Annoying creationists

[Dr Adequate]

kleinman doesn't get the difference between computational time and model time?

Evidently not.

Look at his reply to you.

Don’t you mean generations computed in the model and real generation time? I’ll let Dr Schneider answer this one; this is from his ev blog page:

Schneider lets slip that there is another unrealistic element in his (and indeed all) computer simulations in that it (they) "does not correlate with time":

So? Run the program slower if you want. Make one generation per 20 minutes to match rapid bacterial growth. THIS WILL NOT CHANGE THE FINIAL RESULT!

 

[joobz]

So why do you keep doing so?

Demonic possession, perhaps?

Maybe he's applying "The Secret." Evolution is true because he didn't believe in creationism enough.

 

[kleinman]

Annoying Creationists

Maybe he's applying "The Secret." Evolution is true because he didn't believe in creationism enough.

There’s no “The Secret” here joobz, there is Dr Schneider’s model of evolution by random point mutation and natural selection and there are numerous real examples that show he got the model correct. The auditors are here and your theory of evolution books do not balance. Your theory is bankrupt.

 

[kjkent1]

Oh really little gator?

Yes, small man.

Does Unnamed’s alternative selection algorithm satisfy the necessary generational constraints?

You certainly seemed to think so at the time it was introduced into this thread. Your objection was that the method ignored the non-binding-site region of the genome. However, Unnamed's post of the algorithm shows that it doesn't do anything other than weight each mistake by the value contained in the weight matrix, instead of simply providing a fixed selective weight to the mistake.

Schneider's original algorithm treats each mistake as effectively of equal selective weight. Paul A's mods to the java version permit the weights of mistakes occurring in different regions to be varied. Unnamed's algorithm treats each mistake as having a destructive/constructive value to the organism equal to the mistake's weight as evaluated by the weight matrix.

The point is that it is highly likely that not all mistakes/mutations have equal selective power, because a mistake in a junk region may be selectively neutral while a mistake in another region could produce instant cell death. No one, including Dr. Schneider has determined any model that accurately models this selective power.

You are claiming that ev cannot evolve fast enough to produce the sort of speciation which is found in nature. Assuming this is true, it could easily be because the selection method does not accurately reflect the selective power of individual mistakes. From examining the differences between Schneider's original algorithm, Paul's mods and Unnamed's algorithm, it is obvious that selective weight has a substantial effect on evolutionary change.

The last time I checked, Dr Schneider’s model was peer reviewed and published.

You can continue to harp that ev is peer reviewed, but so what? The original algorithm is plausable -- this doesn't mean it is a perfect replica of natural evolution, nor does it need be in order to be acceptable for publication. Ev may be a "worst case" scenario, but it still proves information gain, and that's all it needs to prove to show that evolution is possible.

Kjkent1, how do you select for something that is not functioning such as a partially completed gene? There is no selection process that can select for something that does not exist.

You claim ev is a plausable model. Ev begins with a random genome, containing unselected material. This is substantially the same as a junk dna region. Given that as a premise, it is an observed fact that genomes of independent life forms exhibit the Rseq ~ Rfreq relationship. So, selection does not need to be for some external function. Selection need only produce genetic sequences where Rseq -> Rfreq, because that apparently is a fundamental property of living organisms.

You may immediately ask why should that be? You may as well ask why the cosmological constant is 2E-121. It doesn't matter why. It only matters that it is so.

I really don't care what your personal beef with Schneider is. If you think he's defamed you, then you should sue his ass and prove your case.

But, on the subject of evolution, there is no doubt that it occurs. The evidence is everywhere. If you want each speciation change to be the product of divine intervention, you can certainly believe that to be true. But, no amount of microscopic examination will show God's index finger pushing base pairs around.

All anyone will ever observe is accidental changes which create speciated life forms.

 

[Ichneumonwasp]

Do you want to explain what the selective pressure were that led to the differences between the human and chimp genes and how these transformations were accomplished because mutation and selection is a profoundly slow mechanism as shown by ev.

So, ev says it couldn't happen, so it didn't happen, is that the thrust of your question?

So increased brain size with larger frontal and temporal lobes with consequent improvements in cognitive ability and communication skills improving our hunting ability is not enough? You want something more than that do you mean?

This is getting silly. You misinterpret Dr. Schneider and continually use him in some weird surrogate appeal to authority anytime anyone claims that perhaps ev doesn't quite model all of evolutionary reality. Dr. Schneider has said, himself, that ev does not model all of evolutionary reality. Whenever we show you some aspect of the real world you trot out ev and say "Well, that can't happen because ev says it's impossible". I'm sorry, bud, but I'm going with the real world.

The model models what it models. It doesn't do windows.

It is not that my view is truncated; it is that your view of mutation and selection is grossly over-extrapolated.

How's that? My view is that mutation and selection does not cover the entire field of endeavor. You cannot disregard these other spheres. Well, let me rephrase that, since you most assuredly have ignored them -- you shouldn't ignore the real world and the way the genome actually works.

My view is supported by a peer reviewed and published mathematical model of mutation and natural selection

Your view consists of the misapplication of a computer model that demonstrates increase in information via mutation and selection. It does not cover wide swaths of the real world, as Dr. Schneider repeats and you continue to quote. It does, most assuredly model the real world -- as it relates to the ability of mutation and selection to account for information gain.

your view is a collection of observations that has no mathematical foundation.

There is plenty of mathematical foundation for the current theory of evolution. I have no idea to what you refer.

In the mean time, I have yet to see these equations you contend that you have. How about showing us? Show us your mathematics so that we can apply them to real world situations. Pretty please?

Crossing over does not create new information in the gene pool, you can change the way the information is expressed by crossing over.

I just gave you in that previous post two mechanisms by which crossing over can increase information. You did read that post, did you not? If so, then what in the world are you talking about?

Are you going to argue that reptiles evolved to birds by crossing over?

There really are some brands with less caffeine these days, Dr. Kleinman. You should try one of them. Or, perhaps you could understand what an example is. And understand that I was referring to your simplistic attempt to suggest that no new information can arise from sexual reproduction. The steps from reptile to bird included several changes, including alterations in one of those big modulatory gene families I earlier mentioned -- hox genes. I would have to look at what has been worked out to see what we know and what we don't know. You'll have to forgive me for having an actual life with a real job. I know my field and not all others. It is easy to ask questions and play dumb and not so easy to know all the answers. I do not pretend to know all the answers. But this really has nothing to do with our topic of discussion originally -- the inadequacy of your claim that ev models HIV triple therapy. You still haven't responded to that issue with any clarity. I have seen hand waving.

Do you think that humans and chimps evolved from the primate precursor by crossing over?

Who knows? Some of the gene changes might have involved that mechanism. It's difficult to tell. That is not the point. You're trying to make it into a big point is rather pointless and excessively silly. Please continue though.

Humans and chimps don’t even have the same number of chromosomes.

