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.

Wednesday, April 13, 2011

Vascular endothelial growth factor (VEGF

more details to keep you confused, I am.
definition:
Vascular endothelial growth factor (VEGF): A substance made by cells that stimulates new blood vessel formation, a mitogen for vascular endothelial (vessel lining) cells.
VEGF is a polypeptide structurally related to platelet-derived growth factor (PDGF). The gene for VEGF is on chromosome 6p12.

Vascular endothelial growth factor (VEGF) stimulates neurogenesis in vitro and in vivo

http://www.pnas.org/content/99/18/11946.full

Abstract

Vascular endothelial growth factor (VEGF) is an angiogenic protein with neurotrophic and neuroprotective effects. Because VEGF promotes the proliferation of vascular endothelial cells, we examined the possibility that it also stimulates the proliferation of neuronal precursors in murine cerebral cortical cultures and in adult rat brain in vivo. VEGF (>10 ng/ml) stimulated 5-bromo-2′-deoxyuridine (BrdUrd) incorporation into cells that expressed immature neuronal marker proteins and increased cell number in cultures by 20–30%. Cultured cells labeled by BrdUrd expressed VEGFR2/Flk-1, but not VEGFR1/Flt-1 receptors, and the effect of VEGF was blocked by the VEGFR2/Flk-1 receptor tyrosine kinase inhibitor SU1498. Intracerebroventricular administration of VEGF into rat brain increased BrdUrd labeling of cells in the subventricular zone (SVZ) and the subgranular zone (SGZ) of the hippocampal dentate gyrus (DG), where VEGFR2/Flk-1 was colocalized with the immature neuronal marker, doublecortin (Dcx). The increase in BrdUrd labeling after the administration of VEGF was caused by an increase in cell proliferation, rather than a decrease in cell death, because VEGF did not reduce caspase-3 cleavage in SVZ or SGZ. Cells labeled with BrdUrd after VEGF treatment in vivo include immature and mature neurons, astroglia, and endothelial cells. These findings implicate the angiogenesis factor VEGF in neurogenesis as well.

Vascular endothelial growth factor (VEGF) is a hypoxia-inducible secreted protein that interacts with receptor tyrosine kinases on endothelial cells to promote angiogenesis. Recent evidence indicates that VEGF can also act directly on neurons to produce neurotrophic and neuroprotective effects. For example, VEGF stimulates axonal outgrowth and improves the survival of cultured superior cervical and dorsal root ganglion neurons (1, 2), enhances the survival of mesencephalic neurons in organotypic explant cultures (3), protects HN33 (mouse hippocampal neuron × neuroblastoma) cells from death induced by serum withdrawal (4), reduces hypoxic death of HN33 cells and cultured cerebral cortical neurons (5), and protects cultured hippocampal neurons from glutamate toxicity (6). Conversely, inhibition of VEGF signaling leads to apoptosis in cortical neuron cultures (7), and deletion of the hypoxia-response element from the VEGF promoter causes motor-neuron degeneration in mice (8), perhaps because of loss of a direct neurotrophic effect of VEGF.

Neurogenesis, the process through which precursor cells differentiate toward a mature neuronal phenotype, persists in discrete regions of the adult brain, including the rostral subventricular zone (SVZ) (9, 10) and the subgranular zone (SGZ) of the hippocampal dentate gyrus (DG) (11). Comparatively little is known regarding the possible role of VEGF in adult neurogenesis, although other growth factors, including epidermal growth factor (EGF) (12), fibroblast growth factor-2 (FGF-2) (13), brain-derived neurotrophic factor (BDNF) (14), and erythropoietin (15), have been implicated. In addition, the VEGF receptor Flk-1 is expressed in neural progenitor cells of the mouse retina (16), and its activation stimulates their differentiation into amacrine neurons and photoreceptor cells (17). Finally, neurogenesis in the adult SGZ appears to occur in intimate association with angiogenesis, suggesting that common factors, such as VEGF, might be involved in both processes (18).

To investigate the possibility that VEGF is a neurogenic as well as an angiogenic factor, we examined its effects in in vitro and in vivo models of neurogenesis, by using the cell-proliferation marker 5-bromodeoxyuridine (BrdUrd). The in vitro model employs primary cultures of embryonic rat cortical neurons, and has been used to identify growth factors involved in hypoxia-induced neurogenesis, including heparin-binding EGF (19). The in vivo model involves intracerebroventricular (i.c.v.) administration of growth factors in the adult rat, and has been used to study the induction of neurogenesis in the brain in vivo by factors such as EGF, FGF-2, and BDNF (20–22).

I would prefer that I not have to go to medical school and do all this on my own. There has to be enough smart people out there who care to completely change stroke rehab (rehab protocols, OT, PT and PMR doctor schooling). I've given up on the stroke associations.