Annoying creationists

[Foster Zygote]

Can you outline where the ability to 'answer questions' makes something right or wrong? I must have missed that in logic class.

This is the bit where T'ai Chi deliberately confuses the definition of "answer questions" as regards the context of science with "answer questions" as regards a statement in response to a query that may or may not be true.

 

[Foster Zygote]

I'm asking if you have real biology rather than some simulation.

I think T'ai is asking for things like examples of speciation in the laboratory or new evolutionary adaptations like Nylon eating microbes. Anyone want to take a steam shovel to this thread and dig 'em up?

 

[kleinman]

Annoying Creationists

It is apparent from a quick perusal of posts made over the weekend that you evolutionists still don’t understand how mutation and selection works either mathematically or empirically. Since you refuse to study Dr Schneider’s simulation of random point mutations and natural selection I’ll have to continue to post real examples of how mutation and selection actually works but I don’t mind this since there is a vast number of these examples to draw from. So let’s see what you evolutionists have to say about mutation and selection. Let’s start with rocketwhomissesthetarget.

Dr Schneider has posted extensively about his ev model including a glossary of his variables used in his calculations.

What does this have to do with whether or not you understand it?

Oh my rocketwhomissesthetarget, I understand how ev works, that’s why I can post hundreds of empirical examples of what Dr Schneider’s model shows. And what Dr Schneider’s model shows is that combination selection pressures profoundly slow the sorting/optimization (mutation/selection) process in his algorithm. This is how mutation and selection works in reality as well.

Why shouldn’t I cite evidence of how mutation and selection actually works? There is an abundance of this evidence available.

And a complete lack of understanding regarding that evidence on your part, which is why you consistently dodge questions by simply posting more citations.

I see, you post no citations which show that n+1 selection pressures evolve more rapidly than n selection pressures and then whine when I post hundreds of citations which show that combination selection pressure profoundly slow the sorting/optimization process of mutation and selection. Just because you don’t have any mathematical or empirical evidence to support your irrational and illogical theory, don’t blame me.

Why don’t you use google and find a citation which shows that n+1 selection pressures evolve more rapidly than n selection pressures?

I don't need google, I simply used all the citations you provided us:

Bacteria -- n pressures, slow mutation.
Bacteria + penicillin -- n + 1 pressures, rapid mutation.

Of course you will deny this somehow...

Sorry about this rocketwhomisses the target, you’ve got you mathematics and empirical evidence wrong. You have already admitted that bacteria in vitro will evolve resistance more quickly than bacteria in vivo. So your mathematics should look like this.
Bacteria (in vivo) – n weak selection pressures, impossibly slow evolution for common descent.
Bacteria (in vivo) + penicillin – n weak selection pressures + 1 strong selection pressure, fairly fast evolution of penicillin resistance but still impossibly slow evolution for common descent.
Bacteria (in vitro) – n-m weak selection pressures, impossibly slow evolution for common descent.
Bacteria (in vitro) + penicillin – n-m weak selection pressures + 1 strong selection pressure, faster evolution of penicillin resistance than with n selection pressures but still impossibly slow evolution for common descent.
Rocketwhomissesthetarget, I do commend you for trying to put some mathematics to your confused understanding of how mutation and selection works, keep working on it, I have great hopes that you can get it right.

Your analogy is not quite correct rocketdodger.

The odds of you actually having any degrees, given your displayed maturity level, are extremely slim.

The odds are much greater that I have those degrees than your theory of evolution is mathematically possible. Not only do I have those degrees, I am licensed as both a physician and an engineer. You are going to have to find another way to defeat my arguments which disprove the theory of evolution since I have all the mathematical and empirical evidence of how mutation and selection works and you have zilch to support your view.

There are no sorting/optimization/iteration problems that work that way which converge more quickly the more sorting/optimization/iteration conditions imposed on the problem.

I agree, there are not. But this has very little to do with evolution, and if you actually tried to explain why you think evolution is merely a sorting/optimization problem you would soon see this. But like I said.. you cannot explain why, because you do not know why. All you know is the nonsense you put together from random google results.

The problem you have in your argument is that Dr Schneider’s peer reviewed and published model of random point mutations and natural selection is simply a sorting/optimization algorithm and the behavior of this algorithm is exactly analogous to what is observed in reality. Sorting/optimization is exactly how mutation and selection works. Mutation and selection is the sorting of beneficial and detrimental mutations with the selection conditions defining the optimization conditions. If you have more than a single selection (optimization) condition, it profoundly slows the process. That is what the mathematics shows and that is what the empirical data shows.

I can't find the link to Kleinman's thesis and background, anyone have it handy?

I’ve already posted the title of my thesis and the publisher on this thread. Do you think you can find it, rocketwhomissesthetarget?

I have published publicly on two topics and you don’t understand the mathematics of either.

I didn't bother reading your publications and judging by the number of citations, nobody else bothered reading them either or found them very useful.

I see, you claim you are going to find irregularities in my PhD thesis, let’s see you do it and prove your mathematical prowess. You would have a better chance in proving there are irregularities in 2+2=4. Joobz, you are incompetent in the mathematics of mutation and selection, ignorant of how the process works empirically and silly in your speculations of how chemistry works. You are nothing more than a big blow hard; you have no science or mathematics to back up your bizarre and strange speculations. Joobz, why don’t you put your money where your mouth is? Let’s make a wager, say $10,000. If you can find a mathematical or empirical irregularity in my PhD thesis, I’ll pay you $10,000; if you can’t you pay me $10,000. Are you ready for that, big mouth?

Hey kjkent1, if you can prove that reptiles evolved into birds one strong selection pressure at a time, go for it.

At the risk of repeating myself: The geological and fossil records demonstrate that evolution has occurred within the generational time available.

Well, it didn’t happen by mutation and selection, we have mathematical and empirical evidence which show how this process works. Perhaps it happened by the string cheese theory?

Well, Kleinman is entitled to critique a model he feels is not reflective of reality, or for whatever other reason. Especially if the people who made the model are trying to convince others it is reflective of reality.

You have misunderstood this thread. While more or less everyone else has understood that the model in question is just a model, which doesn't claim to model all of reality, and which certainly doesn't model all of reality, Kleinman is the person who has repeatedly claimed that it does, or, at least, that it is so accurate and so complete that results from the model, when in conflict with results from reality, counters and supersedes these, and should replace them. Kleinman's "critique" of the model is virtually non-existent, whereas the rest of us have long ago realised the limitations of the model, and act accordingly.

It is not the "evolutionarians" of this thread who are holding this model to be a sacred standard of our way to view the world. I assume you have not read any part of the thread prior to joining in, or you would have spotted this.

