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.

Sunday, November 22, 2015

Intraventricular Infusion of a Low Fraction of Serum Enhances Neurogenesis and Improves Recovery in a Rodent Stroke Model

Is this interesting enough to be proposed for human clinical trials? I want to know whom in the world can answer that question and then follow thru with the research to prove it one way or another. But that won't occur because we have no stroke strategy or stroke leaders at all.
http://www.sciencedirect.com/science/article/pii/S0304394015302573
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Highlights

A serum fraction (100K) was easily derived from serum.
100K/bFGF enhanced cell proliferation at SVZ area and infarcted brain.
100K/bFGF increased the number of MAP-2 cells at infarcted brain in MCAO rat.
100K/bFGF improved animals' motor coordination of MCAO rat.

Abstract

Enhancing endogenous neurogenesis is a potential therapeutic strategy in stroke treatment. We have previously domonstrated that treatment with a fraction of serum with molecular weight of less than 100kDa (100K) combined with bFGF promoted neurogenesis of cultured stem and progenitor cells (NSPCs). In this study, we further evaluated the efficacy of intraventricular administration of 100K with bFGF (100K/bFGF) in a rat model of transient middle cerebral artery occlusion (MCAO). Rats administered 100K/bFGF on post-stroke day 1 exhibited a higher number of Ki67 and Nestin immunoreactive cells at the subventricular zone (SVZ) area and in the infarcted brain, indicating promotion of NSPCs proliferation. The 100K/bFGF treatment also predominantly increased the number of MAP-2 immunoreactive cells rather than GFAP immunoreactive cells at the SVZ area and in the infarcted regions, implying that 100K/bFGF dominated NSPCs differentiating into neurons rather than astrocytes. Importantly, treatment with 100K/bFGF significantly improved the animals' motor coordination. These findings demonstrated that treatment with a low serum fraction and bFGF benefited ischemic stroke likely through promotion of the proliferation and neuronal differentiation of endogenous NSPCs.

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