Vascular health

If it's on your mind and it has to do with multiple sclerosis in any way, post it here.

Postby Terry » Tue Oct 21, 2008 7:14 pm

So what if the vascular issue is the primary cause of MS?
Secondary to that, pathogens.
We all have dormant virus/bacteria. What if at times, for example, during high stress, the blood pressure rises at the same time a dormant bacteria/virus becomes active in the blood stream. The bacteria/virus is leaked/ forced into the CNS, there to grow in its new surroundings.
All the inflammation and attack of myelin, etc is the body trying to rid the CNS of the pathogen and/or the pathogen doing damage.
This would account for variations in the disease. Each pathogen may have a favorite place to hide, and a differing way to survive.
Low body temp, low vit D, low uric acid, what else...could these be triggered by the bacteria trying to survive or triggered by the body using whatever mechanisms it has to stop the attack?
Crazy thoughts? Maybe/ probably. I have a sneaking suspicion that my vascular system is bad. I took aspirin for 4 days and experienced burning pain in the sides of my head and migraines with aura. Had to stop. Is thick blood a protection from the leaking?
Would this fit with what we know or suspect about MS?
If so, how? If not, why?
Please think with/ for me. I'm stuck in this theory.
Terry
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Postby cheerleader » Tue Oct 21, 2008 9:57 pm

Terry...
Everything you mention makes sense to me. Guess we're both crazy. The more I ponder it all, the more I keep coming back 'round to....drum roll, please...
ENDOTHELIAL DYSFUNCTION.
The lining of the blood vessels isn't working properly, and it allows leakage of foreign cells into the body's tissues. Pathogens, C-reactive protein, bacteria, toxins, you name it, it gets in and messes stuff up.

Endothelial dysfunction is implicated in all autoimmune diseases...I think the specific difference in MS is that there is a rupture in the BBB, leading to a leakage into the CNS.

"ED" (no longer erectile dysfunction!) is also at fault for clotting disorders and sticky blood. And guess what causes ED? Low vit. D, bacteria, toxins, oxidative stress, cortisol and all the stuff already implicated in MS.

Sorry the aspirin affected you so nastily...was it a baby aspirin? Maybe try the oils and enzymes instead?

I'm researching ways to heal the endothelium, and will post as I learn more. In the meantime, read up on the endothelium and MS and see whatchya think-

http://cat.inist.fr/?aModele=afficheN&cpsidt=997998

vascularly yours,
AC
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby gibbledygook » Wed Oct 22, 2008 2:02 am

Will also rummage around in PubMed for more on PECAMs and CD31 and CD51. :)

Time to test quercetin in high dose, methinks!
1: Acta Pharmacol Sin. 2001 Sep;22(9):857-60.Links
Effect of quercetin on adhesion of platelets to microvascular endothelial cells in vitro.Fan PS, Gu ZL, Liang ZQ.
Department of Pharmacology, Suzhou University, Suzhou Institute of Chinese Materia Medica, Suzhou 215007, China.

AIM: To study the effect of quercetin(Que) on the adhesion of platelets to microvascular endothelial cells (MVEC) isolated from human skin. METHODS: [3H]-adenine-labeled platelets were incubated with MVEC. Effect of Que on platelet endothelial cell adhesion molecular (PECAM) expression on MVEC was also evaluated using enzyme-linked immunosorbent assay (ELISA). RESULTS: Adhesion of platelet to MVEC reached to maximum at about 30 min. Que inhibited the adhesion of platelets to MVEC in a concentration-dependent manner. Que 5 micromol/L did not show any significant inhibition. When the concentration of Que increased to 10, 20, and 40 micromol/L, the inhibition rate increased to 10.5 %, 20.0 %, and 42.2 %, respectively. Pre-incubation of Que (10 - 40 micromol/L) with labeled platelets for 30 min also inhibited the adhesion but Que 5 micromol/L did not. The inhibition rate of Que 10, 20, and 40 micromol/L was 18.2 %, 29.8 %, and 65.3 % respectively. Expression of PECAM on the endothelial cells was decreased in a concentration-dependent manner when MVEC were treated with Que (10 - 40 micromol/L) for 12 h but Que 5 micromol/L did not significantly affect the expression. CONCLUSION: Que could inhibit the adhesion of platelets to MVEC. This effect may be related to decreased expression of PECAM on MVEC.

