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PostPosted: Thu Nov 05, 2009 6:03 pm 
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skydog wrote:
Bumping this for the newbies and to refresh the memories of the rest. Not a dead horse, Lots of very important info in the Shayk/Sheron posts. Bumping up the good stuff needs to continue. Back to the roots of how we arrived to this point for others to see. M


Thanks so much, Mark...this thread is one of the most important for new folks to read....researchers have known about the connection of slowed perfusion and hypoxic injury to MS brains, but it's never been explained before CCSVI. We finally have a model that confirms the research- and explains why blood flow is slowed leaving the brain. This thread is an oldie, but a goodie :)
Also...glad to know you'll be heading back to Stanford, Mark. I wish you answers and healing.
cheer

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PostPosted: Sat Dec 12, 2009 4:19 pm 
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Bump. :)

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RRMS Dx'd 2007, first episode 2004. Bilateral stent placement, 3 on left, 1 stent on right, at Stanford August 2009. Watch my operation video: http://www.youtube.com/watch?v=cwc6QlLVtko, Virtually symptom free since, no relap


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PostPosted: Sat Dec 12, 2009 4:37 pm 
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Thanks, Mark! I LOVE THIS THREAD.
-was thinking about this the other night....listening to Jeff's smooth, rhythmic breathing while he sleeps. No more gasping for air or sleep apnea since his procedure. His jugulars are open, his brain is getting oxygen throughout the night. I've encouraged Dr. Haacke to include his BOLD technology (oxygenation levels) testing for MS patients before and after jugular opening. I think this is a big part of the puzzle for many MS patients who currently suffer from fatigue and brain fog.
cheer

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dual stents placed 5/09
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PostPosted: Sat Dec 12, 2009 4:53 pm 
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I am stunned and amazed and overwhelmed !! It will take me days to get up to speed on this.. 8O. I didn't join this board until October and so missed out on all the earlier scientific conversations. Needless to say, I haven't taken the time to read all the earlier conversations either.

I am trying to "feed" some researchers the scientific basis and framework for CCSVI and they should see this post and all the links. But if I send them the post I imagine they will just set it aside as just a bunch of know-nothings chatting about something they don't understand. It is clear to me that you all do understand quite a bit. So my quandary is how to be a proper conduit from this discussion to these researcher's minds. I am a bit overwhelmed. I am also very tired, fatigued, headachy and cranky, LOL.

Any suggestions would be most appreciated.

Oh, I forgot to ask... why aren't these paper in the scientific thread ?

ozarkcanoer


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PostPosted: Sat Dec 12, 2009 5:04 pm 
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We have had some good discussion on our threads and this thread is one of the better ones, but I have kept the research thread pretty much focused on the actual Zamboni and related research rather than our speculations. I could link this thread perhaps.......

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PostPosted: Sat Dec 12, 2009 5:27 pm 
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Being focused is a good idea. It is easier to understand Zamboni's main ideas with out all the obfuscating science jargon. Maybe the best thing is just to bump up all the good threads like this one, and we TIMSers can absorb them. Or, I could go back and read all the old threads, digest them and try to communicate the information to my contacts (who, by the way, never seem to want to respond to me :( :( :( ).

ozarkcanoer


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PostPosted: Sat Dec 12, 2009 5:43 pm 
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Yes, thank you for bumping the thread, I had not seen it, but was aware of the selenium, reduced glutathione, etc. An excellent naturopath was my first stop after diagnosis, and she did un incredible job of leveling me out. It very may well be that her protocol has kept the really nasty MS stuff at bay.

The hypoxia seems so very obviously an issue, and it is interesting that there are reports of sleep apnea. I used to meditate myself to sleep, but had to stop, because I would wake up not breathing. I became a little nervous about slowing down my breath and heart. I have had sleep apnea for at least 30 years.
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Imagine this: you are dx'd MS then they give you a good dose of erythropoietin and HCG ( or neupogen or something) to stimulate your stem cells........ while your BBB is still open

a week later you get a dose of Steroid....

then stents.

Total fantasy!! But the idea would be to do some repairative work before closing the BBB up by stopping CCSVI.


This is something that I have been thinking of a lot, and struggling with. Can the iron be scavenged back through the BBB when it is healed? I'm not sure how that would work. Simplistically, I would think that it would be impermeable (to iron) both ways, but that does not quite work in my addled mind.

I have been taking very high doses of fibrin-scouring enzymes for the last 8 months, or so, and started having a very long relapse (very unusual for me) about 6 months ago. It has occurred to me that the plaques might not be scar tissue in the normal sense, but are a buffer secondary to the breached BBB. I have discontinued the enzymes as an experiment.

I have thought about iron chelation, but have wondered if that might also be fuel on the fire, the idea being that pulling the iron out, with no sufficient drainage, could result in that much more iron (in the cerebral vessels) to find other breaches, and cause, perhaps, more wide-spread damage. I suppose that this is some of the research that needs to be done in the long term. Liberation must come first though, and there is a pretty darn convincing body of research and practice on that already.

I wonder if anyone going to Poland has the opportunity to ask Dr. Simka about immediately starting some kind of chelation therapy ie: is it contra-indicated by his after surgery medications? I would ask by e-mail, but he must be half crazy with the level of inquiries, and doesn't need to be pestered by my mental meanderings. I would think that the endothelium would heal quite quickly, within hours, perhaps.

