Gibbledygook's anti-viral log

Tell us what you are using to treat your MS-- and how you are doing.

Postby gibbledygook » Wed Mar 11, 2009 1:35 am

Am looking at shear stress on the endothelium...

1: Mol Cell Biomech. 2008 Mar;5(1):1-8.Links
Role of shear stress direction in endothelial mechanotransduction.Chien S.
UCSD, La Jolla, CA, USA.

Fluid shear stress due to blood flow can modulate functions of endothelial cells (ECs) in blood vessels by activating mechano-sensors, signaling pathways, and gene and protein expressions. Laminar shear stress with a definite forward direction causes transient activations of many genes that are atherogenic, followed by their down-regulation; laminar shear stress also up-regulates genes that inhibit EC growth. In contrast, disturbed flow patterns with little forward direction cause sustained activations of these atherogenic genes and enhancements of EC mitosis and apoptosis. In straight parts of the arterial tree, laminar shear stress with a definite forward direction has anti-atherogenic effects. At branch points, the complex flow patterns with little net direction are atherogenic. Thus, the direction of shear stress has important physiological and pathophysiological effects on vascular ECs.

PMID: 18524241 [PubMed - indexed for MEDLINE]
link


1: Free Radic Res. 2007 Dec;41(12):1364-75. Links
Microcirculation and oxidative stress.Crimi E, Ignarro LJ, Napoli C.
Department of Anesthesia and Critical Care, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. ecrimi@partners.org

The microcirculation is a complex and integrated system, transporting oxygen and nutrients to the cells. The key component of this system is the endothelium, contributing to the local balance between pro and anti-inflammatory mediators, hemostatic balance, as well as vascular permeability and cell proliferation. A constant shear stress maintains vascular endothelium homeostasis while perturbed shear stress leads to changes in secretion of vasodilator and vasoconstrictor agents. Increased oxidative stress is a major pathogenetic mechanism of endothelial dysfunction by decreasing NO bioavailability, promoting inflammation and participating in activation of intracellular signals cascade, so influencing ion channels activation, signal transduction pathways, cytoskeleton remodelling, intercellular communication and ultimately gene expression. Targeting the microvascular inflammation and oxidative stress is a fascinating approach for novel therapies in order to decrease morbidity and mortality of chronic and acute diseases.

PMID: 18075839 [PubMed - indexed for MEDLINE]
link

venotonics include horsechestnut/butchers broom/diosmin etc

1: Clin Hemorheol Microcirc. 2007;37(3):277-90. Links
Leukocyte involvement in the signs and symptoms of chronic venous disease. Perspectives for therapy.Boisseau MR.
Université Victor Segalen Bordeaux 2, 146 rue Léo Saignat, 33076 Bordeaux Cedex, France. m.r.boisseau@wanadoo.fr

Pain intensity in chronic venous disease varies with the stage in the clinical-etiologic-anatomic-pathophysiologic (CEAP) classification but also with patient perception, pain being by definition subjective. The venous hypertension responsible for the varicose veins and trophic changes in CVD has a variety of algogenic repercussions in which leukocytes play a particular role, notably through their ability to roll along the vessel wall. Shear stress, hypoxia and stasis activate the marginated leukocytes to shed L-selectin from their surface and express integrins, matrix metalloproteinase 9, elastase, lactoferrin and free radicals. Meanwhile the endothelium expresses adhesion molecules that permit slow rolling on E-selectin followed by adhesion and tissue transmigration. Vein wall and valve areas in particular attract mast cells, monocyte-macrophages and T lymphocytes, and undergo remodeling. Sympathetic sensory C and Adelta fibers, which wrap around cutaneous venules and are also present in the venous intima and media, are nociceptors sensitive to the pain mediators concentrated within leukocytes, such as mast cell bradykinin, responsible for visceral pain. Neuronal inflammation combined with wall remodeling intensifies symptoms. Yet no direct link has so far been shown between pain and mast cell mediator levels. Leukocyte adhesion is also associated with the increased capillary permeability that leads to edema. Antileukocyte therapies include postural rest and venotonics which alone or in combination with compression have been shown to unstick and inhibit leukocytes. The micronized purified flavonoid fraction (MPFF) protects vascular endothelium against hypoxia and reduces adhesion molecule expression. Unlike other antileukocyte therapies, venotonics do not cause neutropenia.

