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With all due respect...


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#61 mitohunter

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Posted 11 March 2006 - 05:27 AM

well, i am just thinking "outside of the box"...i.e., what if there were a way for cells to produce ATP w/o mitos?
Remember, even if the 13 mito genes were somehow (after years of research dollars) moved to the nucleus, the mitos will still be generating plenty of free radicals.

#62 JonesGuy

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Posted 11 March 2006 - 07:29 AM

The ROS scrubbing mechanisms (similar to what's in our germ cells) would need to be encouraged as well

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#63 mitohunter

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Posted 11 March 2006 - 09:24 PM

What do mitos have to do with ROS scrubbing, i.e., are they in majority control of this process?

another thought:

The other handy thing about mDNA is that it changes much more rapidly than nuclear DNA, about 20 times as fast, because mitochondria lack an efficient proof-reading system to check for errors when DNA is copied. The high mutation rate means that there is plenty of variation in the sequence of mDNA between people, and variation is the lifeblood of genetics

I cannot remember where I found that quote, but wrote it down and had some thoughts (IF that is factual):
that sounds like bs because we all have about the same lifespan...so the implications of variations/proofreading in mitos doesn't really matter.

#64 mitohunter

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Posted 15 March 2006 - 01:12 AM

Since I am presently working in the functional genomics of Zea maize, I still at every time for a free thought wonder how I can use my position to further the WOA. I googled the lifespan of corn and found no definitive answer. I was wondering that, if I could do a Masters in Hort. Sci. and make corn live longer at the same time....maybe I'd end up in Leeuwenburgh's lab that much faster.
comments?

#65 John Schloendorn

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Posted 15 March 2006 - 05:35 AM

I believe that would be a waste of potential talent. I would stay as close to working on human rejuvenation therapies as possible. It is very hard to see where precisely that is, but it is very easy to see that it is not in corn genomics.

#66 maestro949

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Posted 15 March 2006 - 01:13 PM

Maybe he could mix ES from corn and humans and make CornMan no? Questionis, what would be in it's stool? :)

#67 mitohunter

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Posted 22 March 2006 - 03:45 AM

I believe that would be a waste of potential talent. I would stay as close to working on human rejuvenation therapies as possible. It is very hard to see where precisely that is, but it is very easy to see that it is not in corn genomics.


I agree, and do not agree. The Aging Lab @ UF is nascent...still writing grants....but at the same time, their LAB TECHS have Masters and Ph.D. degrees...so I could "fasttrack" to earn the credentials to get in w/in a few years at most.

#68 mitohunter

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Posted 22 March 2006 - 03:47 AM

Maybe he could mix ES from corn and humans and make CornMan no? Questionis, what would be in it's stool? :)

haha, hee, hee

#69 Mark Hamalainen

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Posted 22 March 2006 - 04:53 AM

The other handy thing about mDNA is that it changes much more rapidly than nuclear DNA, about 20 times as fast, because mitochondria lack an efficient proof-reading system to check for errors when DNA is copied. The high mutation rate means that there is plenty of variation in the sequence of mDNA between people, and variation is the lifeblood of genetics


Good for propagation of the species doesn't mean good for lifespan of the individual.

A graduate degree is a big time investment, before you decide what to do it would be worth it to do extensive reading. Trying to start a research project without specific ideas and plans for your experiments is a good way to waste a lot of valuable lab time. Have you gone through the articles at www.sens.org?

#70 mitohunter

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Posted 23 March 2006 - 01:09 AM

Osiris, I am looking at anything that I can. No, I haven't been through all the SENS articles, in fact, have not been looking at them much....which could be a mistake.
I agree that anyone going for a research project w/o any ideas would be inane. Trust that I am not. Last year I read....no, STUDIED, Dr. Leeuwenburgh's publications. After my Masters in horticulture, I will enter into Dr. L's lab with ideas that he himself may not have thought of. From there, I will contribute to our WOA while earning my Ph.D.

#71 John Schloendorn

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Posted 23 March 2006 - 02:25 AM

Ah well... You're not by any chance into bioluminescent houseplants, are you?

#72 mitohunter

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Posted 24 March 2006 - 01:19 AM

Yes John, they are interesting, especially what "house" you are referring to. Dr. Ferl here at IFAS is working with NASA to have a colony on Mars by 2030, based on bioluminescent Arabidosis.

#73 JonesGuy

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Posted 24 March 2006 - 01:32 AM

That's valuable.

There's good reason to pursue what you can, because fresh perspectives are important.

#74 John Schloendorn

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Posted 24 March 2006 - 02:13 AM

Interesting. Can one see the luminescence of these plants with the eye, or is long exposure imaging required? Are they exploring luciferin biosynthesis at all, or will it have to be supplied? Is the reaction localized in the cytosol or an organelle?

#75 zoolander

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Posted 11 April 2006 - 08:02 PM

Is everyone just playing around with this guy? Some of what you are saying mitoHunter makes me think you may be one protein short of a polypeptide. Seriously, destroy mitochondria and find an alternative source of ATP? WTF! and the fact that mitochondria were a seperate cellular entity at one stage is basic biology.

