Annoying creationists

[kleinman]

Annoying Creationists

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.

 

[kleinman]

Annoying Creationists

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.

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]

Annoying Creationists

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]

Annoying Evidence and Testable Predictions

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.

 

[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.