Interesting research

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Interesting research

Postby HarryZ » Mon Aug 24, 2009 7:22 am

You may want to have a look at this link and see what Dr. Lawrence Steinman (co-inventor of Tysabri) is up to in the world of MS research.

http://www.sciencedaily.com/releases/20 ... 184437.htm

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Postby notasperfectasyou » Mon Aug 24, 2009 7:30 am

Thanks Harry, that's interesting. Can't help but see the potential links to CCSVI and ABX in there. Ken
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Postby mose » Mon Aug 24, 2009 8:02 am

notasperfectasyou wrote:Thanks Harry, that's interesting. Can't help but see the potential links to CCSVI and ABX in there. Ken


very interesting on those fronts. On the CCSVI model, as I mentioned in a previous post, establishing that bloodflow correction 'works' will be the first and by far most important step as without that nothing else really matters. Lagging behind will be the question of 'what causes the stenosis in the first place?', which research with regard to angiotensin may be able to shed some light on.
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Potential for Angiotensin Receptor Blockers

Postby GaryRSmith » Mon Feb 01, 2010 12:26 pm

Hello there.

If you are interested in learning more about Angiotensin Receptor Blockers and what seems the likely mechanism of action you might be interested in a couple of review papers that I have written:

Smith, G.R. and S. Missailidis, Cancer, inflammation and the AT1 and AT2 receptors. J Inflamm (Lond), 2004. 1(1): p. 3.

Smith G.R. and S. Missailidis, Learning from cancer: The adaptive growth, wound and immune responses. Gene Therapy and Molecular Biology, 2009. 13(A): p. 158-185

I have been pushing for research into the huge potential for these drugs since 2004 and any help in spreading the message would be appreciated.

I am happy to answer questions.

Best regards, Gary.
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Postby suze » Mon Feb 01, 2010 7:11 pm

Blocking angiotensin, causes lisinopril to be a vasodilator (I think) Hence the connection to CCSVI. Interesting that it stimulates T-cells. I seem to remember that l-argenine is a vasodilator and also stimulates T-cell activity.
It would be interesting to know about other 'products' that dilate veins through blocking angiotensin. I think there is a thread in CCSVI Forum about vasodilators.
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Postby jackD » Mon Feb 01, 2010 7:51 pm

I have been following "Larry" for many many years.

His article in the 1993 Scientific Amercian Special Issue on THE IMMUNE SYSTEM on "HOW MULTIPLE SCLEROSIS PROGRESSES" really got my attention.

The odd thing is that that was two years before I even suspected I had MS.

I bought the Sep 93 SA mag my local supermarket. I am bit of a scientific nerd.

He also, as an extra, mapped out 5 stages in the progression of MS that the disease could be halted. (They are in RED in the SA Sep 93 paper)

It appears that he then went to Isreal to the Wiesman? Institute and did the basic research on some of the major MS drugs that blocked those 5 areas then they were sold to the drug companies fo comercial development.

Here is that article.

http://home.ix.netcom.com/~jdalton/autoimmunity.pdf (it is a bit BIG about 1.7 MB)

Here is another GREAT article by him on the TWO STAGES of MS.

http://home.ix.netcom.com/~jdalton/ms-two-stages.pdf

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Re: Potential for Angiotensin Receptor Blockers

Postby jackD » Mon Feb 01, 2010 8:08 pm

GaryRSmith wrote:Hello there.

If you are interested in learning more about Angiotensin Receptor Blockers and what seems the likely mechanism of action you might be interested in a couple of review papers that I have written:

Smith, G.R. and S. Missailidis, Cancer, inflammation and the AT1 and AT2 receptors. J Inflamm (Lond), 2004. 1(1): p. 3.

Smith G.R. and S. Missailidis, Learning from cancer: The adaptive growth, wound and immune responses. Gene Therapy and Molecular Biology, 2009. 13(A): p. 158-185

I have been pushing for research into the huge potential for these drugs since 2004 and any help in spreading the message would be appreciated.

I am happy to answer questions.

Best regards, Gary.


Just as a point of clairification - Lisinopril is an ACE inhibitor drug.

I certainly do agree with you that some Angiotensin Receptor Blockers do GREAT things.

I asked my doctor put me on this one (Telmisartan) for obvious reasons.

Dr ********

I request that you consider changing my ARB medication from Benicar 20 mg to Telmisartan (brand names Micardis, Kinzal, Pritor) for the reasons of PCa advantages.

I would request the Generic. According to NIH-NLN Pub MED there have been over 16,000 hits on the search "Telmisartan PSA".

I know nothing about it value as a Angiotensin II blocker.My Rx Pharm no is CVS 555555555. Please Email a reply if possible. I am on my way to see the Urologist/Oncoligist today.

