68 replies to this topic

[TheFountain]

Apoptosis regulates the proliferation of disease factors too in some cases, so unless he comes up with a selective version of his formula, he could accelerate these specific disease factors by producing a situation in which these disease cells are left to proliferate. Could this be where autophagy comes in? Or would that be useless in this context?

Edited by TheFountain, 12 October 2010 - 08:56 AM.

[rwac]

Eye lens cells have no mitochondria to speak of or target.
http://www.scienceda...71020111527.htm

That's right, and even if it did, what I don't get is how an antioxidant could reverse damage. If he claimed that it prevented blindness, that would make more sense. But he says it cured blindness dogs and a horse in 2-3 months. The whole thing just smells funny. If the stuff works as well as he says, why continuously bring up and stress the theory that only confuses the matters.

It's possible that cataracts are actually caused by oxidative stress from neighboring tissue. Reducing stress at the source might allow cells to regenerate.

[xEva]

It's possible that cataracts are actually caused by oxidative stress from neighboring tissue. Reducing stress at the source might allow cells to regenerate.

Good point. That became clear from the collection of links given by VidX above. The lens cells start off nucleated, with mitochondria, but lose them as they differentiate. So, the outer lens cells have mitochondria.

Lens cells are epithelial in origin. A single layer of cuboidal cells is found on the anteriour surface of the lens, below the capsule. They are nucleated, actively divide, and account for almost all the metabolic activity of the lens. Cuboidal cells in the equatorial zone of the lens differentiate and elongare into lens fiber cells, and lose their nuclei and intracellular organelles such as mitochondria. Thus, most of the lens consists of mature lens fibers, which lack the ability to perform metabolic functions such as protein synthesis and energy production. The fibers are force toward the interior of the lens and are compressed as new fibers are deposited over them.

[VidX]

The experiments on mice involving this substance are being conducted currently in St. Petersburg. It?s too early to speak of final results, a mouse?s life span is 2.5 to 3 years. So far the results are poor, the mice die anyway, our remedy has no effect on them.

Am I missing something here. If the mice are indeed dieing, what has actually been achieved? This looks like a negative result to me - at least so far. There is no mention of increased lifespan for the mice.

Yeah, I remember reading this (is it from an older interview? Maybe that was a start of animal trials or something).
However it is we can just speculate at the moment as we have no idea how much variables are involved (or not), discussion is interesting of course, anyway... One antioxidant that WORKS (even if just slightly) would be better then all that promoted crap in the media that doesn't do sh*t irl.

[AgeVivo]

The lifetime did not extend too much, the physical process of aging got slower and sometimes it even stoppped. The animals, given our preparation, lived to old age staying in active and healthy condition, and then they died in a few days and even hours.

A translation:
the lifetime did not extend too much : there was no significative increase of lifespan ?
the physical process of aging got slower and sometimes it even stoppped : no significant effect (the mortality rate increased until a plateau, as usual)
lived to old age staying in active and healthy condition : those animals were mice (that generally are active until close to death)
and then they died in a few days and even hours : and then they died

Edited by AgeVivo, 12 October 2010 - 08:15 PM.

[VidX]

A new website: http://www.skulachevs-ions.com

and another one:

http://en.skq-project.ru/

and another:

http://www.nanotech-...?story_id=36942

Edited by VidX, 29 November 2010 - 08:08 AM.

[carlcrott]

http://www.ncbi.nlm....pubmed/19120018

[JLL]

http://www.ncbi.nlm....pubmed/19120018

Looking at the survival graph of the mice, maximum lifespan was only slightly increased. Median lifespan, yes, but if this truly stopped the aging program, wouldn't we have seen an increase in MLS as well?

EDIT: Or is this again a case of mice dying from causes that are not strictly related to aging? The old mouse on the drug does look better than the control mouse.

Edited by JLL, 11 December 2010 - 07:57 PM.

[VidX]

He says that it's not clear why they die, even if keeping traits of "youth" till the last day.