Deans' stroke musings: Intranasal VEGF - A and VEGF - E in a modified Levine model of stroke

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.

Friday, April 19, 2013

Intranasal VEGF - A and VEGF - E in a modified Levine model of stroke

This thesis might not have produced positive results but it did advance the knowledge out there. Something we badly need in order to come up with more hypotheses.

Intranasal VEGF - A and VEGF - E in a modified Levine model of stroke

Intranasal

VEGF

A and VEGF

E in a modified Levine

model of stroke

Jon

athan

Robert Osborne

A thesis submitted for the degree of

Master of Science

at the University of Otago,

Dunedin,

New Zealand

Abstract

VEGF(Vascular endothelial growth factor)-A has been shown to successfully enter the brain via the intranasal pathway and improve symptoms following focal ischemia in rats. However VEGF-A promotes inflammation and vascular permeability which are believed to contribute

to the damage following stroke.

VEGF-E has been shown to produce reduced inflammation

and vascular permeability while still stimulating similar levels of angiogenesis. We aimed to compare intranasal VEGF-A and VEGF-E doses in a modified Levine model of stroke.

VEGF was delivered on days 3, 4 & 5 following hypoxic ischemia.

Infarct was measured on day 14 using cresyl violet stain. Behavioural assessments were performed before hypoxic ischemia and on day 1, 7 and 14. We found that VEGF-A and VEGF-E did not affect behavioural scores or infarct volume.

However, VEGF-E (20μg) reduced weight loss at day 14 after stroke.

These findings suggest that intranasal VEGF-A and VEGF–E are not effective in the modified Levine model used in this study