chromatic & vision sensitivity in hypoxia

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

chromatic & vision sensitivity in hypoxia

Postby Cece » Thu Feb 17, 2011 7:30 pm

http://www.iovs.org/content/49/2/820.abstract
Mild Hypoxia Impairs Chromatic Sensitivity in the Mesopic Range

conclusions. In the mesopic range, mild hypoxia impairs chromatic sensitivity progressively with reducing luminance. Binocular summation of chromatic signals is consistent and independent of the luminance channel. The CAD test is highly sensitive to mild congenital and acquired color vision deficiencies.


http://oai.dtic.mil/oai/oai?verb=getRec ... =ADA129719
Abstract : The effects of sixteen days of sustained hypoxia (4300m equivalent) on the dark adaptation threshold function were studied. Twelve male subjects were measured periodically (days 2,4,6,9,11,13,16 of exposure) over a 20-min test period for both red and green stimuli using a new computerized dark adaptometer. Comparison with sea level performance showed negligible elevations of thresholds for red response, but highly significant impairment of green response (P<00001) over almost the entire dark adaptation function. These losses peaked between the sixth and ninth day followed by little recovery, except at the eleventh day when the subjects descended briefly to 3200m elevation. Impairments developed rapidly again upon return to the original higher altitude. The results differ from previous published findings based on shorted exposure periods which showed only slight impairments of the early segment of dark adaptation. Implications of the results are discussed.

http://www.clinph-journal.com/article/S1388-2457(06)01868-2/abstract
Objective
This study investigated neuroretinal activity under normoxic and hypoxic conditions with the multifocal electroretinogram (mfERG).

Methods
We used two mfERG paradigms, the fast flicker and slow flash stimulation modes, to measure neuroretinal activity in five healthy participants who breathed room air and a reduced oxygen mixture (14% oxygen, balance nitrogen). We analysed concentric ring N1P1 and P1N2 response density amplitudes, the P1 implicit times as well as the local scalar product (SP) response densities.

Results
During hypoxia there was a significant reduction of the scalar product response density for the fast flicker (p<0.001) and for the slow flash mfERG (p<0.001). The N1P1 and P1N2 response densities were lower especially for the central three rings; although these reductions were not significant between the two oxygen conditions, they indicated an overall distortion of the mfERG waveform.

Conclusions
It is demonstrated that a postreceptoral, primarily ON and OFF bipolar cell deficit is evident in the central retina of healthy young people during short term hypoxia.

Significance
Our findings suggest that persons with pre-existing ischaemic eye disease may be at risk when exposed to hypoxic conditions.


http://www.springerlink.com/content/u44986g78877w715/
The effect of a moderate level of hypoxia on human color vision
Algis J. Vingrys and Leon F. Garner

Abstract
This study reports the effect of a moderate level of hypoxia on human color discimination. We found a generalized loss of color vision affecting both red-green and blue-yellow discrimination at an altitude of 12,000 feet. Although the residual color discrimination at this altitude was within age-matched, sea-level norms, a statistically significant increase over sea level error scores was measured on the Farnsworth-Munsell 100-Hue test and the Pickford-Nicolson anomaloscope. An analysis of psychophysical and electrophysiological studies indicates that hypoxia acts by depressing retinal ganglion cell activity and that it can affect photopic visual processes as well as scotopic vision. We conclude that studies evaluating man's visual performance at altitude must consider post-receptoral processes.


http://journals.lww.com/internat-ophtha ... ude.6.aspx
International Ophthalmology Clinics:
Spring 1999 - Volume 39 - Issue 2 - ppg 59-78

The Eye at Altitude


more coming....
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Postby Cece » Thu Feb 17, 2011 7:32 pm

http://www.ingentaconnect.com/content/a ... 1/art00002
Oxygenation State and Twilight Vision at 2438 m
Author: Connolly, Desmond M.

Source: Aviation, Space, and Environmental Medicine, Volume 82, Number 1, January 2011 , pp. 2-8(7)

Abstract:

Connolly DM. Oxygenation state and twilight vision at 2438 m. Aviat Space Environ Med 2011; 82:2-8.

