Annoying creationists [Archive] - Page 22

kjkent1

14th August 2007, 01:53 AM

Dr Schneider recently updated his ev blog site in response to criticism of his ev model found in "Unacknowledged Information Costs in Evolutionary Computing: A Case Study on the Evolution of Nucleotide Binding Sites". In Dr Schneider’s critique of this paper he said the following.
http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/blog-ev.html (http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/blog-ev.html)

Do any of you evolutionarians who think that Dr Schneider’s ev model does not properly model the biology of random point mutation and selection, you will find that author of the program and I are in disagreement with you.Last year, Schneider directly addressed this issue referring to you, in his blog, when he stated:

Large genomes are known to appear by many duplication mechanisms that are not in the Ev model. There are polymerase slippage, illegitimate recombination, transposons, insertion sequences, tetraploidization, and Robertsonain translations. These can all increase genome size rapidly. The mechanisms are currently not part of the Ev/Evj model.So, your claiming that ev is a complete model of evolutionary processes is directly refuted by Schneider. Thus, your claim that you are somehow defending ev in the face of assaults by "evolutionists," is a misrepresentation (some might even call your statement fraudulent, because it is so palpably false).

Dr Schneider and Paul still don’t understand why the model takes such huge number of generations to converge with all but the smallest genomes. The explanation is very simple; it is the multiple simultaneous selection conditions. Simply set the number of selection conditions to one and that single selection condition will evolve in a very small number of generations. This is a fundamental observation seen in any optimization, sorting or iteration problem. Reduce down the number of selection (optimization, sorting or iteration conditions) and the remaining condition is much more rapidly converged upon. This situation becomes much more apparent when the search space becomes massive as seen in large genome life forms.False premise, because you are attempting to compare the entire evolutionary landscape with the limited landscape modeled by ev.

In the over one hundred empirical examples I have presented so far, the type of mutations possible are not limited to random point mutations in these real cases. Despite this, increasing the number of selection pressures still profoundly slows the evolutionary process in these real examples of mutation and selection. These real examples include recombination and any other form of variation you can imagine. Dr Schneider’s computer model may only include random point mutations but it demonstrates the crucial mathematics of mutation and selection properly. It is not the type of mutation which dominates the rate of evolution; it is the number of selection conditions which dominates the mathematics of mutation and selection.One severe mutational event can thwart all possible selection pressures. Were this not true, there would be no evolution of new species, because as you've demonstrated, absent mutations more severe than random point, evolution occurs too slowly to complete in the generational time available.

The huge amount of data available for how mutation and selection works in nature shows that it is not the type of mutation which dominates the mutation and selection process, it is the number of selection conditions which dominates the behavior of this phenomenon. This real fact is seen in infectious and parasitic disease, agriculture, oncology and numerous other scientific fields which address evolution by mutation and selection.First, artificial selection pressures, such as those you cite to, are intended to prevent evolutionary change. Nature doesn't "intend" anything. Natural selection is not generally as harsh as multi-drug therapy, because if it were, then there would no evolutionary change.

Kjkent1, you don’t need this form of mutation in ev to understand the mathematics of mutation and selection. Evolution by mutation and selection is simply a multidimensional optimization problem. If you have only a single optimization condition (selection condition), it is much easier for the system to find a solution. When you have multiple optimization conditions (selection conditions) occurring simultaneously, it is much more difficult for an optimal solution to be found, especially when the search space becomes huge which happens with realistic length genomes.As already demonstrated, the occurrence of a severe mutation, such as a frame shift, alters the landscape and changes the entire optimization problem. This is observed in many of your cited to articles, because resistance frequently appears despite the best efforts of research scientists.

If your theory were correct, the therapies would always be successful. Yet, in real life, there is always a new virus and/or bacteria appearing, and it must have evolved from the existing viruses and bacteria, because the alternative is magic.

Which, of course, is your preference. Viruses and bacteria, for you, have good and/or evil purposes, and they appear instantaneously, via God's divine and magical intervention.

Sorry, Alan, but no one here other than you believes in magic.

Belz...

14th August 2007, 05:38 AM

Belz, you need to read the paragraphs because imbedded in those paragraphs are data from Dr Schneider’s computer simulation of random point mutation and natural selection.

Klein, it is obvious to me that you do not understand what science is, or what mathematics are. That you think a paragraph of plain text can be "imbedded" with data is quite telling.

Either present actual data from the simulation, and calculations to prove your conclusion that evolution is impossible, or retract your claims.

kleinman

14th August 2007, 06:15 AM

Kotatsu, you haven’t defined the selection pressures and the target genes/proteins.Then I will do so a last time:

The relevant selection pressures in the case of the moths and their ears are as follows:
1. Predation by bats using syntonic echo-location.
2. Predation by bats using allotonic echo-location.

Where only one of these are in effect, no specialization of the moth ear has occurred. Where both are in effect, specialization has occurred. This implies that the added selection pressure (2 above) has not halted evolution of the moth ear.

As to which genes/proteins are targeted, that is largely irrelevant to the argument (NOTE: here is your loophole, Kleinman!).
I wouldn’t call your last statement a loophole; I would call it a vast vacuum in which you can place your speculations. We are talking about the mathematics of mutation and selection and the associated empirical evidence which can be precisely measured and supports the mathematics, not some vague speculations about a phenomenon that can not be repeated.
When you do that, we can continue the discussion on your examples. Instead your argument consist of a predator chases a reptile into a tree and the reptile grows wings because it would be beneficial.That is a small part of my argument for an entirely different part of the discussion, yes. Why do you mix the various parts up? Also: what is unlikely in the abbreviated scenario you propose? Do you agree that --- provided evolutionary theory is true --- a reptile for which wings may be beneficial may under some circumstances evolve such structures?

Lastly: have you no comment at all about nested hierarchies?
This is a discussion of the mathematics of mutation and selection centered on Dr Schneider’s ev computer model and the associated empirical data. What Dr Schneider’s model shows is that the mutation and selection process is profoundly slow on all but the shortest genomes. The reason why this process is profoundly slow is the three selection conditions. If you set any two of the three selection conditions to zero, the remaining condition evolves extremely rapidly, even on longer genome cases. What this shows mathematically is that multiple simultaneous selection conditions profoundly slow the mutation and selection process. This affect of multiple simultaneous selection processes slowing evolution is seen and measured by numerous scientists repeatedly under multiple different situations including the evolution of HIV, HBV, HCV, TB, Malaria, cancer cells, weeds, rodents,… Every accurate measurement of the mutation and selection process shows that multiple simultaneous selection pressures slow evolution. That is what Dr Schneider’s ev program demonstrates mathematically and that is what the empirical evidence shows. In your imagination, a reptile evolving wings may be beneficial for the creature but they are not going to appear by mutation and selection. The mutation and selection phenomenon does not work that way.
I don't think it is easily predictable either way. In general, when multiple antibiotics with different mechanisms of action are used the kill rate is so high that there is a very small population left to provide new variations through mutations. This is the primary reason that multiple antibiotic regimens can slow the process of resistance development (the main reason why we use them). It has nothing to do with the number of selection pressures (as Kleinman has been repeatedly told and shown, especially with the HIV example) but with the ability of the selection pressures to decrease the population size.

Since single antibiotic regimens often do not reduce the population size as prfoundly as regimens with multiple agents, one might expect the application of one agent to cause resistance to develop relatively more quickly than application of multiple agents. But it really depends on the "strength" of the selection pressure. The number (of pressures) is relatively irrelevant (there is obviously some relevance since multiple pressures will require multiple genomic changes for resistance to develop and that requires more time in general) when it comes to discussing this issue since it is this ability to reduce population size, and hence variability, that is crucial to the process.

If there is a single agent that places a relatively minor pressure on a population, then resistance will be unlikely to develop. There will be significant variability so that resistance could easily develop, but there isn't much advantage to it (there will simply be many different possible colonies and the one with resistance may or may not survive all the other contingencies of that particular environment; in other words, resistance will almost surely arise, but it may not be selected since there isn't that much advantage gained by it; eventually you would see resistance in the population but it may take more time than you'd expect because of other factors at play).

If a single agent places a huge pressure on a population and significantly reduces population size, then resistance will generally develop fairly quickly to a single agent. The length of time for resistance to develop depends on how big a population is left (how much variability is possible). In this scenario, sequential application of different agents will result in fairly rapid resistance to all three agents. Since it is more difficult for multiple changes to occur within a population that has three antibiotics working on it (if resitance develops to antibiotic one, there are still two working that could potentially keep the population size very low), it will generally take longer for resistance to develop when those agents produce a dramatic reduction in population size than when a single pressure is applied. However, if the three agents are not able to reduce the population to a critically small size and variability is still relatively high, then resistance in that scenario will occur quickly when the three agents are applied. There is a clear example of this with particular kinds of HIV triple therapy which we already showed Kleinman. He ignored it.

So, there is no simple answer to this. It depends on what happens to the population and to the variability in the population. Either coadministration of three agents or sequential administration of three agents could result in the quicker development of resistance.Then I will withdraw my argument.

Thank you for your explanation.
Ichneumonwasp is ignoring the mathematical and empirical data. Dr Schneider’s model does not allow for reduction in population, half the population always survives yet three selection conditions take far more generations to evolve than evolving only a single selection condition in the model. Likewise, combination therapy for HIV exhibits the same behavior in delaying the virus from evolving to all three selection conditions simultaneously. Perhaps Ichneumonwasp will explain why physicians are now continually monitoring people who suffer from HIV for the appearance of resistance to any of the three drugs and as soon as resistance to any of the drugs appears, that ineffective drug is replaced in the combination? Ichneumonwasp does not recognize that the mutation and selection process is simply and optimization problem where the number of conditions optimized has a profound affect on the rate of convergence of these types of problems. Even small populations of HIV can quickly evolve resistance to a single drug. That is why combination therapy is used.
Do any of you evolutionarians who think that Dr Schneider’s ev model does not properly model the biology of random point mutation and selection, you will find that author of the program and I are in disagreement with you. Last year, Schneider directly addressed this issue referring to you, in his blog, when he stated:Large genomes are known to appear by many duplication mechanisms that are not in the Ev model. There are polymerase slippage, illegitimate recombination, transposons, insertion sequences, tetraploidization, and Robertsonain translations. These can all increase genome size rapidly. The mechanisms are currently not part of the Ev/Evj model.So, your claiming that ev is a complete model of evolutionary processes is directly refuted by Schneider. Thus, your claim that you are somehow defending ev in the face of assaults by "evolutionists," is a misrepresentation (some might even call your statement fraudulent, because it is so palpably false).
What you are missing lita’ gator is that you can’t take Dr Schneider’s shopping list of genetic variations and put these mechanisms into a coherent picture of how a reptile would transform into a bird. What you can do is take his computer model and show that multiple simultaneous selection pressures profoundly slow the evolutionary process and then demonstrate this with vast amounts of empirical data. There are no real examples of mutation and selection which demonstrate that any of the above mechanisms would change this mathematical and empirical fact. Have you noticed that Dr Schneider no longer discusses his model on open forums and restricts himself to his own blog site?
Dr Schneider and Paul still don’t understand why the model takes such huge number of generations to converge with all but the smallest genomes. The explanation is very simple; it is the multiple simultaneous selection conditions. Simply set the number of selection conditions to one and that single selection condition will evolve in a very small number of generations. This is a fundamental observation seen in any optimization, sorting or iteration problem. Reduce down the number of selection (optimization, sorting or iteration conditions) and the remaining condition is much more rapidly converged upon. This situation becomes much more apparent when the search space becomes massive as seen in large genome life forms.False premise, because you are attempting to compare the entire evolutionary landscape with the limited landscape modeled by ev.
Simple enough lita’ gator, give us a single real example where any other mechanism of mutation changes the mathematical fact that multiple selection pressures profoundly slow the evolutionary process. It is you who makes the false premise and fail to understand the mathematics of mutation and selection.
In the over one hundred empirical examples I have presented so far, the type of mutations possible are not limited to random point mutations in these real cases. Despite this, increasing the number of selection pressures still profoundly slows the evolutionary process in these real examples of mutation and selection. These real examples include recombination and any other form of variation you can imagine. Dr Schneider’s computer model may only include random point mutations but it demonstrates the crucial mathematics of mutation and selection properly. It is not the type of mutation which dominates the rate of evolution; it is the number of selection conditions which dominates the mathematics of mutation and selection.One severe mutational event can thwart all possible selection pressures. Were this not true, there would be no evolution of new species, because as you've demonstrated, absent mutations more severe than random point, evolution occurs too slowly to complete in the generational time available.
This is a problem you evolutionarians have. You need to claim some bizarre “severe mutational event can thwart all possible selections pressures”. What you are saying is that highly improbable events must occur over and over for the evolution of new species. That is not what the mathematics show and that is not what the empirical data show for the mutation and selection process. The theory of evolution must rest on the following pillars, strange speculations, unsupportable extrapolations, denial of the empirical and mathematical data.
The huge amount of data available for how mutation and selection works in nature shows that it is not the type of mutation which dominates the mutation and selection process, it is the number of selection conditions which dominates the behavior of this phenomenon. This real fact is seen in infectious and parasitic disease, agriculture, oncology and numerous other scientific fields which address evolution by mutation and selection.First, artificial selection pressures, such as those you cite to, are intended to prevent evolutionary change. Nature doesn't "intend" anything. Natural selection is not generally as harsh as multi-drug therapy, because if it were, then there would no evolutionary change.
Do you consider Dr Schneider’s selection pressures to be “artificial”? His model is intended to show how binding sites evolve yet it still demonstrates how multiple selection pressures slow the evolutionary process. What you still do not understand is that mutation and selection is simply and optimization problem, the greater the number of optimization conditions, the slower the process goes. You also need to understand that if a selection pressure is not “harsh”, it does not have a strong affect on the fitness of the population to reproduce and therefore will not have a strong affect on the frequency with which particular genes appear.
Kjkent1, you don’t need this form of mutation in ev to understand the mathematics of mutation and selection. Evolution by mutation and selection is simply a multidimensional optimization problem. If you have only a single optimization condition (selection condition), it is much easier for the system to find a solution. When you have multiple optimization conditions (selection conditions) occurring simultaneously, it is much more difficult for an optimal solution to be found, especially when the search space becomes huge which happens with realistic length genomes.As already demonstrated, the occurrence of a severe mutation, such as a frame shift, alters the landscape and changes the entire optimization problem. This is observed in many of your cited to articles, because resistance frequently appears despite the best efforts of research scientists.

If your theory were correct, the therapies would always be successful. Yet, in real life, there is always a new virus and/or bacteria appearing, and it must have evolved from the existing viruses and bacteria, because the alternative is magic.

Which, of course, is your preference. Viruses and bacteria, for you, have good and/or evil purposes, and they appear instantaneously, via God's divine and magical intervention.

Sorry, Alan, but no one here other than you believes in magic.
The main point about “severe mutations, such as frame shifts” is that they are usually fatal and these types of mutations do not have any impact on the vast amount of data available which demonstrates how mutation and selection actually works and the way it works is that multiple selection pressures profoundly slow the process.
Belz, you need to read the paragraphs because imbedded in those paragraphs are data from Dr Schneider’s computer simulation of random point mutation and natural selection.Klein, it is obvious to me that you do not understand what science is, or what mathematics are. That you think a paragraph of plain text can be "imbedded" with data is quite telling.
Better yet, instead of my reposting the data, I’ll show you how to generate the data. Click the following link http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/evj/evjava/index.html (http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/evj/evjava/index.html) . Start with the baseline case, G=256, mutation rate=1/generation per genome and so on. Click the check box “Pause on perfect creature” and then click the “Run” button. Record the number of generations it takes to evolve a “perfect creature”. Then click the “New” button and set the “Potential sites” (genome size) field to 512 and run this case until a perfect creature is evolved. Again record the number of generations. Repeat this process doubling the “Potential sites” and record the number of generations each time. Then you can tell us what the results are. While you are doing that, here are a couple of more examples which demonstrate how mutation and selection actually works.

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. Resistance is a major problem in many developing countries and may be imported into the UK

http://www.anopheles.org/showabstract.php?pmid=12435448 (http://www.anopheles.org/showabstract.php?pmid=12435448)
Malaria associated anaemia represents a major cause of childhood mortality in sub-Saharan Africa. Prevention of severe anaemia necessitates rapid treatment of symptomatic high density parasitaemia, as well as reduction of asymptomatic parasite prevalence to provide recovery period to restore production of erythrocytes. Both interventions are being increasingly impaired by reduced efficacy of antimalarial treatment due to parasite drug resistance. A new treatment strategy, including combinations of antimalarial drugs with optimal pharmacodynamic and kinetic properties may respond to the need of rapid and radical parasite clearance, temporary protection to re-infection, and prevention of drug resistance.
There it is evolutionarians; once again the empirical evidence shows that combination selection pressures slow evolution. This supports the mathematical results obtained from the peer reviewed and published ev computer model of random point mutations and natural selection. That is how mutation and selection actually works.

kjkent1

14th August 2007, 08:29 AM

Mr. Scott

14th August 2007, 09:31 AM

your argument consist of a predator chases a reptile into a tree and the reptile grows wings because it would be beneficial. [/SIZE][/FONT]

Yikes! That's a textbook example of a strawman argument.

Dr. Kleinman, why does God need help from false witness?

Belz...

14th August 2007, 10:09 AM

Better yet, instead of my reposting the data, I’ll show you how to generate the data.

Oh, no, Klein. By all means. Repost the data and calculations.

Your failure to do so for several pages following countless demands by myself speaks volumes about your inability to understand this issue or support your opinions.

Dr Adequate

14th August 2007, 11:27 AM

A quick perusal shows that you evolutionarians have not made much progress in your understanding of how mutation and selection actually works. So let’s see if we can help draw you out of your quagmire of confused and convoluted thinking. Who’s up first?
Oh, it’s Belz.

Belz, you need to read the paragraphs because imbedded in those paragraphs are data from Dr Schneider’s computer simulation of random point mutation and natural selection. It is this data from the parametric study of Dr Schneider’s very interesting computer model which shows how the various parameters on mutation and selection behave. The ev model shows which are the dominant parameters in the model and how these parameters affect the rate of accumulation of information by mutation and selection. By far, the most dominant parameter in this model is the number of selection pressures. If you are used to seeing algebraic expressions, you have some work to do to learn how to study and understand computer simulations. Most modern scientific problems are studied this way, not with simple algebraic expressions. It is starting to become apparent that I will have to show you how you analyze computer simulations for you to be able comprehend this discussion.

Nothing but the results from a peer reviewed and published model of random point mutation and natural selection which shows that combination selection pressures profoundly slow the evolutionary process. Oh, and let’s not forget over 100 citations which demonstrates this mathematical fact empirically, over and over and over again. But let’s see what you have Adequate.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg

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

Now if you want an example of nothing, that’s the number of empirical examples of your silly graph.

Taffer can’t tell the difference between mutation and natural selection and recombination and natural selection. Taffer’s “carefully” explained argument consist of saying emergence of resistance is not evolution. If you had read more than three or four of these references you would have seen the Taffer is confused about this topic.

How would you know if you have only read three or four of these citations? Paul, since you are having a hard time coming to grips with what your own computer program is showing, there is a huge amount of empirical data available which demonstrates exactly how mutation and selection works. Ask Delphi to explain it to you.

Paul, I’m amazed that when you are confronted with the data from your own computer model and the massive amount of empirical data which demonstrates what your model shows that you still don’t understand how mutation and selection actually works. However, I do understand that this totally shatters your belief system and it will take a while for this to sink in.

Paul, mutation and selection is simply an optimization problem for beneficial and detrimental mutations. As in all optimization problems, the greater the number of optimization conditions the slower the process goes and it does not take very many optimization conditions in the mutation and selection process for this to become profoundly slow because of the huge search space for realistic size genomes. That is the mathematical vise that ev demonstrates and places the theory of evolution in.

Myriad, I appreciate what you are saying here and agree that I should use the word “shows” rather than “proves”. However, you have run numerous cases from ev yourself and are aware that the number of generations for convergence of the ev model goes up very rapidly as you increase genome length. In fact, you proposed a strategy to increase the rate of convergence of the model. If you want the model to converge rapidly, reduce the number of selection conditions to one and that condition will converge very rapidly, even for longer genomes. It is the number of selection conditions which dominates the mathematics of mutation and selection. This is not an extrapolation. These data points are easily computed and this mathematical phenomenon is demonstrated over and over again by the empirical data. As I mention to Paul above, mutation and selection is simply an optimization problem for beneficial and detrimental mutations where the number of optimization conditions dominates the rate of convergence and becomes profoundly slow in the search space of a realistic size genome with multiple selection conditions. This is the way that mutation and selection actually works.

Let’s make this clear. I neither need to nor want to report invalid results from ev or other source to disprove the ridiculous theory of evolution by mutation and selection. Myriad, why don’t you report results from ev that contradict my conclusions. It is clear how the mathematics of mutation and selection actually works with ev and this result is demonstrated over and over again in reality. Adequate’s temper tantrums will not change this mathematical and empirical fact that multiple selection pressures profoundly slow the evolutionary process. If there was any truth to Adequate’s silly graph, he would have posted examples of his strange speculation that multiple selection pressures accelerate evolution. Mutation and selection simply does not work the way Adequate alleges.

Kotatsu, you haven’t defined the selection pressures and the target genes/proteins. When you do that, we can continue the discussion on your examples. Instead your argument consist of a predator chases a reptile into a tree and the reptile grows wings because it would be beneficial.

Only in your dreams Kotatsu, many of the citations I have posted not only identify the specific genes targeted, they identify the locus/loci which are altered by the mutation/selection process. Here’s an example for you and Dr Schneider and the gang over at the National Cancer Institute where the specific locus of mutation is identified and the way to address this mutation/selection process in cancer therapy. After all, if Dr Schneider went next door and spoke with the clinical oncologists, he could learn how mutation and selection actually works.

http://www.hematology.org/meetings/2007/attendee/education_program.cfm (http://www.hematology.org/meetings/2007/attendee/education_program.cfm)

Multiple selection pressures slow evolution, that’s how it works mathematically and that’s how it works empirically.

Dr Schneider recently updated his ev blog site in response to criticism of his ev model found in "Unacknowledged Information Costs in Evolutionary Computing: A Case Study on the Evolution of Nucleotide Binding Sites". In Dr Schneider’s critique of this paper he said the following.
http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/blog-ev.html (http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/blog-ev.html)

Do any of you evolutionarians who think that Dr Schneider’s ev model does not properly model the biology of random point mutation and selection, you will find that author of the program and I are in disagreement with you.

Dr Schneider and Paul still don’t understand why the model takes such huge number of generations to converge with all but the smallest genomes. The explanation is very simple; it is the multiple simultaneous selection conditions. Simply set the number of selection conditions to one and that single selection condition will evolve in a very small number of generations. This is a fundamental observation seen in any optimization, sorting or iteration problem. Reduce down the number of selection (optimization, sorting or iteration conditions) and the remaining condition is much more rapidly converged upon. This situation becomes much more apparent when the search space becomes massive as seen in large genome life forms.

In the over one hundred empirical examples I have presented so far, the type of mutations possible are not limited to random point mutations in these real cases. Despite this, increasing the number of selection pressures still profoundly slows the evolutionary process in these real examples of mutation and selection. These real examples include recombination and any other form of variation you can imagine. Dr Schneider’s computer model may only include random point mutations but it demonstrates the crucial mathematics of mutation and selection properly. It is not the type of mutation which dominates the rate of evolution; it is the number of selection conditions which dominates the mathematics of mutation and selection.

The huge amount of data available for how mutation and selection works in nature shows that it is not the type of mutation which dominates the mutation and selection process, it is the number of selection conditions which dominates the behavior of this phenomenon. This real fact is seen in infectious and parasitic disease, agriculture, oncology and numerous other scientific fields which address evolution by mutation and selection.

Kjkent1, you don’t need this form of mutation in ev to understand the mathematics of mutation and selection. Evolution by mutation and selection is simply a multidimensional optimization problem. If you have only a single optimization condition (selection condition), it is much easier for the system to find a solution. When you have multiple optimization conditions (selection conditions) occurring simultaneously, it is much more difficult for an optimal solution to be found, especially when the search space becomes huge which happens with realistic length genomes.

I wouldn’t call your last statement a loophole; I would call it a vast vacuum in which you can place your speculations. We are talking about the mathematics of mutation and selection and the associated empirical evidence which can be precisely measured and supports the mathematics, not some vague speculations about a phenomenon that can not be repeated.

This is a discussion of the mathematics of mutation and selection centered on Dr Schneider’s ev computer model and the associated empirical data. What Dr Schneider’s model shows is that the mutation and selection process is profoundly slow on all but the shortest genomes. The reason why this process is profoundly slow is the three selection conditions. If you set any two of the three selection conditions to zero, the remaining condition evolves extremely rapidly, even on longer genome cases. What this shows mathematically is that multiple simultaneous selection conditions profoundly slow the mutation and selection process. This affect of multiple simultaneous selection processes slowing evolution is seen and measured by numerous scientists repeatedly under multiple different situations including the evolution of HIV, HBV, HCV, TB, Malaria, cancer cells, weeds, rodents,… Every accurate measurement of the mutation and selection process shows that multiple simultaneous selection pressures slow evolution. That is what Dr Schneider’s ev program demonstrates mathematically and that is what the empirical evidence shows. In your imagination, a reptile evolving wings may be beneficial for the creature but they are not going to appear by mutation and selection. The mutation and selection phenomenon does not work that way.

Ichneumonwasp is ignoring the mathematical and empirical data. Dr Schneider’s model does not allow for reduction in population, half the population always survives yet three selection conditions take far more generations to evolve than evolving only a single selection condition in the model. Likewise, combination therapy for HIV exhibits the same behavior in delaying the virus from evolving to all three selection conditions simultaneously. Perhaps Ichneumonwasp will explain why physicians are now continually monitoring people who suffer from HIV for the appearance of resistance to any of the three drugs and as soon as resistance to any of the drugs appears, that ineffective drug is replaced in the combination? Ichneumonwasp does not recognize that the mutation and selection process is simply and optimization problem where the number of conditions optimized has a profound affect on the rate of convergence of these types of problems. Even small populations of HIV can quickly evolve resistance to a single drug. That is why combination therapy is used.

What you are missing lita’ gator is that you can’t take Dr Schneider’s shopping list of genetic variations and put these mechanisms into a coherent picture of how a reptile would transform into a bird. What you can do is take his computer model and show that multiple simultaneous selection pressures profoundly slow the evolutionary process and then demonstrate this with vast amounts of empirical data. There are no real examples of mutation and selection which demonstrate that any of the above mechanisms would change this mathematical and empirical fact. Have you noticed that Dr Schneider no longer discusses his model on open forums and restricts himself to his own blog site?

Simple enough lita’ gator, give us a single real example where any other mechanism of mutation changes the mathematical fact that multiple selection pressures profoundly slow the evolutionary process. It is you who makes the false premise and fail to understand the mathematics of mutation and selection.

This is a problem you evolutionarians have. You need to claim some bizarre “severe mutational event can thwart all possible selections pressures”. What you are saying is that highly improbable events must occur over and over for the evolution of new species. That is not what the mathematics show and that is not what the empirical data show for the mutation and selection process. The theory of evolution must rest on the following pillars, strange speculations, unsupportable extrapolations, denial of the empirical and mathematical data.

Do you consider Dr Schneider’s selection pressures to be “artificial”? His model is intended to show how binding sites evolve yet it still demonstrates how multiple selection pressures slow the evolutionary process. What you still do not understand is that mutation and selection is simply and optimization problem, the greater the number of optimization conditions, the slower the process goes. You also need to understand that if a selection pressure is not “harsh”, it does not have a strong affect on the fitness of the population to reproduce and therefore will not have a strong affect on the frequency with which particular genes appear.

The main point about “severe mutations, such as frame shifts” is that they are usually fatal and these types of mutations do not have any impact on the vast amount of data available which demonstrates how mutation and selection actually works and the way it works is that multiple selection pressures profoundly slow the process.

Better yet, instead of my reposting the data, I’ll show you how to generate the data. Click the following link http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/evj/evjava/index.html (http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/evj/evjava/index.html) . Start with the baseline case, G=256, mutation rate=1/generation per genome and so on. Click the check box “Pause on perfect creature” and then click the “Run” button. Record the number of generations it takes to evolve a “perfect creature”. Then click the “New” button and set the “Potential sites” (genome size) field to 512 and run this case until a perfect creature is evolved. Again record the number of generations. Repeat this process doubling the “Potential sites” and record the number of generations each time. Then you can tell us what the results are. While you are doing that, here are a couple of more examples which demonstrate how mutation and selection actually works.

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

http://www.anopheles.org/showabstract.php?pmid=12435448 (http://www.anopheles.org/showabstract.php?pmid=12435448)

There it is evolutionarians; once again the empirical evidence shows that combination selection pressures slow evolution. This supports the mathematical results obtained from the peer reviewed and published ev computer model of random point mutations and natural selection. That is how mutation and selection actually works. So you haven't actually thought of any new lies?

But you have written nearly two and a half thousand words of the same old rubbish that failed to deceive us the first few hundred times you posted it.

Ah well, it's not as though your time is valuable.

Dr Adequate

14th August 2007, 03:19 PM

This is a discussion of the mathematics of mutation and selection centered on Dr Schneider’s ev computer model and the associated empirical data. What Dr Schneider’s model shows is that the mutation and selection process is profoundly slow on all but the shortest genomes. The reason why this process is profoundly slow is the three selection conditions. If you set any two of the three selection conditions to zero .... ... then you are evolving something else, and you are not comparing simultaneous selection pressures with the same selection pressures applied in a sequential and cumulative manner, and of course you know this just as well as we do, don't you, you boring lying tosser.

Ichneumonwasp is ignoring the mathematical and empirical data. Dr Schneider’s model does not allow for reduction in population, half the population always survives yet three selection conditions take far more generations to evolve than evolving only a single selection condition in the model. I regret to inform you that your discovery that it takes more time to do more evolution is not the ground-breakingly original idea that you seem to suppose. Perhaps you could explain what you think this has to do with your halfwitted lies about simultaneous selection pressures?

Better yet, instead of my reposting the data, I’ll show you how to generate the data. Click the following link http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/evj/evjava/index.html (http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/evj/evjava/index.html) . Start with the baseline case, G=256, mutation rate=1/generation per genome and so on. Click the check box “Pause on perfect creature” and then click the “Run” button. Record the number of generations it takes to evolve a “perfect creature”. Then click the “New” button and set the “Potential sites” (genome size) field to 512 and run this case until a perfect creature is evolved. Again record the number of generations. Repeat this process doubling the “Potential sites” and record the number of generations each time. Then you can tell us what the results are. While you are doing that, here are a couple of more examples which demonstrate how mutation and selection actually works. The astute reader, i.e. anyone who isn't kleinman, will observe that if you follow these instructions, you will be halving the mutation rate (mutations/base/generation) every time you double the length of the genome, something which does not, of course, happen in nature. Comparison of the correct simulation with kleinman's halfwitted blunder shows that most of the increase in the number of generations which kleinman attributes to increased genome length is in fact a consequence of the reduced mutation rate.

We may note also that 512 bases without a mistake is a different target from 256 bases without a mistake. If the selection conditions were the same in both cases, and if we didn't emulate kleinman's silly blunder over the mutation rate, we would find that genome length per se is not a problem.

Kotatsu

15th August 2007, 02:14 AM

I wouldn’t call your last statement a loophole; I would call it a vast vacuum in which you can place your speculations. We are talking about the mathematics of mutation and selection and the associated empirical evidence which can be precisely measured and supports the mathematics, not some vague speculations about a phenomenon that can not be repeated.

and:

This is a discussion of the mathematics of mutation and selection centered on Dr Schneider’s ev computer model and the associated empirical data. What Dr Schneider’s model shows is that the mutation and selection process is profoundly slow on all but the shortest genomes. The reason why this process is profoundly slow is the three selection conditions. If you set any two of the three selection conditions to zero, the remaining condition evolves extremely rapidly, even on longer genome cases. What this shows mathematically is that multiple simultaneous selection conditions profoundly slow the mutation and selection process. This affect of multiple simultaneous selection processes slowing evolution is seen and measured by numerous scientists repeatedly under multiple different situations including the evolution of HIV, HBV, HCV, TB, Malaria, cancer cells, weeds, rodents,… Every accurate measurement of the mutation and selection process shows that multiple simultaneous selection pressures slow evolution. That is what Dr Schneider’s ev program demonstrates mathematically and that is what the empirical evidence shows. In your imagination, a reptile evolving wings may be beneficial for the creature but they are not going to appear by mutation and selection. The mutation and selection phenomenon does not work that way.

Then this is where I give up. Unless someone goes to your place and physically disables the Ctrl+C and Ctrl+V commands from your keyboard, thee seems to be no reason to approach your posts with anything even remotely resembling seriousness. If I want form answers copied over and over regardless of what I say, I may as well call the Railway Departure Times Information Service and yell at them for a while.

In the history of wastes of time, you, Kleinman, not only get a few chapters of your own, but a large part of the introduction is devoted to you as well, and your face features prominently on the cover.

kleinman

15th August 2007, 11:44 AM

What you are missing lita’ gator is that you can’t take Dr Schneider’s shopping list of genetic variations and put these mechanisms into a coherent picture of how a reptile would transform into a bird. What you can do is take his computer model and show that multiple simultaneous selection pressures profoundly slow the evolutionary process and then demonstrate this with vast amounts of empirical data. There are no real examples of mutation and selection which demonstrate that any of the above mechanisms would change this mathematical and empirical fact. Have you noticed that Dr Schneider no longer discusses his model on open forums and restricts himself to his own blog site?The "coherent picture" that you claim cannot be constructed, "is" the theory of evolution. And, it's entirely coherent. Mutations occur and they change the evolutionary landscape. The evidence for this is overwhelming. The frame shift in Achromobacter guttatus K172 (nylonase producing bacteria) demonstrates one of the microbiological methods by which a reptile can transform into a bird. And, all your arm waiving will not explain it away.
Kjkent1, I have never claimed that mutations don’t occur and that the evolutionary landscape is not altered by these mutations. What I have claimed is this process is far more limited than you evolutionarians allege. Consider your example of a nylonase producing bacteria; how many selection pressures where placed on this bacteria in order to produce this nylonase from an already existing polyermase? The answer to that question is one selection pressure was placed on these bacteria. If you were to place two or more selection pressures on these bacteria, it would be far more difficult to evolve this nylonase from the already existing polymerase. All you have shown is that on rare occasions, a frame shift will alter an already existing polymerase when the population is subjected to a single selection pressure. Now if you show that a nylonase is produced simultaneously with several different resistant genes to several different antibiotics and that it is done more rapidly than when the selection pressures are done sequential, then you will have refuted my argument that simultaneous selection pressures profoundly slow the evolutionary process.
Simple enough lita’ gator, give us a single real example where any other mechanism of mutation changes the mathematical fact that multiple selection pressures profoundly slow the evolutionary process. It is you who makes the false premise and fail to understand the mathematics of mutation and selection.This is a classic strawman. You erect a phony barrier to evolution and then invite your opponents to try to tear it down. You haven't proved that multiple selection pressures prevent evolution from occurring. In order to accomplish this, you must now explain the existence of K172, by something other than magic. The bug exists and it falsifies your theory. So, deal with it, or admit that your theory is built on the foundation that K172 is not just a random accident, but is rather the product of divine intervention (magic).
Lita’ gator, the only thing made of straw in this discussion is your theory of evolution. Showing that a particular strain of bacteria when subjected to a single selection pressure can on rare occasions transform an existing polymerase to another form of the polymerase by a frame shift does not refute the argument that simultaneous selection pressures profoundly slow the evolutionary process.
This is a problem you evolutionarians have. You need to claim some bizarre “severe mutational event can thwart all possible selections pressures”. What you are saying is that highly improbable events must occur over and over for the evolution of new species. That is not what the mathematics show and that is not what the empirical data show for the mutation and selection process. The theory of evolution must rest on the following pillars, strange speculations, unsupportable extrapolations, denial of the empirical and mathematical data.Instead of proclaiming that K172 could not have arisen by random chance, why don't you calculate the probability of it arising. I'll tell you why: you can't, and it's not because you're not a sufficiently talented mathematician. You can't calculate the probability, because the set of possibilities which could lead to the appearance of an enzyme capable of digesting nylon is unknown. What "is" known, however, is that K172 exists -- therefore the probability of its existence is unity, and that falsifies your theory. Deal with it.
Why don’t you suggest to the scientists who developed the strain of bacteria that can digest nylon to repeat the experiment except this time include a second selection pressure like an antibiotic and see what happens?
Do you consider Dr Schneider’s selection pressures to be “artificial”? His model is intended to show how binding sites evolve yet it still demonstrates how multiple selection pressures slow the evolutionary process. What you still do not understand is that mutation and selection is simply and optimization problem, the greater the number of optimization conditions, the slower the process goes. You also need to understand that if a selection pressure is not “harsh”, it does not have a strong affect on the fitness of the population to reproduce and therefore will not have a strong affect on the frequency with which particular genes appear.There is a huge difference between harsh, randomly applied natural selection pressures, and pressures intentionally applied by a conscious being. "Mother Nature" is just a phrase. There is no actual Mother sitting somewhere and applying selection pressures so as to halt evolution. Unless you accept magic as a given --which you do, of course.
Lita’ gator, you are demonstrating your ignorance of the mathematics of mutation and selection. If a selection pressure is very weak, it does not affect the fitness of the population to reproduce and therefore does not change the frequency of genes by very much. You also still have the problem that sorting beneficial and detrimental mutations will still be profoundly slow when you have multiple simultaneous selection pressures.
The main point about “severe mutations, such as frame shifts” is that they are usually fatal and these types of mutations do not have any impact on the vast amount of data available which demonstrates how mutation and selection actually works and the way it works is that multiple selection pressures profoundly slow the process.The frame shift in K172 was not fatal, and it has the impact of falsifying your entire theory.

Unless and until you explain K172's existence (and all the other evidences for extreme beneficial mutations), all of your evidence which you suggest falsifies evolution, is meaningless, because your evidence doesn't explain K172.
You again demonstrate a big problem you evolutionarians have. You try to use exceptional cases to demonstrate your theory. Just because on rare occasions a frame shift mutation is beneficial for a population, does not overcome the fact that multiple simultaneous selection pressures profoundly slow the evolutionary process. This mathematical fact is demonstrated empirically over and over again. Frame shift mutations do not overcome this mathematical fact.
your argument consist of a predator chases a reptile into a tree and the reptile grows wings because it would be beneficial.Yikes! That's a textbook example of a strawman argument.