T’ai, you need to understand that I believe that Dr Schneider properly modeled the essential features of the mutation and selection process and it demonstrates how mutation and selection actually works. I told Dr Schneider in our discussions that once evolutionists understood what his model actually shows, his model would be discredited by evolutionists and that is exactly what his happening. Unfortunately for believers in the evolutionists world view, Dr Schneider’s model predicts how mutation and selection actually works as demonstrated in the hundreds of real citations which I have already posted, all of which show that combination selection pressures profoundly slow the evolutionary process.

No Kotatsu, these are not comments on American popular culture, they are comments on evolutionist popular culture because mutation and selection simply does not work the way you allege, the mathematics and empirical evidence of mutation and selection contradict your scientifically and mathematically baseless speculations and extrapolations.

Actually being biologist, as opposed to you, I must, if I am to believe you, ask what sort of biology text books you read which have "Sesame Street" and "Marvel comics" listed in their evolution sections. These, I understand, are references to American popular culture, but I am unfamiliar with the exact details, never having lived in America. Ask me about Czech and Polish animation from the 80's, instead. They showed heaps of that on Swedish TV when I was a kid.

Kotatsu, I don’t care what you call yourself; you simply don’t understand how mutation and selection works either mathematically or empirically. This mush that you put forth doesn’t qualify as a scientific or mathematical argument of how mutation and selection actually works.

So, now we have the theory of evolution by “sheer coincidence”, Kotatsu, you take speculation to new levels.

So you have no actual answer, is that a correct interpretation?

It is not a correct interpretation if you want to claim that your argument has any scientific basis. Mutation and selection does not work that way either empirically or mathematically.

Oh, that’s right, you said a reptile chased in into a tree and it would be beneficial for that reptile to grow wings. You evolutionists really practice some weird thinking.

No. Your post contains several misinterpretations. I gave you a list of a number of various realistic selection pressures, all of which could plausibly lead to a situation where mutations in genes which for instance aided in horizontal movement between trees would be advantageous compared to alleles without this advantage.

Until you present something that is measurable and repeatable, you present nothing more than mush. The hundreds of citations which I have posted identify explicitly what the selection pressures are, the target genes for the selection pressures and often times identify the specific loci and mutations required for adaptation to the selection pressures. So far, all you have presented is mush.

What you are seeing are connections which are mathematically and empirically impossible. These are extrapolations and speculations that are contradicted by the way mutation and selection actually works.

Yet those trees are constructed using maths... In the simples tree-building algorithm, that of distance, the differences between the various sequences are simply counted, and the tree is constructed in such a way that those sequences most similar to each other are placed next to each other, and so on in a way that forms a nested hierarchy (unless, of course, all sequences are identical, which will instead result in a "comb" polytomy).

Kotatsu, you are trying to make connections where none exist. You don’t have selection pressures which would make these transformations. Mutation and selection simply does not work the way you allege, we have mathematical and empirical evidence which show how mutation and selection actually works. This empirical evidence is measurable and repeatable.

There are many unusual species which evolutionists like you speculate and extrapolate that appear by evolution. However, you are in denial about how mutation and selection actually works. Combination selection pressures confound the evolutionary process. A population can most easily evolve against a single selection pressure directed at a single gene. As soon as multiple selection pressures come into play, these multiple selection pressures confound the evolutionary process. That is what the mathematical evidence shows and that is what the empirical evidence shows.

So now it is no longer impossible for them to evolve against several selection pressures, just not as easy? And multiple selection pressures don't "slow and ultimately stop evolution" any more, but simply confounds it? Marvellous! In a few decades, we'll finally have you on our side!

Kotatsu, you are in denial. Mutation and selection is not an incomprehensible process mathematically. If you ever come to understand that this process is nothing more than a sorting/optimization problem, you would realize that your belief system is wrong. The empirical evidence of how mutation and selection works verifies this. The pictures you draw are based on a mathematically impossible theory.

Mr Scott has not shown that scales transform into feathers, all Mr Scott has shown is that feather can grow on birds in unusual locations when there is a mutation. Kotatsu, have you ever heard of teratomas?

I have now. However, feel free to elaborate, as I believe this may be an area where you can actually display knowledge.

Teratomas are tumors which contain tissues not usually found in that organ. For example, these tumors can arise in the testis or ovaries and grow tissue replete with skin and hair. The point is that the potential for the growth of these tissues was already present in the genome.

Of course I am Kotatsu, here is a note from your lecture: Reptile chased into tree->reptile grows wings.

Good, good. Now, your homework for next week will be to actually read what is being said to you before taking the notes. See if you can do that, and you may actually pass this class!

For some reason I don’t think I’ll ever pass your class in evolutionism or joobz’s class in alchemy.

Why can't I reproduce such a graph using ev? Because as it turns out, ev has nothing to do with selective pressures...at all... so Kleinman, how on Earth are you using ev to support your claim that "combination selection pressures profoundly slow evolution?"

Why don't you think so? You can adjust the strength of three selection criteria, or eliminate them, on the New dialog. The fact that there are three is arbitrary, but they are individually adjustable.

One problem is that Evj has no mechanism for introducing the pressures sequentially. So we can't compare what Dr. A. represented by his red and blue lines. Then again, each of Dr. A's pressures affects a different gene, whereas Evj only has one gene affected by multiple pressures, so the comparison may be moot.

Thank you Paul for setting rocketdodger straight on this issue, it doesn’t matter that you can’t apply the selection pressures in ev sequentially, there is more than enough empirical evidence that shows how this works.

So, has he thought of any new lies?

Adequate, when are you going to stop behaving like a whining brat and start practicing mathematics again? It is now clear that the evolution by mutation and selection is nothing more than a sorting/optimization problem and that Dr Schneider’s properly demonstrates how this process works. How long are you going to cling to your incoherent, irrational and illogical view that n+1 selection pressures evolve more rapidly than n selection pressures? If you do continue to cling to the incoherent, irrational and illogical, stick around, you are my favorite annoyee and obfuscatematician.

So, has he thought of any new lies?

Except for trying again to establish some credibility regarding his math abilities by referencing his meager publications, no.

Put your money where your big mouth is. You said you are going to prove irregularities in my PhD thesis, $10,000 wager says you can’t show any mathematical or empirical irregularities. What do you say big mouth? Or are you a big coward as well as a big mouth?

Adequate can you link me to the model you used to make that graph Kleinman is claiming to be incorrect? I am trying to reproduce the results -- they seem intuitively correct (if one has a clue about math) but I need an actual model or program or something that I can use.