COME ON!

I feel like I'm taking crazy pills.

And then there is that superiority complex of yours. The ONE? When you refer to the ONE are you referring to the ONE from the matrix? The mitochondrial matrix?

I am 6 months away from completing my Ph.D and have starting writing my thesis. My main area of research is looking at the effects of dietary supplements and resistance training on muscle oxidative capacity in aged males. I have been working with mitochodria from the last 4-5 years and believe I know them well.

If anything should happen, it should be mitocondrial biogenesis and not mitochondrial apoptosis. Of course free radical are problematic but that is a part of life. Life, you know, has its negatives.

MitoHunter, how do you propose we find another way to produce ATP? You will need to get this (whatever it is) into the cell. So you are suggesting we devolve and force the mitochondrial out of its biological contract and infect the cell with a new fandangled organelle that will not produce free radicals.

The biggest question is how do you propose to reinvent oxidative phosphorylation?

#76 JonesGuy

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Posted 11 April 2006 - 09:51 PM

How about putting the mtDNA into the nucleus (with a way to migrate to the mitochondria)? That way, the oxidative damage isn't being done to the DNA, and it will last longer?

Lots of species have varying amount of mtDNA in the nucleus.

#77 DukeNukem

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Posted 12 April 2006 - 01:01 AM

Like most conspiracy theories, this one fails because if that cure existed, a significant number of people would have to know about it and the chances of keeping it secret decrease exponentially with each additional person that knows. Besides, there is much more money to be made in treating aging than there is in maintaining the status quo.


Osiris,

o I agree that there's likely not a cure to aging that is being kept under wraps. If someone actually had such a cure, they'd try to make money from it, and there would be a ton of money to be made!

o I don't think that the major drug companies really want to upset their proven, FDA-endorsed license to print money in any hurry. Right now, they are having their way with their FDA lackey, and laughing all the way to the bank. SO, the incentive is not there for them to search for a be-all aging cure that changes everything. (Practically all diseases are cured via prevention, and all of those millions of pills people buy and take each day go in the garbage.) That cure will more likely come from a start-up type of company that has nothing to lose ... and let's hope they are not bought out by Big Pharma because that will likely steer the process away from where we all want it to go.

#78

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Posted 12 April 2006 - 04:09 AM

makes me think you may be one protein short of a polypeptide


[lol]

If anything should happen, it should be mitocondrial biogenesis and not mitochondrial apoptosis. Of course free radical are problematic but that is a part of life. Life, you know, has its negatives.


A more precise solution is to turn up the rate of mitochondrial turnover (incease both mitochondrial autophagy and biogenesis) whilst ensuring the mtDNA polymerase (the enzyme that duplicates mtDNA) is of the less error prone variety.

Alternatively, mtDNA genome repair and stability factors (repair & antioxidant enzymes, mtDNA damage sensors, etc.) can be upregulated or new ones introduced without altering mitochondrial lifecycle.

Either of these proposals would involve only a handful of genes being modified.

#79 marcus

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Posted 12 April 2006 - 06:39 PM

I disagree that there is not an incentive to produce a "be all aging cure that changes everything". Big pharma is a competitive industry and those who develop the most powerful therapies and drugs stand to bring in the most money. There is a constant race going on to develop new/better therapies as this is the main way to take market share from your competitors.

It makes for fun speculation that there is some conspiracy that there are major cures being kept off the market to maintain the status quo, but the economic reality is that the big drug companies are in a constant race with each other(and upstart biotech) to develop better drugs and therapies. The incentive is and has always been there to develop the best therapies/drugs. What is keeping big pharma away from working on proposed treatments like those outlined in SENS is the lack of pre-clinical data to support such development. In their cost/benefit analysis SENS type objectives are still far to risky to make any kind of investment in them. I'm sure down the road big pharma will join the fight to bring these type of advanced therapies to market, but not until much of the risk has gone out of the equation. It's not a matter of big pharma wanting to maintain the status quo, but more a matter of there still being too much risk and uncertainty in some of the new therapies/ideas being developed.

M

#80 JonesGuy

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Posted 12 April 2006 - 07:28 PM

Why don't germline mitos age?

#81 John Schloendorn

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Posted 12 April 2006 - 07:45 PM

Why don't germline mitos age?


First, "aging" is something that happens to organisms, not cells or mitos. If you translate your question into "why don't germline mitos dysfunction?", the question is wrong, because most germ cell mitos that are made clearly do dysfunction soon after. So the answer to what you mean by your question is probably massive selection on the level of the mito, the cell and perhaps also the individual. When they say the germ line is immortal, this is indeed referring to a "line", i.e. an arbitrarily unlikely succession of events consistent with survival. The individual germ cell, let alone the individual germ cell mito is very mortal indeed. Only the luckiest make it.

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#82 Centurion

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Posted 15 August 2006 - 03:18 PM

  I don't see too many with my level of education in imminst,


Forgive me, but that is quite possibly the most arrogant comment I have seen here in a while. By your level of education I assume a degree? I know this post was written a while back, but I don't see people like Zoolander (almost with a doctorate) touting their academic prowess.......




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