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PostPosted: Sat Dec 12, 2009 5:50 pm 
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marie, cheer, Curious, et. al.,

I just emailed my contacts a link to this thread. Sometimes I just have to be bold and reckless. What do I have to lose anyway, LOLOL.

ozarkcanoer


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PostPosted: Sun Dec 13, 2009 12:17 am 
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Lol. I'm just a bumper car. It's fun to go down the rabbit hole. I'd been meaning to "really dig in" since the procedure but have been catching up on life and the kids and such so just trying to keep up with the latest and add to the knowledge base and talk to others and now got both kids full time for Christmas vacation so what I did, was clone myself. Simple.

I think it's a great thread to send to your researchers. Tell em to come on in, the water's fine...

Mark

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RRMS Dx'd 2007, first episode 2004. Bilateral stent placement, 3 on left, 1 stent on right, at Stanford August 2009. Watch my operation video: http://www.youtube.com/watch?v=cwc6QlLVtko, Virtually symptom free since, no relap


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PostPosted: Sun Dec 13, 2009 12:36 am 
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Enjoy your kids , Mark. Isn't that what life is really about?

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PostPosted: Sun Dec 13, 2009 8:14 am 
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Check out this video from Gemany's Max Planck Institute of Biochemistry. It shows the migration of T-Cells through the BBB (T-Cells green spots, vessels = red). This is "live" footage.

http://www.mpg.de/video/MS.avi

This might pretty well be considered evidence supporting the idea that slackened bloodflow makes it easier for buckwild T-Cell gangsters to slip into the brain and terrorize and kill honest brain cells.


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PostPosted: Sun Dec 13, 2009 10:38 am 
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For those with sleep apnea (aka Johnson?)...I think CPAP machine- continuos positive airway pressure- might be a wise choice until jugular veins can be addressed- I found a study showing how CPAP opened up IJVs while in supine position, but can' find the study this am....will look later-
cheer

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PostPosted: Sun Dec 13, 2009 10:41 pm 
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A connection between hypoxia and ferretin in the brain:
More evidence that hypoxic injury might be behind some of the iron deposition in brain tissue-

Quote:
Multiple Sclerosis
Multiple sclerosis is a neuroinflammatory condition in which the oligodendrocyte and its product myelin are the targets of attack by mononuclear cells. By using immunocy to chemical and histochemical staining methods, high concentrations of ferritin and iron are observed in oligodendrocytes. During stresses such as hypoxia, oligodendrocytes can increase their synthesis of ferritin. Ferritin, by releasing iron, is fully capable of providing elements (such as free iron) that through oxidative processes can cause cellular injury. In 1 study, 5 autopsy specimens from patients with multiple sclerosis showed positive iron reactions in sections surrounding demyelinated plaques.


http://ajcp.ascpjournals.org/content/su ... 4.full.pdf

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PostPosted: Sun Dec 13, 2009 11:28 pm 
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Thanks cheerleader.

It all makes perfect sense, the more we find.

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PostPosted: Mon Dec 14, 2009 12:15 am 
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cheerleader wrote:
A connection between hypoxia and ferretin in the brain:
More evidence that hypoxic injury might be behind some of the iron deposition in brain tissue-

Quote:
Multiple Sclerosis
Multiple sclerosis is a neuroinflammatory condition in which the oligodendrocyte and its product myelin are the targets of attack by mononuclear cells. By using immunocy to chemical and histochemical staining methods, high concentrations of ferritin and iron are observed in oligodendrocytes. During stresses such as hypoxia, oligodendrocytes can increase their synthesis of ferritin. Ferritin, by releasing iron, is fully capable of providing elements (such as free iron) that through oxidative processes can cause cellular injury. In 1 study, 5 autopsy specimens from patients with multiple sclerosis showed positive iron reactions in sections surrounding demyelinated plaques.


http://ajcp.ascpjournals.org/content/su ... 4.full.pdf


Is it tight junctions separating + serum iron, or oligo breakdown, mix of both? I mean this makes a bit more sense in a more localized fashion, now does this mean that it is possible that the BBB is NOT breached then since we have a mechanism inside that could explain oligo death? If so what killed the oligos then? Okay wait then it's hypoxia via reflux, then oligo then iron deposition? I know I'm talking in circles. Heck it could be iron from BOTH sources, serum and oligo death... Could it be that the only real thing that reflux contributes in a great way is hypoxia and nothing else? Or is the localized reflux+hypertension enough to get the iron deposited in there all on it's own.

That's why I find that other imaging study interesting because it indicates that there is axonal death and death "markers" like N=acetylaspartate . situated away from lesions, we just don't *see* it/them on normal imaging models, but it's there, diffused across the white matter.

Sometimes this stuff is like a rubber ball in the racquetball court that is my brain. Bounce bounce bounce bounce. I dunno...

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RRMS Dx'd 2007, first episode 2004. Bilateral stent placement, 3 on left, 1 stent on right, at Stanford August 2009. Watch my operation video: http://www.youtube.com/watch?v=cwc6QlLVtko, Virtually symptom free since, no relap


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