PMID: 17726258 [PubMed - indexed for MEDLINE
link

perhaps ultrasound on the stenoses?!

1: Ultrasound Med Biol. 2007 May;33(5):663-71. Epub 2007 Mar 26. Links
Mechanisms by which low-intensity ultrasound improve tolerance to ischemia-reperfusion injury.Bertuglia S.
CNR Institute of Clinical Physiology, Faculty of Medicine, University of Pisa, Pisa, Italy. sibert@ifc.cnr.it

Recent studies show that low-intensity ultrasound (US) increases endothelial nitric oxide (NO) levels in different models both in vitro and in vivo. Ischemia-reperfusion (I/R) injury is characterized by endothelial cell dysfunction, mainly as a result of altered shear stress responses associated with vasoconstriction, reduced capillary perfusion and excessive oxidative stress. This review provides an overview of the microvascular effects of low-intensity US and suggests that US exposure can be a method to provide tolerance to I/R damage. The hamster cheek pouch, extensively used in studies of I/R-induced injury, has been characterized in terms of changes of arteriolar diameter, flow and shear stress. The low-intensity US exposure reduces vasoconstriction and leukocyte adhesion and increases capillary perfusion during postischemic reperfusion. These effects may be the result of enhanced fluctuations in shear stress exerted by the flowing blood on the vessel wall. The fluctuations in turn are due to mechanical perturbations arising from the difference in acoustical impedance between the endothelial cells and the vessel content. We believe that periodic pulses of US may also cause a sustained reduction of oxidative stress and an enhanced endothelial NO level by increasing oscillatory shear stress during postischemic reperfusion. Low-intensity US exposure may represent a safe and novel important therapeutic target for patients with acute coronary syndromes and for treatment of chronic myocardial ischemia.

PMID: 17383799 [PubMed - indexed for MEDLINE]
link


1: World J Surg. 2007 Apr;31(4):733-43. Links
Effect of low shear stress on permeability and occludin expression in porcine artery endothelial cells.Conklin BS, Vito RP, Chen C.
Sections of Leukocyte Biology and Nutrition, Department of Pediatrics, Baylor College of Medicine, Children's Nutrition Research Center, 1100 Bates, Suite 6014, Houston, Texas 77030, USA.

INTRODUCTION: Although both fluid shear stress and mass transport of atherogenic substances into the vascular wall are known to be important factors in atherogenesis, there has been little research on the effect of shear stress on vascular permeability. Therefore, the effects of shear stress on the permeability of arteries and the expression of the endothelial cell tight junction molecule occludin, an important regulator of vascular permeability, were investigated. METHODS: Porcine carotid arteries were perfusion cultured ex vivo with low (1.5 dyne/cm(2)) or physiologic (15 dyne/cm(2)) shear stress and 100 mmHg pressure for 24 hours. Subsequently, 20 nm gold particles in solution were infused into the lumen of vessels at 100 mmHg for 30 minutes. Frozen sections were then cut and stained for gold particles. Image analysis was used to determine the density of the particles in the vessel walls. The expression of endothelial cell occludin mRNA and protein were determined using reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting, respectively. RESULTS: Permeability results showed a 2.8-fold increase in the apparent permeability of vessels cultured with low versus physiologic shear stress. RT-PCR and Western blotting results showed significant decreases in occludin mRNA and protein expression at 12 and 24 hours in vessels cultured with low versus physiologic shear stress. CONCLUSIONS: These results demonstrate that low shear stress increases vascular permeability in porcine carotid arteries, possibly owing to decreased occludin expression. These results may have implications in the preferential formation of atherosclerotic vascular disease adjacent to branches and bifurcations where low mean shear stresses may occur.