Dr. Kleinman, why does God need help from false witness?
Why Edited incivility., where in your textbook is a description of the selection pressure(s) that would transform a reptile to a bird?
Better yet, instead of my reposting the data, I’ll show you how to generate the data. Click the following link http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/evj/evjava/index.html (http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/evj/evjava/index.html) . Start with the baseline case, G=256, mutation rate=1/generation per genome and so on. Click the check box “Pause on perfect creature” and then click the “Run” button. Record the number of generations it takes to evolve a “perfect creature”. Then click the “New” button and set the “Potential sites” (genome size) field to 512 and run this case until a perfect creature is evolved. Again record the number of generations. Repeat this process doubling the “Potential sites” and record the number of generations each time. Then you can tell us what the results are. While you are doing that, here are a couple of more examples which demonstrate how mutation and selection actually works.The astute reader, i.e. anyone who isn't kleinman, will observe that if you follow these instructions, you will be halving the mutation rate (mutations/base/generation) every time you double the length of the genome, something which does not, of course, happen in nature. Comparison of the correct simulation with kleinman's halfwitted blunder shows that most of the increase in the number of generations which kleinman attributes to increased genome length is in fact a consequence of the reduced mutation rate.
To bad you are not an astute reader because an astute reader would know what a realistic mutation rate is. 1 mutation per 256 bases per generation is not a realistic mutation rate, neither is 1 mutation per 512 bases per generation, nor 1 mutation per 1024 bases, nor 1 mutation per 2048 bases, nor 1 mutation per 4096 bases… It is only when you get to 1 mutation per over 10,000 bases that you start to have realistic mutation rates and that is for replication of viruses like HIV which don’t have error correction mechanisms in their reproductive process. For life forms with error correction mechanisms (which is virtually every higher life form than viruses) the mutation rate is closer to 1 mutation per 1,000,000 bases per generation or even less than that.
So you haven't actually thought of any new lies?

But you have written nearly two and a half thousand words of the same old rubbish that failed to deceive us the first few hundred times you posted it.
What is abundantly clear is how easily both of your feet fit in your mouth when you posted this;
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
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.
http://forums.randi.org/images/smilies/doglaugh.gif
Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution cheese wiz?

Edited incivility.

Better yet, instead of my reposting the data, I’ll show you how to generate the data.Oh, no, Klein. By all means. Repost the data and calculations.

Your failure to do so for several pages following countless demands by myself speaks volumes about your inability to understand this issue or support your opinions.
Edited incivility.

[SIZE=3]So here’s some data for you to ponder from ev. Start from the baseline case which Dr Schneider used in his publication, except that we use evolution of a perfect creature as the convergence criteria. Population is 64, number of binding sites is 16, site width is 6 bases, weight width is 5 bases, mutation rate is 1 mutation per genome per generation, the weight factors for each of the three selection conditions is left a the default value of 1 and the genome length is varied by a factor of two. A perfect creature occurs when there are no mistakes in any of the three selection condition, no spurious binding of the weight matrix in the nonbinding site region of the genome, no spurious binding in the gene and no missed binding sites. Using these values you obtain the following data:
Genome Length/Generations for perfect creature
256/662
512/2,412
1,024/18,030
2,048/42,641
4,096/163,722
8,192/710,152
16,384/6,894,433

Now, consider the last case where G=16,384 and the generations for convergence equals 6,894,433. Take this same case and set two of the three selection conditions to zero and you obtain the following data:

Selection condition/generations for convergence to zero mistakes
missed sites/1
spurious binding within gene/223
spurious binding outside gene/223

Evolving all three selection conditions simultaneously for the case G=16,384 takes more than 10,000 times more generations than evolving any one of the individual selection conditions. That is how mutation and selection works. Sorting mutations for multiple simultaneous selection conditions is profoundly slower than sorting mutations for a single selection condition. Let’s see what happens for the case of G=32,768.

Selection condition/generations for convergence to zero mistakes
missed sites/1
spurious binding within gene/115
spurious binding outside gene/403

[FONT=Times New Roman]I’ll let you Edited incivility. try to get the three simultaneous selection conditions converge for the G=32,768 case. Be prepared for your computer to run for weeks on that case.

Now, how does that correlate with empirical data? Here’s another citation that demonstrates this mathematical fact.

http://www.anopheles.org/showabstract.php?pmid=15388456 (http://www.anopheles.org/showabstract.php?pmid=15388456)
Malaria parasites carrying genes conferring resistance to antimalarials are thought to have a selective advantage which leads to higher rates of transmissibility from the drug-treated host. This is a likely mechanism for the increasing prevalence of parasites with resistance to chloroquine (CQ) and sulfadoxine-pyrimethamine in sub-Saharan Africa. Combination therapy is the key strategy being implemented to reduce the impact of resistance, but its effect on the transmission of genetically resistant parasites from treated patients to mosquito vectors has not been measured directly. In a trial comparing CQ monotherapy to the combination CQ plus artesunate (AS) in Gambian children with uncomplicated falciparum malaria, we measured transmissibility by feeding Anopheles gambiae mosquitoes with blood from 43 gametocyte-positive patients through a membrane. In the CQ-treated group, gametocytes from patients carrying parasites with the CQ resistance-associated allele pfcrt-76T prior to treatment produced infected mosquitoes with 38 times higher Plasmodium falciparum oocyst burdens than mosquitoes fed on gametocytes from patients infected with sensitive parasites (P < 0.001). Gametocytes from parasites carrying the resistance-associated allele pfmdr1-86Y produced 14-fold higher oocyst burdens than gametocytes from patients infected with sensitive parasites (P = 0.011). However, parasites carrying either of these resistance-associated alleles pretreatment were not associated with higher mosquito oocyst burdens in the CQ-AS-treated group. Thus, combination therapy overcomes the transmission advantage enjoyed by drug-resistant parasites.
Once again, combination selection pressures are demonstrated to slow the evolutionary process profoundly. That’s how mutation and selection works mathematically as demonstrated by the ev computer simulation of random point mutations and natural selection and that is how mutation and selection works empirically as demonstrated by this citation and the more than 100 other citations I have already posted.

Please remember your Membership Agreement and refrain from personal insults and condescending nicknames. Please, also consider the use of a bit more brevity in your posts.

joobz

15th August 2007, 12:56 PM

:words:
Still haven't figured out how to call a variable? :D

kleinman

15th August 2007, 01:05 PM

Still haven't figured out how to call a variable?
Still haven’t figured out to get any mathematics or scientific data to back up your weird speculations?
Envision a system of millions of forming and destructive chemical reactions. Now, envision that intermediates of there reactions associate through non-covalent means and that this complex becomes protected against the destructive reactive pathway, perhaps by a reversible precipitation. These new complexes result in a localized increased of new chemical species. These chemical species then progress in a new series of reaction... that is what I mean through cooperative means. I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?

Belz...

15th August 2007, 01:07 PM

Alright Belz, get your bib on and we’ll spoon feed you. If you are a good evolutionarian, afterwards we’ll tell you a fairy tale before your nap. Oh, wait, you already know a fairy tale, it’s your theory of evolution.

Somehow I feel comforted by the fact that the only thing you've got to throw at me are insults.

Genome Length/Generations for perfect creature

What's a "perfect creature" in the context of evolution ?

That is how mutation and selection works.

In the simulation, yes.

Care to show that this is how it works in reality ?

Oh, and don't forget to explain how it applies to the types of mutations NOT covered by the simulation.

I’ll let you lazybones Belz try to get the three simultaneous selection conditions converge for the G=32,768 case. Be prepared for your computer to run for weeks on that case.

I have no intention of creating a simulation to fit your fantasies. Now that we have actual numbers in ONE of your posts, I'll let other people dismantle it if they understand anything from what you've posted.

But at least you've FINALLY posted something that could be construed as mathematics.

Good show.

joobz

15th August 2007, 01:14 PM

:words:
Still haven't figured out how to call a variable? :biggrin:
Still haven't had thought of any new lies?
Still don't have an argument that proves me wrong?

kleinman

15th August 2007, 01:50 PM

Edited incivility.

Genome Length/Generations for perfect creatureWhat's a "perfect creature" in the context of evolution ?
A “perfect creature” in the context of ev is simply cute terminology Dr Schneider and Paul use to describe a creature that has adapted to the selection pressures it has been subjected to. In ev, there are three possible selection conditions. One condition is that the weight matrix used to locate binding sites must find the sites where they are expected. If the weight matrix does not locate a binding site where it is expected, it is counted as a mistake. The second selection condition is that a binding site must not be found in the gene area of the genome. If a binding site is found in this region, it is counted as a mistake. The third selection condition is that a binding must not be found in the nonbinding site region of the genome. If a binding site is located in this region of the genome, it is counted as a mistake. Each generation, half the population with the least number of mistakes is allowed to reproduce, the other half dies. The new population of creatures is then subjected to mutations in each of their genomes and mistakes are again counted and the cycle is repeated. A perfect creature has evolved sequences of bases which satisfy the selection conditions it has been subjected to.
That is how mutation and selection works.In the simulation, yes.

Care to show that this is how it works in reality ?

Oh, and don't forget to explain how it applies to the types of mutations NOT covered by the simulation.
The ev simulation is a very good mathematical analogy of the mutation and selection process. What ev is revealing is how difficult it becomes for a population to navigate the fitness landscape when there are multiple selection conditions. This becomes particularly apparent when the search space is enlarged beyond all but the shortest genomes.

Here is an example of how this works in reality. I recently posted this reference but I will use it again because it is particularly clear comparison of what ev is showing.
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. Resistance is a major problem in many developing countries and may be imported into the UK
Monotherapy (single selection conditions) quickly lead to the evolution of resistance. It is the combination therapy which confounds TB from navigating the fitness landscape and evolving resistance to all drugs simultaneously.

These real cases I have been posting are not limited to random point mutations. For example, HIV does recombination but still the evolution of the virus is slowed profoundly when combination therapy is used against it. This is why people now can survive for years with the virus. None of the citations I have posted are limited to random point mutation. Any type of mutation or recombination is available in these cases yet they all demonstrate that multiple simultaneous selection pressures profoundly slow the evolution of the population subjected to these selection pressures. On the other hand, single selection pressures can be quickly adapted to. That is what ev shows and that is what the empirical data shows.
I’ll let you Edited incivility. try to get the three simultaneous selection conditions converge for the G=32,768 case. Be prepared for your computer to run for weeks on that case.I have no intention of creating a simulation to fit your fantasies. Now that we have actual numbers in ONE of your posts, I'll let other people dismantle it if they understand anything from what you've posted.

But at least you've FINALLY posted something that could be construed as mathematics.

Good show.
This isn’t my fantasy, this is Dr Schneider’s peer reviewed and published model of random point mutation and natural selection which shows these results. And what it shows is that multiple simultaneous selection pressures profoundly slow the evolutionary process in his model. The empirical data confirms this result and that is why the theory of evolution is mathematically impossible by mutation and selection. Mutation and selection can not and does not work the way you evolutionarians allege.

This is your second infraction in a very short period of time. Please cease with the personal insults. You should be aware by now that changes have occurred on the Forum, and we expect you to adhere to the Membership Agreement (http://www.randi.org/forum/rules.html). Please review it.

Dr Adequate

15th August 2007, 02:21 PM

Dr Adequate

15th August 2007, 02:46 PM

I have no intention of creating a simulation to fit your fantasies. Now that we have actual numbers in ONE of your posts, I'll let other people dismantle it if they understand anything from what you've posted. Done.

But at least you've FINALLY posted something that could be construed as mathematics. Not really. Are you familiar with the acronym "GIGO"?

kleinman

15th August 2007, 03:18 PM

To bad you are not an astute reader because an astute reader would know what a realistic mutation rate is. 1 mutation per 256 bases per generation is not a realistic mutation rate, neither is 1 mutation per 512 bases per generation, nor 1 mutation per 1024 bases, nor 1 mutation per 2048 bases, nor 1 mutation per 4096 bases… It is only when you get to 1 mutation per over 10,000 bases that you start to have realistic mutation rates and that is for replication of viruses like HIV which don’t have error correction mechanisms in their reproductive process.And what size are their populations?

So how many mutations per base do you get in the population as a whole?

How does that compare to ev?
If you had been an astute reader you would have seen that the population was posted and it was only 64 creatures, yet with only a single selection condition, this tiny population can rapidly evolve to a single selection condition.

The conversion of mutations per genome to mutation per base has been extensively discussed on the Evolutionisdead thread. Dr Schneider has chosen to use either mutations per genome per generation or mutations per number of bases per generation. Because of Dr Schneider’s choice of method for computing mutation rates, you can only approximate the mutation rate per base. If you think that invalidates ev, take the issue up with Dr Schneider. I don’t believe Dr Schneider’s method of computing mutation rate significantly affects the results of the computation.
So here’s some data for you to ponder from ev. Start from the baseline case which Dr Schneider used in his publication, except that we use evolution of a perfect creature as the convergence criteria. Population is 64, number of binding sites is 16, site width is 6 bases, weight width is 5 bases, mutation rate is 1 mutation per genome per generation, the weight factors for each of the three selection conditions is left a the default value of 1 and the genome length is varied by a factor of two. A perfect creature occurs when there are no mistakes in any of the three selection condition, no spurious binding of the weight matrix in the nonbinding site region of the genome, no spurious binding in the gene and no missed binding sites. Using these values you obtain the following data:
Genome Length/Generations for perfect creature
256/662
512/2,412
1,024/18,030
2,048/42,641
4,096/163,722
8,192/710,152
16,384/6,894,433Everyone reading this thread knows the stupid mistake you're making here. So do you, 'cos I explained it to you. Just in case you missed it, I highlighted the point at which you screwed everything up.
Nothing is screwed up except your understanding of ev. If you want a realistic mutation rate for ev when the mutation rate in 1 mutation per genome per generation, you need a genome length of about 1,000,000. That would give an approximate mutation rate per base of 10^-6. Despite the still unrealistically high mutation rates used in these cases, it still takes almost 7 million generations to evolve the three selection conditions on the 16k genome. That is an order of magnitude more generations than the 8k case even though the genome was only doubled and the mutation rate halved. Adequate, you have yet to post a single case from ev, why don’t you do the 32k case from this series?
Now, consider the last case where G=16,384 and the generations for convergence equals 6,894,433. Take this same case and set two of the three selection conditions to zero and you .... ... are evolving something else.

We agree entirely that it takes more time to do more evolution. This is what my model shows, this is what ev shows, and this is bleedin' obvious.

But it has nothing to do with your silly, silly lies about the effect of simultaneous as opposed to sequential cumulative pressures.
Adequate, why don’t you tell us what this “something else” that is evolving when you only use one of the three selection conditions in ev?

You are now saying “that it takes more time to do more evolution”? That’s not what you said with your silly graph. Let’s again remind the readers what you said;
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
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.
http://forums.randi.org/images/smilies/doglaugh.gif
Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?
So tell us Adequate, do more simultaneous selection pressures mean more evolution or less evolution? Give us a real example of your convoluted and contradictory thinking. I have posted over 100 examples of combination selection pressures profoundly slowing evolution whether it is HIV, HBV, HCV, TB, Malaria, weeds, rodents, cancer… Each of these observations have been repeated by numerous scientists and clinicians. You’ve said you have worked on iteration problems, describe a single example of an iteration problem where the more conditions you have to iterate upon, the more rapid the problem converges. Give us an example of an optimization problem where the more conditions you are trying to optimize, the more rapid the optimization proceeds. Give us an example of a database sorting problem where the more conditions upon which you are sorting, the faster the sort proceeds. Mutation and selection is in the same family of mathematical problems. It is the sorting of beneficial and detrimental mutations. The greater the number of selection conditions, the slower the process proceeds. That is what ev shows and that is what reality shows.

joobz

15th August 2007, 04:52 PM

kleinman

15th August 2007, 05:16 PM

You are now saying “that it takes more time to do more evolution”? That’s not what you said with your silly graph. Let’s again remind the readers what you said;Actually that's not at all what he's saying at all. He's commenting on the foolish mistake you have made with mutation rate (a mistake very similar to one that was pointed out to you by myself 100 pages ago).
If you want a real example of foolishness, here it is:
Envision a system of millions of forming and destructive chemical reactions. Now, envision that intermediates of there reactions associate through non-covalent means and that this complex becomes protected against the destructive reactive pathway, perhaps by a reversible precipitation. These new complexes result in a localized increased of new chemical species. These chemical species then progress in a new series of reaction... that is what I mean through cooperative means. I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?
If you want a realistic mutation rate for ev when the mutation rate in 1 mutation per genome per generation, you need a genome length of about 1,000,000.Oh there it is. You assume a constant, unchanging mutation rate. Sorry, no dice.
There you go Dr Schneider, joobz has the solution for why your model converges so slowly, you use a constant mutation rate.
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, why don’t you give us a real example where non-constant mutation rate accelerates evolution?
http://forums.randi.org/images/smilies/doglaugh.gif
Now, here is another citation which shows how multiple selection pressures profoundly slow evolution.
http://www.prn.org/html/authorized/prnpreviews/hepatitisB_HivCoinfectoin.php (http://www.prn.org/html/authorized/prnpreviews/hepatitisB_HivCoinfectoin.php)
HBV infection is a dynamic disease and coinfection with HIV considerably complicates its diagnosis and management. The choice of antiviral therapy should be based on the need for HIV therapy, with control of HBV when HAART is initiated. Combination therapy should be used to avoid development of antiviral resistance. Continuous monitoring of HBV patients, regardless of need for treatment or history of seroconversion, is imperative to recognize reactivation and subsequent need for treatment, and to identify drug resistance and viral breakthrough early. Prompt changes in therapy when resistance emerges will reduce the development of compensatory mutations that will affect our ability to use newer therapies and lead to transmission of drug-resistant viruses in vaccinated individuals.
Joobz, you make a strong case for your argument with all zero of your real examples of how mutation and selection actually works. With enough free energy, anything is possible.
http://forums.randi.org/images/smilies/doglaugh.gif

joobz

15th August 2007, 06:03 PM

if you want a real example of foolishness, here it is:
really, then tell me how i'm wrong. if it is foolshness, then give specific reasons why you state that my admittedly speculative concept is impossibe to the point of foolish. that should be easy.

Joobz, if the sun shines on lead long enough does it turn into gold?

You keep saying this, as though it proves something, but it just shows why you are ignorant of all science. Only the most inept of scientists would confuse nuclear reactions with chemical reactions.

There you go Dr Schneider, joobz has the solution for why your model converges so slowly, you use a constant mutation rate.
again, do you think this is a smart thing to say? seems to be the type of semantic dodge that a person with no intellectual foundation would make.

:words:
Still not able to run Dr. A's code?
still not able to prove that slow=stop.

kleinman

15th August 2007, 06:28 PM

if you really want and example of foolishness, here it is.Envision a system of millions of forming and destructive chemical reactions. Now, envision that intermediates of there reactions associate through non-covalent means and that this complex becomes protected against the destructive reactive pathway, perhaps by a reversible precipitation. These new complexes result in a localized increased of new chemical species. These chemical species then progress in a new series of reaction... that is what I mean through cooperative means. I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?really, then tell me how i'm wrong. if it is foolshness, then give specific reasons why you state that my admittedly speculative concept is impossibe to the point of foolish. that should be easy.
Oh joobz, you are right, anything is possible if you have enough free energy, even turning lead into gold.
http://forums.randi.org/images/smilies/doglaugh.gif
There you go Dr Schneider, joobz has the solution for why your model converges so slowly, you use a constant mutation rate.
again, do you think this is a smart thing to say? seems to be the type of semantic dodge that a person with no intellectual foundation would make.
Well then, why don’t you put a variable mutation rate in ev, the code is available online. You know how to call a variable, don’t you?
http://forums.randi.org/images/smilies/doglaugh.gif
http://forums.randi.org/images/smilies/emot-words.gif
Here’s some words for you joobz, these demonstrate empirically how mutation and selection actually works and its not like you evolutionarians allege.
http://www.diva-portal.org/diva/getDocument?urn_nbn_se_uu_diva-7197-1__fulltext.pdf (http://www.diva-portal.org/diva/getDocument?urn_nbn_se_uu_diva-7197-1__fulltext.pdf)
The dosing strategy based on the MSW concept is to keep drug concentration levels above MPC. This could possibly be achieved by using higher doses and/or shorter dosing intervals than generally needed to cure an infection. Further, the time within the MSW can be narrowed by using com-pounds with reduced differences between MPC and MIC or compounds that quickly pass through the window. However, for some currently available drugs, concentrations above MPC can not be reached in patients due to pharmacokinetic reasons or toxicity limits. One strategy to circumvent this problem could be the use of combination therapy. The simultaneous administration of two antibiotics of different classes would require two concurrent mutations for bacterial growth. For M. tuberculosis, concentrations above MPC can not be attained for most of the first-line agents (Dong et al. 2000). In the case of tuberculosis, treatment duration is long and to minimize the risk of resistance, usually two to four drugs are prescribed. However, in-creasing the dose or using several compounds may also confer problems like toxic side-effects, ecological effects, and higher treatment costs.
And
To preserve the effect of new and existing drugs, it is of also of highest importance that the dosing regimes are carefully selected based on the pharmacokinetic and pharmacodynamic properties that prevent emergence of pre-existing or newly formed mutants of antibiotic resistance. This should be considered by both the pharmaceutical industry and the prescribing clinicians. This thesis support the use of high antibiotic concentrations and optimal antibiotic properties would be a high AUC, low MPC (where this parameter is applicable) and a short time within the (mutant) selective window. When an optimal resistance preventing dosage regimen is limited by the drug’s pharmacokinetics and toxicity, this may be circumvented by using combination therapy. It should be kept in mind that selection of resistance takes place not only among the target pathogens at the infection site, but also in the commensal flora. More studies are needed to characterize how different dosage regimens influence selection of resistance at different body sites. Obviously, the normal flora, e.g. in the gut, constitutes a reservoir for resistance. To reduce transmission of resistant bacteria between individuals, implementation of general hygienic measures may be particularly important during antibiotic therapy.
Combination therapy profoundly slows the evolution of resistance, combination selection pressures slow evolution. That is what ev shows and that is what the empirical data shows.

joobz

15th August 2007, 06:50 PM

:words:
You've offered nothing, my points still stand.

[FONT=Times New Roman][SIZE=3]really, then tell me how i'm wrong. if it is foolshness, then give specific reasons why you state that my admittedly speculative concept is impossibe to the point of foolish. that should be easy.

You keep saying this, as though it proves something, but it just shows why you are ignorant of all science. Only the most inept of scientists would confuse nuclear reactions with chemical reactions.

again, do you think this is a smart thing to say? seems to be the type of semantic dodge that a person with no intellectual foundation would make.

Still not able to run Dr. A's code?
still not able to prove that slow=stop.

kleinman

15th August 2007, 07:15 PM

You've offered nothing, my points still stand.
You are right joobz, I’ve offered nothing but the results of a peer reviewed and published model of random point mutation and natural selection which shows that multiple selection pressures profoundly slow the evolutionary process and a continuous stream of citations which demonstrates this result empirically. And you joobz have offered this;
Envision a system of millions of forming and destructive chemical reactions. Now, envision that intermediates of there reactions associate through non-covalent means and that this complex becomes protected against the destructive reactive pathway, perhaps by a reversible precipitation. These new complexes result in a localized increased of new chemical species. These chemical species then progress in a new series of reaction... that is what I mean through cooperative means. I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?

Here joobz, have another citation which shows that combination selection pressures profoundly slow the evolutionary process. This citation is also for Dr Schneider and the rest of his gang over at the National Cancer Institute. Dr Schneider should step over to the clinical oncology wing of the building; the clinical oncologists will tell him how mutation and selection actually works.
http://www.phrmafoundation.org/research/chabner.pdf (http://www.phrmafoundation.org/research/chabner.pdf)
Ironically, the scenario of evolution of drug resistance has been most elegantly studied for two successful agents, methotrexate (the cytotoxic folate analogue) and imatinib (the highly effective inhibitor of the BCR–ABL tyrosine kinase). In some cases, targeted drugs and conventional antitumour agents can both be affected by a common resistance mechanism involving drug efflux (the MDR transporter)77, or mutations in cell-death pathways. Because of resistance to single agents, combination therapy is essential for tumour eradication and cure. As we have reviewed, even the most successful of the targeted molecules, imatinib, does not fully eradicate the malignant clone. Fortunately, clinical trials have demonstrated potent synergy between targeted molecules, particularly monoclonal antibodies such as rituximab (Rituxan)78, bevacizumab76 and trastuzumab (Herceptin)79, and traditional chemotherapy
Combination therapy slows and can stop the evolution of resistance in cancer cells. Joobz, that is called a cure. You know what that is don’t you? That is extinction of the population of cancer cells.

joobz

15th August 2007, 07:48 PM

You are right joobz, I’ve offered nothing
I agree.

Dr Adequate

15th August 2007, 08:37 PM

If you had been an astute reader you would have seen that the population was posted and it was only 64 creatures ... I am and I did. Now, how does this compare with the population sizes of HIV? Hint: they are much, much larger.

The conversion of mutations per genome to mutation per base has been extensively discussed on the Evolutionisdead thread. Dr Schneider has chosen to use either mutations per genome per generation or mutations per number of bases per generation. Because of Dr Schneider’s choice of method for computing mutation rates, you can only approximate the mutation rate per base. If you think that invalidates ev, take the issue up with Dr Schneider. I don’t believe Dr Schneider’s method of computing mutation rate significantly affects the results of the computation. This gibberish has nothing to do with what I posted. I'll explain it to you one more time, and then I'll put it in the FAQ --- everyone who isn't you will understand how dumb you're being.

If you fix mutations per genome, instead of mutations per base, then every time you double the size of the genome you are halving the mutation rate, which is not what happens in nature.

What part of this don't you understand?

Nothing is screwed up except your understanding of ev. If you want a realistic mutation rate for ev when the mutation rate in 1 mutation per genome per generation, you need a genome length of about 1,000,000. That would give an approximate mutation rate per base of 10^-6. Despite the still unrealistically high mutation rates used in these cases, it still takes almost 7 million generations to evolve the three selection conditions on the 16k genome. If you use an unrealistically low population size, yes.

This was your first cock-up. Remember?

Your other is that you're miscounting the selection pressures, as I've explained to you above.

Adequate, why don’t you tell us what this “something else” that is evolving when you only use one of the three selection conditions in ev? Certainly. If you only apply one selection pressure, then you are evolving something which only satisfies this one selection pressure, rather than something which satisfies all three. These are two different things.

Let me know if there's any part of that you don't understand.

You are now saying “that it takes more time to do more evolution”? That’s not what you said with your silly graph What an incredibly stupid lie. You've posted that graph time and time again --- everyone can see that the number of generations increases monotonically with the number of selection pressures.

Let’s again remind the readers what you said; I don't need your help to show you up as a liar, but feel free.

Everyone can see that my graph shows that more selection pressures take longer.

So tell us Adequate, do more simultaneous selection pressures mean more evolution or less evolution?; More. As do more sequential cumulative selection presures.

Give us a real example ... Example: it takes more evolution to produce a new vertebrate class than a new vertebrate species, and it also takes longer.

More evolution --- more time.

Are you really going to dispute this?

You’ve said you have worked on iteration problems, describe a single example of an iteration problem where the more conditions you have to iterate upon, the more rapid the problem converges. Give us an example of an optimization problem where the more conditions you are trying to optimize, the more rapid the optimization proceeds. Give us an example of a database sorting problem where the more conditions upon which you are sorting, the faster the sort proceeds. Such things do not happen, which is why, of course, I have never claimed that they do.

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

You come here prating about how you're going to teach us about the "mathematics of mutation and selection", and you still need me to explain that more evolution takes more time?

What's the weather like on your planet?

Dr Adequate

15th August 2007, 08:48 PM

You are now saying “that it takes more time to do more evolution”? That’s not what you said with your silly graph. Let’s again remind the readers what you said;
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg This one's definitely going in the FAQ.

If you are genuinely unable to read that graph, I suggest that you sue your primary school.

Dr Adequate

15th August 2007, 09:19 PM

You’ve said you have worked on iteration problems, describe a single example of an iteration problem where the more conditions you have to iterate upon, the more rapid the problem converges. Give us an example of an optimization problem where the more conditions you are trying to optimize, the more rapid the optimization proceeds. Give us an example of a database sorting problem where the more conditions upon which you are sorting, the faster the sort proceeds. Mutation and selection is in the same family of mathematical problems. It is the sorting of beneficial and detrimental mutations. The greater the number of selection conditions, the slower the process proceeds. That is what ev shows and that is what reality shows. Hey, kleinman, will you please read the following passage again until you understand what it is that I've been telling you for what seems like the past zillion years. Pay special attention to the "NOTE FOR COMPLETE MORONS".

Let's see if we can explain it in language that kleinman would understand. Suppose a stupid lunatic thinks he hears a magic sky fairy telling him to gather two of every kind of animal.

Because he's a halfwit, he goes wandering around at random looking for the animals.

Now, consider the following two options:

(1) He collects the animals he stumbles across in strict alphabetical order, starting with aardvarks and working his way along the list. If he happens to see an animal, and it's not the next one on his list, he ignores it.

(2) When he sees an animal, if he hasn't already got a pair, he collects it.

Which method do you think would be faster?

NOTE FOR COMPLETE MORONS, I.E. KLEINMAN: the fact that both methods take longer the more animals there are on the list does not somehow magically mean that the first method is better. If you are still incapable of understanding this, please let me know.

Belz...

16th August 2007, 05:57 AM

A “perfect creature” in the context of ev is simply cute terminology Dr Schneider and Paul use to describe a creature that has adapted to the selection pressures it has been subjected to.

Ah! Therefore it's a misnomer.

Each generation, half the population with the least number of mistakes is allowed to reproduce, the other half dies.

Is that the case in reality, or just in the simulation ?

Because things are rarely that simple.

The ev simulation is a very good mathematical analogy of the mutation and selection process.

Analogy ? I thought you said it was a perfect representation that proved evolution to be impossible ?

What ev is revealing is how difficult it becomes for a population to navigate the fitness landscape when there are multiple selection conditions.

Only when only point mutations are considered...

These real cases I have been posting are not limited to random point mutations.

No but the simulation is.

This isn’t my fantasy, this is Dr Schneider’s peer reviewed and published model of random point mutation and natural selection which shows these results. And what it shows is that multiple simultaneous selection pressures profoundly slow the evolutionary process in his model.

Bolding mine. Thanks.

The empirical data confirms this result and that is why the theory of evolution is mathematically impossible by mutation and selection.

Actually, that's a lie, because we've seen examples in this thread that show this claim to be false.

Mutation and selection can not and does not work the way you evolutionarians allege.

I don't claim anything, and I'm not an "evolutionarian", whatever the hell that means.

Belz...

16th August 2007, 06:00 AM

Not really. Are you familiar with the acronym "GIGO"?

Nope.

Is there some sort of Guinness record for the use of the laughing dog ? I think Klein wins.

joobz

16th August 2007, 08:16 AM

Analogy ? I thought you said it was a perfect representation that proved evolution to be impossible ?

that's Kleinman's elastic definition policy.
Stretch a definition to fill the seive like holes in his theory.
So far we have
Slow=stop
analogy=perfect model
point mutation = all mutations
decreasing model mutation rate = realistic mutation rate
Nuclear reaction = chemical reaction
1st Law of Thermo = Natural Selection
running someone elses simulation = doing maths
observed recorded evolution = microevolution

joobz

16th August 2007, 08:24 AM

Nope.
GIGO= Garbage in, garbage out.

Is there some sort of Guinness record for the use of the laughing dog ? I think Klein wins.Yeah, but seeing it so often, I've built up an immunity to it. You'd think he'd switch to using at least 2 or three images to prevent such adaptations.

cyborg

16th August 2007, 08:26 AM

joobz, kleinman doesn't believe in evolution remember?

kleinman

16th August 2007, 09:42 AM

You are right joobz, I’ve offered nothingI agree.
Joobz attempts to use a sentence fragment but let’s show joobz why his speculation is so foolish. This is joobz’s vision on how abiogenesis occurs.
Envision a system of millions of forming and destructive chemical reactions. Now, envision that intermediates of there reactions associate through non-covalent means and that this complex becomes protected against the destructive reactive pathway, perhaps by a reversible precipitation. These new complexes result in a localized increased of new chemical species. These chemical species then progress in a new series of reaction... that is what I mean through cooperative means. I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?
really, then tell me how i'm wrong. if it is foolshness, then give specific reasons why you state that my admittedly speculative concept is impossibe to the point of foolish. that should be easy.
Your admittedly speculative concept is impossible to the point of foolish because you can’t describe how one of the basic components of life (ribose) can form nonenzymatically despite having virtually unlimited free energy. Do you want to go down the entire list of basic chemicals that are commonly found in living things that you can not describe how could form nonenzymatically despite having virtually unlimited energy? That would make this thread profoundly long. Joobz, that is why your admitted speculation is impossible to the point of foolishness. I’ll tell what joobz, for the sake of brevity, why don’t you describe which basic molecules essential for life easily form nonenzymatically simply because the free energy is available. That will make your discussion of this topic pleasantly short.
If you had been an astute reader you would have seen that the population was posted and it was only 64 creatures ...I am and I did. Now, how does this compare with the population sizes of HIV? Hint: they are much, much larger.
It is miniscule Adequate but once again you have missed the point. Despite this tiny population in ev, each of the individual selection pressures when applied singly rapidly evolve despite this tiny population. Increasing the genome length does not affect convergence of the individual selection pressures in ev. This exact same behavior is seen in HIV. Monotherapy leads to a striking reduction in the HIV population for a week or two but even this suppressed population can quickly evolve to the single selection pressure. Use combination therapy on a suppressed population of HIV viruses and you can inhibit reproduction of the virus for years. If you weren’t so incompetent in the mathematics of mutation and selection you would understand this.
The conversion of mutations per genome to mutation per base has been extensively discussed on the Evolutionisdead thread. Dr Schneider has chosen to use either mutations per genome per generation or mutations per number of bases per generation. Because of Dr Schneider’s choice of method for computing mutation rates, you can only approximate the mutation rate per base. If you think that invalidates ev, take the issue up with Dr Schneider. I don’t believe Dr Schneider’s method of computing mutation rate significantly affects the results of the computation.This gibberish has nothing to do with what I posted. I'll explain it to you one more time, and then I'll put it in the FAQ --- everyone who isn't you will understand how dumb you're being.
Adequate, I don’t care what you put in your FAQ. You are the master of gibberish, let’s remind the readers of your gibberish.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
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.
http://forums.randi.org/images/smilies/doglaugh.gif
Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?
You have only one FAQ and you have no answer for your dumb graph.
If you fix mutations per genome, instead of mutations per base, then every time you double the size of the genome you are halving the mutation rate, which is not what happens in nature.

What part of this don't you understand?
Adequate, you are so slow on this topic. Of course I know that if you use a fixed mutation rate per genome that every time you double the genome length you halve the mutation rate but again you missed the point. Doubling the genome length had a marked affect on evolving all three selection conditions simultaneously but had virtually no affect on evolving the selection conditions when applied singly despite that genome length was doubled and mutation rate was halved. You still can’t see that the number of selection conditions is by far the most dominant parameter in the ev computer simulation. This same affect is seen over and over again in the empirical evidence. Mutation and selection is an optimization problem where the number of optimization conditions dominates the mathematics of this problem. You have a PhD in mathematics yet you still can not recognize this. You have a major blind spot in your understanding of how the mathematics of mutation and selection actually works.
Nothing is screwed up except your understanding of ev. If you want a realistic mutation rate for ev when the mutation rate in 1 mutation per genome per generation, you need a genome length of about 1,000,000. That would give an approximate mutation rate per base of 10^-6. Despite the still unrealistically high mutation rates used in these cases, it still takes almost 7 million generations to evolve the three selection conditions on the 16k genome.If you use an unrealistically low population size, yes.

This was your first cock-up. Remember?

Your other is that you're miscounting the selection pressures, as I've explained to you above.
To the censors on this thread, you let Adequate say cock-up but you censor me what I use the term pussycat? You have strange standards. Now back to Adequate’s misunderstanding of the mathematics of mutation and selection.

Despite the unrealistically low population size in ev, it easily evolves the selection conditions when applied singly. It is only when the selection conditions are applied simultaneously that this tiny population takes profoundly longer to do the optimization.

Now Adequate, the master of ev who has not posted a single case from the model is now claiming that I am miscounting selection pressures. My suggestion to Adequate is that he start Paul’s ev program, go to the advanced features screen and you will find that there are weight factors for the three different selection conditions and each of the selection conditions are different. Adequate, why don’t you tell us how many selection conditions there are in ev and then I’ll explain to you why the three selection conditions each have unique properties?
Adequate, why don’t you tell us what this “something else” that is evolving when you only use one of the three selection conditions in ev?Certainly. If you only apply one selection pressure, then you are evolving something which only satisfies this one selection pressure, rather than something which satisfies all three. These are two different things.

Let me know if there's any part of that you don't understand.
Why Adequate, you are correct. That like saying that if you suppress HIV with a reverse transcriptase inhibitor you wouldn’t expect changes in the proteases and visa versa. So in ev, if you select singly for sequences of bases that don’t have spurious binding in the nonbinding site region of the genome, you wouldn’t expect binding sites to evolve and visa versa. However, both the ev model and treatment of HIV exhibit the same behavior. If you try to evolve all three selection conditions in ev simultaneously, the evolutionary process is profoundly slowed and if you treat HIV with effective three combination therapy, the evolution of the virus is profoundly slowed. That’s how mutation and selection actually works Adequate, its and optimization problem.
You are now saying “that it takes more time to do more evolution”? That’s not what you said with your silly graphWhat an incredibly stupid lie. You've posted that graph time and time again --- everyone can see that the number of generations increases monotonically with the number of selection pressures.
Every time you say this Adequate, I’m going to shove your incredibly stupid graph right back into your face with your incredibly stupid claim, so here it is again.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
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.
http://forums.randi.org/images/smilies/doglaugh.gif
Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?
You can not squirm out of your incredibly stupid claim.
So tell us Adequate, do more simultaneous selection pressures mean more evolution or less evolution?;More. As do more sequential cumulative selection presures.
Adequate, you are slow on this topic of the mathematics of mutation and selection but you are starting to get the point. Populations (even small populations) can more easily evolve to single selection pressures when applied sequentially but apply the pressures simultaneously and the population has a far more difficult time evolving to these simultaneous selection pressures. That is what ev shows and that is what the vast amount of empirical data for mutation and selection shows.
Give us a real example ... Example: it takes more evolution to produce a new vertebrate class than a new vertebrate species, and it also takes longer.

More evolution --- more time.

Are you really going to dispute this?
Adequate, this vague answer reveals that you have no examples for your incredibly stupid graph.
You’ve said you have worked on iteration problems, describe a single example of an iteration problem where the more conditions you have to iterate upon, the more rapid the problem converges. Give us an example of an optimization problem where the more conditions you are trying to optimize, the more rapid the optimization proceeds. Give us an example of a database sorting problem where the more conditions upon which you are sorting, the faster the sort proceeds.Such things do not happen, which is why, of course, I have never claimed that they do.

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

You come here prating about how you're going to teach us about the "mathematics of mutation and selection", and you still need me to explain that more evolution takes more time?

What's the weather like on your planet?
Adequate, you are trying to squirm out of your incredibly stupid claim for your incredibly stupid graph. Let’s post it again so we can see exactly what you said.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
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.
http://forums.randi.org/images/smilies/doglaugh.gif
Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?
So you are contradicting yourself. You said above “More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.”, then you claim in your discussion about your graph, “Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.”