Yeah, Adequate, give rocketdodger a link, google seems to be failing him.

Yawn.

If you're bored, you could really change things up by answering a substantive question about your claims.

Or, you know, keep ignoring reality. I'll just be over here pretending like I'm waiting for an answer that I know will never come...

Yeah T’ai, like Delphi telling us that a temperature change transforms reptiles into birds, all he needs is a hundred million years and the earth as his test tube despite his own reference to Wikipedia fitness landscape contradicts his strange speculations.

Is this thread still active!!??

I really have trouble to keep up, thats for sure...
How many times have we been through this now?

I can’t help it if you evolutionists are slow at learning the mathematics of mutation and selection. Here are some more empirical examples of how the process works for those of you having trouble with the mathematics.
http://aac.asm.org/cgi/content/full/49/10/4305

This is the first report to provide additional evidence that combination therapy with two small-molecule inhibitors may afford an advantage in overcoming the resistance issue. For example, we demonstrated that the frequency of resistance to the combination of A-782759 and BILN-2061 was significantly lower than the frequency of resistance to either single compound alone. In addition, the replicon containing dually resistant mutants had dramatically reduced replication compared to the wild type despite some of the single mutants having replication capacities close to or better than the wild type. Taken together, these findings support the notion that combination therapy will provide an approach to suppress the emergence of resistance and increase the efficacy of HCV therapy.

http://www.journals.uchicago.edu/CID/journal/issues/v45n11/51016/51016.html

Antimicrobial drug resistance in infectious agents occurs by means of several mechanisms; these include genetic changes and the acquisition of genes coding for resistance. Mycobacteria differ from most other bacteria by the presence of a cell wall with unique properties. Exchange of genes across this type of cell wall is difficult. Therefore, development of drug resistance in this group of bacteria evolves mainly from mutational events [1]. Resistance only becomes apparent if the resistant subpopulation of bacteria survives during treatment. To avoid this, patients with tuberculosis (TB) are treated with a combination of drugs. Development of resistance to one of the drugs in the regimen is not relevant to the survival of the bacterium in which that occurred, because there will always be 1 drug to which it is still susceptible. Selection of resistant mutants only happens when patients are treated with inappropriate regimens or when patients become selectively noncompliant by not taking all of the 3 or 4 drugs they were prescribed. The long duration of treatment, as well as the large amount of drugs and their gastrointestinal adverse effects, contribute to a relatively high rate of noncompliance in patients with TB.

And

Figure 1 illustrates how the F15/LAM4/KZN strain developed resistance over time. One can only speculate about the reasons for this development. A general observation in antibacterial therapy is that treatment with fixed combinations of drugs will lead to infections with organisms that are resistant to that combination. This was thought not to be applicable to M. tuberculosis for 2 reasons: (1) combination therapy would prevent in vivo survival of mutants that are resistant to one drug, and the chance of mutations leading to resistance to 2 drugs in the same cell is extremely small; and (2) the loss of fitness of drug-resistant strains limits their transmission [14, 15]. From this it follows that focussing on optimization of the TB-control programs for drug-susceptible TB will prevent resistance to spread. If the vast majority of patients fully adhere to their treatment regimens, no resistance will develop, and drug-resistant strains that develop in the small minority of persons who are not compliant will not spread.

Hey joobz after you lose $10,000 trying to find irregularities in my PhD dissertation, you can notify the authors of the above citation that evolution can not be stopped.

 

[joobz]

Hey joobz after you lose $10,000 trying to find irregularities in my PhD dissertation, you can notify the authors of the above citation that evolution can not be stopped.

Your delusions are getting the best of you. Why would I bother reading your ineffectual paper? 5 citations in ~25 years. 4 of those citations from your group. Meaning, that only 1 other researcher found your work worth enough to cite. Not a very impressive record at all.


but please, tell us again all about you non-linear PDEs. Or better yet, actually present your math that shows evolution is impossible. It's been a year and all we hear is boasts, but you never deliver. I wonder if this is the reason why you only had 2 publications.

 

[delphi_ote]

Lots of posts from T'ai Chi. Still no definition of "complex." Still no acknowledgment that this is a problem with his argument. If you're lurking, do you find this intellectually dishonest?

 

[rocketdodger]

Oh my rocketwhomissesthetarget, I understand how ev works, that’s why I can post hundreds of empirical examples of what Dr Schneider’s model shows. And what Dr Schneider’s model shows is that combination selection pressures profoundly slow the sorting/optimization (mutation/selection) process in his algorithm. This is how mutation and selection works in reality as well.

Congratulations on once again utterly failing to explain why. In other words, you don't understand, you just cite.

I see, you post no citations which show that n+1 selection pressures evolve more rapidly than n selection pressures and then whine when I post hundreds of citations which show that combination selection pressure profoundly slow the sorting/optimization process of mutation and selection. Just because you don’t have any mathematical or empirical evidence to support your irrational and illogical theory, don’t blame me.

Sorry about this rocketwhomisses the target, you’ve got you mathematics and empirical evidence wrong. You have already admitted that bacteria in vitro will evolve resistance more quickly than bacteria in vivo. So your mathematics should look like this.
Bacteria (in vivo) – n weak selection pressures, impossibly slow evolution for common descent.
Bacteria (in vivo) + penicillin – n weak selection pressures + 1 strong selection pressure, fairly fast evolution of penicillin resistance but still impossibly slow evolution for common descent.
Bacteria (in vitro) – n-m weak selection pressures, impossibly slow evolution for common descent.
Bacteria (in vitro) + penicillin – n-m weak selection pressures + 1 strong selection pressure, faster evolution of penicillin resistance than with n selection pressures but still impossibly slow evolution for common descent.

...so, you are saying that n + 1 selection pressures can lead to faster evolution than n pressures... which is exactly the opposite of all your previous claims... welcome back to the Kleinman merry-go-round everyone!

The odds are much greater that I have those degrees than your theory of evolution is mathematically possible. Not only do I have those degrees, I am licensed as both a physician and an engineer.

Oh really? Where? By whom?

If you have more than a single selection (optimization) condition, it profoundly slows the process.

Why? Wait, let me guess.. "because that is what the mathematics and empirical evidence shows." OHHHH WELL THEN ITS ALL CLEARED UP, THANK YOU.

Honestly, Kleinman, I can't bring myself to believe that you could have written a paper on partial differential equations when you are completely unable to show why multiple optimization conditions would slow sorting. It is so simple.. all you have to do is think for a little and explain...

 

[kleinman]

Annoying Creationists

Hey joobz after you lose $10,000 trying to find irregularities in my PhD dissertation, you can notify the authors of the above citation that evolution can not be stopped.