Introduction: Under twilight viewing conditions, hypoxia, equivalent to breathing air at 3048 m (10,000 ft), compromises low contrast acuity, dynamic contrast sensitivity, and chromatic sensitivity. Selected past experiments have been repeated under milder hypoxia, equivalent to altitude exposure below 2438 m (8000 ft), to further define the influence of oxygenation state on mesopic vision. Methods: To assess photopic and mesopic visual function, 12 subjects each undertook three experiments using the Contrast Acuity Assessment test, the Frequency Doubling Perimeter, and the Color Assessment and Diagnosis (CAD) test. Experiments were conducted near sea level breathing 15.2% oxygen (balance nitrogen) and 100% oxygen, representing mild hypobaric hypoxia at 2438 m (8000 ft) and the benefit of supplementary oxygen, respectively. Results: Oxygenation state was a statistically significant determinant of visual performance on all three visual parameters at mesopic, but not photopic, luminance. Mesopic sensitivity was greater with supplementary oxygen, but the magnitude of each hypoxic decrement was slight. Hypoxia elevated mesopic contrast acuity thresholds by ~4%; decreased mesopic dynamic contrast sensitivity by ~2 dB; and extended mean color ellipse axis length by approximately one CAD unit at mesopic luminance (that is, hypoxia decreased chromatic sensitivity). Conclusions: The results indicate that twilight vision may be susceptible to conditions of altered oxygenation at upper-to-mid mesopic luminance with relevance to contemporary night flying, including using night vision devices. Supplementary oxygen should be considered when optimal visual performance is mission-critical during flight above 2438 m (8000 ft) in dim light.
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Postby Cece » Thu Feb 17, 2011 7:34 pm

Br J Ophthalmol 2010;94:1393-1397 doi:10.1136/bjo.2009.178491
Laboratory science

Effects on colour discrimination during long term exposure to high altitudes on Mt Everest

Gabriel Willmann1,2, Iliya V Ivanov3,4, Manuel D Fischer3, Sukhamay Lahiri1, Rohit K Pokharel5, Annette Werner3, Tejvir S Khurana1

Abstract
Aim To investigate changes in colour discrimination as a result of chronic hypoxic exposure induced by extreme altitudes (above 8000 m) during an expedition to Mt Everest.

Methods Colour discrimination thresholds for tritan, protan and deutan axes were measured extensively in two male participants (four eyes) during an expedition to Mt Everest, using a quantitative, computer controlled psychophysical colour vision test (modified version of the Cambridge Colour Test). The tests were carried out over a period of 54 days at altitudes of 1300 m, 3450 m, 4410 m, 5060 m, 5300 m, 6450 m, 7200 m and 8000 m.

Results Colour vision tests 1 week before and 6 months after the expedition indicated normal colour discrimination in both participants. With increasing altitude, colour discrimination thresholds were found to rise, predominantly for the tritan (blue) axes in both observers. Deutan (green) thresholds were minimally elevated at high altitude, whereas protan (red) was altered in one observer. Tritan colour discrimination thresholds decreased as a function of time spent at a given altitude and normalised upon return to low altitude.

Conclusions Chronic hypoxia induced by high altitude exposure transiently affects colour discrimination, in particular tritan axis discrimination. Decreased tritan discrimination is partly reversible upon physiological adaptation to high altitude and completely normalised upon return to low altitude.
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Postby Cece » Thu Feb 17, 2011 7:35 pm

Color Research & Application
Special Issue: The Proceedings of the International Colour Vision Society

Volume 26, Issue S1, pages S277–S280, 2001


Relation between retinal hypoxia and alteration of the chromatic vision in anemias and glaucomas
Maria Mattiello, Marta Maneiro, Ricardo Gastelú

Abstract
Both glaucoma and anemia produce losses in chromatic discrimination. A discrimination loss can frequently be seen prior to changes visible in fundoscopy. The etiology is assumed to be an absence of proper oxygenation due to raised interocular pressure that blocks the blood irrigation system, or to a deficiency in red blood cells, hemoglobin, or total blood volume. Results of this study show that: (a) if there is an appropriate early treatment, the patients with glaucomas and anemias can improve their chromatic vision; (b) the chromatic tests enable a follow-up of both pathologies; (c) early presentation of chromatic deficits could be due to cellular hypoxia; (d) iron-deficit anemias are similar in score values to the open-angle chronic glaucomas with a mild and/or medium loss of visual field. © 2000 John Wiley & Sons, Inc. Col Res Appl, 26, S277–S280, 2001
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Postby Cece » Thu Feb 17, 2011 7:39 pm