PMID: 11749871 [PubMed - indexed for MEDLINE]

link

Cilostazol attenuates PECAM-1:
1: Cardiovasc Res. 2008 Sep 3. [Epub ahead of print] Links
Cilostazol inhibits cytokine-induced nuclear factor-{kappa}B activation via AMP-activated protein kinase activation in vascular endothelial cells.Hattori Y, Suzuki K, Tomizawa A, Hirama N, Okayasu T, Hattori S, Satoh H, Akimoto K, Kasai K.
Department of Endocrinology and Metabolism, Dokkyo University School of Medicine, Mibu, Tochigi 321-0293, Japan.

AIMS: Cilostazol is a selective inhibitor of phosphodiesterase 3 that increases intracellular cyclic AMP (cAMP) levels and activates protein kinase A, thereby inhibiting platelet aggregation and inducing peripheral vasodilation. We hypothesized that cilostazol may prevent inflammatory cytokine induced-nuclear factor (NF)-kappaB activation by activating AMP-activated protein kinase (AMPK) in vascular endothelial cells. METHODS AND RESULTS: Cilostazol was observed to activate AMPK and its downstream target, acetyl-CoA carboxylase, in human umbilical vein endothelial cells (HUVEC). Phosphorylation of AMPK with cilostazol was not affected by co-treatment with an adenylate cyclase inhibitor, SQ 22536, and a cell-permeable cAMP analogue, pCTP-cAMP, did not induce AMPK phosphorylation and had no effect on cilostazol-induced AMPK phosphorylation, suggesting that cilostazol-induced AMPK activation occurs through a signalling pathway independent of cyclic AMP. Cilostazol also dose-dependently inhibited tumour necrosis factor alpha (TNFalpha)-induced NF-kappaB activation and TNFalpha-induced IkappaB kinase activity. Furthermore, cilostazol attenuated the TNFalpha-induced gene expression of various pro-inflammatory and cell adhesion molecules, such as vascular cell adhesion molecule-1, E-selectin, intercellular adhesion molecule-1, monocyte chemoattractant protein-1 (MCP-1), and PECAM-1 in HUVEC. RNA interference of AMPKalpha1 or the AMPK inhibitor compound C attenuated cilostazol-induced inhibition of NF-kappaB activation by TNFalpha. CONCLUSION: In the light of these findings, we suggest that cilostazol might attenuate the cytokine-induced expression of adhesion molecule genes by inhibiting NF-kappaB following AMPK activation.

PMID: 18703532 [PubMed - as supplied by publisher]

link

What is cilostazol? From wikipedia today:
Cilostazol (pronounced /sɨˈlɒstəzɒl/) is a medication used in the alleviation of the symptom of intermittent claudication in individuals with peripheral vascular disease. It is manufactured by Otsuka Pharmaceutical Co. under the trade name Pletal.

Although drugs similar to cilostazol have increased the risk of death in patients with congestive heart failure, studies of significant size have not addressed people without the disease.

Cilostazol is a selective cAMP phosphodiesterase inhibitor. It inhibits platelet aggregation and is a direct arterial vasodilator. Its main effects are dilation of the arteries supplying blood to the legs and decreasing platelet coagulation.


Here's one for lindacarol:
1: Diabetes Metab Res Rev. 2004 May-Jun;20(3):232-8. Links
The antidiabetic agent, gliclazide, reduces high insulin-enhanced neutrophil-transendothelial migration through direct effects on the endothelium.Okouchi M, Okayama N, Omi H, Imaeda K, Fukutomi T, Nakamura A, Itoh M.
Department of Internal Medicine and Bioregulation, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan. okochi@med.nagoya-cu.ac.jp

BACKGROUND AND AIM: Many lines of evidence indicate that hyperinsulinemia might be associated with coronary atherosclerosis, and, currently, there are no effective strategies for preventing this. We previously reported that high insulin enhances neutrophil-transendothelial migration, a process that involves increased surface presentation of platelet endothelial cell adhesion molecule-1 (PECAM-1) through a mitogen-activated protein (MAP) kinase-dependent event. In this current study, we examined if antidiabetic agents, especially K(ATP) channel blockers, might similarly protect against the leukocyte-endothelial cell interactions enhanced by high insulin. METHODS: Neutrophils transmigration across umbilical vein endothelial cells (in high insulin medium) with or without K(ATP) channel blockers was performed. Neutrophil migration was quantified by measuring myeloperoxidase, and surface expression of endothelial PECAM-1 was examined using cell-surface enzyme immunoassay. RESULTS: Neutrophil-transendothelial migration and PECAM-1 expression were enhanced by insulin (100 micro U/mL, 24 h) and were attenuated by gliclazide (20 micro M), but not by other K(ATP) channel blockers (glibenclamide, nateglinide, and glimepiride). Neutrophil migration and PECAM-1 expression were also increased by the mitogen-activated protein (MAP) kinase activator, anisomycin (1 micro M), and also attenuated by gliclazide. Nitric oxide (NO) synthase inhibitors did not modify either gliclazide effect. CONCLUSIONS: Our results suggest that the K(ATP) channel blocker, gliclazide, blocks high insulin-mediated neutrophil migration and PECAM-1 expression. These gliclazide effects may be mediated through the inhibition of MAP kinase activation and are unrelated to NO production. Copyright 2004 John Wiley & Sons, Ltd.