Your delusions are getting the best of you. Why would I bother reading your ineffectual paper? 5 citations in ~25 years. 4 of those citations from your group. Meaning, that only 1 other researcher found your work worth enough to cite. Not a very impressive record at all.

but please, tell us again all about you non-linear PDEs. Or better yet, actually present your math that shows evolution is impossible. It's been a year and all we hear is boasts, but you never deliver. I wonder if this is the reason why you only had 2 publications.

So joobz, not only are you a big mouth who is ignorant of mathematics, you are a coward. You said you could find irregularities in my PhD thesis, put up or shut up. Here’s what you said.

As for his credentials. He's stated that he is Dr. Alan Kleinman. A physician with a PhD in engineering (I do not remember which field). He even posted a link to his thesis as proof of his degree. I could critique his PhD for irregularities in his publication track that raise interesting questions.

$10,000 wager that you can’t find any mathematical or empirical irregularities in my PhD thesis or are you just a big mouth fake? You claim to have a PhD in engineering, how much do you know about PDEs prove my thesis wrong or are you just a big faker? I think you are a faker after posting your nonsense speculations about abiogenesis.

There’s the wager you fake. Why don’t you post your name you coward and let’s have a look at your PhD thesis. Joobz, not only are you a mathematical incompetent in the mathematics of mutation and selection, you are a mathematical incompetent in PDEs. Prove otherwise and take up this $10,000 wager since you have claimed that you can find irregularities in my PhD thesis.

Lots of posts from T'ai Chi. Still no definition of "complex." Still no acknowledgment that this is a problem with his argument. If you're lurking, do you find this intellectually dishonest?

Delphi, the mathematics of mutation is not that complex, you have some understanding of the problem; otherwise you wouldn’t have posted the Wikipedia reference to fitness landscape. Why don’t you tell us how a temperature change can transform hundreds, perhaps thousands of genes simultaneously?

Sorry about this rocketwhomisses the target, you’ve got you mathematics and empirical evidence wrong. You have already admitted that bacteria in vitro will evolve resistance more quickly than bacteria in vivo. So your mathematics should look like this.

Bacteria (in vivo) – n weak selection pressures, impossibly slow evolution for common descent.
Bacteria (in vivo) + penicillin – n weak selection pressures + 1 strong selection pressure, fairly fast evolution of penicillin resistance but still impossibly slow evolution for common descent.
Bacteria (in vitro) – n-m weak selection pressures, impossibly slow evolution for common descent.
Bacteria (in vitro) + penicillin – n-m weak selection pressures + 1 strong selection pressure, faster evolution of penicillin resistance than with n selection pressures but still impossibly slow evolution for common descent.

...so, you are saying that n + 1 selection pressures can lead to faster evolution than n pressures... which is exactly the opposite of all your previous claims... welcome back to the Kleinman merry-go-round everyone!

Read it again rocketwhomissesthetarget.

The odds are much greater that I have those degrees than your theory of evolution is mathematically possible. Not only do I have those degrees, I am licensed as both a physician and an engineer.

Oh really? Where? By whom?

You can find this information if you read the thread. Do you have to be spoon fed everything? Why don’t you tell us what your credentials are, you claim you understand how mutation and selection works, tell us why.

Attack the argument, not the arguer. This thread has calmed down a lot since I last looked in. Try to keep it that way.

Replying to this modbox in thread will be off topic  Posted By: Cuddles

 

[Belz...]

Oh my rocketwhomissesthetarget, I understand how ev works, that’s why I can post hundreds of empirical examples of what Dr Schneider’s model shows.

Actually, you could post those and still don't understand, so that's not a good argument.

 

[Paul C. Anagnostopoulos]

Read it again rocketwhomissesthetarget.

Let me see (emphasis mine):

Bacteria (in vivo) – n weak selection pressures, impossibly slow evolution for common descent.
Bacteria (in vivo) + penicillin – n weak selection pressures + 1 strong selection pressure, fairly fast evolution of penicillin resistance but still impossibly slow evolution for common descent.
Bacteria (in vitro) – n-m weak selection pressures, impossibly slow evolution for common descent.
Bacteria (in vitro) + penicillin – n-m weak selection pressures + 1 strong selection pressure, faster evolution of penicillin resistance than with n selection pressures but still impossibly slow evolution for common descent.

~~ Paul

 

[CFLarsen]

Tsk ? Are you even capable of understanding what we've been telling you ?

How can you possibly know ALL the steps ?

Look at it from T'ai Chi's point of view.

Since T'ai Chi argues that there is an intelligent designer - namely God, who is omniscient - it follows that any explanation that doesn't know all the steps - namely science - has to be inferior as an explanation.

T'ai Chi argues that:

1) The Intelligent Designer (God) knows all the steps.

2) Science doesn't know all the steps.

Ergo:

1) is the truth.

If in doubt, or cornered: see 1).

T'ai seems to think he's hit upon something very clever here. I imagine he thinks it's one of his most devastating coup de grace lines, much like his "but the model is intelligently designed" argument (The model is also constructed within a computer so I guess T'ai Chi has also proved that we all live in the Matrix).

Exactly. Not only is his argument unfalsifiable, it doesn't give us any answers. It only raises more questions, all of which can - and will - be answered with:

"Goddidit".

T'ai Chi may call it "intelligent designer", because he, like all Creationists, is intellectually dishonest, but he means "god".

The only thing I really wonder about is whether he thinks it's truly reasonable to demand that all sciences produce such a ridiculously detailed proof, or if he's actually aware that he's employing an intellectually dishonest dodge by demanding the ludicrous.

Judging from his previous posts, I'd say it is the latter.

 

[kleinman]

Annoying Creationists

Oh my rocketwhomissesthetarget, I understand how ev works, that’s why I can post hundreds of empirical examples of what Dr Schneider’s model shows.

Actually, you could post those and still don't understand, so that's not a good argument.

The point you are missing Belz is that Dr Schneider’s model shows that the reason it so slowly converges is the three selection conditions. If you set two of the three selection conditions to zero in the model then the remaining selection condition can evolve much, much more rapidly. That same behavior of mutation and selection is seen in reality in the numerous citations posted. That is how mutation and selection works mathematically and that is how it works empirically. Mutation and selection is simply a sorting/optimization problem. That is why Dr Schneider’s model behaves the way it does and that is why the citations posted demonstrates the same behavior. You can try to say that I don’t understand how mutation and selection works but I can produce data from a peer reviewed and published computer simulation of random point mutations and natural selection and hundreds of empirical examples which shows the same thing, that is combination selection pressures profoundly slow the evolutionary process. You can try to say the contrary but you can’t produce the mathematical data and you can’t produce the empirical evidence.