PMID: 17372666 [PubMed - indexed for MEDLINE]
link

aspirin might be helpful in reducing stenosis:

1: Shi Yan Sheng Wu Xue Bao. 2003 Apr;36(2):85-90.Links
[Inhibition of vascular smooth muscle cell proliferation by non-steroidal anti-inflammatory drugs][Article in Chinese]


Wang YQ, Brooks G, Harper J, Li YQ, Zhu CB, Yuan WZ, Wu XS.
College of Life Science, Hunan Normal University, Changsha 410081.

Abnormal vascular smooth muscle cell (VSMC) proliferation is known to play an important role in the pathogenesis of atherosclerosis, restenosis and instent stenosis. Recent studies suggest that salicylates, in addition to inhibiting cyclooxygenase activity, exert an antiproliferative effect on VSMC growth both in vitro and in vivo. However, whether all non-steroidal anti-inflammatory drugs (NSAID) exert similar antiproliferative effects on VSMCs, and do so via a common mechanism of action, remains unknown. In the present study, we demonstrated that the NSAIDs, aspirin, ibuprofen and sulindac induced a dose-dependent inhibition of proliferation in rat A10 VSMCs (IC50 = 1666 mumol/L, 937 mumol/L and 520 mumol/L, respectively). These drugs did not show significant cytotoxic effects as determined by LDH release assay, even at the highest concentrations tested (aspirin, 5000 mumol/L; ibuprofen, 2500 mumol/L; and sulindac, 1000 mumol/L). Flow cytometric analyses showed that a 48 h exposure of A10 VSMCs to ibuprofen (1000 mumol/L) and sulindac (750 mumol/L) led to a significant G1 arrest (from 68.7 +/- 2.0% of cells in G1 to 76.6 +/- 2.2% and 75.8 +/- 2.2%, respectively, p < 0.05). In contrast, aspirin (2500 mumol/L) failed to induce a significant G1 arrest (68.1 +/- 5.2%). Clearer evidence of a G1 block was obtained by treatment of cells with the mitotic inhibitor, nocodazole (40 ng/ml), for the final 24 h of the experiment. Under these conditions, aspirin still failed to induce a G1 arrest (from 25.9 +/- 10.9% of cells in G1 to 19.6 +/- 2.3%) whereas ibuprofen and sulindac led to a significant accumulation of cells in G1(51.8% +/- 17.2% and 54.1% +/- 10.6%, respectively, p < 0.05). These results indicate that ibuprofen and sulindac inhibit VSMC proliferation by arresting the cell cycle in the G1 phase whereas the effect of aspirin appears to be independent of any special phase of the cell cycle. Irrespective of mechanism, our results suggest that NSAIDs might be of benefit to the treatment of vascular proliferative disorders.

PMID: 12858504 [PubMed - indexed for MEDLINE]
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3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Postby gibbledygook » Mon Apr 20, 2009 4:30 am

I have returned from South Africa and am very glad as I definitely suffered a disabling relapse just before departing there. The relapse was, I believe, triggered by using just horsechestnut and butchers broom AND then when a new pain developed on just these herbs using too large doses of vasodilating salvia and ginkgo. I reckon the horsechestnut caused too much vasoconstriction inducing reflux/large pressures on vein wall and then salvia caused precipitous dilation and altered haemodynamics which was also damaging to the vein wall. I live and learn! What was most interesting to learn also was that the salvia wasn't as good as last year at reducing the newly developing pain in my left foot but berberine was. I also learnt that on berberine I didn't get spasms on the long haul flights unlike with baclofen which has in the past failed miserably at controlling night spasms on long haul flights.

So now I'm back and after complaining that the salvia and ginkgo made my walking too spongy my Chinese doctor prescribed the following:

1.88g centella asiatica/gotu kola
1.88g ilicis pubescentis
1.25g ginkgo
1.56 taxilli herba
1.25 spatholib caulis
1.56 astragalus radix
1.25 angelica sinensis
0.94 paeoniae
0.94 corni fructus
0.94 cyathulae radix
0.94 crataegi fructus
0.63 chuangxiong

I already have a few trial pots of gotu kola so I shall add this to my curcumin, capsaicin, scutellaria and berberine.
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Postby robbie » Mon Apr 20, 2009 8:06 am

Being 6.5 and having a bad relapse so far from home must have been a scary experience
Had ms for over 19 years now.
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Postby gibbledygook » Tue Apr 21, 2009 12:16 am

Hi Robbie! I think that before the attack my EDSS was about 4 to 5. I was given 6.5 at my last relapse and I think I recovered quite well between then and a month and a half ago. The worst was getting tick bite fever and not being able to get to the toilet and needing the toilet constantly. Some honeymoon!!!