PMID: 15133755 [PubMed - indexed for MEDLINE]

Related ArticlesProtective actions of gliclazide on high insulin-enhanced neutrophil-endothelial cell interactions through inhibition of mitogen activated protein kinase and protein kinase C pathways. [Microvasc Res. 2004] High insulin enhances neutrophil transendothelial migration through increasing surface expression of platelet endothelial cell adhesion molecule-1 via activation of mitogen activated protein kinase. [Diabetologia. 2002] Participation of high glucose concentrations in neutrophil adhesion and surface expression of adhesion molecules on cultured human endothelial cells: effect of antidiabetic medicines. [J Diabetes Complications. 2002] The mechanisms of inhibitory actions of gliclazide on neutrophils-endothelial cells adhesion and surface expression of endothelial adhesion molecules mediated by a high glucose concentration. [J Diabetes Complications. 2003] Cerivastatin ameliorates high insulin-enhanced neutrophil-endothelial cell adhesion and endothelial intercellular adhesion molecule-1 expression by inhibiting mitogen-activated protein kinase activation. [J Diabetes Complications. 2003] » See all Related Articles...

link
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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luteolin reduces vascular permeability

Postby gibbledygook » Wed Oct 22, 2008 6:35 am

1: Planta Med. 2008 Oct 20. [Epub ahead of print]
Anti-Oxidant, Anti-Inflammatory and Anti-Allergic Activities of Luteolin.Seelinger G, Merfort I, Schempp CM.
Medical Services Dr. Seelinger, Berlin, Germany.

Luteolin is a flavone which occurs in medicinal plants as well as in some vegetables and spices. It is a natural anti-oxidant with less pro-oxidant potential than the flavonol quercetin, the best studied flavonoid, but apparently with a better safety profile. It displays excellent radical scavenging and cytoprotective properties, especially when tested in complex biological systems where it can interact with other anti-oxidants like vitamins. Luteolin displays specific anti-inflammatory effects at micromolar concentrations which are only partly explained by its anti-oxidant capacities. The anti-inflammatory activity includes activation of anti-oxidative enzymes, suppression of the NFkappaB pathway and inhibition of pro-inflammatory substances. IN VIVO, luteolin reduced increased vascular permeability and was effective in animal models of inflammation after parenteral and oral application. Although luteolin is only a minor component in our nutrition (less than 1 mg/day) epidemiological studies indicate that it has the potential to protect from diseases associated with inflammatory processes such as cardiovascular disease. Luteolin often occurs in the form of glycosides in plants, but these are cleaved and the aglycones are conjugated and metabolized after nutritional uptake which has to be considered when evaluating IN VITRO studies. Some data for oral and topical bioavailability exist, but more quantitative research in this field is needed to evaluate the physiological and therapeutical potential of luteolin. Akt:serine/threonin protein kinase B COX-2:cyclooxygenase-2 CVD:cardiovascular disease DPPH:2,2-diphenyl-1-picrylhydrazyl EAE:experimental autoimmune encephalomyelitis EGCG:epigallocatechin 3-gallate fMLP:fMetLeuPhe, formyl peptide GSH:glutathione IFN-gamma:interferon gamma IkappaB:Inhibitor of kappa B IL:interleukin iNOS:inducible nitric oxygen synthase IP-10:inducible nitric oxygen synthase IRF:interferon regulatory factor LPS:lipopolysaccharide LysoPAF AcTF:1-lysophospholipide acetyltransferase MAPK:mitogen-activated protein kinase M-CSF:macrophage colony-stimulating factor NFkappaB:nuclear factor kappa B 8-OHdG:8-hydroxy-2'-deoxyguanosine PGE (2):prostaglandin E (2)PMA:phorbol myristate acetate ROS:reactive oxygen species TEAC:trolox equivalent anti-oxidant capacity TNF-alpha:tumor necrosis factor-alpha.

