Annoying creationists

[kleinman]

That could have been better phrased.You're absolutely correct. In my defense, my brain was still reeling from the absolute stupidity of his comments.
What’s the problem Delphi? Did you have a little trouble organizing your sock drawer?
If you'd said "doubles the expected number of a given mutation per generation", then the halfwit would be less unlikely to misunderstand you.Under the assumption that your more precise phrasing would roughly double his chances of understanding, I ran some calculations. Unfortunately, a double isn't precise enough to hold the value.
Since our resident PhD in amathematics now understands that doubling the population does not double the probability of a particular mutation occurring at a particular locus, perhaps he will explain to you why doubling the expectation does not cause huge populations to markedly accelerate the rate of convergence in ev.
The adaptation of organisms to environmental stresses is primarily done by recombination and natural selection, not mutation and natural selection. Recombination and natural selection can give rapid morphological changes, mutation and selection is a profoundly slow process. Ev shows this and reality shows this.Viruses and bacteria no longer evolve quickly. We're all saved!
They don’t when there are multiple selection pressures. Ev shows this, combination therapy of HIV shows this, combination therapy of TB shows this. Of course single selection pressures can give more rapid evolution; this is shown by gonorrhea, MRSA and pseudomonas.
It seems that when you studied alchemical engineering they neglected to teach you anything about the mathematics of coordinate transformations. For example, there are problems that are defined by space and time coordinates (real coordinates) that can be solve by mathematically combining space and time into a single mathematical coordinate (abstract coordinate). These are called similarity solutions. Don’t mistake your ignorance as my lying to you. You have plenty of ignorance of mathematics, especially the mathematics of mutation and selection.And what does this have to do with what I asked you? I'm glad you provided a googled explanation of these concepts, but I was asking you how they relate to the question at hand.
Really, I “googled” this explanation, you have just entered the realm of the fake paranormal. Of course what can you expect from an alchemical engineer?
The fitness landscape is an abstract concept. You are free to select any variable space you wish that makes the computions easier. I was highlighting again your inability to distinguish between the relavent and irrelavent. Your arbitrary space selection has no bearing on the reality that is modeled. Life isn't beholdened to your definitions.
Oh, so you think Dr Schneider’s ev model is “irrelevant”? You think the fitness landscape is “irrelevant”? You think the numerous real examples that show multiple selection pressures are “irrelevant”? What you think is relevant is based on your prejudiced and biased evolutionist world view, you silly mathematically challenged hypocrite.
I’m going to admit you are correct. Malaria affects multiple genetic systems.I am glad to see you admit your mistake about "malaria" being a single selection pressure.So what is the selection pressure that sums up to evolving reptiles into birds?I know what you mean, even if the words are wrong.
Ah, come on, just say it, there is no selection pressure that does this.
I didn’t notice the quote from your HIV database where they recommend returning to monotherapy.A lovely Kleinmanism, thank you. But irrelevant. As with the malaria link above, this paper provides evidence that there are greater than 500 selection pressures acting on the HIV genome alone. And yet it still evolves incredibly fast.
Ok, quote some of these selection pressures and let’s discuss them. With all these selection pressures, perhaps it is HIV that is evolving into birds.
If multiple selection pressures slow evolution, how can there be a measurable selection pressure on each aa codon of the HIV genome?
Ok, let’s talk about this in more detail. What proportion of these selection pressures are stabilizing, what proportion of these selection pressures are directional? Why do HIV drugs have (at least temporarily) a profound effect on the fitness of the virus while these hundreds of other selection pressures do not?
Previously, you claimed that from your ev modeling, 3 selection pressures would render evolution impossible. What do you know believe to be the correct number of selection pressures? 500? 5000?
I know what you mean even though you got the words wrong. Let’s see if you have a point here, start describing some of these hundreds of selection pressures and let’s see how they affect the fitness of the virus. It is clear that these hundreds of selection pressures you are talking about certainly are not causing extinction of the virus yet the antiretroviral medicines have a profound affect on the fitness of the virus. Why don’t these hundreds of selection pressures you are talking about have very little effect on the fitness of the virus?
As you have a detailed mathematical model, answers to within an order of magnitude would be sufficient.
Describe some of these selection pressures in detail. I have said numerous times that ev should be modified to simulate mutation and selection with HIV. Perhaps we can get some answers. As it stands, you are claiming there are hundreds of selection pressures aside from the antiretroviral drugs yet these selection pressures do nothing to slow the disease.
You also still haven’t explained why chimpanzees and humans produce different preproinsulin yet produce identical insulin. This all despite you claim we descended from a common ancestor.And you never defined macroevolution, so you first. If one base pair mutation is a microevolutionary event, how many base pair mutations to make a macroevolutionary event? 2? 10? 100?
If you are going to talk about the differences between the human and chimpanzee, the number isn’t 2, 10, or 100, you’ve got to account for 35,000,000 base pairs to start with and that is just in the homologous portions of the genome.
Then you should understand that multiple selection pressures slow evolution, silly amathematician."Should"? I am under no obligation to believe your halfwitted fantasies.
Another amathematical explanation from the silly amathmetician.
It is you who is wrong on this point; you can not ignore neutral (or silent) mutation.It's not a question of ignoring them, it's a question of how they're represented. They can equivalently be considered component parts of the mutation that does affect a trait. However, that is a moot point; I already told you that you may consider as many dimensions as you like, including all mutations that do not affect the fitness, hence including all silent mutations.
I guess you understood my explanation why you can not ignore silent mutations.
What you still don’t understand is that when you expand the number of dimensions (by increasing the genome length) you are expanding the search space which profoundly slows the search.What you still don't understand is that the "search" space is not the genome space, it is the local neighborhood of the population genomes. Until you realize that, your interpretation of the fitness landscape will remain distorted and your conclusions incorrect.
Mutations occur on the genome level and selection occurs on the genome level.
Selection imposes direction on the search process.It does not and could not possibly, as selection comes into play only after the "search" is complete (after a mutation occurs that does change the fitness).
I don’t agree with your view. A fatal mutation for a creature does not require a search, selection occurs immediately.
You also still haven’t explained why chimpanzees and humans produce different preproinsulin yet produce identical insulin.Um, because, we have different diets and there is big difference in translation efficiency between the two varieties of preproinsulin. Humans need more of it. Look here
That’s an interesting hypothesis, did the selection pressure that caused these differences in the preproinsulin start with the advent of McDonald’s or do we need to go back a few thousand more years when farming started?
I was just thinking. This thread would make an excellent text for anyone wanting to know more about evolution. Thanks, Kleinman, for granting us this opportunity to rehash the important aspects of evolution for a wider audience. I, personally, am learning a ton from all the posters, well except for you, Kleinman.
Rehashing old ideas, that’s the way to learn something new. It must be kjkent1’s string cheese theory that needs a wider audience. Now if you only knew something about ev and the mathematics of mutation and selection. Of course, Dr Richard may prove me wrong with his 500 selection pressures on the HIV virus, none of which seem to affect the fitness of the virus and be of any help to people suffering from the disease.

[joobz]

Really, I “googled” this explanation, you have just entered the realm of the fake paranormal. Of course what can you expect from an alchemical engineer?It's a reasonable hypothesis. You haven't displayed ANY ability in the realm of math or engineering. Why would I expect you to know simple definitions.

Oh, so you think Dr Schneider’s ev model is “irrelevant”? You think the fitness landscape is “irrelevant”?
I never said this, you liar. I said you were harping on an irrelevant point (how you selected your variables, whether it was genome lengths, selection pressures, ect.) Your entire point is wrong. Multiple selection pressures do not halt evolution.
You think the numerous real examples that show multiple selection pressures are “irrelevant”?The numerous real world examples are HIGHLY RELAVENT! and that is why your entire point is completely and TOTALLY blown out of the water.
What you think is relevant is based on your prejudiced and biased evolutionist world view, you silly mathematically challenged hypocrite. sure it is...there, there little Kleinman. :rub:

[kleinman]

Really, I “googled” this explanation, you have just entered the realm of the fake paranormal. Of course what can you expect from an alchemical engineer?It's a reasonable hypothesis. You haven't displayed ANY ability in the realm of math or engineering. Why would I expect you to know simple definitions.
Like your theory of evolution, your “reasonable hypothesis” is wrong. We do like your display of scientific knowledge of abiogenesis when you told us you have no idea how ribose can form nonenzymatically.
Oh, so you think Dr Schneider’s ev model is “irrelevant”? You think the fitness landscape is “irrelevant”?I never said this, you liar. I said you were harping on an irrelevant point (how you selected your variables, whether it was genome lengths, selection pressures, ect.) Your entire point is wrong. Multiple selection pressures do not halt evolution.
This entire thread is based on the results from ev you silly alchemical engineer. Do any selection pressures halt evolution? Do multiple selection pressures slow evolution?
You think the numerous real examples that show multiple selection pressures are “irrelevant”? The numerous real world examples are HIGHLY RELAVENT! and that is why your entire point is completely and TOTALLY blown out of the water.
Really, then why is combination therapy used to treat HIV, why is combination therapy used to treat TB, why are combination pesticides used, why are combination herbicides used, why are combination rodenticides used? They are used because combination selection pressures slow the evolution of resistant strains of these organisms. That is what ev shows, this is what the fitness landscape shows and if you were not such a biased a prejudiced, hypocritical evolutionist you would realize this.
What you think is relevant is based on your prejudiced and biased evolutionist world view, you silly mathematically challenged hypocrite.sure it is...there, there little Kleinman.
Hey joobequate, did you notice what Delphi said,
Doubling the size of the population doubles the chances of a given mutation in the population.
How many times are you going to remind Delphi about his error about probabilities greater than 1, you biased, prejudiced hypocrite.

[Taffer]

Really, tell us how recombination makes new genes?

No comment on the rest of my post?

Very well...

One possible mechanism for new genes to arrise is through duplication of a current gene. With regard to recombination, this can happen when a new organism inherits a recombinant chromosome with two copies of one gene. When this is the case, evolutionary pressures specific to the gene are relaxed (because changes to one of the two copies of the gene are no longer harmful - there is still another functional copy of the gene). When there are relaxed evolutionary pressures, new mutations are not selected aganst as strongly, and so occur in larger quantities. In other words variation "builds up" in the two genes. Eventually, the old gene's function will change, and you have a new gene. Once this happens, selection pressure once again control variation in the original gene, and in the new gene (only one copy of it now exists).

There is huge amounts of evidence to show that this actually happens.

[joobz]

It's a reasonable hypothesis. You haven't displayed ANY ability in the realm of math or engineering. Why would I expect you to know simple definitions.
Like your theory of evolution, your “reasonable hypothesis” is wrong. We do like your display of scientific knowledge of abiogenesis when you told us you have no idea how ribose can form nonenzymatically.
???What is your meaning here? This seems rather non sequitor to me.


I never said this, you liar. I said you were harping on an irrelevant point (how you selected your variables, whether it was genome lengths, selection pressures, ect.) Your entire point is wrong. Multiple selection pressures do not halt evolution.
This entire thread is based on the results from ev you silly alchemical engineer. Do any selection pressures halt evolution? Do multiple selection pressures slow evolution?What are you talking about? another non sequitor. We were talking about your handling of fitness landscape. You are really unraveling it seems. Take a break and collect your thoughts. You are making absolutely no sense.

[quote=me]Really, then why is combination therapy used to treat HIV, why is combination therapy used to treat TB, why are combination pesticides used, why are combination herbicides used, why are combination rodenticides used? They are used because combination selection pressures slow the evolution of resistant strains of these organisms. That is what ev shows, this is what the fitness landscape shows and if you were not such a biased a prejudiced, hypocritical evolutionist you would realize this. this has been addessed here, several times, by more competent biologists than myself. Your denial of the truth doesn't help you any.



Hey joobequate, did you notice what Delphi said,

How many times are you going to remind Delphi about his error about probabilities greater than 1, you biased, prejudiced hypocrite.
Dr. A had already admonished this mistake. Delphi hasn't been the one to pretend infallibility here. He hasn't denied and lied about facts and data when presented. Remember: "first cast out the beam out of thine own eye; and then shalt thou see clearly to cast out the mote out of thy brother's eye."

[Ichneumonwasp]

That’s an interesting hypothesis, did the selection pressure that caused these differences in the preproinsulin start with the advent of McDonald’s or do we need to go back a few thousand more years when farming started?


You must be really running low on your tired quip bag for such a loser. What's wrong? Did the makeshift reply fairie not replenish your stock?:( You do know about the metabolism differences between fructose and glucose do you not?

How very sad.

You tell me. When did the change happen? Oh, wait, it doesn't matter as far as your original question was concerned, now does it? Kleinman quashed again, pretending it was otherwise. It's so sad when Fredric March falls and begins babbling isn't it? You wouldn't know anything about inherting wind now would you?

[kleinman]

Really, tell us how recombination makes new genes?No comment on the rest of my post?
Not until you explain how recombination makes new genes.
One possible mechanism for new genes to arrise is through duplication of a current gene. With regard to recombination, this can happen when a new organism inherits a recombinant chromosome with two copies of one gene. When this is the case, evolutionary pressures specific to the gene are relaxed (because changes to one of the two copies of the gene are no longer harmful - there is still another functional copy of the gene). When there are relaxed evolutionary pressures, new mutations are not selected aganst as strongly, and so occur in larger quantities. In other words variation "builds up" in the two genes. Eventually, the old gene's function will change, and you have a new gene. Once this happens, selection pressure once again control variation in the original gene, and in the new gene (only one copy of it now exists).
Gene duplication does not make a new gene; it only duplicates an existing gene. Only when mutation and selection acts on this duplicated gene do you have any possible mechanism for creating a new gene. Recombination can change the way a gene is expressed but does not create a new gene. Recombination alone can not create a new gene.
How many times are you going to remind Delphi about his error about probabilities greater than 1, you biased, prejudiced hypocrite.Dr. A had already admonished this mistake. Delphi hasn't been the one to pretend infallibility here. He hasn't denied and lied about facts and data when presented. Remember: "first cast out the beam out of thine own eye; and then shalt thou see clearly to cast out the mote out of thy brother's eye."
I admitted this error on the Evolutionisdead forum long ago you hypocrite yet you have brought this up on several occasions.

So now you are an expert in the Bible? If you had read the verse before the one you quoted you would have seen:

MAT:7:2 For with what judgment ye judge, ye shall be judged: and with what measure ye mete, it shall be measured to you again.

You are the hypocrite judge.

[joobz]

I admitted this error on the Evolutionisdead forum long ago you hypocrite yet you have brought this up on several occasions.I do not read that forum. That is only one of the errors I remind you of. Your use of Thermodynamics and your use of fitness landscape are others that I remind you of. I've become tired of giving you allowances. I had in the beginning (reread this thread), but your beligerence simply deserves nothing better.

So now you are an expert in the Bible? If you had read the verse before the one you quoted you would have seen:

MAT:7:2 For with what judgment ye judge, ye shall be judged: and with what measure ye mete, it shall be measured to you again.

You are the hypocrite judge.
You are the utter fool again. I Know full well what the verse is from and what precedes it. I was throwing the hypocrite term back in your face. Yet again, the beam blocks your ability to even see this. Stop playing the fool and I'll stop treating you as such.

[Ichneumonwasp]

Recombination alone can not create a new gene.


Sure it can. You've already been told how it can. More than once. Do you have some form of dementia, Dr, Kleinman?

[Ichneumonwasp]

MAT:7:2 For with what judgment ye judge, ye shall be judged: and with what measure ye mete, it shall be measured to you again.

So, Kleinman, are you saying that your afterlife will consist in you being called an idiot by everyone followed by a constant barrage of insults at your inability to understand selection pressures?

[Taffer]

Not until you explain how recombination makes new genes.

Whatever.

Gene duplication does not make a new gene; it only duplicates an existing gene. Only when mutation and selection acts on this duplicated gene do you have any possible mechanism for creating a new gene.

What if only a portion of a gene is copied? What if the portion of the gene which is copied is a regulartory section, and the new regulatory section on a different gene causes it to have a new function? There is more to genes then just the coding region, kleinman.

Recombination can change the way a gene is expressed but does not create a new gene. Recombination alone can not create a new gene.

"How a gene is expressed". If a gene is expressed differently, then how is it not a new gene? What do you consider a gene to be? Just the coding region? Just the introns and exons? What?

Hint: geneticists do not consider just the coding region to be a gene.

[Ichneumonwasp]

What do you consider a gene to be? Just the coding region? Just the introns and exons? What?


Apparently so. I tried introducing the idea of promoter regions earlier while you were out but it doesn't seem to have sunk in.

Just like he seems to think that humans stayed in the forest with other apes eating only fruit until we magically invented McDonalds. I guess we skipped those long centuries of savannah life where our diet changed from what the common ancestor of us and chimps ate in the mighty forest.

[kjkent1]

Rehashing old ideas, that’s the way to learn something new. It must be kjkent1’s string cheese theory that needs a wider audience.Why don't you tell us why you find Susskind's string theory so humorous?

[Mr. Scott]

What prediction does the theory of evolution make that can be tested?

What prediction does creationism make that can be tested?

What evidence would convince Kleinman that macroevolution without intelligent design accounts for the origin of species?

What evidence would convince evolutionists that god created all genes?

What evidence would convince Keinman that at least one gene arose spontaneously without intelligent design -- evidence that would cause Dr. Alan Kleinman to abandon creationism?

[Dr Adequate]

Since our resident PhD in amathematics now understands ....[/SIZE] "Now" understands?

You dreary lying tosser, we explained it to you.

Why do you lie so much, kleinman?

... perhaps he will explain to you why doubling the expectation does not cause huge populations to markedly accelerate the rate of convergence in ev. If you believe that that phrase has meaning, could you explain why?

Do you post when you're drunk?

alchemical engineer Ooh ... magic words!

Oh, so you think Dr Schneider’s ev model is “irrelevant”? You think the fitness landscape is “irrelevant”? You think the numerous real examples that show multiple selection pressures are “irrelevant”? No, he doesn't, you stupid lying twat.

Your stupid lies about these subjects, however, are worse than irrelevant. They're stupid lies.

Ok, quote some of these selection pressures and let’s discuss them. With all these selection pressures, perhaps it is HIV that is evolving into birds. Drunk or insane?

Ok, let’s talk about this in more detail. What proportion of these selection pressures are stabilizing, what proportion of these selection pressures are directional? Why do HIV drugs have (at least temporarily) a profound effect on the fitness of the virus while these hundreds of other selection pressures do not? You didn't read the article?

I know what you mean even though you got the words wrong. Let’s see if you have a point here, start describing some of these hundreds of selection pressures and let’s see how they affect the fitness of the virus. It is clear that these hundreds of selection pressures you are talking about certainly are not causing extinction of the virus yet the antiretroviral medicines have a profound affect on the fitness of the virus. Why don’t these hundreds of selection pressures you are talking about have very little effect on the fitness of the virus?You know I said you should learn something about genetics?

I never get tired of being right.

As it stands, you are claiming there are hundreds of selection pressures aside from the antiretroviral drugs yet these selection pressures do nothing to slow the disease.


You know I said you should learn something about genetics?

I never get tired of being right.

If you are going to talk about the differences between the human and chimpanzee, the number isn’t 2, 10, or 100, you’ve got to account for 35,000,000 base pairs to start with and that is just in the homologous portions of the genome. And we've done so, and all your whining and lying won't change that.

Another amathematical explanation from the silly amathmetician. Oh, more magic words.

Mutations occur on the genome level and selection occurs on the genome level. Learn some basic genetics.

string cheese Oh look, reality didn't disappear.

And you've said "cheese" so many times. Perhaps ... perhaps there is some flaw in your basic method.

Perhaps however often a creationist halfwit screams nonsense at the Universe, he won't change its nature nor convince the amused onlookers.

[Dr Adequate]

Gene duplication does not make a new gene; it only duplicates an existing gene. Only when mutation and selection acts on this duplicated gene do you have any possible mechanism for creating a new gene. Recombination can change the way a gene is expressed but does not create a new gene. Recombination alone can not create a new gene. The stupid ... IT BURNS!

[Taffer]

The stupid ... IT BURNS!

Sig'd. :D

[delphi_ote]

They don’t when there are multiple selection pressures.
What about when they aren't under multiple selection pressures? Do viruses and bacteria adapt to environmental stresses at all? The type of recombination you've been talking about isn't exactly their schtick, but you seem to believe that recombination is the primary mechanism for adaptation.

You're claiming that the fastest adapting populations should terrible at adaptation. Do you see why I think your ideas are totally divorced from reality?

[Thabiguy]

Mutations occur on the genome level and selection occurs on the genome level.

I don’t agree with your view. A fatal mutation for a creature does not require a search, selection occurs immediately.

So I was wrong. I thought there was some progress here, but there wasn't; Kleinman did not attain a better understanding of the fitness landscape. He just adopted some of my terms and mimicked their usage and that created a temporary illusion of comprehension.

He did not understand that the selection pressures, expressed by the fitness function, define the fitness landscape; that the steepness of its slope in a particular direction is defined by a partial derivative of the fitness function in that direction and so does not generally depend on the number of variables in that function; and that the speed of ascent on the fitness landscape for a given mutation rate is determined only by the steepness of the slope.

He continues to imagine some preexisting fitness landscape that the genomes explore in search of better fitness; that the selection pressures determine the directions in which this "search" is made; and that the overall size of the "search space" (determined by the genome length) profoundly slows down the "search" - but only if the "search" is made in more than one direction (?). I'm not kidding you, this is what he says:
If you have only a single selection pressure (monotherapy) it is much easier for natural selection to find a new optimum on the fitness landscape. The search only requires a single direction. However, when you introduce combination therapy (multiple selection pressures), it is much more difficult for natural selection to find new optimums for each of these selection pressures simultaneously. Several directions must be searched simultaneously and this confounds the search.
...
When you expand the number of dimensions (by increasing the genome length) you are expanding the search space which profoundly slows the search.
...
Only when you have a single selection condition does the length of the genome have little effect on the rate of evolution. As you increase the number of selection pressures, then the length of the genome has a profound effect on rate of evolution.
...
Selection imposes direction on the search process.

I tried to explain where his fundamental misconception is, that the fitness landscape, the fitness function, and the selection pressures are all the same thing, just differently expressed, that it is nonsensical to say that selection determines the direction of the "search" (search of what? - selection pressures are the fitness landscape, the only direction that selection determines is up).

I tried explaining it with calculus, as Kleinman repeatedly expressed his fondness for mathematics, and because the derivative of the fitness function seemed such a natural way of talking about the slope of the fitness landscape. That was like discussing music with a labrador.

I tried talking to him in his own terms of the "search", trying to explain how the notion is wrong and how things actually look like from that (somewhat inconvenient but admissible) perspective. That didn't work either.

I've run out of ways to explain it. Maybe the reason he cannot grasp it is that it's beyond his capabilities (I could understand that, I guess it's beyond the capabilities of many ordinary people), maybe he can understand it but refuses to, because acknowledging the misconception would invalidate his preconceived arguments. Maybe it's both.

Perhaps he will eventually understand (or allow himself to understand) what others are saying to him. For the time being, his attempts to patronize those who try to educate him are... bizarre; amusing, but also kinda sad.

[Dr Richard]

Originally Posted by Kleinman
I’m going to admit you are correct. Malaria affects multiple genetic systems.
Originally Posted by Dr Richard
I am glad to see you admit your mistake about "malaria" being a single selection pressure.
Originally Posted by Kleinman
So what is the selection pressure that sums up to evolving reptiles into birds?
Originally Posted by Dr Richard
I know what you mean, even if the words are wrong.

Ah, come on, just say it, there is no selection pressure that does this.


The truth is contained in the original post Kleinman. Seek, and ye shall find... ;)


Originally Posted by Dr Richard
A lovely Kleinmanism, thank you. But irrelevant. As with the malaria link above, this paper provides evidence that there are greater than 500 selection pressures acting on the HIV genome alone. And yet it still evolves incredibly fast.

Originally Posted by kleinman
Ok, quote some of these selection pressures and let’s discuss them. With all these selection pressures, perhaps it is HIV that is evolving into birds.

I have posted a link to the paper, kleinman. They give a very nice, mathematical definition of how they are calculating selection pressure for each amino acid codon.

Too technical for you?

Perhaps we had better continue your education in the world of evolutionary biology.

What do you understand by the term "selection pressure" when it is applied to a gene or part of a gene?


Originally Posted by Dr Richard
If multiple selection pressures slow evolution, how can there be a measurable selection pressure on each aa codon of the HIV genome?

Originally Posted by kleinman
Ok, let’s talk about this in more detail. What proportion of these selection pressures are stabilizing, what proportion of these selection pressures are directional? Why do HIV drugs have (at least temporarily) a profound effect on the fitness of the virus while these hundreds of other selection pressures do not?

Again, you have woefully misunderstood how the paper calculates selection pressure.

Even though it had maths in it.

By defintion, if a selection pressure exists for a mutation in the amino acid codon, a mutation on it affects the fitness of the virus.


Originally Posted by Dr Richard
Previously, you claimed that from your ev modeling, 3 selection pressures would render evolution impossible. What do you know believe to be the correct number of selection pressures? 500? 5000?

I know what you mean even though you got the words wrong. Let’s see if you have a point here, start describing some of these hundreds of selection pressures and let’s see how they affect the fitness of the virus. It is clear that these hundreds of selection pressures you are talking about certainly are not causing extinction of the virus yet the antiretroviral medicines have a profound affect on the fitness of the virus. Why don’t these hundreds of selection pressures you are talking about have very little effect on the fitness of the virus?

a) see answer above as to how you have misunderstood the paper I cited

b) think about that last question you asked. Can you think of an answer as applied to evolution? I am sure, if you try, you can, and if you do you may begin to understand where you went wrong in your assumptions.


Originally Posted by Dr Richard
As you have a detailed mathematical model, answers to within an order of magnitude would be sufficient.

Describe some of these selection pressures in detail. I have said numerous times that ev should be modified to simulate mutation and selection with HIV. Perhaps we can get some answers. As it stands, you are claiming there are hundreds of selection pressures aside from the antiretroviral drugs yet these selection pressures do nothing to slow the disease.

1. Attempt at evasion noted.

2. Again, please tell me the minimum number of selection pressures you think must operate to slow evolution in the real world based on your extensive mathematical modelling.

3. As to your last comment, reread the paper again.

4. Why should the selection pressures slow the disease?

4. And how do you know they do nothing to slow/accelerate the disease?



Originally Posted by Kleinman
You also still haven’t explained why chimpanzees and humans produce different preproinsulin yet produce identical insulin. This all despite you claim we descended from a common ancestor.
Originally Posted by Dr Richard
And you never defined macroevolution, so you first. If one base pair mutation is a microevolutionary event, how many base pair mutations to make a macroevolutionary event? 2? 10? 100?

If you are going to talk about the differences between the human and chimpanzee, the number isn’t 2, 10, or 100, you’ve got to account for 35,000,000 base pairs to start with and that is just in the homologous portions of the genome.

Evasion noted again Kleinman.

I didnt ask you how many base pair differences there were between chimps and humans, I asked you how many base pair mutations make a macroevolutionary event.

I ask again:

If one base pair mutation is a microevolutionary event, how many base pair mutations to make a macroevolutionary event? 2? 10? 100?


Dr Richard may prove me wrong with his 500 selection pressures on the HIV virus, none of which seem to affect the fitness of the virus and be of any help to people suffering from the disease.

1. Again you repeat your mistunderstanding of the calculation of selection pressure in the paper I cited.

2. Although your last statement is a gem, contained within may be a glimmer of understanding about the host/virus evolutionary interactions that (Taffer?) explained to you many posts ago.

[Paul C. Anagnostopoulos]

Gene duplication does not make a new gene; it only duplicates an existing gene. Only when mutation and selection acts on this duplicated gene do you have any possible mechanism for creating a new gene. Recombination can change the way a gene is expressed but does not create a new gene. Recombination alone can not create a new gene.
Even if it were to catenate a promoter and a partial gene with another partial gene?

You appear to be saying that both recombination and mutation are required for evolution. That may even be somewhat true.

~~ Paul

[Dr Richard]

Originally Posted by Kleinman
Gene duplication does not make a new gene; it only duplicates an existing gene. Only when mutation and selection acts on this duplicated gene do you have any possible mechanism for creating a new gene. Recombination can change the way a gene is expressed but does not create a new gene. Recombination alone can not create a new gene.

Thank you for highlighting this Paul.

It is refreshing to see that Kleinman's knowledge of molecular biology is now only 27 years out of date.

Evolution of a New Enzymatic Function by Recombination within a Gene (http://www.pnas.org/cgi/content/abstract/77/6/3529)

[kleinman]

Ok, quote some of these selection pressures and let’s discuss them. With all these selection pressures, perhaps it is HIV that is evolving into birds.I have posted a link to the paper, kleinman. They give a very nice, mathematical definition of how they are calculating selection pressure for each amino acid codon.
Let me help you with this Dr Richard and I’ll show you how to quote from a paper to support your position:
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1669717&blobname=gkl855e1.jpg
And here is another quote from the paper:
Thus a Ka/Ks = 1 value indicates neutral selection. Ordinarily Ka/Ks is « 1, indicating negative selection against amino acid mutations (far fewer observed than expected under a neutral model). Ka/Ks > 1 is referred to as positive selection (i.e. amino acid mutations increase reproductive fitness) and is observed in rare cases where new evolutionary challenges create strong pressure for rapid evolution of a protein (e.g. immune system genes like MHC that are involved in recognizing pathogenic antigens).
I added the highlighting. So this nice mathematical definition tells us that of your 500 or so selection pressures most are neutral (Ka/Ks = 1) or negative (Ka/Ks is « 1). Note that negative selection pressures are stabilizing selection pressures. Only in rare cases are selection pressures positive (Ka/Ks > 1), that is directional selection pressures. These are the types of selection pressures which evolve drug resistance and lead to evolution.

Thank you Dr Richard, your link again proves my point that multiple selection pressures slows evolution, however I will modify my wording slightly in order to accommodate your contention. Multiple directional selection pressures slow evolution. Neutral and stabilizing selection pressures do not lead to evolution. Dr Richard, stick with us, we will get you up to speed on the mathematics of mutation and selection.

Let me show you evolutionists how to use a links to support your position. In case you have forgotten what I am contending, here it is again:

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*░░░░░░░This is what reality shows.░░░░░░*
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The following quote is from the Guidelines for the Use of Antiretroviral Agents in HIV-1-Infected Adults and Adolescents and can be viewed at http://aidsinfo.nih.gov/contentfiles/AdultandAdolescentGL.pdf (http://aidsinfo.nih.gov/contentfiles/AdultandAdolescentGL.pdf) .
Simultaneously stopping all drugs in a regimen containing these agents may result in functional monotherapy with the NNRTIs, because their half-lives are longer than other agents. This may increase the risk of selection of NNRTI-resistant mutations.
This quote shows that monotherapy of HIV accelerates the evolution of resistant strains of the virus.

Here is an example from Wikipedia on the topic of pesticides and can be viewed at http://en.wikipedia.org/wiki/Pesticide (http://en.wikipedia.org/wiki/Pesticide)
Tankmixing pesticides is the combination of two or more pesticides with different modes of action. This practice may improve individual pesticide application results in addition to the benefit of delaying the onset of or mitigating existing pest resistance.
This quote shows that combining pesticides delays the evolution of pest resistance strains.

This example is from Iowa State University on the topic of herbicides and can be viewed at http://www.weeds.iastate.edu/mgmt/2004/combination.shtml (http://www.weeds.iastate.edu/mgmt/2004/combination.shtml)
The evolution of herbicide resistance within a weed population is based on selection pressure. The more frequently a herbicide is used, the more pressure placed on a weed population, and the sooner resistance will appear at a troublesome level in the population. Using alternative modes of action can reduce the potential for selecting resistant weeds by placing different selection pressures on weed populations. In a system relying only on glyphosate, a weed possessing a trait allowing it to survive glyphosate will rapidly increase in frequency. But if a second herbicide is used with glyphosate, this alternative herbicide may kill the weed with the glyphosate resistant trait and prevent it from increasing within the weed population. Theoretically this approach is sound and can reduce the potential for herbicide resistance.
This quote shows that combining herbicides delays the evolution of weed resistance strains.

This example is from German researchers on the topic of rodenticides and can be viewed at http://72.14.253.104/search?q=cache:rHo5amSD9IAJ:digitalcommons.unl.edu/cgi/viewcontent.cgi%3Farticle%3D1047%26context%3Dvpc16 +combination+rodenticide+resistance&hl=en&ct=clnk&cd=4&gl=us (http://72.14.253.104/search?q=cache:rHo5amSD9IAJ:digitalcommons.unl.edu/cgi/viewcontent.cgi%3Farticle%3D1047%26context%3Dvpc16 +combination+rodenticide+resistance&hl=en&ct=clnk&cd=4&gl=us)
Coumatetralyl (Racumin ) has been known since 1957 as a multiple dose anticoagulant and has been used successfully over many decades. In the seventies and especially the eighties, rats developed an increased resistance to anticoagulants in certain regions of Central Europe. Also, the addition of vitamin K to animal feed (especially to chicken feed) has reduced the efficacy against rats and mice in farm buildings. Combinations of anticoagulants with different types of vitamin D are generally described to increase the efficacy of action against rodents. It was found that especially the combination of coumatetralyl with cholecalciferol (vitamin D3) could overcome the above mentioned problems. Cholecalciferol causes hypercalcemia and, therefore, has a different mode of action compared to anticoagulants. The combination of these active ingredients leads to an obvious increase in efficacy against rodents, even under difficult conditions. The formulation with optimal rodenticidal efficacy contains 0.04 % coumatetralyl and 0.025 % cholecalciferol mixed in rolled oats.
This quote shows that combination rodenticides delay the evolution of rodenticides resistance.

If these links and associated quotes are not sufficient for you evolutionists, google search with the following terms; combination "selection pressures" resistance and you will find a huge number of papers that show that combination selection pressures slow the evolution of resistant strains of a wide variety of different types of life forms.

Now if you evolutionists think that multiple selection pressures accelerate evolution, post your links and associated quotes that support your contention. Posting links with your vague speculations does not cut it here.

[Taffer]

Let me help you with this Dr Richard and I’ll show you how to quote from a paper to support your position:

And here is another quote from the paper:

I added the highlighting. So this nice mathematical definition tells us that of your 500 or so selection pressures most are neutral (Ka/Ks = 1) or negative (Ka/Ks is « 1). Note that negative selection pressures are stabilizing selection pressures. Only in rare cases are selection pressures positive (Ka/Ks > 1), that is directional selection pressures. These are the types of selection pressures which evolve drug resistance and lead to evolution.

Small correction, as I see it. "Positive selection" selects for any mutations which increase reproductive function, it does not drive to any goal. This is important.

Thank you Dr Richard, your link again proves my point that multiple selection pressures slows evolution, however I will modify my wording slightly in order to accommodate your contention.

It does nothing of the sort. I have no idea how you get that from the paper, because it says nothing of the sort whatsoever. Perhaps you could point out exactly where it says that multiple selection pressures slows evolution?

Because that would go against all other evolutionary models we currently have.

Multiple directional selection pressures slow evolution.

No selection is directional, kleinman, so this statement is false. Selection does one thing only: selects against those with a lower reproductive fitness. It does not "select for" anything, becuase evolution is not directional.

Neutral and stabilizing selection pressures do not lead to evolution.

Selection always leads to evolution. Selection acts on variation in a population. In the absense of variation, no evolution can occur. But in the presence of evolution, even "stabalizing" selection changes the ratio of new alleles in a population, which is what evolution is.

Dr Richard, stick with us, we will get you up to speed on the mathematics of mutation and selection.

We sure will, but you won't teach it, because you lack the ability to grasp it.


The following quote is from the Guidelines for the Use of Antiretroviral Agents in HIV-1-Infected Adults and Adolescents and can be viewed at http://aidsinfo.nih.gov/contentfiles/AdultandAdolescentGL.pdf (http://aidsinfo.nih.gov/contentfiles/AdultandAdolescentGL.pdf) .

This quote shows that monotherapy of HIV accelerates the evolution of resistant strains of the virus.


No it doesn't! All it shows is that monotherapy increases the risk of selection of a resistant strain of the virus. Selection of a strain and evolution are different. No-one denies that the presence of a single drug will lead to a population of organisms which are resistant to that drug. Multiple drugs do not slow the evolution of any individual resistances, but require all 3 drugs to be present (assuming, of course, that all drugs are "kill" drugs, which is not the case in real life) in the organism for it to live. But the time for such an organism to arise is the same as the same organism arising through "serial" resistance evolution.

This quote shows that combining pesticides delays the evolution of pest resistance strains.

Yet again you show a lack of understanding of the topic. "Evolution of" and "arisal of" are not the same thing. What multiple pesticides does is reduce the available population for any variation to occur in. But once that variation occurs, evolution happens very rapidly, regardless of single or multiple selection pressures.

Perhaps that's a better way to explain it to you. Multiple drugs reduce variation in a population. Once the variation exists, evolutionary rate is unchanged.

This example is from Iowa State University on the topic of herbicides and can be viewed at [/SIZE][/FONT]http://www.weeds.iastate.edu/mgmt/2004/combination.shtml (http://www.weeds.iastate.edu/mgmt/2004/combination.shtml)

This quote shows that combining herbicides delays the evolution of weed resistance strains.

This is the same quote I gave before which I pointed out states that increased selection pressures increases evolutionary rate! Did you not read my post at all?!

Kleinman, you are confusing evolution. Evolution is "the change in allele frequency in a population over time", not "the arrisal of novel alleles in a population over time". The gain of variation in a population is not "evolution", but "random mutation" and other such things. "Selection pressures" work on "variation" which causes "evolution". Evolution is a combination of all these things, not one without the other. All you have shown is that multiple drugs reduce variation in a population. Fine. Wonderful. That does not slow down evolution!

The rate of evolution is dependent only on the strength of selection.

This example is from German researchers on the topic of rodenticides and can be viewed at [/SIZE][/FONT]http://72.14.253.104/search?q=cache:rHo5amSD9IAJ:digitalcommons.unl.edu/cgi/viewcontent.cgi%3Farticle%3D1047%26context%3Dvpc16 +combination+rodenticide+resistance&hl=en&ct=clnk&cd=4&gl=us (http://72.14.253.104/search?q=cache:rHo5amSD9IAJ:digitalcommons.unl.edu/cgi/viewcontent.cgi%3Farticle%3D1047%26context%3Dvpc16 +combination+rodenticide+resistance&hl=en&ct=clnk&cd=4&gl=us)

This quote shows that combination rodenticides delay the evolution of rodenticides resistance.

Did you even read your own bloody source? It shows that using more then one drug is more effective then only one! It says nothing about resistance arising at a slower rate, only that multiple drugs are useful with already existing resistance.

If these links and associated quotes are not sufficient for you evolutionists, google search with the following terms; combination "selection pressures" resistance and you will find a huge number of papers that show that combination selection pressures slow the evolution of resistant strains of a wide variety of different types of life forms.

Kleinman I have already done this, posted the first 3 pages, and showed why they do not say what you think they do! Ignoring the rest of my post, and respond to more then a single point I rose!

Now if you evolutionists think that multiple selection pressures accelerate evolution, post your links and associated quotes that support your contention. Posting links with your vague speculations does not cut it here.

I have already posted a mathematical model which clearly shows stronger selection increases the rate of evolution. Since you cannot refute this, I think it is evidence enough.

[Dr Richard]

Originally posted by kleinman:

Multiple directional selection pressures slow evolution

priceless

[Taffer]

priceless

How did I miss that? You can't buy this stuff, folks. :D

[Dr Richard]

Let me help you with this Dr Richard and I’ll show you how to quote from a paper to support your position:

I am glad that you have now properly read the paper.

You really should try that before commenting on them, as it would have saved me having waste almost an entire post correcting your previous misconception of the term selection pressure.

As for cutting and pasting from papers, in my undergraduate days we concentrated on understanding the papers we were reading, not assigning random .gifs to macro keys.

And here is another quote from the paper:[/SIZE][/FONT]

I added the highlighting. So this nice mathematical definition tells us that of your 500 or so selection pressures most are neutral (Ka/Ks = 1) or negative (Ka/Ks is « 1). Note that negative selection pressures are stabilizing selection pressures. Only in rare cases are selection pressures positive (Ka/Ks > 1), that is directional selection pressures. These are the types of selection pressures which evolve drug resistance and lead to evolution.

Taffer had already corrected your mistake about a selection pressure of 1.