Unless you claim that increasing the rate of something means that it will take more time for the event, you have directly contradicted yourself.
This one's definitely going in the FAQ.

If you are genuinely unable to read that graph, I suggest that you sue your primary school.
Why would I want to sue my primary school, they did an excellent job teaching me how to read, write and do arithmetic. I also learned how to deal with the school bully out on the playground.
A “perfect creature” in the context of ev is simply cute terminology Dr Schneider and Paul use to describe a creature that has adapted to the selection pressures it has been subjected to.Ah! Therefore it's a misnomer.
Take that one up with Paul and Dr Schneider, I would not have used that terminology.
Each generation, half the population with the least number of mistakes is allowed to reproduce, the other half dies.Is that the case in reality, or just in the simulation ?

Because things are rarely that simple.
Ev is an idealized computer simulation of random point mutation and natural selection. Dr Schneider uses a contrived selection process in order to formulate his model mathematically. It does not evolve any real sequences of bases that would give functional proteins. However what it does properly demonstrate is the mathematics of the mutation and selection optimization problem. Dr Schneider has done an effective defense of this issue of killing off half the population in his selection process and I tend to agree with him on this point. This selection process does not allow for extinction or modeling for more or less intense selection pressures which might kill off more or less than half the population. What Dr Schneider’s model allows you to do is get into the ball park of the mutation and selection process. What the model shows is how difficult it is to optimize multiple selection conditions even when extinction of the population is not possible. It clear demonstrates how easy it is to evolve single selection pressures. The question you should ask is this finding reflected in reality? The answer to this question is yes, there is a vast amount of empirical data which shows this is exactly how mutation and selection actually works. Mutation and selection is a far more limited process than what evolutionarians allege.
The ev simulation is a very good mathematical analogy of the mutation and selection process.Analogy ? I thought you said it was a perfect representation that proved evolution to be impossible ?
If you had read this thread, you would see that I have always described ev as a plausible representation of the mutation and selection process or I have described ev as an idealized model of the mutation and selection process. I don’t know of anyone who said that ev is a perfect representation of mutation and selection. Even Dr Schneider and Paul have only gone so far as to describe ev as representing reality. I agree with this view insofar that the ev model shows how difficult it is to evolve simultaneous selection pressures on all but unrealistically short genomes.
What ev is revealing is how difficult it becomes for a population to navigate the fitness landscape when there are multiple selection conditions.Only when only point mutations are considered...
This argument comes up over and over on this thread. If you think other forms of mutations or recombination will accelerate evolution in ev, put it in the model and prove your point. I have chosen to counter this argument by posting citations of real examples of mutations and selection which are not limited to random point mutations which all show that combination selection pressures profoundly slow the evolutionary process. Mutation and selection is an optimization process. The more optimization conditions that a population faces, the more difficult it is for the population to optimize to these conditions despite the mutations available or recombination. This is the mathematical and empirical fact that you evolutionarians have to come to grips with.
These real cases I have been posting are not limited to random point mutations.No but the simulation is.
Even this limited ev simulation demonstrates what the dominant parameter of the mutation and selection process is. That parameter is the number of selection conditions and that parameter far outweighs the effect of all other parameters in the model.
The empirical data confirms this result and that is why the theory of evolution is mathematically impossible by mutation and selection.Actually, that's a lie, because we've seen examples in this thread that show this claim to be false.
Now Belz, I have reposted data from ev for you, now you repost those examples which you claim show my hypothesis false. The only counter examples posted are Kotatsu’s which don’t describe accurately the selection pressures and target genes and none of Kotatsu’s examples are repeatable. On the other hand all the examples I have posted precisely define the selection pressures and target genes and many of these cases describe the exact loci where mutations occur and these results have been repeated numerous times by numerous scientists. It is your theory of evolution which is the lie.
Mutation and selection can not and does not work the way you evolutionarians allege.I don't claim anything, and I'm not an "evolutionarian", whatever the hell that means.
An evolutionarian is someone who puts his faith in evolutionism.
Not really. Are you familiar with the acronym "GIGO"?Nope.

Is there some sort of Guinness record for the use of the laughing dog ? I think Klein wins.
The laughing dog is the only way I can respond to incredibly stupid claims in this forum; I get censored if I describe anyone as being mathematically challenged. It reveals the hypocrisy of the moderators on this forum. It is all right to make blanket statements that creationists are not scientists. It gives me all the more joy to annoy you evolutionarians with the mathematical and empirical facts of how mutation and selection actually works. Here is another example of how this phenomenon actually works and it is not like the way you evolutionarians allege.

http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowFulltext&ArtikelNr=107110&Ausgabe=233711&ProduktNr=223857 (http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowFulltext&ArtikelNr=107110&Ausgabe=233711&ProduktNr=223857)
Purpose: We investigated whether a 5-fluorouracil (5-FU)-resistant tumor could regain chemosensitivity after the administration of 5-aza-2'-deoxycytidine (DAC) as a demethylating agent. Methods: Human colorectal cancer cells (SW48) are characterized by the hypermethylation of proapoptotic genes. They were transplanted into 20 athymic BALB/c nu/nu mice which were randomly placed into 4 groups (1 = control; 2 = 5-FU alone; 3 = DAC alone; 4 = DAC followed by 5-FU). We evaluated the synergistic effect of DAC and 5-FU on the growth of these xenografts. Reactivation of proapoptotic genes in these cells was analyzed by methylation-specific PCR. Gene expression was determined by a quantitative reverse-transcription PCR assay. Results: Compared with the control group, relative tumor volumes were statistically significantly decreased only in group 4 mice (p = 0.006). In groups 3 and 4, p14, p16 and death-associated protein kinase (DAPK) promoter regions were demethylated and p14 gene expression was gradually increased after DAC administration. Conclusion: DAC could be a useful medicine that breaks the silencing of various genes and recovers some expressions. By pretreating with DAC at a nontoxic level, we confirmed the restoration of 5-FU chemosensitivity and apoptosis induction. The combination of demethylating agents and several cytotoxic drugs has potential in clinical practice.

Belz...

16th August 2007, 10:13 AM

Ev is an idealized computer simulation of random point mutation and natural selection.

Idealised. Good. You're getting closer to admitting that it isn't a very good model, after all.

I don’t know of anyone who said that ev is a perfect representation of mutation and selection.

You implied it, because you said it PROVED that evolution is impossible.

If you think other forms of mutations or recombination will accelerate evolution in ev, put it in the model and prove your point.

Huh ? You think that ADDITIONAL means of mutation will not help accelerate the rate of change ?

This is the mathematical and empirical fact that you evolutionarians have to come to grips with.

I have no idea what an "evolutionarian" is, but I can tell a christian fanatic when I see one.

Now Belz, I have reposted data from ev for you, now you repost those examples which you claim show my hypothesis false.

Contrary to me, you've been around since before those examples were posted. Frankly, I've enough of reposting stuff that people ignore in the CT forum to waste my time doing the same with you.

It is your theory of evolution which is the lie.

For the sake of argument, why do all biologists in the world stick to evolution if it's so obviously a lie ? What's the benefit of continuing to work based on something that's false ?

An evolutionarian is someone who puts his faith in evolutionism.

Ah! Good. Then evolutionarians either do not exist or are few and far between in this forum, because like with the rest of science, FAITH HAS NOTHING TO DO WITH IT.

The laughing dog is the only way I can respond to incredibly stupid claims in this forum

No, all it proves is that you DON'T have an answer outside of your programmed mantra.

I get censored if I describe anyone as being mathematically challenged.

That's what you get when your primary form of argument is insults. You should've learned that in elementary school.

As for your "mathematically challenged", we've already seen the level of mathematics you display.

It is all right to make blanket statements that creationists are not scientists.

Indeed it is, because creationism flies in the face of everything we know. Day and night did NOT appear before the sun did, for sure.

It gives me all the more joy to annoy you evolutionarians with the mathematical and empirical facts of how mutation and selection actually works.

The only thing that's annoying with you is your lack of grasp on reality.

Paul C. Anagnostopoulos

16th August 2007, 11:03 AM

Ah! Therefore it's a misnomer.
The term perfect creature was invented before Evj would let you enable and disable selection pressures. It referred to the fact that the creature could perfectly distinguish binding sites from other positions on the chromosome. It is, now, a misnomer.

Dr Schneider and Paul still don’t understand why the model takes such huge number of generations to converge with all but the smallest genomes. The explanation is very simple; it is the multiple simultaneous selection conditions. Simply set the number of selection conditions to one and that single selection condition will evolve in a very small number of generations. This is a fundamental observation seen in any optimization, sorting or iteration problem. Reduce down the number of selection (optimization, sorting or iteration conditions) and the remaining condition is much more rapidly converged upon. This situation becomes much more apparent when the search space becomes massive as seen in large genome life forms.
This is another lie. Of course it takes longer to evolve a creature with zero mistakes when there are three pressures instead of one. My point, all along, is that these two scenarios cannot be compared because different functions are being evolved. The question of "speed of evolution" makes no sense.

Adequate, why don’t you tell us how many selection conditions there are in ev and then I’ll explain to you why the three selection conditions each have unique properties?
But there is nothing special about three selection conditions. We could have had two or four just as easily.

Back to the beach ...

~~ Paul

joobz

16th August 2007, 11:19 AM

Joobz attempts to use a sentence fragment but let’s show joobz why his speculation is so foolish.
I was simply editing your comments down to the truth.

This is joobz’s vision on how abiogenesis occurs.
[/color]
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?
Again,
nuclear reactions are not chemical reactions. Repeating this phrase makes you look like an imbicile. for your own sake, I suggest you stop it. Unless, of course, you want to look like an imbicile. Then, by all means, carry on.

Your admittedly speculative concept is impossible to the point of foolish because you can’t describe how one of the basic components of life (ribose) can form nonenzymatically despite having virtually unlimited free energy. Hmmm, seems that has already been addressed in the literature.

Sugar synthesis from a gas-phase formose reaction.
Astrobiology. 2007 Jul;7(3):433-42.

Formation of a beta-Pyrimidine Nucleoside by a Free Pyrimidine Base and Ribose in a Plausible Prebiotic Reaction.
J Am Chem Soc. 2007 Aug 8;129(31):9556-9557.

On the Prebiotic Synthesis of Ribonucleotides: Photoanomerisation of Cytosine Nucleosides and Nucleotides Revisited.
Chembiochem. 2007 Jul 9;8(10):1170-1179.

A possible path to the RNA world: enantioselective and diastereoselective purification of ribose.
Orig Life Evol Biosph. 2007 Apr;37(2):167-75. Epub 2006

Prebiotic carbohydrate synthesis: zinc-proline catalyzes direct aqueous aldol reactions of alpha-hydroxy aldehydes and ketones.
Org Biomol Chem. 2005

Do you want to go down the entire list of basic chemicals that are commonly found in living things that you can not describe how could form nonenzymatically despite having virtually unlimited energy? yes, I would love to see the list. I'm sure we can find research being done on all those areas. And if we can't, you've just given people a research area to delve into. It is a very interesting topic.

That would make this thread profoundly long. Joobz, that is why your admitted speculation is impossible to the point of foolishness.
Your repetitious lies and nonsense have made the thread long. Your elastic definitions have exposed your complete lack of rational thought. Your inability to compile a program has shown your inability to even run simulations, let along do math.

If there is something foolish here, it isn't anything I've offered up.

:words:...gibberish.:words:... dumb graph.:words:
number of selection conditions :words:cock-up :words: pussycat? :words:
So, when do you plan on offering this mathematical proof against evolution we keep hearing about? We've been waiting for over a year now.

kleinman

16th August 2007, 01:29 PM

Ev is an idealized computer simulation of random point mutation and natural selection.Idealised. Good. You're getting closer to admitting that it isn't a very good model, after all.
Far from it Belz, I agree with Dr Schneider that it is a good model and I can show that it properly models the affect of multiple selection pressures. In addition, the model properly simulates how population affects the evolutionary process, how genome length affects the evolutionary process and how mutation rate affects the evolutionary process. I also understand the limitations of the model, for example, ev does not allow for extinction. If you don’t think ev is a very good model, perhaps you should contact the peer reviewers at Nucleic Acids Research and tell them your opinion.
I don’t know of anyone who said that ev is a perfect representation of mutation and selection.You implied it, because you said it PROVED that evolution is impossible.
Ev doesn’t have to be a perfect representation of mutation and selection in order to prove that the theory of evolution is mathematically impossible. Since you have no experience with computer simulations, you probably not aware that no computer simulation is a perfect representation of the real system it models. I would never say or imply that any computer simulation is a perfect representation of the system it models. What ev does properly model is the affect of multiple simultaneous selection pressures on the rate of evolution. It profoundly slows this optimization problem and this is demonstrated over and over in the empirical data of mutation and selection.
If you think other forms of mutations or recombination will accelerate evolution in ev, put it in the model and prove your point.Huh ? You think that ADDITIONAL means of mutation will not help accelerate the rate of change ?
The empirical data say that other mechanisms of mutation and recombination do not overcome the affect of multiple selection pressures. The dominant parameter by far in the mutation and selection optimization problem is the number of selection pressures.
This is the mathematical and empirical fact that you evolutionarians have to come to grips with.I have no idea what an "evolutionarian" is, but I can tell a christian fanatic when I see one.
An evolutionarian is a devotee to evolutionism which is a belief system that is mathematically impossible. I happen to be a Christian fanatic who understands the mathematics of mutation and selection and it proves the evolutionarian belief system to be mathematically impossible.
Now Belz, I have reposted data from ev for you, now you repost those examples which you claim show my hypothesis false.Contrary to me, you've been around since before those examples were posted. Frankly, I've enough of reposting stuff that people ignore in the CT forum to waste my time doing the same with you.
So aren’t you the hypocrite.
Ah! Therefore it's a misnomer.The term perfect creature was invented before Evj would let you enable and disable selection pressures. It referred to the fact that the creature could perfectly distinguish binding sites from other positions on the chromosome. It is, now, a misnomer.
It has always been a misnomer that causes confusion. Before you put the enable and disable selection pressure feature in the program, the perfect creature was simply a genome which had evolved to all three selection pressures with no more mistakes. Now that you can enable and disable selection pressures, you can evolve genomes to single selection pressures and ev shows how much more rapidly ev will evolve to single selection pressures than three selection pressures.
Dr Schneider and Paul still don’t understand why the model takes such huge number of generations to converge with all but the smallest genomes. The explanation is very simple; it is the multiple simultaneous selection conditions. Simply set the number of selection conditions to one and that single selection condition will evolve in a very small number of generations. This is a fundamental observation seen in any optimization, sorting or iteration problem. Reduce down the number of selection (optimization, sorting or iteration conditions) and the remaining condition is much more rapidly converged upon. This situation becomes much more apparent when the search space becomes massive as seen in large genome life forms.This is another lie. Of course it takes longer to evolve a creature with zero mistakes when there are three pressures instead of one. My point, all along, is that these two scenarios cannot be compared because different functions are being evolved. The question of "speed of evolution" makes no sense.
Why Mr RcaPaulcity, it takes 10 of thousands of times more generations to evolve all three selection conditions than any one of the selection conditions alone and that is on only a 16k genome. You don’t want to compare the two scenarios because this proves why your theory of evolution is mathematically impossible. The problem for you evolutionarians is that there is a vast amount of empirical data which shows this is exactly how mutation and selection works. You keep trying to squirm out of this mathematical and empirical fact by claiming different functions are being evolved. There are three possible conditions in your model which can be evolved. Binding sites can be evolved where they are expected to be found, spurious binding can be eliminated from the gene and spurious binding can be eliminated outside the binding site. Applying only a single selection condition will still evolve any one of these three conditions very rapidly, even on longer genomes. You are trying to squirm out of this mathematical fact by arguing that there is some different function. You are simply evolving one of the three conditions in the model independently of the other conditions. There is no difference in the function for that selection condition.
Adequate, why don’t you tell us how many selection conditions there are in ev and then I’ll explain to you why the three selection conditions each have unique properties?But there is nothing special about three selection conditions. We could have had two or four just as easily.
Really, why don’t you tell us what those two or four selections are? Then I’ll tell you why three selection conditions are the correct number for your model.
Back to the beach ...
Paul, when you see the sun over the water, do you marvel at how wonderful the primordial soup was?
Joobz, if the sun shines on lead long enough does it turn into gold?Again,
nuclear reactions are not chemical reactions. Repeating this phrase makes you look like an imbicile. for your own sake, I suggest you stop it. Unless, of course, you want to look like an imbicile. Then, by all means, carry on.
Oh, I see joobz; there is not enough free energy for nuclear reactions to occur.
http://forums.randi.org/images/smilies/doglaugh.gif
Your admittedly speculative concept is impossible to the point of foolish because you can’t describe how one of the basic components of life (ribose) can form nonenzymatically despite having virtually unlimited free energy.Hmmm, seems that has already been addressed in the literature.
Oh, I see you don’t know how ribose forms nonenzymatically but somebody else does. Put it in words for us so we can all have a big laugh.
http://forums.randi.org/images/smilies/doglaugh.gif

joobz

16th August 2007, 02:02 PM

kleinman

16th August 2007, 02:18 PM

Oh, I see joobz; there is not enough free energy for nuclear reactions to occur.
Well, of course I'm not saying that. That's a lie you just made up and a rather studpid one. It would imply that nuclear reactions never occur. Since we know that nuclear reaction do occur, this statement is entirely dumb.

It would be almost as stupid as saying chemical and nuclear reactions are equivilent.
You said that if you had enough free energy any chemical reaction is possible; here is what you said;
Envision a system of millions of forming and destructive chemical reactions. Now, envision that intermediates of there reactions associate through non-covalent means and that this complex becomes protected against the destructive reactive pathway, perhaps by a reversible precipitation. These new complexes result in a localized increased of new chemical species. These chemical species then progress in a new series of reaction... that is what I mean through cooperative means. I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.
http://forums.randi.org/images/smilies/doglaugh.gif
So if you have enough free energy any chemical reaction is possible, but not any nuclear reaction is not possible? How could that be? Lead exists, gold exists, they are both made of protons, electrons and neutrons, then one must have evolved from the other, all you need is enough free energy.
Joobz, if the sun shines on lead long enough does it turn into gold?
http://forums.randi.org/images/smilies/doglaugh.gif

joobz

16th August 2007, 02:53 PM

kleinman

16th August 2007, 03:28 PM

You said that if you had enough free energy any chemical reaction is possible; here is what you said;
No, I said As long as there was enough free energy for these reaction[s] to occur.This sentence is not the same as your dumb statement. Do you understand the difference?
Sure I understand what you are saying. You are speculating that all it takes is enough free energy and life spontaneously occurs.
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?Do you really want to keep repeating this most retardly stupid reasoning?
No, I’d rather repeat you simple minded speculation of abiogenesis. Here it is again.
Envision a system of millions of forming and destructive chemical reactions. Now, envision that intermediates of there reactions associate through non-covalent means and that this complex becomes protected against the destructive reactive pathway, perhaps by a reversible precipitation. These new complexes result in a localized increased of new chemical species. These chemical species then progress in a new series of reaction... that is what I mean through cooperative means. I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.
http://forums.randi.org/images/smilies/doglaugh.gif
Oh, why not, joobz here is your FAQ, if the sun shines on lead long enough does it turn into gold?
http://forums.randi.org/images/smilies/doglaugh.gif
I find it very amusing that you compare the nuclear transition of one stable element to another to simple organic chemistry. I'm hoping you keep making this utterly moronic claim. It's Definitely FAQ worthy.
Now joobz thinks that life consists of simple organic chemistry.
http://forums.randi.org/images/smilies/doglaugh.gif

Paul C. Anagnostopoulos

16th August 2007, 04:03 PM

joobz

16th August 2007, 04:27 PM

[snip nonsense]
It is blindingly obvious that none of your statements reflects my views.

However, allow me to explain to others why I find your childish confusion of nuclear and chemical reactions to be....moronic.

Chemical reactions involve the changing of electron orbitals. The sharing seperation of these electrons are what we mean by a chemical reaction. A nuclear reaction involves variation in the nucleus.

Chemical reactions do not result in a change in mass. Also, there is no change in elements present (If you start with 5 oxygens atoms, you'll end with 5 oxygen atoms). Nuclear reactions have a measurable mass change and can result in a change in element content.

Chemical reactions are insensitive to the isotope, Nuclear reactions aren't.

Nuclear reactions result in HUGE amounts of energy change (release or absorbed depending on the reaction). This can be easily 10-100 GigaJoules/mole. Chemical reactions are typically on the order of 1-100 kJ/mole. One of Kleinman's biggest errors.

Chemical reactions are dependant upon the combination of chemicals present, nuclear reactions aren't.

Nuclear reactions can occur spontaneously (low activation energy, think radioactive decay). However, stable isotopes have huge activation energies. This is probably the most laughable aspect of Kleinman's confusion. The conversion of lead to gold would require ENORMOUS energies (due to the energy of nuclear formations required. The closest thing to an actual conversion of lead (actually bismuth) to gold required accellerated carbon12 with a minimum energy of 4.8GeV. This translates (forgive me, nuclear physicists for this crude comparison but...) into a relative 460 Terajoules/Mole used to convert bizmuth to gold (and only in small quantities). or about 1 billion times more energy than your standard chemical reaction.

http://prola.aps.org/abstract/PRC/v23/i3/p1044_1

kleinman

16th August 2007, 04:34 PM

Why Mr RcaPaulcity, it takes 10 of thousands of times more generations to evolve all three selection conditions than any one of the selection conditions alone and that is on only a 16k genome. You don’t want to compare the two scenarios because this proves why your theory of evolution is mathematically impossible.But Alan, a completely different sort of transcription factor is being evolved in the two cases. Surely you can't be suggesting that comparing the "speed of evolution" of these two cases is meaningful? Looking at it another way: Surely you can't be suggesting that it is meaningful to compare two functions with different Rfrequencies?
So what if there is a completely different “transcription factor”? Simply changing the random seed gives different transcription factors. You have previously said that there is more than one perfect creature. Surely I do suggest that comparing the speed of evolution of single selection conditions with multiple selection conditions a valid comparison because that is how mutation and selection actually works. None of the “transcription factors” evolved by ev represents real sequences or proteins. They are simply sequences that evolve to match the selection criteria imposed by the weight matrix.
Really, why don’t you tell us what those two or four selections are? Then I’ll tell you why three selection conditions are the correct number for your model.We could have had only two mistake point controls: missed binding sites and spurious bindings. Or we could have had four: missing binding sites, spurious bindings within the weight matrix, spurious bindings in the threshold, and spurious bindings outside the gene. In fact, we could have had five: missed binding sites, spurious bindings within the weight matrix, spurious bindings in the threshold, spurious bindings in the binding sites but not at the beginning, and spurious bindings elsewhere.
There is a difference between spurious binding outside the gene and in the gene. The gene determines the weight matrix while spurious binding outside the gene has no effect on the weight matrix. Why don’t you try ev with the four or five selection conditions you suggest above and see what it does to the rate of convergence of the model. What do think will happen? Do you think more selection conditions will speed up or slow down the rate of information acquisition?

That’s enough playing with joobz and Paul for one day. Again, for you evolutionarians who graduated from Mathishard University, mutation and selection is simply an optimization or sorting problem. As in all problems of this type, the number conditions upon which you optimize or sort dominates the rate at which you can accomplish such a sort or optimization. This effect is plainly seen in Dr Schneider’s peer reviewed and published model of random point mutations and natural selection. His model has three selection conditions and will only rapidly converge these three conditions on unrealistically short genomes. However if you turn off any two of the three selection conditions, the third condition rapidly converges even on longer genomes. This effect is seen in a huge number of empirical examples including the evolution of resistance in cancer cells. It is interesting that Dr Schneider is not aware of this fact since Dr Schneider works at the National Cancer Institute. I guess Dr Schneider is too busy to talk with the clinical oncologists at the National Cancer Institute because if he did, he would understand this fundamental principle of the mutation and selection process. Dr Schneider would then understand why his model takes huge numbers of generations to converge on all but the unrealistically smallest genomes.

So, here is another empirical example which shows that combination selection pressures profoundly slow the evolutionary process.
http://www.pngimr.org.pg/Editorial%20-%20%20Mar-June%202001.pdf (http://www.pngimr.org.pg/Editorial%20-%20%20Mar-June%202001.pdf)
Combination therapy is well established for the treatment of many illnesses such as HIV infection (6), tuberculosis and other bacterial infections (7), and leukaemia (8). To gain resistance to a drug combination, an organism must simultaneously develop multiple mutations (assuming the drugs have different modes of action). If these mutations arise independently, then the probability of a double mutation arising is the product of the individual probabilities. For example, if a resistance mutation for each of the two drugs arises once per billion divisions, then the double mutation arises once per billion billion. By contrast, if one drug is used alone until resistance develops and is then replaced by the second drug (ie, a policy of drug cycling) then only one billion divisions would be needed for resistance to arise to the first drug, and then only one billion more for resistance to the second drug. In this scenario, the singly-resistant parasites would initially be rare, which would increase the time needed for them to generate the second billion divisions, but nevertheless the overall time to achieve double resistance would in theory be less. Mathematical models (9-12) predict that, under a variety of conditions, a policy of combination therapy is generally better — in terms of delaying drug resistance — than other policies such as cycling of single drugs. This applies to the spread of preexisting mutations, as well as those arising de novo. The only predicted exception occurs when multiple antibiotic resistance mutations are carried on the same plasmid (13), which should not be relevant for Plasmodium. Another benefit of combination therapy can be expected on pharmacological grounds. The combination increases the rate of reduction of the parasites, so the infection is brought under control while the drug concentrations are still relatively high. This reduces the opportunity for selection of resistance, since it exposes parasites to sublethal drug concentrations for a shorter time(14).
Again, empirical evidence shows that single sequential selection pressures cumulatively evolve far more rapidly than simultaneous selection pressures. That is how mutation and selection works in reality.

Now you all have a good weekend and I will be back next week to post more citations which show how mutation and selection actually works and discuss with joobz his thesis for abiogenesis that with enough free energy any chemical reaction is possible but not any nuclear is possible and joobz contention that life is composed of simple organic molecules. I guess alchemical engineers do not get beyond organic chemistry in their training. Joobz, did you ever hear of biochemistry?
http://forums.randi.org/images/smilies/doglaugh.gif

joobz

16th August 2007, 04:39 PM

Now you all have a good weekend and I will be back next week to post more citations which show how mutation and selection actually works and discuss with joobz his thesis for abiogenesis that with enough free energy any chemical reaction is possible but not any nuclear is possible and joobz contention that life is composed of simple organic molecules. I guess alchemical engineers do not get beyond organic chemistry in their training. Joobz, did you ever hear of biochemistry?
http://forums.randi.org/images/smilies/doglaugh.gif
We were discussing Prebiotic formation of nucleic acids. That means a non-biochemical route. Duh.

Paul C. Anagnostopoulos

16th August 2007, 05:36 PM

So what if there is a completely different “transcription factor”? Simply changing the random seed gives different transcription factors.
Oh for crying out loud. Obviously I meant that the transcription factors perform different functions, not that the chromosome base sequences are different.

None of the “transcription factors” evolved by ev represents real sequences or proteins.
Then why does Ev prove mathematically that evolution is impossible?

There is a difference between spurious binding outside the gene and in the gene. The gene determines the weight matrix while spurious binding outside the gene has no effect on the weight matrix. Why don’t you try ev with the four or five selection conditions you suggest above and see what it does to the rate of convergence of the model. What do think will happen? Do you think more selection conditions will speed up or slow down the rate of information acquisition?
Of course spurious bindings outside the gene affect the weight matrix: They have to be eliminated in order to produce a perfect creature.

I don't think the number of selection conditions matters much. You were the one stating that you would "tell [me] why three selection conditions are the correct number for your model."

~~ Paul

Dr Adequate

16th August 2007, 10:08 PM

Adequate, you are trying to squirm out of your incredibly stupid claim for your incredibly stupid graph. Let’s post it again so we can see exactly what you said.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg

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

So you are contradicting yourself. You said above “More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.”, then you claim in your discussion about your graph, “Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.” This is also going in the FAQ.

It is so going in the FAQ.

That is so funny.

And you don't know why, do you?

At what age did you stop studying mathematics?

Did you make it to double figures?

If you really don't know how to divide one number by another, then I suggest that you sue either:

(1) Your primary school --- for negligence.

(2) Your kindergarten --- for letting you eat lead paint.

(3) Your midwife --- for dropping you on your head.

(4) Your parents --- for breeding.

Dr Adequate

16th August 2007, 10:18 PM

Now joobz thinks that life consists of simple organic chemistry. If anyone except kleinman had told this stupid lie, I'd think it strange that anyone should be so stupid as to tell such a stupid lie to an audience every one of which can see that this is a stupid lie and that joobz thinks no such thing.

In kleinman's case, I find it inevitable.

Dr Adequate

17th August 2007, 04:24 AM

Trying to explain basic math to kleinman is beginning to remind me irresistably of Father Ted's attempt to explain perspective to Dougal.

Ted: (Holding a toy cow in front of Dougal.) Dougal, this cow is small. (Points out of the window.) Those cows are far away. Small ... Far away ...

Belz...

17th August 2007, 05:51 AM

Far from it Belz, I agree with Dr Schneider that it is a good model and I can show that it properly models the affect of multiple selection pressures.

I'm starting to doubt your sincerity. In the post I was replying to you said this:

Ev is an idealized computer simulation of random point mutation and natural selection.

So, not only is the model incomplete, it's also idealised, so it doesn't model reality. How can it "mathematically" prove that evolution is impossible, then ?

Ev doesn’t have to be a perfect representation of mutation and selection in order to prove that the theory of evolution is mathematically impossible.

No, but it better take all types of mutation into account, and model things properly, not "ideally".

Since you have no experience with computer simulations

Speculation.

you probably not aware that no computer simulation is a perfect

I'm very much aware that computer simulations are imperfect. That's why I challenge your claim that it proves anything.

The empirical data say that other mechanisms of mutation and recombination do not overcome the affect of multiple selection pressures.

I'm not particularily interested in YOUR interpretation of said data. Do you have a link that supports your interpretation ?

An evolutionarian is a devotee to evolutionism which is a belief system that is mathematically impossible. I happen to be a Christian fanatic who understands the mathematics of mutation and selection and it proves the evolutionarian belief system to be mathematically impossible.

So you admit that you are biased ? You also admit that you believe in a god that is logically, mathematically and physically impossible, and you say evolution is unscientific ?

So aren’t you the hypocrite.

You're the one who's been arguing against those examples since the beginning. Why would you need me to provide them to you ?

Belz...

17th August 2007, 05:53 AM

Oh, I see joobz; there is not enough free energy for nuclear reactions to occur.

I don't think you understand much about nuclear reactions vs chemical ones.

You are speculating that all it takes is enough free energy and life spontaneously occurs.

Somehow I'm sure he isn't.

joobz

17th August 2007, 08:11 AM

I don't think you understand much about nuclear reactions vs chemical ones.

Somehow I'm sure he isn't.
Of course I'm not. I've been quite clear what my position is. He's been projecting his nonsense onto me in hopes that some of it will stick.

After 133 pages of his nonsense, he can't find a single point that I've been horrifically wrong on.
However, his list of "stupid things only a stupid fool would say" keeps growing. He gets annoyed with me, because I remind him of his errors.

Such as
1. 1st law thermo = natural selection
2. No evidence for speciation
3. Probability greater than 1
4. Nuclear and chemical reactions are equivilent
5. Thermodyanmics is a kinetic study
6. slow=stop
7. Unable to compile a program
8. Mutation rate is constant
9. biochemistry is a prebiotic field
10. mutations other than point and Recombination and aren't important

I'm sure there are more, but that's all that is coming to me right now.

cyborg

17th August 2007, 09:09 AM

11. Most mutations are bad because cancer is bad

jimbob

19th August 2007, 08:51 AM

To be a little bit fair. If an organism is well adapted to its environment, then most alterations would make it less well optimised. Of course some will still be improvements. And when the environment changes, the organism is not so well optimised, so there is a higher chance that more changes would be beneficial.

ETA:

Actually that is being far too fair.

Number 6 is the biggie

slow=slow.

If the population is completely wiped out, then evolution stops in that population, otherwise it continues.

Dr Adequate

19th August 2007, 11:27 AM

slow=slow. Oh, now you want to explain an identity to kleinman.

Good luck with that.

kjkent1

19th August 2007, 11:51 AM

Kleinman's entire theory fails at the start, because he attempts to calculate the probability of a particular definite and certain event after it has already occurred.

It's not surprising that Kleinman continues to insist that he is right and everyone else is wrong. The casinos of Las Vegas are built on the bones of those who, after witnessing the occurrence of an incredibly improbable event, pour their life savings into trying to prove that it can or cannot repeat.

Every six-deck Blackjack shoe contains a random order of cards arranged a staggeringly improbable order. Calculated after the fact, the likelihood of any of these orders occurring is "mathematically impossible," given the available time since the beginning of the universe (to borrow from Kleinman).

Yet, those improbable orders of cards occur every ~10 minutes, 24 hours per day, seven days per week, at table after table, in every casino on the "Strip."

The Theory of Evolution is an empirically verified fact, no amount of probability calculations will undo that fact, and only God, if He exists, can prove otherwise.

T'ai Chi

19th August 2007, 11:56 AM

Some mod wrote

"Please, also consider the use of a bit more brevity in your posts."

Uh. What?

Dr Adequate

19th August 2007, 12:22 PM

Some mod wrote

"Please, also consider the use of a bit more brevity in your posts."

Uh. What? So, you're still filling in with stupid until kleinman comes back?

What's it like, temping for idiots?

cyborg

19th August 2007, 03:32 PM

To be a little bit fair. If an organism is well adapted to its environment, then most alterations would make it less well optimised.

jimbob - you do realise that mutations that lead to cancer and mutations in reproduction are quite dissimilar right?

jimbob

19th August 2007, 11:27 PM

Sorry Cyborg, yes of course, I find it hard to read streams-of-conciousness writing on a computer, so have missed much of Kleinman's words...

As I "understood" Kleinman's argument, he is sometimes saying:

"look, these organisms are well-adapted to their environment and deviations from this are always harmful."

He isn't realy arguing that mutations within an organism are inevitrably harmful an cause cancer, so this invalidates evolution... is he?

If the mutations do not happen in reproduction, they won't survive past the death of the individual organism*. However I would say that cancerous mutations show that evolutionary pressures are at workwithin the cellular level of the body. Cancerous cells are good at reproducing, and for many generations their mutations do better than their unmutated parent line; of course they eventually destroy their environment (unless they are benign tumors sommewhere it doesn't matter), but they are successfull for many generations.

*Sometimes these cancer lines actually mange to survive their host's demise by spreading to other animals (http://news.bbc.co.uk/1/hi/world/asia-pacific/6378279.stm), as in the case of Canine transmissible venereal tumour (http://www.sciencedaily.com/releases/2006/08/060811075902.htm) or the tasmanian devil cancer (that we are currently aware of)...

Fine, if somewhat grotesque, examples of evolution at the genetic level, the ultimate expression of the selfish gene.

As you say, this is different from mutations during reproduction...

I have a new idea to explain what the creator was doing.

Obviously the creator is not a sadist that needlessly enjoys blood sports (Thanks Richard Dawkins for the "Cheetah and the Gazelle" argument). But that we are preparing of a type of Ragnarök, where this creation will have to fight against the creations of an axiomatically evil creator. No I can't say why... To perfect the organisms for this fight the best solution is for the creator to use evolutionary algorithms...,

cyborg

20th August 2007, 07:57 AM

"look, these organisms are well-adapted to their environment and deviations from this are always harmful."

He isn't realy arguing that mutations within an organism are inevitrably harmful an cause cancer, so this invalidates evolution... is he?

The former statement credits kleinman far, FAR too much.

His argument is:

"If mutations were any damn good then cancer should be just damn sweet! Explain that idiot evolutionarians!"

kleinman

20th August 2007, 09:26 AM

I can see you evolutionarians have been working hard this last weekend to understand the mathematics of mutation and selection. You keep up your good work. So let’s see what you have to say.

We were discussing Prebiotic formation of nucleic acids. That means a non-biochemical route. Duh.
Discussion, don’t you mean your speculations of the prebiotic formation of nucleic acids? Recall, joobz, you have no idea how ribose could form nonenzymatically and even if you could, ribose is an unstable molecule and would not remain it that form for long. Prebiotic formation of nucleic acids?
http://forums.randi.org/images/smilies/doglaugh.gif
So what if there is a completely different “transcription factor”? Simply changing the random seed gives different transcription factors.Oh for crying out loud. Obviously I meant that the transcription factors perform different functions, not that the chromosome base sequences are different.
Paul, how’s the beach? Do you look at the sun hitting the water and think how wonderful the prebiotic soup was?

So tell us Paul, what do you mean by “transcription factors perform different functions”?
None of the “transcription factors” evolved by ev represents real sequences or proteins.Then why does Ev prove mathematically that evolution is impossible?
Ev demonstrates the mathematical behavior of mutation and selection on a wide variety of different size search spaces with a variety of different of mutation rates and several different number selection conditions. Even though the selection conditions and the mechanism of selection are contrived, they demonstrate how slow this process is on all but the tiniest genomes (search spaces). The empirical data shows that real selection conditions mirror the mathematical behavior of Dr Schneider’s model despite his contrivances. Dr Schneider’s model has the essential elements necessary to demonstrate the mathematics of mutation and selection. What his model shows is that the number of selection conditions dominates the mathematic of mutation and selection.
There is a difference between spurious binding outside the gene and in the gene. The gene determines the weight matrix while spurious binding outside the gene has no effect on the weight matrix. Why don’t you try ev with the four or five selection conditions you suggest above and see what it does to the rate of convergence of the model. What do think will happen? Do you think more selection conditions will speed up or slow down the rate of information acquisition?Of course spurious bindings outside the gene affect the weight matrix: They have to be eliminated in order to produce a perfect creature.
Ok, if there is a mutation in the weight matrix, it will change the number of spurious bindings.
I don't think the number of selection conditions matters much. You were the one stating that you would "tell [me] why three selection conditions are the correct number for your model."
Paul, your own model shows that if you set two of the three selection conditions to zero, the remaining selection condition evolves many orders of magnitude more quickly than all three selection conditions simultaneously. There is nothing magic about three selection conditions other than it is two more optimization conditions than a single selection condition. Four selection conditions are three more optimization conditions than a single selection condition. As in any optimization problem, the more conditions you are trying to optimize, the slower the process goes. In addition, the larger the search space in which you are trying to optimize the multiple conditions, the more difficult it is to carry out the optimization. This is how mutation and selection works and this is what ev is demonstrating
This is also going in the FAQ.
http://forums.randi.org/images/smilies/doglaugh.gif
Let’s remind the readers of your FAQ.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
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.
http://forums.randi.org/images/smilies/doglaugh.gif
Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?
Then you compound your incredibly stupid graph with this quote.
More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.
http://forums.randi.org/images/smilies/doglaugh.gif
To be a little bit fair. If an organism is well adapted to its environment, then most alterations would make it less well optimised.jimbob - you do realise that mutations that lead to cancer and mutations in reproduction are quite dissimilar right?
Really cyborg, how do these examples differ in demonstrating the fitness to reproduce?

Once again, you evolutionarians have demonstrated an inability to understand the mathematics of mutation and selection, which is that multiple selection conditions profoundly slow the evolutionary process. Here are a couple more examples of how mutation and selection actually work and it is not how you evolutionarians allege.

http://www.pnas.org/cgi/content/abstract/94/22/12106 (http://www.pnas.org/cgi/content/abstract/94/22/12106)
The spread of bacteria resistant to antimicrobial agents calls for population-wide treatment strategies to delay or reverse the trend toward antibiotic resistance. Here we propose new criteria for the evaluation of the population-wide effects of treatment protocols for directly transmitted bacterial infections and discuss different usage patterns for single and multiple antibiotic therapy. A mathematical model suggests that the long-term benefit of single drug treatment from introduction of the antibiotic until a high frequency of resistance precludes its use is almost independent of the pattern of antibiotic use. When more than one antibiotic is employed, sequential use of different antibiotics in the population ("cycling") is always inferior to treatment strategies where, at any given time, equal fractions of the population receive different antibiotics. However, treatment of all patients with a combination of antibiotics is in most cases the optimal treatment strategy.
And here is another example for the Dr Schneider and the gang over at the National Cancer Institute.
http://bloodjournal.hematologylibrary.org/cgi/content/abstract/100/3/1068 (http://bloodjournal.hematologylibrary.org/cgi/content/abstract/100/3/1068)
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 BCR-ABL-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.
Once again, the empirical and mathematical data show that multiple selection pressures profoundly slow the evolutionary process. This is how mutation and selection works mathematically and this is how mutation and selection works empirically.

Belz...

20th August 2007, 10:23 AM

I can see you evolutionarians have been working hard this last weekend to understand the mathematics of mutation and selection.

Which is more than we can say about you.

kleinman

20th August 2007, 11:25 AM

I can see you evolutionarians have been working hard this last weekend to understand the mathematics of mutation and selection. Which is more than we can say about you.
Belz, I have to admit you are correct on this point. It is so easy to prove that the theory of evolution is mathematically impossible that I haven’t had to work very hard. When you have amathematicians like Adequate that post incredibly stupid graphs and then contradict themselves, it becomes a trivially easy debate. In addition there is such a vast amount of empirical data available that shows how mutation and selection actually works, it only takes a minute or two to find new citations which show that multiple selection pressures profoundly slow the evolutionary process by mutation and selection.

http://physician.mediwire.com/main/Default.aspx?P=Content&ArticleID=117810 (http://physician.mediwire.com/main/Default.aspx?P=Content&ArticleID=117810)
The problem associated with misdiagnosis is not limited to developing countries. For example, in North America it is estimated that physicians overprescribe antibiotics by 50%. In addition, many health-care providers tend to avoid narrow-spectrum drugs in favor of broader-spectrum antibiotics that have wider applications. Of course, this eventually results in a smaller, more costly arsenal of antimicrobials. Antimicrobials are frequently used in combination to treat life-threatening infections (Table 4), prevent emergence of resistance, treat mixed infections of aerobic and anaerobic bacteria, enhance activity (synergy), or avoid using high doses of the more toxic antimicrobials. Combination therapy can be very effective when used appropriately, but unfortunately many health-care providers use combinations that provide little synergy and no more efficacy than would be produced if only a single agent were employed.
See Belz, how easy it is to find citations which show that multiple simultaneous selection pressures slow evolution. It is too easy to show that the theory of evolution by mutation and selection is mathematically and empirically impossible.

WildCat

20th August 2007, 11:39 AM

It is too easy to show that the theory of evolution by mutation and selection is mathematically and empirically impossible.
And yet you have failed to do so!

And you're the guy arguing that a magical invisible sky fairy exists and created everything...

joobz

20th August 2007, 11:42 AM

Recall, joobz, you have no idea how ribose could form nonenzymatically and even if you could, ribose is an unstable molecule and would not remain it that form for long. Prebiotic formation of nucleic acids?Now you know that's not true. many people have studies this and found many feasible mechanisms.

Sugar synthesis from a gas-phase formose reaction.
Astrobiology. 2007 Jul;7(3):433-42.

Formation of a beta-Pyrimidine Nucleoside by a Free Pyrimidine Base and Ribose in a Plausible Prebiotic Reaction.
J Am Chem Soc. 2007 Aug 8;129(31):9556-9557.

On the Prebiotic Synthesis of Ribonucleotides: Photoanomerisation of Cytosine Nucleosides and Nucleotides Revisited.
Chembiochem. 2007 Jul 9;8(10):1170-1179.

A possible path to the RNA world: enantioselective and diastereoselective purification of ribose.
Orig Life Evol Biosph. 2007 Apr;37(2):167-75. Epub 2006

Prebiotic carbohydrate synthesis: zinc-proline catalyzes direct aqueous aldol reactions of alpha-hydroxy aldehydes and ketones.
Org Biomol Chem. 2005

Why do you tell lies that are so easily easily proven as lies that it makes you look like an inept fool? Do you like to look like an inept fool?
Discussion, don’t you mean your speculations of the prebiotic formation of nucleic acids? For you, changing focus of the conversation is an admission that you realize that what you had said before was completely wrong and stupid. Isn't it? You admit what you said was stupid, right? Shall I remind you? You claimed I was ignoring Biochemistry in my analysis. This was really dumb, wasn't it?
You equated nuclear and chemical reactions. This was even more stupid, wasn't it? Only a complete inept moron would continue such idiocy. Wouldn't they? This is why you changed topics, right?
I hope this is the reason. I'd hate to think you were really this inept.

kleinman

20th August 2007, 11:59 AM

Recall, joobz, you have no idea how ribose could form nonenzymatically and even if you could, ribose is an unstable molecule and would not remain it that form for long. Prebiotic formation of nucleic acids?Now you know that's not true. many people have studies this and found many feasible mechanisms.
Belz, I forgot to mention the incredibly ridiculous speculations of joobz. It is these types of speculations that make this an easy debate. Here is joobz’s strange speculation again.
Envision a system of millions of forming and destructive chemical reactions. Now, envision that intermediates of there reactions associate through non-covalent means and that this complex becomes protected against the destructive reactive pathway, perhaps by a reversible precipitation. These new complexes result in a localized increased of new chemical species. These chemical species then progress in a new series of reaction... that is what I mean through cooperative means. I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?
For you, changing focus of the conversation is an admission that you realize that what you had said before was completely wrong and stupid. Isn't it? You admit what you said was stupid, right? Shall I remind you? You claimed I was ignoring Biochemistry in my analysis. This was really dumb, wasn't it?
You equated nuclear and chemical reactions. This was even more stupid, wasn't it? Only a complete inept moron would continue such idiocy. Wouldn't they? This is why you changed topics, right? I hope this is the reason. I'd hate to think you were really this inept.
Why joobz, if you have enough free energy any chemical reaction is possible but not any nuclear reaction? Perhaps you are suggesting nuclear reactions can’t occur?
http://forums.randi.org/images/smilies/doglaugh.gif
So tell us joobz, if the sun shines on lead long enough does it turn into gold or is there not enough free energy available for this reaction to occur?
http://forums.randi.org/images/smilies/doglaugh.gif

Belz...

20th August 2007, 01:11 PM

It is so easy to prove that the theory of evolution is mathematically impossible that I haven’t had to work very hard.

Which is why, I guess, you failed to take note of your utter defeat.

See Belz, how easy it is to find citations which show that multiple simultaneous selection pressures slow evolution. It is too easy to show that the theory of evolution by mutation and selection is mathematically and empirically impossible

All you've shown is that, when you kill something real quickly, it fails to adapt.

kleinman

20th August 2007, 01:28 PM

It is so easy to prove that the theory of evolution is mathematically impossible that I haven’t had to work very hard.Which is why, I guess, you failed to take note of your utter defeat.
If I have had a failure here it is the failure to teach you evolutionarians how mutation and selection actually works. However, I attribute part of the blame to evolutionarians not reading this thread, the related threat on the Evolutionisdead forum and Dr Schneider’s web page and related papers on the ev computer simulation of random point mutations and natural selection. But don’t worry; you can take the course over until you learn how mutation and selection actually works. At the pace at which you are learning this topic, I expect it to take an number of years.
See Belz, how easy it is to find citations which show that multiple simultaneous selection pressures slow evolution. It is too easy to show that the theory of evolution by mutation and selection is mathematically and empirically impossible.All you've shown is that, when you kill something real quickly, it fails to adapt.
Really Belz, I wasn’t aware that you could treat anyone suffering of HIV by killing the virus. You need to go back and read the citations I have been posting a bit more carefully. In addition, you need to study the ev computer model because in this model, the population is never killed off completely, half the population is always allowed to reproduce.

Again, don’t worry Belz, I am patient, I will show you evolutionarians how mutation and selection actually works and it doesn’t work the way you evolutionarians allege.

joobz

20th August 2007, 02:10 PM

Belz, I forgot to mention the incredibly ridiculous speculations of joobz. It is these types of speculations that make this an easy debate. Here is joobz’s strange speculation again.
[/color]
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?

Why joobz, if you have enough free energy any chemical reaction is possible but not any nuclear reaction? Perhaps you are suggesting nuclear reactions can’t occur?
http://forums.randi.org/images/smilies/doglaugh.gif
So tell us joobz, if the sun shines on lead long enough does it turn into gold or is there not enough free energy available for this reaction to occur?
http://forums.randi.org/images/smilies/doglaugh.gif
Wow, so you are still keeping to the argument that only a complete inept moron would use. Oh well. I'm not shocked. At least you provide entertaining examples of inanity that can use in class.

Dr Adequate

20th August 2007, 03:37 PM

Belz, I have to admit you are correct on this point. It is so easy to prove that the theory of evolution is mathematically impossible that I haven’t had to work very hard. When you have amathematicians like Adequate that post incredibly stupid graphs and then contradict themselves, it becomes a trivially easy debate. In addition there is such a vast amount of empirical data available that shows how mutation and selection actually works, it only takes a minute or two to find new citations which show that multiple selection pressures profoundly slow the evolutionary process by mutation and selection.

http://physician.mediwire.com/main/Default.aspx?P=Content&ArticleID=117810 (http://physician.mediwire.com/main/Default.aspx?P=Content&ArticleID=117810)

See Belz, how easy it is to find citations which show that multiple simultaneous selection pressures slow evolution. It is too easy to show that the theory of evolution by mutation and selection is mathematically and empirically impossible.
Belz, I forgot to mention the incredibly ridiculous speculations of joobz. It is these types of speculations that make this an easy debate. Here is joobz’s strange speculation again.
[/COLOR]
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?

Why joobz, if you have enough free energy any chemical reaction is possible but not any nuclear reaction? Perhaps you are suggesting nuclear reactions can’t occur?
http://forums.randi.org/images/smilies/doglaugh.gif
So tell us joobz, if the sun shines on lead long enough does it turn into gold or is there not enough free energy available for this reaction to occur?
http://forums.randi.org/images/smilies/doglaugh.gif
If I have had a failure here it is the failure to teach you evolutionarians how mutation and selection actually works. However, I attribute part of the blame to evolutionarians not reading this thread, the related threat on the Evolutionisdead forum and Dr Schneider’s web page and related papers on the ev computer simulation of random point mutations and natural selection. But don’t worry; you can take the course over until you learn how mutation and selection actually works. At the pace at which you are learning this topic, I expect it to take an number of years.

Really Belz, I wasn’t aware that you could treat anyone suffering of HIV by killing the virus. You need to go back and read the citations I have been posting a bit more carefully. In addition, you need to study the ev computer model because in this model, the population is never killed off completely, half the population is always allowed to reproduce.

Again, don’t worry Belz, I am patient, I will show you evolutionarians how mutation and selection actually works and it doesn’t work the way you evolutionarians allege. Oh, look, he's back!

Hi, kleinman. Have you figured out how to divide one number by another, or do I have to talk you through it?

To put it another way: are you going to admit that you're an innumerate halfwit?

Dr Adequate

20th August 2007, 03:50 PM

Then you compound your incredibly stupid graph with this quote.

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

Yes, I compound my original offense of telling the truth by telling more truth.

I'm sure that this is perfectly shocking to creationists. Telling the truth, dear me.

But it does kind of earn me kudos amongst people who aren't insane liars.

Dr Adequate

20th August 2007, 03:55 PM

Interesting. Having failed to abolish reality by reciting the word "cheese", kleinman is now attempting to abolish reality by repeatedly showing us a cartoon of a dog.

I predict that this pathetic magical ritual will also fail to abolish reality.

I used to count up how many times he said "cheese" during the course of a week. If he performs the dog ritual much longer, I shall start counting the cartoon dogs.

delphi_ote

20th August 2007, 04:47 PM

But what if he combines them?

cyborg

20th August 2007, 04:48 PM

Kleinman doesn't believe in recombination.

jimbob

20th August 2007, 04:48 PM

http://forums.randi.org/showthread.php?postid=2875386#post2875386

So if you have enough free energy any chemical reaction is possible, but not any nuclear reaction is not possible? How could that be? Lead exists, gold exists, they are both made of protons, electrons and neutrons, then one must have evolved from the other, all you need is enough free energy.
Joobz, if the sun shines on lead long enough does it turn into gold?

There is a difference in the energies required. The Sun produces a lot of UV light were the photons heve energies sufficient to break chemical bonds (That is how oxygen forms ozone, at high altitudes).

Nuclear reactions require far more energy, but some cosmic rays do have the energy to instigate this.

There is a fundamental difference though. Life is a series of chemical processes not nuclear ones. So what does transmutation have to do with anything.

I suspect that you are actually quite clever, Kleinman, so why the emotional attachment to something so obviously wrong?

kleinman

20th August 2007, 05:24 PM

Wow, so you are still keeping to the argument that only a complete inept moron would use. Oh well. I'm not shocked. At least you provide entertaining examples of inanity that can use in class.
Envision a system of millions of forming and destructive chemical reactions. Now, envision that intermediates of there reactions associate through non-covalent means and that this complex becomes protected against the destructive reactive pathway, perhaps by a reversible precipitation. These new complexes result in a localized increased of new chemical species. These chemical species then progress in a new series of reaction... that is what I mean through cooperative means. I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?
Why joobz, I’m simply arguing at the level of your incredibly ridiculous speculations.

I predict that this pathetic magical ritual will also fail to abolish reality.
Well let’s see how good Adequate is at his predictions.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
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.
http://forums.randi.org/images/smilies/doglaugh.gif
Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?
Then you compound your incredibly stupid graph with this quote.
More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.
http://forums.randi.org/images/smilies/doglaugh.gif
Another one of Adequate’s predictions proved wrong. Adequate, have you booked your world tour to tell all the scientists and physicians that multiple selection pressures accelerate evolution? You better hurry because there are an awful lot of them misinterpreting their data. The keep thinking that combination selection pressures slow the evolutionary process. In fact, here are a couple more examples. Adequate, I guess you will have to correct these mathematicians as well.

http://www.people.fas.harvard.edu/~michor/publications/Mathematical%20models%20of%20targeted%20cancer%20t herapy,%20BJC%202006.pdf (http://www.people.fas.harvard.edu/~michor/publications/Mathematical%20models%20of%20targeted%20cancer%20t herapy,%20BJC%202006.pdf)
Araujo et al (2005) used mathematical modelling to investigate combination therapy in which multiple nodes in a signal transduction pathway are targeted simultaneously with specific inhibitors. They demonstrated that the attenuation of signalling is significantly enhanced when several upstream processes are inhibited, and that this weakening is most pronounced in signals downstream of serially connected targets.

http://lib.bioinfo.pl/auth:Komarova,NL (http://lib.bioinfo.pl/auth:Komarova,NL)
Although targeted therapy is yielding promising results in the treatment of specific cancers, drug resistance poses a problem. We develop a mathematical framework that can be used to study the principles underlying the emergence and prevention of resistance in cancers treated with targeted small-molecule drugs. We consider a stochastic dynamical system based on measurable parameters, such as the turnover rate of tumor cells and the rate at which resistant mutants are generated. We find that resistance arises mainly before the start of treatment and, for cancers with high turnover rates, combination therapy is less likely to yield an advantage over single-drug therapy. We apply the mathematical framework to chronic myeloid leukemia. Early-stage chronic myeloid leukemia was the first case to be treated successfully with a targeted drug, imatinib (Novartis, Basel). This drug specifically inhibits the BCR-ABL oncogene, which is required for progression. Although drug resistance prevents successful treatment at later stages of the disease, our calculations suggest that, within the model assumptions, a combination of three targeted drugs with different specificities might overcome the problem of resistance.

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.
So, once again, the mathematical and empirical data show that simultaneous selection pressures profoundly slow the evolutionary process. It is not as Adequate alleges:
Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
http://forums.randi.org/images/smilies/doglaugh.gif
Adequate, you better get a calculator to count up the laughing dog because you are going to see it with your ridiculous fake graph and ridiculous conclusion you draw from you graph. Oh yes, and do go on tour and tell the world “with simultaneous selection pressures the rate of evolution increases with the number of selection pressures”.
http://forums.randi.org/images/smilies/doglaugh.gif
But what if he combines them?
Now Delphi, mixed drinks aren’t good for you either. Just because you made a bad career decision and became an evolutionarian doesn’t mean the end of the world. I do like your work in stop action photography.
Kleinman doesn't believe in recombination.
Now cyborg, you know that isn’t true. If you said that I don’t believe in the cruft theory of evolution, that’s another story. However, since evolution by mutation and selection is mathematically impossible, it gives new life to the cruft theory of evolution.
http://forums.randi.org/images/smilies/doglaugh.gif
So if you have enough free energy any chemical reaction is possible, but not any nuclear reaction is not possible? How could that be? Lead exists, gold exists, they are both made of protons, electrons and neutrons, then one must have evolved from the other, all you need is enough free energy.
Joobz, if the sun shines on lead long enough does it turn into gold?There is a difference in the energies required. The Sun produces a lot of UV light were the photons heve energies sufficient to break chemical bonds (That is how oxygen forms ozone, at high altitudes).
So what; joobz makes this incredibly ridiculous claim that as long as there is sufficient free energy, anything chemical reaction can happen. There are also cosmic rays and alpha particles coming from the sun. There more than enough free energy to change the nucleus of lead to gold but it doesn’t happen. Joobz is the modern version of an alchemist. Joobz can’t even describe how ribose could form in the primordial soup. His unscientific speculations are typical for believers in evolutionism. Now when it comes to mutation and selection, there are more than enough mathematical models and empirical data for us to know exactly how it works. Simultaneous selection pressures profoundly slow the evolutionary process. That is what these models show and that is what the empirical data shows.

Dr Adequate

20th August 2007, 05:52 PM

[/COLOR]
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?
Why joobz, I’m simply arguing at the level of your incredibly ridiculous speculations.

Well let’s see how good Adequate is at his predictions.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg

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

Then you compound your incredibly stupid graph with this quote.

http://forums.randi.org/images/smilies/doglaugh.gif
Another one of Adequate’s predictions proved wrong. Adequate, have you booked your world tour to tell all the scientists and physicians that multiple selection pressures accelerate evolution? You better hurry because there are an awful lot of them misinterpreting their data. The keep thinking that combination selection pressures slow the evolutionary process. In fact, here are a couple more examples. Adequate, I guess you will have to correct these mathematicians as well.

http://www.people.fas.harvard.edu/~michor/publications/Mathematical%20models%20of%20targeted%20cancer%20t herapy,%20BJC%202006.pdf (http://www.people.fas.harvard.edu/~michor/publications/Mathematical%20models%20of%20targeted%20cancer%20t herapy,%20BJC%202006.pdf)

http://lib.bioinfo.pl/auth:Komarova,NL (http://lib.bioinfo.pl/auth:Komarova,NL)

http://www.annals.org/cgi/content/full/128/11/951 (http://www.annals.org/cgi/content/full/128/11/951)

So, once again, the mathematical and empirical data show that simultaneous selection pressures profoundly slow the evolutionary process. It is not as Adequate alleges:

http://forums.randi.org/images/smilies/doglaugh.gif
Adequate, you better get a calculator to count up the laughing dog because you are going to see it with your ridiculous fake graph and ridiculous conclusion you draw from you graph. Oh yes, and do go on tour and tell the world “with simultaneous selection pressures the rate of evolution increases with the number of selection pressures”.
http://forums.randi.org/images/smilies/doglaugh.gif

Now Delphi, mixed drinks aren’t good for you either. Just because you made a bad career decision and became an evolutionarian doesn’t mean the end of the world. I do like your work in stop action photography.

Now cyborg, you know that isn’t true. If you said that I don’t believe in the cruft theory of evolution, that’s another story. However, since evolution by mutation and selection is mathematically impossible, it gives new life to the cruft theory of evolution.
http://forums.randi.org/images/smilies/doglaugh.gif

So what; joobz makes this incredibly ridiculous claim that as long as there is sufficient free energy, anything chemical reaction can happen. There are also cosmic rays and alpha particles coming from the sun. There more than enough free energy to change the nucleus of lead to gold but it doesn’t happen. Joobz is the modern version of an alchemist. Joobz can’t even describe how ribose could form in the primordial soup. His unscientific speculations are typical for believers in evolutionism. Now when it comes to mutation and selection, there are more than enough mathematical models and empirical data for us to know exactly how it works. Simultaneous selection pressures profoundly slow the evolutionary process. That is what these models show and that is what the empirical data shows. So, tell me again, what is it about my model that you don't understand?

Is it the fact that a large number is bigger than a small one, or the fact that x/y is not equal to y?

So far, it appears to be both.

---

Oh, and the pathetic magic ritual with the cartoon dog still hasn't abolished reality. You remember I explained that to you?

joobz

20th August 2007, 05:53 PM

[/color]
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?
Why joobz, I’m simply arguing at the level of your incredibly ridiculous speculations.
[snip]
So what; joobz makes this incredibly ridiculous claim that as long as there is sufficient free energy, anything chemical reaction can happen. There are also cosmic rays and alpha particles coming from the sun. There more than enough free energy to change the nucleus of lead to gold but it doesn’t happen.
This horribly stupid and childishly dumb lie has been played out. It's funny to see you continue to post it,but it doesn't deserve any more comment. (It does deserve a place in your FAQ though). I'll wait till you come up with a new lie before I make fun of you some more.

Joobz is the modern version of an alchemist.
Being a chemical engineer does make me a modern version of an alchemist. Just like being a doctor makes you a modern version of a barber.

The only difference being I'd trust my barber as a doctor before I'd trust you as....well anything except an example of comeplete inanity.

kleinman

20th August 2007, 06:10 PM

So, tell me again, what is it about my model that you don't understand?
I understand your silly graph, it is a fake. Here is what you are claiming.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
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.
http://forums.randi.org/images/smilies/doglaugh.gif
Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?
Then you compound your incredibly stupid graph with this quote.
More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.
http://forums.randi.org/images/smilies/doglaugh.gif
Are you still counting up the doggie laugh cartoons? Too bad you are not as good at counting with mutation and selection.
Joobz is the modern version of an alchemist.Being a chemical engineer does make me a modern version of an alchemist. Just like being a doctor makes you a modern version of a barber.
At least a barber can cut hair, an alchemist never turned lead into gold and you don’t know how to turn inorganic molecules into living things. However you do know how to speculate. Here it is again for the readers.
Envision a system of millions of forming and destructive chemical reactions. Now, envision that intermediates of there reactions associate through non-covalent means and that this complex becomes protected against the destructive reactive pathway, perhaps by a reversible precipitation. These new complexes result in a localized increased of new chemical species. These chemical species then progress in a new series of reaction... that is what I mean through cooperative means. I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?

Now here is how mutation and selection works in reality and it doesn’t work like Adequate’s silly graph. This reference also is dedicated to the Dr Schneider and his crew over at the National Cancer Institute.

http://jco.ascopubs.org/cgi/content/full/23/15/3614 (http://jco.ascopubs.org/cgi/content/full/23/15/3614)

Mapping tumor cell protein networks in vivo will be critical for realizing the promise of patient-tailored molecular therapy. Cancer can be defined as a dysregulation or hyperactivity in the network of intracellular and extracellular signaling cascades. These protein signaling circuits are the ultimate targets of molecular therapy. Each patient's tumor may be driven by a distinct series of molecular pathogenic defects. Thus, for any single molecular targeted therapy, only a subset of cancer patients may respond. Individualization of therapy, which tailors a therapeutic regimen to a tumor molecular portrait, may be the solution to this dilemma. Until recently, the field lacked the technology for molecular profiling at the genomic and proteomic level. Emerging proteomic technology, used concomitantly with genomic analysis, promises to meet this need and bring to reality the clinical adoption of molecular stratification. The activation state of kinase-driven signal networks contains important information relative to cancer pathogenesis and therapeutic target selection. Proteomic technology offers a means to quantify the state of kinase pathways, and provides post-translational phosphorylation data not obtainable by gene arrays. Case studies using clinical research specimens are provided to show the feasibility of generating the critical information needed to individualize therapy. Such technology can reveal potential new pathway interconnections, including differences between primary and metastatic lesions. We provide a vision for individualized combinatorial therapy based on proteomic mapping of phosphorylation end points in clinical tissue material.
And
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.

joobz

20th August 2007, 07:07 PM

:words:
:nope:

kleinman

20th August 2007, 07:21 PM

http://forums.randi.org/images/smilies/emot-words.gif

Misspelled http://forums.randi.org/images/smilies/emot-words.gif
:dl:

Dr Adequate

20th August 2007, 11:53 PM

I understand your silly graph, it is a fake. Here is what you are claiming.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg

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

Then you compound your incredibly stupid graph with this quote.

http://forums.randi.org/images/smilies/doglaugh.gif
Are you still counting up the doggie laugh cartoons? Too bad you are not as good at counting with mutation and selection.

At least a barber can cut hair, an alchemist never turned lead into gold and you don’t know how to turn inorganic molecules into living things. However you do know how to speculate. Here it is again for the readers.
[/COLOR]
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?

Now here is how mutation and selection works in reality and it doesn’t work like Adequate’s silly graph. This reference also is dedicated to the Dr Schneider and his crew over at the National Cancer Institute.

http://jco.ascopubs.org/cgi/content/full/23/15/3614 (http://jco.ascopubs.org/cgi/content/full/23/15/3614)

And
You still don't have an critique of my model so much as ... well ... a picture of a dog.

It's no substitute.

UnrepentantSinner

21st August 2007, 12:21 AM

Joobz, if the sun shines on lead long enough does it turn into gold

Forget the laughing dog, I want a straw man smilie for "questions" like this.

Belz...

21st August 2007, 05:34 AM

If I have had a failure here it is the failure to teach you evolutionarians how mutation and selection actually works. However, I attribute part of the blame to evolutionarians not reading this thread

Kleinman, I'd like you to read the following very carefully:

Very often, someone with unconventional, revolutionary or reactionary ideas will pit his opinions against that of other people, such as happens here all the time. Very often, these opinions will be scoffed at, laughed at or thoroughly demolished by more knowledgeable people that tread these forums. Now, why is it that, faced with such overwhelming hostility or opposition, doesn't the someone with an unconventional, revolutionary or reactionary idea even consider, for an instant, that HE might be the one who's wrong ? Why must you pretty much all, always claim that the OTHER people are the ones blinded by faith, dishonest, paid off, dogmatic or plain evil ?

I ask this in all seriousness. Because UFO proponents, Bigfoot hunters, Conspiracy Theorists, Mediums, mystics, wiccas, homeopaths, creationists and other woo do exactly the same thing. They present their case, are shown wrong or at least shown strong opposition, and react with vitriol instead of pausing to examine the situation.

So, why is it that almost none of you ever want to allow the possibility that you might be wrong ?

Belz...

21st August 2007, 05:36 AM

You need to go back and read the citations I have been posting a bit more carefully. In addition, you need to study the ev computer model because in this model, the population is never killed off completely, half the population is always allowed to reproduce.

Sir, I am not interested in a simulation. I am interested in the real-life examples you've provided and that I was responding to. It would be interesting if you tried to keep up, here.

Belz...

21st August 2007, 05:38 AM

Forget the FAQ, Adequate. Here's MY summary of Klein's argument:

:dl: :dl: :dl: :dl: :dl: :dl: :dl: :dl: :dl: :dl: :dl: :dl: :dl: :dl: :dl: :dl: :dl: :dl: :dl: :dl: :dl: :dl: :dl: :dl: :dl: :dl: :dl: :dl: :dl: :dl:

kleinman

21st August 2007, 06:02 AM

You still don't have an critique of my model so much as ... well ... a picture of a dog.

It's no substitute.
You don’t have a model to critique, only an incredibly silly graph. Let’s see your silly graph again and what you have to say about it.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
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.
http://forums.randi.org/images/smilies/doglaugh.gif
Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?
Then you compound your incredibly stupid graph with this quote.
More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.
http://forums.randi.org/images/smilies/doglaugh.gif
Are you still counting up the doggie laugh cartoons? Too bad you are not as good at counting with mutation and selection.

Now I know that the data from Dr Schneider’s peer reviewed and published model of random point mutations and natural selection and the well over one hundred citations of empirical data which show you to be totally wrong are not much of a substitute for a critique of your incredibly silly graph but it will have to do. Here is another example from a scientist who recognizes how mutation and selection works empirically and it is not the way you evolutionarians claim.

http://www.jpgmonline.com/article.asp?issn=0022-3859;year=2006;volume=52;issue=4;spage=277;epage=2 80;aulast=Shanks (http://www.jpgmonline.com/article.asp?issn=0022-3859;year=2006;volume=52;issue=4;spage=277;epage=2 80;aulast=Shanks)
The growing problem of drug resistance has greatly complicated the treatment for falciparum malaria. Whereas chloroquine and sulfadoxine/pyrimethamine could once cure most infections, this is no longer true and requires examination of alternative regimens. Not all treatment failures are drug resistant and other issues such as expired antimalarials and patient compliance need to be considered. Continuation of a failing treatment policy after drug resistance is established suppresses infections rather than curing them, leading to increased transmission of malaria, promotion of epidemics and loss of public confidence in malaria control programs. Antifolate drug resistance (i.e. pyrimethamine) means that new combinations are urgently needed particularly because addition of a single drug to an already failing regimen is rarely effective for very long. Atovaquone/proguanil and mefloquine have been used against multiple drug resistant falciparum malaria with resistance to each having been documented soon after drug introduction. Drug combinations delay further transmission of resistant parasites by increasing cure rates and inhibiting formation of gametocytes. Most currently recommended drug combinations for falciparum malaria are variants of artemisinin combination therapy where a rapidly acting artemisinin compound is combined with a longer half-life drug of a different class. Artemisinins used include dihydroartemisinin, artesunate, artemether and companion drugs include mefloquine, amodiaquine, sulfadoxine/pyrimethamine, lumefantrine, piperaquine, pyronaridine, chlorproguanil/dapsone. The standard of care must be to cure malaria by killing the last parasite. Combination antimalarial treatment is vital not only to the successful treatment of individual patients but also for public health control of malaria.
Joobz, if the sun shines on lead long enough does it turn into goldForget the laughing dog, I want a straw man smilie for "questions" like this.
The only thing made of straw in this discussion is your theory of evolution by mutation and selection and it is going up in flames.
If I have had a failure here it is the failure to teach you evolutionarians how mutation and selection actually works. However, I attribute part of the blame to evolutionarians not reading this threadKleinman, I'd like you to read the following very carefully:

Very often, someone with unconventional, revolutionary or reactionary ideas will pit his opinions against that of other people, such as happens here all the time. Very often, these opinions will be scoffed at, laughed at or thoroughly demolished by more knowledgeable people that tread these forums. Now, why is it that, faced with such overwhelming hostility or opposition, doesn't the someone with an unconventional, revolutionary or reactionary idea even consider, for an instant, that HE might be the one who's wrong ? Why must you pretty much all, always claim that the OTHER people are the ones blinded by faith, dishonest, paid off, dogmatic or plain evil ?

I ask this in all seriousness. Because UFO proponents, Bigfoot hunters, Conspiracy Theorists, Mediums, mystics, wiccas, homeopaths, creationists and other woo do exactly the same thing. They present their case, are shown wrong or at least shown strong opposition, and react with vitriol instead of pausing to examine the situation.

So, why is it that almost none of you ever want to allow the possibility that you might be wrong ?
Belz, the reason I don’t consider myself wrong about the mathematics of mutation and selection is the vast amount of empirical data which supports this mathematics. I understand that you don’t understand the mathematics of this process of mutation and selection but it actually is not an uncommon problem seen in other areas of mathematics. Mutation and selection is simply and optimization or sorting problem in which the number of optimization or sorting conditions have a profound affect on the rate which these types of problems converge. If you read Delphi’s reference to the fitness landscape on Wikipedia, you would get an idea of what this mathematics is all about. If you understood what Dr Schneider’s model of mutation and selection was showing, you should ask whether this is reflected in the empirical data. The answer to this is yes, over and over. Whether you are talking about virology, parasitology, bacteriology, oncology, agriculture,… Every example of mutation and selection you can find behaves like Dr Schneider’s model shows. Combination simultaneous selection pressures profoundly slow the evolutionary process.
You need to go back and read the citations I have been posting a bit more carefully. In addition, you need to study the ev computer model because in this model, the population is never killed off completely, half the population is always allowed to reproduce. Sir, I am not interested in a simulation. I am interested in the real-life examples you've provided and that I was responding to. It would be interesting if you tried to keep up, here.
Belz, Dr Schneider’s mathematical model of mutation and selection is the subject of this thread. I realize you don’t understand his model and likewise you don’t understand the empirical examples of mutation and selection that I have and will continue to post. Your ignorance of how mutation works both mathematically and empirically is not a suitable defense for your mathematically impossible theory of evolution.

joobz

21st August 2007, 07:55 AM

:words:

:nope:

Belz...

21st August 2007, 08:06 AM

Belz, the reason I don’t consider myself wrong about the mathematics of mutation and selection is the vast amount of empirical data which supports this mathematics.

Klein, I asked you to read what I posted carefully. You obviously haven't.

Your answer boils down to the SAME thing that UFO proponents, Bigfoot hunters, Conspiracy Theorists, Mediums, mystics, wiccas, homeopaths, creationists and other woo say when asked this very question: "I just KNOW it's true, that's how".

It's not enough to know it, you must show it. And so far, you haven't convinced anyone, here. And before you start ranting about dogma, think about biologists and other scientists. To say that they're ALL dogmatic because they disagree with you reeks of paranoia.

So, again, why can't you possibly be wrong ? Why does it boil down to condescension and insults ?

I understand that you don’t understand the mathematics of this process of mutation and selection but it actually is not an uncommon problem seen in other areas of mathematics.

Again with the insults. It is obvious to me that YOU don't understand mathematics. At most, you've proven that you can add numbers together.

Mutation and selection is simply and optimization or sorting problem in which the number of optimization or sorting conditions have a profound affect on the rate which these types of problems converge.

Again, that's the SAME thing you've been saying again and again. Repeating something does not make it true.

Belz, Dr Schneider’s mathematical model of mutation and selection is the subject of this thread.

Yes, and it's been said that the model is not only incomplete but inexact. Hell, even you've admitted that. What's left to say, then ?

I realize you don’t understand his model and likewise you don’t understand the empirical examples of mutation and selection that I have and will continue to post.

AGAIN with the insults. Don't you get tired of acting like a jerk ?

Your ignorance of how mutation works both mathematically and empirically is not a suitable defense for your mathematically impossible theory of evolution.

I'm not defending evolution, or haven't you noticed ? I'm simply asking you to prove your assertions. So far you've just shown that the ev model says what you say it says, but you're a far cry from proving that it represents reality.

Dr Adequate

21st August 2007, 08:22 AM

You don’t have a model to critique What a strange lie. Everyone's seen my model, my assumptions, my data, my math, and my source code. And all you have to say in return ...

, only an incredibly silly graph. Let’s see your silly graph again and what you have to say about it.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg

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

Then you compound your incredibly stupid graph with this quote.

http://forums.randi.org/images/smilies/doglaugh.gif
Are you still counting up the doggie laugh cartoons? Too bad you are not as good at counting with mutation and selection.

Now I know that the data from Dr Schneider’s peer reviewed and published model of random point mutations and natural selection and the well over one hundred citations of empirical data which show you to be totally wrong are not much of a substitute for a critique of your incredibly silly graph but it will have to do. Here is another example from a scientist who recognizes how mutation and selection works empirically and it is not the way you evolutionarians claim.

http://www.jpgmonline.com/article.asp?issn=0022-3859;year=2006;volume=52;issue=4;spage=277;epage=2 80;aulast=Shanks (http://www.jpgmonline.com/article.asp?issn=0022-3859;year=2006;volume=52;issue=4;spage=277;epage=2 80;aulast=Shanks)

The only thing made of straw in this discussion is your theory of evolution by mutation and selection and it is going up in flames.

Belz, the reason I don’t consider myself wrong about the mathematics of mutation and selection is the vast amount of empirical data which supports this mathematics. I understand that you don’t understand the mathematics of this process of mutation and selection but it actually is not an uncommon problem seen in other areas of mathematics. Mutation and selection is simply and optimization or sorting problem in which the number of optimization or sorting conditions have a profound affect on the rate which these types of problems converge. If you read Delphi’s reference to the fitness landscape on Wikipedia, you would get an idea of what this mathematics is all about. If you understood what Dr Schneider’s model of mutation and selection was showing, you should ask whether this is reflected in the empirical data. The answer to this is yes, over and over. Whether you are talking about virology, parasitology, bacteriology, oncology, agriculture,… Every example of mutation and selection you can find behaves like Dr Schneider’s model shows. Combination simultaneous selection pressures profoundly slow the evolutionary process.

Belz, Dr Schneider’s mathematical model of mutation and selection is the subject of this thread. I realize you don’t understand his model and likewise you don’t understand the empirical examples of mutation and selection that I have and will continue to post. Your ignorance of how mutation works both mathematically and empirically is not a suitable defense for your mathematically impossible theory of evolution. ... is a bunch of halfwitted lies and a cartoon picture of a dog.

I have achieved pwnage.

joobz

21st August 2007, 08:46 AM

What a strange lie. Everyone's seen my model, my assumptions, my data, my math, and my source code. And all you have to say in return ...

... is a bunch of halfwitted lies and a cartoon picture of a dog.

I have achieved pwnage.
Ah, so you are also a pwnage addict. It's the only reason why any of us would continue this game.
:deadhorse

kjkent1

21st August 2007, 04:54 PM

I'm not defending evolution, or haven't you noticed ? I'm simply asking you to prove your assertions. So far you've just shown that the ev model says what you say it says, but you're a far cry from proving that it represents reality.Kleinman believes that he has proved his assertions and that anyone who doesn't concede defeat in the face of Kleinman's proof is "ignorant" or "brainwashed."

