Gibbledygook's anti-viral log

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

Postby CureOrBust » Thu Sep 04, 2008 2:45 am

gibbledygook wrote:I went to see the doctor about fertility problems and we looked through some of the hormone levels which have been tested recently.
gibbledygook wrote:Fingers crossed the DHEA is also ok.
Have you told your fertility doctor you are taking DHEA?
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Postby gibbledygook » Thu Sep 04, 2008 3:23 am

Not yet, I haven't yet met the fertility doctor as she's only available in early October but my DHEA levels have been tested recently and they are low end of normal and my progesterone is also below normal levels. Apparently people with MS are generally low in DHEA levels and reading stuff on pubmed and elsewhere it may be worth cautiously introducing and then testing dhea levels. Certainly my tack for month before visiting the fertility quack.
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 Sep 04, 2008 8:56 am

I went back to the Sen shop to return the Er Xian Tang formula which caused such a reaction yesterday and the different doctor again said that Er Xian was too warm for me and he prescribed instead Liu Wei di Huang Wan formula. Eash pill contains 700mg and consists of (taking 9pills daily):
30% rehmannia glutinosa = 1.89g daily
18% cornus officinalis = 1.134g daily
12%alisma acquatica-plantago = .756g daily
12% paeonia suffruticosa = .756g daily
12% poria cocos = .756g daily

The closest thing on fertility I can find is this:
1: J Ethnopharmacol. 1988 Jul-Aug;23(2-3):151-8.Links
Effects of a Chinese herbal medicine, keishi-bukuryo-gan, on the gonadal system of rats.Sakamoto S, Kudo H, Kawasaki T, Kuwa K, Kasahara N, Sassa S, Okamoto R.
Department of Endocrinology, Tokyo Medical and Dental University, Japan.

Keishi-bukuryo-gan (TJ-25) is a traditional Chinese herbal remedy containing five components: bark of Cinnamomum cassia, root of Paeonia lactiflora, seed of Prunus persica or P. persiba var. davidiana, carpophores of Poria cocos and root bark of Paeonia suffruticosa. This preparation has been used in the treatment of gynecological disorders such as hypermenorrhea, dysmenorrhea and infertility. In the present study, the effects of TJ-25 on plasma levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and estradiol (E2), and on uterine wet weight and thymidine kinase (TK) activity were documented in immature rats. Long-term daily oral administration of TJ-25 (300 mg/kg) for 14 days decreased plasma levels of LH, FSH and E2 by 94%, 67% and 50%, respectively, compared to controls. Uterine wet weight and TK activity were reduced to 65% and 64% that of controls, respectively. Short-term effects of TJ-25 on E2 were also examined. Thirty hours after administration of E2 (1.0 micrograms/kg) alone, uterine wet weight and TK activity were elevated 2.4- and 21-fold, respectively, over controls. However, simultaneous administration of TJ-25 (three consecutive doses, every 12 h) with E2 reduced E2-induced increases in uterine wet weight and TK activity by 29% and 39%, respectively. Treatment with TJ-25 also enhanced LH-RH-induced increases in plasma LH and FSH levels 1.2- and 2.5-fold, respectively, as compared with controls. The results obtained in the present study indicate that TJ-25 may act as a LH-RH antagonist and/or as a weak anti-estrogen.

http://tinyurl.com/568twe


Can't say I've noticed any increased tingling so at least it's not affecting my MS but I'm not convinced it will help with the old fertility!

Keep forgetting to update my good progress walking. Today and yesterday I walked 900 meters with a cane supporting my good leg with the achilles problem. The osteo told me to use my cane to support my good leg and work out the bad leg. The walk gets tricky by about 700 meters but considering I could barely manage 5 meters 6 months ago this is phenomenal, in my opinion. I wonder what the neurologist will think when I see him at the end of September. :)
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 » Tue Sep 09, 2008 7:07 am

I have decided to reduce slightly the quantities of salvia and scutellaria as it is kind of depressing looking at such a huge pile of pills 6 times a day! I am therefore going to take 2 600mg pills of salvia, scutellaria and rehmannia 6 times a day with 2 of the life extension curcumin pills 6 times a day. I'm also experimenting with 600mg tablets of nettle today which I'll also reduce to 2 600mg pills 6 times daily. I take bioperine 10mg 3 times daily and the disgusting chinese tea 3 times daily and the fertility formula 3 times daily. I've also ordered some other interesting herbs - berberry, butterbur and horsechestnut for their effects on the blood and capillaries and ginger as an anti-inflammatory, kelp for good bowel and wild yam for fertility.
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 » Wed Sep 10, 2008 5:53 am

Very interesting new developments on the herbal front have led me to the conclusion that platelet formation in MS is a crucial event which can be moderated by the use of capsaicin AND salvia. This is because for the last 2 and a bit weeks I have enjoyed enormous symptomatic relief from the MS after increasing my dose of salvia to 10g daily with also 10g scutellaria, 7g curcumin and about 2g capsaicin. About 2.75 days ago I stopped the capsaicin over possibly unwarranted fertility fears (have just seen the ovarian follicle developing quite normally and all fertility worries are prob overblown). The second night without normal capsaicin I noticed more tingling and tendency to spasm. This was the same last night. I am now right back on the capsaicin!! Here's some pubmed research to support the notion that platelet formation is dysregulated in MS and maybe rectified with salvia and capsaicin:

1: J Neuroinflammation. 2008 Jun 27;5:27. Links
Evidence of platelet activation in multiple sclerosis.Sheremata WA, Jy W, Horstman LL, Ahn YS, Alexander JS, Minagar A.
Multiple Sclerosis Center and Department of Neurology Miller School of Medicine, University of Miami, Miami, Florida, USA. sheremaw@bellsouth.net

OBJECTIVE: A fatality in one multiple sclerosis (MS) patient due to acute idiopathic thrombocytopenic purpura (ITP) and a near fatality in another stimulated our interest in platelet function abnormalities in MS. Previously, we presented evidence of platelet activation in a small cohort of treatment-naive MS patients. METHODS: In this report, 92 normal controls and 33 stable, untreated MS patients were studied. Platelet counts, measures of platelet activation [plasma platelet microparticles (PMP), P-selectin expression (CD62p), circulating platelet microaggragtes (PAg)], as well as platelet-associated IgG/IgM, were carried out. In addition, plasma protein S activity was measured. RESULTS: Compared to controls, PMP were significantly elevated in MS (p < 0.001) and CD62p expression was also markedly elevated (p < 0.001). Both are markers of platelet activation. Platelet-associated IgM, but not IgG, was marginally elevated in MS (p = 0.01). Protein S in MS patients did not differ significantly from normal values. CONCLUSION: Platelets are significantly activated in MS patients. The mechanisms underlying this activation and its significance to MS are unknown. Additional study of platelet activation and function in MS patients is warranted.
link

From wikipedia today, 10.9.08
Platelets, or thrombocytes, are the cells circulating in the blood of mammals that are involved in hemostasis leading to the formation of blood clots. Like red blood cells, platelets have no nucleus.

(Primary hemostasis is the immediate response to injury, which involves platelets. Secondary hemostasis is the next response to injury, which involves other components of the clotting system.)

If the number of platelets is too low, that can cause bleeding. If the numbers of platelets is too high, that can cause blood clots (thrombosis) which block blood vessels, and cause strokes and heart attacks. An abnormality or disease of the platelets is called a thrombocytopathy[1] which could be either a low number (thrombocytopenia), a decrease in function (thrombasthenia) or an increase in number (thrombocytosis).

Platelets are produced in blood cell formation (thrombopoiesis) by budding off from megakaryocytes. This process is regulated by thrombopoietin, a hormone usually produce by liver and kidney. Each megakaryocyte produces between 5,000 and 10,000 platelets.

Platelets circulate for approximately one week, and are then destroyed by the spleen and by Kupffer cells in the liver.

The inner surface of blood vessels is lined with a thin layer of endothelial cells. Under the endothelial layer is a layer of collagen. When the endothelial layer is injured, the collagen is exposed.

When the platelets contact collagen, they are activated. They are also activated by thrombin (primarily through PAR-1), ADP receptors (P2Y1 and P2Y12) expressed on platelets. They can also be activated by a negatively charged surface, such as glass.

Once activated, they release coagulation factors and platelet activating factors. These substances are normally stored in one of two cytoplasmic granules:

either the dense granules (containing ADP or ATP, calcium and serotonin)
or the α-granules (containing platelet factor 4, PDGF, fibronectin, B-thromboglobulin, vWF, fibrinogen, and coagulation factors V and XIII).
Platelet activation further results in the scramblase-mediated transport of negatively charged phospholipids to the platelet surface. These phospholipids provide a catalytic surface (with the charge provided by phosphatidylserine and phosphatidylethanolamine) for the tenase and prothrombinase complexes.