Yet another mathematical error - how many is that now?

To sharpen your skills, lets go back to the basics. How many positive selection pressures do they identify in the paper?


And now back to the questions you are evading:

Again, please tell me the minimum number of selection pressures you think must operate to slow evolution in the real world based on your extensive mathematical modelling.

If one base pair mutation is a microevolutionary event, how many base pair mutations to make a macroevolutionary event? 2? 10? 100?

[kleinman]

I added the highlighting. So this nice mathematical definition tells us that of your 500 or so selection pressures most are neutral (Ka/Ks = 1) or negative (Ka/Ks is « 1). Note that negative selection pressures are stabilizing selection pressures. Only in rare cases are selection pressures positive (Ka/Ks > 1), that is directional selection pressures. These are the types of selection pressures which evolve drug resistance and lead to evolution.Small correction, as I see it. "Positive selection" selects for any mutations which increase reproductive function, it does not drive to any goal. This is important.
Are you not a student of population genetics? Go back to your text book and you will find that population geneticists distinguish three types of selection; they are stabilizing selection, directional selection and disruptive selection. Stabilizing selection favors an intermediate optimum phenotype and selects against phenodeviants. Directional selection is selection directed toward a new intermediate optimum, not at the mean of the population, in response to a new selective challenge. Disruptive selection, rather than favoring any one phenotype, favors two quite different forms and selects against the intermediates; this may be viewed as directional selection of two separate subpopulations, in response to two different sets of environmental conditions. These definitions are taken from the text Genetics in Medicine by Thompson & Thompson. Dr Richard’s link also includes “neutral selection” which essentially occurs with mutations which don’t affect fitness. The goal for directed selection is a new intermediate optimum on the fitness landscape.
Thank you Dr Richard, your link again proves my point that multiple selection pressures slows evolution, however I will modify my wording slightly in order to accommodate your contention.It does nothing of the sort. I have no idea how you get that from the paper, because it says nothing of the sort whatsoever. Perhaps you could point out exactly where it says that multiple selection pressures slows evolution?

Because that would go against all other evolutionary models we currently have.
The reason you don’t understand this is that you don’t understand the different types of selection pressures. Go back to the Ka/Ks equation. When Ka/Ks = 1 you have neutral selection pressure, that is mutations occur which don’t affect the frequency of the particular gene in the gene pool, when Ka/Ks is « 1 you have a stabilizing selection pressure, that is a mutation causes a phenodeviant which is detrimental to the creature and is selected against. When Ka/Ks is « 1, the frequency of that particular mutation is reduced in the gene pool. Only when Ka/Ks > 1 do you have selection which increases the frequency of that mutation in the gene pool. These types of mutations lead to a new optimum on the fitness landscape and are thus directional in nature. The authors have indicated that only in rare cases are selection pressures positive (or directional) (Ka/Ks > 1).

Neutral or stabilizing selection processes do not lead to new strains in the gene pool. Only when you have directional selection do you introduce new strains in the gene pool and again, these authors indicate that directional selection for HIV is rare. When antiretroviral medications are used on HIV, these apply directional selection pressure on the virus. Note that when a resistant strain evolves, that directional selection pressure will become a stabilizing selection pressure if the virus is still exposed to the drug.

Only directional selection pressure leads to genetic evolution. Of the hundreds of selection pressures Dr Richard refers to, only a tiny fraction of these are directional selection pressures. If you want to evolve drug resistance in HIV, use a single directional selection pressure and you can achieve this quickly because of the viruses’ high mutation rate and rapid reproduction. Combine multiple directional selection pressures and you will slow this process.
Multiple directional selection pressures slow evolution.No selection is directional, kleinman, so this statement is false. Selection does one thing only: selects against those with a lower reproductive fitness. It does not "select for" anything, becuase evolution is not directional.
You better go back and re-read your textbooks before you take your final exams.
Neutral and stabilizing selection pressures do not lead to evolution.Selection always leads to evolution. Selection acts on variation in a population. In the absense of variation, no evolution can occur. But in the presence of evolution, even "stabalizing" selection changes the ratio of new alleles in a population, which is what evolution is.
I don’t know what to tell you other than go back to your textbooks and learn what the different forms of selection do.
Dr Richard, stick with us, we will get you up to speed on the mathematics of mutation and selection.We sure will, but you won't teach it, because you lack the ability to grasp it.
If you teach what you are saying here, you will be misleading your students on how mutation and selection works. What can you expect from an evolutionist?
This quote shows that monotherapy of HIV accelerates the evolution of resistant strains of the virus.No it doesn't! All it shows is that monotherapy increases the risk of selection of a resistant strain of the virus. Selection of a strain and evolution are different. No-one denies that the presence of a single drug will lead to a population of organisms which are resistant to that drug. Multiple drugs do not slow the evolution of any individual resistances, but require all 3 drugs to be present (assuming, of course, that all drugs are "kill" drugs, which is not the case in real life) in the organism for it to live. But the time for such an organism to arise is the same as the same organism arising through "serial" resistance evolution.
You still don’t understand the mathematics of mutation and selection. Once you understand what the different forms of selection are, perhaps you will be able to begin to understand the mathematics of mutation and selection.
Multiple directional selection pressures slow evolutionpriceless
If you ever graduate Sesame Street and learn how to count, you will understand how mutation and selection really works. Your own link to The HIV positive selection mutation database shows this but it must be too technical for you to understand.

This is what happens when you try to discuss mathematics with a Sesame Street drop out.

[Dr Richard]

This is the same quote I gave before which I pointed out states that increased selection pressures increases evolutionary rate! Did you not read my post at all?!


Thank you for another gem Taffer. I have taken Kleinman's advice and decided to copy a few quotes from the example he cites:

For herbicide combinations to reduce resistance risks, they both must achieve efficacy that is high enough against all weeds to ensure redundant kill. This redundant kill rarely, if ever, occurs in the real world

Relying on alternative modes of action to reduce resistance risks will rarely result in the redundant kill essential for this strategy to be effective against resistance selection

Thus, for the majority of weed species the described herbicide program has a similar risk of glyphosate resistance as if glyphosate had been used alone

My only regret is that I'm on holiday as of tomorrow and will miss such kleinman komedy moments.

At least this thread will be still be going when I return

And I confidently predict that over the 10 days klienman will continue to evade the questions I have asked him.

[Dr Richard]

This is what happens when you try to discuss mathematics with a Sesame Street drop out.[/FONT]

A bizarre ad hom but evades these two questions: I have numbered them to make them seem mathematical and help you...


1. Again, please tell me the minimum number of selection pressures you think must operate to slow evolution in the real world based on your extensive mathematical modelling.

2. If one base pair mutation is a microevolutionary event, how many base pair mutations to make a macroevolutionary event? 2? 10? 100

[kleinman]

Let me help you with this Dr Richard and I’ll show you how to quote from a paper to support your position:You really should try that before commenting on them, as it would have saved me having waste almost an entire post correcting your previous misconception of the term selection pressure.
Really, what comment did I make on this paper before reading it? Please feel free to quote me.
I added the highlighting. So this nice mathematical definition tells us that of your 500 or so selection pressures most are neutral (Ka/Ks = 1) or negative (Ka/Ks is « 1). Note that negative selection pressures are stabilizing selection pressures. Only in rare cases are selection pressures positive (Ka/Ks > 1), that is directional selection pressures. These are the types of selection pressures which evolve drug resistance and lead to evolution.Taffer had already corrected your mistake about a selection pressure of 1.
Taffer has no idea of what selection pressures are, he needs to go back and read his textbook, perhaps you need to do this as well.
And now back to the questions you are evading:

Again, please tell me the minimum number of selection pressures you think must operate to slow evolution in the real world based on your extensive mathematical modelling.
I haven’t evaded this question; you must have a problem reading this thread. The way the mathematics of mutation and selection works, the more directional selection pressures you have, the slower the evolutionary process goes. If you read your link to The HIV positive selection mutation database carefully, you will see that directional selection pressures are rare for HIV, the other selection pressures are either neutral or stabilizing which do not lead to drug resistance. No wonder advancement in the treatment of HIV is proceeding so slowly due to the distorted and contorted misunderstanding of mutation and selection that you evolutionists put forward. At least infectious disease experts understand that combination therapy slows the evolution of resistant strains of the virus. Someday this reality will sink into your evolutionist brainwashed heads.

[joobz]

I see that the chain gang has been working overtime on the goal posts
My view on this issue is that once you get beyond a single point mutation you are already starting to enter the realm of macroevolution.
to
The way the mathematics of mutation and selection works, the more directional selection pressures you have, the slower the evolutionary process goes

So we no longer have a 2 selection pressures =macroevolution =impossible, but rather a
x number of "directional selection pressures" = slower evolution=???

Slower is rather vague, don't you think? Since when does "slow" equal never?
Using your search criteria has pulled up this little gem from
Phil. Trans. R. Soc. Lond. B (1998) 353, 1787-1795
One myth involves the belief that we can manage resistance. I will maintain that we can only attempt to mitigate resistance because resistance is a natural evolutionary response to environmental stresses. As such, resistance will remain an ongoing dilemma in pest management and we can only delay the onset of resistance to pesticides.

[kleinman]

Slower is rather vague, don't you think? Since when does "slow" equal never?
Using your search criteria has pulled up this little gem from
Phil. Trans. R. Soc. Lond. B (1998) 353, 1787-1795 One myth involves the belief that we can manage resistance. I will maintain that we can only attempt to mitigate resistance because resistance is a natural evolutionary response to environmental stresses. As such, resistance will remain an ongoing dilemma in pest management and we can only delay the onset of resistance to pesticides.
Good for you joobz. I read this article the other day; my first impression was Ms Hoy has never heard of extinction. If you read a little further into the abstract you will see the following quote:
Delaying resistance, whether to traditional pesticides or to transgenic plants containing toxin genes from Bacillus thuringiensis, will require that we develop multi-tactic pest management programmes that incorporate all appropriate pest management approaches.
What does “incorporate all appropriate pest management approaches” mean? Why it means multiple selection pressures, which is how you delay resistance. Sound familiar doesn’t it? I’m glad that Ms Hoy understands this principle, now if only other evolutionists can learn to understand this and then the mathematical impossibility of the theory of evolution will become apparent to you evolutionists.

For those of you who wish to read this paper, it is located at http://links.jstor.org/sici?sici=0962-8436(19981029)353%3A1376%3C1787%3AMMAMOR%3E2.0.CO% 3B2-9 (http://links.jstor.org/sici?sici=0962-8436(19981029)353%3A1376%3C1787%3AMMAMOR%3E2.0.CO% 3B2-9)

Finally, joobz, you are starting to think about the problem. Did you notice all the other links in that google search that also shows that multiple directional selection pressures slow evolution?

[joobz]

Why it means multiple selection pressures, which is how you delay resistance.
NOTE that word, delay. Hoy was talking about delaying the resistance development against pesticides. But Hoy doesn't say, Halt, stop, prevent, abolish, never will happen,.... Hoy says delay. We can only ever delay things, we can't stop evolution.

Repeat after me,
Slow is a relative term.
Slow is a relative term.
Slow doesn't mean stop.
Slow doesn't mean stop.
...

[Paul C. Anagnostopoulos]

Multiple directional selection pressures ...
Ah, now it's multiple directional pressures.

I'm buying stock in a goalpost moving company with lots of big trucks.


I see that the chain gang has been working overtime on the goal posts.
They are moved by chain gangs?! Why, that's just cruel and unusual punishment.

~~ Paul

[delphi_ote]

They are moved by chain gangs?! Why, that's just cruel and unusual punishment.
Of course they're moved by chain gangs. Nobody would willingly sign on for that kind of labor!

Don't worry. It's not cruel and unusual. They're doing the Lord's work.

Slaves, obey your earthly masters with deep respect and fear. Serve them sincerely as you would serve Christ.

Christians who are slaves should give their masters full respect so that the name of God and his teaching will not be shamed. If your master is a Christian, that is no excuse for being disrespectful. You should work all the harder because you are helping another believer by your efforts. Teach these truths, Timothy, and encourage everyone to obey them.

[kleinman]

Why it means multiple selection pressures, which is how you delay resistance.NOTE that word, delay. Hoy was talking about delaying the resistance development against pesticides. But Hoy doesn't say, Halt, stop, prevent, abolish, never will happen,.... Hoy says delay. We can only ever delay things, we can't stop evolution.
This is progress. You finally understand that multiple directional selection pressures slow evolution. We now need to get you to understand two more points. The first point is that evolution does not go on for ever, extinction does occur. The second point is that additional directional selection pressures have a profound affect on the rate of evolution. HIV is an example of a bracketing case for this phenomenon. HIV has a short genome, a high mutation rate and a high reproduction rate, all features which contribute to a relatively rapid adaptation by mutation and selection. Even with these features, the delay in evolution of multiple drug resistance of this virus when using combination therapy can be and is striking when compared to monotherapy. This mechanism of mutation and selection for adaptation to multiple directional selection pressures for creatures with much larger genomes, much slower reproductive rates and lower mutation rates can accomplish nothing in realistic time spans especially evolving reptiles into birds.

I do commend you though for finally understanding that multiple directional selection pressures slow evolution.
Repeat after me,
Slow is a relative term.
Slow is a relative term.
Slow doesn't mean stop.
Slow doesn't mean stop.
Slow is a relative term.
Slow is a relative term.
Slow doesn't mean stop.
Slow doesn't mean stop.
Extinction means stop.
Too slow means the theory of evolution is mathematically impossible.

Now it only remains to show you that extinction does occur and that mutation and multiple directional selection pressures slow evolution too much for the theory to be mathematically impossible.
Multiple directional selection pressures ...Ah, now it's multiple directional pressures.

I'm buying stock in a goalpost moving company with lots of big trucks.
Paul, stop whining about moving goal posts. Ev is demonstrating this exact effect. When you initially start the program with random genomes, the selection conditions are directional. Once you satisfy the selection conditions, the selection conditions become stabilizing selection conditions. Ev is demonstrating exactly how mutation and selection (both directional and stabilizing) works.
I see that the chain gang has been working overtime on the goal posts. They are moved by chain gangs?! Why, that's just cruel and unusual punishment.
I can’t help it that you finding out the truth of your theory of evolution is cruel and unusual punishment. Just think of this as an improvement in the goalposts.

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*░░░░░░░This is what reality shows.░░░░░░*
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[joobz]

This is progress. You finally understand that multiple directional selection pressures slow evolution. I've never said this. I was simply demonstrating your have moved your whole argument into such a nebulous realm that it is meaningless.

Slow is a relative term.
Slow is a relative term.
Slow doesn't mean stop.
Slow doesn't mean stop.
Extinction means stop.
Too slow means the theory of evolution is mathematically impossible.
When did stop=too slow? again, you lack any sense of numerical reasoning.

extinction only means "stop" for that which is extinct. however, all else that survives is still evolving. Complete Global extinction would mean stop. But really, this is not what you have been advocating or defending.

You have claimed that evolution is a myth and that ev shows this. But you now admit that evolution is only "slowed" by your multiple directional pressures. How can something that doesn't exist be slowed?

[Dr Richard]

Really, what comment did I make on this paper before reading it? Please feel free to quote me.

Ok, quote some of these selection pressures and let’s discuss them. With all these selection pressures, perhaps it is HIV that is evolving into birds.

Would appear to have been written by someone who has not read the paper.


Taffer has no idea of what selection pressures are, he needs to go back and read his textbook, perhaps you need to do this as well.

I would love to hear your definition of "selection pressure" klienman.


I'll add it to the list of questions Kleinman can't answer: (I have amended question 1 as you have moved the goalposts from "multiple selection pressures prevent evolution" to "multiple directional selection pressures slow evolution"

1. Again, please tell me the minimum number of "directional "selection pressures you think must operate to prevent macroevolution by slowing microevolution to such an extent that it cannot happen within the timeframe of life on earth in the real world based on your extensive mathematical modelling.

2. If one base pair mutation is a microevolutionary event, how many base pair mutations to make a macroevolutionary event? 2? 10? 100?

3. How many positive selection pressures are listed on the HIV positive selection database for just two of the genes?

4. What is your definition of a "selection pressure"

5. (for old time's sake) What is your definition of macroevolution again? (NB random lists of things you think it is are not acceptable)


Please note the numbering. You seem to be ignoring questions.

[kleinman]

They are moved by chain gangs?! Why, that's just cruel and unusual punishment.Of course they're moved by chain gangs. Nobody would willingly sign on for that kind of labor!
If this is slavery, I’m really enjoying it.
Slaves, obey your earthly masters with deep respect and fear. Serve them sincerely as you would serve Christ.
Christians who are slaves should give their masters full respect so that the name of God and his teaching will not be shamed. If your master is a Christian, that is no excuse for being disrespectful. You should work all the harder because you are helping another believer by your efforts. Teach these truths, Timothy, and encourage everyone to obey them.
Important principles you display here. Delphi, do you know your Master?
This is progress. You finally understand that multiple directional selection pressures slow evolution.I've never said this. I was simply demonstrating your have moved your whole argument into such a nebulous realm that it is meaningless.
Two steps forward, one step back. We will get to the point where you can understand how mutation and selection actually works.
Slow is a relative term.
Slow doesn't mean stop.
Slow doesn't mean stop.
Extinction means stop.
Too slow means the theory of evolution is mathematically impossible.When did stop=too slow? again, you lack any sense of numerical reasoning.
I didn’t say stop=too slow, I said extinction means stop. What I said was too slow means that the theory of evolution is mathematically impossible, you simply do not have enough time to accumulate the information by mutation and selection.
extinction only means "stop" for that which is extinct. however, all else that survives is still evolving. Complete Global extinction would mean stop. But really, this is not what you have been advocating or defending.
What I have been advocating is that the ev computer model shows that the acquisition of information by random point mutation is profoundly slow, too slow to support the theory of evolution. The reason why it is too slow is the competing directional selection conditions which slow the evolutionary process profoundly when realistic genome lengths and mutation rates are used. This is also seen in reality.
You have claimed that evolution is a myth and that ev shows this. But you now admit that evolution is only "slowed" by your multiple directional pressures. How can something that doesn't exist be slowed?
It is the theory of evolution which is the myth, microevolution does occur but extrapolating this phenomenon to the evolution of reptiles into birds is mathematically impossible, that’s the myth.
Really, what comment did I make on this paper before reading it? Please feel free to quote me.Ok, quote some of these selection pressures and let’s discuss them. With all these selection pressures, perhaps it is HIV that is evolving into birds. Would appear to have been written by someone who has not read the paper.
Apparently you didn’t understand your own reference. I asked you do discuss the selection pressures mentioned in the article and you couldn’t. I quote from the article specifically what kinds of selection pressures are computed and they show the vast majority are neutral or stabilizing and only rarely are the selection pressures directional. It is the directional selection pressures which evolve drug resistance.
Taffer has no idea of what selection pressures are, he needs to go back and read his textbook, perhaps you need to do this as well.I would love to hear your definition of "selection pressure" klienman.
If you had read the Taffer post, you would know the definitions that I use. Since you are a lazy reader, I will post these definitions again, just for you.
Go back to your text book and you will find that population geneticists distinguish three types of selection; they are stabilizing selection, directional selection and disruptive selection. Stabilizing selection favors an intermediate optimum phenotype and selects against phenodeviants. Directional selection is selection directed toward a new intermediate optimum, not at the mean of the population, in response to a new selective challenge. Disruptive selection, rather than favoring any one phenotype, favors two quite different forms and selects against the intermediates; this may be viewed as directional selection of two separate subpopulations, in response to two different sets of environmental conditions. These definitions are taken from the text Genetics in Medicine by Thompson & Thompson. Dr Richard’s link also includes “neutral selection” which essentially occurs with mutations which don’t affect fitness. The goal for directed selection is a new intermediate optimum on the fitness landscape.
So let’s discuss your article The HIV positive selection mutation database and your 500 selection pressures in this context and what it means to the mathematics of mutation and selection. You will find that your article supports my contention that multiple directional selection pressures slows evolution.

[Dr Adequate]

The forum editor modified the goalposts so here it is again in proper format.
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****************************************** Here are the goalposts again in case you evolutionists whine that I am moving them.

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*░░░░░░░This is what reality shows.░░░░░░*
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Let’s ask the officials to do an instant replay of the goalposts, and here it is:[/SIZE]

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*░░░░░░░░░This is what ev shows.░░░░░░░░░*
*░░░░░░░This is what reality shows.░░░░░░*
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How about if I paint you a picture:

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*░slows░░░░░░░░░░░░░░░░░░░░░░░░evolution░*
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*░░░░░░░░░This is what ev shows.░░░░░░░░░*
*░░░░░░░This is what reality shows.░░░░░░*
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You don’t have to fill all your gaps in your theory, just fill this one, you know the one:
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*░░|H Multiple Selection Pressures .|░░░░*
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*░slows░░░░░░░░░░░░░░░░░░░░░░░░evolution░*
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*░░░░░░░░░This is what ev shows.░░░░░░░░░*
*░░░░░░░This is what reality shows.░░░░░░*
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Just think of this as an improvement in the goalposts.

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*░░|H Multiple Selection Pressures .|░░░░*
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*░slows░░░░░░░░░░░░░░░░░░░░░░░░evolution░*
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*░░░░░░░░░This is what ev shows.░░░░░░░░░*
*░░░░░░░This is what reality shows.░░░░░░*
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You just can't buy that sort of entertainment.

His goalposts lasted only nine days before he was forced to shift them --- which is fast, considering how obtuse he is.

You will notice, by the way, that kleinman's new lie has already been proven false. We're way ahead of him.

[joobz]

Two steps forward, one step back. We will get to the point where you can understand how mutation and selection actually works.Yes, I'm interested to know how these directional pressures are important and, particularly, how many are needed to stop evolution.

I didn’t say stop=too slow, I said extinction means stop. What I said was too slow means that the theory of evolution is mathematically impossible, you simply do not have enough time to accumulate the information by mutation and selection.Can you put some numbers onto those bolded points you've made. I'm really trying to understand where you see the line being drawn.

What I have been advocating is that the ev computer model shows that the acquisition of information by random point mutation is profoundly slow, too slow to support the theory of evolution. The reason why it is too slow is the competing directional selection conditions which slow the evolutionary process profoundly when realistic genome lengths and mutation rates are used. This is also seen in reality.and no other mutation is possible? no other genetic adaptation scheme matters? this is very interesting...

It is the theory of evolution which is the myth, microevolution does occur but extrapolating this phenomenon to the evolution of reptiles into birds is mathematically impossible, that’s the myth.
So you admit to microevolution. I understand.

Now what is Microevolution? How does it differ from macroevolution?
I remember you saying
My view on this issue is that once you get beyond a single point mutation you are already starting to enter the realm of macroevolution.
but are now saying
The way the mathematics of mutation and selection works, the more directional selection pressures you have, the slower the evolutionary process goes

Several question I have are
1.) If microevolution is real, How does it evade being slowed by "more directional selection pressures"?
2.) How many microevolutionary changes must occur before it is called macroevolution?
3.) How does this all relate to the Fitness Landscape argument that you kept refering to previously?

[Dr Adequate]

So let’s discuss your article The HIV positive selection mutation database and your 500 selection pressures in this context and what it means to the mathematics of mutation and selection. You will find that your article supports my contention that multiple directional selection pressures slows evolution. This is a lie, which is why you cannot quote the article as saying any such thing.

Let's call this one Lie #7, since it seems likely that you're going to recite it over and over without producing a shred of evidence for it.

Have you written the macro yet?

[Dr Adequate]

Can you put some numbers onto those bolded points you've made. I'm really trying to understand where you see the line being drawn. Ah, c'mon, how can he answer that? It's not as if he has some sort of mathematical understanding of mutation and selection --- such as he could get out of a biology textbook if he wasn't so lazy and stupid.

[kjkent1]

It's really simple folks -- let me explain it to you so that you understand, once and for all!

In a big crowd of selection pressures, the directional pressures are hard for the base pairs to spot. So, the directional pressures all wear little tiny badges so that they can be more easily distingushed by the base pairs, than they would be if they were only wearing genes.

This is where God comes in. When God hits a base pair square with the club facing in, this causes a mutation to hook rather than go straight or slice. When God hooks on a dog leg, that's good. When God slices, the dog gets bad knees and must be put down early.

In short, kleinman's problem is that there are no goalposts in golf, and using slaves as caddies is considered bad form -- even by Christian golfers.

[Dr Richard]

Originally Posted by Kleinman reposting for Dr Richard and missing the fact that he asked for a defintion of "selection pressure" not "different types of selection"

Go back to your text book....

And try again. Question 4 still stands. Now have a go at questions 1, 2, 3 and 5.

1. Again, please tell me the minimum number of "directional "selection pressures you think must operate to prevent macroevolution by slowing microevolution to such an extent that it cannot happen within the timeframe of life on earth in the real world based on your extensive mathematical modelling.

2. If one base pair mutation is a microevolutionary event, how many base pair mutations to make a macroevolutionary event? 2? 10? 100?

3. How many positive selection pressures are listed on the HIV positive selection database for just two of the genes?

4. What is your definition of a "selection pressure"

5. (for old time's sake) What is your definition of macroevolution again? (NB random lists of things you think it is are not acceptable)

[cyborg]

You just can't buy that sort of entertainment.

His goalposts lasted only nine days before he was forced to shift them --- which is fast, considering how obtuse he is.

BWAHAHA.

I can't wait to see the next iteration - why bother debunking kleinman when he does the job himself so well? Could there be a more perfect illustration of goal-post shifting?

[Dr Richard]

About multiple selection pressures, given that to address all salient points would risk me missing the impending heat death of the universe.

Much reference has been made to the HIV positive selection database

http://www.bioinformatics.ucla.edu/HIV/

A copy of one of the papers is available here (http://www.bioinformatics.ucla.edu/HIV/Chen,%20Perlina,%20Lee%202004.pdf).

I will firstly summarise what we are discussing here:

Kleinman is claiming (I have reformatted the ASCII art) that:

Directional multiple selection pressures mathematically slows evolution its impossible ev shows this real life shows this

And cites the HIV virus, and in particular the work referenced above, as evidence of this.

Let us consider what these researchers have done.

Firstly, they looked at samples of HIV from 40,000 HIV +ve patients (and had access to another database too).

They have coded the RNA sequence of the protease and reverse transcriptase genes of the (majority) HIV virus for every patient.

They did sufficient checks to ensure that the sequencing was accurate and compared the sequence from every patient to a baseline "reference" sample. A deviation from the baseline sample was counted as a mutation.

What they were interested in was examining the selection pressure acting for every mutation in these genes. They did this by looking at the amino acids produced by the HIV RNA.

This is the clever bit:

3 base pairs of RNA/DNA will code for an amino acid: UUU will get you phenyalanine for instance. A point mutation to UUC will still get you phenylalanine, so the protein produced by the gene will still be the same.

Assuming that a mutation which does not affect the amino acid sequence will have no effect on the fitness of the HIV virus (debatable in higher organisms but reasonable in HIV I feel), this mutation will confer no selective benefit to the virus. Therefore, in a large enough population, this mutation would occur no more often than expected by chance, giving a measure of selection pressure = 1.

However, consider another point mutation to UCU - this would give a serine amino acid, not a phenylalanine. This may have no effect on the function of the overall protein, and would again occur no more often than expected by chance. But, if the mutation confers a "fitness benefit" to the HIV virus, evolutionary theory would expect it to be selected for, and the mutation would be found more often than expected by chance: a selection pressure >1. Likewise, if the mutation is harmful, it will occurs less often than expected by chance: selection pressure <1.

This is what is referred to as Ka/Ks in the paper.

The reason why kleinman is so utterly wrong about this paper is this:

to calculate the selection pressure for a given amino acid mutation the researchers counted the number of times that mutation had occurred in their database

They have to in order to calculate Ka/Ks. From the paper

NY, the count of X3Y mutations observed at that codon,

Now let us go back to Kleinman's original claim:


Directional multiple selection pressures mathematically slows evolution its impossible ev shows this real life shows this

The researchers have calculated Ka/Ks by counting the numbers of real life, existing, forms of HIV which have mutated from the reference sample and increased in frequency as a result of selection. This is evolution.


The evolved forms of HIV, which Kleinman claims are impossible, have actually been counted by this research.

That is why Kleinman is wrong.

That is why this paper does not support his claim.

That is why another of his claims:

Neutral or stabilizing selection processes do not lead to new strains in the gene pool

Is also wrong. If he said "neutral selection processes do not not lead to an increased frequency of new strains in the gene pool over that which would be expected by chance" then he would be right, but he is uttely wrong with his original sentence.

With these errors corrected, I suspect Kleinman will attempt to develop another form of argument about the higher number of negative/neutral selection pressures vs. positive selection pressures shown in this study.

He is too lazy to count them for himself, but if you go to the database linked web page you can do it yourself.

I count about 60-70 positive selection pressures for a single amino acid substitution when one mutation occurs in one dataset. Note that does NOT mean 70 types of HIV that have seen selected for, or even that there were 70 mutated HIV strains found in the study.

Then click on this link (http://www.bioinformatics.ucla.edu/HIV/heatmaps.html).

Here, the researchers have examined the effect on selection pressure if TWO mutations occur. All the blue dots indicate a high Ka/Ks - positive selection pressures, again CALCULATED BY USING THE FREQUENCY OF EVOLVED HIV STRAINS.

Again, multiple selection pressures (as measured by differing Ka/Ks) are not inhibiting the evolution of the HIV virus.


Eventually, as logic takes its toll, kleinmans ASCII art will come to read:

One or more directional multiple selection pressure(s) sufficiently strong to cause "redundant kill" (the minimum level of population death necessary to ensure that the overall (genomic mutation rate)*(surviving population per generation) is too low to adapt to the applied pressure(s) before population death occurs) mathematically slows evolution and renders the population extinct its impossible ev shows this real life shows this

That is why real doctors use triple therapy kleinman.

[kleinman]

Two steps forward, one step back. We will get to the point where you can understand how mutation and selection actually works.Yes, I'm interested to know how these directional pressures are important and, particularly, how many are needed to stop evolution.
There are essentially two different forms of selection pressures, you have stabilizing selection pressures and directional selection pressures. A stabilizing selection pressure favors a particular phenotype increasing the frequency of that phenotype in the population. A directional selection pressure is directed to a new optimum. Note that ev’s selection pressures start out as directional selection pressures seeking the perfect creature. As long as selection is left on in the model, the entire population will evolve to “perfect” creatures. Once this happens, the directionality of the selection pressure ceases and the selection pressure becomes stabilizing, any mutation that causes a creature to no longer be “perfect” is selected out. The new optimum has been found for the population. This is analogous to what happens with HIV. When the HIV virus is exposed to a drug which reduces it’s fitness (ability to reproduce), the drug acts as a directional selection pressure until a strain mutates and becomes resistant to that drug. As long as the drug is in the viruses’ environment, the drug then acts as a stabilizing selection pressure preventing the virus from mutating back to its wild form. Note that wild HIV virus reproduces more rapidly than drug resistant strains of the virus when not in the presence of the drug and will take over the population of viruses in this case. Evolution only occurs under directional selection pressures, not stabilizing selection pressures. This is why Dr Richard’s 500 selection pressures must be distinguished as stabilizing or directional (and neutral) when considering the rate of evolution. The vast majority of the selection pressures in Dr Richard’s reference are not directional. It is the use of combination directional selection pressures (combination therapy) which slows the evolution of drug resistant strains of the virus. Some people with HIV have lived decades longer without active disease using this strategy.
I didn’t say stop=too slow, I said extinction means stop. What I said was too slow means that the theory of evolution is mathematically impossible, you simply do not have enough time to accumulate the information by mutation and selection.Can you put some numbers onto those bolded points you've made. I'm really trying to understand where you see the line being drawn.
The best hard numbers I have are based on the results from ev. Setting two of the three selection conditions to zero will allow the remaining condition to evolve 3 to 5 orders of magnitude more quickly than evolving all three selection conditions simultaneously for genome lengths in the range of HIV. For larger genomes, I expect this number to be far greater. I don’t have quantitative data yet for the real examples I have given but it is clear that people using multiple selection pressures to control HIV, TB, pests, weeds, rodents and so on already know this effect is real.
What I have been advocating is that the ev computer model shows that the acquisition of information by random point mutation is profoundly slow, too slow to support the theory of evolution. The reason why it is too slow is the competing directional selection conditions which slow the evolutionary process profoundly when realistic genome lengths and mutation rates are used. This is also seen in reality.and no other mutation is possible? no other genetic adaptation scheme matters? this is very interesting...
It is the number of directional selection pressures and genome length which dominate the mathematics of mutation and selection. There is no reason to believe that frame shift mutations, translocations, duplications or any other way of scrambling a genome is going to change the underlying mathematics of mutation and selection.
It is the theory of evolution which is the myth, microevolution does occur but extrapolating this phenomenon to the evolution of reptiles into birds is mathematically impossible, that’s the myth.So you admit to microevolution. I understand.
I have admitted to this since the very beginning of this debate. I have also admitted to mutation and selection as a mechanism for increasing genetic information.
Now what is Microevolution? How does it differ from macroevolution?
Microevolutionary events occur, macroevolutionary events do not.
My view on this issue is that once you get beyond a single point mutation you are already starting to enter the realm of macroevolution.but are now sayingThe way the mathematics of mutation and selection works, the more directional selection pressures you have, the slower the evolutionary process goesSeveral question I have are
1.) If microevolution is real, How does it evade being slowed by "more directional selection pressures"?
2.) How many microevolutionary changes must occur before it is called macroevolution?
3.) How does this all relate to the Fitness Landscape argument that you kept refering to previously?
1.) Microevolution does not evade being slowed by more directional pressures, this is demonstrated by ev and the numerous real examples I have presented many times on this thread.
2.) Far too many, the accounting for all the difference between reptiles and birds or even humans and chimpanzees is just too great. Aside from not having selection pressures that would accomplish these transformations, you simply do not have enough reproduction to accomplish these transformations on these very large genome creatures. Mutation and selection just can not get you there, the mathematics does not work.
3.) The fitness landscape is used to describe the path a population subjected to a directional selection pressure must take in order to get to a new optimum. If you have a single directional selection pressure, it is much easier for the population to find this optimum. As soon as you introduce multiple directional selection pressures, the population must find optimums for all these conditions simultaneously. This confounds the mutation and selection process where one selection pressure may cause interference with another selection pressure to find its optimum. You could actually use ev to map out the fitness landscape graphically and watch the fitness function change as the mutation and selection process was occurring. The optimums for this fitness landscape occur when all three selection conditions for the model are satisfied.
In a big crowd of selection pressures, the directional pressures are hard for the base pairs to spot. So, the directional pressures all wear little tiny badges so that they can be more easily distingushed by the base pairs, than they would be if they were only wearing genes.
Oh no, little gator, the directional selection pressures are easier to identify then that, they are the one’s that make the perfect creatures.
1. Again, please tell me the minimum number of "directional "selection pressures you think must operate to prevent macroevolution by slowing microevolution to such an extent that it cannot happen within the timeframe of life on earth in the real world based on your extensive mathematical modelling.
Let’s do one question at a time, otherwise, too many directional selection pressures. I already answered this question but will give it a go again. Ev shows that three directional selection pressures profoundly slow evolution on large genomes. Ev does evolve the three directional selection pressures reasonably quickly on an HIV size genome but not nearly now quickly as a single directional selection pressure. On large genomes, a single directional selection pressure still evolves rapidly in ev. So in answer to your question, based on the mathematics shown by ev, on genomes the size of HIV with equivalent reproductive rates, three directional selective pressures already is slowing microevolution markedly, I suspect a couple more directional selection pressures may give many years more of disease free life. On longer genome creatures such as bacteria I don’t think you will need as many directional selection pressures. The problem here is that most bacteria have been subjected to monotherapy for years. In fact you are taught in medical school not to use combination therapy for the treatment of most bacterial infections. The end result of this line of thinking are multi-drug resistant TB, gonorrhea, MRSA, pseudomonas … I think this line of thinking needs to be reconsidered. Once we finish discussing this question, I’ll go on to your next question.

[Paul C. Anagnostopoulos]

You will notice, by the way, that kleinman's new lie has already been proven false. We're way ahead of him.
There's much to be said for predebunking lies.


This is where God comes in. When God hits a base pair square with the club facing in, this causes a mutation to hook rather than go straight or slice. When God hooks on a dog leg, that's good. When God slices, the dog gets bad knees and must be put down early.
May I have permission to use this in my class on metaphors?

~~ Paul

[Paul C. Anagnostopoulos]

Now what is Microevolution? How does it differ from macroevolution?

Microevolutionary events occur, macroevolutionary events do not.
All righty then, that 'splains it.

~~ Paul

[kleinman]

I count about 60-70 positive selection pressures for a single amino acid substitution when one mutation occurs in one dataset. Note that does NOT mean 70 types of HIV that have seen selected for, or even that there were 70 mutated HIV strains found in the study.
Since Dr Richard does a lousy job explaining his posts, let’s see if we can do a bit better. Let’s start with the equation used to compute the selection pressure at a codon.

http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1669717&blobname=gkl855e1.jpg (http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1669717&blobname=gkl855e1.jpg)

What Dr Richard is confusing is the terminology. Ka/Ks > 1 is called a positive (directional) selection pressure for a codon. When the data for Ka/Ks is plotted for the example for the protease gene, each time Ka/Ks > 1, he counts this as a positive selective pressure.

If you count every codon which shows the results of directional selection pressure with ev when evolving 16 binding sites, 6 bases wide (2 codons wide), you would count 32 positive selection pressures. Dr Richard, each time a particular codon in HIV changes as a result of a directed selection pressure from a protease inhibitor does mean you have additional directed selection pressures. What is happening is a large number of Ka/Ks > 1 for the individual codons in a gene is a measure of the intensity of the directed selection pressure. So if a particular protease inhibitor leads to 60-70 amino acid changes in order to evolve resistance to that drug, it would be a more intense directed selection pressure than another protease inhibitor that only required 30 amino acid changes.

Again, multiple selection pressures (as measured by differing Ka/Ks) are not inhibiting the evolution of the HIV virus.

Eventually, as logic takes its toll, kleinmans ASCII art will come to read:
Dr Richard, you need to do a little more work on your counting.
Microevolutionary events occur, macroevolutionary events do not.All righty then, that 'splains it.
Ev’s helping to ‘slain it. Reptiles to birds is certainly not microevolution.

[kjkent1]

May I have permission to use this in my class on metaphors?

~~ PaulIf you're serious, of course. Send me a PM and I'll give you my ID so I can be properly credited for my work as Rodney Dangerfield's ghostwriter.

LOL!

[kjkent1]

It is the number of directional selection pressures and genome length which dominate the mathematics of mutation and selection. There is no reason to believe that frame shift mutations, translocations, duplications or any other way of scrambling a genome is going to change the underlying mathematics of mutation and selection.What remarkable reasoning powers you have at your disposal, Herr Kleinman.

You have the wisdom of a much younger man.

[Dr Adequate]

Isn't it funny the way he keeps underlining the word he's just learnt?

I wonder why he does that.

Apart from that, there's no new lie of any note; and, of course, no math.

[Dr Adequate]

There is no reason to believe that frame shift mutations, translocations, duplications or any other way of scrambling a genome is going to change the underlying mathematics of mutation and selection. :dl:

Pure gold.

[Dr Richard]

Since Dr Richard does a lousy job explaining his posts, let’s see if we can do a bit better.

Ka/Ks > 1 is called a positive (directional) selection pressure for a codon.

Indeed, as I said, it is a positive selection pressure. I am glad you agree.


When the data for Ka/Ks is plotted for the example for the protease gene, each time Ka/Ks > 1, he counts this as a positive selective pressure.

Which you just agreed it is, acting at the level of the codon.


Dr Richard, each time a particular codon in HIV changes as a result of a directed selection pressure from a protease inhibitor does mean you have additional directed selection pressures.

I am glad you agree again, although your assertion that the positive selection pressures in the protease gene are due to a protease inhibitor is sadly mistaken -see below. But...

kleinman is finally beginning to get it.

This is what happens when you are unable to define selection pressure sufficiently, kleinman.

We can measure "a selection pressure" acting on an individual organism (one selection pressure per organism), a selection of genes, a gene, a part of a gene, an amino acid codon or an individual base pair.

klienman prefers to count selection pressures on a gene, because that is what ev does, but it is not true (see paper under discussion as evidence) that the only selection pressures measurable in real world act purely at the gene level.