Let me see (emphasis mine):

Bacteria (in vivo) – n weak selection pressures, impossibly slow evolution for common descent.

Bacteria (in vivo) + penicillin – n weak selection pressures + 1 strong selection pressure, fairly fast evolution of penicillin resistance but still impossibly slow evolution for common descent.
Bacteria (in vitro) – n-m weak selection pressures, impossibly slow evolution for common descent.
Bacteria (in vitro) + penicillin – n-m weak selection pressures + 1 strong selection pressure, faster evolution of penicillin resistance than with n selection pressures but still impossibly slow evolution for common descent.

Paul, do I have to spell this out for you? Ok, in both the in vitro and in vivo cases you have a single strong selection pressure evolving on the background of weak selection pressures. In the in vivo case, you have n weak selection pressures interfering with the evolution of the single strong selection pressure, whereas in the in vitro case, you have only n-m weak selection pressures interfering with the evolution of the single strong selection pressure. The evolution of the penicillin resistance occurs more rapidly in the in vitro case because there are fewer selection pressures than the in vivo case (the immune response and so on). Rocketdodger realizes this.

Now if you want to try and argue that putting a strong selection pressure on a population will make the weak selection pressures evolve more rapidly then you might have a point but the problem for you is that it is mathematically impossible. Weak selection pressures don’t have a strong impact on the fitness of a population to reproduce but they still interfere with the ability of that population to evolve against a strong selection pressure.

Combination selection pressures profoundly slow the ability of the population to evolve against all these pressures simultaneously. Paul, you should understand this, your own ev model shows this and reality shows this as well. Ev is simply a sorting/optimization algorithm which shows what happens when you have multiple optimization conditions acting on an evolving system simultaneously.

 

[Paul C. Anagnostopoulos]

Paul, do I have to spell this out for you? Ok, in both the in vitro and in vivo cases you have a single strong selection pressure evolving on the background of weak selection pressures. In the in vivo case, you have n weak selection pressures interfering with the evolution of the single strong selection pressure, whereas in the in vitro case, you have only n-m weak selection pressures interfering with the evolution of the single strong selection pressure. The evolution of the penicillin resistance occurs more rapidly in the in vitro case because there are fewer selection pressures than the in vivo case (the immune response and so on). Rocketdodger realizes this.

Aha, I get it. We're assuming that there are m fewer selection pressures in vitro than in vivo. How do we know this?

But sure, let's assume that at least some background selection pressures can interfere with the evolution of a solution to a strong selection pressure. Presumably you have mathematics to show that in the real world the situation is such that only certain (unspecified) biological mechanisms could have evolved in the time available, while other extant mechanisms could not have evolved. This mathematics would surely indicate which mechanisms could have evolved and which could not. Would you be so kind as to present the math?

~~ Paul

 

[Paul C. Anagnostopoulos]

The point you are missing Belz is that Dr Schneider’s model shows that the reason it so slowly converges is the three selection conditions. If you set two of the three selection conditions to zero in the model then the remaining selection condition can evolve much, much more rapidly. That same behavior of mutation and selection is seen in reality in the numerous citations posted.

So in all those citations, they are evolving two completely different mechanisms and then comparing the time required? Because that is what you're doing when you set one or two of Evj's selection conditions to zero. I don't think anyone will argue with you if you say that evolving a "simple" mechanism is easier than evolving a "more complicated" mechanism. In the case of Evj, you are comparing the time to evolve a transcription factor that recognizes any locus with one that recognizes them selectively. All three selection conditions act on a single gene.

~~ Paul

 

[kleinman]

Annoying Creationists

Paul, do I have to spell this out for you? Ok, in both the in vitro and in vivo cases you have a single strong selection pressure evolving on the background of weak selection pressures. In the in vivo case, you have n weak selection pressures interfering with the evolution of the single strong selection pressure, whereas in the in vitro case, you have only n-m weak selection pressures interfering with the evolution of the single strong selection pressure. The evolution of the penicillin resistance occurs more rapidly in the in vitro case because there are fewer selection pressures than the in vivo case (the immune response and so on). Rocketdodger realizes this.

Aha, I get it. We're assuming that there are m fewer selection pressures in vitro than in vivo. How do we know this?

I have posted citations where the scientists intentionally produce resistance to particular therapies in vitro in order to identify the particular mutations which would confer this resistance. The development of these resistant strains are done under controlled conditions and the evolution of resistance can be done in a small number of generations with proper support of the population being evolved and the minimization of other selection pressures on the population.

I have also seen this phenomenon many times in my clinical practice. There have been occasions when I have used particular recommended antibiotics for treating infections and the culture and sensitivity report comes back with the in vitro testing showing that the bacteria is resistant to the drug used yet the infection resolves. The immune system puts tremendous selection pressure on most infections. In addition, some of the citations I have posted show that drugs which when used alone may not have effect on particular populations but when used in combination with other drugs sometimes regain effectiveness.

But sure, let's assume that at least some background selection pressures can interfere with the evolution of a solution to a strong selection pressure. Presumably you have mathematics to show that in the real world the situation is such that only certain (unspecified) biological mechanisms could have evolved in the time available, while other extant mechanisms could not have evolved. This mathematics would surely indicate which mechanisms could have evolved and which could not. Would you be so kind as to present the math?

Paul, ev does present the math. Even with its strong selection pressures (only the best half of the population is allowed to reproduce every generation), the sorting process is still very slow. If you introduce other selection conditions, this would only interfere with the sorting process even more so. It is the multiple simultaneous sorting conditions which slow the evolutionary process in ev, this is strikingly apparent when you set two of the three selection conditions to zero. If you impose another selection condition in ev for example in the nonbinding site region not only do you have no binding sites but also if occurrences of 4 identical bases in a row constitutes a mistake, satisfying this additional condition would slow the sorting process for the other selection conditions.

The fundamental point here in the mathematics of mutation and selection is that the number of selection conditions dominates the mathematical behavior of these systems. Weak selection pressures may not prevent the evolution of a strong selection pressure but they do interfere with the process.

The point you are missing Belz is that Dr Schneider’s model shows that the reason it so slowly converges is the three selection conditions. If you set two of the three selection conditions to zero in the model then the remaining selection condition can evolve much, much more rapidly. That same behavior of mutation and selection is seen in reality in the numerous citations posted.