PMID: 18937165 [PubMed - as supplied by publisher]
link

I tried this supplement once before but without result. Maybe I was taking too modest a quantity.
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 Terry » Wed Oct 22, 2008 6:40 am

So bacteria and viruses can change the body's mechanisms to make the environment safe for themselves. Also, the body counters the bac/viruses by shifting to attack/ protect. How do you distinguish between the two? Is there enough info out there to know the difference?
If you thin the blood, have you made it easier for the bad stuff to leak?
If you supplement, what info do you use to be sure you are not feeding the pathogens or making the environment better for them to proliferate?
Have you figured out WHY the vascular structure is compromised? Do you think it always leaks, or just leaks sometimes?
Do you think we have more pathogens, or a normal amount and the problem is the leaking?
If someone is taking antibiotics, does the antibioltic get into the cns to clear up what has already leaked, or does it just clear it from the "regular" areas so as to keep it from leaking again?
Sorry for all the questions. Just trying to understand.
Terry
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Postby gibbledygook » Wed Oct 22, 2008 7:08 am

Hi Terry,

I think the problem is leaking. I think we probably leak the whole time but in varying amounts and certainly once one is progressive. From my experiments I can tell that too much blood thinning from salvia is bad but that enough felt very good (when I started taking about 10g of salvia it felt great with less spasticity etc). It seems that there is quite a lot of vasoconstriction in MS. Maybe this is because of some pathogen or maybe something else altogether. All I know is that my legs felt great when I started taking a lot of the blood thinner, salvia. Then after taking 14g for a few days I started to feel a lot worse. I'm sure it's a good idea to dilate the vessels a bit and try to take things that prevent permeability or which inhibit things like VEGF and PECAM.
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 » Wed Oct 22, 2008 7:23 am

Terry-
Endothelial Dysfunction is not caused specifically by pathogens, although they do contribute... it is a weakening of the vessel walls by a variety of factors. The major one is oxidative stress from all those unpaired free-radicals bouncing around. I think a multi-modal approach is best at restoring vessel health.

A probiotic would address gut bacteria and reduce pathogens
lots of antioxidants to bind with free radicals,
(Alex mentions quercetin, which has been terrific for Jeff-)
Thinning the blood is not a bad thing and will not allow more pathogens to "leak."
If anything, thinner blood will help vasoconstriction and blood flow

THis study speaks of cerebral-vascular disease, not MS specific-
"Oxidative stress has been implicated in the development of endothelial dysfunction through alterations of the nitric oxide metabolism. A number of evidence suggests a role for phagocytic-cell-mediated oxidative stress in diminished nitric oxide availability that is present in patients with atherosclerotic risk factors such as arterial hypertension. Thus, the combination of an excessive production of reactive oxygen species, namely superoxide anion, with an impaired antioxidant defense capacity leading to oxidative stress may facilitate the development and progression of atherosclerosis. Findings from recent clinical studies suggest that this mechanism can be operative in patients with cerebrovascular disease."
http://content.karger.com/ProdukteDB/pr ... /000107376

There's so much out there about ways to heal the damage to the endothelium....not just supplements (although that's a huge part of it). Laughter, exercise, stress reduction, dietary changes. Too much to go into here, but I'll put together a reference in pdf form with sources and pm you when it's ready.
AC
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby dignan » Wed Oct 22, 2008 10:00 am

AC, I saw this abstract about endothelial cells and neuronal precursor cells and I think it gives more support to what you're saying about the endothelium. It looks to me like stem cell treatment for MS might be moving towards implanting some kind of neuronal precursor cells.


Endothelium-induced proliferation and electrophysiological differentiation of human embryonic stem cell-derived neuronal precursors.

Stem Cells Dev. 2008 Jun;17(3):565-72.
Lai B, Mao XO, Greenberg DA, Jin K.
Buck Institute for Age Research, Novato, CA 94945-0638, USA.

Neurogenesis occurs in a stem cell niche in which vascular elements, including endothelial cells (ECs), are thought to play an important role.

Using co-culture experiments, we investigated the effect of ECs on proliferation and functional neuronal differentiation of human embryonic stem (ES) cell-derived neuronal precursor cells (NPCs). NPCs were cultured for 5 days in medium containing fibroblast growth factor-2 (FGF-2), with or without ECs. FGF-2 and ECs were then removed, and NPCs were maintained in culture for additional periods.

Compared to control NPC cultures, EC-treated NPC cultures showed increased cell proliferation at short intervals (5 days) after withdrawal of FGF-2 and larger tetrodotoxin-sensitive inward membrane currents at longer intervals (10-14 days), but a similar pattern of development of neuronal differentiation markers. The effects of ECs appeared to result from the release of soluble factors rather than from cell contact, because they were observed despite the physical separation of NPCs from ECs by a cell-impermeable membrane.