But that will not deter kleinman:

What is happening is a large number of Ka/Ks > 1 for the individual codons in a gene is a measure of the intensity of the directed selection pressure. So if a particular protease inhibitor leads to 60-70 amino acid changes in order to evolve resistance to that drug, it would be a more intense directed selection pressure than another protease inhibitor that only required 30 amino acid changes.


In other words, kleinman wants to sum the many, many selection pressures observed at the amino acid level into one, for the whole gene, but does not want to sum the gene-operating selection pressures into one for the whole organism (because that creates one selection pressure and ruins his whole multiple selection pressure argument).

What is really funny is his reference to a protease inhibitor as though this is the only selection pressure acting on the protease gene.

Take a look at the HIV positive selection database (http://www.bioinformatics.ucla.edu/HIV/) again klienman

Third graph down, titled "Stanford untreated dataset"

oops, multiple selection pressures measured on the genome in untreated patients

Of course, it is itneresting to compare that to the treated group, where some additional positive selection pressures can be measured.

You may care to hypothesise that these are due to a gene-wide selection pressure exerted by different protease inhibitors, but this does not hold for the others.

So let us finally return to return to the issue of multiple selection pressures and evolution:

Let’s do one question at a time, otherwise, too many directional selection pressures... So in answer to your question, based on the mathematics shown by ev, on genomes the size of HIV with equivalent reproductive rates, three directional selective pressures already is slowing microevolution markedly, I suspect a couple more directional selection pressures may give many years more of disease free life....On longer genome creatures such as bacteria I don’t think you will need as many directional selection pressures

5 selection pressures in HIV treated patients kleinman?

If we are talking about measuring a selection pressure acting at the viron level, there is one, and only for every organism, and the dataset shows it is evolving. Therefore, you are wrong.

If we are talking about measuring selection pressures acting at the gene level, there are 9 or 10 (for HIV, depending on whether you count the LTR), and the dataset shows HIV is evolving. Therefore, you are wrong.

If we are talking about measuring selection pressures acting at the amino acid codon level, there are 15 on untreated patient on the protease gene alone, and the database shows HIV is evolving. Therefore, you are wrong.

Whichever way you look at it - organism, gene or base pair sequence, your maths is faulty.

I am glad you finally came out with the magic number 5. I'll add it to the list of questions as an answer. Please carry on


1. Again, please tell me the minimum number of "directional "selection pressures you think must operate to prevent macroevolution by slowing microevolution to such an extent that it cannot happen within the timeframe of life on earth in the real world based on your extensive mathematical modelling.

kleinman's answer = 5 (3 modelled in ev + "a couple" more) - but less in bacteria! and organisms with a longer genome

2. If one base pair mutation is a microevolutionary event, how many base pair mutations to make a macroevolutionary event? 2? 10? 100?

(3. How many positive selection pressures are listed on the HIV positive selection database for just two of the genes? - question removed as I had to give you the answer - shame, it is the only one you could have easily got right)


4. What is your definition of a "selection pressure"

5. (for old time's sake) What is your definition of macroevolution again? (NB random lists of things you think it is are not acceptable

[Ducky]

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[Taffer]

Are you not a student of population genetics? Go back to your text book and you will find that population geneticists distinguish three types of selection; they are stabilizing selection, directional selection and disruptive selection. Stabilizing selection favors an intermediate optimum phenotype and selects against phenodeviants. Directional selection is selection directed toward a new intermediate optimum, not at the mean of the population, in response to a new selective challenge. Disruptive selection, rather than favoring any one phenotype, favors two quite different forms and selects against the intermediates; this may be viewed as directional selection of two separate subpopulations, in response to two different sets of environmental conditions. These definitions are taken from the text Genetics in Medicine by Thompson & Thompson.

I think I am beginning to understand the depth of your misunderstandings. I will honestly do my best to educate you, as, in this case, it is an easy mistake to make. Please forgive my headings and the like; I'm in a strange mood. :o

=Introduction of key terms=
There are few key terms that we must understand before continuing, these being "variation", "fitness" and "selection".

-Variation-
Variation is a key concept in evolution, one which is vital for evolution if evolution is to occur. If we restrict our example to a single locus on a genome, which we will call the (made up) evo gene. This imaginary gene is 100 basepairs long. To measure genetic variation in a population (the only form of variation I am dealing with because, essentially, all variation arrises from this), we need to know the exact sequence of this gene. In our example, the sequence is the basepair Guanine (G) 100 times.

Genetic variation occurs when there exists different sequences for the evo gene in the population. Say, 20% of our population contains 80 G and then 20 T (lets call this the B allele, and the other (100% G) the A allele). The more variations of the same gene (called "alleles"), the more variation exists in the population.

-Fitness-
Fitness is fairly easy to define, and very difficult to quantify. Fitness, simply put, is a measure of "how well" an organism does compared to another. Generally, this is measured by how many offspring an organism could produce, but naturally this is very hard to judge. In practice, "fitness" is thought of in terms of alleles, not organisms. If we take some samples, and find that the 20% of our imaginary population which have the B allele, when compared to those with the A allele, produce 25% more offspring, then we could conclude (depending on statistical support for these results of course) that the fitness of the A allele is 0.75 that of the B allele. There is a reason why we do not consider the fitness of the B allele to be 1.25 that of the A allele, which I shall get into later.

In mathematical models, the fitness of an allele is given by "1-s", where "s" is the selection coefficient. In our case above, the selection coefficient would be 0.25, thus making the fitness 0.75 (1-0.25=0.75).

-Natural Selection (or "What now?")-
This is where the real bulk of evolution happens; through natural selection. In common language, selection is the force which "weeds out" unsuccessful traits in a population. It is often said that selection "selects against" unsuccessful traits while "selecting for" successful traits. Unfortunately, this is not quite the truth, but rather a close approximation which is easier to explain. Firstly, selection is not a "force" at all, but should rather be considered a phenomenon of nature. It occurs everywhere and always. Secondly, and most importantly, the phenomenon we call "natural selection" is simply the fact that those organisms which are less fit (i.e. have a higher selection coefficient) the others are, on average, less able to reproduce. Thus, they have a lower contrabution of genetic variation to the next generation then those with higher fitness (lower selection coefficients). Over time, therefore, the proportion of alleles in a population with higher levels of fitness will grow, and those with lower fitness will fall. It is this change in allele frequences which is evolution.

Now, kleinman, we come to your (implied) question. What is the difference between "stabilizing selection, directional selection and disruptive selection". The key to understanding this is that the selection occuring in these three different situations is not different in any way. Selection in all three cases provides "negative pressure" on alleles with lower fitnesses. What these different things are, are models of the results of selection, given different allele fitnesses. But natural selection does not change in any way. The equations are still the same. Alleles with high selection coefficients will be strongly selected against, and alleles with low selection coefficients will be weakly selected against. Obviously, alleles with no selection coefficient (i.e. the most "successful" allele) will not be selected against at all. This is important. The "best" allele is not selected "for", it is just not selected against. The difference is very subtle, the result is often the same, but it is fundamental to understanding your misconceptions.

Why does selection not select "for" anything? It is because natural selection is blind. If it were to select "for" something, then it would have an "end product" in mind. It would have a plan. But this is not how natural selection (and evolution), works. It is completely blind, and as such, can only "weed out" the weakest. It is this which drives the change in allele frequences.

To conclude, it is a common misconception that selection is "for" and "against" different alleles (or traits, or whatever). It is often explained as if this is the case. But when you look at the models of selection, and at the science behind selection, what we really see is that selection is only "against" and "not against". The understanding of this difference is key to the understanding of evolutionary theory as a whole.

So, to answer your (implied) questions in a straight forward manner, in the different "modes" of selection, selection is not, in fact, different at all. All that is different is the result, based upon allele fitness.


Dr Richard’s link also includes “neutral selection” which essentially occurs with mutations which don’t affect fitness.

It is an old debate, and one I'm not going to get into, but the general argument goes something like "If it doesn't affect fitness, how can it be selected for? And if it can't be selected for, how is it selection?".

The goal for directed selection is a new intermediate optimum on the fitness landscape.

And right there is your misconception. There is no "goal" for evolution. Nor is there any "goal" for natural selection. Natural selection is only "against" and "not against".

The reason you don’t understand this is that you don’t understand the different types of selection pressures. Go back to the Ka/Ks equation. When Ka/Ks = 1 you have neutral selection pressure, that is mutations occur which don’t affect the frequency of the particular gene in the gene pool, when Ka/Ks is « 1 you have a stabilizing selection pressure, that is a mutation causes a phenodeviant which is detrimental to the creature and is selected against. When Ka/Ks is « 1, the frequency of that particular mutation is reduced in the gene pool. Only when Ka/Ks > 1 do you have selection which increases the frequency of that mutation in the gene pool.

Again, it is your misunderstanding. Selection behaves no different in all three of these cases, only the result of that selection is different. When Ka/Ks = 1, the allele has no selection acting on it at all. When Ka/Ks < 1, the allele is being selected against. When Ka/Ks > 1, selection is not selecting against it. You have to remember that fitness is relative. This is one of the reasons why it is so hard to give a numerical value to fitness. Fitness is not a finite number, but a relative value based on the "optimal" allele fitness. In other words, all alleles' fitnesses are being compared to the "best" allele. The exact same allele (i.e. the same allele with the same genetic sequence) can be Ka/Ks < 1 in one population, and Ka/Ks > 1 in another. I.e. the same allele can have a low fitness in one population, and a high fitness in another. This is because fitness is relative to all other possible alleles in a population, and why all selection models always have one allele with a fitness of 1 (and thus, no selection coefficient).

These types of mutations lead to a new optimum on the fitness landscape and are thus directional in nature.

No. Selection is not directional, because selection does not have a "goal in mind" when it "selects". Selection, and evolution, are blind.

The authors have indicated that only in rare cases are selection pressures positive (or directional) (Ka/Ks > 1).

It is very true that beneficial mutations are rare.

Neutral or stabilizing selection processes do not lead to new strains in the gene pool.

If you mean "Neutral and stabilizing selection processes do not lead to a change in allele frequency", then I agree with one small correction. Alleles which are undergoing neutral selection most certainly do change in frequency. Look up "genetic drift".

Only when you have directional selection do you introduce new strains in the gene pool and again, these authors indicate that directional selection for HIV is rare. When antiretroviral medications are used on HIV, these apply directional selection pressure on the virus. Note that when a resistant strain evolves, that directional selection pressure will become a stabilizing selection pressure if the virus is still exposed to the drug.

Only directional selection pressure leads to genetic evolution. Of the hundreds of selection pressures Dr Richard refers to, only a tiny fraction of these are directional selection pressures. If you want to evolve drug resistance in HIV, use a single directional selection pressure and you can achieve this quickly because of the viruses’ high mutation rate and rapid reproduction. Combine multiple directional selection pressures and you will slow this process.

What slows is not evolution, but the arisal of the correct variation in the population. Evolution does not slow, the levels of variation decrease. Please note that this is only the case in instances where the population is significantly reduced. However, evolution (the change in allele frequency over time) does not slow. What is happening is the level of "unique features" in a smaller population is less.

You better go back and re-read your textbooks before you take your final exams.

Just for your information, I have no more finals. I already have my degree.

Unless you mean my finals for my graduate studies, in which case I can assure you that they will not deal with such basic issues which we are discussing. This stuff was covered in my second year.

I don’t know what to tell you other than go back to your textbooks and learn what the different forms of selection do.

It is you who does not understand, kleinman. The different forms of selection do not "do" anything, they "just are". The different forms are different forms of results, not different ways in which selection works.

If you teach what you are saying here, you will be misleading your students on how mutation and selection works. What can you expect from an evolutionist?

I would expect any evolutionary geneticist to understand these basic principles of genetic evolution, and so naturally I would teach it.

You still don’t understand the mathematics of mutation and selection. Once you understand what the different forms of selection are, perhaps you will be able to begin to understand the mathematics of mutation and selection.

Kleinman, you are wrong. Simply, plainly, and completely, wrong. I do understand "the mathematics of mutation and selection" (insofar as that is actually a meaningful term), and I do understand how selection works. It is you who does not understand, and refuses to learn.

If you ever graduate Sesame Street and learn how to count, you will understand how mutation and selection really works. Your own link to The HIV positive selection mutation database shows this but it must be too technical for you to understand.

This is what happens when you try to discuss mathematics with a Sesame Street drop out.

He has a far greater grasp of all of this then you do, kleinman.

[Taffer]

Taffer has no idea of what selection pressures are, he needs to go back and read his textbook, perhaps you need to do this as well.

You really should go back to school, kleinman. You would learn a lot about evolution. And why you are wrong.

[Taffer]

Finally, joobz, you are starting to think about the problem. Did you notice all the other links in that google search that also shows that multiple directional selection pressures slow evolution?

I already did this search, and showed that the first three of the "many" papers did not agree with you at all. Aren't you going to comment on this?

[Taffer]

...That is why real doctors use triple therapy kleinman.

Perfect. Thank you for a wonderful post.

[Taffer]

Ev’s helping to ‘slain it. Reptiles to birds is certainly not microevolution.

And it certainly has happened. The evidence that reptiles and birds shared a common ancestor is more then the evidence that we went to the moon.

[joobz]

The best hard numbers I have are based on the results from ev. Setting two of the three selection conditions to zero will allow the remaining condition to evolve 3 to 5 orders of magnitude more quickly than evolving all three selection conditions simultaneously for genome lengths in the range of HIV. For larger genomes, I expect this number to be far greater.
which number is far greater? and why do you not include population in this discussion? haven't we established as pop->inf, gen->1?


It is the number of directional selection pressures and genome length which dominate the mathematics of mutation and selection. There is no reason to believe that frame shift mutations, translocations, duplications or any other way of scrambling a genome is going to change the underlying mathematics of mutation and selection.This is your concrete basis for not worring about it?

I think this paper wouldn't have been accepted if that was the case:

Carvajal-Rodriguez A, Crandall KA, Posada D. "Recombination favors the evolution of drug resistance in HIV-1 during antiretroviral therapy." Infect Genet Evol. 2007 Feb 12; [Epub ahead of print]

I can't access the paper yet, but from the abstract:
Using computer simulations we show that the effect of recombination on the evolution of drug resistance depends strongly on the intensity of selection, as well as on the viral population size. Under the high selection pressure expected during antiretroviral therapy, the strength of the Hill-Robertson effect increases and recombination favors the evolution of resistance under a wide range of population sizes, independently of the sign of the epistatic interaction. Our results suggest that recombination plays an important role in the evolution of drug resistance in HIV-1 under various realistic scenarios.
Seems like evolution has a mathematical basis after all.


Microevolutionary events occur, macroevolutionary events do not.
How many microevolutionary steps=macroevolution?
2.) Far too many..
AHhh, evolution doesn't occur because that's how you defined it. very interesting.

3.) The fitness landscape is used to describe the path a population subjected to a directional selection pressure must take in order to get to a new optimum. If you have a single directional selection pressure, it is much easier for the population to find this optimum. you can't know this a priori. intensity of the selection pressure, the independant nature of the pressures will all matter.
As soon as you introduce multiple directional selection pressures, the population must find optimums for all these conditions simultaneously. This confounds the mutation and selection process where one selection pressure may cause interference with another selection pressure to find its optimum. or it may enhance adaptation (e.g., if one pressure enhances the mutation rates.)

[kleinman]

What is happening is a large number of Ka/Ks > 1 for the individual codons in a gene is a measure of the intensity of the directed selection pressure. So if a particular protease inhibitor leads to 60-70 amino acid changes in order to evolve resistance to that drug, it would be a more intense directed selection pressure than another protease inhibitor that only required 30 amino acid changes.In other words, kleinman wants to sum the many, many selection pressures observed at the amino acid level into one, for the whole gene, but does not want to sum the gene-operating selection pressures into one for the whole organism (because that creates one selection pressure and ruins his whole multiple selection pressure argument).
This is what is so illogical about Dr Richard’s way of counting. Notice how you neglected to respond to my final quote from this post. I’ll repeat it here so we can see where your logic leads.
If you count every codon which shows the results of directional selection pressure with ev when evolving 16 binding sites, 6 bases wide (2 codons wide), you would count 32 positive selection pressures. Dr Richard, each time a particular codon in HIV changes as a result of a directed selection pressure from a protease inhibitor does mean you have additional directed selection pressures. What is happening is a large number of Ka/Ks > 1 for the individual codons in a gene is a measure of the intensity of the directed selection pressure. So if a particular protease inhibitor leads to 60-70 amino acid changes in order to evolve resistance to that drug, it would be a more intense directed selection pressure than another protease inhibitor that only required 30 amino acid changes.
Dr Richard, if you want to use your logic, ev does not have three directional selection pressures is has 32 directional selection pressures not 3. You are confusing the results of a directional selection pressure with the meaning of a directional selection pressures.

It’s time for you to answer a couple of questions. The first is what are these 60-70 directional selection pressures? The second is, there is an error in the equation in your link, what is it? If you can’t find it, perhaps the resident James Randi Educational Forum PhD in amathematics can find it.
What is really funny is his reference to a protease inhibitor as though this is the only selection pressure acting on the protease gene.

Take a look at the HIV positive selection database again klienman

Third graph down, titled "Stanford untreated dataset"

oops, multiple selection pressures measured on the genome in untreated patients
If you had read this thread carefully, you would have seen that I had said there is an immune response to HIV (how many directed selection pressures to you want to call this?) that HIV patients can mount but you appear not to know that it is insufficient to stop the disease. A single antibody directed at the protease can lead to all these amino acid substitutions, just as a single drug leads to numerous amino acid substitutions, just as ev’s 3 selection conditions leads to 32 amino acid substitutions. According to your logic, ev has 32 directed selection pressures. Which counting system do you want to work with?
5 selection pressures in HIV treated patients kleinman?
It doesn’t matter how you want to count selection pressures. If you want to count each amino acid substitution as a selection pressure then ev has 32 selection directional pressures and still gives an analogous model of combination therapy of HIV. It is better to describe directional selection pressures by the number of genes impacted, the degree of inhibition of each of the genes involved and the number of amino acid substitutions required to achieve resistance to that directional selection pressure.

What you continue to miss in this discussion Dr Richard is that the underlying mathematics does not change by changing the way you count selection pressures. The more the amino acid substitutions required, the more generations needed to accomplish these changes by mutation and selection. Stabilizing selection pressures interfere with this process. This is why as you lengthen the genome in the ev model it takes more generations to evolve your selection conditions. Ev demonstrates this with spurious binding in the non-binding site region. HIV with its short genome has a much smaller portion of it’s genome being acted on by stabilizing selection pressures than an E Coli size genome or a human size genome. This is why your theory of evolution is mathematically impossible. You don’t have the selection pressure(s) to evolve reptiles into birds and if you did, you don’t have sufficient generations and sufficient populations to accomplish the transformation my mutation and selection. You really ought to study ev, you would learn something about the mathematics of mutation and selection.

Since I have already answered a couple of questions for you, it’s time for you to answer I couple of questions for me.

The first is what are these 60-70 directional selection pressures? The second is, there is an error in the equation in your link, what is it? If you can’t find it, perhaps the resident James Randi Educational Forum PhD in amathematics can find it.

[Mr. Scott]

There is no reason to believe that frame shift mutations, translocations, duplications or any other way of scrambling a genome is going to change the underlying mathematics of mutation and selection.

This is a fairly critical point, Dr. Alan Kleinman, because if you can't mathematically prove that assertion, then you no longer have mathematical proof that evolution was to slow to account for the origin of species.

Your failure to mathematically prove this means the entire thesis you've presented in this thread is terminally busted.

Please present this proof.

(In your response, could you refer to me as "little Tiktaalik (http://news.nationalgeographic.com/news/2006/04/0405_060405_fish.html)?" Thanks!)

[joobz]

Microevolutionary events occur, macroevolutionary events do not.
how many microevolutionary steps = macroevolution?

2.) Far too many
[quote=Dr. Richard]5 selection pressures in HIV treated patients kleinman?
It doesn’t matter how you want to count selection pressures.


The goalpost has again changed yet again.
It has become "Evolution is impossible because Kleinman defines it as such!"

Asking for concrete values and hypotheses are not needed anymore. He's found an endzone that science can't touch. Unfortunately, in the realm of reality it is out of bounds.

[kleinman]

The best hard numbers I have are based on the results from ev. Setting two of the three selection conditions to zero will allow the remaining condition to evolve 3 to 5 orders of magnitude more quickly than evolving all three selection conditions simultaneously for genome lengths in the range of HIV. For larger genomes, I expect this number to be far greater.which number is far greater? and why do you not include population in this discussion? haven't we established as pop->inf, gen->1?
Computer memory requirements limit running large genome with large populations simultaneously. On my computer, the limit is a 1k genome length and a population of 1 meg. With smaller populations, you can run larger genome cases and these cases show that the generations for convergence proportional to about G^2. Adebz has stated that at infinite population, generation for converges goes to 1. If that is true, the data obtained from ev shows that the slope of the generations for convergence/population is so shallow with large populations that you will need unrealistically large populations to get small generations for convergence. Adebz now understands that doubling population does not double the probability of a particular mutation occurring at a particular locus. This effect is demonstrated by ev by it’s rapidly decreasing slope of the generations for convergence/population curve for the larger population series already presented here.

What you need to understand is that if you are going to propose the evolution of reptiles into birds, you don’t have infinite populations; you don’t even have the entire reptile population involved in this so called evolutionary event. If you did, why do we still have reptiles? You have large genome creatures with much longer generation times than HIV or even bacteria with much smaller populations requiring huge numbers of amino acid substitutions in order to accomplish this evolutionary event. You don’t have the selection pressure to accomplish this and you evolutionists think that directional selection pressures are not influenced by stabilizing selection pressures. The mathematics is just not there to support this concept.
It is the number of directional selection pressures and genome length which dominate the mathematics of mutation and selection. There is no reason to believe that frame shift mutations, translocations, duplications or any other way of scrambling a genome is going to change the underlying mathematics of mutation and selection.This is your concrete basis for not worring about it?
Look at this thread joobz, I present the results of Dr Schneider’s peer reviewed and published model and you all attribute this mathematics to me and instantly discredit the results. Why do you think that Dr Schneider stopped publishing on his model? He knows what his model shows. He has put himself in the position of having to retract his statements that his model represents mutation and selection realistically or that his model is showing that information acquisition on longer genomes becomes profoundly slow. There is evidence of this in his web published statements that realistic length genomes cases would take years to run.

It is the responsibility of evolutionists to prove your theory mathematically. If evolutionists think that other mechanisms of mutations will somehow accelerate evolution, put the mechanism in ev and show this. If anything, mutations which cause frame shifts will disrupt the sequences of already evolved binding sites. As it stands right now, ev shows that the rate of information gain by random point mutation and natural selection is far too slow on realistic length genomes to support the theory of evolution. However, ev does a good job in modeling how microevolution works.
I think this paper wouldn't have been accepted if that was the case:

Carvajal-Rodriguez A, Crandall KA, Posada D. "Recombination favors the evolution of drug resistance in HIV-1 during antiretroviral therapy." Infect Genet Evol. 2007 Feb 12; [Epub ahead of print]

I can't access the paper yet, but from the abstract: Using computer simulations we show that the effect of recombination on the evolution of drug resistance depends strongly on the intensity of selection, as well as on the viral population size. Under the high selection pressure expected during antiretroviral therapy, the strength of the Hill-Robertson effect increases and recombination favors the evolution of resistance under a wide range of population sizes, independently of the sign of the epistatic interaction. Our results suggest that recombination plays an important role in the evolution of drug resistance in HIV-1 under various realistic scenarios.
What is the Hill-Robertson effect? Here is the definition from Wikipedia which can be found at: http://en.wikipedia.org/wiki/Hill-Robertson_effect (http://en.wikipedia.org/wiki/Hill-Robertson_effect)
In a finite population subject to natural selection and genetic recombination, genetic drift will create random instances of linkage disequilibrium. Some will be selectively advantageous, others will not. However, the creation of these slows down the progress of selection. Recombination breaks down the disequilibria, allowing selection to act independently on various loci.
So how does this work with HIV? Here is a quote from an article located at http://www.cdc.gov/ncidod/eid/vol3no3/burke.htm (http://www.cdc.gov/ncidod/eid/vol3no3/burke.htm)
Human immunodeficiency virus (HIV)-1, like all retroviruses, is "diploid." Each viral particle contains two RNA strands of positive polarity, each full length and potentially able to replicate (1). No other virus families, RNA or DNA, are diploid. Typically both RNA strands in a retroviral particle derive from the same parent provirus. However, if an infected cell simultaneously harbors two different proviruses, one RNA transcript from each provirus can be encapsidated into a single "heterozygous" virion. When this virion subsequently infects a new cell, the reverse transcriptase may jump back and forth between the two RNA templates so that the newly synthesized retroviral DNA sequence is recombinant between that of the two parents (2). All subsequent progeny virions will be of this recombinant genotype. HIV-1 strains with chimeric genomes thought to have arisen through homologous recombination have recently been discovered in nature (3).
This is a property unique to the retroviruses, are you trying to generalize this phenomenon to the entire theory of evolution? This appears like a baseless extrapolation.
Seems like evolution has a mathematical basis after all.
The microevolution of the HIV virus does.
3.) The fitness landscape is used to describe the path a population subjected to a directional selection pressure must take in order to get to a new optimum. If you have a single directional selection pressure, it is much easier for the population to find this optimum. you can't know this a priori. intensity of the selection pressure, the independant nature of the pressures will all matter.
Ev is a simulation of this process and it show that the search for this optimum becomes profoundly slow with multiple selection pressures and large genomes.
As soon as you introduce multiple directional selection pressures, the population must find optimums for all these conditions simultaneously. This confounds the mutation and selection process where one selection pressure may cause interference with another selection pressure to find its optimum.or it may enhance adaptation (e.g., if one pressure enhances the mutation rates.)
You do know that some mutations are harmful and that stabilizing selection pressures select out those creatures. Perhaps what you suggest here should be put into ev and show mathematically how one selection pressure enhances another. The problem with your logic is that you suggest when sorting a dataset, introducing another sorting condition at the same time will somehow accelerate the original sorting process. I don’t believe there is a mathematical basis for this. If you can give me a few real examples of how this happens, I’ll reconsider my position on your theory. As it stands, you are proposing an exceptional case to try to establish the rule for evolution.

[Mercutio]

In completely unrelated news, the first marsupial genome has been sequenced. (http://abc.net.au/science/news/stories/2007/1918682.htm) Overall, the genome of the opossum (Monodelphis domestica) includes roughly 18,000-20,000 genes, Graves says.

That makes it about the same size as the human genome, although the genes are arranged on a small number of extremely large chromosomes.

Most of the opossum's genes have counterparts in humans and other animals such as mice, the Nature paper shows.

Those that are opossum-specific seem to be related to immunity, sensory perception and detoxification, the researchers say.

"That's to be expected because immune genes evolve very, very fast," Graves says.

"They're under stringent selection every time we meet a new bug." So...lots of selection pressures = fast evolution.

Like I said, just a cool article completely unrelated to the current thread.

[kleinman]

It doesn’t matter how you want to count selection pressures.The goalpost has again changed yet again.
It has become "Evolution is impossible because Kleinman defines it as such!"

Asking for concrete values and hypotheses are not needed anymore. He's found an endzone that science can't touch. Unfortunately, in the realm of reality it is out of bounds.
Joobz, unless you understand Dr Richard’s terminology you can not talk about concrete values. What Dr Richard counts as a directed selection pressure is the number of amino acid substitutions that results from a selection pressure. If you are going to count selection pressures like this, ev has 32 selection pressures (amino acid substitutions) when evolving 16 binding sites each 6 bases wide. I have counted selection pressures as the number of mathematical conditions Dr Schneider uses in ev. This concept is equivalent to the use of a drug for the treatment of HIV which can lead to 60-70 amino acid substitutions to evolve resistance to that drug. You can count the single drug therapy as a single selection pressure that leads to 60-70 amino acid substitutions. A single antibody directed against a protease can do the equivalent. There are concrete values mixed in with all the noise Dr Richard adds to this discussion. When you sort through what he is saying, ev is still a valid analogy for what is happening with combination (or monotherapy) therapy of HIV.

[Dr Richard]

This is what is so illogical about Dr Richard’s way of counting. Notice how you neglected to respond to my final quote from this post. I’ll repeat it here so we can see where your logic leads.

Dr Richard, if you want to use your logic, ev does not have three directional selection pressures is has 32 directional selection pressures not 3. You are confusing the results of a directional selection pressure with the meaning of a directional selection pressures.

I am saying that you can measure a selection pressure acting on the codon.

What is your definition of a selection pressure again kleinman?

You'll have a week to think of one.

It’s time for you to answer a couple of questions. The first is what are these 60-70 directional selection pressures?

Another failure in reading comprehension. But your faith is blinding you to the obvious.

I cannot say for certain, as the paper does not provide this information. But I would say they include (but are not limited to)

1. mutations within the HIV protease gene that improve the efficiency of the gene in an untreated patient

2. mutations within the HIV protease gene that improve the efficiency of the gene in an treated patient

3. mutations within the reverse transcriptase gene that improve the efficiency of the gene in an untreated patient

4. mutations within the reverse transcriptase gene that improve the efficiency of the gene in an treated patient

5. mutations within either gene that improve integration/replication in the host DNA

6. mutations that interact with other mutations in the genome to improve overall fitness


The second is, there is an error in the equation in your link, what is it? If you can’t find it, perhaps the resident James Randi Educational Forum PhD in amathematics can find it.[/SIZE][/FONT]

Which link?


If you had read this thread carefully, you would have seen that I had said there is an immune response to HIV (how many directed selection pressures to you want to call this?) that HIV patients can mount but you appear not to know that it is insufficient to stop the disease. A single antibody directed at the protease can lead to all these amino acid substitutions,

Your lack of knowledge of the immune system does not suprise me.

Are you seriously trying to contend that the whole immune response to HIV infection is due a single antibody? That is very funny.

As stated before, I would count the human immune response as about 3500 selection pressures if we use the kleinman "selection pressure acting at a gene level" method of counting.

I have never claimed that human immune system is effective in all cases at preventing HIV infection.

Although you are again sadly misguided in asserting that it cannot stop the disease: a few seconds of research will tell you that there are individuals who have sufficient immunity to HIV to have immunity: this paper (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=17092330&query_hl=5&itool=pubmed_DocSum)will highlight some more immune mechanisms other than antibodies for you to learn about and explain why some individuals have higher natural resistance than others:


just as a single drug leads to numerous amino acid substitutions, just as ev’s 3 selection conditions leads to 32 amino acid substitutions. According to your logic, ev has 32 directed selection pressures. Which counting system do you want to work with?[/SIZE][/FONT]

You are wrong whichever system you pick: selection pressure acting at the level of the organism, the gene or base pair. Pick one.



It doesn’t matter how you want to count selection pressures. If you want to count each amino acid substitution as a selection pressure then ev has 32 selection directional pressures and still gives an analogous model of combination therapy of HIV. It is better to describe directional selection pressures by the number of genes impacted, the degree of inhibition of each of the genes involved and the number of amino acid substitutions required to achieve resistance to that directional selection pressure.

You are inching towards the light of understanding. Don't stop. But remember to update your goralpost art (getting a little crowded now) and include the other mechanisms of evolutionary change other than amino acid substitutions.


What you continue to miss in this discussion Dr Richard is that the underlying mathematics does not change by changing the way you count selection pressures.

Which why you have always been wrong


The more the amino acid substitutions required, the more generations needed to accomplish these changes by mutation and selection.

These have already been achieved. That is what the database shows. Its entire existence is a refutation of your theory.


Ev demonstrates this with spurious binding in the non-binding site region. HIV with its short genome has a much smaller portion of it’s genome being acted on by stabilizing selection pressures than an E Coli size genome or a human size genome. This is why your theory of evolution is mathematically impossible. You don’t have the selection pressure(s) to evolve reptiles into birds and if you did, you don’t have sufficient generations and sufficient populations to accomplish the transformation my mutation and selection. You really ought to study ev, you would learn something about the mathematics of mutation and selection.

Any evidence for the above list of random assertions? Other than the last 3000+ posts of mindless macro pasting?


Since I have already answered a couple of questions for you, it’s time for you to answer I couple of questions for me.

The first is what are these 60-70 directional selection pressures? The second is, there is an error in the equation in your link, what is it? If you can’t find it, perhaps the resident James Randi Educational Forum PhD in amathematics can find it.

See above.

1. Again, please tell me the minimum number of "directional "selection pressures you think must operate to prevent macroevolution by slowing microevolution to such an extent that it cannot happen within the timeframe of life on earth in the real world based on your extensive mathematical modelling.

kleinman's answer = 5 (3 modelled in ev + "a couple" more) - but less in bacteria and organisms with a longer genome

2. If one base pair mutation is a microevolutionary event, how many base pair mutations to make a macroevolutionary event? 2? 10? 100?

4. What is your definition of a "selection pressure"

5. (for old time's sake) What is your definition of macroevolution again? (NB random lists of things you think it is are not acceptable)

[Dr Richard]

[FONT='Times New Roman']Joobz, unless you understand Dr Richard’s terminology you can not talk about concrete values. What Dr Richard counts as a directed selection pressure is the number of amino acid substitutions that results from a selection pressure.

Wrong

This concept is equivalent to the use of a drug for the treatment of HIV which can lead to 60-70 amino acid substitutions to evolve resistance to that drug.

Wrong

You can count the single drug therapy as a single selection pressure that leads to 60-70 amino acid substitutions.

Wrong

A single antibody directed against a protease can do the equivalent.

Wrong

There are concrete values mixed in with all the noise Dr Richard adds to this discussion. When you sort through what he is saying, ev is still a valid analogy for what is happening with combination (or monotherapy) therapy of HIV.

Wrong.

Not suprised you wrote in a small font; ashamed?

Off on holiday now, good luck with those tricky questions

[kleinman]

"That's to be expected because immune genes evolve very, very fast," Graves says.So...lots of selection pressures = fast evolution.
What are these lots of selection pressures? Are you using Dr Richard’s counting scheme and counting each amino acid substitution as a selection pressure. Do you want to explain how this mechanism works with viruses, bacteria and how do you get these changes into gametes?

[joobz]

Computer memory requirements limit running large genome with large populations simultaneously. On my computer, the limit is a 1k genome length and a population of 1 meg. With smaller populations, you can run larger genome cases and these cases show that the generations for convergence proportional to about G^2. only when point mutation is occuring, mutation rate and kill off rate is fixed. Seems like you are making a baseless extrapolation.
Adebz has stated that at infinite population, generation for converges goes to 1. If that is true, the data obtained from ev shows that the slope of the generations for convergence/population is so shallow with large populations that you will need unrealistically large populations to get small generations for convergence.
only when point mutation is occuring, mutation rate and kill off rate is fixed. Seems like you are making a baseless extrapolation.
Adebz now understands that doubling population does not double the probability of a particular mutation occurring at a particular locus. This effect is demonstrated by ev by it’s rapidly decreasing slope of the generations for convergence/population curve for the larger population series already presented here.
only when point mutation is occuring, mutation rate and kill off rate is fixed. Seems like you are making a baseless extrapolation.

Look at this thread joobz, I present the results of Dr Schneider’s peer reviewed and published model and you all attribute this mathematics to me and instantly discredit the results.
I know full well you haven't done any math. Don't worry. No one has accused you of any model generation.
ev only has point mutation occuring with mutation rate and kill off rate fixed. Seems like you are making a baseless extrapolation.

Why do you think that Dr Schneider stopped publishing on his model? He knows what his model shows. He has put himself in the position of having to retract his statements that his model represents mutation and selection realistically or that his model is showing that information acquisition on longer genomes becomes profoundly slow. There is evidence of this in his web published statements that realistic length genomes cases would take years to run.
You are again confusing simulation time with evolution time. Seems like you are making a baseless extrapolation.


What is the Hill-Robertson effect? Here is the definition from Wikipedia which can be found at: http://en.wikipedia.org/wiki/Hill-Robertson_effect (http://en.wikipedia.org/wiki/Hill-Robertson_effect)

So how does this work with HIV? Here is a quote from an article located at http://www.cdc.gov/ncidod/eid/vol3no3/burke.htm (http://www.cdc.gov/ncidod/eid/vol3no3/burke.htm)
great. But then this completely destroys your earlier assertion


There is no reason to believe that frame shift mutations, translocations, duplications or any other way of scrambling a genome is going to change the underlying mathematics of mutation and selection.
This statements is a baseless extrapolation.

This is a property unique to the retroviruses, are you trying to generalize this phenomenon to the entire theory of evolution? This appears like a baseless extrapolation.thank you for this method of critique.
Unfortunately, you've been using HIV viruses as proof of why evolution is impossible. I show a study where they demonstrate how multiple selection pressures won't HALT HIV evolution, and now you claim that I can't extrapolate this truth to anything else.

Seems like you keep adjusting the playing field to suite your needs. We used YOUR example and found it wanting. Now you claim it's a bad example.

Call the chain gang again, this goal post keeps shifting.

[kleinman]

This is what is so illogical about Dr Richard’s way of counting. Notice how you neglected to respond to my final quote from this post. I’ll repeat it here so we can see where your logic leads.

Dr Richard, if you want to use your logic, ev does not have three directional selection pressures is has 32 directional selection pressures not 3. You are confusing the results of a directional selection pressure with the meaning of a directional selection pressures.I am saying that you can measure a selection pressure acting on the codon.

What is your definition of a selection pressure again kleinman?

You'll have a week to think of one.
I don’t need a week to think about this one. I have been using the concept of a macroscopic selection pressure whether it is Dr Schneider’s selection conditions used in his model or the drugs which are used to treat HIV. These are macroscopic selection pressures. You now try to equate each amino substitution as a directed selection pressure. If you work by that definition, ev has 32 directed selection pressures.
It’s time for you to answer a couple of questions. The first is what are these 60-70 directional selection pressures?
It’s time for you to answer a couple of questions. The first is what are these 60-70 directional selection pressures?Another failure in reading comprehension. But your faith is blinding you to the obvious.

I cannot say for certain, as the paper does not provide this information. But I would say they include (but are not limited to)

1. mutations within the HIV protease gene that improve the efficiency of the gene in an untreated patient

2. mutations within the HIV protease gene that improve the efficiency of the gene in an treated patient

3. mutations within the reverse transcriptase gene that improve the efficiency of the gene in an untreated patient

4. mutations within the reverse transcriptase gene that improve the efficiency of the gene in an treated patient

5. mutations within either gene that improve integration/replication in the host DNA

6. mutations that interact with other mutations in the genome to improve overall fitness
1. What is the selection pressure that increases protease efficiency in an untreated patient?
2. What is the selection pressure that increases protease efficiency in a treated patient?
3. What is the selection pressure that increases reverse transcriptase efficiency in an untreated patient?
4. What is the selection pressure that increases reverse transcriptase efficiency in an treated patient?
5. What is the selection pressure that improves integration/replication in the host DNA?
6. What is the selection pressure that causes mutations in the genome to interact with other mutations to improve overall fitness?

