Garden of Eden lays in the Persian Gulf? Not a religious thread.

[lestatdark]

padib said:

lestatdark said:

Dr.Grass said:

lestatdark said:

Dr.Grass said:

Jumpin said:

All of this arguing about whether Noah's Ark was true or not is silly. Of course this didn't happen. How can people actually consider this a possibility in this day and age? It is ridiculous.

Noah's Ark claimed that there were 2 of every species of animal on board and that Noah was hundreds of years old.

1. It is biologically impossible for a human to reach that age. The oldest people with today's medical technology have not lived much past 110 years, let alone 700 in what was a bronze age civilization.
2. Many species of animals require vast ecosystems that cannot possibly exist on a boat. Not to mention, if the world was flooded, then all marine life would die as well, because the saline levels of water would be incorrect for almost all species of marine life in the world; despite what you may think, a freshwater fish can't live in the ocean.
3. There are about 2 to 3 million species of animal estimated, but some estimates go up to 50 million.
4. There is no evidence of any great flood 4,000 years ago, but we have Civilizations dating back to over 5,000 years, and Neolithic and Paleolithic societies dating back much further. We also have fairly detailed archaeological accounts which detail the migration of modern humans, out of Africa, and into the Western Continents, and this occurred tens of thousands of years ago.
5. Those fossils that are high up are the result of tectonic plate movement, not a whole lot of extra water that mysteriously appeared on Earth.

Please, it is people like you guys with sickeningly primitive beliefs that give ALL religious people a bad name. You focus WAY too much on having obviously mythological and fictional accounts as being "true" that you ignore the true purpose of religion.

1. That's not true. The number of times a cell reproduces is encoded in our genes. Just change that one piece of code and you can live much longer.

Oh dear....

Tell you what, you try and do that and see where that gets you xD. Oh and an heads-up, don't forget to set up the telomerases so that they won't cut the telomeres, or you'll still risk cellular death. Then you'll also have to cut out apoptosis signals, capsases and many other cell-death inducers. Don't also forget to implement a much more efficient DNA repair system, because ours is inefficient after 60 years of divisions, that's why you start having more probability of self-induced cancer and that's not accounting all the external factors that can lead to potential lethal mutation. 

There's no simple "way" to live longer, that must have been the most unscientifical, innacurate thing I've ever read from you.

He said it isn't possible, I said it is. I said nothing about how probable it is.

He has more of a point than you can possibily have. Even if we advance genetic therapy long enough and can somehow eliminate all mutagenical and envorimental issues out of the genetical equation, the best estimatives, before total cellular breakdown and loss of complete capacities of DNA repair in a human being is 150-200 years, at best. 

So 700 years is indeed impossible without any kind of external input, such as cryogenics, repairing nano-machines or other sci-fi related medicinal "advancements".

What in our genes dictates that at 150 (barring out all other factors from the equation), at 150-200 years there is a complete loss of capacities of DNA repair? Is it a gene? Enlighten me.

This may be something you laugh at, but it provides explanations, which is something I understand to be encouraged in the elaboration of theories:

http://www.creationworldview.org/articles_view.asp?id=45

EDIT: I found this link more informative: http://creation.com/living-for-900-years

It's a conjunction of factors. Telomeres have an fixed amount of quadruple-bonds of Guanine that protect the DNA from the degenerative effect of the Nucleases, thus are the primary factors that dictate DNA longetivity and a cell's capacity to divide (if the telomere dissapears, apoptosis is immediatily triggered on the cell to promote it's death, if that is not signalled, the p53 and rb4 genes malfunction and that, with the over-expression of the telomerase enzyme, are the first steps into cancer formation, which is the other end to any cell. 

Also, Mitochondrial function in a cell is limited. As you're aware Mitochondrias have their own set of DNA to create the intra-matrix protein complexes responsible for the oxidative respiration chain and the formation of ATP. In normal conditions, in which the cell is constantly oxigenated and that the mitochondrial DNA is function normally, every mitochondria have a very limited number of divisions. As there are a very varying number of mitochondria per cell (depending on the function of the cell, the tissue that is a part of or shifts in cell stress), they also account for limiting the number of cell divisions. 

Plus, mitochondrias are the primary motor behind the apoptosis signal and the capsases formation. The capsases are enzymes that detect the "check-point" proteins in each of the stages of the cell (there's various stages, but the majority of the cell's life is on the stationary stage, or S). The S state is followed immediatly by the G state, which is the precursor state of the mitosis, the cell division. There are a varied number of "check-points" proteins, which function by varying their number from check-point to check-point. If the number is off, then the cell does not divide and must signal itself for death. 

Then there's also the external signalling that the cell can give to the immunological system by coating some of the oligo-glyco-proteins in the plasmatic membrane with antigens that are recognized by phagocytes and that's the signal for cell degeneration via enzymatical digestion in the phagocyte. This is sort of a last resort method, since this scenario happens almost exclusively in the case of mutations on the aformentioned systems or in the case of early formations of cancer tissue.

The 150-200 limit is a statistical limit. It's extremely improbable that a functional tissue can sustain itself after the extremely high number of divisions 150-200 years of divisions require, free of mutations or without any kind of mutations that the DNA repair systems can detect and remove.

Also, to talk a bit about the DNA repair system in humans (and in the majority of Eukaryotic cells), unlike in bacteria where there are specialized systems that can detect via positive or negative feedback even small localized mutations or even have systems that can create unique immunities against antibiotics and external mutagenical factors with the plasmid DNAs, our DNA repair system is intrinsically tied to the DNA polymerase.

The Eukaryotic DNA polymerase has both the capacity of creating new strands of DNA but also has the capacity to detect localized mutations downstream (5´-> 3´transcription in the leading strand) from the promotor sites after the AUG initialization site. When and if mutations are detected, the polymerase activates another of it's functions, the (3´ -> 5´) endonuclease enzymatic action, in which the lagging portions of the polymerase, via hidrolysis, remove not only the affected localized mutation but also a big chunk of the DNA sequences upstream and downstream of that mutation. To exemplify, you have the following DNA sequence with a localized mutation (in blank):

5' - AGGGATTTCCTCATTCGA - 3'    
3' - TCCCTAAAGGCGTAAGCT - 5' 

After the endonuclease removal:    5' - AGGGATT                    CGA - 3'  
                                                                  3' - TCCCTAAAGGCGTAAGCT - 5'    

After repairing:  5' - AGGGATTTCCGCATTCGA - 3'
                               3' - TCCCTAAAGGCGTAAGCT - 5'

As you can see, in the first one, there's a localized mutation in the 11th pair, since T and G don't pair up. The polymerase recognizes it, cuts out a chunk of it (the second sequence) and then it repairs it to the correct pair G - C. 

Well since these are the basics of DNA repair in our cells in a single mismatched pair (the simplest localized mutation), then it gets all more complicated (i shall not go in depth with the T-T dimers which are one of the most complicated localized mutations and one of the most proeminent causes of cancerous mutations).
At any given moment, up to 10^4 mutations ocurr in a random point in our DNA. Since we have 46 chromossomes (23 pairs), up to 4.6 billion base pairs in each chromossome and since only a small fraction of our DNA is being currently used to create proteins, there's a huge margin of probability that a lot of those mutations will not be detected by a polymerase and thus will be continualy propagating themselves in every cell division. Now, point mutations on transcription-locked genes are not that big of a deal, since most of those genes are only used in the early stages of the cell (embrionic formation), but imagine that one of those mutations are in a gene that code for a specific mitosis characteristic that only happens in the 2000 or so cellular division and that mutation has been propagating since the first cellular division with no removal happening. When the 2000 or so cellular division happens, the cell finally detects it and it either signals itself for death or the cell becomes non-functional if the mutation is critical or can even become a cancerous cell post-division. 

There's also another problem with our DNA repair systems. Each DNA polymerase endonuclease capacity is very limited (can only detect and repair succesfully up to 10^6 mutations before creating errors itself) and even with the high number and type of DNA polymerases in Eukaryotic cells (the Pol B - for Beta - is the most functional of all), every statistical model predicts that mutations can and will start to pile up within a cell. Even if you overcome the problems of aging and the metabolical requirements for living up to 150 - 200 years (and those are two distincitvely different problems that could take me pages to explain as well), at that plateau the number of mutations surmount to such a critical amount that there's no possibility that a viable cell exists that can divide itself without signaling for death or go cancerous.

In summary, there's no single gene responsible for controlling whether or not we can live much longer than we live now, heck there's not even a single chromossome that we can manipulate to enhance our living span. The only real way we would ever be able to do it, is if there were artificial ways to repair the cell (either by massive gene therapy with stem cells to restore the DNA within our cells to an initial state, creating nanoscale machines that replace our DNA polymerases with much better capacities than them or even wilder, Sci-Fi realm techniques). 

And yeah, I did do a quick view on your links. If that's considered science within some circles, then I dread to be with those so called "scientists". Even my 8 year old cousin is a better "scientist" than those people.