Annoying creationists

[kleinman]

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.
So joobz, tell us which of your proofs was the most devastating? Was it your Madagascar rainforest citation or was it your speculation about abiogenesis?

Hey joobz, who is Santa’s little helper in your avatar?

[joobz]

So joobz, tell us which of your proofs was the most devastating? Was it your Madagascar rainforest citation or was it your speculation about abiogenesis?Once you learn the way multiple selection pressures actually work, you'll see that they do not remain constant in magnitude and number. This is a fact which makes evolution quite possible and permits the wide genetic variety seen in madagascar. Your theory has been quite effective at demonstrating this.

Hey joobz, who is Santa’s little helper in your avatar?
He is baby new theory. He represents the rebirth of the concept of multiple selection pressures and the fact that evolution is quite real and possible.

[Shalamar]

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, Kleinman, you're the only evolutionist I know who thinks it works the way you do.

[kleinman]

So joobz, tell us which of your proofs was the most devastating? Was it your Madagascar rainforest citation or was it your speculation about abiogenesis?Once you learn the way multiple selection pressures actually work, you'll see that they do not remain constant in magnitude and number. This is a fact which makes evolution quite possible and permits the wide genetic variety seen in madagascar. Your theory has been quite effective at demonstrating this.
The results for your speculations were obtained from the JooBz (Just Baloney) computer simulation of mutation and speculation.
Hey joobz, who is Santa’s little helper in your avatar?He is baby new theory. He represents the rebirth of the concept of multiple selection pressures and the fact that evolution is quite real and possible.
Looks like you are going to get coal in your stocking this year.
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, Kleinman, you're the only evolutionist I know who thinks it works the way you do.
I can’t help it if you evolutionists don’t understand how the mutation and selection sorting/optimization process works. Here is a citation for you Shalamar that may help you understand how the mutation and selection sorting/optimization process works.
http://jvi.asm.org/cgi/reprint/JVI.01624-06v1.pdf (http://jvi.asm.org/cgi/reprint/JVI.01624-06v1.pdf)
A treatment strategy to prevent the evolution of significant or complete resistance could be combination therapy of several mutagens or of a mutagen in combination with other antiviral drugs.
Joobz, you better tell these authors that you can’t stop evolution.

[joobz]

The results for your speculations were obtained from the JooBz (Just Baloney) computer simulation of mutation and speculation.Not at all. I simply used your theory of multiple selection pressures slowing evolution (which I believe represents an accurate explanation as to how multiple drug therapy works) demonstrates clearly how evolution is quite possible. Varying the number and intensity of pressures will rapidly accelerate evolution.


Looks like you are going to get coal in your stocking this year.Baby new theory gives out diamonds to everyone who understands the nature of variable multiple selection pressures and how it accelerates evolution.



http://jvi.asm.org/cgi/reprint/JVI.01624-06v1.pdf (http://jvi.asm.org/cgi/reprint/JVI.01624-06v1.pdf)

Joobz, you better tell these authors that you can’t stop evolution.
Thank you kleinman for that reference, it also agrees with the concept that variable pressures and optimal mutation rate can accelerate evolution.

This latter case is potentially a worry because the elevated mutation rate might facilitate evolution to a part of the fitness landscape that was otherwise not likely to be accessed. In general, if mutagenesis
increases the mutation rate closer to the mutation-rate optimum for the virus, then mutagenesis will presumably be counterproductive for treatment. This possibility seems unlikely for RNA viruses, as their intrinsic mutation rates are so high. However, the relevant parameters are not adequately known to exclude this possibility, so the caution seems warranted.

[Myriad]

If the sun shines on lead long enough does it turn into gold?


Kleinman keeps asking this irrelevant question, but he has it backwards. Sunshine turns lighter elements into gold, and gold into lead, through the fast neutron capture process.

Of course, you need a lot of sunshine. The neutron flux has to be sufficient to outpace beta decay, so the rate (not just the absolute accumulated amount over time) of sunshine is important. Generally the only places that have enough sunshine are the cores of supernovas, colliding neutron stars, and similar environments. The rate of sunshine needed for heavy nucleosynthesis would simultaneously crush and vaporize any living creature on earth in an instant, but in the end I can state that yes, enough sunshine acting on iron wil turn it into gold, and the gold into lead.

Given that the necessary trace elements are already present on earth when the planet forms, turning N2, H20, and CO2 into organic compounds, amino acids, and the rest of the stuff I'm made of takes a lot less energy. Well within the capabilities of ordinary earthside sunshine.

Respectfully,
Myriad

[Kotatsu]

Kotatsu, have you made a phylogenic tree specifically for humans?

I invite you to explain the relevance of your question, and also to perhaps answer the questions I had about what you mean by "a higher branch". Further, I'd like to know what part of the following statement:

"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."

it is you oppose.

To answer your question: yes, I have made a phylogenetic tree which included humans, but was not specifically targeted only at humans. It included sequences from all apes, some monkeys, and an assortment of other mammals. The results of the analysis of that tree, as I recall, was exactly as predicted. The analysis included jackknifing, bootstrapping, distance, and a plain parsimony analysis, and was part of my systematics education.

[Belz...]

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.

Your puny religion has been around for 2000 years and it still can't explain how the sun shines.

[Belz...]

I am literally speechless.

Can you translate what he said ?

[Belz...]

I can’t help it if you evolutionists don’t understand how the mutation and selection sorting/optimization process works.

:D

I knew you'd say that.

[Kotatsu]

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?

DNA.

DNA is a sequence of naturally occurring molecules which, by undergoing various mechanisms of adjustment, have slowly changed what would once be recognised as "some kind of reptile" into present day birds.

You are getting stupider by the minute, Kleinman.

[Kotatsu]

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 ?

Copycat. (http://forums.randi.org/showthread.php?postid=3097753#post3097753)

:D

[Mr. Scott]

What I'm starting to infer here is that Kleinman believes evolution is an adaptive process but not a creative process.

For example, he apparently believes a bacterium that encounters penicillin has some sort of mechanism in which it declares “Oh my, this toxin is going to kill me. I better mutate my genome so that it won’t.” However, if three antibiotics are simultaneously present, the bacterium becomes overwhelmed and dies. There is, of course, no evidence for any such mechanism.

This is, by the way, a Lysenkoist (http://en.wikipedia.org/wiki/Lysenkoism) theory, based not on science but on ideology, and when followed in communist Russia and China caused mass starvation. A similar Kleinmanist theory of antibiotic adaptation, if adopted, would similarly lead to massive spread of disease, since it is also based on ideology, not science.

The purpose of Ev was to show how mutation and natural selection was indeed a creative process. It has succeeded. It was not intended, nor is it particularly useful in predicting the absolute “speed” of the real world evolutionary creative process, because the whole world of nature is, for the time being, beyond the capacity of any simulation.

There is, nevertheless, a mountain of consistent evidence for the creative process of evolution, including the Ev simulation. That we can confound evolution is some instances with carefully targeted intense multiple antibiotic or antiviral selection pressures does nothing to refute Darwin’s theory of evolution.

Because evolution is a creative process (especially by gene duplication and mutation) evolving a dinosaur into a bird is feasible if new genes endow the genome with reproductive advantages. Genetic and geologic evidence confirm dino-to-bird evolution. We’ve seen creative adaptations in recent human history (Flavobacterium Sp. K172 in 1975) so the theory of evolution is quite alive and well, growing in evidential support and academic acceptance daily. Kleinman’s google-bombing here has only one effect -- to make him look deluded and ignorant.

[Paul C. Anagnostopoulos]

Of course you admit that ev is not evolving real binding sites because it isn’t.
So then why in the name of all that is holy do you keep saying things like "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."?


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.
I don't think we're refusing to accept that some things are harder to evolve than others. I think what we're refusing to accept is the conclusions you are drawing from comparing two different functions.


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.
How, exactly?


Likewise, if you run ev long enough you long enough, you can evolve a perfect creature when Rf>Rcapacity.
Agreed. The point is that there is a discontinuity in the number of generations required when Rcapacity is exceeded.


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.
That sounds about right.


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.
Yes, it should take longer because Rseq can drift above Rfreq even with a few mistakes remaining.

~~ Paul

[Paul C. Anagnostopoulos]

So, joobz, your speculation that variable mutation rate has a profound affect on the rate of evolution is exactly just that, speculation.
The data for mutations vs. generations to perfect creature fits:

$88{,}680 x^{-.71}$

If you ignore the last point, it fits:

$102{,}786 x^{-.80}$


~~ Paul

[Paul C. Anagnostopoulos]

Can you translate what he said ?
Me wanna know, too.

~~ Paul

[Belz...]

Copycat. (http://forums.randi.org/showthread.php?postid=3097753#post3097753)

:D

Hey! I had no idea!!

[Belz...]

What I'm starting to infer here is that Kleinman believes evolution is an adaptive process but not a creative process.

For example, he apparently believes a bacterium that encounters penicillin has some sort of mechanism in which it declares “Oh my, this toxin is going to kill me. I better mutate my genome so that it won’t.” However, if three antibiotics are simultaneously present, the bacterium becomes overwhelmed and dies. There is, of course, no evidence for any such mechanism.

Those creationists DO appear to be stuck with Lamarckism, don't they ?

[Mr. Scott]

Those creationists DO appear to be stuck with Lamarckism, don't they ?

Cognitive dissonance (http://en.wikipedia.org/wiki/Cognitive_dissonance) at work. Even monkeys do it (http://www.world-science.net/othernews/071106_rationalize.htm).

[Mr. Scott]

Those creationists DO appear to be stuck with Lamarckism, don't they ?

Kleinman seems to be arguing for:

...the second component of Lamarck's theory of evolution ... the adaptation of organisms to their environment. This could move organisms sideways from the ladder of progress .. it could also drive organisms into evolutionary blind alleys, where the organism became so finely adapted that no further change could occur.

...hence three adaptative micro-evolutions and the organism strikes out.

Jean-Baptiste Lamarck linky (http://en.wikipedia.org/wiki/Lamark#Le_pouvoir_de_la_vie:_The_complexifying_for ce)

[kjkent1]

The data for mutations vs. generations to perfect creature fits:

http://www.randi.org/latexrender/latex.php?$88{,}680 x^{-.71}$

If you ignore the last point, it fits:

http://www.randi.org/latexrender/latex.php?$102{,}786 x^{-.80}$


~~ PaulI'm not understanding why you contnue to argue with kleinman over the evolutionary times to "perfect creature" with any mistake weight set at zero. Seems to me that the definition of "perfect creature" is completely different as soon as any mistake weight is zeroed out, because the algorithm stops looking for the zeroed-out errors in the genome.

A "perfect creature" with all three mistake weights set to zero is identical to the random genome that ev starts with, because the algorithm can't distinguish the existence of any mistakes. That's why it halts at generation 1.

[kleinman]

The results for your speculations were obtained from the JooBz (Just Baloney) computer simulation of mutation and speculation.Not at all. I simply used your theory of multiple selection pressures slowing evolution (which I believe represents an accurate explanation as to how multiple drug therapy works) demonstrates clearly how evolution is quite possible. Varying the number and intensity of pressures will rapidly accelerate evolution.
Joobz, varying the number and intensity of pressures will rapidly accelerate evolution only when you reduce down the number of selection pressures to a single strong selection pressure and start with less than lethal selection intensity and slowly increase the intensity. I understand your misinterpretation of this principle because evolution is not your field. Your understanding of the theory of evolution is on par with your understanding of abiogenesis.
Looks like you are going to get coal in your stocking this year.Baby new theory gives out diamonds to everyone who understands the nature of variable multiple selection pressures and how it accelerates evolution.
The only problem with your mythical story is that in order to make diamonds you need pressure and joobz, you don’t have the pressure.
Joobz, you better tell these authors that you can’t stop evolution.Thank you kleinman for that reference, it also agrees with the concept that variable pressures and optimal mutation rate can accelerate evolution.This latter case is potentially a worry because the elevated mutation rate might facilitate evolution to a part of the fitness landscape that was otherwise not likely to be accessed. In general, if mutagenesis
increases the mutation rate closer to the mutation-rate optimum for the virus, then mutagenesis will presumably be counterproductive for treatment. This possibility seems unlikely for RNA viruses, as their intrinsic mutation rates are so high. However, the relevant parameters are not adequately known to exclude this possibility, so the caution seems warranted.
Joobz forgot to post this part of the citation.
http://jvi.asm.org/cgi/reprint/JVI.01624-06v1.pdf (http://jvi.asm.org/cgi/reprint/JVI.01624-06v1.pdf)
A treatment strategy to prevent the evolution of significant or complete resistance could be combination therapy of several mutagens or of a mutagen in combination with other antiviral drugs.
Joobz still doesn’t understand that it is the number of selection pressures which dominate the behavior of the mutation and selection sorting/optimization problem. Changing the mutation rate has only a slight effect on the rate of evolution when compared by the profound affect that increasing the number of selection pressure has on the rate of convergence. The fact that evolution is not joobz’s field makes it understandable that he wouldn’t know that most mutations are harmful and that introducing a mutagen to a population is generally harmful to a population. On the other hand, joobz is an alchemical engineer and he should know that many chemicals are mutagens and cause cancer and death.
If the sun shines on lead long enough does it turn into gold?Kleinman keeps asking this irrelevant question, but he has it backwards. Sunshine turns lighter elements into gold, and gold into lead, through the fast neutron capture process.
This analogy is totally relevant Myriad because joobz has claimed that any chemical reaction is possible if you have enough free energy. Sunlight also decomposes organic molecules. If you don’t believe this, look at what happens to tires exposed to sunlight for a few years. It is joobz’s type of idiotic unscientific logic that drives the theory of evolution. The failure of evolutionists to properly elucidate the mutation and selection sorting/optimization process has caused and will continue to cause the premature deaths of millions of people suffering from diseases subject to the phenomenon of mutation and selection.
Kotatsu, have you made a phylogenic tree specifically for humans?I invite you to explain the relevance of your question, and also to perhaps answer the questions I had about what you mean by "a higher branch". Further, I'd like to know what part of the following statement:

"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."

it is you oppose.

To answer your question: yes, I have made a phylogenetic tree which included humans, but was not specifically targeted only at humans. It included sequences from all apes, some monkeys, and an assortment of other mammals. The results of the analysis of that tree, as I recall, was exactly as predicted. The analysis included jackknifing, bootstrapping, distance, and a plain parsimony analysis, and was part of my systematics education.
I’m just trying to find out if you are a closet eugeneticist. By your analysis, some humans are more evolutionarily advanced than others. So Kotatsu, tell us which humans constitute the super race?
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?DNA.
So now DNA becomes a selection pressure. Kotatsu do you want to explain to us how DNA is a selection pressure?
Of course you admit that ev is not evolving real binding sites because it isn’t.So then why in the name of all that is holy do you keep saying things like "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."?
I continue to point this out because Dr Schneider and you have adopted sloppy terminology for your computer simulation. The sequences of bases that Dr Schneider’s sorting algorithm evolves have nothing whatsoever to do with binding sites. They are simply sequences of bases which satisfy the selection conditions. Here is what Dr Schneider said in the abstract from his paper:
http://nar.oxfordjournals.org/cgi/content/full/28/14/2794 (http://nar.oxfordjournals.org/cgi/content/full/28/14/2794)
How do genetic systems gain information by evolutionary processes? Answering this question precisely requires a robust, quantitative measure of information. Fortunately, 50 years ago Claude Shannon defined information as a decrease in the uncertainty of a receiver. For molecular systems, uncertainty is closely related to entropy and hence has clear connections to the Second Law of Thermodynamics. These aspects of information theory have allowed the development of a straightforward and practical method of measuring information in genetic control systems. Here this method is used to observe information gain in the binding sites for an artificial ‘protein’ in a computer simulation of evolution. The simulation begins with zero information and, as in naturally occurring genetic systems, the information measured in the fully evolved binding sites is close to that needed to locate the sites in the genome. The transition is rapid, demonstrating that information gain can occur by punctuated equilibrium.
I added the highlighting. Ev is not evolving binding sites for an artificial ‘protein’. Ev is only sorting sequences of bases which satisfy the sorting conditions, nothing more and nothing less. And what ev shows is that only extremely simple sorting conditions sort quickly in the model. This is reflected in real examples of mutation and selection. Add additional sorting conditions to any mutation and selection sorting/optimization process profoundly slow the process. That is the mathematical and empirical fact of life you evolutionists refuse to acknowledge and the end result of this denial is the premature death of millions of people suffering from diseases subject to the principles of mutation and selection. If you want to teach children about evolution, teach them how mutation and selection actually works, not your irrational and illogical concept of common descent.
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.I don't think we're refusing to accept that some things are harder to evolve than others. I think what we're refusing to accept is the conclusions you are drawing from comparing two different functions.
You continue to make this idiotic statement that somehow ev is evolving function. Ev is simply a sorting algorithm, sorting sequences of bases which satisfy the sorting conditions, which shows that sorting multiple conditions simultaneously are far more difficult than sorting single conditions at a time. This is the mathematical and empirical fact of life you are in denial of. Your distorted and irrational concept of mutation and selection has nothing to do with mathematics or science.
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.How, exactly?
Irrational and illogical assertions like Adequate’s and rocketdodger’s that n+1 selection pressures evolve more rapidly than n selection pressures is a perfect example. If infectious disease experts listened to this nonsense, they would not use combination therapy to treat HIV, HBV, HCV, Malaria, TB,… Your irrational assertion that ev is somehow evolving function when all ev is doing is sorting sequences of bases and shows that this sorting process becomes profoundly slow when you have multiple simultaneous sorting conditions. Ev properly shows how the mutation and selection sorting process works and you are refusing to acknowledge that the dominant parameter in this sorting problem is the number of selection conditions contributes to the confusion evolutionists have in understanding how mutation and selection actually works. You evolutionists have no right to teach your irrational belief system to children and if you do succeed in doing so, you will raise another generation who do not understand how the mutation and selection sorting/optimization process actually works.
Likewise, if you run ev long enough you long enough, you can evolve a perfect creature when Rf>Rcapacity.Agreed. The point is that there is a discontinuity in the number of generations required when Rcapacity is exceeded.
Paul, there is no discontinuity in the convergence of ev when you use only a single selection condition. It is the increased complexity of multiple sorting conditions that profoundly slows the ability of ev to do the sort. And Paul, if you read the hundreds of citations of real examples of mutation and selection posted, you would find the same result.
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.Yes, it should take longer because Rseq can drift above Rfreq even with a few mistakes remaining.
And that in fact is what is shown by the data I posted last night. I stopped the case for 30 mutations/G/gen at 1,000,000 generations. It was hovering between 3-5 mistakes. But the bottom line on this series of cases shows that joobz speculation that varying the mutation rate will overcome the effect of combined selection pressures is wrong. Mutation rate has only a tiny effect on the rate of sorting when compared to the profound effect that the number of selection conditions has on the mutation and selection sorting/optimization process.
So, joobz, your speculation that variable mutation rate has a profound affect on the rate of evolution is exactly just that, speculation.The data for mutations vs. generations to perfect creature fits: 88,680x^-.71
Paul why don’t you do a curve fit for the generations for convergence as a function of the number of selection pressures? Oh, that’s right; you have made the idiotic assertion that sorting based on only one of the three selection conditions gives a different function. Paul, do you want to claim that giving three drug combination therapy for the treatment of HIV gives different function than giving the drugs one at a time sequentially?

Paul, this idiotic understanding of the mutation and selection sorting/optimization process that evolutionists assert has caused and will continue to cause the premature deaths of millions of people suffering from diseases subject to the phenomenon of the mutation and selection sorting/optimization process. Paul, perhaps you can confuse another generation with these idiotic assertions so that they to do not understand how the mutation and selection sorting/optimization process actually works.

How can I end a post without another citation which show that combination selection pressures profoundly slow the evolutionary process.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1533841 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1533841)
This improved understanding of the evolution of drug resistance has come from a relatively simple situation. Until recently, the number of antimalaria drugs in common use was small: chloroquine and sulfadoxine-pyrimethamine in Africa and the Americas, with mefloquine and more recently, mefloquine-artesunate in Southeast Asia[13]. As chloroquine and sulfadoxine-pyrimethamine have lost their efficacy, combination drugs have been strongly endorsed as the most effective next step [14]. In response to this emphasis, many different combination drugs, most containing an artemisinin derivative are being used in various countries, especially in East Africa (Figure 1. Many of these combinations have shown excellent initial efficacy in drug trials [13], but only mefloquine/artesunate has a long enough history to allow a strong prediction of the useful therapeutic life of these combinations [15]. It is particularly important to establish a baseline for effectiveness of new drugs and combinations so that any subsequent changes can be seen. This complex situation underlines the importance of regional surveillance of drug use, efficacy and effectiveness as these new combinations are tried in a variety of demographic and ecological settings. What has worked well for a long time in Thailand may not be so long lived in Tanzania [16]!

[joobz]

Joobz, varying the number and intensity of pressures will rapidly accelerate evolution only when you reduce down the number of selection pressures to a single strong selection pressure and start with less than lethal selection intensity and slowly increase the intensity.Not just 1 strong selection. This is wrong. Multiple selections with variable intensity. We know that nature provides such systems continuously.

I see that you have been brainwashed into thinking that multiple selection pressures are magically constant and unwavering. This is ok. It can be quite hard overcoming your belief systems. All I can do is demonstrate the evidence that exists in the real world. Thankfully all evidence you have presented support this.



The only problem with your mythical story is that in order to make diamonds you need pressure and joobz, you don’t have the pressure.Sure there are many pressures in the environment. They aren't constant. that's all. That is what accelerates the growth of this diamond, the theory of evolution.

Joobz still doesn’t understand that it is the number of selection pressures which dominate the behavior of the mutation and selection sorting/optimization problem. Changing the mutation rate has only a slight effect on the rate of evolution when compared by the profound affect that increasing the number of selection pressure has on the rate of convergence. The fact that evolution is not joobz’s field makes it understandable that he wouldn’t know that most mutations are harmful and that introducing a mutagen to a population is generally harmful to a population. On the other hand, joobz is an alchemical engineer and he should know that many chemicals are mutagens and cause cancer and death.yes they do. interesting that, isn't it. You'll also notice that many cancers/bacteria/viruses can adapt to their environment when variable selection pressures are enacted. This is what all disease treatment models show and what is present in nature. You are obviously just ignorant of the theory of multiple selection pressures.

[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 just gonna post this over and over... it is a priceless gem of a statement.

[Henners]

<<I understand your misinterpretation of this principle because evolution is not your field. >>

The figure of speech being employed here is ...

(a) tinny

(b) sticky

(c) irony

[Belz...]

I am just gonna post this over and over... it is a priceless gem of a statement.

I still don't know what it's supposed to mean. How are you supposed to alter a molecule's ability ?

"Hey, man. This molecule of H20 doesn't quite taste like water!"

[kleinman]

Joobz, varying the number and intensity of pressures will rapidly accelerate evolution only when you reduce down the number of selection pressures to a single strong selection pressure and start with less than lethal selection intensity and slowly increase the intensity.Not just 1 strong selection. This is wrong. Multiple selections with variable intensity. We know that nature provides such systems continuously.

I see that you have been brainwashed into thinking that multiple selection pressures are magically constant and unwavering. This is ok. It can be quite hard overcoming your belief systems. All I can do is demonstrate the evidence that exists in the real world. Thankfully all evidence you have presented support this.
Unfortunately for you joobz you only have your speculations to support your argument. Even just two less than fatal selection pressures when combined can still cause extinction of the population. It is you who is brainwashed that somehow selection pressures cooperate with each other in the mutation and selection sorting/optimization process. Your irrational and illogical thinking about how mutation and selection works fits well with your irrational and illogical concept of cooperative chemistry for abiogenesis. You have no mathematics and no empirical evidence to support your speculations.
The only problem with your mythical story is that in order to make diamonds you need pressure and joobz, you don’t have the pressure.Sure there are many pressures in the environment. They aren't constant. that's all. That is what accelerates the growth of this diamond, the theory of evolution.
Poor joobz, all that speculation and no mathematics or empirical evidence to substantiate his speculations; ok joobz, tell us what that pressure is that would evolve a gene de novo? Your theory doesn’t qualify as diamond, it doesn’t even qualify as paste.
Joobz still doesn’t understand that it is the number of selection pressures which dominate the behavior of the mutation and selection sorting/optimization problem. Changing the mutation rate has only a slight effect on the rate of evolution when compared by the profound affect that increasing the number of selection pressure has on the rate of convergence. The fact that evolution is not joobz’s field makes it understandable that he wouldn’t know that most mutations are harmful and that introducing a mutagen to a population is generally harmful to a population. On the other hand, joobz is an alchemical engineer and he should know that many chemicals are mutagens and cause cancer and death.yes they do. interesting that, isn't it. You'll also notice that many cancers/bacteria/viruses can adapt to their environment when variable selection pressures are enacted. This is what all disease treatment models show and what is present in nature. You are obviously just ignorant of the theory of multiple selection pressures.
Joobz, you have made a claim that variability of selection pressures is what makes the theory of evolution work. Tell us how it happens both mathematically and empirically. Or is this just a minor gap in your speculations?
I am just gonna post this over and over... it is a priceless gem of a statement.I still don't know what it's supposed to mean.
Rocketdodger does not understand how selection pressures affect the sequences of DNA.
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.
You don’t need molecules to interact directly with the DNA in order to influence the selection of particular mutations in DNA. Of course, what can you expect from someone who thinks that the more selection pressures imposed on a system the faster the sorting process for these selection conditions proceeds. Oh, rocketdodger, feel free to post that citation as many times as you want. After all, I have some oldies but goodies for you, like 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 http://forums.randi.org/images/smilies/frown.gif
and
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.
Rocketdodger, you haven’t made much progress on the mutation and selection sorting/optimization process since you made these posts.

Rocketdodger, perhaps you can convince infectious diseases experts that n+1 selection pressures evolve more rapidly than n selection pressures and they will stop using combination therapy.
http://forums.randi.org/images/smilies/doglaugh.gif

[Belz...]

Rocketdodger does not understand how selection pressures affect the sequences of DNA.

That's okay. You don't understand how molecules work.

[Belz...]

After all, I have some oldies but goodies for you, like this:

That's why you're stuck with Lamarckism, Klein. You can't let go of obsolete statements.

Tell me, do you prefer red M&Ms ?

[kleinman]

Rocketdodger does not understand how selection pressures affect the sequences of DNA.That's okay. You don't understand how molecules work.
Oh, that’s right, you have proven that molecules beggaminases.
After all, I have some oldies but goodies for you, like this:That's why you're stuck with Lamarckism, Klein. You can't let go of obsolete statements.
You are the one stuck on the obsolete theory of evolution. Modern mathematics and computers enables the modeling of the mutation and selection sorting/optimization process and modern science enables the sequencing and identifying the consequences of the mutation and selection sorting/optimization process. These modern technologies show that the mutation and selection sorting/optimization process is profoundly slowed when you have more than a single selection condition acting. That’s what the peer reviewed and published model or random point mutations and natural selection ev shows and that is what the hundreds of real examples of mutation and selection cited demonstrate. So Belz, you are the one stuck with the obsolete theory.

[Mr. Scott]

I’m just trying to find out if you are a closet eugeneticist. By your analysis, some humans are more evolutionarily advanced than others. So Kotatsu, tell us which humans constitute the super race?

My day doesn't start until Kleinman, the Kwazy Kweationist posts. Can I answer this one?

The Chinese are more evolutionarily advanced. There are more of them, so their genes are more prevalent. My Chinese friends seem to be more advanced than us whites, and a mixed Chinese/white kid I know is good at both math and sports!

By the way, are the Chinese a race... or a kind? Did Noah have to keep a mating pair on his ark? Or did God smite Mandarin into one of the slaves building the Tower of Babel?

[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 don't really see any point in arguing with a mind capable of producing something like the above paragraph.

[joobz]

Unfortunately for you joobz you only have your speculations to support your argument. Even just two less than fatal selection pressures when combined can still cause extinction of the population. It is you who is brainwashed that somehow selection pressures cooperate with each other in the mutation and selection sorting/optimization process. Your irrational and illogical thinking about how mutation and selection works fits well with your irrational and illogical concept of cooperative chemistry for abiogenesis. You have no mathematics and no empirical evidence to support your speculations.This isn't my theory. I am simply applying the theory you presented, which shows that strong, multiple stable selection pressures prevents the population from adapting and thereby go extinct. I thank you for presenting this. Unfortunately, you are unable to see the reality of what that theory shows because your belief system prevents you from seeing it.

That multiple variable selection pressures can accelerate the evolutionary process and that nature provides a constant stream of variable pressures.

Poor joobz, all that speculation and no mathematics or empirical evidence to substantiate his speculations; ok joobz, tell us what that pressure is that would evolve a gene de novo? Your theory doesn’t qualify as diamond, it doesn’t even qualify as paste.

Joobz, you have made a claim that variability of selection pressures is what makes the theory of evolution work. Tell us how it happens both mathematically and empirically. Or is this just a minor gap in your speculations? I have presented this. Don't be lazy and go back and read the papers that I gave you. The ones you like to mock becuase you don't understand them.

Also, all papers that you present show this as well. Afterall, I am simply applying the theory you have developed. It is quite clear that the variable multiple selection pressures in nature provides an accelerated chance for evolution to occur. Coupled this with a variable mutation rate, and evolution is quite real and possible

Thank you for this paper as well.
increases the mutation rate closer to the mutation-rate optimum for the virus, then mutagenesis will presumably be counterproductive for treatment. This possibility seems unlikely for RNA viruses, as their intrinsic mutation rates are so high. However, the relevant parameters are not adequately known to exclude this possibility, so the caution seems warranted.

[Mr. Scott]

I’m just trying to find out if you are a closet eugeneticist. By your analysis, some humans are more evolutionarily advanced than others. So Kotatsu, tell us which humans constitute the super race?

I'd like to respond to this seriously. It seems to be an appeal to emotions. That eugenics and master race ideas are horrific have no bearing on whether or not Darwinian evolution occurred. The social implications of a theory are independent of the correctness of the theory. Dr. Kleinman, you've just exemplified how creationists are not just annoying and unscientific, but also despicable and dishonest.

[Belz...]

Oh, that’s right, you have proven that molecules beggaminases.

:rolleyes: Now you're just being stupid, Kleinman. Feel free to argue like a five year-old if you want.

You are the one stuck on the obsolete theory of evolution.

You are the one stuck on the obselete theory of special creation.

These modern technologies show that the mutation and selection sorting/optimization process is profoundly slowed when you have more than a single selection condition acting.

Except when you're using sorting/optimisation processes OTHER than ev, right ?

[Kotatsu]

I’m just trying to find out if you are a closet eugeneticist.

Rest assured that I am not.

By your analysis, some humans are more evolutionarily advanced than others.

By my analysis, no such conclusions could be drawn, as there were too few individuals of each species to give any kind of useful resolution at that level. What could be seen was a nested hierarchy of the normal kind, in which the various taxa were positioned as would be predicted. Note that with "normal kind" I mean that all branches were of equal length (apart from the distance analysis, of course), which does not in any way imply that any taxon is more advanced than any other.

Is there any field of knowledge which you actually have mastered? Or are you this dumb all over?

So Kotatsu, tell us which humans constitute the super race?

I have no idea, but my money would be on whatever "race" you're not.

So now DNA becomes a selection pressure. Kotatsu do you want to explain to us how DNA is a selection pressure?

If that was what you were asking for, your wording was poor, clumsy, insane or deliberately obscure.

[Paul C. Anagnostopoulos]

I'm not understanding why you contnue to argue with kleinman over the evolutionary times to "perfect creature" with any mistake weight set at zero. Seems to me that the definition of "perfect creature" is completely different as soon as any mistake weight is zeroed out, because the algorithm stops looking for the zeroed-out errors in the genome.
That particular dataset is from a series of experiments with all mistake counts set to 1.

~~ Paul

[Paul C. Anagnostopoulos]

I continue to point this out because Dr Schneider and you have adopted sloppy terminology for your computer simulation. The sequences of bases that Dr Schneider’s sorting algorithm evolves have nothing whatsoever to do with binding sites. They are simply sequences of bases which satisfy the selection conditions.
Perhaps you haven't noticed that when someone creates a computer model of a natural process, they tend to talk about the components and aspects of the model using the same terminology used for the natural process. In no case that I know of do they think that the model is the actual thing.


