The Marshall Protocol Study Site Home

Search
   
Members

Calendar

Help

Home
Search by username
   Not logged in - Login | Register 


Reflections on my visit to China
 Moderated by: Prof Trevor Marshall Page:  First Page Previous Page  1  2  3  4   
 

New Topic

Reply

Print
AuthorPost
paulalbert
Research Team


Joined: Thu Jul 15th, 2004
Location: New York USA
Posts: 1034
Status:  Offline
 Posted: Fri Jan 9th, 2009 19:56

Quote

Reply
The transcript of the clinical talk is up on the KB:
http://mpkb.mp-dev.com/doku.php/home:publications:marshall_westchina_2008

Thank you very much to Margaret who did this. If you notice mistakes in the transcription, feel free to change them.

Paul



____________________
Diag CFS 6.03 / sympt since 9.02 / exercise, food intol, sleep prob / 1,25D: 16, 4.06; 1,25D:27, 25D:26 7.04; 1,25D:43, 25D:6 6.05; 1,25D:17, 25D:8 8.05; / MP: 7.04 / Ph. 3 / Bacteriality
Frans
Member*


Joined: Sun Feb 20th, 2005
Location: Near Rotterdam, Netherlands
Posts: 1034
Status:  Offline
 Posted: Sat Jan 10th, 2009 08:24

Quote

Reply
Interesting study, finding P. Acnes in Sarc and also correllating it to ACE levels:

The number of genomes of P. acnes in BAL cells was correlated with the serum angiotensin-converting enzyme (ACE) level and the percentage of macrophages in BAL fluid from patients with sarcoidosis. CONCLUSIONS: The amount of P. acnes DNA in BAL cells from patients with sarcoidosis was significantly higher than that in BAL cells from patients with other pulmonary diseases. P. acnes may be involved in the pathogenesis of sarcoidosis.

(PMID 19070256)

Best, Frans

Last edited on Sat Jan 10th, 2009 08:25 by Frans



____________________
Burn-out/nervous breakdown Jan01 125D 48 25D8.48 Ph1Nov06 ModPh2Jan07 Ph2Apr08 Cipramil Seroquel NoIRs lite exp r/t work cover up 25D3.9(Oct07)
Gus
inactive member
 

Joined: Tue Dec 19th, 2006
Location: United Kingdom
Posts: 15
Status:  Offline
 Posted: Mon Jan 12th, 2009 01:38

Quote

Reply
Also in SLE. P acnes is of course a cell-wall deficient bacterium

see http://www3.interscience.wiley.com/journal/119555659/abstract

Gus



____________________
Pre MP, Symptoms typical FMS or Lyme (tick bite 1964) 25D 1.4 ng/ml 1,25D 29pg/ml, Noirs on order, avoiding D but not sun/lights, Benicar/Mino available but start date not decided.
Prof Trevor Marshall
Foundation Staff


Joined: Fri Jul 9th, 2004
Location: Thousand Oaks, California USA
Posts: 15734
Status:  Offline
 Posted: Wed Feb 25th, 2009 18:40

Quote

Reply
Janet has finished a printable transcript of the West China Hospital Presentation. This is an important one to print for Doc, as it deals with clinical aspects I usually don't cover in the scientific presentations.

http://AutoimmunityResearch.org/transcripts/WCH_2008_seminar_transcript.pdf
 
(the video is at http://www.vimeo.com/2599416 )
 

neldawhite
member


Joined: Wed Feb 20th, 2008
Location: Elk Grove, California USA
Posts: 58
Status:  Offline
 Posted: Thu Feb 26th, 2009 10:14

Quote

Reply
Hello Dr. Marshall,

I'm in Phase 2 and just sat down with my very supportive husband and read the transcript on your visit to China. I had already watched the video.  My husband focused on an answer you gave and was curious about all the IP that I have been professing.  The question we have is where you say "Therefore, the dietary VD has to be kept below 15nan, or there won't be any immunopatholgy, there won't be any bug killing".  We were under the assumption there  would be less bug-killing if the VD levels were not low but  not any bug-killing.

So the question is; Am I really experiencing IP from bug-killing if my VD is at 28nan?  I'm still assuming there is great benefit in activating the VDR with Benicar, but have I been killing any bugs so far?  And if not what is causing my IP like symptoms? 

Thanks you,

Nelda



____________________
MP start Oct'08 (no breaks) | Fibromyalgia, Sjogren's, Deg.Disc Disease, | anxiety, sinusitis, eye issues, hot flashes, calcium deposits | last 25D= 10ng/mL Apr'10
Prof Trevor Marshall
Foundation Staff


Joined: Fri Jul 9th, 2004
Location: Thousand Oaks, California USA
Posts: 15734
Status:  Offline
 Posted: Thu Feb 26th, 2009 15:43

Quote

Reply
That is a case where I was being over-zealous to get my message through.

