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The Marshall Protocol Study Site > PROF. MARSHALL'S PERSPECTIVE > Prof. Marshall's Perspective > Understanding Aging - Conference at UCLA, June 27-29


Understanding Aging - Conference at UCLA, June 27-29
 Moderated by: Prof Trevor Marshall Page:  First Page Previous Page  1  2  3   
 

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Prof Trevor Marshall
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 Posted: Tue Jul 8th, 2008 03:26

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It was some sort of caramel thingy wrapped in a thin shell of chocolate. Very nice indeed:):):)
 

Joyful
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 Posted: Tue Jul 8th, 2008 03:35

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Ahh, chocolate... a favorite topic all around these parts... :)

One other question ... was it really as loud in the poster presentation area as the video seemed to make to be?

I can't imagine how a person could have a real conversation with all the background noise. (Or is that my neuro-herx/IP making up reaility again?)



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Prof Trevor Marshall
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 Posted: Tue Jul 8th, 2008 04:12

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It is usually pretty loud in poster sessions. The room used at UCLA was smallish, and the free alcohol tended to add to the volume even more. It was nevertheless easy enough to hold a conversation when one was focused upon doing that (and not de-focused by the alcohol).
 
The poster sessions ran from 9pm-11.30pm-ish both evenings. Lectures started at 9am, Long days indeed...
 
 

Last edited on Tue Jul 8th, 2008 04:14 by Prof Trevor Marshall

Ruth Goold
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 Posted: Wed Jan 14th, 2009 08:36

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Here is an interesting study indicating one of the possible anti-aging mechanisms in which nuclear hormone receptors may participate.  It shows the involvement of an orphan nuclear receptor, Essrb (estrogen related receptor beta), as a transcription factor involved in the induction of fibroblasts (differentiated cells) into stem cells (undifferentatied cells).  Essrb interacts with the glucocorticoid receptor (GR) and at least the alpha form of this gene (Essra) possesses a vitamin D reponse element and is therefore likely regulated by the VDR. 

Reprogramming of fibroblasts into induced pluripotent stem cells with orphan nuclear receptor Esrrb.  Nature Cell Biology.  Feng et al.  PMID: 19136965.

See also:

Nuclear receptors in regulation of mouse ES cell pluripotency and differentiation. Mullen et al. PPAR research.  PMID: 18274628.

 



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jlunn247
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 Posted: Wed Jan 14th, 2009 22:57

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Could they possibly repeat that study here in Michigan or the U.S.?:shock:

 I would love to volunteer. Maybe they could use cord blood.

My kidneys could handle it.:)

Wait do men have estrogen receptors?

Last edited on Wed Jan 14th, 2009 23:01 by jlunn247



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Prof Trevor Marshall
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 Posted: Wed Jan 14th, 2009 23:27

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do men have estrogen receptors

I hope so, because it is the Estrogen-beta-receptor which expresses VDR. And VDR expresses the Estrogen-alpha-receptor. So men would get into quite a mess without Estradiol...
 
http://en.wikipedia.org/wiki/Estradiol
 
 

Last edited on Wed Jan 14th, 2009 23:30 by Prof Trevor Marshall

Ruth Goold
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 Posted: Wed Dec 1st, 2010 11:46

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Hope this is the right thread for new ageing info - just wanted to mention a nice (mouse) study that confirms the MP viewpoint that ageing is indeed reversible.  The study is:
Telomerase reactivation reverses tissue degeneration in aged telomerase-deficient mice.
published today in Nature by Jaskelioff et al.         PMID: 21113150

 The title pretty much says it all but here is some info pulled from the Nature page abstract:

The question: 
"Unanswered is whether elimination of intrinsic instigators driving age-associated degeneration can reverse, as opposed to simply arrest, various afflictions of the aged."

The answer:
"Telomerase reactivation in such late generation TERT-ER mice extends telomeres, reduces DNA damage signalling and associated cellular checkpoint responses, allows resumption of proliferation in quiescent cultures, and eliminates degenerative phenotypes across multiple organs including testes, spleens and intestines. Notably, somatic telomerase reactivation reversed neurodegeneration with restoration of proliferating Sox2+ neural progenitors, Dcx+ newborn neurons, and Olig2+ oligodendrocyte populations."

The conclusion:
"Accumulating evidence implicating telomere damage as a driver of age-associated organ decline and disease risk1, 3 and the marked reversal of systemic degenerative phenotypes in adult mice observed here support the development of regenerative strategies designed to restore telomere integrity."