negative results in this one, but some review of other studies and mention of the hue test:
Among other methods to detect colour
vision defects, Farnsworth-Munsell 100 Hue (FM-
100) test is the preferred method at high altitude or
simulating laboratory environments [7, 8]. Error
scores by the FM-100 Hue test are reported to increase
at moderate altitude (3600m) when compared with
sea-level scores; it was suggested that hypoxia at high
altitudes can depress retinal ganglion cell activity and
can affect photopic as well as scotopic vision [8].

http://www.erciyestipdergisi.org/pdf/pdf_EMJ_175.pdf
It's the full pdf of the article.
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Postby Cece » Thu Feb 17, 2011 7:42 pm

http://circ.ahajournals.org/cgi/content ... 16/24/2818

(Circulation. 2007;116:2818-2829.)
© 2007 American Heart Association, Inc.

--------------------------------------------------------------------------------

Molecular Cardiology


Age Decreases Endothelial Progenitor Cell Recruitment Through Decreases in Hypoxia-Inducible Factor 1 Stabilization During Ischemia
Eric I. Chang, MD*; Shang A. Loh, MD*; Daniel J. Ceradini, MD; Edward I. Chang, MD; Shin-e Lin, MD; Nicholas Bastidas, MD; Shahram Aarabi, MD; Denise A. Chan, PhD; Michael L. Freedman, MD; Amato J. Giaccia, PhD; Geoffrey C. Gurtner, MD
From the Department of Surgery (Eric I. Chang, S.A.L., D.J.C., Edward I. Chang, S.L., N.B., S.A., G.C.G.) and Department of Radiation Biology (D.A.C., A.J.G.), Stanford University, Stanford, Calif; and Department of Medicine (M.L.F.), New York University, New York, NY.

Correspondence to Geoffrey C. Gurtner, MD, Stanford University, PSRL–GK201, 257 Campus Dr, Stanford, CA 94305-5148. E-mail ggurtner@stanford.edu

Received May 16, 2007; accepted September 28, 2007.

Background— Advanced age is known to impair neovascularization. Because endothelial progenitor cells (EPCs) participate in this process, we examined the effects of aging on EPC recruitment and vascular incorporation.

Methods and Results— Murine neovascularization was examined by use of an ischemic flap model, which demonstrated aged mice (19 to 24 months) had decreased EPC mobilization (percent mobilized 1.4±0.2% versus 0.4±0.1%, P<0.005) that resulted in impaired gross tissue survival compared with young mice (2 to 6 months). This decrease correlated with diminished tissue perfusion (P<0.005) and decreased CD31+ vascular density (P<0.005). Gender-mismatched bone marrow transplantation demonstrated significantly fewer chimeric vessels in aged mice (P<0.05), which confirmed a deficit in bone marrow–mediated vasculogenesis. Age had no effect on total EPC number in mice or humans. Reciprocal bone marrow transplantations confirmed that impaired neovascularization resulted from defects in the response of aged tissue to hypoxia and not from intrinsic defects in EPC function. We demonstrate that aging decreased hypoxia-inducible factor 1 stabilization in ischemic tissues because of increased prolyl hydroxylase–mediated hydroxylation (P<0.05) and proteasomal degradation. This resulted in a diminished hypoxia response, including decreased stromal cell–derived factor 1 (P<0.005) and vascular endothelial growth factor (P<0.0004). This effect can be reversed with the iron chelator deferoxamine, which results in hypoxia-inducible factor 1 stabilization and increased tissue survival.

Conclusions— Aging impairs EPC trafficking to sites of ischemia through a failure of aged tissues to normally activate the hypoxia-inducible factor 1–mediated hypoxia response.

this one has nothing to do with vision but it came up and it's interesting; does aging diminish our ability to cope with hypoxia on a cellular level?
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Postby Cece » Thu Feb 17, 2011 7:49 pm

Medicine Graefe's Archive for Clinical and Experimental Ophthalmology
Volume 237, Number 5, 377-380, DOI: 10.1007/s004170050247
CLINICAL INVESTIGATION

Colour vision disturbances in chronic smokers
C. Erb, Thilo Nicaeus, Martin Adler, Jutta Isensee, Eberhart Zrenner and Hans-Jürgen Thiel


Abstract
· Purpose: The aim of the present study was to test the influence of smoking on colour perception. · Subjects and methods: At the University Eye Hospital Tübingen, 76 generally healthy smokers with inconspicuous ophthalmological findings (visual acuity, refraction, intraocular pressure, morphology) were examined by the cap-sorting test, Roth 28-hue desaturated. Group 1 was comprised of smokers (n=20; M 9, F 11; mean age 28.1±10.3 years) with a smoking consumption of less than one packet of cigarettes per day (8.4±5.3 cigarettes/day) for 9.1±8.3 years. Group 2 consisted of smokers (n=32; M 22, F 10; mean age 28.6±9.7 years) with a smoking consumption of one or more than one packet per day (30±8.4 cigarettes/day) for 9.5±8.3 years. Generally healthy and ophthalmologically normal non-smokers served as a control group (n=76; M 41, F 35; mean age 30±9 years). · Results: The average error score of the control group was (median±mean absolute deviation) 42±18. Group 1 showed no difference to the control group (51±27; P=0.42). On the other hand, group 2 had a significantly higher error score than the control group (102±45; P<0.0001). · Conclusion: Otherwise healthy smokers with a cigarette consumption of less than 20 cigarettes per day do not show any disturbances in colour vision. Smokers who consume more than 20 cigarettes per day may suffer colour vision defects as a result.

please don't smoke if you have MS, it adds hypoxia to hypoxia
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Postby cheerleader » Thu Feb 17, 2011 7:53 pm

I can see clearly now the rain is gone
I can see all obstacles in my way
Gone are the dark clouds that had me blind
It's gonna be a bright, bright sunshinin' day
It's gonna be a bright, bright sunshinin' day

Oh yes, I can make it now the pain is gone
All of the bad feelings have disappeared
Here is the rainbow I've been praying for
It's gonna be a bright, bright sunshinin' day


Reading thru your research, I heard this song, Cece :)
Great job collecting the papers on hypoxia and color vision. There is so much linking relief of diffuse cerebral hypoxia to all of the improvements you CCSVI-ers are having immediately after angioplasty. Relief of fatigue, spasms, cognitive fog, improved vision, color and detail preception, return of dreaming. And I can't take credit for the revelation, it was Dr. Dake who put it together, since he'd seen this in his patients he'd treated for relief of vena cava syndrome.

We're going to need doctors to publish these results. We need the BOLD fmri results of blood flow from Dr. Haacke. The anecdotes continue to increase. Thanks for sharing your story with all of us, Cece....keep healing!
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Postby Cece » Thu Feb 17, 2011 8:14 pm

That is a fun song for this, Cheer.

I quoted Dr. Dake's results to my husband tonight, from ISET, where in his RR patients fatigue continued to improve even up to the one year mark. Lots of healing ahead....

There are a thousand (or more) research papers needing to be written on CCSVI, but I think this Farnsworth-Munsell 100 Hue test could be administered before and after the procedure, it would be interesting.
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Postby bluesky63 » Sat Feb 19, 2011 6:34 am

The vision test is a great idea. :-) Anything objective and reproducible will be wonderful.

I have seen a distinct improvement in my night vision. And I know I keep going on about black and white movies vs. color, but that really is how it feels.

The song . . . look at my user name -- can you tell I love it? The optimism in it was one of many reasons I chose my name. :-) And it's a perfect image for the liberati!

Thanks for the posts and the awesome energy and research and commitment, everyone! What a difference from a year ago, from two years ago! Where will we be in 2012?
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Postby ThisIsMA » Sat Feb 19, 2011 12:29 pm

This quote from one of the studies Cece quoted in this thread jumped out at me:

We demonstrate that aging decreased hypoxia-inducible factor 1 stabilization in ischemic tissues because of increased prolyl hydroxylase–mediated hydroxylation (P<0.05) and proteasomal degradation. This resulted in a diminished hypoxia response, including decreased stromal cell–derived factor 1 (P<0.005) and vascular endothelial growth factor (P<0.0004). This effect can be reversed with the iron chelator deferoxamine, which results in hypoxia-inducible factor 1 stabilization and increased tissue survival.