So in all those citations, they are evolving two completely different mechanisms and then comparing the time required? Because that is what you're doing when you set one or two of Evj's selection conditions to zero. I don't think anyone will argue with you if you say that evolving a "simple" mechanism is easier than evolving a "more complicated" mechanism. In the case of Evj, you are comparing the time to evolve a transcription factor that recognizes any locus with one that recognizes them selectively. All three selection conditions act on a single gene.

That’s not correct Paul, the selection conditions in ev evolve sequences of bases which match the weight matrix at certain locations in the genome and eliminate these sequences in the gene and nonbinding site region. That is all that the ev sort/optimization algorithm does.

 

[joobz]

So joobz, not only are you a big mouth who is ignorant of mathematics, you are a coward. You said you could find irregularities in my PhD thesis, put up or shut up. Here’s what you said.

again, reading comprehension fails you.

I could critique his PhD for irregularities in his publication track that raise interesting questions. But, I see no reason to doubt him or this. As it is irrelevant. His terrible arguments and woefully terrible understanding of science is much more telling.

I know full well what I said. I was referring to the track record. I was calling your publication track of only 2 papers, neither of which had the same advisor, an irregularity. I could care less how accurate the papers were. It is obvious by their impact that they were unimportant. your inability to argue your case effectively here has been much more indicative of your skills than anything else.

$10,000 wager that you can’t find any mathematical or empirical irregularities in my PhD thesis or are you just a big mouth fake? You claim to have a PhD in engineering, how much do you know about PDEs prove my thesis wrong or are you just a big faker? I think you are a faker after posting your nonsense speculations about abiogenesis.

none of this is meaningful. Care to state where I was "fake"? can you actually present anything meaningful as an arugment, or will you resort to personal attacks?

There’s the wager you fake. Why don’t you post your name you coward and let’s have a look at your PhD thesis. Joobz, not only are you a mathematical incompetent in the mathematics of mutation and selection, you are a mathematical incompetent in PDEs. Prove otherwise and take up this $10,000 wager since you have claimed that you can find irregularities in my PhD thesis.

I see no reason to trust anything about you. it is obvious you are a dishonest person who will resort to these silly attacks because you have no foundation to any argument you make. Why would I want to share anything with you?

 

[rocketdodger]

You can find this information if you read the thread. Do you have to be spoon fed everything?

This is pretty ironic, coming from you of all people. I don't feel like combing through a thread with thousands and thousands of posts -- what is so hard about just telling me? I think your refusal speaks volumes about your character.

Why don’t you tell us what your credentials are, you claim you understand how mutation and selection works, tell us why.

I am a video game programmer, employed by Activision, with a B.S. in Computer Science that includes credits in molecular biology. Is that outstanding? Not at all. But it is the truth.

How does mutation and selection work? Here is an example of a coherent, well thought out, and easy to follow argument -- the kind you are incapable of producing Kleinman. I could be wrong on many points, but at least I put my ideas into a form readable by others so they have the opportunity to show me where I am wrong.

---------------------------------------------------------------------------------------

Given a population and environment, any mutation in any individual of the population can be measured by the change in relative reproductive fitness of the individual as affected by that mutation. Mutations that increase relative reproductive fitness are termed "beneficial," while those that decrease it are termed "harmful." Furthermore, the relative change in fitness can be "strong" or "weak," depending on just how large the change is.

When relative reproductive fitness is increased, an individual has a relatively higher chance to propagate its DNA to the next generation by having offspring. When decreased, the opposite occurs. These offspring, in turn, have the same fate. Over time, the changed percentages (relative to the other individuals in the population) lead to the mutation either being present in the vast majority of individuals' genomes (evolution) or hardly any (no evolution). This is "selection."

That is it. There is nothing more to evolution.

Where does "optimization/sorting" fall in this process? Clearly, the selection process can be viewed as a type of sorting, because individuals with higher relative reproductive fitness tend to be placed "ahead" of those with lower. Furthermore, the selection process can be said ` There are two important distinctions from a typical sorting algorithm, however, that are very important.

First, the individuals sort themselves, not some external entity. Thus, there is no such thing as the "sorting slowing down" -- it always proceeds at a rate determined by the species life cycle and nothing else.

Second, selection is fact not simple sorting. Rather, it is a process that can be viewed as somewhat analagous to sorting. The sorting influences the results of selection, but selection happens every generation regardless.

What does this mean for evolution and multiple selective pressures?

First of all we need to define exactly what we mean by "rate of evolution." For this discussion, it means "rate of fixation of mutations into the species' genome," or in other words, how long it takes on avearge for a given mutation to spread so that a good majority of the individuals in the population carry it.

Second, we need to define "selective pressure," which for this discussion is simply a factor in the environment that, when paired with a mutation, leads to a given change in relative reproductive fitness. A "stronger" pressure results in a larger change than a "weaker" pressure, given the same pairing.

Knowing all of this, generating some fairly accurate ideas of what will happen to a population subjected to multiple selective pressures of varying strengths is not difficult.

The individuals still sort themselves according to relative reproductive fitness, in the same amount of time as before. Those with the most/strongest beneficial mutations will tend to have the most offspring, those with the fewest/weakest beneficial mutations will tend to have the least, and vica versa for harmful mutations.

The difference is that, because a single mutation is not responsible for determining relative fitness anymore, it will take more generations for a given mutation to either spread throughout the population or disappear from the population, depending on the difference that mutation affects in relative fitness.

The change still happens, however, and furthermore, the distribution of all the mutations changes in parallel. This brings us to Adequate's graph. Because the distribution of all mutations is changing at once, in parallel, the extra time it takes for any one of them to be fixed in the genome is more than made up for. Adequate's graph shows the results that this fact leads to.

Suppose you have 50 pressures, and each of them takes on average 100 generations to result in their corresponding mutations being fixed (evolution). Then if you apply them all back to back, one at a time, it will take 50 x 100 or 5000 generations for all the mutations to be fixed and the evolution completed. Now suppose you apply them all at once. It doesn't matter that it may take much, much longer for each mutation to be fixed -- as long as they are all finished by generation 4999, the average number of generations to fixation will be less than before. And that means a faster rate of evolution. Does this actually happen? Adequate says it does, and I will whip up a little simulation of my own to see for myself. My hunch is "yes, it does."

In the context of all the studies Kleinman cites, this doesn't matter -- the goal of the pressures is to actually kill off the population, and so taking longer for a resistance mutation to be fixed is extremely damaging. If the entire population is dead by generation 2000, then obviously evolution will be profoundly slowed.

ETA: Everyone, please critique these ideas if they seem wrong in any way -- I want to show Kleinman what an intelligent discussion between educated people actually looks like.