Are there any stabilizing selection pressures acting on HIV and if so, how many are there? Are there neutral selection pressures acting on HIV and if so, how many are there?
The second is, there is an error in the equation in your link, what is it? If you can’t find it, perhaps the resident James Randi Educational Forum PhD in amathematics can find it.Which link?
It’s in The HIV positive selection mutation database link the one you said you read so carefully. Here, I’ll post the equation again for you. Once you find the error, explain to us this equation. You brought up the reference. Let’s see if you can explain to us your own links. If it is too technical for you, don’t bother. We already have enough evolutionists posting URLs on this thread that they can’t explain.
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1669717&blobname=gkl855e1.jpg

[kleinman]

Computer memory requirements limit running large genome with large populations simultaneously. On my computer, the limit is a 1k genome length and a population of 1 meg. With smaller populations, you can run larger genome cases and these cases show that the generations for convergence proportional to about G^2.only when point mutation is occuring, mutation rate and kill off rate is fixed. Seems like you are making a baseless extrapolation.
Large population cases are done with unrealistically high mutation rates in order to get as fast a convergence as possible. Even under these circumstances the largest of population cases takes hundreds of hours of cpu time on a 2.3GHz machine. Do you think slowing down the mutation rate will speed up evolution? No matter what the mutation rate, half the population always survives. What do you think happens when a living thing is exposed to a mutagen?
Adebz has stated that at infinite population, generation for converges goes to 1. If that is true, the data obtained from ev shows that the slope of the generations for convergence/population is so shallow with large populations that you will need unrealistically large populations to get small generations for convergence.only when point mutation is occuring, mutation rate and kill off rate is fixed. Seems like you are making a baseless extrapolation.
If you think that other mutation mechanism will accelerate evolution, prove it. Otherwise you are the one making the baseless extrapolation. Ev shows that point mutations and natural selection doesn’t support the theory of evolution. If you contend that other mechanisms of mutations will correct what ev is showing, put this in the model and prove it. Otherwise, the theory of evolution is founded on baseless speculations and extrapolations.
Adebz now understands that doubling population does not double the probability of a particular mutation occurring at a particular locus. This effect is demonstrated by ev by it’s rapidly decreasing slope of the generations for convergence/population curve for the larger population series already presented here.only when point mutation is occuring, mutation rate and kill off rate is fixed. Seems like you are making a baseless extrapolation.
Let’s see if Adebz can show that frame shift mutations increase the probability of a particular mutation occurring at a particular location. Maybe you want to try to do this probability problem?
Look at this thread joobz, I present the results of Dr Schneider’s peer reviewed and published model and you all attribute this mathematics to me and instantly discredit the results.I know full well you haven't done any math. Don't worry. No one has accused you of any model generation.
ev only has point mutation occuring with mutation rate and kill off rate fixed. Seems like you are making a baseless extrapolation.
What I have done is what Dr Schneider suggested to me privately and publicly suggested in his published paper on ev. That is do a parametric study with his computer simulation of random point mutation and natural selection. I guess alchemical engineers do not do parametric studies with their computer models.
Why do you think that Dr Schneider stopped publishing on his model? He knows what his model shows. He has put himself in the position of having to retract his statements that his model represents mutation and selection realistically or that his model is showing that information acquisition on longer genomes becomes profoundly slow. There is evidence of this in his web published statements that realistic length genomes cases would take years to run.You are again confusing simulation time with evolution time. Seems like you are making a baseless extrapolation.
No joobz, I’m not confusing simulation time with evolution time. If you studied and understood ev, you would know this. Dr Schneider and Paul understand this principle even if you don’t.
What is the Hill-Robertson effect? Here is the definition from Wikipedia which can be found at: http://en.wikipedia.org/wiki/Hill-Robertson_effect (http://en.wikipedia.org/wiki/Hill-Robertson_effect)

So how does this work with HIV? Here is a quote from an article located at [/URL]http://www.cdc.gov/ncidod/eid/vol3no3/burke.htm (http://www.cdc.gov/ncidod/eid/vol3no3/burke.htm) great. But then this completely destroys your earlier assertion
No it doesn’t, it only shows that you know how to make a baseless extrapolation.
There is no reason to believe that frame shift mutations, translocations, duplications or any other way of scrambling a genome is going to change the underlying mathematics of mutation and selection.This statements is a baseless extrapolation.
Simple enough; put any mutation mechanism you want in ev and prove this. Otherwise your theory of evolution started and remains without a mathematical basis. Of course, that is not a baseless extrapolation in the brainwashed mind of an evolutionist.
This is a property unique to the retroviruses, are you trying to generalize this phenomenon to the entire theory of evolution? This appears like a baseless extrapolation.thank you for this method of critique.
Unfortunately, you've been using HIV viruses as proof of why evolution is impossible. I show a study where they demonstrate how multiple selection pressures won't HALT HIV evolution, and now you claim that I can't extrapolate this truth to anything else.
What you continue to miss in this discussion is that recombination does not create new genes. You must still evolve the resistant gene by mutation and selection. Once you evolve the gene, recombination can spread the gene though the gene pool but recombination does not make new gene.
Seems like you keep adjusting the playing field to suite your needs. We used YOUR example and found it wanting. Now you claim it's a bad example.
I see, when evolutionists adjust their theory, this is scientific research, when I adjust my theory, I’m moving the goal posts. Well let’s see. I started saying that the theory of evolution is mathematically impossible as shown by the results of the peer reviewed published model of random point mutation and natural selection. Then I adjusted my statement by saying that the reason why ev shows the theory of evolution is mathematically impossible is that multiple selection pressures slow the process of evolution and then shame of shames, I said it is multiple [U]directional selection pressures which slow evolution. Do you think stabilizing selection pressures accelerate evolution?

I’ve put forth a simple mathematical hypothesis based on the results of an evolutionist written, peer reviewed and published model of mutation and selection. I have presented numerous real examples of this phenomenon. If you think that multiple directional selection pressures accelerate evolution, prove it. Complaining about moving goalposts will not win this debate.

[Paul C. Anagnostopoulos]

... the first marsupial genome has been sequenced.
All hail the mighty little grey, short-tailed opossum!

~~ Paul

[kleinman]

... the first marsupial genome has been sequenced.All hail the mighty little grey, short-tailed opossum!
Paul, do you know how to tell the difference between the opossum and the theory of evolution?

The opossum plays dead, the theory of evolution is dead.

[joobz]

For clarity, I have summarized the key points of this conversation. I think we have a new lie here.

If you studied ev, you would understand this. If you examined the real cases of combination therapy for the treatment of HIV, combination therapy for the treatment of TB, combination pesticides, combination herbicides, combination rodenticides, you would see real examples of what ev demonstrates and what the fitness landscape requires. Mutation and selection can not and does not do what evolutionists allege, it is mathematically impossible.


It is the number of directional selection pressures and genome length which dominate the mathematics of mutation and selection. There is no reason to believe that frame shift mutations, translocations, duplications or any other way of scrambling a genome is going to change the underlying mathematics of mutation and selection.


This is your concrete basis for not worring about it?

I think this paper wouldn't have been accepted if that was the case:

Carvajal-Rodriguez A, Crandall KA, Posada D. "Recombination favors the evolution of drug resistance in HIV-1 during antiretroviral therapy." Infect Genet Evol. 2007 Feb 12; [Epub ahead of print]

I can't access the paper yet, but from the abstract:
Using computer simulations we show that the effect of recombination on the evolution of drug resistance depends strongly on the intensity of selection, as well as on the viral population size. Under the high selection pressure expected during antiretroviral therapy, the strength of the Hill-Robertson effect increases and recombination favors the evolution of resistance under a wide range of population sizes, independently of the sign of the epistatic interaction. Our results suggest that recombination plays an important role in the evolution of drug resistance in HIV-1 under various realistic scenarios
Seems like evolution has a mathematical basis after all.






So how does this work with HIV? Here is a quote from an article located at http://www.cdc.gov/ncidod/eid/vol3no3/burke.htm (http://www.cdc.gov/ncidod/eid/vol3no3/burke.htm)
Human immunodeficiency virus (HIV)-1, like all retroviruses, is "diploid." Each viral particle contains two RNA strands of positive polarity, each full length and potentially able to replicate (1). No other virus families, RNA or DNA, are diploid. Typically both RNA strands in a retroviral particle derive from the same parent provirus. However, if an infected cell simultaneously harbors two different proviruses, one RNA transcript from each provirus can be encapsidated into a single "heterozygous" virion. When this virion subsequently infects a new cell, the reverse transcriptase may jump back and forth between the two RNA templates so that the newly synthesized retroviral DNA sequence is recombinant between that of the two parents (2). All subsequent progeny virions will be of this recombinant genotype. HIV-1 strains with chimeric genomes thought to have arisen through homologous recombination have recently been discovered in nature (3).

This is a property unique to the retroviruses, are you trying to generalize this phenomenon to the entire theory of evolution? This appears like a baseless extrapolation.
Unfortunately, you've been using HIV viruses as proof of why evolution is impossible. I show a study where they demonstrate how multiple selection pressures won't HALT HIV evolution, and now you claim that I can't extrapolate this truth to anything else.
No it doesn’t, it only shows that you know how to make a baseless extrapolation.

I see, when evolutionists adjust their theory, this is scientific research, when I adjust my theory, I’m moving the goal posts.

This isn't an "adjustment of a theory". This is intellectual dishonesty.

We have been discussing how multiple pressures doesn't stop evolution using HIV as an example. I give evidence that states mathematically that this isn't the case. And now you claim that it doesn't apply.
This is the worst form of professional behavior.

[Ichneumonwasp]

Joobz, yeah, he pulled that with me several pages ago when I pushed him into the same corner, which is why I bowed out of the debate. There is simply no sense in continuing a conversation with someone who is so dishonest.

[kjkent1]

Paul, do you know how to tell the difference between the opossum and the theory of evolution?

The opossum plays dead, the theory of evolution is dead.I guess that the Christian theory of creation is dead, too, because there are no opossum in Africa or the middle east and never have been. And, even if opossum were on Noah's Ark, how did they manage to get from Africa to South America?

http://forums.randi.org/imagehosting/14913461a70fa119db.jpg

[kleinman]

For clarity, I have summarized the key points of this conversation. I think we have a new lie here.
You say something with clarity? This almost makes me want to post a gif or jpeg. Your idea of clarity is that abiogenesis is true because of cooperative chemistry and your idea that evolution is true because of cooperative selection pressures. Sorry, I’m not going to cooperate with this type of nonsense. However, I will listen to your story of how the sun beating down on the primordial soup cooperates to chemically produce life. Everyone enjoys a good fairy tale.

But feel free to include the other mutation mechanisms in ev an show how they cooperate to accelerate evolution.
Joobz, yeah, he pulled that with me several pages ago when I pushed him into the same corner, which is why I bowed out of the debate. There is simply no sense in continuing a conversation with someone who is so dishonest.
Really, is that the reason why you are bowing out of the debate? It wouldn’t have any thing to do with you have no idea of the mathematics of mutation and selection which you don’t.

[joobz]

You say something with clarity? This almost makes me want to post a gif or jpeg. Your idea of clarity is that abiogenesis is true because of cooperative chemistry and your idea that evolution is true because of cooperative selection pressures.
No I didn't, you little liar. I simply gave an example of a possible mechanism. I never said that this "proved" abiogenesis.

Sorry, I’m not going to cooperate with this type of nonsense. However, I will listen to your story of how the sun beating down on the primordial soup cooperates to chemically produce life. Everyone enjoys a good fairy tale.

You can't even insult me without lieing. I suggest going back to making fun of my spelling and grammar. At least that's honest.

I've proven you to be an intellectually dishonest little liar. Do you wish to revisit how HIV proves evolution is impossible?

[Ichneumonwasp]

Really, is that the reason why you are bowing out of the debate? It wouldn’t have any thing to do with you have no idea of the mathematics of mutation and selection which you don’t.

Yes, your dishonesty is the precise reason for my bowing out. That and the subtle embarassment that I think everyone feels at watching you make such a complete fool of yourself. It is quite sad to watch.

[kleinman]

Paul, do you know how to tell the difference between the opossum and the theory of evolution?

The opossum plays dead, the theory of evolution is dead.I guess that the Christian theory of creation is dead, too, because there are no opossum in Africa or the middle east and never have been. And, even if opossum were on Noah's Ark, how did they manage to get from Africa to South America?
I keep telling you red herring man that I’m here to prove to you that the theory of evolution is mathematically impossible. I’m not here to prove to you that God exists scientifically.

Anyway, your explanation for how opossum came about by evolution doesn’t have a mathematical basis. Use your imagination and you can probably figure a way opossum can migrate. You know how good your evolutionist imagination is. Perhaps they evolved wings traveled to South America and then devolved their wings once they arrived.

What is it with you evolutionists, you all say you are bowing out of this discussion and yet you keep on posting. You are a mysterious group, whiny and thin skinned but your faith in your belief system is amazing.

[joobz]

I keep telling you red herring man that I’m here to prove to you that the theory of evolution is mathematically impossible. I’m not here to prove to you that God exists scientifically.that's right. I remember how science works now. Foolishly trash theories that you don't understand and don't defend the one you beleive in. interesting.

What is it with you evolutionists, you all say you are bowing out of this discussion and yet you keep on posting. You are a mysterious group, whiny and thin skinned but your faith in your belief system is amazing.
Why do you lie so much? We haven't all stated this?

[kleinman]

I keep telling you red herring man that I’m here to prove to you that the theory of evolution is mathematically impossible. I’m not here to prove to you that God exists scientifically.that's right. I remember how science works now. Foolishly trash theories that you don't understand and don't defend the one you beleive in. interesting.
You liar! I am only trashing one theory, your dumb theory of evolution and I’m using an evolutionist written and peer reviewed model of mutation and natural selection to show it is mathematically impossible, well that and a series of real examples of what the model shows. And the author of this model got it right. Now if only you evolution cultists would come to understand this. I’m patient; we will get the message through to you and free you from the bondage of your mathematically impossible theory.
What is it with you evolutionists, you all say you are bowing out of this discussion and yet you keep on posting. You are a mysterious group, whiny and thin skinned but your faith in your belief system is amazing.Why do you lie so much? We haven't all stated this?
Will it still be a lie when you bow out?

[kjkent1]

I keep telling you red herring man that I’m here to prove to you that the theory of evolution is mathematically impossible. I’m not here to prove to you that God exists scientifically.

Anyway, your explanation for how opossum came about by evolution doesn’t have a mathematical basis. Use your imagination and you can probably figure a way opossum can migrate. You know how good your evolutionist imagination is. Perhaps they evolved wings traveled to South America and then devolved their wings once they arrived.

What is it with you evolutionists, you all say you are bowing out of this discussion and yet you keep on posting. You are a mysterious group, whiny and thin skinned but your faith in your belief system is amazing.I don't "believe" in evolution. I review the observed evidence and conclude that evolution is the only sane possibility, because the alternative is a guy in a white robe and a beard blowing life into dust.

Schneider's model shows how information gain from a random start occurs. It does not show how abiogenesis has culminated in homo sapiens.

For you to extrapolate one from the other is, in my opinion, mentally disordered, because you are applying ev as the model for all observed evolutionary evidence that fits the ev model -- while excluding all observed evidence that does not fit.

You may as well say that since Newton's equations don't fit with the observation of the Michelson-Morley experiment, that the experiment is mathematically impossible, and Newton is correct.

In retrospect, knowing that Einstein's equations exist to explain reality, it's easy to say that Newton's formulas are wrong as applied to certain relativistic effects. But, if we place ourselves in time prior to Einstein, and conduct the Mchelson experiment, that would be the equivalent to what you are attempting to do with ev and evolution.

You have a formula that you think explains everything, and wherever it doesn't explain something observed in nature, you insist that what it does not explain is mathematically impossible.

Seek professional help, Alan.

[joobz]

You liar! You even calling me a liar on this point is a lie. Wow, that's like a russian doll of lies. Do you really think you are fooling anyone?
I am only trashing one theory, your dumb theory of evolution ...[snip incoherent rambling]It's not my theory. I haven't published any work in the area. It is the best working model to describe species. I'd be willing to entertain alternatives, if one existed that fit the data better. But what would you know of that.
Will it still be a lie when you bow out????
So you are now trying to obtain truth by attrition? I can easily get a lie detector bot to match your liar bot and let them duke it out. Funny thing is, that won't change reality.

[kleinman]

I don't "believe" in evolution. I review the observed evidence and conclude that evolution is the only sane possibility, because the alternative is a guy in a white robe and a beard blowing life into dust.
Oh, I understand, how many alternative universes have you observe? And how often have you observed the sun giving rise to life in the primordial soup? Kjkent1, it is all belief. Which belief can be shown is mathematically impossible?
Schneider's model shows how information gain from a random start occurs. It does not show how abiogenesis has culminated in homo sapiens.
Really? I love when you make posts like this, it gives me an opportunity of showing how Dr Schneider used the results from his model in his publication Ev Evolution of Biological Information.
Second, the probability of finding 16 sites averaging 4 bits each in random sequences is 2^(-4x16)~=5x10^-20 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 ~4x10^9 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.
Care to include diverse world wide population, sexual recombination and interspecies genetic transfers in ev and correct his estimate?
For you to extrapolate one from the other is, in my opinion, mentally disordered, because you are applying ev as the model for all observed evolutionary evidence that fits the ev model -- while excluding all observed evidence that does not fit.
Perhaps you should include panspermia in your observations or our beloved string cheese theory of evolution. Would you care for a bowl of primordial soup to go with your string cheese?
You may as well say that since Newton's equations don't fit with the observation of the Michelson-Morley experiment, that the experiment is mathematically impossible, and Newton is correct.
Ok, I’ll take some red herring with that string cheese. This is really a hearty meal.
In retrospect, knowing that Einstein's equations exist to explain reality, it's easy to say that Newton's formulas are wrong as applied to certain relativistic effects. But, if we place ourselves in time prior to Einstein, and conduct the Mchelson experiment, that would be the equivalent to what you are attempting to do with ev and evolution.
I knew that the Einstein’s equations were related to the theory of evolution. Recombination is the way you get relatives, relatively speaking.
You have a formula that you think explains everything, and wherever it doesn't explain something observed in nature, you insist that what it does not explain is mathematically impossible.
Dr Schneider’s computer doesn’t explain everything, it only explains the theory of evolution by random point mutations and natural selection is mathematically impossible. However, I believe if you combine the string cheese theory of evolution with Dr Schneider’s work, you would really have something. You have observed alternative universes, haven’t you?
Seek professional help, Alan.
Are there any plumbers out there? We have a bunch of evolutionists with blocked up pipes and we need professional help immediately.
You liar!You even calling me a liar on this point is a lie. Wow, that's like a russian doll of lies. Do you really think you are fooling anyone?
Don’t be silly, I don’t need to fool anyone. I have the results of an evolutionist written, peer reviewed and published model of random point mutation and natural selection and numerous real examples which show why the theory of evolution is mathematically impossible. I have no need to fool anyone, only to get you evolutionists to understand what this model says and what the real examples of the model show.
I am only trashing one theory, your dumb theory of evolution ...[snip incoherent rambling]It's not my theory. I haven't published any work in the area. It is the best working model to describe species. I'd be willing to entertain alternatives, if one existed that fit the data better. But what would you know of that.
I see, you prefer a mathematically impossible theory to no theory at all. That’s shows real scientific acumen.
Will it still be a lie when you bow out?So you are now trying to obtain truth by attrition? I can easily get a lie detector bot to match your liar bot and let them duke it out. Funny thing is, that won't change reality.
You evolutionists repeat your speculations over and over (usually stamping your foot while you are doing this) until you finally get tired. I’ll keep on repeating the results of ev calmly, and throw in real examples of what it is showing.

In the mean time, you evolutionists have a good weekend. And watch out for those directional selection pressures. Too many of them can kill you and if they don’t, they will really slow you down. If you can survive them, you may find yourself at a new optimum.

[joobz]

I’ll keep on repeating the results of ev calmly, and throw in real examples of what it is showing.

Oh so this is your version of "real examples". Continue to spout lies. They just pile up and up and up.
For clarity, I have summarized the key points of this conversation. I think we have a new lie here.

If you studied ev, you would understand this. If you examined the real cases of combination therapy for the treatment of HIV, combination therapy for the treatment of TB, combination pesticides, combination herbicides, combination rodenticides, you would see real examples of what ev demonstrates and what the fitness landscape requires. Mutation and selection can not and does not do what evolutionists allege, it is mathematically impossible.


It is the number of directional selection pressures and genome length which dominate the mathematics of mutation and selection. There is no reason to believe that frame shift mutations, translocations, duplications or any other way of scrambling a genome is going to change the underlying mathematics of mutation and selection.


This is your concrete basis for not worring about it?
I think this paper wouldn't have been accepted if that was the case:
Carvajal-Rodriguez A, Crandall KA, Posada D. "Recombination favors the evolution of drug resistance in HIV-1 during antiretroviral therapy." Infect Genet Evol. 2007 Feb 12; [Epub ahead of print]
I can't access the paper yet, but from the abstract:

Using computer simulations we show that the effect of recombination on the evolution of drug resistance depends strongly on the intensity of selection, as well as on the viral population size. Under the high selection pressure expected during antiretroviral therapy, the strength of the Hill-Robertson effect increases and recombination favors the evolution of resistance under a wide range of population sizes, independently of the sign of the epistatic interaction. Our results suggest that recombination plays an important role in the evolution of drug resistance in HIV-1 under various realistic scenarios

Seems like evolution has a mathematical basis after all.


So how does this work with HIV? Here is a quote from an article located at http://www.cdc.gov/ncidod/eid/vol3no3/burke.htm

Human immunodeficiency virus (HIV)-1, like all retroviruses, is "diploid." Each viral particle contains two RNA strands of positive polarity, each full length and potentially able to replicate (1). No other virus families, RNA or DNA, are diploid. Typically both RNA strands in a retroviral particle derive from the same parent provirus. However, if an infected cell simultaneously harbors two different proviruses, one RNA transcript from each provirus can be encapsidated into a single "heterozygous" virion. When this virion subsequently infects a new cell, the reverse transcriptase may jump back and forth between the two RNA templates so that the newly synthesized retroviral DNA sequence is recombinant between that of the two parents (2). All subsequent progeny virions will be of this recombinant genotype. HIV-1 strains with chimeric genomes thought to have arisen through homologous recombination have recently been discovered in nature (3).
This is a property unique to the retroviruses, are you trying to generalize this phenomenon to the entire theory of evolution? This appears like a baseless extrapolation.


Unfortunately, you've been using HIV viruses as proof of why evolution is impossible. I show a study where they demonstrate how multiple selection pressures won't HALT HIV evolution, and now you claim that I can't extrapolate this truth to anything else.


No it doesn’t, it only shows that you know how to make a baseless extrapolation.


I see, when evolutionists adjust their theory, this is scientific research, when I adjust my theory, I’m moving the goal posts.
This isn't an "adjustment of a theory". This is intellectual dishonesty.
We have been discussing how multiple pressures doesn't stop evolution using HIV as an example. I give evidence that states mathematically that this isn't the case. And now you claim that it doesn't apply.
This is the worst form of professional behavior.

[kleinman]

I was going to stop for the weekend but I happened to take a look at Dr Schneider’s ev blog page an note that he has spoken up about ev for the first time in months.

In case you evolutionists think that Dr Schneider has abandoned his ev model, he has not. The following was posted on his ev blog page earlier this month at http://www-lmmb.ncifcrf.gov/~toms/paper/ev/blog-ev.html (http://www-lmmb.ncifcrf.gov/~toms/paper/ev/blog-ev.html)
The key test [for Intellegent Design] is show me a process that generates information, and large amounts of specified information, without the guidance of an intelligent agent.

Ev does that.
I find this a bit of a strange statement since the basic premise for Intelligent Design is that it requires intelligence. However, I’m glad that Dr Schneider has not abandoned his model. I wonder if he will ever discuss publicly how much information is generated by his model of random point mutations and natural selection. Since I believe his model shows that information can be generated but at far more limited values than necessary to accomplish the huge genetic changes to evolve reptiles into bird or even humans and chimpanzees from a primate precursor. His model does properly capture the fact that multiple (directed) selection pressures slows down the acquisition of information by this process, especially with longer genomes.

[Taffer]

So I see you have gone on to simply ignoring my posts, kleinman. Is this because I actually know what I'm talking about, and you cannot lie your way through an argument with me?

ETA: Please note that I haven't forgotten all the unanswered questions you have simply ignored, kleinman. For example, where I used a certain word you accused me of misspelling. Or why you haven't commented on the three first search returns from your own search, and why they do not support your position.

[Dr Adequate]

I’m here to prove to you that the theory of evolution is mathematically impossible. Really?

When are you planning to start?

[Dr Adequate]

In case you evolutionists think that Dr Schneider has abandoned his ev model, he has not. Why on earth would we think that? The model is still, as it has always been, "a process that generates information, and large amounts of specified information, without the guidance of an intelligent agent". No-one has pointed out any flaws in this claim since he first produced it. Why, then, should he abandon it; or we suppose that he has?

You do come out with some nutty stuff.

I find this a bit of a strange statement ... Whereas I find it simple and lucid.

If you'll tell me which aspect of it you're too dumb to understand, I'll explain it in nice short words for you.

[Taffer]

1. What is the selection pressure that increases protease efficiency in an untreated patient?

Nothing. Selection pressures and blind, unguided and have no goal. There is selection against unfit traits, and that is all.

2. What is the selection pressure that increases protease efficiency in a treated patient?

Nothing. Selection pressures and blind, unguided and have no goal. There is selection against unfit traits, and that is all.

3. What is the selection pressure that increases reverse transcriptase efficiency in an untreated patient?

Nothing. Selection pressures and blind, unguided and have no goal. There is selection against unfit traits, and that is all.

4. What is the selection pressure that increases reverse transcriptase efficiency in an treated patient?

Nothing. Selection pressures and blind, unguided and have no goal. There is selection against unfit traits, and that is all.

5. What is the selection pressure that improves integration/replication in the host DNA?

Nothing. Selection pressures and blind, unguided and have no goal. There is selection against unfit traits, and that is all.

6. What is the selection pressure that causes mutations in the genome to interact with other mutations to improve overall fitness?

Nothing. Selection pressures and blind, unguided and have no goal. There is selection against unfit traits, and that is all.

Are there any stabilizing selection pressures acting on HIV and if so, how many are there? Are there neutral selection pressures acting on HIV and if so, how many are there?

There is only selection, kleinman. There is no such thing as "stabilizing selection pressures", only selection against unfit traits. There is no such thing as "neutral selection pressures", only selection against unfit traits. What we call "stabilizing selection" (note the lack of the word "pressures") is the situation wherein all available variants of a sequence are less fit then the most common allele. What we call "disruptive selection" is the situation wherein the alleles which are the two rarest are the least unfit, and thus increase in frequency over time. What we call "directional selection" is the situation wherein one rare allele is less unfit the all others, and thus increases in frequency over time. Please note that in all these situations, selection works exactly the same. All selection ever does is cause the less unfit organisms to contribute fewer genes to the next generation. All selection ever does is select "against" those who are unfit.

[Dr Adequate]

Oh, I understand, how many alternative universes have you observe? And how often have you observed the sun giving rise to life in the primordial soup? Kjkent1, it is all belief. Which belief can be shown is mathematically impossible?

Really? I love when you make posts like this, it gives me an opportunity of showing how Dr Schneider used the results from his model in his publication Ev Evolution of Biological Information.

Care to include diverse world wide population, sexual recombination and interspecies genetic transfers in ev and correct his estimate?

Perhaps you should include panspermia in your observations or our beloved string cheese theory of evolution. Would you care for a bowl of primordial soup to go with your string cheese?

Ok, I’ll take some red herring with that string cheese. This is really a hearty meal.

I knew that the Einstein’s equations were related to the theory of evolution. Recombination is the way you get relatives, relatively speaking.

Dr Schneider’s computer doesn’t explain everything, it only explains the theory of evolution by random point mutations and natural selection is mathematically impossible. However, I believe if you combine the string cheese theory of evolution with Dr Schneider’s work, you would really have something. You have observed alternative universes, haven’t you?

Are there any plumbers out there? We have a bunch of evolutionists with blocked up pipes and we need professional help immediately.

Don’t be silly, I don’t need to fool anyone. I have the results of an evolutionist written, peer reviewed and published model of random point mutation and natural selection and numerous real examples which show why the theory of evolution is mathematically impossible. I have no need to fool anyone, only to get you evolutionists to understand what this model says and what the real examples of the model show.

I see, you prefer a mathematically impossible theory to no theory at all. That’s shows real scientific acumen.

You evolutionists repeat your speculations over and over (usually stamping your foot while you are doing this) until you finally get tired. I’ll keep on repeating the results of ev calmly, and throw in real examples of what it is showing.

In the mean time, you evolutionists have a good weekend. And watch out for those directional selection pressures. Too many of them can kill you and if they don’t, they will really slow you down. If you can survive them, you may find yourself at a new optimum. So ... same old lies ... check ... same old ravings ... check ... same old magic words ... check.

No sign of any math.

Situation nominal.

[Dr Adequate]

Really? I love when you make posts like this, it gives me an opportunity of showing how Dr Schneider used the results from his model in his publication Ev Evolution of Biological Information. What do you find so loveable about a quote which shows you up as a liar and a fool?

Let me guess --- the fact that you didn't understand a word of it. Am I right?

It's the Lie #5 fiasco all over again, isn't it?

[joobz]

So ... same old lies ... check ... same old ravings ... check ... same old magic words ... check.

No sign of any math.

Situation nominal.
I don't know. I thought the change from
"HIV is proof evolution is impossible" to
"HIV is not representative of evolution"
was a very humorous transition.

[Mr. Scott]

There is no reason to believe that frame shift mutations, translocations, duplications or any other way of scrambling a genome is going to change the underlying mathematics of mutation and selection.

Dr. Adequate, I really like this one. Can we assign it a lie number?

[Skeptic Ginger]

I keep telling you red herring man that I’m here to prove to you that the theory of evolution is mathematically impossible. ...Mathematically, how did all the animals today evolve from the minuscule number that could have fit on Noah's Arc?

The Enclopedia of Life Project (http://www.ngbw.org/eol/index.html) expects to catalogue 1.8 million known species of living things on Earth and the actual number is estimated to be 10 million. (I also saw a new estimate that on the sea floor alone there are probably another 10 million unknown species but we'll let you slide on that since those life forms wouldn't have necessarily died in the big flood, ignoring the salt water/fresh water issues as well of course.)

So can you have it both ways? Not enough time for evolution in 3.5 billion years but enough in the last 6,000 to evolve from the Ark survivors?

.....Use your imagination and you can probably figure a way opossum can migrate. You know how good your evolutionist imagination is. Perhaps they evolved wings traveled to South America and then devolved their wings once they arrived......Did you miss the plate tectonics lectures in school too?

[Dr Adequate]

Dr. Adequate, I really like this one. Can we assign it a lie number? Yes, I think this would be Lie #8.

Lie #8: in simulating evolution, it's only necessary to simulate selection and point mutation, everything else is irrelevant. Hence ev is a good model of the whole evolutionary process.

Truth #8: It should be obvious even to a dork like kleinman that evolutionary history cannot be explained exclusively by mutations which conserve the length of the genome. Moreover, the idea that the processes modelled by ev are all that matters has been rejected by the creators of ev; by Dr Schneider ---

[L]arge environmentally diverse worldwide populations, sexual recombination and interspecies genetic transfer ... are undoubtedly important in accounting for human evolution.

--- and by Paul C. Anagnostopoulos (see this thread, passim).

[Dr Adequate]

Did you miss the plate tectonics lectures in school too? The movement of continents which we observe is just micromovement. There's no way that lots of micromovement can add up to macromovement, as you silly amathematical tectonicists claim. I can prove this mathematically, using a method whereby I never do any actual math or calculations but shout about cheese a lot instead. We call it "kleinmath".

[kjkent1]

Dr Schneider’s computer doesn’t explain everything, it only explains the theory of evolution by random point mutations and natural selection is mathematically impossible.If this is your position, then no one in this thread would disagree with you.

Evolution, from abiogenesis to present day life form diversity, solely by random point mutation and ev's version of selection, is very likely impossible.

But, to repeat again, that's not what Schneider's paper intended to prove. The paper shows info gain from a random start using point mutation and natural selection. So there's really no argument. And now you can go away.However, I believe if you combine the string cheese theory of evolution with Dr Schneider’s work, you would really have something. You have observed alternative universes, haven’t you?
Of course I have. Haven't you? When you close your eyes and pray to Jesus, are you not communicating with an alternate universe?

You certainly aren't communicating with anyone in this universe, because if you were, then God would be mortal.

Here's a new question for ya, little Alan: suppose you were able to convince the entire scientific community that evolution is mathematically impossble. What scientific theory would you substitute to explain all the observed evidence?

[Dr Adequate]

I don't know. I thought the change from
"HIV is proof evolution is impossible" to
"HIV is not representative of evolution"
was a very humorous transition. Ooh, yes!

* claps hands *

And look at the reason he gives.

It undergoes recombination!

:dl:

Apparently that makes a b-i-i-i-g difference ...

Did you get that folks?

(1) We're not allowed to claim that recombination makes evolution more powerful in diploid species (like dinosaurs and birds, or apes and humans) because point mutation and selection are all that matters. 'Cos Kleinman said so and then shouted about cheese a lot, so it must be true.

(2) We're not allowed to use HIV as a model for how evolution works because it's diploid (like dinosaurs and birds, or apes and humans) and undergoes recombination, which makes evolution more powerful. 'Cos kleinman says so, and behold his word is as law, possibly the one about not shaving thy camels on the Sabbath, and lo, righteousness shineth forth from his holy sphincter.

[Skeptic Ginger]

The movement of continents which we observe is just micromovement. There's no way that lots of micromovement can add up to macromovement, as you silly amathematical tectonicists claim. I can prove this mathematically, using a method whereby I never do any actual math or calculations but shout about cheese a lot instead. We call it "kleinmath".

:D

[Paul C. Anagnostopoulos]

The movement of continents which we observe is just micromovement. There's no way that lots of micromovement can add up to macromovement, as you silly amathematical tectonicists claim. I can prove this mathematically, using a method whereby I never do any actual math or calculations but shout about cheese a lot instead. We call it "kleinmath".
I believe the cheese thing is restricted to evolution. If we begin to discuss plate tectonics, the thing will be pizza, not just cheese. Or possibly tacos.

~~ Paul

[kleinman]

So I see you have gone on to simply ignoring my posts, kleinman. Is this because I actually know what I'm talking about, and you cannot lie your way through an argument with me?

ETA: Please note that I haven't forgotten all the unanswered questions you have simply ignored, kleinman. For example, where I used a certain word you accused me of misspelling. Or why you haven't commented on the three first search returns from your own search, and why they do not support your position.
I’m not ignoring any of you questions. I’m still waiting for you to explain how recombination creates new genes. So far, all you speculated is that duplicated genes acted on by mutation and selection creates new genes. I’m waiting for you to explain how recombination alone can make new genes.
There is no reason to believe that frame shift mutations, translocations, duplications or any other way of scrambling a genome is going to change the underlying mathematics of mutation and selection.Dr. Adequate, I really like this one. Can we assign it a lie number?
Only a pussycat who has been at the cat nip too much is going to believe that these other mutation mechanisms are going to change the underlying mathematics of mutation and selection.
I keep telling you red herring man that I’m here to prove to you that the theory of evolution is mathematically impossible. ...Mathematically, how did all the animals today evolve from the minuscule number that could have fit on Noah's Arc?
I’ll tell you what red herring girl. Once you evolutionists understand and accept what the mathematics of mutation and selection, you can start a new thread on this question and we can discuss this.
.....Use your imagination and you can probably figure a way opossum can migrate. You know how good your evolutionist imagination is. Perhaps they evolved wings traveled to South America and then devolved their wings once they arrived......Did you miss the plate tectonics lectures in school too?
There you go kjkent1.
Dr Schneider’s computer doesn’t explain everything, it only explains the theory of evolution by random point mutations and natural selection is mathematically impossible.If this is your position, then no one in this thread would disagree with you.
Really, evolutionists agree the theory of evolution by random point mutations and natural selection is mathematically impossible?
Evolution, from abiogenesis to present day life form diversity, solely by random point mutation and ev's version of selection, is very likely impossible.
I have never heard this statement in any course or read it any textbook on evolution. Tell us, which mechanism of mutation will improve the mathematical possibility of the theory of evolution the most? And what version of selection will change the probabilities for the theory? Unnamed is not defending his selection process.
But, to repeat again, that's not what Schneider's paper intended to prove. The paper shows info gain from a random start using point mutation and natural selection. So there's really no argument. And now you can go away.
Dr Schneider’s published statements are not in agreement with what you are saying here, would you like me to post them again here? I’ll go away when the theory of evolution goes away.
However, I believe if you combine the string cheese theory of evolution with Dr Schneider’s work, you would really have something. You have observed alternative universes, haven’t you?Of course I have. Haven't you? When you close your eyes and pray to Jesus, are you not communicating with an alternate universe?
Of course not, I am praying to the Creator of everything.
Here's a new question for ya, little Alan: suppose you were able to convince the entire scientific community that evolution is mathematically impossble. What scientific theory would you substitute to explain all the observed evidence?
This is a new question for me? Not, little gator.
The movement of continents which we observe is just micromovement. There's no way that lots of micromovement can add up to macromovement, as you silly amathematical tectonicists claim. I can prove this mathematically, using a method whereby I never do any actual math or calculations but shout about cheese a lot instead. We call it "kleinmath".I believe the cheese thing is restricted to evolution. If we begin to discuss plate tectonics, the thing will be pizza, not just cheese. Or possibly tacos.
It’s nice to see that Adebz has posted a gif again. His gif and awe strategy in this discussion is so effective---at boring everyone to death. It’s nice to know that Adebz now finally understands how population affects the probabilities in the mutation and selection mathematics. I wonder if Adebz will tell us what the error in the equation of Dr Richard’s reference is or whether Dr Richard will find it.

So, Dr Schneider has spoken up on his web site for the first time in months about his ev model.
The key test [for Intellegent Design] is show me a process that generates information, and large amounts of specified information, without the guidance of an intelligent agent.

Ev does that.
Does Dr Schneider believe that ev shows that random point mutations and natural selection can generate large enough amounts of specified information to make the theory of evolution mathematically possible? Dr Schneider does not offer an explanation why the rate of information gain becomes profoundly slow in his model when realistic length genomes are used. I wonder if Dr Schneider will discuss what a parametric of ev shows? Perhaps he will try to defend Paul’s Rcapacity concept.

[Taffer]

I’m not ignoring any of you questions. I’m still waiting for you to explain how recombination creates new genes. So far, all you speculated is that duplicated genes acted on by mutation and selection creates new genes. I’m waiting for you to explain how recombination alone can make new genes.

Mate, I never said it did. I have no idea where you get the thought that I ever claimed that recombination alone can make new genes.

I'm still waiting for responses to at least 2 posts.

[kleinman]

I’m not ignoring any of you questions. I’m still waiting for you to explain how recombination creates new genes. So far, all you speculated is that duplicated genes acted on by mutation and selection creates new genes. I’m waiting for you to explain how recombination alone can make new genes.Mate, I never said it did. I have no idea where you get the thought that I ever claimed that recombination alone can make new genes.
Is that an admission that recombination alone does not and can not create new genes? We are talking about mathematical precision in this discussion of mutation and selection, not the sloppy speculations that you evolutionists use to explain your theory.

Once you accept this point, then we can go on to your next misunderstanding of recombination and natural selection. That is that recombination and natural selection can cause the loss of alleles from the gene pool and thus the loss of information from the gene pool.

[tojohndillonesq]

Not disagreeing with anything stated here. In fact, you will find that many creationists do not disagree with anything you have said here.

Any valid argument requires a high degree of specificity. Creationists fall into a number of quite disparate groups:

1) Young Earth Creationists who believe the Earth is less than ~20,000 years old.
2) Old Earth Creationists who do not dispute the evidence that the Earth is over three billion and the universe is over 30 billion years old, but believe that some aspects of Creation were "miraculous" in the sense that they occured outside all known laws of physics and outside any possible scientific explanation.
3) Creationists who do not dispute ANY of the scientific evidence about the origins of life, evolution, the age of the universe, etc.

Note that the third group encompasses virtually all Hindus and Buddhists, as well as a number of Christians. Hence is it by far the largest of the three segments. To lump the three groups together is inaccurate.

The group you are really attacking, and rightly so, is the Young Earth Creationists. The ones who deny the evidence of evolution, carbon dating, the time it took light to reach us from stars more than 20K light years away, etc. I propose a set of labels.

Group 1 is YEC. No sense of scienctific process or evidentiary procedure.
Group 2 is OEC. Want to believe in the unexplainable.
Group 3 is Deists. Believe in a God who originated the whole thing, and believe that saying evolution led to man is like saying "rain falls from clouds."

Hostility is, of course, a sign of fear. The hostility to science shown by YEC and OEC is caused by their fear of losing their faith in God. They shout about their faith to drown their own doubts.

When a scientist is hostile to YEC or OEC, it is like being hostile to a child who believes in Santa. It is not only illogical, but unproductive and unkind. the truly intelligent person is bigger than that. Attaching negative emotions to ideas or facts is... a flawed mental process.

The last thing I would like to point out is that to hate God is to believe in Him. You can hate what the idea of God has done to the world - the ignorance and violence it has caused - but in that case you must also take into account the good things as well. Just as with science. Bombs and penicillin Yin and Yang.

Sometimes these annoying creationists just piss me off:

http://www.evolutionisdead.com/forum/viewtopic.php?p=11670&sid=3406e76df02b7fb9f60af262a63c3a63#11670

~~ Paul

[Paul C. Anagnostopoulos]

Is that an admission that recombination alone does not and can not create new genes?
Do you know for a fact that the portions of DNA that make up one gene cannot end up being recombined?

