Annoying creationists

[kjkent1]

Whoa there! That's MY $10,000 you're after!

Unless you'd like to make multiple wagers, kleinman? It's a GREAT opportunity to make a profit off all of us dumb evolutionists.kleinman's an M.D. I'm sure he's good for at least $20K.

[kleinman]

Ok, we have a bet, if ev takes more than three times longer to evolve all three selection conditions simultaneously for a G=20,000 bases than it takes to evolve each of the three selection conditions individually than you owe me $10,000. If ev evolves the three selection conditions singly in more than three times the sum of the number of generations for each of the selection conditions than it take for all three selection conditions simultaneously, than I owe you $10,000.I think I'd like to take you up on your wager, Dr. Kleinman.

The wager, as I understand it is: if ev evolves a genome in fewer generations with all three mistake counts set to non-zero values, than it evolves the same genome with only one of the three mistake counts set to non-zero, then you will pay $10,000, otherwise I will pay you $10,000.
That’s a G=20,000 genome lita’ gator.
If that's the bet, then I'll take it, providing that (1) the measurement of evolution is based solely on Rseq >= Rfreq, (2) the test is run with 10 different random seeds, and the results are averaged, and (3) the loser agrees to pay all reasonable costs incurred in enforcing the contract.
Ok
If you accept, I will need your mailing address so that I can send you a written contract for your signature. Feel free to send me a private message.
You already have my mailing address.
Sol, you are squirming.Not at all - except with anticipation of my $10,000.
You mean the anticipation of loosing your $10,000.
The rate is determined by the number of generations necessary to evolve a particular selection condition. When multiple conditions are imposed simultaneously, it takes far more generations for a population to evolve to these conditions simultaneously than if these conditions are imposed singly.So you agree to use more conditions - say 100? According to you, the time required to evolve to conform to 100 selection conditions is at least 100 times the time required to evolve to 1? Is that right, or are you admitting you were WRONG all along?
Ev doesn’t have 100 selection conditions; you are already trying to squirm out of the wager.
I think I'd like to take you up on your wager, Dr. Kleinman.Whoa there! That's MY $10,000 you're after!

Unless you'd like to make multiple wagers, kleinman? It's a GREAT opportunity to make a profit off all of us dumb evolutionists.
I don’t think you are dumb, I think you are ignorant of how ev and mutation and selection works.

[kjkent1]

That’s a G=20,000 genome lita’ gator.Will you accept a smaller value for G -- say 2048?

[rocketdodger]

If that’s not enough for you rocketdodger, I have more citations which show the same.

All of those studies only reinforce my argument you sad little man.

You are simply incapable of understanding this -- one cannot measure the rate of fixation in a population that is nonexistent.

You claim adding selective pressures confounds the sorting mechanism and messes with the trajectory on the fitness landscape and blah blah blah -- none of that even matters when the population is gone. How can you not see this? How can you claim the sorting is confounded when there is nothing left to sort?

Can you show us any studies in which the pressures are not designed to destroy the population?

[joobz]

I see you are evading my questions with silly betting diversions. I also see you evading actually taking bets by offering insults.

I request no money from you. I simply ask that you justify your model assumptions. That should be easy for someone who is so smart they can solve nonlinear PDEs numerically using a computer program.

[sol invictus]

Ev doesn’t have 100 selection conditions; you are already trying to squirm out of the wager.

The version I'm looking at seems to allow an arbitrary number.

Anyway, let's be a little more specific, shall we? The bet is we run ev with 20,000 potential binding sites (which is going to be slow, but as you will). Now for some reason you want only 3 binding sites. I don't see why you want such a small number if you actually believe your own claim. It would be much better to run with a large number to decrease the risk of a statistical fluctuation screwing this up. But as you will.

So after agreeing on mutation rates etc., we run until a perfect creature is produced. If number of generations required is G(3) (the 3 for 3 binding sites), your claim is that G(3) > 3 G(1), is that correct?

Clearly this will need to be done quite a few times to get a good average, with a true random seed on each run. I assume you agree on that?

If so, what do you propose for mutation rate, population, and site width?


I don’t think you are dumb, I think you are ignorant of how ev and mutation and selection works.

Dumb or ignorant, either way you can take our money.

[kleinman]

That’s a G=20,000 genome lita’ gator.Will you accept a smaller value for G -- say 2048?
Kjkent1, convergence can not be based on Rseq >= Rfreq because as Paul has said:
The problem with using Rs > Rf as the test, rather than the perfect creature, is that there is no selection pressure to reach Rs > Rf. There is only pressure to reach a perfect creature. There is no Rs > Rf selection pressure in nature, either.
Convergence must be based on zero mistakes. Then G=2048 is acceptable. Send me the contract.
Can you show us any studies in which the pressures are not designed to destroy the population?
Rocketwhomissesthetarget, all selection pressures impair the fitness of a population to reproduce.
I request no money from you. I simply ask that you justify your model assumptions. That should be easy for someone who is so smart they can solve nonlinear PDEs numerically using a computer program.
There you go again joobz; you are calling ev my model.
You had it correct when you said to Paul:
I swear I'm going to release a new version of Evj that does not use the term perfect creature. And I'm going to do it soon.While you are at it, can you include a list of model assumptions made in evj and explain that ANY extrapolation that is made that exceeds the bounds of the assumptions is inherently wrong?
Why don’t you ask Dr Schneider what his assumptions are? Then you will realize that the assumptions are not limiting the real examples that I have cited.
Ev doesn’t have 100 selection conditions; you are already trying to squirm out of the wager.The version I'm looking at seems to allow an arbitrary number.
Sol, I have a suggestion for you, take your money and buy a savings bond or cd.

[joobz]

There you go again joobz; you are calling ev my model.
You had it correct when you said to Paul:

Why don’t you ask Dr Schneider what his assumptions are? Then you will realize that the assumptions are not limiting the real examples that I have cited.

Why do you keep avoiding answering my question? Do you not understand the model you are trying to present, or do you think by avoiding me you will not look as foolish as you do?

[kjkent1]

Kjkent1, convergence can not be based on Rseq >= Rfreq because as Paul has said:The problem with using Rs > Rf as the test, rather than the perfect creature, is that there is no selection pressure to reach Rs > Rf. There is only pressure to reach a perfect creature. There is no Rs > Rf selection pressure in nature, either.Convergence must be based on zero mistakes. Then G=2048 is acceptable. Send me the contract.I can see you're trying to squirm out of the bet.

YOU are the person who has consistently lauded Schneider's peer-reviewed, published paper: Evolution of Biological Information. The conclusion of said paper is:

"The results, which show the successful simulation of binding site evolution, can be used to address both scientific and pedagogical issues. Rsequence approaches and remains around Rfrequency(Figure), supporting the hypothesis that the information content at binding sites will evolve to be close to the information needed to locate those binding sites in the genome, as observed in natural systems [footnotes]."

There is NOTHING in the above conclusion, nor anything in Schneider's paper which refers to a "perfect creature." In fact, nowhere in the paper does the word "perfect" appear.

So, with apologies to Paul, if your position is that Schneider's paper and experiment is valid, then the idea of a "perfect creature" is not relevant to this discussion or to the wager at hand.

The ONLY relevant measurement of evolution of information to be found in Schneider's paper and ev is the relationship of Rseq ~ Rfreq.

Now, I have provided you with an opportunity to prove your point. I will bet you $10,000, $100,000, $1 million, or whatever is your present net worth, that as soon as you set any one of the ev mistake weights to zero, convergence of Rseq -> Rfreq will NEVER occur, except by random chance -- while convergence with all three mistake weights set to any non-zero number will cause convergence, when using the ev default settings and a G=2048.

Of course, you already know that this is true, so there is ZERO chance that you will accept my wager now.

It's one thing to constantly claim that your right and others are wrong because you say so. It's another thing to put up real money and defend your position in the real world.


So, what's it gonna be, Alan? If you accept the bet, you will lose your life savings, and your belief system. If you don't, all you'll lose is what remains of your credibility.

[sol invictus]

Sol, I have a suggestion for you, take your money and buy a savings bond or cd.

You're backing out? That was even faster than expected.

You have two choices here, kleinman - either continue with this, or admit you've been wrong all along.

Do you or do you not maintain that the number of generations to a perfect creature with binding sites set to N, is greater than N times the number of generations to perfect creature with binding sites set to 1? (N=3 is fine if you insist - we'll just have to run more trials to take the average.)


YES OR NO?

[rocketdodger]

Rocketwhomissesthetarget, all selection pressures impair the fitness of a population to reproduce.


Your ignorance is boundless. Google "selection pressure definition" and tell me how many hits contain anything like "impair the fitness of a population to reproduce" -- I DARE YOU

If all selection pressures impair the fitness of a population to reproduce then why does ev use a constant population size? Can you answer that Kleinman?

[kleinman]

There you go again joobz; you are calling ev my model.
You had it correct when you said to Paul:

Why don’t you ask Dr Schneider what his assumptions are? Then you will realize that the assumptions are not limiting the real examples that I have cited.Why do you keep avoiding answering my question? Do you not understand the model you are trying to present, or do you think by avoiding me you will not look as foolish as you do?
Well joobz, since you are too lazy to investigate ev yourself or what Dr Schneider has said about ev, I’ll do it again for you. Since all I have done is taken the ev model and studied what it shows when the input parameters are varied and what it shows is the mutation and selection sorting/optimization process is profoundly slowed when you have combination selection pressures in the model. In addition, I have posted hundreds of citations which demonstrate the same behavior as Dr Schneider’s peer reviewed and published model shows. So what has Dr Schneider said about his model? You can find the answers at the following URLs:
What was Dr Schneider’s intention for the use of his model?
http://nar.oxfordjournals.org/cgi/content/full/28/14/2794 (http://nar.oxfordjournals.org/cgi/content/full/28/14/2794)
Variations of the program could be used to investigate how population size, genome length, number of sites, size of recognition regions, mutation rate, selective pressure, overlapping sites and other factors affect the evolution.
Then what does Dr Schneider say about ev as a simulation of how mutation and selection works in reality?
http://www.lecb.ncifcrf.gov/~toms/paper/ev/faq-for-ev.html (http://www.lecb.ncifcrf.gov/~toms/paper/ev/faq-for-ev.html)
Briefly, what is Ev? Ev is a computer program that allows one to model the way that information is gained in living organisms by natural selection. The example used is the patterns in DNA to which proteins bind to regulate genes. This is a well-understood system and so it makes a good demonstration of evolution. Also, the mathematics is precise and gives quantitative results that match the results seen in nature.
and
Where is the environment in this picture of evolution of binding sites? The size of the genome and number of required sites is the 'environment' from the viewpoint of the binding site recognizer. This is, of course, an exact mirror of the situation in nature. DNA recognition proteins can be activated to bind or blocked from binding DNA by outside factors (e.g. LacI) but once that has taken place, the recognizers function by locating positions on the DNA. So they are buffered from the external environment and they only face the problem of locating their sites on the genome. The Ev organism recognizers have the same challenge.
and
If you had a different recognition method would you get a different result? No, so long as the recognition function gives a finely graded and ordered response to input sequences. In the Ev program, recognition is done using a numerical matrix of numbers, encoded in the genomes. In nature, DNA is copied to RNA, the RNA is translated into a polypeptide and then the polypeptide folds to make a protein. Finally, the protein recognizes the binding sites by physical interactions with the DNA. We already know that when the recognition method is the natural one, Rsequence is close to Rfrequency (see Schneider 1986, flexrbs). Even these vastly different mechanisms give the same results, so the answer is no. However, you are quite welcome to put a different recognition method into the Ev program source code and see what happens. If you do that you might be able to publish the results!
Dr Schneider is correct about this. The citations which I have posted show that the different recognizers that occur in real examples of mutation and selection have the same behavior as his mathematical model which is combination selection pressures profoundly slow the evolutionary process.
Why don't you do a real biological experiment instead of just a computer model? The primary reason is that we don't have infinite resources and time. If you have the resources (a molecular biology lab), are interested in doing an experiment, and would like to discuss it please contact me. The second reason is that nature has already done experiments, and we generally see that Rsequence is close to Rfrequency in real examples (Schneider 1986, flexrbs). The third reason is that many people have already done related evolutionary experiments, such as SELEX and similar experiments ( J Am Chem Soc. 2004 Apr 28;126(16):5130-7. Informational complexity and functional activity of RNA structures. Carothers JM, Oestreich SC, Davis JH, Szostak JW.) though to my knowledge no one has tested whether Rsequence evolves to Rfrequency in vivo.
What Dr Schneider fails to recognize here is that real biological experiments of his simulation are done all the time including in his own organization, the National Cancer Institute. Real examples of the mutation and selection sorting/optimization process are being done all the time and they all show that combination selection pressures profoundly slow this sorting/optimization process. This is in agreement with what his model shows.
Isn't the Ev mutation rate much higher than natural rates? It's only 10 fold faster than HIV. Interestingly, there are mutations in the bacteriophage T4 DNA polymerase that reduce mutation rates. So the rate of mutation is itself under evolutionary control (though not in the ev program).
Now joobz, you can ask Dr Schneider yourself if mutation rates will change the underlying mathematical fact that combination selection pressures profoundly slow the evolutionary process. If you studied ev, you would find out that mutation rates do not change the fact that the number of optimization conditions dominates the mathematics of the mutation and selection sorting/optimization process.
Won't a slower evolution take too long in nature? No. For practical reasons we usually use a tiny population in Ev, generally only 16 organisms. In nature there are usually populations of millions. For example, in the lab a single cubic centimeter (ml, a milliliter) of E. coli culture can easily contain 108 bacteria. (That's 100 million.) With an error rate of one in 10^6 (i.e., one in a million) at each genetic location, there will be plenty of variation to drive evolution. Notice that we have 6 billion people on the planet, so there is lots of opportunity for us to continue evolving. (Have you been wearing your seatbelt? People who don't wear seatbelts are being selected against ...)
Dr Schneider has not done the studies that he suggested for his model. If he had, he would find out that huge populations have a much more limited effect on the evolutionary process than he is claim here. Is Dr Schneider claiming that there was a population of 6 billion primate precursors for the evolution of humans and chimpanzees?
If you had a reasonable sized genome would you find that there won't be an information gain? No. Don't be lazy, go try it yourself! But notice that it will take a lot more computation, and the runs may take some years unless you write a version that uses parallel processors.
Why does it take huge numbers of generations to evolve his system? It is the combined selection pressures which makes it an extremely slow process to find a trajectory on the fitness landscape to his “perfect creature” local optimum. In fact, in many if not most cases, a “perfect creature” local optimum can not be achieved because the population gets stranded at other “non-perfect creature” local optima.
Why are there so few mistakes at the beginning? Cristi asked:

I ran the program with a few different seeds, and the best organism is at the first step already in a great shape, with only around 20 mistakes. I think that is not a reasonable starting state for the population; the best organism at the first step should have at least about 200 mistakes, if not be even closer to the maximum number of mistakes. (Unfortunately, I cannot modify the threshold to deal with that, and I am not going to try more seeds either, since it does not appear to go anywhere far from those values.)

You didn't say what your parameters were, but suppose that you have 16 sites and 64 organisms as in the standard java run. Sorting gives the best organism, of course, so right away you have a strong bias. Why 20? I guess that this is most easily "accomplished" by having a weight matrix that does not recognize ANYTHING, or has little recognition capability. If it didn't recognize anything there would be exactly 16 mistakes. This could happen by having a very high initial threshold. If it accidently recognized 4 more sites in the wrong locations that would account for your 20. This is a hypothesis and so you can test it by looking closely at the organism that has that situation. I do agree it is a somewhat curious effect. Would it happen in nature? Sure. All that has to happen is a recognition protein is duplicated (apparently a common occurance since we see lots of nearly identical genes in various organisms and the recombination mechanism for doing this is pretty well understood). Then one copy diverges so that it doesn't recognize much at all on the DNA. As it then starts to locate a few spots, if it matches, WHOSH selection takes over and it locks on. This effect occurs in Ev too of course.
I added the highlighting. Here Dr Schneider acknowledges that ev is simply a sorting/optimization algorithm. If he had done the studies that he suggested himself, he would have discovered that this sorting process is profoundly slowed because of his combination selection conditions. This is demonstrated over and over by real examples of mutation and selection.

Now joobz, if this is not enough for you, here is what Dr Schneider has said on his ev blog cite located at: http://www.lecb.ncifcrf.gov/~toms/paper/ev/blog-ev.html (http://www.lecb.ncifcrf.gov/~toms/paper/ev/blog-ev.html)

Fred Williams complains that the "program is not real-world, not even close. New information was not created naturalistically." It is not clear what he means by 'real-world' or 'naturalistically'. If you read the Ev paper carefully you will note that the model parallels the natural situation. There are places on the genome where having a binding site would be advantageous whether or not there is a site there. Genomes are of a certain size. These two factors determine Rfrequency in natural genomes and the situation is the same in the ev simulation. So Fred Williams needs to be explicit about what his problems are. I suggest that he do some honest work and write his own program. I think he will find when he does this that the Ev program is about the minimum coding that one can do that still matches the natural world. Sure, you could do molecular modelling in three dimensions of molecules diffusing through space and binding. Unfortunately you won't have enough computer power to do this simulation. So replace the molecular modelling with a model of a sequence recognizer - a weight matrix. These are well recognized in the molecular biology literature, if you read even a few papers! The sequence does not need to be three dimensional, it can be a string in the computer. That does not alter the computation of the Shannon information at all, so it is still a good model.
Again I added highlighting. Dr Schneider is again correct, his model shows what combination selection pressures do to the mutation and selection sorting/optimization process.
"Schneider's paper is misleadingly titled: "Evolution of biological information". But it is just a *computer* simulation. No actual *biological* materials (e.g. genomes of nucleic acids, proteins, etc) were used, nor does Schneider propose that his simulation be tested with *real* genomes or proteins.Actual biological materials were used to determine the original hypothesis. Read the literature: Schneider1986.
On p.2796 this "gene" is only "125" bases long. There are AFAIK *no* biological genes 125 bases long, nor are their organisms that have "a genome size of 256 bases" with a gene of 125 bases. So again, this is *not* a "simulation" of a *real* "biological" organism.tRNA genes are typically 76 bases long. Lots of small RNAs have been discovered in the the last few years. This is a huge topic in modern biology. But that doesn't really matter because this is a model. Again, Dr. Jones can run the program with sizes that he would prefer. A clear prediction is that the program will give similar results for larger geneomes and gene sizes.
Once again, Dr Schneider makes a claim for large genomes. What is not similar is the astronomically huge number of generations required to evolve his simple system on all but the tiniest genomes because of the combined selection pressures. If Dr Schneider had done the studies he called for in his own publication on ev, he would realize that the dominant parameter in the mutation and selection sorting/optimization process is the number of sorting conditions applied simultaneously.
In the rest of the paper he uses the single word "selection". I take this as a tacit admission that his model is not a simulation of *real* biological natural selection.No. A rose is a rose by any other name. Selection is selection whether it be natural (generally meaning the environment of earth), breeding (by humans usually, though perhaps some ants select their fungi), SELEX or in a computer simulation. Of COURSE it is a simulation of natural selection! The paper would not be relevant to biology and would not have been published in a major scientific journal if it were not!
Again, Dr Schneider is correct about this. His model does properly capture the behavior of the mutation and selection sorting/optimization problem. The crucial point the Dr Schneider has missed is that the number of selection conditions dominates the mathematical behavior of his model. This is also reflected in real examples of mutation and selection. Hundreds of real examples have been cited already on this thread.
Even if Schneider did eventually test his computer simulation against the real worldSee above. First, Dr. Jones neglected to read the scientific literature and so didn't understand why the program was written. Second, there are already natural data that Ev is designed to simulate. Third, instead of complaining Dr. Jones can do his own simulations.
Again, Dr Schneider speaks rightly. Ev does properly model the mutation and selection sorting/optimization process. There are many examples of what his model shows, which is, multiple selection pressures profoundly slow the evolutionary sorting/optimization process.
There are many other examples which I could quote from Dr Schneider’s web site where he defends the reality of his model. Joobz, if you have a problem with Dr Schneider’s model, you can contact him at toms@ncifcrf.gov (toms@ncifcrf.gov?subject=Tom%20Schneider's%20Home %20Page%20(index.html)) .

Kjkent1, convergence can not be based on Rseq >= Rfreq because as Paul has said:The problem with using Rs > Rf as the test, rather than the perfect creature, is that there is no selection pressure to reach Rs > Rf. There is only pressure to reach a perfect creature. There is no Rs > Rf selection pressure in nature, either.Convergence must be based on zero mistakes. Then G=2048 is acceptable. Send me the contract.I can see you're trying to squirm out of the bet.
You want to use a convergence criterion that the author says in not a realistic criterion. Perhaps this is the reason you are having such a difficult time understanding how mutation and selection sorting/optimization actually works.
Sol, I have a suggestion for you, take your money and buy a savings bond or cd.You're backing out? That was even faster than expected.
No Sol, it is clear you have no idea how ev actually works. I don’t need to take money from an ignoramus.

[Belz...]

Belz, just because you are ignorant of the mathematics of mutation and selection, calling me either mentally ill or a chatbot is not going to increase your understanding of the topic.

That's not even a sentence, which is exactly what I expect from a chatbot.

I’ll continue to give you empirical examples which demonstrate how the mutation and selection sorting/optimization process actually works

"Continue" ? You mean "start", right ?

Sure I understand Belz, no matter what mathematical or empirical evidence is presented to you about how mutation and selection actually works; you are going to deny the truth.

That has nothing to do with what we were talking about. Once more you're losing track of your replies. We're talking about statistical probabilities of one theory vs another.

You are not a scientist

That's true. I'm not a scientist. Whatever gave you THAT idea ?

you are an evolutionist religious zealot.

In order for me to be a zealot, I'd have to actually care.

You don’t have the selection pressures and even if you did, you can’t transform the huge number of genes necessary to change a reptile population into a bird population.

How many genes do you think need to be changed for that to happen ? You're the one who's claiming this.

Belz, as much as you are committed to the theory of evolution and common descent, the mathematical and scientific evidence shows that it can’t happen.

Not according to everybody else on the planet, Galileo.

It is not my job to debug and correct programming errors that every evolutionist zealot comes up with.

Which programming errors ? I'm sure you can point them out. See, I'm not a scientist, but I AM a computer programmer.

If they think they can prove that n+1 selection pressures evolve more quickly than n selection pressures, produce the data.

They have.

[Belz...]

You haven’t presented any results other than this:

I found a combination of parameters last night that led to over 100 pressures being faster than a single one, but I forgot what it was

That’s the parametric study you presented. It is this kind of slop that evolutionists like to call science.

Well, you lying little troll. You KNOW you're lying, too.

What a pathetic thing you are, chatbot.

[kleinman]

You haven’t presented any results other than this:I found a combination of parameters last night that led to over 100 pressures being faster than a single one, but I forgot what it wasThat’s the parametric study you presented. It is this kind of slop that evolutionists like to call science.Well, you lying little troll. You KNOW you're lying, too.
Belz, let me give you an example of how to collect data for a parametric study of ev.
Start Paul’s well written online version of ev. Use all the default parameters that Dr Schneider used for his single published case except set the number of sites (G, the genome length) to 16,384 and for the convergence criterion click the check box for perfect creature (zero mistakes) and run this case. You will find that it takes 6,894,433 generations to evolve all three selection conditions simultaneously. Now reset this example keeping all input parameters the same except set the weight factors for spurious sites in gene to 0 and spurious sites in the non-binding site region to 0. It only takes a single generation to evolve a creature that has evolved all the binding sites. Now reset this case except set the weight factor for missed binding sites to 0 and spurious binding in the gene to 0 while spurious binding in the non-binding site region to 1. This case takes 223 generations to eliminate spurious binding in the non-binding site region. Now reset this case except set the weight factor for missed binding sites to 0 and spurious binding in the non-binding site region to 0 while spurious binding in the gene to 1. This case also happens to take 223 generations to eliminate mistakes in the gene region.

Belz, you can do the same thing for 32k and 64k genome lengths. I’ll let you run the three selection condition cases, but I’ll give you the results for the single selection condition cases.

G/gens missed site/gens spurious binding within gene/gens spurious binding outside gene
16384/1/223/223
32768/1/115/403
65536/1/788/1026

Belz, not only do I know I am not lying. I neither need to nor want to lie to prove your mathematically and empirically irrational theory wrong. These results are obtained from the peer reviewed and published model written by the head of computational molecular biology at the National Cancer Institute. These results explain how the mutation and selection sorting/optimization problem works that is combination selection pressures profoundly slow the mutation and selection sorting/optimization process. In the simple case presented above, it takes more than six orders of magnitude more generations to evolve all three selection conditions simultaneously than evolving the single selection conditions alone.

Belz, the theory of evolution by mutation and selection is mathematically and empirically impossible. The theory of evolution by mutation and selection is a mathematically and empirically irrational and illogical theory.

[kjkent1]

You want to use a convergence criterion that the author says in not a realistic criterion. Perhaps this is the reason you are having such a difficult time understanding how mutation and selection sorting/optimization actually works.The AUTHOR of ev is Tom Schneider. Paul is Schneider's agent -- unless Paul "is" Schneider.

And, all of a sudden, when it will absolutely crush your argument, the paper: Evolution of Biological Information, is no longer good enough as the authority for your argumen. Now, you want to use non-peer reviewed criteria to support your position.

You are such an unbelievable hypocrite, Alan!

Regardless, why don't we ask Paul whether Rseq -> Rfreq is the requisite test measurement of evolutionary change in ev.

Yo...PAUL!!!

[kleinman]

You want to use a convergence criterion that the author says in not a realistic criterion. Perhaps this is the reason you are having such a difficult time understanding how mutation and selection sorting/optimization actually works.The AUTHOR of ev is Tom Schneider. Paul is Schneider's agent -- unless Paul "is" Schneider.
And Paul is the author of evj.
And, all of a sudden, when it will absolutely crush your argument, the paper: Evolution of Biological Information, is no longer good enough as the authority for your argumen. Now, you want to use non-peer reviewed criteria to support your position.
Really, that’s what Dr Schneider’s paper on ev says? You obviously didn’t read the paper very carefully.
http://nar.oxfordjournals.org/cgi/content/full/28/14/2794 (http://nar.oxfordjournals.org/cgi/content/full/28/14/2794)
When the program starts, the genomes all contain random sequence, and the information content of the binding sites, Rsequence, is close to zero. Remarkably, the cyclic mutation and selection process leads to an organism that makes no mistakes in only 704 generations (Fig. 2a).
You are such an unbelievable hypocrite, Alan!
You are the one who is arguing that satisfying the selection conditions should not be the measure of convergence. Rs->Rf is a peculiar result from Dr Schneider’s selection conditions but has no correlation with reality. Now are you trying to squirm out of our wager by calling for a convergence condition that has no basis in reality?

[sol invictus]

You're backing out? That was even faster than expected.

You have two choices here, kleinman - either continue with this, or admit you've been wrong all along.

Do you or do you not maintain that the number of generations to a perfect creature with binding sites set to N, is greater than N times the number of generations to perfect creature with binding sites set to 1? (N=3 is fine if you insist - we'll just have to run more trials to take the average.)


YES OR NO?

So, kleinman, you admit you were wrong and agree that the fixation rate under N+1 selection pressures is higher than the rate under N?

Game over, I guess.

[kleinman]

You're backing out? That was even faster than expected.

You have two choices here, kleinman - either continue with this, or admit you've been wrong all along.

Do you or do you not maintain that the number of generations to a perfect creature with binding sites set to N, is greater than N times the number of generations to perfect creature with binding sites set to 1? (N=3 is fine if you insist - we'll just have to run more trials to take the average.)

YES OR NO?
Sol, go home, your mother is calling you.

[kjkent1]

Evolution of Biological Information, Schneider, 2001: "When the program starts, the genomes all contain random sequence, and the information content of the binding sites, Rsequence, is close to zero. Remarkably, the cyclic mutation and selection process leads to an organism that makes no mistakes in only 704 generations (Fig. 2a)."And, then in the next sentence (which you conveniently omitted): "Although the sites can contain a maximum of 2L = 12 bits, the information content of the binding sites rises during this time until it oscillates around the predicted information content, Rfrequency = 4 bits, with Rsequence = 3.983 ± 0.399 bits during the 1000 to 2000 generation interval (Fig. 2b)."
You are the one who is arguing that satisfying the selection conditions should not be the measure of convergence. Rs->Rf is a peculiar result from Dr Schneider’s selection conditions but has no correlation with reality. Now are you trying to squirm out of our wager by calling for a convergence condition that has no basis in reality?No basis in reality? Again, from Schneider’s paper:
“To test the hypothesis that Rsequence can evolve to match Rfrequency, the evolutionary process was simulated by a simple computer program, ev, for which I will describe one evolutionary run.”

The above quote seems pretty conclusive to me. The ev program is designed “to test the hypothesis that Rseq can evolve to match Rfreq…”
Why don’t you just admit that you’re wrong and we can move on, Alan. You’re very clearly demonstrating that you’re both deceitful and hypocritical --- inadmirable traits for a self-professed Christian.

In fact, what you're doing is precisely the reason why design/creation advocates, such as yourself, are routinely laughed out of the courtroom: judges can tell when someone is being intentionally misleading -- and they don't put up with it.

[kjkent1]

So, kleinman, you admit you were wrong and agree that the fixation rate under N+1 selection pressures is higher than the rate under N?

Game over, I guess.Sol, we're wasting are energy. kleinman knows he's wrong, but his low self image won't permit him to admit it. This little game with the $10K wager is proof of why kleinman doesn't publish in the scientific community. That would require him to back his propositions with testable proof, and to accept reasonable criticism of his theories.

kleinman can't do either, and this thread is testament to the fact.

[sol invictus]

Sol, go home, your mother is calling you.

Let's summarize the small part of this unwieldy thread that I've participated in.

Kleinman proposes a simple probabilistic model for evolution, and claims it demonstrates that multiple selection pressures slow the rate of fixations. He gives a nonsensical answer for the rate. I spend five minutes thinking about his model and find the correct answer - which is that the rate of fixation under N pressures scales as N/Log(N), an increasing function of N. Put another way, the time required for N fixations only grows as Log(N), so 1,000,000 fixations take only about 14 times as long as 1.

I point this out to kleinman, who first denies it, and then admits he was wrong, saying

I don’t claim to be an expert in probability theory.

But after admitting that, he flipflops back and continues to claim that the rate decreases (while continuing to ignore all evidence to the contrary, which is all evidence). This is clearly not rational behavior, and there are two possibilities: that he knows he is wrong and is simply lying, or that he is in denial and truly believes. If he's lying he will refuse a bet with real money, but if he actually believes he is correct he should accept eagerly.

Therefore I offer him a bet on the subject, which, after some prodding he accepts (or rather he accepts his own version of it). He wants to bet using the program ev, which is more or less just a complicated version of the simple model I had analyzed.

After it becomes clear that I'm entirely serious on betting real money, he pauses to think and realizes again that he's wrong (probably by experimenting with ev and finding it out for himself - something you'd have thought he would have done around 6,000 posts ago). So then he chickens out, flipflops yet again, and withdraws from the bet, hence proving himself both a hypocrite and a liar.

So, folks, what's next for the amazing kleinman? How many more flipflops will he take? Will the thread continue, now that he's admitted twice that his core contention is wrong? Will the repeated humiliations finally take their toll and shame him into silence? Or will he be forced by foolish pride into accepting this bet, costing himself $10,000?

Any predictions?

[rocketdodger]

Any predictions?

"mathematical and empirical evidence"
"hundreds of examples"
"mathematically and empirically impossible"
"mathematical and empirical evidence"
"hundreds of examples"
"mathematically and empirically impossible"
"mathematical and empirical evidence"
"hundreds of examples"
"mathematically and empirically impossible"
"mathematical and empirical evidence"
"hundreds of examples"
"mathematically and empirically impossible"
"mathematical and empirical evidence"
"hundreds of examples"
"mathematically and empirically impossible"
"mathematical and empirical evidence"
"hundreds of examples"
"mathematically and empirically impossible"
"mathematical and empirical evidence"
"hundreds of examples"
"mathematically and empirically impossible"
"mathematical and empirical evidence"
"hundreds of examples"
"mathematically and empirically impossible"
"mathematical and empirical evidence"
"hundreds of examples"
"mathematically and empirically impossible"
"mathematical and empirical evidence"
"hundreds of examples"
"mathematically and empirically impossible"
"mathematical and empirical evidence"
"hundreds of examples"
"mathematically and empirically impossible"

[sol invictus]

Sol, we're wasting are energy. kleinman knows he's wrong, but his low self image won't permit him to admit it. This little game with the $10K wager is proof of why kleinman doesn't publish in the scientific community. That would require him to back his propositions with testable proof, and to accept reasonable criticism of his theories.

kleinman can't do either, and this thread is testament to the fact.

Yes, I think you're right. The wager was my attempt to differentiate between a well-meaning but deluded kleinman and a cynical and hypocritical lying kleinman.

It worked.

[delphi_ote]

Now delphi, I don’t want you to worry, you have a promising career making stop action movies of human skateboards, but I will distract you with another citation which shows that combination selection pressures profoundly slow the evolutionary process.
Pete and Repeat were in a boat. Pete fell out. Who was left?

[kleinman]

Sol, go home, your mother is calling you.Let's summarize the small part of this unwieldy thread that I've participated in.
That’s your problem, you have given only superficial study of how mutation and selection works mathematically and you are ready to throw your money away on this superficial analysis.
Sol, we're wasting are energy. kleinman knows he's wrong, but his low self image won't permit him to admit it. This little game with the $10K wager is proof of why kleinman doesn't publish in the scientific community. That would require him to back his propositions with testable proof, and to accept reasonable criticism of his theories.Yes, I think you're right. The wager was my attempt to differentiate between a well-meaning but deluded kleinman and a cynical and hypocritical lying kleinman.
Kjkent1 is no better at reading my mind than you are Sol at understanding how ev works. Do you really want me to take your money Sol? Then you are on, the wager is $10,000 that you can’t prove with ev that n+1 selection pressures evolve more rapidly than n selection pressures. Your ignorance of ev and mutation and selection is going to cost you.

Let me give you a few more citations of real examples which show that combination selection pressures profoundly slow the evolutionary process. Sol, you are too ignorant to understand how it works mathematically.
http://aac.asm.org/cgi/content/full/45/6/1607 (http://aac.asm.org/cgi/content/full/45/6/1607)
The emergence of antibiotic resistance in mycobacteria involves the selection of mutant variants within a susceptible bacterial population. However, it is unclear whether antimycobacterial drugs act just as selective agents or can influence the rate of appearance of resistant mutants. The present study was initiated to address this issue by monitoring the effects of antimicrobial agents on the appearance and growth of clarithromycin (CLR)-resistant (CLRr) bacilli in broth cultures of Mycobacterium avium. Preexposure of M. avium to CLR had a significant dose effect on the emergence of resistance, with concentrations of 4 to 8 µg/ml resulting in a maximal (~104-fold) increase in the number of CLRr bacilli after a 4-day incubation. In addition, a dose effect was found with azithromycin. The use of combinations of CLR with either ethambutol (EMB) or rifabutin (RFB) resulted in fewer resistant bacilli compared to the use of CLR alone. The lowest active concentration of EMB (4 µg/ml) was equivalent to the EMB MIC (4 to 8 µg/ml) for the parental CLRs strain and the emergent CLRr variants, and thus, the antiresistance effect was probably the result of the bacteriostatic effect of EMB on CLRr bacilli. However, RFB was an order of magnitude more active (0.05 µg/ml) at reducing resistance than suggested by the MIC of this agent (0.5 to 1 µg/ml). These results indicate that the emergence of resistance was not simply the selection of a preexisting subpopulation of resistant bacilli. Further analysis suggested that early events in the emergence of resistance involved organisms (progenitors) that acquired a resistance phenotype. In addition, the progenitors appeared to be in a transient state, able to develop into a stable resistant lineage in the presence of CLR, or able to revert to the wild type in nonselective conditions.
http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed&cmd=Retrieve&list_uids=11030464 (http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed&cmd=Retrieve&list_uids=11030464)
Hepatitis B virus (HBV) was identified as a cause of viral hepatitis more than 30 years ago and hepatitis B vaccines have been available for almost 20 years, but HBV infection continues to be a global health problem, responsible for about 1.2 million deaths annually. By the end of this year, almost 400 million people--about 5% of the world's population and more than ten times the number infected with human immunodeficiency virus (HIV)--will be infected with HBV. Chemotherapy remains the only treatment option for controlling chronic HBV infection once acquired, but none of the many different chemotherapeutic strategies used in the past has proven consistently successful. Prospects for successful treatment of HBV have improved dramatically during the past decade due to the development of new, well tolerated and efficacious anti-HBV drugs, and to advances in our understanding of HBV replication and pathogenesis. The newer anti-HBV drugs are capable of reducing viral loads very rapidly, but the initial response is invariably followed by very much slower elimination of residual virus. As more effective anti-HBV drugs become available, the emergence of drug resistance during the slower phase of HBV elimination will probably become the most significant obstacle in the way of eventual control of HBV infection. Experience with HIV indicates that combination chemotherapy may suppress or eliminate drug resistance and methods for pre-clinical and clinical assessment of anti-HBV drug combinations are being developed. Basic research into mechanisms of drug action and interaction should assist in the design and optimisation of combination chemotherapy for HBV infection, for which additional new anti-HBV drugs will undoubtedly be required in future.
You are an ignoramus Sol, so let’s see you produce the data from ev which shows that n+1 selection pressures evolve more rapidly than n selection pressures.