 

[kjkent1]

The fundamental point here in the mathematics of mutation and selection is that the number of selection conditions dominates the mathematical behavior of these systems. Weak selection pressures may not prevent the evolution of a strong selection pressure but they do interfere with the process.

This is such baloney, Alan. A pack of wolves will eat loads of sheep, regardless of the number of missing or spurious binding sites in the genomes of those sheep.

The selection pressures found in ev, are relatively equal, even where the weights are set to the extremes, vis-a-vis real life application of selective pressure.

Your examples show this, because as soon as you expose a bacteria or virus to a single wolf-sized selection pressure, resistance appears.

By analogy, if you put wolves, bears and humans into hunting down those sheep, pretty quickly, there won't be any evolutionary change, because there won't be any sheep left.

You may be terrific at doing non-linear differential equations -- but you just suck at seeing the obvious.

 

[Paul C. Anagnostopoulos]

I have posted citations where the scientists intentionally produce resistance to particular therapies in vitro in order to identify the particular mutations which would confer this resistance. The development of these resistant strains are done under controlled conditions and the evolution of resistance can be done in a small number of generations with proper support of the population being evolved and the minimization of other selection pressures on the population.

You're sure they are minimizing selection pressures in general, or just ones they think will interfere with what they are trying to accomplish? Are you sure they aren't introducing other pressures?

Paul, ev does present the math.

Sorry, Ev doesn't display a single math equation that I know of.

That’s not correct Paul, the selection conditions in ev evolve sequences of bases which match the weight matrix at certain locations in the genome and eliminate these sequences in the gene and nonbinding site region. That is all that the ev sort/optimization algorithm does.

Yes, indeed, when all three selection conditions are turned on. When one or two are turned off, that is not the function that evolves. The fact that evolving a different function takes fewer generations is not as interesting as you make it out to be.

~~ Paul

 

[kleinman]

Annoying Creationists

I have posted citations where the scientists intentionally produce resistance to particular therapies in vitro in order to identify the particular mutations which would confer this resistance. The development of these resistant strains are done under controlled conditions and the evolution of resistance can be done in a small number of generations with proper support of the population being evolved and the minimization of other selection pressures on the population.

You're sure they are minimizing selection pressures in general, or just ones they think will interfere with what they are trying to accomplish? Are you sure they aren't introducing other pressures?

These scientists are trying to isolate and identify the mutations that give resistance to particular drugs. Why would they introduce other selection pressures which would interfere with what they are trying to identify? They grow their populations in incubators with plenty of resources needed by the population and introduce the drugs slowly so as not to kill the entire population.

Paul, ev does present the math.

Sorry, Ev doesn't display a single math equation that I know of.

Paul, you are not going to make a point here by being cute. Ev is a collection of equations and conditional statements which produces data from its sorting/optimization algorithm which simulates the mutation and selection process. Dr Schneider’s equations are there, I have seen the code and it does a good job of simulating how the mutation and selection process works.

That’s not correct Paul, the selection conditions in ev evolve sequences of bases which match the weight matrix at certain locations in the genome and eliminate these sequences in the gene and nonbinding site region. That is all that the ev sort/optimization algorithm does.

Yes, indeed, when all three selection conditions are turned on. When one or two are turned off, that is not the function that evolves. The fact that evolving a different function takes fewer generations is not as interesting as you make it out to be.

Stop being silly Paul, there is no function being evolved in ev. There are only sequences of bases which satisfy the selection conditions determined by matches to the weight matrix evolving in ev. Of course you can claim that ev is evolving real binding sites, then you can explain to us what the function of a binding site is for a gene that evolves binding sites. That would be an amusing story for you to tell us.

You can find this information if you read the thread. Do you have to be spoon fed everything?

This is pretty ironic, coming from you of all people. I don't feel like combing through a thread with thousands and thousands of posts -- what is so hard about just telling me? I think your refusal speaks volumes about your character.

So you want to make my character the issue in this discussion rather than what I post based on the results from ev and the hundreds of real examples of how mutation and selection actually works. How would you know what speaks volumes and what doesn’t since you are too lazy to read the volumes? Mutation and selection is not a trivial mathematical subject. Why don’t you read what Dr Schneider has written about the ev program instead of trying to figure out my PhD dissertation is all about? Then perhaps you will be prepared to carry out an intelligent discussion on the topic.

How does mutation and selection work? Here is an example of a coherent, well thought out, and easy to follow argument -- the kind you are incapable of producing Kleinman. I could be wrong on many points, but at least I put my ideas into a form readable by others so they have the opportunity to show me where I am wrong.

---------------------------------------------------------------------------------------

Given a population and environment, any mutation in any individual of the population can be measured by the change in relative reproductive fitness of the individual as affected by that mutation. Mutations that increase relative reproductive fitness are termed "beneficial," while those that decrease it are termed "harmful." Furthermore, the relative change in fitness can be "strong" or "weak," depending on just how large the change is.

When relative reproductive fitness is increased, an individual has a relatively higher chance to propagate its DNA to the next generation by having offspring. When decreased, the opposite occurs. These offspring, in turn, have the same fate. Over time, the changed percentages (relative to the other individuals in the population) lead to the mutation either being present in the vast majority of individuals' genomes (evolution) or hardly any (no evolution). This is "selection."

That is it. There is nothing more to evolution.

Rocketdodger, you are wrong about this, there is one thing more that you have to add to your description. How does this mutation and selection process work mathematically and empirically? Dr Schneider wrote a computer simulation of this process which can show you how the process works mathematically and there is a vast amount of empirical evidence which show how this process works empirically.

Where does "optimization/sorting" fall in this process? Clearly, the selection process can be viewed as a type of sorting, because individuals with higher relative reproductive fitness tend to be placed "ahead" of those with lower. Furthermore, the selection process can be said ` There are two important distinctions from a typical sorting algorithm, however, that are very important.

First, the individuals sort themselves, not some external entity. Thus, there is no such thing as the "sorting slowing down" -- it always proceeds at a rate determined by the species life cycle and nothing else.

Again rocketdodger, you are wrong about this, the environment does the sort. The individuals who have the best fitness in given environment are able to reproduce; this is not determined by the individuals themselves. If you consider for example HIV in an environment that has PIs and RTIs, only those viruses that can adapt to these selection pressures will be able to reproduce. It is an empirical fact that if you use only single drug therapy, the HIV population can evolve resistance to that single selection pressure rapidly while multiple drug therapy profoundly slows the virus population’s ability to reproduce. The sorting of beneficial and detrimental mutations is strongly dependent on the number of selection pressures. For single selection pressures, the ability of the population to sort beneficial and detrimental mutations is very easy and the sort occurs very rapidly, for multiple selection pressures, this sorting process becomes profoundly slow. This is a mathematical and empirical fact of life for mutation and selection process.