~~ Paul

[kleinman]

Hostility is, of course, a sign of fear. The hostility to science shown by YEC and OEC is caused by their fear of losing their faith in God. They shout about their faith to drown their own doubts.
Let’s see, kjkent1 thinks I’m doing this thread to build my self esteem, now we have tojohndillionesq who thinks I’m hostile to the theory of evolution out of fear. How about this alternative, the theory of evolution by mutation and selection is bad science that is mathematically impossible based on the results of an evolutionist written and peer reviewed computer model of random point mutation and natural selection. The reason why it is mathematically impossible is that multiple selection pressures slow the evolutionary process. This mathematical result is demonstrated by numerous real examples of this phenomenon.

Now tojohndillionesq, you appear hostile to the mathematics of mutation and selection and the numerous real examples of this mathematics. Is this because you are frightened of losing your faith in the theory of evolution?

[kleinman]

Is that an admission that recombination alone does not and can not create new genes? Do you know for a fact that the portions of DNA that make up one gene cannot end up being recombined?
You can have errors in the recombination process that can make new sequences of bases. Are you proposing this as the mutation mechanism that will solve the deficiencies which ev reveals for the theory of evolution?

[Paul C. Anagnostopoulos]

You can have errors in the recombination process that can make new sequences of bases. Are you proposing this as the mutation mechanism that will solve the deficiencies which ev reveals for the theory of evolution?
You didn't answer my question: Do you know for a fact that the portions of DNA that make up one gene cannot end up being recombined?

~~ Paul

[Dr Adequate]

How about this alternative, the theory of evolution by mutation and selection is bad science that is mathematically impossible based on the results of an evolutionist written and peer reviewed computer model of random point mutation and natural selection. The reason why it is mathematically impossible is that multiple selection pressures slow the evolutionary process. This mathematical result is demonstrated by numerous real examples of this phenomenon. Well, we know that "alternative" to be a load of bulldung. We need a plausible hypothesis as to why you lie so much.

Now tojohndillionesq, you appear hostile to the mathematics of mutation and selection and the numerous real examples of this mathematics. You're wrong. He's actually hostile to people who bleat out stupid lies on this subject.

I'd try to explain to you what's wrong with lying, but I fear it would be like trying to describe color to a blind man.

[Dr Adequate]

Only a pussycat who has been at the cat nip too much is going to believe that these other mutation mechanisms are going to change the underlying mathematics of mutation and selection. Then why did you make such a big deal out of HIV recombining, you stupid two-faced liar?

Once you evolutionists understand and accept what the mathematics of mutation and selection, you can start a new thread on this question and we can discuss this. Cool. I'll start the thread and see if you're lying about this too.

Here you go. Kleinman's Noah's Ark Rubbish (http://forums.randi.org/showthread.php?t=82190) --- for all your lying-about-imaginary-magic-boats needs.

Really, evolutionists agree the theory of evolution by random point mutations and natural selection is mathematically impossible? Yes, and we agree that the inventor of this "theory", one Dr Alan Kleinman --- perhaps you've heard of him --- is a lying halfwit.

I have never heard this statement in any course or read it any textbook on evolution. Perhaps you should read one.

It’s nice to know that Adebz now finally understands how population affects the probabilities in the mutation and selection mathematics. "Finally"? You stupid lying twat, I have been explaining the effect of population size to you ever since you started lying about it.

If you finally agree that I'm right, cheers. But I doubt it. To realise that I'm right, you'd have to know at least as much probability theory as most teenagers manage to understand in high school.

I wonder if Adebz will tell us what the error in the equation of Dr Richard’s reference is or whether Dr Richard will find it. Dr Richard has given several references containing several equations.

In one of them, I suspect that a typesetter has dropped a subscript. Well, that's biology finished then.

---

Hey, remember last time you thought you'd found an error in a peer-reviewed paper?

And you'd dropped a zero from the length of the human genome and forgotten that it was diploid?

That was funny.

Does Dr Schneider believe that ev shows that random point mutations and natural selection can generate large enough amounts of specified information to make the theory of evolution mathematically possible? He says explicitly that his model does not include various important factors and processes, as you would know if you stopped screaming stupid lies about what he wrote and actually read it.

[kleinman]

You can have errors in the recombination process that can make new sequences of bases. Are you proposing this as the mutation mechanism that will solve the deficiencies which ev reveals for the theory of evolution?You didn't answer my question: Do you know for a fact that the portions of DNA that make up one gene cannot end up being recombined?
Transposition and recombination of genes or parts of genes is done all the time in immunocytes for the production of antibodies. This is a very active and precise process. Do you think this process occurs in meiosis or the recombination that is associated with HIV or other creatures? Do you have any examples where this type of recombination occurs in the reproductive process? Do you think this is the mutation mechanism that will solve the deficiencies which ev reveals for the theory of evolution?

[tojohndillonesq]

Lets be clear about what we mean by "hostile." I meant to imply anger and hatred. The OED says ("unfriendly" or "enemy.") What I meant to say was that an angry or hateful opposition is quite different from logical opposition.

When you question the intelligence or honesty of the opposing side, it is an inherently hostile and illogical argument. The only possible logical response to that is to say: "What you say about me may be true, but you have not addressed the merits of my argument."

I regret that you think I am hostile to your mathematics. I am not sure what I wrote to cause that... I don't see where I wrote any angry or insulting comments. Just as importantly, I don't see where you thought I disagreed with you?! I have a CS degree with a minor in math and I am not remotely qualifed to comment decisively on those things; few people are.

I would further point out that those in my third segment, the Deists, do not reject arguments of mathematics. Reviewing my posting I see that I was not as clear as I could have been on that point. Deists do not reject scientific evidence from either side. leaving that to the experts. (Which, if you do not have a Doctorate and numerous articles published on the subject, you probably are not. I find Behe to be a highly credible source, whether I agree with him or not.)

I firmly believe that science can and will explain everything. If evolution is disproven, it will be disproven through scientific evidence such as you present. It will be highly interesting to me, but not salient to the question of God.

"No one ever had his mind changed by being insulted."
--- A. Scott Walker

If I ... know all mysteries and all knowledge ... but do not have love, I am nothing.
--- Paul

[joobz]

If evolution is disproven, it will be disproven through scientific evidence such as you present.
Here is where you are slightly mistaken. Kleinman has yet to offer anything that remotely approaches a notion that could even begin to be considered an inkling of a scientific argument.
I refer you to the kleinman FAQ (http://forums.randi.org/showpost.php?p=2533858&postcount=3669), to his moving of goalposts (http://forums.randi.org/showpost.php?p=2588328&postcount=4041), and to his overall lack of intellectual honesty (http://forums.randi.org/showpost.php?p=2591274&postcount=4079).

[kleinman]

When you question the intelligence or honesty of the opposing side, it is an inherently hostile and illogical argument. The only possible logical response to that is to say: "What you say about me may be true, but you have not addressed the merits of my argument."
Why don’t you do a simple count of how many times the word liar (or forms of the word) has been used in this thread and who has used it and report that result back to us.
I firmly believe that science can and will explain everything. If evolution is disproven, it will be disproven through scientific evidence such as you present. It will be highly interesting to me, but not salient to the question of God.
Really, science will explain everything? Science has come up with the theory of evolution by mutation and selection but the basic premise of the theory does not obey simple bookkeeping rules.
If evolution is disproven, it will be disproven through scientific evidence such as you present.Here is where you are slightly mistaken. Kleinman has yet to offer anything that remotely approaches a notion that could even begin to be considered an inkling of a scientific argument.
I refer you to the kleinman FAQ, to his moving of goalposts, and to his overall lack of intellectual honesty.
Tojohndillionesq, when you do your count for the word liar, don’t forget to include terminology like “lack of intellectual honesty”. What I would say about joobz is that he is either ignorant or in denial of the mathematics of mutation and natural selection and the numerous real examples of this mathematics that I have presented.

[joobz]

Why don’t you do a simple count of how many times the word liar (or forms of the word) has been used in this thread and who has used it and report that result back to us.

Really, science will explain everything? Science has come up with the theory of evolution by mutation and selection but the basic premise of the theory does not obey simple bookkeeping rules.

Tojohndillionesq, when you do your count for the word liar, don’t forget to include terminology like “lack of intellectual honesty”. What I would say about joobz is that he is either ignorant or in denial of the mathematics of mutation and natural selection and the numerous real examples of this mathematics that I have presented.
If you don't want to be called a liar, then don't lie.

[Dr Adequate]

When you question the intelligence or honesty of the opposing side, it is an inherently hostile and illogical argument. There is nothing "illogical" about pointing out that a stupid liar is a stupid liar.

As for "hostile", yes, certainly. I am hostile towards stupid liars.

The only possible logical response to that is to say: "What you say about me may be true, but you have not addressed the merits of my argument." But if kleinman said that it would not be true. We've made mincemeat of his "argument", such as it was. And much of his "argument" consists of telling stupid lies, a fact hard to convey without at least hinting that he's a stupid liar.

[kleinman]

Here are some more references that show that multiple selection pressures slow the evolution of resistance to those selection pressures.

The first example is from a paper on the treatment of Malaria that can be located at: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1796884 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1796884)

The half-lives of the single drugs amodiaquine (7–21 days[18]) and mefloquine (14–21 days[19]) are in the range of the sensitivity analysis shown in Figure 2d, which shows their expected results are similar to those of sulfadoxine-pyrimethamine (bearing in mind the assumption that the same drug is used for IPT as for non-IPT therapy). However, when mutations in multiple unlinked genes are needed for resistance, breakdown of their association by recombination will undermine the impact of selection on the spread of resistance.

The following is another reference to combination therapy for HIV located at: http://www.medscape.com/viewarticle/494361_3 (http://www.medscape.com/viewarticle/494361_3)
There may be several reasons for the favored emergence of L74V after M184V during selection by abacavir: the extent of resistance conferred may be greater (hence selection favors it), the mutation may be more prevalent in quasispecies at baseline, or this mutation pair may have greater fitness than M184V plus K65R (or M184 plus Y115F). Coadministration of abacavir with a thymidine analogue prevents or dramatically reduces the frequency with which L74V, K65R, and Y115F are observed.[21]

The following is from a paper that addresses drug therapy for malaria in rodents and multiple selection pressures and is located at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12803854&dopt=Abstract (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12803854&dopt=Abstract)
The influence of combinations containing the blood schizontocides chloroquine (CQ) or mefloquine (MEF), together with the 8-aminoquinolines (8AQ) primaquine (PQ) or the new, long-acting compound, tafenoquine (TAF), on the rate of selection of resistance to the individual compounds was examined using the asexual, intra-erythrocytic stages in rodent malaria models.
and
It is concluded that, whereas use of an 8AQ alone carries a high risk of selecting resistance, combinations containing 8AQ may have a place in the protection of blood schizontocides that are to be deployed in endemic areas.

Here is another paper that reference malaria treatment in humans and is located at: http://www.rff.org/rff/Documents/RFF-Resources-160-malaria.pdf (http://www.rff.org/rff/Documents/RFF-Resources-160-malaria.pdf)
The hope is that combined drug therapies can be implemented more widely in affected areas. Like the AIDS “cocktail” that has transformed that illness from an automatic death sentence to something that can be aggressively managed, at least in industrialized countries, the new malaria combination therapies are believed to be more effective at delaying the emergence of resistance when compared to single drugs used as stand-alone treatments, which are rapidly losing their effectiveness.
Here is another article that addresses combination selection pressures and the evolution of resistance in weeds and is located at: http://www.plantprotection.org/hrac/Bindex.cfm?doc=Partnership.html (http://www.plantprotection.org/hrac/Bindex.cfm?doc=Partnership.html)
Mixtures or sequences of herbicides with differing modes of action are important especially to prevent or overcome resistance based on target site differences. To be effective the herbicides used in mixtures or sequences must have similar efficacy against the target weed. If the resistance is based on enhanced metabolism, this technique may also be useful, as the metabolic processes may be specific to certain types of molecule, but an empirical approach is needed to determine the best herbicide combinations.
The following is a reference which discusses multiple selection pressures exhibited by a single drug on e coli. This article is interesting because it shows an example of a single selection pressure which when intensified acts like multiple selection pressures. This article is located at http://jac.oxfordjournals.org/cgi/content/full/49/6/925 (http://jac.oxfordjournals.org/cgi/content/full/49/6/925)
In E. coli, fluoroquinolones, including ciprofloxacin, primarily inhibit DNA gyrase (GyrA) with topoisomerase IV (ParC) as a secondary target.19 Single-site mutations at codon 83 or 87 of the gyrA QRDR are sufficient to confer low-level ciprofloxacin resistance, whereas higher levels of resistance either require double (codons 83 and 87) mutations in gyrA, or gyrA mutations in combination with parC or marA mutations, the latter enhancing drug efflux via the AcrAB–TolC system and reducing influx by suppressing expression of the outer membrane protein OmpF.20,21 Thus, at low concentrations ciprofloxacin has a high endogenous resistance potential, but at higher selective concentrations there is a requirement to generate simultaneous mutations in two or more loci4 and the agent consequently displays low endogenous resistance potential.

Multiple selection pressures slow evolution. This is what ev shows, this is what the Wikipedia reference to fitness landscape shows and this is what these real examples show. Do you evolutionists have any mathematical model or real examples that contradict this hypothesis? Otherwise, the evidence continues to pile up that the theory of evolution is mathematically impossible.

[joobz]

You understand that your plastic definition of SLOW and MULTIPLE are trite. All the references that you present say is that EVEN WITH multiple selection pressures, EVOLUTION STILL HAPPENS. ADAPTATION STILL HAPPENS. Please show more data of this kind, It just proves this point. And all of this in a timescale observable for a lab experiment.

You need to show that evolution will STOP with multiple selection pressures, and YOU need to show that this is the case for millions of years.

Sorry Kleinman, I know you thought you'd get away with bending definitions between slow and stop and few to multiple (which you still seem to not want to assign a real number to).


But again, thank you for presenting work that supports reality.

[Paul C. Anagnostopoulos]

Transposition and recombination of genes or parts of genes is done all the time in immunocytes for the production of antibodies. This is a very active and precise process. Do you think this process occurs in meiosis or the recombination that is associated with HIV or other creatures? Do you have any examples where this type of recombination occurs in the reproductive process? Do you think this is the mutation mechanism that will solve the deficiencies which ev reveals for the theory of evolution?
Yes, those are the questions I asked you. Could you answer them?

~~ Paul

[Paul C. Anagnostopoulos]

Let's see what we can find ...

Recombinant allele composed of gene and pseudogene:

http://www.springerlink.com/content/2gqnd5bcgwaw0tqf/

Complex alleles from unequal crossover:

http://www.clinchem.org/cgi/content/full/51/11/2167


and, oh my, Gaucher disease:

http://www.journals.uchicago.edu/AJHG/journal/issues/v72n3/024533/024533.web.pdf

Oh look, and Fabry disease, too:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=2539398&query_hl=9&itool=pubmed_DocSum

And:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=AbstractPlus&list_uids=3195594&query_hl=9&itool=pubmed_DocSum

~~ Paul

[kleinman]

You understand that your plastic definition of SLOW and MULTIPLE are trite. All the references that you present say is that EVEN WITH multiple selection pressures, EVOLUTION STILL HAPPENS. ADAPTATION STILL HAPPENS. Please show more data of this kind, It just proves this point. And all of this in a timescale observable for a lab experiment.
What’s the matter? All these examples are experiments that are done on observable timescales. They all demonstrate that single selection pressures evolve more rapidly than multiple selection pressures and that multiple selection pressures is the strategy to stop evolution of resistant strains of bacteria, parasites, pests, weeds, pests… If multiple selection pressures can not stop evolution, why do all theses scientists advocate its usage? So what is the selection pressure that evolves reptiles into birds or humans and chimpanzees from a primate precursor? You are still ignorant of or in denial of the mathematics of mutation and selection, perhaps both. You should study ev a little, you can get some education on this topic.
Transposition and recombination of genes or parts of genes is done all the time in immunocytes for the production of antibodies. This is a very active and precise process. Do you think this process occurs in meiosis or the recombination that is associated with HIV or other creatures? Do you have any examples where this type of recombination occurs in the reproductive process? Do you think this is the mutation mechanism that will solve the deficiencies which ev reveals for the theory of evolution?Yes, those are the questions I asked you. Could you answer them?
The recombination that occurs with production of antibodies occurs in somatic cells, not in gametes. If you think this is the mechanism which will counter the hypothesis that multiple selection pressures slow the evolutionary process, describe how this works explicitly and quote from your links to support your argument. The ultimate way of showing this would be to include this feature in ev and accelerate the profoundly slow acquisition of information on realistic length genomes. I do think that a mechanism of gene rearrangement that in half your links cause life threatening diseases doesn’t make for a very strong speculation for how the theory of evolution works, but if you can make a plausible explanation of how it works, I’m willing to listen.

[Dr Adequate]

Here are some more references that show that multiple selection pressures slow the evolution of resistance to those selection pressures.

The first example is from a paper on the treatment of Malaria that can be located at: http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1796884 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1796884)



The following is another reference to combination therapy for HIV located at: http://www.medscape.com/viewarticle/494361_3 (http://www.medscape.com/viewarticle/494361_3)


The following is from a paper that addresses drug therapy for malaria in rodents and multiple selection pressures and is located at: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12803854&dopt=Abstract (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12803854&dopt=Abstract)

and


Here is another paper that reference malaria treatment in humans and is located at: http://www.rff.org/rff/Documents/RFF-Resources-160-malaria.pdf (http://www.rff.org/rff/Documents/RFF-Resources-160-malaria.pdf)

Here is another article that addresses combination selection pressures and the evolution of resistance in weeds and is located at: http://www.plantprotection.org/hrac/Bindex.cfm?doc=Partnership.html (http://www.plantprotection.org/hrac/Bindex.cfm?doc=Partnership.html)

The following is a reference which discusses multiple selection pressures exhibited by a single drug on e coli. This article is interesting because it shows an example of a single selection pressure which when intensified acts like multiple selection pressures. This article is located at http://jac.oxfordjournals.org/cgi/content/full/49/6/925 (http://jac.oxfordjournals.org/cgi/content/full/49/6/925)


Multiple selection pressures slow evolution. This is what ev shows, this is what the Wikipedia reference to fitness landscape shows and this is what these real examples show. Do you evolutionists have any mathematical model or real examples that contradict this hypothesis? Otherwise, the evidence continues to pile up that the theory of evolution is mathematically impossible. So, you're still trying to prop up lies you can't justify by citing random paragraphs from articles you don't understand?

[kleinman]

So, you're still trying to prop up lies you can't justify by citing random paragraphs from articles you don't understand?
Oh don’t be silly Adebz; it is random paragraphs and natural selection.

[Dr Adequate]

If multiple selection pressures can not stop evolution, why do all theses scientists advocate its usage? Because reducing population size reduces the rate of evolution, as you've had explained to you half-a-dozen times, you stupid twat.

But "multiple selection pressures" in general do not "stop" evolution, what is why you can't quote a single one of these scientists saying so.

'Cos they're not retarded liars, you see.

[Dr Adequate]

Oh don’t be silly Adebz; it is random paragraphs and natural selection. I suppose posting this gibberish was easier than finding an article which supports your lies in any way.

[joobz]

What’s the matter? Your lies.

All these examples are experiments that are done on observable timescales.
yup

They all demonstrate that single selection pressures evolve more rapidly than multiple selection pressures and that multiple selection pressures is the strategy to stop evolution of resistant strains of bacteria, parasites, pests, weeds, pests… No, they don't show this. They show simply that the can reduce the likelyhood of adaptation, this doesn't mean stop. I know in your head, you think it does, but that has no bearing on reality.


If multiple selection pressures can not stop evolution, why do all theses scientists advocate its usage?
Because they try to stave off resistance. Is that a hard concept to understand for you?

So what is the selection pressure that evolves reptiles into birds or humans and chimpanzees from a primate precursor? You honestly think this is a valid argument? What's the exact mechanism of gravity?
We know it happened, the how is still not known (as far as I understand).
http://www.talkorigins.org/faqs/comdesc/section1.html#morphological_intermediates_ex1 (http://www.talkorigins.org/faqs/comdesc/section1.html#morphological_intermediates_ex1)


You are still ignorant of or in denial of the mathematics of mutation and selection, perhaps both. You should study ev a little, you can get some education on this topic.
Yawn.

[kleinman]

If multiple selection pressures can not stop evolution, why do all theses scientists advocate its usage?Because they try to stave off resistance. Is that a hard concept to understand for you?
Of course it is not hard for me to understand, it is the entire premise of my argument. Multiple selection pressures stave off the ability of creatures to evolve resistance to those selection pressures. Understand rubberband?

[joobz]

Of course it is not hard for me to understand, it is the entire premise of my argument. Multiple selection pressures stave off the ability of creatures to evolve resistance to those selection pressures. Understand rubberband?
Oh thank you for the rubberband comment. I thought I had already addressed this point.
You understand that your plastic definition of SLOW and MULTIPLE are trite. All the references that you present say is that EVEN WITH multiple selection pressures, EVOLUTION STILL HAPPENS. ADAPTATION STILL HAPPENS. Please show more data of this kind, It just proves this point. And all of this in a timescale observable for a lab experiment.

You need to show that evolution will STOP with multiple selection pressures, and YOU need to show that this is the case for millions of years.

Sorry Kleinman, I know you thought you'd get away with bending definitions between slow and stop and few to multiple (which you still seem to not want to assign a real number to).


But again, thank you for presenting work that supports reality.
Yup, still true. YOU need to SHOW how evolution is STOPPED. you haven't done that.

[kleinman]

Yup, still true. YOU need to SHOW how evolution is STOPPED. you haven't done that.
I don’t have to show that evolution is stopped; I only have to show that it is slowed down sufficiently that it is mathematically impossible to occur in the time available. You know that Paul said this and I agree with him:
You do realize you're saying that evolution simply never occurs, because certainly there are millions of selection pressures in the real world.
Look what two or three selection pressures do to the evolution of viruses and bacteria. What do you think will happen with millions of selection pressures on much more complex creatures? If you studied ev a little, you would have some idea of the answer to this question. The mathematics of mutation and selection shows something completely different than what evolutionists allege.

[Taffer]

Is that an admission that recombination alone does not and can not create new genes? We are talking about mathematical precision in this discussion of mutation and selection, not the sloppy speculations that you evolutionists use to explain your theory.

Once you accept this point, then we can go on to your next misunderstanding of recombination and natural selection. That is that recombination and natural selection can cause the loss of alleles from the gene pool and thus the loss of information from the gene pool.

No, kleinman, stop your strawmen. It is possible for recombination to create new genes. But I never claimed that it does regularly, nor did I even use that as a part of my argument. I have given you a mathematical model for selection, and you said it was "recombination and selection", which is utter rubbish. Recombination creates variation. Mutations create variation. Reproduction creates variation. Gene flow creates variation. Selection only acts on variation, and it matters not how this variation arose.

So stop blathering on about "recombination and selection", and address my posts.

[Taffer]

You can have errors in the recombination process that can make new sequences of bases.

Yes. And you can also have recombination occuring inside of genes. It does not occur at specific locations, you realise.

Are you proposing this as the mutation mechanism that will solve the deficiencies which ev reveals for the theory of evolution?

There are no deficiencies, only misconceptions on your part. Recombination creates variation. Mutation creates variation. Reproduction creates variation. Gene flow creates variation. Selection acts on this variation in the same way no matter whence that variation arose.

Ev only includes a single form of variation, which is why it does not model the entire phenomenon of evolution by natural selection.

[joobz]

I don’t have to show that evolution is stopped; I only have to show that it is slowed down sufficiently that it is mathematically impossible to occur in the time available. And you are wrong. but what's new.

You know that Paul said this and I agree with him:
You do realize you're saying that evolution simply never occurs, because certainly there are millions of selection pressures in the real world.
Look what two or three selection pressures do to the evolution of viruses and bacteria. What do you think will happen with millions of selection pressures on much more complex creatures? If you studied ev a little, you would have some idea of the answer to this question. The mathematics of mutation and selection shows something completely different than what evolutionists allege.
:D :D :D
And Paul was making fun of you when he said that, unfortunately you were too foolish to realize. Let's see if I can explain this SLOWLY.
You have those MILLONS of selection pressures ALL THE TIME. Yet we still see adaptation.

[Taffer]

Transposition and recombination of genes or parts of genes is done all the time in immunocytes for the production of antibodies.

This is a completely different type of recombination then that which happenes during meiosis.

This is a very active and precise process.

No, it isn't.

Somatic recombination, also known as V(D)J recombination, of immunoglobulins involves the random selection and combination of genes encoding each segment of the immunoglobulin variable region in a manner that generates a huge repertoire of antibodies with different paratopes.

Emphasis mine. Source. (http://en.wikipedia.org/wiki/Antibody)

Do you think this process occurs in meiosis or the recombination that is associated with HIV or other creatures?

Recombination which occurs during meiosis is a completely different mechanism.

Do you have any examples where this type of recombination occurs in the reproductive process?

No, because it is a completely different mechanism.

Do you think this is the mutation mechanism that will solve the deficiencies which ev reveals for the theory of evolution?

No, because it happens in somatic cells, and thus is not passed on to the next generation. I'm beginning to think you really don't know what recombination is.

Meiotic recombination can, and does, happen inside a gene. Not that it even matters. Your whole argument is pointless, because recombination creates variation, and it is variation which selection acts upon.

[Dr Adequate]

I don’t have to show that evolution is stopped; I only have to show that it is slowed down sufficiently that it is mathematically impossible to occur in the time available. Really? So:

(a) Why don't you try to show that evolution is "slowed down sufficiently"?

Let me guess, because that would require actual math rather than hysterics and ravings about "cheese" and "joobequate" and "herrings" and "fecal matter".

(b) Why do you keep lying about how evolution is "stopped", if all you have to do is prove that it is "slowed down sufficiently"?

Let me guess, because you find that telling the same lie over and over is easier than doing the math.

(c) Why don't your actions correspond in any way to your windy, empty boasts?

I guess that one answers itself.

[Dr Adequate]

Look what two or three selection pressures do to the evolution of viruses and bacteria. What do you think will happen with millions of selection pressures on much more complex creatures? If you studied ev a little, you would have some idea of the answer to this question. The mathematics of mutation and selection shows something completely different than what evolutionists allege. Now, when you say "the mathematics of mutation and selection", you're not referring to any mathematics, are you?

You're referring to the crazy crap you think up in your head.

[Taffer]

Now, when you say "the mathematics of mutation and selection", you're not referring to any mathematics, are you?

You're referring to the crazy crap you think up in your head.

Given that he thinks that "the mathematics of mutation and selection" and "the mathematics of recombination and selection" are different things, I'm fairly certain we can answer that question.

[Paul C. Anagnostopoulos]

You know that Paul said this and I agree with him:

You do realize you're saying that evolution simply never occurs, because certainly there are millions of selection pressures in the real world.
I'm glad you agree with my statement about what you said, otherwise you'd be disagreeing with yourself. And that would just be weird.

So you're saying that bacteria, for example, have never evolved?

~~ Paul

[joobz]

I'm glad you agree with my statement about what you said, otherwise you'd be disagreeing with yourself. And that would just be weird.:D
Although, it would be par for the course.

[kleinman]

Is that an admission that recombination alone does not and can not create new genes? We are talking about mathematical precision in this discussion of mutation and selection, not the sloppy speculations that you evolutionists use to explain your theory.

Once you accept this point, then we can go on to your next misunderstanding of recombination and natural selection. That is that recombination and natural selection can cause the loss of alleles from the gene pool and thus the loss of information from the gene pool.No, kleinman, stop your strawmen. It is possible for recombination to create new genes. But I never claimed that it does regularly, nor did I even use that as a part of my argument. I have given you a mathematical model for selection, and you said it was "recombination and selection", which is utter rubbish. Recombination creates variation. Mutations create variation. Reproduction creates variation. Gene flow creates variation. Selection only acts on variation, and it matters not how this variation arose.
Make sure you stamp your foot when you say this. If you are so sure that recombination makes new genes, add this feature to ev and show us how the theory of evolution works mathematically.
So stop blathering on about "recombination and selection", and address my posts.
Hey, I’m not telling you to stop your blathering, I’m telling you to prove your blathering mathematically.
You can have errors in the recombination process that can make new sequences of bases.Yes. And you can also have recombination occuring inside of genes. It does not occur at specific locations, you realise.
Really, you think that crossing over during meiosis does not occur at specific locations? If you think that non-homologous crossing over is the mutation process that drives the your theory of evolution, put the feature into ev and prove it mathematically.
Are you proposing this as the mutation mechanism that will solve the deficiencies which ev reveals for the theory of evolution?There are no deficiencies, only misconceptions on your part. Recombination creates variation. Mutation creates variation. Reproduction creates variation. Gene flow creates variation. Selection acts on this variation in the same way no matter whence that variation arose.
There is a deficiency in your understanding in the theory of evolution by mutation and selection. That is that multiple selection pressures slow the evolutionary process. Ev shows this and now we have more than ten papers that show that this is how mutation and selection works. If you think that recombination and selection will change this fact, include this in ev and show us. Remember this though, we already have real examples of combination rodenticides slow the evolution of resistant strains of rodents and these creatures use recombination in their reproduction.
Ev only includes a single form of variation, which is why it does not model the entire phenomenon of evolution by natural selection.
What you still don’t understand about the mathematics of mutation and selection is that multiple selection pressures slow the evolutionary process. If you think that other forms of variations will somehow changes this fact that multiple selection pressures slow the evolutionary process, you need to show how this works mathematically.
I don’t have to show that evolution is stopped; I only have to show that it is slowed down sufficiently that it is mathematically impossible to occur in the time available.And you are wrong. but what's new.
I guess you evolutionists can increase the age of the earth to a squillion years.
You do realize you're saying that evolution simply never occurs, because certainly there are millions of selection pressures in the real world.Look what two or three selection pressures do to the evolution of viruses and bacteria. What do you think will happen with millions of selection pressures on much more complex creatures? If you studied ev a little, you would have some idea of the answer to this question. The mathematics of mutation and selection shows something completely different than what evolutionists allege.And Paul was making fun of you when he said that, unfortunately you were too foolish to realize. Let's see if I can explain this SLOWLY.
Hey Paul, is joobz a mind reader? Most of those selection pressures are stabilizing selection pressures which reduce variation in the population.
You have those MILLONS of selection pressures ALL THE TIME. Yet we still see adaptation.
I wonder who is going to be the last person on this thread to understand the mathematics of mutation and selection, you or Adebz?
Transposition and recombination of genes or parts of genes is done all the time in immunocytes for the production of antibodies.This is a completely different type of recombination then that which happenes during meiosis.
Occasionally, you can have non-homologous recombination during reproduction. Include whatever form of variation in ev you want and show us that it can overcome the effect that multiple selection pressures has on the mathematics of mutation (or variation) and selection.

We now have a horse race, who will be the last evolutionist to understand the mathematics of mutation and selection. Will it be Taffer, joobz or Adebz? The race has started, they are off and mumbling. Adebz lurches into the lead by posting a gif that temporarily puts us in awe, joobz lumbers up with “can’t everyone just cooperate and adapt”, and here comes Taffer stamping his hoof and whinnies recombination is variation! Stay tuned and find out who wins this race and becomes the last evolutionist to understand the mathematics of mutation and selection.
You know that Paul said this and I agree with him: You do realize you're saying that evolution simply never occurs, because certainly there are millions of selection pressures in the real world.I'm glad you agree with my statement about what you said, otherwise you'd be disagreeing with yourself. And that would just be weird.

So you're saying that bacteria, for example, have never evolved?
Of course bacteria evolve but only in a very limited sense. It is the evolutionists who make weird extrapolations. The thought that bacteria transformed into humans is lets say, a mathematically baseless extrapolation.

[Taffer]

:rolleyes:

Why even bother? You're so convinced you're right, that nothing we say will ever convince you. Kleinman, I've already shown mathematically how increased selection pressure speeds evolution. I've already shown why every single one of your 'supporting' papers do not support you. You have ignored both those posts. I have explained multiple times that you do not understand evolutionary theory, and that selection acts on variation, and it makes no difference where this variation comes from. I've already told you more times then I can remember that ev only models a single process, not all of evolution.

How about you respond to my previous posts, instead of your endless arm waving, shouting "evolution slows, so you're wrong!".

[joobz]

Hey Paul, is joobz a mind reader? Most of those selection pressures are stabilizing selection pressures which reduce variation in the population.ahh, they don't count because you say so. How scientific.

Of course bacteria evolve but only in a very limited sense. limited, interesting. Please explain this word. Many, slow, limited,... Your language has all the hallmarks of numeric accuracy. You must be using maths.

Again, what prevents evolution from going too far?
Do you consider bacteria and viruses that switch from being airborne communicable to contact communicable a "limited evolutionary change"? Do you conisder diseases that switch between species of infection a "limited evolutionary change"?

[Paul C. Anagnostopoulos]

Of course bacteria evolve but only in a very limited sense. It is the evolutionists who make weird extrapolations. The thought that bacteria transformed into humans is lets say, a mathematically baseless extrapolation.
Okay, so you do disagree with yourself.

~~ Paul

[Dr Adequate]

Make sure you stamp your foot when you say this. If you are so sure that recombination makes new genes, add this feature to ev and show us how the theory of evolution works mathematically.

Hey, I’m not telling you to stop your blathering, I’m telling you to prove your blathering mathematically.

Really, you think that crossing over during meiosis does not occur at specific locations? If you think that non-homologous crossing over is the mutation process that drives the your theory of evolution, put the feature into ev and prove it mathematically.

There is a deficiency in your understanding in the theory of evolution by mutation and selection. That is that multiple selection pressures slow the evolutionary process. Ev shows this and now we have more than ten papers that show that this is how mutation and selection works. If you think that recombination and selection will change this fact, include this in ev and show us. Remember this though, we already have real examples of combination rodenticides slow the evolution of resistant strains of rodents and these creatures use recombination in their reproduction.

What you still don’t understand about the mathematics of mutation and selection is that multiple selection pressures slow the evolutionary process. If you think that other forms of variations will somehow changes this fact that multiple selection pressures slow the evolutionary process, you need to show how this works mathematically.

I guess you evolutionists can increase the age of the earth to a squillion years.

Hey Paul, is joobz a mind reader? Most of those selection pressures are stabilizing selection pressures which reduce variation in the population.

I wonder who is going to be the last person on this thread to understand the mathematics of mutation and selection, you or Adebz?

Occasionally, you can have non-homologous recombination during reproduction. Include whatever form of variation in ev you want and show us that it can overcome the effect that multiple selection pressures has on the mathematics of mutation (or variation) and selection.

We now have a horse race, who will be the last evolutionist to understand the mathematics of mutation and selection. Will it be Taffer, joobz or Adebz? The race has started, they are off and mumbling. Adebz lurches into the lead by posting a gif that temporarily puts us in awe, joobz lumbers up with “can’t everyone just cooperate and adapt”, and here comes Taffer stamping his hoof and whinnies recombination is variation! Stay tuned and find out who wins this race and becomes the last evolutionist to understand the mathematics of mutation and selection.

Of course bacteria evolve but only in a very limited sense. It is the evolutionists who make weird extrapolations. The thought that bacteria transformed into humans is lets say, a mathematically baseless extrapolation. So, you still haven't done any actual math?

Your lies, your gibberish, your tantrums, your magic words and your plaintive dreary whining about your betters are not a substitute.

[kleinman]

Why even bother? You're so convinced you're right, that nothing we say will ever convince you. Kleinman, I've already shown mathematically how increased selection pressure speeds evolution. I've already shown why every single one of your 'supporting' papers do not support you. You have ignored both those posts. I have explained multiple times that you do not understand evolutionary theory, and that selection acts on variation, and it makes no difference where this variation comes from. I've already told you more times then I can remember that ev only models a single process, not all of evolution.
I’m convinced that I understand how ev works and that it properly models the mathematics of random point mutations and natural selection. What it shows is that the dominant parameters in the model are the number of selection conditions and the length of the genome. You have not shown mathematically how increased selection pressure speeds up evolution. If you think you have, show how you did it to Paul. I think he would be thrilled to know how to speed up ev. Use anything you want with ev, recombination, indels, transpositions, whatever and show how this speeds up evolution. I have already listed ten or twelve references of real examples how multiple selection pressures slow evolution. These real examples are not limited to random point mutations.
How about you respond to my previous posts, instead of your endless arm waving, shouting "evolution slows, so you're wrong!".
I may be arm waving and shouting but I’ve also posted the data from a peer reviewed model of random point mutations and natural selection which substantiates my contention and numerous real examples of multiple selection pressures slowing evolution. I’m waiting for you to post data from your peer reviewed and published model of mutation and natural selection or real examples which show that multiple selection pressures speed evolution.
Hey Paul, is joobz a mind reader? Most of those selection pressures are stabilizing selection pressures which reduce variation in the population.ahh, they don't count because you say so. How scientific.
How about if I give you a quote from my genetics text, Genetics in Medicine, by Thompson and Thompson.
Of the three types of selection, stabilizing selection appears to play the major role. It may be viewed as a tendency to maintain the status quo.
The three types of selection are stabilizing, directional and disruptive. I gave you the definitions earlier in the thread.
Of course bacteria evolve but only in a very limited sense.limited, interesting. Please explain this word. Many, slow, limited,... Your language has all the hallmarks of numeric accuracy. You must be using maths.
Bacteria can evolve resistance to drugs and other selection pressures, but bacteria certainly didn’t evolve into humans. Evolutionists like to use the term unlimited when talking about mutation and selection. That type of thinking has no hallmarks of numeric accuracy. They like to say that a series of microevolutionary steps leads to a macroevolutionary steps. This type of process is limited by the selection pressure(s), fitness landscape and time.
Again, what prevents evolution from going too far?
Selection pressure(s), fitness landscape and time.
Do you consider bacteria and viruses that switch from being airborne communicable to contact communicable a "limited evolutionary change"? Do you conisder diseases that switch between species of infection a "limited evolutionary change"?
I don’t know what you mean by this question. All infections agents require contact of some type with the host and a proper portal of entry.
Of course bacteria evolve but only in a very limited sense. It is the evolutionists who make weird extrapolations. The thought that bacteria transformed into humans is lets say, a mathematically baseless extrapolation.Okay, so you do disagree with yourself.
I do that occasionally. I then argue with both sides and then hopefully come to agreement with the one who is correct. Sometimes the answer is none of the above. However, whenever I think about bacteria evolving into humans--- nah.

I see that the James Randi Forum resident PhD in amathematics really wants to be the last evolutionist on this thread to understand the mathematics of mutation and selection.

[Dr Adequate]

I’m convinced that I understand how ev works and that it properly models the mathematics of random point mutations and natural selection. What it shows is that the dominant parameters in the model are the number of selection conditions and the length of the genome. You have not shown mathematically how increased selection pressure speeds up evolution. If you think you have, show how you did it to Paul. I think he would be thrilled to know how to speed up ev. Use anything you want with ev, recombination, indels, transpositions, whatever and show how this speeds up evolution. I have already listed ten or twelve references of real examples how multiple selection pressures slow evolution. These real examples are not limited to random point mutations.

I may be arm waving and shouting but I’ve also posted the data from a peer reviewed model of random point mutations and natural selection which substantiates my contention and numerous real examples of multiple selection pressures slowing evolution. I’m waiting for you to post data from your peer reviewed and published model of mutation and natural selection or real examples which show that multiple selection pressures speed evolution.

How about if I give you a quote from my genetics text, Genetics in Medicine, by Thompson and Thompson.

The three types of selection are stabilizing, directional and disruptive. I gave you the definitions earlier in the thread.

Bacteria can evolve resistance to drugs and other selection pressures, but bacteria certainly didn’t evolve into humans. Evolutionists like to use the term unlimited when talking about mutation and selection. That type of thinking has no hallmarks of numeric accuracy. They like to say that a series of microevolutionary steps leads to a macroevolutionary steps. This type of process is limited by the selection pressure(s), fitness landscape and time.

Selection pressure(s), fitness landscape and time.

I don’t know what you mean by this question. All infections agents require contact of some type with the host and a proper portal of entry.

I do that occasionally. I then argue with both sides and then hopefully come to agreement with the one who is correct. Sometimes the answer is none of the above. However, whenever I think about bacteria evolving into humans--- nah.
So, you still haven't done any math.

Why do you keep whining about mathematics? You're just drawing attention to your deficiencies.