[kjkent1]

Kjkent1 is no better at reading my mind than you are Sol at understanding how ev works. I know you well enough to be able to prove you wrong throughout this thread. That's good enough for me.

[kleinman]

Now delphi, I don’t want you to worry, you have a promising career making stop action movies of human skateboards, but I will distract you with another citation which shows that combination selection pressures profoundly slow the evolutionary process.Pete and Repeat were in a boat. Pete fell out. Who was left?
It can’t be delphi ote because he has not given a single example of combination selection pressures accelerating evolution. Delphi, you have nothing to repeat. Delphi, you have sunk along with the theory of evolution. It is a Titanic sinking of a Titanic theory, sunk after striking against a mathematical iceberg. Hey delphi, thank you for your reference to the Wikipedia fitness landscape reference. It is worth repeating.
http://en.wikipedia.org/wiki/Fitness_landscape (http://en.wikipedia.org/wiki/Fitness_landscape)
Apart from the field of evolutionary biology, the concept of a fitness landscape has also gained importance in evolutionary optimization methods such as genetic algorithms or evolutionary strategies. In evolutionary optimization, one tries to solve real-world problems (e.g., engineering or logistics problems) by imitating the dynamics of biological evolution. For example, a delivery truck with a number of destination addresses can take a large variety of different routes, but only very few will result in a short driving time. In order to use evolutionary optimization, one has to define for every possible solution s to the problem of interest (i.e., every possible route in the case of the delivery truck) how 'good' it is. This is done by introducing a scalar-valued function f(s) (scalar valued means that f(s) is a simple number, such as 0.3, while s can be a more complicated object, for example a list of destination addresses in the case of the delivery truck), which is called the fitness function or fitness landscape. A high f(s) implies that s is a good solution. In the case of the delivery truck, f(s) could be the number of deliveries per hour on route s. The best, or at least a very good, solution is then found in the following way. Initially, a population of random solutions is created. Then, the solutions are mutated and selected for those with higher fitness, until a satisfying solution has been found.

Evolutionary optimization techniques are particularly useful in situations in which it is easy to determine the quality of a single solution, but hard to go through all possible solutions one by one (it is easy to determine the driving time for a particular route of the delivery truck, but it is almost impossible to check all possible routes once the number of destinations grows to more than a handful).

The concept of a scalar valued fitness function f(s) also corresponds to the concept of a potential or energy function in physics. The two concepts only differ in that physicists traditionally think in terms of minimizing the potential function, while biologists prefer the notion that fitness is being maximized. Therefore, multiplying a potential function by -1 turns it into a fitness function, and vice versa.
Now Sol thinks he is going to get a more rapid optimization to 100 conditions than to 99. Little does Sol realize that obtaining an optimal solution for more than a “handful” of conditions become “almost impossible”. Thanks for this reference delphi!
Kjkent1 is no better at reading my mind than you are Sol at understanding how ev works.I know you well enough to be able to prove you wrong throughout this thread. That's good enough for me.
You had better stick with ambulance chasing if you want to make a living, you will go broke as a mind reader.

[joobz]

Talk about being a phony. I asked YOU to justify YOUR assumptions and here you present someone else's model assumptions.


Dr Schneider is correct about this. The citations which I have posted show that the different recognizers that occur in real examples of mutation and selection have the same behavior as his mathematical model which is combination selection pressures profoundly slow the evolutionary process.
I've noticed that you fail to explain what profoundly slow means.

Now joobz, you can ask Dr Schneider yourself if mutation rates will change the underlying mathematical fact that combination selection pressures profoundly slow the evolutionary process. If you studied ev, you would find out that mutation rates do not change the fact that the number of optimization conditions dominates the mathematics of the mutation and selection sorting/optimization process.You keep using the relative term, slow.
higher mutation rate will result in fewer generations than equivilent settings with lower mutation rate.

Dr Schneider has not done the studies that he suggested for his model. If he had, he would find out that huge populations have a much more limited effect on the evolutionary process than he is claim here. Is Dr Schneider claiming that there was a population of 6 billion primate precursors for the evolution of humans and chimpanzees?
Dr. A proved that increased population size reduces the number of generations needed for convergence. Or were you hoping I forgot that fact?

Why does it take huge numbers of generations to evolve his system? It is the combined selection pressures which makes it an extremely slow process to find a trajectory on the fitness landscape to his “perfect creature” local optimum. In fact, in many if not most cases, a “perfect creature” local optimum can not be achieved because the population gets stranded at other “non-perfect creature” local optima.
you are again confusing computation time with the number of generations needed to converge. an infitine population will converge in 1 generation, but the ability for a computer to do the sort will take a very long time. BUt, of course you know this. You are simply hoping I forgot that we had already talked about this. And again, this has nothing to do with YOUR ASSUMPTIONS!

I'll stop there, because none of those statements actually deal with the assumptions you need for your statements to be true.

Please explain why a variable environment doesn't increase the rate of adaptation. Remember, we have presented papers that demonstrate that this is the case.

Now, will you stop being a phony and actually justify YOUR ASSUMPTIONS!

[kjkent1]

You had better stick with ambulance chasing if you want to make a living, you will go broke as a mind reader.I don't practice personal injury law. And, it doesn't require a mind reader to predict your responses.

You can't admit the possibility that you may be in error on any substantive issue. This is a well-known characteristic of someone with extremely low self esteem.

You've achieved all these marvelous academic credentials during your life, yet no one will take you seriously. That must be absolutely punishing and degrading. I can't imagine how humiliating it must be for you to know that no matter how hard you fight for positive recognition, the only recognition you receive is negative.

I can certainly understand why you would need a God to comfort you. Without God, you would be totally lost.

How truly sad for you.

If you only understood that the reason why you receive negative recognition is because you cannot objectively assess yourself in the world. If you could, you wouldn't need to post here -- you would be satisfied with your medical practice and your Christian works on behalf of society.

But, here you are -- suffering endlessly and not understanding why.

I forgive you, as does your Lord. Hopefully, you will someday be able to forgive yourself.

[kleinman]

Talk about being a phony. I asked YOU to justify YOUR assumptions and here you present someone else's model assumptions.
Joobz, I wasn’t talking about your model for abiogenesis, we haven’t forgotten this bizarre bit of speculation. Let’s remind the readers of your weird view of how chemistry works.
Envision a system of millions of forming and destructive chemical reactions. Now, envision that intermediates of there reactions associate through non-covalent means and that this complex becomes protected against the destructive reactive pathway, perhaps by a reversible precipitation. These new complexes result in a localized increased of new chemical species. These chemical species then progress in a new series of reaction... that is what I mean through cooperative means. I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?
We are not talking about your bizarre bit of alchemy; we are talking about Dr Schneider’s ev computer simulation of random point mutations and natural selection. That’s the model which proves the theory of evolution mathematically impossible. Of course joobz, you can speculate that “cooperative” selection pressures exist which accelerate evolution.
http://forums.randi.org/images/smilies/doglaugh.gif

[joobz]

Joobz, I wasn’t talking about your model for abiogenesis, we haven’t forgotten this bizarre bit of speculation. Let’s remind the readers of your weird view of how chemistry works.
[/color]
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?
We are not talking about your bizarre bit of alchemy; we are talking about Dr Schneider’s ev computer simulation of random point mutations and natural selection. That’s the model which proves the theory of evolution mathematically impossible. Of course joobz, you can speculate that “cooperative” selection pressures exist which accelerate evolution.
http://forums.randi.org/images/smilies/doglaugh.gif
I see. You are simply remaining a scared little man.
You are afraid to take the bets offered you.
You are afraid to actually justify your assumptions.

Why are you such a phony?

[rocketdodger]

Now Sol thinks he is going to get a more rapid optimization to 100 conditions than to 99. Little does Sol realize that obtaining an optimal solution for more than a “handful” of conditions become “almost impossible”. Thanks for this reference delphi!

I guess I will add this to the long list of questions Kleinman can't answer -- Can you show us why obtaining an optimal solution, as opposed to any other sub-optimal solution, has anything to do with fixation rate?

[kleinman]

I see. You are simply remaining a scared little man.
Joobz, your speculation is frightening, all zero of your citations which show that combination selection pressures evolve more rapidly than single selection pressures leaves me trembling in fear and I am horrified by your spelling. Could you soothe us by telling us how letting sun light hitting lead will turn it into gold?
http://forums.randi.org/images/smilies/doglaugh.gif
Now Sol thinks he is going to get a more rapid optimization to 100 conditions than to 99. Little does Sol realize that obtaining an optimal solution for more than a “handful” of conditions become “almost impossible”. Thanks for this reference delphi!I guess I will add this to the long list of questions Kleinman can't answer -- Can you show us why obtaining an optimal solution, as opposed to any other sub-optimal solution, has anything to do with fixation rate?
I guess you didn’t read this citation so I’ll post it again for you.

“Darwinian Evolution Can Follow Only Very Few Mutational Paths to Fitter Proteins”
Daniel M Weinreich, Nigel F Delaney, Mark A DePristo, Daniel L Hartl. Science. Washington: Apr 7, 2006. Vol. 312, Iss. 5770; pg. 111
Five point mutations in a particular Beta-lactamase allele jointly increase bacterial resistance to a clinically important antibiotic by a factor of ~100,000. In principle, evolution to this high-resistance Beta-lactamase might follow any of the 120 mutational trajectories linking these alleles. However, we demonstrate that 102 trajectories are inaccessible to Darwinian selection and that many of the remaining trajectories have negligible probabilities of realization, because four of these five mutations fail to increase drug resistance in some combinations. Pervasive biophysical pleiotropy within the Beta-lactamase seems to be responsible, and because such pleiotropy appears to be a general property of missense mutations, we conclude that much protein evolution will be similarly constrained. This implies that the protein tape of life may be largely reproducible and even predictable.
Rocketdodger, this example is of only a single selection pressure directed at the Beta-lactamase allele. The trajectories for the evolution of resistance to this single selection pressure are limited. When you add more selection pressures and the fitness landscape becomes more irregular, the trajectories become even more limited. This is why combination selection pressures profoundly slow the evolution of multiple selection pressures. This is one of the many lessons of mutation and selection you still don’t understand.

[Paul C. Anagnostopoulos]

Kjkent1, convergence can not be based on Rseq >= Rfreq because as Paul has said:
Neither can it be based on zero mistakes, because the two models you are comparing do not produce the same genetic function and so the meaning of mistakes is completely different in each case. Surely you agree that if an absence of selection pressure is a reason to reject Rs > Rf, then a lack of common function is a reason to reject zero mistakes.

~~ Paul

[rocketdodger]

Rocketdodger, this example is of only a single selection pressure directed at the Beta-lactamase allele. The trajectories for the evolution of resistance to this single selection pressure are limited. When you add more selection pressures and the fitness landscape becomes more irregular, the trajectories become even more limited. This is why combination selection pressures profoundly slow the evolution of multiple selection pressures. This is one of the many lessons of mutation and selection you still don’t understand.

Can you show us why obtaining an optimal solution, as opposed to any other sub-optimal solution, has anything to do with fixation rate?

Or in language you can understand, Kleinman:

What does reaching your destination have to do with the total distance you have traveled?

[Paul C. Anagnostopoulos]

Regardless, why don't we ask Paul whether Rseq -> Rfreq is the requisite test measurement of evolutionary change in ev.
Indeed it is, but it is a passive measurement in the sense that there is no pressure to attain Rs > Rf. It simply embodies the prediction and observation that the amount of information that evolves as only the binding sites are matched approaches the theoretical amount of information required for the match. If you are not evolving a perfect matching situation, then all the R values are irrelevant.

~~ Paul

[kleinman]

Rocketdodger, this example is of only a single selection pressure directed at the Beta-lactamase allele. The trajectories for the evolution of resistance to this single selection pressure are limited. When you add more selection pressures and the fitness landscape becomes more irregular, the trajectories become even more limited. This is why combination selection pressures profoundly slow the evolution of multiple selection pressures. This is one of the many lessons of mutation and selection you still don’t understand.Can you show us why obtaining an optimal solution, as opposed to any other sub-optimal solution, has anything to do with fixation rate?
Rocketdodger, I’ll explain it to you as many times as you need. There are not a huge number of “sub-optimal” solutions. That’s what the citation is all about. In order for a trajectory on a fitness landscape to be accessible to a population, each step on the fitness landscape has to give improved fitness to the population. This is why ev stops evolving in many cases. The population gets stuck at a local optimum where every step away from this local optimum reduces the fitness of the population. Fitness landscapes with many selection conditions have many peaks and valleys. The only local optima accessible to the population are those with trajectories that always give improving fitness. These are few and far between as described by the citation I just reposted.
Regardless, why don't we ask Paul whether Rseq -> Rfreq is the requisite test measurement of evolutionary change in ev.Indeed it is, but it is a passive measurement in the sense that there is no pressure to attain Rs > Rf. It simply embodies the prediction and observation that the amount of information that evolves as only the binding sites are matched approaches the theoretical amount of information required for the match. If you are not evolving a perfect matching situation, then all the R values are irrelevant.
Thank you Paul for clarifying that for kjkent1. And kjkent1, why don’t you save yourself the postage and just send the check for $10,000 since we already know how ev and mutation and selection actually works.

[joobz]

Joobz, your speculation is frightening, all zero of your citations which show that combination selection pressures evolve more rapidly than single selection pressures leaves me trembling in fear and I am horrified by your spelling. Could you soothe us by telling us how letting sun light hitting lead will turn it into gold?.
No justifications then? Ready to admit you have nothing?

[sol invictus]

Do you really want me to take your money Sol? Then you are on, the wager is $10,000 that you can’t prove with ev that n+1 selection pressures evolve more rapidly than n selection pressures. Your ignorance of ev and mutation and selection is going to cost you.

Great - we're back on! On again, off again - I'm getting dizzy...

So, here are the terms:

we will run ev for a (large) number of trials. Each trial will consist of two runs: one with (say) 20 binding sites, and one with 10. Feel free to change those numbers if you don't like them. All other ev parameters will remain fixed between the two runs, and throughout the trials. Each run on each trial will be seeded with a new, true random seed (we can use stock prices in the newspaper that day or something).

On each run, we will record the number of generations required to reach a perfect creature. Let's call that number G(20) for the runs with 20 binding sites, and G(10) for the runs with 10 sites. We will then compute the arithmetic mean of G(20), call it |G(20)|, and the mean of G(10), |G(10)|, across all the trials.

You are betting $10,000 that |G(20)| > (20/10) * |G(10)| = 2 |G(10)|. If you prefer to change the numbers 10 and 20 to N1 and N2, with N2>N1, your bet is that |G(N2)| > (N2/N1) * |G(N1)|. I am betting the opposite - that |G(20)| < (20/10) * |G(10)| (or the equivalent for any N2 > N1). In the unlikely event of equality, I'll be generous - you win the bet.

Do you agree to these preliminary terms? If so, we will continue and choose the other ev parameters, number of trials to average over, method for choosing the seeds, and finalize the bet. At that point I'm going to consult a lawyer to see how best to ensure you pay me the $10,000 after you lose.

OK, kleinman? Have you got the balls?

[kleinman]

Joobz, your speculation is frightening, all zero of your citations which show that combination selection pressures evolve more rapidly than single selection pressures leaves me trembling in fear and I am horrified by your spelling. Could you soothe us by telling us how letting sun light hitting lead will turn it into gold?No justifications then? Ready to admit you have nothing?
Only a peer reviewed and published model of random point mutations and natural selection which show that combination selection pressures profoundly slow the evolutionary process and hundreds of real examples of mutation and selection which demonstrates what ev shows mathematically. Here joobz, have another citation.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=90683 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=90683)
The potential for selection of new drug-resistant HBV mutants highlights the need to develop additional anti-HBV drugs and therapeutic strategies (7, 13, 41). Reliable in vitro systems that are capable of detecting drug resistance as it arises are required, as are assays that are capable of predicting which drug combinations are optimal for delaying or preventing resistance and for controlling resistance if it develops (13). On the other hand, in vitro studies are not always accurate predictors of effectiveness in vivo, and clinical trials are the ultimate test of treatment efficacy.
Joobz, you better tell these authors that ‘delay’ does not mean ‘prevent’.

Now joobz, if I only had your skills at speculation then with enough free energy, anything is possible.

[kjkent1]

Regardless, why don't we ask Paul whether Rseq -> Rfreq is the requisite test measurement of evolutionary change in ev.Indeed it is, but it is a passive measurement in the sense that there is no pressure to attain Rs > Rf. It simply embodies the prediction and observation that the amount of information that evolves as only the binding sites are matched approaches the theoretical amount of information required for the match. If you are not evolving a perfect matching situation, then all the R values are irrelevant.Thank you Paul for clarifying that for kjkent1. And kjkent1, why don’t you save yourself the postage and just send the check for $10,000 since we already know how ev and mutation and selection actually works.You need to work on your reading comprehension, Alan. Paul answered the question of whether Rseq-> Rfreq is the requiste test measurement of evolutionary change in ev, as follows:

INDEED IT IS.

Let me repeat that, just in case you missed it:

Paul, is Rseq -> Rfreq the requiste test measurement of evolutionary change in ev?

Paul's answer:

INDEED IT IS.

Now that we've got that out of the way, Alan -- if you still want the wager based on the REQUISTE TEST MEASUREMENT of ev, then let's go, because I'm gonna own everything thing that you currently own, and unlike the others who are playing with you, if you bet, and you lose, I will be enforcing my winnings via a judgment from the California Superior Court.

Just in case anyone's wondering, this particular wager is not based primarily on chance, thus it is not voided by the public policy in California against gambling, and therefore it is an enforceable contract.

[kleinman]

Do you really want me to take your money Sol? Then you are on, the wager is $10,000 that you can’t prove with ev that n+1 selection pressures evolve more rapidly than n selection pressures. Your ignorance of ev and mutation and selection is going to cost you.Great - we're back on! On again, off again - I'm getting dizzy...
Sol, you were dizzy before you ever started posting on this thread.
So, here are the terms:

we will run ev for a (large) number of trials. Each trial will consist of two runs: one with (say) 20 binding sites, and one with 10. Feel free to change those numbers if you don't like them. All other ev parameters will remain fixed between the two runs, and throughout the trials. Each run on each trial will be seeded with a new, true random seed (we can use stock prices in the newspaper that day or something).
Sol, the number of binding sites is not a selection pressure. If you read Dr Schneider’s papers on ev, the number of binding sites is the variable gamma. I have already done a series and studied the affect of varying gamma. Other than ev will not converge if gamma is too small, varying the number of binding sites has little affect on the generations for convergence. Increasing gamma has a small effect on reducing the generations for convergence but nothing like reducing the number of selection pressures to only a single pressure. Do you want me to post the data?
You are betting $10,000 that |G(20)| > (20/10) * |G(10)| = 2 |G(10)|. If you prefer to change the numbers 10 and 20 to N1 and N2, with N2>N1, your bet is that |G(N2)| > (N2/N1) * |G(N1)|. I am betting the opposite - that |G(20)| < (20/10) * |G(10)| (or the equivalent for any N2 > N1). In the unlikely event of equality, I'll be generous - you win the bet.
Sol, you are a ding-a-ling. You don’t know the difference between the number of selection pressures and the number of binding sites in ev.

[kleinman]

Indeed it is, but it is a passive measurement in the sense that there is no pressure to attain Rs > Rf. It simply embodies the prediction and observation that the amount of information that evolves as only the binding sites are matched approaches the theoretical amount of information required for the match. If you are not evolving a perfect matching situation, then all the R values are irrelevant.You need to work on your reading comprehension, Alan. Paul answered the question of whether Rseq-> Rfreq is the requiste test measurement of evolutionary change in ev, as follows:

INDEED IT IS.

Let me repeat that, just in case you missed it:

Paul, is Rseq -> Rfreq the requiste test measurement of evolutionary change in ev?
Only a lawyer can turn the word ‘passive’ into the word ‘requisite’. The active selection condition in ev is the number of mistakes. R values are irrelevant otherwise.

[sol invictus]

Sol, you are a ding-a-ling. You don’t know the difference between the number of selection pressures and the number of binding sites in ev.

Rather than point out why you're wrong (which I'm sure would be futile), why don't you tell me which ev parameter is "the number of selection pressures" so we can proceed?

[kjkent1]

Only a lawyer can turn the word ‘passive’ into the word ‘requisite’. The active selection condition in ev is the number of mistakes. R values are irrelevant otherwise.I didn't change any words. The fact is that when you set a mistake count in ev to zero, the ev algorithm no longer counts that type of mistake. This causes the program to report no mistakes even though those mistakes are observed in the genome.

This is easy to prove. When you set all three mistake counts to zero, the program immediately reports a "perfect creature" in the first generation, i.e., one completely free of mistakes, even though the sequence logo graphic displays totally random noise, because that's what ev starts with at instantiation: a randomly arranged genome.

So, the report of a "perfect creature" by ev is incorrect -- the creature isn't perfect. No information gain has occured, and the proof is that Rseq is nowhere near Rfreq.

Rseq ~ Rfreq is the ONLY meaningful measurement in ev. It accurately reports the state of the genome in terms of its information content regardless of any mistake count setting.

Now, if you want to create a new counter that actually measures the number of mistakes, regardless of any mistake count setting, then we can use that. But, the result will be functionally identical to that which is reported by Rseq.

Are you ready to concede your error, or do you prefer to continue to twist in the wind?

[Belz...]

Belz, let me give you an example of how to collect data for a parametric study of ev.

I'm going to ignore the rest of your post because it has nothing to do with what I said. Again, you know this, and this dodging amounts to dishonesty.

You know full well what Rocketdodger was talking about.

Sol, go home, your mother is calling you.

How utterly adolescent of you.

[Belz...]

It can’t be delphi ote because he has not given a single example of combination selection pressures accelerating evolution.

Chatbot.

[Paul C. Anagnostopoulos]

Thank you Paul for clarifying that for kjkent1. And kjkent1, why don’t you save yourself the postage and just send the check for $10,000 since we already know how ev and mutation and selection actually works.
You appear to have missed this statement:


Neither can it be based on zero mistakes, because the two models you are comparing do not produce the same genetic function and so the meaning of mistakes is completely different in each case. Surely you agree that if an absence of selection pressure is a reason to reject Rs > Rf, then a lack of common function is a reason to reject zero mistakes.

~~ Paul

[Paul C. Anagnostopoulos]

Rather than point out why you're wrong (which I'm sure would be futile), why don't you tell me which ev parameter is "the number of selection pressures" so we can proceed?
There is no way to continuously vary the number of pressures. There are three pressures with relative weights. You can vary the weights or turn off the pressures. And the pressures all pertain to one gene. I think you have to give up on experiments that involve a variable number of pressures.

~~ Paul

[Paul C. Anagnostopoulos]

Only a lawyer can turn the word ‘passive’ into the word ‘requisite’. The active selection condition in ev is the number of mistakes. R values are irrelevant otherwise.
He didn't do that, but you know that.

The active selection condition is the number of mistakes, but the number of mistakes is not a measure of evolving information content. This is because the number of mistakes means something different when all three pressures are active as opposed to only one or two of them. Therefore, when comparing models with different numbers of pressures, mistake count is meaningless.

Furthermore, the R numbers are meaningless when running models with fewer than three selection pressures. This is because no attempt is being made to evolve a creature that matches binding sites but no other positions.

And so we conclude that there is no way to compare Ev models with different numbers of pressures.

~~ Paul

[sol invictus]

There is no way to continuously vary the number of pressures. There are three pressures with relative weights. You can vary the weights or turn off the pressures. And the pressures all pertain to one gene. I think you have to give up on experiments that involve a variable number of pressures.

~~ Paul

What are the three?

Perhaps I misunderstood the algorithm, but I thought each time the recognizer misses a site, that counts as a mistake, and that the creatures with more than the median number of mistakes are killed.

If that's correct, each site constitutes a selection pressure... unless we're using that phrase differently? What I mean is that each site constitutes a trait that is subject to selection - if the site has the wrong sequence it is selected against, and if it has the correct sequence (or close enough) it isn't.

So I would say increasing the number of sites increases the number of selection pressures. Do you disagree with that? I suppose it's complicated in ev by non-sites being mistakenly identified also acting as a pressure, but that's not going to affect the scaling with the number of sites very much. Anyway, that can presumably be turned off by setting the corresponding weight to zero?

[joobz]

Joobz, you better tell these authors that ‘delay’ does not mean ‘prevent’.

It seems the authors already know the difference, otherwize they wouldn't have said "delay or prevent".

Now, when will you actually man up and defend your theory. I state clearly taht your argument is bogus becuase the selection conditions are neither constant in magnitude or number. That this fact will result in increased emergence of adaptation.

This is merely 2 of the points you have to fight against.
consider this a softball pitch.

[rocketdodger]

Perhaps I misunderstood the algorithm, but I thought each time the recognizer misses a site, that counts as a mistake, and that the creatures with more than the median number of mistakes are killed.

That is basically it -- the "three" pressures Kleinman is obsessed with are just variations of how to count a "mistake."

If that's correct, each site constitutes a selection pressure... unless we're using that phrase differently? What I mean is that each site constitutes a trait that is subject to selection - if the site has the wrong sequence it is selected against, and if it has the correct sequence (or close enough) it isn't.


Yes, you are correct. It depends on how you want to look at it.

In this case, it would be equivalent to consider a pressure for every site. In reality, though, it is pretty hard to determine just which bases are targeted by a given pressure -- even if a mutation increases relative fitness, there could be many many more waiting to happen that never do.

It is worth noting, also, that local optima only exist on a fitness landscape if pressures are considered in an aggregate sense, I.E. targeting more than one base and changing relative fitness in more than one possible way.

[Belz...]

In this case, it would be equivalent to consider a pressure for every site. In reality, though, it is pretty hard to determine just which bases are targeted by a given pressure

Ridiculous, Dodger. Kleinman has himself claimed that he could easily identify which pressures act on which genes and how many pressures there are. If Kleinman says it, we must accept it as true, because we can't possibly expect him to back up any of his statements.

[kleinman]

You evolutionists still haven’t figured out that mutation and selection is simply a sorting/optimization problem, the behavior of which is dominated by the number of selection conditions. Dr Schneider understands this, he has written about this on his web site. So we’ll just have to correct this evolutionist misunderstanding. So let’s start with Sol.
Sol, you are a ding-a-ling. You don’t know the difference between the number of selection pressures and the number of binding sites in ev.Rather than point out why you're wrong (which I'm sure would be futile), why don't you tell me which ev parameter is "the number of selection pressures" so we can proceed?
Sol, I’m not wrong, you just don’t understand how ev works. You see there is a difference between you and I. I spent several months studying ev, reading Dr Schneider’s publications about ev, discussing the model with Dr Schneider and Paul and running hundreds of cases with ev before I took this discussion public. You have done none of these things but seem to think you know how ev works. Gamma, the number of binding sites in ev are not the selection conditions. There are three selection conditions in ev based on the match of a weight matrix to sequences of bases. If a match is not found where a match is expected (the binding site), this is counted as a mistake. If there is a match in the gene region of the genome, this is counted as a mistake. And if there is a match in the non-binding portion of the genome this is counted as a mistake. The half of the population with the fewest number of mistakes is allowed to reproduce each generation with random mutations occurring at a user specified amount each generation. You can access the properties for the selection conditions by first clicking the “New” button in the upper left of the main window of ev, this opens the “New Model Parameters” window. In the lower right corner is the “Advanced>>” button. Click the “Advanced>>” button and you will see the user modifiable properties for the three selection conditions.
Only a lawyer can turn the word ‘passive’ into the word ‘requisite’. The active selection condition in ev is the number of mistakes. R values are irrelevant otherwise.I didn't change any words. The fact is that when you set a mistake count in ev to zero, the ev algorithm no longer counts that type of mistake. This causes the program to report no mistakes even though those mistakes are observed in the genome.
Of course when you remove a selection condition, it no longer affects the frequency of genetic sequences. That’s how the mutation and selection process works. They are only mistakes if there is a selection condition which affects the fitness to reproduce. What you are having a hard time understanding is that if you increase the number of selection conditions, it becomes much more difficult to sort beneficial and detrimental mutations. But kjkent1, that is the mathematical and empirical fact of life.
This is easy to prove. When you set all three mistake counts to zero, the program immediately reports a "perfect creature" in the first generation, i.e., one completely free of mistakes, even though the sequence logo graphic displays totally random noise, because that's what ev starts with at instantiation: a randomly arranged genome.
What you don’t understand about this kjkent1 is that is how it works empirically as well. If you place a population in an environment with as few selection pressures as possible, you get more diversity of population. Members of the population who could not reproduce in a more stressful environment can survive and reproduce in this low stress environment. Add stress (selection conditions) to the population and the least fit are the first to be removed from the population.
So, the report of a "perfect creature" by ev is incorrect -- the creature isn't perfect. No information gain has occured, and the proof is that Rseq is nowhere near Rfreq.
Kjkent1, you are confused by Dr Schneider’s and Paul’s sloppy use of terminology. A “perfect creature” is simply a creature that has zero mistakes for a given set of selection conditions. What has occurred under these circumstances is that sequences of bases have been selected which satisfy the selection condition(s). Information in the genome has increased; the genomes are no longer random.
Rseq ~ Rfreq is the ONLY meaningful measurement in ev. It accurately reports the state of the genome in terms of its information content regardless of any mistake count setting.
When this debate first started, we were using Rs>=Rf as the condition for convergence. That is when Paul argued that “perfect creature” should be used as the convergence criterion. I accepted his argument and have used this criterion since. Now that you realize that this doesn’t suit you purposes, you want to return to this passive measure as your convergence criterion. What you don’t realize is that any of the selection conditions in ev increase the information content in the genomes. The genomes are no longer random. They have sequences of bases that specifically satisfy the selection conditions.
Now, if you want to create a new counter that actually measures the number of mistakes, regardless of any mistake count setting, then we can use that. But, the result will be functionally identical to that which is reported by Rseq.
Ok, the convergence criterion for ev is when it evolves the hemoglobin gene.
Are you ready to concede your error, or do you prefer to continue to twist in the wind?
The only thing twisting in the wind is the theory of evolution as it hangs from the mathematical gallows the Dr Schneider has written.
Thank you Paul for clarifying that for kjkent1. And kjkent1, why don’t you save yourself the postage and just send the check for $10,000 since we already know how ev and mutation and selection actually works.You appear to have missed this statementNeither can it be based on zero mistakes, because the two models you are comparing do not produce the same genetic function and so the meaning of mistakes is completely different in each case. Surely you agree that if an absence of selection pressure is a reason to reject Rs > Rf, then a lack of common function is a reason to reject zero mistakes.
Why Paul, you wouldn’t be back peddling again on your previous statement?
The problem with using Rs > Rf as the test, rather than the perfect creature, is that there is no selection pressure to reach Rs > Rf. There is only pressure to reach a perfect creature. There is no Rs > Rf selection pressure in nature, either.
Setting two of the three selection conditions to zero still is evolving a portion of the three selection condition model. It simply shows how slow evolving combination selection conditions is when compared to evolving only a single selection condition. This is the lesson that ev is teaching and this is the lesson that the empirical data teaches as well. Mutation and selection is simply a sorting/optimization problem. The ability of a population to sort beneficial and detrimental mutations is strongly dependent on the number of sorting conditions. The sorting process is by far most easily done it there is only a single sorting condition. When you combine multiple sorting conditions, it becomes profoundly slow. Your own model shows this.
Rather than point out why you're wrong (which I'm sure would be futile), why don't you tell me which ev parameter is "the number of selection pressures" so we can proceed?There is no way to continuously vary the number of pressures. There are three pressures with relative weights. You can vary the weights or turn off the pressures. And the pressures all pertain to one gene. I think you have to give up on experiments that involve a variable number of pressures.
Paul, don’t educate Sol until he sends me the $10,000. However, you can vary the number of pressures in ev. You can change the number of selection pressures from three to one and show that the remaining selection pressure evolves many orders of magnitude faster than all three selection conditions when combined. Of course this makes too much sense for those of you who have embraced the evolutionist dogma.
Only a lawyer can turn the word ‘passive’ into the word ‘requisite’. The active selection condition in ev is the number of mistakes. R values are irrelevant otherwise.He didn't do that, but you know that.

The active selection condition is the number of mistakes, but the number of mistakes is not a measure of evolving information content. This is because the number of mistakes means something different when all three pressures are active as opposed to only one or two of them. Therefore, when comparing models with different numbers of pressures, mistake count is meaningless.
Sure kjkent1 changed your word ‘passive’ to ‘requisite’ in his argument. Paul, each of the selection conditions take the initially random genomes and reduce the disorder. Any of the individual selection conditions reduce the disorder in the genomes. They give sequences of bases which satisfy the selection conditions, decrease the disorder in the genome and therefore increase the information content in the genome.
Furthermore, the R numbers are meaningless when running models with fewer than three selection pressures. This is because no attempt is being made to evolve a creature that matches binding sites but no other positions.

And so we conclude that there is no way to compare Ev models with different numbers of pressures.
You are correct when you say that R numbers are meaningless when running models with fewer than three selection pressures, but you are wrong when you conclude that there is no way to compare Ev models with different numbers of pressures. All you have to do is put in the input parameters which show that ev can evolve any single selection condition very rapidly but when evolving all three conditions simultaneously it takes many, many orders of magnitude more generations to sort the beneficial and detrimental mutations. You may not want to do the comparison because it shows why the mutation and selection sorting/optimization process becomes so profoundly slow when you have combination selection pressures but you can do the comparison. The empirical data shows the same affect, combination selection pressures have a profound impact on the ability of the population to evolve to these combined pressures. Paul, you are taking a position that is in contradiction to the mathematical behavior of your own sorting/optimization algorithm and the empirical data which show how mutation and selection works in reality.
Joobz, you better tell these authors that ‘delay’ does not mean ‘prevent’.It seems the authors already know the difference, otherwize they wouldn't have said "delay or prevent".
English lesson for joobz, synonyms for the word delay-holdup, wait, stoppage, setback, impediment, hindrance, interruption, interruption, synonyms for the word prevent-stop, put off, avert, avoid, foil, thwart, check, put a stop to.
Perhaps I misunderstood the algorithm, but I thought each time the recognizer misses a site, that counts as a mistake, and that the creatures with more than the median number of mistakes are killed.That is basically it -- the "three" pressures Kleinman is obsessed with are just variations of how to count a "mistake."
Sol, it is not perhaps, you do misunderstand the ev algorithm and rocketwhomissesthetarget, I am not obsessed with three selection pressures. It is just a mathematical reality that if you are trying to sort and optimize on conditions, the more conditions imposed the profoundly slower the sort/optimization process becomes. Of course you have claimed you have a model which shows otherwise. I remember the results of your parametric study.
I found a combination of parameters last night that led to over 100 pressures being faster than a single one, but I forgot what it was http://forums.randi.org/images/smilies/frown.gif
If that's correct, each site constitutes a selection pressure... unless we're using that phrase differently? What I mean is that each site constitutes a trait that is subject to selection - if the site has the wrong sequence it is selected against, and if it has the correct sequence (or close enough) it isn't.Yes, you are correct. It depends on how you want to look at it.
Rocketwhomissesthetarget, you are in the dark yet you would call it the light of day.
In this case, it would be equivalent to consider a pressure for every site. In reality, though, it is pretty hard to determine just which bases are targeted by a given pressure -- even if a mutation increases relative fitness, there could be many many more waiting to happen that never do.
If you understood how ev works, you would realize that every locus is tested by the weight matrix for a match. Only in your imagination rocketwhomissesthetarget are there many more mutations which increase relative fitness of the population. We have the mathematical behavior of the ev model which shows otherwise. Of course that is what the theory of evolution by mutation and selection is formed by, “imagination”. When you study the mathematical and empirical behavior of the mutation and selection sorting/optimization problem, you find out that it works entirely differently than what comes from the imaginations of evolutionists.
It is worth noting, also, that local optima only exist on a fitness landscape if pressures are considered in an aggregate sense, I.E. targeting more than one base and changing relative fitness in more than one possible way.
Too bad for your theory that the mathematical and empirical evidence contradicts what comes from your imaginations. Didn’t you read this citation?