When I first started reviewing Dr. Kleinman's assertions, I was admittedly a little perturbed that someone with his credentials could maintain that Dr. Schneider's ev program was seriously flawed to the point where it might actually falsify what it was attempting to prove.

However, after researching the issue myself, I realized that ev's key (implied) finding, i.e., that Rseq evolves over time to ~ Rfreq in all genetically autonomous organisms, ignores the fact that when a peculiarly new mutation first occurs, that mutation drives Rfreq and Rseq apart numerically. Whereafter, generational evolution, as modeled by ev, then proceeds to cause the two values to converge again.

Thus, Kleinman's statement that evolution is mathematically impossible, as modeled by ev, may indeed be true -- but, only because ev ignores the other part of evolutionary change: the major (or dare I say "macro") mutation that causes a substantial modification to an existing organism.

This sort of mutation is precisely that which Dr. Schneider stated to Dr. Kleinman in June 06, is not modeled by ev (i.e., translocation, addition, deletion, frame shift, duplication, fusion, etc.).

So, it's little wonder that Dr. Kleinman insists that Dr. Schneider got it right and that ev proves that evolution is impossible in the generational time available, by point mutation alone. Because, it "is" impossible without the more extreme mutations, all of which are simply absent from ev.

If Dr. Kleinman really wants to disprove evolutionary theory by mathematical model, then he should find genetically autonomous organisms with very recent substantial mutations, calculate their respective Rfreq and Rseq values, and then compare these values against the measured values found in organisms which have not substantially changed over a long period of time.

Reason suggests that the more recently evolved changes to an organism should produce greater differences between Rseq and Rfreq for that organism, relative to organisms which have not displayed recent evolutionary change.

And, if this difference does not appear, then that would suggest either that (1) only major mutations which do not substantially separate Rfreq and Rseq are valid from an evolutionary perspective, or (2) that evolution is mathematically impossible.

This would still leave Kleinman with the task of disproving (1) above. But, that could be accomplished by artificially inserting mutations into an existing organism to see what sort of changes would cause the organism to survive, vis-a-vis die. Ultimately, it should be possible to demonstrate the specific conditions necessary for evolution of the sort hypothesized by the theory of evolution to occur.

And, if all attempts at inserting mutations into an organism fail to permit the organism to survive the change, then that would prove evolution impossible.

However, Kleinman's present argument proves nothing, except that he's not willing to objectively consider the evidence, wherever that evidence tends to prove that God is not involved in the evolutionary process.

Kotatsu

21st August 2007, 11:29 PM

The "View first unread" button took me to a Kleinman post. The forum software is obviously lying to me or mocking me.

Belz...

22nd August 2007, 05:54 AM

Kleinman believes that he has proved his assertions and that anyone who doesn't concede defeat in the face of Kleinman's proof is "ignorant" or "brainwashed."

Of course. Again, that's how woo-woos do it. They HAVE to convince themselves that their opponents are wrong, in some way that explains their overwhelming numbers.

Also, I don't understand how Klein can miss the fact that only point mutations are part of the model.

kleinman

22nd August 2007, 08:12 AM

Belz, the reason I don’t consider myself wrong about the mathematics of mutation and selection is the vast amount of empirical data which supports this mathematics.Klein, I asked you to read what I posted carefully. You obviously haven't.
Belz, I am sure I read your post more carefully than you have read this thread, the related thread on the Evolutionisdead forum and Dr Schneider’s web site and supporting documents for the ev computer program.
Your answer boils down to the SAME thing that UFO proponents, Bigfoot hunters, Conspiracy Theorists, Mediums, mystics, wiccas, homeopaths, creationists and other woo say when asked this very question: "I just KNOW it's true, that's how".

It's not enough to know it, you must show it. And so far, you haven't convinced anyone, here. And before you start ranting about dogma, think about biologists and other scientists. To say that they're ALL dogmatic because they disagree with you reeks of paranoia.

So, again, why can't you possibly be wrong ? Why does it boil down to condescension and insults ?
When you “boil” down my answer, don’t forget to include the data from a peer reviewed and published mathematical model of mutation and selection and the huge amount of empirical data from multiple different scientists in a wide variety of different scientific disciplines that show that multiple simultaneous selection profoundly slow the evolutionary process. Why does Dr Schneider’s model and reality demonstrate this mathematical and empirical fact? It is very simple Belz, evolution by mutation and selection is an optimization problem and like all optimization problems, the number of optimization conditions dominates the rate of convergence. It doesn’t bother me that you evolutionarians disagree with this mathematical and empirical fact now. This is such a profoundly contradictory finding to your belief system that it will take time for this mathematical and empirical fact to soak into your brainwashed and biased minds.
I understand that you don’t understand the mathematics of this process of mutation and selection but it actually is not an uncommon problem seen in other areas of mathematics.Again with the insults. It is obvious to me that YOU don't understand mathematics. At most, you've proven that you can add numbers together.
Belz, mutation and selection actually is a bookkeeping problem. Dr Schneider did this bookkeeping with his model. What Dr Schneider’s model shows is that the theory of evolution does not add up.
Mutation and selection is simply and optimization or sorting problem in which the number of optimization or sorting conditions have a profound affect on the rate which these types of problems converge.Again, that's the SAME thing you've been saying again and again. Repeating something does not make it true.
Belz, since you don’t understand the mathematics of mutation and selection and you have shown no interest in doing so, I’ll try to describe to you in words why mutation and selection is simply and optimization problem. Mutation and selection is an optimization problem because reproductive fitness must choose between beneficial and detrimental mutations. It is this sorting or optimization process which becomes profoundly slow when you have multiple different selection conditions acting simultaneously. Mutations for single selection conditions are much more easily sorted or optimized for than when there are multiple simultaneous selection conditions. This is the mathematical fact that ev shows and this is what the citations I have been posting demonstrate empirically.
Belz, Dr Schneider’s mathematical model of mutation and selection is the subject of this thread.Yes, and it's been said that the model is not only incomplete but inexact. Hell, even you've admitted that. What's left to say, then ?
Belz, you are demonstrating your ignorance of computer simulations when you say something like this. No computer simulation is a perfect representation of reality; however the essential features of reality can be modeled successfully. Yesterday the space shuttle landed safely despite a gouge in the thermal protection system. The decision to land the space shuttle despite the damage to the thermal protection system was made based on imperfect computer simulations and empirical data. I agree with Dr Schneider when he said the following.
A good simulation does not attempt to simulate everything; only the essential components are modeled. For the issue at hand, the form of the genetic code is not relevant; information measured by Shannon's method is more general than that.
Dr Schneider properly modeled the essentials of mutation and selection; that is why the results of his model fit the empirical data so well.
Your ignorance of how mutation works both mathematically and empirically is not a suitable defense for your mathematically impossible theory of evolution.I'm not defending evolution, or haven't you noticed ? I'm simply asking you to prove your assertions. So far you've just shown that the ev model says what you say it says, but you're a far cry from proving that it represents reality.
Belz, my assertion is very simple. What I am asserting is that multiple simultaneous selection pressures profoundly slow the evolutionary process. Dr Schneider’s ev computer model demonstrates this assertion mathematically and the huge number of citations which I have and will continue to post more of demonstrates the validity of this assertion empirically. Study the mathematics of mutation and selection or study the empirical data (better yet, study both) and find out that what I am asserting is true.
You don’t have a model to critique, only an incredibly silly graph. What a strange lie. Everyone's seen my model, my assumptions, my data, my math, and my source code. And all you have to say in return ...
Oh yes, you posted this along with all zero of your citations showing real examples of your incredibly silly graph. So let’s again post all your assumptions, all of your data, all of your math and all of your source code.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
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.
http://forums.randi.org/images/smilies/doglaugh.gif
Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?
And here is your silly source code fragment.

function t(selected: integer; genes: integer): integer;

var genome: array[0 .. 1, 1 .. pop, 1 .. 10] of boolean;
fitness: array[0 .. 1, 1 .. pop] of real;
c, g, h, g1, g2, i, j, o, n, fixed, generations: integer;
flag: boolean;

begin

o:=0; n:=1;
for i:=1 to pop do for j:=1 to genes do genome[0,i,j]:=false;
for i:=1 to pop do fitness[0,i]:=1;

generations:=0;

repeat
c:=0;

repeat
c:=c+1;
g1:=1+random(pop);
g2:=1+random(pop);
if fitness[o,g1]*random > fitness[o,g2]*random then g:=g1 else g:=g2;
for j:=1 to genes do genome[n,c,j]:=genome[o,g,j];
fitness[n,c]:=fitness[o,g];
if random(50)=0 then
begin
j:=1+random(10);
genome[n,c,j]:=not(genome[n,c,j]);
if (genome[n,c,j]) and (j<=selected) then fitness[n,c]:=fitness[n,c]*1.25 else fitness[n,c]:=fitness[n,c]/1.25;
end;
until c=pop;

fixed:=0;
for j:=1 to selected do
begin
flag:=true;
for i:=1 to pop do flag:=flag and genome[n,i,j];
if flag then fixed:=fixed+1;
end;
if fixed=selected then
begin
selected:=selected+1;
if selected<=genes then
for i:=1 to pop do if genome[n,i,selected] then fitness[n,i]:=fitness[n,i]*1.25;
end;

o:=1-o; n:=1-n;
generations:=generations+1;

until (fixed=genes);

t:=generations;

end;

Too bad your code fragment doesn’t compile without errors and too bad you don’t have any empirical examples of your silly graph and too bad that you contradict yourself when you say the following:
Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.

And

More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.
http://forums.randi.org/images/smilies/doglaugh.gif
I'm not defending evolution, or haven't you noticed ? I'm simply asking you to prove your assertions. So far you've just shown that the ev model says what you say it says, but you're a far cry from proving that it represents reality.Kleinman believes that he has proved his assertions and that anyone who doesn't concede defeat in the face of Kleinman's proof is "ignorant" or "brainwashed."
Now kjkent1, there is another possibility, evolutionarians can be both "ignorant" and "brainwashed" on the topic of the mutation and selection; "ignorant" of the mathematics of mutation and selection and "brainwashed" so as not to accept the vast amount of empirical data which show how mutation and selection actually works.
When I first started reviewing Dr. Kleinman's assertions, I was admittedly a little perturbed that someone with his credentials could maintain that Dr. Schneider's ev program was seriously flawed to the point where it might actually falsify what it was attempting to prove.
Why kjkent1, is that what I said? Perhaps you would be willing to post my quotes where you claim I am saying this. In fact, I think Dr Schneider properly modeled the essential parameters of the mutation and selection process. You will find that I have posted this contention numerous times.
However, after researching the issue myself, I realized that ev's key (implied) finding, i.e., that Rseq evolves over time to ~ Rfreq in all genetically autonomous organisms, ignores the fact that when a peculiarly new mutation first occurs, that mutation drives Rfreq and Rseq apart numerically. Whereafter, generational evolution, as modeled by ev, then proceeds to cause the two values to converge again.
Kjkent1, did your research show that Rseq evolves over time to ~ Rfreq for only unrealistically short genomes?
Thus, Kleinman's statement that evolution is mathematically impossible, as modeled by ev, may indeed be true -- but, only because ev ignores the other part of evolutionary change: the major (or dare I say "macro") mutation that causes a substantial modification to an existing organism.
Kjkent1, where are all your empirical examples of these "macro" mutations because I have posted well over one hundred empirical examples which show that combination selection pressures profoundly slow the evolutionary process.
This sort of mutation is precisely that which Dr. Schneider stated to Dr. Kleinman in June 06, is not modeled by ev (i.e., translocation, addition, deletion, frame shift, duplication, fusion, etc.).
Dr Schneider has also failed to post a single empirical example of his contention as well. I will continue to post empirical evidence which show that multiple simultaneous selection pressures profoundly slow the evolutionary process while you and Dr Schneider can make claims for which there is no empirical evidence. Perhaps Dr Schneider will add some of the mutation mechanisms which you list above and at least try to give mathematical evidence of his contention, but I doubt he will because it is now understood why ev converges so slowly for all but the most unrealistically small genomes. It is the number of selection conditions which dominates the mathematics of mutation and selection.
So, it's little wonder that Dr. Kleinman insists that Dr. Schneider got it right and that ev proves that evolution is impossible in the generational time available, by point mutation alone. Because, it "is" impossible without the more extreme mutations, all of which are simply absent from ev.
Kjkent1, you continue to ignore the fact that empirical data of mutation and selection does not support your allegation.
If Dr. Kleinman really wants to disprove evolutionary theory by mathematical model, then he should find genetically autonomous organisms with very recent substantial mutations, calculate their respective Rfreq and Rseq values, and then compare these values against the measured values found in organisms which have not substantially changed over a long period of time.
Kjkent1, there is an abundance of empirical data already available which show how mutation and selection actually works. The data from Dr Schneider’s mathematical model is already in agreement with this empirical data. The ball is already in the evolutionarian court. Your mathematical model already shows that the theory of evolution is mathematically impossible and the empirical data demonstrate that the data from your mathematical model correctly models the process of mutation and selection. Kjkent1, you can either try to refute these findings by modifying your model to show some different result or give real empirical examples which counters the mathematical and empirical fact of how mutation and selection actually works. So far, you have done neither.
The "View first unread" button took me to a Kleinman post. The forum software is obviously lying to me or mocking me.
Kotatsu, you have been listening to evolutionarian tales for so long that you are having trouble discerning the truth. Let me give you a couple of more empirical examples of how mutation and selection actually works. And the way mutation and selection works both mathematically and empirically is that combination selection pressures profoundly slow the evolutionary process.

http://www.cnio.es/eventos/descargas/Meeting/160329_524,38_booklet.pdf (http://www.cnio.es/eventos/descargas/Meeting/160329_524,38_booklet.pdf)
These findings in extensive preclinical studies led to dozens of clinical trials of C225, both as monotherapy and in combination with chemotherapy or radiotherapy. Results from Phase I and II trials involving thousands of patients are promising, and data from two Phase III trials have been reported. In a randomized study C225 was added to therapy for patients with colorectal cancer progressing on Irinotecan chemotherapy, or chemotherapy alone was continued. The results for combination treatment were 22.9% partial response and 4.1 months time to progression; the results for chemotherapy alone were 10.8% partial response and 1.5 months time to progression. In a Phase III study of radiotherapy plus or minus C225 for patients with locally advanced head and neck cancer, the combination therapy extended median survival to 54 months, whereas radiation alone extended median survival 28 months – a highly significant difference.

The FDA approval of 5-azacytidine for the treatment of MDS and the favorable clinical results obtained with 5-aza-2’-deoxycytidine in various hematologic malignancies transform hypomethylation therapy of cancer from concept to clinical reality. Numerous questions regarding this approach remain unanswered – dose, patient selection, mechanisms of response, mechanisms of resistance, safety and combination therapy. Data from several clinical and translational trials in hematologic malignancies will be presented arguing for the use of a low dose approach to favor the hypomethylation effect, and suggesting that part of the mechanism of response is hypomethylation triggering apoptosis. Resistance to 5-aza-2’-deoxycytidine in-vitro and in-vivo appears to be biologic (i.e. resistance to apoptosis) rather than pharmacologic (i.e. resistance to hypomethylation induction), and there are as yet no reliable pre-treatment markers to predict sensitivity to these agents. The future of hypomethylation therapy will clearly entail combinations of drugs to (i) enhance gene reactivation and (ii) exploit gene reactivation, and clinical trials of such approaches are ongoing.

Dr Adequate

22nd August 2007, 09:35 AM

So let’s again post all your assumptions, all of your data, all of your math and all of your source code. I notice that despite you saying this, you didn't actually do so.

Too bad your code fragment doesn’t compile without errors ...

You mean you still haven't figured out how to declare constants in Pascal? Gosh golly, is there no limit to the things you can't do?

Look, in the declarations for the main body of the program, declare const pop = 20; (or however large you want the effective population).

If you will follow my instructions, you will be able to call the function. If you are too stubborn, stupid, and lazy to do so, then this is the fault of your stubbornness, stupidity, and laziness, not of my model.

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.

Why can't you produce any counterexamples, kleinman?

and too bad that you contradict yourself when you say the following: Those two statements are not mutually contradictory, as you will find out the moment you bother to read them.

In the meantime, listening to you claim that they are is one of the principal pleasures of this thread.

You remind me rather of one of those scenes in cartoons where the guy doesn't fall until he's noticed that he's walked off the cliff.

Go on, read the two statements which you claim contradict one another.

Meanwhile, I'm just gonna sit here laughing my evolutionarianismistite tushie off.

kleinman

22nd August 2007, 10:16 AM

So let’s again post all your assumptions, all of your data, all of your math and all of your source code.I notice that despite you saying this, you didn't actually do so.
Edited out rule 12 breach.
Too bad your code fragment doesn’t compile without errors ...You mean you still haven't figured out how to declare constants in Pascal? Gosh golly, is there no limit to the things you can't do?

Look, in the declarations for the main body of the program, declare const pop = 20; (or however large you want the effective population.

If you will follow my instructions, you will be able to call the function. Edited out rule 12 breach.
It is not my job to debug your incredibly silly code fragment. Edited out rule 12 breach.
[FONT=Times New Roman][SIZE=3]What is obvious is that you have no idea how the mathematics of mutation and selection works.
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.

Why can't you produce any counterexamples, kleinman?
The reason why the precise experiment has not been done is that mutation and selection does not work the way you allege in your model. There are a vast number of experiments which demonstrate how mutation and selection actually works. I have posted well over one hundred examples of this and post another example below. When are you going to post your real first example of your incredibly silly graph?
and too bad that you contradict yourself when you say the following:Those two statements are not mutually contradictory, as you will find out the moment you bother to read them.
So let’s read them again:
Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.

And

More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.
http://forums.randi.org/images/smilies/doglaugh.gif
In the meantime, listening to you claim that they are is one of the principal pleasures of this thread.

You remind me rather of one of those scenes in cartoons where the guy doesn't fall until he's noticed that he's walked off the cliff.
Why Adequate, don’t you realize that mathematics and empirical data shows that the theory of evolution has fallen into the abyss?
Go on, read the two statements which you claim contradict one another.

Meanwhile, I'm just gonna sit here laughing my evolutionarianismistite tushie off.
Sure Adequate, let’s read your contradictory statements again, it gives everyone a good laugh.
Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.

And

More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.
http://forums.randi.org/images/smilies/doglaugh.gif
Now here is another real example of how mutation and selection actually works. This is another example dedicated to Dr Schneider and his cohort over at the National Cancer Institute where combination selection pressures slow the evolution of resistance in cancer cells.

http://www.translational-medicine.com/content/5/1/38 (http://www.translational-medicine.com/content/5/1/38)
Lenalidomide and Sorafenib inhibit HUVEC ability to migrate and form tubes and when used in combination the inhibition is increased. The agents alone and in combination inhibit outgrowth in the rat aortic ring model. The combination of the agents improved the inhibition over either single agent. In a xenograft model, combination therapy inhibited tumor growth over inhibition by single agent alone in a significant fashion (p < 0.004: lenalidomide and p < 0.0035: sorafenib). Furthermore, spontaneous lung metastasis development was completely inhibited in the combination treated animals. Sixty percent of vehicle treated animals developed lung metastases compared to 50% of lenalidomide treated animals, and 33% of sorafenib treated animals.
See how easy it works Adequate, list a URL and post a quote from the site which supports your hypothesis.

Mr. Scott

22nd August 2007, 10:25 AM

Dr. Kleinman, do you have any mathematical or empirical proof that only point mutations are significant?

kjkent1

22nd August 2007, 11:01 AM

Now kjkent1, there is another possibility, evolutionarians can be both "ignorant" and "brainwashed" on the topic of the mutation and selection; "ignorant" of the mathematics of mutation and selection and "brainwashed" so as not to accept the vast amount of empirical data which show how mutation and selection actually works.
Demonstrably incorrect logical analysis. A person who is brainwashed doesn't know the truth, because the ability to recognize truth has been removed by the brainwashing.

A person who is ignorant is merely unaware of the truth, but can still recognize it. Thus, as the brainwashed person cannot recognize truth, he/she cannot be ignorant. Therefore, such a person cannot be both ignorant and brainwashed.
Why kjkent1, is that what I said? Perhaps you would be willing to post my quotes where you claim I am saying this. In fact, I think Dr Schneider properly modeled the essential parameters of the mutation and selection process. You will find that I have posted this contention numerous times.
What you say, repeatedly, is that ev proves evolution impossible. That is precisely the opposite of what Schneider asserts. Thus, my comment, that you seek to use ev to falsify precisely what it attempts to prove, is true.
Kjkent1, did your research show that Rseq evolves over time to ~ Rfreq for only unrealistically short genomes?
If we consider the typical genome which has already reached a point where Rseq ~ Rfreq, and then insert a large mutational change, then the convergence of Rseq ~ Rfreq need only occur within that mutated section, which is relatively small -- because if it were too large, the mutation would likely kill the host organism.
Kjkent1, where are all your empirical examples of these "macro" mutations because I have posted well over one hundred empirical examples which show that combination selection pressures profoundly slow the evolutionary process.
The fossil record demonstrates how profoundly fast evolution has proceeded. You may choose to believe that the reason why the changes occurred so quickly, is that divine intervention, rather than random chance, was responsible. But, the former position is a return to a belief in magic, which are outside the scope of scientific investigation.
Dr Schneider has also failed to post a single empirical example of his contention as well.
I've already provided the K172 (nylonase producing bacteria) as a modern example of evolutionary change, which is not modeled by ev. You have yet to show why this bacteria's achievement does not falsify your theory. Until you explain K172's existence, scientifically, and similarly explain the fossil record, your theory is conclusively falsified.
I will continue to post empirical evidence which show that multiple simultaneous selection pressures profoundly slow the evolutionary process while you and Dr Schneider can make claims for which there is no empirical evidence.
Your posts are irrelevant, because they do not address the fossil record or K172. Until you address these issues, your theory is falsified.
Perhaps Dr Schneider will add some of the mutation mechanisms which you list above and at least try to give mathematical evidence of his contention, but I doubt he will because it is now understood why ev converges so slowly for all but the most unrealistically small genomes.
I don’t read Dr. Schneider’s mind. If you really want to discover the truth, you would attempt to do so, without relying on anyone else, by creating a model which considers all, rather than only some, of the relevant issues. Instead, you hide your head in the sand and ignore any evidence which falsifies your theory.
It is the number of selection conditions which dominates the mathematics of mutation and selection.
The fossil record and K172, inter alia, prove that your conclusion here is false.
Kjkent1, you continue to ignore the fact that empirical data of mutation and selection does not support your allegation.
On the contrary, I see that the empirical data you provide is too narrow to draw the conclusion that you do, and that the empirical evidence that you ignore, falsifies your theory.
Kjkent1, there is an abundance of empirical data already available which show how mutation and selection actually works. The data from Dr Schneider’s mathematical model is already in agreement with this empirical data. The ball is already in the evolutionarian court. Your mathematical model already shows that the theory of evolution is mathematically impossible and the empirical data demonstrate that the data from your mathematical model correctly models the process of mutation and selection. Kjkent1, you can either try to refute these findings by modifying your model to show some different result or give real empirical examples which counters the mathematical and empirical fact of how mutation and selection actually works. So far, you have done neither.
As I have explained, above, your theory is falsified and your conclusion does not follow from the evidence.

Dr Adequate

22nd August 2007, 11:24 AM

It is not my job to debug your incredibly silly code fragment. I know that you are incompetent to make it work. This is why I just told you how.

Why would I want to following the instructions ... In order to be able to check that my model does what I say.

If you don't want to do so, why do you keep whining about your inability to do so?

Sure Adequate, let’s read your contradictory statements again, it gives everyone a good laugh. You can't read them again unless you've read them once

Read them.

In the meantime, you are indeed giving everyone a good laugh --- just not for the reasons you'd like. You're as good as a circus. It's true, you're only one clown ...

See how easy it works Adequate, list a URL and post a quote from the site which supports your hypothesis. If it's that easy, why can't you find a single counterexample?

Dr Adequate

22nd August 2007, 11:31 AM

Apparently kleinman's new magic words are "incredibly silly".

Actually, all kleinman's magic words are incredibly silly.

Oh damn, I've broken the use-mention distinction, has anyone got any glue?

Belz...

22nd August 2007, 01:15 PM

Belz, I am sure I read your post more carefully than you have read this thread

It's not showing, since your replies look like what would be written by an automatic word bot.

When you “boil” down my answer, don’t forget to include the data from a peer reviewed and published mathematical model of mutation and selection and the huge amount of empirical data from multiple different scientists in a wide variety of different scientific disciplines that show that multiple simultaneous selection profoundly slow the evolutionary process.

If it's THAT obvious, then WHY, oh WHY hasn't the whole scientific community accepted these findings, thrown the theory of evolution out the window and started looking for another one ?

And you still haven't answered my question: Could you be wrong ?

This is such a profoundly contradictory finding to your belief system that it will take time for this mathematical and empirical fact to soak into your brainwashed and biased minds.

Don't try to fancy yourself a psychologist. You've already failed miserably at being a mathematician and a biologist.

Belz, mutation and selection actually is a bookkeeping problem. Dr Schneider did this bookkeeping with his model. What Dr Schneider’s model shows is that the theory of evolution does not add up.

Klein, you've ADMITTED that the model only shows a PORTION of what evolution is. The only reason why you put it on such a pedestal is because it supports your already-decided, religious opinion.

Belz, since you don’t understand the mathematics of mutation and selection and you have shown no interest in doing so, I’ll try to describe to you in words why mutation and selection is simply and optimization problem.

I haven't seen any mathematics that I could understand, let alone NOT understand. All I've seen is you showing numbers. Not really doing anything with them, mind you. Just putting them up.

Mutation and selection is an optimization problem because reproductive fitness must choose between beneficial and detrimental mutations.

It has no such obligation.

It is this sorting or optimization process which becomes profoundly slow when you have multiple different selection conditions acting simultaneously.

That's your claim, Klein. I see you understand nothing about the scientific method. Claim <> Evidence.

Belz, you are demonstrating your ignorance of computer simulations when you say something like this. No computer simulation is a perfect representation of reality

Strawman. I said it was INEXACT. Not imperfect. The model does not represent reality in any way, shape or form.

What I am asserting is that multiple simultaneous selection pressures profoundly slow the evolutionary process. Dr Schneider’s ev computer model demonstrates this assertion mathematically

No, it demonstrates it in a simulation. It's mathematics DO NOT MODEL REALITY.

and the huge number of citations which I have and will continue to post more of demonstrates the validity of this assertion empirically.

At most, only in some instances. You have not shown that this is always true.

joobz

22nd August 2007, 01:25 PM

Don't try to fancy yourself a psychologist. You've already failed miserably at being a mathematician and a biologist.
...and a chemist....and an engineer....and a statistician...and an immunologist....and a computer programmer....

kleinman

22nd August 2007, 05:07 PM

Dr. Kleinman, do you have any mathematical or empirical proof that only point mutations are significant?
Well kitty cat, I have never argued that only point mutations are significant. What I have said is that other forms of mutations such as insertion/deletion mutations tend to be far more harmful. It is you evolutionarians who have contended that other forms of mutations will somehow correct your theory from what is shown by ev. That is multiple simultaneous selection pressures profoundly slow the rate of evolution. I have shown and will continue to show empirical examples of mutation and selection which are not limited to point mutation, all of which show that multiple simultaneous selection pressures profoundly slow the evolutionary process. If you want a little discussion about point mutations, I refer you to Wikipedia on that topic.
http://en.wikipedia.org/wiki/Point_mutation (http://en.wikipedia.org/wiki/Point_mutation)
A point mutation, or substitution, is a type of mutation that causes the replacement of a single base nucleotide with another nucleotide. Often the term point mutation also includes insertions or deletions of a single base pair (which have more of an adverse effect on the synthesized protein due to nucleotides still being read in triplets, but in different frames- a mutation called a frameshift mutation).
Kitty cat, I leave it to you to prove that other forms of mutations besides point mutations overcome the mathematical fact which ev demonstrates, that is multiple simultaneous selection profoundly slows the evolutionary process. You will also have to overcome the vast amount of empirical data which is not limited to point mutations which shows that multiple simultaneous selection pressures profoundly slow the evolutionary process. What you are having trouble coming to grips with is that the dominant parameter in the mutation and selection process is not the type of mutation but the number of selection conditions.
Now kjkent1, there is another possibility, evolutionarians can be both "ignorant" and "brainwashed" on the topic of the mutation and selection; "ignorant" of the mathematics of mutation and selection and "brainwashed" so as not to accept the vast amount of empirical data which show how mutation and selection actually works.Demonstrably incorrect logical analysis. A person who is brainwashed doesn't know the truth, because the ability to recognize truth has been removed by the brainwashing.

A person who is ignorant is merely unaware of the truth, but can still recognize it. Thus, as the brainwashed person cannot recognize truth, he/she cannot be ignorant. Therefore, such a person cannot be both ignorant and brainwashed.
A person who is brainwashed is programmed to believe a particular belief system. What you have to do is overcome this programming with overwhelming and irrefutable evidence, especially evidence which those adherents develop themselves. A person who can choose to be ignorant of the facts because it conflicts with their belief system, this is called denial. What is being done here is Dr Schneider’s own computer model is being used to show the fallacy of the theory of evolution and the data from this is being substantiated with the vast amount of empirical data which shows that the results from Dr Schneider’s model is correct.
Why kjkent1, is that what I said? Perhaps you would be willing to post my quotes where you claim I am saying this. In fact, I think Dr Schneider properly modeled the essential parameters of the mutation and selection process. You will find that I have posted this contention numerous times.What you say, repeatedly, is that ev proves evolution impossible. That is precisely the opposite of what Schneider asserts. Thus, my comment, that you seek to use ev to falsify precisely what it attempts to prove, is true.
If you read Dr Schneider’s paper carefully, what you will find is that he used the rate of information gain on an unrealistically short genome with an unrealistically high mutation rate to estimate the evolution of a human genome. Dr Schneider did an invalid extrapolation from the results of a single case from his model. If Dr Schneider had done a careful parametric study with his model, he would have found the correct interpretation of his mathematical model. You can not understand the behavior of mutation and selection from ev based on a single case.
Kjkent1, did your research show that Rseq evolves over time to ~ Rfreq for only unrealistically short genomes?If we consider the typical genome which has already reached a point where Rseq ~ Rfreq, and then insert a large mutational change, then the convergence of Rseq ~ Rfreq need only occur within that mutated section, which is relatively small -- because if it were too large, the mutation would likely kill the host organism.
What you are still ignoring is that Rseq ~ Rfreq in a relatively small number of generations only on short genomes with huge reproduction rates. These types of numbers are only achieved with viruses and bacteria. The combination selection pressures of ev require huge number of generations to converge on all but the shortest genomes. Only single selection conditions converge rapidly on longer genomes. This is the lesson that ev teaches and this is what the empirical data show.
Kjkent1, where are all your empirical examples of these "macro" mutations because I have posted well over one hundred empirical examples which show that combination selection pressures profoundly slow the evolutionary process.The fossil record demonstrates how profoundly fast evolution has proceeded. You may choose to believe that the reason why the changes occurred so quickly, is that divine intervention, rather than random chance, was responsible. But, the former position is a return to a belief in magic, which are outside the scope of scientific investigation.
The fossil record is the evolutionarian version of the Rorschach test. You evolutionarians see what you want to see in the fossil record. On the other hand, this discussion is about the mathematics of mutation and selection and the empirical data which supports this mathematics. Why don’t you take your fossil record and describe the selection conditions and genes which are impacted by these selection conditions? What you will find is that there are huge genetic differences between birds and reptiles and you don’t have the selection conditions that would make such a transformation. Even if you could imagine the selection conditions, it would take astronomically huge numbers of generations to make the transformation.
Dr Schneider has also failed to post a single empirical example of his contention as well.I've already provided the K172 (nylonase producing bacteria) as a modern example of evolutionary change, which is not modeled by ev. You have yet to show why this bacteria's achievement does not falsify your theory. Until you explain K172's existence, scientifically, and similarly explain the fossil record, your theory is conclusively falsified.
That is an example of a bacterial population subjected to a single selection condition in which a polymerase is transformed into a different polymerase. There is nothing unusual about your example except perhaps this is a rare example of a frame shift mutation providing a beneficial mutation. Now if you subject this population to multiple selection pressures besides limiting their food source to nylon and this shows that the multiple selection pressures accelerate evolution, then you would have an argument.
I will continue to post empirical evidence which show that multiple simultaneous selection pressures profoundly slow the evolutionary process while you and Dr Schneider can make claims for which there is no empirical evidence.Your posts are irrelevant, because they do not address the fossil record or K172. Until you address these issues, your theory is falsified.
How about the evolutionarian interpretation of the fossil record and your example of K172 are irrelevant? When the mathematical and empirical data show that the theory of evolution is mathematically impossible by mutation and selection because combination selection pressures profoundly slow the evolutionary process.
Perhaps Dr Schneider will add some of the mutation mechanisms which you list above and at least try to give mathematical evidence of his contention, but I doubt he will because it is now understood why ev converges so slowly for all but the most unrealistically small genomes.I don’t read Dr. Schneider’s mind. If you really want to discover the truth, you would attempt to do so, without relying on anyone else, by creating a model which considers all, rather than only some, of the relevant issues. Instead, you hide your head in the sand and ignore any evidence which falsifies your theory.
Until one of you evolutionarians includes these other mechanisms of mutations to ev, you have an open door to speculate whatever you want. There is one problem though; the empirical evidence contradicts your speculations.
Kjkent1, you continue to ignore the fact that empirical data of mutation and selection does not support your allegation.On the contrary, I see that the empirical data you provide is too narrow to draw the conclusion that you do, and that the empirical evidence that you ignore, falsifies your theory.
Why don’t you expand the empirical data and post an example which shows that combination selection conditions accelerate evolution? That would make this a much more challenging discussion since I have already posted over 100 citations which show that multiple simultaneous selection pressures profoundly slow evolution.
Kjkent1, there is an abundance of empirical data already available which show how mutation and selection actually works. The data from Dr Schneider’s mathematical model is already in agreement with this empirical data. The ball is already in the evolutionarian court. Your mathematical model already shows that the theory of evolution is mathematically impossible and the empirical data demonstrate that the data from your mathematical model correctly models the process of mutation and selection. Kjkent1, you can either try to refute these findings by modifying your model to show some different result or give real empirical examples which counters the mathematical and empirical fact of how mutation and selection actually works. So far, you have done neither.As I have explained, above, your theory is falsified and your conclusion does not follow from the evidence.
Let’s see, you have K172 (a bacterial population which transforms a polymerase to a polymerase subject to a single selection pressure) and the evolutionarian interpretation of the fossil record and I have a peer reviewed and published model of random point mutation and natural selection which shows that multiple simultaneous selection conditions profoundly slow the evolutionary process. In addition, I have posted over one hundred citations of empirical evidence which verifies this finding. Lita’ gator, I like my closing argument over your closing argument any day of the week.
It is not my job to debug your incredibly silly code fragment.I know that you are incompetent to make it work. This is why I just told you how.
If you want incompetence, let’s show the readers incompetence.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
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.
http://forums.randi.org/images/smilies/doglaugh.gif
Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?
And then you said this.
More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.
http://forums.randi.org/images/smilies/doglaugh.gif
Now Adequate, you are demonstrating incompetence.
When you “boil” down my answer, don’t forget to include the data from a peer reviewed and published mathematical model of mutation and selection and the huge amount of empirical data from multiple different scientists in a wide variety of different scientific disciplines that show that multiple simultaneous selection profoundly slow the evolutionary process.If it's THAT obvious, then WHY, oh WHY hasn't the whole scientific community accepted these findings, thrown the theory of evolution out the window and started looking for another one ?

And you still haven't answered my question: Could you be wrong ?
What makes you think that no one else in the scientific community accepts these findings? I’m taking this argument to hard core evolutionarians who have been steeped in evolutionism for years. It will take a while for these mathematical and empirical facts to sink into the minds of those who have been thoroughly programmed for years.

With respects to your question, could I be wrong about the mathematics of mutation and selection. The answer to your question is no. I have worked with this type of mathematics before in different forms and presented in different formats. Mutation and selection is simply an optimization problem. These types of problems converge much more slowly when you have more than a single optimization condition. In addition, there is a vast amount of empirical data which verifies what Dr Schneider’s model is showing. Now Belz, why don’t you answer the same question, do you think you could be wrong about how mutation and selection actually works?

Now, here are a couple more empirical examples of how mutation and selection actually works and it works the way Dr Schneider’s ev model shows, that is multiple simultaneous selection pressures profoundly slow the evolutionary process.

http://vir.sgmjournals.org/cgi/content/full/85/11/3173?ck=nck (http://vir.sgmjournals.org/cgi/content/full/85/11/3173?ck=nck)
Treatment response.
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.

http://gut.bmj.com/cgi/content/abstract/49/6/860?ck=nck (http://gut.bmj.com/cgi/content/abstract/49/6/860?ck=nck)
BACKGROUND Strategies for prevention of liver graft reinfection by hepatitis B virus (HBV) have been developed during recent years. Initially, passive immunoprophylaxis with high titre HBV immunoglobulin (HBIg), followed by lamivudine prophylaxis, and then the combination of lamivudine and HBIg have been employed. However, suboptimal use of the combination may be associated with failure of prophylaxis reflected by the emergence of HBV species with genetic changes that confer resistance to lamivudine and HBIg. Reinfection of the graft by HBV can be associated with rapid development of liver failure.
CASE REPORT A 43 year old HBV infected man received lamivudine before transplantation, and lamivudine and HBIg after transplantation. Despite prophylaxis, graft reinfection and severe hepatitis were observed. The observed serological evolution and genetic sequencing of the emergent HBV species suggested selection of lamivudine resistant and surface antigen escape mutants consecutively. Adefovir treatment began after the devlopment of graft failure.
OUTCOME A rapid exponential decline in serum HBV titre was observed. Liver function tests normalised and signs of liver failure resolved.
CONCLUSION The use of HBIg and lamivudine permits prevention of graft reinfection by HBV for the majority of patients. Adefovir, a potent inhibitor of lamivudine resistant HBV, should be used when failure of prophylaxis is associated with graft hepatitis.

Dr Adequate

22nd August 2007, 05:43 PM

Well, that was two thousand eight hundred and forty-one words of the same old crap, wasn't it?

kjkent1

22nd August 2007, 05:45 PM

A person who is brainwashed is programmed to believe a particular belief system. What you have to do is overcome this programming with overwhelming and irrefutable evidence, especially evidence which those adherents develop themselves. A person who can choose to be ignorant of the facts because it conflicts with their belief system, this is called denial. What is being done here is Dr Schneider’s own computer model is being used to show the fallacy of the theory of evolution and the data from this is being substantiated with the vast amount of empirical data which shows that the results from Dr Schneider’s model is correct.You are now showing a cognitive inability to logically analyze a problem. You stated that it was possible for a person to be simultaneously ignorant and brainwashed about the same subject matter. Since a necessary condition of ignorance is the ability to recognize the truth upon its presentation, and a necessary condition of brainwashing is the inability to recognize that same truth, your statement is logically impossible, and false.