I so wish I had enough background in science to know what they were talking about, but my intuition is that this might have something to do with the reason why people with MS get increased disabiltity as we age. And that CCSVI treatment followed by iron chelation might fight that.
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Postby Cece » Sat Feb 19, 2011 12:37 pm

ThisIsMA wrote:This quote from one of the studies Cece quoted in this thread jumped out at me:

We demonstrate that aging decreased hypoxia-inducible factor 1 stabilization in ischemic tissues because of increased prolyl hydroxylase–mediated hydroxylation (P<0.05) and proteasomal degradation. This resulted in a diminished hypoxia response, including decreased stromal cell–derived factor 1 (P<0.005) and vascular endothelial growth factor (P<0.0004). This effect can be reversed with the iron chelator deferoxamine, which results in hypoxia-inducible factor 1 stabilization and increased tissue survival.


I so wish I had enough background in science to know what they were talking about, but my intuition is that this might have something to do with the reason why people with MS get increased disabiltity as we age. And that CCSVI treatment followed by iron chelation might fight that.

wow - I didn't know that was in there!
Deferoxamine results in hypoxia-inducible factor 1 stabilization and increased tissue survival.

here's one study:
12 patients with advanced multiple sclerosis were given deferoxamine for a period of 3 months.
4 patients showed significant improvement, 2 had moderate improvement and 3 were slightly
improved

http://tinyurl.com/6f9s62m
I dont' have access to the full paper though.

another one, seemingly without results but short-term and no control group:
http://www.ncbi.nlm.nih.gov/pubmed/10875447
Cell Mol Biol (Noisy-le-grand). 2000 Jun;46(4):865-9.

A multiple course trial of desferrioxamine in chronic progressive multiple sclerosis.
Lynch SG, Fonseca T, Levine SM.

Department of Neurology, University of Kansas Medical Center, Kansas City 66160, USA. slynch@kumc.edu

Abstract
Chronic progressive multiple sclerosis (MS) is a debilitating disease that is often refractory to treatment. We have previously published a pilot study using a single 2-week course of the iron chelating drug, desferrioxamine (DFO), as a candidate drug for treatment of this form of MS. In this study, we gave 9 patients up to 8 courses of this regimen over 2 years. The patients tolerated the medication well. During the study, 1 patient improved, 3 remained stable, and 5 worsened by 0.5 on the Kurtzke expanded disability status scale (EDSS). These results suggest that, while the drug is well tolerated, no effect on disease progression can be identified at this dosage level. A more continuous dosage schedule could be studied as a candidate for treatment in this disease process.

It did show that the drug was well tolerated.

I agree with you about aging, ThisIsMA.
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Postby Cece » Sat Feb 19, 2011 1:03 pm

Deferoxamine has been shown to suppress experimental allergic encephalomyelitis (Pedchenko and LeVine 1998), an animal model of multiple sclerosis, and thus might be useful in the treatment of dismyelinating disorders.

http://onlinelibrary.wiley.com/doi/10.1 ... 507.x/full
(not in the abstract, but it comes up in the search results in google since google must be searching the full paper)

If EAE had anything to do with MS, this one would be exciting....

What ThisIsMA pointed out is exciting because it's not the chelating properties that is the focus, it's the impact on the hypoxia factor that was mentioned in that research. A different mechanism of action for the results to be coming from and one that fits in well with CCSVI/hypoxia.

http://www.annals.org/content/120/6/490.abstract
Iron-Chelating Agents in Non-Iron Overload Conditions
E. E. Voest; G. Vreugdenhil; and J. J. M. Marx

...Deferoxamine improved the deleterious effects of experimental allergic encephalomyelitis in
rats [108]. This model was used to study multiple sclerosis. Consequently, a clinical trial investigating the effects of deferoxamine in multiple sclerosis was begun [109].