Thanks

JackD



Oncol Rep. 2008 Aug;20(2):295-300.

Telmisartan is a potent target for prevention and treatment in human prostate cancer.
Funao K, Matsuyama M, Kawahito Y, Sano H, Chargui J, Touraine JL, Nakatani T, Yoshimura R.

Department of Urology, Osaka City University Graduate School of Medicine, Osaka 545-8585, Japan.

Angiotensin II receptor blockers (ARBs) are widely used as hypertensive therapeutic agent. Recent studies have reported that ARBs have the potential to inhibit the growth of prostate cancer (PC) cells. Moreover, it was recently reported that Telmisartan (a kind of ARB) has peroxisome proliferator-activated receptor (PPAR)-gamma activation. We previously reported that PPAR-gamma ligand induces growth arrest of PC cells through apoptosis. In this study, we evaluated the effects of the Telmisartan and other ARBs on cell proliferation in several PC cell lines. We used normal prostate stromal cell (NPC), human hormone-refractory PC (PC3), androgen-independent PC (DU-145) and androgen-dependent PC (LNCaP) cell lines. Effects of Telmisartan and other ARBs (Candesartan, Valsartan, Irbesartan and Losartan) on PC cell growth were examined by MTT assay. Flow cytometry and Hoechst staining were used to determine whether or not ARBs induce apoptosis. [b]Telmisartan caused marked inhibition of PC cells in concentration-dependent and time-dependent manner. PC cells with treatment of 100 microM Telmisartan induced early apoptosis and DNA fragmentation. [/b]However, NPC with treatment of 100 microM Telmisartan did not induce apoptosis or DNA fragmentation. Furthermore, other ARBs had no effect on cell proliferation in the PC cells and NPC. [b]Telmisartan may mediate potent antiproliferative effects against PC cells through PPAR-gamma.
Thus, Telmisartan is a potent target for prevention and treatment in PC.[/b]

PMID: 18636189 [PubMed - indexed for MEDLINE]

Regarding ONE ACE inhibitor I also demanded this specific ACE inhibitor captopril from my doctor.

Prostate. 2004 Jan 1;58(1):50-6.

Association between captopril, other antihypertensive drugs and risk of prostate cancer.
Ronquist G, Rodríguez LA, Ruigómez A, Johansson S, Wallander MA, Frithz G, Svärdsudd K.

Department of Medical Sciences, Clinical Chemistry, University Hospital, Uppsala, Sweden.

BACKGROUND: There has been some debate on the existence of an association between hypertension, antihypertensive medications and cancer risk. METHODS: We performed a nested case-control study to assess the association between the risk of prostate cancer and the use of the angiotensin converting enzyme (ACE)-inhibitor captopril, and other antihypertensive drugs. We used data from the General Practice Research Database in UK.

RESULTS: We found an incidence rate of prostate cancer of 1.61 per 1,000 person-years among male patients aged 50-79 years old. Patients with a history of benign prostatic hyperplasia and/or prostatism carried a two-fold greater risk of prostate cancer than those without such antecedents. None of the other studied co-morbidities were associated with prostate cancer. We found that users of captopril had a relative risk of 0.7 (95% CI: 0.4-1.2) to develope prostate cancer. None of the other studied individual ACE-inhibitors shared a similar effect with the one observed for captopril.

CONCLUSIONS: No clear association was apparent between the use of antihypertensive drugs and prostate cancer. However, specific focus on users of captopril showed a lower risk of subsequent prostate cancer. Further research is needed to explore this association. Copyright 2003 Wiley-Liss, Inc.

PMID: 14673952 [PubMed - indexed for MEDLINE]

Scand J Urol Nephrol. 2009;43(1):32-6.

Captopril may reduce biochemical (prostate-specific antigen) failure following radical prostatectomy for clinically localized prostate cancer.
Ronquist G, Frithz G, Wang YH, Lindeborg T.

Department of Medical Sciences, Clinical Chemistry, Uppsala University, Uppsala, Sweden. gunnar.ronquist@akademiska.se

OBJECTIVE: A prior report suggested that individuals medicated with captopril showed a decreased incidence of prostate cancer. This study therefore investigated whether captopril given postoperatively had any preventive effect on biochemical recurrence for patients treated with radical prostatectomy. MATERIAL AND METHODS: Data were prospectively reviewed for 62 men subjected to radical retropubic prostatectomy due to biopsy-confirmed, clinically localized prostate cancer and comparisons were made between two groups, those receiving captopril postoperatively (12.5 mg twice daily; captopril group, n=32) and those not receiving any captopril (control group, n=30). One surgeon carried out the surgery.