This is an excellent demonstration of your general lack of objectivity re the science surrounding evolution: you are so emotionally attached to your religious beliefs, that you cannot concede an opponent's most trivial correction to your thought process.

So, let's try it again...

Q: is it possible to be both ignorant and brainwashed about the same subject matter simultaneously (Y/N)?

Until you can correctly answer the above question, there is little point in discussing anything more complex.

Dr Adequate

22nd August 2007, 06:14 PM

Since a necessary condition of ignorance is the ability to recognize the truth upon its presentation ... I question the premise. A goat, for example, is ignorant of algebra.

kleinman

22nd August 2007, 06:33 PM

Well, that was two thousand eight hundred and forty-one words of the same old crap, wasn't it?
Here is some real crap.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
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.
http://forums.randi.org/images/smilies/doglaugh.gif
Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?
And then you said this.
More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.
http://forums.randi.org/images/smilies/doglaugh.gif
Now Adequate, you are demonstrating real crap.
Q: is it possible to be both ignorant and brainwashed about the same subject matter simultaneously (Y/N)?

Until you can correctly answer the above question, there is little point in discussing anything more complex.

Edited out rule 12 breach.

Once again, I will explain to you evolutionarians how the mathematics of mutation and selection works. Mutation and selection is simply a sorting or optimization problem for the selection of beneficial and detrimental mutations. Like all sorting or optimization problems, the number of selection conditions has a profound affect on the rate of convergence of these problems. What ev demonstrates is how difficult it is to sort mutations for three selection conditions on all but the shortest genomes. With more realistic length genomes, the search space becomes massive for anything more than a single selection condition. Single selection conditions can be converged easily on even the longer genome cases when multiple selection condition requires many orders of magnitude more generations to converge. Edited out rule 12 breach.

joobz

22nd August 2007, 07:20 PM

kjkent1

22nd August 2007, 08:49 PM

Kjkent1, the answer is Y, you are the perfect example of this. You are ignorant of the mathematics of mutation and selection and you have been brainwashed (programmed by evolutionism).That's the wrong answer, Alan. You need to get some behavioral therapy if you are actually unable to understand the logical contridiction in my question.

kjkent1

22nd August 2007, 08:50 PM

...

kjkent1

22nd August 2007, 08:54 PM

...

Belz...

23rd August 2007, 05:35 AM

Well kitty cat, I have never argued that only point mutations are significant.

Therefore you admit that the ev model is inadequate ?

With respects to your question, could I be wrong about the mathematics of mutation and selection. The answer to your question is no.

Then you have no place in a debate of any kind, because your mind is incapable of adapting to new data. You are doomed to have the same dogmatic view of the universe for the rest of your life.

Enjoy your religious fantasy.

Dr Adequate

23rd August 2007, 06:35 AM

Here is some real crap. You're right, and let's look at the most fecal aspect of your dreary nonsense.

Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?

And then you said this.

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

Are you really trying to pretend that this:

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

was a response to this:

Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?

rather than to this:

You’ve said you have worked on iteration problems, describe a single example of an iteration problem where the more conditions you have to iterate upon, the more rapid the problem converges. Give us an example of an optimization problem where the more conditions you are trying to optimize, the more rapid the optimization proceeds.

If so, I have restored the links in the posts so that people can see what a sordid, squalid, stupid liar you are.

Dr Adequate

23rd August 2007, 06:51 AM

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

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

Now Adequate, you are demonstrating real crap. You think that the proposition that more optimisation takes more time is "real crap"?

This is going to be fun.

Please, please lecture us on this aspect of "the mathematics of mutation of selection" some more, and explain this point in full.

It's popcorn time!

http://img452.imageshack.us/img452/3044/popcornkj3.jpg

Mr. Scott

23rd August 2007, 07:26 AM

Well kitty cat, I have never argued that only point mutations are significant. What I have said is that other forms of mutations such as insertion/deletion mutations tend to be far more harmful.

OK, laughing dog, you slipped out through an ambiguity in my question. I'll clarify it:

Do you have mathematical proof that evolution is significantly advanced by point mutations only?

Your claim above "other forms of mutations such as insertion/deletion mutations tend to be far more harmful" isn't mathematical. It's incorrect when it applies to insertions/deletions on duplications, and there is an ever growing body of empirical evidence that shows unambiguously that insertions/deletions on duplications significantly advance evolution and even result in new genes. They've been observed in our lifetimes, and have had tens of millions of lifetimes to evolve the variety of life on Earth -- and this is empirically and mathematically confirmed.

Additionally, the insertions of viral DNA in the primate genome pretty much prove to virtual mathematical certainty that humans and apes share common ancestors.

Even you, Kleinman, have stated that most mutations are harmful. You agree with evolutionarians on that! The non-harmful mutations are behind macro evolution.

I'll ask my clarified yes/no question again:

Do you have mathematical proof that evolution is significantly advanced only by point mutations?

kleinman

23rd August 2007, 08:53 AM

You are now showing a cognitive inability to logically analyze a problem.I disagree. There has been over a year of posts demonstrating his cognitive inability to logically analyze a problem. This is far from the first instance of it.
Let’s review joobz cognitive (cognitive? how about his speculative abilities).
Envision a system of millions of forming and destructive chemical reactions. Now, envision that intermediates of there reactions associate through non-covalent means and that this complex becomes protected against the destructive reactive pathway, perhaps by a reversible precipitation. These new complexes result in a localized increased of new chemical species. These chemical species then progress in a new series of reaction... that is what I mean through cooperative means. I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold? Joobz, why don’t you describe to us the chemistry of any organic molecule that might arise in your speculative primordial soup and demonstrate your cognitive, whoops speculative ability?
Kjkent1, the answer is Y, you are the perfect example of this. You are ignorant of the mathematics of mutation and selection and you have been brainwashed (programmed by evolutionism).That's the wrong answer, Alan. You need to get some behavioral therapy if you are actually unable to understand the logical contridiction in my question.
The real contradiction in this discussion is the theory of evolution; it is contradicted by both the mathematical and empirical facts.
Well kitty cat, I have never argued that only point mutations are significant.Therefore you admit that the ev model is inadequate ?
Of course not, the ev model contains the essential features necessary to describe the mathematics of mutation and selection. Only in the confused thinking of evolutionarians do you think that somehow other forms of more destructive mutations will somehow overcome the mathematical fact that the dominant parameter in the mathematics of mutation and selection is the number of simultaneous selection conditions. The next most dominant parameter is the genome length.
With respects to your question, could I be wrong about the mathematics of mutation and selection. The answer to your question is no.Then you have no place in a debate of any kind, because your mind is incapable of adapting to new data. You are doomed to have the same dogmatic view of the universe for the rest of your life.
I understand how annoyed you evolutionarians become when mathematical and empirical facts are introduced into your belief system but if you want to understand how mutation and selection actually works, that is what you have to do.
Enjoy your religious fantasy.
Why Belz, the only religious fantasy on this thread is evolutionism.
Well kitty cat, I have never argued that only point mutations are significant. What I have said is that other forms of mutations such as insertion/deletion mutations tend to be far more harmful.OK, laughing dog, you slipped out through an ambiguity in my question. I'll clarify it:

Do you have mathematical proof that evolution is significantly advanced by point mutations only?
What’s the matter kitty cat, you don’t like empirical evidence? I’ll let Dr Schneider and you other evolutionarians satisfy yourselves that other forms mutations do not overcome the mathematical fact the number of simultaneous selection pressures is the dominant parameter in the mathematics of mutation and selection. I do this because you evolutionarians are already trying to attribute Dr Schneider’s work to me. I’ll just continue to post the empirical data which refutes your silly theory.
Now kitty cat, you have yet to answer my question. What are the lies your parents told you?
Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
and
More optimisation takes more time. This is what my model shows. More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.Now Adequate, you are demonstrating real crap.You think that the proposition that more optimisation takes more time is "real crap"?
Of course I don’t think that more optimization takes more time is “real crap”. What I am enjoying is you trying to squirm out of your totally contradictory statements about your silly graph. I must admit that you look good with both of your feet in your mouth.
http://forums.randi.org/images/smilies/doglaugh.gif
Please, please lecture us on this aspect of "the mathematics of mutation of selection" some more, and explain this point in full.

It's popcorn time!
http://img452.imageshack.us/img452/3044/popcornkj3.jpg
Adequate, listen! You can hear the theory of evolution popping. So you want another lesson on “the mathematics of mutation and selection”, ok here is another lesson on the contrast of simultaneous selection pressures and sequential selection pressures.

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=24062 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=24062)
Exposure to 3TC of HIV-1 mutant strains containing non-nucleoside reverse transcriptase inhibitor (NNRTI)-specific mutations in their reverse transcriptase (RT) easily selected for double-mutant viruses that had acquired the characteristic 184-Ile mutation in their RT in addition to the NNRTI-specific mutations. Conversely, exposure of 3TC-resistant 184-Val mutant HIV-1 strains to nine different NNRTIs resulted in the rapid emergence of NNRTI-resistant virus strains at a time that was not more delayed than when wild-type HIV-1(IIIB) was exposed to the same compounds. The RTs of these resistant virus strains had acquired the NNRTI-characteristic mutations in addition to the preexisting 184-Val mutation. Surprisingly, when the 184-Ile mutant HIV-1 was exposed to a variety of NNRTIs, the 188-His mutation invariably occurred concomitantly with the 184-Ile mutation in the HIV-1 RT. Breakthrough of this double-mutant virus was markedly accelerated as compared with the mutant virus selected from the wild-type or 184-Val mutant HIV-1 strain. The double (184-Ile + 188-His) mutant virus showed a much more profound resistance profile against the NNRTIs than the 188-His HIV-1 mutant. In contrast with the sequential chemotherapy, concomitant combination treatment of HIV-1-infected cells with 3TC and a variety of NNRTIs resulted in a dramatic delay of virus breakthrough and resistance development.
See Adequate, the empirical data shows that it is much easier for life forms to evolve to single selection conditions than to combination selection conditions. Now, here is another lesson for you, that is simultaneous combination selection pressures profoundly slow the evolutionary process.

http://aac.asm.org/cgi/content/full/49/5/1671 (http://aac.asm.org/cgi/content/full/49/5/1671)
Combination antiretroviral therapy (ART) has dramatically decreased morbidity and mortality among human immunodeficiency virus (HIV) type 1 (HIV-1)-infected patients through the durable suppression of viral replication to undetectable levels (22). Although ART has changed significantly in the decades since the advent of monotherapy, nucleoside and nucleotide reverse transcriptase (RT) inhibitors (NRTIs and NtRTIs, respectively) remain important foundations of therapy. The current guidelines for the treatment of HIV infection in the United States and the United Kingdom recommend dual NRTI and NtRTI therapy in combination with a protease inhibitor (PI) or a nonnucleoside reverse transcriptase inhibitor (NNRTI) for most patients (1, 3). New NRTI and NtRTI options for HIV therapy include two new fixed-dose once-daily combinations, abacavir (ABC) plus lamivudine (3TC) and tenofovir disoproxil fumarate (TDF) plus emtricitabine (FTC).
and
The inclusion of ZDV with ABC, 3TC, and TDF as quadruple therapy appears to result in a greater degree of viral suppression than that seen with the suboptimal triple combination of ABC, 3TC, and TDF, although these regimens have not been directly compared. It is conceivable that the inclusion of ZDV with ABC, 3TC, and TDF provided sufficient antiviral coverage to prevent selection of the K65R substitution. A possible reason for the early virologic nonresponsiveness with certain of these triple-NRTI regimens is a low genetic barrier to resistance on the part of the combination that allows the rapid emergence of M184V with or without K65R. The combination of TDF and ddI or TDF and ABC, either in a triple-NRTI regimen or as the dual-NRTI backbone in combination with a PI or NNRTI, are currently not recommended. In contrast, the 3TC and ABC combination and the 3TC and TDF combination seem to be effective NRTI backbones when they are used together with an NNRTI or a PI. Triple-NRTI regimens containing ZDV continue to play an important role in ART as an alternative to PI- and NNRTI-containing regimens as initial therapy, as simplified therapy, and in some quadruple regimens (5, 21, 25, 29; J. A. Bartlett, J. Johnson, G. Herrera, N. Sosa, A. E. Rodriguez, and M. S. Shaefer, Abstr. XIV Int. AIDS Conf., abstr. TuOrB1189, 2002; M. Markowitz, J. M. Lang, E. DeJesus, C. Hill-Zabala, E. R. Lanier, Q. Liao, K. Pappa, and M. Shaefer, Abstr. Int. AIDS Soc. 2nd Conf. Pathogen. Treatment, abstr. 42, 2003). Evidence also suggests that a triple-NRTI regimen that includes ZDV remains a rational treatment approach for many patients, especially those who initiate therapy with low viral loads (Ait Khaled et al., Abstr. XI Int. HIV Drug Res. Workshop; Melby et al., Abstr. 8th Conf. Retrov. Opportunistic Infect.). Several studies have suggested that the triple combination of ZDV, ABC, and 3TC is less potent than two NRTIs plus either a PI or an NNRTI (12, 25, 29). Although the difference in potency between PIs and triple NRTIs may often be overcome by an adherence advantage among patients with lower baseline viral loads, this may not be the case when regimens consisting of triple NRTIs are compared with those containing EFV and two NRTIs (12, 25, 29).
See Adequate, multiple simultaneous selection pressures profoundly slow the evolutionary process. The more selection conditions imposed, the more difficult it is for the population to navigate the fitness landscape.

Pop goes the theory of evolution.

christie malry

23rd August 2007, 09:29 AM

I have afeeling I'm going to regret this, but I'm going to ask anyway...

Hi Kleinman, assume that I can in no way be bothered to read the preceding 134 pages of this debate in its entirety, can you please point me to where your opponents are asking you about whether increased selection pressures increase or decrease the rate of evolution? It just doesn't seem to be on this page.

And why you think that evolution can't work when you seem to be relying on it in the post you just made?

You don't have to answer me in detail, you can just point me in the right general direction and I'll go and have a look for myself. It's just that I'm not sure what you're saying or why, but it sounds kind of interesting.

Cheers in advance.

ETA: Oh, found it on page 2. Christ, this has been going on a while. Are you still the only person who believes this, Kleinman?

joobz

23rd August 2007, 10:08 AM

Let’s review joobz cognitive (cognitive? how about his speculative abilities).
Thank you. Since the research literature has been supportng my speculations, This proves that my ability to theorize is quite solid.

A new approach for the cooperative chemical evolution of nucleic acids and proteins under the primitive earth environment.
Nucleic Acids Res Suppl. 2002;(2):279-80.

Adenine synthesis in interstellar space: mechanisms of prebiotic pyrimidine-ring formation of monocyclic HCN-pentamers.
Astrobiology. 2007 Jun;7(3):455-70.

From geochemistry and biochemistry to prebiotic evolution...we necessarily enter into Ganti's fluid automata.
Genet Mol Res. 2007 Jun 20;6(2):258-73.

Amino Acid Interaction with and Adsorption on Clays: FT-IR and Mossbauer Spectroscopy and X-ray Diffractometry Investigations.
Orig Life Evol Biosph. 2007 Jun 20; [Epub ahead of print

Emergence of homochirality in far-from-equilibrium systems: mechanisms and role in prebiotic chemistry.
Chirality. 2007 Aug;19(8):589-600. Review.

Stochastic innovation as a mechanism by which catalysts might self-assemble into chemical reaction networks.
Proc Natl Acad Sci U S A. 2007 Jun 12;104(24):10098-103. Epub 2007 Jun 4.

Formation of potentially prebiotic amphiphiles by reaction of beta-hydroxy-n-alkylamines with cyclotriphosphate.
Angew Chem Int Ed Engl. 2007;46(22):4166-8.

Joobz, if the sun shines on lead long enough does it turn into gold?
Ah, why do you continue to say things that have been proven wrong to the point absurdity? It just make you look like a complete idiot? Is it because you ARE a complete idiot, or are you simply some sort of intellectual masochist who enjoys being the fool?

Joobz, why don’t you describe to us the chemistry of any organic molecule that might arise in your speculative primordial soup and demonstrate your cognitive, whoops speculative ability?
Don't be silly. I have already.

Mr. Scott

23rd August 2007, 10:36 AM

What’s the matter kitty cat, you don’t like empirical evidence? I’ll let Dr Schneider and you other evolutionarians satisfy yourselves that other forms mutations do not overcome the mathematical fact the number of simultaneous selection pressures is the dominant parameter in the mathematics of mutation and selection. I do this because you evolutionarians are already trying to attribute Dr Schneider’s work to me. I’ll just continue to post the empirical data which refutes your silly theory.

That in answer to my clear yes/no question? That you change the subject to "empirical data" is telling.

Your claim that evolution is mathematically impossible requires that only point mutations are significant in the forward progress of evolution. Do you, or do you not have mathematical proof of this?

Now kitty cat, you have yet to answer my question. What are the lies your parents told you?

You refused to answer one of my questions on the grounds that it was off topic, yet you ask me that in this thread and expect an answer?

Do you, or do you not have mathematical proof that only point mutations are significant in the progress of evolution?

...and while we are asking on-topic questions you refuse to answer directly, I'll ask again: Why does God need help from false witness?

Belz...

23rd August 2007, 10:48 AM

Of course not, the ev model contains the essential features necessary to describe the mathematics of mutation and selection.

So... the model eschews other, significant (those are your words) sources of mutation, but somehow it still contains the "essential" features necessary to describe mutation and selection ?

How can you contain the essentials and STILL exclude them ?

Only in the confused thinking of evolutionarians do you think that somehow other forms of more destructive mutations...

Duplicate genes are "more" destructive than point mutations ?

will somehow overcome the mathematical fact that the dominant parameter in the mathematics of mutation and selection is the number of simultaneous selection conditions.

Is it, now ?

It's the DOMINANT parameter ? Proof ?

I understand how annoyed you evolutionarians become when mathematical and empirical facts are introduced into your belief system but if you want to understand how mutation and selection actually works, that is what you have to do.

I'm sorry, but that had NOTHING to do with what I said, which isn't surprising because you're currently caught between two impossible options.

1) Admit that you're wrong, which you've said you cannot do.
2) Continue to defend your claim, which you've SHOWN you cannot do.

Why Belz, the only religious fantasy on this thread is evolutionism.

Rhetoric is a poor argumentative tool, Klein.

Pop goes the theory of evolution.

Yeah, that's right. Kleinman, avenger of Christianism, who took down the goliath of science all on his own.

kjkent1

23rd August 2007, 10:58 AM

Dear Paul A.:

How much will it cost me to get you to shut the door on this thread?

Otherwise, I may be forced to attend Kleinmans Anonymous.

Thanks in advance,

kjkent1

kleinman

23rd August 2007, 11:55 AM

Joobz, why don’t you describe to us the chemistry of any organic molecule that might arise in your speculative primordial soup and demonstrate your cognitive, whoops speculative ability? Don't be silly. I have already.
Yes, I remember. Here is how you describe the formation of ribose in the primordial soup.
You can’t even explain how ribose can form nonenzymatically. How is the RNA world going to come about without ribose?Got me, I couldn't.
http://forums.randi.org/images/smilies/doglaugh.gif
[quote="Mr Scott"]Your claim that evolution is mathematically impossible requires that only point mutations are significant in the forward progress of evolution. Do you, or do you not have mathematical proof of this?
Why kitty cat, where is your mathematical proof that these other form of mutations make your theory mathematically possible. I have the mathematical proof that point mutations show that the theory of evolution is mathematically impossible and the empirical evidence that other forms of mutation do not make a difference. Now tell us the lies your parents told you.
Of course not, the ev model contains the essential features necessary to describe the mathematics of mutation and selection.[quote="Belz…"]So... the model eschews other, significant (those are your words) sources of mutation, but somehow it still contains the "essential" features necessary to describe mutation and selection ?

How can you contain the essentials and STILL exclude them ?
Belz, I don’t exclude any form of mutations from the theory of evolution. What Dr Schneider’s model shows is that point mutations and natural selection is such a slow process for increasing information that the theory of evolution is mathematically impossible. If you think that other forms of mutations which scramble the genome more severely will somehow rescue your theory, present the model. I have chosen to use real examples of mutation and selection that are not limited to random point mutations to demonstrate why your theory is impossible. Why don’t you and Mr Scott get together and add the other forms of mutations to ev and make your point.
Dear Paul A.:
How much will it cost me to get you to shut the door on this thread?
Otherwise, I may be forced to attend Kleinmans Anonymous.
Thanks in advance,
kjkent1
Don’t tell me that I have annoyed an evolutionarian. Did you notice that Adequate has taken his graph down? I’ll have to resort to my ascii art again to restore his work of art.
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http://forums.randi.org/images/smilies/doglaugh.gif

I have afeeling I'm going to regret this, but I'm going to ask anyway...
Why should you regret asking a question?
Hi Kleinman, assume that I can in no way be bothered to read the preceding 134 pages of this debate in its entirety, can you please point me to where your opponents are asking you about whether increased selection pressures increase or decrease the rate of evolution? It just doesn't seem to be on this page.
Now I know why you regret asking the question. You are a student who can’t be bothered to read. I’ll still try to address your question but not by directing you to the page(s) where this topic was discussed. Your question happens to be a good question even though it happens to be a bit vague. When you ask about increased selection pressures, you have to define what you mean by increased selection pressure. Perhaps it would help if we defined more precisely what increased selection pressure is. I’ll list what I believe are the variables which contribute to increased selection pressure and you can try to add or subtract from this list.

The first variable (and my personal favorite) when describing the magnitude or intensity of selection pressure is the number of selection conditions imposed on a population. This is what is used Dr Schneider’s ev model and this is the variable that is described in the citations that I have been posting. It is this variable (the number of selection conditions) which I am arguing is the dominant parameter in the mutation and selection process.

Another variable that is involved in the magnitude or intensity of selection pressure is the ability of the selection pressure to depress the reproductive fitness of the population. A selection pressure that has overwhelming power to depress the reproductive fitness of the population will drive that population to extinction. If an overwhelming selection pressure does not drive a population to extinction, it will certainly reduce the diversity of the population allowing only those members to survive that have a phenotype which allows them to survive such a selection pressure. A selection pressure that has only a very slight affect on the reproductive fitness of the population will only cause very slight changes in the frequency of particular genes.

A third variable which affects the magnitude or intensity of a selection pressure is the number of loci which must mutate in order for members of the population to adapt to the selection pressure. A selection pressure which requires only a mutation at a single locus to adapt will be of less intensity than a selection pressure which requires mutations at multiple loci in order for the population to adapt.

Perhaps you can think of other variables which would affect the intensity or magnitude of a selection pressure. Then you evolutionarians have to put together these variables into a form that would allow the transformation of reptile to birds. It is my contention that the number of selection conditions is the dominant parameter in the mathematics of mutation and selection. Dr Schneider’s model does not allow extinction but his model only allows half the population to reproduce in every generation. That is an intense selection criterion. Despite this intense selection criterion, the three selection conditions in his model still can only evolve on unrealistically small genomes. When you reduce the number of selection conditions to one, the model easily and rapidly evolves that single condition.
And why you think that evolution can't work when you seem to be relying on it in the post you just made?
I have never said that evolution can’t work. What I am saying is that evolution by mutation and selection is a far more limited phenomenon than alleged by evolutionarians. I support my hypothesis with Dr Schneider’s peer reviewed and published computer simulation of random point mutation and natural selection and the vast amount of empirical data which demonstrates the results of his model. What evolution by mutation and selection is simply an optimization problem for sorting beneficial and detrimental mutations. If you ever take the time to study optimization or sorting problems, you will find that the mathematics of these problems is dominated by the optimization or sorting conditions. This condition is demonstrated by Dr Schneider’s ev computer simulation and this affect is demonstrated in reality. The gross extrapolation of mutation and selection to the evolution of reptiles to birds does not make mathematical sense. Not only do evolutionarians not have selection conditions that would accomplish this type of transformation, the number of genetic systems that would have to be transformed would give such a horrendously complex fitness landscape that no population could navigate such a landscape. Look what happens to the evolution of HIV when the virus is subjected to only three selection conditions despite the virus’s extremely high reproductive rate and mutation rate.
You don't have to answer me in detail, you can just point me in the right general direction and I'll go and have a look for myself. It's just that I'm not sure what you're saying or why, but it sounds kind of interesting.
It is an interesting topic but it will not change the fundamental mathematical defect in the theory of evolution. What is important about this topic is that if you want to stop the evolution of HIV completely, you will need combination selection pressures that suppress the reproductive fitness of the virus strongly and require as many mutations as possible to evolve resistance to these selection pressures.
ETA: Oh, found it on page 2. Christ, this has been going on a while. Are you still the only person who believes this, Kleinman?
Christie, is has been going on for a while. I don’t know if I am the only one who believes this. Delphi, (an ardent evolutionarian) has taken to arranging his sock drawer and Adequate (a fanatical evolutionarian) has taken to throwing temper tantrums but it’s ok, I don’t mind being the only one posting on this forum arguing this point. It is actually a very easy position to take on evolution. The mathematics is clear and there is a vast amount of empirical data with which to annoy evolutionarians. In fact, here is another empirical example of how mutation and selection actually works. This is another citation dedicated to Dr Schneider and his crew over at the National Cancer Institute which show that combination simultaneous selection pressures profoundly slow the evolutionary process while sequential selection pressures are much easier for populations to adapt to.

http://www.medpagetoday.com/HematologyOncology/LeukemiaLymphoma/tb/6437 (http://www.medpagetoday.com/HematologyOncology/LeukemiaLymphoma/tb/6437)
NEW YORK, Aug. 17 -- A double-barreled initial approach to chronic myelogenous leukemia with both imatinib (Gleevec) and dasatinib (SPRYCEL) may prevent treatment-resistant genetic mutations. Action Points

Explain to interested patients that the study was small and included primarily patients with advanced disease, but it suggests that combination kinase inhibitor therapy could provide advantages over sequential therapy.

Dasatinib is approved as second-line treatment of chronic myelogenous leukemia with resistance or intolerance to prior therapy including imatinib.

Conventional use of dasatinib only after imatinib fails allows for compound drug-resistant mutations that synergistically increase tumor growth, found Charles L. Sawyers, M.D., of Memorial Sloan-Kettering Cancer Center here, and colleagues.

Frontline kinase inhibitor combination therapy could "substantially improve both the depth and durability of clinical responses," particularly in advanced phases of disease, they wrote online in the Journal of Clinical Investigation.

Furthermore, "it is likely that other cancers being treated with kinase inhibitor therapy will benefit from a similar treatment strategy," they added.

Mutations conferring kinase inhibitor resistance have become increasingly common not just in chronic myelogenous leukemia but also in gastrointestinal stromal tumor and lung cancer. As clinical experience with dasatinib grows, some patients have begun to experience relapse on second-line dasatinib, the researchers said.

One mechanism anticipated for prior studies is selection for the T315I mutation, a "gatekeeper" mutation that confers resistance to imatinib, dasatinib, and the related investigational compound nilotinib.

So, the researchers assessed it and other mutations in dasatinib failure. They studied 17 consecutive patients treated at a single center who developed dasatinib resistance after imatinib treatment.

Analysis of their blood samples at relapse showed that all patients had new mutations in the BCR-ABL protein. Twelve had the T315I mutation and one had the relatively resistant F317L mutation.

Six patients had the imatinib-sensitive, dasatinib-resistant mutations V299L, T315A, or F317I.

Two had only the V299L mutation and responded to retreatment with imatinib or nilotinib.

One of these patients responded only briefly to an escalated dose of dasatinib and then returned to imatinib, which effectively reduced myeloblasts from 52% to 12% until starting chemotherapy for a planned allogeneic marrow transplant. The other patient temporarily responded to high-dose imatinib but had a sustained complete hematologic response on investigational nilotinib.

"However, this strategy of cycling between kinase inhibitors is potentially limited by the emergence of compound mutations that, when paired in the same molecule, confer resistance to both drugs," the researchers said.

"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 [new mutations] with enhanced oncogenic potency," they added.

And, that's what they found.

Of the 17 patients, five developed compound mutations -- two or more changes in the same mRNA -- with a new dasatinib-resistant mutation occurring on the background of their original imatinib-resistant substitution.

Two patients had more than one mutation develop during dasatinib treatment, but separately rather than as a compound mutation.

The compound mutations were likely caused by selective pressure from sequential therapy, Dr. Sawyers and colleagues said.

One patient had a triple compound mutation conferring resistance to both compounds. And, the triple mutation from sequential therapy synergistically made tumor cells grow faster in vitro than expected.

This patient, left without other treatment options, turned to combined imatinib and dasatinib therapy and had a hematologic response sustained for at least two months.

"These findings make a case for upfront therapy with a cocktail of kinase inhibitors that collectively cover a broad range of mutations and prevent the emergence of resistance," the researchers wrote.

However, studies would need to address tolerability and "whether the potential benefit of preventing resistance is outweighed by additional toxicities," they added. Larger, longer studies also need to determine whether sequential therapy has the same effect in early-stage CML.

"Targeted therapy of human malignancies is still in its infancy," the researchers concluded. "Optimal patient management in the future will likely require periodic genotyping to determine the likelihood of response to a particular kinase inhibitor."

Dr Adequate

23rd August 2007, 12:17 PM

Of course I don’t think that more optimization takes more time is “real crap”. Then why did you describe my statement that more optimization takes more time as "real crap"?

Are you just in love with telling lies?

What I am enjoying is you trying to squirm out of your totally contradictory statements about your silly graph. Edited out rule 12 breach.
Everyone reading this thread can see that I am not trying to "squirm out" of any statement I have made about my model.

Why do you lie when you know that you're going to get caught?

I particular, I stand by both of the statements which you claim are "contradictory", because they are both very obviously true. Everyone reading this thread can see that they are not contradictory just by glancing at the graph which they both accurately describe ---- except possibly you, Edited out rule 12 breach.

Dr Adequate

23rd August 2007, 12:20 PM

Yes, I remember. Here is how you describe the formation of ribose in the primordial soup.

You can’t even explain how ribose can form nonenzymatically. How is the RNA world going to come about without ribose?Got me, I couldn't.
http://forums.randi.org/images/smilies/doglaugh.gif

Why kitty cat, where is your mathematical proof that these other form of mutations make your theory mathematically possible. I have the mathematical proof that point mutations show that the theory of evolution is mathematically impossible and the empirical evidence that other forms of mutation do not make a difference. Now tell us the lies your parents told you.

Belz, I don’t exclude any form of mutations from the theory of evolution. What Dr Schneider’s model shows is that point mutations and natural selection is such a slow process for increasing information that the theory of evolution is mathematically impossible. If you think that other forms of mutations which scramble the genome more severely will somehow rescue your theory, present the model. I have chosen to use real examples of mutation and selection that are not limited to random point mutations to demonstrate why your theory is impossible. Why don’t you and Mr Scott get together and add the other forms of mutations to ev and make your point.

Don’t tell me that I have annoyed an evolutionarian. Did you notice that Adequate has taken his graph down? I’ll have to resort to my ascii art again to restore his work of art.
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http://forums.randi.org/images/smilies/doglaugh.gif

Why should you regret asking a question?

Now I know why you regret asking the question. You are a student who can’t be bothered to read. I’ll still try to address your question but not by directing you to the page(s) where this topic was discussed. Your question happens to be a good question even though it happens to be a bit vague. When you ask about increased selection pressures, you have to define what you mean by increased selection pressure. Perhaps it would help if we defined more precisely what increased selection pressure is. I’ll list what I believe are the variables which contribute to increased selection pressure and you can try to add or subtract from this list.

The first variable (and my personal favorite) when describing the magnitude or intensity of selection pressure is the number of selection conditions imposed on a population. This is what is used Dr Schneider’s ev model and this is the variable that is described in the citations that I have been posting. It is this variable (the number of selection conditions) which I am arguing is the dominant parameter in the mutation and selection process.

Another variable that is involved in the magnitude or intensity of selection pressure is the ability of the selection pressure to depress the reproductive fitness of the population. A selection pressure that has overwhelming power to depress the reproductive fitness of the population will drive that population to extinction. If an overwhelming selection pressure does not drive a population to extinction, it will certainly reduce the diversity of the population allowing only those members to survive that have a phenotype which allows them to survive such a selection pressure. A selection pressure that has only a very slight affect on the reproductive fitness of the population will only cause very slight changes in the frequency of particular genes.

A third variable which affects the magnitude or intensity of a selection pressure is the number of loci which must mutate in order for members of the population to adapt to the selection pressure. A selection pressure which requires only a mutation at a single locus to adapt will be of less intensity than a selection pressure which requires mutations at multiple loci in order for the population to adapt.

Perhaps you can think of other variables which would affect the intensity or magnitude of a selection pressure. Then you evolutionarians have to put together these variables into a form that would allow the transformation of reptile to birds. It is my contention that the number of selection conditions is the dominant parameter in the mathematics of mutation and selection. Dr Schneider’s model does not allow extinction but his model only allows half the population to reproduce in every generation. That is an intense selection criterion. Despite this intense selection criterion, the three selection conditions in his model still can only evolve on unrealistically small genomes. When you reduce the number of selection conditions to one, the model easily and rapidly evolves that single condition.

I have never said that evolution can’t work. What I am saying is that evolution by mutation and selection is a far more limited phenomenon than alleged by evolutionarians. I support my hypothesis with Dr Schneider’s peer reviewed and published computer simulation of random point mutation and natural selection and the vast amount of empirical data which demonstrates the results of his model. What evolution by mutation and selection is simply an optimization problem for sorting beneficial and detrimental mutations. If you ever take the time to study optimization or sorting problems, you will find that the mathematics of these problems is dominated by the optimization or sorting conditions. This condition is demonstrated by Dr Schneider’s ev computer simulation and this affect is demonstrated in reality. The gross extrapolation of mutation and selection to the evolution of reptiles to birds does not make mathematical sense. Not only do evolutionarians not have selection conditions that would accomplish this type of transformation, the number of genetic systems that would have to be transformed would give such a horrendously complex fitness landscape that no population could navigate such a landscape. Look what happens to the evolution of HIV when the virus is subjected to only three selection conditions despite the virus’s extremely high reproductive rate and mutation rate.

It is an interesting topic but it will not change the fundamental mathematical defect in the theory of evolution. What is important about this topic is that if you want to stop the evolution of HIV completely, you will need combination selection pressures that suppress the reproductive fitness of the virus strongly and require as many mutations as possible to evolve resistance to these selection pressures.

Christie, is has been going on for a while. I don’t know if I am the only one who believes this. Delphi, (an ardent evolutionarian) has taken to arranging his sock drawer and Adequate (a fanatical evolutionarian) has taken to throwing temper tantrums but it’s ok, I don’t mind being the only one posting on this forum arguing this point. It is actually a very easy position to take on evolution. The mathematics is clear and there is a vast amount of empirical data with which to annoy evolutionarians. In fact, here is another empirical example of how mutation and selection actually works. This is another citation dedicated to Dr Schneider and his crew over at the National Cancer Institute which show that combination simultaneous selection pressures profoundly slow the evolutionary process while sequential selection pressures are much easier for populations to adapt to.

http://www.medpagetoday.com/HematologyOncology/LeukemiaLymphoma/tb/6437 (http://www.medpagetoday.com/HematologyOncology/LeukemiaLymphoma/tb/6437)
2251 words of your usual dreary crap, then?

Dr Adequate

23rd August 2007, 12:26 PM

Oh, wait, it isn't just the same old stinking crap, you also thought of a new insane halfwitted lie:

Did you notice that Adequate has taken his graph down? I have not, of course, done any such thing, you Removed word liar, as everyone reading this thread can check.

Everyone can see that that it's still exactly where I posted it, right here (http://forums.randi.org/showthread.php?p=2607145).

Everyone can see that you're lying, kleinman.

Why do you lie when you know you're going to get caught?

Removed personal attack

Or perhaps you've just become so frightened of my model that you can't bear to look at the data any more, and snivelled out this wretched stupid lie out as a lame excuse. Removed personal attack

Or, sheesh, perhaps you've been possessed by Satan Father of Lies?

Why do you lie when you know you're going to get caught?

Dr. A; Please keep in mind your membership agreement; I have removed and edited out several words and even sentences that were violations of Rule 12, leaving in the challenges to Kleinman.

Dr Adequate

23rd August 2007, 12:37 PM

ETA: Oh, found it on page 2. Christ, this has been going on a while. Are you still the only person who believes this, Kleinman? Assuming, of course, that he has at least managed to deceive himself with his own puke and drivel.

Otherwise no-one believes it.

Dr Adequate

23rd August 2007, 12:55 PM

I’ll have to resort to my ascii art again to restore his work of art.
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|_______________________________________ Now, since everyone can in fact see my graph, everyone can see that your stupid crap is not what I posted, can't they?

So everyone reading this thread knows that you're a liar.

Why do you lie when you know that you're going to be caught, kleinman?

Dr Adequate

23rd August 2007, 12:57 PM

Rhetoric is a poor argumentative tool, Klein. Which is appropriate, because so is kleinman.

tracer

23rd August 2007, 01:00 PM

http://img452.imageshack.us/img452/3044/popcornkj3.jpg

Damn you, Dr. A!
Now you've made me want some popcorn.

Belz...

23rd August 2007, 01:15 PM

Belz, I don’t exclude any form of mutations from the theory of evolution.

No, you just claim they're all bad and therefore pointless to the discussion at hand.

What Dr Schneider’s model shows is that point mutations and natural selection is such a slow process for increasing information that the theory of evolution is mathematically impossible.

You are lying. Not only doesn't it show that conclusively, but the very FACT that there are other sources of mutation makes the simulation irrelevant. At best.

If you think that other forms of mutations which scramble the genome more severely will somehow rescue your theory, present the model.

Present the model ? Do I look like the kind of person who will spend so much time making a simulation when what YOU need to do is prove YOUR theory ?

I have chosen to use real examples of mutation and selection that are not limited to random point mutations to demonstrate why your theory is impossible. Why don’t you and Mr Scott get together and add the other forms of mutations to ev and make your point.[/QUOTE]

kleinman

23rd August 2007, 01:17 PM

Did you notice that Adequate has taken his graph down?I have not, of course, done any such thing, you retarded liar, as everyone reading this thread can check.
Glad to see you got your graph back. We wouldn’t want the readers to be deprived of this:
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
The red line shows generations to achieve fixation of n alleles acted on by n selection pressures, the n+1th selection pressure being introduced only after the nth allele is fixed.