“Darwinian Evolution Can Follow Only Very Few Mutational Paths to Fitter Proteins”
Daniel M Weinreich, Nigel F Delaney, Mark A DePristo, Daniel L Hartl. Science. Washington: Apr 7, 2006. Vol. 312, Iss. 5770; pg. 111
Five point mutations in a particular Beta-lactamase allele jointly increase bacterial resistance to a clinically important antibiotic by a factor of ~100,000. In principle, evolution to this high-resistance Beta-lactamase might follow any of the 120 mutational trajectories linking these alleles. However, we demonstrate that 102 trajectories are inaccessible to Darwinian selection and that many of the remaining trajectories have negligible probabilities of realization, because four of these five mutations fail to increase drug resistance in some combinations. Pervasive biophysical pleiotropy within the Beta-lactamase seems to be responsible, and because such pleiotropy appears to be a general property of missense mutations, we conclude that much protein evolution will be similarly constrained. This implies that the protein tape of life may be largely reproducible and even predictable.
In this case, it would be equivalent to consider a pressure for every site. In reality, though, it is pretty hard to determine just which bases are targeted by a given pressureRidiculous, Dodger. Kleinman has himself claimed that he could easily identify which pressures act on which genes and how many pressures there are. If Kleinman says it, we must accept it as true, because we can't possibly expect him to back up any of his statements.
Belz, it’s not me saying this; it’s what is shown in the hundreds of citations which I have posted. Here is another example combination selection pressures work.
http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed&cmd=Retrieve&list_uids=10681317 (http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed&cmd=Retrieve&list_uids=10681317)
Penciclovir (9-[2-hydroxy-1-(hydroxymethyl)-ethoxymethyl]guanine [PCV]), lamivudine ([-]-beta-L-2',3'-dideoxy-3'-thiacytidine [3TC]), and adefovir (9-[2-phosphonylmethoxyethyl]-adenine [PMEA]) are potent inhibitors of hepatitis B virus (HBV) replication. Lamivudine has recently received approval for clinical use against chronic human HBV infection, and both PCV and PMEA have undergone clinical trials against HBV in their respective prodrug forms (famciclovir and adefovir dipivoxil [bis-(POM)-PMEA]). Since multidrug combinations are likely to be used to control HBV infection, investigation of potential interactions between PCV, 3TC, and PMEA is important. Primary duck hepatocyte cultures which were either acutely or congenitally infected with the duck hepatitis B virus (DHBV) were used to investigate in vitro interactions between PCV, 3TC, and PMEA. Here we show that the anti-DHBV effects of all the combinations containing PCV, 3TC, and PMEA are greater than that of each of the individual components and that their combined activities are approximately additive or synergistic. These results may underestimate the potential in vivo usefulness of PMEA-containing combinations, since there is evidence that PMEA has immunomodulatory activity and, at least in the duck model of chronic HBV infection, is capable of inhibiting DHBV replication in cells other than hepatocytes, the latter being unaffected by treatment with either PCV or 3TC. Further investigation of the antiviral activities of these drug combinations is therefore required, particularly since each of the component drugs is already in clinical use.
Of course you evolutionists have your imaginations and beggaminases to support your argument.

[Belz...]

Belz, it’s not me saying this; it’s what is shown in the hundreds of citations which I have posted. Here is another example combination selection pressures work.

I think you forgot to read what I wrote. To back to school, chatbot.

Of course you evolutionists have your imaginations and beggaminases to support your argument.

Beggaminase is a VERB, you dolt.

[joobz]

English lesson for joobz, synonyms for the word delay-holdup, wait, stoppage, setback, impediment, hindrance, interruption, interruption, synonyms for the word prevent-stop, put off, avert, avoid, foil, thwart, check, put a stop to.

BWA HA HA HA HA!!!!

I think you really are becoming more and more incoherent.

Why would the authors say "to delay or prevent" if they were the same thing? That would be like writing, "To delay or delay". Considering the authors are probably not brain dead moron, they understand that delaying something doesn't mean the same thing as preventing something.

Slow doesn't equal stop.

Now, any chance you'll actually try to justify your assumptions? Or will you continue to post things that makes you look even more inept?

[rocketdodger]

It is just a mathematical reality that if you are trying to sort and optimize on conditions, the more conditions imposed the profoundly slower the sort/optimization process becomes.

Can you show us mathematical proof of this claim?


If you understood how ev works, you would realize that every locus is tested by the weight matrix for a match. Only in your imagination rocketwhomissesthetarget are there many more mutations which increase relative fitness of the population. We have the mathematical behavior of the ev model which shows otherwise.

Yes, which is why I used the qualifier "in reality' in that statement, you stupid fool.


Too bad for your theory that the mathematical and empirical evidence contradicts what comes from your imaginations. Didn’t you read this citation?

Yes, I did. Unless my eyes deceive me, they explicitly say that five (thats 5, or 1 + 1 + 1 + 1 + 1, or 5 * 1) mutations are required to acquire resistance in that study. Because you are, as we know, mathematically incompetent, I will also point out for you that 120 (the number of trajectories on the fitness landscape in this case) is 5! (thats "five factorial" which means 5 * 4 * 3 * 2 * 1 in case you didn't know you genius), or the total number of ways one can arrange five items.

Now I could be wrong, Kleinman, but it seems to me that "targeting one base" does not mean "targeting five bases." I stated that if only a single base is targeted, there are no local optima. This is equivalent to saying there is only a single trajectory to the goal. And, SURPRISE, "single" = 1!. In other words, there is only one way you can arrange one item. I guess reality doesn't contradict what I said after all, does it.

[kleinman]

Belz, it’s not me saying this; it’s what is shown in the hundreds of citations which I have posted. Here is another example combination selection pressures work.I think you forgot to read what I wrote. To back to school, chatbot.
I’ve been reading evolutionist nonsense for years, you say nothing new.
Of course you evolutionists have your imaginations and beggaminases to support your argument.Beggaminase is a VERB, you dolt.
Sorry I don’t have a copy of the Belzford English dictionary. So I googled your word “beggaminases” and all it does is point back to this thread. Your evolutionist confabulation doesn’t work here; we are looking at the mathematical and empirical evidence of how mutation and selection sorting/optimization work. Just listen to how you evolutionists shriek and cry when you are confronted by these mathematical and empirical facts of how the mutation and selection sorting/optimization problems actually works.
English lesson for joobz, synonyms for the word delay-holdup, wait, stoppage, setback, impediment, hindrance, interruption, interruption, synonyms for the word prevent-stop, put off, avert, avoid, foil, thwart, check, put a stop to. BWA HA HA HA HA!!!!

I think you really are becoming more and more incoherent.
Perhaps you think “BWA HA HA HA HA” is a coherent response but what can you expect from a grammatically challenged alchemical engineer.
It is just a mathematical reality that if you are trying to sort and optimize on conditions, the more conditions imposed the profoundly slower the sort/optimization process becomes.Can you show us mathematical proof of this claim?
Of course, I have already demonstrated this with ev. Many of the citations I have posted are for mathematical models of the mutation and selection problem and they show this result as well. Even Adequate says the following:
More optimisation takes more time.
It is only mathematical incompetents like you who suggest that more sorting conditions accelerate the process.

[joobz]

Perhaps you think “BWA HA HA HA HA” is a coherent response but what can you expect from a grammatically challenged alchemical engineer.
Yes, it is. It was me laughing at your condensention while simultaneously demonstrating your poor reading comprehension. Are you illiterate as well as innumerate?

Perhaps you'd like to explain again how the authors believe that delay and prevent mean the same thing. Why don't you email them and ask for that explanation. I'm sure they would humor you.

BTW, I've noticed again that you have completely and totally avoided my request. What are your justifications for all of your theory assumptions? You've avoided this question for over 3 months now. To use your words, why do you continue to be a such a phony?

[kleinman]

I've noticed again that you have completely and totally avoided my request. What are your justifications for all of your theory assumptions? You've avoided this question for over 3 months now.
Joobz, don’t blame me if you are ignorant of how the mutation and selection sorting/optimization problem works. I’ve posted Dr Schneider’s justifications for his model and just because evolution is not your field, don’t whine to me that you don’t understand how Dr Schneider’s program works. Do your homework and come up to speed on the topic, then you have a chance of understanding how the mutation and selection sorting/optimization problem works, that is if you can set aside your silly speculations which is doubtful for someone so deeply indoctrinated in the evolutionist belief system.

[joobz]

... I’ve posted Dr Schneider’s justifications...[snip pointless diatribe]
Yes you did. But this is not the same as YOUR justifications! Don't confuse Dr. Schneider, a successful published researcher, with yourself, an ineffectual PhD with only 2 publications to his name.

Now, when will you actually man up and defend your theory. I state clearly taht your argument is bogus becuase the selection conditions are neither constant in magnitude or number. That this fact will result in increased emergence of adaptation.

[rocketdodger]

Of course, I have already demonstrated this with ev.

No, you have not. Even if your interpretations of ev were correct, they say nothing about sorting algorithms in general.

If you disagree, Kleinman, then feel free to post the relevant portions of the source code (which is publicly available at the ev site) that you feel are representative of all sorting algorithms.

Many of the citations I have posted are for mathematical models of the mutation and selection problem and they show this result as well.

I don't recall any citations that mention sorting algorithms always being confounded by additional sorting conditions. If I am wrong, please re-post them and highlight the sentences where such a thing is stated.

Even Adequate says the following:

That statement is correct. If you weren't an idiot, you would realize that there are more factors contributing to the rate of a process than simply how long it takes.

It is only mathematical incompetents like you who suggest that more sorting conditions accelerate the process.

First, quote me stating that a sorting process is accelerated by additional sorting conditions.

When you fail to do so (because I never said it), please show us why "increasing the rate of a process" is equivalent to "accelerating a process."

[kjkent1]

You are correct when you say that R numbers are meaningless when running models with fewer than three selection pressures, but you are wrong when you conclude that there is no way to compare Ev models with different numbers of pressures. All you have to do is put in the input parameters which show that ev can evolve any single selection condition very rapidly but when evolving all three conditions simultaneously it takes many, many orders of magnitude more generations to sort the beneficial and detrimental mutations. You may not want to do the comparison because it shows why the mutation and selection sorting/optimization process becomes so profoundly slow when you have combination selection pressures but you can do the comparison. The empirical data shows the same affect, combination selection pressures have a profound impact on the ability of the population to evolve to these combined pressures. Paul, you are taking a position that is in contradiction to the mathematical behavior of your own sorting/optimization algorithm and the empirical data which show how mutation and selection works in reality.kleinman, YOU are the person who is ignorant about the reality of evolution. It is an observed, empirical fact that substantially all independently living organisms have genomes where Rseq ~ Rfreq.

Thus, there is no real-world evolution without convergence. There may be some sorting and optimizing in a mathematical model that has no correlation with reality, but there is no evolution, i.e., no information gain.

The whole point of Schneider's software and paper is to display a means of measuring evolutionary change, i.e., information gain, at the genome level. Your desire to concentrate on some definition of zero mistakes that allows for a genetic structure that looks nothing like anything found in nature, is a demonstration that you don't know what you're talking about.

That's about the sloppiest science anyone could propose. In simpliciter, if we adopt your position, then we should be able to cobb together a random string of bases, inject it into a cell membrane, and some new life should immediately appear.

In fact, if we adopt your position, then your entire theory falls flat, because it would mean that selection is no longer a criterion for evolutionary change -- all that's needed is mutation!

The only rational mathematical measurement of evolutionary change is Rseq -> Rfreq. Frankly, if you were able to concede the obvious, you would have a new and perhaps more sound argument against evolution, i.e., if large-scale mutations are responsible for macroevolutionary change, then what is the probability that such mutations will interfere with the relationship of Rseq ~ Rfreq. Because, if there is too much interference, then modern genomes should not display the Rseq~Rfreq relationship, because there hasn't been sufficient time for this integration to occur.

Or, perhaps, the only large-scale mutations which are beneficial are those that just happen to maintain a reasonable relationship between Rseq and Rfreq?

Either way, it gives everyone something with a foundation to chew on. Whereas, your current hypothesis is based on your misunderstanding of the computational effect of setting a mistake count to zerio in computer program -- not very inspired, and in fact, pretty droll.

[Paul C. Anagnostopoulos]

If that's correct, each site constitutes a selection pressure... unless we're using that phrase differently? What I mean is that each site constitutes a trait that is subject to selection - if the site has the wrong sequence it is selected against, and if it has the correct sequence (or close enough) it isn't.
Yes, that is correct. I wouldn't think of those as separate selection pressures, but then again the term selection pressure is a bit goosey.


So I would say increasing the number of sites increases the number of selection pressures. Do you disagree with that? I suppose it's complicated in ev by non-sites being mistakenly identified [spurious bindings] also acting as a pressure, but that's not going to affect the scaling with the number of sites very much. Anyway, that can presumably be turned off by setting the corresponding weight to zero?
If you turn off mistake points for spurious bindings, the entire genome ends up being matched by the gene. It happens very quickly. This is why Alan keeps saying that fewer pressures result in faster evolution.

~~ Paul

[Paul C. Anagnostopoulos]

Why Paul, you wouldn’t be back peddling again on your previous statement?
No, I would not. The pressure is to reduce the number of mistakes. That does not mean that it is meaningful to compare the number of mistakes between two models with different ways of calculating the mistake count.

~~ Paul

[Belz...]

I’ve been reading evolutionist nonsense for years, you say nothing new.

That's okay. We've been reading YOUR nonsense for over a year, now, and you've NEVER said anything new.

Sorry I don’t have a copy of the Belzford English dictionary. So I googled your word “beggaminases” and all it does is point back to this thread. Your evolutionist confabulation doesn’t work here

You're the one who asked me for another word. The fact that you can't understand that makes you the most stupid person on this thread.

Incidently, I can see you looking at mathematical problems:

Kleinman: (reading) "Where 'X' is the number of years ? What the hell are they talking about ? 'X' is not a synonym of 'year' ! Stoopid mathematicians."

[Belz...]

Of course, I have already demonstrated this with ev.

And what do you make of the OTHER programs ?

Gee, I can't expect an answer to that one.

[sol invictus]

Sol, I’m not wrong

Sorry, but yes, you are.

you just don’t understand how ev works.

My understanding of it was and is correct, as far as I can tell. It's not very complicated.

Gamma, the number of binding sites in ev are not the selection conditions.

You can use whatever terms you like, but what you are referring to as selection conditions are actually the weights of a whole set of pressures. The fact is that each binding site constitutes a selection pressure, with strength given by the weight for "Missed Site". With the other weights also non-zero there are additional selection pressures - but many such pressures for each of the three non-zero weights, not one.

When you set some of the weights to 0 you are changing the number of selection pressures by a very large amount. For example if you set the weight for "Missed Sites" to 0, you have reduced the number of selection pressures by gamma. Failing to comprehend this basic point may partially explain why you have misunderstood the model so badly.

Anyway, you've now acknowledged that ev demonstrates that increasing the number of selection pressures does NOT significantly increase the time required to evolve a perfect creature:


I have already done a series and studied the affect of varying gamma. Other than ev will not converge if gamma is too small, varying the number of binding sites has little affect on the generations for convergence.

There, you have just agreed that increasing the number of pressures does not affect the time required very strongly.

GAME OVER.

Now, would you still like to lose your $10,000?

[Paul C. Anagnostopoulos]

For example if you set the weight for "Missed Sites" to 0, you have reduced the number of selection pressures by gamma.
I do not understand what you mean by this.

Also, I'm not sure we are distinguishing selection pressures from their genetic targets correctly. I don't even know what the correct distinction is.

~~ Paul

[sol invictus]

Yes, that is correct. I wouldn't think of those as separate selection pressures, but then again the term selection pressure is a bit goosey.

Understood. There is some semantic fuzziness here, but the algorithm is clear.


If you turn off mistake points for spurious bindings, the entire genome ends up being matched by the gene. It happens very quickly. This is why Alan keeps saying that fewer pressures result in faster evolution.


Well, it does result in faster evolution - just not very much faster, so long as the total number of pressures remains reasonably large. Of course if you simply turn off all the pressures, evolution is instantaneous... which seems to be kleinman's great discovery.

[sol invictus]

I do not understand what you mean by this.


In the simple model kleiman proposed a while back, you simply waited for a given mutation to happen at a given place in the genome. Once that mutation occurred it was absolutely fixed (and it never mutated back again). Then you asked how long it took for a specific set of N such mutations to occur. The answer scales as log(N). That simple model appears to describe these more complicated algorithms reasonably well.

In ev, as far as I understand, each binding site that doesn't match is counted as a mistake. Therefore each binding site acts as a selection pressure - in any creature where it doesn't match it contributes to selecting against that creature. However if you set the weight (meaning the mistake point value for missed sites) to 0, it has no effect on selection. That holds for all the sites, so by setting the weight to zero you have reduced the number of selection pressures by gamma.

Now I agree that this counting is a little ill-defined in this particular model, but not in any way that seems to affect things substantially.

[kleinman]

... I’ve posted Dr Schneider’s justifications...[snip the facts about the mutation and selection sorting/optimization problem that joobz doesn’t understand which is virtually everything]Yes you did. But this is not the same as YOUR justifications! Don't confuse Dr. Schneider, a successful published researcher, with yourself, an ineffectual PhD with only 2 publications to his name.
I’m the one who agrees with Dr Schneider’s model and his justifications for his model. It is you evolutionists who are now discrediting his model now that you understand what it shows about the mutation and selection sorting/optimization problem. The only problem with your attacks on his model is that it shows how the mutation and selection sorting/optimization problem actually works in real examples of mutation and selection, that is combination selection pressures profoundly slow the sorting/optimization process. Of course joobz, you can propose cooperative selection pressures to go along with your cooperative chemistry nonsense. That kind of bizarre speculation fits your belief system.
Of course, I have already demonstrated this with ev.No, you have not. Even if your interpretations of ev were correct, they say nothing about sorting algorithms in general.
If you don’t believe me, here is what Adequate says about these problems.
More optimisation takes more time.
Many of the citations I have posted are for mathematical models of the mutation and selection problem and they show this result as well.I don't recall any citations that mention sorting algorithms always being confounded by additional sorting conditions. If I am wrong, please re-post them and highlight the sentences where such a thing is stated.
Don’t blame me for you failure of reading comprehension. So I’ll repost some of these citations of mathematical models which show that combination selection pressures profoundly slow the evolutionary process.
http://www.blackwell-synergy.com/doi/pdf/10.1046/j.1365-3156.2001.00800.x (http://www.blackwell-synergy.com/doi/pdf/10.1046/j.1365-3156.2001.00800.x)
Resistance genes are generally assumed to be biologically less efficient than the normal susceptible type. For example, an enzyme may escape drug action by a mutation that alters the drug-binding site. As this mutation probably also affects its catalytic capacity, the mutation will be removed from the population by natural selection and their frequency in the naive, non-drug-treated, population will be determined by a mutation/selection balance (Hastings 1997; Koella 1998). If drugs are used in combination, then the frequency of parasites resistant to both drugs will be
very low. For example, if 0.1% are resistant to drug A and 0.005% are resistant to drug B, then parasites resistant to both will initially be present at a frequency of 0.1 x 0.05% = 0.00005% (assuming that the same gene cannot encode resistance to both drugs). Thus using drugs in combination from the outset may greatly increase the useful therapeutic lifespan of the drug, because lowering the starting frequency delays the point at which a significant amount of resistance emerges.
And
One important general point from the models is that use of combination therapy in their initial deployment is invariably better than introducing one drug alone, followed by introduction of the second-line drug once the first becomes ineffective (see, for example, Curtis & Otoo 1986; Smith 1990; Bonhoeffer et al. 1997; for malaria, helminths and bacteria, respectively).
And
If parasites reach high numbers within hosts, then spontaneous mutations to resistance may occur. Infections of P. falciparum may reach 10^11-10^12 individual parasites per host and it seems logical that a small subpopulation may have mutated to drug resistance (for example if the mutation rate to resistance is 10^-8 then there would be 1000±10 000 resistant parasites) which then expands to dominate the infection. This argument seems logically plausible and receives support from observations of humans treated with the antimalarial drug atovaquone, where an infection which was originally susceptible disappears below detectable levels before recrudescing as a resistant infection (Looareesuwan et al. 1996). Measurements of drug sensitivity in vitro before and after treatment show greatly increased levels of resistance in the recrudescent infection. It seems plausible that the same effects may occur in other parasites that reach high population numbers within a host. Once again the effect can be minimized or even eliminated by using drugs in combination. In the above example of 10^11 parasites, mutation rates to resistance of 10^-8, and assuming two drugs were used in combination, then resistance would arise in only 10^16 parasites, in effect rendering the frequency of spontaneous mutations negligible. The implications for the evolution of drug resistance are discussed in Lipsitch and Levin (1997) and White (1999 and references therein).
http://www.billingpreis.mpg.de/hbp04/mybil.pdf (http://www.billingpreis.mpg.de/hbp04/mybil.pdf)
Despite the approval of almost 20 antiretroviral drugs and the use of combination therapy, successful treatment of HIV-infections is hampered by the emergence of drug-resistant genetic variants in response to therapy. Finding a new potent drug combination after treatment failure is considered challenging, because most accumulated mutations confer resistance to multiple drugs. We present three computational tools for the analysis and simulation of viral genomic sequences, phenotypic drug resistance, and clinical outcomes. Mtreemix is a software package for estimating and using mixture models of trees that describe probabilistically the evolution of drug resistance. Geno2pheno is a web-based system for the prediction of phenotypic resistance from viral genotypes. It also implements normalization methods that make these predictions comparable between different drugs. Finally, theo predicts virological response within a patient from the infecting viral strain and the selected drug combination. Together these models and programs provide a quantitative picture of the evolution of drug resistance and support the design of individualized antiviral therapies.
and
We mention a clinical study from De Luca, Cozzi-Lepri, Perno, Balotta, Di Giambenedetto, Orani, Mussini, Toti & d’Arminio Monforte (2003) to demonstrate the benefit of predicting phenotypic resistance for the selection of new antiretroviral regimens. These researchers analyze therapy changes accompanied by a genotypic resistance tests in 332 previously untreated patients. Phenotypes are predicted with geno2pheno for the components of the combination therapies, and each drug is scored as active if the virus is predicted susceptible to it. Using a Cox proportional hazards model, they show that patients with a combination therapy consisting of ≤ 2 active drugs have a significantly higher risk of virological failure (sustained virus load increase) than patients receiving ≥ 3 active drugs (p < 0.004). The authors also compare the performance of 11 rules-based interpretation systems and our data-driven approaches. Genotypic scoring based on the SVM predictions as implemented in geno2pheno turns out to be the only interpretation system that provides significant predictions of virological failure after 24 weeks of treatment (De Luca, Cingolani, Di Giambenedetto, Trotta, Baldini, Rizzo, Bertoli, Liuzzi,Narciso, Murri, Ammassari, Perno & Antinori 2003
These authors are answering the correct question Sol.
Here is another citation on the same topic which shows mathematically how mutation and selection works.
http://bioinformatics.oxfordjournals.org/cgi/content/full/21/21/3943 (http://bioinformatics.oxfordjournals.org/cgi/content/full/21/21/3943)
Summary: The development of drug resistance is a major obstacle to successful treatment of HIV infection. The extraordinary replication dynamics of HIV facilitates its escape from selective pressure exerted by the human immune system and by combination drug therapy. We have developed several computational methods whose combined use can support the design of optimal antiretroviral therapies based on viral genomic data.
and
Suppose we have estimated a mutagenetic tree model for the development of resistance to a certain drug. In particular, this model can be used to compute transition probabilities between mutational patterns. As described in the previous section we can predict the resistance phenotype from the genotype. Using a classifier restricted to the set of n mutations we predict each mutational pattern to be either susceptible or resistant. Now, for a given virus we may ask what the transition probability to any resistant state is. In fact, this question is crucial for minimizing the risk of resistance development with the next regimen. We refer to the genetic barrier as the probability of not reaching any resistant state after a fixed time period under therapy. This quantity can be calculated as the sum of the probabilities of all mutational patterns predicted as susceptible. Thus, a higher genetic barrier indicates that the virus is less likely to become resistant.

For example, Table 2 shows the genetic barriers to both low level and high level zidovudine resistance of the wild type virus under three different regimens, namely zidovudine monotherapy, double therapy with zidovudine plus lamivudine, and double therapy with zidovudine plus didanosine. The underlying mutagenetic tree model is the tree displayed in Figure 1 scaled to a mean sampling time of 96 weeks. As expected, the genetic barrier to zidovudine is always higher under the combination of zidovudine plus lamivudine than under zidovudine alone, because these drugs do not share any resistance mutations. More surprisingly, we find that zidovudine resistance appears to develop faster under zidovudine plus didanosine than under zidovudine monotherapy. This effect may be explained by the stronger selective pressure exerted by the double therapy and the cross-resistance profile of zidovudine and didanosine (Beerenwinkel et al., 2005b; Brun-Vezinet et al., 1997). Thus, the genetic barrier is a useful concept for designing effective treatment strategies.
and
In order to support clinical decision making on the basis of viral genomic data, we have developed and applied several computational methods and tools. Specifically, we have addressed data integration and management (Arevir database), prediction of drug resistance and co-receptor usage from genotypes (geno2pheno), modeling of the evolution of drug resistance and the genetic barrier by mutagenetic trees (mtreemix), and selection of optimal drug combinations (theo). The integration of various types of genomic, phenotypic and clinical data as well as the coupling of different computational models yields predictive models of therapy outcome that may support the design of combination therapies.
http://www.biology.emory.edu/research/Levin/pubs/97cycle.pdf (http://www.biology.emory.edu/research/Levin/pubs/97cycle.pdf)
ABSTRACT: The spread of bacteria resistant to antimicrobial agents calls for population-wide treatment strategies to delay or reverse the trend toward antibiotic resistance. Here we propose new criteria for the evaluation of the population-wide effects of treatment protocols for directly transmitted bacterial infections and discuss different usage patterns for single and multiple antibiotic therapy. A mathematical model suggests that the long-term benefit of single drug treatment from introduction of the antibiotic until a high frequency of resistance precludes its use is almost independent of the pattern of antibiotic use. When more than one antibiotic is employed, sequential use of different antibiotics in the population (‘‘cycling’’) is always inferior to treatment strategies where, at any given time, equal fractions of the population receive different antibiotics. However, treatment of all patients with a combination of antibiotics is in most cases the optimal treatment strategy.
http://www.blackwell-synergy.com/doi/abs/10.1046/j.1365-3180.2003.00355.x (http://www.blackwell-synergy.com/doi/abs/10.1046/j.1365-3180.2003.00355.x)
A simulation study was conducted to examine the effect of pattern of herbicide use on development of resistance to two herbicides with different modes of action in finite weed populations. The effects of the size of the treatment area (analogous to initial weed population), germination fraction and degree of self-pollination in the weed were investigated. The results indicate that the probability of developing resistance to one or both herbicides decreases as the size of the area/initial population decreases. For treatment areas of 100 ha or less with an initial weed seedbank of 100 seeds m2 and initial frequencies of the resistance genes of 106, development of resistance to both herbicides (double-resistance) is uncommon within 50 years for all types of weeds if both herbicides are used in all years (used in combination). If herbicides are used in alternate years (rotated) double-resistance almost always occurs in 100 ha areas but is uncommon in areas of 1 ha or less. The results suggest that adoption of practices that limit movement of weeds in conjunction with using herbicides in combination rather than in rotation can substantially delay development of herbicide resistance.
http://dimacs.rutgers.edu/Workshops/TumorModeling/abstracts.html (http://dimacs.rutgers.edu/Workshops/TumorModeling/abstracts.html)
The genetic instability of tumor cells renders them the ability to rapidly become resistant to many chemotherapies. As a result, there is great interest in selecting combination chemotherapeutic regimens that will overcome resistance and exert synergistic therapeutic activity.
http://www.springerlink.com/content/ahe70qmqg2f5ukxl/ (http://www.springerlink.com/content/ahe70qmqg2f5ukxl/)
In this paper we discuss some questions of applying evolutionary algorithms to multiobjective optimization problems with continuous variables. A main question of transforming evolutionary algorithms for scalar optimization into those for multiobjective optimization concerns the modification of the selection step. In an earlier article we have analyzed special properties of selection rules called efficiency preservation and negative efficiency preservation.

Here, we discuss the use of these properties by applying an accordingly modified selection rule to some test problems. The number of efficient alternatives of a population for different test problems provides a better understanding of the change of data during the evolutionary process. Also effects of the number of objective functions are treated. We also analyze the influence of the number of objectives and the relevance of these results in the context of the 1/5 rule, a mutation control concept for scalar evolutionary algorithms which cannot easily be transformed into the multiobjective case.
http://www.ecologyandsociety.org/vol3/iss2/art12/manuscript.html (http://www.ecologyandsociety.org/vol3/iss2/art12/manuscript.html)
Essentially, all of these drugs, if used as single antiviral therapy, lead to the emergence of resistant virus mutants. The pattern is often similar. Initially, there is a decay in virus abundance, but after some time, the virus resurges. The decisive treatment breakthrough was to combine several drugs at once. For about 2 years, this combination therapy has proved to be a tremendous success. In many patients, virus abundance in the blood decays below detection limit within weeks of treatment and can remain undetectable for years.

Mathematical models have been developed to describe the dynamics of resistance in order to understand the factors that determine when and if resistant virus will emerge in a patient. The mathematical theory also provides a definition of viral resistance. Earlier, I mentioned the basic reproductive ratio, R0, as a measure of the intrinsic growth potential of the virus. Let us now apply this notion to individual virus mutants and let us consider a patient who has just started on antiviral treatment. A particular virus mutant is resistant to therapy if its R0 value during therapy exceeds one. Such a mutant will not decline to zero abundance, but will persist during treatment. Therefore, resistance is not simply determined by the susceptibility of the virus mutant to inhibition by the drug, but by its intrinsic growth rate (or fitness) during antiviral therapy. An important consequence of this notion is that resistance is not only a property of the virus, but also a combined property of virus and host (Bonhoeffer et al. 1997). A particular virus mutant may be resistant in a patient with a weak immune response and may be eliminated in a patient with a strong immune response. Furthermore, test tube measurements of levels of inhibition by various drug concentrations are not sufficient to determine whether a particular virus mutant will be resistant to antiviral therapy.

Mathematical models show that the main problem of resistance is whether or not resistant virus mutants are present in a patient prior to treatment. Treatment will work if the R0 values of all virus mutants present in a patient at the time when therapy starts are below one. An interesting mathematical result is that the probability that a particular mutant will emerge during effective therapy is less than the probability that this mutant was already present before treatment. Therefore, treatment must be designed to minimize the probability that resistant variants exist in a patient at the time when treatment commences. This can be achieved by treating patients early in infection, when virus load and diversity are low and the immune system remains intact. In addition, it is essential to use many drugs at once, because a virus that is resistant to several drugs simultaneously will require many specific mutations. In fact, the more drugs are deployed, the better the chances of success. Of course, the limiting conditions will be the adverse side effects and the cost of therapy. Thus, mathematical models support the notion of ''treating hard and early.''
http://www.pngimr.org.pg/Editorial%20-%20%20Mar-June%202001.pdf (http://www.pngimr.org.pg/Editorial%20-%20%20Mar-June%202001.pdf)
Combination therapy is well established for the treatment of many illnesses such as HIV infection (6), tuberculosis and other bacterial infections (7), and leukaemia (8). To gain resistance to a drug combination, an organism must simultaneously develop multiple mutations (assuming the drugs have different modes of action). If these mutations arise independently, then the probability of a double mutation arising is the product of the individual probabilities. For example, if a resistance mutation for each of the two drugs arises once per billion divisions, then the double mutation arises once per billion billion. By contrast, if one drug is used alone until resistance develops and is then replaced by the second drug (ie, a policy of drug cycling) then only one billion divisions would be needed for resistance to arise to the first drug, and then only one billion more for resistance to the second drug. In this scenario, the singly-resistant parasites would initially be rare, which would increase the time needed for them to generate the second billion divisions, but nevertheless the overall time to achieve double resistance would in theory be less. Mathematical models (9-12) predict that, under a variety of conditions, a policy of combination therapy is generally better — in terms of delaying drug resistance — than other policies such as cycling of single drugs. This applies to the spread of preexisting mutations, as well as those arising de novo. The only predicted exception occurs when multiple antibiotic resistance mutations are carried on the same plasmid (13), which should not be relevant for Plasmodium. Another benefit of combination therapy can be expected on pharmacological grounds. The combination increases the rate of reduction of the parasites, so the infection is brought under control while the drug concentrations are still relatively high. This reduces the opportunity for selection of resistance, since it exposes parasites to sublethal drug concentrations for a shorter time(14).
http://dimacs.rutgers.edu/Workshops/TumorModeling/abstracts.html (http://dimacs.rutgers.edu/Workshops/TumorModeling/abstracts.html)
The genetic instability of tumor cells renders them the ability to rapidly become resistant to many chemotherapies. As a result, there is great interest in selecting combination chemotherapeutic regimens that will overcome resistance and exert synergistic therapeutic activity. Traditional analysis of drug combination effects on cells is based on a number of assumptions and idealizations. A more rational mechanistic modeling approach may accelerate the search for effective drug combinations that are tailored to individual responses. The chemotherapeutic drugs, carmustine and etoposide, each nominally induces G2 phase arrest and, secondarily, apoptosis. Despite this similarity in mechanism, we found that the pharmacodynamic responses to these agents is dramatically different on human glioma cell lines. We have developed a cell cycle structured model of chemotherapeutic activity based on the dynamic transitions of cells along the phases of the cell cycle. We show that our mathematical model is able to explain the shapes of the dose response curves of multiple cell lines to these agents. We are able to predict with the model the effects of drug combinations, taking into account variable dose and timing regimens, to determine the most effective strategy. Using this model, we are able to explain several non-intuitive experimental observations involving combinations of chemotherapeutic drugs on glioma-derived cell lines.
http://cohesion.rice.edu/Engineering/bioe/emplibrary/Physics_Today_Jan07.pdf (http://cohesion.rice.edu/Engineering/bioe/emplibrary/Physics_Today_Jan07.pdf)
At the molecular level, what are the likely escape mutants that lead to new viral strains or new antibiotic-resistant bacteria? To be specific, I’ll consider viruses. The immune system recognizes regions of viral proteins, and it develops the ability to clear the virus from the body based on that recognition. If not completely eradicated from the human(and possibly animal) population, the surviving virus will tend to accumulate mutations in the region of the genetic sequence that codes for those recognizable protein pieces and thus avoid immune recognition. Predicting which mutations are likely in the surviving virus could allow vaccination against potential future strains—the escape mutants—and more effective control of the virus in the population. Similarly, the ability to predict at the molecular level which changes may lead to resistance against a drug can aid in the design of improved drugs or suggest optimal combinations of existing drugs to mitigate the evolution of resistance and eradicate the pathogen.
That’s just a few of the citations of mathematical models which show that combination selection pressures slow the evolutionary process. So not only are you ignorant of how this mathematics works of mutation and selection works, you are inattentive. That is not a good combination rocketwhomissesthetarget.
Why Paul, you wouldn’t be back peddling again on your previous statement?No, I would not. The pressure is to reduce the number of mistakes. That does not mean that it is meaningful to compare the number of mistakes between two models with different ways of calculating the mistake count.
Since you enjoy painting yourself into corners so much, why don’t you tell us what the difference is between calculating mistakes for three selection conditions versus a single selection condition in ev.