Hypoxia Alters Iron Homeostasis and Induces Ferritin Synthesis in Oligodendrocytes
Yan Qi1, Tejal M. Jamindar3, Glyn Dawson1,2,*Article first published online: 23 NOV 2002

DOI: 10.1046/j.1471-4159.1995.64062458.x

Abstract: Both iron and the major iron-binding protein ferritin are enriched in oligodendrocytes compared with astrocytes and neurons, but their functional role remains to be determined. Progressive hypoxia dramatically induces the synthesis of ferritin in both neonatal rat oligodendrocytes and a human oligodendroglioma cell line. We now report that the release of iron from either transferrin or ferritin-bound iron, after a decrease in intracellular pH, also leads to the induction of ferritin synthesis. The hypoxic induction of ferritin synthesis can be blocked either with iron chelators (deferoxamine or phenanthroline) or by preventing intracellular acidification (which is required for the release of transferrin-bound iron) with weak base treatment (ammonium chloride and amantadine). Two sources of exogenous iron (hemin and ferric ammonium citrate) were able to stimulate ferritin synthesis in both oligodendrocytes and HOG in the absence of hypoxia. This was not additive to the hypoxic stimulation, suggesting a common mechanism. We also show that ferritin induction may require intracellular free radical formation because hypoxia-mediated ferritin synthesis can be further enhanced by cotreatment with hydrogen peroxide. This in turn was blocked by the addition of exogenous catalase to the culture medium. Our data suggest that disruption of intracellular free iron homeostasis is an early event in hypoxic oligodendrocytes and that ferritin may serve as an iron sequestrator and antioxidant to protect cells from subsequent iron-catalyzed lipid peroxidation injury.

...(from google, same article) The hypoxic induction of ferritin synthesis can be blocked either with iron chelators (deferoxamine
or phenanthro- line) or by preventing ...


Eur Neurol 1994, 26:310-323. 12. Guy
J, Mcgorray S, Qi XP, Fitzsimmons J, Mancuso A, Rao N: Conjugated deferoxamine reduces the blood-brain barrier disruption in experimental optic neuritis.
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Postby cheerleader » Sat Feb 19, 2011 1:33 pm

And I will take this moment to plug my favorite anti-oxidant, BBB permeating chelating agent and hypoxia protective supplement---
EGCG
or, green tea.

The fountain of youth.

Evidence to link abnormal metal (iron, copper and zinc) metabolism and handling with Parkinson’s and Alzheimer’s diseases pathology has frequently been reported. The capacity of free iron to enhance and promote the generation of toxic reactive oxygen radicals has been discussed numerous times. Metal chelation has the potential to prevent iron-induced oxidative stress and aggregation of alpha-synuclein and beta-amyloid peptides. The efficacy of iron chelators depends on their ability to penetrate the subcellular compartments and cellular membranes where iron dependent free radicals are generated. Thus, natural, non-toxic, brain permeable neuroprotective drugs, are preferentially advocated for “ironing out iron” from those brain areas where it preferentially accumulates in neurodegenerative diseases. This review will discuss the most recent findings from in vivo and in vitro studies concerning the transitional metal (iron and copper) chelating property of green tea and its major polyphenol, (−)-epigallocatechin-3-gallate with respect to their potential for the treatment of neurodegenerative diseases.

http://www.springerlink.com/content/j6808g63382p0656/

and it protects the brain from hypoxic injury---

Unilateral common carotid artery occlusion followed by global hypoxia caused extensive neuronal damage in the ipsilateral hemisphere of the brain, particularly in the hippocampus and cerebral cortex, as evidenced by hematoxylin and eosin staining. The mean volume of infarction was 99.6  15.6 mm3. There was no apparent neuronal damage in the contralateral hemisphere.
EGCG (50 mg/kg) i.p. treatment for 4 days beginning 1 day prior to HI significantly (P0.05) reduced the mean volume of infarction (38.016.4 mm3). Hippocampus and cortical structures were protected by
EGCG administration.

http://www.fasebj.org/content/19/2/258.full.pdf

It also makes a tasty beverage. And no, I'm not selling it on my website :) But Jeff's been taking it for over 3 years, and he's a fan--
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Postby ThisIsMA » Sat Feb 19, 2011 1:38 pm

Cece, Wow! I think you're on to something. You are an amazing researcher!

Again I wish I could fully understand the technical details of the science, but the articles you're quoting seem right on target.

Maybe someone should pass these research articles on to Dr. Zamboni just in case he isn't already aware of this particular line of research regarding the relationship between hypoxia, iron, antioxidants, and oligodendrocytes?

I know he's a big proponent of the significance of the iron/ms association. Also Dr. Haacke might be interested?

Very exciting stuff!

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