You're completely lost now aren't you? Do you honestly think that crossing over has something to do with chimps and humans mating? Have we really sunk to that level of ridiculousness?

You can not create new information in the gene pool without mutation and selection.

Sure you can. New information means new proteins. New proteins can arise through numerous mechanisms, including alternative splicing. New information may take the form of protein a being in contact with protein b during development (when previously they were expressed at completely different times), a change that depends on a feedback mechanism that determines the timing of expression. That change can occur in an intron rather than an exon, so mutations needn't involve exons at all for alterations in the real world to happen. There are many different ways that "junk" DNA adds to the regulation of promoter regions. Increase production of a protein and that gene can go from what we call recessive to what we call dominant. Move a promoter to a region that was not previously expressed and presto we've got a new gene just waiting to do its thing. Copy promoters all over the place and new proteins sprout like daisies on a warm summer day. Nature is just cool like that.

There is no other mechanism for creating new genes

Complete and utter BS. Hey, I've got a classic one for you -- just copy a gene and let the new copy mutate. That's lots of new information with no loss of information. That should satisfy you. But, whoa, what if the DNA sequence is a promoter region and it is copied several times in front of a piece of DNA that was never used before in that species but is perfectly capable of producign a protein. Whoops, there we go with that new information sprouting up.

there is no selection pressure that can create a gene from the beginning

What selection pressure is needed aside from the new gene itself? If it makes copies, it can. Selection.

Recombination can alter the way genes are expressed but you can not create new genes this way.

Only if you think one dimensionally. Get real. You do know something about genetics don't you?

Recombination and natural selection can cause the loss of alleles (and thus reduce the diversity of a species). That is what “crossing over” gives to the theory of evolution. Feel free to put recombination with crossing over in ev. You will find you can’t create new genes this way.

You're really funny sometimes, Dr. Kleinman. Someone might actually think you are being serious with completely ignorant statements like this, but you aren't really serious, are you?

Well, the peer reviewers at Nucleic Acids Research don’t seem to agree with you.

Don't seem to agree with me how? Now let's see, what was the title and the first lines of that abstract again? Oh Yeah:

Evolution of biological information

How do genetic systems gain information by evolutionary processes? Answering this question precisely requires a robust, quantitative measure of information.

It's a model of information gain. It does not model evolution in all its particulars, as Dr. Schneider repeatedly says. In particular the model does not say that the only means of gaining information is through mutation and selection. What he said is that it is a way of gaining information because creationists argued that no information could possibly be gained through this means. He proved the creationists wrong. You are wrong for inappropriately applying his model. Shame on you, Dr. Kleinman.

 

[kleinman]

Annoying Creationists

Does Unnamed’s alternative selection algorithm satisfy the necessary generational constraints?

You certainly seemed to think so at the time it was introduced into this thread. Your objection was that the method ignored the non-binding-site region of the genome. However, Unnamed's post of the algorithm shows that it doesn't do anything other than weight each mistake by the value contained in the weight matrix, instead of simply providing a fixed selective weight to the mistake.

Now don’t forget to mention these quotes:

In addition, there is no selection process for a partially completed gene.

I don't think that's true, but if it were, then my change would be meaningless.

It seems Unnamed has abandoned this debate as well as his unrealistic selection scheme. He probably realized there is no way to select for a gene that is not functional.

Schneider's original algorithm treats each mistake as effectively of equal selective weight. Paul A's mods to the java version permit the weights of mistakes occurring in different regions to be varied. Unnamed's algorithm treats each mistake as having a destructive/constructive value to the organism equal to the mistake's weight as evaluated by the weight matrix.

What Unnamed is doing with his selection process is equivalent to setting the weight factor for spurious binding to zero. I point this out to Unnamed and we had the following exchange.

Unnamed, what you are doing here is ignoring errors in the non-binding site region.

No I'm not, unless I was doing it by mistake.

I think if you keep track of the value of valuation[p] in the following equation,
sv += Math.abs(valuation[p] - threshold);
you will see that this number will be much larger in the binding site region due to the good match of the weight matrix. In the non-binding site region this value will remain small. You are effectively giving a higher weight to good mutations in the binding site region than to harmful mutations in the non-binding site region. You can achieve the same effect if you set the value for the variable gene=1 and nongene=0 and still sort on the variable “mistakes”.

Unnamed abandoned the discussion after this exchange. It seems that evolutionists don’t like the debate on the mathematics of mutation and selection.

The point is that it is highly likely that not all mistakes/mutations have equal selective power, because a mistake in a junk region may be selectively neutral while a mistake in another region could produce instant cell death. No one, including Dr. Schneider has determined any model that accurately models this selective power.

Of course selection pressures can have varying intensities. The way Paul has varied the intensity ignores the fact that highly potent selection pressures will suppress reproduction by increasing the death rate. Increasing selection pressures in ev does not affect death rates. In fact, if you increase the weights uniformly, you get the same generations for convergence no matter what the weights are. Intense selection pressures will slow evolution more, ev does not include this effect.

You are claiming that ev cannot evolve fast enough to produce the sort of speciation which is found in nature. Assuming this is true, it could easily be because the selection method does not accurately reflect the selective power of individual mistakes. From examining the differences between Schneider's original algorithm, Paul's mods and Unnamed's algorithm, it is obvious that selective weight has a substantial effect on evolutionary change.

Reducing the number of selection pressures as Unnamed did does accelerate evolution.

The last time I checked, Dr Schneider’s model was peer reviewed and published.

You can continue to harp that ev is peer reviewed, but so what? The original algorithm is plausable -- this doesn't mean it is a perfect replica of natural evolution, nor does it need be in order to be acceptable for publication. Ev may be a "worst case" scenario, but it still proves information gain, and that's all it needs to prove to show that evolution is possible.

Ev shows how microevolution occurs and that macroevolution is impossible. How does ev show this? It shows this by revealing how rapidly single selection conditions evolve even on longer genomes and how slowly multiple selection conditions evolve even on short genomes. There are numerous real examples of this.

Kjkent1, how do you select for something that is not functioning such as a partially completed gene? There is no selection process that can select for something that does not exist.

You claim ev is a plausable model. Ev begins with a random genome, containing unselected material. This is substantially the same as a junk dna region. Given that as a premise, it is an observed fact that genomes of independent life forms exhibit the Rseq ~ Rfreq relationship. So, selection does not need to be for some external function. Selection need only produce genetic sequences where Rseq -> Rfreq, because that apparently is a fundamental property of living organisms.

Selection is a response to an external function. Turn off selection in ev and see what happens to Rseq.

You may immediately ask why should that be? You may as well ask why the cosmological constant is 2E-121. It doesn't matter why. It only matters that it is so.

Oh tell me why the stars do shine?

I really don't care what your personal beef with Schneider is. If you think he's defamed you, then you should sue his ass and prove your case.

I don’t have a beef with Dr Schneider; in fact, I may be the last person on earth that believes he modeled mutation and selection properly. IDers questioned the validity of ev for years and now evolutionists are abandoning his work in droves including his own programmer. The only thing I take issue with Dr Schneider is his use of an extremely short genome and an extremely high mutation rate to estimate the rate of information gain for a human genome. This was a big boo boo. I actually think ev is a useful tool that can me modified to more exactly model HIV treatment and drug resistance.

But, on the subject of evolution, there is no doubt that it occurs. The evidence is everywhere. If you want each speciation change to be the product of divine intervention, you can certainly believe that to be true. But, no amount of microscopic examination will show God's index finger pushing base pairs around.

All anyone will ever observe is accidental changes which create speciated life forms.

Now if only ev showed this was mathematically possible.

Do you want to explain what the selective pressure were that led to the differences between the human and chimp genes and how these transformations were accomplished because mutation and selection is a profoundly slow mechanism as shown by ev.

So, ev says it couldn't happen, so it didn't happen, is that the thrust of your question?

Think of ev as an accounting tool. What ev does is keep track of beneficial, neutral and detrimental mutations. Sequencing of human and chimp DNA shows at least 35,000,000 base substitutions in the homologous regions of the genomes. You have about 500,000 generations to accomplish all these changes. Ev shows that even on short genomes, 500,000 generations are not sufficient to evolve binding sites (100 loci) on a 32k genome and human and chimp genomes number in the billions of base pairs. The mathematics just doesn’t work out.

So increased brain size with larger frontal and temporal lobes with consequent improvements in cognitive ability and communication skills improving our hunting ability is not enough? You want something more than that do you mean?

Mutation and selection does not explain these differences. Does it require mutation and selection to achieve the changes you describe? Maybe you should argue these type of differences can be achieved with recombination and selection.

This is getting silly. You misinterpret Dr. Schneider and continually use him in some weird surrogate appeal to authority anytime anyone claims that perhaps ev doesn't quite model all of evolutionary reality. Dr. Schneider has said, himself, that ev does not model all of evolutionary reality. Whenever we show you some aspect of the real world you trot out ev and say "Well, that can't happen because ev says it's impossible". I'm sorry, bud, but I'm going with the real world.

Mutation and selection is a bookkeeping problem. When you apply these rules of bookkeeping, you can not account for all the genetic differences between living things. In particular, multiple selection pressures slow the evolutionary process. This is a mathematical fact shown by ev and there are numerous real examples of this including the use of combination therapy to treat HIV.

The model models what it models. It doesn't do windows.

Ev gives us a window on mutation and natural selection. You ought to take a look through this window.

It is not that my view is truncated; it is that your view of mutation and selection is grossly over-extrapolated.

How's that? My view is that mutation and selection does not cover the entire field of endeavor. You cannot disregard these other spheres. Well, let me rephrase that, since you most assuredly have ignored them -- you shouldn't ignore the real world and the way the genome actually works.

Mutation and selection can accomplish small events such as drug resistance with microbes. There are real examples of these phenomena. However, to extrapolate these types of phenomena to the evolution of birds from reptiles or humans and chimps from a primate ancestor by mutation and selection has no mathematical foundation. You simply do not have sufficient number of generations and populations to accomplish all the genetic changes required. In the real world, the books have to balance. In addition to the fact that multiple selection pressures slow down evolution, there are no selection pressures that can evolve a gene from the beginning. You are the one ignoring the real world and you do this by extrapolating mutation and selection far beyond what it is mathematically capable of doing.

My view is supported by a peer reviewed and published mathematical model of mutation and natural selection.

Your view consists of the misapplication of a computer model that demonstrates increase in information via mutation and selection. It does not cover wide swaths of the real world, as Dr. Schneider repeats and you continue to quote. It does, most assuredly model the real world -- as it relates to the ability of mutation and selection to account for information gain.

I did exactly what Dr Schneider suggested publicly and privately to me. I varied genome length, selection pressures, mutation rates, population as well as other parameters in his program. What it showed was that genome length and the number of selection pressures are the dominate variables in the mutation and selection process. There are many real examples which demonstrate this finding. Look through the window and see.

your view is a collection of observations that has no mathematical foundation.

There is plenty of mathematical foundation for the current theory of evolution. I have no idea to what you refer.

Where is this mathematics of mutation and selection you are talking about?

In the mean time, I have yet to see these equations you contend that you have. How about showing us? Show us your mathematics so that we can apply them to real world situations. Pretty please?

I have the mathematics of a peer reviewed and published computer model of mutation and natural selection. Now where is this mathematical cornucopia that forms the foundation of your theory?

Crossing over does not create new information in the gene pool, you can change the way the information is expressed by crossing over.

I just gave you in that previous post two mechanisms by which crossing over can increase information. You did read that post, did you not? If so, then what in the world are you talking about?

Crossing over does not increase information in a genome; it is simply a rearrangement of existing genes in the gene pool. You not created any new genes.

Are you going to argue that reptiles evolved to birds by crossing over?

There really are some brands with less caffeine these days, Dr. Kleinman. You should try one of them. Or, perhaps you could understand what an example is. And understand that I was referring to your simplistic attempt to suggest that no new information can arise from sexual reproduction. The steps from reptile to bird included several changes, including alterations in one of those big modulatory gene families I earlier mentioned -- hox genes. I would have to look at what has been worked out to see what we know and what we don't know. You'll have to forgive me for having an actual life with a real job. I know my field and not all others. It is easy to ask questions and play dumb and not so easy to know all the answers. I do not pretend to know all the answers. But this really has nothing to do with our topic of discussion originally -- the inadequacy of your claim that ev models HIV triple therapy. You still haven't responded to that issue with any clarity. I have seen hand waving.

What you continue to have difficulty with is the mathematics of mutation and selection. The massive number of differences between reptile and bird genomes can not be accomplished by mutation and selection. Not only is there no selection pressure that would do this, there is no way to account for all the required changes needed by mutation and selection. One unique gene difference between birds and reptiles is enough to prove the impossibility of evolution. What is the selection pressure that would evolve this unique gene?

Do you think that humans and chimps evolved from the primate precursor by crossing over?

Who knows? Some of the gene changes might have involved that mechanism. It's difficult to tell. That is not the point. You're trying to make it into a big point is rather pointless and excessively silly. Please continue though.

This seems to be the sum total of the evolutionist argument, you don’t know how it happened but you know it did. Well, I know it didn’t happen by mutation and selection, ev shows how slow this process is and that the theory of evolution by mutation and selection is mathematically impossible.

Humans and chimps don’t even have the same number of chromosomes.

You're completely lost now aren't you? Do you honestly think that crossing over has something to do with chimps and humans mating? Have we really sunk to that level of ridiculousness?

What still hasn’t sunk in with you is that recombination without error can not increase information in the gene pool and that recombination with natural selection can cause the loss of information in the gene pool due to loss of alleles.

You can not create new information in the gene pool without mutation and selection.

Sure you can. New information means new proteins. New proteins can arise through numerous mechanisms, including alternative splicing. New information may take the form of protein a being in contact with protein b during development (when previously they were expressed at completely different times), a change that depends on a feedback mechanism that determines the timing of expression. That change can occur in an intron rather than an exon, so mutations needn't involve exons at all for alterations in the real world to happen. There are many different ways that "junk" DNA adds to the regulation of promoter regions. Increase production of a protein and that gene can go from what we call recessive to what we call dominant. Move a promoter to a region that was not previously expressed and presto we've got a new gene just waiting to do its thing. Copy promoters all over the place and new proteins sprout like daisies on a warm summer day. Nature is just cool like that.

Really now, do you think this occurs with reproduction? You are now extrapolating the production of immunoglobins to reproduction. And do you want to explain how coping promoters all over the place speeds up the evolutionary process?

There is no other mechanism for creating new genes.

Complete and utter BS. Hey, I've got a classic one for you -- just copy a gene and let the new copy mutate. That's lots of new information with no loss of information. That should satisfy you. But, whoa, what if the DNA sequence is a promoter region and it is copied several times in front of a piece of DNA that was never used before in that species but is perfectly capable of producign a protein. Whoops, there we go with that new information sprouting up.

Copy a gene and you have two copies of the same gene. A new gene requires mutation. So now you have a copy of a gene that is slightly altered and low and behold, it performs an entirely new function like growing feathers on a lizard. It requires mutations to make a new gene and ev shows this is a profoundly slow process even if you have a selection process that could make the new gene and you don’t. You are in complete denial of the mathematics of mutation and selection and how it works. Study ev and learn how the mathematics of mutation and selection works instead of making your wild unscientific extrapolations.

there is no selection pressure that can create a gene from the beginning

What selection pressure is needed aside from the new gene itself? If it makes copies, it can. Selection.

I haven’t posted this for a while so for your benefit, I will repost why your concept is impossible.

A gene is to evolve. The first base in the sequence for the gene is laid down on the genome. One base codes for nothing so there is nothing for natural selection to act upon. A second base added by random chance is laid down in the sequence. Still nothing to code for, natural selection can not act on this sequence. A third base in the sequence is laid down. You now have enough bases to form a codon for a single amino acid. A single amino acid has no functional use so there is still nothing for natural selection to act upon. So bases must be added randomly until you have a long enough sequence of bases to produce a functional polypeptide and then natural selection can act. Adding bases randomly yield probabilities so infinitesimally small that evolution is mathematically impossible.

Recombination can alter the way genes are expressed but you can not create new genes this way.

Only if you think one dimensionally. Get real. You do know something about genetics don't you?

In which dimension do you dwell where recombination can create a new gene?

Recombination and natural selection can cause the loss of alleles (and thus reduce the diversity of a species). That is what “crossing over” gives to the theory of evolution. Feel free to put recombination with crossing over in ev. You will find you can’t create new genes this way.

You're really funny sometimes, Dr. Kleinman. Someone might actually think you are being serious with completely ignorant statements like this, but you aren't really serious, are you?

Simple enough, tell us how recombination without error can create new genes and I’ll tell you how recombination and natural selection can cause the loss of alleles. Of course you can’t tell us how recombination without error can create new genes but I can tell you how recombination and natural selection can cause the loss of alleles.

Well, the peer reviewers at Nucleic Acids Research don’t seem to agree with you.

Don't seem to agree with me how? Now let's see, what was the title and the first lines of that abstract again? Oh Yeah:

How do genetic systems gain information by evolutionary processes? Answering this question precisely requires a robust, quantitative measure of information.

You really need to read beyond the abstract for this one, if you had you would have seen:

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

If you had investigated ev as Dr Schneider suggested, you would have more than a superficial understanding of the mathematics of mutation and selection. Anything more than a superficial investigation of ev reveals the mathematical impossibility of the theory of evolution.

It's a model of information gain. It does not model evolution in all its particulars, as Dr. Schneider repeatedly says. In particular the model does not say that the only means of gaining information is through mutation and selection. What he said is that it is a way of gaining information because creationists argued that no information could possibly be gained through this means. He proved the creationists wrong. You are wrong for inappropriately applying his model. Shame on you, Dr. Kleinman.

If you had read the paper beyond the abstract you would realize that you are limiting the scope of ev because it suits your belief system, not because that was the intention of Dr Schneider. If you had read these threads you would have seen from the very beginning that I acknowledged that you can gain information by mutation and selection. The only shame in this is that you think you can understand the mathematics of mutation and selection without doing your homework. Read Dr Schneider’s works completely and read these threads completely, otherwise you reveal that you are superficial in your analysis, of course, that is the only type of analysis the theory of evolution can stand up to.

 

[Paul C. Anagnostopoulos]

Reducing the number of selection pressures as Unnamed did does accelerate evolution.

Are you sure he did that?

If you had read the paper beyond the abstract you would realize that you are limiting the scope of ev because it suits your belief system, not because that was the intention of Dr Schneider.

Now you're just being ridiculous.

~~ Paul

 

[Paul C. Anagnostopoulos]

I did exactly what Dr Schneider suggested publicly and privately to me. I varied genome length, selection pressures, mutation rates, population as well as other parameters in his program. What it showed was that genome length and the number of selection pressures are the dominate variables in the mutation and selection process.

Hey Dr. Adequate, you have to assign this a lie number. Kleinman didn't know he could vary the mistake counts until a few weeks ago. Before that, the goalpost was somewhere else.

~~ Paul

 

[kjkent1]

I think if you keep track of the value of valuation[p] in the following equation,
sv += Math.abs(valuation[p] - threshold);
you will see that this number will be much larger in the binding site region due to the good match of the weight matrix. In the non-binding site region this value will remain small. You are effectively giving a higher weight to good mutations in the binding site region than to harmful mutations in the non-binding site region. You can achieve the same effect if you set the value for the variable gene=1 and nongene=0 and still sort on the variable “mistakes”.

Little man, you're inventing what you think the algorithm does.

The code line that you quote above is exactly the same in the portion of the algorithm that deals with binding sites (siteInd[p]) as it is in the portion that deals with the non-binding sites (!siteInd[p]). In both cases, the algorithm gives the creature a selective value (sv) equal to the absolute value of the location minus the threshold.

Thus, Unnamed's algorithm treats both binding and non-binding site regions identically as to mistake weight.

What the algorithm does to speed up the evolutionary process, is to use the absolute value difference between the weight at the binding site location and the threshold value, whereas Schneider's original algorithm treated every mistake and binding as worth one (1) point.

So, when the algorithm sorts the creatures, creatures with mistakes are killed faster, and creatures without live longer, because they are more harshly penalized for their errors.

And, until you can quantify how important an error vs. no error is to a creature's survival, you can't say whether Schneider's approach or Unnamed's is more reasonable.

What you CAN say, is that harsher selective pressures speed up evolution.

Which, by the way, is proof of exactly the opposite of what you contend with your multiple selctive pressures slowing evolution argument.

 

[kleinman]

Annoying Creationists

Reducing the number of selection pressures as Unnamed did does accelerate evolution.

Are you sure he did that?

Yes, and this is the equation that does this:

sv += Math.abs(valuation[p] - threshold);

valuation[p] (the value of the dot product of the weight matrix with the positions on the genome) will almost always be a small number in the nonbinding site region of the genome. This is equivalent of ignoring the spurious binding in the nonbinding site region.

If you had read the paper beyond the abstract you would realize that you are limiting the scope of ev because it suits your belief system, not because that was the intention of Dr Schneider.

Now you're just being ridiculous.

So, since you are Dr Schneider’s coworker, why don’t you tell us what he meant when he said this:

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

He must have meant that only variations that support the theory of evolution should be investigated. Paul, I love it when you squirm.

I did exactly what Dr Schneider suggested publicly and privately to me. I varied genome length, selection pressures, mutation rates, population as well as other parameters in his program. What it showed was that genome length and the number of selection pressures are the dominate variables in the mutation and selection process.

Hey Dr. Adequate, you have to assign this a lie number. Kleinman didn't know he could vary the mistake counts until a few weeks ago. Before that, the goalpost was somewhere else.

Righto Mr Rcapacity, you don’t lie, you just back pedal at the speed of light. Oh, that’s right; you evolutionists go faster than the speed of light. Let’s see, it started less than two years ago when you said this:

I think Ev rankles the IDers because it is a model of actual life, and also because Schneider is fairly good at advertising it.

Then you said this:

It works like real life in a simulation of a limited situation. It covers maybe 1/100 of 1% of the complexity of real life.

Then you said this:

You seem to be saying something different than what Dr Schneider has said and what I have heard evolutionists say for years, that is random mutation and natural selection is the driving force for evolution. Now you are saying that random mutation and natural selection covers only 1/100 of 1% of the complexity of real life.

That's not what I said at all. I said that Ev only simulates a tiny fraction of the richness of the evolutionary landscape.

Then you said this:

Are you going to retract your extrapolation that 16 binding sites on a 100k genome take 200,000,000 generations to evolve?

Why? It is an extrapolation using the Ev model. We don't know how much it has to do with real life.

And so your view of ev evolves.

Just what does ev show now? You certainly aren’t saying the same thing that the author of the program has said which is unfortunate because I think he got this mathematical model of mutation and selection correct. Since random point mutation and natural selection represents 1/100 of 1% of your theory of evolution, care to tell us what the other 99.99% is?

The code line that you quote above is exactly the same in the portion of the algorithm that deals with binding sites (siteInd[p]) as it is in the portion that deals with the non-binding sites (!siteInd[p]). In both cases, the algorithm gives the creature a selective value (sv) equal to the absolute value of the location minus the threshold.

Why don’t you tell us what valuation[p] is computing?

You all have a good weekend, and don’t let your view of ev evolve too much. Dr Schneider won’t have anything left to advertise.

 

[joobz]

Ugh, Dr. Kleinman, you've become boring again. You've reverted to your original goalpost lies which have already been exposed and discounted.

Please be a little more inventive. Otherwise, this thread will die.

 

[kjkent1]

Yes, and this is the equation that does this:

sv += Math.abs(valuation[p] - threshold);

valuation[p] (the value of the dot product of the weight matrix with the positions on the genome) will almost always be a small number in the nonbinding site region of the genome. This is equivalent of ignoring the spurious binding in the nonbinding site region.

That's really funny. Since the entire genome is being randomly mutated and selected for/against at the same time, but only the binding site region is being monitored for threshold bindings, why would any portion of the genome produce smaller or larger selective valuations?

Answer: they wouldn't. The only differnce between the results in the binding and non-binding region is that the program is tracking the results in one and not in the other.

And, if you run ev and look at the valuations in the non-binding site region, you will immediately recognize that there are just as many large valuations therein as occurs in the binding site region. So, your conclusion above is false. Unnamed's algorithm does not ignore the non-binding site region.

Why don’t you tell us what valuation[p] is computing?

I don't need to, because you just explained it at the beginning of your last post.

It's really a pity that you don't take anyone seriously other than yourself. You might actually help make a contribution to society, if you weren't so dead set on trying to overcome your self esteem issues.

 

[Ichneumonwasp]

Think of ev as an accounting tool. What ev does is keep track of beneficial, neutral and detrimental mutations. Sequencing of human and chimp DNA shows at least 35,000,000 base substitutions in the homologous regions of the genomes. You have about 500,000 generations to accomplish all these changes. Ev shows that even on short genomes, 500,000 generations are not sufficient to evolve binding sites (100 loci) on a 32k genome and human and chimp genomes number in the billions of base pairs. The mathematics just doesn’t work out.

Last time I checked you said that we should not compare apples and oranges, but that is precisely what you are doing.

Ev begins with random "bases" in no particular order and evolves sequences that fit predefined binding site information. It begins from scratch, so to speak, and moves toward a defined pre-set goal (as a way to determine the emergence of information).

The change from chimp to human begins with approximately 25,000 to 35,000 already pre-existing genes. A small number of those genes change over time, with most of the alterations occurring in regulatory regions or in feedback loops concerned with the timing of gene expression during development. There is no "de novo evolution of binding sites". The alterations occur and if they allow more offspring to survive, then they are expressed at higher frequency. Many of the changes were in gene deletions or gene duplications with and without modification. A simple gene duplication near a promoter that is active at a different time of development you would see as no new information (same gene), but the reality is that considerable morphological change can occur with gene expressions at different times (see bone morphogenic protein for a stark example). Other changes are single base substitutions, as with FOXP2, not the evolution of completely novel binding sites from scratch using a simple mutation and selection. The comparison with ev is absolute and complete bunk. Analogies don't work when they are not analogous.

Ev basically models what the early biosphere could have been like. It has set genome lengths and only allows mutations with no other sharing of genetic material between varying entities. Yet, under these extremely restricted conditions, it shows that information can develop over time. It's relationship to evolution of primates or any animal -- almost zero.

Mutation and selection does not explain these differences. Does it require mutation and selection to achieve the changes you describe? Maybe you should argue these type of differences can be achieved with recombination and selection.

What is your point? You recently told me that no new information could arise from recombination and selection. Yet now you wish to tell me that increased brain size and new communications abilities arise from the very situation that you earlier claimed could not create information? What?

