed in this thesis
will be broadly useful for improving the quality of a wide array of molecular and cellular
based revascularization therapies