RESULTS: The two groups were comparable as regards age at surgery, prostate volume, preoperative prostate-specific antigen values, pathological stage, Gleason score, organ-confined disease, occurrence of positive surgical margins and extraprostatic extension. The incidence of biochemical failure was three out of 32 patients in the captopril group and 10 out of 30 in the control group (p=0.034) during a mean observational time of 29 months.

CONCLUSIONS: A lower rate of biochemical recurrence was observed in men subjected to radical prostatectomy treated with captopril postoperatively than in those not receiving captopril.

These results were based on only 32 observations; a larger study may show no evidence of an association.

PMID: 18932051 [PubMed - indexed for MEDLINE]

Ann N Y Acad Sci. 2008 Sep;1138:65-72.

Captopril as a potential inhibitor of lung tumor growth and metastasis.
Attoub S, Gaben AM, Al-Salam S, Al Sultan MA, John A, Nicholls MG, Mester J, Petroianu G.

Department of Pharmacology, Faculty of Medicine and Health Sciences, UAE University, Al Ain, United Arab Emirates. samir.attoub@uaeu.ac.ae

Lung cancer is the most common form of cancer in the world, and 90% of patients die from their disease. The angiotensin converting enzyme (ACE) inhibitors are used widely as antihypertensive agents, and it has been suggested that they decrease the risk of some cancers, although available data are conflicting. Accordingly, we investigated the anticancer activity of the ACE inhibitor, captopril, in athymic mice injected with highly tumorigenic LNM35 human lung cells as xenografts. Using this model, we demonstrated that daily IP administration of captopril (2.8 mg/mouse) for 3 weeks resulted in a remarkable reduction of tumor growth (58%, P < 0.01) and lymph node metastasis (50%, P= 0.088). There were no undesirable effects of captopril treatment on animal behavior and body weight. In order to determine the mechanism by which captopril inhibited tumor growth, we investigated the impact of this drug on cell proliferation, apoptosis, and angiogenesis. Immunohistochemical analysis demonstrated that captopril treatment significantly reduced the number of proliferating cells (Ki-67) in the tumor samples but was not associated with inhibition of tumor angiogenesis (CD31). Using cell viability and fluorescent activated cell sorting analysis tests, we demonstrated that captopril inhibited the viability of LNM35 cells by inducing apoptosis, providing insight about the mechanisms underlying its antitumorigenic activities.

In view of these experimental findings, we conclude that captopril could be a promising option for the treatment of lung cancer.

PMID: 18837885 [PubMed - indexed for MEDLINE]
Last edited by jackD on Fri Feb 05, 2010 10:20 pm, edited 3 times in total.
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Postby jackD » Mon Feb 01, 2010 9:49 pm

I had 1st asked my doctor to change my ACE inhibitor
to captopril after finding this abstract in pub-med.

After having a prostate cancer scare I had him double the dose.

He was quite pleased to learn about the positive lung
cancer effects.

jackD

Immunopharmacol Immunotoxicol. 1995 Aug;17(3):471-91.

Effects of the angiotensin converting enzyme inhibitor captopril on experimental autoimmune encephalomyelitis.

Constantinescu CS, Ventura E, Hilliard B, Rostami A.

Department of Neurology, University of Pennsylvania, Philadelphia 19104, USA.

Angiotensin converting enzyme (ACE)1 mediates inflammation, participates in T cell stimulation by certain antigenic peptides, and influences the permeability of the blood brain barrier (BBB).

ACE is elevated in multiple sclerosis (MS), an autoimmune disease of the central nervous system (CNS), characterized by increased BBB permeability. ACE inhibitor captopril suppresses certain immune functions and inhibits inflammatory or autoimmune diseases.

We studied the effect of captopril on Lewis rat EAE, an animal model of MS. Fourteen rats with EAE were treated with captopril 30 mg/kg daily from immunization to day 21 post-immunization, and compared with 14 untreated rats. Severity scores and lymphocyte reactivity to myelin basic protein and mitogen were measured.

There was a statistically significant (p < 0.05) difference between the mean and cumulative clinical scores of captopril-treated and untreated animals. Lymphocytes from captopril treated EAE rats at the peak of disease severity had diminished responses to MBP and concanavalin A.

The data suggest a significant beneficial effect of captopril in Lewis rat EAE. Further studies including other inhibitors of ACE or of other peptidases with immune, inflammatory or BBB role, may identify potentially valuable immunopharmacologic agents.

PMID: 8576541 [PubMed - indexed for MEDLINE]
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Postby shye » Fri Feb 05, 2010 9:29 am

JackD,
you post is informative--many would like to see that info I am sure--they won't if you leave the post here (odd place to post this)--
You need to post this as a separate thread--with a good title to get across the idea quickly--such as: ACE high in MS/increases BBB permeability..
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