So, let's look at the actual information. FOXP2 underwent a base substitution to become the new gene that it is. So, whoops, mutation and selection can account for that change. The protocadherin story is more complicated but may well simply result from mutation as well. There are desert regions surrounding the gene family that are thought to be involved in regulatory functions. They are probably transcription factor binding sites, etc. that are involved in regulating the expression of this and other local genes. The change in protocadhedrin is not in the protein itself -- that is conserved -- but in those regulatory regions that are considered otherwise non-coding, changing the expression of this protein during development. The big changes between chimp and human brain are in the networks of proteins involved in the developmental process. If you only look at the genes and do not consider the local milieu or the extraordinary differences that arise from alternative splicing the you only will see a bare fraction of what is responsible for the difference between us and chimps.

Mutation and selection is a bookkeeping problem. When you apply these rules of bookkeeping, you can not account for all the genetic differences between living things. In particular, multiple selection pressures slow the evolutionary process. This is a mathematical fact shown by ev and there are numerous real examples of this including the use of combination therapy to treat HIV.

So, you've just shot yourself in the foot? Yes, mutation and selection cannot account for all the genetic differences between living things. That is one of the things I am trying to tell you. Thank you for arguing my side. What this shows is that your "mathematical fact" of ev is no fact at all, but complete bunk. If you cannot account for all the genetic differences by use of your model that uses only mutation and selection, then the answer is clear. The model cannot account for all genetic differences. The model is insufficient. You cannot use the model to argue the impossibility of evolution. You have just proved wrong your entire premise and hung yourself with your own words.

End of story.

I'll get to the rest later. This looks like it will need to be a very long post, though I'm not sure there is much sense in continuing since even you seem to see that your argument is fundamentally flawed. An inadequate model is an inadequate model. The model (ev) was very good for what it was designed to to -- in fact I think it was brilliantly conceived -- but it is, even by your own admission, inadequate for the task you have set it.

 

[Ichneumonwasp]

Mutation and selection can accomplish small events such as drug resistance with microbes. There are real examples of these phenomena. However, to extrapolate these types of phenomena to the evolution of birds from reptiles or humans and chimps from a primate ancestor by mutation and selection has no mathematical foundation. You simply do not have sufficient number of generations and populations to accomplish all the genetic changes required. In the real world, the books have to balance. In addition to the fact that multiple selection pressures slow down evolution, there are no selection pressures that can evolve a gene from the beginning. You are the one ignoring the real world and you do this by extrapolating mutation and selection far beyond what it is mathematically capable of doing.

Load of bunk. Mutation and selection can accomplish small events, big events, grand events, deathly events, whatever. It all depends on what genes and gene networks are involved. You are again showing your incredibly one-dimensional view of the genome. Single base changes in regulatory genes or in regions for promoter or transcription factors can have a huge impact on morphology. It is absolute and complete misrepresentation to say anything else.

I am not extrapolating mutation and selection beyond what it is mathematically incapable of doing. You seem to have no grasp whatsoever of the actual genome of actual living beings. We have seen huge changes in organisms over time that you seem to think are impossible mathematically. Yet you do not fault the mathematical model? Why? Because you have a preset notion that evolution cannot occur. Schneider based his model on a subset of information from living creatures. He did not model the genomic behavior of all living beings. I'm sure we can contact him about this issue?

Hey, Paul, would you mind asking Schneider if he designed his model to cover all living beings?

You're beginning to screech, Dr. Kleinman. Your argument from a model against reality. That's a truly stupid thing to do.

Where is this mathematics of mutation and selection you are talking about?

Your biases are showing Dr. Kleinman. I said there were plenty of mathematical models of the current theory of evolution, not merely of mutation and selection. You, who are the mathematical genius of the century, are aware of all this work, are you not, Dr. Kleinman? I can barely read a paper on evolutionary theory without being inundated with mathematical modelling of this, that, and the other.

I have the mathematics of a peer reviewed and published computer model of mutation and natural selection. Now where is this mathematical cornucopia that forms the foundation of your theory?

You haven't read any of the literature, have you? OK, I'll start posting links in the morning as I pull up individual articles. How many do you want? There are mathematical models galore. You know this. Why are you acting dumb about it?

Crossing over does not increase information in a genome; it is simply a rearrangement of existing genes in the gene pool. You not created any new genes.

Pseudogenes, not previously expressed in an organism, now expressed in the presence of a promoter, repeat, rinse. Move transcription factor to new gene so that it is expressed in new milieu and suddenly the protein balance is changed. We're talking morphological changes here, Dr. Kleinman. You know, the stuff that natural selection actually works on.

What you continue to have difficulty with is the mathematics of mutation and selection. The massive number of differences between reptile and bird genomes can not be accomplished by mutation and selection. Not only is there no selection pressure that would do this, there is no way to account for all the required changes needed by mutation and selection.

Well gosh and golly jeepers, name me one person who actually thinks that all the changes between reptile and bird occurred by simplistic models of mutation and selection. I'd actually like to meet this mythical creature rarer than a phoenix-unicorn hybrid. Your mathematics are useless in this situation, Dr. Kleinman. Just how far do you intend to carry this straw man?

One unique gene difference between birds and reptiles is enough to prove the impossibility of evolution. What is the selection pressure that would evolve this unique gene?

What? I have no idea what you are on about now.

This seems to be the sum total of the evolutionist argument, you don’t know how it happened but you know it did. Well, I know it didn’t happen by mutation and selection, ev shows how slow this process is and that the theory of evolution by mutation and selection is mathematically impossible.

Well, isn't that nice. We agree on something. I know it didn't happen according to the simple outline you propose too. Evolution is much more complex than simple mutation and selection. There is no argument here.

What still hasn’t sunk in with you is that recombination without error can not increase information in the gene pool and that recombination with natural selection can cause the loss of information in the gene pool due to loss of alleles.

Oh, really? Yet up above you said that I should be arguing for recombination with selection for the development of the human brain. I guess the human brain is just a degenerate version of something that has lost information from that wonder of the world, the human-chimp common ancestor. I'll get the press on the line and let them know.

Really now, do you think this occurs with reproduction? You are now extrapolating the production of immunoglobins to reproduction. And do you want to explain how coping promoters all over the place speeds up the evolutionary process?

Didn't even mention immunoglobulins or hypervariable regions, but we could go there next. How do I explain it? I already have. You obviously didn't understand. Do you know what a promoter region is? Do you know what a transcription factor site is?

If a promoter is placed near a pseudo gene, then that pseudogene can lose its paltry pseudo status and join the rest of the club in the smoking car, the place where all the big boy genes hang out.

Copy a gene and you have two copies of the same gene. A new gene requires mutation. So now you have a copy of a gene that is slightly altered and low and behold, it performs an entirely new function like growing feathers on a lizard. It requires mutations to make a new gene and ev shows this is a profoundly slow process even if you have a selection process that could make the new gene and you don’t. You are in complete denial of the mathematics of mutation and selection and how it works. Study ev and learn how the mathematics of mutation and selection works instead of making your wild unscientific extrapolations.

