Yesterday at 10:28 PM Jeptha said this in Post #158
http://www.endeav.org/evolut/text/ta1/
I've read the paper. Interesting, but
nowhere in the paper does the author discuss delta S, or entropy. All the discussions are on delta G, or free energy. Therefore the statement in the abstract is not supported by the data in the paper itself.
Also, I'm surprised you are using this paper, since this paragraph directly contradicts your major thesis -- that macroevolution is contrary to thermodynamics.
"Let us stress once more that the principle of stability of chemical substances is a thermodynamic principle. It correlates with the principle of structural stabilization (Gladyshev, 1997) and states that the trend of a biological system in evolution (ontogeny and phytogeny) to the appearance of relatively more stable structures of higher hierarchies leads to the selection of relatively less stable structures of lower hierarchies.
This evolutionary trend of biological systems seems to rejuvenate the lower hierarchic structures (preserves the optimal stability of these structures) and causes a practically unlimited development of the biological world."
In trying to "win" the small point, you have posted a paper that contradicts your main point. Thank you for showing that macroevolution is
not contrary to thermodynamics.
"His idea has met with much experimental success, and is now considered a major theory of aging.
And this contradicts your assertion that Harman doesn't understand thermodynamics and that his theory is about thermodynamics.
JEP: Im trying to ascertain where you are coming from. Did I not make it clear to you in previous posts that aging via destruction of organelles is disorder and an increase in entropy?? Even such mainstream publications such as the Merck Manual attribute cellular necrosis to increased entropy.
First, increased entropy is a result of necrosis. Perhaps the word "necrosis" confused you, but Merck is saying the same thing I am: when cells die there is an increase in entropy. Necrosis is cell death. Prior to that point the cell is at lower entropy than the surroundings. If it weren't, it wouldn't be alive.
JEP: Er
.Right. That was what we were talking about. Remember??
The discussion is whether the free radical theory is an increase in entropy of the organism. It isn't. It's about cellular damage caused by the production of free radicals during ox-phos. The cell itself is still an area of
lower entropy compared to the surroundings. It is a
local reduction in entropy.
"It's not clear why reducing caloric intake should reduce the amount of free radicals produced in cells, although there are some candidate explanations. But George Roth, who heads the National Institutes of Aging study on calorically restricted monkeys, suspects that free radicals are part of the more general story of aging."
JEP: But its clear now that I walked you through the formula for ATP production, isnt it?
I walked
you through the production of ATP, remember? Production of ATP means providing high energy bonds that can do work inside the cell -- reducing entropy in the process by taking more disordely small molecules and making macromolecules of reduced disorder.
Free radicals are a side effect of that reaction when electrons are transferred to oxygen but not to make H2O, instead O3 or H2O2.
This is not part of thermodynamics, but the result of an inadequate amount of telomerase.
JEP: Not at all true. This happens to everyone and is a normal part of aging. See below.
BTW, this is not part of the"entropy" theory, but a separate theory of aging first proposed by Leonard Hayflick in the 1960s. It means that cells have a finite number of divisions. It was thought, for a while, that telomerase controlled this. There are 2 problems here:
1. Stem cells have adequate telomerase and have unlimited cell divisions.
2. In many cell types, telomere length is not related to the number of cell divisions remaining.
JEP: Really? Tell me. What is this entropy theory? I didnt know there was one since entropy is just a measure of SLOT.
The "entropy theory" is the one you and Roth are proposing. Don't you remember your own position? Here, let me refresh your memory from this post:
"Did I not make it clear to you in previous posts that aging via destruction of organelles is disorder and an increase in entropy?? "
The shortening of telomeres of DNA is not "destruction of organelles" and therefore
not part of your theory.
One biologic mechanism for Hayflick's limit is now understood. Telomeres are stretches of DNA at the end of chromosomes that serve as handles by which chromosomes are moved during the telophase of meiosis. Telomeres are irreversibly shortened each time a cell divides. When the telomeres become too short, the cell can no longer divide.
Again, this is
not irreversibly shortened. In the presence of the enzyme telomerase, the telomere length is maintained. If you are going to be a self-proclaimed "semi-literate creationist", then you have to start reading
all the data and not just that which agrees with your position. Some papers you want to see are:
1: Allsopp RC, Morin GB, DePinho R, Harley CB, Weissman IL.
Telomerase is required to slow telomere shortening and extend replicative
lifespan of HSC during serial transplantation.
Blood. 2003 Mar 27 [epub ahead of print]
PMID: 12663456 [PubMed - as supplied by publisher]
2: Cherif H, Tarry JL, Ozanne SE, Hales CN.