These findings indicate that ECs can regulate the proliferation and electrophysiological neuronal differentiation of human NPCs.

Pubmed link
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Postby cheerleader » Wed Oct 22, 2008 3:55 pm

dignan wrote:AC, I saw this abstract about endothelial cells and neuronal precursor cells and I think it gives more support to what you're saying about the endothelium. It looks to me like stem cell treatment for MS might be moving towards implanting some kind of neuronal precursor cells.


Thanks for this, Dignan. Exciting news about EC stem cells. I'd read about some research which was being done using umbilical cord blood EC cells, and it's encouraging to see that ECs can differentiate into neuronal precursor cells.

I was never able to understand the concept of rogue killer T-cells breaking through a barrier on their own, attacking myelin. Autoimmunity doesn't make sense to me. Over-simplistically, it seemed to me that something must be wrong with the gatekeeper, that being the endothilial cells that line all of our blood and lymph vessels and communicate directly with the immune system.

It's amazing to see all the modern environmental factors that damage ECs...I've put together a list which includes plastics, cigarette smoke, diesel smog, free radicals, chronic bacterial infections, mercury and cadium exposure, saturated fats, sedentary lifestyle, cortisol from stress,lack of vitamin D, etc...etc. Our endothelium are breaking down, and all autoimmune diseases have shown EC dysfunction. Partial healing of ECs thru diet and lifestyle changes may explain partial remissions in MS.
AC
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby Terry » Thu Oct 23, 2008 5:33 am

but I'll put together a reference in pdf form with sources and pm you when it's ready.


Thanks, Cheer. I appreciate it.

Terry
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Postby Sharon » Thu Oct 23, 2008 10:57 am

Cheer -

Would you send me the .pdf also? I would be interested in the information you have gathered.

Thanks
Sharon
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Postby cheerleader » Thu Oct 23, 2008 11:21 am

Terry, Sharon and anyone else interested in "endothilial health."
I'm not able to add attachments to my pms-
If you want, pm me your e-mails, and I'll send along the pdf of my research.
If you're not comfortable with that, I'll see if Jeff can figure out a way
to host me on his web site.
It's been an amazing journey putting this together.
AC
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Postby Terry » Thu Oct 23, 2008 3:50 pm

By amazing journey do you mean pain in the ass? :lol:

...email address on the way.
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Postby Terry » Thu Oct 23, 2008 6:33 pm

Cheer,

Good reading! Thanks so much.
I will use it as reference.
and btw, I have NEVER finished a sudoku puzzle.
Thanks for your help.

Terry
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Butcher's broom

Postby gibbledygook » Fri Oct 24, 2008 4:02 am

Gonnae get me some bootcher's broom:
1: Clin Hemorheol Microcirc. 1997 Sep-Oct;17(5):385-8. Links
Antipermeability effects of Cyclo 3 Fort in hamsters with moderate diabetes.Svensjö E, Bouskela E, Cyrino FZ, Bougaret S.
Laboratório de Pesquisas em Microcirculação, State University of Rio de Janeiro, Brazil.

Ruscus aculeatus extract (the active principle of Cyclo 3 Fort) is used to increase venous tone in patients with venous disease. In these experiments, the effects of oral Cyclo 3 Fort on capillary permeability were studied in hamsters with moderate diabetes induced by two intraperitoneal injections of streptozotocin (40 mg/kg). Hamsters were treated with a placebo or Cyclo 3 Fort, 2, 10 or 50 mg/kg/day, for 4 weeks starting 3 days after induction of diabetes. Intravital microscopy of cheek pouch preparations was performed using fluorescein-labelled dextran (FITC-dextran) as a marker for plasma exudation (leak formation). Plasma levels of glucose were measured prior to experiments. Following preparation for intravital microscopy, each cheek pouch was subjected to two applications of histamine, 5 x 10(-6) M for 5 min at 30-minute intervals. Plasma exudation (number of leaks/cm2) was significantly reduced in animals receiving Cyclo 3 Fort at doses of 10 mg/kg or above. The mean number of leaks was 258 +/- 17 in the placebo group, compared with 253 +/- 12, 125 +/- 7 (p < 0.01) and 99 +/- 7 (p < 0.01) in animals receiving Cyclo 3 Fort, 2, 10 or 50 mg/kg, respectively. Blood glucose levels did not differ between groups. Thus, oral Cyclo 3 Fort inhibited histamine-induced plasma exudation in hamsters with mild diabetes without affecting the glycaemia.

PMID: 9502536 [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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