[rocketdodger]

That’s just a few of the citations of mathematical models which show that combination selection pressures slow the evolutionary process. So not only are you ignorant of how this mathematics works of mutation and selection works, you are inattentive. That is not a good combination rocketwhomissesthetarget.

I will repeat my statement because you obviously didn't read it the first time:

I don't recall any citations that mention sorting algorithms always being confounded by additional sorting conditions. If I am wrong, please re-post them and highlight the sentences where such a thing is stated.

Among the highlighted sentences in that turd of a post you just made, Kleiman, I count the number of times terms such as "sort" or "sorting" appear as ..... zero. Care to try again?

[joobz]

I’m the one who agrees with Dr Schneider’s model and his justifications for his model. It is you evolutionists who are now discrediting his model now that you understand what it shows about the mutation and selection sorting/optimization problem. The only problem with your attacks on his model is that it shows how the mutation and selection sorting/optimization problem actually works in real examples of mutation and selection, that is combination selection pressures profoundly slow the sorting/optimization process. Of course joobz, you can propose cooperative selection pressures to go along with your cooperative chemistry nonsense. That kind of bizarre speculation fits your belief system.None of this is an answer to what I asked. I know What Dr. Scneider says. I'm asking YOU for YOU to justify YOUR assumptions. This is not the same thing as showing me what someone else says. Why are you so afraid to answer my questions?

BTW, none of the quotes you gave say that evolution stops with multiple selection pressures. More importantly, none of them claim that the emergence of resistence is permanently prevented.

So, will you be a man, or continue to be a scared phony?

[joobz]

I will repeat my statement because you obviously didn't read it the first time:

Among the highlighted sentences in that turd of a post you just made, Kleiman, I count the number of times terms such as "sort" or "sorting" appear as ..... zero. Care to try again?
The game is
You, I or anyone else: ASK A DIRECT QUESTION
Kleinman: Flings feces at the keyboard and pretends it is an answer
You, I or anyone else: Ask question again, with hope of different outcome
Kleinman: Flings feces at the keyboard and pretends it is an answer

[kleinman]

I found a combination of parameters last night that led to over 100 pressures being faster than a single one, but I forgot what it was http://forums.randi.org/images/smilies/frown.gif
In the meantime, I’ll continue to post real examples of mutation and selection which shows that you are wrong.

And your understanding of ev is best expressed by the following:
I am eager to participate in this discussion but I don't know the mathematical details of the topic, only general ideas. Paul, is there a good introductory source (assuming I am fluent in mathematics) where I can learn what this equation you guys are talking about represents? All this Rseq~ and Rfreq~ stuff is lost on me.
Rocketwhomissesthetarget, you are a slow learner on this topic. You did give Sol good advice to not wager the $10,000.

[rocketdodger]

Kleinman, you are living proof that homo sapiens descended from apes. There really isn't anything else to say at this point.

[sol invictus]

You did give Sol good advice to not wager the $10,000.

So kleinman, have you backed out yet again? It's really getting hard to keep track of your flipflopping and squirming.

If not, what's your wager? Will you still bet that increasing the number of selection pressures slows the rate of evolution, even though you just admitted it doesn't?

[kleinman]

Here’s something you evolutionists don’t have for your mathematically impossible theory, real examples which show that combination selection pressures profoundly slow the evolutionary process.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=9517926 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=9517926)
The selection of bacterial resistance was examined in relationship to antibiotic pharmacokinetics (PK) and organism MICs in the patients from four nosocomial lower respiratory tract infection clinical trials. The evaluable database included 107 acutely ill patients, 128 pathogens, and five antimicrobial regimens. Antimicrobial pharmacokinetics were characterized by using serum concentrations, and culture and sensitivity tests were performed daily on tracheal aspirates to examine resistance. Pharmacodynamic (PD) models were developed to identify factors associated with the probability of developing bacterial resistance. Overall, in 32 of 128 (25%) initially susceptible cases resistance developed during therapy. An initial univariate screen and a classification and regression tree analysis identified the ratio of the area under the concentration-time curve from 0 to 24 h to the MIC (AUC0–24/MIC) as a significant predictor of the development of resistance (P < 0.001). The final PK/PD model, a variant of the Hill equation, demonstrated that the probability of developing resistance during therapy increased significantly when antimicrobial exposure was at an AUC0–24/MIC ratio of less than 100. This relationship was observed across all treatments and within all organism groupings, with the exception of β-lactamase-producing gram-negative organisms (consistent with type I β-lactamase producers) treated with β-lactam monotherapy. Combination therapy resulted in much lower rates of resistance than monotherapy, probably because all of the combination regimens examined had an AUC0–24/MIC ratio in excess of 100. In summary, the selection of antimicrobial resistance appears to be strongly associated with suboptimal antimicrobial exposure, defined as an AUC0–24/MIC ratio of less than 100.
http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed&cmd=Retrieve&list_uids=9214473 (http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed&cmd=Retrieve&list_uids=9214473)
Lamivudine ([-]-beta-L-2',3'-dideoxy-3'-thiacytidine [3TC]) and penciclovir (9-[2-hydroxy-1-(hydroxymethyl)ethoxymethyl]guanine [PCV]) are potent inhibitors of hepatitis B virus (HBV) replication. Both drugs have entered phase III clinical trials for treatment of chronic HBV infection. 3TC and PCV are deoxycytidine and deoxyguanosine analogs, respectively, and their modes of action and how they interact are matters of both theoretical and practical interest. We compared the antiviral activities of 3TC and PCV alone and in combination in primary duck hepatocyte (PDH) cultures derived from ducklings congenitally infected with the duck hepatitis B virus (DHBV). 3TC and PCV inhibited DHBV replication to a comparable extent when used alone (50% inhibitory concentrations with 95% confidence intervals were 0.55 [0.50-0.59] micromol/L for 3TC and 0.35 [0.27-0.43] micromol/L for PCV), and in combination, the two nucleoside analogs acted synergistically over a wide range of clinically relevant concentrations. Synergy between PCV and 3TC was also observed in acutely infected cells and in "washout" experiments designed to assess the persistence of antiviral activity after drug removal. Furthermore, the combination was more effective in reducing the normally recalcitrant viral covalently closed circular (CCC) DNA form of DHBV than either drug alone. These results suggest that combinations of 3TC and PCV may act synergistically against HBV in vivo.
Of course you evolutionists have lots of speculations and lots of mathematical data which you happened to forget. Oh yes, you evolutionist crybabies have no shortage of foul language. That is sure to convince everyone of your dedication to your belief system.
http://forums.randi.org/images/smilies/doglaugh.gif

[joobz]

Here’s something you evolutionists don’t have for your mathematically impossible theory, real examples which show that combination selection pressures profoundly slow the evolutionary process.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=9517926 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=9517926)

http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed&cmd=Retrieve&list_uids=9214473 (http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed&cmd=Retrieve&list_uids=9214473)

Of course you evolutionists have lots of speculations and lots of mathematical data which you happened to forget. Oh yes, you evolutionist crybabies have no shortage of foul language. That is sure to convince everyone of your dedication to your belief system.
http://forums.randi.org/images/smilies/doglaugh.gif
you seem to be projecting.

You've resorted to igoring all comments (becuase they completely destroy your imaginary world) and will post a bunch of quotes that say nothing to support your argument. This is spamming and is against forum rules.

Why are you so afaid to debate us?

[kleinman]

You've resorted to igoring all comments (becuase they completely destroy your imaginary world) and will post a bunch of quotes that say nothing to support your argument. This is spamming and is against forum rules.
…Flings feces … Flings feces
It’s good to see that you have expanded your vocabulary joobz.

You can’t find a citation that would support your mathematically and empirically impossible world view, so you resort to what you know best.

[joobz]

It’s good to see that you have expanded your vocabulary joobz.

You can’t find a citation that would support your mathematically and empirically impossible world view, so you resort to what you know best.
Funny how you quote that post, but continue to ignore the countless posts that I ask you to defend your theory. What would you call such behavior?

SO Agian, do you have any support for your *ahem* Ideas *ahem*, or will you continue to throw out non sequitors and derision?

Really, the choice is yours; be a man or continue to be a petulant boy.

[kjkent1]

You can’t find a citation that would support your mathematically and empirically impossible world view, so you resort to what you know best.You could just debate the substantive issues instead of carrying on a lecture from the pulpit. There are people here with more than half a brain, but by treating everyone like they're moronic, you're just making yourself look like an ass to the world.

We're all tired of reading your citations. The bottom line is that you have a theory about evolution that does not explain all of the physical evidence. And, you are selecting a small portion of evidence and summarily declaring that your evidence is the only evidence that matters.

Your reconciliation for this discrepancy is that divine will intercedes to make the impossible occur.

However, neither the scientific nor the legal communities permit a resort to magic as a means of resolving questions of fundamental importance.

So, either produce evidence that resolves all of the evidentiary issues or accept that your conclusion is not warranted from the evidence thus far produced.

Real-world evolution requires convergence of Rseq -> Rfreq. Setting ev's mistake weights to zero does not permit this to occur, therefore zeroing the mistake weights is invalid. Ev is useless as a mathematical model unless it's modeling something approaching reality.

You're wrong, Alan -- deal with it and debate the issue intelligently.

[Paul C. Anagnostopoulos]

Well, it does result in faster evolution - just not very much faster, so long as the total number of pressures remains reasonably large. Of course if you simply turn off all the pressures, evolution is instantaneous... which seems to be kleinman's great discovery.
Oh no, it's much faster. With a genome of size 1024, it takes thousands of generations to evolve a perfect creature. If you turn off spurious binding mistake points, it takes only 1. Or else I'm misunderstanding you.


In ev, as far as I understand, each binding site that doesn't match is counted as a mistake. Therefore each binding site acts as a selection pressure - in any creature where it doesn't match it contributes to selecting against that creature. However if you set the weight (meaning the mistake point value for missed sites) to 0, it has no effect on selection. That holds for all the sites, so by setting the weight to zero you have reduced the number of selection pressures by gamma.
Oh, right, gamma! I was thinking of G.

~~ Paul

[Paul C. Anagnostopoulos]

Since you enjoy painting yourself into corners so much, why don’t you tell us what the difference is between calculating mistakes for three selection conditions versus a single selection condition in ev.
When there are three selection conditions, mistakes are counted for missing bindings and two kinds of spurious bindings. When there is only a single condition, mistakes are counted for only one of those three things.

You know that, right?

~~ Paul

[sol invictus]

With a genome of size 1024, it takes thousands of generations to evolve a perfect creature. If you turn off spurious binding mistake points, it takes only 1.


We're in perfect agreement - that's what I meant when I said it would be instantaneous.

Oh, right, gamma! I was thinking of G.

Yeah, sorry if that was the wrong letter. I was referring to the number of actual binding sites per creature (as opposed to the genome size).

[sol invictus]

Here’s something you evolutionists don’t have for your mathematically impossible theory, real examples which show that combination selection pressures profoundly slow the evolutionary process.

Of course you evolutionists have lots of speculations and lots of mathematical data which you happened to forget.

This is really great... clearly kleinman has realized he's been wrong about ev all along, not to mention his own little model. So now he's reduced to ignoring all of the stuff he said before and simply quoting a bunch of abstracts of papers that have nothing to do with his contention.

Kleinman, FYI, no one is reading those abstracts anymore. I did at first, but after the third or fourth one turned out to have nothing to do with what you said it did, I stopped looking, and now I just skip over those parts of your posts. I'm sure everyone else does the same.

So kleinman - will you bet me that the rate of evolution decreases as the number of selection pressures increases? We can use ev (as YOU proposed), or the simpler model YOU proposed, or rocketdodger's model, or any other reasonable model for evolution. $10,000 on the line!

So?

[joobz]

This is really great... clearly kleinman has realized he's been wrong about ev all along, not to mention his own little model. So now he's reduced to ignoring all of the stuff he said before and simply quoting a bunch of abstracts of papers that have nothing to do with his contention.

Kleinman, FYI, no one is reading those abstracts anymore. I did at first, but after the third or fourth one turned out to have nothing to do with what you said it did, I stopped looking, and now I just skip over those parts of your posts. I'm sure everyone else does the same.

That is exactly his plan. By posting quotes to sites that have nothing to do with his argument, he is now deliberately spamming the thread. From what I can gather, I think he hopes to be kicked off the forum. I think that he would like that, so he could claim that the evil evolutionists didn't want to here his troff.

He knows that the abstracts do not say what he says, he knows that they do not support his theory. All he hopes to do is to annoy us with his antics. Unfortunately for him, no one here is annoyed. We simply are waiting for him to grow up.

[kleinman]

You can’t find a citation that would support your mathematically and empirically impossible world view, so you resort to what you know best.You could just debate the substantive issues instead of carrying on a lecture from the pulpit. There are people here with more than half a brain, but by treating everyone like they're moronic, you're just making yourself look like an ass to the world.
Your argument that there are 10^500 alternative universes speaks for itself.
Since you enjoy painting yourself into corners so much, why don’t you tell us what the difference is between calculating mistakes for three selection conditions versus a single selection condition in ev.When there are three selection conditions, mistakes are counted for missing bindings and two kinds of spurious bindings. When there is only a single condition, mistakes are counted for only one of those three things.

You know that, right?
That is correct. And the point of this result is that more selection conditions being imposed simultaneously, the more difficult it is for a population to find a trajectory on the fitness landscape to satisfy all the conditions simultaneously. The number of selection conditions is the dominant parameter in the mutation and selection sorting/optimization process. This is clearly what ev is showing. This is also what is shown by the empirical data of mutation and selection. Where I disagree with you on this point is with your argument that these are completely different models. The difference between the two cases is that in one instance you are evolving three selection conditions simultaneously while in the other instance you are evolving only one of the conditions at a time. In one case you are trying to sort and optimize the entire genome, in the other case you are only trying to sort and optimize a portion of the genome. The former instance requires vastly more generations, the later instance take only a trivially small number of generations. This is reflected in the real examples of mutation and selection. Targeting a single gene with a single selection pressure is much easier for a population to evolve to. When you target two or more genes with multiple selection pressures, the evolutionary process for the population is far more difficult. This is in agreement with the results from ev. This is why combination therapy is used for treating HIV and I believe this will become the standard of care for treating other diseases subject to mutation and selection. It just depends how long it will take for the mathematical and empirical facts of how the mutation and selection sorting/optimization actually works to sink into the evolutionist mentality which at this time dominates the field of biology. This irrational mentality damages the scientific understanding how mutation and selection actually works.

[kjkent1]

Your argument that there are 10^500 alternative universes speaks for itself.To repeat myself for the umpteenth time, that particular argument is advanced by Dr. Leonard Susskind, Ph.D., Felix Bloch professor of physics, Stanford University. So, if you don't like the theory, then contact Susskind and take it up with him. Alternatively, you could discuss the issue with Sol (who, unless I'm very much mistaken, shares some of the same mental space with Dr. Susskind).

...the point of this result is that more selection conditions being imposed simultaneously, the more difficult it is for a population to find a trajectory on the fitness landscape to satisfy all the conditions simultaneously. The number of selection conditions is the dominant parameter in the mutation and selection sorting/optimization process. This is clearly what ev is showing. This is also what is shown by the empirical data of mutation and selection. Where I disagree with you on this point is with your argument that these are completely different models. The difference between the two cases is that in one instance you are evolving three selection conditions simultaneously while in the other instance you are evolving only one of the conditions at a time. In one case you are trying to sort and optimize the entire genome, in the other case you are only trying to sort and optimize a portion of the genome. The former instance requires vastly more generations, the later instance take only a trivially small number of generations. This is reflected in the real examples of mutation and selection. Targeting a single gene with a single selection pressure is much easier for a population to evolve to. When you target two or more genes with multiple selection pressures, the evolutionary process for the population is far more difficult. This is in agreement with the results from ev. This is why combination therapy is used for treating HIV and I believe this will become the standard of care for treating other diseases subject to mutation and selection. It just depends how long it will take for the mathematical and empirical facts of how the mutation and selection sorting/optimization actually works to sink into the evolutionist mentality which at this time dominates the field of biology. This irrational mentality damages the scientific understanding how mutation and selection actually works.This is some of the most utter rubbish I've ever read! If ev's performance with only one mistake count enabled were duplicated by a real world organism, we would routinely see HIV morphing into butterflies and turtles during every drug trial.

There is NO real world evolution unless Rseq -> Rfreq.

[rocketdodger]

It just depends how long it will take for the mathematical and empirical facts of how the mutation and selection sorting/optimization actually works to sink into the evolutionist mentality which at this time dominates the field of biology. This irrational mentality damages the scientific understanding how mutation and selection actually works.

*laugh*

[tsig]

Well joobz, since you are too lazy to investigate ev yourself or what Dr Schneider has said about ev, I’ll do it again for you. Since all I have done is taken the ev model and studied what it shows when the input parameters are varied and what it shows is the mutation and selection sorting/optimization process is profoundly slowed when you have combination selection pressures in the model. In addition, I have posted hundreds of citations which demonstrate the same behavior as Dr Schneider’s peer reviewed and published model shows. So what has Dr Schneider said about his model? You can find the answers at the following URLs:
What was Dr Schneider’s intention for the use of his model?
http://nar.oxfordjournals.org/cgi/content/full/28/14/2794 (http://nar.oxfordjournals.org/cgi/content/full/28/14/2794)

Then what does Dr Schneider say about ev as a simulation of how mutation and selection works in reality?
http://www.lecb.ncifcrf.gov/~toms/paper/ev/faq-for-ev.html (http://www.lecb.ncifcrf.gov/~toms/paper/ev/faq-for-ev.html)

and

and

Dr Schneider is correct about this. The citations which I have posted show that the different recognizers that occur in real examples of mutation and selection have the same behavior as his mathematical model which is combination selection pressures profoundly slow the evolutionary process.

What Dr Schneider fails to recognize here is that real biological experiments of his simulation are done all the time including in his own organization, the National Cancer Institute. Real examples of the mutation and selection sorting/optimization process are being done all the time and they all show that combination selection pressures profoundly slow this sorting/optimization process. This is in agreement with what his model shows.

Now joobz, you can ask Dr Schneider yourself if mutation rates will change the underlying mathematical fact that combination selection pressures profoundly slow the evolutionary process. If you studied ev, you would find out that mutation rates do not change the fact that the number of optimization conditions dominates the mathematics of the mutation and selection sorting/optimization process.

Dr Schneider has not done the studies that he suggested for his model. If he had, he would find out that huge populations have a much more limited effect on the evolutionary process than he is claim here. Is Dr Schneider claiming that there was a population of 6 billion primate precursors for the evolution of humans and chimpanzees?

Why does it take huge numbers of generations to evolve his system? It is the combined selection pressures which makes it an extremely slow process to find a trajectory on the fitness landscape to his “perfect creature” local optimum. In fact, in many if not most cases, a “perfect creature” local optimum can not be achieved because the population gets stranded at other “non-perfect creature” local optima.

I added the highlighting. Here Dr Schneider acknowledges that ev is simply a sorting/optimization algorithm. If he had done the studies that he suggested himself, he would have discovered that this sorting process is profoundly slowed because of his combination selection conditions. This is demonstrated over and over by real examples of mutation and selection.

Now joobz, if this is not enough for you, here is what Dr Schneider has said on his ev blog cite located at: http://www.lecb.ncifcrf.gov/~toms/paper/ev/blog-ev.html (http://www.lecb.ncifcrf.gov/~toms/paper/ev/blog-ev.html)


Again I added highlighting. Dr Schneider is again correct, his model shows what combination selection pressures do to the mutation and selection sorting/optimization process.


Once again, Dr Schneider makes a claim for large genomes. What is not similar is the astronomically huge number of generations required to evolve his simple system on all but the tiniest genomes because of the combined selection pressures. If Dr Schneider had done the studies he called for in his own publication on ev, he would realize that the dominant parameter in the mutation and selection sorting/optimization process is the number of sorting conditions applied simultaneously.

Again, Dr Schneider is correct about this. His model does properly capture the behavior of the mutation and selection sorting/optimization problem. The crucial point the Dr Schneider has missed is that the number of selection conditions dominates the mathematical behavior of his model. This is also reflected in real examples of mutation and selection. Hundreds of real examples have been cited already on this thread.

Again, Dr Schneider speaks rightly. Ev does properly model the mutation and selection sorting/optimization process. There are many examples of what his model shows, which is, multiple selection pressures profoundly slow the evolutionary sorting/optimization process.
There are many other examples which I could quote from Dr Schneider’s web site where he defends the reality of his model. Joobz, if you have a problem with Dr Schneider’s model, you can contact him at toms@ncifcrf.gov (toms@ncifcrf.gov?subject=Tom%20Schneider's%20Home %20Page%20(index.html)) .


You want to use a convergence criterion that the author says in not a realistic criterion. Perhaps this is the reason you are having such a difficult time understanding how mutation and selection sorting/optimization actually works.

No Sol, it is clear you have no idea how ev actually works. I don’t need to take money from an ignoramus.

The program you can't grasp

The facts you cannot see

And the color of the spine speaks for itself

[Mr. Scott]

I hope you all had a wonderful thanksgiving. It seems though that you evolutionist still haven’t figured out how mutation and selection actually works so let’s have some leftover theory of evolution turkey.

You know, during Thanksgiving I had a premonition that Kleinman would resume this thread with a line like that. I think he's exhibiting some kind of pathological addictive OCD that compels him to provoke evolutionists. The stark evidence of this is how, on the very day his summary judgment in his malpractice case was reversed, he posted here to rant against evolution. I'd really like to know if Dr. Levin is aware of how many hours he spends at the clinic, on the payroll and using clinic computers for posting his creationist rants instead of caring for his patients. Perhaps if he wasn't so obsessed with the threat evolution poses to the Garden of Eden fairy tale, he'd have been able to concentrate sufficiently on his work to followed up on Mr. Powell's MRI and avoid his legal nightmare.

Here's a video summarizing that case: Powell v. Kleinman, M.D. (http://www.dailycasereport.com/index.php?q=adv_sheet_by_case/1395)

Overall, I must say this thread has been a great resource for explaining evolution theory and creationist pathology. I've learned more in this year on this than at any other time in my life, and am more confident than ever that I could argue creationists into a corner. Thanks, Alan!

[Kotatsu]

Well now Kotatsu, not only have you explained “Invasion of the Body Snatchers”, you have now explained why annelids are more evolutionarily advanced than humans.

Well, as there are several thousand species of Annelids alive today, and only one species of human, I'd say that yes, yes they are more "evolutionary advanced". They can reproduce asexually, live at the bottom of the sea, or in a heavily polluted sludge. They can form cysts and virtually cease living when conditions are bad and then revive later on when conditions have improved (1). They can be both male and female at the same time (2), they can live in the earth or in glaciers.

Humans, on the other hand, have to share species with you.

---
(1) And not just three days later, as is that (so far unsubstantiated) record among humans.
(2) And what man among us has never played with the idea of having his own breats?

[sphenisc]

(2) And what man among us has never played with the idea of having his own breats?

I think I can honestly say I've never played with the idea of having my own breats.









Well not until now..

[Belz...]

That’s just a few of the citations of mathematical models which show that combination selection pressures slow the evolutionary process.

Actually, they show that, when you kill off entire populations, they don't tend to reproduce.

Nice going.

[Belz...]

In the meantime, I’ll continue to post real examples of mutation and selection which shows that you are wrong.

You really are a liar, Kleinman. A chronic liar, too.

I think you need medical attention. Seriously.

[Paul C. Anagnostopoulos]

Yeah, sorry if that was the wrong letter. I was referring to the number of actual binding sites per creature (as opposed to the genome size).
Gamma is correct. I was just reading it as G.

~~ Paul

[Belz...]

Your argument that there are 10^500 alternative universes speaks for itself.

Why ? What's wrong with it, specifically ?

The number of selection conditions is the dominant parameter in the mutation and selection sorting/optimization process. This is clearly what ev is showing.

Don't you find it odd that it's only clear to you ?

[Belz...]

Perhaps if he wasn't so obsessed with the threat evolution poses to the Garden of Eden fairy tale, he'd have been able to concentrate sufficiently on his work to followed up on Mr. Powell's MRI and avoid his legal nightmare.

He's a real doctor, then ?

Well, I wouldn't want to consult him. Spending so much time on this thread must affect his work. Or vice-versa...


Patient: "I have a sharp pain here, now."
Klein: "Well, it seems your condition has beggaminased!"
Patient: "What ?"

[Belz...]

(2) And what man among us has never played with the idea of having his own breats?

Me.

You're disgusting! :p

[kjkent1]

You know, during Thanksgiving I had a premonition that Kleinman would resume this thread with a line like that. I think he's exhibiting some kind of pathological addictive OCD that compels him to provoke evolutionists. The stark evidence of this is how, on the very day his summary judgment in his malpractice case was reversed, he posted here to rant against evolution. I'd really like to know if Dr. Levin is aware of how many hours he spends at the clinic, on the payroll and using clinic computers for posting his creationist rants instead of caring for his patients. Perhaps if he wasn't so obsessed with the threat evolution poses to the Garden of Eden fairy tale, he'd have been able to concentrate sufficiently on his work to followed up on Mr. Powell's MRI and avoid his legal nightmare.

Here's a video summarizing that case: Powell v. Kleinman, M.D. (http://www.dailycasereport.com/index.php?q=adv_sheet_by_case/1395)

Overall, I must say this thread has been a great resource for explaining evolution theory and creationist pathology. I've learned more in this year on this than at any other time in my life, and am more confident than ever that I could argue creationists into a corner. Thanks, Alan!Well, I never thought that I'd discover a new way to earn Mandatory Continuing Legal Education (MCLE) credit in this thread.

Thank you, Mr. Scott -- you've actually managed to save me some time and money!

Oh, and thank you Dr. Kleinman for the quarter-hour worth of civil procedure credit!

ROFLMAO!

[kleinman]

Your argument that there are 10^500 alternative universes speaks for itself.To repeat myself for the umpteenth time, that particular argument is advanced by Dr. Leonard Susskind, Ph.D., Felix Bloch professor of physics, Stanford University. So, if you don't like the theory, then contact Susskind and take it up with him. Alternatively, you could discuss the issue with Sol (who, unless I'm very much mistaken, shares some of the same mental space with Dr. Susskind).
You are the one who raised this issue here. All you have to do is tell us how many of these 10^500 alternative universes you have visited.

I on the other hand am discussing Dr Schneider’s peer reviewed and published computer simulation of random point mutations and natural selection which I am assuming is correct. A parametric study of his model shows that the dominant parameter affecting the convergence of this sorting/optimization algorithm is the number of selection pressures. This is in complete agreement with the empirical data.
Well now Kotatsu, not only have you explained “Invasion of the Body Snatchers”, you have now explained why annelids are more evolutionarily advanced than humans.Well, as there are several thousand species of Annelids alive today, and only one species of human, I'd say that yes, yes they are more "evolutionary advanced". They can reproduce asexually, live at the bottom of the sea, or in a heavily polluted sludge. They can form cysts and virtually cease living when conditions are bad and then revive later on when conditions have improved (1). They can be both male and female at the same time (2), they can live in the earth or in glaciers.
There you go Kotatsu; you have just proven that annelids evolved from humans.
That’s just a few of the citations of mathematical models which show that combination selection pressures slow the evolutionary process.Actually, they show that, when you kill off entire populations, they don't tend to reproduce.
I guess you missed the lecture in your biology class where they tell you that there are no antiviral medications which kill the virus. They only impair the ability of the virus to reproduce. When are you evolutionists going to learn what a selection pressure is?
Yeah, sorry if that was the wrong letter. I was referring to the number of actual binding sites per creature (as opposed to the genome size).Gamma is correct. I was just reading it as G.
And neither G nor gamma are selection pressures. Keep at it though Sol, you can learn how ev works. Then perhaps you will learn how the mutation and selection sorting/optimization process actually works. And it doesn’t work in the irrational and illogical way that evolutionists allege.

[joobz]

You are the one who raised this issue here. All you have to do is tell us how many of these 10^500 alternative universes you have visited.

I on the other hand am discussing Dr Schneider’s peer reviewed and published computer simulation of random point mutations and natural selection which I am assuming is correct. A parametric study of his model shows that the dominant parameter affecting the convergence of this sorting/optimization algorithm is the number of selection pressures. This is in complete agreement with the empirical data.

There you go Kotatsu; you have just proven that annelids evolved from humans.

I guess you missed the lecture in your biology class where they tell you that there are no antiviral medications which kill the virus. They only impair the ability of the virus to reproduce. When are you evolutionists going to learn what a selection pressure is?

And neither G nor gamma are selection pressures. Keep at it though Sol, you can learn how ev works. Then perhaps you will learn how the mutation and selection sorting/optimization process actually works. And it doesn’t work in the irrational and illogical way that evolutionists allege.
why look at that. You never attempted to answer my questions. Will you now justify your assumptions or will you continue to be a scared man saying how you are only using Schneider's model?

[sol invictus]

And neither G nor gamma are selection pressures. Keep at it though Sol, you can learn how ev works. Then perhaps you will learn how the mutation and selection sorting/optimization process actually works. And it doesn’t work in the irrational and illogical way that evolutionists allege.

I see - so binding sites are not selection pressures in ev? That's interesting, because last time I looked at the code, it assigned mistake points for each missed site. Then it culled the population on the basis of those mistake points.

Hmm... sounds an awful lot like a selection pressure, doesn't it, kleinman?

Your position is totally incoherent. You believe that the weight assigned to each binding site IS a selection pressure, but somehow the individual binding sites themselves are not. Suppose ev allowed you to set weights for each individual binding site, rather than having a single equal weight for all of them. What would you call those weights?

[rocketdodger]

Holy sh-- ... Kleinman had a malpractice lawsuit filed against him!!!!!!!!!!!!!!!!!!!

Apparently the people on this thread aren't the only ones who find him to be incapable.

[Belz...]

I guess you missed the lecture in your biology class where they tell you that there are no antiviral medications which kill the virus. They only impair the ability of the virus to reproduce.

Well, gee, nothing kills viruses, then, because antibodies just impair the ability of the virus to reproduce.

[kleinman]

You never attempted to answer my questions. Will you now justify your assumptions or will you continue to be a scared man saying how you are only using Schneider's model?
I’m not scared of a silly alchemist. The only assumption I’m making with Dr Schneider’s ev computer simulation is that it is a valid representation of the mutation and selection sorting/optimization problem. I then did a parametric study with his model as he suggested in his publication on ev. Dr Schneider’s peer reviewed and published model of random point mutations and natural selection clearly shows that the number of selection conditions dominates the rate of convergence of his algorithm. This is in fact what happens in real cases of mutation and selection. Joobz, you should study the model and learn how the mutation and selection sorting/optimization process actually works.
And neither G nor gamma are selection pressures. Keep at it though Sol, you can learn how ev works. Then perhaps you will learn how the mutation and selection sorting/optimization process actually works. And it doesn’t work in the irrational and illogical way that evolutionists allege.I see - so binding sites are not selection pressures in ev? That's interesting, because last time I looked at the code, it assigned mistake points for each missed site. Then it culled the population on the basis of those mistake points.
You don’t have this right Sol. All you are doing when you increase the number of binding sites (gamma) is changing the fraction of the genome where not locating a match to the weight matrix is counted as a mistake. If you reduce gamma, then finding a match in that portion of the genome is now counted as a mistake. Here are the results of a series where I varied gamma and its effect on the rate of convergence. G=2048, mutation rate=1/G/generation, site width=6.
Gamma/Generations for Rs >= Rf
2/500000 stopped
3/500000 stopped
4/500000 stopped
5/79738
6/32553
7/75235
8/80923
9/32700
10/56148
11/14895
12/52949
13/22090
14/38615
15/54498
16/35486
17/49832
18/54845
19/26543
20/37769
40/19458
80/19613
160/19112
200/17910
All you are doing when changing gamma is changing the portion of the genome where you are sorting for or against a match of the weight matrix.
Hmm... sounds an awful lot like a selection pressure, doesn't it, kleinman?
It sounds like nothing of the kind and once you understand how ev works, you will realize this as well.
Your position is totally incoherent. You believe that the weight assigned to each binding site IS a selection pressure, but somehow the individual binding sites themselves are not. Suppose ev allowed you to set weights for each individual binding site, rather than having a single equal weight for all of them. What would you call those weights?
Again, it sounds incoherent to you because you don’t understand how ev works. The selection pressures in ev are simply based on matches of a weight matrix to a sequence of bases. In some cases these matches are considered mistakes and in other cases the lack of a match is considered a mistake.

The more complex you make the sorting conditions for ev, the more difficult you will make it for the algorithm to do the sort. Single selection conditions sort the most easily for the algorithm and this is reflected in real cases of mutation and selection. Here is a real example which demonstrates what ev shows mathematically.
http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed&cmd=Retrieve&list_uids=10697872 (http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed&cmd=Retrieve&list_uids=10697872)
Resistance to antimalarial drugs arises when spontaneously occurring mutants with gene mutations or amplifications which confer reduced drug susceptibility are selected, and are then transmitted. Simultaneous use of two or more antimalarials with different modes of action and which therefore do not share the same resistance mechanisms will reduce the chance of selection, because the chance of a resistant mutant surviving is the product of the parasite mutation rates for the individual drugs, multiplied by the number of parasites in an infection that are exposed to the drugs. The artemisinin derivatives are very active antimalarials, which produce large reductions in parasite biomass per asexual cycle, and reduce malaria transmissibility. To date no resistance to these drugs has been reported. These drugs therefore make particularly effective combination partners. This suggests that antimalarial drugs should not be used alone in treatment, but always in combination, as in the treatment of tuberculosis or HIV, and that the combination should include artemisinin or one of its derivatives.
Sol, you keep working at it and you will be able to understand how ev and the mutation and selection sorting/optimization process actually works.

[Kotatsu]

There you go Kotatsu; you have just proven that annelids evolved from humans.

How, if at all, does your mind work, Kleinman? There is nothing in what I wrote that would suggest that either group derived directly from the other. Given the most basic knowledge of the respective groups (1), what I wrote would actually suggest quite the opposite, as several of the characteristics mentioned cannot be found among mammals. This suggests that they are not closely related at all.

Also: any man who says he has never wanted a set of breats of his own is by lying. Real men want them. Now you know.

---
(1) And I believe this is where I give you too much credit.

[joobz]

I’m not scared of a silly alchemist. The only assumption I’m making with Dr Schneider’s ev computer simulation is that it is a valid representation of the mutation and selection sorting/optimization problem.
Then you have made a false assumption. because as I have clearly stated, selection pressures are neither constant in magnitude or number in real environments. And we know (because you like to reference the paper) that variably changing pressures can accelerate adaptation and thereby evolution.

that wasn't so hard now was it. And that was merely 2 of the faulty assumptions you've made. I do not even need to bother going over all the other ones.
Thank you for playing.

[rocketdodger]

Well, gee, nothing kills viruses, then, because antibodies just impair the ability of the virus to reproduce.

To be precise, though, isn't that killing a virus? Virii are so simple that their ability to reproduce is a necessary condition for them to be considered alive (unlike animals, which are obviously alive even if they can't reproduce anymore).

I could argue, if I wanted, that virii who can't reproduce are dead. I don't really care, though, because you and I and everyone who isn't an idiot knows I was talking about a population being destroyed, which can easily be done by greatly inhibiting the individuals' reproduction.

Kleinman, on the other hand, seems to think populations that can't reproduce 1) never die off, as if microorganisms are somehow immortal now, and 2) that mutation and selection can take place in the absence of reproduction. Go figure.

[Belz...]

Kleinman is in confirmation bias mode. Anything that disagrees with him is silly or somehow irrelevant. The rest he can safely misinterpret.

[Belz...]

To be precise, though, isn't that killing a virus? Virii are so simple that their ability to reproduce is a necessary condition for them to be considered alive (unlike animals, which are obviously alive even if they can't reproduce anymore).

I wanted to point that out, but then I wished to avoid whatever crap Kleinman was going to answer.