I added the highlighting. Ev is not evolving binding sites for an artificial ‘protein’. Ev is only sorting sequences of bases which satisfy the sorting conditions, nothing more and nothing less.
But then, if we continue to use your odd sorting approach, that is all that is happening in nature, too. So why keep harping on it?


You continue to make this idiotic statement that somehow ev is evolving function. Ev is simply a sorting algorithm, sorting sequences of bases which satisfy the sorting conditions, ...
... and ultimately evolving a gene with the function of binding to binding sites but no other positions.


Irrational and illogical assertions like Adequate’s and rocketdodger’s that n+1 selection pressures evolve more rapidly than n selection pressures is a perfect example. If infectious disease experts listened to this nonsense, they would not use combination therapy to treat HIV, HBV, HCV, Malaria, TB,
Their assertion contributes to the premature death of millions of people?

Your irrational assertion that ev is somehow evolving function when all ev is doing is sorting sequences of bases and shows that this sorting process becomes profoundly slow when you have multiple simultaneous sorting conditions.
This assertion of mine contributes to the premature death of millions of people?


Paul, there is no discontinuity in the convergence of ev when you use only a single selection condition. It is the increased complexity of multiple sorting conditions that profoundly slows the ability of ev to do the sort.
But why are there discontinuities when you have three pressures?


Paul why don’t you do a curve fit for the generations for convergence as a function of the number of selection pressures? Oh, that’s right; you have made the idiotic assertion that sorting based on only one of the three selection conditions gives a different function.
Do you think you end up with the same result regardless of the number of pressures?

~~ Paul

[kleinman]

I’m just trying to find out if you are a closet eugeneticist. By your analysis, some humans are more evolutionarily advanced than others. So Kotatsu, tell us which humans constitute the super race?I'd like to respond to this seriously. It seems to be an appeal to emotions. That eugenics and master race ideas are horrific have no bearing on whether or not Darwinian evolution occurred. The social implications of a theory are independent of the correctness of the theory. Dr. Kleinman, you've just exemplified how creationists are not just annoying and unscientific, but also despicable and dishonest.
Mr Scott, you say that about everyone including your parents. So now you are claim that Darwinian evolution does not apply to humans and some humans are not more fit than others? Your irrational and illogical speculation of how the mutation and selection sorting/optimization process actually works is worse than the evolutionist concepts of eugenics and master race. More people will die prematurely who suffer from diseases subject to the phenomenon of mutation and selection because evolutionists like you want to teach your irrationality to school children. The mutation and selection sorting/optimization process is profoundly slowed by combination selection pressures. A peer reviewed and published model of random point mutations and natural selection shows this and hundreds of real examples of mutation and selection show this. You don’t believe what your parents told you, you don’t believe the mathematics of mutation and selection and you don’t believe the empirical data of mutation and selection. You only believe the evolutionist dogma and it is wrong.
I’m just trying to find out if you are a closet eugeneticist.Rest assured that I am not.
So then you don’t believe some humans are more fit than others. How do humans evolve? While you are trying to figure out how humans will evolve, here is another citation which show that combination selection pressures slow evolution by the mutation and selection sorting/optimization process.
http://aac.asm.org/cgi/content/full/46/3/863 (http://aac.asm.org/cgi/content/full/46/3/863)
Our results show that some antibiotic treatments can select for mutator bacteria present at low frequencies among all wild-type populations. Actually, by selecting for a resistance allele, the antibiotic selective pressure also selected for a mutator allele as the mechanism that generated the resistance. Moreover, mutators could also facilitate the modification of the active sites of detoxification enzymes to shift the resistance from resistance to a low dose to resistance to a high dose (17) and extend their resistance spectra (12). It could also rapidly accumulate compensatory mutations that limit the cost to the bacteria associated with the resistance alleles (1). Mutator bacteria can be considered risk markers for antibiotic therapy. If corroborated by epidemiological data, our results would suggest that, in the case of a first therapeutic failure and if time allows, a diagnostic assay for the presence of mutators should determine the next therapeutic step. If a drug is available for which mutational events can very rarely generate antibiotic resistance, such as AMP at a high concentration used against the bacteria in the present study, then it is the first choice for use against the mutators. Otherwise, the use of a combination therapy seems to be the best alternative. As the selection of mutator bacteria is favored by several bacterial and environmental factors (18), some conditions (e.g., a large bacterial population) allow the selection of such strains more than others. In these cases, if possible, therapies should be initiated directly with a protocol that limits the risk of selection of mutators. For example, the use of antibiotics that inhibit a single enzyme should probably be set aside, even when used in combination therapies, as we did in the present work.

[joobz]

So then you don’t believe some humans are more fit than others. How do humans evolve? While you are trying to figure out how humans will evolve, here is another citation which show that combination selection pressures slow evolution by the mutation and selection sorting/optimization process.
http://aac.asm.org/cgi/content/full/46/3/863 (http://aac.asm.org/cgi/content/full/46/3/863)

I see you are having trouble understanding the nature of multiple selection pressures. This is something I expect, because your belief structure prevents you from seeing what the reality is.

When there are multiple constant, strong pressures exhibited on a population, that population will go extinct. however, when multiple pressures are placed on the population in varying fashion, the evolutionary process can accelerate. This is seen in nature, since nature does not possess a constant number of selection pressures.

Also, thank you for presenting another article which says quite clearly, that evolution is possible and quite real.

The emergence of antibiotic resistance during therapy can increase the rate of secondary bacteremia, hospitalization costs, and mortality (3 (http://aac.asm.org/cgi/content/full/46/3/863#R3)). Bacterial resistance can be acquired either by chromosomal mutations or by horizontal transfer of plasmid-borne resistance genes. In sensitive, strictly clonal bacterial populations (plasmid bearing or not), the generation of antibiotic resistance depends on the rate of emergence of resistant mutants, i.e., on the bacterial mutation rate (8 (http://aac.asm.org/cgi/content/full/46/3/863#R8), 9 (http://aac.asm.org/cgi/content/full/46/3/863#R9)). A correlation between high mutation rate and antibiotic resistance has been reported in the case of Pseudomonas aeruginosa isolated from the lungs of cystic fibrosis patients (11 (http://aac.asm.org/cgi/content/full/46/3/863#R11)). We used a model of bacterial colonization of germfree mice to assess in vivo the risk of emergence of antibiotic-resistant mutants due to mutator bacteria in the course of antibiotic treatment.

perhaps you better tell the authors that these bacteria aren't actually evolving.

[kleinman]

I continue to point this out because Dr Schneider and you have adopted sloppy terminology for your computer simulation. The sequences of bases that Dr Schneider’s sorting algorithm evolves have nothing whatsoever to do with binding sites. They are simply sequences of bases which satisfy the selection conditions.Perhaps you haven't noticed that when someone creates a computer model of a natural process, they tend to talk about the components and aspects of the model using the same terminology used for the natural process. In no case that I know of do they think that the model is the actual thing.
“Perfect creature” and “binding sites” is not reflective of what the ev sorting algorithm is modeling. All that ev is doing is sorting sequences based on sorting conditions and it shows how profoundly slow the process is when multiple sorting conditions are used simultaneously. This also is what happens in nature as the hundreds of citations posted shows.
I added the highlighting. Ev is not evolving binding sites for an artificial ‘protein’. Ev is only sorting sequences of bases which satisfy the sorting conditions, nothing more and nothing less.But then, if we continue to use your odd sorting approach, that is all that is happening in nature, too. So why keep harping on it?
What is odd about the sorting approach that I am using with your model? All I am doing is showing you what you model does when the sorting conditions are simplified. I will continue harping on this and posting more citations which substantiates this because this is how the mutation and selection sorting/optimization process actually works. You evolutionists are in denial.
You continue to make this idiotic statement that somehow ev is evolving function. Ev is simply a sorting algorithm, sorting sequences of bases which satisfy the sorting conditions, ...... and ultimately evolving a gene with the function of binding to binding sites but no other positions.
And I’ll continue to tell you that ev is not evolving any function or any binding sites. Ev is simply a sorting algorithm that demonstrates how slow the sorting process is when multiple sorting conditions are applied simultaneously.
Irrational and illogical assertions like Adequate’s and rocketdodger’s that n+1 selection pressures evolve more rapidly than n selection pressures is a perfect example. If infectious disease experts listened to this nonsense, they would not use combination therapy to treat HIV, HBV, HCV, Malaria, TB,Their assertion contributes to the premature death of millions of people?
Yes, because evolutionists believe this nonsense and will teach it to children. It will slow the understanding of how mutation and selection actually works.
Your irrational assertion that ev is somehow evolving function when all ev is doing is sorting sequences of bases and shows that this sorting process becomes profoundly slow when you have multiple simultaneous sorting conditions.This assertion of mine contributes to the premature death of millions of people?
Yes, because it obfuscates the understanding of how the mutation and selection sorting/optimization process actually works.
Paul, there is no discontinuity in the convergence of ev when you use only a single selection condition. It is the increased complexity of multiple sorting conditions that profoundly slows the ability of ev to do the sort.But why are there discontinuities when you have three pressures?
What discontinuity? Ev still converges when you have three pressures; it just doesn’t converge on your perfect creature. You have this mistaken belief that ev has only a single local optimum.
Paul why don’t you do a curve fit for the generations for convergence as a function of the number of selection pressures? Oh, that’s right; you have made the idiotic assertion that sorting based on only one of the three selection conditions gives a different function.Do you think you end up with the same result regardless of the number of pressures?
Of course I don’t think that. I no more think that you will have the same result with ev when using 1 versus 3 selection conditions than I think you will have the same result when treating HIV with monotherapy versus 3 drug combination therapy. If you increase the number of selection conditions in ev to 4, you will slow the sorting process even more so, just as the evidence is now starting to appear that 4 drug therapy for HIV works better than 3 drug therapy. How surprising that the mutation and selection sorting/optimization process would work like this.

[Mr. Scott]

Mr Scott, you say that about everyone including your parents. So now you are claim that Darwinian evolution does not apply to humans and some humans are not more fit than others? Your irrational and illogical speculation of how the mutation and selection sorting/optimization process actually works is worse than the evolutionist concepts of eugenics and master race.

That's incredibly bizarre and off-target. Your delusions seem boundless. My athiest parents never lied to me about evolution. I never claimed Darwinian evolution did not apply to humans or that some humans were not more fit than others. I called you on your appeal to emotions (which was also a veiled ad hominem). Evolution is not wrong just because eugenics is abhorrent. If the social consequences of a scientific theory were relevant to the validity of the theory, then the atom bomb couldn't have worked because it would kill, maim, and terrify so many people. Are you attempting to build a straw man tall enough to reach heaven? Remember how your god punishes hubris?

You didn't answer my questions:

Did Noah carry a mating pair of Chinese people on the ark? Or did God smite a Tower builder at Babel with Mandarin? Your creation story is in the same book as the ridiculous Noah and Babel fairy tales. Do you assign them equal validity?

[Kotatsu]

So then you don’t believe some humans are more fit than others. How do humans evolve?

Well, obviously some humans are more fit than others, as evidences for example by different susceptibility to mortal or sterilising diseases, differences in amount of young conceived and reared, and so on. However, these are generally differences which do not align themselves to perceived racial categories.

Also, implied in the term "eugenicist" is the will to actively sort out the individuals perceived to be less fit for the betterment of the species as a whole. Phylogenetics have nothing to do with this, nor does, indeed, the whole field of evolutionary science. If you want examples of wanton slaying of people not belonging to the ingroup, you need look no further than your own religion, sir.

[joobz]

What is odd about the sorting approach that I am using with your model? All I am doing is showing you what you model does when the sorting conditions are simplified. I will continue harping on this and posting more citations which substantiates this because this is how the mutation and selection sorting/optimization process actually works. You evolutionists are in denial.

And I’ll continue to tell you that ev is not evolving any function or any binding sites. Ev is simply a sorting algorithm that demonstrates how slow the sorting process is when multiple sorting conditions are applied simultaneously.It is good that you continue demonstrating these things. You've hit upon a feature that proves the fact that evolution is possible. You've shown that constant severe multiple selection pressures results in arrested evolution and/or extinction. However, your theory also shows that variable pressures (in number and strength) provides Ideal conditions for the accelerated adaptation. This is substantiated by the numerous examples of resistence emergence that you have presented over and over again. Since nature only provides random highly variable pressures, we know that evolution is quite possible.

Unfortunately, your delusions prevent you from seeing this reality just yet. That's ok, I'll keep presenting information that demonstrates this fact.

[Belz...]

Your irrational and illogical speculation of how the mutation and selection sorting/optimization process actually works is worse than the evolutionist concepts of eugenics and master race.

May I ask to which concepts of eugenics and master race you're refering to ?

[Belz...]

If you want examples of wanton slaying of people not belonging to the ingroup, you need look no further than your own religion, sir.

Touché.

[Paul C. Anagnostopoulos]

What is odd about the sorting approach that I am using with your model? All I am doing is showing you what you model does when the sorting conditions are simplified. I will continue harping on this and posting more citations which substantiates this because this is how the mutation and selection sorting/optimization process actually works. You evolutionists are in denial.
Is there any chance you could answer a question rather than just repeating your mantra?


Yes, because it obfuscates the understanding of how the mutation and selection sorting/optimization process actually works.
And so I'm contributing to the deaths of millions of people, yet all you do about it is waste your time on this forum. You have the opportunity to out someone as bad as Hitler, yet all you do is waste your time on this forum.

Who is it that is contributing to the deaths of millions of people, you *********** moron?


What discontinuity? Ev still converges when you have three pressures; it just doesn’t converge on your perfect creature. You have this mistaken belief that ev has only a single local optimum.
Converging on the same local optimum as a parameter is varied, and then suddenly converging on a different local optimum is a discontinuity. Your mantra has taken over your brain, Alan.


Of course I don’t think that. I no more think that you will have the same result with ev when using 1 versus 3 selection conditions ...
And yet you will not let me say that we end up with two different functions.

~~ Paul

[Paul C. Anagnostopoulos]

Your irrational and illogical speculation of how the mutation and selection sorting/optimization process actually works is worse than the evolutionist concepts of eugenics and master race.
You're over the top, Alan.

~~ Paul

[Mr. Scott]

You're over the top, Alan.

~~ Paul

It's an hour before Kleinman the Great arrives at his clinic and, instead of following up on his patients' MRIs or saving the world from monotherapy, debates us Devils of Darwinism on an "obscure Internet forum."

Let me get his first cracks out of the way so he can get down to business.

It is you deluded evolutionists who are over the top with your mathematically impossible theory of mutation and selection, shown impossible by Dr. Schneider's peer-reviewed program and the hundreds of real world examples I've posted.

(Try this: The universe is a sorting and optimization problem. A computer simulation to model every atomic particle would run profoundly slowly. Therefore, an invisible all-powerful being runs it.)

Am I catching on?

You evolutionists want to talk about anything but the mathematics of mutation and natural selection.

It's too easy. After a year of this, I too have spawned a kleinbot function in my brain. Actually, Kleinman has evolved, although profoundly slowly. Read the first few pages of this thread and you will see obsolete arguments. Notice how he doesn't use the words macro- or mico-evolution any more?

[kjkent1]

“Perfect creature” and “binding sites” is not reflective of what the ev sorting algorithm is modeling. All that ev is doing is sorting sequences based on sorting conditions and it shows how profoundly slow the process is when multiple sorting conditions are used simultaneously. This also is what happens in nature as the hundreds of citations posted shows.Once upon a time in this thread, kleinman took the position that "ev is plausible model" of evolution, "Schneider got it right with ev," and that "I'll defend Schneider's work even if none of you evolutionists will."

Now, slowly but surely, ev has become nothing more than a sequence sorting program, which doesn't require any relevant biological premises. It doesn't matter that the whole purpose of the ev experiment is to show that binding sites can evolve and gain information. All that matters is that point mutation and selection is profoundly slow, and multiple relatively severe selection pressures slow evolution.

Wow, that last conclusion is really mind numbing! How could anyone seriously think that if they were to spread 3-4 different weed killers on their lawn, that there would be a lawn left at the end of the week!

True brilliance is the stuff of which kleinman is made.

[kleinman]

Mr Scott, you say that about everyone including your parents. So now you are claim that Darwinian evolution does not apply to humans and some humans are not more fit than others? Your irrational and illogical speculation of how the mutation and selection sorting/optimization process actually works is worse than the evolutionist concepts of eugenics and master race.That's incredibly bizarre and off-target. Your delusions seem boundless. My athiest parents never lied to me about evolution. I never claimed Darwinian evolution did not apply to humans or that some humans were not more fit than others. I called you on your appeal to emotions (which was also a veiled ad hominem). Evolution is not wrong just because eugenics is abhorrent. If the social consequences of a scientific theory were relevant to the validity of the theory, then the atom bomb couldn't have worked because it would kill, maim, and terrify so many people. Are you attempting to build a straw man tall enough to reach heaven? Remember how your god punishes hubris?
So your parents were atheists and could prove that there is no God. They did lie to you.

Certainly eugenics is abhorrent but the concept of eugenics is a valid deduction from the theory of evolution. If it is survival of fittest then some humans are more fit than others. Of course you could deny that humans are not evolving but how do you reconcile that with the rest of your belief system. Your mathematically impossible theory of evolution is an abhorrent theory.
So then you don’t believe some humans are more fit than others. How do humans evolve?Well, obviously some humans are more fit than others, as evidences for example by different susceptibility to mortal or sterilising diseases, differences in amount of young conceived and reared, and so on. However, these are generally differences which do not align themselves to perceived racial categories.
Ok, so your argument there is survival of the fittest.
Also, implied in the term "eugenicist" is the will to actively sort out the individuals perceived to be less fit for the betterment of the species as a whole. Phylogenetics have nothing to do with this, nor does, indeed, the whole field of evolutionary science. If you want examples of wanton slaying of people not belonging to the ingroup, you need look no further than your own religion, sir.
Don’t species actively sort out the individuals less fit? Why shouldn’t humans?

Wanton slaying of people saying they are doing it in the name of god don’t hold a candle to the work of evolutionists like Hitler, Stalin, and Mao. Then how many abortionists are also evolutionists? It is your mathematically impossible theory which is abhorrent. Of course evolutionists redeem themselves by starting hospitals all over the world. Didn’t we just see the opening of the “Evolutionist Hospital of the Most Fit”?

[joobz]

Your mathematically impossible theory of evolution is an abhorrent theory.So you are against personalized medicine. You believe that everyone is equal and will, therefore, respond equally to any disease treatment. Unfortunately, you are completely unaware of the modern trends in medicine which will account for the known population variations and will one day, provide the idealized best care for each patient. Soon, gone will be the days where doctors guessed which medicine(out of several) a patient should have becuase the average population works well on that drug. It seems that you are in need of some continuing education courses to maintain your MD.

Wanton slaying of people saying they are doing it in the name of god don’t hold a candle to the work of evolutionists like Hitler, Stalin, and Mao. Then how many abortionists are also evolutionists? It is your mathematically impossible theory which is abhorrent. Of course evolutionists redeem themselves by starting hospitals all over the world. Didn’t we just see the opening of the “Evolutionist Hospital of the Most Fit”?
Now this is just silly. You simply need to learn a bit more about the way variable multiple selection pressures work and that nature is a variable environment in order to understand that not only is the evolutionary theory possible, it is real.

[kjkent1]

Wanton slaying of people saying they are doing it in the name of god don’t hold a candle to the work of evolutionists like Hitler, Stalin, and Mao. Then how many abortionists are also evolutionists? It is your mathematically impossible theory which is abhorrent. Of course evolutionists redeem themselves by starting hospitals all over the world. Didn’t we just see the opening of the “Evolutionist Hospital of the Most Fit”?You mean that because Stalin killed millions in the name of communism, that it's okay that the Christian settlers of the new world slaughtered nearly the entire native american population?

Similar for Mao vs. Cortez and the Aztecs. Similar for Hitler (who by the way thought he was authorized by God to wipe out the Jews) vs. King Richard.

Oh, and let's not forget that the Antebellum South justified slavery by reference to Exodus 21.

Apparently, your theory is that as long as your God isn't the worst murderer on the block, that means he should be exonerated.

That's pretty ill, Alan. Stay away from philosophy discussions -- you're gonna hurt yourself.

[Belz...]

[B]Wanton slaying of people saying they are doing it in the name of god don’t hold a candle to the work of evolutionists like Hitler, Stalin, and Mao. Then how many abortionists are also evolutionists? It is your mathematically impossible theory which is abhorrent. Of course evolutionists redeem themselves by starting hospitals all over the world. Didn’t we just see the opening of the “Evolutionist Hospital of the Most Fit”?

I'd like you to show how Hitler and the others were representative of darwinism in general. I'd also remind you that Hitler was a Christian, so he actually adds up with the Crusades and the Inquisition.

It's also interesting to see how your argument is slowly shifting towards appeals to emotion and personal attacks rather than evidence, since it's been shown for over a year now that you don't have any.

[Shalamar]

People. Klienman is a broken record. He does not believe in the Scientific Theory of Evolution, because he doesn't believe in it! Yes. Its circular. He ignores the fact that most medicines are developed using evolutionary practices. He ignores the problems in hospitals due to bacteria, and other illnesses developing resistances to anti-biotics.

He is TERRIFIED of Evolution, because he feels it will destroy his faith. He gets it so very wrong, and he continues to focus on small things, and yet, he has yet to prove, and show his math that it is 'mathematically abhorrent'.

Now he's using eugenetics to 'prove' that Evolution is immoral, and evil.

As for hospitals, I was not aware that each and every hospital in the world was solely religious based. I'm sure there are scores of medical researchers who would be horrified that Klienman finds them to be 'abhorrent' because they use evolutionary principles to do their work. They should all Just pray for everything to be cured! I'm sure Klienman uses no medicines at all, and just uses prayer, as medicine would be abhorrent...

[kleinman]

What is odd about the sorting approach that I am using with your model? All I am doing is showing you what you model does when the sorting conditions are simplified. I will continue harping on this and posting more citations which substantiates this because this is how the mutation and selection sorting/optimization process actually works. You evolutionists are in denial.Is there any chance you could answer a question rather than just repeating your mantra?
I am answering the question which Dr Schneider asked in his own paper.
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.
Sorry you don’t like the answer because it doesn’t fit your world view.
Yes, because it obfuscates the understanding of how the mutation and selection sorting/optimization process actually works.And so I'm contributing to the deaths of millions of people, yet all you do about it is waste your time on this forum. You have the opportunity to out someone as bad as Hitler, yet all you do is waste your time on this forum.

Who is it that is contributing to the deaths of millions of people, you *********** moron?
My, my Paul, a moderator violating the forum’s rules, you are setting a bad example. Yes Paul, you are obfuscating how Dr Schneider’s sorting algorithm works and Dr Schneider’s sorting algorithm works just like it does in the real world. Combination selection pressures profoundly slow the mutation and selection sorting/optimization process. In order to find cures for diseases subject to the principles of mutation and selection, it requires understanding how this process works. Paul, you are in denial of how this process works as shown by your own computer model. Hitler was an evolutionist; he advanced the concept of a super race which is a simple deduction of the concept of survival of the fittest.
What discontinuity? Ev still converges when you have three pressures; it just doesn’t converge on your perfect creature. You have this mistaken belief that ev has only a single local optimum.Converging on the same local optimum as a parameter is varied, and then suddenly converging on a different local optimum is a discontinuity. Your mantra has taken over your brain, Alan.
I have my mantras and you have your mantras. You are making claims about Rcapacity without producing the data. What if changing the binding site width changes the fitness landscape from one appearing more like mountain ranges to a different fitness landscape that looks like rolling plains. If you want the answer to this question you need to map out the fitness landscape. You may be able to get some idea of the shape of the fitness landscape by tracking the mistake counts for each of the selection conditions and avoid the massive computational effort of generating the fitness landscape. From my point of view though, it makes no difference. Ev is either profoundly slow to converge or it doesn’t converge at all.
Of course I don’t think that. I no more think that you will have the same result with ev when using 1 versus 3 selection conditions ...And yet you will not let me say that we end up with two different functions.
All right Paul, I’m going to relent to you on this point. The mutation and selection sorting/optimization process is profoundly slowed when evolving multiple functions simultaneously. It is much easier to evolve a single function based on a single selection pressure than to evolve three functions to three simultaneous selection pressures. This is exactly analogous to using monotherapy for the treatment of HIV verses 3 drug combination therapy for treating the disease.
Your irrational and illogical speculation of how the mutation and selection sorting/optimization process actually works is worse than the evolutionist concepts of eugenics and master race.You're over the top, Alan.
Why? More people will die prematurely from the consequences of diseases subject to the principles of mutation and selection than from those who espouse the concept of a master race.
Your mathematically impossible theory of evolution is an abhorrent theory.So you are against personalized medicine. You believe that everyone is equal and will, therefore, respond equally to any disease treatment. Unfortunately, you are completely unaware of the modern trends in medicine which will account for the known population variations and will one day, provide the idealized best care for each patient. Soon, gone will be the days where doctors guessed which medicine(out of several) a patient should have becuase the average population works well on that drug. It seems that you are in need of some continuing education courses to maintain your MD.
Joobz, what do you know about the practice of medicine? Tell us all about your training and experience.
Wanton slaying of people saying they are doing it in the name of god don’t hold a candle to the work of evolutionists like Hitler, Stalin, and Mao. Then how many abortionists are also evolutionists? It is your mathematically impossible theory which is abhorrent. Of course evolutionists redeem themselves by starting hospitals all over the world. Didn’t we just see the opening of the “Evolutionist Hospital of the Most Fit”?I'd like you to show how Hitler and the others were representative of darwinism in general. I'd also remind you that Hitler was a Christian
Why Belz, didn’t you know that Hitler continually advanced the concept that the Germans were the master race, more highly evolved, more fit. Where do you find those concepts in Christianity? Now Hitler wasn’t the only mass murderer who embraced evolutionism. Stalin and Mao, both communists followed the teaching of Marx who adopted evolutionism.
http://pubs.socialistreviewindex.org.uk/isj71/darwin.htm (http://pubs.socialistreviewindex.org.uk/isj71/darwin.htm)
The impact of Charles Darwin's theory of evolution was undoubtedly revolutionary. Marx's response to the appearance of The Origin of Species in 1859 is well known. In a letter to Ferdinand Lassalle he wrote:

Darwin's book is very important and serves me as a natural-scientific basis for the class struggle in history... Despite all deficiencies, not only is the death-blow dealt for the first time here to 'teleology' in the natural sciences, but its rational basis is empirically explained.2
http://emporium.turnpike.net/C/cs/hscom.htm (http://emporium.turnpike.net/C/cs/hscom.htm)
Both Karl Marx and Friedrich Engels were evolutionists before they encountered Darwin's "The Origin of Species" - (Dec 12, 1859) Engels wrote to Marx: "Darwin who I am now reading, is splendid" (Morris 1989, 83 quoting Zirkle). Like Darwin, "Marx thought he had discovered the law of development. He saw history in stages, as the Darwinists saw geological strata and successive forms of life... In keeping with the feelings of the age, both Marx and Darwin made struggle the means of development" (Morris 1989, 83 quoting Borzin). "There was truth in Engel's eulogy on Marx: 'Just as Darwin had discovered the law of evolution in organic nature so Marx discovered the law of evolution in human history'" (Morris 1989, 83 quoting Himmelfarb).

"It is commonplace that Marx felt his own work to be the exact parallel of Darwin's. He even wished to dedicate a portion of Das Kapital to the author of The Origin of Species" (Morris 1989, 83 quoting Barzum). Indeed, Marx wished to dedicate parts of his famous book to Darwin but "Darwin 'declined the honor' because, he wrote to Marx, he did not know the work, he did not believe that direct attacks on religion advanced the cause of free thought, and finally because he did not want to upset 'some members of my family'" (Morris 1989, 83 quoting Jorafsky).

Other Soviet Communist leaders are evolutionists as well. Lenin, Trostsky, and Stalin were all atheistic evolutionists. A soviet think tank founded in 1963 developed a one-semester course in "Scientific Atheism" which was introduced in 1964. Also, a case can be made that Darwinism was influential in propagating communism in China.
http://www.marxists.org/reference/archive/morgan-lewis/ancient-society/foreword.htm (http://www.marxists.org/reference/archive/morgan-lewis/ancient-society/foreword.htm)
Commenting on this outstanding book in the light of which he had written ‘The Origin of Family, Private Property and State’ which again contains a summary of the important facts established by Morgan in “Ancient Society,” Engels says, “Morgan’s great merit lies in the fact that he discovered and re-constructed in its main lines the pre-historic basis of our written history; so long as no important additional material makes changes necessary, his classification will undoubtedly remain in force.” In a letter to Kautsky (February 16, 1884) he says, “There exists a definitive book on the origins of society, as definitive as Darwin’s work for Biology, and it is, naturally, again Marx who has discovered it: it is Morgan, Ancient Society, 1877. Marx spoke to me of it but I had other matters on my mind and he did not return to the subject. This surely pleased him for I can see by his very detailed extracts that he wanted to introduce it to the Germans himself. Within the limits set by his subject, Morgan spontaneously discovered Marx’s materialist conception of history, and his conclusions with regard to present-day society are absolutely communist postulates. The Roman and Greek gens is for the first time fully explained by those of savages, especially the American Indians, and this gives a solid base to primitive history.”
http://en.wikipedia.org/wiki/Evolutionary_theory_and_the_political_left (http://en.wikipedia.org/wiki/Evolutionary_theory_and_the_political_left)
When Karl Marx read Darwin's work on evolution he immediately believed that it supported his worldview and theory of class struggle. Karl Marx sent Darwin an autographed copy of his Das Kapital; Darwin responded with a polite "thank you" letter, but never read the book[1]. Marx believed that Darwin's work both helped to explain the internal struggles of human society, and provided a material explanation for the processes of nature, something which his philosophy was heavily based on.
So not only is the theory of evolution mathematically impossible, evolutionism is the religion of mass murderers. All you evolutionists have a good weekend trying to disconnect your theory of evolution from the greatest mass murderers in history. I’ll return next week to post more citations which show your theory to be mathematically impossible. Dr Schneider’s ev computer simulation shows this and reality demonstrates what ev shows.

[rocketdodger]

All you evolutionists have a good weekend trying to disconnect your theory of evolution from the greatest mass murderers in history. I’ll return next week to post more citations which show your theory to be mathematically impossible. Dr Schneider’s ev computer simulation shows this and reality demonstrates what ev shows.

Don't bother. Frankly, I am done arguing with the hopelessly incompetent mass of defunct neurons a medical examiner might call your brain. I will check in from time to time to see what remarkable stupidity you have drooled into the numerous posts you make, but don't expect me to take anything you say seriously.

[Belz...]

Why Belz, didn’t you know that Hitler continually advanced the concept that the Germans were the master race, more highly evolved, more fit.

And yet he was a Christian.

Where do you find those concepts in Christianity?

In the thought that believers are "better" than nonbelievers.

Now Hitler wasn’t the only mass murderer who embraced evolutionism. Stalin and Mao, both communists followed the teaching of Marx who adopted evolutionism.

I see you've invented your own definition of "evolutionism". If, by that, you mean any endeavour to improve upon anything, no matter by what means, then congratulations: you've just invented a useless word.

So not only is the theory of evolution mathematically impossible, evolutionism is the religion of mass murderers.

Okay, that's a stundie.

All you evolutionists have a good weekend trying to disconnect your theory of evolution from the greatest mass murderers in history.

Appeal to emotions, again.

[Paul C. Anagnostopoulos]

He's toast.

~~ Paul

[cyborg]

I thought he'd made the "evolution is bad therefore wrong" argument already?

[joobz]

Joobz, what do you know about the practice of medicine? Tell us all about your training and experience.I am very aware of the NIH's roadmap for health and know that personalized medicine is the morally advanced and appropriate method of care. This is why so much research is going into it.

However, you choose believe that everyone is physiologically equal and respond equally to all medicines. I'm not certain your understanding of health care is as solid as it should be. It seems your belief system (that evolution and genetic variation is not real) may get in the way of your care.