Platelet aggregation is the clumping of platelets together, using fibrin as the connecting agent. Activated platelets have fibrin receptors on their surfaces. Platelet adhesion is the process of platelets sticking to the damaged inner surface of the vessel wall. Adhesion can occur because collagen in the vessel wall is exposed when the endothelial surface lining the vessel is breached, and activated platelets have collagen receptors on their surfaces. Aggregation and adhesion act together to form the platelet plug. The high concentration of myosin and actin filaments in platelets are stimulated to contract during aggregation, further reinforcing the plug.

The most abundant platelet aggregation receptor is glycoprotein (GP) IIb/IIIa; this is a calcium-dependent receptor for fibrinogen, fibronectin, vitronectin, thrombospondin and von Willebrand factor (vWF). Other receptors include GPIb-V-IX complex (vWF) and GPVI (collagen).

Platelet aggregation is stimulated by ADP, thromboxane and α2 receptor-activation, but inhibited by other inflammatory products like PGI2 and PGD2.

Besides being the chief cellular effector of hemostasis, platelets are rapidly deployed to sites of injury or infection and potentially modulate inflammatory processes by interacting with leukocytes and by secreting cytokines, chemokines and other inflammatory mediators[3] [4] [5] [6].

It also secretes e.g. platelet-derived growth factor (PDGF).

A normal platelet count in a healthy person is between 150,000 and 400,000 per mm³ (microlitre) of blood (150–400 x 109/L).[7] 95% of healthy people will have platelet counts in this range. Some will have statistically abnormal platelet counts while having no abnormality, although the likelihood increases if the platelet count is either very low or very high.

Both thrombocytopenia (or thrombopenia) and thrombocytosis may present with coagulation problems. Generally, low platelet counts increase bleeding risks (although there are exceptions, e.g. immune heparin-induced thrombocytopenia) and thrombocytosis (high counts) may lead to thrombosis (although this is mainly when the elevated count is due to myeloproliferative disorder).

Low platelet counts are generally not corrected by transfusion unless the patient is bleeding or the count has fallen below 5 x 109/L; it is contraindicated in thrombotic thrombocytopenic purpura (TTP) as it fuels the coagulopathy. In patients having surgery, a level below 50 x 109/L) is associated with abnormal surgical bleeding, and regional anaesthetic procedures such as epidurals are avoided for levels below 80-100.

Normal platelet counts are not a guarantee of adequate function. In some states the platelets, while being adequate in number, are dysfunctional. For instance, aspirin irreversibly disrupts platelet function by inhibiting cyclooxygenase-1 (COX1), and hence normal hemostasis; Platelets have no DNA and are unable to produce new cyclooxygenase. Normal platelet function will not return until the aspirin has ceased and enough of the affected platelets have been replaced by new ones, which can take over a week. Ibuprofen, another NSAID, does not have such a long duration effect, with platelet function returning in 24 hours [8], and taking ibuprofen before aspirin will prevent the irreversible effects of aspirin[9]. Uremia (a consequence of renal failure) leads to platelet dysfunction that may be ameliorated by the administration of desmopressin.


1: Eur J Pharmacol. 1991 Sep 4;202(1):129-31. Links
Inhibition of platelet aggregation by capsaicin. An effect unrelated to actions on sensory afferent neurons.Hogaboam CM, Wallace JL.
Faculty of Medicine, University of Calgary, Alberta, Canada.

The effects of capsaicin on the ability of platelets to aggregate in response to thrombin, platelet-activating factor or calcium ionophore (A23187) were examined. At concentrations previously shown to activate sensory afferent neurons, capsaicin markedly inhibited the responsiveness of platelets to the three agonists. The effects of capsaicin on platelet aggregation were reversible, and could be observed if capsaicin was added after platelets had begun to aggregate in response to the agonist. Capsaicin did not affect the shape change which occurs in response to the agonists, a process which is calcium-independent. These results demonstrate that capsaicin, at concentrations which are frequently used to 'selectively' activate sensory afferent neurons, is also capable of affecting the function of the platelet. Such non-specific effects of capsaicin must be considered when this substance is used as a pharmacological probe of sensory afferent nerve function.

PMID: 1786800 [PubMed - indexed for MEDLINE]
link

and salvia:
1: Am J Chin Med. 2008;36(2):313-28. Links
Interaction of salvianolic acids and notoginsengnosides in inhibition of ADP-induced platelet aggregation.Yao Y, Wu WY, Liu AH, Deng SS, Bi KS, Liu X, Guo DA.
Shanghai Research Center for Modernization of Traditional Chinese Medicine, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai, China.

Salvia miltiorrhiza and Panax notoginseng were both considered to be beneficial to cardiovascular diseases in traditional Chinese medicine and often used in combination. To examine the possible interaction between them, the effects of the active fractions of these two herbs, salvianolic acids (SA) and notoginsengnosides (NG), on platelet aggregation were checked respectively or in combination in vitro and in vivo. Both the platelet aggregation of platelet rich plasma (PRP) and washed platelet after ADP induction were checked. In vitro study showed that both SA and NG had an inhibitory effect on platelet aggregation. However, there is no synergistic effect of the combination of SA and NG in vitro. In vivo study showed that i.g. 550 mg/kg/day SA or NG for 5 days could significantly inhibit ADP-induced platelet aggregation of PRP. Moreover, combination of SA and NG at a ratio of 5:1 had a synergistic effect on platelet aggregation of PRP. The mechanism for the synergism of SA and NG in vivo was not clear. High performance liquid chromatography analysis of the plasma of rats received SA, NG or combination of SA and NG showed that co-administration of NG caused change in the plasma distribution profile of SA. The influence of combination on the absorption and/or metabolism of SA may be one of the reasons for the synergism of SA and NG in vivo.
link

May have to try ginseng!
1: Zhongguo Zhong Xi Yi Jie He Za Zhi. 2007 Jul;27(7):589-92.Links
[Clinical study on effect of total panax notoginseng saponins on immune related inner environment imbalance in rheumatoid arthritis patients][Article in Chinese]


Zhang JH, Wang JP, Wang HJ.
Department of Rheumatology, Gansu Provincial People's Hospital, Lanzhou. qisecaihong89@126.com

OBJECTIVE: To study the therapeutic effect and possible mechanism of total panax notoginseng saponins (PNS) for treatment of rheumatoid arthritis (RA), and to observe its safety and influence on RA immune related inner environment. METHODS: Eighty-four patients were randomly assigned to two groups. All were treated with the routine therapy with diclofenac sodium, Leflunomide and prednisone, but for the 43 patients in the treatment group PNS was given additionally. The therapeutic course was 28 days for both groups. Clinical efficacy and change of indexes including platelet counts, immnuoglobulins (IgG, IgA, IgM), complement (C)3, rheumatoid factor (RF), C-reactive protein (CRP), ceruloplasmin (CER), haptoglobin (HPT), and alpha1-acid glycoprotein (AAG) were observed. RESULTS: Significant improvement of clinical symptoms, including the joint swelling index, joint tenderness index, joint pain index, time of morning stiffness and VAS revealed in both groups after treatment, and the effect in the treatment group was better (P<0.05 or P<0.01). PLT, CER, AAG, HPT, CRP, IgG, IgA, IgM, C3 and RF were lowered in both groups (P<0.01), but the lowering in PLT, CER, AAG and CRP in the treatment group was more significant than that in the control group respectively (P < 0.05 or P < 0.01). CONCLUSION: PNS can significantly improve the condition of patients, enhance the therapeutic effect in treating RA, through regulating the disordered immunity and improving the effect of anti-inflammatory and analgesia.

PMID: 17717913 [PubMed - in process
link
Last edited by gibbledygook on Wed Sep 10, 2008 7:13 am, edited 2 times 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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another interesting herb in my tea

Postby gibbledygook » Wed Sep 10, 2008 6:03 am

Another interesting herb in my chinese tea is ligustrum lucidi fructus or ligustrum seed or grossy privet fruit. This is because of the way it upregulates the vitamin d gene expression:

1: Menopause. 2008 May-Jun;15(3):558-65. Links
Fructus ligustri lucidi extract improves calcium balance and modulates the calciotropic hormone level and vitamin D-dependent gene expression in aged ovariectomized rats.Zhang Y, Dong XL, Leung PC, Che CT, Wong MS.
Shenzhen Research Institute, The Hong Kong Polytechnic University, State Key Laboratory of Chinese Medicine and Molecular Pharmacology, Shenzhen, People's Republic of China.