He clearly doesn't understand any science at all, anyway.

[rocketdodger]

The only assumption I’m making with Dr Schneider’s ev computer simulation is that it is a valid representation of the mutation and selection sorting/optimization problem.

I find it interesting that you would say this, Kleinman, after you have said:

Rocketwhomissesthetarget, all selection pressures impair the fitness of a population to reproduce.

I could be wrong, but I seem to recall that in ev population size is held constant for the duration of a run. So even though it doesn't, according to you, model reality at all in this respect, you find it to be a valid representation?

[kleinman]

There you go Kotatsu; you have just proven that annelids evolved from humans.How, if at all, does your mind work, Kleinman? There is nothing in what I wrote that would suggest that either group derived directly from the other. Given the most basic knowledge of the respective groups (1), what I wrote would actually suggest quite the opposite, as several of the characteristics mentioned cannot be found among mammals. This suggests that they are not closely related at all.
So when you said this;
.Well, as there are several thousand species of Annelids alive today, and only one species of human, I'd say that yes, yes they are more "evolutionary advanced". They can reproduce asexually, live at the bottom of the sea, or in a heavily polluted sludge. They can form cysts and virtually cease living when conditions are bad and then revive later on when conditions have improved (1). They can be both male and female at the same time (2), they can live in the earth or in glaciers.
You weren’t talking about common descent? Kotatsu, your weird connections you make with your phylogenic trees ignores the mathematical and empirical facts of how mutation and selection actually works.
I’m not scared of a silly alchemist. The only assumption I’m making with Dr Schneider’s ev computer simulation is that it is a valid representation of the mutation and selection sorting/optimization problem.Then you have made a false assumption. because as I have clearly stated, selection pressures are neither constant in magnitude or number in real environments. And we know (because you like to reference the paper) that variably changing pressures can accelerate adaptation and thereby evolution.
The only thing you have clearly stated is this:
If there was a "sticky" thread on drug delivery, biomaterials or polymer chemistry, I'd be there instantly.But evolution isn't my field.
So when it comes to whose claims to accept, Dr Schneider, the peer reviewed and published author of ev who many times has claimed his model simulates reality, or you who admits that evolution isn’t your field, I’ll accept Dr Schneider’s claim on this topic over you any day. If you think you have a valid criticism of Dr Schneider’s model, you should contact him at toms@ncifcrf.gov (toms@ncifcrf.gov?subject=Tom%20Schneider's%20Home %20Page%20(index.html)) , he is an ardent defender of his computer simulation. In the meantime, I’ll continue to post citations of what his model shows mathematically, that is the mutation and selection sorting/optimization problem is profoundly slowed by combination selection pressures. Here is another citation which demonstrates this very behavior.
http://aac.asm.org/cgi/content/full/43/6/1497?ck=nck (http://aac.asm.org/cgi/content/full/43/6/1497?ck=nck)
The target of all rifamycins is the DNA-directed RNA polymerase, mostly the -subunit encoded by the rpoB gene (4). An amino acid exchange encoded in a 69-bp region (codons 511 to 533) of the rpoB gene in mycobacteria (7, 12) or in codons 507 to 533, 563 to 572, and 687 in Escherichia coli (9) induces resistance. For different bacteria, rpoB mutations have been described (1-3, 6, 11, 13). It was shown that a triple therapy containing RBU is effective in the eradication of H. pylori after the failure of other therapies and in spite of resistance to other antibiotics (8). The success rate of a combination of 40 mg of pantoprazole twice daily, 1 g of amoxicillin twice daily, and 400 mg of RBU once daily was 78.6%. Because no resistant clinical isolates in Germany were identified (n = 81), resistant mutants were selected by serial passage in vitro of H. pylori ATCC 43504 and analyzed for mutations in the rpoB gene in this study.

[Myriad]

Folks, I'd suggest leaving the malpractice lawsuit out of this discussion.

It's not on topic, and furthermore the suit itself does not appear to have a great deal of merit. One judge summarily dismissed it, an appeals judge disagrees, but overall my (non-professional, either in medicine or law) impression is still that the case is weak.

Even if the plaintiff wins the case in the end, one oversight, even a tortious one, does not imply professional incompetence. That's why all MDs, even the best ones, pay for malpractice insurance.

Plus, there's remarkably little evidence that the person you're corresponding with in this thread is actually Alan Kleinman, MD. I've worked with MDs and have close relatives who are MDs, and in talking to any of them, bits of medical terminology and points of medical expertise leak into their conversation. The same is true for the MDs who post in these forums. Not so with our Dr. Kleinman. Not a trace of professional medical knowledge in any of his posts.

Respectfully,
Myriad

[kjkent1]

You are the one who raised this issue here. All you have to do is tell us how many of these 10^500 alternative universes you have visited.This is the typical response of someone who has serious self esteem issues. You tell me I raised the issue, and then you "pronounce" the only means by which I may redeem myself -- as if only you are in a position to judge the validity of other views.

I don't have to do sh__ at your command, Alan. However, I think it's fair to suggest that the amount of time you spend arguing nonsense here, indicates that you are not concentrating on your patients -- and that the result of that cavalier attitude will very likely end in your loss of licensure.

I on the other hand am discussing Dr Schneider’s peer reviewed and published computer simulation of random point mutations and natural selection which I am assuming is correct. A parametric study of his model shows that the dominant parameter affecting the convergence of this sorting/optimization algorithm is the number of selection pressures. This is in complete agreement with the empirical data.Your parametric study is flawed, because it depends on your insertion of an invalid parameter -- a parameter which, at the extreme causes a random arranged genome to be reported as a "perfect creature."

It takes a certain kind of "irrational exuberance" to be able to willfully fail to recognize an error of such striking proportion.

[rocketdodger]

Folks, I'd suggest leaving the malpractice lawsuit out of this discussion.

It's not on topic, and furthermore the suit itself does not appear to have a great deal of merit. One judge summarily dismissed it, an appeals judge disagrees, but overall my (non-professional, either in medicine or law) impression is still that the case is weak.

Even if the plaintiff wins the case in the end, one oversight, even a tortious one, does not imply professional incompetence. That's why all MDs, even the best ones, pay for malpractice insurance.

Plus, there's remarkably little evidence that the person you're corresponding with in this thread is actually Alan Kleinman, MD. I've worked with MDs and have close relatives who are MDs, and in talking to any of them, bits of medical terminology and points of medical expertise leak into their conversation. The same is true for the MDs who post in these forums. Not so with our Dr. Kleinman. Not a trace of professional medical knowledge in any of his posts.

Respectfully,
Myriad

Please do not be offended by my post Myriad. I know how frivolous malpractice suits are these days and I would never judge a doctor based on anecdotal evidence that someone has filed one against them.

My post was in jest -- I am convinced that whoever is behind the screen name "Kleinman" in this thread is definitely not a real doctor nor a real engineer. He/she has offered me zero proof of those claims other than "I already posted my references somewhere, go find them yourself."

Furthermore, as you point out, there is no way in hell any state in my country would let someone like this become a professional doctor or engineer. I dare say there is no way such a fool could get into grad school, never mind complete it.

My post was just a poke, implying that it is kind of ironic that the persona "Kleinman" choose to fraudulently impersonate had a malpractice suit filed against him.

BTW, further evidence that this real Kleinman is not our "Kleinman" is the fact that the real Kleinman seems to specialize in neurobiology -- he wrote a book on mental health around the world and the content of the lawsuit Mr. Scott pointed out seems to deal with spinal cord health or something along those lines.

[Mr. Scott]

Plus, there's remarkably little evidence that the person you're corresponding with in this thread is actually Alan Kleinman, MD. I've worked with MDs and have close relatives who are MDs, and in talking to any of them, bits of medical terminology and points of medical expertise leak into their conversation. The same is true for the MDs who post in these forums. Not so with our Dr. Kleinman. Not a trace of professional medical knowledge in any of his posts.


Dr. Kleinman is the topic of this thread. He is the "Annoying Creationist" who inspired the original post.

There is considerable evidence that the Dr. Alan Kleinman of this thread is the same as the Dr. Alan Kleinman of the malpractice suit in my earlier post, and that our Krazy Kreationist wants us to know exactly who he is. He in fact derides those on JREF who don't post under their real names. The evidence is buried in this 6000+ post thread, in which Kleinman, among other things, called a small child he stitched up a "whining crybaby" like us evolutionists. He is, indeed, a practicing medical doctor and wants us to know it. Any medical knowledge he has that conflicts with creationist doctrine he dismisses, which makes me wonder if in some areas, like the evolution of the spine and its consequences, his expertise is compromised.

The specific person who inspired this thread is, indeed, on topic, though I don't plan to dwell on it.

[Kotatsu]

So when you said this;You weren’t talking about common descent?

Um, no? Whatever gave you that idea. I wrote that they were more "evolutionary advanced", by which I mean that annelids, as a group, are more successful, flexible and versatile than humans, as a group, are. How you get this to imply that annelids are descended from humans, I have no idea.

[Mr. Scott]

further evidence that this real Kleinman is not our "Kleinman" is the fact that the real Kleinman seems to specialize in neurobiology

No that's Joel Kleinman. Our friend here is Alan Kleinman. The evidence is buried in this thread (which I've followed since post #1) and the thread on the "evolutionisdead" forum, which I've browsed.

[rocketdodger]

No that's Joel Kleinman. Our friend here is Alan Kleinman. The evidence is buried in this thread (which I've followed since post #1) and the thread on the "evolutionisdead" forum, which I've browsed.

...but...but....he is so.....I don't even have a word for it...

The only explanation for the behavior we have seen, from an individual who supposedly went through grad school and got an M.D., is a degrading mental illness.

If that is your diagnosis, then I might agree. I do not think a healthy person could exhibit such a duality in cognitive ability.

[Mr. Scott]

remember google is watching you

Yes, Dr. Kleinman, we all know google is watching. However, the thread between you and Paul on the "evolutionisdead" forum is now a dead link. That creationists chose to erase your arguments but evolutionists continue to provoke them is food for thought.

[kleinman]

You are the one who raised this issue here. All you have to do is tell us how many of these 10^500 alternative universes you have visited.This is the typical response of someone who has serious self esteem issues. You tell me I raised the issue, and then you "pronounce" the only means by which I may redeem myself -- as if only you are in a position to judge the validity of other views.
Don’t tell me you are one of those “self esteem” crybabies?
I on the other hand am discussing Dr Schneider’s peer reviewed and published computer simulation of random point mutations and natural selection which I am assuming is correct. A parametric study of his model shows that the dominant parameter affecting the convergence of this sorting/optimization algorithm is the number of selection pressures. This is in complete agreement with the empirical data.Your parametric study is flawed, because it depends on your insertion of an invalid parameter -- a parameter which, at the extreme causes a random arranged genome to be reported as a "perfect creature."
Sorry to hurt your “self esteem” but Dr Schneider clearly said the following in his paper on ev;
http://nar.oxfordjournals.org/cgi/content/full/28/14/2794 (http://nar.oxfordjournals.org/cgi/content/full/28/14/2794)
Variations of the program could be used to investigate how population size, genome length, number of sites, size of recognition regions, mutation rate, selective pressure, overlapping sites and other factors affect the evolution.
I added the highlighting so as not hurt your “self esteem”. Now kjkent1, I have gone out of my way not to hurt your “self esteem”, now the least you could do for us is tell us what it is like in those 10^500 alternative universes.
So when you said this;You weren’t talking about common descent?Um, no? Whatever gave you that idea. I wrote that they were more "evolutionary advanced", by which I mean that annelids, as a group, are more successful, flexible and versatile than humans, as a group, are. How you get this to imply that annelids are descended from humans, I have no idea.
So the annelids are on a higher branch of your phylogenic tree?
remember google is watching youYes, Dr. Kleinman, we all know google is watching. However, the thread between you and Paul on the "evolutionisdead" forum is now a dead link. Why creationists chose to erase your arguments but evolutionists continue to provoke them is food for thought.
Google isn’t the only One watching or is that one of the lies your parents told you.

This interesting discussion warrants another example of mutation and selection which shows that combination selection pressures slow the evolutionary process.
http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed&cmd=Retrieve&list_uids=11196485 (http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed&cmd=Retrieve&list_uids=11196485)
The development of resistance to drugs poses one of the greatest threats to malaria control. In Africa, the efficacy of readily affordable antimalarial drugs is declining rapidly, while highly efficacious drugs tend to be too expensive. Cost-effective strategies are needed to extend the useful life spans of antimalarial drugs. Observations in South-East Asia on combination therapy with artemisinin derivatives and mefloquine indicate that the development of resistance to both components is slowed down. This suggests the possibility of a solution to the problem of drug resistance in Africa, where, however, there are major obstacles in the way of deploying combination therapy effectively. The rates of transmission are relatively high, a large proportion of asymptomatic infection occurs in semi-immune persons, the use of drugs is frequently inappropriate and ill-informed, there is a general lack of laboratory diagnoses, and public health systems in sub-Saharan Africa are generally weak. Furthermore, the cost of combination therapy is comparatively high. We review combination therapy as used in South-East Asia and outline the problems that have to be overcome in order to adopt it successfully in sub-Saharan Africa.

[Myriad]

Yes, Dr. Kleinman, we all know google is watching. However, the thread between you and Paul on the "evolutionisdead" forum is now a dead link. That creationists chose to erase your arguments but evolutionists continue to provoke them is food for thought.


Interesting. It looks like the whole Information Theory subforum (all but 2 threads) at EiD got wiped out at some point. Probably not deliberately, and it's very unlikely that Kleinman's thread was singled out. Maintenance there has always been a little dodgy.

Respectfully,
Myriad

[Mr. Scott]

google is watching you

I think Kleinman sees his year on this thread as an exercise in google bombing and little else.

[rocketdodger]

Sorry to hurt your “self esteem” but Dr Schneider clearly said the following in his paper on ev;
http://nar.oxfordjournals.org/cgi/content/full/28/14/2794


Variations of the program could be used to investigate how population size, genome length, number of sites, size of recognition regions, mutation rate, selective pressure, overlapping sites and other factors affect the evolution.

Kleinman, seriously, pull your head out of your a--.

A VARIATION of a program is not "an identical program with different input."

A VARIATION is a DIFFERENT program that can be shown to be based on the original program.

If you have modified any of the source code of ev, leading to a VARIATION, then please show us what you did. I DARE YOU.

[kleinman]

If you have modified any of the source code of ev, leading to a VARIATION, then please show us what you did. I DARE YOU.
I didn’t have to rocketwhomissesthetarget. Paul did it for me. Now I DOUBLE-DARE YOU to show n+1 selection pressures evolve more quickly than n selection pressures. Wait, make that a TRIPLE-DARE YOU. And while you are hitting your head against the wall, let’s amuse ourselves with another citation which shows that combination selection pressures profoundly slow the mutation and selection sorting/optimization process.
http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed&cmd=Retrieve&list_uids=11132385 (http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed&cmd=Retrieve&list_uids=11132385)
Following a marked decline in the efficacy in vivo of mefloquine between 1990 and 1994, a combination of artesunate (4 mg/kg/d for 3 d) and mefloquine (25 mg/kg) has been used as first line treatment of uncomplicated falciparum malaria in camps for displaced persons located along the north-western border of Thailand. Antimalarial drug susceptibility of fresh isolates of Plasmodium falciparum from this population was evaluated using a radioisotope microdilution assay between 1995 and 1999. In total, 268 isolates were collected, of which 189 were from primary infections and 79 from recrudescent infections. The geometric mean 50% inhibitory concentration (IC50) values from primary infections were: dihydroartemisinin 1.2 ng/mL, artesunate 1.6 ng/mL, artemether 4.8 ng/mL, atovaquone 0.4 ng/mL, lumefantrine 32 ng/mL, chloroquine 149 ng/mL, quinine 354 ng/mL, mefloquine 27 ng/mL and halofantrine 4.1 ng/mL. A significant positive correlation was found between the susceptibility in vitro to artesunate and quinine (r = 0.43, P < 0.001), mefloquine (r = 0.46, P < 0.001), and halofantrine (r = 0.51, P < 0.001). These levels of resistance in vitro are among the highest reported and confirm continuing high level multidrug resistance in this area. Despite intensive use of the combination between 1995 and 1999 there has been a significant improvement in mefloquine sensitivity (P < 0.001) and artesunate sensitivity (P < 0.001). This supports observations in vivo that the combination of artesunate and mefloquine has reversed the previous decline in mefloquine sensitivity.

[joobz]

So when it comes to whose claims to accept, Dr Schneider, the peer reviewed and published author of ev who many times has claimed his model simulates reality, or you who admits that evolution isn’t your field, I’ll accept Dr Schneider’s claim on this topic over you any day.
And your acceptance of his model isn't in question. In fact, this is a bizarre non-sequitor. Also, you should point out my admittedly novice understanding of evolution. It only makes you look more foolish. Indeed, as a lay person, for me to find such glaringly stupid errors on your part only demonstrates how wrothless your entire argument is. Is that really what you want people to see?

So, Are you going to answer my question or will you give another nonsequitor evasion and continue to be a silly child?

[Myriad]

Dr. Kleinman is the topic of this thread. He is the "Annoying Creationist" who inspired the original post.


I thought someone might point that out... :p However, I'm not sure that whether or not he's Dr. Kleinman, or a doctor, or an effective doctor, has any bearing on how annoying he is. I could be wrong...

There is considerable evidence that the Dr. Alan Kleinman of this thread is the same as the Dr. Alan Kleinman of the malpractice suit in my earlier post, and that our Krazy Kreationist wants us to know exactly who he is.


Well, I'd say he wants us to think that we know who he is. Claiming that he points out his identity begs the question of whather he's telling the truth about that identity.

He in fact derides those on JREF who don't post under their real names.


Yep. In fact he derides those on JREF for doing all kinds of things that he does himself. Such as having difficulty understanding simple math. Given his evident propensity for doing so, in fact, I'd sat that his deriding other posters for not using their real names is evidence in favor of the hypothesis that he's not using his own.

The evidence is buried in this 6000+ post thread, in which Kleinman, among other things, called a small child he stitched up a "whining crybaby" like us evolutionists. He is, indeed, a practicing medical doctor and wants us to know it. Any medical knowledge he has that conflicts with creationist doctrine he dismisses, which makes me wonder if in some areas, like the evolution of the spine and its consequences, his expertise is compromised.


Again, he certainly wants us to think it but that's as far as the evidence goes. I have followed the whole thread, and was active in the precursor EvolutionIsDead thread well over a year ago. I vaguely remember the stiched-up child story, and as I recall it was not convincing. It lacked any authentic detail. There was nothing in it that set off "this couldn't possibly be an M.D." alarm bells but it was the kind of anecdote that someone just imagining in his head what a doctor does all day would likely make up. For example, a pediatrician or general/family practitioner (and who else would be stitching up an injured child? Dr. K is too old to be an ER resident, and his main practice is listed as Occupational Medicine, so if he's treating a child at all it would most likely be in a health clinic setting acting as a GP) probably sees a lot more children being whining crybabies about getting vaccination shots than about getting stitches. Wouldn't one of those examples have made his point better? By contrast, many children are quite brave when it comes to serious injury (though of course, there are all kinds and he might have lucked into the whining one that day).

The specific person who inspired this thread is, indeed, on topic, though I don't plan to dwell on it.


I don't mind anyone talking about our Dr. Kleinman all you want. My only concern was the malpractice suit, and the likely possibility that discussing it is dragging some total stranger's dirty laundry through a public forum.

Respectfully,
Myriad

[rocketdodger]

I didn’t have to rocketwhomissesthetarget. Paul did it for me.

Err... no, he didn't... because he has been telling you that his additions aren't meant to show what you contend they show.

It is only your utterly unmatched foolishness that leads you to think you know, better than the very programmer who wrote the code, what the code represents.

Now I DOUBLE-DARE YOU to show n+1 selection pressures evolve more quickly than n selection pressures. Wait, make that a TRIPLE-DARE YOU.

I did, within the context of my own program. Adequate has done so within the context of his. We all have shown you in the context of the ev program. You will undoubtedly respond to these statements in a childish way, demanding the evidence and presenting obsolete quotes from Adequate and I, but everyone knows such a response is nothing more than a pathetic diversion from a sad creature who has run out of options.

It is interesting to note that although you consistently state that we are all wrong you have also consistently failed to show us why.

[joobz]

I thought someone might point that out... :p However, I'm not sure that whether or not he's Dr. Kleinman, or a doctor, or an effective doctor, has any bearing on how annoying he is. I could be wrong...

Well, I'd say he wants us to think that we know who he is. Claiming that he points out his identity begs the question of whather he's telling the truth about that identity.

Yep. In fact he derides those on JREF for doing all kinds of things that he does himself. Such as having difficulty understanding simple math. Given his evident propensity for doing so, in fact, I'd sat that his deriding other posters for not using their real names is evidence in favor of the hypothesis that he's not using his own.

Again, he certainly wants us to think it but that's as far as the evidence goes. I have followed the whole thread, and was active in the precursor EvolutionIsDead thread well over a year ago. I vaguely remember the stiched-up child story, and as I recall it was not convincing. It lacked any authentic detail. There was nothing in it that set off "this couldn't possibly be an M.D." alarm bells but it was the kind of anecdote that someone just imagining in his head what a doctor does all day would likely make up. For example, a pediatrician or general/family practitioner (and who else would be stitching up an injured child? Dr. K is too old to be an ER resident, and his main practice is listed as Occupational Medicine, so if he's treating a child at all it would most likely be in a health clinic setting acting as a GP) probably sees a lot more children being whining crybabies about getting vaccination shots than about getting stitches. Wouldn't one of those examples have made his point better? By contrast, many children are quite brave when it comes to serious injury (though of course, there are all kinds and he might have lucked into the whining one that day).

I don't mind anyone talking about our Dr. Kleinman all you want. My only concern was the malpractice suit, and the likely possibility that discussing it is dragging some total stranger's dirty laundry through a public forum.

Respectfully,
Myriad
Interesting. Actually, I did find it odd that he kept referring to his "published thesis" rather than his actual peer reviewer journal articles as proof of his credentials. Any PhD I know would rather brag about the # of pubs with a # of citations rather than their solitary thesis. Most of the time, the papers generated by the thesis are a better indicator of the thesis quality.

Nah, I have no problem thinking he his what he says he is. There are people with MDs and PhDs that don't deserve them. I don't think he's any worse than they are.

[kleinman]

Dr. Kleinman is the topic of this thread. He is the "Annoying Creationist" who inspired the original post.I thought someone might point that out... However, I'm not sure that whether or not he's Dr. Kleinman, or a doctor, or an effective doctor, has any bearing on how annoying he is. I could be wrong...
You are the same Myriad that claimed he could get ev to converge more quickly by giggling, oops jiggling the weight factors? Well you were correct, jiggle two of the three weight factors to zero and ev can evolve the remaining selection condition in a trivially small number of generations. That’s the key to the mathematics of the mutation and selection sorting/optimization problem. It is the multiple selection conditions which slows the convergence of ev. It works that way in reality as well.
I didn’t have to rocketwhomissesthetarget. Paul did it for me.Err... no, he didn't... because he has been telling you that his additions aren't meant to show what you contend they show.
Of course it wasn’t Paul’s intention to disprove the theory of evolution but such is life, the changes he made show just that. They demonstrate that combination selection pressures profoundly slow the mutation and selection sorting/optimization problem.
Now I DOUBLE-DARE YOU to show n+1 selection pressures evolve more quickly than n selection pressures. Wait, make that a TRIPLE-DARE YOU.I did, within the context of my own program. Adequate has done so within the context of his. We all have shown you in the context of the ev program. You will undoubtedly respond to these statements in a childish way, demanding the evidence and presenting obsolete quotes from Adequate and I, but everyone knows such a response is nothing more than a pathetic diversion from a sad creature who has run out of options.
Oh, that’s right; you proved your contention with the following:
I found a combination of parameters last night that led to over 100 pressures being faster than a single one, but I forgot what it was http://forums.randi.org/images/smilies/frown.gif
And Adequate made his point with the following (I prefer to think of his quote as an oldie but goodie, not obsolete):
The red line shows generations to achieve fixation of n alleles acted on by n selection pressures, the n+1th selection pressure being introduced only after the nth allele is fixed.

The blue line shows generations to achieve fixation of n alleles acted on by n selection pressures simultaneously.

All other features and parameters of the two models are identical. The model is designed so that the relative advantage of n+1 new genes over n (when selection is acting) is the same for all n, i.e. each new allele carries the same advantage.

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
And then Adequate goes on to say this:
More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.
http://forums.randi.org/images/smilies/doglaugh.gif
Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?
And
So far as I know, no-one has done the experiment.
and
and too bad you don’t have any empirical examples of your silly graph ...[quote="Adequate"]As I have explained to you, I produced the model because I've not heard of this precise experiment being done.
So what are my options since you evolutionists have made such a convincing argument that n+1 selection conditions evolve more quickly than n conditions? It’s simple! Post more examples of how mutation and selection works in reality. I know how much you evolutionists love to read these citations.
http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed&cmd=Retrieve&list_uids=11491008 (http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed&cmd=Retrieve&list_uids=11491008)
[quote="Resistance of Plasmodium falciparum to antimalarial drugs in a highly endemic area of southern Viet Nam: a study in vivo and in vitro."] To assess the antimalarial sensitivity of Plasmodium falciparum in vivo and in vitro in a highly endemic area of southern Viet Nam, a field study was conducted (in 1999) at a rubber plantation in Binh Phuoc Province north of Ho Chi Minh City. Fifty patients were treated with either artesunate (4 mg/kg on day 0, then 2 mg/kg on day 1 to 4) or mefloquine (10 mg/kg at 0 h, then 5 mg/kg at 6 h), and their progress was followed for 28 days under standard WHO protocols. Blood spots were taken at baseline from all patients, as well as from those who redeveloped parasitaemia during follow-up, for polymerase chain reaction (PCR) determination of parasite genotypes to assist differentiation of re-infection from recrudescence. Both treatments cleared parasites within 5 days. Of the 25 mefloquine-treated patients, 2 (8%) re-presented with probable re-infections. For artesunate, 4 patients (16%) had re-infections and 5 (20%) had recrudescences. Sensitivity tests in vitro of pre-treatment P. falciparum isolates showed geometric mean IC50 values of 29, 38, 209 and 15 nmol/L for chloroquine (n = 32), mefloquine (n = 33), quinine (n = 31) and artemisinin (n = 31), respectively. There were significant correlations between IC50s for artemisinin and mefloquine (r = 0.72, P = 0.004), and chloroquine and quinine (r = 0.44, P = 0.05). These data show that, although mefloquine has been used for 10 years in Binh Phuoc Province, it remains fully effective, perhaps because an artemisinin derivative is commonly given at the same time. The recrudescence rate for artesunate is similar to those reported in other epidemiological contexts. The present in-vitro data imply that quinine remains effective and that reduced drug pressure has been associated with increased sensitivity of local strains of P. falciparum to chloroquine. Although from one hyperendemic area, these results may have implications for antimalarial prophylaxis and treatment strategies for residents and travellers to southern Viet Nam.

[rocketdodger]

rofl

[sol invictus]

You don’t have this right Sol. All you are doing when you increase the number of binding sites (gamma) is changing the fraction of the genome where not locating a match to the weight matrix is counted as a mistake. If you reduce gamma, then finding a match in that portion of the genome is now counted as a mistake. Here are the results of a series where I varied gamma and its effect on the rate of convergence. G=2048, mutation rate=1/G/generation, site width=6.

For once you're saying something that's almost correct, although I've already pointed it out. As I said before, gamma is not exactly the number of selection pressures because of the effect you refer to here. However when gamma*site width is small compared to G, this effect is irrelevant.

I don't have time now for a more complete post - that will follow later.

[kleinman]

You don’t have this right Sol. All you are doing when you increase the number of binding sites (gamma) is changing the fraction of the genome where not locating a match to the weight matrix is counted as a mistake. If you reduce gamma, then finding a match in that portion of the genome is now counted as a mistake. Here are the results of a series where I varied gamma and its effect on the rate of convergence. G=2048, mutation rate=1/G/generation, site width=6. For once you're saying something that's almost correct, although I've already pointed it out. As I said before, gamma is not exactly the number of selection pressures because of the effect you refer to here. However when gamma*site width is small compared to G, this effect is irrelevant.

I don't have time now for a more complete post - that will follow later.
You still don’t have it correct Sol. It is totally relevant. If you hold gamma*site width constant and increase G, the generations for convergence increases exponentially. Try running a series of cases where you do this, it would be educational for you. What you will find is that it is the mistakes in the non-binding site region which slow the convergence. What is happening is the search space for the local optimum is increasing at 4^G. The only way to reduce the size of the search space is to reduce the portion of the genome subject to selection. This is why combination therapy works in the real world. Therapy which targets a single gene is only applying selection pressure against a small portion of the genome. Adding additional selection pressures to other portions of the genome confounds the populations’ ability to find a trajectory that would satisfy all the selection conditions. This is the nature of the sorting/optimization problem and this is why the theory of evolution is mathematically impossible. You can’t transform entire genome simultaneously. It is mathematically impossible to transform hundreds of genes simultaneously by the mutation and selection sorting/optimization process. It is only barely possible to transform two genes simultaneously. As you continue your studies with ev, you will learn this.

It’s been another fun week discussing the theory of evolution with you evolutionists; I leave you until next week when we can continue this interesting and informative discussion. Here for your enjoyment is another citation which shows that the mutation and selection sorting/optimization problem is profoundly slowed by combination selection pressures.

Effectiveness of Antimalarial Drugs
J Kevin Baird. The New England Journal of Medicine. Boston: Apr 14, 2005. Vol. 352, Iss. 15; pg. 1565, 15 pgs
Combined therapies, which constitute a widely practiced strategy in the treatment of diseases such as leprosy, tuberculosis, and infection with the human immunodeficiency virus and which have long been known to be effective against malaria,110 have rarely been used in its treatment until recently.111 The use of more than one agent successfully requires separate mechanisms of action against the same stage of the parasite. Thus, because both sulfadoxine and pyrimethamine are folate antagonists, they would not be considered a combined therapy. Similarly, combining a blood-stage schizonticide with primaquine is not considered combined therapy, because the drugs attack different stages of the parasite. The fixed combination of atovaquone-chloroguanide, which affects mitochondrial electron transport and folate metabolism in asexual blood stages, represents true combination therapy.112

Combined antimalarial therapies include old and new drugs - old drugs in new combinations (chloroquine and sulfadoxine-pyrimethamine), an old drug combined with a new drug (amodiaquine and artesunate), and new drugs in combination (lumefantrine and artemether).113,114 Combination therapy that includes artemisinin appears to be potent and particularly useful in endemic regions; extracted from the weed Artemesia annua, the artemisinins (primarily artemether, artesunate, and dihydroartemisinin) were developed in China during the 1960s.

The artemisinins act very rapidly, reducing parasitemia by a factor of 10^sup 4^ with each cycle. Thus, for a parasite burden in the range of 10^sup 12^, only three cycles are required to abolish parasitemia. The artemisinins are rapidly eliminated, and daily administration for a period of seven days (three cycles) is required. Episodes of recrudescence follow briefer regimens, but a seven-day regimen is considered to be impractical. Therefore, treatment for a period of three days with artemisinin combined with a slowly eliminated companion blood-stage schizonticide has been adopted. This three-day regimen of artemisinin reduces the parasite burden by a factor of 10^sup 8^ (leaving only 0.000001 percent of parasites surviving to be abolished by mefloquine) (Fig. 3). The artemisinins also exert activity against gametocytes, reducing the probability of transmission.

The use of combination therapies with artemisinin does not preclude the onset of drug resistance, particularly since patients may not take the medication as directed. Thus, the multiple doses needed with such combined therapies (typically six doses over a period of three days) represent an important potential pitfall. The emergence of resistant strains may already be in progress. In vitro studies indicate diminished susceptibility to artesunate among Asian isolates.41 Isolates from western Cambodia, where combination therapies with artemisinin derivatives are widely used, show diminished susceptibility to the combination of mefloquine and artesunate, as compared with isolates from eastern Cambodia.115 In contrast, in the 1990s in some regions bordering western Thailand, combination therapies with artemisinin derivatives were deployed as first-line therapy with excellent efficacy (more than 90 percent), and this success appears to be stable.116 Where more resources are available, including medications, resistant strains have been slower to develop. Where both medication and an effective health care infrastructure are present, resistance can be controlled. Such economic and personnel issues may explain the contrasting findings with regard to rates of resistance to combination therapies with artemisinin derivatives.117 Thus, supplying these therapies in the setting of an adequate health care infrastructure would seem the best way to prevent the onset of resistance.
You all have a good weekend.

[joobz]

I leave you until next week when we can continue this interesting and informative discussion.
Discussion requires interactivity. I have yet to see you actually contribute something useful or new or actually respond to any question.

How many times have I asked for the exact same thing, and each time you are simply to afraid to do it. Why are you so afraid?

[Dr Adequate]

So, has kleinman done anything new this week?

[Paul C. Anagnostopoulos]

You don’t have this right Sol. All you are doing when you increase the number of binding sites (gamma) is changing the fraction of the genome where not locating a match to the weight matrix is counted as a mistake.
True, but you are also increasing the number of mistake points that can be assigned when bindings are missed. One could, as Sol suggested, have a separate mistake point spinner for each binding site, allowing the user to assign more mistakes points to sites closer to the gene and fewer mistake points to sites farther away (for example). Would we now say that we had gamma + 2 pressures instead of just 3? Why not?

~~ Paul

[rocketdodger]

So, has kleinman done anything new this week?

Nope. Just more out of context and misinforming repostings of the honest statements you and I have made regarding the limitations of our programs, followed by that ******* laughing dog gif.

As usual, we put forth valid questions and counter-arguments, and he responds by "throwing feces at the keyboard" as joobz would say.

[PBTree]

Even as a lay person, I love this thread. I make sure that everyday I come in and read where we are up to. I am still confused though.

Is the argument:

Evolutionists state that evolution is the only way it could have happened but don't know all of the answers, and;

now that the creationists have been shown that evolution is the only way, they have decided the un-answered questions are all due to to some made up chap called god?


More than happy to accept a good slapping and told to p..s off if I am interfering in a good old scientific broohaha.

[Olowkow]

Looks more like a lot of "obsfuctating" non science to me...but what do I know?
It all comes down to how much stuff (sheer tonnage) could you fit on Noah's ark? (do the calculations for goodness sake) let alone catch and corral and feed all these millions of species. Just sit down and watch National Geographic shows about the Galapagos sometime...remarkable instances of evolution and adaptation. Obvious! Trying to prove evolution could not have happened is pointless, masturbatory, theistic (and, yes, annoying) thinking, and vicious verbosity is not going to change that.
I am not an expert in evolution nor a mathematician, but I do know that a proof in math is either right or wrong, no in between. Just like electronics, you plug it in and it works or it doesn't. The god stuff never works.

[kjkent1]

Even as a lay person, I love this thread. I make sure that everyday I come in and read where we are up to. I am still confused though.

Is the argument:

Evolutionists state that evolution is the only way it could have happened but don't know all of the answers, and;

now that the creationists have been shown that evolution is the only way, they have decided the un-answered questions are all due to to some made up chap called god?


More than happy to accept a good slapping and told to p..s off if I am interfering in a good old scientific broohaha.The argument is simply that there is an incredible amount of geological, fossil, genetic, radiologic, mathematical, etc. evidence supporting mutation and selection as the means by which the variety of modern biological life forms appear on Earth.

Along comes Alan M. Kleinman, PhD, M.D., who summarily declares that because (1) a computer model, called ev, cannot evolve its programmed genome using only random point mutation in a number of generations sufficient to permit evolution to have occured in the amount of time which has passed since life first arose, and (2) because there are lots of studies which show that if a virus, bacteria or parasite is attacked by several strong toxins at once, that resistance will develop more slowly than if the attack is conducted with only one strong toxin; that, evolution is thus impossible, and therefore, God is responsible for the variety of life.

So, all of us frustrated thinkers lob shells at Alan between Sunday and Thursday, and he skillfully dodges them by judging us as a bunch of brainwashed "evolushunists" who must soon come to Jesus or be roasted on the spit of Satan for all eternity.

Kind of makes us all a little weird, huh? But, hey, it's more efficient than hangin' out at the Barber Shop on Main Street. Or maybe not. At least there you could actually get a haircut when you needed one!