Ageing and telomeres: a study into organ- and gender-specific telomere
shortening.
Nucleic Acids Res. 2003 Mar 1;31(5):1576-83.
PMID: 12595567 [PubMed - indexed for MEDLINE]
3: Ramirez RD, Herbert BS, Vaughan MB, Zou Y, Gandia K, Morales CP, Wright WE,
Shay JW.
Bypass of telomere-dependent replicative senescence (M1) upon overexpression of
Cdk4 in normal human epithelial cells.
Oncogene. 2003 Jan 23;22(3):433-44.
PMID: 12545164 [PubMed - indexed for MEDLINE]
4: Allsopp RC, Cheshier S, Weissman IL.
Telomerase activation and rejuvenation of telomere length in stimulated T cells
derived from serially transplanted hematopoietic stem cells.
J Exp Med. 2002 Dec 2;196(11):1427-33.
And these are only the recent ones. From the abstract to the last paper:
"We now show that stimulation of T cells derived from serially transplanted HSC results in a telomerase-dependent elongation of telomere length to a size similar to that observed in T cells isolated directly from young mice. ... Together, these results imply that one role for telomerase in T cells may be to renew or extend replicative potential via the rejuvenation of telomere length."
So, as much as you rely on the Merck Index, sometimes it is wrong. This paper shows that telomere length
is reversible.
JEP: The addition of telemorase can inhibit this shortening but it is not the lack of it that causes it.
Yes and no. Telomeres are shortened because the DNA polymerases don't go to the end of the DNA strand. However, it is the job of telomerase to restore the telomere length to the DNA. Only in cells lacking telomerase is the shortening seen.
First, the premise that Dolly aged very rapidly is not supported by the data.
Jep: Really? You better tell all the newspapers this because this was headline news for about a month: LONDON, Feb. 14 Dolly the cloned sheep was put to death Friday, after premature aging and disease marred her short existence and raised questions about the practicality of copying life.
http://www.msnbc.com/news/872966.asp
It was in the scientific literature. What you have demonstrated is that the papers got it wrong. Not unknown in journalism, especially journalism on science.
"However, Ian Wilmut, who pioneered the research, said the early indications were that Dolly, cloned from a breast cell and named after the singer Dolly Parton, had contracted the disease from other animals in a shared pen.
"There is always a greater risk if you have animals inside that infections will spread, so we had been concerned about this," Professor Wilmut said."
http://www.theage.com.au/articles/2003/02/17/1045330539301.html
Normal sheep lifetimes are not known
JEP: *chuckle* Thats a good one. I used to raise lambs in Colorado. Boy wouldnt I be an incompetent shepherd if I didnt even know how long sheep were supposed to live. Sheep live a natural life from 11 to 16 years at the max.
You got this from the web. My apologies for not including the phrase "in these living conditions", but lifetimes of sheep in pens is shorter, as the incidence of arthritis is higher because they are walking on concrete floors.
JEP: And isnt this interesting that Dolly was cloned from a six year old sheep and lived 6.5 years before they had to put her to sleep:
Irrelevant, since she did not die of old age, but a lung infection.
JEP: Ill give you a friendly warning like I did the physicist. If you keep calling me on this stuff and quoting pseudo-science to support it, the dum kreationist is going to make the medical doctor look really silly. No disrespect intended, just being fair to you.

I'm not worried.
There is no logical connection between telomeres and entropy.
JEP: Sure there is. Full to empty is a classic example of logical entropy just as concentrated to diffused is.
You haven't shown that shorter telomeres have less entropy than long ones. Where are your calculations?
The damage from free radicals doesn't occur in the mitochondria anyway, so this is irrelevant.
JEP: Sheeze
.Where do you get your material.
From the scientific literature. Some of the damage does occur there, but a lot of it occurs to cell membranes since free radicals react with the double bonds of lipids there.
The mitochondria is the ONLY place in the cell where this reaction occurs:
ROFL! You would have done better to state that mitochondria are
one place where free radicals react. Remember, part of the damage caused by free radicals is supposed to be to
nuclear DNA.
Dr. Harman feels that getting antioxidants into mitochondria is critical because of the vast number of free radical reactions produced in these organelles, which literally explode with the kind of dynamic chain-crackling chemical activity that Harman believes is a major cause of aging.
As I said,
one place. But you claimed "ONLY place".
Somewhere in all this, Jeptha, you seem to have lost your point. Life itself is a local decrease in entropy.
Continued in next post.