So not only is the theory of evolution mathematically impossible, evolutionism is the religion of mass murderers. All you evolutionists have a good weekend trying to disconnect your theory of evolution from the greatest mass murderers in history. I’ll return next week to post more citations which show your theory to be mathematically impossible. Dr Schneider’s ev computer simulation shows this and reality demonstrates what ev shows.
I see you have switched arguments from proving evolution is impossible to saying it is immoral. This tactic change indicates to me that you realize what your argument shows. That multiple variable selection pressures can accelerate the adaption response making evolution quite possible. Since nature is a variable environment, evolution is a possible and true.

Soon, you will also come to understand that your belief system, that made you unable to see the truth around you, is also confusing your sense of morality. Eventually you will see that your religious dogma prevents you from properly treating patients as individuals. Unfortuantely, your current practice is amoral and hopefully will change.

You will soon realize that genetically variable is not equivalent to value variable. But this is a concept that seems to extend beyond your grasp right now. So, we'll just work with what we got.

[joobz]

He's toast.

~~ Paul
Definitely. His change in attack is an obvious admission in him becoming aware of what his constant multiple selection pressure argument shows. That the natural environment provides the variability which allows for evolution to occur in a realistic timescale.

[kjkent1]

Look at all them "peace loving" annoying creationists!

http://upload.wikimedia.org/wikipedia/commons/thumb/a/af/Klan-in-gainesville.jpg/300px-Klan-in-gainesville.jpg (http://en.wikipedia.org/wiki/Image:Klan-in-gainesville.jpg)

[Kotatsu]

Ok, so your argument there is survival of the fittest.

My argument is that annelids have a more useful and generally evolutionary fit bauplan than humans do, as evidenced by their far greater diversity, numbers, and ranges, and the fact that while the "worm" bauplan can be found in almost all phyla, then human bauplan can be found only in one, and that's one of the smaller and less significant ones to boot.

The rest of this part of the discussion is fluff you have added because you have no idea what I am talking about, are physically or mentally unable to educate yourself, and haven't decided upon a suitable "funny" nickkname based on my screen name despite having communicated with me for about a year. I am disappointed in you.

Don’t species actively sort out the individuals less fit? Why shouldn’t humans?

They do? Tell me, how many species (apart from humans) do you know that actively judge which individual members of the group are less fit, and then go forth to execute or otherwise neutralise them? By what mechanisms do they do this? Can you name even one?

And regardless of if you eventually find one, I would just like to make clear already now that existence of a trait in one given species does by no means imply that that trait is desirable, extant, or even possible in another given species.

Wanton slaying of people saying they are doing it in the name of god don’t hold a candle to the work of evolutionists like Hitler, Stalin, and Mao.

Hitler was a Christian, so any and all killings he is responsible for counts equally for both sides, at the very least. Unlike the benevolent Christians who conquered the Americas ad Australia, however, Hitler never managed to more or less clear a continent of its original inhabitants. Of course, he was only one person, while the Christian colonizers were many.

Then how many abortionists are also evolutionists?

I have no idea, and see no relevance in the question, unless you can show me that the majority of abortionists (by which I assume you mean those who actually either go through or perform an abortion, rather than just those who support it) do this out of a desire to better the species.

It is your mathematically impossible theory which is abhorrent. Of course evolutionists redeem themselves by starting hospitals all over the world. Didn’t we just see the opening of the “Evolutionist Hospital of the Most Fit”?

While Christians have been reported to refuse to give aid to tsunami victims unless they first convert to Christianity.

See? It's easy to point out acts of rotten eggs regardless of to what groups they belong. This, however, has no bearing at all on the veracity of evolution and the validity of the theory aiming to describe the mechanisms by which it occurs. So cease this idiotic appeal to various emotions, and instead present your data.

[Kotatsu]

Why? More people will die prematurely from the consequences of diseases subject to the principles of mutation and selection than from those who espouse the concept of a master race.

Then you should just get God to stop all that mutation and selection, so that the scales will be tipped the other way and you can blame more deaths on the secret cabal of evil evolutionists who are even now weeding out the lesser men (i.e., believers) in order to create a master race of evolutionist God-deniers, shouldn't you?

As people have asked before, why are you wasting your time here? We are obviously lost cases.

[Belz...]

He's toast.

~~ Paul

Yeah, Godwin and all.

[Henners]

<<So not only is the theory of evolution mathematically impossible, evolutionism is the religion of mass murderers. All you evolutionists have a good weekend trying to disconnect your theory of evolution from the greatest mass murderers in history.>>

Oh, dear, dear, Mr K.

In fact, you'll find that driving on the right is a better predictor than theories taken out of context.

Might I suggest that your own temperament would be greatly improved if you were to start driving on the left asap.

[kjkent1]

See? It's easy to point out acts of rotten eggs regardless of to what groups they belong. This, however, has no bearing at all on the veracity of evolution and the validity of the theory aiming to describe the mechanisms by which it occurs. So cease this idiotic appeal to various emotions, and instead present your data.Amen to that, brother!

[delphi_ote]

Sorry, kleinman.
http://i71.photobucket.com/albums/i133/delphi_ote/fail-5.jpg
People already thought of that kind of argument (http://en.wikipedia.org/wiki/Association_fallacy). You've also got a little bit of this (http://en.wikipedia.org/wiki/Appeal_to_consequences) mixed in there. Nice try, though.

[Paul C. Anagnostopoulos]

Oh, the pops are sweeter and the taste is new.
They're shot with sugar, through and through.

~~ Paul

[Mercutio]

It has been a while since I checked in on this sub-forum. I almost hoped that this thread might have miraculously dropped from the front page.... no such luck.

Anyway, I only just today ran across this (http://www.nytimes.com/2007/07/01/books/review/Dawkins-t.html?ex=1340942400&en=a8d3b05b1f9ae784&ei=5090&partner=rssuserland&emc=rss), which directly applies to Kleinman's (original) argument (I know it has evolved since then, having been subject to multiple selection pressures). I did not know that Kleinman agreed so well with Behe. Live and learn...

[Dr Adequate]

Oooh, kleinman thought of a new lie!

Stalin and Mao, both communists followed the teaching of Marx who adopted evolutionism. And yet Stalin banned the theory of evolution and murdered its advocates. I don't know where Mao stood, though I'm certain that he was a committed twoplustwoequalsfourist. Is that why you hate math so much?

Now Hitler wasn’t the only mass murderer who embraced evolutionism. This is my favorite creationist lie. Not just because it's so stupid, not just because it stinks so much, but also because it gives me a legitimate excuse to point out that Hitler was a devout creationist.

"The fox remains always a fox, the goose remains a goose, and the tiger will retain the character of a tiger." - Adolf Hitler, Mein Kampf, vol. ii, ch. xi

"For it was by the Will of God that men were made of a certain bodily shape, were given their natures and their faculties." - Adolf Hitler, Mein Kampf, vol. ii, ch. x

"From where do we get the right to believe, that from the very beginning Man was not what he is today? Looking at Nature tells us, that in the realm of plants and animals changes and developments happen. But nowhere inside a kind shows such a development as the breadth of the jump , as Man must supposedly have made, if he has developed from an ape-like state to what he is today." - Adolf Hitler, Hitler's Tabletalk (Tischgesprache im Fuhrerhauptquartier)

"The most marvelous proof of the superiority of Man, which puts man ahead of the animals, is the fact that he understands that there must be a Creator." - Adolf Hitler, Hitler's Tabletalk (Tischgesprache im Fuhrerhauptquartier)

"My feeling as a Christian points me to my Lord and Savior as a fighter. It points me to the man who once in loneliness, surrounded only by a few followers, recognized these Jews for what they were and summoned men to fight against them." - Adolf Hitler, speech, April 12 1922, published in My New Order

All you evolutionists have a good weekend trying to disconnect your theory of evolution from the greatest mass murderers in history. It doesn't take all weekend to show up your silly lies. Coupla minutes?

Now I shall find something more entertaining to do.

[sol invictus]

Hitler was an evolutionist; he advanced the concept of a super race which is a simple deduction of the concept of survival of the fittest.

http://img394.imageshack.us/img394/7072/godwinslaw7qt.gif

[Olowkow]

Wow! I should have documented the fact that I long ago predicted this discussion would decay to "Well, evolutionists/atheists are just evil, so there!", despite the facts. I could have qualified for the MDC!

I agree, "he's toast".

[rocketdodger]

It has been a while since I checked in on this sub-forum. I almost hoped that this thread might have miraculously dropped from the front page.... no such luck.

Anyway, I only just today ran across this (http://www.nytimes.com/2007/07/01/books/review/Dawkins-t.html?ex=1340942400&en=a8d3b05b1f9ae784&ei=5090&partner=rssuserland&emc=rss), which directly applies to Kleinman's (original) argument (I know it has evolved since then, having been subject to multiple selection pressures). I did not know that Kleinman agreed so well with Behe. Live and learn...

Everything makes sense now.

I have long wondered how someone as stupid as Kleinman could have come up with a <incorrect> theory on their own. Now I know -- it isn't his.

So Kleinman has just jumped on another creationist bandwagon and doesn't know anything about what he speaks of? This has kind of been evident from the get-go, but now it makes perfect sense to me. Of course he can't address our arguments directly, he is nothing more than a messenger boy.

[delphi_ote]

I have long wondered how someone as stupid as Kleinman could have come up with a <incorrect> theory on their own. Now I know -- it isn't his.
Sorry. I should've mentioned he was parroting Behe pages ago. Great link, Mercurtio!

[jimbob]

http://img394.imageshack.us/img394/7072/godwinslaw7qt.gif

The inimitable XKCD:

http://imgs.xkcd.com/comics/regarding_mussolini.png

The author encourages hotlinking:

Permanent link to this comic: http://xkcd.com/261/
Image URL (for hotlinking/embedding): http://imgs.xkcd.com/comics/regarding_mussolini.png

Edit: Of course, the above is a special case...

[joobz]

What I'd like to know is what made kleinman go down the hitler road.

[delphi_ote]

What I'd like to know is what made kleinman go down the hitler road.
I'd say a combination of frustration, inability to think critically, blind devotion to a hopeless cause, ignorance of history, and desperation.

[Kotatsu]

Everything makes sense now.

I have long wondered how someone as stupid as Kleinman could have come up with a <incorrect> theory on their own. Now I know -- it isn't his.

So Kleinman has just jumped on another creationist bandwagon and doesn't know anything about what he speaks of? This has kind of been evident from the get-go, but now it makes perfect sense to me. Of course he can't address our arguments directly, he is nothing more than a messenger boy.

Does anyone have a more complete reference to the Miller paper he mentions?

[Belz...]

It has been a while since I checked in on this sub-forum. I almost hoped that this thread might have miraculously dropped from the front page.... no such luck.

Hey, Mercutio!

No, Kleinman has not given up. In fact now his argument is that evolution is a religion of mass murderers. Why ? Why because Hitler and Stalin and Mao were evilutionists! Why ? Why because the concept of a master race is an idea of Darwin's!

This serves to show how poorly creationists understand evolution. There is no such thing as a "more evolved", "superior" or "better" species and the fact that they don't understand this, one of the most basic implications of evolutionary theory, is quite telling of their unwillingness to keep themselves informed about an issue that is otherwise so crucial to them.

The fact that Kleinman also tries to educate the rest of us about a theory he knows nothing about, is downright ironic.

[kjkent1]

All right Paul, I’m going to relent to you on this point. The mutation and selection sorting/optimization process is profoundly slowed when evolving multiple functions simultaneously. It is much easier to evolve a single function based on a single selection pressure than to evolve three functions to three simultaneous selection pressures. This is exactly analogous to using monotherapy for the treatment of HIV verses 3 drug combination therapy for treating the disease.

I can't let the above baloney go unanswered.

Alan, when Paul refers to different functions, he is explaining that when you set a mistake weight to zero, it changes the definition of a perfect creature. Examples:

1. A perfect creature with three non-zero mistake weights, has an absence of missing and/or spurious bindings, inside and out of the binding site region.

2. A perfect creature with the missing binding site mistake count set to zero is filled with missing bindings.

3. A perfect creature with the spurious binding site mistake count inside the binding site region set to zero is filled with spurious bindings in the binding site region.

4. A perfect creature with the spurious binding site mistake count outside the binding site region set to zero is filled with spurious bindings outside the binding site region.

5. A perfect creature with all three mistake counts set to zero is filled with totally random noise.

No one should have to enumerate what's taking place in ev for every single combination of mistake weights in order for you to acknowledge that your attempt to compare the evolutionary times which occur when a mistake weight is zero vis-a-vis when all mistake weights are non-zero, is absurd.

Stop jerking around on this issue. Setting a mistake weight to zero changes the definition of perfect creature in ev (i.e., moves the goalpost), and makes evolutionary time comparisons meaningless.

Which is one of the reasons why I argue that Rseq -> Rfreq is the only available measurement -- because it is unaffected by zeroing out a mistake weight.

Also, because convergence is the formal methodology by which Schneider's paper measures evolutionary change.

[Paul C. Anagnostopoulos]

Which is one of the reasons why I argue that Rseq -> Rfreq is the only available measurement -- because it is unaffected by zeroing out a mistake weight.
Except that those values don't make sense when we're not evolving a creature that distinguishes binding sites from other positions. Rfrequency is precisely the measure of the amount of information required to do so.

Sometime soon I will get off my butt and change "perfect creature" to "zero mistakes". I will also add the mistake counts to the Data & Statistics panel. Here's an idea: I will put a short message below the sequence logo if any mistake counts are zero.

~~ Paul

[kjkent1]

Except that those values don't make sense when we're not evolving a creature that distinguishes binding sites from other positions. Rfrequency is precisely the measure of the amount of information required to do so.

Sometime soon I will get off my butt and change "perfect creature" to "zero mistakes". I will also add the mistake counts to the Data & Statistics panel. Here's an idea: I will put a short message below the sequence logo if any mistake counts are zero.

~~ PaulI understand your point. My point is that the whole idea of ev is to support the conclusion of Schneider's paper: to measure evolutionary information gain -- which is what the Rfreq -> Rseq relationship is all about. kleinman is way too smart to not recognize that he's been mistaken on this issue for the past year, and he just keeps on dancing around it.

This is an obvious point, that kleinman simply refuses to acknowledge, because, after all, he "is" the annoying creationist.

[Cuddles]

Derail split here (http://forums.randi.org/showthread.php?t=100796).

[kleinman]

Any of you evolutionists figure out how the mutation and selection sorting/optimization process actually works this weekend? I guess they didn’t teach you how this mathematics works in Evolutionist Mythematics 101. So we’ll fill this gigantic vacuum in your training.
All you evolutionists have a good weekend trying to disconnect your theory of evolution from the greatest mass murderers in history. I’ll return next week to post more citations which show your theory to be mathematically impossible. Dr Schneider’s ev computer simulation shows this and reality demonstrates what ev shows.Don't bother. Frankly, I am done arguing with the hopelessly incompetent mass of defunct neurons a medical examiner might call your brain. I will check in from time to time to see what remarkable stupidity you have drooled into the numerous posts you make, but don't expect me to take anything you say seriously.
It’s no bother rocketdodger, in fact I quite enjoy showing you that your irrational and illogical theory is mathematically impossible. Now rocketdodger, why should I expect an evolutionist to take mathematical and empirical data seriously? Do you have any new data from your model that shows n+1 selection pressures evolve more rapidly than n selection pressures or did you:
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
He's toast.
It goes well with the flame roasted theory of evolution. Care to have some evolutionist whine to go with your dinner?
So not only is the theory of evolution mathematically impossible, evolutionism is the religion of mass murderers. All you evolutionists have a good weekend trying to disconnect your theory of evolution from the greatest mass murderers in history. I’ll return next week to post more citations which show your theory to be mathematically impossible. Dr Schneider’s ev computer simulation shows this and reality demonstrates what ev shows.I see you have switched arguments from proving evolution is impossible to saying it is immoral. This tactic change indicates to me that you realize what your argument shows. That multiple variable selection pressures can accelerate the adaption response making evolution quite possible. Since nature is a variable environment, evolution is a possible and true.
The theory of evolution succeeds on both counts joobz. Your claim that multiple simultaneous selection conditions accelerate evolution carries as much weight as Adequate’s and rocketdodger’s mythematics. Now Dr Schneider’s peer reviewed and published model of mutation and selection does properly show how mutation and selection actually works and I have a couple more empirical examples of this mathematical fact.
Ok, so your argument there is survival of the fittest.My argument is that annelids have a more useful and generally evolutionary fit bauplan than humans do, as evidenced by their far greater diversity, numbers, and ranges, and the fact that while the "worm" bauplan can be found in almost all phyla, then human bauplan can be found only in one, and that's one of the smaller and less significant ones to boot.
What a strange form of eugenics you practice. So is survival of the fittest true or not?
It has been a while since I checked in on this sub-forum. I almost hoped that this thread might have miraculously dropped from the front page.... no such luck.
Luck has nothing to do with it Mercutio, of course you wouldn’t understand that because you believe in a mathematically irrational and illogical theory. Hey Mercutio, are you ready to tell us what the components of the DNA replicase system were doing before DNA could be replicated? In particular, could you tell us what helicase and gyrase were doing before DNA existed?
Stalin and Mao, both communists followed the teaching of Marx who adopted evolutionism.And yet Stalin banned the theory of evolution and murdered its advocates. I don't know where Mao stood, though I'm certain that he was a committed twoplustwoequalsfourist. Is that why you hate math so much?
Stalin was an equal opportunity survival of the fittest practitioner. Or don’t you believe that some evolutionists are more fit than others?

Adequate, I don’t hate mathematics, that’s why I challenge your irrational and illogical mythematics. You above all should understand how the mutation and selection sorting/optimization problem works, especially since you claim to understand how iteration problems work. As long as you continue to claim the following:
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.
Your irrational nonsense will contribute to the premature deaths of people suffering from HIV and other diseases subject to the principles of mutation and selection. You are doing a good job helping write the newest bloody chapter in the history of evolutionism.
Which is one of the reasons why I argue that Rseq -> Rfreq is the only available measurement -- because it is unaffected by zeroing out a mistake weight.Except that those values don't make sense when we're not evolving a creature that distinguishes binding sites from other positions. Rfrequency is precisely the measure of the amount of information required to do so.

Sometime soon I will get off my butt and change "perfect creature" to "zero mistakes". I will also add the mistake counts to the Data & Statistics panel. Here's an idea: I will put a short message below the sequence logo if any mistake counts are zero.
Be careful Paul, somebody may figure out how the mutation and selection sorting/optimization process actually works if you make these kinds of changes, well everyone but kjkent1, he will spend his life looking for a legal loophole for the theory.

Well, not much progress this weekend but I have hope for you. Here are a couple more examples which demonstrate how the mutation and selection sorting/optimization problem actually works and what it shows is that combination selection pressures profoundly slow the evolutionary process.
http://aac.asm.org/cgi/content/abstract/AAC.01123-07v1 (http://aac.asm.org/cgi/content/abstract/AAC.01123-07v1)
Combination therapy is the most effective strategy to prevent emergence of resistance during tuberculosis (TB) treatment. Another strategy, albeit theoretical, is to limit the time that drug concentrations fall in the "mutant selection window" (MSW) between the MIC and the mutant prevention concentration (MPC). Drug concentrations above the MPC prevent selective amplification of resistant mutants in vitro even with single drug exposure. The MSW concept has been validated using fluoroquinolones against Mycobacterium tuberculosis in vitro, but not in vivo. Using a mouse model in which serum moxifloxacin (MXF) concentrations were maintained above the MPC, we tested whether this strategy prevents selection of MXF-resistant mutants.

Beginning 2 weeks after aerosol infection with M. tuberculosis, when the mean lung log10 CFU count was 7.9 ± 0.2, mice received no treatment or MXF in the diet at 0.25%, to approximate the conventional human dose, or 1.5%, to maintain serum concentrations above the MPC (8 µg/ml). After 56 days of treatment, lung CFU counts were 3.5 ± 0.8 and 0.9 ± 0.6 in 0.25% and 1.5% MXF-treated mice, respectively. In mice given 0.25% MXF, MXF-resistant mutants were selected by Day 28 and detected in 16% (3/19) of mice tested on Day 56. No selection of MXF-resistant mutants was detected in mice given 1.5% MXF.

We conclude that maintaining serum concentrations of MXF above the MPC prevents selection of MXF-resistant mutants. Although this target cannot be achieved clinically with MXF, it might be possible with new fluoroquinolones with more potent activity and/or improved pharmacokinetics.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=127422 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=127422)
Our observation that the HBV mutants most commonly associated with LMV and/or famciclovir resistance remain sensitive to both AT-61 and AT-130 justifies the further development of these compounds or their derivatives for eventual clinical use. These compounds appear to have the potential to arrest the replication of known drug-resistant HBV strains and thus, in combination with nucleoside/nucleotide analogs (4, 5) and/or other drugs, may help reduce, or perhaps even prevent, the development of drug resistance (27).

[Kotatsu]

I see you have ceased to make sense at all. How curious. Still, it's a moderately free country, I suppose.

What a strange form of eugenics you practice.

To an observer without your mental qualities, I guess it might even look as if I don't practice eugenics at all!

So is survival of the fittest true or not?

That is statistically what generally happens to a population, yes, regardless of intervention.

[joobz]

Oh it's sad to see that you are so indoctrinated into your theory that evolution is impossible that you are unable to reason. That's ok. We'll help you along and eventually get you to see how in fact multiple variable selection pressures actually work.The theory of evolution succeeds on both counts joobz. You are correct. the evolutionary theory does succeed. It succeeds at explaining how life developed on this planet and how life continues to exist on this planet.

Your claim that multiple simultaneous selection conditions accelerate evolution carries as much weight as Adequate’s and rocketdodger’s mythematics. Now Dr Schneider’s peer reviewed and published model of mutation and selection does properly show how mutation and selection actually works and I have a couple more empirical examples of this mathematical fact. This is completely correct. All of these points demonstrate clearly how evolution works. Your theory of multiple stable selection pressures inhibiting emergence is correct. That is indeed what happens. It also shows that when these pressures fail to remain strong and consistent, resisitence can rapidly emerge. This was clearly explained in a paper published in PNAS and is the basis for all references you site. Nature is a variable selection pressure system.

From your own citation:
Combination therapy is the most effective strategy to prevent emergence of resistance during tuberculosis (TB) treatment. Another strategy, albeit theoretical, is to limit the time that drug concentrations fall in the "mutant selection window" (MSW) between the MIC and the mutant prevention concentration (MPC). Drug concentrations above the MPC prevent selective amplification of resistant mutants in vitro even with single drug exposure. The MSW concept has been validated using fluoroquinolones against Mycobacterium tuberculosis in vitro, but not in vivo. Using a mouse model in which serum moxifloxacin (MXF) concentrations were maintained above the MPC, we tested whether this strategy prevents selection of MXF-resistant mutants. Even a single strong pressure can block emergence. However, had they varied this pressure, emergence would evolve. Thank you for this paper, it further proves that evolution occurs in nature and nicely explains the diversity of life on this planet.

and thank you for this one as well
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=127422 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=127422)
LMV, a deoxycytidine analog, is a safer and more effective inhibitor of HBV replication, but its effects are rarely sustained after short-term treatment, and its long-term use frequently results in the emergence of drug-resistant HBV strains. I'm glad you are referencing sources that understand that evolution occurs and is real. It would be quite immoral for a doctor to ignore these basic facts of medical science.

[kleinman]

What a strange form of eugenics you practice.To an observer without your mental qualities, I guess it might even look as if I don't practice eugenics at all!
You practice eugenics that is obvious.
So is survival of the fittest true or not?That is statistically what generally happens to a population, yes, regardless of intervention.
So, who are the fittest humans?
Combination therapy is the most effective strategy to prevent emergence of resistance during tuberculosis (TB) treatment. Another strategy, albeit theoretical, is to limit the time that drug concentrations fall in the "mutant selection window" (MSW) between the MIC and the mutant prevention concentration (MPC). Drug concentrations above the MPC prevent selective amplification of resistant mutants in vitro even with single drug exposure. The MSW concept has been validated using fluoroquinolones against Mycobacterium tuberculosis in vitro, but not in vivo. Using a mouse model in which serum moxifloxacin (MXF) concentrations were maintained above the MPC, we tested whether this strategy prevents selection of MXF-resistant mutants.Even a single strong pressure can block emergence.
Joobz, now that you figured out the obvious that a single selection pressure can cause extinction, how do you reconcile this with your claim that evolution can not be stopped?

Here is another example of how the mutation and selection sorting/optimization process actually works and it is not the way you evolutionists allege.
http://www.bumc.bu.edu/www/busm/Ll/PDFs/Gleevec.pdf (http://www.bumc.bu.edu/www/busm/Ll/PDFs/Gleevec.pdf)
Several principles have been developed to manage the troublesome occurrence of mutations in human immunodeficiency virus-1 (HIV) RT, which may be of value if applied to the case of chemoresistance in CML. An important principle in the treatment of HIV with chemical agents is the simultaneous introduction of combinations of anti-viral drugs that have not been used previously for a particular patient (41). In CML, partial cytogenetic or hematologic responses are actually exceedingly dangerous states, because ongoing genetic instability in the surviving CML clones provides an ideal mechanism for the strong selection of resistant mutations under the pressure of a single anti-cancer drug. Therefore, the repopulation of the marrow and peripheral blood with resistant clones is almost inevitable. Deininger and Druker (2) have acknowledged that Gleevec’s selective pressure favors the outgrowth of pre-existing resistant clones, similar to a bacterial culture treated with a single antibiotic. However, the pace of basic research into drug design for the next generation of chemical inhibitors of Abl suggests that there will soon be a respectable arsenal of agents available for physician choice, such as AP23464 (Ariad Pharmaceuticals), BMS-354825 (Bristol-Myers Squibb;42,43), SKI606 (Wyeth), PD180970 (Parke Davis), CGP76030 and AMN107 (Novartis; 43), VX-680 (Vertex Pharmaceuticals/Merck;44). Other targeted agents such as SU11248 (Pfizer), have value against Kit and platelet derived growth factor receptor α form (16).
and
Absent successful allogeneic stem cell transplantation, it is likely that clinicians will be forced to confront the problem of invariable relapse in CML, and will continue to depend upon chemical agents. The experience of HIV anti-viral drug resistance suggests the following analogous principles should be applied to CML therapy:
1. Several combinations of Abl-directed drugs should be used simultaneously, even if specificity is not optimal, provided that the combination can be tolerated.
2. Patients should be carefully monitored for the emergence of resistance, and new agents
quickly substituted as they become available.
3. If a combination treatment protocol fails, it is important to change more than one component of the protocol. Substitution of a single agent, even Gleevec, may promote resistance to new agents by increasing the strength of the drug selective pressure.
4. Single agent therapy, such as Gleevec alone, should be avoided, given the obvious risk for the development of drug resistance.

[rocketdodger]

So, who are the fittest humans?

It is hard to say who the most fit are. It is much easier to say who the least fit are.

For example, any of the poor blokes who made the remarkably bad choice of placing their faith in your abilities. They must be very unhealthy indeed.

[joobz]

Joobz, now that you figured out the obvious that a single selection pressure can cause extinction, how do you reconcile this with your claim that evolution can not be stopped?
I see your blind devotion to a lie has made you unable to read. I never said evolution can't be stopped. I agree that strong, constant multiple pressures will block emergence and likely result in extinction.

I am simply saying that nature doesn't provide such an environment. Nature is highly variable and accelerates the evolutionary process. You even agreed to this fact last week. These conclusions extend directly from your arguments. I hope you aren't moving deeper into your delusions and will start to claim that nature doesn't have weather.

[kleinman]

Joobz, now that you figured out the obvious that a single selection pressure can cause extinction, how do you reconcile this with your claim that evolution can not be stopped?I see your blind devotion to a lie has made you unable to read. I never said evolution can't be stopped. I agree that strong, constant multiple pressures will block emergence and likely result in extinction.

I am simply saying that nature doesn't provide such an environment. Nature is highly variable and accelerates the evolutionary process. You even agreed to this fact last week. These conclusions extend directly from your arguments. I hope you aren't moving deeper into your delusions and will start to claim that nature doesn't have weather.
You still are a mathematical incompetent for the mutation and selection sorting/optimization process. Ev does not allow extinction yet the three selection conditions take hundreds of millions of generations to evolve the three conditions on a 100k genome. Now you are claiming that these strong selection pressures don’t exist in nature. Do you want to give us an example of the weak selection pressures that you speculate accelerate evolution? Or is this argument just a remake of your cooperative chemistry speculations for abiogenesis.

[Belz...]

So is survival of the fittest true or not?

Nope.

Gosh, you don't really understanding anything about evolution, don't you ?

So, who are the fittest humans?

Nope.

Say, shouldn't you stop annoying people whom you think are mass murderers ? Isn't that a bad idea ?

[joobz]

You still are a mathematical incompetent for the mutation and selection sorting/optimization process. Ev does not allow extinction yet the three selection conditions take hundreds of millions of generations to evolve the three conditions on a 100k genome. Now you are claiming that these strong selection pressures don’t exist in nature. Do you want to give us an example of the weak selection pressures that you speculate accelerate evolution? Or is this argument just a remake of your cooperative chemistry speculations for abiogenesis.This is very sad, but understandable. The foundations of your belief system are being shaken. It is likely for you to be resistant to this information. You've been programmed this whole time to believe a lie, that evolution doesn't exist.

Now, why would you demand evidence? You've seen it. All of the references you've presented have demonstrated that evolution occurs. They are all working in attempts to try and stop the process. Indeed, all of those researchers are fairly certain that it takes much much more effort to halt emergence than let evolution take its course.

In the mean time, Have you figured out that weather provides multiple variable selection pressures?

[Belz...]

You still are a mathematical incompetent for the mutation and selection sorting/optimization process. Ev does not allow extinction yet the three selection conditions take hundreds of millions of generations to evolve the three conditions on a 100k genome. Now you are claiming that these strong selection pressures don’t exist in nature. Do you want to give us an example of the weak selection pressures that you speculate accelerate evolution? Or is this argument just a remake of your cooperative chemistry speculations for abiogenesis.

Gee, Klein. If evolution doesn't work, then why do we have such a hard time with HIV ?

[kleinman]

You still are a mathematical incompetent for the mutation and selection sorting/optimization process. Ev does not allow extinction yet the three selection conditions take hundreds of millions of generations to evolve the three conditions on a 100k genome. Now you are claiming that these strong selection pressures don’t exist in nature. Do you want to give us an example of the weak selection pressures that you speculate accelerate evolution? Or is this argument just a remake of your cooperative chemistry speculations for abiogenesis.Now, why would you demand evidence? You've seen it. All of the references you've presented have demonstrated that evolution occurs. They are all working in attempts to try and stop the process. Indeed, all of those researchers are fairly certain that it takes much much more effort to halt emergence than let evolution take its course.
No, I don’t have any examples of weak selection pressures that I speculate would accelerate evolution. I am making the same kind of speculation of cooperative chemistry causing abiogenesis as weak selection pressures cooperating to accelerate evolution. You can’t get too much of an irrational and illogical idea to explain a mathematically impossible theory. ..

[kjkent1]

Be careful Paul, somebody may figure out how the mutation and selection sorting/optimization process actually works if you make these kinds of changes, well everyone but kjkent1, he will spend his life looking for a legal loophole for the theory.Actually, everyone here but you has figured out how evolution works. None of us have any problem understanding the process.

The theory of evolution is well-supported by geological, fossil, radiological, genetic, mathematical, etc., evidence -- and your hopeless devotion to a new religion that declares the theory impossible based solely on your own misuse of a mathematical model make you appear to suffer from a serious mental illness.

But, being as this is Christmas, what I want to know is how you can worship a sadistic, misogynist, slaver as your God? For my money, you're working for the wrong deity.

Santa Claus is definitely a preferable icon for a holiday of giving and hope for the future.

[joobz]

..
Look at that. you said absolutely nothing in your last post. It must be hard having your entire world view start to shatter around you. Don't worry. It's only truth that is breaking in.

Allow me to help truth in a bit more. Here's some of the proof that you asked for. Realize, almost all of these have come from your own posts. The truth has been there all along, you simply are not able to see past your delusion.

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 then provided multiple examples of groups trying to stop evolution. Why would they try to stop something that, according to you, doesn't happen?

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=127422 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=127422)
LMV, a deoxycytidine analog, is a safer and more effective inhibitor of HBV replication, but its effects are rarely sustained after short-term treatment, and its long-term use frequently results in the emergence of drug-resistant HBV strains.

http://jvi.asm.org/cgi/reprint/JVI.01624-06v1.pdf (http://jvi.asm.org/cgi/reprint/JVI.01624-06v1.pdf)
This latter case is potentially a worry because the elevated mutation rate might facilitate evolution to a part of the fitness landscape that was otherwise not likely to be accessed. In general, if mutagenesis
increases the mutation rate closer to the mutation-rate optimum for the virus, then mutagenesis will presumably be counterproductive for treatment. This possibility seems unlikely for RNA viruses, as their intrinsic mutation rates are so high. However, the relevant parameters are not adequately known to exclude this possibility, so the caution seems warranted.


http://www.pubmedcentral.nih.gov/articlerender.fcgi?&pubmedid=15793111 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?&pubmedid=15793111)

We report here the case of a patient who experienced an infection caused by E. aerogenes that became resistant to imipenem during treatment through a decrease in porin synthesis. We document the step-by-step in vivo emergence of imipenem- and polymyxin-resistant variants during sequential antibiotic therapy. This report reinforces the anxiety associated with the lack of research into new antibacterial agents

[kleinman]

You still are a mathematical incompetent for the mutation and selection sorting/optimization process. Ev does not allow extinction yet the three selection conditions take hundreds of millions of generations to evolve the three conditions on a 100k genome. Now you are claiming that these strong selection pressures don’t exist in nature. Do you want to give us an example of the weak selection pressures that you speculate accelerate evolution? Or is this argument just a remake of your cooperative chemistry speculations for abiogenesis. Gee, Klein. If evolution doesn't work, then why do we have such a hard time with HIV ?
That’s easy Belz, years of treatment of HIV with monotherapy has introduced huge populations of resistant strains in the HIV gene pool. This would not have occurred if you evolutionists hadn’t done such a lousy job in describing how the mutation and selection sorting/optimization process actually works. Thanks to the evolutionists erroneous description of the mutation and selection sorting/optimization process, millions of people will die prematurely from HIV and other diseases subject to the principles of mutation and selection.
Be careful Paul, somebody may figure out how the mutation and selection sorting/optimization process actually works if you make these kinds of changes, well everyone but kjkent1, he will spend his life looking for a legal loophole for the theory.Actually, everyone here but you has figured out how evolution works. None of us have any problem understanding the process.
Yes kjkent1, your string cheese theory of evolution is quite convincing, 10^500 alternative universes explains it all.
Joobz tries to find anything to support his speculations:
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=127422 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=127422)
LMV, a deoxycytidine analog, is a safer and more effective inhibitor of HBV replication, but its effects are rarely sustained after short-term treatment, and its long-term use frequently results in the emergence of drug-resistant HBV strains.
Our observation that the HBV mutants most commonly associated with LMV and/or famciclovir resistance remain sensitive to both AT-61 and AT-130 justifies the further development of these compounds or their derivatives for eventual clinical use. These compounds appear to have the potential to arrest the replication of known drug-resistant HBV strains and thus, in combination with nucleoside/nucleotide analogs (4, 5) and/or other drugs, may help reduce, or perhaps even prevent, the development of drug resistance (27).
Of course single drug therapy frequently results in the emergence of drug-resistant HBV strains.
http://jvi.asm.org/cgi/reprint/JVI.01624-06v1.pdf (http://jvi.asm.org/cgi/reprint/JVI.01624-06v1.pdf)
This latter case is potentially a worry because the elevated mutation rate might facilitate evolution to a part of the fitness landscape that was otherwise not likely to be accessed. In general, if mutagenesis increases the mutation rate closer to the mutation-rate optimum for the virus, then mutagenesis will presumably be counterproductive for treatment. This possibility seems unlikely for RNA viruses, as their intrinsic mutation rates are so high. However, the relevant parameters are not adequately known to exclude this possibility, so the caution seems warranted.
A treatment strategy to prevent the evolution of significant or complete resistance could be combination therapy of several mutagens or of a mutagen in combination with other antiviral drugs.
Joobz, since you are an expert in the practice of medicine, perhaps you could tell us where these types of drugs are already being used. And joobz, since you are an expert in the mathematics of evolution, perhaps you could tell us how mutation rate affects the mutation and selection process.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?&pubmedid=15793111 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?&pubmedid=15793111)
We report here the case of a patient who experienced an infection caused by E. aerogenes that became resistant to imipenem during treatment through a decrease in porin synthesis. We document the step-by-step in vivo emergence of imipenem- and polymyxin-resistant variants during sequential antibiotic therapy. This report reinforces the anxiety associated with the lack of research into new antibacterial agents
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.
Here’s a perfect example of how to accelerate the evolutionary process, use sequential antibiotic treatments. If you want to profoundly slow the evolutionary process, use the antibiotics in combination therapy. Thanks for pointing that out for us joobz.

[joobz]

Here’s a perfect example of how to accelerate the evolutionary process, use sequential antibiotic treatments. If you want to profoundly slow the evolutionary process, use the antibiotics in combination therapy. Thanks for pointing that out for us joobz.
Very good, kleinman. We'll make an scientist out of you yet. Now you are starting to see why evolution occurs in nature. Nature provides a variable environment where multiple selection pressures do not remain constant and in place. When they do, we have extinctions.

[kleinman]

Here’s a perfect example of how to accelerate the evolutionary process, use sequential antibiotic treatments. If you want to profoundly slow the evolutionary process, use the antibiotics in combination therapy. Thanks for pointing that out for us joobz.Very good, kleinman. We'll make an scientist out of you yet. Now you are starting to see why evolution occurs in nature. Nature provides a variable environment where multiple selection pressures do not remain constant and in place. When they do, we have extinctions.
So now you are ready to tell us what those thousands of sequential selection pressures are that transformed a reptile population into a bird population. Of course we know that all these selection pressures cooperate with each other, it’s the same physical force that causes chemicals to cooperate with each other to bring about abiogenesis.

[kjkent1]

...years of treatment of HIV with monotherapy has introduced huge populations of resistant strains in the HIV gene pool. This would not have occurred if you evolutionists hadn’t done such a lousy job in describing how the mutation and selection sorting/optimization process actually works. Thanks to the evolutionists erroneous description of the mutation and selection sorting/optimization process, millions of people will die prematurely from HIV and other diseases subject to the principles of mutation and selection.Rebuttal:

Were it not for God, no one would ever die. Thus, God, and not evolutionists, is responsible for every death that has ever occurred, since the beginning of time.

Everyone is "profoundly" tired of your philosophic rant, Alan. Try something different -- like maybe thinking before you put your fingers to the keyboard.

[joobz]

So now you are ready to tell us what those thousands of sequential selection pressures are that transformed a reptile population into a bird population. Of course we know that all these selection pressures cooperate with each other, it’s the same physical force that causes chemicals to cooperate with each other to bring about abiogenesis.
Ah, so you finally come back to changing topics as a means of defense. This is a good sign. It usually happens when a person feels that they are on uncertain ground. And, your theory that evolution is impossible is certainly thin ice.

I think you are starting to realize what your multiple selection pressure argument was showing. that evolution isn't just possible, but the natural environment provides the perfect conditions for it to occur.

[kleinman]

So now you are ready to tell us what those thousands of sequential selection pressures are that transformed a reptile population into a bird population. Of course we know that all these selection pressures cooperate with each other, it’s the same physical force that causes chemicals to cooperate with each other to bring about abiogenesis.Ah, so you finally come back to changing topics as a means of defense. This is a good sign. It usually happens when a person feels that they are on uncertain ground. And, your theory that evolution is impossible is certainly thin ice.
I have no idea what those thousands of selection pressures are but I am sure that all these selection pressures cooperated because it is my speculation. And my theory of evolution is just like the Titanic, it has hit a mathematical iceberg.
I think you are starting to realize what your multiple selection pressure argument was showing. that evolution isn't just possible, but the natural environment provides the perfect conditions for it to occur.
http://forums.randi.org/images/smilies/doglaugh.gif

[sol invictus]

Hitler was an evolutionist; he advanced the concept of a super race which is a simple deduction of the concept of survival of the fittest.

http://img394.imageshack.us/img394/7072/godwinslaw7qt.gif

[joobz]

http://forums.randi.org/images/smilies/doglaugh.gif
See, You again said absolutely nothing. We both know that if you actually found a flaw in the theory you would have presented it. Instead, you present only a laughing dog. All this means is that you are reacting strongly to the theory you helped develop.

I really hope that you'll break through this delusion you have established. At best, it will have no effect except keep you living in a fantasy world. At worst, it will effect your patient care by thinking that resistence can't emerge in bacteria becuase evolution doesn't occur. Or by thinking that people are all the same and have the exact same reactions to medicine.

[kleinman]

Hitler was an evolutionist; he advanced the concept of a super race which is a simple deduction of the concept of survival of the fittest.http://img394.imageshack.us/img394/7072/godwinslaw7qt.gif
Sol, weren’t you going to demonstrate to us how ev shows that n+1 selection pressures evolves more rapidly than n selection pressures? Have you even figured out the difference between gamma and the number of selection conditions?
http://forums.randi.org/images/smilies/doglaugh.gifSee, You again said absolutely nothing. We both know that if you actually found a flaw in the theory you would have presented it. Instead, you present only a laughing dog. All this means is that you are reacting strongly to the theory you helped develop.
I’ll let my citations speak for me. Here is another one which shows that combination selection pressures profoundly slow the evolutionary process.
http://bloodjournal.hematologylibrary.org/cgi/reprint/100/3/1068.pdf (http://bloodjournal.hematologylibrary.org/cgi/reprint/100/3/1068.pdf)
The development of chronic myeloid leukemia (CML) is dependent on the deregulated tyrosine kinase of the oncoprotein BCR-ABL. STI571 (imatinib mesylate), an abl tyrosine kinase inhibitor, has proven remarkably effective for the treatment of CML. However, resistance to STI571 because of enhanced expression or mutation of the BCR-ABL gene has been detected in patients. In the current study we show that the farnesyl transferase inhibitor (FTI) SCH66336 (lonafarnib) inhibits the proliferation of STI571-resistant BCRABL–positive cell lines and hematopoietic colony formation from peripheral blood samples of STI571-resistant patients with CML. Moreover, SCH66336
enhances STI571-induced apoptosis in STI571-sensitive cells and, in patients with
STI571 resistance from gene amplification, cooperates with STI571 to induce
apoptosis. Our data provide a rationale for combination clinical trials of STI571
and SCH66336 in CML patients and suggest that combination therapy may be effective in patients with STI571 resistance. (Blood. 2002;100:1068-1071)

[sol invictus]

Sol, weren’t you going to demonstrate to us how ev shows that n+1 selection pressures evolves more rapidly than n selection pressures? Have you even figured out the difference between gamma and the number of selection conditions?

I already demonstrated that obvious fact in several different ways, offered to bet on it, and you refused to back up your "beliefs" with money. Meaning you don't have faith even in your own lies.

That proves you're a lying hypocrite troll, and so from now on I'll participate in this thread only to mock your ridiculous statements whenever I have a whim to.

Have a nice day.

[joobz]

I’ll let my citations speak for me. Here is another one which shows that combination selection pressures profoundly slow the evolutionary process.
http://bloodjournal.hematologylibrary.org/cgi/reprint/100/3/1068.pdf (http://bloodjournal.hematologylibrary.org/cgi/reprint/100/3/1068.pdf)

Your first sentence contradicts your second sentence. The reference does speak for itself. It says,
EVOLUTION IS REAL AND OCCURS!

Thank you for providing another proof of this.

STI571 (imatinib mesylate; Gleevec) represents a promising therapy for BCR-ABL–positive leukemia, but clinical resistance to STI571 can confound disease treatment. Multiple mechanisms account for clinical resistance, some involving alterations in BCR-ABL itself.
Reactivation of BCR-ABL signaling either through point mutation or gene amplification of BCR-ABL has been observed in STI571- resistant patients1-3 and in a number of STI571-resistant BCR-ABL– positive cell lines.4-6 Some mechanisms of clinical STI571 resistance
may be BCR-ABL independent, arising from altered drug
uptake or metabolism, as demonstrated in a nude mouse model.7 Secondary genetic alterations in leukemic cells, which typically accompany chronic myeloid leukemia (CML) progression,8,9 may also confer drug resistance because the survival of late-stage CML leukemic cells may be less dependent on BCR-ABL tyrosine kinase activity

kleinman, I hope your inability to understand the way variable multiple selection pressures actually work isn't a permanent problem. It truly does represent a danger to your work.

[kleinman]

Sol, weren’t you going to demonstrate to us how ev shows that n+1 selection pressures evolves more rapidly than n selection pressures? Have you even figured out the difference between gamma and the number of selection conditions?I already demonstrated that obvious fact in several different ways, offered to bet on it, and you refused to back up your "beliefs" with money. Meaning you don't have faith even in your own lies.
You must have taken lessons on ev from rocketdodger. He forgot.
That proves you're a lying hypocrite troll, and so from now on I'll participate in this thread only to mock your ridiculous statements whenever I have a whim to.
You mean you were serious before? You better stay away from the entrance to my cave.
Have a nice day.
Why thank you sol. You have a nice day as well.

[Paul C. Anagnostopoulos]

Sol, weren’t you going to demonstrate to us how ev shows that n+1 selection pressures evolves more rapidly than n selection pressures? Have you even figured out the difference between gamma and the number of selection conditions?
No, but please enlighten us. What if we allowed the user to set the mistake points for each binding site? How many selection pressures would there be then?

~~ Paul

[sol invictus]

You better stay away from the entrance to my cave.

Not that kind of troll, kleinman.

You're the kind with florescent hair that middle-school kids used to attach to their backpacks:

http://eatourbrains.com/EoB/wp-content/uploads/2007/05/troll.jpg

[kleinman]

Sol, weren’t you going to demonstrate to us how ev shows that n+1 selection pressures evolves more rapidly than n selection pressures? Have you even figured out the difference between gamma and the number of selection conditions?No, but please enlighten us.
Don’t you remember when sol got gamma and G mixed up?
What if we allowed the user to set the mistake points for each binding site? How many selection pressures would there be then?
Sounds like an interesting and fairly easy concept to implement. Since it is fairly easy for ev to find binding sites it’s probably not going to have a huge affect on the fitness landscape. It takes only a few generations to identify all binding sites. I don’t think sorting the sequences at the binding site locations is what slows the convergence in ev. I think it is the elimination of the weight matrix matches in the non-binding site region that slows and ultimately stops the convergence of ev. The mutation and selection sorting/optimization process is strongly dependent on how much of the genome you are trying to sort. This is the lesson you evolutionists need to learn. This is why single drug therapy is the easiest selection situation for a population to evolve to. As more and more of the genome is targeted by more and more drugs, it complicates the sorting process and trajectory on the fitness landscape. The mutation and selection sorting/optimization process works only when sorting a small fraction of the genome. This occurs with a single selection pressure targeting a single gene.
You better stay away from the entrance to my cave.Not that kind of troll, kleinman.

You're the kind with florescent hair that middle-school kids used to attach to their backpacks:
http://eatourbrains.com/EoB/wp-content/uploads/2007/05/troll.jpg
I used to have that much hair but now I can wash my hair with a washcloth and dry my head with a squeegee.

[sol invictus]

Don’t you remember when sol got gamma and G mixed up?

You're the one mixed up about that, klein. Of course you never answered any of the many questions we asked you about it - you just lied and ducked and spouted nonsense about Hitler.

I used to have that much hair but now I can wash my hair with a washcloth and dry my head with a squeegee.[/SIZE][/FONT]

Wow, pretending to have a sense of humor. That's rather sophisticated - your degree must be in advanced trolling.

[kleinman]

Don’t you remember when sol got gamma and G mixed up?You're the one mixed up about that, klein. Of course you never answered any of the many questions we asked you about it - you just lied and ducked and spouted nonsense about Hitler.
Sure I answer you questions, you just don’t want to listen. Next thing you are going to tell us is that Hitler didn’t believe in an Aryan super race. You know what that’s all about, survival of the fittest.
I used to have that much hair but now I can wash my hair with a washcloth and dry my head with a squeegee.Wow, pretending to have a sense of humor. That's rather sophisticated - your degree must be in advanced trolling.
Sol, didn’t you know I’m not here to humor you, I’m here to annoy you and you sound very annoyed. I’m having fun showing you evolutionists how the mutation and selection sorting/optimization process works and that your irrational and illogical theory of evolution is mathematically impossible.

[Shalamar]

Have any proof yet Klienman?

I see from your posts that you have no proof. Just technobabble.

You claim it is mathematically impossible. Please. Show your Math.

In other words, Put up, or shut up.

[Mercutio]

On topic. (http://scienceblogs.com/gnxp/2007/12/accelerated_adaptive_human_evo.php)

[joobz]

Sure I answer you questions, you just don’t want to listen. Next thing you are going to tell us is that Hitler didn’t believe in an Aryan super race. You know what that’s all about, survival of the fittest.

Sol, didn’t you know I’m not here to humor you, I’m here to annoy you and you sound very annoyed. I’m having fun showing you evolutionists how the mutation and selection sorting/optimization process works and that your irrational and illogical theory of evolution is mathematically impossible.
The only super race here is the race to see how long it will take you to learn the simple functioning of variable multiple selection pressures.

I must thank you, though. You've clearly demonstrated how this is possible.

[sol invictus]

Do you have any new data from your model that shows n+1 selection pressures evolve more rapidly than n selection pressures

klienman, you are living proof that sometimes no evolution at all occurs, even when the pressures are trivial mathematics and basic Aristotelian logic, not to mention overwhelming evidence.

Survival of the stupidest, I guess.

[kleinman]

On topic.
Read the associated link which describes the model.
http://www.genetics.org/cgi/content/full/156/3/1437 (http://www.genetics.org/cgi/content/full/156/3/1437)
We present a theoretical framework within which to analyze the results of experimental evolution. Rapidly evolving organisms such as viruses, bacteria, and protozoa can be induced to adapt to laboratory conditions on very short human time scales. Artificial adaptive radiation is characterized by a list of common observations; we offer a framework in which many of these repeated questions and patterns can be characterized analytically. We allow for stochasticity by including rare mutations and bottleneck effects, demonstrating how these increase variability in the evolutionary trajectory. When the product Np, the population size times the per locus error rate, is small, the rate of evolution is limited by the chance occurrence of beneficial mutations; when Np is large and selective pressure is strong, the rate-limiting step is the waiting time while existing beneficial mutations sweep through the population. We derive the rate of divergence (substitution rate) and rate of fitness increase for the case when Np is large and illustrate our approach with an application to an experimental data set. A minimal assumption of independent additive fitness contributions provides a good fit to the experimental evolution of the bacteriophage X174.
They are modeling only a single strong selection pressure. They are making the same error that Dr Schneider makes with his amplification (replication) concept. It only occurs with a single strong selection pressure. As soon as you target multiple genes the amplification effect is removed.

You evolutionists still need to learn that the number of selection pressures dominates the mutation and selection sorting/optimization process.

[kjkent1]

Read the associated link which describes the model.
http://www.genetics.org/cgi/content/full/156/3/1437 (http://www.genetics.org/cgi/content/full/156/3/1437)

They are modeling only a single strong selection pressure. They are making the same error that Dr Schneider makes with his amplification (replication) concept. It only occurs with a single strong selection pressure. As soon as you target multiple genes the amplification effect is removed.

You evolutionists still need to learn that the number of selection pressures dominates the mutation and selection sorting/optimization process.Perhaps you should respond to the blog and correct the author. Maybe you can dialog and something may be gained.

Or, maybe you can just chant "Alakazam" and the author will suddenly come to "know" of your supreme brilliance, and he will adopt your position.

[delphi_ote]

kleinman isn't even trying to hide his trolling anymore. He keeps Godwining the thread to upset people and then replying to their responses with complaints that they've strayed from the topic. All he wants to do is get a rise out of people at this point.

If this is an example of Christian ethics, no thanks.

[joobz]

kleinman isn't even trying to hide his trolling anymore. He keeps Godwining the thread to upset people and then replying to their responses with complaints that they've strayed from the topic. All he wants to do is get a rise out of people at this point.

If this is an example of Christian ethics, no thanks.
Ever Since his own argument has turned out to prove the fact that evolution is not only possible but what nature shows, he has become rather disjointed. He realizes the futlity of his position, but is still not yet willing to accept the facts.

It's ok. I think we should be here for him and help him through this trying time. His belief system has just been shaken, he could become rather irritable and angry.

[kjkent1]

Ever Since his own argument has turned out to prove the fact that evolution is not only possible but what nature shows, he has become rather disjointed. He realizes the futlity of his position, but is still not yet willing to accept the facts.

It's ok. I think we should be here for him and help him through this trying time. His belief system has just been shaken, he could become rather irritable and angry.The only thing that would actually annoy kleinman would be if he were to get the same attention here that he receives in the real world: none.

Completely ignoring him would destroy him. He lives for the attention he gets in this thread.

[PBTree]

I think you are all going about this the wrong way. Why don't we go to the supposed source.

I have sent a personal email to one:

Mr. P. Ope
c/- The Vatican

and asked him to explain the whole situation. Being Mr. Bigs representative on the Blue Planet, I am sure he will be able to solve this all with a couple of well chosen paragraphs about Selection Pressure and those damn mutations. (He calls them protestants)

I mean, imagine the selection pressure he was under a couple of years ago. Just before the smoke out of the chimney. He is bound to be an expert and if not, it will be in this big book he has out back.

I love this thread.....

[Kotatsu]

You practice eugenics that is obvious.

Would you care to enlighten me about exactly how I practice eugenics? Against which group?

So, who are the fittest humans?

The most fittest humans would be those who leave the largest amount of descendants.

[Kotatsu]

Say, shouldn't you stop annoying people whom you think are mass murderers ? Isn't that a bad idea ?

I guess he feels safe because I am across the Atlantic.

[Kotatsu]

That’s easy Belz, years of treatment of HIV with monotherapy has introduced huge populations of resistant strains in the HIV gene pool. This would not have occurred if you evolutionists hadn’t done such a lousy job in describing how the mutation and selection sorting/optimization process actually works. Thanks to the evolutionists erroneous description of the mutation and selection sorting/optimization process, millions of people will die prematurely from HIV and other diseases subject to the principles of mutation and selection.

Don't forget that it's also because a large bunch of Christians have decided that abstinence is a better way to battle HIV than any kind of protection ever will be, because protection is an abomination against God.

[delphi_ote]

His belief system has just been shaken, he could become rather irritable and angry.
I find it funny that he has fought tooth and nail in hundreds of posts for some rather trivial Christian dogma outlined in the first couple pages of Genesis, but he never seems to follow anything close to the Christian ethics outlined in later chapters. It's almost like he never bothered to read the book he is spending so much time defending.

Oh. Did I say "funny"? I meant "tragic".

[Belz...]

That’s easy Belz, years of treatment of HIV with monotherapy has introduced huge populations of resistant strains in the HIV gene pool.

Monotherapy doesn't mean that NO OTHER selection pressures are at work, Klein. Try again.

Thanks to the evolutionists erroneous description of the mutation and selection sorting/optimization process, millions of people will die prematurely from HIV and other diseases subject to the principles of mutation and selection.

Appeal to emotion. Gee, you like those feelings, don't you ?

[kleinman]

You claim it is mathematically impossible. Please. Show your Math.
You are making an error here, it is not my mathematics, it is the mathematics of Dr Tom Schneider, head of computational molecular biology at the National Cancer Institute. Dr Schneider has documented his mathematics extensively online and can be found at:
http://nar.oxfordjournals.org/cgi/content/full/28/14/2794 (http://nar.oxfordjournals.org/cgi/content/full/28/14/2794)
The above URL gives the basic description of Dr Schneider’s model and presents the results of a single case.
http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/ (http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/)
The above URL gives access to the online version of Dr Schneider’s model written by Paul Anagnostopoulos, moderator and discussant on this site.

There are many links at Dr Schneider’s site which help explain his model but don’t be surprised if it takes several months of study to understand what he is doing.
Read the associated link which describes the model.
http://www.genetics.org/cgi/content/full/156/3/1437 (http://www.genetics.org/cgi/content/full/156/3/1437) Perhaps you should respond to the blog and correct the author. Maybe you can dialog and something may be gained.

Or, maybe you can just chant "Alakazam" and the author will suddenly come to "know" of your supreme brilliance, and he will adopt your position.
Fair enough legal beagle, I sent an email to one of the authors and informed this author of the mathematical fact of how combination selection pressures profoundly slow a populations ability to find a trajectory to a new local optimum.
kleinman isn't even trying to hide his trolling anymore. He keeps Godwining the thread to upset people and then replying to their responses with complaints that they've strayed from the topic. All he wants to do is get a rise out of people at this point.

If this is an example of Christian ethics, no thanks.
Delphi, you are so immersed in the lie of evolutionism that you have lost the ability to recognize the truth about how the mutation and selection sorting/optimization process actually works. It is not my job to win you to God; it is my job to tell you the truth about the mutation and selection process. If that gets a rise out of you, so be it. Christ calls us to be salt, not sugar. So stop whining and use your skills as a scientist and seek the truth.
It's ok. I think we should be here for him and help him through this trying time. His belief system has just been shaken, he could become rather irritable and angry.The only thing that would actually annoy kleinman would be if he were to get the same attention here that he receives in the real world: none.

Completely ignoring him would destroy him. He lives for the attention he gets in this thread.
Joobz, this discussion doesn’t make me irritable or angry; in fact I’m enjoying this discussion. You have to put up with a lot of whining but that is all right. Now legal beagle’s psychoanalysis couldn’t be more wrong. I look forward to the day when it is finally understood by the scientific community how the mutation and selection sorting/optimization process actually works and I can return to a quiet life.
You practice eugenics that is obvious.Would you care to enlighten me about exactly how I practice eugenics? Against which group?
Anyone who isn’t segmented or sucks blood.
So, who are the fittest humans?The most fittest humans would be those who leave the largest amount of descendants.
What do you think about birth control?
That’s easy Belz, years of treatment of HIV with monotherapy has introduced huge populations of resistant strains in the HIV gene pool. This would not have occurred if you evolutionists hadn’t done such a lousy job in describing how the mutation and selection sorting/optimization process actually works. Thanks to the evolutionists erroneous description of the mutation and selection sorting/optimization process, millions of people will die prematurely from HIV and other diseases subject to the principles of mutation and selection.Don't forget that it's also because a large bunch of Christians have decided that abstinence is a better way to battle HIV than any kind of protection ever will be, because protection is an abomination against God.
You’ve just said that the most fit have the most descendants and now you want to prevent births. Kotatsu, you do believe in eugenics.
That’s easy Belz, years of treatment of HIV with monotherapy has introduced huge populations of resistant strains in the HIV gene pool.Monotherapy doesn't mean that NO OTHER selection pressures are at work, Klein. Try again.
Belz, read the following citation and learn how wrong you are.
http://www.annals.org/cgi/content/full/128/11/951 (http://www.annals.org/cgi/content/full/128/11/951)
First, using drugs that require the virus to undergo multiple mutations to achieve high-level resistance maximizes the efficacy of the drug for the existing viral population and minimizes the probability of breakthrough. In this respect, a drug to which resistance develops after only a single amino acid substitution is expected to be more vulnerable to resistance than an equipotent drug that requires the virus to undergo multiple mutations to achieve the same degree of resistance.

Second, the need for multiple mutations can be increased further by combining different drugs that inhibit independent targets. Three distinct therapeutic classes of drugs with nonoverlapping sets of resistance determinants exist: protease inhibitors, nucleoside inhibitors, and non-nucleoside reverse transcriptase inhibitors. There is no evidence that mutations compromising the effects of members of one class will reduce the utility of members of any other class. This is one of the most important benefits of divergent combination therapy: When many simultaneous mutations are required, the probability of preexisting resistance in a therapy-naive patient becomes negligible and the effect of the drug combination is maximized.

However, many patients are not naive to therapy. Their extensive drug experience and the consequent resistance of their viruses to multiple drugs may be the greatest obstacle to long-term viral suppression. The presence of preexisting resistance mutations in the viral population effectively lowers the genetic barrier to resistance with respect to a wide variety of possible treatment regimens and sometimes even to the most efficacious combination therapies.
I have posted other citations which show the same thing. Do you want me to repost them?
http://www.jci.org/cgi/content/full/117/9/2562 (http://www.jci.org/cgi/content/full/117/9/2562)
Molecularly targeted kinase inhibitor cancer therapies are currently administered sequentially rather than simultaneously. We addressed the potential long-term impact of this strategy in patients with chronic myelogenous leukemia (CML), which is driven by the fusion oncogene BCR-ABL. Analysis of BCR-ABL genotypes in CML patients who relapsed after sequential treatment with the ABL inhibitors imatinib and dasatinib revealed evolving resistant BCR-ABL kinase domain mutations in all cases. Twelve patients relapsed with the pan-resistant T315I mutation, whereas 6 patients developed novel BCR-ABL mutations predicted to retain sensitivity to imatinib based on in vitro studies. Three of these patients were retreated with imatinib (or the chemically related compound nilotinib) and responded; however, selection for compound mutants (2 or 3 BCR-ABL mutations in the same molecule) can substantially limit the potential effectiveness of retreating patients with inhibitors that have previously failed. Furthermore, drug-resistant mutations, when compounded, can increase oncogenic potency relative to the component mutants in transformation assays. The Aurora kinase inhibitor VX-680, currently under clinical evaluation based on its activity against the T315I mutation, is also effective against the other commonly detected dasatinib-resistant mutation in our analysis, V299L. Our findings demonstrate the potential hazards of sequential kinase inhibitor therapy and suggest a role for a combination of ABL kinase inhibitors, perhaps including VX-680, to prevent the outgrowth of cells harboring drug-resistant BCR-ABL mutations.
And
Of particular concern is the strong selective pressure for compound drug-resistant mutants in the context of sequential cancer therapy in a substantial proportion of patients. (These mutants could emerge by selection of preexisting clones or generation of new mutations.) Compound mutants not only diminish the chance of retaining sensitivity to a hypothetical "third-generation" inhibitor due to their potential complexity but also carry the risk of creating novel kinase alleles with enhanced oncogenic potency. Prevention of selection for such compound mutants will likely require up-front combination therapy utilizing compounds that can collectively suppress all single point mutations. To this end, we have provided evidence that VX-680, which is undergoing clinical evaluation and has shown early efficacy in T315I-associated cases (10), can inhibit the kinase activity of the most common dasatinib-resistant mutants. Future studies will need to address the tolerability of such combinations and whether the potential benefit of preventing resistance is outweighed by additional toxicities. In addition, our analysis was focused primarily on advanced-phase CML (since these patients were the first to relapse). Although compound mutations were identified at the time of dasatinib failure in both chronic phase patients studied in this analysis, longer follow-up on a larger number of patients is required to discern the impact of sequential ABL kinase inhibitor therapy in early-stage CML.
The use of monotherapy gives rapids evolution of resistance. In the case of HIV, these viruses are exchanged by carriers of the disease and interfere with combination therapy. The failure of evolutionists to acknowledge and teach this mathematical and empirical fact of how the mutation and selection sorting/optimization process works will cause the premature death of millions of people suffering from diseases subject to the principles of mutation and selection.

[Shalamar]

You are making an error here, it is not my mathematics, it is the mathematics of Dr Tom Schneider, head of computational molecular biology at the National Cancer Institute. Dr Schneider has documented his mathematics extensively online and can be found at:

So.. That would be a reply of 'I don't actually have any proof, or math to back up my claim that evolution is impossible'.

Gotcha.

Besides, your claim that multiple selection pressures slow down evolution (To make it impossible) is only one part of the evidence that makes up the Scientific Theory of Evolution. I understand your faith screams that it MUST be false, but Evolution is a fact. Terribly sorry. In fact, a story just came out talking about the evidence that evolution is humanity is FASTER than it ever has been.

[delphi_ote]

Delphi, you are so immersed in the lie of evolutionism that you have lost the ability to recognize the truth about how the mutation and selection sorting/optimization process actually works.
"Thou shalt not bear false witness against thy neighbour." Exodus 20:16
It is not my job to win you to God;
"And Jesus said unto them, Come ye after me, and I will make you to become fishers of men." Mark 1:17
"Now then we are ambassadors for Christ, as though God did beseech you by us: we pray you in Christ's stead, be ye reconciled to God." 2 Corinthians 5:20
it is my job to tell you the truth about the mutation and selection process.
Odd. I couldn't find any bible verses about this one.
If that gets a rise out of you, so be it. Christ calls us to be salt, not sugar.
"But in your hearts set apart Christ as Lord. Always be prepared to give an answer to everyone who asks you to give the reason for the hope that you have. But do this with gentleness and respect" 1 Peter 3:15
So stop whining and use your skills as a scientist and seek the truth.
The truth is, you're so caught up on a narrow-minded, literal interpretation of Genesis, you've acted unethically to ignore basic scientific facts. If Christianity means denying reality and acting like a jerk, I'll take atheism any day.

[joobz]

You are making an error here, it is not my mathematics, it is the mathematics of Dr Tom Schneider, head of computational molecular biology at the National Cancer Institute. Dr Schneider has documented his mathematics extensively online and can be found at:
http://nar.oxfordjournals.org/cgi/content/full/28/14/2794 (http://nar.oxfordjournals.org/cgi/content/full/28/14/2794)
The above URL gives the basic description of Dr Schneider’s model and presents the results of a single case.
http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/ (http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/)
The above URL gives access to the online version of Dr Schneider’s model written by Paul Anagnostopoulos, moderator and discussant on this site.

There are many links at Dr Schneider’s site which help explain his model but don’t be surprised if it takes several months of study to understand what he is doing.Don't be so modest. You presented a very nice description of the way multiple selection pressures determine the rate at which a popluation may adapt. With this model, it becomes clear that a variable multiple selection pressures accelerate the rate of evolutionary adaptation. With a consistent, nonchanging level of strong multiple selection pressures do we see a slow down in this adaptation capacity(potentially leading to extinction).
Since nature is a variable environment, we know that evolution is not only possible, it is real.

[Belz...]

It is not my job to win you to God

Sorry to be the one to tell you this, then, but you're not going to Heaven.

[Belz...]

Don't be so modest. You presented a very nice description of the way multiple selection pressures determine the rate at which a popluation may adapt. With this model, it becomes clear that a variable multiple selection pressures accelerate the rate of evolutionary adaptation. With a consistent, nonchanging level of strong multiple selection pressures do we see a slow down in this adaptation capacity(potentially leading to extinction). [/SIZE][/FONT]
Since nature is a variable environment, we know that evolution is not only possible, it is real.



Yeah, Klein. Thanks for that.

[Kotatsu]

Anyone who isn’t segmented or sucks blood.

Oh really? I actively prevent non-annelids from mating in order to make them the dominant life-form? Well, I must do that in my sleep, I guess, because there's certainly no time for that during the days.

Also: if by "sucks blood" you are referring to leeches, you are being redundant, as leeches are segmented as well. That's part of the whole "Annelida" thing.

What do you think about birth control?

I believe that's up to the couple in question. If they want to have kids, that's fine by me. If they just want to have sex and use some kind of birth control to be able to do so without the possibility of conception, that's fine, too. It's really not my business to advocate or prevent other people from having sex the way they want to.

You’ve just said that the most fit have the most descendants and now you want to prevent births. Kotatsu, you do believe in eugenics.

That is also not true, Kleinman. I have no desire to prevent births, but I do have a desire to prevent the spreading of HIV as it is a horrible disease (even though to my knowledge no one I know has contracted it).

[kleinman]

You are making an error here, it is not my mathematics, it is the mathematics of Dr Tom Schneider, head of computational molecular biology at the National Cancer Institute. Dr Schneider has documented his mathematics extensively online and can be found at:So.. That would be a reply of 'I don't actually have any proof, or math to back up my claim that evolution is impossible'.
Nothing other than a peer reviewed and published model of random point mutations and natural selection and hundreds of citations, all which show that combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process.
Gotcha.
You mean to say Gotnotheoryofevolutionbymutationandselection.
Delphi, you are so immersed in the lie of evolutionism that you have lost the ability to recognize the truth about how the mutation and selection sorting/optimization process actually works."Thou shalt not bear false witness against thy neighbour." Exodus 20:16
Keep going delphi, let’s hear your sermon.
It is not my job to win you to God;"And Jesus said unto them, Come ye after me, and I will make you to become fishers of men." Mark 1:17
"Now then we are ambassadors for Christ, as though God did beseech you by us: we pray you in Christ's stead, be ye reconciled to God." 2 Corinthians 5:20
Certainly we are to be fishers and ambassadors but it is the Spirit of God which wins the soul. If you want a better understanding of this, read Matthew 13.
it is my job to tell you the truth about the mutation and selection process.Odd. I couldn't find any bible verses about this one.
It’s in there, keep looking.
If that gets a rise out of you, so be it. Christ calls us to be salt, not sugar."But in your hearts set apart Christ as Lord. Always be prepared to give an answer to everyone who asks you to give the reason for the hope that you have. But do this with gentleness and respect" 1 Peter 3:15
I have had to sew up injuries on children; they did not think I did this with gentleness and respect. My hope is that your injuries are not fatal.
So stop whining and use your skills as a scientist and seek the truth.The truth is, you're so caught up on a narrow-minded, literal interpretation of Genesis, you've acted unethically to ignore basic scientific facts. If Christianity means denying reality and acting like a jerk, I'll take atheism any day.
Your refusal to understand how the mutation and selection sorting/optimization process works will cause the premature death of millions of people suffering from diseases subject to the principles of mutation and selection. This is what your faith in atheism brings. Here are some more of the basic scientific facts of how the mutation and selection sorting/optimization process actually works.
http://clincancerres.aacrjournals.org/cgi/content/full/11/19/6987?ijkey=c66726d59a1d21f01b056c518c06abf33d95798 4 (http://clincancerres.aacrjournals.org/cgi/content/full/11/19/6987?ijkey=c66726d59a1d21f01b056c518c06abf33d95798 4)
The most immediate potential benefit of combined Abl inhibitor therapy is that an inhibitor cocktail may target a wider range of resistant clones than either single agent and thereby prohibit or delay the onset of acquired drug resistance. For example, mutations that confer resistance to BMS-354825 but not to imatinib have been identified in vitro (25). The goals of this type of approach are different from combination strategies directed against distinct cellular targets (34–37) but similar to strategies using combinations of protease or reverse transcriptase inhibitors for HIV (38). Due to the enhanced inhibitory activity of combined Abl inhibitor therapy, this strategy may also improve molecular response rates in newly diagnosed patients and patients with imatinib-resistant CML. In the clinical setting, it is possible that use of imatinib-Src/Abl inhibitor combinations will lead to increased toxicity in normal tissues, and this will require careful monitoring. Consideration must be given to the tolerability of such drug regimens and to the potential emergence of new resistance mechanisms that circumvent this strategy. In addition, this approach does not solve the problem of mutants that are resistant to both drugs, such as T315I. However, these studies suggest that clinical trials of these drug combinations should be pursued.

http://jco.ascopubs.org/cgi/content/full/23/15/3614 (http://jco.ascopubs.org/cgi/content/full/23/15/3614)
Although cancer therapy has been directed at a single molecular target, in the future we can imagine targeting an entire set of interconnected kinase-driven events all along a deranged signaling pathway.38 Interconnecting points within a signaling cascade are interdependent. This is because a downstream phosphorylation event is driven by upstream events leading to the activation of the kinase acting on the target substrate. For example, as shown in Figure 2, phosphorylation of ERK is dependent on the activity of MEK, which is in turn driven by an entire series of upstream events. Consequently, in the context of this active pathway, a potential combinatorial therapeutic strategy would use an MEK inhibitor (the readout being ERK phosphorylation) and a Raf farnesyltransferase inhibitor (the readout being MEK phosphorylation). Given that the molecular network signaling pathways share an interacting and interdependent linkage, strategically selected combinatorial therapies could be given at a potentially lower dose, which could result in reduced toxicity compared with that seen using either agent alone. The potential reduction in toxicity combined with increased therapeutic efficacy is a promising hallmark of the potential for combinatorial therapeutics. Moreover, the likelihood of a tumor developing resistance to a cocktail of inhibitors that target an entire pathway could be significantly less probable.
By the way delphi, keep your atheistic religion out of our public schools.

[Shalamar]

I see he managed to ignore everything else posted, including the evidence countering HIS evidence.

It also seems that he uses the Bible as 'proof' against evolution. Frightening. The Bible isn't science.

By the way delphi, keep your atheistic religion out of our public schools.

Atheism isn't a religion.

By the way, Klienman, keep your religion out of our public schools.

Evolution DOES NOT equal Atheism!

[kleinman]

By the way delphi, keep your atheistic religion out of our public schools.Atheism isn't a religion.
Go for it Shalamar, prove to us there is no God.

I can prove how the mutation and selection sorting/optimization process works both mathematically and empirically and it shows the theory of evolution to be mathematically impossible. Now let’s see you prove mathematically and empirically there is no God.

[delphi_ote]

It’s in there, keep looking.
Sorry. It doesn't work that way. You either show us or hush.

If you have a better way of modeling AIDS, stop wasting time posting here and go invent a better drug. Again, either prove it or hush.

The rest of your post is rude nonsense that I'll do you the favor of completely ignoring. Your current behavior, however, exemplifies everything I found wrong with the Christian church. You're fishing without bait.

[delphi_ote]

Go for it Shalamar, prove to us there is no God.
Prove to us there is no Krishna, Thor, Allah, Zeus, Santa Claus, or Gandalf.

[Mister Agenda]

I admit I'm not competent to follow Kleinman's math. Am I correct in saying that his basic point is that natural selection tends to keep species stable, slowing the rate of evolution to a point that it can't account for observed speciation?

If so, I tend to agree, except that when conditions change, natural selection no longer necessarily favors the status quo, speeding the rate of evolution. Am I making a valid point or am I confused?

[cyborg]

I admit I'm not competent to follow Kleinman's math.

That's okay: it's incompetent math.

Am I correct in saying that his basic point is that natural selection tends to keep species stable, slowing the rate of evolution to a point that it can't account for observed speciation?

No - his basic point is that if that if everything that allows evolution to occur is suppressed such that evolution does not occur then evolution is impossible.

I think this might be easily analogised by saying that it is impossible to score a goal in football if you keep cutting off the player's legs and therefore concluding that football is an impossible game.

[Belz...]

You’ve just said that the most fit have the most descendants and now you want to prevent births. Kotatsu, you do believe in eugenics.

What a pack of lies.

[joobz]

Nothing other than a peer reviewed and published model of random point mutations and natural selection and hundreds of citations, all which show that combination selection pressures profoundly slow evolution by the mutation and selection sorting/optimization process.
Of course. your description of multiple selection pressures has been invaluable in showing how a variable environment can accelerate the evolutionary process. Indeed, you have helped prove that nature provides the ideal conditions for the evolutionary derived diversity that we see today. You have directly helped advance the understanding of evolution and helped to prove that it is both possible and real.

All of your references merely strengthen this point. Thank you!

[kleinman]

It’s in there, keep looking.Sorry. It doesn't work that way. You either show us or hush.
You are in denial about how the mutation and selection sorting/optimization process works and you don’t know the Bible as well as you think. Delphi study both some more and perhaps you will understand. But you are showing us that skills as a censor.
If you have a better way of modeling AIDS, stop wasting time posting here and go invent a better drug. Again, either prove it or hush.
Dr Schneider’s model all ready shows the essential behavior of the mutation and selection sorting/optimization process, which is combination selection pressures profoundly slow the evolutionary process. Despite the mathematical data from ev which show that combination selection pressures profoundly slow the evolutionary process and the hundreds of citations I have posted which demonstrates the same thing and your citation to Wikipedia and the fitness landscape you still won’t acknowledge the mathematical and empirical facts which show that the theory of evolution is mathematically impossible. So, instead you try censorship.
The rest of your post is rude nonsense that I'll do you the favor of completely ignoring. Your current behavior, however, exemplifies everything I found wrong with the Christian church. You're fishing without bait.
An atheist finds it rude to post mathematical and empirical data which shows that the theory of evolution is mathematically impossible. Sorry that reality doesn’t fit with your belief system.
Go for it Shalamar, prove to us there is no God.Prove to us there is no Krishna, Thor, Allah, Zeus, Santa Claus, or Gandalf.
It is you atheists which claim to know there is no God. What I am claiming here is that the mutation and selection sorting/optimization process is so profoundly slow that the theory of evolution is mathematically impossible. I am using Dr Schneider’s peer reviewed and published model of random point mutations to show this mathematically, hundreds of empirical examples which demonstrate the same thing and of course your Wikipedia reference to the fitness landscape. Don’t worry delphi, you will always have a career in the stop action movie business.
I admit I'm not competent to follow Kleinman's math. Am I correct in saying that his basic point is that natural selection tends to keep species stable, slowing the rate of evolution to a point that it can't account for observed speciation?
First of all, it is not my mathematics; it is the mathematics of Dr Tom Schneider, head of computational molecular biology at the National Cancer Institute. While it is true that most selection pressures are stabilizing, what I am contending is that Dr Schneider’s computer simulation shows that combination selection pressures profoundly slow the mutation and selection sorting/optimization process. You only get rapid evolution of a population when there is only a single strong selection pressure. When additional selection pressures are added to a population subjected to the single strong selection pressure, it slows the ability of the population to sort beneficial and detrimental mutations. This is what real examples of mutation and selection demonstrates as well.
If so, I tend to agree, except that when conditions change, natural selection no longer necessarily favors the status quo, speeding the rate of evolution. Am I making a valid point or am I confused?
You are making a valid point but the mutation and selection sorting/optimization process is far too slow to allow adaptation to multiple selection conditions simultaneously. That is what the mathematics shows and that is what real examples of mutation and selection demonstrates.
I admit I'm not competent to follow Kleinman's math.That's okay: it's incompetent math.
Cyborg, that’s not a nice or true thing to say about Dr Schneider’s mathematical model.
Am I correct in saying that his basic point is that natural selection tends to keep species stable, slowing the rate of evolution to a point that it can't account for observed speciation?No - his basic point is that if that if everything that allows evolution to occur is suppressed such that evolution does not occur then evolution is impossible.
Cyborg, I’ll let you defend your cruft theory of evolution and I’ll defend my hypothesis that combination selection pressures profoundly slow the evolutionary process.

Mister Agenda, once you understand that mutation and selection is simply a sorting/optimization problem where beneficial and detrimental mutations are sorted based on one or more selection conditions, then you will understand why combination selection conditions profoundly slow the process. The more selection conditions that the population is subjected to; the more difficult it is for the population to do the sort. A simple analogy would be if I asked you to sort the phone book but not just by name but also by address and phone number and at the same time you introduce random errors into the data. It is much more difficult to sort by multiple conditions simultaneously.
I think this might be easily analogised by saying that it is impossible to score a goal in football if you keep cutting off the player's legs and therefore concluding that football is an impossible game.
The only thing accurate about your analogy is the theory of evolution is the player and it no longer has legs, the mutation and selection process simply doesn’t work the way you allege.

Here is another example how the mutation and selection sorting/optimization process actually works.

RNA virus mutations and fitness for survival
E Domingo, J J Holland. Annual Review of Microbiology. Palo Alto: 1997. Vol. 51 pg. 151, 28 pgs
The fact that very few viral pathogens can be effectively controlled, either by vaccination or by antiviral therapies, attests to the need to understand the mechanisms by which viruses overcome the pressures that are intended to limit their replication. Current evidence suggests that the origins of such an ability include: the frequent generation of mutations by RNA viruses, the continuous competition among variant genomes, and the selection of those variants which are best adapted to each particular environment (51,51a, 53,55,91). Many questions remain, however, such as: Which factors affect genetic stability and which affect rapid change? What are the mechanisms of long-term persistence versus those of extinction? What mutation pathways are required to reach high fitness values? What is the relevance of viral variability to pathogenesis? Progress in understanding the implications of high mutation rates and the population dynamics of RNA viruses has already provided a basis for the preference of some types of treatments over others: combination antiretroviral therapy over monotherapy (34,43,50) or multicomponent complex vaccines over simple, peptide vaccines (43, 50, 83,146,189a, 202). Yet, the broad implications of the complexities of RNA genetics for RNA virus adaptability, viral emergence, and disease control are only beginning to be comprehended.
You evolutionists are overwhelming me with all zero of your citations which show that combination selection pressures accelerate evolution.

[joobz]

You evolutionists are overwhelming me with all zero of your citations which show that combination selection pressures accelerate evolution.
You are so right. a Stable combination of strong selection pressures can lead to extinction or at the very least a dramatic supression of resistence emergence. This is an invaluable part of your description and one you should be proud of. You are simply missing the true meaning of what is being said, and this is simply because your dogma prevents you from it.

A variable environment of multiple selection conditions leads to much faster emergence of adapted traits than the stable counterpart. This is a very important realization you helped me come to.

It proves why the variable natural environment is so important!

And thank you for your new evidence. It only futher supports this conclusion.

The fact that very few viral pathogens can be effectively controlled, either by vaccination or by antiviral therapies, attests to the need to understand the mechanisms by which viruses overcome the pressures that are intended to limit their replication. Current evidence suggests that the origins of such an ability include: the frequent generation of mutations by RNA viruses, the continuous competition among variant genomes, and the selection of those variants which are best adapted to each particular environment (51,51a, 53,55,91). Many questions remain, however, such as: Which factors affect genetic stability and which affect rapid change? What are the mechanisms of long-term persistence versus those of extinction? What mutation pathways are required to reach high fitness values? What is the relevance of viral variability to pathogenesis? Progress in understanding the implications of high mutation rates and the population dynamics of RNA viruses has already provided a basis for the preference of some types of treatments over others: combination antiretroviral therapy over monotherapy (34,43,50) or multicomponent complex vaccines over simple, peptide vaccines (43, 50, 83,146,189a, 202). Yet, the broad implications of the complexities of RNA genetics for RNA virus adaptability, viral emergence, and disease control are only beginning to be comprehended.

If only you would stop confusing religion with the reality of evolution that you helped prove, you would see the beauty of your argument.

[kleinman]

The fact that very few viral pathogens can be effectively controlled, either by vaccination or by antiviral therapies, attests to the need to understand the mechanisms by which viruses overcome the pressures that are intended to limit their replication.
Progress in understanding the implications of high mutation rates and the population dynamics of RNA viruses has already provided a basis for the preference of some types of treatments over others: combination antiretroviral therapy over monotherapy (34,43,50) or multicomponent complex vaccines over simple, peptide vaccines
Joobz, your speculations on the mutation and selection sorting/optimization process matches your speculations on abiogenesis. They are illogical, irrational and mathematically and empirically impossible.

[rocketdodger]

No - his basic point is that if that if everything that allows evolution to occur is suppressed such that evolution does not occur then evolution is impossible.

I think this might be easily analogised by saying that it is impossible to score a goal in football if you keep cutting off the player's legs and therefore concluding that football is an impossible game.

Awesome.

[joobz]

Joobz, your speculations on the mutation and selection sorting/optimization process matches your speculations on abiogenesis. They are illogical, irrational and mathematically and empirically impossible.
these aren't my speculations Kleinman. It's your theory. This is simply the logical conclusion from the elegant theory you have created. I thank you for it. I'm certain everyone here thanks you for your efforts at proving evolution for us.

Afterall, your theory has clearly demostrated what happens under a constant unchanging number of combined selection pressures.

It's a good thing nature isn't a constant environment. I mean, you can't be so confused with your dogmatic anti-evolutionist views to believe that there is no such thing as weather.

[delphi_ote]

An atheist finds it rude to post mathematical and empirical data which shows that the theory of evolution is mathematically impossible.
:notm:
You've retreated every time from presenting a mathematical argument of any sort for your position. Your conclusions about anything resembling empirical evidence have been demonstrated time and time again to be wrong. Nothing to worry about there.

What I find it rude, hypocritical and dishonest is that you've ignored all of this and started hiding behind ad hominems and association fallacies.

For all of your complaining about atheism and evolution leading to unethical behavior, you are setting a terrible example of how to behave. If you had any interest about the truth or respect for your fellow man, you wouldn't waste all of our time calling people Hitler. It's amazing that your critical thinking skills so catastrophically bad that you can't even reconcile your arguments with your own behavior. By all means, please post another ridiculously long message on this organization's website (which very vocally supports the theory of evolution) and gripe about evolutionists censoring you.

[Shalamar]

Go for it Shalamar, prove to us there is no God.

I can prove how the mutation and selection sorting/optimization process works both mathematically and empirically and it shows the theory of evolution to be mathematically impossible. Now let’s see you prove mathematically and empirically there is no God.

I have yet to see any 'mathematical' proof from you that the Theory of Evolution is impossible. Please, show us your math.

God can not be disproven. God also can not be proven. False statements regarding evolution, and atheism.

Please provide your math.

[Kotatsu]

What a pack of lies.

Fortunately, he seems to have stopped responding to me at all. Maybe he's getting scared because he's not segmented?

And thanks!

[sol invictus]

Strange - I thought Klienman said multiple selection pressures slow evolution? I guess I must have misunderstood.

Rapid acceleration in human evolution described
...
Many of the recent genetic changes reflect differences in the human diet brought on by agriculture, as well as resistance to epidemic diseases that became mass killers following the growth of human civilizations, the researchers said.

For example, Africans have new genes providing resistance to malaria. In Europeans, there is a gene that makes them better able to digest milk as adults. In Asians, there is a gene that makes ear wax more dry.

The changes have been driven by the colossal growth in the human population -- from a few million to 6.5 billion in the past 10,000 years -- with people moving into new environments to which they needed to adapt, added Henry Harpending, a University of Utah anthropologist.

"The central finding is that human evolution is happening very fast -- faster than any of us thought," Harpending said in a telephone interview.

"Most of the acceleration is in the last 10,000 years, basically corresponding to population growth after agriculture is invented," Hawks said in a telephone interview.

[Mr. Scott]

You practice eugenics that is obvious.

You lie, that is obvious, and you don't follow your god's law to not lie (Commandment #9). You don't turn the other cheek as Christ commands, nor do you treat your neighbors here on JREF as you would like them to treat you. You cherry-pick the bible, that is obvious. Shame on you for your hypocrisy, Dr. Kleinman.

[Mr. Scott]

It is not my job to refute every misinterpretation [of evidence for evolution] that you evolutionists come up with.

Your modus operandi is to check scientific evidence against the Bible.

This is a thoroughly worthless way to do science, and if science had always proceeded that way, we'd be still in the bronze age with no science of medicine at all. They thought diseases were manifestations of God's will, and the Bible never mentions the microbes so central to your refutation of evolution. Faith, prayer, and other nonsense were the only "medicine" they had.

Science follows the evidence, wherever that leads, and if it leads us away from present biblical interpretation, then we must change our biblical interpretations.

It's the scientific method (following the evidence) that you have to thank for your career as a healer.

There is a mountain of consistent evidence that evolution is real, and there's no evidence against it. Why an educated person ignores good scientific evidence just because it disagrees with some old fairy tales is a testament to the extreme irrationality we are capable of...

...and it's very, very bad science.

[Henners]

So, who are the fittest humans?

Catholics, obviously.

They belong to a religion that does not practice contraception and therefore have a higher reproductive success.

If you, yourself, kleinman, have ever used any form of contraception, I must congratulate you on making a very wise and selfless eugenic decision for the benefit of the rest of humanity.

[Belz...]

Fortunately, he seems to have stopped responding to me at all. Maybe he's getting scared because he's not segmented?

We ALL want to be segmented.






... what the hell am I saying ??

[Belz...]

Why an educated person ignores good scientific evidence just because it disagrees with some old fairy tales is a testament to the extreme irrationality we are capable of...

Yes, you evolutionists are indeed capable of extreme irrationality when believing in your old fairy tale of evolution.

Meanwhile, I'll continue to post hundreds of real-life examples of how mutation and selection really work.

[Kotatsu]

We ALL want to be segmented.
... what the hell am I saying ??

You're just saying what's on everyone's mind! The truth will out!

And now that you have expressed a wish to be segmented, I will graciously allow you to reproduce, as long as you have no more than 30-40 descendants.

[Mr. Scott]

Yes, you evolutionists are indeed capable of extreme irrationality when believing in your old fairy tale of evolution.

Meanwhile, I'll continue to post hundreds of real-life examples of how mutation and selection really work.

Yes, it's too easy. Kleinman has evolved himself into a dead end and is now completely predictable.

It is you whining cry baby evolutionists who are now completely predictable

No! How do you turn this thing off? Help!!!

[Paul C. Anagnostopoulos]

Don’t you remember when sol got gamma and G mixed up?
That was me.


It takes only a few generations to identify all binding sites. I don’t think sorting the sequences at the binding site locations is what slows the convergence in ev. I think it is the elimination of the weight matrix matches in the non-binding site region that slows and ultimately stops the convergence of ev.
Say what? When you run the standard model, it takes one generation to eliminate spurious bindings and 661 more generations to match the binding sites. With a random seed of 1, it takes 6 generation to eliminate spurious bindings and 871 more generation to match the binding sites.

It's easy to eliminate spurious bindings: Just find a weight matrix and threshold that put every position on the genome below the threshold.

~~ Paul

[Belz...]

You're just saying what's on everyone's mind! The truth will out!

And now that you have expressed a wish to be segmented, I will graciously allow you to reproduce, as long as you have no more than 30-40 descendants.

Woah. I've gotta be careful in avoiding n+1 selection pressures, then.

No! How do you turn this thing off? Help!!!

You don't. You gotta shoot its brain. Problem is, it doesn't have any.

[joobz]

Woah. I've gotta be careful in avoiding n+1 selection pressures, then.

You don't. You gotta shoot its brain. Problem is, it doesn't have any.

Oh, come on everyone. While Kleinman has been extremely abrasive, he has raised a very important point. Indeed, it is true, that with a stable combined number of strong selection pressures, the ability for a population to evolve becomes greatly reduced. Indeed, such considtions can readily lead to extinctions. Kleinman is exactly right on this.

His argument highlights the importance of a variably changing environment in the acceleration of population emergence. Indeed, since nature provides such an environment, evolutionary theory isn't only mathematically possible, all evidence shows that it is real.

This is a wonderful contribution to the layman's understanding of evolution and kleinman must be thanked for advancing it for us.

Afterall, creationist now must prove that weather doesn't exist in order to claim that evolution in nature is impossible.

Kleinman has single handedly negated one of ID's arguments against evolution.

[kleinman]

An atheist finds it rude to post mathematical and empirical data which shows that the theory of evolution is mathematically impossible.http://forums.randi.org/images/smilies/sno.gif
You've retreated every time from presenting a mathematical argument of any sort for your position. Your conclusions about anything resembling empirical evidence have been demonstrated time and time again to be wrong. Nothing to worry about there.
Delphi, it appears you have forgotten what you said previously. Let me remind you.
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.
It is clear from ev that the shape of the fitness landscape is strongly dependent on the number of selection pressures. It is this mathematical fact that ev demonstrates that you are in denial of. The hundreds of empirical examples I have posted of the mutation and selection sorting/optimization process demonstrates this as well. It is the number of selection conditions which dominates the mathematics of the mutation and selection sorting/optimization process. Reread your own Wikipedia reference to the fitness landscape of you have trouble grasping this mathematical and empirical fact of life.
What I find it rude, hypocritical and dishonest is that you've ignored all of this and started hiding behind ad hominems and association fallacies.
The mathematical and empirical evidence of how the mutation and selection sorting/optimization process works is clear. It is the number of selection pressures which dominates the behavior of this process. Your denial of these mathematical and empirical facts contributes to the premature death of millions of people suffering from diseases that are subject to the mutation and selection process.
For all of your complaining about atheism and evolution leading to unethical behavior, you are setting a terrible example of how to behave. If you had any interest about the truth or respect for your fellow man, you wouldn't waste all of our time calling people Hitler. It's amazing that your critical thinking skills so catastrophically bad that you can't even reconcile your arguments with your own behavior. By all means, please post another ridiculously long message on this organization's website (which very vocally supports the theory of evolution) and gripe about evolutionists censoring you.
Just because many people support the theory of evolution does not make the theory correct. The mathematical and empirical data show that you are wrong about how the mutation and selection sorting/optimization process works. And you incorrect interpretation of the mutation and selection sorting/optimization process contributes to the premature death of millions of people suffering from diseases subject to the principles of mutation and selection. I think you are the rude one in this debate.
Go for it Shalamar, prove to us there is no God.

I can prove how the mutation and selection sorting/optimization process works both mathematically and empirically and it shows the theory of evolution to be mathematically impossible. Now let’s see you prove mathematically and empirically there is no God.I have yet to see any 'mathematical' proof from you that the Theory of Evolution is impossible. Please, show us your math.
If you had read this thread, you would see the proof. Here’s an opportunity for you to learn for yourself how the mutation and selection sorting/optimization process works. Start Dr Schneider’s ev computer simulation of random point mutations and natural selection. Leave all the parameters at their baseline values except G, set G to 16384 and click the stop on “perfect creature”. Run the model until a “perfect creature” is evolved. Then restart the model using all the same parameters except under the advanced features of the model, set any two of the three weights for the selection conditions to zero. What you are doing when you set two of the three weight factors to zero is that you are reducing down the number of selection conditions from three to one. Tell us what values you get.
You practice eugenics that is obvious.You lie, that is obvious
You think everyone lies to you including your parents.
You don't turn the other cheek as Christ commands, nor do you treat your neighbors here on JREF as you would like them to treat you.
Are you going to teach us on the Bible? Teach us on John 18:19-23. Then perhaps you will understand Matthew 5:38-39.
Don’t you remember when sol got gamma and G mixed up?That was me.
After all this time you mixed up G and gamma? Paul, you need a power nap.
It takes only a few generations to identify all binding sites. I don’t think sorting the sequences at the binding site locations is what slows the convergence in ev. I think it is the elimination of the weight matrix matches in the non-binding site region that slows and ultimately stops the convergence of ev.Say what? When you run the standard model, it takes one generation to eliminate spurious bindings and 661 more generations to match the binding sites. With a random seed of 1, it takes 6 generation to eliminate spurious bindings and 871 more generation to match the binding sites.
Is this the case of G=256? If so, then the portion of the genome which represents binding sites, gene and non-binding site region are very close. Try the cases of G=16384, G=32768 and G=65536 and do selection based only on location of binding sites. The message here is that the only way to speed up the mutation and selection sorting/optimization process is to reduce down the size of the search space. You do that by reducing the number of selection conditions and the genes targeted by the selection conditions. That’s what your model shows and that’s what real examples of mutation and selection shows.
It's easy to eliminate spurious bindings: Just find a weight matrix and threshold that put every position on the genome below the threshold.
You are drawing a conclusion based on a single case. You would think that after all this time you would learn that trying to draw conclusions from ev based on a single case leads you astray. The mathematical fact of life which ev sorting algorithm demonstrates is that the mutation and selection sorting/optimization process is strongly dependent on the number of selection conditions. This mathematical fact of life is also demonstrated in the hundreds of real examples of mutation and selection.

Here is another real example which demonstrates this mathematical fact of life.
http://www.translational-medicine.com/content/5/1/38 (http://www.translational-medicine.com/content/5/1/38)
Lenalidomide is an IMiD which can inhibit the function of endothelial cells in vitro, can block the outgrowth of cells from a rat aortic ring mimicking the inhibition of cells in the tumor microenvironment, and can inhibit the growth of a primary tumor as well as inhibit the growth of metastases in a human ocular melanoma xenograft model. Sorafenib likewise can inhibit endothelial cells in vitro, ex vivo and can inhibit tumor growth in vivo. Further, the combination of lenalidomide and a tyrosine kinase inhibitor like sorafenib is a viable combination which targets multiple aspects of the tumor microenvironment in vitro, ex vivo and in vivo. Based on our pre-clinical results, we believe that this combination and this strategy warrant testing in a clinical setting against ocular melanoma.

[Paul C. Anagnostopoulos]

After all this time you mixed up G and gamma? Paul, you need a power nap.
I'm Greek. Gamma and G are the same thing.


Is this the case of G=256? If so, then the portion of the genome which represents binding sites, gene and non-binding site region are very close. Try the cases of G=16384, G=32768 and G=65536 and do selection based only on location of binding sites.
What? That's the silliest damn thing I've heard in a long time. Of course if you are not trying to distinguish binding sites from other positions, it won't take long to identify the binding sites. That's because the gene will bind everywhere. You said:

It takes only a few generations to identify all binding sites.
You meant to say "It takes only a few generations to match all binding positions [when that's all you're trying to do]."


You are drawing a conclusion based on a single case.
Hardy har har.

~~ Paul

[Paul C. Anagnostopoulos]

Further, the combination of lenalidomide and a tyrosine kinase inhibitor like sorafenib is a viable combination which targets multiple aspects of the tumor microenvironment in vitro, ex vivo and in vivo. Based on our pre-clinical results, we believe that this combination and this strategy warrant testing in a clinical setting against ocular melanoma.
You know, you keep citing these sorts of experiments. Now I will agree that the progression of cancer is something like evolution, but it is not evolution. Could you show us the mathematical proof that it is enough like evolution to make your examples relevant?

~~ Paul

[kjkent1]

What? That's the silliest damn thing I've heard in a long time. Of course if you are not trying to distinguish binding sites from other positions, it won't take long to identify the binding sites. That's because the gene will bind everywhere.It's just incredible that kleinman keeps trying to justify his position by disabling part of the ev algorithm.

Alan, how do you explain the extreme case, where all three mistake weights are zero, and ev reports a perfect creature in the 1st generation?

You cannot honestly believe that the "zero mistakes"/"perfect creature" reported by ev with all mistakes disabled (set to zero) is the same organism as reported when all three mistakes are enabled (non-zero)?

You may as well say that there's no difference between a Shakespeare play and a bag full of Scrabble tiles!

PS. It appears that someone is about to publish a rather detailed empirical rebuttal to your theory:

http://johnhawks.net/weblog/topics/evolution/selection/acceleration_embargo_ends_2007.html

You had better contact Mr. Hawks and set him straight!

[kleinman]

After all this time you mixed up G and gamma? Paul, you need a power nap.I'm Greek. Gamma and G are the same thing.
I guess if you were Hebrew, gimmel and G would be the same thing.
Is this the case of G=256? If so, then the portion of the genome which represents binding sites, gene and non-binding site region are very close. Try the cases of G=16384, G=32768 and G=65536 and do selection based only on location of binding sites.What? That's the silliest damn thing I've heard in a long time. Of course if you are not trying to distinguish binding sites from other positions, it won't take long to identify the binding sites. That's because the gene will bind everywhere. You said:
That’s the point, one who confuses Gamma and G. It is much, much more difficult to evolve more complex function. This is what your ev sorting algorithm shows. This is why it takes huge numbers of generations to evolve all three sorting conditions simultaneously on all but the tiniest genomes and evolving only a single selection condition is extremely easy, even on genomes which won’t evolve all three selection conditions simultaneously.
It takes only a few generations to identify all binding sites.You meant to say "It takes only a few generations to match all binding positions [when that's all you're trying to do]."
That’s correct Paul, simple function is the easiest for your sorting algorithm to accomplish, and complex function is much, much more difficult for your sorting algorithm to accomplish. That’s how the mutation and selection sorting/optimization process actually works. Ev properly demonstrates this mathematical fact.
Further, the combination of lenalidomide and a tyrosine kinase inhibitor like sorafenib is a viable combination which targets multiple aspects of the tumor microenvironment in vitro, ex vivo and in vivo. Based on our pre-clinical results, we believe that this combination and this strategy warrant testing in a clinical setting against ocular melanoma.You know, you keep citing these sorts of experiments. Now I will agree that the progression of cancer is something like evolution, but it is not evolution. Could you show us the mathematical proof that it is enough like evolution to make your examples relevant?
Paul, are you now going to claim that the evolution of cancer cells to resistance to the drugs used to treat these cancers is not an example of the mutation and selection sorting/optimization process? You would learn something about the mutation and selection sorting/optimization process if you read the citations I have posted like this:
http://www.bumc.bu.edu/www/busm/Ll/PDFs/Gleevec.pdf (http://www.bumc.bu.edu/www/busm/Ll/PDFs/Gleevec.pdf)
Several principles have been developed to manage the troublesome occurrence of mutations in human immunodeficiency virus-1 (HIV) RT, which may be of value if applied to the case of chemoresistance in CML. An important principle in the treatment of HIV with chemical agents is the simultaneous introduction of combinations of anti-viral drugs that have not been used previously for a particular patient (41). In CML, partial cytogenetic or hematologic responses are actually exceedingly dangerous states, because ongoing genetic instability in the surviving CML clones provides an ideal mechanism for the strong selection of resistant mutations under the pressure of a single anti-cancer drug. Therefore, the repopulation of the marrow and peripheral blood with resistant clones is almost inevitable. Deininger and Druker (2) have acknowledged that Gleevec’s selective pressure favors the outgrowth of pre-existing resistant clones, similar to a bacterial culture treated with a single antibiotic. However, the pace of basic research into drug design for the next generation of chemical inhibitors of Abl suggests that there will soon be a respectable arsenal of agents available for physician choice, such as AP23464 (Ariad Pharmaceuticals), BMS-354825 (Bristol-Myers Squibb;42,43), SKI606 (Wyeth), PD180970 (Parke Davis), CGP76030 and AMN107 (Novartis; 43), VX-680 (Vertex Pharmaceuticals/Merck;44). Other targeted agents such as SU11248 (Pfizer), have value against Kit and platelet derived growth factor receptor α form (16).
and
Absent successful allogeneic stem cell transplantation, it is likely that clinicians will be forced to confront the problem of invariable relapse in CML, and will continue to depend upon chemical agents. The experience of HIV anti-viral drug resistance suggests the following analogous principles should be applied to CML therapy:
1. Several combinations of Abl-directed drugs should be used simultaneously, even if specificity is not optimal, provided that the combination can be tolerated.
2. Patients should be carefully monitored for the emergence of resistance, and new agents
quickly substituted as they become available.
3. If a combination treatment protocol fails, it is important to change more than one component of the protocol. Substitution of a single agent, even Gleevec, may promote resistance to new agents by increasing the strength of the drug selective pressure.
4. Single agent therapy, such as Gleevec alone, should be avoided, given the obvious risk for the development of drug resistance.
Cancer therapy and HIV are simply two of the many examples of the mutation and selection sorting/optimization process. A process which you own computer model shows that when trying to evolve complex function is much, much slower than when evolving simple function.

Paul, you need to watch your G’s and Gamma’s.

[Belz...]

There HAS to be a way to MAKE that damn ev program support my argument!

[Shalamar]

Klienman, you keep saying that you can prove mathematically that Evolution is impossible.
I ask you for the math. The calculations. Instead, you point me at a SIMULATION.

Show me the math. I wish to see the actual calculations.

[Paul C. Anagnostopoulos]

That’s the point, one who confuses Gamma and G. It is much, much more difficult to evolve more complex function. This is what your ev sorting algorithm shows.
Yes, blah blah blah. But in the future, please don't say stuff like this:

It takes only a few generations to identify all binding sites. I don’t think sorting the sequences at the binding site locations is what slows the convergence in ev. I think it is the elimination of the weight matrix matches in the non-binding site region that slows and ultimately stops the convergence of ev.
You didn't mean "identify all binding sites," you meant "match every position." And you meant to say the opposite of what you said in the last two sentences.


That’s correct Paul, simple function is the easiest for your sorting algorithm to accomplish, and complex function is much, much more difficult for your sorting algorithm to accomplish.
I agree, for some definition of simple.


Paul, are you now going to claim that the evolution of cancer cells to resistance to the drugs used to treat these cancers is not an example of the mutation and selection sorting/optimization process?
No, I'm going to claim that it's not particularly relevant to real-world evolution of species. I'm going to claim that calling everything a sort/optimization process has caused it all to become a fuzzy blur in your mind.

~~ Paul

[joobz]

Klienman, you keep saying that you can prove mathematically that Evolution is impossible.
I ask you for the math. The calculations. Instead, you point me at a SIMULATION.

Show me the math. I wish to see the actual calculations.
In Kleinman's world, running simulations=doing the math. But this is ok, becuase it is obvious that he has helped strengthen the argument FOR evolution.

We should all thank him for proving that we need a variable environment to see a rapid emergence. Thank god nature is such an environment, otherwise we wouldn't be here.

[Shalamar]

In Kleinman's world, running simulations=doing the math. But this is ok, becuase it is obvious that he has helped strengthen the argument FOR evolution.

We should all thank him for proving that we need a variable environment to see a rapid emergence. Thank god nature is such an environment, otherwise we wouldn't be here.

I figured that out a long time ago. But he repeats 'I can prove that Evolution is Mathematically impossible'. When brought to task for this, he points to a website, and says 'Run the simulation'. Unless the simulation spans 4 billion years, and copies the earth, and nature perfectly, I'm not interested.

EV is an interesting program that shows ways it might happen, but it is still limited. Which is why biologists work in nature, and not in computers.

[rocketdodger]

Indeed, it is true, that with a stable combined number of strong selection pressures, the ability for a population to evolve becomes greatly reduced. Indeed, such considtions can readily lead to extinctions. Kleinman is exactly right on this.

You mean a combined number of strong destructive selection pressures.

Of course it is a mute point because Kleinman firmly believes, despite clear examples to the contrary, that all selection pressures must "reduce the fitness of a population to reproduce." In his mind there is no such thing as non-destructive selection pressures.

[joobz]

You mean a combined number of strong destructive selection pressures.

Of course it is a mute point because Kleinman firmly believes, despite clear examples to the contrary, that all selection pressures must "reduce the fitness of a population to reproduce." In his mind there is no such thing as non-destructive selection pressures.
Ah yes. Actually as Kleinman would term them,
Multiple DIRECTIONAL selection pressures.

[kleinman]

Klienman, you keep saying that you can prove mathematically that Evolution is impossible. I ask you for the math. The calculations. Instead, you point me at a SIMULATION.
It’s clear that you don’t understand how modern complex mathematical problems are solved. The mutation and selection sorting/optimization process is a complex interaction of many parameters that can not be described by a simple closed form algebraic equation. The mutation and selection sorting/optimization process is a cyclical process of mutation->selection->reproduction and back to mutation. This process is repeated over and over. Ev is an application of this concept. The closest you can get to write an equation for this process is to write it in functional form. I doubt you have any knowledge of functional analysis but that’s how you study a model like ev. When you do functional analysis of the mutation and selection sorting/optimization process, it reveals that the dominant parameter in this mathematical process is the number of selection conditions. This mathematical fact is demonstrated by the hundreds of real examples of the mutation and selection sorting/optimization process. To understand how ev works, you need to do a parametric study of the model. This is what Dr Schneider recommended in his publication on ev. Dr Schneider did a parametric study of his model but never published the results. I believe he did not publish his results because he didn’t understand why it took such huge numbers of generations to converge for anything other the tiniest genome lengths. He could not understand why amplification was not occurring in his model. The reason why amplification does not occur in his model is the multiple simultaneous selection conditions. Set any two of the three selection conditions in his model and you get the amplification phenomenon.
Show me the math. I wish to see the actual calculations.
You can start at this URL http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/ (http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/) . There are many links on this page that not only talk about the equations used but also you can download the source code for the model.
That’s the point, one who confuses Gamma and G. It is much, much more difficult to evolve more complex function. This is what your ev sorting algorithm shows.Yes, blah blah blah. But in the future, please don't say stuff like this:
Paul, don’t you remember when you blah blah blahed the following statement?
But a portion of a whole function is not the same function as the whole function, is it? Lots of things in life are made easier by only doing part of the whole task.
Your model shows that it is much easier to evolve simple function than complex function. Somewhere in your evolutionist dream world you think that a reptile population can evolve to a bird population. This is a mathematical and empirical impossibility. Even your simple three selection condition model shows how slow this process is. There is no way to transform thousands of genes simultaneously by mutation and selection. Your model shows it can barely evolve three selection conditions on only the tiniest genomes.
It takes only a few generations to identify all binding sites. I don’t think sorting the sequences at the binding site locations is what slows the convergence in ev. I think it is the elimination of the weight matrix matches in the non-binding site region that slows and ultimately stops the convergence of ev.You didn't mean "identify all binding sites," you meant "match every position." And you meant to say the opposite of what you said in the last two sentences.
Whatever. And no I did not mean to say the opposite in the last two sentences. Evolving simple function is much, much easier than evolving complex function. And the mathematical behavior of evolving simple function versus complex function is far from linear. That is what your mathematical model of the mutation and selection sorting/optimization process shows.
That’s correct Paul, simple function is the easiest for your sorting algorithm to accomplish, and complex function is much, much more difficult for your sorting algorithm to accomplish.I agree, for some definition of simple.
Why not start with your own sorting/optimization algorithm? Sorting for any single simple sorting condition in your model takes trivially small number of generations when compared to the more complex sorting condition based on all three sorting condition simultaneously.
Paul, are you now going to claim that the evolution of cancer cells to resistance to the drugs used to treat these cancers is not an example of the mutation and selection sorting/optimization process?No, I'm going to claim that it's not particularly relevant to real-world evolution of species. I'm going to claim that calling everything a sort/optimization process has caused it all to become a fuzzy blur in your mind.
Your evolutionist indoctrination interferes with understanding how the mutation and selection process actually works. You don’t see in a fuzzy blur, you are blind. Perhaps another citation which shows how the mutation and selection sorting/optimization process works might help.
http://pathogens.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.ppat.0030046&ct=1 (http://pathogens.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.ppat.0030046&ct=1)
Combination antiretroviral therapy is effective in reducing, but not eliminating, HIV-1 replication. Residual viremia during suppressive antiretroviral therapy may arise from a number of sources, including reservoirs of long-lived virus-producing cells, or ongoing complete cycles of viral replication. Here, we used a new, more sensitive assay of HIV-1 RNA to measure residual viremia in a large cohort of patients with prolonged suppression on antiretroviral therapy. We found a persistent, stable level of viremia in patients on prolonged therapy that correlated with pretherapy levels of HIV-1. Over 80% of patients had viremia 1 copy/ml plasma, and the level of viremia was independent of the drug regimen patients were taking. These data strongly suggest that persistent viremia on antiretroviral therapy is likely derived from reservoirs of long-lived virus-producing cells that are not affected by currently available drugs that target new cycles of viral replication. New antiviral strategies that eradicate this reservoir will be necessary to cure HIV-1 infection.

[Henners]

So you don't actually have the Mathematics, then, and cannot articulate it either.

That means that you have nothing to communicate but your childhood indoctrination.

Shame. On the other hand, it explains everything - all the way from the patronising to the panic.

[joobz]

Your evolutionist indoctrination interferes with understanding how the mutation and selection process actually works. You don’t see in a fuzzy blur, you are blind. Perhaps another citation which shows how the mutation and selection sorting/optimization process works might help.
http://pathogens.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.ppat.0030046&ct=1 (http://pathogens.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.ppat.0030046&ct=1)


Again, you are so close to understanding the truth, but your dogmatic beliefs are getting in the way. Eventually you will understand the concepts behind multiple selection pressures and how a variable environment is capable of accelerating the evolutionary process.

Your only chance now to prove evolution is impossible is to prove that there is no such thing as weather. I can only assume that your dogmas are so ingrained that you actually believe that.

Thank you for presenting more evidence that supports the fact that evolutionary emergence is real and occurs in nature.
http://pathogens.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.ppat.0030046&ct=1 (http://pathogens.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.ppat.0030046&ct=1)

Combination antiretroviral therapy is effective in reducing, but not eliminating, HIV-1 replication. Residual viremia during suppressive antiretroviral therapy may arise from a number of sources, including reservoirs of long-lived virus-producing cells, or ongoing complete cycles of viral replication. Here, we used a new, more sensitive assay of HIV-1 RNA to measure residual viremia in a large cohort of patients with prolonged suppression on antiretroviral therapy. We found a persistent, stable level of viremia in patients on prolonged therapy that correlated with pretherapy levels of HIV-1. Over 80% of patients had viremia 1 copy/ml plasma, and the level of viremia was independent of the drug regimen patients were taking. These data strongly suggest that persistent viremia on antiretroviral therapy is likely derived from reservoirs of long-lived virus-producing cells that are not affected by currently available drugs that target new cycles of viral replication. New antiviral strategies that eradicate this reservoir will be necessary to cure HIV-1 infection.

[Belz...]

So you don't actually have the Mathematics, then, and cannot articulate it either.

I've been telling him this for a year, now.

[rocketdodger]

Ah yes. Actually as Kleinman would term them,
Multiple DIRECTIONAL selection pressures.

Errr, I mean, "pressures that don't result in a smaller population size after each generation."

Kleinman claims all directional selection pressures decrease population size each generation.

This is pretty stupid because the population size in ev is held constant, yet Kleinman relies on ev for most of his argument.

Adequate, I, and ev have shown that fixation rates increase as one adds pressures as long as those pressures don't decrease population size.

[kleinman]

Your evolutionist indoctrination interferes with understanding how the mutation and selection process actually works. You don’t see in a fuzzy blur, you are blind. Perhaps another citation which shows how the mutation and selection sorting/optimization process works might help.
http://pathogens.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.ppat.0030046&ct=1 (http://pathogens.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.ppat.0030046&ct=1) Again, you are so close to understanding the truth, but your dogmatic beliefs are getting in the way. Eventually you will understand the concepts behind multiple selection pressures and how a variable environment is capable of accelerating the evolutionary process.
Joobz’s concept of a variable environment is simply sequential rather than simultaneous selection pressures. This effect is well demonstrated by MRSA, multidrug resistant HIV, TB and so forth. Now if joobz could demonstrate how sequential selection pressures could transform a reptile population into a bird population. Of course there are cooperative selection pressures that would do this, this fits well with his speculation of cooperative chemistry for abiogenesis.
Combination antiretroviral therapy is effective in reducing, but not eliminating, HIV-1 replication. Residual viremia during suppressive antiretroviral therapy may arise from a number of sources, including reservoirs of long-lived virus-producing cells, or ongoing complete cycles of viral replication. Here, we used a new, more sensitive assay of HIV-1 RNA to measure residual viremia in a large cohort of patients with prolonged suppression on antiretroviral therapy. We found a persistent, stable level of viremia in patients on prolonged therapy that correlated with pretherapy levels of HIV-1. Over 80% of patients had viremia 1 copy/ml plasma, and the level of viremia was independent of the drug regimen patients were taking. These data strongly suggest that persistent viremia on antiretroviral therapy is likely derived from reservoirs of long-lived virus-producing cells that are not affected by currently available drugs that target new cycles of viral replication. New antiviral strategies that eradicate this reservoir will be necessary to cure HIV-1 infection.
Of course combination selection pressures do not work unless they are applied to a population. Notice how joobz did not highlight the sentence I highlighted in blue because joobz does not believe that evolution can be stopped.

[joobz]

Joobz’s concept of a variable environment is simply sequential rather than simultaneous selection pressures. This effect is well demonstrated by MRSA, multidrug resistant HIV, TB and so forth. Now if joobz could demonstrate how sequential selection pressures could transform a reptile population into a bird population. Of course there are cooperative selection pressures that would do this, this fits well with his speculation of cooperative chemistry for abiogenesis.

Of course combination selection pressures do not work unless they are applied to a population. Notice how joobz did not highlight the sentence I highlighted in blue because joobz does not believe that evolution can be stopped.
Kleinman, you have an extremely easy task in front of you. All you need to do to prove evolution is impossible is to prove that there is no such thing as weather.

[joobz]

Errr, I mean, "pressures that don't result in a smaller population size after each generation."

Kleinman claims all directional selection pressures decrease population size each generation.

This is pretty stupid because the population size in ev is held constant, yet Kleinman relies on ev for most of his argument.

Adequate, I, and ev have shown that fixation rates increase as one adds pressures as long as those pressures don't decrease population size. Don't forget to add Delphi_Ote to your list. he had wrote a bit of code showing an example of emergence occuring more rapidly under multiple pressures than one single pressure. He simply had the one single pressure be much stronger than the others.

This point and your point highlight the concept of exactly how many assumptions must be made for kleinman's theory to work. He's simply helped prove that since nature doesn't fit in with his assumptions, we can completely dismiss the argument that evolution is mathematically impossible.

I thank Kleinman for making it so clearly obvious that evolution is real.

[Paul C. Anagnostopoulos]

Whatever. And no I did not mean to say the opposite in the last two sentences. Evolving simple function is much, much easier than evolving complex function.
That's not what you said:

I don’t think sorting the sequences at the binding site locations is what slows the convergence in ev. I think it is the elimination of the weight matrix matches in the non-binding site region that slows and ultimately stops the convergence of ev.
This is wrong. It is precisely the binding site locations that take time, when you are evolving a creature that distinguishes them. When evolving a creature that makes no distinction, nothing takes much time. That would be because no distinction is being made, and so there isn't really anything evolving at all.


Sorting for any single simple sorting condition in your model takes trivially small number of generations when compared to the more complex sorting condition based on all three sorting condition simultaneously.
I don't believe anyone has argued this fact with you.

~~ Paul

[Mr. Scott]

And you incorrect interpretation of the mutation and selection sorting/optimization process contributes to the premature death of millions of people suffering from diseases subject to the principles of mutation and selection. I think you are the rude one in this debate.


That is A) an appeal to emotion, and B) a claim for which you have never provided evidence.

Your links to combination therapy don't qualify as evidence because they are in accord (not in conflict) with standard evolutionary theory.

Please present your evidence that Darwin's theory of evolution contributes to the death of millions. What claims of evolutionists result in millions of deaths by disease? What claims of creationists will save these lives? What evidence do you have to support these claims?

[kleinman]

Whatever. And no I did not mean to say the opposite in the last two sentences. Evolving simple function is much, much easier than evolving complex function.That's not what you said:I don’t think sorting the sequences at the binding site locations is what slows the convergence in ev. I think it is the elimination of the weight matrix matches in the non-binding site region that slows and ultimately stops the convergence of ev.This is wrong. It is precisely the binding site locations that take time, when you are evolving a creature that distinguishes them. When evolving a creature that makes no distinction, nothing takes much time. That would be because no distinction is being made, and so there isn't really anything evolving at all.
Paul, you have been confused on this topic for quite a while. Do you recall when you started this thread?
http://www.randi.org/forumlive/showthread.php?t=67488 (http://www.randi.org/forumlive/showthread.php?t=67488)
You could not understand why the convergence of ev slowed as you increase G.
So I ran a set of experiments with a fixed population (64) and a fixed chromosome length (1000). I varied the mutation rate from 1/1 million bases down to 1/200 bases. The number of generations to converge on a creature with perfect DNA binding varied according to the equation g=.9m^1.02, which is just about linear, as one would expect. I therefore conclude that high mutation rates can be extrapolated to lower ones with no fuss. Then, for some reason, I decided to run another series of experiments with a fixed population (64) and a fixed number of mutations per base (1/16,000). I'm varying the chromosome length from 512 bases by factors of 2. I would expect the number of generations to evolve a perfect creature to remain constant, because the probability of mutating any non-junk DNA base in the chromosome remains constant. However, I'm seeing what appears to be a factor of 2 increase in the number of generations required as the chromosome increases in length by a factor of 2.Paul, I believe you now understand why the number of generations for convergence does not increase linearly with genome length even when you use a mutation rate that is fixed to a specific number of bases. For the sake of others that are trying to follow this issue, the reason the number of generations increase supra-linearly is the form of the selection process Dr Schneider uses in his program.

Selection is based on the number of errors that occur on a genome. There are two types of errors. The first type of error is the failure of the weight matrix to identify a binding site in the binding site region of the genome. The second type of error is the weight matrix identifying a binding site in the non-binding site region of the genome.

As you lengthen the genome in the model while keeping the mutation rate per locus constant, you are increasing the possible number of errors which can occur in the non-binding site region. That is what causes the generations for convergence to increase at a greater than linear rate.

Paul likes to complain that ev does not model reality in its entirety and I am going to have to agree with him on this point when it comes to the selection process Dr Schneider employs in his model.

In the early phase of the evolutionary process in ev, an error in the non-binding site region is less likely to select out that organism because there are so many errors in the binding site region. As the evolutionary process continues and more and more binding sites are properly identified, a single error in the non-binding site region can cause the selection out of that organism. Because of this effect, the early stages of evolution occur much more rapidly than the later stages of the process. Errors in the non-binding site of the genome have greater affect in the selection process late in the evolution of the binding sites than early in the evolutionary process.

If the selection process specified that any error in the non-binding site region will cause selection out of that creature regardless of how many or few binding sites are properly recognized in the binding site region would more accurately represent reality. If you employ this condition, the rate of evolution would markedly slow but I believe would be more representative of reality.
The mutation and selection sorting/optimization process is dominated by the number of selection conditions. Increasing G in the model also slows the convergence of the model. After all this time you still don’t understand this.
Sorting for any single simple sorting condition in your model takes trivially small number of generations when compared to the more complex sorting condition based on all three sorting condition simultaneously.I don't believe anyone has argued this fact with you.
Paul, have you been reading this thread? Adequate and rocketdodger have been arguing that n+1 selection pressures evolve more rapidly than n selection pressures. Your model and the hundreds of real examples of the mutation and selection sorting/optimization process I have posted and now your statement directly contradicts their assertions. You are slow at this Paul but finally you are starting to understand that the dominant parameter in the mutation and selection sorting/optimization process is the number of selection conditions applied to the population.

[joobz]

Paul, you have been confused on this topic for quite a while. Do you recall when you started this thread?
http://www.randi.org/forumlive/showthread.php?t=67488 (http://www.randi.org/forumlive/showthread.php?t=67488)
You could not understand why the convergence of ev slowed as you increase G.

The mutation and selection sorting/optimization process is dominated by the number of selection conditions. Increasing G in the model also slows the convergence of the model. After all this time you still don’t understand this.

Paul, have you been reading this thread? Adequate and rocketdodger have been arguing that n+1 selection pressures evolve more rapidly than n selection pressures. Your model and the hundreds of real examples of the mutation and selection sorting/optimization process I have posted and now your statement directly contradicts their assertions. You are slow at this Paul but finally you are starting to understand that the dominant parameter in the mutation and selection sorting/optimization process is the number of selection conditions applied to the population.
Still no luck proving that weather doesn't exist, eh?

Let me see if I can help, ***looks outside***, hmm It's raining but it wasn't yesterday. Hmm, looks like evidence suggests that weather is real. If weather is real, than the number of selection pressures that acts in nature isn't constant in number or magnitude. Therefore, based upon your own theory that you have so adequately presented, evolution in nature is both possible and real.

[rocketdodger]

Adequate and rocketdodger have been arguing that n+1 selection pressures evolve more rapidly than n selection pressures.

No, we have not, you stupid lying fool. That is why you cannot quote either Dr. Adequate or I as having said so.

Show us a quote linking to the post where we said it or stop lying.

Show us a quote linking to the post where we said it or stop lying.

Show us a quote linking to the post where we said it or stop lying.

Show us a quote linking to the post where we said it or stop lying.

Show us a quote linking to the post where we said it or stop lying.

Show us a quote linking to the post where we said it or stop lying.

Show us a quote linking to the post where we said it or stop lying.

Show us a quote linking to the post where we said it or stop lying.

[tsig]

I admit I'm not competent to follow Kleinman's math. Am I correct in saying that his basic point is that natural selection tends to keep species stable, slowing the rate of evolution to a point that it can't account for observed speciation?

If so, I tend to agree, except that when conditions change, natural selection no longer necessarily favors the status quo, speeding the rate of evolution. Am I making a valid point or am I confused?

SpecialK has never posted a mathematical formula so if you followed his math you would be following a large white rabbit.

[tsig]

We ALL want to be segmented.






... what the hell am I saying ??

I can haz

sygmnts?

[tsig]

You're just saying what's on everyone's mind! The truth will out!

And now that you have expressed a wish to be segmented, I will graciously allow you to reproduce, as long as you have no more than 30-40 descendants.

I, for one, bow sequentially to our segmented overlourd.

[Paul C. Anagnostopoulos]

You could not understand why the convergence of ev slowed as you increase G.
Indeed, I was confused when I posted that. Notice my next post:

I may have opened my big mouth too soon. Nothing to see here until I run more cases...



The mutation and selection sorting/optimization process is dominated by the number of selection conditions. Increasing G in the model also slows the convergence of the model. After all this time you still don’t understand this.
What does this have to do with the fact that you said:

I don’t think sorting the sequences at the binding site locations is what slows the convergence in ev. I think it is the elimination of the weight matrix matches in the non-binding site region that slows and ultimately stops the convergence of ev.
That statement is simply incorrect. Run an Evj model with all three mistakes counts nonzero. The spurious bindings are eliminated quite quickly as compared to the missing bindings.



Paul, have you been reading this thread? Adequate and rocketdodger have been arguing that n+1 selection pressures evolve more rapidly than n selection pressures. Your model and the hundreds of real examples of the mutation and selection sorting/optimization process I have posted and now your statement directly contradicts their assertions.
They have been arguing about the real world, and not saying what you think they are anyway. You were talking about Ev:

Sorting for any single simple sorting condition in your model takes trivially small number of generations when compared to the more complex sorting condition based on all three sorting condition simultaneously.
I don't think anyone is arguing that the mistakes go to zero faster when counting mistakes for only one condition than when counting mistakes for three conditions. And you still haven't addressed the question of the correlation between a mistake count and a pressure. What if we add a mistake count for each binding site?

~~ Paul

[kleinman]

Adequate and rocketdodger have been arguing that n+1 selection pressures evolve more rapidly than n selection pressures.Show us a quote linking to the post where we said it or stop lying.
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
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 let’s not forget this little gem.
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.
So not only are you incompetent in the mathematics of the mutation and selection sorting/optimization problem, you can’t even remember what you have said.
SpecialK has never posted a mathematical formula so if you followed his math you would be following a large white rabbit.
You evolutionists don’t have much experience solving functional equations. If you did, you would know that the solution isn’t in terms of an algebraic equation. The solution is in the form of data, and I have posted plenty of data from Dr Schneider’s peer reviewed and published model of random point mutations and natural selection. And what Dr Schneider’s model shows is that combination selection pressures profoundly slow the evolutionary process unlike what rocketdodger and Adequate assert. Here is another citation which shows how the mutation and selection sorting/optimization process actually works.
http://www.ecologyandsociety.org/vol3/iss2/art12/manuscript.html (http://www.ecologyandsociety.org/vol3/iss2/art12/manuscript.html)
An important contribution of biomedical research in this century was the discovery of antibiotics, which effectively inhibit reproduction of bacteria. As a consequence, many otherwise fatal bacterial infections could be treated. Until recently, however, no potent medication was available against viral infections. (A prominent exception is acyclovir, which inhibits herpes simplex virus.) In 1989, it became clear that a drug called zidovudine, which was originally developed against cancer, was effective against HIV. Clinical trials showed that the drug increased the life expectancy of AIDS patients by about 6 months. The drug works as an inhibitor of the reverse transcriptase, which is a viral enzyme that rewrites the genetic information of HIV from the RNA into the DNA alphabet. Unfortunately, the beneficial effect of the drug is only short-lived, because the virus rapidly develops resistance: mutations in the reverse transcriptase gene can render the enzyme insensitive to inhibition by the drug. Thus, the virus can escape from drug treatment in a way that is similar to its escape from immune responses. More recently, further anti-HIV drugs have been developed. Some of the new drugs are reverse transcriptase inhibitors, and others are directed against the viral protease, an enzyme essential for the formation of infectious virus particles from infected cells. All anti-HIV drugs prevent the virus from reproducing: they do not kill virus particles or infected cells (Figs. 4 and 5).

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.''
The mutation and selection sorting/optimization process does not work like the irrational and illogical assertion made by rocketdodger and Adequate, n+1 selection pressures evolve more rapidly than n selection. In fact they have got it completely backwards. This is why the theory of evolution is mathematically impossible and the irrational and illogical interpretation of the mutation and selection sorting/optimization process that evolutionists try to advance will cause the premature death of millions of people suffering from diseases subject to the principles of the mutation and selection process.

[tsig]

Delphi, it appears you have forgotten what you said previously. Let me remind you.

It is clear from ev that the shape of the fitness landscape is strongly dependent on the number of selection pressures. It is this mathematical fact that ev demonstrates that you are in denial of. The hundreds of empirical examples I have posted of the mutation and selection sorting/optimization process demonstrates this as well. It is the number of selection conditions which dominates the mathematics of the mutation and selection sorting/optimization process. Reread your own Wikipedia reference to the fitness landscape of you have trouble grasping this mathematical and empirical fact of life.

The mathematical and empirical evidence of how the mutation and selection sorting/optimization process works is clear. It is the number of selection pressures which dominates the behavior of this process. Your denial of these mathematical and empirical facts contributes to the premature death of millions of people suffering from diseases that are subject to the mutation and selection process.

Just because many people support the theory of evolution does not make the theory correct. The mathematical and empirical data show that you are wrong about how the mutation and selection sorting/optimization process works. And you incorrect interpretation of the mutation and selection sorting/optimization process contributes to the premature death of millions of people suffering from diseases subject to the principles of mutation and selection. I think you are the rude one in this debate.

If you had read this thread, you would see the proof. Here’s an opportunity for you to learn for yourself how the mutation and selection sorting/optimization process works. Start Dr Schneider’s ev computer simulation of random point mutations and natural selection. Leave all the parameters at their baseline values except G, set G to 16384 and click the stop on “perfect creature”. Run the model until a “perfect creature” is evolved. Then restart the model using all the same parameters except under the advanced features of the model, set any two of the three weights for the selection conditions to zero. What you are doing when you set two of the three weight factors to zero is that you are reducing down the number of selection conditions from three to one. Tell us what values you get.

You think everyone lies to you including your parents.

Are you going to teach us on the Bible? Teach us on John 18:19-23. Then perhaps you will understand Matthew 5:38-39.

After all this time you mixed up G and gamma? Paul, you need a power nap.

Is this the case of G=256? If so, then the portion of the genome which represents binding sites, gene and non-binding site region are very close. Try the cases of G=16384, G=32768 and G=65536 and do selection based only on location of binding sites. The message here is that the only way to speed up the mutation and selection sorting/optimization process is to reduce down the size of the search space. You do that by reducing the number of selection conditions and the genes targeted by the selection conditions. That’s what your model shows and that’s what real examples of mutation and selection shows.

You are drawing a conclusion based on a single case. You would think that after all this time you would learn that trying to draw conclusions from ev based on a single case leads you astray. The mathematical fact of life which ev sorting algorithm demonstrates is that the mutation and selection sorting/optimization process is strongly dependent on the number of selection conditions. This mathematical fact of life is also demonstrated in the hundreds of real examples of mutation and selection.

Here is another real example which demonstrates this mathematical fact of life.
http://www.translational-medicine.com/content/5/1/38 (http://www.translational-medicine.com/content/5/1/38)


You are ignoing the emperical evidence that proves that segmentation is true.

I can segment before your very eyes, is this proof?

Why?

[rocketdodger]

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 :(

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.

Show us where we say n+1 selection pressures "evolve more rapidly" than n pressures or stop lying. And INCLUDE A LINK OR NUMBER FOR THE ORIGINAL POST YOU SCUMBAG, so PEOPLE CAN SEE WHY YOU ARE LYING.

Show us where we say n+1 selection pressures "evolve more rapidly" than n pressures or stop lying. And INCLUDE A LINK OR NUMBER FOR THE ORIGINAL POST YOU SCUMBAG, so PEOPLE CAN SEE WHY YOU ARE LYING.

Show us where we say n+1 selection pressures "evolve more rapidly" than n pressures or stop lying. And INCLUDE A LINK OR NUMBER FOR THE ORIGINAL POST YOU SCUMBAG, so PEOPLE CAN SEE WHY YOU ARE LYING.

Show us where we say n+1 selection pressures "evolve more rapidly" than n pressures or stop lying. And INCLUDE A LINK OR NUMBER FOR THE ORIGINAL POST YOU SCUMBAG, so PEOPLE CAN SEE WHY YOU ARE LYING.

[kleinman]

You could not understand why the convergence of ev slowed as you increase G.Indeed, I was confused when I posted that. Notice my next post:I may have opened my big mouth too soon. Nothing to see here until I run more cases...
Of course you were and are confused about the mutation and selection sorting/optimization process. Your own mathematical model is showing that the theory of evolution by mutation and selection is mathematically impossible. Combination selection pressures profoundly slow the ability of a population to evolve to those selection pressures.
The mutation and selection sorting/optimization process is dominated by the number of selection conditions. Increasing G in the model also slows the convergence of the model. After all this time you still don’t understand this.What does this have to do with the fact that you said:I don’t think sorting the sequences at the binding site locations is what slows the convergence in ev. I think it is the elimination of the weight matrix matches in the non-binding site region that slows and ultimately stops the convergence of ev.That statement is simply incorrect. Run an Evj model with all three mistakes counts nonzero. The spurious bindings are eliminated quite quickly as compared to the missing bindings.
Don’t be silly Paul. Are you now going to argue that evolution occurs without selection? What ev shows is that it is much, much easier to sort for a single selection condition than for all three selection conditions simultaneously.
Paul, have you been reading this thread? Adequate and rocketdodger have been arguing that n+1 selection pressures evolve more rapidly than n selection pressures. Your model and the hundreds of real examples of the mutation and selection sorting/optimization process I have posted and now your statement directly contradicts their assertions.They have been arguing about the real world, and not saying what you think they are anyway. You were talking about Ev:
You must be talking about one of kjkent1’s 10^500 alternative universes because when I asked Adequate to give us a real example of his graph, he said this.
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 ...As I have explained to you, I produced the model because I've not heard of this precise experiment being done.
Paul, perhaps you want to give us a real example of this illogical and irrational assertion.
Sorting for any single simple sorting condition in your model takes trivially small number of generations when compared to the more complex sorting condition based on all three sorting condition simultaneously.I don't think anyone is arguing that the mistakes go to zero faster when counting mistakes for only one condition than when counting mistakes for three conditions. And you still haven't addressed the question of the correlation between a mistake count and a pressure. What if we add a mistake count for each binding site?
Paul, I don’t know why it is such a mystery to you that the mistake count is simply based on a match of the weight matrix and sorting for minimum number of mistakes is much faster when you limit number of conditions for which the algorithm is sorting. Real examples of the mutation and selection sorting/optimization process behave in the analogous manner. Add any form of mistake count you want. You will find that the more complex you make the sorting conditions, the much, much slower the sorting process will become. This is why the theory of evolution is mathematically impossible.

[tsig]

It’s clear that you don’t understand how modern complex mathematical problems are solved. The mutation and selection sorting/optimization process is a complex interaction of many parameters that can not be described by a simple closed form algebraic equation. The mutation and selection sorting/optimization process is a cyclical process of mutation->selection->reproduction and back to mutation. This process is repeated over and over. Ev is an application of this concept. The closest you can get to write an equation for this process is to write it in functional form. I doubt you have any knowledge of functional analysis but that’s how you study a model like ev. When you do functional analysis of the mutation and selection sorting/optimization process, it reveals that the dominant parameter in this mathematical process is the number of selection conditions. This mathematical fact is demonstrated by the hundreds of real examples of the mutation and selection sorting/optimization process. To understand how ev works, you need to do a parametric study of the model. This is what Dr Schneider recommended in his publication on ev. Dr Schneider did a parametric study of his model but never published the results. I believe he did not publish his results because he didn’t understand why it took such huge numbers of generations to converge for anything other the tiniest genome lengths. He could not understand why amplification was not occurring in his model. The reason why amplification does not occur in his model is the multiple simultaneous selection conditions. Set any two of the three selection conditions in his model and you get the amplification phenomenon.

You can start at this URL http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/ (http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/) . There are many links on this page that not only talk about the equations used but also you can download the source code for the model.

Paul, don’t you remember when you blah blah blahed the following statement?

Your model shows that it is much easier to evolve simple function than complex function. Somewhere in your evolutionist dream world you think that a reptile population can evolve to a bird population. This is a mathematical and empirical impossibility. Even your simple three selection condition model shows how slow this process is. There is no way to transform thousands of genes simultaneously by mutation and selection. Your model shows it can barely evolve three selection conditions on only the tiniest genomes.

Whatever. And no I did not mean to say the opposite in the last two sentences. Evolving simple function is much, much easier than evolving complex function. And the mathematical behavior of evolving simple function versus complex function is far from linear. That is what your mathematical model of the mutation and selection sorting/optimization process shows.

Why not start with your own sorting/optimization algorithm? Sorting for any single simple sorting condition in your model takes trivially small number of generations when compared to the more complex sorting condition based on all three sorting condition simultaneously.

Your evolutionist indoctrination interferes with understanding how the mutation and selection process actually works. You don’t see in a fuzzy blur, you are blind. Perhaps another citation which shows how the mutation and selection sorting/optimization process works might help.
http://pathogens.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.ppat.0030046&ct=1 (http://pathogens.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.ppat.0030046&ct=1)


I was blind but now I sea.

[sol invictus]

I'm Greek. Gamma and G are the same thing.

Yassou! Ti kaneis? With a name like Anagnostopoulos I had assumed you were Chinese :).

Oh, come on everyone. While Kleinman has been extremely abrasive, he has raised a very important point. Indeed, it is true, that with a stable combined number of strong selection pressures, the ability for a population to evolve becomes greatly reduced. Indeed, such considtions can readily lead to extinctions. Kleinman is exactly right on this.


I can only assume you're being sarcastic. Klienman's "argument" rests on simulations in which the population size doesn't change and extinction is impossible. Those simulations show clearly that increasing the number of pressures increases the rate of evolution. The reason for that is obvious, and it's trivial to prove mathematically (as I did a little while back in this thread).

Back in the real world, I agree that enough pressures can simply wipe out a population entirely. There have been many examples of that in the history of the world. However that certainly does not translate into any statement about n+1 pressures causing the rate of evolution to be slower than n... it's plainly much more complicated than that.

In fact if we define the rate of evolution to mean the number of desirable mutations per generation per creature, I doubt there will ever be a case in which more pressures slows the rate, even taking extinctions into account.

[kleinman]

Show us where we say n+1 selection pressures "evolve more rapidly" than n pressures or stop lying. And INCLUDE A LINK OR NUMBER FOR THE ORIGINAL POST YOU SCUMBAG, so PEOPLE CAN SEE WHY YOU ARE LYING.
http://forums.randi.org/showpost.php?p=3210379&postcount=6952 (http://forums.randi.org/showpost.php?p=3210379&postcount=6952)
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.
http://forums.randi.org/showpost.php?p=3170363&postcount=6644 (http://forums.randi.org/showpost.php?p=3170363&postcount=6644)
Do you even know what a fitness landscape looks like, Kleinman? Here is a hint for you -- regardless of the number of selective pressures, the landscape is always a convex shape. There is no such thing as local optima that the population can "get stuck on" or whatever nonsense it is that you assert.
http://forums.randi.org/showpost.php?p=3169325&postcount=6615 (http://forums.randi.org/showpost.php?p=3169325&postcount=6615)
While you wait for a real example of n+1 pressures evolving faster than n pressures (which we have shown you time and time again, by the way, you genius) we will be waiting for you to show us a real example of whatever it is you claim generated life as we know it.
http://forums.randi.org/showpost.php?p=3126277&postcount=6348 (http://forums.randi.org/showpost.php?p=3126277&postcount=6348)
At first, it appeared as though Kleinman might be right -- adding selective pressures in low numbers really does slow the average rate of fixation way down. However, once a "critical mass" has been reached, adding pressures actually drives the rate back up. Eventually, with enough pressures, you get to a point where the average rate of fixation is equal to or faster than it is under only a single pressure.
http://forums.randi.org/showpost.php?p=3127246&postcount=6359 (http://forums.randi.org/showpost.php?p=3127246&postcount=6359)
Actually, Adequate and I sort of are. My simulation shows that if you introduce enough strong pressures, and if you measure the rate of fixation on average, then fixation is just as fast (or even faster).
http://forums.randi.org/images/smilies/doglaugh.gif

[kjkent1]

Paul, I don’t know why it is such a mystery to you that the mistake count is simply based on a match of the weight matrix and sorting for minimum number of mistakes is much faster when you limit number of conditions for which the algorithm is sorting. Real examples of the mutation and selection sorting/optimization process behave in the analogous manner. Add any form of mistake count you want. You will find that the more complex you make the sorting conditions, the much, much slower the sorting process will become. This is why the theory of evolution is mathematically impossible.If it's impossible, then how come this new report seems to be finding so much evolutionary change in the human population?

http://johnhawks.net/weblog/topics/evolution/selection/acceleration_embargo_ends_2007.html

Just another brainwashed evolutionist?

[Shalamar]

Klienman, you keep saying that you can prove mathematically that Evolution is impossible.
I ask you for the math. The calculations. Instead, you point me at a SIMULATION.

Show me the math. I wish to see the actual calculations.

Unless you can show the actual equations, and the mathematics, you have NO evidence, or proof, beyond your own dogmatic beliefs.

[sol invictus]

Klienman, you keep saying that you can prove mathematically that Evolution is impossible.
I ask you for the math. The calculations. Instead, you point me at a SIMULATION.

And it's a simulation that shows the opposite of what he claims.


Show me the math. I wish to see the actual calculations.

He did propose a mathematical model for this a while back, and claimed some totally incorrect results using it. I analyzed it correctly and showed that it predicts that increasing the number of pressures increases the rate of evolution. The rate scales as N/Log(N) for N pressures. kLIEnman admitted he had been incorrect - and has ignored that model and what he said about it ever since.

[kleinman]

Paul, I don’t know why it is such a mystery to you that the mistake count is simply based on a match of the weight matrix and sorting for minimum number of mistakes is much faster when you limit number of conditions for which the algorithm is sorting. Real examples of the mutation and selection sorting/optimization process behave in the analogous manner. Add any form of mistake count you want. You will find that the more complex you make the sorting conditions, the much, much slower the sorting process will become. This is why the theory of evolution is mathematically impossible.If it's impossible, then how come this new report seems to be finding so much evolutionary change in the human population?
Wow, an evolutionist says we have evolved. How could Dr Schneider’s mathematics be so wrong? I wonder if John Hawks knows anything about the mathematics of the mutation and selection sorting/optimization process? I doubt it.

[rocketdodger]

http://forums.randi.org/showpost.php?p=3210379&postcount=6952 (http://forums.randi.org/showpost.php?p=3210379&postcount=6952)
[/SIZE][/FONT]

Please explain how anything I state in that post is equivalent to saying "n+1 selection pressures evolve more rapidly than n selection pressures," you lying troll.

http://forums.randi.org/showpost.php?p=3170363&postcount=6644 (http://forums.randi.org/showpost.php?p=3170363&postcount=6644)
[/SIZE][/FONT]

Please explain how anything I state in that post is equivalent to saying "n+1 selection pressures evolve more rapidly than n selection pressures," you lying troll.

http://forums.randi.org/showpost.php?p=3169325&postcount=6615 (http://forums.randi.org/showpost.php?p=3169325&postcount=6615)
[/SIZE][/FONT]

Please explain how anything I state in that post is equivalent to saying "n+1 selection pressures evolve more rapidly than n selection pressures," you lying troll.

http://forums.randi.org/showpost.php?p=3126277&postcount=6348 (http://forums.randi.org/showpost.php?p=3126277&postcount=6348)
[/SIZE][/FONT]

Please explain how anything I state in that post is equivalent to saying "n+1 selection pressures evolve more rapidly than n selection pressures," you lying troll.

http://forums.randi.org/showpost.php?p=3127246&postcount=6359 (http://forums.randi.org/showpost.php?p=3127246&postcount=6359)
[/SIZE][/FONT]

Please explain how anything I state in that post is equivalent to saying "n+1 selection pressures evolve more rapidly than n selection pressures," you lying troll.

[joobz]

(http://forums.randi.org/showpost.php?p=3127246&postcount=6359)

http://forums.randi.org/images/smilies/doglaugh.gif
I see you haven't figured out how to prove that there is no such thing as weather. Too bad.

I must say, Your theory has been an excellent help in proving evolution is quite possible. THANK YOU!

[kjkent1]

Wow, an evolutionist says we have evolved. How could Dr Schneider’s mathematics be so wrong? I wonder if John Hawks knows anything about the mathematics of the mutation and selection sorting/optimization process? I doubt it.As you have, since the outset of your communications with Schneider, completely misunderstood how ev works, you have no idea that there is no contradiction between Hawks' empirical evidence and Schneider's algorithm.

All you need to do to understand your mistake, is to explain why ev reports no mistakes at the first generation with all three mistake weights set to zero.

Your view that the sorting conditions are simpler is irrelevant, because once you disable a mistake count, ev no longer represents a model of genetic evolution. Thus, your examples are rendered meaningless.

Ev is only a relevant model when all three mistake counts are non-zero. Otherwise, you may as well be trying to prove that a bingo card can spring to life if the correct numbers are selected.

You have yet to actually respond to Hawks' contention, other than via ridicule. Hawks' paper is relevant. It falls to you to defeat it.

http://johnhawks.net/weblog/topics/evolution/selection/acceleration_embargo_ends_2007.html

[Shalamar]

Wow, an evolutionist says we have evolved. How could Dr Schneider’s mathematics be so wrong? I wonder if John Hawks knows anything about the mathematics of the mutation and selection sorting/optimization process? I doubt it.

Amazing. A scientist doing work in his field! Ok. You don't like science. At all.

Can you show me the mathematics of the mutation and selection sorting/optimization process? Please show all your work, and all equations.

[Paul C. Anagnostopoulos]

Don’t be silly Paul. Are you now going to argue that evolution occurs without selection? What ev shows is that it is much, much easier to sort for a single selection condition than for all three selection conditions simultaneously.
Is it possible for you to stop repeating your mantra long enough to address the actual posts people make? You said:

I don’t think sorting the sequences at the binding site locations is what slows the convergence in ev. I think it is the elimination of the weight matrix matches in the non-binding site region that slows and ultimately stops the convergence of ev.
That is wrong.


Paul, I don’t know why it is such a mystery to you that the mistake count is simply based on a match of the weight matrix and sorting for minimum number of mistakes is much faster when you limit number of conditions for which the algorithm is sorting.
I agreed with that, didn't I? However, if I give each binding site its own mistake count, then I have added "conditions." But when those mistake counts are set to 1, the perfect creature will arise in exactly the same number of generations.


Add any form of mistake count you want. You will find that the more complex you make the sorting conditions, the much, much slower the sorting process will become. This is why the theory of evolution is mathematically impossible.
Ah, so now there is a measure of the complexity of the sorting conditions. It's not simply a question of how many of them there are. Excellent.

~~ Paul

[Paul C. Anagnostopoulos]

Yassou! Ti kaneis? With a name like Anagnostopoulos I had assumed you were Chinese
Kala. I'm assuming you're Roman. Is that correct?

~~ Paul

[sol invictus]

Kala. I'm assuming you're Roman. Is that correct?

Sic, amicus graecum. A Kleinman: aut insanit homo, aut versus facit.

[kleinman]

Klienman, you keep saying that you can prove mathematically that Evolution is impossible.
I ask you for the math. The calculations. Instead, you point me at a SIMULATION.

Show me the math. I wish to see the actual calculations.

Unless you can show the actual equations, and the mathematics, you have NO evidence, or proof, beyond your own dogmatic beliefs.
Dr Schneider’s computer simulation is a mathematical model of the mutation-selection-reproduction cycle. That is the physical phenomenon that Dr Schneider is modeling. Modern science uses simulations to study the behavior of complex systems. Engineers study the behavior of bridges by writing simulations based on force equals mass time acceleration or the thermal behavior of complex systems by writing simulation based on conservation of energy and so on. Biologists have been slow to apply these types of modern analytical tools but Dr Schneider has finally done this with the mutation-selection-reproduction cycle. The following is Dr Schneider’s calculations for the mutation-selection-reproduction cycle in Pascal format. I am not sure how clear this will present so you can find the original at [URL="ftp://ftp.ncifcrf.gov/pub/delila/ev.p
This calculation will compile using the GNU Pascal compiler which is available free online. It is calculations like this that will bring the field of Biology into the 21st century and show why a 19th century theory is mathematically impossible.

If you've posted a link you don't need to post the whole thing.

Breach of Rule 6.

[rocketdodger]

Since you are confident enough in you abilities now, Kleinman, to post source code for a "calculation," would you be so kind as to illustrate what, in the code, Paul is wrong about?

Since you claim to know better than him what the "calculation" does, I am sure you will be able to show us quickly.

Don't let us down, Kleinman! Show us what you can do!

[Shalamar]

So Sorry. But that is computer code.

I am not interested in a simulation. You have said repeatedly that you can prove that evolution is mathematically impossible. You have failed to show your math, or the equations.

You said you have proof. Please show us this mathematical proof. Please post the equations.

[joobz]

This calculation will compile using the GNU Pascal compiler which is available free online. It is calculations like this that will bring the field of Biology into the 21st century and show why a 19th century theory is mathematically impossible.
It's obvious you still haven't grasped what your theory of multiple selection pressures really is saying. It says that a constant number of multiple strong selection pressures hinders the evolutionary process greatly. This is very true. And it also shows that when these pressures are not constant but varying, the evolutionary process speeds up drastically.

Since nature provides a variable environment of pressures, evolution is not only possible, it is real.

To help you understand this point, I'll start presenting examples of weather.

[kleinman]

Since you are confident enough in you abilities now, Kleinman, to post source code for a "calculation," would you be so kind as to illustrate what, in the code, Paul is wrong about?
I’ve never said either Paul or Dr Schneider have done something wrong in their code. I have consistently said that Dr Schneider has properly modeled the essential features of the mutation and selection process.
Since you claim to know better than him what the "calculation" does, I am sure you will be able to show us quickly.

Don't let us down, Kleinman! Show us what you can do!
Sure rocketdodger, I will do this for you---again and again and again.

Take Dr Schneider’s baseline case except set G=16384 and set the stop on “perfect creature” (zero mistake condition). You will find that it takes 6,894,433 generations to evolve (sort) to zero mistakes. Then run this case again and set the weight factors for spurious binding in the non-binding site region and spurious binding in the gene region to 0 and leave the weight factor for missed binding sites at 1. You find that this single sorting condition evolves in only a single generation. Now run the same case again but set the weight factors for spurious binding in the non-binding site region and missed binding sites 0 and set the weight factor spurious binding in the gene to 1. This case takes only 223 generations to evolve (sort). And now again take the same case but set the weight factors for spurious binding in the gene region and missed binding sites 0 and set the weight factor spurious binding in the non-binding site region to 1. This case also only takes 223 generations to evolve (sort).

Ev is demonstrating how profoundly the number of selections condition affects the ability of this sorting algorithm to converge. Ev will easily sort a single selection condition but the multiple sorting condition case is more than five orders of magnitude slower. This effect becomes more pronounced as you increase G in the simulation. In fact when ev stops converging for all three sorting conditions, you can still easily converge any of the individual sorting conditions in a small number of generation.

I have no problem with Dr Schneider’s and Paul’s computer code. In fact I believe that they have properly modeled the mutation and selection sorting/optimization process. And what their model shows is that combination selection pressures profoundly slow the evolutionary process. That’s the mathematical and empirical fact of life that you evolutionists are in denial of.
I am not interested in a simulation. You have said repeatedly that you can prove that evolution is mathematically impossible. You have failed to show your math, or the equations.
We will just have to leave it at that for you. Keep following the discussion and perhaps you will understand.
Since nature provides a variable environment of pressures, evolution is not only possible, it is real.
What you don’t realize joobz is that evolution occurs more rapidly in vitro than it does in vivo. The reason this happens is that the weak selection pressures are removed from the population in the in vitro case and reducing the number of selection pressures allows a single strong selection pressure to evolve more rapidly. Add additional selection pressures and the mutation and selection sorting/optimization process is profoundly slowed.
Don’t be silly Paul. Are you now going to argue that evolution occurs without selection? What ev shows is that it is much, much easier to sort for a single selection condition than for all three selection conditions simultaneously.Is it possible for you to stop repeating your mantra long enough to address the actual posts people make? You said:I don’t think sorting the sequences at the binding site locations is what slows the convergence in ev. I think it is the elimination of the weight matrix matches in the non-binding site region that slows and ultimately stops the convergence of ev.That is wrong.
Paul, I’m going to agree with you. It is not the elimination of the weight matrix matches in the non-binding site region that slows and ultimately stops the convergence of ev. It is the combination of eliminating of the weight matrix matches in the non-binding site region along with eliminating of the weight matrix matches in the gene regions and selection for weight matrix matches in the binding site region that slows and ultimately stops the convergence of ev. Any one of the three alone can easily be sorted for.
Paul, I don’t know why it is such a mystery to you that the mistake count is simply based on a match of the weight matrix and sorting for minimum number of mistakes is much faster when you limit number of conditions for which the algorithm is sorting.I agreed with that, didn't I? However, if I give each binding site its own mistake count, then I have added "conditions." But when those mistake counts are set to 1, the perfect creature will arise in exactly the same number of generations.
If you assign each binding site its own mistake count, what you will find that setting the weights to values other than one will only alter the shape of the fitness landscape and the trajectory the population must take to get to the nearest local optimum. It will not change the mathematical fact that the more complex you make your sorting conditions, the much, much slower the sorting process becomes.
Add any form of mistake count you want. You will find that the more complex you make the sorting conditions, the much, much slower the sorting process will become. This is why the theory of evolution is mathematically impossible.Ah, so now there is a measure of the complexity of the sorting conditions. It's not simply a question of how many of them there are. Excellent.
After all this time working with your model, you still don’t recognize that there is a measure of the complexity of the sorting conditions. That measure is dependent on the number of loci the sorting conditions must evolve in order to get to a local optimum and the availability of a trajectory for the population to get to that local optimum. Ev clearly show that restricted sorting conditions are by far the most easy to evolve. This is reflected in every real empirical, measurable, repeatable example of mutation and selection known. Your theory of evolution by mutation and selection is a fantasy trip which is contradicted by your own mathematical model and all the actual evidence of mutation and selection available.

http://vir.sgmjournals.org/cgi/content/full/85/11/3173?ck=nck (http://vir.sgmjournals.org/cgi/content/full/85/11/3173?ck=nck)
Beginning with observational data, the clearest difference between genotypes is in their susceptibility to treatment with IFN monotherapy or IFN/ribavirin (RBV) combination therapy. Typically, only 10–20 and 40–50 % of individuals infected chronically with genotype 1 HCV on monotherapy and combination therapy, respectively, exhibit complete and permanent clearance of virus infection. This long-term response rate is much lower than the rates of 50 and 70–80 % that are observed on treatment of HCV genotype 2 or 3 infections (reviewed by Pawlotsky, 2003a; Zeuzem, 2004). This difference has proved to be highly significant in patient management and has led to the use of higher doses and longer durations of treatment for type 1 (and type 4) infections, in order to achieve acceptable efficacy. In numerous multivariate analyses, genotype-specific differences in treatment response have been shown to be independent of host variables, such as stage of disease progression, age, duration of infection, sex and HIV and other virus co-infections. It is similarly independent of virus-specific factors, such as pre-treatment viral load, although this also correlates independently (inversely) with response.
Note that this article identifies that HCV does recombination, yet combination therapy is still more effective than single drug therapy.

[OnlyTellsTruths]

version = 4.05; (* of ev.p 2006 Jun 28
2006 Jun 28,4.05; increase maximum genome allowed
2006 Jun 28,4.04; mutations specified: per genome or per base.
2006 Jun 24,4.03; halt on 0 mistakes not working - fixed.
2006 Jun 24,4.02; clean up
2006 Jun 24,4.01; halt on condition: report to list
2006 Jun 24,4.00; halt on condition: implement all parameters
2006 Jun 24,3.99; halt on condition: implemented Rs>=Rf and mistakes = 0
2006 Jun 24,3.98; halt on condition: introduce parameter
2005 Jul 17,3.95; use 'model' instead of 'simulation'
2005 Jun 27,3.88: ok.ok. G is a bad idea. Name it something else to
avoid the base g! (A conflict occured in evd.)
2005 Jun 15,3.83: rename the variable 'genome' to be G.
2005 May 07,3.81: modify score function
2005 May 07,3.80: sigma score function more logical
2005 Mar 27,3.79: Paul C. Anagnostopoulos pointed out that in
makeprecalc the following should be bases per site:
writeln(output,' width = ', width:5,' bits per site');
2005 Mar 23,3.78: rename evp.original as ev.original.evp; set up others
2005 Mar 15,3.77: document version in parameter file description
2004 Sep 9,3.76: upgrade for GPC
3.76 [2003 Jul 23] fix note about clearing all
3.73 [2003 Jul 23] fix comment on hg
3.72 [2002 Apr 3] Nearly 10x speed increase! See technical notes.
3.71 [2002 Mar 28] remove namelength const and alpha type which were not used
3.70 [2001 Jun 8] upgrade documentation
3.69 [2001 Jun 6] upgrade documentation
3.68 [2001 Jun 6] SPECIAL RULE can be turned off by parameter
3.66 [2000 Jul 16] upgrade documentation
3.64 [2000 Jul 16] upgrade documentation
3.63 [2000 Jul 15] upgrade documentation
3.62 [2000 Jul 10] add more evp examples
3.61 [2000 Jul 9] upgrade documentation for publication release
3.57 [1999 Jul 24] clean up code a bit
3.55 [1999 Jul 22] Hg gets small sample correction.
3.42 [1999 Feb 17] sigma implemented
3.42 [1999 Feb 17] version number of program in parameter file
3.36 [1999 Feb 17] ability to only mutate the newly replicated half of the
population. This preserves good mutations. (variable mutatehalf)
This takes longer and is not a good idea!
1999 Feb 17: upgrade to more modern time modules, solve y2k problem
1998 March 7: upgrade to allow random placement of sites.
previous change: 1989 December 14
origin: 1984 april 17. --

[kleinman]

version = 4.05; (* of ev.p 2006 Jun 28
2006 Jun 28,4.05; increase maximum genome allowed
2006 Jun 28,4.04; mutations specified: per genome or per base.
2006 Jun 24,4.03; halt on 0 mistakes not working - fixed.
2006 Jun 24,4.02; clean up
2006 Jun 24,4.01; halt on condition: report to list
2006 Jun 24,4.00; halt on condition: implement all parameters
2006 Jun 24,3.99; halt on condition: implemented Rs>=Rf and mistakes = 0
2006 Jun 24,3.98; halt on condition: introduce parameter
2005 Jul 17,3.95; use 'model' instead of 'simulation'
2005 Jun 27,3.88: ok.ok. G is a bad idea. Name it something else to
avoid the base g! (A conflict occured in evd.)
2005 Jun 15,3.83: rename the variable 'genome' to be G.
2005 May 07,3.81: modify score function
2005 May 07,3.80: sigma score function more logical
2005 Mar 27,3.79: Paul C. Anagnostopoulos pointed out that in
makeprecalc the following should be bases per site:
writeln(output,' width = ', width:5,' bits per site');
2005 Mar 23,3.78: rename evp.original as ev.original.evp; set up others
2005 Mar 15,3.77: document version in parameter file description
2004 Sep 9,3.76: upgrade for GPC
3.76 [2003 Jul 23] fix note about clearing all
3.73 [2003 Jul 23] fix comment on hg
3.72 [2002 Apr 3] Nearly 10x speed increase! See technical notes.
3.71 [2002 Mar 28] remove namelength const and alpha type which were not used
3.70 [2001 Jun 8] upgrade documentation
3.69 [2001 Jun 6] upgrade documentation
3.68 [2001 Jun 6] SPECIAL RULE can be turned off by parameter
3.66 [2000 Jul 16] upgrade documentation
3.64 [2000 Jul 16] upgrade documentation
3.63 [2000 Jul 15] upgrade documentation
3.62 [2000 Jul 10] add more evp examples
3.61 [2000 Jul 9] upgrade documentation for publication release
3.57 [1999 Jul 24] clean up code a bit
3.55 [1999 Jul 22] Hg gets small sample correction.
3.42 [1999 Feb 17] sigma implemented
3.42 [1999 Feb 17] version number of program in parameter file
3.36 [1999 Feb 17] ability to only mutate the newly replicated half of the
population. This preserves good mutations. (variable mutatehalf)
This takes longer and is not a good idea!
1999 Feb 17: upgrade to more modern time modules, solve y2k problem
1998 March 7: upgrade to allow random placement of sites.
previous change: 1989 December 14
origin: 1984 april 17.
OnlyTellsTruths, didn’t you know that Paul is Dr Schneider’s co-worker?

[joobz]

What you don’t realize joobz is that evolution occurs more rapidly in vitro than it does in vivo. The reason this happens is that the weak selection pressures are removed from the population in the in vitro case and reducing the number of selection pressures allows a single strong selection pressure to evolve more rapidly. Add additional selection pressures and the mutation and selection sorting/optimization process is profoundly slowed.
I completely realize that we can set up conditions in a lab that speeds up the process. I also know that we can artifically inhibit the process using a stable set of strong multiple selection pressures.

