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PostPosted: Thu Oct 04, 2012 7:03 pm 
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Interesting to ponder how this might play into CCSVI.

You have a protein in mice studies ( pigment epithelium-derived factor ) that supposedly, again in mice,
assists in oligo/myelin production: http://www.futurity.org/health-medicine/protein-could-undo-ms-nerve-damage/
HEALTH & MEDICINE - Posted by Charles Casey-UC Davis on Thursday, October 4, 2012
Protein could undo MS nerve damage


“What’s unique about our findings is that we demonstrated that the continuous administration of recombinant PEDF into the normal adult mouse brain enhances production of glial cells in a critical portion of the brain,” says Jiho Sohn, a post-doctoral scholar and lead study author.
“In addition, we noted the maturation of oligodendrocyte progenitors in the bundle of nerve fibers that connect the left and right hemispheres of the brain.” The study also documented that PEDF infusion enhances production of oligodendroglial progenitor cells from endogenous neural stem cells in mice with corpus callosum demyelinative lesions."

....... All well and good and a possible future therapy in repairing our nerves.

However, this PEDF is also (as mentioned in the article) useful for the inhibition of tumor growth, and for macular degeneration, by inhibiting blood vessel growth!

Now who knows if that applies directly to the venous system or is strictly on the arterial side, a search on "pedf blood vessels" deals mainly with diabetic retinopathy, macular degeneration, vessel growth in tumors etc.

One would think that vessels are vessels but who knows?

Is this protein active in the brain or just the eyes and/or tumors?

To wit:
"Dr. Bouck said that blood supply in the eye seemed to be controlled by the balance between a pair of substances, PEDF, which inhibits new blood vessel growth, and a factor called VEGF (pronounced veg-eff), which stimulates vessel growth.

"When oxygen is low, as happens in certain eye diseases, less PEDF is produced, allowing blood vessels to invade and more oxygen to come in. When oxygen is sufficient, the pigment epithelial cells step up production of PEDF, which suffuses the eye and banishes blood vessels, Dr. Bouck said."

I'm wondering how this protein plays into say collateral growth, certainly not something we would want to inhibit in those with compromised venous flow..

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PostPosted: Thu Oct 04, 2012 9:24 pm 
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There's something more than excess blood vessel growth in tumours. I think it's some kind of mutation that results not just in uncontrolled growth, but in growth that fails to follow the normal fractal pattern of splitting of blood vessels. This, I think, is a genetic mutation which will happen eventually due to the entropy of age.

I agree that collateral growth is sometimes necessary; sometimes it's the response to a low-oxygen situation (stenosis?). Some of the collaterals I've seen don't look very well-ordered, and I think the seeming inability of cancer and "MS" to coexist might be related to why they don't end up tumourous. They seem to end up stringy, not splitting in two much.

If we are going to start messing with this VEGF/PEDF balance, let's say I'd prefer it were done to mice first...

Oligodendrocytes maturing does sound like a good thing if you're needing myelin... My corpus callosum is atrophic, too.

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