OBJECTIVE: Fructus ligustri lucidi (FLL) is a widely used herb in China that is classically included in antiaging formulas for the treatment of age-related symptoms. Our laboratory previously showed that FLL could regulate calcium balance in young ovariectomized (OVX) rats. In the present study, we aimed to determine whether FLL could regulate calcium balance in aged OVX rats and to study the potential mechanisms that mediate its action in vivo. DESIGN: Aged OVX rats were orally administered an ethanol extract of FLL and its vehicle and fed with diets containing different levels of calcium [low calcium diet (LCD), 0.1% Ca; medium calcium diet (MCD), 0.6% Ca; and high calcium diet (HCD), 1.2% Ca] for 12 weeks. RESULTS: Significant reductions in urinary and fecal calcium excretion were found in the FLL-treated animals, resulting in a significant induction of calcium retention in rats fed with the MCD and HCD. FLL treatment significantly increased the serum 1,25-dihydroxyvitamin D3 level and slightly decreased the serum parathyroid hormone level in OVX rats fed with the MCD and HCD. When OVX rats were challenged by LCD, the inductions of serum parathyroid hormone and 1,25-dihydroxyvitamin D3 were decreased by FLL administration. FLL treatment significantly up-regulated duodenal vitamin D receptor and calcium transport protein 1 mRNA expression in rats fed with the HCD. FLL treatment reduced the expression of renal vitamin D receptor and 25-hydroxyvitamin D-24-hydroxylase mRNA in OVX rats fed with the LCD and MCD. CONCLUSIONS: Twelve weeks of FLL treatment could reduce calcium loss, modulate the parathyroid hormone-vitamin D axis, and increase vitamin D-dependent calcium transport in aged OVX rats, suggesting that FLL might be useful as an alternative medicine for improving calcium balance in postmenopausal women.
link

it also regulates the blood glucose:
1: Can J Physiol Pharmacol. 2007 Nov;85(11):1076-83. Links
Antidiabetic potential of oleanolic acid from Ligustrum lucidum Ait.Gao D, Li Q, Li Y, Liu Z, Liu Z, Fan Y, Han Z, Li J, Li K.
Department of Biological Engineering, College of Environment and Chemistry Engineering, Yanshan University, Qinhuangdao 066004, China.

Ligustrum lucidum Ait. has been used in traditional Chinese medicine for over 1000 years because of its anti-tumor, antimutagenic, antidiabetic, and hepatoprotective properties. The aim of this study was to determine whether oleanolic acid (OA) is the principal active compound of L. lucidum responsible for its antidiabetic properties, and to examine its effect on the expression of thyroid hormones and insulin secretion, thus revealing the mechanism by which L. lucidum modulates insulin levels in diabetes. When rats with streptozotocin-induced diabetes were treated with OA (100 and 200 mg/kg body mass per day, for 40 days), the changes in blood glucose levels and in oral glucose tolerance tests showed that hypoglycemia was more pronounced in OA-treated groups than in the diabetic control rats, and that the levels of triglyceride, total cholesterol, and low-density lipoportein cholesterol in OA-treated rats were lower than those in the diabetic control rats, whose high-density lipoprotein cholesterol increased. OA-treated rats also gained weight, and exhibited increased serum insulin levels. In contrast, OA treatment did not effect the levels of thyroid hormone or TSH in rats with streptozotocin-induced diabetes. These results indicate that OA has hypoglycemic and hypolipidemic effects. OA treatment might stimulate insulin release, and consequently, results in the modulation of glucose levels and regulation of lipid metabolism.
link

doesn't seem bad on reproduction either:
1: Asian J Androl. 2001 Mar;3(1):71-3.Links
Effect of ligustrum fruit extract on reproduction in experimental diabetic rats.Feng SL, Li SH, Wang Y, Chen CC, Gao B.
Liaoning Provincial Diabetes Treatment Center, Shenyang, China.

AIM: To study the effect of ligustrum fruit on spermatogenesis and blood gonadal hormones in diabetic rats. METHODS: Experimental diabetes was induced in male Wistar rats with streptozotocin. Ligustrum fruit extract was given by gastric gavage at a dose of crude drug 30 g x kg(-1) x d(-1) for 110 days. The serum gonadadotropic hormones and testosterone were determined on d 60 and testicular histology examined on d 110. RESULTS: In the control diabetic rats, the seminiferous tubules were dilated and the spermatogenic cells irregularly arranged. Spermatogenesis was arrested with the number of spermatids highly reduced and spermatozoa not observed. In the treated rats, all types of spermatogenic cells were practically normal. The serum luteinizing hormone (LH), follicle-stimulating hormone (FSH) and testosterone levels were higher in the treated than in the control rats, but the difference was insignificant. CONCLUSION: In experimental diabetic rats, ligustrum fruit extract protects the damaging effect of experimental diabetes on spermatogenesis.
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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more on coagulation

Postby gibbledygook » Wed Sep 10, 2008 7:09 am

People with MS have coagulation disorder:
1: BMC Neurol. 2007 Oct 18;7:36. Links
Clinical and neuroimaging correlates of antiphospholipid antibodies in multiple sclerosis: a preliminary study.Bidot CJ, Horstman LL, Jy W, Jimenez JJ, Bidot C Jr, Ahn YS, Alexander JS, Gonzalez-Toledo E, Kelley RE, Minagar A.
Wallace H. Coulter Platelet Laboratory, University of Miami Dept. of Medicine, Miller School Of Medicine, Miami, FL, USA. cbidot@med.miami.edu

BACKGROUND: The presence of antiphospholipid antibodies (APLA) in multiple sclerosis (MS) patients has been reported frequently but no clear relationship between APLA and the clinical and neuroimaging features of MS have heretofore been shown. We assessed the clinical and neuroimaging features of MS patients with plasma APLA. METHODS: A consecutive cohort of 24 subjects with relapsing-remitting (RR) MS were studied of whom 7 were in remission (Rem) and 17 in exacerbation (Exc). All subjects were examined and underwent MRI of brain. Patients' plasma was tested by standard ELISA for the presence of both IgM and IgG antibodies using a panel of 6 targets: cardiolipin (CL), beta2 glycoprotein I (beta2GPI), Factor VII/VIIa (FVIIa), phosphatidylcholine (PC), phosphatidylserine (PS) and phosphatidylethanolamine (PE). RESULTS: In exacerbation up to 80% of MS subjects had elevated titers of IgM antibodies directed against the above antigens. However, in remission, less than half of MS patients had elevated titers of IgM antibodies against one or more of the above antigens. This difference was significant, p < 0.01, for all 6 target antigens. Interestingly, none of the MS patients had elevated plasma titers of IgG against any of the target antigens tested. Correlation analysis between MRI enhancing lesions and plasma levels of APLA revealed high correlation for aPC, aPS and aFVIIa (p </= 0.0065), a trend for aPE and aCL (p = 0.056), and no correlation for abeta2GP1. The strongest correlation was for aFVIIa, p = 0.0002. CONCLUSION: The findings of this preliminary study show that increased APLA IgM is associated with exacerbations of MS. Currently, the significance of this association in pathogenesis of MS remains unknown. However, systematic longitudinal studies to measure APLA in larger cohorts of patients with relapsing-remitting MS, particularly before and after treatment with immunomodulatory agents, are needed to confirm these preliminary findings.
link

from wikipedia today 10.9.08
Antiphospholipid syndrome (APS or APLS) or antiphospholipid antibody syndrome is a disorder of coagulation, which causes blood clots (thrombosis) in both arteries and veins, as well as pregnancy-related complications such as miscarriage, preterm delivery, or severe preeclampsia. The syndrome occurs due to the autoimmune production of antibodies against phospholipid (aPL), a cell membrane substance. In particular, the disease is characterised by antibodies against cardiolipin (anti-cardiolipin antibodies) and β2 glycoprotein I.

The term "primary antiphospholipid syndrome" is used when APS occurs in the absence of any other related disease. APS is commonly seen in conjunction with other autoimmune diseases; the term "secondary antiphospholipid syndrome" is used when APS coexists with other diseases such as systemic lupus erythematosus (SLE). In rare cases, APS leads to rapid organ failure due to generalised thrombosis and a high risk of death; this is termed "catastrophic antiphospholipid syndrome".

Antiphospholipid syndrome is sometimes referred to as Hughes syndrome after the rheumatologist Dr. Graham R.V. Hughes (St. Thomas' Hospital, London, UK) who worked at the Louise Coote Lupus Unit at St Thomas' Hospital in London.

...
Antiphospholipid syndrome is an autoimmune disease, in which "antiphospholipid antibodies" (Anticardiolipin antibodies and Lupus anticoagulant) react against proteins that bind to anionic phospholipids on plasma membranes. Like many autoimmune diseases, it is more common in women than in men. The exact cause is not known, but activation of the system of coagulation is evident. Clinically important antiphospholipid antibodies (those that arise as a result of the autoimmune process) are associated with thrombosis and vascular disease. The syndrome can be divided into primary (no underlying disease state) and secondary (in association with an underlying disease state) forms. The main target of anti-cardiolipin antibodies is apolipoprotein H (commonly referred to as β2Glycoprotein 1) and the main target of Lupus anticoagulant is prothrombin. Other targets of anti-phospholipid antibodies are protein S, protein C and annexin A5.

The Lupus anticoagulant antibodies are those that show the closest association with thrombosis, those that target β2glycoprotein 1 have a greater association with thrombosis than those that target prothrombin. Anticardiolipin antibodies are associated with thrombosis at moderate to high titres (>40 GPLU or MPLU). Patients with both Lupus anticoagulant antibodies and moderate/high titre anticardiolipin antibodies show a greater risk of thrombosis than with one alone.
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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angelica sinensis

Postby gibbledygook » Wed Sep 10, 2008 7:29 am

Looking throuch pubmed, ginseng seems a bit immuno stimulatory which may be why it's not in my tea prescription. Angelica sinensis, however, is in the prescription. It seems to increase vascular endothelial growth factor, which sounds good:
1: Am J Chin Med. 2008;36(3):541-54. Links
Angiogenic effects of the extracts from Chinese herbs: Angelica and Chuanxiong.Meng H, Guo J, Sun JY, Pei JM, Wang YM, Zhu MZ, Huang C.
Department of Physiology, The Fourth Military Medical University, Xi'an 710032, China.

Angelica and ChuanXiong are used to cure ischemic heart disease in China. Previous studies found that these two herbs could increase myocardial blood flow, oxygen-supply and keep myocardial oxygen balance, etc. However, the mechanisms of angiogenic effects of these two herbs are not well-known. The purpose of this study was to assess the effects of Angelica and ChuanXiong on vascular endothelial growth factor (VEGF) expression in rat myocardial infarction, on endothelial cell proliferation and quantity of vessels on chick embryo chorioallantoic membrane (CAM). In this study, rats were divided randomly into either pre-treatment or acute-treatment group and sacrificed at the end of the treatments. VEGF expression using Western blot analysis was significantly increased in the groups pre-treated with ChuanXiong and Angelica when compared to the control group (p < 0.05). There was significant increase in VEGF expression in the rats treated acutely with Angelica (p < 0.05). In the contrary, the rats treated with ChuanXiong showed a decrease in VEGF expression when compared to the acute-treatment control group (p < 0.05). Similar results were observed in immunohistochemistry of VEGF expression in the myocardia. Our study also demonstrated that these two herbs significantly enhanced endothelial cell proliferation (p < 0.05) and revascularity in CAM (p < 0.05). The data showed that Angelica and ChuanXiong could affect VEGF expression in rat myocardial infarction, promote endothelial cell proliferation and stimulate quantity of vessels on CAM model. The results suggest that Angelica and ChuanXiong have angiogenic effects, and may provide some mechanisms for the treatment of myocardial infarction and peripheral ischemia.

PMID: 18543387 [PubMed - indexed for MEDLINE]
link

from wikipedia today 10.9.09:
Vascular endothelial growth factor (VEGF) a sub-family of growth factors, more specifically of platelet-derived growth factor family of cystine-knot growth factors. They are important signaling proteins involved in both vasculogenesis (the de novo formation of the embryonic circulatory system) and angiogenesis (the growth of blood vessels from pre-existing vasculature).As its name implies, VEGF-A activity has been mostly studied on cells of the vascular endothelium, although it does have effects on a number of other cell types (e.g. stimulation monocyte/macrophage migration, neurons, cancer cells, kidney epithelial cells). In vitro, VEGF-A has been shown to stimulate endothelial cell mitogenesis and cell migration. VEGF-A is also a vasodilator and increases microvascular permeability and was originally referred to as vascular permeability factor.


but it may not be so good:
1: J Clin Immunol. 2007 May;27(3):246-56. Epub 2007 Mar 6. Links
Vascular endothelial growth factor (VEGF) in autoimmune diseases.Carvalho JF, Blank M, Shoenfeld Y.
Rheumatology Division, São Paulo University, School of Medicine, São Paulo, Brazil.

Vascular endothelial growth factor (VEGF) is a potent stimulating factor for angiogenesis and vascular permeability. There are eight isoforms with different and sometimes overlapping functions. The mechanisms of action are under investigation with emerging insights into overlapping pathways and cross-talk between other receptors such as the neuropilins, which were not previously associated to angiogenesis. VEGF has important physiological actions on embryonic development, healing, and menstrual cycle. It also has a great role in pathological conditions that are associated to autoimmune diseases. There is considerable evidence in various autoimmune diseases such as in systemic lupus erythematosus, rheumatoid arthritis, and multiple sclerosis of an interrelationship between the VEGF system and theses disorders. Serum levels of VEGF correlate with disease activity in a large number of autoimmune diseases and fall with the use of standard therapy. We raised the possible future therapeutic strategies in autoimmune diseases with the anti-VEGF or anti-VEGFR (receptor). So far, this therapy has been used in cancer and macular ocular degeneration in diabetes. This review outlines the evidence for VEGF participation in various autoimmune diseases and proposes lines for future research in this field.
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neuroprotective:
1: Exp Brain Res. 2008 Jan;184(3):307-12. Epub 2007 Aug 24. Links
Protection against hydrogen peroxide-induced injury by Z-ligustilide in PC12 cells.Yu Y, Du JR, Wang CY, Qian ZM.
Department of Pharmacology and Key Laboratory of Drug Targeting, Education Ministry, West China School of Pharmacy, Sichuan University, Chengdu, 610041, People's Republic of China.

Z-ligustilide (Z-LIG) is the primary lipophilic compound of the Chinese medicine Danggui (Radix Angelica sinensis). Previous studies demonstrated that Z-LIG had significant neuroprotective potential in both transient and permanent cerebral ischemia, possibly through antioxidant and anti-apoptotic mechanisms. The present study examined the mechanisms of Z-LIG on hydrogen peroxide (H(2)O(2))-induced injury in PC12 cells. Following exposure of the cells to H(2)O(2 )(500 microM), a significant reduction in cell survival and total antioxidant capacity (TAC), as well as increased intracellular reactive oxygen species (ROS), were observed. In addition, H(2)O(2 )treatment significantly upregulated Bax expression, cleaved-caspase 3, and cytosolic cytochrome-c, and decreased Bcl-2 protein levels. Pretreatment of the cells with Z-LIG (0.1, 1.0, 2.5, or 5.0 microg/ml) significantly attenuated H(2)O(2)-induced cell death, attenuated increased intracellular ROS levels, and decreased Bax expression, cleaved-caspase 3, and cytochrome-c. Further, Z-LIG improved cellular TAC and concentration-dependently upregulated Bcl-2 expression. These results demonstrate that Z-LIG has a pronounced protective effect against H(2)O(2)-induced cytotoxicity, at least partly through improving cellular antioxidant defense and inhibiting the mitochondrial apoptotic pathway. These findings suggest that Z-LIG may be useful in the treatment of neurodegenerative disorders in which oxidative stress and apoptosis are mainly implicated.
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mast cell activity weakens BBB

Postby gibbledygook » Wed Sep 10, 2008 8:25 am

1: Front Biosci. 2007 Jan 1;12:1615-28.Links
Corticotropin-releasing hormone and the blood-brain-barrier.Theoharides TC, Konstantinidou AD.
Department of Pharmacology and Experimental Therapeutics, Tufts University School of Medicine and Tufts-New England Medical Center, 136 Harrison Avenue, Boston, MA 02111, USA. theoharis.theoharides@tufts.edu

Increased blood-brain-barrier (BBB) permeability precedes any clinical or pathologic signs and is critical in the pathogenesis of multiple sclerosis (MS) and brain metastases. CD4+ TH1 cells mediate demyelination in MS, but how they get sensitized and enter the brain to induce brain inflammation remains obscure. TH2 cytokines associated with allergic disorders have recently been implicated in MS, while genes upregulated in MS plaques include the mast cell-specific tryptase, the IgE receptor (Fc-epsilon-RI) and the histamine-1 receptor. Mast cell specific tryptase is elevated in the CSF of MS patients, induces microvascular leakage and stimulates protease-activated receptors (PAR), leading to widespread inflammation. BBB permeability, MS and brain metastases appear to worsen in response to acute stress that leads to the local release of corticotropin-releasing hormone (CRH), which activates brain mast cells to selectively release IL-6, IL-8 and vascular endothelial growth factor (VEGF). Acute stress increases BBB permeability that is dependent on CRH and mast cells. Acute stress shortens the time of onset of experimental alleric encephalomyelitis (EAE) that does not develop in W/W mast cell deficient or CRH -/- mice. Brain mast cell inhibition and CRHR antagonists offer novel therapeutic possibilities.
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Is the blood brain barrier permeable owing to vasoconstriction in ms? This article suggests so:
1: Klin Oczna. 2007;109(7-9):317-20.Links
[Glaucoma neuropathy and neuropathy in multiple sclerosis--common elements of pathogenesis?][Article in Polish]


Jankowska-Lech I, Terelak-Borys B, Grabska-Liberek I, Palasik W.
Kliniki Okulistyki Centrum Medycznego Kształcenia Podyplomowego w Warszawie.

The optic neuropathy in multiple sclerosis and glaucoma neuropathy are very common ophthalmological diseases. Multiple sclerosis /MS/ is the chronic inflammatory central nervous system demyelinisation disease with an autoimmunological ethiology. The last investigation of multiple sclerosis indicate the molecular and cellular autoimmunisation aspects. Te role of vasoactive factors is underlines in its pathogenesis which also suggests the common elements of glaucoma and MS pathogenesis. The over expressed vasoconstrictive mechanisms in both diseases can conduct to optic nerve injury. The aim of this study is evaluation of the optic disc morphological changes in sclerosis multiplex patients /MS/ with or without neuritis optica in anamnesis in glaucoma "remodeling" aspects. MATERIAL AND METHODS: We present two patients with coexsist sclerosis multiplex and glaucoma neuropathy, which underwent retrobulbar neuritis. CONCLUSION: Coexistance of glaucoma neuropathy and multiple sclerosis neuropathy may indicate common elements of glaucoma and SM pathogenesis. The authors recommend precise morphological optic disc evaluation in multiple sclerosis patients because glaucoma neuropathy may appear.

PMID: 18260288 [PubMed - indexed for MEDLINE]
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as does this article:
1: Eur Neurol. 2003;49(3):164-8. Links
Extraocular blood flow and endothelin-1 plasma levels in patients with multiple sclerosis.Pache M, Kaiser HJ, Akhalbedashvili N, Lienert C, Dubler B, Kappos L, Flammer J.
University Eye Clinic Basel, University Hospital Basel, Basel, Switzerland.

In order to evaluate whether plasma levels of the potent vasoconstrictor endothelin-1 (ET-1) are increased in patients with multiple sclerosis (MS) and whether these patients exhibit an ET-1-mediated vascular dysregulation, ET-1 plasma levels were measured in 30 patients with MS. Blood flow velocities in the ophthalmic artery, central retinal artery, central retinal vein, short lateral posterior ciliary artery, and short medial posterior ciliary artery were assessed in parallel. ET-1 plasma levels were significantly increased in MS patients when compared to sex- and age-matched healthy controls (2.0 +/- 0.4 pg/ml, range 1.1-2.8 vs. 1.5 +/- 0.2 pg/ml, range 0.9-2.0; p < 0.001). Moreover, the patients exhibited significant alterations of extraocular blood flow. The role of ET-1 in the inflammatory process remains to be clarified. Copyright 2003 S. Karger AG, Basel
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as does this one:
1: Brain. 2002 Nov;125(Pt 11):2446-59. Links
TNF-alpha reduces cerebral blood volume and disrupts tissue homeostasis via an endothelin- and TNFR2-dependent pathway.Sibson NR, Blamire AM, Perry VH, Gauldie J, Styles P, Anthony DC.
MRC Biochemical and Clinical Magnetic Resonance Unit, Department of Biochemistry, University of Oxford, UK. niki@bioch.ox.ac.uk

TNF-alpha expression is elevated in a variety of neuropathologies, including multiple sclerosis, cerebral malaria and HIV encephalitis. However, the consequences of such high cerebral TNF-alpha expression remain unresolved. Here, using MRI, we demonstrate that a focal intrastriatal injection of TNF-alpha causes a significant, acute reduction (15-30%) in cerebral blood volume (CBV), which is dependent on TNF-alpha-type 2 receptor (TNFR2) activation, and can be ameliorated by pre-treatment with a non-specific endothelin (ET) receptor antagonist. An acute breakdown of the blood-cerebrospinal fluid barrier (B-CSF-B) and a delayed breakdown of the blood-brain barrier (BBB) were also observed using contrast-enhanced MRI. Furthermore, a significant reduction in tissue water diffusion was apparent 24 h after intrastriatal injection of TNF-alpha injection, which may indicate compromise of tissue energy metabolism. Prolonged expression of endogenous TNF-alpha, achieved through the use of an adenoviral vector expressing TNF-alpha cDNA (Ad5TNF-alpha(m)), caused a sustained depression in CBV in accordance with the single TNF-alpha bolus data. These findings identify vasoconstriction, disrupted tissue homeostasis and damage to the BBBs as adverse effects of TNF-alpha within the brain, and suggest that antagonists of the endothelin and TNF-alpha type 2 receptors may be therapeutic in TNF-alpha-associated neuropathologies.

PMID: 12390971 [PubMed - indexed for MEDLINE]

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And certainly this one:
1: J Neuroophthalmol. 2001 Mar;21(1):37-8. Links
Increased endothelin-1 plasma levels in patients with multiple sclerosis.Haufschild T, Shaw SG, Kesselring J, Flammer J.
University Eye Clinic, Basel, Switzerland.

OBJECTIVE: We tested the hypothesis that the plasma level of endothelin-1 (ET-1) is increased in patients with multiple sclerosis (MS). The peptide ET-1 is one of the most potent known vasoconstrictors. An increased level of endothelin could explain some of the vascular symptoms of these patients. MATERIALS AND METHODS: A specific radioimmunoassay was used to determine ET-1 plasma levels. Twenty patients with MS were compared to 20 age- and sex-pair-matched healthy subjects. RESULTS: The plasma ET-1 levels were, on average, 224% higher in the patients with MS than in the controls (p < 0.005). The mean ET-1 levels (mean +/- standard deviation [SD]) were 3.5 +/- 0.83 pg/mL (min 2.13, max 5.37 pg/mL) in patients with MS and 1.56 +/- 0.3 pg/mL (min 0.9, max 2.13 pg/mL) in healthy volunteers. Neither the different forms nor stages of MS had an influence on the results. The ET-1 level was also not correlated with the duration of the disease. CONCLUSIONS: The plasma ET-1 level is markedly and significantly increased in patients with MS. Neither the cause of such an increase nor the pathogenetic role is known.

PMID: 11315981 [PubMed - indexed for MEDLINE]

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but this article suggests that vasodilation is the problem!
1: J Magn Reson Imaging. 2000 May;11(5):495-505. Links
Dynamic susceptibility contrast MR imaging of plaque development in multiple sclerosis: application of an extended blood-brain barrier leakage correction.Haselhorst R, Kappos L, Bilecen D, Scheffler K, Möri D, Radü EW, Seelig J.
Biocenter and MR Center of the University, CH-4056 Basel, Switzerland.

Since the pathogenesis of multiple sclerosis (MS) lesions is not yet fully understood, we investigated the potential of dynamic susceptibility contrast (DSC) magnetic resonance (MR) perfusion imaging for a better characterization of lesion pathology. Twenty-five MS patients were examined on a 1.5 T scanner. A single dose of gadolinium (Gd)-DOTA contrast agent was injected, and echoplanar images were acquired every 0.5 seconds for 1 minute. From the signal intensity-versus-time curves, the relative cerebral blood volume (rCBV) was evaluated for regions in plaques and in gray and white matter. The rCBV calculated for acute, Gd-enhancing plaques was corrected for the effects of blood-brain barrier leakage, using a new correction algorithm. Acute plaques had significantly higher blood volumes than normal-appearing white matter (P < = 0.01). Chronic plaques that appeared hypointense on T(1)-weighted images had lower rCBV than T(1)-isointense plaques (P < = 0.03). Our results indicate that the acute phase in MS is accompanied by vasodilation. In later stages of gliosis, the perfusion decreases with increasing axonal injury. Although the DSC technique is less sensitive than conventional MR imaging, the information provided is essentially different from that obtained with any other MR method.

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I guess the only way to find out which herbs to take is to experiment. Horsechestnut seems to be vasoconstrictive:
1: Pharmacol Res. 2001 Sep;44(3):183-93. Links
Aescin: pharmacology, pharmacokinetics and therapeutic profile.Sirtori CR.
Department of Pharmacological Sciences, University of Milano, Via Balzaretti 9, 20133 Milano, Italy. cesare.sirtori@unimi.it

Aescin, the major active principle from Aesculus hippocastanum (Hippocastanaceae) the horse chestnut tree, has shown satisfactory evidence for a clinically significant activity in chronic venous insufficiency (CVI), haemorrhoids and post-operative oedema. In one controlled trial aescin was shown to be as effective as compression therapy as an alternative to medical treatment for CVI. The therapeutic benefit is well supported by a number of experimental investigations in different animal models, indicative of clearcut anti-oedematous, anti-inflammatory and venotonic properties, mainly related to the molecular mechanism of the agent, allowing improved entry of ions into channels, thus raising venous tension in both in vitro and in vivo conditions. Other mechanisms, i.e. release of PGF(2) from veins, antagonism to 5-HT and histamine, reduced catabolism of tissue mucopolysaccharides, further underline the wide ranging mechanisms of the therapeutic activity of aescin. The excellent tolerability of aescin in the clinic indicates this treatment is of definite clinical benefit in patients with clinical conditions resulting in CVI, haemorrhoids or peripheral oedema formation. Copyright 2001 Academic Press.
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1: Altern Med Rev. 2001 Apr;6(2):126-40. Links
Hemorrhoids and varicose veins: a review of treatment options.MacKay D.
Thorne Research, 4616 SE 30th, Portland, OR 97202, USA. mackaynd@earthlink.net

Hemorrhoids and varicose veins are common conditions seen by general practitioners. Both conditions have several treatment modalities for the physician to choose from. Varicose veins are treated with mechanical compression stockings. There are several over-the-counter topical agents available for hemorrhoids. Conservative therapies for both conditions include diet, lifestyle changes, and hydrotherapy which require a high degree of patient compliance to be effective. When conservative hemorrhoid therapy is ineffective, many physicians may choose other non-surgical modalities: injection sclerotherapy, cryotherapy, manual dilation of the anus, infrared photocoagulation, bipolar diathermy, direct current electrocoagulation, or rubber band ligation. Injection sclerotherapy is the non-surgical treatment for primary varicose veins. Non-surgical modalities require physicians to be specially trained, own specialized equipment, and assume associated risks. If a non-surgical approach fails, the patient is often referred to a surgeon. The costly and uncomfortable nature of treatment options often lead a patient to postpone evaluation until aggressive intervention is necessary. Oral dietary supplementation is an attractive addition to the traditional treatment of hemorrhoids and varicose veins. The loss of vascular integrity is associated with the pathogenesis of both hemorrhoids and varicose veins. Several botanical extracts have been shown to improve microcirculation, capillary flow, and vascular tone, and to strengthen the connective tissue of the perivascular amorphous substrate. Oral supplementation with Aesculus hippocastanum, Ruscus aculeatus, Centella asiatica, Hamamelis virginiana, and bioflavonoids may prevent time-consuming, painful, and expensive complications of varicose veins and hemorrhoids.

PMID: 11302778 [PubMed - indexed for MEDLINE]
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1: Acta Pharmacol Sin. 2004 Jul;25(7):869-75.Links
Effects of sodium beta-aescin on expression of adhesion molecules and migration of neutrophils after middle cerebral artery occlusion in rats.Hu XM, Zhang Y, Zeng FD.
Institute of Clinical Pharmacology, Tongji Medical College of Huazhong University of Science and Technology, Wuhan 430030, China.

AIM: To investigate the effects of sodium beta-aescin on neutrophil migration and expression of adhesion molecules (ICAM-1 and E-selectin) after middle cerebral artery occlusion (MCAO) in rats. METHODS: Rats were pretreated with sodium beta-aescin for 7 d and then subjected to cerebral ischemia/reperfusion (I/R) injury induced by an MCAO. After a 2-h ischemia and a 24-h reperfusion, the infarct volume and neurological deficit were determined by the method of TTC staining and the Longa's score. The effect of sodium beta-aescin on the migration of neutrophils was evaluated by measuring the activity of myeloperoxidase (MPO) enzyme. The expressions of adhesion molecules were determined by immunohistochemistry and Western blot. RESULTS: Sodium beta-aescin significantly reduced the cerebral infarct volume and ameliorated the neurological deficit (P<0.05 or P<0.01). The MPO activity and the expressions of ICAM-1 and E-selectin in the vehicle-treated rats were increased significantly (P<0.01) after cerebral I/R. After treatment with sodium beta-aescin, the enzymatic activity of MPO and the expressions of these adhesion molecules were significantly reduced compared with the vehicle-treated group (P<0.05 or P<0.01). CONCLUSION: Sodium beta-aescin can attenuate brain injury, down-regulate the protein expressions of ICAM-1 and E-selectin, and reduce the migration of neutrophils after cerebral I/R.

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I'm going to look into ICAM-1 later
1: Vascul Pharmacol. 2007 Jul;47(1):68-73. Epub 2007 Apr 21. Links
Endothelium protectant and contractile effects of the antivaricose principle escin in rat aorta.Carrasco OF, Vidrio H.
Department of Pharmacology School of Medicine, Universidad Nacional Autónoma de México, Apartado Postal 70297, 04510 Mexico, D.F. Mexico.

The triterpene saponin escin is the active component of the extract of seeds of Aesculus hippocastanum used in the treatment of chronic venous insufficiency. Escin is also used experimentally to increase membrane permeability in isolated cells. Since endothelial dysfunction is postulated to be involved in venous insufficiency, the possible endothelium-protectant effect of escin was explored in rat aortic rings, a model widely used to study such effects with cardiovascular agents. Escin enhanced endothelium-dependent relaxation induced by acetylcholine when such relaxation had been reduced by exposure to the superoxide ion generator pyrogallol. This effect was attributed to enhanced nitric oxide production by endothelial nitric oxide synthase, a calcium-dependent enzyme, activated by the increased endothelial cell permeability to calcium induced by escin. Another effect of escin thought to contribute to its therapeutic activity is its ability to produce venous contraction. The compound was found to induce concentration-related contraction also in rat aortic rings. This response was partially inhibited by removal of the endothelium or by preincubation with indomethacin, and was completely abolished by incubation in a calcium-free perfusion fluid. Contraction was considered to be due mainly to the aforementioned effect on calcium permeability, with some mediation by release of endothelial vasoconstrictor prostanoids. It was concluded that, in rat aorta, escin possesses an endothelium-protectant action and a direct contractile effect. The former could contribute to its beneficial effect in the treatment of venous insufficiency, while the latter could constitute a limiting side effect.

PMID: 17512261 [PubMed - indexed for MEDLINE
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1: Planta Med. 2007 Mar;73(3):285-8. Epub 2007 Feb 19.Links
Aescin protection of human vascular endothelial cells exposed to cobalt chloride mimicked hypoxia and inflammatory stimuli.Montopoli M, Froldi G, Comelli MC, Prosdocimi M, Caparrotta L.
Department of Pharmacology and Anaestesiology, University of Padova, Padova, Italy.

Human vascular endothelial cells (HUVECs) were exposed to CoCl2 as an in vitro model of hypoxia. Expression of VCAM-1 (vascular cell adhesion molecule), reduction of PECAM-1 (platelet endothelial cell adhesion molecule) and cytoskeletal changes without alterations in cell viability were observed. HUVECs were also exposed to Escherichia coli lipopolysaccaride (LPS) as an in vitro model of inflammation: significant IL-6 release was measured. Pre-treatment of HUVECs with aescin prevented, in a concentration-dependent fashion (0.1-1 microM), the action of CoCl2 on VCAM-1 and PECAM-1, also preserving endothelial cell morphology. Furthermore, aescin pre-treatment reduced IL-6 release from LPS-activated vascular endothelium.

PMID: 17310430 [PubMed - indexed for MEDLINE]
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and butterbur appears to be vasodilatory:
1: Eur J Pharmacol. 2008 Sep 28;593(1-3):79-86. Epub 2008 Jul 10. Links
S-petasin and butterbur lactones dilate vessels through blockage of voltage gated calcium channels and block DNA synthesis.Sheykhzade M, Smajilovic S, Issa A, Haunso S, Christensen SB, Tfelt-Hansen J.
Department of Pharmacology and Pharmacotherapy, Faculty of Pharmaceutical Sciences, University of Copenhagen, Copenhagen, Denmark.

Eremophilanlactones isolated from roots of Petasites hybridus (L.) G.M. et Sch. (Asteraceae) and S-petasin have vasodilatory effects with pD(2) -log (EC(50)) values of 6.01+/-0.08, 5.24+/-0.10, 4.74+/-0.13, and 5.43+/-0.06 for S-petasin, the (Z)-3-methylthioacrylic ester of 2beta-hydroxy-8betaH-7(11)-eremophilene-12,8-olide, the angelic ester of 2beta-hydroxy-8alphaH-7(11)-eremophilene-12,8-olide, and the angelic ester of 2beta-hydroxy-8betaH-7(11)-eremophilene-12,8-olide, respectively, in the mesenteric arteries. The pD(2) values were somewhat lower for all compounds in aortic segments. The vasodilation was caused by a blockage of the voltage gated calcium channels. S-petasin, (Z)-3-methylthioacrylic ester of 2beta-hydroxy-8betaH-7(11)-eremophilene-12,8-olide, and the angelic ester of 2beta-hydroxy-8alphaH-7(11)-eremophilene-12,8-olide displayed similar potencies in inhibiting DNA synthesis in cardiomyocytes and vascular smooth muscle cells.

PMID: 18655785 [PubMed - in process]
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and berberine seems vasodilatory and overcomes the transient vasoconstriction of coffee:

1: Eur J Pharmacol. 2000 Jul 7;399(2-3):187-96. Links
Vasorelaxant and antiproliferative effects of berberine.Ko WH, Yao XQ, Lau CW, Law WI, Chen ZY, Kwok W, Ho K, Huang Y.
Department of Physiology, Faculty of Medicine, Chinese University of Hong Kong, Shatin, Hong Kong, People's Republic of China.

The present study was intended to examine the relaxant effects of berberine in rat isolated mesenteric arteries. Berberine produced a rightward shift of the concentration-response curve to phenylephrine and significantly reduced the maximal contractile response to phenylephrine. Berberine (10(-7)-3x10(-5) M) also relaxed the phenylephrine- and 9,11-dideoxy-11alpha, 9alpha-epoxy-methanoprostaglandin F(2alpha)-precontracted arteries with respective IC(50) values of 1.48+/-0.16x10(-6) and 2.23+/-0. 22x10(-6) M. Removal of a functional endothelium significantly attenuated the berberine-induced relaxation (IC(50): 4.73+/-0. 32x10(-6) M) without affecting the maximum relaxant response. Pretreatment with N(G)-nitro-L-arginine methyl ester (L-NAME) or methylene blue reduced the relaxant effect of berberine, and L-arginine (10(-3) M) partially antagonized the effect of L-NAME. In contrast, pretreatment with 10(-6) M glibenclamide or 10(-5) M indomethacin had no effect. Berberine (10(-5) M) reduced over by 50% the transient contraction induced by caffeine or phenylephrine in endothelium-denuded rings bathed in Ca(2+)-free Krebs solution. Pretreatment with putative K(+) channel blockers, such as tetrapentylammonium ions (1-3x10(-6) M), 4-aminopyridine (10(-3) M), or Ba(2+) (3x10(-4) M), significantly attenuated the berberine-induced relaxation in endothelium-denuded arteries. In contrast, tetraethylammonium ions (3x10(-3) M), charybdotoxin (10(-7) M) or glibenclamide (10(-6) M) were without effect. Berberine reduced the high-K(+)-induced sustained contraction and the relaxant response to berberine was greater in rings with endothelium (IC(50): 4.41+/-0.47x10(-6) M) than in those without endothelium (IC(50): 8.73+/-0.74x10(-6) M). However, berberine (10(-6)-10(-4) M) did not affect the high-K(+)-induced increase of intracellular [Ca(2+)] in cultured aortic smooth muscle cells. Berberine did not affect active phorbol ester-induced contraction in Ca(2+)-free Krebs solution. In addition, berberine inhibited proliferation of cultured rat aortic smooth muscle cells with an IC(50) of 2.3+/-0.43x10(-5) M. These findings suggest that berberine could act at both endothelium and the underlying vascular smooth muscle to induce relaxation. Nitric oxide from endothelium may account primarily for the berberine-induced endothelium-dependent relaxation, while activation of tetrapentylammonium-, 4-aminopyridine- and Ba(2+)-sensitive K(+) channels, inhibition of intracellular Ca(2+) release from caffeine-sensitive pools, or a direct relaxant effect, is likely responsible for the berberine-induced endothelium-independent relaxation. Mechanisms related to either Ca(2+) influx or protein kinase C activation may not be involved. Both vasorelaxant and antiproliferative effects may contribute to a long-term benefit of berberine in the vascular system.

PMID: 10884519 [PubMed - indexed for MEDLINE
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My hunch is that people with MS generally have vasoconstriction but during relapse the endothelial suffers from a sort of burst dam effect. I'm going to start with the vasodilators. 8)
Last edited by gibbledygook on Thu Sep 11, 2008 9:58 am, edited 4 times in total.
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ICAM-1

Postby gibbledygook » Thu Sep 11, 2008 8:50 am

Reducing ICAM-1 with horsechestnut sounds like a good idea:
1: J Neurosci. 2007 Nov 14;27(46):12531-9. Links
A promising therapeutic approach for multiple sclerosis: recombinant T-cell receptor ligands modulate experimental autoimmune encephalomyelitis by reducing interleukin-17 production and inhibiting migration of encephalitogenic cells into the CNS.Sinha S, Subramanian S, Proctor TM, Kaler LJ, Grafe M, Dahan R, Huan J, Vandenbark AA, Burrows GG, Offner H.
Neuroimmunology Research, Veterans Affairs Medical Center, Portland, Oregon 97239, USA.

Recombinant T-cell receptor ligands (RTLs) can prevent and reverse clinical and histological signs of experimental autoimmune encephalomyelitis (EAE) in an antigen-specific manner and are currently in clinical trials for treatment of subjects with multiple sclerosis (MS). To evaluate regulatory mechanisms, we designed and tested RTL551, containing the alpha1 and beta1 domains of the I-A(b) class II molecule covalently linked to the encephalitogenic MOG-35-55 peptide in C57BL/6 mice. Treatment of active or passive EAE with RTL551 after disease onset significantly reduced clinical signs and spinal cord lesions. Moreover, RTL551 treatment strongly and selectively reduced secretion of interleukin-17 and tumor necrosis factor alpha by transferred green fluorescent protein-positive (GFP+) MOG-35-55-reactive T-cells and almost completely abrogated existent GFP+ cellular infiltrates in affected spinal cord sections. Reduced inflammation in spinal cords of RTL551-treated mice was accompanied by a highly significant downregulation of chemokines and their receptors and inhibition of VCAM-1 (vascular cell adhesion molecule-1) and ICAM-1 (intercellular adhesion molecule-1) expression by endothelial cells. Thus, RTL therapy cannot only inhibit systemic production of encephalitogenic cytokines by the targeted myelin oligodendrocyte glycoprotein-reactive T-cells but also impedes downstream local recruitment and retention of inflammatory cells in the CNS. These findings indicate that targeted immunotherapy of antigen-specific T-cells can result in a reversal of CNS lesion formation and lend strong support to the application of the RTL approach for therapy in MS.

PMID: 18003831 [PubMed - indexed for MEDLINE]
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ICAM-1 could do with being downregulated:
1: Mult Scler. 2007 Jul;13(6):701-7. Epub 2007 Mar 15. Links
Cell surface adhesion molecules and cytokine profiles in primary progressive multiple sclerosis.Ukkonen M, Wu K, Reipert B, Dastidar P, Elovaara I.
Department of Neurology, Tampere University Hospital, Tampere, Finland. maritta.ukkonen@pshp.fi

OBJECTIVE: We evaluated the utility of adhesion molecule (AM) and cytokine/chemokine expressions in blood and cerebrospinal fluid (CSF) as markers of disease activity in primary progressive multiple sclerosis (PPMS). METHODS: The expressions of AMs and the levels of 17 cytokines in patients with PPMS (n = 25) were compared with those in secondary progressive MS (SPMS) (n = 18) and controls (n =11) and correlated with the volumes of focal and atrophic changes on MRI. RESULTS: The expressions of very late activation antigen 4 (VLA-4), lymphocyte function-associated antigen 1 (LFA-1) and intercellular adhesion molecule 1 (ICAM-1) in blood and CSF were higher in PPMS than in controls. Comparison between PPMS and SPMS showed higher levels of ICAM-1 in blood and CSF in PPMS, while the level of the vascular adhesion molecule (VCAM-1) was higher only in blood. There was no difference in the levels of cytokines in serum or CSF between PPMS and SPMS or controls, but evidence suggesting intrathecal synthesis of interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) was found in PPMS. The expressions of CSF VLA-4 in PPMS correlated with the total volume of cerebral lesions and the number of diffuse brain lesions in MRI, while the amount of LFA-1 in CSF correlated with the number of spinal T2 lesions. The level of serum MIP-1beta correlated with the T2 lesion load and EDSS score in PPMS. CONCLUSIONS: The upregulated expressions of AMs in blood and CSF and evidence for intrathecal synthesis of MCP-1 and IL-8 in PPMS indicate the importance of inflammatory changes in the pathogenesis of PPMS.

PMID: 17613596 [PubMed - indexed for MEDLINE
link

1: J Immunol. 2007 Jan 15;178(2):851-7. Links
Intercellular adhesion molecule-1 expression is required on multiple cell types for the development of experimental autoimmune encephalomyelitis.Bullard DC, Hu X, Schoeb TR, Collins RG, Beaudet AL, Barnum SR.
Department of Genetics, University of Alabama at Birmingham, 845 19th Street South, Birmingham, AL 35294, USA.

Many members of the Ig superfamily of adhesion molecules, such as ICAM-1 and VCAM-1, have been implicated in the pathogenesis of multiple sclerosis. Although it is well-established that VCAM-1/VLA-4 interactions can play important roles in mediating CNS inflammatory events in multiple sclerosis patients and during the development of experimental allergic encephalomyelitis (EAE), the contributions of ICAM-1 are poorly understood. This is due in large part to conflicting results from Ab inhibition studies and the observation of exacerbated EAE in ICAM-1 mutant mice that express a restricted set of ICAM-1 isoforms. To determine ICAM-1-mediated mechanisms in EAE, we analyzed ICAM-1 null mutant mice (ICAM-1(null)), which express no ICAM-1 isoforms. ICAM-1(null) mice had significantly attenuated EAE characterized by markedly reduced spinal cord T cell infiltration and IFN-gamma production by these cells. Adoptive transfer of Ag-restimulated T cells from wild-type to ICAM-1(null) mice or transfer of ICAM-1(null) Ag-restimulated T cells to control mice failed to induce EAE. ICAM-1(null) T cells also showed reduced proliferative capacity and substantially reduced levels of IFN-gamma, TNF-alpha, IL-4, IL-10, and IL-12 compared with that of control T cells following myelin oligodendrocyte glycoprotein 35-55 restimulation in vitro. Our results indicate that ICAM-1 expression is critical on T cells and other cell types for the development of demyelinating disease and suggest that expression of VCAM-1 and other adhesion molecules cannot fully compensate for the loss of ICAM-1 during EAE development.
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alpha lipoic acid reduces ICAM-1 and VCAM

Postby gibbledygook » Thu Sep 11, 2008 9:22 am

1: J Neuroimmunol. 2006 Jun;175(1-2):87-96. Epub 2006 Apr 27. Links
Lipoic acid inhibits expression of ICAM-1 and VCAM-1 by CNS endothelial cells and T cell migration into the spinal cord in experimental autoimmune encephalomyelitis.Chaudhary P, Marracci GH, Bourdette DN.
Department of Neurology, L226, Oregon Health & Science University, 3181 SW Sam Jackson Park Road, Portland, 97239, USA. chaudhare@ohsu.edu

Lipoic acid (LA) suppresses and treats murine experimental autoimmune encephalomyelitis (EAE), which models multiple sclerosis. However, the mechanisms by which LA mediates its effects in EAE are only partially known. In the present study, LA (25, 50 and 100 microg/ml) inhibited upregulation of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) in tumor necrosis factor-alpha (TNF-alpha) stimulated cultured brain endothelial cells. Immunohistochemical analysis of spinal cords from SJL mice that had received LA (100 mg/kg/day) following immunization to induce EAE exhibited markedly reduced expression of ICAM-1 and VCAM-1 compared with that of EAE mice receiving saline. Co-localization analysis showed that ICAM-1 and VCAM-1 expression increased over endothelial cells (staining positive for von Willebrand factor, vWF) in EAE and that LA decreased the expression levels to that observed in naïve mice. Spinal cords from mice receiving LA had significantly reduced inflammation (decreased CD4 and CD11b staining) as compared to EAE mice that received saline. Overall, our data suggest that the anti-inflammatory effects of LA in EAE may be partly due to inhibition of ICAM-1 and VCAM-1 expression by central nervous system (CNS) endothelial cells.

PMID: 16644024 [PubMed - indexed for MEDLINE]
Well, I've been taking this supplement for some time but evidently in insufficient dosage. I shall have to quadruple it to see if there's any effect:
[quote][/quote]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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Adding in berberine

Postby gibbledygook » Fri Sep 12, 2008 4:07 am

I'm feeling quite intrepid with my herbal explorations. I added berberine 1.8g last night and this morning to the salvia, capsaicin, curcumin, scutellaria and rehmannia and after about 2 hours I felt quite light-headed. It was as though my blood pressure dropped. And indeed, checking through pubmed I see that berberine reduces sistolic pressure and arterial constriction. Wow and it also looks like one shouldn't take too much of it. So I am, hooray, now going to reduce the amounts of all the herbs to 3 times daily and in total 5.4g of barberine, salvia, scutellaria and rehmannia and 4.8g of the life extension curcumin and up to 1.8g of the capsaicin. This seems a much more manageable amount. Both legs feel different this morning with much reduced tingling in the left.
Last edited by gibbledygook on Wed Sep 17, 2008 12:32 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 gibbledygook » Fri Sep 12, 2008 5:11 am

Just as I teeter on the brink of major MS improvement via the vasodilators my Chinese doctor tells me that berberine is bad for pregnancy! Merde! However dan shen/salvia is okay. He wasn't too keen on curcumin either for pregnancy. Drat and blast. Still he recommended continuing with herbs for the pregnancy (if it comes) but only certain herbs. Amazing. I have total respect for Chinese medicine now.
He said that MS fell into 4 types. One of them, into which I fall, is blood stasis. Hence the anti-platelet/vasodilatory success of dan shen. I think I'm going to try to learn Mandarin! 8)
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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Pregnancy suitable herbs

Postby gibbledygook » Sat Sep 13, 2008 5:44 am

The chinese tea suitable for pregnancy and with blood stasis MS has arrived and consists of the following daily quantities of herbs:
3.6g of rehmannia
2.2g of peony
2.7g of angelica sinensis
1.3g of chuanxiong rhizome
3.1g of taxilli herba
2.7g of spatholobi caulis
2.2g of salviae miltiorrhiza
3.6gof codonopsis radix
2.2g of poria
2.7g of polygoni multflori caulis
1.8g of dipsaci radix
1.8g of cynomorii herba

this includes some new herbs for me and an increased amount of codonopsis which I'm sure somebody else is trialling.

I'm glad that I've reduced my other herbs to the reduced amount of about 6g daily. When I introduced the barberry in largeish dose yesterday I had such a noticeable lightheadedness that I was quite shocked. I guess some herbs are very potent whilst others, like curcumin for instance, are pretty harmless in large quantities.

This is what wikipedia says today of codonopsis:
Codonopsis pilosula (党参; pinyin: dǎngshēn), also known as dang shen or poor man's ginseng, is a perennial species of flowering plant native to Northeast Asia and Korea and usually found growing around streambanks and forest openings under the shade of trees. The plant is shrubby and dense and has a tendency to climb, producing heart shaped leaves, light green five pointed bell shaped flowers with prominent yellow or light purple veins. The plant can grow up to 8-10 feet in height with roots 1-3 cm thick.

The roots of C. pilosula (radix) are used in traditional Chinese medicine to lower blood pressure, increase red and white blood cell count, cure appetite loss, strengthen the immune system, and replenish qi. The roots are harvested from the plant during the third or fourth year of growth and dried prior to sale.

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 » Wed Sep 17, 2008 12:31 am

I think that 3 600g pills of salvia miltiorrhiza/dan shen 3 times daily (5.4g) isn't quite enough as I noticed a bit more stiffness in the leg yesterday and used my cane which I haven't wanted in weeks so I'm going to increase to maybe up to 5 times daily. However I think the other herbs I'll still only take 3 times daily.
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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