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

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

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
And then Adequate goes on to say this:
More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.
http://forums.randi.org/images/smilies/doglaugh.gif
Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?
I find your graph precious and your comments about your graph delightful. You keep up the good work Adequate.
http://forums.randi.org/images/smilies/doglaugh.gif
So let’s give another example of how mutation and selection actually works. As precious as Adequate’s graph is and as delightful are his comments about his graph, alas, mutation and selection does not work the way his twisted imagination works.

http://www.sciencemag.org/cgi/content/abstract/269/5224/696 (http://www.sciencemag.org/cgi/content/abstract/269/5224/696)
Combinations of antiretroviral drugs that prevent or delay the appearance of drug-resistant human immunodeficiency virus-type 1 (HIV-1) mutants are urgently required. Mutants resistant to 3'-azidothymidine (AZT, zidovudine) became phenotypically sensitive in vitro by mutation of residue 184 of viral reverse transcriptase to valine, which also induced resistance to (-)2'-deoxy-3'-thiacytidine (3TC). Furthermore, AZT-3TC coresistance was not observed during extensive in vitro selection with both drugs. In vivo AZT-3TC combination therapy resulted in a markedly greater decreased in serum HIV-1 RNA concentrations than treatment with AZT alone, even though valine-184 mutants rapidly emerged. Most samples assessed from the combination group remained AZT sensitive at 24 weeks of therapy, consistent with in vitro mutation studies.
How could this be Adequate, I found a citation (well, hundreds of citations) that contradicts your incredibly silly graph and your incredibly silly comments about your graph. How could this be? Combination selection pressures slow the evolutionary process? How could Adequate’s graph be so wrong?
http://forums.randi.org/images/smilies/doglaugh.gif

Dr Adequate

23rd August 2007, 01:30 PM

joobz

23rd August 2007, 01:36 PM

Yes, I remember. Here is how you describe the formation of ribose in the primordial soup.
[quote="Kleinman"]You can’t even explain how ribose can form nonenzymatically. How is the RNA world going to come about without ribose?[quote="joobz"]Got me, I couldn't.
hmm, you quote something from over a year ago, when I didn't know. But, you ignore the references I provided from a week ago that prove you your claim wrong.

After 133 pages of his nonsense, you can't find a single point that I've been horrifically wrong on.
However, your list of "stupid things only a stupid fool would say" keeps growing.

Such as
1. 1st law thermo = natural selection
2. No evidence for speciation
3. Probability greater than 1
4. Nuclear and chemical reactions are equivilent
5. Thermodyanmics is a kinetic study
6. slow=stop
7. Unable to compile a program
8. Mutation rate is constant
9. biochemistry is a prebiotic field
10. mutations other than point and Recombination and aren't important
11. Unable to read a graph

kleinman

23rd August 2007, 01:39 PM

So your only critique of my model, besides your stupid lie about having produced counterexamples, is that I've made two obviously true statements about the data output?

I admit it, I have indeed, pointed out the completely obvious. I don't see that this is an objection.
Adequate has a model of mutation and selection?
http://forums.randi.org/images/smilies/doglaugh.gif
You do have a precious graph with some delightful commentary, here it is again.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
The red line shows generations to achieve fixation of n alleles acted on by n selection pressures, the n+1th selection pressure being introduced only after the nth allele is fixed.

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

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

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
And then Adequate goes on to say this:
More optimisation takes more time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.
http://forums.randi.org/images/smilies/doglaugh.gif
Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution?
Adequate, your art work is darling and your rhetoric describing your art work is cherished.
http://forums.randi.org/images/smilies/doglaugh.gif

kleinman

23rd August 2007, 01:45 PM

Yes, I remember. Here is how you describe the formation of ribose in the primordial soup.Got me, I couldn't.hmm, you quote something from over a year ago, when I didn't know. But, you ignore the references I provided from a week ago that prove you your claim wrong.
Let’s hear how an alchemist describes abiogenesis.
Envision a system of millions of forming and destructive chemical reactions. Now, envision that intermediates of there reactions associate through non-covalent means and that this complex becomes protected against the destructive reactive pathway, perhaps by a reversible precipitation. These new complexes result in a localized increased of new chemical species. These chemical species then progress in a new series of reaction... that is what I mean through cooperative means. I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?
Maybe Adequate can help you with a graph to go along with your silly speculations.
http://forums.randi.org/images/smilies/doglaugh.gif

Dr Adequate

23rd August 2007, 01:52 PM

Adequate has a model of mutation and selection?
http://forums.randi.org/images/smilies/doglaugh.gif
You do have a precious graph with some delightful commentary, here it is again.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg

And then Adequate goes on to say this:

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

Adequate, your art work is darling and your rhetoric describing your art work is cherished.
http://forums.randi.org/images/smilies/doglaugh.gif So now you have no counterarguments, not even ones with lies in.

You're just going to quote me pointing out the truth.

Good, good, carry on. Every time you do so, everyone can see that what I say is true.

Dr Adequate

23rd August 2007, 01:58 PM

11. Unable to read a graph And it goes deeper than that, 'cos I've told him what it shows. He's quoted the relevant passages dozens of times. He's even highlighted them in red. And he just can't get his head round it.

It's amazing, isn't it? I can't imagine being like that, it must be like being color-blind or something.

slyjoe

23rd August 2007, 02:16 PM

And it goes deeper than that, 'cos I've told him what it shows. He's quoted the relevant passages dozens of times. He's even highlighted them in red. And he just can't get his head round it.

It's amazing, isn't it? I can't imagine being like that, it must be like being color-blind or something.

No, that defense won't work for him either. I'm color blind and I can see the highlighted parts just fine, thank you very much. :)

kjkent1

23rd August 2007, 03:00 PM

Don’t tell me that I have annoyed an evolutionarian.Okay, I won't tell you that.

Instead, I will simply suggest that you get some psychological counseling, because you obviously have a serious problem with admitting the possibility of error. This could very negatively affect your ability to practice medicine at the standard of care.

Anticipating your response that it is "evolutionarians" who have the problem admitting error, I will reply now, that I have a very open mind, but you have not proved your case. You simply rattle out the same old stuff, post after post, and even someone such as myself, who has no special scientific education, can immediately find the very substantial holes in your assertions.

Point being, that even were I to concede that the theory of evolution is wrong, this would not be an admission that the Kleinman theory is correct. Instead, I would be left with "I dunno" as the answer to any question concerning the existence of life on Earth.

Fortunately, it's rather obvious to me that your theory is wrong and evolution is correct. The facts speak for themselves -- as does your apparently endless capacity for "tilting at windmills."

Darat

23rd August 2007, 03:03 PM

First and final warning.

kleinman & Dr Adequate - please read the new Membership Agreement, you are both repeatedly breaching the new Rule 12.

If this thread cannot continue without breaching the new rules I will permanently close it. In the meantime I am closing it for 24 hours to allow some of the heat to dissipate.

Once I re-open it I will issue suspensions to any Member that continues to breach Rule 12.

kleinman

27th August 2007, 09:52 AM

Dr Schneider has posted on his ev blog web site located at http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/blog-ev.html (http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/blog-ev.html) and again is arguing that his model refutes Professor Behe’s irreducible complexity hypothesis. Professor Behe has added the term “necessarily” to his definition for irreducible complexity. Dr Schneider says the following.
Essentially, the word 'necessarily' was added. The changes do not appear to alter the definition sufficiently to escape the challenge from Ev (which Behe did not respond to). As pointed out in the discussion of of the Ev paper (page 2797), the organisms in Ev match this definition exactly, but they evolved. This completely destroys Behe's thesis.
So, what did Dr Schneider say in his paper that refutes the hypothesis of irreducible complexity?
The ev model can also be used to succinctly address two other creationist arguments. First, the recognizer gene and its binding sites co-evolve, so they become dependent on each other and destructive mutations in either immediately lead to elimination of the organism. This situation fits Behe's [34] definition of `irreducible complexity' exactly (``a single system composed of several well-matched, interacting parts that contribute to the basic function, wherein the removal of any one of the parts causes the system to effectively cease functioning'', page 39), yet the molecular evolution of this `Roman arch' is straightforward and rapid, in direct contradiction to his thesis. Second, the probability of finding 16 sites averaging 4 bits each in random sequences 2^-4*16 @ 5 10^-20 is yet the sites evolved from random sequences in only ~10^3 generations, at an average rate of 1 bit per 11 generations. Because the mutation rate of HIV is only 10 times slower, it could evolve a 4 bit site in 100 generations, about 9 months [35], but it could be much faster because the enormous titer (10^10 new virions/day/person [17]) provides a larger pool for successful changes. Likewise, at this rate, roughly an entire human genome of ~4 * 10^9 bits (assuming an average of 1 bit/base, which is clearly an overestimate) could evolve in a billion years, even without the advantages of large environmentally diverse worldwide populations, sexual recombination and interspecies genetic transfer. However, since this rate is unlikely to be maintained for eukaryotes, these factors are undoubtedly important in accounting for human evolution. So, contrary to probabilistic arguments by Spetner [36,32], the ev program also clearly demonstrates that biological information, measured in the strict Shannon sense, can rapidly appear in genetic control systems subjected to replication, mutation and selection [33].
Dr Schneider continues to misinterpret his own model. He is arguing from his single unrealistic case of a population with genome length of only 256 bases. It is only this unrealistic case which shows the rapid accumulation of information. Dr Schneider knows well that any realistic length genome would require huge numbers of generations to acquire the same amount of information that his unrealistic case demonstrates. Is Dr Schneider trying to argue that he has modeled the de nova evolution of binding sites? Does Dr Schneider want to explain why his model takes huge number of generations to converge when realistic parameters are used? Apparently not, because he has chosen his own web site to advertise his model where he is not exposed to direct challenge to his assertions.

Well, the James Randi Educational forum provides a venue from which to challenge Dr Schneider, head of computational molecular biology at the National Cancer Institute and his unrealistic assertions. What Dr Schneider’s model actually shows is how slowly mutation and selection accumulates information when multiple selection conditions are applied simultaneously. This mathematical finding has important implications for the treatment of cancer as well as infectious diseases, agriculture and other fields of science and medicine. Dr Schneider’s model demonstrates the mutation/selection optimization problem and how profoundly slowly it converges with multiple selection conditions. It is worthwhile to review what his model shows.

Consider Dr Schneider’s baseline case of population=64, genome length=64, binding sites=16, site width=6, weight width=5 and mutation rate=1 per genome per generation. You obtain the following data from his model for generation for convergence as a function of genome length. The convergence condition is that each of the three selection conditions is satisfied simultaneously without mistakes.

Genome length/generations to convergence for all three selection conditions no mistakes
256/662
512/2,412
1,024/18,030
2,048/42,641
4,096/163,722
8,192/710,152
16,384/6,894,433

When you set any two of the three selection conditions to zero, the remaining selection condition evolves far more rapidly than all three selection conditions simultaneously. This is demonstrated by the following data obtained from the model.

Genome length/no missed binding sites/no spurious binding in gene/no spurious binding outside gene
16,384/1/223/223
32,768/1/115/403
65,536/1/788/1,026

This series of cases demonstrates the import feature of the mutation/selection optimization process. It takes far more generations to converge all three selection conditions simultaneously than any one of the three selection conditions alone. This is clearly demonstrated even on genomes four times longer with one fourth the mutation rate than the largest genome case computed with simultaneous selection pressures.

The importance of this mathematical finding is reflected in the empirical data. In particular, I will focus on examples from the field of oncology since Dr Schneider works at the National Cancer Institute.

http://caonline.amcancersoc.org/cgi/content/full/54/3/150 (http://caonline.amcancersoc.org/cgi/content/full/54/3/150)
Advanced premalignant lesions have a high risk of transformation to malignancy as well as resistance to single-agent retinoid therapy. Biochemoprevention, which combined retinoids with interferon (IFN) and -tocopherol, 195 was therefore designed to target this group. Papadimitrakopoulou et al. conducted a nonrandomized clinical trial in 36 patients with advanced premalignant lesions using IFN-, -tocopherol, and 13cRA for one year.195 Biochemoprevention prevented laryngeal lesions but had no effect on oral cavity lesions (P = 0.009). From biopsy specimens at different time points in this trial, it was discovered that patients with high p53 expression had lower complete response rates (P = 0.04) and higher disease progression rates (P =0.02) than patients with low p53 expression.196 Based on this study, another trial using biochemoprevention induction therapy for one year followed by two years of maintenance fenretinide or placebo is underway.

http://carcin.oxfordjournals.org/cgi/content/full/21/3/485 (http://carcin.oxfordjournals.org/cgi/content/full/21/3/485)
Although mutations in death receptors are rare events in human tumors, changes accompanying tumorigenesis can alter the regulation of these pathways. Mitogenic oncogenes like c-myc and E1A can increase sensitivity to Fas and TNF- in cultured cells (159,160), and many human tumors have alterations in TRAIL-mediated death pathways (19). TRAIL is a TNF-related protein that initiates p53-independent apoptosis by binding to its receptors DR4 or DR5. Normal cells are resistant to TRAIL-induced apoptosis, apparently because these cells express `decoy' receptors that compete with DR4 and DR5 for TRAIL but do not transmit a death-inducing signal (161,162). Through an unknown mechanism, the expression of the decoy receptor 1 seems to be widely lost on tumor cells, making them exquisitely susceptible to TRAIL-mediated cell death. Because DR5 is a p53-responsive gene, combination therapy with TRAIL and classic cytotoxic agents may be particularly effective in treating tumors with functional p53 (73).

http://www.rxpgnews.com/cancer/lung/article_4344.shtml (http://www.rxpgnews.com/cancer/lung/article_4344.shtml)
By University of California - Los Angeles, An early phase study pairing an experimental targeted therapy with a common anti-inflammatory produced promising results in patients with advanced lung cancer, researchers at UCLA's Jonsson Cancer Center reported.

Pairing the targeted therapy Tarceva with the anti-inflammatory drug Celebrex increased response rates in lung cancer patients by about three-fold, said Dr. Karen Reckamp, an assistant professor of hematology/oncology and lead author of the study. The research appears in the June 1 issue of Clinical Cancer Research, the peer-reviewed journal of the American Association of Cancer Research.

Previous laboratory studies at UCLA showed that a cell signaling pathway known as COX-2 may be linked to resistance to drugs like Tarceva, which block tumor cell growth by targeting the protein EGFR, or epidermal growth factor receptor. Researchers theorized that giving Tarceva with Celebrex, a COX-2 inhibitor, would help battle resistance and prove to be an affective combination against lung cancer.

Typically, about 10 percent of lung cancer patients respond to Tarceva. In Reckamp's study of the combination therapy, about 33 percent of patients responded.

"Tarceva alone is a great drug and has a lot of clinical benefits, but for a small proportion of patients," Reckamp said. "With this drug combination, we saw an increase in response rates, indicating we are overcoming some resistance. We also may be beginning to understand the mechanisms of that resistance."

http://www.pnas.org/cgi/content/full/100/3/776 (http://www.pnas.org/cgi/content/full/100/3/776)
The presence of thousands of mutations in single cancer cells suggests that among the 108 cells in a human tumor at the time of diagnosis there are billions of different mutations, and that mutations in most, if not every, gene and regulatory sequence are present in one or more cells within a tumor. On exposure to a chemotherapeutic agent, tumor cells with preexisting mutations that render them resistant would preferentially proliferate and could eventually repopulate the tumor, thus accounting for the efficiency with which tumors acquire drug resistance. The efficacy of combination chemotherapy is usually rationalized on the basis of reduced toxicities, each agent being given in subtoxic amounts; killing of tumor cells is additive, but toxicity is not. The presence of random mutations within a tumor provides another rationalization to account for the utility of combined chemotherapy. Combined regimens may elicit a therapeutic response, even in the presence of preexisting mutations that defeat single-agent therapy, because resistance would require that the same tumor cell harbor mutations that confer resistance to each agent.

Most chemotherapeutic agents target either DNA synthesis or mitosis. Thus, it has been difficult to postulate mechanisms for specificity, because these processes occur with the same frequencies in cancer cells as in some rapidly dividing normal cells. It is interesting to consider that most chemotherapeutic agents are potent mutagens, and presumably induce mutations in both normal and malignant cells. The presence of large numbers of preexisting mutations in tumor cells increases the likelihood that additional mutations might exceed a maximum level consistent with viability. Thus, further mutagenesis might be selectively lethal for tumor cells that contain large numbers of mutations. It seems plausible that there is an error threshold for cell viability, and it is interesting to speculate that some anticancer drugs may introduce a sufficient number of mutations in cancer cells that already harbor multiple mutations to exceed this threshold (51).

The importance of understanding the mathematics of mutation and selection goes beyond just proving that the theory of evolution is mathematically impossible. The mathematics of mutation and selection has important implications in battling cancer as well as infectious diseases. What the mathematics of mutation and selection shows is that combined simultaneous selection pressures profoundly slows the evolutionary process. This is the reason ev converges so slowly when all but the tiniest genome lengths are used in the model and this is what the empirical data shows. This empirical data is not limited to the field of oncology but is also revealed in virology, bacteriology, parasitology and agriculture as well.

kjkent1

27th August 2007, 03:08 PM

kleinman

27th August 2007, 05:08 PM

I wonder if the the slowness of ev's evolutionary process could be attributed to the fact that (1) the model only uses random point mutation, which excludes all of the other well-established and scientifically verified mutations which appear in real-world organisms, and (2) the selection conditions of the ev environment are fixed and unchanging -- entirely unlike any environment found in the real-world?
Ev’s evolutionary process is not slow if you use only a single selection condition. Consider the data in the previous post. The single selection condition series on a 64k genome still is able converge any of the selection conditions in about a thousand generations or less with a population of only 64. How would more extreme scrambling of the genome such as insertions and deletions or translocations accelerate the evolutionary process for three selection conditions? You then have to consider the vast amount of empirical data in which the evolutionary mechanism is not limited to point mutations and natural selection. These real cases demonstrate that multiple simultaneous selection conditions slow the evolutionary process profoundly. You are correct that the selection conditions in ev are fixed and unchanging and that in the “real world” this is not the case. Consider what happens when there is incomplete adherence with combination treatment for HIV. Resistant viruses appear. Now how do you carry your concept of changing selection conditions to evolution of a birds from reptiles. You have an extremely complex fitness landscape this precursor population of reptiles must traverse to metamorphose to a population of birds with an ever changing set of selection pressures. There is no mathematical or empirical basis on which to postulate such huge genetic transformations.
On the subject of multi-drug therapies and their ability to target and slow the onslaught of various otherwise lethal diseases, I have a bit of empirical evidence to share. I have a very good friend who has been fighting HIV for about 15 years now. He has had many different therapies prescribed during that time period, and his disease has eventually mutated to avoid each and every one. At the moment, his current three-drug cocktail has once again failed, and he is now suffering from terminal lymphoma. His projected survival time is less than six months.
I am sorry to hear about your friend. However, he would not have lived these 15 years with monotherapy and the virus would have evolved resistance far more rapidly if monotherapy treatment had been used. Again, you must consider that HIV is one of the most extreme examples of evolution by mutation and selection. It has a very short genome, very short generation times, huge populations and extremely high mutation rates. In addition this virus does recombination. How do you carry over these extreme mathematical advantages that the HIV virus has in the evolutionary process to reptiles which has much longer genomes, much longer generation times, much smaller populations and a much lower mutation rate. In addition, you can’t define the “wild” selection pressures that would accomplish this metamorphosis of a reptile population to a bird population?
Dr. Kleinman, your theory is thus empirically falsified. Period.
Perhaps you could explain how combination therapy extending your friend’s life 15 years falsifies my theory?

Here is another study which shows that combination therapy slows the evolution of resistant HIV viruses.
http://content.nejm.org/cgi/content/abstract/335/15/1081 (http://content.nejm.org/cgi/content/abstract/335/15/1081)
Background This double-blind study evaluated treatment with either a single nucleoside or two nucleosides in adults infected with human immunodeficiency virus type 1 (HIV-1) whose CD4 cell counts were from 200 to 500 per cubic millimeter.

Methods We randomly assigned 2467 HIV-1–infected patients (43 percent without prior antiretroviral treatment) to one of four daily regimens: 600 mg of zidovudine; 600 mg of zidovudine plus 400 mg of didanosine; 600 mg of zidovudine plus 2.25 mg of zalcitabine; or 400 mg of didanosine. The primary end point was a >50 percent decline in the CD4 cell count, development of the acquired immunodeficiency syndrome (AIDS), or death.

Results Progression to the primary end point was more frequent with zidovudine alone (32 percent) than with zidovudine plus didanosine (18 percent; relative hazard ratio, 0.50; P<0.001), zidovudine plus zalcitabine (20 percent; relative hazard ratio, 0.54; P<0.001), or didanosine alone (22 percent; relative hazard ratio, 0.61; P<0.001). The relative hazard ratios for progression to an AIDS-defining event or death were 0.64 (P = 0.005) for zidovudine plus didanosine, as compared with zidovudine alone, 0.77 (P = 0.085) for zidovudine plus zalcitabine, and 0.69 (P = 0.019) for didanosine alone. The relative hazard ratios for death were 0.55 (P = 0.008), 0.71 (P = 0.10), and 0.51 (P = 0.003), respectively. For zidovudine plus zalcitabine, the benefits were limited to those without previous treatment.

Conclusions Treatment with zidovudine plus didanosine, zidovudine plus zalcitabine, or didanosine alone slows the progression of HIV disease and is superior to treatment with zidovudine alone. Antiretroviral therapy can improve survival in patients with 200 to 500 CD4 cells per cubic millimeter.
Perhaps some day, sufficient number and intensity of selection pressures will be put on the HIV virus to completely stop the evolution of the virus.

kjkent1

27th August 2007, 10:51 PM

articulett

27th August 2007, 11:20 PM

Rule 12 breach removed.

Belz...

28th August 2007, 05:31 AM

Klein, what about those species that we can see evolve in real life, not in a simulation, despite several selection pressures ?

Belz...

28th August 2007, 05:33 AM

Perhaps some day, sufficient number and intensity of selection pressures will be put on the HIV virus to completely stop the evolution of the virus.

Why would intensity enter in the equation ? You said the NUMBER of pressures was sufficient. Now it's about intensity ? Did the ev model take this into account ? How does that affect your claim ?

Dr Adequate

28th August 2007, 05:38 AM

The evolution of HIV would be stopped by any pressures sufficient to render it extinct.

Note that every living creature is a member of a lineage which has not gone extinct.

Dr Adequate

28th August 2007, 05:41 AM

This mathematical finding has important implications for the treatment of cancer as well as infectious diseases, agriculture and other fields of science and medicine.. What would you do if you thought that you were telling the truth?

Dr Schneider’s model demonstrates the mutation/selection optimization problem and how profoundly slowly it converges with multiple selection conditions. It is worthwhile to review what his model shows.

Consider Dr Schneider’s baseline case of population=64, genome length=64, binding sites=16, site width=6, weight width=5 and mutation rate=1 per genome per generation. You obtain the following data from his model for generation for convergence as a function of genome length. The convergence condition is that each of the three selection conditions is satisfied simultaneously without mistakes.

Genome length/generations to convergence for all three selection conditions no mistakes
256/662
512/2,412
1,024/18,030
2,048/42,641
4,096/163,722
8,192/710,152
16,384/6,894,433

When you set any two of the three selection conditions to zero, the remaining selection condition evolves far more rapidly than all three selection conditions simultaneously. This is demonstrated by the following data obtained from the model.

Genome length/no missed binding sites/no spurious binding in gene/no spurious binding outside gene
16,384/1/223/223
32,768/1/115/403
65,536/1/788/1,026

This series of cases demonstrates the import feature of the mutation/selection optimization process. It takes far more generations to converge all three selection conditions simultaneously than any one of the three selection conditions alone. This is clearly demonstrated even on genomes four times longer with one fourth the mutation rate than the largest genome case computed with simultaneous selection pressures.

The importance of this mathematical finding is reflected in the empirical data. In particular, I will focus on examples from the field of oncology since Dr Schneider works at the National Cancer Institute.

http://caonline.amcancersoc.org/cgi/content/full/54/3/150 (http://caonline.amcancersoc.org/cgi/content/full/54/3/150)

http://carcin.oxfordjournals.org/cgi/content/full/21/3/485 (http://carcin.oxfordjournals.org/cgi/content/full/21/3/485)

http://www.rxpgnews.com/cancer/lung/article_4344.shtml (http://www.rxpgnews.com/cancer/lung/article_4344.shtml)

http://www.pnas.org/cgi/content/full/100/3/776 (http://www.pnas.org/cgi/content/full/100/3/776)

The importance of understanding the mathematics of mutation and selection goes beyond just proving that the theory of evolution is mathematically impossible. The mathematics of mutation and selection has important implications in battling cancer as well as infectious diseases. What the mathematics of mutation and selection shows is that combined simultaneous selection pressures profoundly slows the evolutionary process. This is the reason ev converges so slowly when all but the tiniest genome lengths are used in the model and this is what the empirical data shows. This empirical data is not limited to the field of oncology but is also revealed in virology, bacteriology, parasitology and agriculture as well. I've already debunked this nonsense, remember --- we all know you're lying.

cyborg

28th August 2007, 04:58 PM

So the kleinman hypothesis in a nutshell is:

"If everything is dead evolution stops."

Thanks for that insight.

kleinman

29th August 2007, 09:06 AM

Ev’s evolutionary process is not slow if you use only a single selection condition. Consider the data in the previous post. The single selection condition series on a 64k genome still is able converge any of the selection conditions in about a thousand generations or less with a population of only 64. How would more extreme scrambling of the genome such as insertions and deletions or translocations accelerate the evolutionary process for three selection conditions?The thing that continues to evade you is that in the real world, we actually see very substantial mutations in organisms that survive to reproduce. Most times, these mutations are either of neutral or detrimental selective value. But, sometimes they're not. And, when they're not, the organism leaps forward in its survival ability as compared to its peers.
Why don’t you list some examples of these very substantial mutations that survive to reproduce?
Such mutations are frequently the result of a change other than point mutation, and they completely avoid all of the selection pressures that natural environments impose. The fact that these mutations occur show that point mutation is not sufficient to described real-world evolution.
So far you have listed only a single example of a bacteria which can now digest nylon because of an insertion deletion. This example does not contradict my hypothesis that multiple simultaneous selection pressures slow the evolutionary process.
You don't like any of these examples, and whenever someone suggests one you immediately jump to an argument from incredulity. This won't make the examples vanish, and everyone else knows that they exist. So, if you refuse to acknowledge the exceptions which make evolution happen, then that makes your conclusions unreasonable.
Do you mean all one of your examples which shows that a population of bacteria when subjected to starvation will mutate a polymerase to digest nylon? What you are missing with your single example is that it does not refute my hypothesis that combination selection pressures slow the evolutionary process profoundly. Ev shows this and the well over one hundred citations show this.
The second thing that you continuously avoid is the reality that evolution has no goal. You cannot calculate the probabilities of a future event that is inherently unpredictable. No particular organism had to occur and every one is a completely random accident.
Certainly evolution has a goal; that goal is the most fit population reproduces the most. This is the cause and effect relationship that drives the evolutionary process. When you examine the mathematics and the empirical evidence of this process you find that when you have more than a single selection pressure, the process is slowed markedly. You have no examples which show that multiple selection pressures accelerates the evolutionary process.
The analogy is That you insist that evolution is a roulette wheel with a nearly infinite number of slots and you try to calculate the probability of the ball falling into a particular location.
That’s not quite the correct analogy. What you have is a roulette wheel with up to billions of slots and you try to calculate the probability of the numerous particular balls falling in numerous particular locations. That is what you are trying to do when you have simultaneous selection pressures.
But, what evolution really is, is a roulette wheel with a nearly infinite number of slots and the proper calculation is the probability that the ball will fall into "any" slot. Because, no matter the slot "something" will evolve. It might not be a human being or an artichoke -- all evolution promises is that it will be something, which, if it survives and reproduces long enough, will eventually fit well very well within its environment.
So you believe there are no harmful mutations? So why do mutagens kill things?
You then have to consider the vast amount of empirical data in which the evolutionary mechanism is not limited to point mutations and natural selection. These real cases demonstrate that multiple simultaneous selection conditions slow the evolutionary process profoundly. You are correct that the selection conditions in ev are fixed and unchanging and that in the “real world” this is not the case. Consider what happens when there is incomplete adherence with combination treatment for HIV. Resistant viruses appear. Now how do you carry your concept of changing selection conditions to evolution of a birds from reptiles. You have an extremely complex fitness landscape this precursor population of reptiles must traverse to metamorphose to a population of birds with an ever changing set of selection pressures. There is no mathematical or empirical basis on which to postulate such huge genetic transformations.See above. The transformation from reptile to bird was an accident.
Really, the transformation from reptile to bird was an accident? So now we have the theory of evolution by accident. Do you care to describe all the accidents in your theory? What were the accidents that created all the different phyla?
I am sorry to hear about your friend. However, he would not have lived these 15 years with monotherapy and the virus would have evolved resistance far more rapidly if monotherapy treatment had been used. Again, you must consider that HIV is one of the most extreme examples of evolution by mutation and selection. It has a very short genome, very short generation times, huge populations and extremely high mutation rates. In addition this virus does recombination. How do you carry over these extreme mathematical advantages that the HIV virus has in the evolutionary process to reptiles which has much longer genomes, much longer generation times, much smaller populations and a much lower mutation rate. In addition, you can’t define the “wild” selection pressures that would accomplish this metamorphosis of a reptile population to a bird population?Reptile to bird was a random accident -- as is the existence of HIV.
Science studies the principles of cause and effect. You put your faith in how life transforms as simply a collection of accidents. You have abandoned scientific principles with this argument. At least with the theory of evolution by mutation and selection you have measurable quantities, genome lengths, mutation rates, populations and so on. You have now transformed your theory to the theory of evolution by accidents.
Perhaps you could explain how combination therapy extending your friend’s life 15 years falsifies my theory?Your theory is that multiple selection pressures prevents evolution. Multiple selection pressures have failed to save my friend. He will be dead soon, either from the lymphoma or from the chemotherapy.
You are misstating my hypothesis. What I have said is that multiple simultaneous selection pressures profoundly slow the evolutionary process and that with sufficient number of selection pressures then you will completely stop the evolutionary process.

You need to understand something about the treatment of HIV. The medications that are used to treat this infection are not totally benign. Some people will not take all their medications because of adverse reactions. Some people forget to take their medicines. There was a time that monotherapy was used to treat HIV and large number of resistant strains already exist in the gene pool. It is clear that the only way to slow the evolution of resistance of HIV to these selection pressures is to use these medications in combination. This understanding on the part of infectious disease experts has given your friend many more years of life than he would have had otherwise.
Perhaps some day, sufficient number and intensity of selection pressures will be put on the HIV virus to completely stop the evolution of the virus.Maybe, but, I can think of a single selection pressure which would stop it dead in its tracks -- kill all the hosts. Not, a particularly satisfying solution, but definitely a single selection pressure. And, once again, your theory is falsified.
Why would you want to kill people just because they are ill?
Klein, what about those species that we can see evolve in real life, not in a simulation, despite several selection pressures ?
I have posted well over one hundred real examples of evolution by mutation and selection which all show that multiple simultaneous selection pressures slow the evolutionary process. Why don’t you give us some specific examples of what you are talking about? Certainly there are examples of evolution by mutation and selection but you are extrapolating these examples far beyond what the mathematics and empirical evidence would allow.
Perhaps some day, sufficient number and intensity of selection pressures will be put on the HIV virus to completely stop the evolution of the virus.Why would intensity enter in the equation ? You said the NUMBER of pressures was sufficient. Now it's about intensity ? Did the ev model take this into account ? How does that affect your claim ?
Ev does allow changing the weights on the selection pressures but does not allow the selection pressures to cause extinction. More intense selection pressures (that is pressures which cause extinction) only worsens the evolutionist argument. Dr Schneider’s assumption in his model that the population can never go extinct is the best case scenario for the evolutionist position. Do you think that selection pressures that cause extinction will accelerate evolution? What his model shows and what the empirical evidence shows is that the number of selection pressures profoundly slow the evolutionary process. In addition, Dr Schneider’s model shows for all practical purposes that evolution stops when you apply his three selection pressures on any realistic length genome despite the fact the population does not go extinct.
So the kleinman hypothesis in a nutshell is:

"If everything is dead evolution stops."
I think you have the wrong nutshell. It is kjkent1 who is arguing this point. My argument is that ev shows that multiple simultaneous selection pressures profoundly slow the evolutionary process and that the empirical evidence demonstrates this mathematical fact. Here is another citation which demonstrates this mathematical fact empirically.

http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=10669360&dopt=AbstractPlus (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=10669360&dopt=AbstractPlus)
Hepatitis B virus (HBV) drug resistance to lamivudine is always accompanied by mutations in the viral polymerase gene at position 550, termed group 1 (M550V with L526M) or group 2 (M550I) mutations. The latter mutation has not been associated with famciclovir resistance. Thus, the addition of famciclovir to lamivudine therapy in persons with group 2 lamivudine resistance may lead to virus suppression. The effect of lamivudine/famciclovir combination therapy on HBV infection was monitored in 5 lamivudine-resistant patients by quantitative polymerase chain reaction and polymerase gene sequencing of serum virus. No patients treated with combination therapy had a decline in HBV load >1 log10. Continual evolution of the viral polymerase was detected in association with virologic resistance to both drugs. Cloning experiments identified the preexistence of these multidrug-resistant virus variants as minority species prior to addition of famciclovir therapy. HBV resistance to lamivudine monotherapy is associated with a complex mixture of variants that limit the efficacy of second-line nucleoside-analogue therapy. First-line potent combination therapy may reduce the emergence of HBV drug resistance.
This is what the mathematics of ev shows and this what the empirical evidence of real examples of mutation and selection show.

joobz

29th August 2007, 10:10 AM

Why don’t you list some examples of these very substantial mutations that survive to reproduce?

So far you have listed only a single example of a bacteria which can now digest nylon because of an insertion deletion. This example does not contradict my hypothesis that multiple simultaneous selection pressures slow the evolutionary process.

Do you mean all one of your examples which shows that a population of bacteria when subjected to starvation will mutate a polymerase to digest nylon? What you are missing with your single example is that it does not refute my hypothesis that combination selection pressures slow the evolutionary process profoundly. Ev shows this and the well over one hundred citations show this.

Certainly evolution has a goal; that goal is the most fit population reproduces the most. This is the cause and effect relationship that drives the evolutionary process. When you examine the mathematics and the empirical evidence of this process you find that when you have more than a single selection pressure, the process is slowed markedly. You have no examples which show that multiple selection pressures accelerates the evolutionary process.

That’s not quite the correct analogy. What you have is a roulette wheel with up to billions of slots and you try to calculate the probability of the numerous particular balls falling in numerous particular locations. That is what you are trying to do when you have simultaneous selection pressures.

So you believe there are no harmful mutations? So why do mutagens kill things?

Really, the transformation from reptile to bird was an accident? So now we have the theory of evolution by accident. Do you care to describe all the accidents in your theory? What were the accidents that created all the different phyla?

Science studies the principles of cause and effect. You put your faith in how life transforms as simply a collection of accidents. You have abandoned scientific principles with this argument. At least with the theory of evolution by mutation and selection you have measurable quantities, genome lengths, mutation rates, populations and so on. You have now transformed your theory to the theory of evolution by accidents.

You are misstating my hypothesis. What I have said is that multiple simultaneous selection pressures profoundly slow the evolutionary process and that with sufficient number of selection pressures then you will completely stop the evolutionary process.

You need to understand something about the treatment of HIV. The medications that are used to treat this infection are not totally benign. Some people will not take all their medications because of adverse reactions. Some people forget to take their medicines. There was a time that monotherapy was used to treat HIV and large number of resistant strains already exist in the gene pool. It is clear that the only way to slow the evolution of resistance of HIV to these selection pressures is to use these medications in combination. This understanding on the part of infectious disease experts has given your friend many more years of life than he would have had otherwise.

Why would you want to kill people just because they are ill?

I have posted well over one hundred real examples of evolution by mutation and selection which all show that multiple simultaneous selection pressures slow the evolutionary process. Why don’t you give us some specific examples of what you are talking about? Certainly there are examples of evolution by mutation and selection but you are extrapolating these examples far beyond what the mathematics and empirical evidence would allow.

Ev does allow changing the weights on the selection pressures but does not allow the selection pressures to cause extinction. More intense selection pressures (that is pressures which cause extinction) only worsens the evolutionist argument. Dr Schneider’s assumption in his model that the population can never go extinct is the best case scenario for the evolutionist position. Do you think that selection pressures that cause extinction will accelerate evolution? What his model shows and what the empirical evidence shows is that the number of selection pressures profoundly slow the evolutionary process. In addition, Dr Schneider’s model shows for all practical purposes that evolution stops when you apply his three selection pressures on any realistic length genome despite the fact the population does not go extinct.

I think you have the wrong nutshell. It is kjkent1 who is arguing this point. My argument is that ev shows that multiple simultaneous selection pressures profoundly slow the evolutionary process and that the empirical evidence demonstrates this mathematical fact. Here is another citation which demonstrates this mathematical fact empirically.

http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=10669360&dopt=AbstractPlus (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=10669360&dopt=AbstractPlus)

This is what the mathematics of ev shows and this what the empirical evidence of real examples of mutation and selection show.
Your central claim "multiple pressures slow evolution" is irrelavent. Slow doesn't equal stop. You rely on too many assumptions (known mutation rates, constant mutation rates, only point mutation matters, known number of pressures, constant number of pressures, etc.) to be able to make any claim that evolution occurs so slowly that 570 million years wasn't enough time. Coupled with the fact that the fossil records complete disprove this claim, you are left with no argument.

Any further reitterations of the same already falsified arguments will be simply spamming the boards.

Do you have any new arguments to make, or can we consider this thread dead?

Belz...

29th August 2007, 10:10 AM

I have posted well over one hundred real examples of evolution by mutation and selection which all show that multiple simultaneous selection pressures slow the evolutionary process.

That has nothing to do with what I asked you. You're repeating yourself for the sake of reading your own arguments again.

Why don’t you give us some specific examples of what you are talking about?

Peppered moths. Nylon-eating baceria. That kind of things. Oh, yeah. HUMANS.

Certainly there are examples of evolution by mutation and selection but you are extrapolating these examples far beyond what the mathematics and empirical evidence would allow.

Wait... wait a minute. You're saying that there ARE examples of evolution by mutation and selection ? I thought you said that evolution was MATHEMATICALLY IMPOSSIBLE.

Ev does allow changing the weights on the selection pressures but does not allow the selection pressures to cause extinction.

Does not allow extinction. How can it stop evolution, then ?

More intense selection pressures (that is pressures which cause extinction) only worsens the evolutionist argument.

According to you, gravity worsens the "evolutionist" argument.

I thought it was "evolutionarian" ?

Do you think that selection pressures that cause extinction will accelerate evolution?

One claim at a time, Klein.

What his model shows and what the empirical evidence shows is that the number of selection pressures profoundly slow the evolutionary process.

What the model shows is point mutations. You keep pointing out the fact that the ev model is flawed. I wonder why you keep using it to support your argument.

Dr Adequate

29th August 2007, 10:54 AM

Why don’t you list some examples of these very substantial mutations that survive to reproduce?

So far you have listed only a single example of a bacteria which can now digest nylon because of an insertion deletion. This example does not contradict my hypothesis that multiple simultaneous selection pressures slow the evolutionary process.

Do you mean all one of your examples which shows that a population of bacteria when subjected to starvation will mutate a polymerase to digest nylon? What you are missing with your single example is that it does not refute my hypothesis that combination selection pressures slow the evolutionary process profoundly. Ev shows this and the well over one hundred citations show this.