This bit on CVI caught my interest:


Nees focuses on the role of the smaller vessels and their endothelium, as opposed to the venous valves, as the starting point for CVI.

The venular endothelium possesses a unique property, which gives it a specific role in the development of CVI. It is, unlike the endothelium of other vessels, a contractile tissue actively regulating the width of its intercellular gaps. Especially inflammatory mediators open these gaps [11,12].

Opening of the venular gaps leads to an outflow of blood and plasma components to the surrounding interstitial tissues and forms the microscopic correlate to the oedema observed clinically. Thrombogenic factors, e.g. tissue factors, induce interstitial inflammation and thrombosis, which spread to the venular lumen, possibly via the open gaps, reducing or cutting off perfusion. This inflammation may maintain the opening of the venular gaps, thus resulting in a circulus vitiosus, a chronic situation. Thrombocytes, polymorphonuclear granulocytes, T-lymphocytes, and monocytes are attracted to the site of inflammation and secrete aggressive oxidative or hydrolytic enzymes. Due to the reduced blood flow and damage in the venular endothelium they are insufficiently diluted [11].

This scenario may also occur in the vasa venorum, i.e. the supply vessels of the larger veins [13]. This is especially relevant for the promotion to the later stages of CVI. Microthrombi and inflammation of the venules, in the direct neighbourhood of the larger veins, may compromise the normal metabolism of venous wall structures, e.g. of the venous valves, eventually leading to their destruction. Histological evaluation of veins from later stages of CVI supports this hypothesis [14,15].

It remains still unclear which factors lead to an opening of the venular gaps in the first place. Hypotheses include immunological attacks of unknown origin, hypoxia, nutritive or toxic causes, infections, and acquired or genetic metabolic factors [7,11,16].

In an attempt to find causative forms of therapy for CVI, Nees et al. evaluated the influence of horse-chestnut seeds extracts (HCSE) on the contractility of the venular endothelial cells [11]. They examined the permeability of guinea pig venular endothelium to water applied under pressure (hydraulic conductivity). Application of polymorphonuclear granulocytes and activated thrombocytes to the endothelial cells increased their hydraulic conductivity by a factor of approximately 15 vs. control. This reflected the opening of the endothelial gaps, which could also be observed directly by scanning electron microscopy.

The parallel addition of HCSE inhibited the increase in conductivity in a dose dependant manner and almost completely in a concentration of 0.01 or 0.1 mg/ml (depending on extract used). The addition of the extracts, ten minutes after the polymorphonuclear granulocytes and thrombocytes, even restituted the increased conductivity almost to baseline values. These effects were observed and verified also by scanning electron microscopy. These findings were replicable also in human venular endothelium [Nees, personal communication].

HCSE required the presence of and probably the binding to serum proteins to show an effect (serum proteins alone did not show any effect and were used as a negative control). Possibly serum concentrations of free HCSE in man do not correspond to therapeutic efficacy [11].

Conclusion
We conclude that in early stages of CVI, when the veins and their wall structures have not yet suffered any permanent damage, pharmacological methods may be sufficient to interact with the disease process. Closure of the venular endothelial gaps interrupts the circulus vitiosus. If venules and surrounding tissues have not yet been permanently damaged they have a chance to regenerate.

Also in the later stages of CVI, HCSE may still close the venular endothelial gaps and thus can reduce oedema to some extent, as shown in Study #2 (Figure 1). At this time, however, the disease process has already involved the larger veins, with irreversible damage.

Adequate therapy in this stage of CVI is compression. It increases blood velocity by mechanically reducing the cross-section of the larger veins. Additionally the increased perivascular pressure inhibits the outflow of blood and plasma factors from the endothelial venular gaps, which reduces contact with tissue factor and thus the initial steps of coagulation and thrombosis [11,17,18].