I'm in complete denial of your lunacy for thinking you have "the mathematics of mutation and selection". Copy a gene and its expression can increase. It can also be associated with different transcription factors so that it is expressed at different times. You know, the whole proteomics bit. Making completely different morphologies -- having genes expressed in different places, different times.

And yes, single gene mutations in newly copied genes works too. But, again, there is no analogy to ev, since ev models numerous changes in the same place and all those changes have to fit a pre-determined state. The new mutation in a gene copy only has to advance survival. Ev does not model that behavior.

A gene is to evolve. The first base in the sequence for the gene is laid down on the genome. One base codes for nothing so there is nothing for natural selection to act upon. A second base added by random chance is laid down in the sequence. Still nothing to code for, natural selection can not act on this sequence. A third base in the sequence is laid down. You now have enough bases to form a codon for a single amino acid. A single amino acid has no functional use so there is still nothing for natural selection to act upon. So bases must be added randomly until you have a long enough sequence of bases to produce a functional polypeptide and then natural selection can act. Adding bases randomly yield probabilities so infinitesimally small that evolution is mathematically impossible.

What an interesting just so story.

And if we begin with peptides that serve as templates for RNA? There is already a relationship between amino acid and RNA in that scenario. The other way around makes no sense -- starting with RNA and/or DNA and expecting it to code for an amino acid. That is a silly story.

Simple enough, tell us how recombination without error can create new genes and I’ll tell you how recombination and natural selection can cause the loss of alleles. Of course you can’t tell us how recombination without error can create new genes but I can tell you how recombination and natural selection can cause the loss of alleles.

Are you an ostrich with its head in the sand. I've already given you several scenarios for this and you pretend that I haven't. Try something new. Your screeching is growing old.

If you had read the paper beyond the abstract you would realize that you are limiting the scope of ev because it suits your belief system, not because that was the intention of Dr Schneider. If you had read these threads you would have seen from the very beginning that I acknowledged that you can gain information by mutation and selection. The only shame in this is that you think you can understand the mathematics of mutation and selection without doing your homework. Read Dr Schneider’s works completely and read these threads completely, otherwise you reveal that you are superficial in your analysis, of course, that is the only type of analysis the theory of evolution can stand up to.

Um, no. I have read the paper completely, just today again. I see in it just how wrong you are, as reflected in some responses above. You, of course, will either not understand them or will pretend not to understand them, or will neglect the issue and continue to put your head in the sand. Whatever you want bro.

So, how about this. You publish this excellent work of yours. Put up now or shut up. You have the answer, so you think. It's time for peer review. I can't wait for the chuckles.

ETA

But, frankly, no one here needs me to repeat the same arguments that you have ignored since the beginning of this thread. This whole fiasco reads -- ev shows that evolution couldn't happen; no, you're wrong and here's the evidence to show where you are wrong; but ev shows that evolution couldn't happen; no, you're wrong and here's more evidence to show where you are wrong; rinse, repeat.

My only contribution was to argue against your use of HIV. I've served that purpose. You are now returning to arguments that began on page 2 of the thread and needn't be rehashed.

 

[BPScooter]

Peer review. A wonderful tradition. It works.

 

[Dr Adequate]

Now don’t forget to mention these quotes:

It seems Unnamed has abandoned this debate as well as his unrealistic selection scheme. He probably realized there is no way to select for a gene that is not functional.

What Unnamed is doing with his selection process is equivalent to setting the weight factor for spurious binding to zero. I point this out to Unnamed and we had the following exchange.

I think if you keep track of the value of valuation[p] in the following equation,
sv += Math.abs(valuation[p] - threshold);
you will see that this number will be much larger in the binding site region due to the good match of the weight matrix. In the non-binding site region this value will remain small. You are effectively giving a higher weight to good mutations in the binding site region than to harmful mutations in the non-binding site region. You can achieve the same effect if you set the value for the variable gene=1 and nongene=0 and still sort on the variable “mistakes”.

Unnamed abandoned the discussion after this exchange. It seems that evolutionists don’t like the debate on the mathematics of mutation and selection.

Of course selection pressures can have varying intensities. The way Paul has varied the intensity ignores the fact that highly potent selection pressures will suppress reproduction by increasing the death rate. Increasing selection pressures in ev does not affect death rates. In fact, if you increase the weights uniformly, you get the same generations for convergence no matter what the weights are. Intense selection pressures will slow evolution more, ev does not include this effect.

Reducing the number of selection pressures as Unnamed did does accelerate evolution.

Ev shows how microevolution occurs and that macroevolution is impossible. How does ev show this? It shows this by revealing how rapidly single selection conditions evolve even on longer genomes and how slowly multiple selection conditions evolve even on short genomes. There are numerous real examples of this.

Selection is a response to an external function. Turn off selection in ev and see what happens to Rseq.

Oh tell me why the stars do shine?

I don’t have a beef with Dr Schneider; in fact, I may be the last person on earth that believes he modeled mutation and selection properly. IDers questioned the validity of ev for years and now evolutionists are abandoning his work in droves including his own programmer. The only thing I take issue with Dr Schneider is his use of an extremely short genome and an extremely high mutation rate to estimate the rate of information gain for a human genome. This was a big boo boo. I actually think ev is a useful tool that can me modified to more exactly model HIV treatment and drug resistance.


Now if only ev showed this was mathematically possible.

Think of ev as an accounting tool. What ev does is keep track of beneficial, neutral and detrimental mutations. Sequencing of human and chimp DNA shows at least 35,000,000 base substitutions in the homologous regions of the genomes. You have about 500,000 generations to accomplish all these changes. Ev shows that even on short genomes, 500,000 generations are not sufficient to evolve binding sites (100 loci) on a 32k genome and human and chimp genomes number in the billions of base pairs. The mathematics just doesn’t work out.

Mutation and selection does not explain these differences. Does it require mutation and selection to achieve the changes you describe? Maybe you should argue these type of differences can be achieved with recombination and selection.

Mutation and selection is a bookkeeping problem. When you apply these rules of bookkeeping, you can not account for all the genetic differences between living things. In particular, multiple selection pressures slow the evolutionary process. This is a mathematical fact shown by ev and there are numerous real examples of this including the use of combination therapy to treat HIV.

Ev gives us a window on mutation and natural selection. You ought to take a look through this window.

Mutation and selection can accomplish small events such as drug resistance with microbes. There are real examples of these phenomena. However, to extrapolate these types of phenomena to the evolution of birds from reptiles or humans and chimps from a primate ancestor by mutation and selection has no mathematical foundation. You simply do not have sufficient number of generations and populations to accomplish all the genetic changes required. In the real world, the books have to balance. In addition to the fact that multiple selection pressures slow down evolution, there are no selection pressures that can evolve a gene from the beginning. You are the one ignoring the real world and you do this by extrapolating mutation and selection far beyond what it is mathematically capable of doing.