My question:
I've wondered a couple of times about monitoring (the likely restoration of) of telomere integrity as a marker for recovery on the MP.  I suspect Trevor and colleagues have considered this - any comments on the feasibility?

Thanks,
Ruth



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NickBowler
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 Posted: Sat Apr 16th, 2011 04:29

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http://www.economist.com/node/18526881

Yes, just how feasible and practical might a telomere length (or telomerase activity) study of pre and post MP candidates be?



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NickBowler
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 Posted: Sat Apr 16th, 2011 06:10

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http://mct.aacrjournals.org/content/2/8/739.full

http://scholarcommons.usf.edu/etd/1094/

It seems to be a worthwhile study area



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 Posted: Sat Apr 16th, 2011 06:15

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Mol Med Report. 2011 Mar; vol. 4(2) pp. 255-60

Change of telomere length in angiotensin ii-induced human glomerular mesangial cell senescence and the protective role of losartan.


Feng X, Wang L, Li Y
Telomeres are DNA repeats at the ends of linear chromosomes in eukaryotic cells; they form cap-like specialized structures at chromosome ends to protect them from digestion and degradation. With each cell division, somatic cell telomeres progressively wear and shorten, leading to cell senescence. Various environmental factors, such as oxidative stress and inflammation, can accelerate telomere shortening. The renin angiotensin system seems to be the key mechanism involved in aging. Our previous studies demonstrated that treatment of human glomerular mesangial cells (GMCs) with angiotensin II (AngII) caused cell senescence. It is important to understand whether AngII accelerates telomere shortening in GMCs and further promotes aging. Therefore, this study was designed to investigate the change in telomere length in AngII-induced GMC senescence and the role of the AngII receptor antagonist losartan in delaying this process. The cells were synchronized and divided into a normal control group, an AngII group (AngII, 10-6 mol/l) and an AngII + losartan group (losartan, 10-5 mol/l), and were then cultured for 72 h. The telomere lengths were analyzed by Southern blot analysis, cell morphology was monitored, the cell cycle and β-galactosidase staining were determined, and the expression of P53 and P21 proteins was assessed by Western blotting. Compared with the control group, the AngII group exhibited a markedly reduced telomere length, cell cycle arrest, enhanced β-galactosidase staining, and elevated expression of P53 and P21. The AngII + losartan group displayed longer telomere lengths, further reduced β-galactosidase staining and decreased P53 and P21 expression compared to the AngII group. This study confirms that AngII induces the shortening of telomere lengths, P53 and P21 expression, cell cycle arrest, and the resulting cell senescence in GMCs. In addition, losartan significantly reduced telomere shortening and cell senescence.

Ruth Goold
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 Posted: Sat Apr 16th, 2011 09:22

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Phillyguy:

Interesting study - I've wondered off and on about the possibility of monitoring telomere length as a biomarker of progress on the MP given its apparent overall 'anti-ageing' effect.  However, I haven't investigated the technical feasibility of selecting an appropriate type of cell to monitor and sampling them in living subjects.  But, how hard could it be...?  ;)

Ruth



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Phillyguy
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 Posted: Sat Apr 16th, 2011 15:32

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The ARBs also boost circulating endothelial progenitor cells (vascular stem cells). Olmesartan appears to increase this cell type more than the other ARBs by about 100%.

Joyful
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 Posted: Fri Apr 22nd, 2011 11:50

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Phillyguy wrote: The ARBs also boost circulating endothelial progenitor cells (vascular stem cells). Olmesartan appears to increase this cell type more than the other ARBs by about 100%.
Good to know!



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NickBowler
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 Posted: Wed Nov 7th, 2012 11:21

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The evidence builds:

http://www.cmaj.ca/content/early/2012/11/05/cmaj.120233



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 Posted: Thu Nov 8th, 2012 13:16

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I was very pleased indeed to find a 4 column article about this publication in our Dutch newspaper (Volkskrant, 7 Nov 2012). The title was: "No additional vitamin D needed to live longer." One of the key sentences in this article: "It is not always clear in these studies what is cause and what is consequence"

The real vitD story starts to be communicated to a greater public!
Jan



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 Posted: Fri Nov 9th, 2012 00:17

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Jan, is there an online version of that article?

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 Posted: Fri Nov 9th, 2012 12:08

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Ron,
I am afraid the article can be viewed only if you are registered member of the newspaper.
Jan



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Park.meds started Nov09(L-dopa/Carbidopa), no Olmesartan break (22Sept2008-23
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 Posted: Sat Nov 10th, 2012 03:19

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Bummer..


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