Nevertheless compression cannot restitute destroyed venous structures, but remains a mainly symptomatic therapy. Especially when taking into account the reduced quality of life under compression therapy, patients in the early stages of CVI should be offered pharmacological treatment rather than to wait until the only help is compression.
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Postby gibbledygook » Thu May 07, 2009 9:32 am

Cheereo's progress with Jeff sounds sooooo exciting.

I'm about to take an oral course of steroids as my leg has really suffered quite a set back during the trip to Africa what with tick bite fever and a relapse. This has also had an impact on my brain and have suffered quite a bit of brain fog for the first time in ages. The humidity is kicking in as well so all in all not a good update. I have only been taking curcumin, scutellaria and capsaicin as the vasodilators are too strong when taken during relapse.

I've been trying to get London doctors interested in scanning my veins to no avail so I think I shall just have to go to the states as I'm beginning to consider this CCSVS as a bit of a medical emergency.

I have finally managed to adjust my bed to the requisite 6 inches higher at the head and will be glad not to sleep on rather lumpy pillows. I think Andrew's theory is intriguing and certainly worth a go.
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Postby gibbledygook » Thu May 14, 2009 8:47 am

I've been on the roids for 4 days and on a properly inclined bed since last week and my urine is very dark. I don't recall that on the steroids before. Mmm. My prescription is also quite low for roids - only 250mg daily for 5 days of methylprednisolone. In the past I've had 1000mg intravenously daily for 3 days. So I would guess that maybe 1) I'm not drinking enough (don't think so) 2) it's something to do with the inclined bed therapy.
The other noticeable thing is I am not needing the toilet at all during the night but in Africa I needed to go every half hour practically especially during the worst of the tick bite fever.
Also hardly a night spasm in the legs.
Finally both my feet feel much much better and the pain that appeared before visiting Africa has vanished thus far whilst the stiffness and malcoordination of the right leg seems better.
Perhaps IBT AND steroids is a bit much for the kidneys but is very good for the MS?

I continue with curcumin, capsaicin, scutellaria, astaxanthin, NAC, vit D, zinc, silicon etc but am still not back on the dilators as they seem to make things worse during exacerbation. I think I will resume on a rather more ad hoc basis after a few weeks and depending on my legs. Still no progress finding willing/able doctors to scan all the veins in the UK. :evil:
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Postby gibbledygook » Fri May 22, 2009 12:57 am

I have now been off the steroids for a week and the night bladder trips have returned with at least one trip a night but better than when I was in South Africa. However I'm back to where I was before the relapse and tick bite fever so I can't really conclude much from the inclined bed.

I had a very strange sensation on the roids this time around which may be related to the inclined bed and it was a strong sensation of pressure in the brain. It wasn't a painful headache type sensation but one of pressure on the skull. Weird. This has since abated but I am now more conscious of an ongoing pressure in my skull. This may be what others call brain fog but to me it feels like pressure.


I have kept off the vasodilators for the time being as I think that since last August 08 I went a bit crazy for them and the vasculature just needs a bit of a rest before I take them in more conservative dosages! What remains clear from my recent experiments is that horsechestnut, a vasoconstrictor, is DANGEROUS to take without a dilator. I've tried it before when on lots of dilators and didn't then have a relapse but took it alone this time in moderate dose and it triggered a new pain and malcoordination in the foot which was then exacerbated by a sudden switch to the dilators. This probably caused huge changes in blood pressure and haemodynamics. If CCSVI isn't a prime factor in MS I will eat my hat! All my experience of vasoactive herbs (horsechestnut, salvia miltiorrhiza, ginkgo, quercetin etc) tells me that the vasculature is a principal factor in the whole MS process. I remember Dr Giovannoni confirming that the reason beta-interferon is effective in MS isn't the immune modulation but its healing of the blood brain barrier...Oh for the Zamboni conclusions next year!
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Postby gibbledygook » Mon Jun 08, 2009 11:40 am

