LIIPAT - Section for Vascular Endothelial Cells (Haraldsen Group)
Vascular endothelial cells line the inside of blood vessels. Once activated, they follow different programs, either getting sticky and recruiting leukocytes to sites of inflammation, or leaving the vessels themselves to build new blood levels. We focus on molecular mechanisms of endothelial cells differentiation with special emphasis on properties that enable leukocyte recruitment in immunity and inflammation, as well as those that enable vascular morphogenesis.


The current model of leukocyte adhesion to the vascular wall is viewed as a multi-step adhesion pathway. Chemokines presented at the endothelial cell surface enable the transition of leukocyte behaviour from rolling to firm adhesion, and are the focus of interest because they attract different subclasses of leukocytes. At sites of acute injury, leukocyte recruitment can occur rapidly, partly explained by the fact that endothelial cells store and rapidly release preformed chemokines to the vascular surface upon exposure to histamine or thrombin. We are currently studying the sorting profile of different chemokines in endothelial cells and the molecular mechanisms of their sorting.

To understand the biology of endothelial cells in different vascular segments and organs we compare the gene expression profile of endothelial cells of different tissue origins, having identified the first nuclear factor of a specialized subtype of vascular endothelial cells (NF-HEV), the characterization of which is ongoing.

In a different approach to understanding of vascular differentiation, we also developed a model for the adoptive transfer of endothelial cells. This technique is based on transferring single human endothelial cells to subcutaneous gels in immunodeficient mice in which they assemble to complex, functional vessels that make xenogeneic contact with the murine vascular system. Importantly, phenotypic properties that are lost in vitro are partly regained upon transfer, and by means of local, osmotic pump-delivery of soluble mediators to these gels, our method is a powerful tool for exploring the regulation of endothelial differentiation through direct experimental manipulation in vivo .







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Editors: Editorial board, patologi-post@labmed.uio.no
Document created: 06.11.2001, modified: 10.02.2005, certified: 06.11.2001
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Dear Vicc,

I have been back on my COQ10 for the last couple weeks.

http://ajpheart.physiology.org/cgi/c...ct/278/4/H1084

I turly am in 100% agreement that the Chambers need people very compatent. As well I think we need complete Pulmonary testing. Each one of us are oxygen levels could be different. I feel a T. Vascular surgeon should also be consulted.

I have heard of a couple people going into remission with this HBOT treatment. But why only a couple?

Not only have I heard the nerves and blood work together but I have also been told the lung and heart work together as well.

As far as Drexel University, I have seened Maleki MD. He is very knowledgeable and has a heart truly in the right place. He did not promise me remission, but pain control. He also uses Ketamine. I was in his office for about a hour he charged me barely anything.

Vicc, have you talked to any T. Vascular surgeons on this therapy? Because some that I spoke with are very aware that RSD has a vascular component.

We are all bonded by this RSD stuff. I know in your heart you want to see all of us cured. I thank you for that from the bottom of my heart. Big Hugs, Roz

Hi Everyone,

Just another article. Please read the whole thing. What I have copied is about 1/3 down.

http://www.emedicine.com/neuro/topic602.htm

IL-6 in clinical stroke

Several clinical studies in patients with stroke have found an association between CSF and plasma IL-6 levels and infarct size and neurologic outcome. Some of these studies have yielded conflicting results.

Fassbender et al (1994) found that plasma levels of IL-6 showed a significant increase within the first few hours following stroke onset, peaking at 10 hours. This increased level of IL-6 significantly correlated with the volume of the brain lesion and was associated with a poor functional neurologic outcome. In contrast, serum levels of IL-1b and TNFa did not increase.

Different results were obtained by Tarkowski et al (1995). In this study, CSF levels of IL-6 were elevated significantly by day 2 and were correlated with the volume of infarct observed; serum levels of IL-6 did not correlate with the size of brain lesion. This study did not find any measurable levels of plasma IL-1b. Finally, Kim et al (1996) measured IL-6 levels in 29 patients with acute stroke. They found the level of IL-6 to be highest (49±16 pg/mL) at 24 hours after onset, remaining high (14±4 pg/mL) for at least 7 days.

The role of cytokines in clinical stroke also has been investigated. Plasma levels in vivo of IL-6 and the naturally occurring IL-1ra were measured using ELISA in 50 patients with acute stroke (4±2 days after onset) and in 20 age-matched healthy controls.

Levels of both IL-6 and IL-1ra were significantly higher in the stroke population (4.6±4.2 pg/mL and 354±270 pg/mL, respectively) than in controls (1.0±0.9 pg/mL and 139±113 pg/mL). The levels of both cytokines were significantly higher in patients who had infarcts measuring more than 3 cm on CT scans. We also found that the level of IL-6 is elevated not only in the acute stroke period, but it remains elevated for up to a year (compared to controls) upon longitudinal follow-up (Coull, 1993).

The acute IL-6 elevation and its ability to predict neurologic recovery from stroke has been investigated. In this study, plasma levels of IL-6, fibrinogen, and albumin along with white blood cell (WBC) count were measured within 4±2 days of onset in 131 patients with stroke. Standard clinical predictors of outcome also were obtained, including neurologic assessments and head CT infarct sizes.

Peak levels of IL-6 were correlated significantly (r=0.18) with 6-month outcome as assessed by the Glasgow Outcome Scale. Taken together, the acute-phase response variables strongly predicted 6-month recovery (R2=0.31) and were nearly as strong a predictor as the standard clinical predictors (R2=0.38). Recent clinical studies have confirmed these findings and found that IL-6 values strongly correlated with C reactive protein (Smith et al, 2004). Acalovschi et al (2003) recently confirmed the robust elevation of serum IL-6 post clinical stroke but found that the soluble receptors (antagonists) for IL-6 were downregulated. These clinical results suggest that the acute-phase response, in particular IL-6, is strongly associated with acute ischemic stroke; the acute-phase response also appears to be correlated with initial infarct size and degree of long-term recovery.

Cytokines - Conclusions

Taken together, the aforementioned observations strongly suggest that the

Roz -

A friend of mine just sent me the full text of "Dietary coenzyme Q10 supplement renders swine hearts resistant to ischemia-reperfusion injury." At the bottom of the first page there's the following notation:

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby
marked ‘‘advertisement’’ in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Do you have any idea what that means? Is it something other than a peer reviewed article, notwithstanding the fact that it was published by the American Physiological Society?

Mike


P.S. If anyone wants a copy of this by email, drop me a pm by no later than 9:00 a.m. Pacific time on December 28th with your email address and I'll be glad to send it on. Otherwise it will have to wait until I get back from a 12 -day meditation retreat.

Hi Everyone,
Here is the Full Article on "Dietary coenzyme Q10 supplement renders swine hearts resistant to ischemia-reperfusion injury." If anyone has any opinions on this I would appreciate it. Big Hugs, Roz

http://ajpheart.physiology.org/cgi/c...ll/278/4/H1084

Looks like if they catch it quickly, and start the treatment there is a good chance of not having any damage to the heart. This would help the thousands of people that suffer heart attacks, and strokes every year.

Im not sure how it would help people that already have the damage, or people suffering with RSD. Unless it would somehow help the damage from spread?

Great news though, and I hope it gets to helping people soon!