[Dr Adequate]

It all comes down to how much stuff (sheer tonnage) could you fit on Noah's ark? (do the calculations for goodness sake) ... Creationists have done the calculations for us --- all we have to figure out are the consequences.

See here: Life on the Ark

[Belz...]

You are the same Myriad that claimed he could get ev to converge more quickly by giggling, oops jiggling the weight factors? Well you were correct, jiggle two of the three weight factors to zero and ev can evolve the remaining selection condition in a trivially small number of generations. That’s the key to the mathematics of the mutation and selection sorting/optimization problem. It is the multiple selection conditions which slows the convergence of ev. It works that way in reality as well.

Of course it wasn’t Paul’s intention to disprove the theory of evolution but such is life, the changes he made show just that. They demonstrate that combination selection pressures profoundly slow the mutation and selection sorting/optimization problem.

Oh, that’s right; you proved your contention with the following:

And Adequate made his point with the following (I prefer to think of his quote as an oldie but goodie, not obsolete):

And then Adequate goes on to say this:

http://forums.randi.org/images/smilies/doglaugh.gif

And

and
and too bad you don’t have any empirical examples of your silly graph ...As I have explained to you, I produced the model because I've not heard of this precise experiment being done.
So what are my options since you evolutionists have made such a convincing argument that n+1 selection conditions evolve more quickly than n conditions? It’s simple! Post more examples of how mutation and selection works in reality. I know how much you evolutionists love to read these citations.
http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed&cmd=Retrieve&list_uids=11491008 (http://www.ncbi.nlm.nih.gov/sites/entrez?db=PubMed&cmd=Retrieve&list_uids=11491008)


Well, Dodger. You were right.

[Belz...]

So, has kleinman done anything new this week?

Nothing whatsoever. He still quotes Dodger's century-old forgetting of the ev parameters, he still lies, he still uses the laughing dog, he still uses the same HIV examples, he still doesn't understand a thing, he still insults instead of adresses, etc.

[Olowkow]

Creationists have done the calculations for us --- all we have to figure out are the consequences.

See here: Life on the Ark

First thanks to kjkent1 for the post. And to PBTree for asking. Good summary, I was getting lost.

And Dr. Adequate, (I'm a fan by the way) thanks for that. Very cool. Enough to make a believer out of Pat Condell, or Ingersoll. Just about blows me out of the... water. Not quite though.

From SW:
"Authorities on biological taxonomy estimate there are less than 18,000 species of mammals, birds, reptiles, and amphibians living in the world today"

From InfoPlease (www,infoplease,com/ce6/sci/A0858838,html):
"There are about 900,000 known insect species, three times as many as all other animal species together, and thousands of new ones are described each year"

Hmmm. A wee bit of a discrepancy here. So either 18,000 or 300,000. I'll need to check this out further. Ok, whatever, in my zeal I got carried away with "millions" (I really meant "zillions") of species...we need lots of bottles and shelves for bugs anyway. Even if they fly, they can't fly for a year. Oh yes, heavy water-filled fish tanks for the salt water, or fresh water, fish (depending on how much dilution of the seas took place). Please don't forget the filters and aerating pumps or they die in just days (and oh, the Ph control!), and most sharks have to keep moving or they die. Ok, put them on leashes trailing the ark...did the ark have sails? Not sure.

Well, well, well. Oh my! Perhaps "zillions" is correct:

"Furthermore, there are currently about 1.5 to 1.8 million named species, but it is estimated that the actual number of species in the world ranges from 5 to 10 million (May et al. 1995)."

"So far scientists have named and classified more than 1½ million animals. Over half of these are types of insects and other species are discovered each year. Scientists believe there may be from 2 million to as many as 50 million kinds of animals alive today." {"Animal." World Book Encyclopedia. 16 vols. Chicago: World Book, 2003}

"The most commonly quoted estimate is somewhere between 30 and 50 millions based on Erwin's (1988,1997) study of tropical insects." {Wolosz, Thomas. How Many Species are There? Center for Earth & Environmental Sciences, SUNY at Plattsburgh, 1988.}

"Right now we can only guess that the correct answer for the total number of species lies between 2 and 100 million,' says [Michael] Rosenzweig." {Just How Many Species Are There, Anyway? Society For Conservation Biology. 26 May 2003.} NO FAIR! JUST A GUESS!

From SW:
"If you add 3,000 more animals for the 5 extra of the clean animals {huh???} this would bring the total to 75,000 animals far less than the 136,560 animals that could have been taken on the Ark. This means that only 60% of the Ark would have been filled allowing plenty of room for Noah, his family, and all the provisions needed for their voyage"

From Answers in Genesis:

"In fact, of the two million known species, 98% are invertebrates, which include a variety of animals from sponges, worms and jellyfish, to mollusks and insects. The remaining 2% are vertebrates and number approximately 40,000 species.2 This number is further reduced when the 25,000 marine vertebrates3 and four thousand amphibians4 are discounted, since they clearly do not fit into any of the categories of animals listed in Genesis 2:20."

OK. I give up!

Oops! But wait, I forgot the PLANTS! They can't have been too happy living for a year under thousands of meters of water. Got to check how many "kinds". They all deserved it (especially those Venus fly traps)... the sinners!

Hic ergo obfusco carborundum sum!

Or, as Monty Python would have it..."There! I've run rings around you logically!"

[rocketdodger]

Well, Dodger. You were right.

:)

[Dr Adequate]

Well, Dodger. You were right. Interesting. It seems that he goes on whining about me all week, without me even having to post to goad him on, in posts that (unless, as in this case, you quote 'em) I'll never bother to read.

His delusions about me have become a permanent part of his monomania.

Should I be flattered, I wonder?

[delphi_ote]

Even as a lay person, I love this thread. I make sure that everyday I come in and read where we are up to. I am still confused though.
Feel free to ask about anything posted! The thread goes a little fast, but I'd be more than happy to share my understanding of anything with you.
Evolutionists state that evolution is the only way it could have happened but don't know all of the answers, and;

now that the creationists have been shown that evolution is the only way, they have decided the un-answered questions are all due to to some made up chap called god?
This argument definitely has something to do with kleinman's assertions, but this particular creationist is also being incredibly intellectually dishonest about what science has answered. He's claiming that certain scientific theories are impossible, despite repeatedly being shown evidence that he is wrong.

If we took his argument to the theory of gravitation, it would look something like this, "Newtonists are wrong about the THEROY of gravitation. It is mathematically impossible, because this computer simulation shows that apples can't fall on people's heads!" Our response goes something like, "Multiple independent lines of evidence support the theory of gravitation, you're wrong about what the simulation shows, and here is a video tape of an apple falling on someone's head."
More than happy to accept a good slapping and told to p..s off if I am interfering in a good old scientific broohaha.
NO WAY! Stick around and chat (if you can stand Kleinman's lame jokes, of course...) Things with Kleinman aren't going anywhere anytime soon, and it sounds like you're genuinely curious.

[Dr Adequate]

If we took his argument to the theory of gravitation, it would look something like this, "Newtonists are wrong about the THEROY of gravitation. It is mathematically impossible, because this computer simulation shows that apples can't fall on people's heads!" Our response goes something like, "Multiple independent lines of evidence support the theory of gravitation, you're wrong about what the simulation shows, and here is a video tape of an apple falling on someone's head." At which point he'd spam the forums with a thousand citations proving that apples will stay on trees indefinitely if you attach them with superglue and Scotch tape and string, and declare that this is mathematical proof that gravity is impossible.

[rocketdodger]

Interesting. It seems that he goes on whining about me all week, without me even having to post to goad him on, in posts that (unless, as in this case, you quote 'em) I'll never bother to read.

Its more than interesting -- its hilarious. I reminded him, yet again, that both you and I have independently disproved his claim about sorting. Then, in the next sentence, I predicted he would reply, not with an argument of his own, but by quoting only the statements of ours that, when taken out of context, could be interpreted (only by an idiot) as invalidating our programs. Of course, I predicted 100% correctly.

Just for fun, I will repeat those statements of ours as well, out of context!

I found a combination of parameters last night that led to over 100 pressures being faster than a single one, but I forgot what it was :(

More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.

So far as I know, no-one has done the experiment.

Wow... I guess since we said those things, our programs and the algorithms we implemented in them must be useless. Wait, here is one about joobz as well!

If there was a "sticky" thread on drug delivery, biomaterials or polymer chemistry, I'd be there instantly.But evolution isn't my field.

I guess all of joobz's arguments are invalid as well now.

Should I be flattered, I wonder?

Actually, yes. It must take quite a bit of time for Kleinman to organize all his quoted replies and scan citations for nonsense -- why he does it, I don't know. Certainly, I wouldn't stick around on a forum full of Kleinmans -- I only stay here because there are other rational participants that I can learn from.

[rocketdodger]

At which point he'd spam the forums with a thousand citations proving that apples will stay on trees indefinitely if you attach them with superglue and Scotch tape and string, and declare that this is mathematical proof that gravity is impossible.

And of course, these citations would be anything google returns when you search for "superglue OR 'Scotch tape' OR string," and Kleinman would highlight in bright red any sentences suggesting that superglue, scotch tape, or string can be used to secure objects from fallling.

Because, as anyone who can understand the mathematics of securing knows, the fact that a certain brand of superglue can hold X pounds per square centimeter shows gravity to be impossible. This is what the mathematics show, and this is what hundreds of real examples show. Gravity is mathematically and empirically impossible. I hope you gravitists had a pleasant Thanksgiving and are ready to see why the only thing falling down in this world is the theory of gravity.

===INSERT STUPID LAUGHING ANIMAL GIF HERE===

[Belz...]

At which point he'd spam the forums with a thousand citations proving that apples will stay on trees indefinitely if you attach them with superglue and Scotch tape and string, and declare that this is mathematical proof that gravity is impossible.

Please don't give him the idea. Then we'll have to show him that if you set two of either "scotch tape", "superglue" or "string" to zero, gravity can proceed!

[sol invictus]

True, but you are also increasing the number of mistake points that can be assigned when bindings are missed. One could, as Sol suggested, have a separate mistake point spinner for each binding site, allowing the user to assign more mistakes points to sites closer to the gene and fewer mistake points to sites farther away (for example). Would we now say that we had gamma + 2 pressures instead of just 3? Why not?


kleinman, I'm waiting for your answer to this (and the same question in my earlier post).

[delphi_ote]

gravitists
We attractionists prefer to call such silly dogmatic scientists Newtonists or gravitationists. You can find out more about the truth by reading this ancient text (http://etext.library.adelaide.edu.au/a/aristotle/physics/).

[PBTree]

Thanks for the answers and welcomes (kjkent1 and delphi ote). I now know why I am not a scientist.

Still think that the creationist summation line will be: "Dunno the ansa, must'a been a god that did it".
+


Off track for one second:



From SW:
"Authorities on biological taxonomy estimate there are less than 18,000 species of mammals, birds, reptiles, and amphibians living in the world today"

From InfoPlease (www,infoplease,com/ce6/sci/A0858838,html):
"There are about 900,000 known insect species, three times as many as all other animal species together, and thousands of new ones are described each year"


How about the insects on the ark that only have a short life cycle. eg Mayfly, 24 hours. (Wind powered Cryogenics methinks?)

Day 2 no more mayflies
Day 10 no more houseflies
Day ~55 no more moths etc etc...
Noah would have spent most of his time performing burials at sea, or did his kids flush them down the toilet :)

[joobz]

I think you'll find that creationists will claim it unnecessary to provide a detailed explanation of how it is possible. Well, with faith, you can move mountains and all.


Now, you may think that this is a bit hypocritical considering their favorite tactic is to demand a detailed point for point proof of evolution, but when has that stopped them?

[delphi_ote]

Still think that the creationist summation line will be: "Dunno the ansa, must'a been a god that did it".
In the end, that's basically their logic. "You are wrong about this detail, therefore I am right about everything." But Kleinman makes it even worse by claiming that a lot of things we do know are unknown. That makes his argument basically, "I am wrong about this detail, therefore I am right about everything."

[kjkent1]

kleinman, I'm waiting for your answer to this (and the same question in my earlier post).Sol, historically, kleinman only posts on Sun through Thurs.

[joobz]

Sol, historically, kleinman only posts on Sun through Thurs.
Sol, historically, kleinman refuses to answer questions in the posts he makes Sun through Thurs.

[sol invictus]

Sol, historically, kleinman only posts on Sun through Thurs.

That's OK - I don't mind waiting a bit for my $10,000.

Sol, historically, kleinman refuses to answer questions in the posts he makes Sun through Thurs.

How could you say such a thing!?!?!? :jaw-dropp

And here I thought I'd been debating with someone that answers inconvenient questions and engages in open and honest debates without a political motive...

[kjkent1]

Hey, sol, I have a tangential question for your physicist brain:

Suppose the Creator really does plop new species down on Earth "in a puff of smoke."

How much energy would be required in the neighorhood of that new species, for the Creator to open a hole in this universe and squeeze that life form through?

Pick a small life form. I don't want to incinerate the planet on the first try!

[sol invictus]

Suppose the Creator really does plop new species down on Earth "in a puff of smoke."

How much energy would be required in the neighorhood of that new species, for the Creator to open a hole in this universe and squeeze that life form through?


Couldn't she just sneeze on some mud or something?

[PBTree]

Couldn't she just sneeze on some mud or something?

Big call that god is a she and that she would allow mud in her house.


I was looking out the window just the other day and made a remark to a colleague that god had to be a man. He wanted to know how I knew that and I said, pointing to the outside,

"there is no way a woman would have chosen those colours".

:)

[Kotatsu]

So the annelids are on a higher branch of your phylogenic tree?

I have no idea what you mean by a "higher branch". That the branch which eventually leads to present-day annelids is nested further within the metazoan tree than that which eventually leads to present-day humans? Or that it is longer (i.e., "reaches higher")?

My position is that annelids, by maintaining and improving a successful bauplan --- one which can be found in most greater phyla --- has been able to utilise more different habitats than humans, and to reach greater diversity and numbers.

[kleinman]

I hope you all had a good weekend. Did any of you evolutionists finally figure out how mutation and selection works, mathematically and empirically? Let’s take an excursion into the evolutionist dream world and find out.
I leave you until next week when we can continue this interesting and informative discussion.Discussion requires interactivity.
Joobz, if we are having difficulty with interactivity it is because your speculations are neither interesting nor informative. Put some empirical or mathematical basis to your speculations and then perhaps we can have some interactions. You claim that Dr Schneider’s ev computer simulation is not a valid simulation of the mutation and selection process. Produce the mathematical and empirical data to show why your allegations should be considered. In the meantime, I will continue to post citations which show that combination selection profoundly slow evolution by the mutation and selection sorting/optimization process.
So, has kleinman done anything new this week?
Only more citations which show that combination selection pressures profoundly slow the mutation and selection sorting/optimization process; I have also shown that you have a PhD in mythematics. Of course Adequate, feel free to post a real example of your mythematical model where you allege that n+1 selection pressures evolve more rapidly than n selection pressures.
You don’t have this right Sol. All you are doing when you increase the number of binding sites (gamma) is changing the fraction of the genome where not locating a match to the weight matrix is counted as a mistake.True, but you are also increasing the number of mistake points that can be assigned when bindings are missed. One could, as Sol suggested, have a separate mistake point spinner for each binding site, allowing the user to assign more mistakes points to sites closer to the gene and fewer mistake points to sites farther away (for example). Would we now say that we had gamma + 2 pressures instead of just 3? Why not?
Paul, I’m surprised I have to explain this to you. In Dr Schneider’s model, the weight matrix is traversed along the genome base to base. The weight matrix either finds a match or doesn’t find a match at each position along the genome. A mistake is then determined depending on whether it is a binding site or not a binding site and whether a match is made or not made. If it is a binding site and a match of the weight matrix does not occur, it is a mistake and if it is not a binding site and a match of the weight matrix does occur, it is a mistake. Increasing gamma only increases the possibility of more binding site errors but also reduces the possible number of non-binding site errors at the same time.

Consider Dr Schneider’s published case of G=256. In that case, the maximum number of mistakes would be 256 where all binding sites are not matched by the weight matrix and all non-binding sites have matches to the weight matrix. Changing the value of gamma does not change the total possible number of mistakes which could occur, it just changes the number of possible missed binding sites and erroneous non-binding site matches. The bottom line in this is that the only way you can accelerate the mutation and selection sorting/optimization process is to reduce the total portion of the genome which is being targeted by the selection pressures, not by changing the selection conditions for different parts of the genome as you are doing when you change the value of gamma. This is demonstrated strikingly by setting two of three weight factors in your model to zero.
Even as a lay person, I love this thread. I make sure that everyday I come in and read where we are up to. I am still confused though.

Is the argument:

Evolutionists state that evolution is the only way it could have happened but don't know all of the answers, and;

now that the creationists have been shown that evolution is the only way, they have decided the un-answered questions are all due to to some made up chap called god?


More than happy to accept a good slapping and told to p..s off if I am interfering in a good old scientific broohaha.
Welcome PBTree, I’m glad you are enjoying this thread. You probably enjoy watching mud-wrestling as well. Now, you are a bit misinformed when you say that evolutionist don’t know all the answers when it comes to the mathematics of the mutation and selection sorting/optimization problem. Evolutionists don’t know any answers. Don’t worry about interfering. Evolutionists need all the help they can get.
Looks more like a lot of "obsfuctating" non science to me...but what do I know?
It all comes down to how much stuff (sheer tonnage) could you fit on Noah's ark? (do the calculations for goodness sake) let alone catch and corral and feed all these millions of species. Just sit down and watch National Geographic shows about the Galapagos sometime...remarkable instances of evolution and adaptation. Obvious! Trying to prove evolution could not have happened is pointless, masturbatory, theistic (and, yes, annoying) thinking, and vicious verbosity is not going to change that.
I am not an expert in evolution nor a mathematician, but I do know that a proof in math is either right or wrong, no in between. Just like electronics, you plug it in and it works or it doesn't. The god stuff never works.
Hey Olowcow, it is Adequate who has the PhD in Obfuscamatics. The problem with watching National Geographic is that on the topic of evolution is that it has transformed itself into Jurassic Park in a white lab coat. Mutation and selection can not do mathematically what evolutionists allege and the empirical evidence of mutation and selection verifies this. You can learn something about the mathematics of the mutation selection sorting/optimization problem by studying the peer reviewed and published model of random point mutations and natural selection, ev. It all comes down to simple bookkeeping. Dr Schneider properly modeled the bookkeeping rules and it shows why common descent is mathematically impossible.
The argument is simply that there is an incredible amount of geological, fossil, genetic, radiologic, mathematical, etc. evidence supporting mutation and selection as the means by which the variety of modern biological life forms appear on Earth.
Evolutionists have been concocting their mythology now for 150 years. It is now clear that the mathematical and empirical evidence of the mutation and selection sorting/optimization problem does not support the concept of common descent. The foundation for the theory of evolution, mutation and selection, has been removed from the theory of evolution. The rest of the house of cards collapses without the foundation cornerstone.
Even as a lay person, I love this thread. I make sure that everyday I come in and read where we are up to. I am still confused though.Feel free to ask about anything posted! The thread goes a little fast, but I'd be more than happy to share my understanding of anything with you.
Don’t forget to share this understanding of yours delphi;
Unless we're talking about a real population. High enough selection pressure will slow the rate of evolution because the population will die off.

Also, if you think about it, it's possible the earlier mutations in a series of smooth mutations to adapt to one selection pressure might be maladaptive to a different selection pressure. This is possible, but I can't think of a natural case where this is likely.

In the end, the number of selection pressures don't matter. It's the shape of the resulting fitness landscape that matters. We can only really talk about fitness landscape in a concrete way in terms of simulations like ev.
Delphi, you are completely wrong about the number of selection pressures. The number of selection pressures are the dominant factor in determining the shape of the fitness landscape and for the ability of a population to find a trajectory to a new local optimum. This is obvious when you look at simulations like ev and empirical examples of mutation and selection.
Evolutionists state that evolution is the only way it could have happened but don't know all of the answers, and;

now that the creationists have been shown that evolution is the only way, they have decided the un-answered questions are all due to to some made up chap called god?This argument definitely has something to do with kleinman's assertions, but this particular creationist is also being incredibly intellectually dishonest about what science has answered. He's claiming that certain scientific theories are impossible, despite repeatedly being shown evidence that he is wrong.

If we took his argument to the theory of gravitation, it would look something like this, "Newtonists are wrong about the THEROY of gravitation. It is mathematically impossible, because this computer simulation shows that apples can't fall on people's heads!" Our response goes something like, "Multiple independent lines of evidence support the theory of gravitation, you're wrong about what the simulation shows, and here is a video tape of an apple falling on someone's head."
What evidence have you shown delphi? The only citation I recall you posting was the Wikipedia reference to the fitness landscape and that citation supports my hypothesis. The only similarity between Newton’s theory of gravitation and the theory of evolution is that one describes attraction, the other sucks.
gravitistsWe attractionists prefer to call such silly dogmatic scientists Newtonists or gravitationists.
Perhaps we should call you evolutionists, suctionists.
Still think that the creationist summation line will be: "Dunno the ansa, must'a been a god that did it".
Oh no PBTree, my summation line is evolutionbymutationandselectiondidn’tdoit. That’s what the mathematics of the mutation and selection sorting/optimization problem shows and that is what the empirical evidence shows.
In the end, that's basically their logic. "You are wrong about this detail, therefore I am right about everything." But Kleinman makes it even worse by claiming that a lot of things we do know are unknown. That makes his argument basically, "I am wrong about this detail, therefore I am right about everything."
That’s a bit of an understatement delphi, after all, mutation and selection is the foundation principle for the theory of evolution. You are wrong about how the foundation principle for how your theory works.
Sol, historically, kleinman only posts on Sun through Thurs.That's OK - I don't mind waiting a bit for my $10,000.
I’m warning you again Sol, put your money into a savings bond or cd before you lose it.
So the annelids are on a higher branch of your phylogenic tree?I have no idea what you mean by a "higher branch". That the branch which eventually leads to present-day annelids is nested further within the metazoan tree than that which eventually leads to present-day humans? Or that it is longer (i.e., "reaches higher")?

My position is that annelids, by maintaining and improving a successful bauplan --- one which can be found in most greater phyla --- has been able to utilise more different habitats than humans, and to reach greater diversity and numbers.
Kotatsu, have you made a phylogenic tree specifically for humans?

Still no rational arguments from you evolutionists which contradicts that combination selection pressures profoundly slow the evolutionary process so I might as well keep posting more citations which demonstrate this mathematical fact.
http://jvi.asm.org/cgi/content/full/jvi;77/10/5721 (http://jvi.asm.org/cgi/content/full/jvi;77/10/5721)
To evaluate human immunodeficiency virus type 1 (HIV-1) replication and selection of drug-resistant viruses during seemingly effective highly active antiretroviral therapy (HAART), multiple HIV-1 env and pol sequences were analyzed and viral DNA levels were quantified from nucleoside analog-experienced children prior to and during a median of 5.1 (range, 1.8 to 6.4) years of HAART. Viral replication was detected at different rates, with apparently increasing sensitivity: 1 of 10 by phylogenetic analysis; 2 of 10 by viral evolution with increasing genetic distances from the most recent common ancestor (MRCA) of infection; 3 of 10 by selection of drug-resistant mutants; and 6 of 10 by maintenance of genetic distances from the MRCA. When four- or five-drug antiretroviral regimens were given to these children, persistent plasma viral rebound did not occur despite the accumulation of highly drug-resistant genotypes. Among the four children without genetic evidence of viral replication, a statistically significant decrease in the genetic distance to the MRCA was detected in three, indicating the persistence of a greater number of early compared to recent viruses, and their HIV-1 DNA decreased by 0.9 log10, resulting in lower absolute DNA levels (P = 0.007). This study demonstrates the variable rates of viral replication when HAART has suppressed plasma HIV-1 RNA for years to a median of <50 copies/ml and that combinations of four or five antiretroviral drugs suppress viral replication even after short-term virologic failure of three-drug HAART and despite ongoing accumulation of drug-resistant mutants. Furthermore, the decrease of cellular HIV-1 DNA to low absolute levels in those without genetic evidence of viral replication suggests that monitoring viral DNA during HAART may gauge low-level replication.
and
In summary, analysis of viral population genetics over a median of 5.1 years of effective HAART detected ongoing replication in a significant subset of children, with the most sensitive indicators being a selection of new or an increasing frequency of preexisting drug-resistant mutants in PBMC and maintenance of the mean genetic distance from the MRCA of infection. Among children with ongoing selection of drug-resistant mutants documented, viral rebound appeared to be limited by potent four- and five-drug HAART regimens, presumably by selection of viruses with impaired replication capacity. Furthermore, subjects without genetic evidence of viral replication had a greater persistence of viral genotypes typical of early infection compared to recently evolved viral sequences. In addition, their HIV-1 DNA levels decreased markedly with HAART and to lower absolute levels compared to subjects with ongoing viral replication, providing a rationale for studies evaluating whether HIV-1 DNA levels predict subsequent virologic failure among subjects with plasma HIV-1 RNA levels of <50 copies/ml.
You evolutionists (or should I say suctionists) are overwhelming me with all zero of your citations which show that n+1 selection conditions evolves more rapidly than n selection conditions.

[rocketdodger]

You evolutionists (or should I say suctionists) are overwhelming me with all zero of your citations which show that n+1 selection conditions evolves more rapidly than n selection conditions.

You are overwhelming us with all zero of your posts that contain intelligent arguments responding to our own.

Oh, and selection conditions don't evolve you fool. You have been told about using this incorrect terminology multiple times. Perhaps one day you will learn to communicate and then maybe this thread will make progress. I doubt it, though.

[joobz]

Joobz, if we are having difficulty with interactivity it is because your speculations are neither interesting nor informative. Put some empirical or mathematical basis to your speculations and then perhaps we can have some interactions.This is simply an insult and a lie.
You claim that Dr Schneider’s ev computer simulation is not a valid simulation of the mutation and selection process. Produce the mathematical and empirical data to show why your allegations should be considered. Here you go. This is a gross error on your part. I have stated quite clearly that your extention of his model is wrong. Becuase the assumptions you use to make that extention is wrong. Will you man up and justify your assumptions? Why do you feel the need to hide and avoid this question? Why are you so afraid to justify the theory you claim proves evolution false?

In the meantime, I will continue to post citations which show that combination selection profoundly slow evolution by the mutation and selection sorting/optimization process.
this is a lie.

[delphi_ote]

What evidence have you shown delphi?
Let's see... blast results, computer code for two fitness landscapes that directly contradict your claim about selection pressures, some information theory equations, plant evolutionary relationships...

I could go on, but why bother? You ignore all evidence which contradicts your beliefs. Instead, here's another funny animated GIF I found.
http://i71.photobucket.com/albums/i133/delphi_ote/l_e1874c871070585b55e33121dd33c290.gif

[kleinman]

You evolutionists (or should I say suctionists) are overwhelming me with all zero of your citations which show that n+1 selection conditions evolves more rapidly than n selection conditions.You are overwhelming us with all zero of your posts that contain intelligent arguments responding to our own.

Oh, and selection conditions don't evolve you fool. You have been told about using this incorrect terminology multiple times. Perhaps one day you will learn to communicate and then maybe this thread will make progress. I doubt it, though.
Oh no, I’m picking up your habits.
I found a combination of parameters last night that led to over 100 pressures being faster than a single one, but I forgot what it was http://forums.randi.org/images/smilies/frown.gif
Hey rocketwhomissesthetarget, pressures are faster?

We all know what is being talked about here, (well maybe everyone but joobz). I am contending that the greater the number of selection pressures a population is subjected to, the slower the evolutionary process proceeds. You contend that the greater the number of selection pressures a population is subjected to the faster the evolutionary process proceeds. Dr Schneider’s simulation of random point mutation and natural selection supports my contention. It is very easy to obtain the data from his model which shows this. And it is very easy for me to post empirical examples which demonstrate the same behavior as Dr Schneider’s mathematical model shows. So when is your memory going to be restored rocketwhomissesthetarget and you post the data or empirical examples which shows that the greater the number of selection conditions the faster the evolutionary process proceeds.

[sol invictus]

Paul, I’m surprised I have to explain this to you. In Dr Schneider’s model, the weight matrix is traversed along the genome base to base. The weight matrix either finds a match or doesn’t find a match at each position along the genome. A mistake is then determined depending on whether it is a binding site or not a binding site and whether a match is made or not made. If it is a binding site and a match of the weight matrix does not occur, it is a mistake and if it is not a binding site and a match of the weight matrix does occur, it is a mistake. Increasing gamma only increases the possibility of more binding site errors but also reduces the possible number of non-binding site errors at the same time.

You didn't answer the question. Perhaps you didn't understand it, but I think you did and simply don't want to face the consequences of the answer. In any case, it's pretty evident that you do not actually believe what you are saying - and that's what makes you unwilling to bet on it. That also makes you both a liar and a hypocrite. Your continued participation in this thread after so long stamps you as an uber-troll as well.

Having demonstrated that clearly I'm going to bow out of this thread, which is really pretty boring.

Have a nice day!

[kleinman]

What evidence have you shown delphi?Let's see... blast results, computer code for two fitness landscapes that directly contradict your claim about selection pressures, some information theory equations, plant evolutionary relationships...
I must be talking too much with rocketwhomissessthetarget. The only code I recall you posting is a little code snippet that you haven’t run. Or perhaps you are talking about Adequate’s silly graph? You couldn’t be talking about rocketwhomissesthetarget’s claimed vaporware? Delphi, your only valid citation you have posted on the topic of mutation and selection is your Wikipedia reference to the fitness landscape and that citation clearly supports my contention.
I could go on, but why bother? You ignore all evidence which contradicts your beliefs. Instead, here's another funny animated GIF I found.
Do go on delphi but make sure you have a designated driver when you head home.

do not use misspellings or alterations of other forum members' handles to mock or insult.

[rcronk]

So, I try to visit this thread every 1000 posts or so. We're almost at 7000! Any progress yet?

I have a request as a neutral observer. Could those on kleinman (maybe it's just kleinman) post the top 2 arguments that support your point of view and anyone on the other side, please post your top 2 strongest arguments against kleinman's point of view? If you will let me, I'd like to pull the arguments out of the people and put them on the table to reduce the ad hominem going on here. We can then take counter arguments and see where we stand.

Well - should we do that or do you guys want to just keep going on as is? Let me know. Thanks.

[joobz]

So, I try to visit this thread every 1000 posts or so. We're almost at 7000! Any progress yet?

I have a request as a neutral observer. Could those on kleinman (maybe it's just kleinman) post the top 2 arguments that support your point of view and anyone on the other side, please post your top 2 strongest arguments against kleinman's point of view? If you will let me, I'd like to pull the arguments out of the people and put them on the table to reduce the ad hominem going on here. We can then take counter arguments and see where we stand.

Well - should we do that or do you guys want to just keep going on as is? Let me know. Thanks.
My strongest argument is simply to ask kleinman to support his argument. He contends that ev shows evolution takes too long. To know this, he must prove that the rate of diversification/evolution under all conditions is too slow to have occured in the 500,000,000+ years it took.

His argument relies on several key assumptions
1. rate of mutation/adaption is known and is constant (doesn't accellerate/decellerate under any conditions)
2.) the number of pressures (which determines the rate of adaptation) is constant and remains of equal magnitude.
3.) That only point mutation drives evolution. that no other mutation/adaptation mechanism will speed the process up.
4.) That slow is the same as saying stopped.
(i've combined the previous into logical groups)

Now, I can say that models have shown that variable environmental conditions (alternating, varing selection pressures) speeds up the evolutionary process.
(see Nadav Kashtan, Elad Noor, and Uri Alon Varying environments can speed up evolution PNAS 2007 104: 13711-13716)

This model was confirmed by the evalution of evolution in hypervariable environments, such as madagascar.
(See Robert E. Dewar and Alison F. Richard Evolution in the hypervariable environment of Madagascar PNAS 2007 104: 13723-13727)

These two points kill assumptions 1 and 2. Therefore we are forced to dissmiss his entire theory. Unless, of course, he can provide other justifications that disprove my argument. I repeatedly ask Kleinman to justify his assumptions of his theory, he fails to do so. Mainly becuase he knows he has no justification.

[rocketdodger]

Let's see... blast results, computer code for two fitness landscapes that directly contradict your claim about selection pressures, some information theory equations, plant evolutionary relationships...

Just for sh--ts and giggles, I am going to organize all of the outstanding questions (from my posts) that Kleinman has dodged. When he is ready to answer any of them, maybe this discussion can move forward.

Kleinman, you claim that all sorting algorithms are confounded by multiple sorting conditions. Dr. Adequate and I have independently written programs that 1) make use of sorting algorithms and 2) are not confounded by additional sorting conditions. Can you show anyone here why the algorithms used by Adequate and myself in our programs are not sorting algorithms?

Kleinman, you claim that all selective pressures reduce the fitness of a population to reproduce. You also claim that ev is a fairly accurate model of mutation and selection. Can you explain why the population size is held constant in ev, despite the fact that this is never the case in reality, especially when strong pressures are present?

Kleinman, all the studies you cite utilize pressures that are severely destructive to the populations in question. Can you cite any real world studies that don't rely on pressures that destroy the populations under study?

Kleinman, you claim n+1 pressures always result in slower evolution than n pressures. Can you explain why populations develop resistance to drugs, given that this is equivalent to adding another pressure to an existing group of n pressures?

Kleinman, you claim that ev shows an orders of magnitude difference between convergence times when the number of pressures is increased from one to two, or one to three. Can you explain why setting the other two weights to anything other than zero does NOT result in an "orders of magnitude" difference?

Kleinman, you claim that multiple trajectories on a fitness landscape always lead to a slower rate of evolution. Can you explain why the trajectory on a fitness landscape is the only variable that dictates the rate of evolution?

Kleinman, you claim that failure to reach a global optimum on a fitness landscape results in a slower rate of evolution. Can you show us why failure to reach a global optimum has anything to do with the rate of evolution?

Kleinman, you claim that additional selective pressures increase the amount of local optima that a population might become trapped in on a fitness landscape. Can you show us why being in the local optima of one pressure would affect the population's ability to evolve against any other pressure?

[delphi_ote]

The only code I recall you posting is a little code snippet that you haven’t run.
If you understand anything about fitness landscapes, you don't need to run the code to know the outcome! And I notice you're still pretending the BLAST results don't exist. How very intellectually dishonest of you.

[Olowkow]

Originally Posted by delphi ote
<<I could go on, but why bother? You ignore all evidence which contradicts your beliefs.>>

I know very little about the subject, and yet this much is obvious to me. So what is the point of continuing? Maybe it's time for a poll to find out who is winning....

Reminds me of the Monty Python skit, "I came here for an argument!" "No you didn't!"

[rocketdodger]

I have a request as a neutral observer. Could those on kleinman (maybe it's just kleinman) post the top 2 arguments that support your point of view and anyone on the other side, please post your top 2 strongest arguments against kleinman's point of view?

1) Kleinman bases his theory on the mathematical assumption that all sorting algorithms are slowed down by additional sorting conditions. He has not, however, defined what he means by "slow down." Dr. Adequate and myself have independently written simulation programs which utilize a sorting algorithm and, if you measure the results the right way, are not slowed down by additional condidtions. If you measure them another way, they are slowed down -- but Kleinman consistently dodges the issue of defining his terms.

2) Kleinman claims that for all n, n+1 pressures "evolve slower" than n pressures. We point out to him that every study he cites is predicated on the fact that this is false -- if you add penicillin to a bacteria population, you have n+1 pressures where before you only had n, and penicllin resistance can develop quite rapidly, much faster than it would if the penicillin weren't present. Kleinman wiggles out of this example by refusing to define "selective pressure" and "evolve slower" as well as claiming that we need to define what the "n" pressures are for the example to be valid. This is where the assumptions joobz has been tracking come into play.

[Belz...]

You evolutionists (or should I say suctionists) are overwhelming me with all zero of your citations which show that n+1 selection conditions evolves more rapidly than n selection conditions.

Selections evolve, now ?