What you fail to realize is that in nature, we typically do not have such settings. The natural environment provides a wide variety of selection pressures that are transient in nature, which helps accelerate emergence of resistence against those pressures.

It seems you are still in doubt about whether or not weather exists.

Allow me to post some more examples of variable weather patterns in the world.

From the NOAA site of historical weather data. A search on peurto Rico from January 1st,2007 to march 31, 2007, the following major weather events occured.
1 PRZ007 - 007 01/02/200706:23 PMWildfire N/A000K0K
2 PRZ006 - 006 02/12/200712:00 PMWildfire N/A000K0K
3 PRZ007 - 011 02/26/200704:39 PMWildfire N/A000K0K
4 PRZ002 03/01/200703:30 PMWildfire N/A000K0K
5 PRZ001 03/08/200712:00 AMVolcanic Ashfall N/A000K0K
6 San Sebastian 03/19/200711:45 PMHeavy Rain N/A000K0K
7 Guaynabo 03/26/200704:30 PMFlood N/A000K0K
8 Arecibo 03/26/200704:35 PMFlood N/A000K0K
9 Vega Alta 03/28/200706:51 PMFlash Flood N/A000K0K
10 Arecibo 03/28/200707:12 PMFlash Flood N/A000K0K
11 Caguas 03/29/200707:05 PMFlood N/A000K0K
12 Gurabo 03/29/200707:11 PMFlood N/A000K0K
13 PRZ001 - 004 03/29/200709:30 PMLandslide N/A000K0K
14 Vega Alta 03/29/200712:27 PMFlood N/A002K0K

I'll keep posting this information, to help you realize that the natural environment is variable.

[Shalamar]

We will just have to leave it at that for you. Keep following the discussion and perhaps you will understand.

YOU have made the claim. YOU need to provide the Math, or retract your statement that you can prove that evolution is mathematically impossible.

It is not up to us to do your work for you.

You have claimed that you can prove that evolution is mathematically impossible. Please show us your math, and all equations.

[rocketdodger]

Sure rocketdodger, I will do this for you---again and again and again.

But you haven't yet... and you sure don't here... I am not asking for parameters you fool.

Paul has told you over and over that setting the weights to zero leads invariably leads to meaningless results. You dispute this, claiming that it is perfectly acceptable to use weight distributions like 1-0-0, 0-1-0, and 0-0-1.

So, show us (and Paul, in particular) the portion of the source code Paul is interpreting incorrectly and why. If you can't, or won't, then there is no reason any of us should take you seriously. Are you going to man up actually address this, or will you simply ignore the challenge like you have ignored every other one we have presented.


I have no problem with Dr Schneider’s and Paul’s computer code. In fact I believe that they have properly modeled the mutation and selection sorting/optimization process. And what their model shows is that combination selection pressures profoundly slow the evolutionary process. That’s the mathematical and empirical fact of life that you evolutionists are in denial of.

You don't even understand their code, you lying buffoon.

This is not surprising, however, as the typical behavior of both creationists and buffoons alike is to pretend to understand things of which they actually know nothing.

[Paul C. Anagnostopoulos]

After all this time working with your model, you still don’t recognize that there is a measure of the complexity of the sorting conditions. That measure is dependent on the number of loci the sorting conditions must evolve in order to get to a local optimum and the availability of a trajectory for the population to get to that local optimum.
Most excellent. Now we know that when we argue about whether n+1 pressures are faster or slower than n, we are arguing simplistically.

~~ Paul

[kleinman]

What you don’t realize joobz is that evolution occurs more rapidly in vitro than it does in vivo. The reason this happens is that the weak selection pressures are removed from the population in the in vitro case and reducing the number of selection pressures allows a single strong selection pressure to evolve more rapidly. Add additional selection pressures and the mutation and selection sorting/optimization process is profoundly slowed.I completely realize that we can set up conditions in a lab that speeds up the process. I also know that we can artifically inhibit the process using a stable set of strong multiple selection pressures.
And that process is sped up by reducing the number of strong selection pressures to a single pressure and then applying a sequence of single strong selection pressures. That’s how to produce MRSA, multidrug resistant gonorrhea, malaria, TB, HIV, multi-herbicide weeds, multi-pesticide resistant insects…
What you fail to realize is that in nature, we typically do not have such settings. The natural environment provides a wide variety of selection pressures that are transient in nature, which helps accelerate emergence of resistence against those pressures.
What you fail to realize is that there are no cooperative selection pressures for evolution and there is no cooperative chemistry that brings about abiogenesis. These are bizarre speculations that you have no mathematical or empirical evidence to support your weird belief system. If you have any mathematical or empirical evidence to support your weird speculations, present it. Oh, wait, you do have evidence; it’s the Madagascar rainforest and plate tectonics.
We will just have to leave it at that for you. Keep following the discussion and perhaps you will understand.YOU have made the claim. YOU need to provide the Math, or retract your statement that you can prove that evolution is mathematically impossible.
Keep reading Shalamar. I’ll spoon feed it to you as much as possible but your inexperience in the mathematics and biology of this problem is making it difficult for you to understand. I’ll continue to provide you empirical examples of the mathematics of evolution by the mutation and selection sorting/optimization process and perhaps you will understand it is the number of selection conditions (sorting conditions) that dominates the behavior of this phenomenon. Here is a recent example from the field of oncology.
http://www.hematology.org/meetings/2007/attendee/education_program.cfm (http://www.hematology.org/meetings/2007/attendee/education_program.cfm)
The development of new therapies for chronic myeloid leukemia continues at a rapid pace with the addition of second- and third-generation Abl kinase inhibitors. Despite these newer agents, imatinib remains the front-line drug of choice based on its outstanding long-term remission rate at five years. Yet acquired resistance to imatinib remains a problem, and the second-line inhibitors, such as dasatinib, fail to cover the T315I-resistant mutant. Many investigational agents with activity against T315I BCR-ABL have been identified and are showing promise in early-phase clinical studies, raising the possibility of triple drug combination therapy for chronic myeloid leukemia (CML), analogous to rationally designed cocktails of antiretroviral therapy for HIV.
And
The management of multiple myeloma has undergone dramatic change in the last ten years. The integration of novel therapies, first into relapsed and refractory myeloma, then early relapse, maintenance, and, most recently, initial treatment, has revolutionized the therapeutic paradigm. This session will focus on recent advances in our understanding of disease biology focusing on genetics. The opportunity for risk, adaptation, and tailoring of therapy will be addressed, as will the role of transplant, where the one-size-fits-all approach no longer applies. The management of the relapsed and refractory patient remains a considerable challenge, but the use of combination therapies utilizing backbone agents, such as bortezomib, thalidomide, and lenalidomide, with glucocorticoids and conventional cytotoxic therapy, as well as a new generation of novel approaches, continue to improve patient outcome.
And
It is clear that acute myeloid leukemia (AML) is a heterogeneous disease with a wide spectrum of phenotypic, cytogenetic, and molecular characteristics. Furthermore, these are not evenly distributed over the age range. Patients are mostly treated with standard combination chemotherapy with minimal modification based on cytogenetic or molecular characteristics. The new knowledge relating to molecular defects offers new prognostic stratification and potential targets for therapy. In younger patients, most clinical trials suggest that treatment outcomes have improved, and some treatment decisions (e.g., stem cell transplantation), are based on cytogenetically-based risk definition. In older patients, who represent the major population with the disease, treatment improvement has been modest, and prognostic factors substantially comprise patient-related features. Clinical studies are now emerging that either more specifically target treatment to the leukemic clone or to groups of patients with particular prognostic characteristics.
And
Current approaches to the treatment of large B-cell lymphomas, Burkitt lymphoma and mantle-cell lymphoma are largely based on empiric combination chemotherapy. However, recent insights into the immunobiology and molecular signatures of these aggressive B-cell lymphomas are leading to the identification of new rational treatment targets and the clinical testing of candidate target inhibitors in these diseases. This session will focus on the expanding treatment options for these lymphoid malignancies and the clinical analyses of promising rational target inhibitors.

[Henners]

We used to call it SUMS when we were little.

Is that any help?

Goods?

[Henners]

This is not surprising, however, as the typical behavior of both creationists and buffoons alike is to pretend to understand things of which they actually know nothing.

To be fair, that is also an attribute of struck-off medics.

[joobz]

And that process is sped up by reducing the number of strong selection pressures to a single pressure and then applying a sequence of single strong selection pressures. That’s how to produce MRSA, multidrug resistant gonorrhea, malaria, TB, HIV, multi-herbicide weeds, multi-pesticide resistant insects…

What you fail to realize is that there are no cooperative selection pressures for evolution and there is no cooperative chemistry that brings about abiogenesis. These are bizarre speculations that you have no mathematical or empirical evidence to support your weird belief system. If you have any mathematical or empirical evidence to support your weird speculations, present it. Oh, wait, you do have evidence; it’s the Madagascar rainforest and plate tectonics.
Now you are switching topics because you are starting to see the truth of what I'm saying. Your own dogmatic views are preventing you from understanding what occurs in nature.

If you want to keep to your beliefs, prove that there is no such thing as weather.

This will be hard, because of the multitudes of data that weather exists.
Here's some more examples, a photo of rain and a photo of snow.

Do you think this changing weather pattern doesn't change the number and magnitude of selection conditions in the environment?

[Shalamar]

Keep reading Shalamar. I’ll spoon feed it to you as much as possible but your inexperience in the mathematics and biology of this problem is making it difficult for you to understand. I’ll continue to provide you empirical examples of the mathematics of evolution by the mutation and selection sorting/optimization process and perhaps you will understand it is the number of selection conditions (sorting conditions) that dominates the behavior of this phenomenon. Here is a recent example from the field of oncology.[/SIZE][/FONT]
http://www.hematology.org/meetings/2007/attendee/education_program.cfm (http://www.hematology.org/meetings/2007/attendee/education_program.cfm)

And

And

And



I read all of that. All I saw was a strong support for the Theory of Evolution.

I see no Math, I see no equations.

Please show your proof on how Evolution is mathmatically impossible. Show all your work, and equations.

Otherwise, it seems you have no proof to back your claims, thus, you have been lying. I understand your faith causes you to do this, and to close your mind. But I suggest you actually show the math you claim as proof.

[kleinman]

Keep reading Shalamar. I’ll spoon feed it to you as much as possible but your inexperience in the mathematics and biology of this problem is making it difficult for you to understand. I’ll continue to provide you empirical examples of the mathematics of evolution by the mutation and selection sorting/optimization process and perhaps you will understand it is the number of selection conditions (sorting conditions) that dominates the behavior of this phenomenon. Here is a recent example from the field of oncology.
http://www.hematology.org/meetings/2007/attendee/education_program.cfm (http://www.hematology.org/meetings/2007/attendee/education_program.cfm)
.
.
.I read all of that. All I saw was a strong support for the Theory of Evolution.
Of course evolution by mutation and selection occurs but in a very limited manner. What these citations show is that populations can only evolve easily against single selection pressures targeting single genes. As soon as you subject populations to more than a single selection pressure targeting multiple genes it impairs the ability of the population to evolve to these combined selection pressures. The greater the number of selection pressures a population is subjected to; it is much, much more difficult for the population to evolve to these simultaneous selection pressures. That’s the message you continue to miss.

Evolutionists can not describe the selection pressures that would lead to the transformation of a reptile population to a bird population and now that the mathematics and empirical evidence shows that combination selection pressures profoundly slow the evolutionary process, there is no way to transform the thousands of genes necessary to morph reptiles into birds. You can only transform a single gene at a time rapidly by the mutation and selection process. As soon as more than a single gene is to be transformed by mutation and selection, the process is profoundly slowed. This is what the real empirical evidence of mutation and selection shows. This is why the theory of evolution is mathematically and empirically impossible.
I see no Math, I see no equations.
That’s because you are unable or unwilling to see the equations. I posted Dr Schneider’s computer model and you are not satisfied. Do you want me to repost Dr Schneider’s entire web site on this thread? Go read his web site at http://www.ccrnp.ncifcrf.gov/~toms/ (http://www.ccrnp.ncifcrf.gov/~toms/) . You will find all the equations and description of his model there.

[joobz]

Of course evolution by mutation and selection occurs but in a very limited manner. What these citations show is that populations can only evolve easily against single selection pressures targeting single genes. As soon as you subject populations to more than a single selection pressure targeting multiple genes it impairs the ability of the population to evolve to these combined selection pressures. The greater the number of selection pressures a population is subjected to; it is much, much more difficult for the population to evolve to these simultaneous selection pressures. That’s the message you continue to miss.
You keep forgeting to mention that those pressures must remain stable and constant in order for evolution resistence to emerge. If, for instance, one of those pressures decreases and comes back, you'll greatly accellerate evolutionary adaptation.

Now, you still seem to think that weather doesn't exist. Here's another example of changes in selection pressures that are quite common in nature.

www.wish-tv.com/weather/graphics/5day.jpg (http://www.wish-tv.com/weather/graphics/5day.jpg)

[rocketdodger]

Evolutionists can not describe the selection pressures that would lead to the transformation of a reptile population to a bird population and now that the mathematics and empirical evidence shows that combination selection pressures profoundly slow the evolutionary process, there is no way to transform the thousands of genes necessary to morph reptiles into birds.

If we can't describe the pressures, then how do you know there is no way?

You can only transform a single gene at a time rapidly by the mutation and selection process. As soon as more than a single gene is to be transformed by mutation and selection, the process is profoundly slowed. This is what the real empirical evidence of mutation and selection shows. This is why the theory of evolution is mathematically and empirically impossible.

How can it be impossible if you can't even enumerate all the necessary mutations?

[kleinman]

Evolutionists can not describe the selection pressures that would lead to the transformation of a reptile population to a bird population and now that the mathematics and empirical evidence shows that combination selection pressures profoundly slow the evolutionary process, there is no way to transform the thousands of genes necessary to morph reptiles into birds.If we can't describe the pressures, then how do you know there is no way?
Oh, so you acknowledge that evolutionism is based on faith? The problem with your faith is that reality contradicts your beliefs. The mutation and selection sorting/optimization process is limited to sorting mutations for a tiny number of genes at any time. Even the evolution of the rapidly reproducing HIV virus is profoundly slowed when only two genes are targeted.
You can only transform a single gene at a time rapidly by the mutation and selection process. As soon as more than a single gene is to be transformed by mutation and selection, the process is profoundly slowed. This is what the real empirical evidence of mutation and selection shows. This is why the theory of evolution is mathematically and empirically impossible.How can it be impossible if you can't even enumerate all the necessary mutations?
People are enumerating these necessary mutations and showing how limited the trajectories are for populations on a fitness landscape. Here is a particular example:
“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.
This example illustrates how limited the trajectories are for a population on a fitness landscape. This also helps explains why using a beta-lactam antibiotic in combination with a second effective antibiotic brings the evolutionary process to a virtual standstill. The population can not evolve against two selection pressures simultaneously.

For you pleasure, I present you with a few more citations which show that combination selection pressures profoundly slow the evolutionary process.
http://www.dcp2.org/pubs/DCP/55/Section/8167 (http://www.dcp2.org/pubs/DCP/55/Section/8167)
In this section, we discuss interventions to address the challenge of drug resistance (table 55.3). Many interventions to address the problem of resistance are the same as those that reduce the burden of disease (these are discussed in detail in the relevant disease-specific chapters in this volume). Reducing disease diminishes the need for drug treatment and, therefore, lowers the likelihood that resistant strains will emerge. Some interventions, such as the use of drug combinations, reduce the likelihood that resistance will emerge, whereas other interventions, such as improvements in drug prescribing and patient compliance with dosing, reduce the likelihood that a resistant pathogen will survive and proliferate. Prolonging the effective therapeutic life of existing drugs is not sufficient, however. Increasing incentives for pharmaceutical firms to bring new drugs to markets may also be called for.
And
The appropriate choice of drug treatment is an important step in delaying the evolution of drug resistance. Drug combinations that include drugs with different targets were first used in the treatment of tuberculosis and have now become routine practice in the treatment of cancer and HIV/AIDS. Combinations of artemisinin and its derivatives with other antimalarials, notably mefloquine, have accelerated recoveries, increased cure rates, and reduced transmissibility. In the refugee camps on the western border of Thailand, where most of the recent studies with artemisinin combinations have been conducted, the use of combinations delayed the development of resistance and reduced the incidence of disease (Nosten and others 2000). The rationale behind drug combinations is that, if resistance results from spontaneous genetic mutations, the chance that a parasite will emerge that is simultaneously resistant to two drugs with unrelated modes of action (that is, drug targets) is the mathematical product of the individual parasite mutation frequencies multiplied by the total number of parasites exposed to the drugs (White 1998, 1999). Combinations, therefore, reduce enormously the probability that a resistant mutant will arise. Sequential deployment of the drugs is much less effective, because it does not exploit the multiplicative reduction in selection risk.

In the context of antibiotics, combinations have typically been used to broaden the spectrum of antimicrobial coverage rather than to reduce the likelihood of the emergence of resistance. With the development of new penicillins and cephalosporins with broader spectra of activity a decade ago, most serious infections have been treated with monotherapy. The use of combination therapy to preserve new classes of antibiotics from the emergence of resistance at a societal level may be rational, but it has not been implemented because of cost concerns and the potential for enhanced toxicity associated with the use of more agents than necessary to effect a cure in an individual patient.
http://lib.bioinfo.pl/auth:J%C3%A4nne,PA (http://lib.bioinfo.pl/auth:J%C3%A4nne,PA)
The EGFR T790M mutation has been identified in tumors from lung cancer patients that eventually develop resistance to erlotinib. In this study, we generated a mouse model with doxycycline-inducible expression of a mutant EGFR containing both L858R, an erlotinib-sensitizing mutation, and the T790M resistance mutation (EGFR TL). Expression of EGFR TL led to development of peripheral adenocarcinomas with bronchioloalveolar features in alveoli as well as papillary adenocarcinomas in bronchioles. Treatment with an irreversible EGFR tyrosine kinase inhibitor (TKI), HKI-272, shrunk only peripheral tumors but not bronchial tumors. However, the combination of HKI-272 and rapamycin resulted in significant regression of both types of lung tumors. This combination therapy may potentially benefit lung cancer patients with the EGFR T790M mutation.
http://www.publications.doh.gov.uk/pub/docs/doh/smacsyn2.pdf (http://www.publications.doh.gov.uk/pub/docs/doh/smacsyn2.pdf)
Tuberculosis (TB) remains the commonest bacterial cause of morbidity and mortality world-wide, with nearly 8 million new cases and 3 million deaths annually, mostly in developing countries. A steady decline in clinical cases in the developed world ceased or reversed in the mid-l980s.

Tuberculosis is treated with combinations of three or four agents for at least 6 months. Monotherapy leads rapidly to resistance by selecting spontaneous mutants. Even with combination therapy, resistance emerges when there is poor concordance by the patient, incorrect dosage or malabsorption of the drugs.
It is this type of empirical evidence along with the mathematical evidence from the peer reviewed and published mathematical model of random point mutations and selection, ev, written by Dr Tom Schneider, head of computational molecular biology at the National Cancer Institute which shows that the mutation and selection sorting/optimization process is profoundly slowed when more than a single selection pressure is applied to a population and therefore the theory of evolution is mathematically and empirically impossible.

Now you all have a good weekend and I’ll be back next week to post more citations which show the theory of evolution is mathematically and empirically impossible and hopefully you evolutionists will learn how the mutation and selection sorting/optimization process actually works.

[joobz]

For you pleasure, I present you with a few more citations which show that combination selection pressures profoundly slow the evolutionary process.
http://www.dcp2.org/pubs/DCP/55/Section/8167 (http://www.dcp2.org/pubs/DCP/55/Section/8167)

And

http://lib.bioinfo.pl/auth:J%C3%A4nne,PA (http://lib.bioinfo.pl/auth:J%C3%A4nne,PA)

http://www.publications.doh.gov.uk/pub/docs/doh/smacsyn2.pdf (http://www.publications.doh.gov.uk/pub/docs/doh/smacsyn2.pdf)

It is this type of empirical evidence along with the mathematical evidence from the peer reviewed and published mathematical model of random point mutations and selection, ev, written by Dr Tom Schneider, head of computational molecular biology at the National Cancer Institute which shows that the mutation and selection sorting/optimization process is profoundly slowed when more than a single selection pressure is applied to a population and therefore the theory of evolution is mathematically and empirically impossible.

Now you all have a good weekend and I’ll be back next week to post more citations which show the theory of evolution is mathematically and empirically impossible and hopefully you evolutionists will learn how the mutation and selection sorting/optimization process actually works.
Over the weekend, see if you can make weather disappear. Otherwise, your belief that evolution is impossible will disappear.

[rocketdodger]

Oh, so you acknowledge that evolutionism is based on faith? The problem with your faith is that reality contradicts your beliefs.

Err, no, because my belief is in nothing but reality. The faith we have in evolutionism is the same faith we have in the rest of the products of the scientific method.

People are enumerating these necessary mutations and showing how limited the trajectories are for populations on a fitness landscape. Here is a particular example:

Oh they are? Then you agree that we will eventually know how reptiles evolved into birds? Well I never thought I would hear you say that.

It is this type of empirical evidence along with the mathematical evidence from the peer reviewed and published mathematical model of random point mutations and selection, ev, written by Dr Tom Schneider, head of computational molecular biology at the National Cancer Institute which shows that the mutation and selection sorting/optimization process is profoundly slowed when more than a single selection pressure is applied to a population and therefore the theory of evolution is mathematically and empirically impossible.

So let me see if I understand this -- you put Schneider on a pedestal and throw his title around in this forum as if it somehow makes his work more important, and then proceed to claim that his interpretation of his own project is incorrect.

If Scheider is the head of computational molecular biology at NCI, with peer reviewed and published material, what makes you think you know more about his area of expertise than he does?

[Mr. Scott]

And you incorrect interpretation of the mutation and selection sorting/optimization process contributes to the premature death of millions of people suffering from diseases subject to the principles of mutation and selection. I think you are the rude one in this debate.

That is A) an appeal to emotion, and B) a claim for which you have never provided evidence.

Your links to combination therapy don't qualify as evidence because they are in accord (not in conflict) with standard evolutionary theory.

Please present your evidence that Darwin's theory of evolution contributes to the deaths of millions. What claims of evolutionists result in millions of deaths by disease? What claims of creationists will save these lives? What evidence do you have to support this claim?

[Shalamar]

Ok. I've tried.

Klienman, you've insulted me, and insulted others here. Indirectly, yes, but you've done it, and you know you have done it.

You say I 'Can not see the equations'. That is because they are not there. You can not prove using math, without the equations.

Now. You have made many many assumptions here, and most are false. Many of these are due to your faith, and you transplant your faith onto science.

Your faith is written on stone tablets a mile high, with letters of fire that spell out exactly what you should believe. So you do so.

Science is written in Sand. Sand on a beach with the tide constantly coming in. Sometimes the letters are washed away, and need to be re-written. Sometimes the words stand up to the waves. This is science.

Now. You can not prove something does not exist. You are attempting to prove that evolution does not exist. You can no more prove that evolution does not exist, than you can prove that I do not have an invisible elf living in my backyard.

Neither Evolution, or the Theory of Evolution are faiths (Yes, They are two separate things). The people who trust in the science no more believe in evolution than they do in their dining room tables. They exist. That is all.

Your attempts with mutation and selection are interesting. I do not fault that, but they seem to be misguided. Even if your hypothesis were fully tested, and shoiwn to be the best fit, they would not invalidate the Theory of Evolution.

Why?

Because the Theory of Evolution is more than that. It is also genetics. It is also the Fossil record, and a great number of other things. The best you could hope for is the brief re-writing of the Theory of Evolution, but Evolution itself would still stand.

In order to invalidate Evolution itself, you would need to present evidence, and a great deal of it in favour of what YOU think is the way it happened.

Now. You claim that n+1 strong selection pressures prove that evolution is mathmatically impossible.

While an interesting claim, there is no math there, nor equations. No matter how much you believe them to be there. And you statement is flawed. It should read more like the following, with information gained from you, and the others on the board:

"It is likely that when multiple (1+n) selections pressures of unknown, but equal strength are applied to simple (viral) organisms in an artificial environment, that this may slow down evolutionary processes to the point of extinction of the organisms involved. However, not knowing how many pressures (n) in nature, and considering the possible variable nature of unequal strengths in nature, it is likely that (1+n) pressures of varying, and unequal strengths may allow the organisms to adapt more rapidly to the pressures, increasing the speed at which evolutionary processes occur."

Nothing is written in absolutes in science. Or rather, they shouldn't be (Only Sith deal in absolutes!) Science is ever changing, and ever challenged. Your claim is a valid, and interesting one, and would likely make a fantastic thesis or lab paper. But you can not confine your 'proofs' to artificial ones only. You need to evaluate what actually occurs in nature as well, to have something to compare your results to. The simulation is a part, but it far from the end all and be all. Creatures are far more complex than mere models.

You have a start, but just a start. You need to read what everyone else here has said, and follow through with broader and more complex experiments.

You can not just point to the results of others, and scream "THERE IS THE MATH! YOU ARE STUPID TO NOT SEE IT!" Where there is no math to be had.

I am curious if what I said is spot on, or flawed. I know klienman will toss that laughing dog at me, so I can ignore that. He just needs to see Science what it is, stop looking at it as faith.

[a_unique_person]

Now this is a real creationism debate.

http://www.theage.com.au/news/national/jail-for-creationist-row-killer/2007/12/14/1197568239761.html



An English backpacker who killed a Scottish tourist at a NSW caravan park after a row over creationism versus evolution has been sentenced to a minimum three years' jail.
Alexander Christian York, 33, was found guilty in July of manslaughter over the 2006 stabbing death of Scottish tourist Rudi Boa, after being acquitted of the more serious charge of murder.
Mr Boa, 28, died on January 27 after an altercation with York at the Blowering Holiday Park, near Tumut in southern NSW.
The incident occurred after the pair and Mr Boa's girlfriend Gillian Brown had spent the night drinking at the Star Hotel in Tumut, and an argument broke out between Mr Boa and York about creationism and evolution.
When Mr York and the couple returned to the caravan park separately later that night, a scuffle broke out between the two men.







They don't say which side won.

[Kotatsu]

Evolutionists can not describe the selection pressures that would lead to the transformation of a reptile population to a bird population

Yet at least one evolutionist has done so repeatedly in this very thread. I listed about 30 selection pressures that alone or in combination would lead to the evolution of birds from a dinosaur ancestor. These posts still stand, so you can go back and read them again, if you like to.

[Kotatsu]

They don't say which side won.

Well, obviously the side that was more fit survived, and thereby won.

But then again, I am apparently a practitioner and proponent of eugenics, so maybe these things are more obvious to me than to the population in general. No disrespect meant.

[Belz...]

(lies)

So, now we have "cooperative" selection pressures ?

Gee, Kleinman, you could revolutionise science with all these new terms.

[Mr. Scott]

Now this is a real creationism debate.

http://www.theage.com.au/news/national/jail-for-creationist-row-killer/2007/12/14/1197568239761.html

They don't say which side won.

It took a bit of googling, but it looks like the creationist made the evolutionist a martyr.

The couple, both biomedical scientists, had been arguing the case of evolution, while York [the killer] had taken a more biblical view of history.

Evolution vs creation row ends in stabbing (http://www.theaustralian.news.com.au/story/0,25197,22924256-12377,00.html)

[Belz...]

I must've missed the commandment that says "Thou shalt kill the disbelievers."

Why is this subject so infuriating ?

[Shalamar]

I must've missed the commandment that says "Thou shalt kill the disbelievers."

Why is this subject so infuriating ?

Because there are two distinctly different types of people in the subject.

There are the scientists. They don't care what the outcome is, all the care about is the evidence. They work at it, examine it, experiment, and see where it all leads. They publish for peer review, and other scientists use the evidence to see if it is accurate.

There has been a lot of work on evolution, and I imagine it is infurating to see ones lifes work reduced to 'Oh.. ,That can't POSSIBLY be real. How can you be so stupid?'

And then you have the theistic views. The 'God did it all', the 'I'm insulted that you say my grandparents are apes'. They fight tooth and nail against evolution because they think it demeans them, or lessens them, or threatens their faith.

And scientists don't really see the point. Science isn't faith. It isn't believed. It is trusted, and experimented until a conclusion is arrived at. And so much work has been done on evolution that you can't just look at one little part of it (Like mutation and selection). You have to look at it ALL. There there is a lot!

Mostly, people don't look at the evidence, and they fight passionately against it, because they can't bring themselves to believe in evolution. Scientists fight passionately for it, because the evidence overwhelmingly supports it!

[rocketdodger]

I fight passionately because the evil and stupidity that creationism (and most religious hogwash in general) breeds is extremely threatening.

One Kleinman, across the country from me, is tolerable. Being surrounded by millions of them is not. It simply can't be allowed to go that far.

[rocketdodger]

So, now we have "cooperative" selection pressures ?

Gee, Kleinman, you could revolutionise science with all these new terms.

Well actually there are cooperative selection pressures, which are defined to be selection pressures that target the same bases. If the target mutation occurs, then both pressures are closer to being satisfied. I would be money such a thing is pretty common.

The FUNNY thing is that when I brought this up about 20 pages ago, Kleinman of course dismissed the idea as nonsense, saying 1) it would be impossible for selective pressures to share targets, even just partially, and 2) if not, then give him a real world example.

[kjkent1]

I must've missed the commandment that says "Thou shalt kill the disbelievers."

Why is this subject so infuriating ?"Of all the creatures that inhabit this planet, only man knows that he will die." -- Phillip Wylie, "The Magic Animal"

Humans are alone in the knowledge of their mortality. But, we have the same basic drive of every other biological organism: survival.

These two concepts are irreconcilable contradictions.

The theist, especially the Christian theist, has solved the contradiction by replacing it with a convenient lie, which must be accepted as absolutely true, regardless of any other personal cost. Otherwise, his/her immortality is lost.

The above is the entire "theory" of Christianity. Everything else is a detail. Only through Jesus can man obtain immortality. Abandon your faith and you will perish.

Once you understand the truth, the allegory of scripture becomes utterly transparent.

Most people need the lie to fight their way through life. It makes the warrior stronger to know that when he goes into battle, he does it to preserve the immortality of his clan.

Thus, the trait of "belief in an afterlife" is literally a "selective" advantage, and we have been selecting for it ever since the first human looked down and recognized that his/her companion was dead.

...and so ends the lesson for today.

[Belz...]

"Of all the creatures that inhabit this planet, only man knows that he will die." -- Phillip Wylie, "The Magic Animal"

Humans are alone in the knowledge of their mortality.

Not sure I agree with that, but I've been aware of the contradiction for a while.

I still don't get why killing the atheist seems like a good way to keep one's faith. What, silencing your opponents is the same as negating their arguments ? Weird.

[rocketdodger]

Its not a big deal.

If you read the article, it says that 1) the stabbing was done during a scuffle, the instigation of which the evolutionist is just as much responsible for and 2) the guy didn't intend to hurt him, it was an accident that it was as bad as it was.

[cyborg]

What, silencing your opponents is the same as negating their arguments ? Weird.

If the contradictory information is not presented it has no power.

[joobz]

Yet at least one evolutionist has done so repeatedly in this very thread. I listed about 30 selection pressures that alone or in combination would lead to the evolution of birds from a dinosaur ancestor. These posts still stand, so you can go back and read them again, if you like to.
Kotatsu, Have no worries. I did not ignore your posts and have learned from you. Your input is not in vain.


Kleinman simply rejects any information that contradicts his dogma. I simply hope he doesn't do the same thing in all parts of his life. Such behavior is quite dangerous.


Besides, I do thank him for presenting the multiple selection pressure argument. I find it very amusing that his theory helps prove that evolution is possible. He contends, rightly, that a set of strong selection pressures can create an environment where no adaptation is possible. His then must pretend that nature is a constant set of extremely high selection pressures for his theory to be accurate.

The pure and simple fact that nature isn't constant disproves his claim and his theory helps support the reality, that evolutionary adaptation is real.

I'll continue to post examples of weather to help him realize that the natural environment(where life exists) is almost never constant.