I've been on an inclined bed now for circa 3 weeks and I have been taking curcumin, capsaicin, scutellaria, zinc, vitamin d etc and anti-histamines for hayfever but little in way of vasodilators. Except alcohol. And of that there has been altogether rather too much. Taking a well-earned break for my husband has meant considerable wine and song. Curiously this has not had nearly as bad an effect on the walking as I had thought and my husband keeps remarking that I'm doing much better and am getting better and better. I don't think he's right but I do seem more mobile both on a hangover and when I'm on the sauce. However I still have this odd sensation of pressure in my skull. A sort of dull ache which changes when moving the head. Almost as if there is liquid sloshing around there. Wine on the brain maybe.

I haven't set out on any walks beyond 400m yet but intend to do so shortly.

I have also had very good bladder control at night in spite of the alcohol which I generally increases my need to go during the night. Yet these last few nights I've been fast asleep until the morning.
This is my second year on Grazax, a new hayfever treatment and I think that this year it is working. Normally by now I need a surgical mask on to filter out the pollen. I also won't have slept much since the pollen seems to start rising in the middle of the night just about when I've pulled the surgical mask off my face. I also will have avoided going outside and will have got through about 1 box of tissues every day. Last year I started rubbing capsaicin on the nasal mucosa in order to alleviate the pain. This year, I have, so far, touch wood, hardly sneezed AT ALL. I have been taking quite a few anti-histamines at the same time and I do have slightly itchy eyes which suggests that the pollen is there but my nose remains almost completely unaffected. This is EXTREMELY unexpected since last year, when I started the Grazax the hayfever was as bad as usual and only capsaicin seemed to offer any relief. Maybe the inclined bed is helping too.
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Postby peekaboo » Mon Jun 08, 2009 1:18 pm

Gibbs -

I have read in thisisms that during the pollen seasons, a relaspe may occur..

Stinging Nettle and quercetin will help Quercetin for the eyes
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Postby gibbledygook » Sun Jun 21, 2009 7:14 am

Yesterday I walked quite a few kilometers with a cane in San Francisco. Although I didn't do any better in one fell swoop than my maximum in London (1.1km) I did manage to walk about 3km with several breaks over the course of about 2 hours in very hilly terrain. I was however using a cane. I think that the inclined bed therapy may have been a contributory factor in this improvement. I haven't walked that far in such difficult terrain in a very vey long time.

I'm going to Stanford today. :D
Last edited by gibbledygook on Mon Jul 06, 2009 6:02 am, edited 1 time in total.
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Postby LR1234 » Sun Jun 21, 2009 8:36 am

Wow Alex! I can't believe you are in America already:)) Good luck with it all, I am really rooting for you and hoping you have lots of things that are easily fixed xxxx
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Postby Sharon » Sun Jun 21, 2009 11:25 am

Alex-

Good luck at Stanford - I must have been "out to lunch" - I did not know that you were planning a trip. We will all look forward to your report.

Hey, congrats on your walking in San Francisco!! "Them thar hills" are not easy for someone who doesn't have MS.

Look forward to hearing from you.

Sharon
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Postby gibbledygook » Sun Jun 21, 2009 11:54 am

Thanks, everyone. I'll set up a new log in the appropriate section once I've had the MRVs.
3 years antibiotics, 06/09 bilateral jug stents at C1, 05/11 ballooning of both jug valves, 07/12 stenting of renal vein, azygos & jug valve ballooning,
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Postby cheerleader » Sun Jun 21, 2009 4:12 pm

Alex!
So glad you are in SF, walking about that beautiful town. Jeff and I lived there for six years, and those are some steep hills! My mom told me you were heading to Stanford (she reads the boards) and I couldn't believe it!

I'm excited for you, and look forward to hearing how it all goes. Please give regards to Dr. Dake and Angela and the Stanford team for all of us here....
thinking of you (-your partner in crime and supplements)
Cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby peekaboo » Mon Jun 22, 2009 6:45 am

WOW You are quite a traveler...It is really fine that you are in California and meeting Dr Dake & staff. Dake & Staff will treat you with geat respect. I wish the best and am looking forward to your test results and intervention if any.
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