I see that the James Randi Forum resident PhD in amathematics really wants to be the last evolutionist on this thread to understand the mathematics of mutation and selection. As I recall, when you use the phrase "understand the mathematics of mutation and selection" you mean "be fooled by kleinman's snivelling innumerate lies".

I think I can guarantee you that this will never happen to any of us.

But thanks for playing.

[kleinman]

Here are some more references to combination selection pressures slowing evolution. The following reference can be found at http://www.journals.uchicago.edu/cgi-bin/resolve?JID990624PDF (http://www.journals.uchicago.edu/cgi-bin/resolve?JID990624PDF)
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.
And
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.
Here is another reference from Wikipedia on combination retroviral therapy for HIV located at http://en.wikipedia.org/wiki/Antiretroviral_drug (http://en.wikipedia.org/wiki/Antiretroviral_drug)
Combinations of antiretrovirals create multiple obstacles to HIV replication to keep the number of offspring low and reduce the possibility of a superior mutation. If a mutation arises that conveys resistance to one of the drugs being taken, the other drugs continue to suppress reproduction of that mutation. With rare exceptions, no individual antiretroviral drug has been demonstrated to suppress an HIV infection for long; these agents must be taken in combinations in order to have a lasting effect. As a result the standard of care is to use combinations of antiretroviral drugs. Combinations usually comprise two nucleoside-analogue RTIs and one non-nucleoside-analogue RTI or protease inhibitor.[2]
Here is another abstract on combination therapy for HIV located at http://adsabs.harvard.edu/abs/1993Natur.365..451L (http://adsabs.harvard.edu/abs/1993Natur.365..451L)
Reports of synergy17–19 and lack of cross-resistance between reverse transcriptase inhibitors (refs 7, 9, 10, 12–14, 17, 18, 20, 21), plus the reversal of AZT resistance by mutations induced by ddl7 and NNRTIs14, have indicated that specific drug combinations directed at reverse transcriptase might curtail resistance. Chow et al.22 extended this concept in a report that specific multiple combinations of resistance mutations in the reverse transcriptase can significantly impair HIV-1 replication. They concluded that evolutionary limitations may exist to prevent the emergence of multidrug resistance to inhibitors of reverse transcriptase22. We report here that HIV-1 co-resistant to AZT, ddl and the NNRTI nevirapine23 can be readily selected in cell culture starting with dual AZT- and ddl-resistant virus. We found no evidence for 'replication incompatible' combinations of resistance mutations, although a mutation (M184-->V) conferring oxathiolane-cytosine nucleoside resistance in reverse transcriptase24,25 completely sup-pressed AZT resistance in a triple-resistant background. These in vitro observations suggest that triple drug combination therapy might ultimately result in co-resistant HIV-1, although they do not preclude assessment of such combinations for treatment of HIV-1 disease.
Here is a line from the abstract from a paper reporting on the treatment of malaria which is located at http://www.ajtmh.org/cgi/reprint/68/5/608.pdf (http://www.ajtmh.org/cgi/reprint/68/5/608.pdf)
Based on the results of this study and with the objective of slowing the development of resistance, the Peruvian Ministry of Health has decided to revise its malaria treatment policy and recommend combination therapy with MQ-AS as the new first-line treatment of uncomplicated P. falciparum malaria in the Amazon region.

[Dr Adequate]

Here are some more references to combination selection pressures slowing evolution. The following reference can be found at http://www.journals.uchicago.edu/cgi-bin/resolve?JID990624PDF (http://www.journals.uchicago.edu/cgi-bin/resolve?JID990624PDF)

And

Here is another reference from Wikipedia on combination retroviral therapy for HIV located at http://en.wikipedia.org/wiki/Antiretroviral_drug (http://en.wikipedia.org/wiki/Antiretroviral_drug)

Here is another abstract on combination therapy for HIV located at http://adsabs.harvard.edu/abs/1993Natur.365..451L (http://adsabs.harvard.edu/abs/1993Natur.365..451L)

Here is a line from the abstract from a paper reporting on the treatment of malaria which is located at http://www.ajtmh.org/cgi/reprint/68/5/608.pdf (http://www.ajtmh.org/cgi/reprint/68/5/608.pdf)
So, you're back to telling stupid lies about the meaning of papers you don't understand?

Still no math, I notice.

[joobz]

Of course bacteria evolve but only in a very limited sense. It is the evolutionists who make weird extrapolations. The thought that bacteria transformed into humans is lets say, a mathematically baseless extrapolation.
Do you consider bacteria and viruses that switch from being airborne communicable to contact communicable a "limited evolutionary change"? Do you conisder diseases that switch between species of infection a "limited evolutionary change"?



I don’t know what you mean by this question. All infections agents require contact of some type with the host and a proper portal of entry.
Think Bird Flu. What is the primary concern? That the virus can become transmissble to humans. This requires an evolutionary adaptation to occur. Do you consider such a minor change with HUGE implications a "Limited evolutionary change"?

[joobz]

How about if I give you a quote from my genetics text, Genetics in Medicine, by Thompson and Thompson.

The three types of selection are stabilizing, directional and disruptive. I gave you the definitions earlier in the thread.
If you honestly think this is a logical response to my post, there is nothing I can do for you.

[kleinman]

So, you're back to telling stupid lies about the meaning of papers you don't understand?
Let’s see if Adebz can tell us what the real meaning of these papers is. Then he might not win the race to be the last evolutionist to understand the real meaning of the mathematics of mutation and selection.
How about if I give you a quote from my genetics text, Genetics in Medicine, by Thompson and Thompson.

The three types of selection are stabilizing, directional and disruptive. I gave you the definitions earlier in the thread.If you honestly think this is a logical response to my post, there is nothing I can do for you.
Of course my response to your post was logical. Evolutionists know that most selection pressures are stabilizing. That is why I quoted this line from an evolutionist written text on genetics. Now if evolutionists learn the mathematics of mutation and selection and come to understand that multiple selection pressures slow the evolutionary process, then we can finally lay the theory of evolution to rest. This is substantiated by an evolutionist written and peer reviewed model of random point mutation and natural selection, the Wikipedia reference on fitness landscape and numerous real examples of multiple selection pressures slowing evolution. I will continue looking for more real examples of how multiple selection pressures slow evolution. You evolutionists can look for examples of where multiple selection pressures accelerate evolution, which would spice up this discussion.

[joobz]

Of course my response to your post was logical. Evolutionists know that most selection pressures are stabilizing. That is why I quoted this line from an evolutionist written text on genetics. Now if evolutionists learn the mathematics of mutation and selection and come to understand that multiple selection pressures slow the evolutionary process, then we can finally lay the theory of evolution to rest. This is substantiated by an evolutionist written and peer reviewed model of random point mutation and natural selection, the Wikipedia reference on fitness landscape and numerous real examples of multiple selection pressures slowing evolution. I will continue looking for more real examples of how multiple selection pressures slow evolution. You evolutionists can look for examples of where multiple selection pressures accelerate evolution, which would spice up this discussion.

Yawn. You say a lot of words, but none address the challenge at your feet. Show how evolution is impossible mathematically. that's it.

All you have presented are generalities (limited, slow, multiple,...) and claimed this is math.

[Taffer]

Here are some more references to combination selection pressures slowing evolution. The following reference can be found at http://www.journals.uchicago.edu/cgi-bin/resolve?JID990624PDF (http://www.journals.uchicago.edu/cgi-bin/resolve?JID990624PDF)

And

Here is another reference from Wikipedia on combination retroviral therapy for HIV located at http://en.wikipedia.org/wiki/Antiretroviral_drug (http://en.wikipedia.org/wiki/Antiretroviral_drug)

Here is another abstract on combination therapy for HIV located at http://adsabs.harvard.edu/abs/1993Natur.365..451L (http://adsabs.harvard.edu/abs/1993Natur.365..451L)

Here is a line from the abstract from a paper reporting on the treatment of malaria which is located at http://www.ajtmh.org/cgi/reprint/68/5/608.pdf (http://www.ajtmh.org/cgi/reprint/68/5/608.pdf)


Emergence does not mean evolution, kleinman. I think it's about time you realised that.

[Taffer]

I’m convinced that I understand how ev works and that it properly models the mathematics of random point mutations and natural selection. What it shows is that the dominant parameters in the model are the number of selection conditions and the length of the genome. You have not shown mathematically how increased selection pressure speeds up evolution. If you think you have, show how you did it to Paul. I think he would be thrilled to know how to speed up ev. Use anything you want with ev, recombination, indels, transpositions, whatever and show how this speeds up evolution. I have already listed ten or twelve references of real examples how multiple selection pressures slow evolution. These real examples are not limited to random point mutations.

In every single one of your examples, kleinman, you misinterpret what they say. Emergence does not mean evolution.

Secondly, I have already shown how increased selection pressures speed up evolution. Please turn your attention to my mathematical model I posted earlier. An increase in selection pressure (i.e. an increase in the selection coefficient) leads to a faster change in allele frequency. What's that? Change in allele frequency is evolution? Oh dear, I think I've just proved you wrong...

I may be arm waving and shouting but I’ve also posted the data from a peer reviewed model of random point mutations and natural selection which substantiates my contention and numerous real examples of multiple selection pressures slowing evolution. I’m waiting for you to post data from your peer reviewed and published model of mutation and natural selection or real examples which show that multiple selection pressures speed evolution.

Every single one of those papers, kleinman, every single one, simply shows that killing off a population will lead to the emergence of antibacterial resistance at a later time. There is no-one denying that. By emergence is not evolution.

How about you use an example which isn't resistance to something? Can you show that evolution has slowed in another example?

How about if I give you a quote from my genetics text, Genetics in Medicine, by Thompson and Thompson.

The three types of selection are stabilizing, directional and disruptive. I gave you the definitions earlier in the thread.

Haven't I already explained to you what this means? Selection does not differ, then pattern of allele frequency changes. Selection is not a 'thing' which can change. It is a phenomenon.

Also, I notice you are still ignoring several of my posts. I would like a response to them.

[Taffer]

Let’s see if Adebz can tell us what the real meaning of these papers is. Then he might not win the race to be the last evolutionist to understand the real meaning of the mathematics of mutation and selection.

Given that he actually understands what evolutionary theory teaches, I suspect he will understand better then you.

To wit: emergence does not mean evolution.

[kleinman]

Of course my response to your post was logical. Evolutionists know that most selection pressures are stabilizing. That is why I quoted this line from an evolutionist written text on genetics. Now if evolutionists learn the mathematics of mutation and selection and come to understand that multiple selection pressures slow the evolutionary process, then we can finally lay the theory of evolution to rest. This is substantiated by an evolutionist written and peer reviewed model of random point mutation and natural selection, the Wikipedia reference on fitness landscape and numerous real examples of multiple selection pressures slowing evolution. I will continue looking for more real examples of how multiple selection pressures slow evolution. You evolutionists can look for examples of where multiple selection pressures accelerate evolution, which would spice up this discussion.Yawn. You say a lot of words, but none address the challenge at your feet. Show evolution how evolution is impossible mathematically. that's it.
Go back and reread this thread and the related thread on the Evolutionisdead forum. You will find the parametric studies done with ev that show that as you increase genome lengths in the model, the number of generations required for evolving the selection conditions becomes huge as you try to approach realistic genome lengths. If you limit the number of selection conditions in the model to a single selection condition that selection condition can evolve very rapidly even with large genomes. This is exactly analogous to what we see in the numerous real examples which I have posted where multiple directed selection pressures slow the creatures ability to evolve resistance to those selection pressures. The Wikipedia reference on fitness landscape presents the same concept in different terminology. This is how mutation and selection works. Stabilizing selection pressures maintain the status quo and directed selection pressures interfere with each other. There are no directed selection pressures that can evolve reptiles into birds or a primate precursor into humans and chimpanzees. It requires too many directed selection pressures which only two or three are sufficient to slow the evolutionary process profoundly even on HIV which has a very high mutation rate, very short generation times, very large reproduction rates and a very short genome length. You can’t evolve binding sites on a genome the length of a typical reptile in a reasonable number of generations using ev. The problem has nothing to do with only allowing random point mutations; the problem is the three selection conditions. How do you expect to evolve the huge number of genetic differences between reptiles and birds with their much lower mutation rates, much longer generation times, much smaller reproduction rates and much longer genome lengths than HIV? The mathematics is not there to support this. Mutation and selection does not work the way evolutionists allege. I will continue to post references to how mutation and selection actually works.

[Dr Adequate]

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.

[Dr Adequate]

Go back and reread this thread and the related thread on the Evolutionisdead forum. You will find the parametric studies done with ev that show that as you increase genome lengths in the model, the number of generations required for evolving the selection conditions becomes huge as you try to approach realistic genome lengths. If you limit the number of selection conditions in the model to a single selection condition that selection condition can evolve very rapidly even with large genomes. This is exactly analogous to what we see in the numerous real examples which I have posted where multiple directed selection pressures slow the creatures ability to evolve resistance to those selection pressures. The Wikipedia reference on fitness landscape presents the same concept in different terminology. This is how mutation and selection works. Stabilizing selection pressures maintain the status quo and directed selection pressures interfere with each other. There are no directed selection pressures that can evolve reptiles into birds or a primate precursor into humans and chimpanzees. It requires too many directed selection pressures which only two or three are sufficient to slow the evolutionary process profoundly even on HIV which has a very high mutation rate, very short generation times, very large reproduction rates and a very short genome length. You can’t evolve binding sites on a genome the length of a typical reptile in a reasonable number of generations using ev. The problem has nothing to do with only allowing random point mutations; the problem is the three selection conditions. How do you expect to evolve the huge number of genetic differences between reptiles and birds with their much lower mutation rates, much longer generation times, much smaller reproduction rates and much longer genome lengths than HIV? The mathematics is not there to support this. Mutation and selection does not work the way evolutionists allege. I will continue to post references to how mutation and selection actually works. So, the same old lies and no actual math?

[Dr Adequate]

Let’s see if Adebz can tell us what the real meaning of these papers is. Sure. They mean what they actually say, none of which supports stupid lies like the following:

Then he might not win the race to be the last evolutionist to understand the real meaning of the mathematics of mutation and selection. Of course my response to your post was logical. Evolutionists know that most selection pressures are stabilizing. That is why I quoted this line from an evolutionist written text on genetics. Now if evolutionists learn the mathematics of mutation and selection and come to understand that multiple selection pressures slow the evolutionary process, then we can finally lay the theory of evolution to rest. This is substantiated by an evolutionist written and peer reviewed model of random point mutation and natural selection, the Wikipedia reference on fitness landscape and numerous real examples of multiple selection pressures slowing evolution. I will continue looking for more real examples of how multiple selection pressures slow evolution. You evolutionists can look for examples of where multiple selection pressures accelerate evolution, which would spice up this discussion. We all know you're lying, kleinman. 'Cos you've babbled out these lies before, remember? And we showed you up as a liar, remember?

[Taffer]

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 simulataneously.

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.

Wonderful. QED.

[Dr Adequate]

Wonderful. Elementary.

I told kleinman this would happen several pages back, on the basis of probability theory.

But thanks.

[Dr Adequate]

I've updated the graph to show the effects of recombination.

http://img337.imageshack.us/img337/1540/genegraphnb7.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 these 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.

The green line shows simultaneous selection pressures with the same parameters, but with recombination between successful organisms.

Note how with simultaneous selection pressures, with or without recombination, the rate of evolution (fixations/generation) increases with the number of selection pressures.

Note that recombination also increases the rate of evolution.

---

I should have mentioned, perhaps, that each data point is the average of 10,000 trials.

[joobz]

Well, that should about sum it up.

The goal post was, multiple "directional" selection pressures slow evolution, which means evolution is impossible.

DR. A. demonstrated, mathematically, that multiple "directional" selection pressures can indeed speed up evolution, which means evolution is possible.

Ok, Kleinman, this is done with. It is now time for you to explain how Noah's ark was mathematically possible. (http://forums.randi.org/showthread.php?t=82190)

[kleinman]

http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
Adebz is trying to do his mathematics by gif and awe. At least this brainwashed, prejudiced and biased evolutionist is trying. What he is trying to do is be the last evolutionist to understand the mathematics of mutation and selection. He thinks that a graph that does not include genome size, mutation rate, population, description of selection pressures, real examples of what he is trying to demonstrate, and a derivation of the model with assumptions used is somehow going to convince anyone reading this thread that multiple selection pressures accelerates evolution. Wait, it does convince Taffer. So we still have a horse race, its Adebz and Taffer neck and neck to be the last evolutionists on this thread to understand the mathematics of mutation and selection.

To wit: emergence does not mean evolution.
Taffer tries to make a point using semantics.

Here is another link which discusses the attempted extinction of mosquito larve and can be found at http://faculty.ucr.edu/~walton/bacteria.htm (http://faculty.ucr.edu/~walton/bacteria.htm) . Note that this author does not use the word emergence in describing the evolution of resistance to these selection pressures.
Two Bacillus are currently used for mosquito control in California; however, because Bacillus thuringiensis subsp. israelensis (Bti) is comparatively less effective against mosquitoes inhabiting the organically enriched waters of treatment wetlands, Bacillus sphaericus currently offers a viable alternative for microbial control of mosquitoes in organically-enriched treatment wetlands (Walton et al. 1998). Unlike Bti which contains multiple toxins that limit the potential for the rapid evolution of resistance in mosquitoes, the two toxin precursors in B. sphaericus act as a single toxin following ingestion and partial digestion by mosquito larvae. Bti has been used for nearly 30 years in large-scale mosquito and black fly control programs and resistance had not been detected in mosquito populations in nature that have been subjected to selection from Bti toxins. Nevertheless, mosquitoes, such as the southern house mosquito Culex quinquefasciatus, can evolve resistance to the full complement of Bti toxins when under strong selection pressure in the laboratory. Resistance to Bti was recently detected in a closely related species Culex pipiens in Syracuse, New York (see: Paul et al. 2005. Journal of the American Mosquito Control Association 21: 305-309). In contrast to the findings for Bti, resistance to B. sphaericus has been observed in several places (Brazil, China, France, India and Thailand). Mosquitoes can evolve resistance to B. sphaericus very rapidly (>10,000-fold in 7-8 generations), especially when the mosquitoes commonly found in often polluted urban environments, such as catch basins and wastewater contaminated by human sewage, are routinely exposed to B. sphaericus toxins.

[joobz]

Taffer tries to make a point using semantics.
BWA HA HA HA HA HA!!!! Another one for the completely insane irony department, Mr. "directional" selection pressures.

So we so far have
1.) HIV doesn't count (even though it used to be the perfect example) because it uses recombination and therefore disproves Kleinman's theory
2.) Stabilizing pressures don't count because they are already in equilibrium and therefore are no longer a factor (even though deviations from other pressures can result in these pressures becoming a selection force again)
3.) Dr. A's model doesn't count becuase he's using assumptions that demonstrate how multiple pressures speed evolution, and obviously only Klienman is allowed to decide on what is allowed.

[Dr Adequate]

Adebz is trying to do his mathematics by gif and awe. At least this brainwashed, prejudiced and biased evolutionist is trying. What he is trying to do is be the last evolutionist to understand the mathematics of mutation and selection. He thinks that a graph that does not include genome size, mutation rate, population, description of selection pressures, real examples of what he is trying to demonstrate, and a derivation of the model with assumptions used is somehow going to convince anyone reading this thread that multiple selection pressures accelerates evolution. Wait, it does convince Taffer. So we still have a horse race, its Adebz and Taffer neck and neck to be the last evolutionists on this thread to understand the mathematics of mutation and selection. Wow, I've prompted a lot of hysterics, haven't I?

Do you have any questions about the model, or would you rather scream and twitch and froth and lie and babble gibberish?

Hey, why do I even bother asking?

Carry on with the lies and the gibberish.

[kleinman]

Taffer tries to make a point using semantics.BWA HA HA HA HA HA!!!! Another one for the completely insane irony department, Mr. "directional" selection pressures.
Hold on folks, this is really becoming a horse race; joobz is coming along from the outside. Who will be the last evolutionist on this thread to understand the mathematics of mutation and selection? These evolutionists really have heart; none of them are willing to give up on their mathematically impossible theory. Stay tuned for the finish of this thrilling race.

[Dr Adequate]

Hold on folks, this is really becoming a horse race; joobz is coming along from the outside. Who will be the last evolutionist on this thread to understand the mathematics of mutation and selection? These evolutionists really have heart; none of them are willing to give up on their mathematically impossible theory. Stay tuned for the finish of this thrilling race. Rather than speculate on who will be the last person to be fooled by the stupid innumerate gibberish of lies which you have the mendacity to call "the mathematics of mutation and selection", you should instead turn your attention to the question of whether anyone will ever thus be deceived.

[Dr Adequate]

Here is another link which discusses the attempted extinction of mosquito larve and can be found at http://faculty.ucr.edu/~walton/bacteria.htm . Note that this author does not use the word emergence in describing the evolution of resistance to these selection pressures. Heh heh. You didn't read that, did you?

It has nothing to do with your halfwitted fantasies, you silly little man.

[kleinman]

Here is another link which discusses the attempted extinction of mosquito larve and can be found at http://faculty.ucr.edu/~walton/bacteria.htm. Note that this author does not use the word emergence in describing the evolution of resistance to these selection pressures. Heh heh. You didn't read that, did you?
Sure I did, that’s why I can post quotes like this from the link:
Unlike Bti which contains multiple toxins that limit the potential for the rapid evolution of resistance in mosquitoes, the two toxin precursors in B. sphaericus act as a single toxin following ingestion and partial digestion by mosquito larvae.
And
In contrast to the findings for Bti, resistance to B. sphaericus has been observed in several places (Brazil, China, France, India and Thailand). Mosquitoes can evolve resistance to B. sphaericus very rapidly (>10,000-fold in 7-8 generations), especially when the mosquitoes commonly found in often polluted urban environments, such as catch basins and wastewater contaminated by human sewage, are routinely exposed to B. sphaericus toxins.
Single selection pressure gives rapid evolution of resistance.
Unlike Bti which contains multiple toxins that limit the potential for the rapid evolution of resistance in mosquitoes, the two toxin precursors in B. sphaericus act as a single toxin following ingestion and partial digestion by mosquito larvae.
And
Bti has been used for nearly 30 years in large-scale mosquito and black fly control programs and resistance had not been detected in mosquito populations in nature that have been subjected to selection from Bti toxins. Nevertheless, mosquitoes, such as the southern house mosquito Culex quinquefasciatus, can evolve resistance to the full complement of Bti toxins when under strong selection pressure in the laboratory. Resistance to Bti was recently detected in a closely related species Culex pipiens in Syracuse, New York (see: Paul et al. 2005. Journal of the American Mosquito Control Association 21: 305-309).
Multiple selection pressures slow evolution of resistance. In this case, it goes from 7 to 8 generations for the single selection pressure to 30 years for multiple selection pressures.

Now if you read your URLs that you post, you would be able to quote from them (if they had anything worthwhile to quote to support your position).

And Adebz surges into the lead. Who will win this race to be the last evolutionist to understand the mathematics of mutation and selection?

[Mr. Scott]

Multiple selection pressures slow evolution of resistance. In this case, it goes from 7 to 8 generations for the single selection pressure to 30 years for multiple selection pressures.

Well, it's quite obvious that the intensity of selection pressures strongly affects the evolution of traits like resistance to antibiotics. A case in point is non-compliance with medication, which is known to encourage resistant populations.

I think we have another unchallenged assumption: that selection pressures are constant and numerous on long time scales in nature.

Why are we assuming this? In nature populations of creatures like primates go through periods of intense selection pressures and periods of little or no selection pressure. There are occasional droughts, food shortages, space shortages, breakouts of infections and predators, and so on and so forth. Individuals will break off from a colony and start other colonies, sometimes in hostile territory with one or more intense selection pressures, sometimes in environments where food is plentiful and selective pressures are absent. Separate colonies will have meetings of individuals which have developed advantageous traits separately and mate to combine them, resulting in parallel, not serial evolution.

And, all those factors not modeled at all in Ev, a simplified model intended only to prove information gain which creationists had previously claimed could not occur.

Another unchalleneged assumption: that an infectious agent like gonorrhea reproduces in a homogeneous environment, as if in a petri dish. Multiple environments with multiple intensities and types of selective pressures in the same organism will resulted in multiple directions of evolution, and cells re-converging after such individual evolutions are known to exchange DNA and combine resistances - as long as selective presures are not so intense as to cause extinction.

All that, again, is not modeled by Ev.

Any assertion that any process proven to occur in real world evolution that Ev doesn't model is unimportant needs to be backed up with mathematical proof, or else, Ev cannot be considered mathematical proof evolution can't account for the origin of species.

Keinman's primary thesis is: Considering only processes modeled by Ev, evolution is to slow to account for the genetic and geological records. I don't think there is any disagreement if stated as such.

[kleinman]

Multiple selection pressures slow evolution of resistance. In this case, it goes from 7 to 8 generations for the single selection pressure to 30 years for multiple selection pressures.Well, it's quite obvious that the intensity of selection pressures strongly affects the evolution of traits like resistance to antibiotics. A case in point is non-compliance with medication, which is known to encourage resistant populations.
I hear and read this type of terminology when evolutionists talk about selection pressures. Do you want to enumerate and elaborate on the variables that determine the intensity of selection pressures?
I think we have another unchallenged assumption: that selection pressures are constant and numerous on long time scales in nature.
Give us some examples of this. Do you propose that a selection pressure doesn’t have to be present long enough for at least some individuals in the population to have adapted to that pressure, for example antibiotic resistance?
Why are we assuming this? In nature populations of creatures like primates go through periods of intense selection pressures and periods of little or no selection pressure. There are occasional droughts, food shortages, space shortages, breakouts of infections and predators, and so on and so forth. Individuals will break off from a colony and start other colonies, sometimes in hostile territory with one or more intense selection pressures, sometimes in environments where food is plentiful and selective pressures are absent. Separate colonies will have meetings of individuals which have developed advantageous traits separately and mate to combine them, resulting in parallel, not serial evolution.
Rapid adaptation occurs by recombination and natural selection, not mutation and natural selection. Recombination and natural selection is what Darwin was observing when he reported on the differences in finch beaks. Recombination and natural selection works with selection of alleles, small populations and small numbers of generations. This is where Stephen Gould’s hypothesis of punctuated equilibrium has application. However, the mathematics of mutation and selection shows it is a far slower mechanism of adaptation that requires much larger populations and much more generations to accomplish its task. Recombination without errors does not increase information in the gene pool; recombination with natural selection can reduce the information in the gene pool.
And, all those factors not modeled at all in Ev, a simplified model intended only to prove information gain which creationists had previously claimed could not occur.
Add any feature you want to ev, whether it is recombination, any or all forms of mutations and show us how your theory works mathematically. Show us how these mechanisms overcome the problem for your theory that multiple selection pressures slow evolution.
Another unchalleneged assumption: that an infectious agent like gonorrhea reproduces in a homogeneous environment, as if in a petri dish. Multiple environments with multiple intensities and types of selective pressures in the same organism will resulted in multiple directions of evolution, and cells re-converging after such individual evolutions are known to exchange DNA and combine resistances - as long as selective presures are not so intense as to cause extinction.

All that, again, is not modeled by Ev.
Add this feature to ev and show us mathematically how the theory of evolution works.
Any assertion that any process proven to occur in real world evolution that Ev doesn't model is unimportant needs to be backed up with mathematical proof, or else, Ev cannot be considered mathematical proof evolution can't account for the origin of species.
I haven’t asserted that they are unimportant; I assert that they won’t overcome the fact that multiple selection pressures slow evolution. This is what is discussed in Delphi’s Wikipedia reference to the fitness landscape and the numerous real examples of multiple selection pressures that I have posting on this thread. These real examples are not limited to random point mutations. Joobz pointed out that HIV does recombination. Certainly rodents use recombination. Any mechanism of mutation or recombination is available to these creatures discussed in the links presented here.

In fact, here are more examples of how multiple selection pressures slow evolution. These are not examples derived from a mathematical model; they demonstrate what is shown in the ev mathematical model.

Here is an article that discusses the treatment of Hepatitis C http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1472602 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1472602) . Again, these authors report that multiple selection pressures slow the evolution of resistant strains of this virus as reported in this quote:
The effective treatment of HCV infection will likely require multiple antiviral drugs with different resistance profiles to delay the emergence of resistance, as has been shown in human immunodeficiency virus (35). In the present study, treatment with either a thumb or a palm inhibitor alone rendered large numbers of resistant replicon colonies in vitro, a potential indication of the likely rapid emergence of HCV-resistant variants upon initiation of monotherapy. Importantly, by combining two inhibitors binding to the thumb and to the palm sites of the HCV polymerase we observed a greater-than-additive inhibitory effect of replicon RNA replication.
I include the following quote from this paper just for Taffer who thinks that “emergence” somehow does not refer to “evolution”.
Mutants Ile482Leu, Met423Ile, and Met423Val were observed at different sequential passages, illustrating the plasticity and evolution of the quasispecies population in the presence of inhibitor's selective pressure (Table 2).
Here is another paper that discusses combination selection pressures for the treatment of malaria. It is located at http://www.ajtmh.org/cgi/content/full/72/2/163 (http://www.ajtmh.org/cgi/content/full/72/2/163) .
The goal of combination therapy (CT) is to delay the emergence and spread of drug resistance. The strategy is supported empirically by the success of CT in treating tuberculosis and human immunodeficiency virus infections, and by mathematical models.1 The rationale for CT is simple. If two drugs have independent mechanisms of action, mutations that confer resistance to each drug will only rarely co-exist in the same parasite. By this logic, drug combinations should both improve treatment cure rate, and delay the emergence of drug resistance.2
Again, I include the following quote for Taffer so that he know that the emergence of resistance is by evolution.
These equations enable the frequencies of dhfr mutations to be tracked over the time course of the evolution of resistance as described in more detail elsewhere.4

[Dr Adequate]

I hear and read this type of terminology when evolutionists talk about selection pressures. Do you want to enumerate and elaborate on the variables that determine the intensity of selection pressures?

Give us some examples of this. Do you propose that a selection pressure doesn’t have to be present long enough for at least some individuals in the population to have adapted to that pressure, for example antibiotic resistance?

Rapid adaptation occurs by recombination and natural selection, not mutation and natural selection. Recombination and natural selection is what Darwin was observing when he reported on the differences in finch beaks. Recombination and natural selection works with selection of alleles, small populations and small numbers of generations. This is where Stephen Gould’s hypothesis of punctuated equilibrium has application. However, the mathematics of mutation and selection shows it is a far slower mechanism of adaptation that requires much larger populations and much more generations to accomplish its task. Recombination without errors does not increase information in the gene pool; recombination with natural selection can reduce the information in the gene pool.

Add any feature you want to ev, whether it is recombination, any or all forms of mutations and show us how your theory works mathematically. Show us how these mechanisms overcome the problem for your theory that multiple selection pressures slow evolution.

Add this feature to ev and show us mathematically how the theory of evolution works.

I haven’t asserted that they are unimportant; I assert that they won’t overcome the fact that multiple selection pressures slow evolution. This is what is discussed in Delphi’s Wikipedia reference to the fitness landscape and the numerous real examples of multiple selection pressures that I have posting on this thread. These real examples are not limited to random point mutations. Joobz pointed out that HIV does recombination. Certainly rodents use recombination. Any mechanism of mutation or recombination is available to these creatures discussed in the links presented here.

In fact, here are more examples of how multiple selection pressures slow evolution. These are not examples derived from a mathematical model; they demonstrate what is shown in the ev mathematical model.

Here is an article that discusses the treatment of Hepatitis C http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1472602 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1472602) . Again, these authors report that multiple selection pressures slow the evolution of resistant strains of this virus as reported in this quote:

I include the following quote from this paper just for Taffer who thinks that “emergence” somehow does not refer to “evolution”.

Here is another paper that discusses combination selection pressures for the treatment of malaria. It is located at http://www.ajtmh.org/cgi/content/full/72/2/163 (http://www.ajtmh.org/cgi/content/full/72/2/163) .

Again, I include the following quote for Taffer so that he know that the emergence of resistance is by evolution.
So, the same old lies and no math.

How did I guess.

[kleinman]

So, the same old lies and no math.
Folks, we are back at our horserace to find out who will be the last evolutionist who understands the mathematics of mutation and selection. And we find that Adebz has surged ahead by a tale.

[joobz]

Folks, we are back at our horserace to find out who will be the last evolutionist who understands the mathematics of mutation and selection. And we find that Adebz has surged ahead by a tale.
Hey, so where's your analysis of Dr. Adaquate's simulations? Or do you generally just ignore all evidence that clearly shows how rediculous you are?

[Dr Adequate]

Folks, we are back at our horserace to find out who will be the last evolutionist who understands the mathematics of mutation and selection. And we find that Adebz has surged ahead by a tale. If you can't think of any new lies, I don't see why I should bother with a new smackdown. Rather than speculate on who will be the last person to be fooled by the stupid innumerate gibberish of lies which you have the mendacity to call "the mathematics of mutation and selection", you should instead turn your attention to the question of whether anyone will ever thus be deceived.

[Dr Adequate]

Hey, so where's your analysis of Dr. Adaquate's simulations? Or do you generally just ignore all evidence that clearly shows how rediculous you are? Well, to be fair, he did scream a lot of hysterical halfwitted nonsense about it, which is as near as kleinman comes to noticing that his fantasy world is under threat.

[kleinman]

Folks, we are back at our horserace to find out who will be the last evolutionist who understands the mathematics of mutation and selection. And we find that Adebz has surged ahead by a tale.Hey, so where's your analysis of Dr. Adaquate's simulations? Or do you generally just ignore all evidence that clearly shows how rediculous you are?
And here comes joobz riding on Adebz’s example of gif and awe. Folks, this is a thrilling horserace, who is going to win it?

[Dr Adequate]

And here comes joobz riding on Adebz’s example of gif and awe. Folks, this is a thrilling horserace, who is going to win it? So, more magic words and gibberish --- but no math.

[kleinman]

Hey, so where's your analysis of Dr. Adaquate's simulations? Or do you generally just ignore all evidence that clearly shows how rediculous you are?Well, to be fair, he did scream a lot of hysterical halfwitted nonsense about it, which is as near as kleinman comes to noticing that his fantasy world is under threat.
And here comes Adebz back into the lead and he is riding his horse backwards! He does leave us hysterical, hysterically laughing.

[joobz]

And here comes Adebz back into the lead and he is riding his horse backwards! He does leave us hysterical, hysterically laughing.
Kleinman, You've reached your Master's Magic number in post count. And after the six hundred and sixty six posts you've made, you have done nothing but establish your incompetance and foolishness.

Where was the magic proof you had for us? Where's the math? Would you prefer to discuss Noah's arc? That thread is still open for your wisdom.

[Dr Adequate]

I wish kleinman would submit a paper for peer review, my colleagues would enjoy the laugh.

---

HOW I PROVED EVOLUTION MATHEMATICALLY IMPOSSIBLE IN MY SPARE TIME, OF WHICH I HAVE TOO MUCH

by Dr Alan Kleinman, mental age 8¾

Cheese! Cheese herrings cheese! Gif and awe, joobaquate, adebz, alchemy. Cheese, fecal matter, diapers, cheese!

Cheese joobequate cruft cheese cheese, horses, herrings, cheese.

Amathematician, cheese, alchemy, cheese whine cheese herrings cheese.

Cheese cheese CHEESE!

Olly-olly-olly home free.

CHEESE!

The author would like to thank his macros for writing most of this for him.

[Dr Adequate]

And here comes Adebz back into the lead and he is riding his horse backwards! He does leave us hysterical, hysterically laughing. Gibberish. No math. Frickin' predictable, aren't you?

[kleinman]

I wish kleinman would submit a paper for peer review, my colleagues would enjoy the laugh.
Peer review by a group of brainwashed, cultist, mathematically challenged evolutionists that is hysterical.

Here is an example of the use of multiple selection pressures to control the evolution of resistance in diamondback moth and beef armyworm. This article is located at http://trec.ifas.ufl.edu/research_ento_nemato_veg_projs.shtml (http://trec.ifas.ufl.edu/research_ento_nemato_veg_projs.shtml) .
Plutella xylostella[/I] (Linnaeus)"]It is very essential to address resistance problem in diamondback moth. In most instances, development of resistance is directly related to the intense selective pressure due to excessive use of a specific insecticide. This selection pressure will be reduced by rotating insecticides of various classes in the management program of diamondback moth.
and
Frequent use of any insecticides for controlling beet armyworm will be reduced by rotating multiple insecticides in the proposed management program. Bt based insecticides will be applied to control early development stages of beet armyworm. Conventional chemical insecticides will be applied to control late stage larvae after every two applications of Bt based insecticides. This practice will significantly delay development of resistance in beet armyworms against any insecticides.
Here is an article about fungicides. This article is located at http://ipm.ncsu.edu/apple/chptr4.html (http://ipm.ncsu.edu/apple/chptr4.html) .
To avoid development of resistance to the DMI fungicides, apply these fungicides only in combination with a broad spectrum, protectant fungicide such as captan or the EBDC fungicides (metiram or mancozeb).

[Dr Adequate]

So, you've got nothing?

[joobz]

Peer review by a group of brainwashed, cultist, mathematically challenged evolutionists that is hysterical.

WAHHH, peer review is hard!! Waaaa, It's all political.. Waaa, I'm expected to actually present something. Waaa.

[Dr Adequate]

If he submitted this crap to the freakin' Discovery Institute, do you suppose they'd touch it?

We can but hope.

[Taffer]

http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
Adebz is trying to do his mathematics by gif and awe. At least this brainwashed, prejudiced and biased evolutionist is trying. What he is trying to do is be the last evolutionist to understand the mathematics of mutation and selection. He thinks that a graph that does not include genome size, mutation rate, population, description of selection pressures, real examples of what he is trying to demonstrate, and a derivation of the model with assumptions used is somehow going to convince anyone reading this thread that multiple selection pressures accelerates evolution.

Do you know why that is, kleinman? It is simply because that graph is based upon the same equations that the formula I gave a few pages ago was. By the way, the formula I gave is proven, mathematically. You claim there is no maths. You are, therefore, completely ignorant of the entire field of population and evolutionary genetics. We have already solved these equations. Many, many, years ago. Dr. Adequate's graph does not include things like genome size because it is not relevant at all. The change in allele frequency in a population depends on only two things: frequency of that allele in the generation before, and the selection coefficient of that particular allele. You don't need to describe any selection pressures, because you have a selection coefficient. You only need the selection coefficient, becuase it is the sum of all selection pressures acting upon the allele.

Wait, it does convince Taffer.

It convinced me two years ago, when I studied these basic principles of population genetics, kleinman. It convinced me because it is correct. You do not convince me because you are not correct.

So we still have a horse race, its Adebz and Taffer neck and neck to be the last evolutionists on this thread to understand the mathematics of mutation and selection.

:rolleyes:

Taffer tries to make a point using semantics.

Emergence is not evolution, kleinman. No matter how much you wave your arms, it isn't going to make it so.

[Taffer]

Here is another link which discusses the attempted extinction of mosquito larve and can be found at [http://faculty.ucr.edu/~walton/bacteria.htm. Note that this author does not use the word emergence in describing the evolution of resistance to these selection pressures.

Two Bacillus are currently used for mosquito control in California; however, because Bacillus thuringiensis subsp. israelensis (Bti) is comparatively less effective against mosquitoes inhabiting the organically enriched waters of treatment wetlands, Bacillus sphaericus currently offers a viable alternative for microbial control of mosquitoes in organically-enriched treatment wetlands (Walton et al. 1998). Unlike Bti which contains multiple toxins that limit the potential for the rapid evolution of resistance in mosquitoes, the two toxin precursors in B. sphaericus act as a single toxin following ingestion and partial digestion by mosquito larvae. Bti has been used for nearly 30 years in large-scale mosquito and black fly control programs and resistance had not been detected in mosquito populations in nature that have been subjected to selection from Bti toxins. Nevertheless, mosquitoes, such as the southern house mosquito Culex quinquefasciatus, can evolve resistance to the full complement of Bti toxins when under strong selection pressure in the laboratory. Resistance to Bti was recently detected in a closely related species Culex pipiens in Syracuse, New York (see: Paul et al. 2005. Journal of the American Mosquito Control Association 21: 305-309). In contrast to the findings for Bti, resistance to B. sphaericus has been observed in several places (Brazil, China, France, India and Thailand). Mosquitoes can evolve resistance to B. sphaericus very rapidly (>10,000-fold in 7-8 generations), especially when the mosquitoes commonly found in often polluted urban environments, such as catch basins and wastewater contaminated by human sewage, are routinely exposed to B. sphaericus toxins.