Indeed, even if the 25-D is in the 30's it is capable of being displaced by a sufficient Benicar dose.

My point was that 25-D does not leave the arena until it falls below about 12 ng/ml :):)
 

neldawhite
member


Joined: Wed Feb 20th, 2008
Location: Elk Grove, California USA
Posts: 58
Status:  Offline
 Posted: Sat Feb 28th, 2009 10:38

Quote

Reply
:) Thank you now I can go back to being pampered through my very real IP.



____________________
MP start Oct'08 (no breaks) | Fibromyalgia, Sjogren's, Deg.Disc Disease, | anxiety, sinusitis, eye issues, hot flashes, calcium deposits | last 25D= 10ng/mL Apr'10
Bane
Research Team


Joined: Sat Jan 26th, 2008
Location: Norway
Posts: 974
Status:  Offline
 Posted: Fri Apr 2nd, 2010 08:12

Quote

Reply
Dr Trevor Marshall wrote: As the recent 'Kidney Intl' paper I cited in my West China Hospital seminar pointed out, "Renal Failure" is a condition which is associated with VDR activation.

At the moment "failure" is described entirely by misbehavior of a few metabolites, GFR particularly.  I think that Medicine will find it hard to cope with the concept that kidney function is so closely related to the immune system, and that "kidney failure" can reverse itself without any requirement for intervention or dialysis. 


 

Of course they don't know olmesartan is an agonist of the vdr;)

 
Costimulation with angiotensin II and interleukin 6 augments angiotensinogen expression in cultured human renal proximal tubular cells

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2494515/

Augmented intrarenal ANG II stimulates IL-6, which contributes to renal injury. The expression of intrarenal angiotensinogen (AGT) is enhanced by increased intrarenal ANG II in human renin/human AGT double transgenic mice. ANG II also augments AGT expression in hepatocytes and cardiac myocytes. However, the mechanisms underlying AGT augmentation by ANG II and the contribution of IL-6 to this system are poorly understood. This study was performed in human renal proximal tubular epithelial cells (HRPTECs) to test the hypothesis that IL-6 contributes to the upregulation of AGT expression by ANG II. Human kidney-2 (HK-2) cells, immortalized HRPTECs, were incubated with 10-7 M ANG II and/or 10 ng/ml IL-6 for up to 24 h. AGT mRNA and protein expressions were measured by real-time RT-PCR and ELISA, respectively. The activities of NF-κB and STAT3 were evaluated by Western blotting and EMSA. Stimulation with either ANG II or IL-6 did not significantly alter AGT mRNA or protein expression. In contrast, costimulation with ANG II and IL-6 significantly increased AGT mRNA and protein expressions (1.26 ± 0.10 and 1.16 ± 0.13 over control, respectively). Olmesartan, an ANG II type 1 receptor blocker, and an IL-6 receptor antibody individually inhibited this synergistic effect. NF-κB was also activated by costimulation with ANG II and IL-6. Phosphorylation and activity of STAT3 were increased by stimulation with IL-6 alone and by costimulation. The present study indicates that IL-6 plays an important role in ANG II-mediated augmentation of AGT expression in human renal proximal tubular cells.

 

Combination therapy with AT1 blocker and vitamin D analog markedly ameliorates diabetic nephropathy: Blockade of compensatory renin increase

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2562415/

Treatment of the diabetic mice with losartan or paricalcitol (19-nor-1,25-dihydroxyvitamin D2, an activated vitamin D analog) alone moderately ameliorated kidney injury; however, combined treatment with losartan and paricalcitol completely prevented albuminuria, restored glomerular filtration barrier structure, and markedly reduced glomerulosclerosis. The combined treatment suppressed the induction of fibronection, TGF-β, and MCP-1 and reversed the decline of slit diaphragm proteins nephrin, Neph-1, ZO-1, and α-actinin-4. These were accompanied by blockade of intrarenal renin and Ang II accumulation induced by hyperglycemia and losartan. These data demonstrate that inhibition of the RAS with combination of vitamin D analogs and RAS inhibitors effectively prevents renal injury in diabetic nephropathy.



Last edited on Fri Apr 2nd, 2010 08:54 by Bane

Bane
Research Team


Joined: Sat Jan 26th, 2008
Location: Norway
Posts: 974
Status:  Offline
 Posted: Fri Apr 2nd, 2010 14:03

Quote

Reply
Posted before, a reminder;)

Comparison of the long-term effects of candesartan and olmesartan on plasma angiotensin II and left ventricular mass index in patients with hypertension.

http://www.ncbi.nlm.nih.gov/pubmed/19927151

These findings indicate that replacing candesartan with olmesartan decreased LVMI in association with a sustained decrease of plasma Ang II over a 12-month period without changing blood pressure or plasma aldosterone in patients with essential hypertension.