Certainly evolution has a goal; that goal is the most fit population reproduces the most. This is the cause and effect relationship that drives the evolutionary process. When you examine the mathematics and the empirical evidence of this process you find that when you have more than a single selection pressure, the process is slowed markedly. You have no examples which show that multiple selection pressures accelerates the evolutionary process.

That’s not quite the correct analogy. What you have is a roulette wheel with up to billions of slots and you try to calculate the probability of the numerous particular balls falling in numerous particular locations. That is what you are trying to do when you have simultaneous selection pressures.

So you believe there are no harmful mutations? So why do mutagens kill things?

Really, the transformation from reptile to bird was an accident? So now we have the theory of evolution by accident. Do you care to describe all the accidents in your theory? What were the accidents that created all the different phyla?

Science studies the principles of cause and effect. You put your faith in how life transforms as simply a collection of accidents. You have abandoned scientific principles with this argument. At least with the theory of evolution by mutation and selection you have measurable quantities, genome lengths, mutation rates, populations and so on. You have now transformed your theory to the theory of evolution by accidents.

You are misstating my hypothesis. What I have said is that multiple simultaneous selection pressures profoundly slow the evolutionary process and that with sufficient number of selection pressures then you will completely stop the evolutionary process.

You need to understand something about the treatment of HIV. The medications that are used to treat this infection are not totally benign. Some people will not take all their medications because of adverse reactions. Some people forget to take their medicines. There was a time that monotherapy was used to treat HIV and large number of resistant strains already exist in the gene pool. It is clear that the only way to slow the evolution of resistance of HIV to these selection pressures is to use these medications in combination. This understanding on the part of infectious disease experts has given your friend many more years of life than he would have had otherwise.

Why would you want to kill people just because they are ill?

I have posted well over one hundred real examples of evolution by mutation and selection which all show that multiple simultaneous selection pressures slow the evolutionary process. Why don’t you give us some specific examples of what you are talking about? Certainly there are examples of evolution by mutation and selection but you are extrapolating these examples far beyond what the mathematics and empirical evidence would allow.

Ev does allow changing the weights on the selection pressures but does not allow the selection pressures to cause extinction. More intense selection pressures (that is pressures which cause extinction) only worsens the evolutionist argument. Dr Schneider’s assumption in his model that the population can never go extinct is the best case scenario for the evolutionist position. Do you think that selection pressures that cause extinction will accelerate evolution? What his model shows and what the empirical evidence shows is that the number of selection pressures profoundly slow the evolutionary process. In addition, Dr Schneider’s model shows for all practical purposes that evolution stops when you apply his three selection pressures on any realistic length genome despite the fact the population does not go extinct.

I think you have the wrong nutshell. It is kjkent1 who is arguing this point. My argument is that ev shows that multiple simultaneous selection pressures profoundly slow the evolutionary process and that the empirical evidence demonstrates this mathematical fact. Here is another citation which demonstrates this mathematical fact empirically.

http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=10669360&dopt=AbstractPlus (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=10669360&dopt=AbstractPlus)

This is what the mathematics of ev shows and this what the empirical evidence of real examples of mutation and selection show. Almost two thousand words, if we include the irrelevant quotations.

And you're still reciting the same old stupid crap, aren't you?

kjkent1

29th August 2007, 10:56 AM

Why don’t you list some examples of these very substantial mutations that survive to reproduce?Been there -- done that. This thread is a testament to listing examples of mutations which have survived to reproduce. You simply reject them all, because they destroy your hypothesis. Every substantial change in the morphology of a life form is the product of a substantial mutation that has survived to reproduce.

You know this, of course -- and, if it didn't happen the way I describe, then tell us all how it did happen. Come on, Alan, explain scientifically how the various species have come to appear on Earth. We're all waiting for you to expose your theory: Genesis 1:1. How very scientific.

So far you have listed only a single example of a bacteria which can now digest nylon because of an insertion deletion. This example does not contradict my hypothesis that multiple simultaneous selection pressures slow the evolutionary process.You mean it doesn't contradict your hypothesis, because you proclaim it to be so? How very scientific of you, Alan. Very impressive.

Do you mean all one of your examples which shows that a population of bacteria when subjected to starvation will mutate a polymerase to digest nylon? What you are missing with your single example is that it does not refute my hypothesis that combination selection pressures slow the evolutionary process profoundly. Ev shows this and the well over one hundred citations show this.Your hypothesis that multiple selection pressures slow point mutation is irrelevant, because the empirical fossil, genetic, etc., evidence shows that evolutionary change occurs despite the existence of multiple selection pressures. If this were not true, then each of your posted citations would be a perfect cure for the disease that it attempts to resolve. But, all of the diseases just continue to appear in new and different forms. How do you explain this behavior in view of your hypothesis that claims it cannot happen ? Genesis 1:1 happened long ago, so what's happening today -- does Satan creates new life forms? I wasn't aware that He had such power.

Certainly evolution has a goal; that goal is the most fit population reproduces the most. This is the cause and effect relationship that drives the evolutionary process. When you examine the mathematics and the empirical evidence of this process you find that when you have more than a single selection pressure, the process is slowed markedly. You have no examples which show that multiple selection pressures accelerates the evolutionary process.I have the entire fossil and genetic record, and I have the continued discovery of new species, which is reported routinely in scientific publications. All of this evidence falsifies your theory that macroevolution does not occur. Of course it does. And, when someone reports an example, such as K172, you can't explain it, so you just reject it by proclamation.

That’s not quite the correct analogy. What you have is a roulette wheel with up to billions of slots and you try to calculate the probability of the numerous particular balls falling in numerous particular locations. That is what you are trying to do when you have simultaneous selection pressures.Selection seeks a local optimum. Mutation seeks nothing, and there is no barrier to the evolution of any novel feature -- except the death of the host prior to reproduction -- which is by no means guaranteed by any selection method or number of selection pressures.

If it were guaranteed, then there would be only one life form: whichever one appeared first. Or, would you like to propose some other theory as to how life appears in its myriad forms? Wait, I forgot. That would be the Genesis 1:1 theory, for which you have zero scientific evidence, right?

So you believe there are no harmful mutations? So why do mutagens kill things?A harmful mutation is one that kills its host prior to reproduction. All other mutations are either neutral or beneficial in the extant environment. I would think that this fact would be obvious to you as an MD.

Really, the transformation from reptile to bird was an accident? So now we have the theory of evolution by accident. Do you care to describe all the accidents in your theory? What were the accidents that created all the different phyla?When was the theory of evolution anything other than a theory of accidental change refined by environmental pressure? Maybe you don't really understand what evolution is. That would certainly account for your continuing misrepresentations.

Science studies the principles of cause and effect. You put your faith in how life transforms as simply a collection of accidents. You have abandoned scientific principles with this argument. At least with the theory of evolution by mutation and selection you have measurable quantities, genome lengths, mutation rates, populations and so on. You have now transformed your theory to the theory of evolution by accidents.Sorry to disappoint you, but Quantum Mechanics demonstrates that some things cannot be predicted with certainty in advance. Einstein lost this battle 90 years ago. Science is the act of verifying a hypothesis by repeatable experiment. Sometimes the effect of an action can only be predicted within limits. Thus an experiment may be repeated to find only a statistical pattern, rather than certainty.

Evolution is exactly such a mechanism. Organisms mutate -- this is verifiable. The outcome of the mutation is unpredictable random accident. It cannot be measured with certainty, but it can be measured within limits. A dinosaur will not mutate in one generation into a cockatoo. But, it can mutate into a cockatoo after many generations, because we have the evidence that it did just that. You are, of course, free to ignore said evidence, in favor of the completely unscientific theory of Genesis 1:1. But, if anything isn't science, Genesis 1:1 is it. So, don't try and suggest that I don't know what science is, while attempting to prop up Jesus on the cross, because that just makes you appear to be a jackass.

You are misstating my hypothesis. What I have said is that multiple simultaneous selection pressures profoundly slow the evolutionary process and that with sufficient number of selection pressures then you will completely stop the evolutionary process.Explain this to my dying friend. I'm certain he will be amused.

You need to understand something about the treatment of HIV. The medications that are used to treat this infection are not totally benign. Some people will not take all their medications because of adverse reactions. Some people forget to take their medicines. There was a time that monotherapy was used to treat HIV and large number of resistant strains already exist in the gene pool. It is clear that the only way to slow the evolution of resistance of HIV to these selection pressures is to use these medications in combination. This understanding on the part of infectious disease experts has given your friend many more years of life than he would have had otherwise.But, he's going to die of HIV anyway -- proof positive that evolution occurs despite furious attempts to prevent it. Or, is the Devil busy in my friend's genome?

Why would you want to kill people just because they are ill?I wouldn't, and your suggesting that I would, is insulting. Grow up, Alan.

I have posted well over one hundred real examples of evolution by mutation and selection which all show that multiple simultaneous selection pressures slow the evolutionary process. Why don’t you give us some specific examples of what you are talking about? Certainly there are examples of evolution by mutation and selection but you are extrapolating these examples far beyond what the mathematics and empirical evidence would allow.Do you dispute the evidence showing that chromosome 1 and 2 in chimpanzees are fused in humans? Do you have a scientific explanation for this other than that it is an accidental mutation? Well...do you??? Let's see it, Alan.

Keep in mind the Membership Agreement and do not use personal attacks or insults to argue your point.

kleinman

29th August 2007, 12:00 PM

Your central claim "multiple pressures slow evolution" is irrelavent. Slow doesn't equal stop. You rely on too many assumptions (known mutation rates, constant mutation rates, only point mutation matters, known number of pressures, constant number of pressures, etc.) to be able to make any claim that evolution occurs so slowly that 570 million years wasn't enough time. Coupled with the fact that the fossil records complete disprove this claim, you are left with no argument.
Of course slow doesn’t equal stop but you miss the point that beyond a single selection pressure, each additional selection pressure has a profound affect on the mutation and selection process. Ev shows this mathematically and the numerous citations I have and will continue to post show this empirically. Are you trying to imply that non-constant mutation rates overcomes the effect of multiple selection pressures? If so, demonstrate this either mathematically or empirically. Otherwise this is just another of your speculations. I can understand why you want to bring in the fossil record into a discussion of the mathematics of mutation and selection because you can’t present any mathematical or empirical evidence for your speculations about mutation and selection. I have presented mathematical evidence from a peer reviewed and published model of random point mutation and natural selection which shows that multiple selection pressures has a profound slowing effect on evolution and I have posted well over one hundred empirical examples with quotes from these citations posted on this thread which demonstrate this mathematical fact. Your interpretation of the fossil record will always be suspect unless you can show how mutation and selection can accomplish these far fetched transformations for reptiles to birds. We have a vast amount of empirical data which show exactly how mutation and selection works and what this data shows is that simultaneous selection pressures profoundly slow the evolutionary process. Oh, and by the way joobz, extinction does occur when there is sufficient selection pressure.
Any further reitterations of the same already falsified arguments will be simply spamming the boards.
Neither your violations of rule 12 or your false accusations of spamming will stop the presentation of the mathematical fact of how mutation and selection actually works. If you want an example of spamming, look at your own post. You quote my entire previous post and then want to start talking about the fossil record.
Do you have any new arguments to make, or can we consider this thread dead?
Nobody is forcing you to post on this thread. I’ll continue to post more new citations of mutation and selection actually works and your violations of rule 12 and false accusations will not stop me. Start another thread if you want to talk about the fossil record. This thread is about the mathematics of mutation and selection as demonstrated by the ev computer simulation of random point mutations and the empirical evidence
I have posted well over one hundred real examples of evolution by mutation and selection which all show that multiple simultaneous selection pressures slow the evolutionary process.That has nothing to do with what I asked you. You're repeating yourself for the sake of reading your own arguments again.
You have already expressed that you have no interest in the mathematics of mutation and selection and now you are not interested in the empirical evidence of how mutation and selection actually works. Your question has been asked and answered.
Why don’t you give us some specific examples of what you are talking about?Peppered moths. Nylon-eating baceria. That kind of things. Oh, yeah. HUMANS.
Ok Belz, now describe the selection pressure(s) on peppered moths, nylon-eating bacteria and oh yeah, HUMANS and the genes on which mutation and selection is acting and show us how combination selection pressures accelerate evolution.
Certainly there are examples of evolution by mutation and selection but you are extrapolating these examples far beyond what the mathematics and empirical evidence would allow.Wait... wait a minute. You're saying that there ARE examples of evolution by mutation and selection ? I thought you said that evolution was MATHEMATICALLY IMPOSSIBLE.
Belz, if you had read this thread, I wouldn’t have to answer this (again and again). There are many examples of mutation and selection however this is a much more limited phenomenon than evolutionists allege. The mathematics of mutation and selection as show by ev demonstrates this and the empirical evidence demonstrated by ev substantiates this mathematical finding. Mutation and selection is a profoundly slow process if you have more than a single selection condition. That is what the mathematical and empirical data show.
Ev does allow changing the weights on the selection pressures but does not allow the selection pressures to cause extinction.Does not allow extinction. How can it stop evolution, then ?
As you lengthen the genome in the model, the number of generations needed to satisfy the three selection conditions becomes greater and greater until the model simple stops converging. If you ran a few cases with ev, it is very easy to demonstrate this affect.
More intense selection pressures (that is pressures which cause extinction) only worsens the evolutionist argument.According to you, gravity worsens the "evolutionist" argument.

I thought it was "evolutionarian" ?
What is it with you? Joobz wants to talk about the fossil record, you want to talk about gravity. Can’t you stay on topic?
Do you think that selection pressures that cause extinction will accelerate evolution?One claim at a time, Klein.
You complain that I don’t answer your questions. Let me help you with the answer to this question. It is obvious that selection pressures which cause extinction do not accelerate evolution. Dr Schneider’s model which does not allow for extinction despite how unfit the population is a best case scenario for the evolutionist argument. Yet even with this extremely beneficial assumption, the evolutionary process is still profoundly slow with all three selection conditions when the model is run with all but the smallest genomes.
What his model shows and what the empirical evidence shows is that the number of selection pressures profoundly slow the evolutionary process.What the model shows is point mutations. You keep pointing out the fact that the ev model is flawed. I wonder why you keep using it to support your argument.
The empirical evidence demonstrates the same behavior that Dr Schneider’s model demonstrates. What is being demonstrated is that multiple selection pressures slow the evolutionary process profoundly. This despite the fact that these real empirical examples are not limited to random point mutations but can have any mutation you can imagine and many of these real cases include recombination (such as HIV) yet they all show that combination selection pressures profoundly slow evolution.
Why don’t you list some examples of these very substantial mutations that survive to reproduce?Been there -- done that. This thread is a testament to listing examples of mutations which have survived to reproduce. You simply reject them all, because they destroy your hypothesis. Every substantial change in the morphology of a life form is the product of a substantial mutation that has survived to reproduce.
Are you talking about all one of your examples, the nylon eating bacteria? You still haven’t described the selection pressures and the genes involved in all one of your examples. As soon as you do, you will find out that all one of your examples is simply a single selection pressure and a single target gene.
You know this, of course -- and, if it didn't happen the way I describe, then tell us all how it did happen. Come on, Alan, explain scientifically how the various species have come to appear on Earth. We're all waiting for you to expose your theory: Genesis 1:1. How very scientific.
Let’s see, joobz wants to talk about the fossil record, Belz wants to talk about gravity and you want to talk about the Bible. Don’t any of you want to talk about the mathematics of mutation and selection and the empirical evidence demonstrated by this mathematics?
So far you have listed only a single example of a bacteria which can now digest nylon because of an insertion deletion. This example does not contradict my hypothesis that multiple simultaneous selection pressures slow the evolutionary process.You mean it doesn't contradict your hypothesis, because you proclaim it to be so? How very scientific of you, Alan. Very impressive.
I don’t do this by proclamation, I do this with the scientific evidence. Your example of a nylon eating bacteria is an example of a single selection pressure with a single target gene. Now if you want to demonstrate the evolution of a nylon eating gene while at the same time evolving resistance to antibiotics and this occurring more rapidly that when either selection pressure is applied sequentially, then you would have a point.
Do you mean all one of your examples which shows that a population of bacteria when subjected to starvation will mutate a polymerase to digest nylon? What you are missing with your single example is that it does not refute my hypothesis that combination selection pressures slow the evolutionary process profoundly. Ev shows this and the well over one hundred citations show this.Your hypothesis that multiple selection pressures slow point mutation is irrelevant, because the empirical fossil, genetic, etc., evidence shows that evolutionary change occurs despite the existence of multiple selection pressures. If this were not true, then each of your posted citations would be a perfect cure for the disease that it attempts to resolve. But, all of the diseases just continue to appear in new and different forms. How do you explain this behavior in view of your hypothesis that claims it cannot happen ? Genesis 1:1 happened long ago, so what's happening today -- does Satan creates new life forms? I wasn't aware that He had such power.
Having a bit of trouble staying on topic aren’t you kjkent1.
Certainly evolution has a goal; that goal is the most fit population reproduces the most. This is the cause and effect relationship that drives the evolutionary process. When you examine the mathematics and the empirical evidence of this process you find that when you have more than a single selection pressure, the process is slowed markedly. You have no examples which show that multiple selection pressures accelerates the evolutionary process.I have the entire fossil and genetic record, and I have the continued discovery of new species, which is reported routinely in scientific publications. All of this evidence falsifies your theory that macroevolution does not occur. Of course it does. And, when someone reports an example, such as K172, you can't explain it, so you just reject it by proclamation.
Unless you can explain how this all occurs by mutation and selection, all your interpretations of the fossil and genetic record are called into question. However, kjkent1, I don’t blame you for wanting to changing the subject. The mathematical and empirical evidence of how mutation and selection actually works is quite damaging to the theory of evolution.
That’s not quite the correct analogy. What you have is a roulette wheel with up to billions of slots and you try to calculate the probability of the numerous particular balls falling in numerous particular locations. That is what you are trying to do when you have simultaneous selection pressures.Selection seeks a local optimum. Mutation seeks nothing, and there is no barrier to the evolution of any novel feature -- except the death of the host prior to reproduction -- which is by no means guaranteed by any selection method or number of selection pressures.
If you read Delphi’s reference to Wikipedia and the fitness landscape you would get some understanding why it is so difficult for a population to find a local optimum on the fitness landscape when you have multiple selection conditions. Do you want me to repost this text?
If it were guaranteed, then there would be only one life form: whichever one appeared first. Or, would you like to propose some other theory as to how life appears in its myriad forms? Wait, I forgot. That would be the Genesis 1:1 theory, for which you have zero scientific evidence, right?
Do you still want to talk about the Bible rather than the mathematics of mutation and selection and the empirical evidence associated with this mathematics? Keep pushing those goalposts kjkent1.
So you believe there are no harmful mutations? So why do mutagens kill things?A harmful mutation is one that kills its host prior to reproduction. All other mutations are either neutral or beneficial in the extant environment. I would think that this fact would be obvious to you as an MD.
And as an MD, I know that beneficial mutations are very rare events. This is why I advise people to avoid mutatgens.
Really, the transformation from reptile to bird was an accident? So now we have the theory of evolution by accident. Do you care to describe all the accidents in your theory? What were the accidents that created all the different phyla?When was the theory of evolution anything other than a theory of accidental change refined by environmental pressure? Maybe you don't really understand what evolution is. That would certainly account for your continuing misrepresentations.
So kjkent1, is the theory of evolution by mutation and natural selection now the theory of evolution by accidental change and natural selection?
Science studies the principles of cause and effect. You put your faith in how life transforms as simply a collection of accidents. You have abandoned scientific principles with this argument. At least with the theory of evolution by mutation and selection you have measurable quantities, genome lengths, mutation rates, populations and so on. You have now transformed your theory to the theory of evolution by accidents.Sorry to disappoint you, but Quantum Mechanics demonstrates that some things cannot be predicted with certainty in advance. Einstein lost this battle 90 years ago. Science is the act of verifying a hypothesis by repeatable experiment. Sometimes the effect of an action can only be predicted within limits. Thus an experiment may be repeated to find only a statistical pattern, rather than certainty.
Are you now arguing that quantum mechanics is not an attempt to describe a cause and effect principle? Perhaps you would describe to us the relationship of information theory and the quantum mechanical definition of entropy?
Evolution is exactly such a mechanism. Organisms mutate -- this is verifiable. The outcome of the mutation is unpredictable random accident. It cannot be measured with certainty, but it can be measured within limits. A dinosaur will not mutate in one generation into a cockatoo. But, it can mutate into a cockatoo after many generations, because we have the evidence that it did just that. You are, of course, free to ignore said evidence, in favor of the completely unscientific theory of Genesis 1:1. But, if anything isn't science, Genesis 1:1 is it. So, don't try and suggest that I don't know what science is, while attempting to prop up Jesus on the cross, because that just makes you appear to be a jackass.
Well, we’ll stop here in our discussion with you since you show no respect for rule 12.

Let’s finish this post with another example of how mutation and selection actually works and that is multiple selection pressures profoundly slow the evolutionary process.

http://www.behindthemedicalheadlines.com/articles/drug-resistant-malaria-and-its-treatment (http://www.behindthemedicalheadlines.com/articles/drug-resistant-malaria-and-its-treatment)
In the past few years, the richer world has become more conscious of the huge morbidity and mortality caused by malaria. Money is now available through the Global fund to fight AIDS, TB and Malaria 9 which is assisting poorer countries to buy effective treatments for these diseases, and more efforts are being made by drug companies and academic institutions to find new drugs. In Africa, by the end of 2005, 17 countries had adopted treatment policies to use artemether-lumefantrine for uncomplicated malaria. For many of these countries, this policy is yet to be implemented due to a lack of availability of the drug; and there is currently a shortage of the drug on the world market. The artemisinins are a powerful weapon in the armamentarium against malaria, which we must use wisely within combination therapies if we are to delay, or even halt, the development of resistance. At the same time, we must continue to develop new antimalarials so that we are not reliant on one class of drug for which the malaria parasite has not yet developed resistance.

joobz

29th August 2007, 12:16 PM

Dr Adequate

29th August 2007, 12:35 PM

Of course slow doesn’t equal stop but you miss the point that beyond a single selection pressure, each additional selection pressure has a profound affect on the mutation and selection process. Ev shows this mathematically and the numerous citations I have and will continue to post show this empirically. Are you trying to imply that non-constant mutation rates overcomes the effect of multiple selection pressures? If so, demonstrate this either mathematically or empirically. Otherwise this is just another of your speculations. I can understand why you want to bring in the fossil record into a discussion of the mathematics of mutation and selection because you can’t present any mathematical or empirical evidence for your speculations about mutation and selection. I have presented mathematical evidence from a peer reviewed and published model of random point mutation and natural selection which shows that multiple selection pressures has a profound slowing effect on evolution and I have posted well over one hundred empirical examples with quotes from these citations posted on this thread which demonstrate this mathematical fact. Your interpretation of the fossil record will always be suspect unless you can show how mutation and selection can accomplish these far fetched transformations for reptiles to birds. We have a vast amount of empirical data which show exactly how mutation and selection works and what this data shows is that simultaneous selection pressures profoundly slow the evolutionary process. Oh, and by the way joobz, extinction does occur when there is sufficient selection pressure.

Neither your violations of rule 12 or your false accusations of spamming will stop the presentation of the mathematical fact of how mutation and selection actually works. If you want an example of spamming, look at your own post. You quote my entire previous post and then want to start talking about the fossil record.

Nobody is forcing you to post on this thread. I’ll continue to post more new citations of mutation and selection actually works and your violations of rule 12 and false accusations will not stop me. Start another thread if you want to talk about the fossil record. This thread is about the mathematics of mutation and selection as demonstrated by the ev computer simulation of random point mutations and the empirical evidence

You have already expressed that you have no interest in the mathematics of mutation and selection and now you are not interested in the empirical evidence of how mutation and selection actually works. Your question has been asked and answered.

Ok Belz, now describe the selection pressure(s) on peppered moths, nylon-eating bacteria and oh yeah, HUMANS and the genes on which mutation and selection is acting and show us how combination selection pressures accelerate evolution.

Belz, if you had read this thread, I wouldn’t have to answer this (again and again). There are many examples of mutation and selection however this is a much more limited phenomenon than evolutionists allege. The mathematics of mutation and selection as show by ev demonstrates this and the empirical evidence demonstrated by ev substantiates this mathematical finding. Mutation and selection is a profoundly slow process if you have more than a single selection condition. That is what the mathematical and empirical data show.

As you lengthen the genome in the model, the number of generations needed to satisfy the three selection conditions becomes greater and greater until the model simple stops converging. If you ran a few cases with ev, it is very easy to demonstrate this affect.

What is it with you? Joobz wants to talk about the fossil record, you want to talk about gravity. Can’t you stay on topic?

You complain that I don’t answer your questions. Let me help you with the answer to this question. It is obvious that selection pressures which cause extinction do not accelerate evolution. Dr Schneider’s model which does not allow for extinction despite how unfit the population is a best case scenario for the evolutionist argument. Yet even with this extremely beneficial assumption, the evolutionary process is still profoundly slow with all three selection conditions when the model is run with all but the smallest genomes.

The empirical evidence demonstrates the same behavior that Dr Schneider’s model demonstrates. What is being demonstrated is that multiple selection pressures slow the evolutionary process profoundly. This despite the fact that these real empirical examples are not limited to random point mutations but can have any mutation you can imagine and many of these real cases include recombination (such as HIV) yet they all show that combination selection pressures profoundly slow evolution.

Are you talking about all one of your examples, the nylon eating bacteria? You still haven’t described the selection pressures and the genes involved in all one of your examples. As soon as you do, you will find out that all one of your examples is simply a single selection pressure and a single target gene.

Let’s see, joobz wants to talk about the fossil record, Belz wants to talk about gravity and you want to talk about the Bible. Don’t any of you want to talk about the mathematics of mutation and selection and the empirical evidence demonstrated by this mathematics?

I don’t do this by proclamation, I do this with the scientific evidence. Your example of a nylon eating bacteria is an example of a single selection pressure with a single target gene. Now if you want to demonstrate the evolution of a nylon eating gene while at the same time evolving resistance to antibiotics and this occurring more rapidly that when either selection pressure is applied sequentially, then you would have a point.

Having a bit of trouble staying on topic aren’t you kjkent1.

Unless you can explain how this all occurs by mutation and selection, all your interpretations of the fossil and genetic record are called into question. However, kjkent1, I don’t blame you for wanting to changing the subject. The mathematical and empirical evidence of how mutation and selection actually works is quite damaging to the theory of evolution.

If you read Delphi’s reference to Wikipedia and the fitness landscape you would get some understanding why it is so difficult for a population to find a local optimum on the fitness landscape when you have multiple selection conditions. Do you want me to repost this text?

Do you still want to talk about the Bible rather than the mathematics of mutation and selection and the empirical evidence associated with this mathematics? Keep pushing those goalposts kjkent1.

And as an MD, I know that beneficial mutations are very rare events. This is why I advise people to avoid mutatgens.

So kjkent1, is the theory of evolution by mutation and natural selection now the theory of evolution by accidental change and natural selection?

Are you now arguing that quantum mechanics is not an attempt to describe a cause and effect principle? Perhaps you would describe to us the relationship of information theory and the quantum mechanical definition of entropy?

Well, we’ll stop here in our discussion with you since you show no respect for rule 12.

Let’s finish this post with another example of how mutation and selection actually works and that is multiple selection pressures profoundly slow the evolutionary process.

http://www.behindthemedicalheadlines.com/articles/drug-resistant-malaria-and-its-treatment (http://www.behindthemedicalheadlines.com/articles/drug-resistant-malaria-and-its-treatment)
Wow, you posted nearly three thousand words and couldn't come up with one new lie.

kleinman

29th August 2007, 01:12 PM

Of course slow doesn’t equal stop but you miss the point that beyond a single selection pressure, each additional selection pressure has a profound affect on the mutation and selection process.what is that profound effect? hmm?
Let’s start with the obvious examples first. The evolution of all three selection conditions on a 16k takes about 7,000,000 generations. Evolution of a one of the three selection conditions takes less than three hundred generations. Increase the genome size to 32k or 64k and the maximum number of generations is still only about 1,000 to evolve any of the three selection conditions singly. If I recall, Paul’s estimate for evolving all three selection on the 32k genome would be quite a bit more than 7,000,000 generations. Perhaps you want to run this case to get a sense what the profound effect is. But let’s look at the empirical examples. Monotherapy for HIV only delays the evolution of the virus for weeks while combination therapy delays the evolution of the virus for decades. Or how about the previous citation I posted.
The artemisinins are a powerful weapon in the armamentarium against malaria, which we must use wisely within combination therapies if we are to delay, or even halt, the development of resistance. At the same time, we must continue to develop new antimalarials so that we are not reliant on one class of drug for which the malaria parasite has not yet developed resistance.
These authors seem to think that there is the possibility to halt the evolution of resistance of malaria. Do you want to tell oncologists that they can not halt the evolution of cancer cells?
Ev shows this mathematically and the numerous citations I have and will continue to post show this empirically. Are you trying to imply that non-constant mutation rates overcomes the effect of multiple selection pressures? If so, demonstrate this either mathematically or empirically.Wrong. Science doesn't work that way. You've made false assumptions. Conclusions based upon those assumptions are false. Therefore your entire argument is false.
Joobz, I missed the mathematical data you posted that refutes the results from ev. I also missed your post where you showed that combined selection pressures accelerates evolution. What a minute, I never missed these posts because you never posted this. Your science is based on raw speculation. You have admitted this. My science is based on the mathematical results from a peer reviewed a published model of mutation and selection and the vast amount of empirical data which substantiates this mathematical finding. Without you speculations you have nothing to support your viewpoint.
Neither your violations of rule 12 or your false accusations of spamming will stop the presentation of the mathematical fact of how mutation and selection actually works. If you want an example of spamming, look at your own post. You quote my entire previous post and then want to start talking about the fossil record.Report me if you feel I have attacked you. I've simply explained taht your whole argument has been falsified. You repeat the same nonsense. Calling your arguments nonsense and foolish is not a personal attack.
I did report you and you were censored. I’ll just keep posting citations which demonstrate how mutation and selection actually works while you continue to post your unscientific speculations.
I’ll continue to post more new citations of mutation and selection actually works and your violations of rule 12 and false accusations will not stop me. Start another thread if you want to talk about the fossil record. This thread is about the mathematics of mutation and selection as demonstrated by the ev computer simulation of random point mutations and the empirical evidenceSorry, but the fossil record IS evidence that you are wrong.
posting links ad nauseum with the exact same easily dissmissable faulty premise is still spamming. Until you can provide a better argument without false assumptions, you are simply repeating the exact same debunked argument.
So let’s see, kjkent1 has transformed the theory of evolution by mutation and selection to the theory of evolution by accident and no you transform the theory of evolution by mutation and selection to the theory of evolution by fossil record. Your strange speculations about the fossil record are in complete contradiction to how mutation and selection actually works. Data are measured daily on how mutation and selection works and it does not support your strange interpretation of the fossil record. However, I don’t blame you for not wanting to talk about how mutation and selection actually works. It is so contradictory to your theory of evolution by fossil record.

So let’s review again how mutation and selection actually works mathematically. Mutation and selection is an optimization or sorting problem of beneficial and detrimental mutations. Like all mathematical problems of this type, the number of optimization or sorting conditions (selection conditions) has a profound affect on the rate at which these types of problems converge. Ev demonstrates how profound this affect is with three selection conditions and how long it takes for the model to converge with only a 16k genome. A single selection condition converges very rapidly for the equivalent conditions. This mathematical effect is demonstrated over and over in the empirical data. It doesn’t matter whether you consider the evolution of HIV, HBV, HCV, TB, Malaria, cancer cells, weeds or rodents. The evolution of all these life forms are profoundly slowed when they are subjected to multiple selection pressures. This is the mathematical and the empirical fact of how mutation and selection actually works. This is not like joobz’s strange speculations about the fossil record. This is mathematically and empirically measured fact.

Belz...

29th August 2007, 01:14 PM

You have already expressed that you have no interest in the mathematics of mutation and selection

Link to a post where I said this ? You won't find it, because I've never said so.

and now you are not interested in the empirical evidence of how mutation and selection actually works. Your question has been asked and answered.

Your answer had NOTHING to do with the question. Just because you feel the need to repeat yourself doesn't mean I will ignore the fact that you're preaching to me.

Ok Belz, now describe the selection pressure(s) on peppered moths, nylon-eating bacteria and oh yeah, HUMANS and the genes on which mutation and selection is acting and show us how combination selection pressures accelerate evolution.

You're asking me to describe the selection pressures ? Are you now saying that some life-forms are only subject to ONE selection pressure, thereby allowing evolution ?

Are you saying that, though "several selection pressures slow or even stop evolution", there are instances of species only subject to ONE ? In that case your original argument is lost.

As you lengthen the genome in the model, the number of generations needed to satisfy the three selection conditions becomes greater and greater until the model simple stops converging.

Satisfy the selection conditions ? Since when is that a yes or no question ?

Evolution isn't about survival of the fittest, but about survival of the barely fit.

What is it with you? Joobz wants to talk about the fossil record, you want to talk about gravity. Can’t you stay on topic?

I never said I wanted to talk about gravity. Your complete lack of reading comprehension is showing more and more.

Please read what I said again.

You complain that I don’t answer your questions. Let me help you with the answer to this question. It is obvious that selection pressures which cause extinction do not accelerate evolution.

That's highly debatable. Extinction, even MASS extinctions, could actually help the evolution of the surviving species.

The empirical evidence demonstrates the same behavior that Dr Schneider’s model demonstrates.

Explain peppered moths, nylon-eating bacteria and humans. And please don't try to claim that there's only one selection pressure at work.

This despite the fact that these real empirical examples are not limited to random point mutations but can have any mutation you can imagine and many of these real cases include recombination (such as HIV) yet they all show that combination selection pressures profoundly slow evolution.

Unfortunately for you, case scenarios and empirical examples do not make anything mathematically possible or impossible.

kjkent1

29th August 2007, 01:18 PM

Are you talking about all one of your examples, the nylon eating bacteria? You still haven’t described the selection pressures and the genes involved in all one of your examples. As soon as you do, you will find out that all one of your examples is simply a single selection pressure and a single target gene.K172 was not created by scientists in a controlled environment. It was discovered in a pool of waste product in a manufacturing plant. K172 exists despite all of the purportedly natural selection pressures which you claim make its existence impossible.

K172 is the product of a frame shift -- not a point mutation. It exists in contravention to your entire theory. So, either explain where K172 came from, or admit that its existence falsifies your theory that macroevolution is mathematically impossible.

Now, in the interest of "science," I'll refrain from addressing the remainder of your post, until you directly address the substance of the above.

kleinman

29th August 2007, 01:59 PM

You have already expressed that you have no interest in the mathematics of mutation and selection Link to a post where I said this ? You won't find it, because I've never said so.
Belz, you said the following.
Mathematics < Reality.
What ev shows coincides with reality. If you had interest in the mathematics of mutation and selection, you would study ev and looked at how the results of this model coincides with reality.
and now you are not interested in the empirical evidence of how mutation and selection actually works. Your question has been asked and answered.Your answer had NOTHING to do with the question. Just because you feel the need to repeat yourself doesn't mean I will ignore the fact that you're preaching to me.
What is it, do you want to talk about gravity. If so, that is not the topic of this thread.
Ok Belz, now describe the selection pressure(s) on peppered moths, nylon-eating bacteria and oh yeah, HUMANS and the genes on which mutation and selection is acting and show us how combination selection pressures accelerate evolution.You're asking me to describe the selection pressures ? Are you now saying that some life-forms are only subject to ONE selection pressure, thereby allowing evolution ?

Are you saying that, though "several selection pressures slow or even stop evolution", there are instances of species only subject to ONE ? In that case your original argument is lost.
Give whatever number of selection pressures you want and whatever genes you want those selection pressures to act on. The citations I post describe explicitly what the selection pressures are and often defines which loci in the gene must mutate in order for adaptation to occur. You have give vague examples without defining what the selection pressures are and the genes affected by these selection pressures. Until you do this, you only have this fuzzy, ill-defined argument of how mutation and selection actually works.
As you lengthen the genome in the model, the number of generations needed to satisfy the three selection conditions becomes greater and greater until the model simple stops converging.Satisfy the selection conditions ? Since when is that a yes or no question ?

Evolution isn't about survival of the fittest, but about survival of the barely fit.
Until you study ev a bit, you will not understand my argument. Start with Dr Schneider’s published case a simply start lengthening the genome and see how long it takes to evolve a perfect creature.
What is it with you? Joobz wants to talk about the fossil record, you want to talk about gravity. Can’t you stay on topic?I never said I wanted to talk about gravity. Your complete lack of reading comprehension is showing more and more.

Please read what I said again.
So let’s see what you said:
.According to you, gravity worsens the "evolutionist" argument.

I thought it was "evolutionarian" ?
So what is it that you want to talk about if it isn’t gravity?
You complain that I don’t answer your questions. Let me help you with the answer to this question. It is obvious that selection pressures which cause extinction do not accelerate evolution.That's highly debatable. Extinction, even MASS extinctions, could actually help the evolution of the surviving species.
How does it help the species that went extinct? It seems like the remaining species after a MASS extinction would have less selection pressure because of the elimination of competition. Are you arguing that removal of selection pressure accelerates evolution?
The empirical evidence demonstrates the same behavior that Dr Schneider’s model demonstrates.Explain peppered moths, nylon-eating bacteria and humans. And please don't try to claim that there's only one selection pressure at work.
You brought up these examples, you explain what the selection pressures are and the genes acted on by these selection pressures. I’ll explain the examples I cite and you explain the examples you cite.
This despite the fact that these real empirical examples are not limited to random point mutations but can have any mutation you can imagine and many of these real cases include recombination (such as HIV) yet they all show that combination selection pressures profoundly slow evolution.Unfortunately for you, case scenarios and empirical examples do not make anything mathematically possible or impossible.
Sure they do, all these examples show that combination selection pressures profoundly slow the evolutionary process. Of course this is what is demonstrated by the ev computer simulation of random point mutation and natural selection. It is the three selection conditions which profoundly slow the evolutionary process in this computer model on all but the smallest genomes.
Are you talking about all one of your examples, the nylon eating bacteria? You still haven’t described the selection pressures and the genes involved in all one of your examples. As soon as you do, you will find out that all one of your examples is simply a single selection pressure and a single target gene.K172 was not created by scientists in a controlled environment. It was discovered in a pool of waste product in a manufacturing plant. K172 exists despite all of the purportedly natural selection pressures which you claim make its existence impossible.

K172 is the product of a frame shift -- not a point mutation. It exists in contravention to your entire theory. So, either explain where K172 came from, or admit that its existence falsifies your theory that macroevolution is mathematically impossible.

Now, in the interest of "science," I'll refrain from addressing the remainder of your post, until you directly address the substance of the above.
So what were the selection pressures and genes being acted on by your example? You brought up this example, so define the selection pressures and genes acted on by these selection pressures and show that multiple selection pressures accelerate evolution.