(All emphasis added.)

Learn to read your own citations. First, this is not from a peer review journal.

Secondly, turn your attention to the section highlighted in red. If you notice the bolded section, you will see it says "the potential for" evolution is reduced. Not actual evolution itself. It does not say evolution slowed, but that there is less chance to evolve. What does this mean? It means that variation has been reduced, and the population size is smaller. This is most definately not the same as evolution slowing. He is saying here, without using these words, that "the emergence of resistance is slowed". Emergence is not evolution.

Thirdly, note the two sections highlighted in red. You will find the bolded sections especially interesting. This paper does not agree with you, as it states that increased selection pressure and many selection pressure (I think we can all agree that a "very polluted urban environment" contains lots of selection pressures) lead to rapid evolution.

Nice try.

[Dr Adequate]

Do you know why that is, kleinman? It is simply because that graph is based upon the same equations that the formula I gave a few pages ago was. To be precise, it's because the computer simulation I used to produce the graph is a model of evolution, and so are the equations. I used a simulated population, just like ev.

I must have missed it when you posted the equations, by the way. I didn't realise quite how often this particular bit of kleinman's nonsense has been debunked.

[Taffer]

Sure I did, that’s why I can post quotes like this from the link:
Unlike Bti which contains multiple toxins that limit the potential for the rapid evolution of resistance in mosquitoes, the two toxin precursors in B. sphaericus act as a single toxin following ingestion and partial digestion by mosquito larvae.

See above. "Potential" for rapid evolution is not putting a limit on evolution itself. It is limiting the emergence of resitance. Emergence is not evolution.

AndIn contrast to the findings for Bti, resistance to B. sphaericus has been observed in several places (Brazil, China, France, India and Thailand). Mosquitoes can evolve resistance to B. sphaericus very rapidly (>10,000-fold in 7-8 generations), especially when the mosquitoes commonly found in often polluted urban environments, such as catch basins and wastewater contaminated by human sewage, are routinely exposed to B. sphaericus toxins.

As stated above, polluted environments have many sources of selection pressure.

Single selection pressure gives rapid evolution of resistance.
Unlike Bti which contains multiple toxins that limit the potential for the rapid evolution of resistance in mosquitoes, the two toxin precursors in B. sphaericus act as a single toxin following ingestion and partial digestion by mosquito larvae.

Read your own source. It says nowhere that "single selection pressure gives rapid evolution of resistance".

AndBti has been used for nearly 30 years in large-scale mosquito and black fly control programs and resistance had not been detected in mosquito populations in nature that have been subjected to selection from Bti toxins. Nevertheless, mosquitoes, such as the southern house mosquito Culex quinquefasciatus, can evolve resistance to the full complement of Bti toxins when under strong selection pressure in the laboratory. Resistance to Bti was recently detected in a closely related species Culex pipiens in Syracuse, New York (see: Paul et al. 2005. Journal of the American Mosquito Control Association 21: 305-309).

Here it says that the use of a single toxin has not shown the evolution of resistance, except when it is really strong. Read your own sources, idiot.

Multiple selection pressures slow evolution of resistance. In this case, it goes from 7 to 8 generations for the single selection pressure to 30 years for multiple selection pressures.

The 30 years quoted was a) for a single "selection pressure", not multiple, and b) the "30 years" would have been a weak selection pressure. Or do you now also claim that strong selection slows evolution too?

Now if you read your URLs that you post, you would be able to quote from them (if they had anything worthwhile to quote to support your position).

Given that I have never seen a single quote from you that supports your position, I find this laughable. Especially because, most often, the quoted paper says the exact opposite of your position.

And Adebz surges into the lead. Who will win this race to be the last evolutionist to understand the mathematics of mutation and selection?

:rolleyes:

[Taffer]

To be precise, it's because the computer simulation I used to produce the graph is a model of evolution, and so are the equations. I used a simulated population, just like ev.

Very true.

I must have missed it when you posted the equations, by the way. I didn't realise quite how often this particular bit of kleinman's nonsense has been debunked.

A few pages back, or so. Kleinman wanted a mathematical model for "multiple selection". Since that concept is redundant (insofar as the model is concerned), I used the model for heterozygote advantage. I then pointed out that increasing selection pressure (one way of which is to increase the number of selection pressures) speeds up evolution, from the very equation.

If I recall, his response was "that models recombination and selection, not mutation and selection". :rolleyes:

[Taffer]

I hear and read this type of terminology when evolutionists talk about selection pressures. Do you want to enumerate and elaborate on the variables that determine the intensity of selection pressures?

Now we are getting somewhere. The degree of selection can be calculated in a number of different ways. Generally, it is measured as a relative selection coefficient of the less fit allele being compared. The more fit allele has a fitness of 1, and the less fit allele has a fitness of 1-s (s being the selection coefficient). One way to calculate the selection coefficient is to compare the number of offspring, on average, produced by those with one allele compared to those with another allele.

Give us some examples of this. Do you propose that a selection pressure doesn’t have to be present long enough for at least some individuals in the population to have adapted to that pressure, for example antibiotic resistance?

Organisms have to be alive for the correct variation to arrise in a population. Smaller populations have less variation (not entirely true, but true enough for our purposes).

Rapid adaptation occurs by recombination and natural selection, not mutation and natural selection.[/quote]

Nonsense. Both recombination and mutation create variation in a population. Selection acts on that variation, and it makes no difference how that variation arose.

Recombination and natural selection is what Darwin was observing when he reported on the differences in finch beaks.

You do not know what recombination is. You are utterly wrong.

Recombination and natural selection works with selection of alleles, small populations and small numbers of generations.

You are wrong.

This is where Stephen Gould’s hypothesis of punctuated equilibrium has application.

Punctuated equilibrium has nothing to do with recombination, and everything to do with selection acting upon variation in a population.

However, the mathematics of mutation and selection shows it is a far slower mechanism of adaptation that requires much larger populations and much more generations to accomplish its task.

Nonsense. Variation is variation, no matter where it came from.

Recombination without errors does not increase information in the gene pool; recombination with natural selection can reduce the information in the gene pool.

Nonsense. First, define "information". Second, explain how recombination which splits a gene in half does not add information.

Add any feature you want to ev, whether it is recombination, any or all forms of mutations and show us how your theory works mathematically. Show us how these mechanisms overcome the problem for your theory that multiple selection pressures slow evolution.

We already have a model. I have given one equation for it. Dr. Adequate has given a graph using its equations. When will you get it through your thick skull that you are wrong, and that we do have mathematical models for evolution? Ev. is only one small part, and you are not even using it correctly. See Dr. Adequate's debunking of your armwaving "mathematics".[

Add this feature to ev and show us mathematically how the theory of evolution works.

Please refer to both my and Dr. Adequate's posts.

I haven’t asserted that they are unimportant; I assert that they won’t overcome the fact that multiple selection pressures slow evolution. This is what is discussed in Delphi’s Wikipedia reference to the fitness landscape and the numerous real examples of multiple selection pressures that I have posting on this thread. These real examples are not limited to random point mutations. Joobz pointed out that HIV does recombination. Certainly rodents use recombination. Any mechanism of mutation or recombination is available to these creatures discussed in the links presented here.

Multiple selection pressures does not slow evolution. You have yet to provide a single citation which agrees with you. Stop your armwaving blathering and either provide your own mathematics, or admit you are wrong. We have provided mathematics which proves "multiple selection pressures" (read: stronger selection) increases the rate of evolution.

[In fact, here are more examples of how multiple selection pressures slow evolution. These are not examples derived from a mathematical model; they demonstrate what is shown in the ev mathematical model.

This ought to be fun.

Here is an article that discusses the treatment of Hepatitis C [/SIZE][/FONT]http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1472602 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1472602) . Again, these authors report that multiple selection pressures slow the evolution of resistant strains of this virus as reported in this quote:The effective treatment of HCV infection will likely require multiple antiviral drugs with different resistance profiles to delay the emergence of resistance, as has been shown in human immunodeficiency virus (35). In the present study, treatment with either a thumb or a palm inhibitor alone rendered large numbers of resistant replicon colonies in vitro, a potential indication of the likely rapid emergence of HCV-resistant variants upon initiation of monotherapy. Importantly, by combining two inhibitors binding to the thumb and to the palm sites of the HCV polymerase we observed a greater-than-additive inhibitory effect of replicon RNA replication.

Emergence is not evolution, kleinman.


I include the following quote from this paper just for Taffer who thinks that “emergence” somehow does not refer to “evolution”.Mutants Ile482Leu, Met423Ile, and Met423Val were observed at different sequential passages, illustrating the plasticity and evolution of the quasispecies population in the presence of inhibitor's selective pressure (Table 2).

Well done! You have provided a citation which actually talks about evolution! Too bad it doesn't agree with you.

Here is another paper that discusses combination selection pressures for the treatment of malaria. It is located at http://www.ajtmh.org/cgi/content/full/72/2/163 (http://www.ajtmh.org/cgi/content/full/72/2/163) .

Emergence is not evolution, kleinman.

Again, I include the following quote for Taffer so that he know that the emergence of resistance is by evolution.


Well done! They talk about evolution in this paper as well as emergence! Too bad it doesn't say anything about what you're blathering on about.

Kleinman, face it. You do not understand what you're waving your arms about. Emergence and evolution are different things. Emergence is when a trait appears. Evolution is the change in allele ratios over time. Get this into your head.

[Taffer]

Peer review by a group of brainwashed, cultist, mathematically challenged evolutionists that is hysterical.

You should go to the CT forum. :rolleyes:

Here is an example of the use of multiple selection pressures to control the evolution of resistance in diamondback moth and beef armyworm. This article is located at [/SIZE][/FONT]http://trec.ifas.ufl.edu/research_ento_nemato_veg_projs.shtml (http://trec.ifas.ufl.edu/research_ento_nemato_veg_projs.shtml)
It is very essential to address resistance problem in diamondback moth. In most instances, development of resistance is directly related to the intense selective pressure due to excessive use of a specific insecticide. This selection pressure will be reduced by rotating insecticides of various classes in the management program of diamondback moth.

Oh look, kleinman, it doesn't say what you think it does! Surprise surprise. It says that evolution occurs rapidly in the presence of strong selection pressure. Oh, but you don't think that, do you? Also note, it talks about rotation of insecticides. In other words, completely stopping one and using another, utterly different, drug. So it only ever has 1 selection pressure at a time. Funny how that slows down evolution! :rolleyes:

Learn to read your sources.


andFrequent use of any insecticides for controlling beet armyworm will be reduced by rotating multiple insecticides in the proposed management program. Bt based insecticides will be applied to control early development stages of beet armyworm. Conventional chemical insecticides will be applied to control late stage larvae after every two applications of Bt based insecticides. This practice will significantly delay development of resistance in beet armyworms against any insecticides.

Only one selection pressure at a time, kleinman. You just refuted your own argument with your own citation. Not that that's surprising.

Learn to read your sources.

Here is an article about fungicides. This article is located at [/SIZE][/FONT]http://ipm.ncsu.edu/apple/chptr4.html (http://ipm.ncsu.edu/apple/chptr4.html) .
To avoid development of resistance to the DMI fungicides, apply these fungicides only in combination with a broad spectrum, protectant fungicide such as captan or the EBDC fungicides (metiram or mancozeb).

Emergence is not evolution, kleinman. How many times must we explain that to you?

[Dr Adequate]

A few pages back, or so. Kleinman wanted a mathematical model for "multiple selection". Since that concept is redundant (insofar as the model is concerned), I used the model for heterozygote advantage. Ah yes.

But we are not talking about the same thing, then. You are counting the number of selection pressures acting on a single site; I am counting the number of sites at which a new mutation, if it occurred, would be favored by natural selection (the x-axis of my graph), since that seems to be what kleinman is counting, or rather what he's counting this week.

[Taffer]

Ah yes.

But we are not talking about the same thing, then. You are counting the number of selection pressures acting on a single site; I am counting the number of sites at which a new mutation, if it occurred, would be favored by natural selection (the x-axis of my graph), since that seems to be what kleinman is counting, or rather what he's counting this week.

Ah yes, so I see. :o

[kleinman]

So, you've got nothing?
Nothing but the results from a peer reviewed and published model of random point mutation and natural selection, the Wikipedia reference to fitness landscape and numerous references that show that multiple selection pressures slow evolution profoundly.
Peer review by a group of brainwashed, cultist, mathematically challenged evolutionists that is hysterical.WAHHH, peer review is hard!! Waaaa, It's all political.. Waaa, I'm expected to actually present something. Waaa.
It’s not hard for evolutionists to get their papers published. Tell the peer reviewers what they want to hear and you get it published. This is how professors get their tenure in the field of biology. This is why the theory of evolution is bad for the study of biology. If you don’t join the cult, you don’t get your papers published and you don’t get tenure.
Wait, it does convince Taffer.It convinced me two years ago, when I studied these basic principles of population genetics, kleinman. It convinced me because it is correct. You do not convince me because you are not correct.
What you still don’t understand is that ev is a direct simulation of random point mutation and natural selection where you can vary parameters such as genome length, population, mutation rate and number of selection pressures and the results from this model match what happens in reality. And that reality is that multiple selection pressures slow evolution profoundly.
Taffer tries to make a point using semantics.Emergence is not evolution, kleinman. No matter how much you wave your arms, it isn't going to make it so.
Then tell us how resistance emerges.
Here is another link which discusses the attempted extinction of mosquito larve and can be found at http://faculty.ucr.edu/~walton/bacteria.htm. Note that this author does not use the word emergence in describing the evolution of resistance to these selection pressures.Two Bacillus are currently used for mosquito control in California; however, because Bacillus thuringiensis subsp. israelensis (Bti) is comparatively less effective against mosquitoes inhabiting the organically enriched waters of treatment wetlands, Bacillus sphaericus currently offers a viable alternative for microbial control of mosquitoes in organically-enriched treatment wetlands (Walton et al. 1998). Unlike Bti which contains multiple toxins that limit the potential for the rapid evolution of resistance in mosquitoes, the two toxin precursors in B. sphaericus act as a single toxin following ingestion and partial digestion by mosquito larvae. Bti has been used for nearly 30 years in large-scale mosquito and black fly control programs and resistance had not been detected in mosquito populations in nature that have been subjected to selection from Bti toxins. Nevertheless, mosquitoes, such as the southern house mosquito Culex quinquefasciatus, can evolve resistance to the full complement of Bti toxins when under strong selection pressure in the laboratory. Resistance to Bti was recently detected in a closely related species Culex pipiens in Syracuse, New York (see: Paul et al. 2005. Journal of the American Mosquito Control Association 21: 305-309). In contrast to the findings for Bti, resistance to B. sphaericus has been observed in several places (Brazil, China, France, India and Thailand). Mosquitoes can evolve resistance to B. sphaericus very rapidly (>10,000-fold in 7-8 generations), especially when the mosquitoes commonly found in often polluted urban environments, such as catch basins and wastewater contaminated by human sewage, are routinely exposed to B. sphaericus toxins. (All emphasis added.)

Learn to read your own citations. First, this is not from a peer review journal.
Let’s see if we can read this citation properly. The text you highlighted in red is clearly saying that multiple selection pressures (Bti) limits the evolution of resistance whereas B. sphaericus which has only a single acting selection pressure. In your second blue highlighted text, it states that resistance to this single selection pressure evolve “>10,000-fold” more rapidly. Your first blue highlighted text states that under controlled laboratory conditions, you can get resistance to the multiple selection pressures of Bti. Real life does not occur in controlled laboratory conditions.

Ev is from a peer reviewed journal, why don’t you believe the results from this model? Anyway, I have given numerous references from peer reviewed journals that shows that multiple selection pressures slow evolution.

Taffer, if your argument for your case comes down to emergence is not evolution, only a devout evolutionist will agree with your case, everyone else will realize that emergence of resistance comes about by evolution and that multiple selection pressures slow emergence of resistance and therefore slow evolution. HIV is the prime example of the way evolution by random mutation and natural selection works. There are numerous peer reviewed papers that publish this result. This is the reality of how mutation and selection actually works.

Here are some more links to multiple selection pressures slowing evolution. The first discusses preventing resistance to fungicides and can be found at http://www.teagasc.ie/publications/2007/20070131/ntc2007paper05.htm (http://www.teagasc.ie/publications/2007/20070131/ntc2007paper05.htm) .
Mix or alternate fungicides with different modes of action.
and
Triazole fungicides should be used in mixtures with non cross-resistant partner fungicides in order to reduce the risk of resistance developing in the target pathogens.
Here is another article that discusses the evolution of weed resistance to herbicides and can be found at http://www.ag.uidaho.edu/potato/research/files/Volume%2038/Hutchinson2.pdf (http://www.ag.uidaho.edu/potato/research/files/Volume%2038/Hutchinson2.pdf)
Repeat herbicide applications with the same site of action to the same or different crops.
Single selection pressures evolve more quickly and
Herbicides used without other weed control options (e.g. cultivation) and are considered "stand alone" weed control programs.
Multiple selection pressures evolve more slowly.

[joobz]

It’s not hard for evolutionists to get their papers published. Tell the peer reviewers what they want to hear and you get it published. This is how professors get their tenure in the field of biology. This is why the theory of evolution is bad for the study of biology. If you don’t join the cult, you don’t get your papers published and you don’t get tenure.

I now understand why you had so few publications from your thesis.:rolleyes:

[Dr Adequate]

Nothing but the results from a peer reviewed and published model of random point mutation and natural selection, the Wikipedia reference to fitness landscape and numerous references that show that multiple selection pressures slow evolution profoundly.

It’s not hard for evolutionists to get their papers published. Tell the peer reviewers what they want to hear and you get it published. This is how professors get their tenure in the field of biology. This is why the theory of evolution is bad for the study of biology. If you don’t join the cult, you don’t get your papers published and you don’t get tenure.

What you still don’t understand is that ev is a direct simulation of random point mutation and natural selection where you can vary parameters such as genome length, population, mutation rate and number of selection pressures and the results from this model match what happens in reality. And that reality is that multiple selection pressures slow evolution profoundly.

Then tell us how resistance emerges.

Let’s see if we can read this citation properly. The text you highlighted in red is clearly saying that multiple selection pressures (Bti) limits the evolution of resistance whereas B. sphaericus which has only a single acting selection pressure. In your second blue highlighted text, it states that resistance to this single selection pressure evolve “>10,000-fold” more rapidly. Your first blue highlighted text states that under controlled laboratory conditions, you can get resistance to the multiple selection pressures of Bti. Real life does not occur in controlled laboratory conditions.

Ev is from a peer reviewed journal, why don’t you believe the results from this model? Anyway, I have given numerous references from peer reviewed journals that shows that multiple selection pressures slow evolution.

Taffer, if your argument for your case comes down to emergence is not evolution, only a devout evolutionist will agree with your case, everyone else will realize that emergence of resistance comes about by evolution and that multiple selection pressures slow emergence of resistance and therefore slow evolution. HIV is the prime example of the way evolution by random mutation and natural selection works. There are numerous peer reviewed papers that publish this result. This is the reality of how mutation and selection actually works.

Here are some more links to multiple selection pressures slowing evolution. The first discusses preventing resistance to fungicides and can be found at http://www.teagasc.ie/publications/2007/20070131/ntc2007paper05.htm (http://www.teagasc.ie/publications/2007/20070131/ntc2007paper05.htm) .

and

Here is another article that discusses the evolution of weed resistance to herbicides and can be found at http://www.ag.uidaho.edu/potato/research/files/Volume%2038/Hutchinson2.pdf (http://www.ag.uidaho.edu/potato/research/files/Volume%2038/Hutchinson2.pdf)

Single selection pressures evolve more quickly and

Multiple selection pressures evolve more slowly. Same old rubbish. A little less coherent. "Multiple selection pressures evolve more slowly"? Sheesh. The phrase "not even wrong" comes to mind. Can't you even remember what it is you're meant to be lying about?

Still no math, I notice.

[kleinman]

Still no math, I notice.
We need a designated driver for Adebz. He has drunk so much of his own whine that he completely missed the mathematics of ev. We are now showing examples of this mathematics. Delphi, can you drive Adebz back to the beginning of this thread so he can see the mathematics of ev and why don’t you take him over to Wikipedia so he can take a look at the mathematics of the fitness landscape. What the mathematics of ev shows is that multiple selection pressures profoundly slow evolution. This mathematical fact is revealed in the treatment of HIV, Hepatitis C, TB, pesticide usage, herbicide usage, fungicide usage, rodenticides usage… What is that selection pressure that evolved reptile into birds?

[joobz]

We need a designated driver for Adebz. He has drunk so much of his own whine that he completely missed the mathematics of ev. We are now showing examples of this mathematics. Delphi, can you drive Adebz back to the beginning of this thread so he can see the mathematics of ev and why don’t you take him over to Wikipedia so he can take a look at the mathematics of the fitness landscape. What the mathematics of ev shows is that multiple selection pressures profoundly slow evolution. This mathematical fact is revealed in the treatment of HIV, Hepatitis C, TB, pesticide usage, herbicide usage, fungicide usage, rodenticides usage… What is that selection pressure that evolved reptile into birds?(bolding mine)

You've lost all form of logic and reason or your lie macro is on the fritz again.

Remember your little, HIV doesn't count cause I say so game? (http://forums.randi.org/showpost.php?p=2592246&postcount=4091)
If, HIV counts, it proves you wrong. If, HIV doesn't count(because of some bizarro stipulations you make), then why refer to it?

[kleinman]

We need a designated driver for Adebz. He has drunk so much of his own whine that he completely missed the mathematics of ev. We are now showing examples of this mathematics. Delphi, can you drive Adebz back to the beginning of this thread so he can see the mathematics of ev and why don’t you take him over to Wikipedia so he can take a look at the mathematics of the fitness landscape. What the mathematics of ev shows is that multiple selection pressures profoundly slow evolution. This mathematical fact is revealed in the treatment of HIV, Hepatitis C, TB, pesticide usage, herbicide usage, fungicide usage, rodenticides usage… What is that selection pressure that evolved reptile into birds?(bolding mine)

You've lost all form of logic and reason or your lie macro is on the fritz again.
HIV is the prime and best example of how mutation and selection works. You need a short genome with a rapid reproduction rate and still combination therapy (multiple selection pressures) can and does stymie the evolutionary process. It is simple arithmetic joobz. This is what the peer reviewed and published model of mutation and selection shows, this is what the Wikipedia reference to fitness landscape shows and this is what reality shows. Do you want me to post quotes from these references again to prove my point? Now if you want to show us how multiple selection pressures accelerate evolution, I think everyone would be interested in you showing how this can occur. But alas, your response will be the same as your response as how ribose can be created nonenzymatically.

In case you don’t think that combination therapy (combination selection pressures) does not suppress evolution of resistant strains of HIV, here is a link to the National Institute of Health at http://www.niaid.nih.gov/factsheets/treat-hiv.htm (http://www.niaid.nih.gov/factsheets/treat-hiv.htm) .
As HIV reproduces itself, different strains of the virus emerge, some that are resistant to antiretroviral drugs. Therefore, doctors recommend patients infected with HIV take a combination of antiretroviral drugs known as HAART. This strategy, which typically combines drugs from at least two different classes of antiretroviral drugs, has been shown to effectively suppress the virus when used properly. Developed by NIAID-supported researchers, HAART has revolutionalized how we treat people infected with HIV by successfully suppressing the virus and decreasing the rate of opportunistic infections.
I found this site by using google with the key words “HIV” “combination” and “treatment”. There were over a million hits to this search. I’ll start posting links and quotes from those links that show that multiple selection pressures suppress the evolution of HIV. This is a prime example how the mathematics of mutation and selection works in reality.

Joobz, you are still one of the favorites to win the horserace as the last evolutionist on this thread to understand the mathematics of mutation and selection.

[Dr Adequate]

HIV is the prime and best example of how mutation and selection works. You need a short genome with a rapid reproduction rate and still combination therapy (multiple selection pressures) can and does stymie the evolutionary process. It is simple arithmetic joobz. This is what the peer reviewed and published model of mutation and selection shows, this is what the Wikipedia reference to fitness landscape shows and this is what reality shows. Do you want me to post quotes from these references again to prove my point? Now if you want to show us how multiple selection pressures accelerate evolution, I think everyone would be interested in you showing how this can occur. But alas, your response will be the same as your response as how ribose can be created nonenzymatically.

In case you don’t think that combination therapy (combination selection pressures) does not suppress evolution of resistant strains of HIV, here is a link to the National Institute of Health at http://www.niaid.nih.gov/factsheets/treat-hiv.htm (http://www.niaid.nih.gov/factsheets/treat-hiv.htm) .

I found this site by using google with the key words “HIV” “combination” and “treatment”. There were over a million hits to this search. I’ll start posting links and quotes from those links that show that multiple selection pressures suppress the evolution of HIV. This is a prime example how the mathematics of mutation and selection works in reality.

Joobz, you are still one of the favorites to win the horserace as the last evolutionist on this thread to understand the mathematics of mutation and selection. Same old bollocks, same halfwitted conflation of demographic pressures and selection pressures, no math.

I'm sorry, kleinman, you're going to have to retake third grade.

[Dr Adequate]

We need a designated driver for Adebz. He has drunk so much of his own whine that he completely missed the mathematics of ev. We are now showing examples of this mathematics. Delphi, can you drive Adebz back to the beginning of this thread so he can see the mathematics of ev and why don’t you take him over to Wikipedia so he can take a look at the mathematics of the fitness landscape. What the mathematics of ev shows is that multiple selection pressures profoundly slow evolution. This mathematical fact is revealed in the treatment of HIV, Hepatitis C, TB, pesticide usage, herbicide usage, fungicide usage, rodenticides usage… What is that selection pressure that evolved reptile into birds? So, it's still the same old lies, the same old gibberish, the same old magic words --- and no math.

[joobz]

HIV is the prime and best example of how mutation and selection works.
You are correct, HIV proves evolution exists. thank you! So will you retract this bit of nonsense you did?

For clarity, I have summarized the key points of this conversation. I think we have a new lie here.

If you studied ev, you would understand this. If you examined the real cases of combination therapy for the treatment of HIV, combination therapy for the treatment of TB, combination pesticides, combination herbicides, combination rodenticides, you would see real examples of what ev demonstrates and what the fitness landscape requires. Mutation and selection can not and does not do what evolutionists allege, it is mathematically impossible.

It is the number of directional selection pressures and genome length which dominate the mathematics of mutation and selection. There is no reason to believe that frame shift mutations, translocations, duplications or any other way of scrambling a genome is going to change the underlying mathematics of mutation and selection.

This is your concrete basis for not worring about it?

I think this paper wouldn't have been accepted if that was the case:
Carvajal-Rodriguez A, Crandall KA, Posada D. "Recombination favors the evolution of drug resistance in HIV-1 during antiretroviral therapy." Infect Genet Evol. 2007 Feb 12; [Epub ahead of print]
I can't access the paper yet, but from the abstract:

Using computer simulations we show that the effect of recombination on the evolution of drug resistance depends strongly on the intensity of selection, as well as on the viral population size. Under the high selection pressure expected during antiretroviral therapy, the strength of the Hill-Robertson effect increases and recombination favors the evolution of resistance under a wide range of population sizes, independently of the sign of the epistatic interaction. Our results suggest that recombination plays an important role in the evolution of drug resistance in HIV-1 under various realistic scenarios
Seems like evolution has a mathematical basis after all.

So how does this work with HIV? Here is a quote from an article located at http://www.cdc.gov/ncidod/eid/vol3no3/burke.htm

Human immunodeficiency virus (HIV)-1, like all retroviruses, is "diploid." Each viral particle contains two RNA strands of positive polarity, each full length and potentially able to replicate (1). No other virus families, RNA or DNA, are diploid. Typically both RNA strands in a retroviral particle derive from the same parent provirus. However, if an infected cell simultaneously harbors two different proviruses, one RNA transcript from each provirus can be encapsidated into a single "heterozygous" virion. When this virion subsequently infects a new cell, the reverse transcriptase may jump back and forth between the two RNA templates so that the newly synthesized retroviral DNA sequence is recombinant between that of the two parents (2). All subsequent progeny virions will be of this recombinant genotype. HIV-1 strains with chimeric genomes thought to have arisen through homologous recombination have recently been discovered in nature (3).
This is a property unique to the retroviruses, are you trying to generalize this phenomenon to the entire theory of evolution? This appears like a baseless extrapolation.

Unfortunately, you've been using HIV viruses as proof of why evolution is impossible. I show a study where they demonstrate how multiple selection pressures won't HALT HIV evolution, and now you claim that I can't extrapolate this truth to anything else.

No it doesn’t, it only shows that you know how to make a baseless extrapolation.

I see, when evolutionists adjust their theory, this is scientific research, when I adjust my theory, I’m moving the goal posts.
This isn't an "adjustment of a theory". This is intellectual dishonesty.
We have been discussing how multiple pressures doesn't stop evolution using HIV as an example. I give evidence that states mathematically that this isn't the case. And now you claim that it doesn't apply.
This is the worst form of professional behavior.

[kleinman]

HIV is the prime and best example of how mutation and selection works.You are correct, HIV proves evolution exists. thank you! So will you retract this bit of nonsense you did?
Certainly evolution by mutation and selection exists. Ev models this quite nicely and explains how it works mathematically. Mutation and selection is a profoundly slow process. You need large populations with large reproduction rates and small genome lengths to accomplish anything. HIV fits these parameters perfectly. Even with these conditions, combination therapy (multiple selection pressures) slows the evolution process profoundly. The real nonsense in this discussion is you believe that reptiles evolved into birds. You have much smaller populations with much lower reproduction rates and much, much larger genomes than in the case of HIV. In addition, you need large numbers of selection pressures (none of which you can describe and mathematically has been shown would interfere with each other) to transform the huge number of genes necessary to morph a reptile genome into a bird genome. That is the nonsense in this discussion and that is what you claim has happened. It is mathematically impossible; the evolution process can not work quickly enough in the time available and you don’t have the selection processes necessary to accomplish the type of transformations you evolutionists allege. If you understood the mathematics of mutation and selection you would understand why the theory of evolution is impossible. You are both ignorant and in denial of these mathematical facts.

[joobz]

Certainly evolution by mutation and selection exists.
So, I'm right and you simply remain intellectually dishonest because it suits your needs. At least that's the only thing that explains this.

For clarity, I have summarized the key points of this conversation. I think we have a new lie here.

If you studied ev, you would understand this. If you examined the real cases of combination therapy for the treatment of HIV, combination therapy for the treatment of TB, combination pesticides, combination herbicides, combination rodenticides, you would see real examples of what ev demonstrates and what the fitness landscape requires. Mutation and selection can not and does not do what evolutionists allege, it is mathematically impossible.

It is the number of directional selection pressures and genome length which dominate the mathematics of mutation and selection. There is no reason to believe that frame shift mutations, translocations, duplications or any other way of scrambling a genome is going to change the underlying mathematics of mutation and selection.

This is your concrete basis for not worring about it?

I think this paper wouldn't have been accepted if that was the case:
Carvajal-Rodriguez A, Crandall KA, Posada D. "Recombination favors the evolution of drug resistance in HIV-1 during antiretroviral therapy." Infect Genet Evol. 2007 Feb 12; [Epub ahead of print]
I can't access the paper yet, but from the abstract:

Using computer simulations we show that the effect of recombination on the evolution of drug resistance depends strongly on the intensity of selection, as well as on the viral population size. Under the high selection pressure expected during antiretroviral therapy, the strength of the Hill-Robertson effect increases and recombination favors the evolution of resistance under a wide range of population sizes, independently of the sign of the epistatic interaction. Our results suggest that recombination plays an important role in the evolution of drug resistance in HIV-1 under various realistic scenarios
Seems like evolution has a mathematical basis after all.

So how does this work with HIV? Here is a quote from an article located at http://www.cdc.gov/ncidod/eid/vol3no3/burke.htm

Human immunodeficiency virus (HIV)-1, like all retroviruses, is "diploid." Each viral particle contains two RNA strands of positive polarity, each full length and potentially able to replicate (1). No other virus families, RNA or DNA, are diploid. Typically both RNA strands in a retroviral particle derive from the same parent provirus. However, if an infected cell simultaneously harbors two different proviruses, one RNA transcript from each provirus can be encapsidated into a single "heterozygous" virion. When this virion subsequently infects a new cell, the reverse transcriptase may jump back and forth between the two RNA templates so that the newly synthesized retroviral DNA sequence is recombinant between that of the two parents (2). All subsequent progeny virions will be of this recombinant genotype. HIV-1 strains with chimeric genomes thought to have arisen through homologous recombination have recently been discovered in nature (3).
This is a property unique to the retroviruses, are you trying to generalize this phenomenon to the entire theory of evolution? This appears like a baseless extrapolation.

Unfortunately, you've been using HIV viruses as proof of why evolution is impossible. I show a study where they demonstrate how multiple selection pressures won't HALT HIV evolution, and now you claim that I can't extrapolate this truth to anything else.

No it doesn’t, it only shows that you know how to make a baseless extrapolation.

I see, when evolutionists adjust their theory, this is scientific research, when I adjust my theory, I’m moving the goal posts.
This isn't an "adjustment of a theory". This is intellectual dishonesty.
We have been discussing how multiple pressures doesn't stop evolution using HIV as an example. I give evidence that states mathematically that this isn't the case. And now you claim that it doesn't apply.
This is the worst form of professional behavior.

[kleinman]

Certainly evolution by mutation and selection exists.So, I'm right and you simply remain intellectually dishonest because it suits your needs. At least that's the only thing that explains this.
The only thing you have been right about in this discussion is when you said you had no idea how ribose could form nonenzymatically. Of course that’s your idea of how to prove abiogenesis is true.

You think that the theory of evolution is mathematically possible. You have no idea how it occurs. You have no mathematical model to substantiate your view. You have no real examples of how it occurs. On the other hand, I have a peer reviewed and published mathematical model of mutation and selection to substantiate my argument. What the model shows is that multiple selection pressures profoundly slow evolution. I have posted about 15 references which demonstrate in reality what the mathematical model shows and why the theory of evolution is mathematically impossible. You don’t even have intellectual dishonesty; you only have ignorance and denial.

I’ll continue to post more references to how multiple selection pressures slow evolution profoundly and we can all wait while you try to find a single example of where multiple selection pressures accelerates evolution.

[kjkent1]

...the theory of evolution is mathematically impossible.Don't mean to intrude on your fun with joobz, but there is no such thing as proof that any real world process is mathematically impossible, and you are being either deceitful or willfully ignorant in suggesting otherwise.

A mathematical model is nothing more than the use of symbols to describe reality. Just because someone manages to craft an equation which successfully describes the information gain produced via random point mutation and one possible method of selection, doesn't mean that this model accurately describes all forms of real-world evolutionary activity -- any more than Newton's laws accurately describe relativistic behavior, or than Einstein's equations accurately describe quantum behavior.

The only thing you've managed to prove is that you are unwilling to actually test your own hypothesis. If you were so willing, then you wouldn't wait for others to modify the ev selection algorithm or modify the types of mutational errors which occur. Instead, you would model these forces yourself, and risk the possibility of falsifying your conclusion.

Your voluntarily choosing to avoid testing your theories demonstrates to me that you don't actually believe your own hypotheses.

So, go right on ahead and continue to claim that Schneider has done all the work necessary, and that there is no reason for you to do any of the work, and the only attention you will receive will be ridicule of others who read your protestations in this forum.

Outside of this forum, in the real world, where things actually matter -- you and your ideas will remain unknown and/or ignored.

[joobz]

The only thing you have been right about in this discussion is when you said you had no idea how ribose could form nonenzymatically. Of course that’s your idea of how to prove abiogenesis is true.

You think that the theory of evolution is mathematically possible. You have no idea how it occurs. You have no mathematical model to substantiate your view. You have no real examples of how it occurs. On the other hand, I have a peer reviewed and published mathematical model of mutation and selection to substantiate my argument. What the model shows is that multiple selection pressures profoundly slow evolution. I have posted about 15 references which demonstrate in reality what the mathematical model shows and why the theory of evolution is mathematically impossible. You don’t even have intellectual dishonesty; you only have ignorance and denial.

I’ll continue to post more references to how multiple selection pressures slow evolution profoundly and we can all wait while you try to find a single example of where multiple selection pressures accelerates evolution.
Shall we remind you why you are found wanting?
No math....Check
No new Lies....Check
Still, fully and wholeheartedly a intellecutal coward...Check.
can you comment on your desire to just out right lie and contridict yourself? here's the example one more time.

For clarity, I have summarized the key points of this conversation. I think we have a new lie here.

If you studied ev, you would understand this. If you examined the real cases of combination therapy for the treatment of HIV, combination therapy for the treatment of TB, combination pesticides, combination herbicides, combination rodenticides, you would see real examples of what ev demonstrates and what the fitness landscape requires. Mutation and selection can not and does not do what evolutionists allege, it is mathematically impossible.

It is the number of directional selection pressures and genome length which dominate the mathematics of mutation and selection. There is no reason to believe that frame shift mutations, translocations, duplications or any other way of scrambling a genome is going to change the underlying mathematics of mutation and selection.

This is your concrete basis for not worring about it?

I think this paper wouldn't have been accepted if that was the case:
Carvajal-Rodriguez A, Crandall KA, Posada D. "Recombination favors the evolution of drug resistance in HIV-1 during antiretroviral therapy." Infect Genet Evol. 2007 Feb 12; [Epub ahead of print]
I can't access the paper yet, but from the abstract:

Using computer simulations we show that the effect of recombination on the evolution of drug resistance depends strongly on the intensity of selection, as well as on the viral population size. Under the high selection pressure expected during antiretroviral therapy, the strength of the Hill-Robertson effect increases and recombination favors the evolution of resistance under a wide range of population sizes, independently of the sign of the epistatic interaction. Our results suggest that recombination plays an important role in the evolution of drug resistance in HIV-1 under various realistic scenarios
Seems like evolution has a mathematical basis after all.

So how does this work with HIV? Here is a quote from an article located at http://www.cdc.gov/ncidod/eid/vol3no3/burke.htm

Human immunodeficiency virus (HIV)-1, like all retroviruses, is "diploid." Each viral particle contains two RNA strands of positive polarity, each full length and potentially able to replicate (1). No other virus families, RNA or DNA, are diploid. Typically both RNA strands in a retroviral particle derive from the same parent provirus. However, if an infected cell simultaneously harbors two different proviruses, one RNA transcript from each provirus can be encapsidated into a single "heterozygous" virion. When this virion subsequently infects a new cell, the reverse transcriptase may jump back and forth between the two RNA templates so that the newly synthesized retroviral DNA sequence is recombinant between that of the two parents (2). All subsequent progeny virions will be of this recombinant genotype. HIV-1 strains with chimeric genomes thought to have arisen through homologous recombination have recently been discovered in nature (3).
This is a property unique to the retroviruses, are you trying to generalize this phenomenon to the entire theory of evolution? This appears like a baseless extrapolation.

Unfortunately, you've been using HIV viruses as proof of why evolution is impossible. I show a study where they demonstrate how multiple selection pressures won't HALT HIV evolution, and now you claim that I can't extrapolate this truth to anything else.

No it doesn’t, it only shows that you know how to make a baseless extrapolation.

I see, when evolutionists adjust their theory, this is scientific research, when I adjust my theory, I’m moving the goal posts.
This isn't an "adjustment of a theory". This is intellectual dishonesty.
We have been discussing how multiple pressures doesn't stop evolution using HIV as an example. I give evidence that states mathematically that this isn't the case. And now you claim that it doesn't apply.
This is the worst form of professional behavior.

[joobz]

Don't mean to intrude on your fun with joobz, but there is no such thing as proof that any real world process is mathematically impossible, and you are being either deceitful or willfully ignorant in suggesting otherwise.
No intrusion. I welcome you to remind him of this error. I became tired of doing so. He has no explanation for the fossil record, no explanation on why microevolution can occur multiple times over but can never result in "macro evolution", can not refute the earlier postings of examples of macroevolution presented by Mr. Scott (I believe), and has no explanation why ANY of his assumptions would be considered valid. Check back to earlier claims for "realistic" mutation rates.

I'm simply going to keep demonstrating his outright lies and missrepresentations in response to his ALREADY debunked claims.

There really is nothing to see here.