 

1,25-Dihydroxyvitamin D3 suppresses high glucose-induced angiotensinogen expression in kidney cells by blocking the NF-{kappa}B pathway.

http://www.ncbi.nlm.nih.gov/pubmed/19193728

The renin-angiotensin system (RAS) is a major mediator of renal injury in diabetic nephropathy. Our previous studies demonstrated that 1,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] plays a renoprotective role by suppressing the RAS, with renin and angiotensinogen (AGT) as the main targets. The mechanism whereby 1,25(OH)(2)D(3) transcriptionally suppresses renin gene expression has been elucidated; however, how vitamin D regulates AGT remains unknown. Exposure of mesangial cells or podocytes to high glucose (HG; 30 mM) markedly stimulated AGT expression. In mesangial cells, the stimulation was inhibited by 1,25(OH)(2)D(3) (20 nM) or NF-kappaB inhibitor BAY 11-7082, suggesting the involvement of NF- kappaB in HG-induced AGT expression and the interaction between 1,25(OH)(2)D(3) and NF-kappaB in the regulation. Plasmid pNF-kappaB-Luc luciferase reporter assays showed that 1,25(OH)(2)D(3) blocked HG-induced NF-kappaB activity. EMSA and ChIP assays demonstrated increased p65/p50 binding to a NF-kappaB binding site at -1734 in the AGT gene promoter upon high glucose stimulation, and the binding was disrupted by 1,25(OH)(2)D(3) treatment. Overexpression of p65/p50 overcame 1,25(OH)(2)D(3) suppression, and mutation of this NF-kappaB binding site blunted 1,25(OH)(2)D(3) suppression of the promoter activity. In mice lacking the vitamin D receptor, AGT mRNA expression in the kidney was markedly increased compared with wild-type mice, and AGT induction in diabetic mice was suppressed by treatment with a vitamin D analog. These data indicate that 1,25(OH)(2)D(3) suppresses hyperglycemia-induced AGT expression by blocking NF-kappaB-mediated pathway.



Last edited on Fri Apr 2nd, 2010 14:43 by Bane

TikBitten
inactive member
 

Joined: Wed Mar 12th, 2008
Location: USA
Posts: 81
Status:  Offline
 Posted: Fri Apr 2nd, 2010 16:27

Quote

Reply
Well alright then, problem solved...

;) 
TB 



____________________
Dx:Neurborreliosis 8/05|25D=46 1,25D=62 10/07|Avoid Sun&VitD since 10/07|Started Ph1&NoIRs 3/08|25D=18 3/08|25D=17 6/08|ModPh2 6/08|Ph2 9/08 stopped NoIRs|Ph3 1/09|25D=13 3/09|25D=10 5/09|25D=11 7/09|25D=15 9/09|25D=9 4/11
TikBitten
inactive member
 

Joined: Wed Mar 12th, 2008
Location: USA
Posts: 81
Status:  Offline
 Posted: Fri Apr 2nd, 2010 16:29

Quote

Reply
Anyone going to take a stab at translating that into English...



____________________
Dx:Neurborreliosis 8/05|25D=46 1,25D=62 10/07|Avoid Sun&VitD since 10/07|Started Ph1&NoIRs 3/08|25D=18 3/08|25D=17 6/08|ModPh2 6/08|Ph2 9/08 stopped NoIRs|Ph3 1/09|25D=13 3/09|25D=10 5/09|25D=11 7/09|25D=15 9/09|25D=9 4/11
Bane
Research Team


Joined: Sat Jan 26th, 2008
Location: Norway
Posts: 974
Status:  Offline
 Posted: Sat Apr 3rd, 2010 02:18

Quote

Reply
TikBitten wrote: Anyone going to take a stab at translating that into English...
Dr Trevor Marshall wrote: VDR is key to kidney function, based on the transcription data from Wang et al, a recent feature in Kidney International has explained the links in exquisite detail.

"Expanding targets of vitamin D receptor activation: downregulation of several RAS components in the kidney"
http://www.ncbi.nlm.nih.gov/pubmed/19008907
http://www.ncbi.nlm.nih.gov/pubmed/18813285







..Trevor..
 


 Current time is 11:48
Page:  First Page Previous Page  1  2  3  4   



* We can help you understand chronic disease, but only your physician is licensed to give you medical care *

Powered by WowBB 1.7 - Entire site Copyright © 2004-2019 Autoimmunity Research Foundation, All Rights Reserved
Click here to view our PRIVACY POLICY
Page processed in 0.5043 seconds (98% database + 2% PHP). 19 queries executed.