I did exactly what Dr Schneider suggested publicly and privately to me. I varied genome length, selection pressures, mutation rates, population as well as other parameters in his program. What it showed was that genome length and the number of selection pressures are the dominate variables in the mutation and selection process. There are many real examples which demonstrate this finding. Look through the window and see.

Where is this mathematics of mutation and selection you are talking about?

I have the mathematics of a peer reviewed and published computer model of mutation and natural selection. Now where is this mathematical cornucopia that forms the foundation of your theory?

Crossing over does not increase information in a genome; it is simply a rearrangement of existing genes in the gene pool. You not created any new genes.

What you continue to have difficulty with is the mathematics of mutation and selection. The massive number of differences between reptile and bird genomes can not be accomplished by mutation and selection. Not only is there no selection pressure that would do this, there is no way to account for all the required changes needed by mutation and selection. One unique gene difference between birds and reptiles is enough to prove the impossibility of evolution. What is the selection pressure that would evolve this unique gene?

This seems to be the sum total of the evolutionist argument, you don’t know how it happened but you know it did. Well, I know it didn’t happen by mutation and selection, ev shows how slow this process is and that the theory of evolution by mutation and selection is mathematically impossible.

What still hasn’t sunk in with you is that recombination without error can not increase information in the gene pool and that recombination with natural selection can cause the loss of information in the gene pool due to loss of alleles.

Really now, do you think this occurs with reproduction? You are now extrapolating the production of immunoglobins to reproduction. And do you want to explain how coping promoters all over the place speeds up the evolutionary process?

Copy a gene and you have two copies of the same gene. A new gene requires mutation. So now you have a copy of a gene that is slightly altered and low and behold, it performs an entirely new function like growing feathers on a lizard. It requires mutations to make a new gene and ev shows this is a profoundly slow process even if you have a selection process that could make the new gene and you don’t. You are in complete denial of the mathematics of mutation and selection and how it works. Study ev and learn how the mathematics of mutation and selection works instead of making your wild unscientific extrapolations.

I haven’t posted this for a while so for your benefit, I will repost why your concept is impossible.

A gene is to evolve. The first base in the sequence for the gene is laid down on the genome. One base codes for nothing so there is nothing for natural selection to act upon. A second base added by random chance is laid down in the sequence. Still nothing to code for, natural selection can not act on this sequence. A third base in the sequence is laid down. You now have enough bases to form a codon for a single amino acid. A single amino acid has no functional use so there is still nothing for natural selection to act upon. So bases must be added randomly until you have a long enough sequence of bases to produce a functional polypeptide and then natural selection can act. Adding bases randomly yield probabilities so infinitesimally small that evolution is mathematically impossible.

In which dimension do you dwell where recombination can create a new gene?

Simple enough, tell us how recombination without error can create new genes and I’ll tell you how recombination and natural selection can cause the loss of alleles. Of course you can’t tell us how recombination without error can create new genes but I can tell you how recombination and natural selection can cause the loss of alleles.


You really need to read beyond the abstract for this one, if you had you would have seen:

If you had investigated ev as Dr Schneider suggested, you would have more than a superficial understanding of the mathematics of mutation and selection. Anything more than a superficial investigation of ev reveals the mathematical impossibility of the theory of evolution.

If you had read the paper beyond the abstract you would realize that you are limiting the scope of ev because it suits your belief system, not because that was the intention of Dr Schneider. If you had read these threads you would have seen from the very beginning that I acknowledged that you can gain information by mutation and selection. The only shame in this is that you think you can understand the mathematics of mutation and selection without doing your homework. Read Dr Schneider’s works completely and read these threads completely, otherwise you reveal that you are superficial in your analysis, of course, that is the only type of analysis the theory of evolution can stand up to.

No new lies here then.

We've debunked all this crap. Go back to the hind end of the bull and fetch us some more.

 

[Dr Adequate]

Interesting admission from kleinman here:

Kleinman, is there a reason you continuously misspell joobz name as joozb? This is not intended to address your little quibble here. I've noticed that you've done the same misspelling constantly for the last few posts. I was just wondering if it is intentional or a very consistent typo. If intentional, is it meant to mean something, because I'm not seeing it.

Nothing intentional meant here. I use macros and do a lot of cutting and pasting because the same points are raised over and over. I misspelled his name unintentionally in an earlier post and it just has been carried forward.

If anyone's been getting the feeling that we're being spammed by an electronic lying machine devoid of knowledge and reason, that would be because we're being spammed by an electronic lying machine devoid of knowledge and reason.

 

[Paul C. Anagnostopoulos]

Yes, and this is the equation that does this:

sv += Math.abs(valuation[p] - threshold);

valuation[p] (the value of the dot product of the weight matrix with the positions on the genome) will almost always be a small number in the nonbinding site region of the genome. This is equivalent of ignoring the spurious binding in the nonbinding site region.

Why do you always speak in absolutes when things aren't absolute? At the beginning of a run, the valuations of loci are almost immediately all less than the threshold. I'd be happy to discuss this further if someone can refresh my memory about Unnamed's selection method, but I don't think he's ignoring anything.

He must have meant that only variations that support the theory of evolution should be investigated. Paul, I love it when you squirm.

He must have meant that? You're a psychologist now?

Just what does ev show now? You certainly aren’t saying the same thing that the author of the program has said which is unfortunate because I think he got this mathematical model of mutation and selection correct. Since random point mutation and natural selection represents 1/100 of 1% of your theory of evolution, care to tell us what the other 99.99% is?

Everything else.

~~ Paul

 

[Paul C. Anagnostopoulos]

That's really funny. Since the entire genome is being randomly mutated and selected for/against at the same time, but only the binding site region is being monitored for threshold bindings, why would any portion of the genome produce smaller or larger selective valuations?

No, every position in the entire genome is evaluated and used to tally mistakes.

And, if you run ev and look at the valuations in the non-binding site region, you will immediately recognize that there are just as many large valuations therein as occurs in the binding site region. So, your conclusion above is false. Unnamed's algorithm does not ignore the non-binding site region.

Now I'm confused. You appear to have contradicted yourself here.

I think I misunderstood what you wrote.

~~ Paul

 

[Mr. Scott]

Annoying Bots

Interesting admission from kleinman here:

Nothing intentional meant here. I use macros and do a lot of cutting and pasting because the same points are raised over and over. I misspelled his name unintentionally in an earlier post and it just has been carried forward.

If anyone's been getting the feeling that we're being spammed by an electronic lying machine devoid of knowledge and reason, that would be because we're being spammed by an electronic lying machine devoid of knowledge and reason.

Very revealing! Kleinman is only a computer simulation/model of a creationist, and was never intended to model the whole landscape of creationist nonsense. That explains why he seems to be failing the Turning Test: no matter how much new information evolutionists present, he just keeps repeating the same old lies. He's a creationist-bot.

A very adequate catch, Dr.