[kleinman]

So, I try to visit this thread every 1000 posts or so. We're almost at 7000! Any progress yet?
Yes, there has been progress, delphi has organized his sock drawer, Paul has reached his Rcapacity, Adequate finally realizes more optimization takes more time and that combination therapy for HIV is appropriate (of course he still doesn’t realize why). Progress has been much slower with kjkent1, he still hasn’t sent us any postcards from the 10^500 alternative universes he has visited, joobz still hasn’t told us how to turn lead into gold by letting the sun shine on it, rocketwhomissesthetarget has become a candidate for a trial of Aricept and sol invictus is looking for a way to lose $10,000.
I have a request as a neutral observer. Could those on kleinman (maybe it's just kleinman) post the top 2 arguments that support your point of view and anyone on the other side, please post your top 2 strongest arguments against kleinman's point of view? If you will let me, I'd like to pull the arguments out of the people and put them on the table to reduce the ad hominem going on here. We can then take counter arguments and see where we stand.
Let’s see if we can get you out of neutral and put you into gear. My argument has been consistent since post 1. The mutation and selection sorting/optimization process is far too slow for the theory of evolution to be mathematically possible. The reason why the mutation and selection sorting/optimization process is so profoundly slow is that any more than a single selection condition targeting a single gene confounds the ability of a population to evolve to these simultaneous selection pressures. The mathematical behavior of the peer reviewed and published mathematical model of random point mutations and natural selection written by Dr Tom Schneider, the head of computational molecular biology at the National Cancer Institute shows this and hundreds of peer reviewed citations of the mutation and selection process demonstrates this empirically. So, even if evolutionists could imagine selection conditions that would transform a reptile population into a bird population, there is no way to transform the thousands of genes simultaneously.

Then, there is no way to evolve a gene de novo. There is no such thing as selection for something that doesn’t exist.

Rcronk, allow me to post a third argument. The only basis for abiogenesis is ignorant speculation.
Well - should we do that or do you guys want to just keep going on as is? Let me know. Thanks.
Come on rcronk, we live in the era of multitasking.
The only code I recall you posting is a little code snippet that you haven’t run.If you understand anything about fitness landscapes, you don't need to run the code to know the outcome! And I notice you're still pretending the BLAST results don't exist. How very intellectually dishonest of you.
I know lots about fitness landscapes, more so thanks to you. I know the BLAST results exists, your head isn’t going to blow up again, is it?

[Belz...]

Yes, there has been progress, delphi has organized his sock drawer, Paul has reached his Rcapacity, Adequate finally realizes more optimization takes more time and that combination therapy for HIV is appropriate (of course he still doesn’t realize why). Progress has been much slower with kjkent1, he still hasn’t sent us any postcards from the 10^500 alternative universes he has visited, joobz still hasn’t told us how to turn lead into gold by letting the sun shine on it, rocketwhomissesthetarget has become a candidate for a trial of Aricept and sol invictus is looking for a way to lose $10,000.

And Kleinman needs his medecine, apparently.

[joobz]

My argument has been consistent since post 1.
Being consistently wrong isn't something to brag about.

[rcronk]

So what's the deal here? Why are we so unable to come together after almost 7000 posts? Why the unwillingness to find common ground or make significant progress by working through each item? Is it that underlying belief systems are really what are at (ad hominem) war here?

Is this really just a theist/atheist argument disguised in "evolution" clothing? Have we attached atheism to evolution and theism to non-evolution and because of the strong theist/atheist beliefs neither side is willing to give any ground because it (mistakenly) threatens the core beliefs? Let's drop the defenses and be rigorously honest for just a moment, shall we?

[delphi_ote]

I know lots about fitness landscapes, more so thanks to you. I know the BLAST results exists, your head isn’t going to blow up again, is it?
If you know about both, you're not being honest about either.

[kleinman]

So what's the deal here? Why are we so unable to come together after almost 7000 posts? Why the unwillingness to find common ground or make significant progress by working through each item? Is it that underlying belief systems are really what are at (ad hominem) war here?
Evolutionists don’t comprehend that they have developed a belief system. They think they are the sole arbiter of science. They have become so entrenched in this dogma that the have lost the ability to make progress with the way the mutation and selection sorting/optimization process actually works. Of course evolutionism is at war with God.
Is this really just a theist/atheist argument disguised in "evolution" clothing? Have we attached atheism to evolution and theism to non-evolution and because of the strong theist/atheist beliefs neither side is willing to give any ground because it (mistakenly) threatens the core beliefs? Let's be rigorously honest for a moment, shall we?
Rcronk, evolutionists arrogantly believe that they can explain everything by natural forces. They have used mutation and selection as the main process for their theory for decades. The mathematical and empirical data contradicts their speculations and extrapolations that evolutionists try to use concerning this process. It is an easy matter for me to continue post real examples of mutation and selection which contradicts the concept of common descent. More and more data is becoming available all the time. Projects like the human genome project and the sequencing of other life forms continues to flow in at an increasing rate. This in addition to the problems that we face due to the mutation and selection sorting/optimization problems will force this issue to be better understood. The question is whether evolutionists will interfere with this better understanding of the process or will they continue to insist that their mathematically and empirically irrational dogma be taught to school children.

[Shalamar]

There has also been no evidence for anything else presented to be an alternative to the Scientific Theory of Evolution.

[rocketdodger]

Why the unwillingness to find common ground or make significant progress by working through each item?

That is what most of us want to know.

Is this really just a theist/atheist argument disguised in "evolution" clothing?

No, this is more of an argument between a group of scientifically honest folks who enjoy learning new things and a slimeball, misinforming, cheap-shotting, rhetoric abusing liar. In "evolution" clothing.

Have we attached atheism to evolution and theism to non-evolution and because of the strong theist/atheist beliefs neither side is willing to give any ground because it (mistakenly) threatens the core beliefs?

Our only core belief is honesty. Kleinman's only core belief is dishonesty. That is the root of the communication problem and that is why after 7000 posts this thread has only gotten worse.

Let's drop the defenses and be rigorously honest for just a moment, shall we?

We have been, from day 1. Take a look at any page of this lumbering sh--fest if you don't believe me.

[Paul C. Anagnostopoulos]

Paul, I’m surprised I have to explain this to you. In Dr Schneider’s model, the weight matrix is traversed along the genome base to base. The weight matrix either finds a match or doesn’t find a match at each position along the genome. A mistake is then determined depending on whether it is a binding site or not a binding site and whether a match is made or not made. If it is a binding site and a match of the weight matrix does not occur, it is a mistake and if it is not a binding site and a match of the weight matrix does occur, it is a mistake. Increasing gamma only increases the possibility of more binding site errors but also reduces the possible number of non-binding site errors at the same time.
This paragraph is not a response to my question.


Consider Dr Schneider’s published case of G=256. In that case, the maximum number of mistakes would be 256 where all binding sites are not matched by the weight matrix and all non-binding sites have matches to the weight matrix. Changing the value of gamma does not change the total possible number of mistakes which could occur, it just changes the number of possible missed binding sites and erroneous non-binding site matches. The bottom line in this is that the only way you can accelerate the mutation and selection sorting/optimization process is to reduce the total portion of the genome which is being targeted by the selection pressures, not by changing the selection conditions for different parts of the genome as you are doing when you change the value of gamma. This is demonstrated strikingly by setting two of three weight factors in your model to zero.
Try running the standard model, but with missed site mistake points set to 10.

~~ Paul

[Paul C. Anagnostopoulos]

Reminds me of the Monty Python skit, "I came here for an argument!" "No you didn't!"
I like this one:

I was hoping to settle this without avoiding some sort of argument.

Parse that, you maniacs!

~~ Paul

[kleinman]

There has also been no evidence for anything else presented to be an alternative to the Scientific Theory of Evolution.
What’s the problem Shalamar? Just because I can use an evolutionist’s computer model which shows how mutation and selection sorting/optimization problem actually works and show that the theory of evolution is mathematically impossible and support this finding with hundreds of real examples of mutation and selection which demonstrates the same thing, I am not obliged to give you an alternative understanding of how we came to be here. All I have done is shown that the theory of evolution is mathematically and scientifically irrational and illogical and that evolutionism interferes with the understanding of how the mutation and selection sorting/optimization process actually works. This irrationality on the part of evolutionists leads to the denial of how the mutation and selection sorting/optimization process actually works as demonstrated by another of hundreds (have I gotten to a thousand yet?) of citations.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?&pubmedid=15793111 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?&pubmedid=15793111)
Our results illustrate the flexibility of the responses of some bacterial pathogens to antibiotics. Colistin or imipenem alone was not efficient to avoid emergence of resistant E. aerogenes variants. As a consequence, with the recovery of imipenem susceptibility observed in the final isolates, we suggest the use of a combination therapy, e.g., imipenem-colistin, for severe E. aerogenes infection to circumvent the emergence of resistance mechanisms.

[joobz]

What’s the problem Shalamar?
I would say the problem is that you avoid the questions which you know destroy your arguments.

We know your tactics. They are transparent and childish. Are you going to remain childish and transparent?

[kjkent1]

Evolutionists have been concocting their mythology now for 150 years. It is now clear that the mathematical and empirical evidence of the mutation and selection sorting/optimization problem does not support the concept of common descent. The foundation for the theory of evolution, mutation and selection, has been removed from the theory of evolution. The rest of the house of cards collapses without the foundation cornerstone.The purported clarity of your claim above, is clear only to you.

Or else you must have a very, very long nose.

[kleinman]

Consider Dr Schneider’s published case of G=256. In that case, the maximum number of mistakes would be 256 where all binding sites are not matched by the weight matrix and all non-binding sites have matches to the weight matrix. Changing the value of gamma does not change the total possible number of mistakes which could occur, it just changes the number of possible missed binding sites and erroneous non-binding site matches. The bottom line in this is that the only way you can accelerate the mutation and selection sorting/optimization process is to reduce the total portion of the genome which is being targeted by the selection pressures, not by changing the selection conditions for different parts of the genome as you are doing when you change the value of gamma. This is demonstrated strikingly by setting two of three weight factors in your model to zero.Try running the standard model, but with missed site mistake points set to 10.
I’ve run the case and it took 316 generations to evolve eliminate mistakes. Now you run the same case with erroneous bindings in the gene and erroneous bindings in the non-binding site region set to 0.

If the point you are trying to make is that changing gamma or changing the weights for the selection conditions will alter the fitness landscape, you won’t get an argument from me on that point. But you still have trouble comprehending that the number of selection conditions dominates the shaping of the fitness landscape and if you run the case I suggest above, you will see evidence of this. By the way, I got 6 generations for ev to eliminate the mistakes for this case.

[rcronk]

Ok - let me try one experiment then. Anybody give me one (1) simple and direct question to ask kleinman that you think he has avoided in the past that hurts his case and let's see if he will answer it. If so, then let's do another question from kleinman back to everyone else that he thinks have been dodged, etc.

If this does not force progress, then I request this thread be closed by the moderators as it has become a stalled ad hominem frenzy. The first question I get wins.

[rocketdodger]

Ok - let me try one experiment then. Anybody give me one (1) simple and direct question to ask kleinman that you think he has avoided in the past that hurts his case and let's see if he will answer it. If so, then let's do another question from kleinman back to everyone else that he thinks have been dodged, etc.

If this does not force progress, then I request this thread be closed by the moderators as it has become a stalled ad hominem frenzy. The first question I get wins.

Given a bacterial population prior to an experiment, there are n pressures being exerted on it. After the addition of a strong pressure (antibiotics, for instance), there is rapid evolution of resistance to that antibiotic where there was no evolution before.

This is clearly an example of n+1 pressures leading to faster evolution than n pressures. All of the studies Kleinman has cited are predicated on this fact. How can he claim that adding a pressure always slows down evolution?

[joobz]

Ok - let me try one experiment then. Anybody give me one (1) simple and direct question to ask kleinman that you think he has avoided in the past that hurts his case and let's see if he will answer it. If so, then let's do another question from kleinman back to everyone else that he thinks have been dodged, etc.

If this does not force progress, then I request this thread be closed by the moderators as it has become a stalled ad hominem frenzy. The first question I get wins.
What are kleinman's justifications of his model for point 1,2,3 and 4 that I listed above?

[rcronk]

And the winner is...

Given a bacterial population prior to an experiment, there are n pressures being exerted on it. After the addition of a strong pressure (antibiotics, for instance), there is rapid evolution of resistance to that antibiotic where there was no evolution before.

This is clearly an example of n+1 pressures leading to faster evolution than n pressures. All of the studies Kleinman has cited are predicated on this fact. How can he claim that adding a pressure always slows down evolution?

Kleinman - please answer just this one question and bring up nothing else. Everybody else be vewwy vewwy quiet...

[kleinman]

Ok - let me try one experiment then. Anybody give me one (1) simple and direct question to ask kleinman that you think he has avoided in the past that hurts his case and let's see if he will answer it. If so, then let's do another question from kleinman back to everyone else that he thinks have been dodged, etc.

If this does not force progress, then I request this thread be closed by the moderators as it has become a stalled ad hominem frenzy. The first question I get wins.Given a bacterial population prior to an experiment, there are n pressures being exerted on it. After the addition of a strong pressure (antibiotics, for instance), there is rapid evolution of resistance to that antibiotic where there was no evolution before.

This is clearly an example of n+1 pressures leading to faster evolution than n pressures. All of the studies Kleinman has cited are predicated on this fact. How can he claim that adding a pressure always slows down evolution?
Rocketdodger, I have answered this before and will answer it as many times as you need. The case you are presenting is not the evolution of a population to n+1 selection pressures. It is the evolution of a population to a single selection pressure on the background of n weak selection pressures. The n weak selection pressures to not speed up the evolution of the population to this single strong selection pressure. In fact these weak selection pressures slow the evolutionary process of the strong selection pressures as you acknowledged when I posed the case of evolution of resistance to an antibiotic in vivo where the bacterial population is subject to the immune system versus evolution of resistance in vitro which you acknowledged would occur more rapidly. Selection pressures both weak and strong slow the evolutionary process when the selection pressures are applied in combination. This is a mathematical and empirical fact of life.

Now rcronk, what skin is it off your nose if this thread continues or does not continue? It doesn’t bother me that these evolutionists call me names. It just shows that don’t have any scientific or mathematical basis to support their theory. Do you have something against posting real examples of how the mutation and selection sorting/optimization process actually works? Or do you make yourself the world’s censor?

[rocketdodger]

Rocketdodger, I have answered this before and will answer it as many times as you need. The case you are presenting is not the evolution of a population to n+1 selection pressures. It is the evolution of a population to a single selection pressure on the background of n weak selection pressures.

Um... so n weak pressures and one strong pressure combined isn't n+1 pressures? I could be wrong, but last time I took kindergarten arithmetic, n and one put together is n+1.

The n weak selection pressures to not speed up the evolution of the population to this single strong selection pressure.

Duh. We are not talking about evolution to relieve the weak pressures. We are talking about evolution to relieve the strong pressure that was added last. And the facts are simple, Kleinman. Before that last pressure is added, there is by definition zero evolution to relieve it. After it is added, there is rapid evolution to relieve it.

You keep switching to this strawman about the weaker pressures slowing down the strong one. So what? We are not comparing a system of one strong pressure with the n+1 system -- we are comparing the system of n pressures with the n+1 system.

[joobz]

Yes, we've been down this alley before. When Kleinman would post an ASCII image of a goalpost, in attempts to mock us. He had "Multiple Selection Pressures" as the posts. But within a week, had changed the ASCII image to say "Multiple Directional Selection pressures". The humor of him moving the goalposts wasn't lost on anyone.

This was one of the reasons for my starting to attack his assumptions. He has continually created a series of arguments which isn't false. Sure, you place enough restrictions on a populations, that population will go extinct. It isn't shocking at all. The difference is he hopes to avoid a clear definition of his assumptions so that he may extrapolate this highly specific case to all of reality. This doesn't work.

For that reason, I ask, Kleinman Justify your model/theory assumptions. I have a list of 9, but will only ask 1. Prove that the number of pressures remain constant in number and magnitude. This must be the case for your theory to be correct, that evolution is too slow to be possible.

[rcronk]

kleinman - I actually would like to see some good solid progress on this thread. This is my selfish attempt to achieve that progress, that's all.

Ok, so there doesn't look like there's progress on the n+1 issue. How about Joobz' issue:

Prove that the number of pressures remain constant in number and magnitude. This must be the case for your theory to be correct, that evolution is too slow to be possible.

Kleinman? If we don't make progress on this one, we'll try it the other way round with kleinman asking a question. I just want to build a case that there is no progress being made here - or make some progress, which I would prefer...

[kleinman]

kleinman - I actually would like to see some good solid progress on this thread. This is my selfish attempt to achieve that progress, that's all.
Threatening to try to get this thread closed is not the way to achieve progress. Evolutionists posting on this thread have tried to do this for months. As far as I know, I am the only one invited to post on this topic on this forum by a moderator. Since that has happened, crybaby evolutionists have been trying to shut down this thread. They are responding as the dogmatic religious zealots they are, not as reasonable and rational scientists or mathematicians.
Ok, so there doesn't look like there's progress on the n+1 issue. How about Joobz' issue:

Prove that the number of pressures remain constant in number and magnitude. This must be the case for your theory to be correct, that evolution is too slow to be possible.
I have never made this assumption. This is one of joobz’s speculations. In fact what I have done with ev is study how mutation rate affects the mutation and selection process, something which joobz has not done. In fact, the mutation rate has only a small affect on the mutation and selection sorting/optimization process. Here is a typical series of cases from ev based on variation of mutation rate on the generations for convergence. G=4096, all other parameters held to baseline case and mutation rate was varied.
Muts #/G/gen | Generations Rs>=Rf
1|162892
2|37782
3|57212
4|23422
5|19514
6|21400
7|12230
8|15984
9|13353
10|8545
11|12462
12|7598
13|11891
14|11774
15|9583
16|7570
17|9934
18|7639
19|6594
20|7308
21|6761
22|4871
23|4735
24|7628
25|13438
26|4617
27|7790
28|10079
29|33519
30|35630
31|78740
32|9606
33|57316
34|264952
This series is typical of eight other series I have run studying the affects of mutation rates on the generations for convergence. Extremely high mutation rates to not affect the generations for convergence in any way close to the way reducing down the number of selection pressures does in the ev model. The hundreds of real examples I have cited do not restrict the mutation rate in any way. These are actual examples of mutation and selection and they all show that combination selection pressures profoundly slow the mutation and selection sorting/optimization process.
Kleinman? If we don't make progress on this one, we'll try it the other way round with kleinman asking a question. I just want to build a case that there is no progress being made here - or make some progress, which I would prefer...
Now the question that I pose to you evolutionists is can you present a real example where n+1 selection pressures evolve more rapidly for a population than n selection pressures? And not talking about rocketdodger’s confused interpretation of a population under n weak selection pressures being subjected to a single strong selection pressure and the population evolving rapidly to that single strong selection pressure. I’m talking about a population evolving more rapidly to two strong selection pressures more rapidly than a single strong selection pressures. If you evolutionists can’t do this, your theory of evolution is mathematically and empirically impossible. You evolutionists need to identify the selection pressures and the target genes for these pressures and show that they are true simultaneous selection pressures.

[rcronk]

ok - rocketdodger, you have kleinman's question. Answer it.

kleinman - Again, I really don't want this thread to shut down, I want to see progress. The last few posts have been much better in the way of less ad hominem attacks and I have hope that if we can keep it clean, some progress can be made.

[Paul C. Anagnostopoulos]

I’ve run the case and it took 316 generations to evolve eliminate mistakes. Now you run the same case with erroneous bindings in the gene and erroneous bindings in the non-binding site region set to 0.
I don't need to. I was simply contradicting your statement:

The bottom line in this is that the only way you can accelerate the mutation and selection sorting/optimization process is to reduce the total portion of the genome which is being targeted by the selection pressures, not by changing the selection conditions for different parts of the genome ...

~~ Paul

[Paul C. Anagnostopoulos]

Muts #/G/gen | Generations Rs>=Rf
So now you are using Rseq >= Rfreq instead of mistakes = 0. As I've pointed out before, there is no pressure to reach Rseq >= Rfreq, only to get the mistakes to 0. That is the reason why your data is all over the place.

Why don't you rerun those experiments stopping on mistakes = 0 instead?

~~ Paul

[rocketdodger]

Why should I answer anything? That entire paragraph Kleinman wrote is exactly the kind of scumball bullsh-- I have been talking about. It is a blatant attempt at subversion.

First, nobody here has claimed that there are studies showing multiple selection pressures of the same magnitude leads to more rapid evolution. We have REPEATEDLY told Kleinman that RATE is not equal to SPEED and he still refuses to change his wording. F--- that, man.

Second, nobody has even claimed that IN REALITY the RATE of evolution under multiple pressures increases. We have simply shown that mathematically this is what would be expected to happen, given the accepted model of mutation and selection (the model that Kleinman agrees upon, mind you). Because our mathetmatics, which we clearly explain, show Kleinman's nonsense theory to be wrong at the most basic level, he consistently redirects attention to the lack of real world studies done to support our arguments rather than dealing with the mathematical arguments directly.

Third, why would failing to produce such a study be evidence that evolution is impossible? Putting such a statement in the question is nothing but cheap rhetoric and everyone knows it. Even if multiple strong pressures slow evolution, so what? Kleinman would have to show that every population throughout history has been under nothing other than multiple strong pressures. Can he do that? We all know the answer.

So why does he ask these questions? Because he knows he is wrong, and instead of owning up to it, he blows smoke. Everyone here can see that.

[Paul C. Anagnostopoulos]

I tried running a series like Kleinman's, except with a genome size of 2048. I stopped on mistakes = 0 (perfect creature).

mutations/generation, generations

.5, 48480
1, 42641
2, 22234
4, 6049
6, 9708
8, 5382
12, 3952
14, 8932
16, mutational overload, no convergence


~~ Paul

[joobz]

I have never made this assumption. You do not claim to make it, but it is NEEDED for your theory to work. As I have already said, (which you ignored because you know it destroys everything you've been saying).
Models have shown that variable environmental conditions (alternating, varing selection pressures) speeds up the evolutionary process.
(see Nadav Kashtan, Elad Noor, and Uri Alon Varying environments can speed up evolution PNAS 2007 104: 13711-13716)

This model was confirmed by the evalution of evolution in hypervariable environments, such as madagascar.
(See Robert E. Dewar and Alison F. Richard Evolution in the hypervariable environment of Madagascar PNAS 2007 104: 13723-13727)


This is one of joobz’s speculations. In fact what I have done with ev is study how mutation rate affects the mutation and selection process, something which joobz has not done. In fact, the mutation rate has only a small affect on the mutation and selection sorting/optimization process. Here is a typical series of cases from ev based on variation of mutation rate on the generations for convergence. G=4096, all other parameters held to baseline case and mutation rate was varied.none of this has any relationship to what I asked. Funny how you keep evading it.

[kleinman]

I’ve run the case and it took 316 generations to evolve eliminate mistakes. Now you run the same case with erroneous bindings in the gene and erroneous bindings in the non-binding site region set to 0.I don't need to. I was simply contradicting your statement:The bottom line in this is that the only way you can accelerate the mutation and selection sorting/optimization process is to reduce the total portion of the genome which is being targeted by the selection pressures, not by changing the selection conditions for different parts of the genome ...
Ok Paul let’s run with your logic here. You can take Dr Schneider’s published baseline model and change the generations for converge from around 700 to 316 generations by setting the weight of the binding sites to 10. That’s for G=256. I can take your case and set the two erroneous binding mistake conditions to 0 and the generations for convergence goes to 6. Let’s see you build you your theory of evolution from this case.

You know well that ev models a stochastic process and the data generated from the model is noisy. Show us that your case is more than an example of some variation in noisy data. Dr Schneider made some claims about ev based on his single case. Let’s see if you do any better. On the other hand, I’ve presented hundreds of cases from Dr Schneider and your model of the mutation and selection sorting/optimization process and it clearly shows that the dominant parameter in the model is the number of selection pressures. Let’s see you take this case of yours and prove otherwise. I think we will be waiting for this longer than rocketdodger producing a real case of combination selection pressures evolving more rapidly than single selection pressures.
Muts #/G/gen | Generations Rs>=Rf So now you are using Rseq >= Rfreq instead of mistakes = 0. As I've pointed out before, there is no pressure to reach Rseq >= Rfreq, only to get the mistakes to 0. That is the reason why your data is all over the place.

Why don't you rerun those experiments stopping on mistakes = 0 instead?
I ran all these cases before you argued that “perfect creature” should be the convergence criterion. I thought your moving the goal posts was reasonable and accepted your argument. Once you did this, a ran many cases comparing both Rs>=Rf and perfect creature. When comparing the convergence results when using all three selection conditions, the values were close. Now Paul, if you think using the “perfect creature” convergence criterion will give a different result for these cases that show the behavior of ev based on mutation rate, I’ll rerun these cases just to show you that you are wrong about your own model.

Rcronk, it seems we already have rocketdodger’s answer.
Why should I answer anything? That entire paragraph Kleinman wrote is exactly the kind of scumball bullsh-- I have been talking about. It is a blatant attempt at subversion.
Rocketdodger, here’s some more subversion for you.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=90535 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=90535)
Although lamivudine, famciclovir, and adefovir have proved to be safe and efficacious suppressors of in vivo HBV replication in the short term, there is little, if any, evidence that they affect HBV CCC DNA which persists in the nuclei of infected cells. Elimination of viral CCC DNA is likely to require very long-term therapy—probably longer than several half-lives of the infected cell population (9, 37, 40, 60). To achieve successful long-term control of HBV replication, additional antiviral agents will be required; fortunately, several potentially useful agents, some of which have progressed to clinical trials, are currently being developed (9, 60). In the future, these will probably be used in combination(s), rather than alone, to minimize the risk of development of viral resistance (10, 11, 28, 60). Unfortunately, the fact that HBV resistance to adefovir has not yet been observed is no guarantee that it will not occur.
Rcronk, the theory of evolution by the mutation and selection sorting/optimization process is mathematically impossible. This is why rocketdodger or any other evolutionist can not find a single example of a population evolving more rapidly to combination selection pressures than to single selection conditions. On the other hand, I have presented hundreds of real cases of mutation and selection where combination selection pressures profoundly slow the evolutionary process. This is how the mutation and selection sorting/optimization process actually works.

[Mr. Scott]

So what's the deal here? Why are we so unable to come together after almost 7000 posts? Why the unwillingness to find common ground or make significant progress by working through each item? Is it that underlying belief systems are really what are at (ad hominem) war here?

Is this really just a theist/atheist argument disguised in "evolution" clothing? Have we attached atheism to evolution and theism to non-evolution and because of the strong theist/atheist beliefs neither side is willing to give any ground because it (mistakenly) threatens the core beliefs? Let's drop the defenses and be rigorously honest for just a moment, shall we?

I'll tell you what I see here.

Kleinman says all scientific evidence that evolution accounts for the origin of species is misinterpreted if it disagrees with his holy book.

There is a mountain of consistent evidence that evolution happened pretty much as Darwin suggested. When confronted with this evidence, Kleinman says it's "misinterpreted" but refuses to detail how. He says it's not his job. It's his way of saying "I don't know and I don't care. My interpretation of the bible is the true one. Period."

So, we have the scientific method which has given us trips to the moon, the Internet, modern medicine, etc., etc., but according to Kleinman a book written by ignorant goat herders trumps science regarding the origin of species.

He has found very thin evidence against macro-evolution, which has been soundly refuted, but it makes no difference to him. He is really only here to google-bomb -- repeating his flimsy hypothesis and denigrading evolution and its supporters. He is not here to engage in an honest discussion to elucidate any scientific truth.

Still, the remarks of Kleinman's detractors continue to inform and educate.

[kleinman]

He has found very thin evidence against macro-evolution which has been soundly refuted, but it makes no difference to him. He is really only here to google-bomb his flimsy hypothesis and denigrade evolution and its supporters. He is not here to engage in an honest argument to tease elucidate any scientific truth.
That thin evidence consists of a peer reviewed and published computer model written by the head of computational molecular biology at the National Cancer Institute which shows that combination selection pressures profoundly slow the mutation and selection sorting/optimization process. In addition I have bombed you evolutionists and will continue to bomb you with hundreds of real examples of mutation and selection that demonstrate this mathematical fact. I do denigrate you evolutionists for your irrational and illogical interpretation of the mutation and selection process because this destructive interpretation of how this phenomenon actually works has and will continue to cause the premature deaths of millions of people suffering from diseases subject to the principles of mutation and selection.

Mr Scott, perhaps your parents didn’t lie to you.

[sol invictus]

Mr Scott, perhaps your parents didn’t lie to you.

Santa Claus is real too???


http://www.harrythecat.com/graphics/b/dog42.gif

[Mr. Scott]

Santa Claus is real too???


http://www.harrythecat.com/graphics/b/dog42.gif

I have irrefutable evidence that I once believed in the tooth fairy.

[Paul C. Anagnostopoulos]

Ok Paul let’s run with your logic here. You can take Dr Schneider’s published baseline model and change the generations for converge from around 700 to 316 generations by setting the weight of the binding sites to 10. That’s for G=256. I can take your case and set the two erroneous binding mistake conditions to 0 and the generations for convergence goes to 6. Let’s see you build you your theory of evolution from this case.
I am evolving a creature that distinguishes binding sites from other positions on the genome. You are not. That's all there is to it.


I ran all these cases before you argued that “perfect creature” should be the convergence criterion. I thought your moving the goal posts was reasonable and accepted your argument. Once you did this, a ran many cases comparing both Rs>=Rf and perfect creature. When comparing the convergence results when using all three selection conditions, the values were close. Now Paul, if you think using the “perfect creature” convergence criterion will give a different result for these cases that show the behavior of ev based on mutation rate, I’ll rerun these cases just to show you that you are wrong about your own model.
Yes, please do. Among other things, you'll find a point where mutational overload occurs. I'm guessing around 32 mutations/generation.

~~ Paul

[rocketdodger]

This is why rocketdodger or any other evolutionist can not find a single example of a population evolving more rapidly to combination selection pressures than to single selection conditions.

And of course, the fact that it is impossible for a single selection condition to exist in the real world has nothing to do with the lack of examples. Kleinman, you are brilliant!

On the other hand, I have presented hundreds of real cases of mutation and selection where combination selection pressures profoundly slow the evolutionary process. This is how the mutation and selection sorting/optimization process actually works.

Yes, hundreds of examples of evolution actually happening in the real world. This is how the mutation and selection sorting/optimization process actually works. What was your theory again, Kleinman?

[Belz...]

This paragraph is not a response to my question.

I hope you're not surprised in any way.

[Belz...]

Rocketdodger, I have answered this before and will answer it as many times as you need. The case you are presenting is not the evolution of a population to n+1 selection pressures. It is the evolution of a population to a single selection pressure on the background of n weak selection pressures.

What a volte-face ! So, now, "weak" equals zero ?

The n weak selection pressures to not speed up the evolution of the population to this single strong selection pressure. In fact these weak selection pressures slow the evolutionary process of the strong selection pressures

How do they do that if they're insignificant ? If what you said above is correct, then what you say here is false.

[Belz...]

That thin evidence consists of a peer reviewed and published computer model written by the head of computational molecular biology at the National Cancer Institute which shows that combination selection pressures profoundly slow the mutation and selection sorting/optimization process.

Against all the REST of the evidence, I'd say it's very thin, indeed.

[joobz]

What a volte-face ! So, now, "weak" equals zero ?We'll if Slow=stop, why not?:rolleyes:

How do they do that if they're insignificant ? If what you said above is correct, then what you say here is false.
This is becuase Kleinman hopes we'll all forget that he switches and changes definitions on the fly. This is the reason I harp on one simple question. I know I sound like a broken record, but challenging his assumptions is the only way I know to keep him focused and prevent him from the variable definition game. It's the reason why he fails to answer my one simple question. He knows what the answer means, and doesn't want to end his game.

[rocketdodger]

This is becuase Kleinman hopes we'll all forget that he switches and changes definitions on the fly. This is the reason I harp on one simple question. I know I sound like a broken record, but challenging his assumptions is the only way I know to keep him focused and prevent him from the variable definition game. It's the reason why he fails to answer my one simple question. He knows what the answer means, and doesn't want to end his game.

This goes for all of us. In fact, in my spare time today, I am going to make a list of all the slimeball debate tactics that kleinman has used on this thread.

[kleinman]

Before I go on with today’s posting, I would like to thank rcronk for demonstrating that it is evolutionists who have abandoned mathematical and scientific method for describing the mutation and selection sorting/optimization problem. Evolutionists only have speculation and unrealistic extrapolation to support their mathematically and empirically impossible theory.
Mr Scott, perhaps your parents didn’t lie to you.Santa Claus is real too???
There is a lot of similarity between the story of Santa Claus and theory of evolution. There really was a person name Nicholas who showed generosity to the poor. This story was perverted into the myth we have today. There really is a phenomenon of the mutation and selection sorting/optimization process and evolutionists have perverted it into the myth we have today.
Ok Paul let’s run with your logic here. You can take Dr Schneider’s published baseline model and change the generations for converge from around 700 to 316 generations by setting the weight of the binding sites to 10. That’s for G=256. I can take your case and set the two erroneous binding mistake conditions to 0 and the generations for convergence goes to 6. Let’s see you build you your theory of evolution from this case.I am evolving a creature that distinguishes binding sites from other positions on the genome. You are not. That's all there is to it.
Paul, you keep repeating this idiotic statement. Ev is not evolving binding sites, ev is sorting sequences of bases to satisfy the selection conditions imposed. If you think ev is really evolving binding sites, why don’t evolutionists genetically engineer these sequences of bases into a bacteria and show that they really are functional binding sites. All that ev demonstrates is that increasing the complexity of the selection conditions profoundly slows the mutation and selection sorting/optimization problem. It is irrational and illogical hogwash to believe that ev actually is evolving binding sites. Once again Paul, you show that you are not a scientist but an evolutionist dogmatist.
I ran all these cases before you argued that “perfect creature” should be the convergence criterion. I thought your moving the goal posts was reasonable and accepted your argument. Once you did this, a ran many cases comparing both Rs>=Rf and perfect creature. When comparing the convergence results when using all three selection conditions, the values were close. Now Paul, if you think using the “perfect creature” convergence criterion will give a different result for these cases that show the behavior of ev based on mutation rate, I’ll rerun these cases just to show you that you are wrong about your own model.Yes, please do. Among other things, you'll find a point where mutational overload occurs. I'm guessing around 32 mutations/generation.
So Paul, not only do you have your Rcapacity, we also have Mcapacity. You have already admitted that there are sequences of bases that will satisfy the 3 selection conditions in ev when Rfrequency > Rcapacity. Do you also admit that there are sequences of bases that will satisfy the selection conditions even when Mcapacity is exceeded? I also think you meant to say 32 mutations/256 bases/generation. Now you imply the problem is a point mutational overload. Do you want to suggest another mutation process that would correct this point mutational overload? At your request I will rerun all these mutation cases and we will continue your education on your own computer model which proves that the theory of evolution is mathematically impossible.
This is why rocketdodger or any other evolutionist can not find a single example of a population evolving more rapidly to combination selection pressures than to single selection conditions.And of course, the fact that it is impossible for a single selection condition to exist in the real world has nothing to do with the lack of examples. Kleinman, you are brilliant!On the other hand, I have presented hundreds of real cases of mutation and selection where combination selection pressures profoundly slow the evolutionary process. This is how the mutation and selection sorting/optimization process actually works.Yes, hundreds of examples of evolution actually happening in the real world. This is how the mutation and selection sorting/optimization process actually works. What was your theory again, Kleinman?
I’ll be patient with you on this topic rocketdodger because we know how slow you are on the topic of mutation and selection sorting/optimization. The hypothesis is that combination selection pressures profoundly slow the evolutionary process, too slow to make the theory of evolution to be mathematically possible. And of course, this is what ev shows and this what these hundreds of examples of mutation and selection shows. It is an unrealistic extrapolation that evolutionist make when they take these cases of mutation and selection and draw the conclusion that common descent can occur. There are no selection pressures that can transform a population of reptiles into a population of birds and even if there was, you can not transform thousands of genes simultaneously by the mutation and selection sorting/optimization process.
Rocketdodger, I have answered this before and will answer it as many times as you need. The case you are presenting is not the evolution of a population to n+1 selection pressures. It is the evolution of a population to a single selection pressure on the background of n weak selection pressures.What a volte-face ! So, now, "weak" equals zero ?
No it doesn’t Belz, great creator of the beggaminases theory of evolution, weak selection pressures are those that have little affect on the fitness of a population to reproduce. These weak selection pressures have little influence on changing the sequences of bases in the population.
The n weak selection pressures to not speed up the evolution of the population to this single strong selection pressure. In fact these weak selection pressures slow the evolutionary process of the strong selection pressuresHow do they do that if they're insignificant ? If what you said above is correct, then what you say here is false.
Belz, you are the one using the word insignificant to describe weak selection pressures. Let’s see if I can clarify this issue for you by presenting you with a thought experiment. Consider two in vitro bacterial growth experiments. Everything is equal in the two experiments except the nutrient fed to one bacterial population requires more work for that population to use that nutrient to grow and reproduce. You then subject both populations to an antibiotic which strongly impairs the fitness to reproduce of both populations. Which population will have a better chance to evolve resistance to this antibiotic?
That thin evidence consists of a peer reviewed and published computer model written by the head of computational molecular biology at the National Cancer Institute which shows that combination selection pressures profoundly slow the mutation and selection sorting/optimization process.Against all the REST of the evidence, I'd say it's very thin, indeed.
What evidence of mutation and selection have you evolutionists presented? Your evidence is non-existent on this topic; this is why you post your fossil Rorschach tests. You can’t present hard mathematical scientific evidence that mutation and selection can perform what you evolutionists claim. On the other hand, I have easily found hundreds of real citations along with a peer reviewed published model of random point mutations and natural selection which shows that combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process and this is the foundation principle for the theory of evolution.

We all have noticed that Dr Schneider is not willing to enter in this discuss but he has posted more than enough information on his views that it is not necessary for him to contribute directly to this discussion. I now remind readers what Dr Schneider has said on the following URL:
http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/williams/ (http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/williams/)
Here's a challenge for the creationists: Stop complaining and do a scientific test of your own ideas. Rewrite Ev so that the total number of mistakes of all organisms is computed. Divide the number of mistakes of each organism by this total to get relative mistake scores. Then alter the sorting algorithm to sort probabilistically based on these relative mistake scores. One way to implement this would be to sum the mistakes of two organisms that are being compared and divide each organism's mistakes by that pair wise total. Then pick a random number between 0 and 1 and compare it to that total. Use this to determine whether or not the organisms switch places in the sort. (Note you will have to deal with the special case of zero.) In other words, make the selective process be probabilistic so that there is nothing at all like truncation.

What do you predict will happen?
Will the evolution still occur?
Will Rsequence still approach Rfrequency?
This gauntlet was thrown on the ground on 2005 May 15.

Notice that, since creatioinists stop complaining when defeated, the most extremely difficult part of the challenge above is "do a scientific test of your own ideas"!
and
2006 Nov 28: Solution to the Challenge.
No creationist responded to this by doing the hard work. However a few moments of thought shows that the programming is not necessary. When one adds the mistakes of two organisms and divides by the total the sorting order is preserved. Therefore the results will be the same: Rsequence will still evolve to match Rfrequency.
Dr Schneider, I have taken up the gauntlet and have shown that your computer simulation of random point mutations and natural selection shows that the theory of evolution is mathematically impossible. I will now show you where your error in understanding the mutation and selection sorting/optimization process occurs. This error is demonstrated on your following page.
http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/AND-multiplication-error.html (http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/AND-multiplication-error.html)
The multiplication rule. It is well known from elementary probability theory that if two events are independent, then we may multiply the probabilities of each event to determine the probability of having both events occur. Suppose that there are two events A and B, with the probability of occurrence for A being PA and the probability of occurrence for B being PB. Further assume that the events neither influence each other nor do they both have a common source of influence. Then the probability that both events occur is PA x PB. That is, when the events A and B are independent, the probability that event A AND event B both occur is found by multiplying the probabilities of the individual events.

Example: A single die is a cube having 6 numbered faces, numbered by dots. The probability of getting a single dot from an unbiased die is 1 out of 6 or 1/6. The probability of getting two dice each to have one dot (snake eyes) is 1/6 multiplied by 1/6 or 1/36 = 0.028. Consider now a case where the two dice are glued together so that on one side there is a snake eyes. We toss the two and only read them if they don't end up on the end as a stack one on top of the other. Since there are 4 sides, the probability of 'snake eyes' is 1/4 = 0.25. The non-independence dramatically increased the probability of the event nine fold.
So far so good Dr Schneider.
The multiplication rule does not apply to biological evolution. A common error in the non-scientific literature and poorly written papers is to assume that probabilities multiply for computing components of living things such as proteins. A typical argument notes that proteins are about 300 amino acids long and that there are 20 different kinds of amino acids. If such a string were to be generated using independent selection of the amino acids, then the probability of generating any particular string is 20-300, a very small number indeed. While this may be true for random strings, it does not directly apply to proteins found in living organisms. Why? Because individual mutations accumulate one-at-a-time and there is amplification (replication) between steps. That is, if one starts with a given amino acid string, the mutations in the genome (from which the string is derived) are sequential. A mutation occurs, perhaps changing the amino acid string. If the change is bad, which is true for the majority of changes, the organism dies and its genes are gone. (In diploids, recessive defects will be removed more slowly since they are only exposed when an organism becomes homozygous for the mutation.) If a rare lucky change occurs that has some advantage (or at best is neutral or only slightly deleterious) then the organism may survive to produce offspring. The possibility of appearance and acceptance (by natural selection processes) of mutations in the offspring therefore depends strongly on whether the previous generation survived and on the number of progeny. Genetic algorithm experiments, such as the Ev evolution program demonstrate clearly that the probability of generating what would be an extremely rare genetic string if the steps were independent, can be high. So the evolution of a 300 amino acid protein is reasonably easy to attain.
I added the highlighting. Here is where you go wrong Dr Schneider. The amplification which you talk about only occurs when you have single selection conditions targeting a small area of the genome. When you have multiple selection conditions, this amplification effect is defeated. This is demonstrated by your own ev simulation of random point mutations and natural selection. Ev does not demonstrate that the evolution of a 300 amino acid protein is reasonably easy to attain, it demonstrates the exact opposite.

Dr Schneider, you have erred in your interpretation of how the mutation and selection sorting/optimization process works. Your failure to correct this error is contributing to the premature death of millions of people suffering from diseases subject to the principles of mutation and selection. This includes people suffering from cancer, a disease which the governmental organization you work for, The National Cancer Institute is dedicated to find cures. You are using tax payer dollars to improperly teach how the mutation and selection sorting/optimization process works. You are working against the cure for cancer by your erroneous teaching and interpretation of the mutation and selection sorting/optimization process.

[Belz...]

No it doesn’t Belz, great creator of the beggaminases theory of evolution, weak selection pressures are those that have little affect on the fitness of a population to reproduce.

You mean, exactly the kind we've been telling you demolish your theory ?

These weak selection pressures have little influence on changing the sequences of bases in the population.

So you say now. A little while ago you claimed they didn't exist.

Belz, you are the one using the word insignificant to describe weak selection pressures. Let’s see if I can clarify this issue for you by presenting you with a thought experiment. Consider two in vitro bacterial growth experiments. Everything is equal in the two experiments except the nutrient fed to one bacterial population requires more work for that population to use that nutrient to grow and reproduce. You then subject both populations to an antibiotic which strongly impairs the fitness to reproduce of both populations. Which population will have a better chance to evolve resistance to this antibiotic?

I don't see that any of the two does, but I'm no biologist.

But I see where you're going with this. Since you've been proven wrong, numerous times, about the absence of selection pressures in a bacterium's natural environment, you now claim that these pressures are, for all intents and purposes, equal to zero. This is a nice way to maintain your opinion, but all it does is prove that n+1 selection pressures do not ALWAYS slow down evolution. You've just drawn the "go to jail" card. Do not pass go.

You are working against the cure for cancer by your erroneous teaching and interpretation of the mutation and selection sorting/optimization process.

Appeal to emotion.

[Paul C. Anagnostopoulos]

Paul, you keep repeating this idiotic statement. Ev is not evolving binding sites, ev is sorting sequences of bases to satisfy the selection conditions imposed. If you think ev is really evolving binding sites, why don’t evolutionists genetically engineer these sequences of bases into a bacteria and show that they really are functional binding sites. All that ev demonstrates is that increasing the complexity of the selection conditions profoundly slows the mutation and selection sorting/optimization problem. It is irrational and illogical hogwash to believe that ev actually is evolving binding sites. Once again Paul, you show that you are not a scientist but an evolutionist dogmatist.
Let's review exactly what I said:

"I am evolving a creature that distinguishes binding sites from other positions on the genome."

Oh look, I did not say "Ev is evolving binding sites." I said exactly what is going on when all three mistake points are greater than zero. I am no longer the idiot.


So Paul, not only do you have your Rcapacity, we also have Mcapacity. You have already admitted that there are sequences of bases that will satisfy the 3 selection conditions in ev when Rfrequency > Rcapacity. Do you also admit that there are sequences of bases that will satisfy the selection conditions even when Mcapacity is exceeded? I also think you meant to say 32 mutations/256 bases/generation. Now you imply the problem is a point mutational overload. Do you want to suggest another mutation process that would correct this point mutational overload? At your request I will rerun all these mutation cases and we will continue your education on your own computer model which proves that the theory of evolution is mathematically impossible.
Yes, I am sure that if you run Ev long enough, you can evolve a perfect creature even in the face of mutational overload. What does that have to do with the price of beans?

I'm pretty sure I mean 32 mutations per generation for a 4096-base genome.

I'm not implying anything about "the problem." I'm only pointing out that there is no pressure to evolve Rsequence > Rfrequency, so you ought to run experiments that stop on perfect creature.

~~ Paul

[Belz...]

Alright. I'm getting tired of asking Kleinman questions that never get answered.

So I'm just going to invent my own proxy-Klein and have IT tell me the answers I should get.

Okay. Let's go.

Belz...: Alright, Klein. So far, you've dodged most of my questions by using ridicule and changing the subject. Let's see if we can get somewhere, now. First, do you deny that all the "hundreds of real-life citations" you post assume that evolution does work as described by the theory ?

Klein: The only thing I deny is you evolutionists' mathematically-impossible theory of evolution by mutation and selection, which has been proven by a peer-reviewed simulation and hundreds of empirical examples to be profoundly slowed by the addition of more selection pressures.

Belz...: (Okay, maybe I made him a little too perfect) That kinda doesn't answer my question, Kleinman.

Klein: That's because your question didn't self-beggaminases!

Belz...: What ? How about answering me, proxy-klein ?

Klein: If you don't understand how mutation and selection really work, Belz, it's not my job explaining it to you.

Belz...: And if I did understand, you wouldn't have to. How convenient.

Klein: The only thing that's convenient is how you ignore how mutation and selection really work.

Belz...: This is getting us nowhere, Kleinbot. Why don't you just answer my question ?

Klein: You're right. It isn't getting us anywhere, because your mathematically-challenged evolutionarians can't grasp how mutation and selection really work.

Belz...: Ugh. The question, Alan ? Do you deny that all the "hundreds of real-life citations" you post assume that evolution does work as described by the theory ?

Klein: The only thing I deny is you evolutionists' mathematically-impossible theory of evolution by mutation and selection, which has been proven by a peer-reviewed simulation and hundreds of empirical examples to be profoundly slowed by the addition of more selection pressures.

Belz...: Didn't you just say that ?

Klein: Sure I did, and it's true.

Belz...: What the ? That STILL doesn't answer my question!

Klein: What ALSO doesn't answer your question is how much in trouble your theory of evolution is!

Belz...: Would you mind if we got to the point, Klein ? My question wasn't too difficult, was it ?

Klein: No, what's difficult is for you to understand that the theory of evolution is dead.

Belz...: ****, even Kleinman simulations are impossible to talk to.

Klein: The only person that's impossible to talk to is a mathematically-challenged evolutionist!

Belz...: :mad:

[rocketdodger]

There are no selection pressures that can transform a population of reptiles into a population of birds and even if there was, you can not transform thousands of genes simultaneously by the mutation and selection sorting/optimization process.

Can you show us why it would be necessary to transform thousands of genes simultaneously, as opposed to one gene at a time?

Belz, you are the one using the word insignificant to describe weak selection pressures. Let’s see if I can clarify this issue for you by presenting you with a thought experiment. Consider two in vitro bacterial growth experiments. Everything is equal in the two experiments except the nutrient fed to one bacterial population requires more work for that population to use that nutrient to grow and reproduce. You then subject both populations to an antibiotic which strongly impairs the fitness to reproduce of both populations. Which population will have a better chance to evolve resistance to this antibiotic?

Can you show us why "chance to evolve resistance" has anything to do with "overall rate of evolution?"

[rocketdodger]

Alright. I'm getting tired of asking Kleinman questions that never get answered.

So I'm just going to invent my own proxy-Klein and have IT tell me the answers I should get.

Okay. Let's go.

...Snip...


ROFL

Awesome job Belz.... it speaks volumes about Kleinman that one can impersonate him so perfectly.

[kleinman]

Paul, you keep repeating this idiotic statement. Ev is not evolving binding sites, ev is sorting sequences of bases to satisfy the selection conditions imposed. If you think ev is really evolving binding sites, why don’t evolutionists genetically engineer these sequences of bases into a bacteria and show that they really are functional binding sites. All that ev demonstrates is that increasing the complexity of the selection conditions profoundly slows the mutation and selection sorting/optimization problem. It is irrational and illogical hogwash to believe that ev actually is evolving binding sites. Once again Paul, you show that you are not a scientist but an evolutionist dogmatist.Let's review exactly what I said:

"I am evolving a creature that distinguishes binding sites from other positions on the genome."

Oh look, I did not say "Ev is evolving binding sites." I said exactly what is going on when all three mistake points are greater than zero. I am no longer the idiot.
Of course you admit that ev is not evolving real binding sites because it isn’t. The ability of ev to evolve (sort) sequences that are distinguished from other sequences on the genome is profoundly slower than simply evolving (sorting) for that sequence alone. This is the mathematical and empirical reality that you evolutionists are refusing to accept. The failure of you evolutionists to acknowledge this mathematical and empirical fact of the mutation and selection sorting/optimization process contributes the premature death of millions of people suffering from diseases subject to the principles of mutation and selection. Dr Schneider and other evolutionists are contributing this misunderstanding. You evolutionists have succeeded in institutionalizing your irrational and illogical theory, the results of this is the premature death of millions of people. Not only is the theory of evolution wrong,
So Paul, not only do you have your Rcapacity, we also have Mcapacity. You have already admitted that there are sequences of bases that will satisfy the 3 selection conditions in ev when Rfrequency > Rcapacity. Do you also admit that there are sequences of bases that will satisfy the selection conditions even when Mcapacity is exceeded? I also think you meant to say 32 mutations/256 bases/generation. Now you imply the problem is a point mutational overload. Do you want to suggest another mutation process that would correct this point mutational overload? At your request I will rerun all these mutation cases and we will continue your education on your own computer model which proves that the theory of evolution is mathematically impossible.Yes, I am sure that if you run Ev long enough, you can evolve a perfect creature even in the face of mutational overload. What does that have to do with the price of beans?

I'm pretty sure I mean 32 mutations per generation for a 4096-base genome.

I'm not implying anything about "the problem." I'm only pointing out that there is no pressure to evolve Rsequence > Rfrequency, so you ought to run experiments that stop on perfect creature.
Likewise, if you run ev long enough you long enough, you can evolve a perfect creature when Rf>Rcapacity.

Actually if you look at the data for generations for convergence as a function of mutation rate, you find that once you get past 4 or 5 mutations/256 bases/generations interferes with the sorting process in ev.

I’m doing the cases again with perfect creature as the convergence criterion and so far it takes more generations to achieve this criterion than Rs>Rf. I’ll have the data generated in a day or two.
There are no selection pressures that can transform a population of reptiles into a population of birds and even if there was, you can not transform thousands of genes simultaneously by the mutation and selection sorting/optimization process.Can you show us why it would be necessary to transform thousands of genes simultaneously, as opposed to one gene at a time?
Sure rocketdodger, as soon as you describe what these thousands of sequential selection pressures are which would transform a reptile into a bird.

[rocketdodger]

Sure rocketdodger, as soon as you describe what these thousands of sequential selection pressures are which would transform a reptile into a bird.

I have no idea what they are, that is why I asked you.

Can you show us why it would be necessary to transform thousands of genes simultaneously, as opposed to one gene at a time? YOU seem to know exactly what such pressures would be -- otherwise, how could you elucidate how the process would need to have happened?

[sol invictus]

Belz...: This is getting us nowhere, Kleinbot. Why don't you just answer my question ?
...

:p

I think kleinman's posts in this thread are proof that evolution is impossible!

[kleinman]

Sure rocketdodger, as soon as you describe what these thousands of sequential selection pressures are which would transform a reptile into a bird.I have no idea what they are, that is why I asked you.
Of course you don’t have any idea what these selection pressures might be because there no scientific evidence of the existence of such selection pressures. Delphi ote speculated that a temperature change may have driven such a transformation. It is true that biological molecules such as enzymes are strongly temperature dependent and that such a biological stress (selection pressure) such as an environmental temperature change would shift these biological molecules off of there local optima. However, now you must sort mutations for all these genes simultaneously and ev shows how profoundly slow this process is, so do the empirical examples which I have posted. It is much more rational to think that such a stress as a temperature change would lead to a migration or perhaps some adaptation by recombination and selection but to think that mutation and selection could accomplish anything to such a stress is like thinking that a life form can evolve resistance to bleach.
Can you show us why it would be necessary to transform thousands of genes simultaneously, as opposed to one gene at a time? YOU seem to know exactly what such pressures would be -- otherwise, how could you elucidate how the process would need to have happened?
Rocketdodger, there is no scientific evidence that such selection pressures exist. If you want to speculate that they do, that’s fine but don’t call it science and don’t teach it to children as if it is science.

Rocketdodger, the mutation and selection sorting/optimization process is a mathematically understandable phenomenon. You evolutionists are avoiding this understanding because it completely undermines the theory of evolution. The consequence of this denial is the premature deaths of millions of people suffering from diseases subject to the principles of mutation and selection. This is the price that people are paying for the irrational and illogical interpretation of the mutation and selection sorting/optimization process by evolutionists.

[rocketdodger]

There are no selection pressures that can transform a population of reptiles into a population of birds and even if there was, you can not transform thousands of genes simultaneously by the mutation and selection sorting/optimization process.

Bold mine.

even if there was... Can you show us why it would be necessary to transform thousands of genes simultaneously, as opposed to one at time?

[kleinman]

There are no selection pressures that can transform a population of reptiles into a population of birds and even if there was, you can not transform thousands of genes simultaneously by the mutation and selection sorting/optimization process.Bold mine.

even if there was... Can you show us why it would be necessary to transform thousands of genes simultaneously, as opposed to one at time?
Let’s see if we can apply a little bit of logic in order for you to get some understanding of what the mathematical dilemma is for you evolutionists.
We start with the fact that there are thousands of differences between the genes of reptiles and birds. If you doubt this, check back in this thread where I posted data which shows that the length of the average genome for reptiles is significantly different than the average genome for birds.

We now know both mathematically and empirically that the transformation of more than a single gene at a time by the mutation and selection sorting/optimization is profoundly slowed. There are only a few life forms which reproduce extremely rapidly such as HIV that have any chance of evolving against three selection pressures simultaneously.

Thus, the transformation of any genome by the mutation and selection sorting/optimization process is limited to only a small portion of the genome at any time. This forces evolutionists like you rocketdodger into the position of claiming that the transformation occurs one gene at a time.

Once you take this position, you need selection conditions that somehow would target these genes one at a time. We have a massive amount of evidence of what it requires to target a single gene. It requires a molecule which has the capability to bind to the protein that the gene produces which then changes the conformation of the protein and impairs its ability to function properly. This is a targeted selection pressure which is demonstrated by the hundreds of citations which I have and will continue to post. Rocketdodger, you need a sequence of molecules targeted to each of the individual reptile genes that would transform these genes one at a time until you have a bird. These molecules do not exist.

By the way, I just realized I haven’t posted any citations today. Here is another citation which shows what is required to target a single gene at time and what happens when you target two genes simultaneously.
http://jvi.asm.org/cgi/content/full/74/19/9028 (http://jvi.asm.org/cgi/content/full/74/19/9028)
Interferon (IFN) monotherapy leads to sustained virological responses in less than 20% of chronic hepatitis C cases (47). The recent introduction of IFN plus ribavirin combination therapy has significantly improved response rates (8, 38). In multivariate analyses, HCV genotype and high viral load are two important virologic factors that independently predict the likelihood of treatment failure (37, 39), stressing the importance of virologic factors in determining response to IFN therapy. Unfortunately, therapeutic intervention strategies are evolving at a faster rate than the understanding of the molecular mechanisms by which patients fail therapy. Understanding the molecular mechanisms of antiviral resistance to IFN therapy may lead to the design of better treatment strategies and/or new antiviral compounds. Furthermore, similar HCV-encoded mechanisms may be operational during manifestation of resistance to new antivirals, such as IFN plus ribavirin combination therapy and therapy with pegylated IFN.

[Belz...]

There are no selection pressures that can transform a population of reptiles into a population of birds and even if there was, you can not transform thousands of genes simultaneously by the mutation and selection sorting/optimization process.

Uh-huh, and ?

We now know both mathematically and empirically that the transformation of more than a single gene at a time by the mutation and selection sorting/optimization is profoundly slowed.

No, I don't think "we" know this.

[Belz...]

ROFL

Awesome job Belz.... it speaks volumes about Kleinman that one can impersonate him so perfectly.

Suddenly, I feel like fighting fire with fire.

[Belz...]

Let’s see if we can apply a little bit of logic in order for you to get some understanding of what the mathematical dilemma is for you evolutionists.

The only person who doesn't understand the mathematical dilemma is you.

We start with the fact that there are thousands of differences between the genes of reptiles and birds.

Isn't God profoundly slowed by this, too ?

We now know both mathematically and empirically that the transformation of more than a single gene at a time by the mutation and selection sorting/optimization is profoundly slowed.

The only thing we know is that you can't present an argument properly. The hundreds of real-life empirical examples you've provided and will continue to provide shows that evolution proceeds as described by the theory.

Thus, the transformation of any genome by the mutation and selection sorting/optimization process is limited to only a small portion of the genome at any time.

At least the genome transforms through time, which can't be said of your religion.

This forces evolutionists like you rocketdodger into the position of claiming that the transformation occurs one gene at a time.

The only position it forces us into is one of disbelief at how incapable you are of grasping how mutation and selection really works.

Rocketdodger, you need a sequence of molecules targeted to each of the individual reptile genes that would transform these genes one at a time until you have a bird. These molecules do not exist.

The only thing that doesn't exist here is your understanding of how mutation and selection really work.

By the way, I just realized I haven’t posted any citations today.

Don't worry, Klein. You never have.

Here is another citation which shows what is required to target a single gene at time and what happens when you target two genes simultaneously.

The only thing it demonstrates is that you don't understand how mutation and selection really work.



Well, that felt good.

[rocketdodger]

Rocketdodger, you need a sequence of molecules targeted to each of the individual reptile genes that would transform these genes one at a time until you have a bird. These molecules do not exist.

WHAT IF GOD MADE THE MOLECULES?

[kleinman]

Rocketdodger, you need a sequence of molecules targeted to each of the individual reptile genes that would transform these genes one at a time until you have a bird. These molecules do not exist.WHAT IF GOD MADE THE MOLECULES?
What is the problem rocketdodger, can’t you think of a sequence of naturally occurring molecules which would transform a reptile into a bird by the mutation and selection sorting/optimization process?

[rocketdodger]

What is the problem rocketdodger, can’t you think of a sequence of naturally occurring molecules which would transform a reptile into a bird by the mutation and selection sorting/optimization process?

I don't need to, for two reasons.

First, the "theory of evolution," isn't even close to complete. Right now science is still in the midst of laying the foundations. The lack of direct and complete evidence for every step in the chain between reptiles and birds has nothing to do with its validity.

Second, your very own citations show clearly that pressures can target individual mutations without interacting directly with the DNA at all. Your claim to the contrary is utter nonsense.

When a pressure "targets" a gene, Kleinman, all it means is that if certain bases in the gene mutate the right way it will contribute to relieving the pressure. If you knew anything about biology you would have known this, but you are a lying fraud and it shows more and more with each post you produce.

[kleinman]

What is the problem rocketdodger, can’t you think of a sequence of naturally occurring molecules which would transform a reptile into a bird by the mutation and selection sorting/optimization process?I don't need to, for two reasons.

First, the "theory of evolution," isn't even close to complete. Right now science is still in the midst of laying the foundations. The lack of direct and complete evidence for every step in the chain between reptiles and birds has nothing to do with its validity.
The theory of evolution has been around for more than 150 years and you evolutionists have done a lousy job elucidating how the mutation and selection sorting/optimization process actually works. Yet you evolutionists like to claim that the theory is established verified science. You are correct that you evolutionists are still in the midst of laying the foundation for your theory but now you don’t have the mutation and selection sorting/optimization process as a mechanism for your theory. You have no evidence of mutation and selection that would explain the chain between reptiles and birds. You do like to trot out an occasional fossil Rorschach image and claim this is your evidence.
Second, your very own citations show clearly that pressures can target individual mutations without interacting directly with the DNA at all. Your claim to the contrary is utter nonsense.
Rocketdodger, there is a clear cut mechanism for the interaction of selection pressures and the change in frequency between particular sequences of bases in the genome. That mechanism is that molecules which target particular enzymes and bind to these enzymes impairing their function translates back to mutated genomes which alter the shape of these particular enzymes and reducing the ability of these molecules to bind to the mutated forms of the enzymes. The cause and effect relationship is clear.
When a pressure "targets" a gene, Kleinman, all it means is that if certain bases in the gene mutate the right way it will contribute to relieving the pressure. If you knew anything about biology you would have known this, but you are a lying fraud and it shows more and more with each post you produce.
You really are slow at learning how the mutation and selection sorting/optimization process actually works. If you understood how the process works, you would know that targeting two different parts of the genome simultaneously confounds the ability of a population to “mutate the right way” in order to relieve both selection pressures simultaneously. Here’s another citation which reveals this mathematical and empirical facts of life how the mutation and selection sorting/optimization process actually works.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?&pubmedid=16731953 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?&pubmedid=16731953)
Using the HCV subgenomic replicon system, we report here the selection and characterization of HCV variants resistant to a thiophene-2-carboxylic acid (NNI-1) which binds to the thumb I site. Through combination studies of NNI-1 with a potent polymerase inhibitor which binds to the palm domain (NNI-3), we have studied the effect of targeting simultaneously different sites of the NS5B polymerase. Upon long-term treatment with both inhibitors, a small number of replicon colonies were isolated. Only 65% of the replicon variants from those replicon colonies contained multiple mutations on the same genome conferring dual resistance to both classes of inhibitors. Further characterization provided initial insights into the potential mutational threshold of the HCV NS5B, with important implications for combination drug therapy for the treatment of HCV infection. The identification of mutations in the HCV polymerase gene responsible for resistance to these structurally different HCV inhibitors alone or in combination is important for the design of future combination therapies.
You are slow at understanding this rocketdodger but I’ll be patient with you and continue to show you how the mutation and selection sorting/optimization process actually works.

[joobz]

Let’s see if we can apply a little bit of logic
:dl::dl::dl:

[kleinman]

http://forums.randi.org/images/smilies/doglaugh.gif
Envision a system of millions of forming and destructive chemical reactions. Now, envision that intermediates of there reactions associate through non-covalent means and that this complex becomes protected against the destructive reactive pathway, perhaps by a reversible precipitation. These new complexes result in a localized increased of new chemical species. These chemical species then progress in a new series of reaction... that is what I mean through cooperative means. I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?

Hey joobz, I see you are posting these citations again.
Models have shown that variable environmental conditions (alternating, varing selection pressures) speeds up the evolutionary process.
(see Nadav Kashtan, Elad Noor, and Uri Alon Varying environments can speed up evolution PNAS 2007 104: 13711-13716)

This model was confirmed by the evalution of evolution in hypervariable environments, such as madagascar.
(See Robert E. Dewar and Alison F. Richard Evolution in the hypervariable environment of Madagascar PNAS 2007 104: 13723-13727)
You are aware now that the citation, Varying environments can speed up evolution has nothing to do with the weather, aren’t you? I like this citation you brought up. In your ignorance of evolution by the mutation and selection sorting/optimization process, this citation clearly shows that sequential single selection conditions evolve much more rapidly than combination selection pressures. I do thank you for the citation. As for your other citation, I’ll let you sit out in the Madagascar rainforest and make your ridiculous speculations. This is as ridiculous as your bizarre and illogical speculations about abiogenesis.
http://forums.randi.org/images/smilies/doglaugh.gif

[joobz]

[/color]
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?
why don't you
"apply some logic" to my questions?
I challenge you to justify your assumptions. Use your great logical intellect.


Hey joobz, I see you are posting these citations again.

You are aware now that the citation, Varying environments can speed up evolution has nothing to do with the weather, aren’t you? are you saying that changes in weather don't change the number of selection pressures? really?

I like this citation you brought up. In your ignorance of evolution by the mutation and selection sorting/optimization process, this citation clearly shows that sequential single selection conditions evolve much more rapidly than combination selection pressures. changes in selection conditions will do that. Good thing reality isn't constant.
I do thank you for the citation. As for your other citation, I’ll let you sit out in the Madagascar rainforest and make your ridiculous speculations. This is as ridiculous as your bizarre and illogical speculations about abiogenesis.
http://forums.randi.org/images/smilies/doglaugh.gif

the second citation is REAL WORLD EVIDENCE on the reality of the first citation. I'm glad you are happy with them. Afterall, they destroy your theory. You'd see that if you were to "apply a little logic" to the problem.
:D

[kleinman]

Joobz, if the sun shines on lead long enough does it turn into gold?why don't you "apply some logic" to my questions?
Better yet, why don’t I give you the data from a peer reviewed and published model of the random point mutation and sorting/optimization process. Here is how mutation rate affects the convergence rate for this sorting algorithm. G=4096, all other parameters held at the baseline case except mutation rate:
Muts/G/gen|Gen Rs>Rf|Gen Perf Creat
1|162892|163722
2|37782|48755
3|57212|57212
4|23422|30316
5|19514|19675
6|21400|23306
7|12230|17689
8|15984|21947
9|13353|13328
10|8545|8935
11|12462|16043
12|7598|10225
13|11891|17029
14|11774|16052
15|9583|17186
16|7570|7715
17|9934|14761
18|7639|8772
19|6594|12152
20|7308|8806
21|6761|7647
22|4871|6724
23|4735|4959
24|7628|4096
25|13438|13463
26|4617|8325
27|7790|8067
28|10079|17877
29|33519|46876
So, joobz, your speculation that variable mutation rate has a profound affect on the rate of evolution is exactly just that, speculation. The affect of combination selection conditions has a far more dominating affect on the rate of convergence of these mutation and selection sorting/optimization problems.
You are aware now that the citation, Varying environments can speed up evolution has nothing to do with the weather, aren’t you?are you saying that changes in weather don't change the number of selection pressures? really?
So joobz, why don’t you tell us what the target genes are to weather changes? You are claiming that it speeds up evolution by the mutation and selection sorting/optimization process. Tell us how and show us how much you know about the evolutionary process.
I like this citation you brought up. In your ignorance of evolution by the mutation and selection sorting/optimization process, this citation clearly shows that sequential single selection conditions evolve much more rapidly than combination selection pressures.changes in selection conditions will do that. Good thing reality isn't constant.
So then expert in speculations, tell us what the sequence of selection pressures were that transformed a reptile population into a bird population.
I do thank you for the citation. As for your other citation, I’ll let you sit out in the Madagascar rainforest and make your ridiculous speculations. This is as ridiculous as your bizarre and illogical speculations about abiogenesis.the second citation is REAL WORLD EVIDENCE on the reality of the first citation. I'm glad you are happy with them. Afterall, they destroy your theory. You'd see that if you were to "apply a little logic" to the problem.
Why don’t you point out these selection conditions from the Madagascar rainforest citation and the target genes for these selection pressures which destroy the hypothesis that combination selection pressures profoundly slow the evolutionary process? And while you are trying to find these quotes, consider this:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1235844 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1235844)
An understanding of the mechanisms of development of resistance is essential in order to maximize the clinical benefit of new antiretroviral agents. In vitro selection experiments can be a useful indicator of the genetic barrier to the development of resistance and the resistance profile of a drug. They may therefore guide the selection of drug combinations and the effective sequencing of drugs in patients.
And
In conclusion, TMC125 is a potent and unique new investigational NNRTI characterized by a high genetic barrier to the development of resistance in vitro. It is active against viruses with either of the signature mutations for efavirenz and nevirapine and can prevent the emergence of resistant HIV-1 from them. We have demonstrated that TMC125 selects for a variety of NNRTI-associated mutations in vitro but that resistance generally requires the presence of at least two of these mutations. Several novel substitutions, most notably V179F, were identified in resistant strains and are the subject of further studies.

In vivo data from short-term trials with TMC125 in treatment-naive and treatment-experienced HIV-1-infected subjects with NNRTI resistance support the clinical relevance of these results (13, 15).
Hey joobz, these authors seem to think they can stop the evolution of resistance to other drugs with their drug. Shouldn’t you contact them and tell them that you can’t stop evolution?
http://forums.randi.org/images/smilies/doglaugh.gif

[joobz]

Better yet, why don’t I give you the data from a peer reviewed and published model of the random point mutation and sorting/optimization process. Here is how mutation rate affects the convergence rate for this sorting algorithm. G=4096, all other parameters held at the baseline case except mutation rate:
Muts/G/gen|Gen Rs>Rf|Gen Perf Creat
1|162892|163722
2|37782|48755
3|57212|57212
4|23422|30316
5|19514|19675
6|21400|23306
7|12230|17689
8|15984|21947
9|13353|13328
10|8545|8935
11|12462|16043
12|7598|10225
13|11891|17029
14|11774|16052
15|9583|17186
16|7570|7715
17|9934|14761
18|7639|8772
19|6594|12152
20|7308|8806
21|6761|7647
22|4871|6724
23|4735|4959
24|7628|4096
25|13438|13463
26|4617|8325
27|7790|8067
28|10079|17877
29|33519|46876
So, joobz, your speculation that variable mutation rate has a profound affect on the rate of evolution is exactly just that, speculation. The affect of combination selection conditions has a far more dominating affect on the rate of convergence of these mutation and selection sorting/optimization problems.That's a bunch of stupid. I've already proved the model isn't a perfect representation of life. The focus is on you needing to prove that all of life has constant number and strength of selection pressures under all conditions. Otherwise your argument is false. good luck:)

So joobz, why don’t you tell us what the target genes are to weather changes?
why do they matter? ARe you saying that changing weather conditions do NOT affect gene expression? Are you saying that changing weather patterns aren't changes in selection pressures (magnitude and the number)? please, prove that. :)

[rocketdodger]

Rocketdodger, there is a clear cut mechanism for the interaction of selection pressures and the change in frequency between particular sequences of bases in the genome. That mechanism is that molecules which target particular enzymes and bind to these enzymes impairing their function translates back to mutated genomes which alter the shape of these particular enzymes and reducing the ability of these molecules to bind to the mutated forms of the enzymes. The cause and effect relationship is clear.

I am literally speechless.

[kleinman]

Rocketdodger, there is a clear cut mechanism for the interaction of selection pressures and the change in frequency between particular sequences of bases in the genome. That mechanism is that molecules which target particular enzymes and bind to these enzymes impairing their function translates back to mutated genomes which alter the shape of these particular enzymes and reducing the ability of these molecules to bind to the mutated forms of the enzymes. The cause and effect relationship is clear.I am literally speechless.
No problem rocketdodger, keep reading and studying and you will learn how the mutation and selection sorting/optimization process actually works. It certainly doesn’t work the way evolutionists allege.

[joobz]

No problem rocketdodger, keep reading and studying and you will learn how the mutation and selection sorting/optimization process actually works. It certainly doesn’t work the way evolutionists allege.
Well, i've proven that it DEFINITELY doesn't work the way you claim.
Thanks for that, BTW. wouldn't have been possible without your willingness to apply logic.:)