[kleinman]

...the theory of evolution is mathematically impossible.Don't mean to intrude on your fun with joobz, but there is no such thing as proof that any real world process is mathematically impossible, and you are being either deceitful or willfully ignorant in suggesting otherwise.
We all know about your string cheese theory. Anything is possible in 10^500 alternative universes. Let’s teach that to naïve preschoolers. Instead, I will continue to give you references to why ev shows the theory of evolution to be mathematically impossible.
The only thing you've managed to prove is that you are unwilling to actually test your own hypothesis. If you were so willing, then you wouldn't wait for others to modify the ev selection algorithm or modify the types of mutational errors which occur. Instead, you would model these forces yourself, and risk the possibility of falsifying your conclusion.
Let’s let the real world do the test. These references which show that multiple selection pressures slow evolution are not limited to random point mutations. These are real living creatures which when they reproduce can have any mutation you can imagine.

Here is another example from the prime case of combination therapy for the slowing of the evolution of resistant strains of HIV http://gateway.nlm.nih.gov/MeetingAbstracts/102225407.html (http://gateway.nlm.nih.gov/MeetingAbstracts/102225407.html)
The combined antiviral effects of indinavir and RT inhibitors dramatically suppressed the emergence of resistance to these agents, in a bi-directional fashion, relative to the rates observed during inhibition of the protease or RT alone. This suggests that the durability of viral inhibition can be increased by combining indinavir with one or more inhibitors of the reverse transcriptase, suppressing the viral replication that drives the evolution of resistance.

Here is an example of the use of combination antibacterial agents to delay the evolution of resistant e coli. http://www.nature.com/nature/journal/v446/n7136/abs/nature05685.html (http://www.nature.com/nature/journal/v446/n7136/abs/nature05685.html)
Multidrug combinations are increasingly important in combating the spread of antibiotic-resistance in bacterial pathogens1, 2, 3. On a broader scale, such combinations are also important in understanding microbial ecology and evolution4, 5. Although the effects of multidrug combinations on bacterial growth have been studied extensively, relatively little is known about their impact on the differential selection between sensitive and resistant bacterial populations1, 6, 7. Normally, the presence of a drug confers an advantage on its resistant mutants in competition with the sensitive wild-type population1. Here we show, by using a direct competition assay between doxycycline-resistant and doxycycline-sensitive Escherichia coli, that this differential selection can be inverted in a hyper-antagonistic class of drug combinations. Used in such a combination, a drug can render the combined treatment selective against the drug's own resistance allele. Further, this inversion of selection seems largely insensitive to the underlying resistance mechanism and occurs, at sublethal concentrations, while maintaining inhibition of the wild type. These seemingly paradoxical results can be rationalized in terms of a simple geometric argument. Our findings demonstrate a previously unappreciated feature of the fitness landscape for the evolution of resistance and point to a trade-off between the effect of drug interactions on absolute potency and the relative competitive selection that they impose on emerging resistant populations.

Here is another reference to HIV and combination vs monotherapy http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8595505&dopt=Abstract (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8595505&dopt=Abstract)
Monotherapy does not give long-term suppression of viral replication and evolution, and combination therapy is viewed as a potentially more effective long-term approach based on increased and more durable suppression of HIV replication.

Here is another example of combination fungicides to delay the evolution of resistance. http://www.apsnet.org/education/advancedplantpath/topics/Resistan/Resistan_Lesson_5.html (http://www.apsnet.org/education/advancedplantpath/topics/Resistan/Resistan_Lesson_5.html)
Many manufacturers of systemic, single-site fungicides are now marketing them formulated as combinations with multi-site fungicides, with the intent of "preventing" the evolution of resistance to the systemic fungicides. Similarly, alternate applications of fungicides with different modes of action or "cocktails" of two or more fungicides applied in the same spray or have been used as a means of combating fungicide resistance. The often-stated rationale for these fungicide combinations is that they prevent the buildup of resistance because the multi-site fungicide in the spray program kills any mutants resistant to the single-site fungicide.

This explanation of the effectiveness of fungicide combinations is not entirely correct, since a multi-site fungicide such as captan is no more effective against a benomyl-resistant Venturia population than it is against the wild-type population. However, even partial suppression of the resistant population will reduce the rate of selection of fungicide resistance and give the grower time to react before there is a catastrophic crop failure. Fungicide combinations, therefore, are a good tactic, not because they prevent resistance, but because they slow down the selection of resistance and thus can prevent crop loss.

This one is for Taffer who complained that a previous reference on this particular topic was not from a peer reviewed journal. Note how in the laboratory, by reducing the number of selection pressures, resistant strains of the mosquito larvae can be evolved when they don’t appear in nature. This is a clear example how single selection pressures applied sequentially will much more rapidly evolve resistance than when the selection pressures are applied simultaneously.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219)
Although no resistance to B. thuringiensis subsp. israelensis has been reported under field conditions, studies in the laboratory have shown that high levels of resistance can be developed when larval populations are selected against recombinant bacilli that produce only one, two, or three of this bacterium's mosquitocidal Cry proteins. For example, when populations of C. quinquefasciatus were selected against a strain producing only Cry11Aa at a concentration that killed 95% (LC95) of the larvae, the level of resistance was 1,000-fold after 28 generations (9). When the same species was selected at the same level with a strain of B. thuringiensis subsp. israelensis that produced Cry11Aa, Cry4Aa, and Cry4Ba, resistance was 217-fold after the same number of generations (9). Interestingly, the level of resistance was only 3.3-fold when C. quinquefasciatus was selected with wild-type B. thuringiensis subsp. israelensis which, in addition to the Cry endotoxins, produces Cyt1Aa (9). The implication of these results is that combinations of Cry endotoxins, and especially combinations of Cry endotoxins and Cyt1Aa, are responsible for delaying resistance.

I’ll keep my eyes open looking for more of these informative links which show that selection pressures in combination slow evolution. I will also watch for examples of where combination selection pressures accelerate evolution but so far, none have appeared. I wonder how many of these references I will have to post before you evolutionists figure out that multiple selection pressures slow evolution. In case you evolutionists haven’t figured it out, I’m patient and the google search I used to find the above references (combination selection evolution resistance) gave over a million hits and the ones above were from the first page. This is going to be fun. We’ll continue on with this next week.

[kjkent1]

We all know about your string cheese theory. Anything is possible in 10^500 alternative universes. Let’s teach that to naïve preschoolers. Instead, I will continue to give you references to why ev shows the theory of evolution to be mathematically impossible.Ahem -- your statement here is either intentionally deceitful or willfully ignorant. I have explained numerous times, that the version of string theory that I have suggested is the creation of Dr. Leonard Susskind, Ph.D, Professor of Physics, Stanford University. I don't see you attempting to challenge his math as impossible. Instead, you refer to it as string cheese. Well, that's your opinion -- worthless as it may be.

Let’s let the real world do the test. These references which show that multiple selection pressures slow evolution are not limited to random point mutations. These are real living creatures which when they reproduce can have any mutation you can imagine.Yes, let's see if I, the unscientific lawyer, can pick out the flaws in your various assertions.

Here is another example from the prime case of combination therapy for the slowing of the evolution of resistant strains of HIV http://gateway.nlm.nih.gov/MeetingAbstracts/102225407.html (http://gateway.nlm.nih.gov/MeetingAbstracts/102225407.html) OK, the error here is pretty obvious: the combination therapy is expressly designed to inhibit replication. And, where there is no replication there is no evolution -- rather there is extinction. So, the therapy attacks not the ability of the organism to evolve, but rather its ability to reproduce.

Also, something not so obvious: the "biosphere" for an HIV-1 colony is a human being. Ultimately, the therapy is intended to reduce replication of the virus as a means of lengthening the existence of the "biosphere." But, if we were to place the virus in a biosphere with a lifetime of billions of years, rather than ~100, would the therapy slow evolution, over the long run? Doubtful, because as soon as the virus did evolve any resistance, it would then start replicating wildly as before, and return to a more natural evolutionary process.

You are unreasonably extrapolating a limited therapeutic effect and applying to nature. In nature, no set of precisely targeted selective mechanisms is working in combination to inhibit the growth of the HIV virus. Instead, the selective mechanisms are randomly applied via a relatively stable environment, and the result is an HIV organism ready to take over an unsuspecting host.

I will not bother to analyze your other citations, because they will all necessarily suffer from the one inescapable error: that the natural landscape, until the emergence of homo sapiens, did not have intelligent selection mechanisms precisely targeting organisms in the environment with the purpose of limiting their reproduction. No amount of naturally hostile conditions could possibly amount to the sort of environmental stress as is being artificially applied in all of your examples of medical intervention.

Sorry, but you lose again. Bend over and assume the position.

[Taffer]

Kleinman, I see you have ignored my posts, and did not read the cited paper. I explained to you why it does not say what you think it does. Remember: many people on this forum actually understand biology, genetics, and evolutionary theory. You, clearly, do not. You are a waste of time.

Good day.

[Dr Adequate]

The only thing you have been right about in this discussion is when you said you had no idea how ribose could form nonenzymatically. Of course that’s your idea of how to prove abiogenesis is true.

You think that the theory of evolution is mathematically possible. You have no idea how it occurs. You have no mathematical model to substantiate your view. You have no real examples of how it occurs. On the other hand, I have a peer reviewed and published mathematical model of mutation and selection to substantiate my argument. What the model shows is that multiple selection pressures profoundly slow evolution. I have posted about 15 references which demonstrate in reality what the mathematical model shows and why the theory of evolution is mathematically impossible. You don’t even have intellectual dishonesty; you only have ignorance and denial. You are lying to us, about us. Whom do you hope to deceive?

I’ll continue to post more references to how multiple selection pressures slow evolution profoundly .... Continue? You fatuous liar, you have not given one case where selection pressures per se slow evolution --- and yet you claim it as a general rule.

You don't tell us how you would get from this imaginary rule to "mathematically impossible", and I predict that you never will.

[Dr Adequate]

Let’s let the real world do the test. These references which show that multiple selection pressures slow evolution are not limited to random point mutations. These are real living creatures which when they reproduce can have any mutation you can imagine.

Here is another example from the prime case of combination therapy for the slowing of the evolution of resistant strains of HIV http://gateway.nlm.nih.gov/MeetingAbstracts/102225407.html (http://gateway.nlm.nih.gov/MeetingAbstracts/102225407.html)


Here is an example of the use of combination antibacterial agents to delay the evolution of resistant e coli. http://www.nature.com/nature/journal/v446/n7136/abs/nature05685.html (http://www.nature.com/nature/journal/v446/n7136/abs/nature05685.html)


Here is another reference to HIV and combination vs monotherapy http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8595505&dopt=Abstract (http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8595505&dopt=Abstract)


Here is another example of combination fungicides to delay the evolution of resistance. http://www.apsnet.org/education/advancedplantpath/topics/Resistan/Resistan_Lesson_5.html (http://www.apsnet.org/education/advancedplantpath/topics/Resistan/Resistan_Lesson_5.html)


This one is for Taffer who complained that a previous reference on this particular topic was not from a peer reviewed journal. Note how in the laboratory, by reducing the number of selection pressures, resistant strains of the mosquito larvae can be evolved when they don’t appear in nature. This is a clear example how single selection pressures applied sequentially will much more rapidly evolve resistance than when the selection pressures are applied simultaneously.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219)


I’ll keep my eyes open looking for more of these informative links which show that selection pressures in combination slow evolution. I will also watch for examples of where combination selection pressures accelerate evolution but so far, none have appeared. I wonder how many of these references I will have to post before you evolutionists figure out that multiple selection pressures slow evolution. In case you evolutionists haven’t figured it out, I’m patient and the google search I used to find the above references (combination selection evolution resistance) gave over a million hits and the ones above were from the first page. This is going to be fun. We’ll continue on with this next week. You are producing cases in which humans imposing artificial demographic pressures on a population slow evolution as though this could serve as evidence that as a general rule multiple selection pressures slow evolution.

This is like showing us photographs of a pig in a helicopter as evidence that all pigs fly round the sky on delicate silvery wings.

You are not going to fool anyone with this garbage, because we all recognise the nature of the deceit.

You say that you are going to "continue on" with posting similarly irrelevant articles. I have no doubt of it. I have never known anyone to persevere as you do in pointless, worthless, fatuous actions. But I might as well let you know in advance that you will deceive no-one.

[Dr Adequate]

Certainly evolution by mutation and selection exists. Ev models this quite nicely and explains how it works mathematically. Mutation and selection is a profoundly slow process. You need large populations with large reproduction rates and small genome lengths to accomplish anything. HIV fits these parameters perfectly. Even with these conditions, combination therapy (multiple selection pressures) slows the evolution process profoundly. The real nonsense in this discussion is you believe that reptiles evolved into birds. You have much smaller populations with much lower reproduction rates and much, much larger genomes than in the case of HIV. In addition, you need large numbers of selection pressures (none of which you can describe and mathematically has been shown would interfere with each other) to transform the huge number of genes necessary to morph a reptile genome into a bird genome. That is the nonsense in this discussion and that is what you claim has happened. It is mathematically impossible; the evolution process can not work quickly enough in the time available and you don’t have the selection processes necessary to accomplish the type of transformations you evolutionists allege. If you understood the mathematics of mutation and selection you would understand why the theory of evolution is impossible. You are both ignorant and in denial of these mathematical facts. I observe that your stupid lies about "mathematics" are unleavened by any actual math.

[Ichneumonwasp]

Joobz, you are still one of the favorites to win the horserace as the last evolutionist on this thread to understand the mathematics of mutation and selection.

You can't possibly be so vain as to think that others will no longer debate you because they believe a word you are saying. How far does your vanity reach, Kleinman? We are embarrassed by your ignorance and obvious mistakes.

[Ducky]

http://www.youtube.com/watch?v=wOe7EuHclyo


Even a comedian could pwn kleinman.







(Though I can't get the yt tags to work.)

[kjkent1]

http://www.youtube.com/watch?v=wOe7EuHclyo

Even a comedian could pwn kleinman.

(Though I can't get the yt tags to work.)Lewis Black is hilarious. Thanks!

[kleinman]

Let’s let the real world do the test. These references which show that multiple selection pressures slow evolution are not limited to random point mutations. These are real living creatures which when they reproduce can have any mutation you can imagine.Yes, let's see if I, the unscientific lawyer, can pick out the flaws in your various assertions.
All you have to know is how to count to understand that the theory of evolution is mathematically impossible. Lawyers do know how to count, don’t they little gator?
Here is another example from the prime case of combination therapy for the slowing of the evolution of resistant strains of HIV http://gateway.nlm.nih.gov/MeetingAb...102225407.htmlOK, the error here is pretty obvious: the combination therapy is expressly designed to inhibit replication. And, where there is no replication there is no evolution -- rather there is extinction. So, the therapy attacks not the ability of the organism to evolve, but rather its ability to reproduce.
All selection pressures inhibit replication. That is by definition what a selection pressure is, it is a stress on life forms that reduce its fitness to reproduce. If that stress is sufficient, it causes extinction.
Also, something not so obvious: the "biosphere" for an HIV-1 colony is a human being. Ultimately, the therapy is intended to reduce replication of the virus as a means of lengthening the existence of the "biosphere." But, if we were to place the virus in a biosphere with a lifetime of billions of years, rather than ~100, would the therapy slow evolution, over the long run? Doubtful, because as soon as the virus did evolve any resistance, it would then start replicating wildly as before, and return to a more natural evolutionary process.
The biosphere or environment is what it is. If small pox were not kept in the laboratory, it would be extinct.
You are unreasonably extrapolating a limited therapeutic effect and applying to nature. In nature, no set of precisely targeted selective mechanisms is working in combination to inhibit the growth of the HIV virus. Instead, the selective mechanisms are randomly applied via a relatively stable environment, and the result is an HIV organism ready to take over an unsuspecting host.
The example of combination therapy of HIV slowing the evolution of the virus is only one of many examples of how multiple selection pressures slow and ultimately stops evolution as show by the example below.
I will not bother to analyze your other citations, because they will all necessarily suffer from the one inescapable error: that the natural landscape, until the emergence of homo sapiens, did not have intelligent selection mechanisms precisely targeting organisms in the environment with the purpose of limiting their reproduction. No amount of naturally hostile conditions could possibly amount to the sort of environmental stress as is being artificially applied in all of your examples of medical intervention.
You don’t need to do the analysis; I’ll do it for you. Somehow you think that man made selection pressures behave in a different mathematical manner than natural selection pressures. Do you care to give us an example of this? Do any of you evolutionist care to give us an example of multiple natural selection pressures accelerating evolution?
Kleinman, I see you have ignored my posts, and did not read the cited paper. I explained to you why it does not say what you think it does. Remember: many people on this forum actually understand biology, genetics, and evolutionary theory. You, clearly, do not. You are a waste of time.
Taffer, I appreciate your complaint about my citing a link from a non-peer reviewed article about bacteria being used to suppress the evolution of resistant mosquito larvae. Below is an example from a peer reviewed journal of how multiple selection pressures stops evolution of mosquito larvae. All mechanisms of mutation and recombination are available to the mosquito larvae yet resistance only occurs when the number of selection pressures are reduced.
Joobz, you are still one of the favorites to win the horserace as the last evolutionist on this thread to understand the mathematics of mutation and selection.You can't possibly be so vain as to think that others will no longer debate you because they believe a word you are saying. How far does your vanity reach, Kleinman? We are embarrassed by your ignorance and obvious mistakes.
Ichneumonwasp joins the competition to be the last evolutionist to understand the mathematics of mutation and selection. Perhaps if he realizes there is no way that multiple selection pressures accelerates evolution he may avoid the winner’s circle of ignorance and denial of the mathematics of mutation and selection.
NOTE that word, delay. Hoy was talking about delaying the resistance development against pesticides. But Hoy doesn't say, Halt, stop, prevent, abolish, never will happen,.... Hoy says delay. We can only ever delay things, we can't stop evolution.
Joobz thinks that evolution can not be stopped. If he reads this article carefully http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219) he will find that if evolution is not stopped, it delayed for a long period of time. Here is how evolution is stopped.
Insecticides based on Bacillus thuringiensis subsp. israelensis have been used for mosquito and blackfly control for more than 20 years, yet no resistance to this bacterium has been reported.
What hasn’t resistance evolved?
The mosquitocidal bacterium Bacillus thuringiensis subsp. israelensis is highly effective as a larvicide against a wide range of mosquito (Diptera: Culicidae) and blackfly species (Diptera: Simuliidae) and has been used routinely in many pest and vector control programs for more than 20 years (1, 10, 12, 30). The principal insecticidal component of B. thuringiensis subsp. israelensis is a spherical parasporal body produced during sporulation and composed of four major endotoxin proteins, Cyt1Aa, Cry4Aa, Cry4Ba, and Cry11Aa (6, 11).
There are four agents acting on the larva. How can the larvas evolve resistance to these toxins?
Although no resistance to B. thuringiensis subsp. israelensis has been reported under field conditions, studies in the laboratory have shown that high levels of resistance can be developed when larval populations are selected against recombinant bacilli that produce only one, two, or three of this bacterium's mosquitocidal Cry proteins.
Reduce down the number of selection pressures and the evolutionary process can proceed. Multiple selection conditions slow the evolutionary process and in this case four selection conditions stop the evolutionary process in a real situation. This is exactly analogous with what ev shows. The question is, how many real examples of the mathematical behavior of mutation and selection which ev shows before evolutionists finally understand this fact? Just how wide and deep is this river of ignorance and denial of the mathematics of mutation and selection that flows out of the theory of evolution?

[kjkent1]

You don’t need to do the analysis; I’ll do it for you. Somehow you think that man made selection pressures behave in a different mathematical manner than natural selection pressures. Do you care to give us an example of this?Hmmm, I must have missed your analysis. I wonder if that's because you forgot to do it, between telling me that I don't need to do any and where you ask me to give you an example to refute your non-existent analysis.

Do you tell your patients when you're practicing faith healing in favor of medicine?Do any of you evolutionist care to give us an example of multiple natural selection pressures accelerating evolution?I already did that, twice in this thread -- using ev, and I posted the data. Of course, you immediately disregarded both examples -- but, that's not my problem.

Seek professional help, Alan.

[Taffer]

Kleinman, when you post a citation which actually states what you think it does, then we can have a discussion. But your refusal to realise that what every single citation is saying is not what you think it is leads this discussion to a dead end. You have not provided a single paper which shows that the rate of evolution slows as a result of multiple selection pressures. All you have shown is that the rate of emergence of a trait can be slowed, which is blindingly obvious. Yet again, emergence is not evolution. Emergence is that chance of a specific trait actually appearing in a population, and it is governed by such things as population size, the effect of the drug, and so-on. What you still fail to realise is that the rate of evolution is increased by heavy selection pressures. Our models show this. Reality shows this. Stop confusing emergence with the rate of evolution. All you have shown is that using many drugs makes the emergence of a multi-resistant individual less likely. Of course it does, because the number of allelic variations in the population is reduce. But evolution is the change in allele frequency over time. It doesn't matter how those alleles arose, once they exist evolution acts the same. More selection pressures do not slow this process. What is lowered is the amount of available variation to 'work with', so to speak.

[Dr Adequate]

All you have to know is how to count to understand that the theory of evolution is mathematically impossible. Lawyers do know how to count, don’t they little gator?

All selection pressures inhibit replication. That is by definition what a selection pressure is, it is a stress on life forms that reduce its fitness to reproduce. If that stress is sufficient, it causes extinction.

The biosphere or environment is what it is. If small pox were not kept in the laboratory, it would be extinct.

The example of combination therapy of HIV slowing the evolution of the virus is only one of many examples of how multiple selection pressures slow and ultimately stops evolution as show by the example below.

You don’t need to do the analysis; I’ll do it for you. Somehow you think that man made selection pressures behave in a different mathematical manner than natural selection pressures. Do you care to give us an example of this? Do any of you evolutionist care to give us an example of multiple natural selection pressures accelerating evolution?

Taffer, I appreciate your complaint about my citing a link from a non-peer reviewed article about bacteria being used to suppress the evolution of resistant mosquito larvae. Below is an example from a peer reviewed journal of how multiple selection pressures stops evolution of mosquito larvae. All mechanisms of mutation and recombination are available to the mosquito larvae yet resistance only occurs when the number of selection pressures are reduced.

Ichneumonwasp joins the competition to be the last evolutionist to understand the mathematics of mutation and selection. Perhaps if he realizes there is no way that multiple selection pressures accelerates evolution he may avoid the winner’s circle of ignorance and denial of the mathematics of mutation and selection.

Joobz thinks that evolution can not be stopped. If he reads this article carefully http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219) he will find that if evolution is not stopped, it delayed for a long period of time. Here is how evolution is stopped.

What hasn’t resistance evolved?

There are four agents acting on the larva. How can the larvas evolve resistance to these toxins?

Reduce down the number of selection pressures and the evolutionary process can proceed. Multiple selection conditions slow the evolutionary process and in this case four selection conditions stop the evolutionary process in a real situation. This is exactly analogous with what ev shows. The question is, how many real examples of the mathematical behavior of mutation and selection which ev shows before evolutionists finally understand this fact? Just how wide and deep is this river of ignorance and denial of the mathematics of mutation and selection that flows out of the theory of evolution? No new lies, no math, but at least "all you have to know is how to count" is quite funny.

[Paul C. Anagnostopoulos]

All selection pressures inhibit replication. That is by definition what a selection pressure is, it is a stress on life forms that reduce its fitness to reproduce. If that stress is sufficient, it causes extinction.
Selection pressure is defined as the intensity of the selection acting on a population of (presumably variable) organisms. It makes no sense to say that all selection pressures inhibit replication.

~~ Paul

[Dr Richard]

Selection pressure is defined as the intensity of the selection acting on a population of (presumably variable) organisms. It makes no sense to say that all selection pressures inhibit replication.

~~ Paul

Since when did anything kleinman said make sense?

I asked him for a defintion of selection pressure over a week ago; seems he still can't get it right. Guess there is no chance of him answering the other questions put to him...

[Mr. Scott]

Since when did anything kleinman said make sense?

I asked him for a defintion of selection pressure over a week ago; seems he still can't get it right. Guess there is no chance of him answering the other questions put to him...

Dr. Kleinman will answer an uncomfortable question, or state some kind of reason why he won't (e.g. "it's none of your business") if your question is the only part of a posting. He is likely to ignore uncomfortable questions if they are within a post that has another comment or question.

A question I'd like to ask him is, "What transpired in your latest communication with Jesus about your efforts to undermine evolution?"

[kleinman]

You don’t need to do the analysis; I’ll do it for you. Somehow you think that man made selection pressures behave in a different mathematical manner than natural selection pressures. Do you care to give us an example of this?Hmmm, I must have missed your analysis. I wonder if that's because you forgot to do it, between telling me that I don't need to do any and where you ask me to give you an example to refute your non-existent analysis.
You have, rather than repeating it again, I’ll show you how to do it using ev. Start by using Dr Schneider’s baseline case that he used in his publication. Then use his suggestion that he published to vary genome length, mutation rates, population, selection etc. and if you systemically tabulate the generations for convergence as you vary these parameters, you will find that the dominant parameters in the model are the genome length and the number of selection pressures. That is the analysis that you have missed.
Do you tell your patients when you're practicing faith healing in favor of medicine?
If you practice medicine for any length of time, you will find that faith has a major impact. The terminology used is placebo/nocebo effect. When you are practicing law, does it matter what you and your clients are putting your faith in?
Do any of you evolutionist care to give us an example of multiple natural selection pressures accelerating evolution?I already did that, twice in this thread -- using ev, and I posted the data. Of course, you immediately disregarded both examples -- but, that's not my problem.
Where is Unnamed to defend his selection scheme? What happens to the data when using Unnamed’s selection scheme and you set two of the three weight factors to zero? What are the real examples that you can give us that demonstrate Unnamed’s selection scheme? This is why I disregard what you have posted. In contrast, the data I post is from Dr Schneider’s peer reviewed and published model of mutation and selection and I have posted 15-20 real examples of this mathematical behavior shown by ev.
Seek professional help, Alan.
I am, I’m still looking for a plumber to clean the clog pipes in your brainwashed cultist evolutionist minds. Then perhaps you will understand the mathematics that ev demonstrates and the numerous real examples of this mathematics that I have posted.
Kleinman, when you post a citation which actually states what you think it does, then we can have a discussion. But your refusal to realise that what every single citation is saying is not what you think it is leads this discussion to a dead end. You have not provided a single paper which shows that the rate of evolution slows as a result of multiple selection pressures. All you have shown is that the rate of emergence of a trait can be slowed, which is blindingly obvious. Yet again, emergence is not evolution. Emergence is that chance of a specific trait actually appearing in a population, and it is governed by such things as population size, the effect of the drug, and so-on. What you still fail to realise is that the rate of evolution is increased by heavy selection pressures. Our models show this. Reality shows this. Stop confusing emergence with the rate of evolution. All you have shown is that using many drugs makes the emergence of a multi-resistant individual less likely. Of course it does, because the number of allelic variations in the population is reduce. But evolution is the change in allele frequency over time. It doesn't matter how those alleles arose, once they exist evolution acts the same. More selection pressures do not slow this process. What is lowered is the amount of available variation to 'work with', so to speak.
The only dead end in this discussion is the one for the theory of evolution. Once you comprehend that the emergence of a trait occurs by evolution and that is slowed by the introduction of more selection pressures you to will realize that the theory of evolution is a dead end. Huge populations won’t rescue your theory but at least you now realize that recombination and natural selection can and does reduce the number of alleles and thus the amount of information in the gene pool. You really need to study ev, you will learn something about the mathematics of mutation and selection.
All selection pressures inhibit replication. That is by definition what a selection pressure is, it is a stress on life forms that reduce its fitness to reproduce. If that stress is sufficient, it causes extinction.Selection pressure is defined as the intensity of the selection acting on a population of (presumably variable) organisms. It makes no sense to say that all selection pressures inhibit replication.
Tell that to the editors of Wikipedia:
Evolutionary pressure or selection pressure can be formalized as an external pressure applied to a process, thereby pushing that process in a distinct direction.

A process driven by evolutionary pressure is, for example, the natural selection for erythrocytes carrying the sickle cell hemoglobin gene mutation (Hb S)—causing sickle cell anaemia—in areas where malaria is a major health concern, which grants some resistance to this infectious disease. Therefore, the concept can be described as the application of Charles Darwin's principle of "survival of the fittest" (which actually should be understood as "extinction of the un-fittest") via some selection mechanism.
Paul, would you give us an example of a selection pressure that increases replication?
Selection pressure is defined as the intensity of the selection acting on a population of (presumably variable) organisms. It makes no sense to say that all selection pressures inhibit replication.Since when did anything kleinman said make sense?

I asked him for a defintion of selection pressure over a week ago; seems he still can't get it right. Guess there is no chance of him answering the other questions put to him...
Stop whining Sesame Street dropout. I just posted the Wikipedia definition for selection pressure. I had already posted the definitions used in Genetics in Medicine, by Thompson and Thompson. So, Sesame Street dropout, when are you going to point out the error in the equation from the link you posted that computes selection pressures and then to explain the equation from your link? Once you learn how to count, everything I say will make sense to you.
Since when did anything kleinman said make sense?

I asked him for a defintion of selection pressure over a week ago; seems he still can't get it right. Guess there is no chance of him answering the other questions put to him...Dr. Kleinman will answer an uncomfortable question, or state some kind of reason why he won't (e.g. "it's none of your business") if your question is the only part of a posting. He is likely to ignore uncomfortable questions if they are within a post that has another comment or question.

A question I'd like to ask him is, "What transpired in your latest communication with Jesus about your efforts to undermine evolution?"
I’m not uncomfortable with any question asked in this thread, pussycat. Do you think I should feel bad when mathematics and reality show the theory of evolution to be untrue? The answer to your question is Matthew 25:23.

[joobz]

You have, rather than repeating it again, I’ll show you how to do it using ev...[snip]
Rather than repeating it again, You'll repeat it again?
We know your position and it has been refuted. Come up with something new to present.

[kleinman]

You have, rather than repeating it again, I’ll show you how to do it using ev...[snip]Rather than repeating it again, You'll repeat it again?
We know your position and it has been refuted. Come up with something new to present.
Joobz, not only have you failed to refute my hypothesis, I have given you a real case where multiple selection pressures stops evolution. I will continue to present new references that show that multiple selection pressures slow and ultimately stop evolution. This is what ev shows and this is what reality shows. This is how the mathematics of mutation and selection works. You are still in the running to be the last evolutionist to understand how the mathematics of mutation and selection works. If you don’t want to win this race of denial and ignorance, study ev.

Here are a couple of more references which show that combination selection pressures slow evolution (and in one case appears to reverse evolution of drug resistance).

http://www.bioone.org/perlserv/?request=get-document&doi=10.1603%2F0022-2585(2003)040%5B0985%3AEFSOIR%5D2.0.CO%3B2 (http://www.bioone.org/perlserv/?request=get-document&doi=10.1603%2F0022-2585(2003)040%5B0985%3AEFSOIR%5D2.0.CO%3B2)
Pyrethroid-treated nets are an efficient tool for reducing malaria transmission and morbidity. The recent evolution of pyrethroid resistance in several Anopheles species represents a major threat for the future success of roll back malaria in Africa. The possible use of nonpyrethroid insecticides, such as carbamates, on nets is a promising alternative solution because these insecticides are effective against susceptible and pyrethroid-resistant populations of Anopheles and Culex mosquitoes. Unfortunately, carbamate resistance as a result of insensitive acetylcholinesterase has recently been detected in Anopheles gambiae s.s. populations from Côte d’Ivoire. Using biochemical assays on surviving Anopheles mosquitoes from an experimental hut trial, we showed evidence for selection for an insensitive acetylcholinesterase mechanism by carbamate impregnated bednets. However, no such selection has been found with nets treated with pyrethroid alone or pyrethroid/carbamate “two-in-one”-treated nets. Because pyrethroid-impregnated nets were suspected to select for the Kdr mutation in An. gambiae, we propose that use of two-in-one nets could be a promising alternative strategy for the management of insecticide resistance in malaria vectors.
I added the highlighting.

http://www.ucsf.edu/synapse/content/51007/bacteria.html (http://www.ucsf.edu/synapse/content/51007/bacteria.html)
The elegant principles of evolution by natural selection pose a major problem throughout the world’s hospitals. Whenever an antibiotic is given to treat an infection, a small proportion of the bacteria present in the patient’s body may possess mutations, accessory genes or other genetic changes that protect them from the antibiotic. As the drug kills the susceptible bacteria, the few resistant organisms find that their competition for scarce resources in the environment of the patient’s body has greatly decreased. They proliferate more aggressively than before, resulting in the drug resistance mutation becoming more common. Therefore, the use of antibiotics commonly results in the spread of organisms resistant to them. The problem is compounded by the fact that this evolution occurs not only for the disease-causing organism, but potentially for all the bacteria present in the patient, some of which may cause disease later. In recent years, the spread of resistance has outpaced the development of new antibiotics, making many infections ever more difficult to treat. This process can be slowed to some extent by judicious use of antibiotics, but not eliminated.

Against this background, a welcome study appearing in the April 5 issue of Nature suggests that some carefully chosen combinations of antibiotics might actually reverse the problem of resistance, selecting for antibiotic-sensitive organisms over resistant ones. Antibiotic combinations can have a range of effects. If two drugs are synergistic, each is more effective at any given dose when they are used in combination. This is often used as a rationale for combining antibiotics in clinical practice. However, it is also possible for antibiotics to partially antagonize each other’s effects, so that higher concentrations are needed than if the drugs were used separately. In the most extreme case, adding a second drug (antibiotic B) can actually cause the bacteria to survive and grow better than they did under treatment with a single antibiotic A. This effect is called suppression, and is, of course, generally avoided in clinical practice.
This link is particularly interesting since it appears that the evolution of drug resistance can be reversed.

[joobz]

Joobz, not only have you failed to refute my hypothesis, I have given you a real case where multiple selection pressures stops evolution. Really??? Hmm, I seem to remember things a bit differently. And look, the thread remembers it differently too.


For clarity, I have summarized the key points of this conversation. I think we have a new lie here.

If you studied ev, you would understand this. If you examined the real cases of combination therapy for the treatment of HIV, combination therapy for the treatment of TB, combination pesticides, combination herbicides, combination rodenticides, you would see real examples of what ev demonstrates and what the fitness landscape requires. Mutation and selection can not and does not do what evolutionists allege, it is mathematically impossible.

It is the number of directional selection pressures and genome length which dominate the mathematics of mutation and selection. There is no reason to believe that frame shift mutations, translocations, duplications or any other way of scrambling a genome is going to change the underlying mathematics of mutation and selection.

This is your concrete basis for not worring about it?

I think this paper wouldn't have been accepted if that was the case:
Carvajal-Rodriguez A, Crandall KA, Posada D. "Recombination favors the evolution of drug resistance in HIV-1 during antiretroviral therapy." Infect Genet Evol. 2007 Feb 12; [Epub ahead of print]
I can't access the paper yet, but from the abstract:

Using computer simulations we show that the effect of recombination on the evolution of drug resistance depends strongly on the intensity of selection, as well as on the viral population size. Under the high selection pressure expected during antiretroviral therapy, the strength of the Hill-Robertson effect increases and recombination favors the evolution of resistance under a wide range of population sizes, independently of the sign of the epistatic interaction. Our results suggest that recombination plays an important role in the evolution of drug resistance in HIV-1 under various realistic scenarios
Seems like evolution has a mathematical basis after all.

So how does this work with HIV? Here is a quote from an article located at http://www.cdc.gov/ncidod/eid/vol3no3/burke.htm

Human immunodeficiency virus (HIV)-1, like all retroviruses, is "diploid." Each viral particle contains two RNA strands of positive polarity, each full length and potentially able to replicate (1). No other virus families, RNA or DNA, are diploid. Typically both RNA strands in a retroviral particle derive from the same parent provirus. However, if an infected cell simultaneously harbors two different proviruses, one RNA transcript from each provirus can be encapsidated into a single "heterozygous" virion. When this virion subsequently infects a new cell, the reverse transcriptase may jump back and forth between the two RNA templates so that the newly synthesized retroviral DNA sequence is recombinant between that of the two parents (2). All subsequent progeny virions will be of this recombinant genotype. HIV-1 strains with chimeric genomes thought to have arisen through homologous recombination have recently been discovered in nature (3).
This is a property unique to the retroviruses, are you trying to generalize this phenomenon to the entire theory of evolution? This appears like a baseless extrapolation.

Unfortunately, you've been using HIV viruses as proof of why evolution is impossible. I show a study where they demonstrate how multiple selection pressures won't HALT HIV evolution, and now you claim that I can't extrapolate this truth to anything else.

No it doesn’t, it only shows that you know how to make a baseless extrapolation.

I see, when evolutionists adjust their theory, this is scientific research, when I adjust my theory, I’m moving the goal posts.
This isn't an "adjustment of a theory". This is intellectual dishonesty.
We have been discussing how multiple pressures doesn't stop evolution using HIV as an example. I give evidence that states mathematically that this isn't the case. And now you claim that it doesn't apply.
This is the worst form of professional behavior.
This won't go away becuase you wish it to. Your argument is without basis.

This link is particularly interesting since it appears that the evolution of drug resistance can be reversed.
:D :D :D :D Please explain what reverse evolution is and how it is different from plain ol' regular evolution?

[kleinman]

Joobz, not only have you failed to refute my hypothesis, I have given you a real case where multiple selection pressures stops evolution.Really??? Hmm, I seem to remember things a bit differently. And look, the thread remembers it differently too.
Of course your brainwashed and prejudiced evolutionist’s mind remembers things differently. Now if you can only recall your mathematical training that was required of you in order to obtain your degree in alchemical engineering, we can free you from your unscientific bias.
This link is particularly interesting since it appears that the evolution of drug resistance can be reversed.Please explain what reverse evolution is and how it is different from plain ol' regular evolution?
Po’ old joobz can’t understand the link so I have to spell it out for him.
http://www.ucsf.edu/synapse/content/51007/bacteria.html (http://www.ucsf.edu/synapse/content/51007/bacteria.html)
The elegant principles of evolution by natural selection pose a major problem throughout the world’s hospitals. Whenever an antibiotic is given to treat an infection, a small proportion of the bacteria present in the patient’s body may possess mutations, accessory genes or other genetic changes that protect them from the antibiotic. As the drug kills the susceptible bacteria, the few resistant organisms find that their competition for scarce resources in the environment of the patient’s body has greatly decreased. They proliferate more aggressively than before, resulting in the drug resistance mutation becoming more common. Therefore, the use of antibiotics commonly results in the spread of organisms resistant to them. The problem is compounded by the fact that this evolution occurs not only for the disease-causing organism, but potentially for all the bacteria present in the patient, some of which may cause disease later. In recent years, the spread of resistance has outpaced the development of new antibiotics, making many infections ever more difficult to treat. This process can be slowed to some extent by judicious use of antibiotics, but not eliminated.

Against this background, a welcome study appearing in the April 5 issue of Nature suggests that some carefully chosen combinations of antibiotics might actually reverse the problem of resistance, selecting for antibiotic-sensitive organisms over resistant ones. Antibiotic combinations can have a range of effects. If two drugs are synergistic, each is more effective at any given dose when they are used in combination. This is often used as a rationale for combining antibiotics in clinical practice. However, it is also possible for antibiotics to partially antagonize each other’s effects, so that higher concentrations are needed than if the drugs were used separately. In the most extreme case, adding a second drug (antibiotic B) can actually cause the bacteria to survive and grow better than they did under treatment with a single antibiotic A. This effect is called suppression, and is, of course, generally avoided in clinical practice.
I added the highlighting.
Researchers from Harvard Medical School reasoned that suppressive antibiotic combinations might create an opportunity for favoring the growth of drug-sensitive organisms over drug-resistant ones. Suppose that two antibiotics, A and B, interact in a suppressive manner as described above. According to the definition of suppression, organisms that are sensitive to the effects of drug B will experience increased survival and growth when drug B is added to drug A, compared to when drug A is used alone. Organisms that are resistant to drug B will not be affected by its presence, and will be inhibited by drug A just as effectively as before. Therefore, the addition of drug B will select for B-sensitive organisms over B-resistant ones. At the end of treatment, the surviving bacterial population (if any) will have evolved to be more sensitive to drug B, reversing the problem of evolution of drug resistance.

The researchers tested this hypothesis using two strains of the common pathogen Escherichia coli that were tagged with fluorescent proteins of different colors, permitting their survival and growth to be measured separately. One strain was resistant to the antibiotic doxycycline, while the other was sensitive to this drug, which acted as “drug B” in the above scenario