Second, selection is fact not simple sorting. Rather, it is a process that can be viewed as somewhat analagous to sorting. The sorting influences the results of selection, but selection happens every generation regardless.

Rocketdodger, mutation and selection is not somewhat analogous to sorting, it is exactly analogous. Mutation and selection is a sorting of beneficial and detrimental mutations based on the optimization of fitness of the population and these types of problems are extremely sensitive to the number of selection conditions.

First of all we need to define exactly what we mean by "rate of evolution." For this discussion, it means "rate of fixation of mutations into the species' genome," or in other words, how long it takes on avearge for a given mutation to spread so that a good majority of the individuals in the population carry it.

And the rate can be measured by the number of generations required to evolve a given number of loci for a given size genome, population, mutation rate and number of selection conditions. If read the earlier portions of this thread, you will see that was what was done with ev.

Second, we need to define "selective pressure," which for this discussion is simply a factor in the environment that, when paired with a mutation, leads to a given change in relative reproductive fitness. A "stronger" pressure results in a larger change than a "weaker" pressure, given the same pairing.

You are missing an important point. The way selection pressures affect the population is by changing the frequency of particular sequences of bases. That’s how a population finds a trajectory on the fitness landscape to a new local optimum.

Knowing all of this, generating some fairly accurate ideas of what will happen to a population subjected to multiple selective pressures of varying strengths is not difficult.

The individuals still sort themselves according to relative reproductive fitness, in the same amount of time as before. Those with the most/strongest beneficial mutations will tend to have the most offspring, those with the fewest/weakest beneficial mutations will tend to have the least, and vica versa for harmful mutations.

That’s pretty much how the sort works rocketdodger. When you plug in the numbers like Dr Schneider did, you can watch how this process works mathematically.

The difference is that, because a single mutation is not responsible for determining relative fitness anymore, it will take more generations for a given mutation to either spread throughout the population or disappear from the population, depending on the difference that mutation affects in relative fitness.

That’s not correct rocketdodger. Every mutation has affect on the process but not nearly as much as the number of selection conditions.

The change still happens, however, and furthermore, the distribution of all the mutations changes in parallel. This brings us to Adequate's graph. Because the distribution of all mutations is changing at once, in parallel, the extra time it takes for any one of them to be fixed in the genome is more than made up for. Adequate's graph shows the results that this fact leads to.

The only problem is that Adequate has no empirical evidence for his graph. All the empirical evidence shows that when a population is trying to evolve to selection pressures in parallel, the process is profoundly slowed. So does Dr Schneider’s model, evolving all three selection conditions simultaneously takes huge numbers of generations, however any one of the selection conditions alone evolves very quickly. That’s how the mutation and selection sorting process works.

Suppose you have 50 pressures, and each of them takes on average 100 generations to result in their corresponding mutations being fixed (evolution). Then if you apply them all back to back, one at a time, it will take 50 x 100 or 5000 generations for all the mutations to be fixed and the evolution completed. Now suppose you apply them all at once. It doesn't matter that it may take much, much longer for each mutation to be fixed -- as long as they are all finished by generation 4999, the average number of generations to fixation will be less than before. And that means a faster rate of evolution. Does this actually happen? Adequate says it does, and I will whip up a little simulation of my own to see for myself. My hunch is "yes, it does."

You can run the numbers in Dr Schneider’s model. To evolve all three selection conditions simultaneously for a 16k genome takes more than 5,000,000 generations while each of the individual selection pressures when applied singly only take at most 100 generations. Your hunch is wrong.

In the context of all the studies Kleinman cites, this doesn't matter -- the goal of the pressures is to actually kill off the population, and so taking longer for a resistance mutation to be fixed is extremely damaging. If the entire population is dead by generation 2000, then obviously evolution will be profoundly slowed.

Rocketdodger, what you don’t realize is that it doesn’t take huge populations to evolve to single selection pressures. If you are going to advocate the concept of common descent, how are you going to explain the transformation of thousands of genes? All the mathematical and empirical evidence show that transforming more than a single gene at a time is extremely difficult for any size population. Here’s another example of how the process works empirically.
http://www.journals.uchicago.edu/JID/journal/issues/v181n4/990745/990745.html

Prolonged administration of nucleoside analogues for chronic hepatitis B may result in the emergence of hepatitis B viral polymerase mutants. To gain insight into the mechanism involved in the virus's resistance to famciclovir, the amino acid sequences of the terminal protein and reverse-transcriptase (RT) domains of the viral polymerase were determined during therapy among 28 patients. The antiviral response was independent of viral genotypes, and nonresponse to famciclovir was associated with a complex variability of the RT domain. No mutation in the YMDD motif was observed, whereas an L528M mutation was clearly selected by famciclovir treatment in 2 patients, as well as 14 novel mutations in 7 patients. Clone sequence analysis of the RT domains of patients undergoing retreatment with famciclovir and/or lamivudine showed the selection of a preexisting drug-resistant mutant in one case and indicated that sequential antiviral therapy may allow the rapid selection of resistant strains.

and

New findings were also obtained by longitudinal studies of viral sequences, obtained from PCR products and PCR clones, in 4 patients who received a second course of antiviral therapy with famciclovir and/or lamivudine (figure 4). Two cases were of particular interest in terms of drug resistance. In the first case (patient 23), an L528M mutant was found as a minor virus population before therapy and was partially selected during the first course of treatment. This mutant became rapidly dominant during the second course of famciclovir in < 6 months. In the second patient (patient 2), the L528M mutation was selected during famciclovir monotherapy. When the patient's treatment was changed to a combination of famciclovir and lamivudine, a rapid selection (6 months) of the double mutation L528M/M552V occurred, conferring resistance to both antivirals. These data demonstrate that nucleoside analogue administration may favor the outgrowth of drug-resistant mutants that preexisted as a minor viral species before therapy and that the L528M change is clearly associated with famciclovir resistance in vivo. Furthermore, these observations emphasize that sequential antiviral therapy with nucleoside analogues may allow the rapid selection of drug-resistant strains. Our observation also suggests that the selection of the L528M mutant conferring resistance to famciclovir may favor the selection of the double L528M/M552V mutant that is cross-resistant to famciclovir and lamivudine.

and

In conclusion, we report a longitudinal study of HBV polymerase sequence during antiviral treatment of chronic hepatitis B with a nucleoside analogue. Our findings give new insight in the dynamics of viral polymerase sequence evolution in relation to drug resistance. