Annoying creationists

[rocketdodger]

Originally Posted by kleinman

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]

Originally Posted by Kleinman

There you go again joobz; you are calling ev my model.

Originally Posted by Kleinman

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.

Originally Posted by joobz

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

Originally Posted by Dr Schneider in his publication on ev

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

Originally Posted by Dr Schneider from his faq site for ev

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

Originally Posted by Dr Schneider from his faq site for ev

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

Originally Posted by Dr Schneider from his faq site for ev

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.

Originally Posted by Dr Schneider from his faq site for ev

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.

Originally Posted by Dr Schneider from his faq site for ev

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.

Originally Posted by Dr Schneider from his faq site for ev

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?

Originally Posted by Dr Schneider from his faq site for ev

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.

Originally Posted by Dr Schneider from his faq site for ev

Why are there so few mistakes at the beginning? Cristi asked:

Originally Posted by Dr Schneider from his faq site for ev

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

Originally Posted by Dr Schneider from his blog site for ev

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.

Originally Posted by Steven E. Jones

"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.

Originally Posted by Dr Schneider from his blog site for ev

Actual biological materials were used to determine the original hypothesis. Read the literature: Schneider1986.

Originally Posted by Steven E. Jones

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.

Originally Posted by Dr Schneider from his blog site for ev

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.

Originally Posted by Steven E. Jones

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.

Originally Posted by Dr Schneider from his blog site for ev

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.

Originally Posted by Steven E. Jones

Even if Schneider did eventually test his computer simulation against the real world

Originally Posted by Dr Schneider from his blog site for ev

See 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 .

Originally Posted by Kleinman

Kjkent1, convergence can not be based on Rseq >= Rfreq because as Paul has said:

Originally Posted by Paul

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.

Originally Posted by Kleinman

Convergence must be based on zero mistakes. Then G=2048 is acceptable. Send me the contract.

Originally Posted by kjkent1

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.

Originally Posted by Kleinman

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

Originally Posted by sol invictus

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...]

Originally Posted by kleinman

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.

Quote:

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 ?

Quote:

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.

Quote:

You are not a scientist

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

Quote:

you are an evolutionist religious zealot.

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

Quote:

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.

Quote:

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.

Quote:

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.

Quote:

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

They have.

[Belz...]

Originally Posted by kleinman

You haven’t presented any results other than this:

Originally Posted by Rocketdodger on something entirely different

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]

Originally Posted by Kleinman

You haven’t presented any results other than this:

Originally Posted by rocketdoger’s idea of a 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

Originally Posted by Kleinman

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

Originally Posted by Belz’s attempt to defend the irrational and illogical

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]

Originally Posted by 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, 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]

Originally Posted by 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.

Originally Posted by kjkent1

The AUTHOR of ev is Tom Schneider. Paul is Schneider's agent -- unless Paul "is" Schneider.

And Paul is the author of evj.

Originally Posted by kjkent1

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

Originally Posted by Dr Schneider in Ev: Evolution of Biological Information

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).

Originally Posted by kjkent1

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]

Originally Posted by 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]

Originally Posted by sol invictus

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

Originally Posted by sol invictus

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]

Originally Posted by Kleinman

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)."

Originally Posted by kleinman

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]

Originally Posted by sol invictus

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]

Originally Posted by kleinman

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

Originally Posted by kleinman

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]

Originally Posted by sol invictus

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]

Originally Posted by kjkent1

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]

Originally Posted by 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?

[kleinman]

Originally Posted by Kleinman

Sol, go home, your mother is calling you.

Originally Posted by sol invictus

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.

Originally Posted by kjkent1

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.

Originally Posted by sol invictus

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

Originally Posted by Effect of Drug Concentration on Emergence of Macrolide Resistance in Mycobacterium avium

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

Originally Posted by Combination chemotherapy for hepatitis B virus: the path forward?

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]

Originally Posted by kleinman

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]

Originally Posted by 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.

Originally Posted by delphi ote

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

Originally Posted by Fitness landscapes in evolutionary optimization

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.

Originally Posted by Fitness landscapes in evolutionary optimization

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!

Originally Posted by Kleinman

Kjkent1 is no better at reading my mind than you are Sol at understanding how ev works.

Originally Posted by kjkent1

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.

Originally Posted by kleinman

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.

Originally Posted by kleinman

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.

Originally Posted by kleinman

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?

Originally Posted by kleinman

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]

Originally Posted by kleinman

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]

Originally Posted by joobz

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.

Originally Posted by joobz

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.

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.

[joobz]

Originally Posted by kleinman

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://www.internationalskeptics.com...s/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://www.internationalskeptics.com...s/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]

Originally Posted by kleinman

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]

Originally Posted by joobz

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?

Originally Posted by Kleinman

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!

Originally Posted by rocketdodger

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

Originally Posted by Abstract

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]

Originally Posted by Kleinman

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]

Originally Posted by 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?

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]

Originally Posted by 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.

~~ Paul

[kleinman]

Originally Posted by 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.

Originally Posted by rocketdodger

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.

Originally Posted by kjkent1

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

Originally Posted by Paul

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]

Originally Posted by 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?

[sol invictus]

Originally Posted by 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...

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]

Originally Posted by 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?

Originally Posted by joobz

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

Originally Posted by In Vitro Susceptibilities of Wild-Type or Drug-Resistant Hepatitis B Virus to (−)-β-d-2,6-Diaminopurine Dioxolane and 2′-Fluoro-5-Methyl-β-l-Arabinofuranosyluracil

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]

Originally Posted by kjkent1

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

Originally Posted by Paul

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.

Originally Posted by kleinman

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]

Originally Posted by 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.

Originally Posted by sol invictus

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.

Originally Posted by sol invictus

So, here are the terms:

Originally Posted by sol invictus

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?

Originally Posted by sol invictus

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]

Originally Posted by Paul

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.

Originally Posted by kjkent1

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:

Originally Posted by Paul

Originally Posted by kjkent1

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]

Originally Posted by kleinman

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]

Originally Posted by kleinman

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...]

Originally Posted by kleinman

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.

Quote:

Sol, go home, your mother is calling you.

How utterly adolescent of you.

[Belz...]

Originally Posted by kleinman

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

Chatbot.

[Paul C. Anagnostopoulos]

Originally Posted by Kleinman

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:

Originally Posted by me

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]

Originally Posted by Sol

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