I dont see how liquid Mag. Oxide would do the trick, personally. I have used a product called "Homozone", which is a powder. After taking it, you also follow it with fresh lemon juice (acidic). It bubbles up in you stomach, and all through your intestines. The pack has a warning to plan your day around it, as it can be very effective. I do not really notice anything with other forms of mag either.Loobie wrote:I used up an entire bottle of of Carlson Liquid Magnesium (it was Mag. oxide) and also Solgar Mag Citrate and it did nothing for the ol' bowels. So I'll try what seems to be working for others.
I just rung this lab, to see how they were going. I spoke to the receptionist, which knew me as the "MS Guy", which makes me hopeful that it has some visibility within the clinic. She told me that the sonographer is still discussing it with the vascular docs (who would of been back today for the first time). Its 1pm in the afternoon now. She also re-took my contact details, just in case.CureOrBust wrote:For the lab I am referred to, I have spoke to a sonographer (face to face on the 1st Monday they were open for the year), but she would like to speak to one of the Vascular doctors in the clinic. These guys will not be back in the office until next week. So that lab is "on hold" till about mid next week.
I also asked / confirmed how many sonographers they had at the practice, and the receptionist said there was only one, not two.CureOrBust wrote:... she said the sonographer at that clinic was very capable. However, after talking a little further, it became clear that they had two sonographers at the clinic, with the other more concerned with cardiac type of doppler investigations.
Interesting to get your "nurses" viewpoint. Although I do not pretend to understand all the text, I felt that it seemed fairly easy and well explained for someone who worked on this day-in-day-out. I am thinking I will get the other 4 tests done (hopefully) then get a copy of this book for my sonographer, if she is interested, and does not know how to do the second test(s).mrhodes40 wrote:Boy, that book looks like serious studying for the sonographer, but it seems like it is possible to do.
My first aim is to get the tests scheduled/done, then see a vascular Dr with my results and the published article. You may end up seeing one first so feel free to use them , or if someone else agrees they are interesting questions, and has a vascular doc for a contactmrhodes40 wrote:I like the questions you plan to ask.
I am simply going off the fact that the sonographer I spoke to in the hospital appeared very knowledgeable, and she said I may have problems getting the 2nd test performed.mrhodes40 wrote:Is your comment that the DCV's will be the hardest related to your understanding it is rare and difficult to do in general, or just that it is not done locally?
link1: Tohoku J Exp Med. 1999 Dec;189(4):259-65. Links
Elevated plasma level of plasminogen activator inhibitor-1 (PAI-1) in patients with relapsing-remitting multiple sclerosis.Onodera H, Nakashima I, Fujihara K, Nagata T, Itoyama Y.
Department of Neurology, Tohoku University School of Medicine, Sendai, Japan. email@example.com
Multiple sclerosis (MS) is an inflammatory demyelinating disease of the central nervous system and one of the earliest changes in inflammatory focus involves the activation of vascular endothelial cells. We determined the plasma level of plasminogen activator inhibitor-1 (PAI-1), a key regulator of fibrinolysis and cell migration, in patients with MS. The level of plasma PAI-1 was significantly higher in active MS cases when compared to stable MS and controls. Plasma concentrations of tissue plasminogen activator, transforming growth factor beta-1, and lipoprotein-a remained normal in spite of disease activity. These results suggested that PAI-1 plasma levels are associated with MS disease activity and is a good marker for MS relapse.
PMID: 10739162 [PubMed - indexed for MEDLINE]
link1: Vasa. 2001 Jul;30(3):184-7.Links
Coagulation and fibrinolysis in chronic venous insufficiency.Blomgren L, Johansson G, Siegbahn A, Bergqvist D.
