Where are they? They're programming the simulation.

X-Message-Number: 14453
From: 
Date: Tue, 12 Sep 2000 12:25:30 EDT
Subject: Where are they? They're programming the simulation.

In a message dated 9/12/00 4:03:23 AM Central Daylight Time, Doug Skrecky 
writes:

<< 2.  ETI's are in fact already here.
     This has an interesting varient:
 2A. We exist in a cyberspace.
  >>

  It is obvious that any real universe containing intelligent life will also 
contain a much greater number of simulations of intelligent life. So the odds 
are that any given intelligent being is living in a simulation, perhaps even 
a simulation within a simulation. Thus the importance of cryonics; it allows 
you to reach a future where the universe is being run under an improved 
operating system. Perhaps the operating system will eventually be made "open" 
(i.e. we will be able to access it.)
  Unfortunately this simulation is likely to be terminated like a bad TV 
series if we don't start doing something more entertaining than discussing 
the origins of the universe (based on our massive knowledge of the cosmos; we 
haven't even explored two solar systems yet!) while our telomeres continue to 
shorten and our lives continue to be run by the likes of Algore and George 
the Second. So, let's focus, people, focus! There's some smart simulated 
minds on Cryonet, let's use them to keep our 'series' on the air. We may be 
the multiverse equivalent of South Park, but multiverses need entertainment 
too. Resetting our telomeres and exploring the universe is entertaining; 
philosophizing while dying of hideous diseases is boring (obviously, or the 
Middle Ages would still be tops in the ratings.)

  So, how about that study at Bethesda that claims that homocysteine shortens 
telomeres and causes artery cells to senesce and cause atherosclerosis  (see 
below for abstract)? I note that Xu used mixed D-L homocysteine, which I 
assume is not physiologically correct (?) Still, if he's right, we should all 
get our homocysteine tested immediately and start taking SAMe and the other 
cofactors immediately to lower our homocysteine levels. Anyone know of any 
similar studies done with L-homocysteine?
  I also note that Southwest Medical Center researchers have extended the 
lives of fibroblasts by using a cDNA to temporarily produce telomerase in the 
cells. This sort of technology seems relatively easy to apply to humans, 
though it might require temporary immunosuppression. It would also be very 
suitable for use in out-of-FDA-jurisdiction clinics (as you would only need 
to have your telomeres reset every fifty years or so.) Hey Saul, aren't you 
just about due for this process? How about building a little telomere reset 
clinic in Guyana (it could go right next to the 25,000-acre Beal Aerospace 
spaceport, also built to escape US regulations)?

  Sorry if I seem impatient (I'm sure that seems pretty funny to Ettinger, 
who has been waiting for the billionaires to wake up and smell the telomeres 
for what, fifty years?)


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FEBS Lett 2000 Mar 17;470(1):20-4 

Homocysteine accelerates endothelial cell senescence. 

Xu D, Neville R, Finkel T 

Laboratory of Molecular Biology, NHLBI, NIH, Bldg 10/7B-15, 10 Center Drive, 
Bethesda, MD 20892-1650, USA.

In this study we demonstrate that exposure of cultured endothelial cells to 
homocysteine significantly accelerates the rate of endothelial senescence. 
Examination of telomere length demonstrates that homocysteine increases the 
amount of telomere length lost per population doubling. The effects of 
homocysteine on both senescence and telomere length are inhibited by 
treatment with the peroxide scavenger catalase. Chronic exposure of 
endothelial cells to homocysteine also increases the expression of two 
surface molecules linked to vascular disease, intracellular adhesion 
molecule-1 (ICAM-1) and plasminogen activator inhibitor-1 (PAI-1). 
Interestingly, the level of expression of both ICAM-1 and PAI-1 correlates 
with the degree of endothelial senescence. Taken together, these results 
suggest that homocysteine accelerates the rate of cellular senescence through 
a redox-dependent pathway. In addition, it suggests that chronic oxidative 
stress in the vessel wall may hasten the rate of senescence and that the 
senescent endothelial cell may in turn be pro-atherogenic.

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