Department of Surgery, St Görans Hospital, Stockholm, Sweden. lena@firstname.lastname@example.org
BACKGROUND: Varicose veins (VV) are common, but only some patients will develop chronic venous insufficiency (CVI) with skin changes or venous ulcer. The pathophysiology of venous ulcer development is complex, and may involve abnormalities in coagulation, fibrinolysis and proinflammatory cytokines. The purpose of this study was to correlate plasma markers within these systems and skin pathology. METHOD: A group of twenty consecutive patients with active or recent venous ulcer were matched for sex and age with further three groups of individuals i.e. controls and patients with VV with and without skin changes respectively. Blood samples were analysed for hemoglobin (HB), total platelet count (TPC), C-reactive protein (CRP), activated partial thromboplastin time (APTT), prothrombin complex (PT), fibrinogen, interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF alpha), D-dimer, tissue plasminogen activator (t-PA), plasminogen activator inhibitor 1 (PAI-1), prothrombin fragments 1 and 2 (F1 + 2), and thrombin antithrombin III complex (TAT). RESULTS AND CONCLUSION: There was an increase of systemic levels of PAI-1 activity and tPA with progressive skin pathology in patients with CVI, and in the group with active ulcer there was an elevation of F1 + 2. Those findings could reflect a defect fibrinolysis, a thrombotic potential or a damaged endothelium.
PMID: 11582948 [PubMed - indexed for MEDLINE]
link1: J Vasc Surg. 2005 Feb;41(2):303-11. Links
An animal model of venous hypertension: the role of inflammation in venous valve failure.Pascarella L, Schmid-Schönbein GW, Bergan J.
Department of Surgery, University of California, San Diego, USA.
BACKGROUND: Clinical observation suggests that chronic venous insufficiency is related to failure of venous valves. Duplex ultrasound studies of lower extremity superficial veins regularly show valve failure and venous reflux. Gross morphologic observation of venous valves in surgical specimens shows tearing, splitting, scarring, and disappearance of valves. HYPOTHESIS: Venous valve damage is acquired, linked with venous hypertension, and affected by inflammation. OBJECTIVE: The objective of this study was to investigate the inflammatory process in valve remodeling associated with acute and chronic venous hypertension. METHODS: A femoral arteriovenous fistula was created in study animals (Wistar rats, n = 60), and animals without an arteriovenous fistula were studied as controls (n = 5). At 1, 7, 21, and 42 days animals with the femoral arteriovenous fistula were anesthetized, and systemic pressure, the pressure in the femoral vein distal to fistula, and the pressure of the femoral vein in the contralateral hind limb were measured. Timed collection of blood backflow after division of the femoral vein distal to the fistula and in the alive, anesthetized animal was collected, measured, and calculated per unit time to be used as an indicator of valve insufficiency. The femoral vein distal to the fistula was harvested; valvular structures were examined and measured. Specimens were processed, and longitudinal sections were made and challenged with immunostaining antibodies against matrix metalloprotease (MMP)-2 and MMP-9. Sections were examined, and expression of molecular markers was determined by light absorption measurements after image digitization. RESULTS: One week after the procedure, all animals exhibited some degree of hind limb edema ipsilateral to the arteriovenous fistula. Pressure in the femoral vein distal to the fistula was markedly increased on average to 96 +/- 9 mm Hg. Reflux was increased in a time-dependent manner, with the 21-day and 42-day groups showing the highest values. Valves just distal to the fistula showed an increased diameter of the valvular annulus and a shortening of the annular height. Venous wall findings included fibrosis and fusion of the media and adventitia and scarring and disappearance of valves principally in the 21- and 42-day specimens. Immunolabeling for MMP-2 showed an increased level in the 21- and 42-day groups. MMP-9 showed an increased level at 1 day, followed by a more marked level in the 21- and 42-day groups. CONCLUSIONS: In this animal model of venous hypertension the findings of limb edema, increasing valvular reflux, and morphologic changes of increased annulus diameter and valve height are seen. Histologic changes included massive fibrosis of media and fusion with adventitia. Inflammatory markers MMP-2 and MMP-9 are strongly represented, and valve disappearance occurs after these markers are present. The gross morphologic changes seen are quite similar to those observed in human surgical specimens removed in treatment of venous insufficiency. CLINICAL RELEVANCE: When observed angioscopically at the time of vein stripping, saphenous vein valves show severe deformities including shortening, scarring, and tearing. The current model of induced venous hypertension demonstrates early venous valve changes that replicate those observed in humans. This observation provides a link from venous hypertension to an induced inflammatory reaction that stimulates the valve damage. Thus the model could be useful for defining the fundamental mechanisms that cause venous valve failure and varicose veins and in pharmacologic testing to prevent or treat venous insufficiency.
PMID: 15768014 [PubMed - indexed for MEDLINE
neurologists connected with the labs.
This observation provides a link from venous hypertension to an induced inflammatory reaction that stimulates the valve damage.
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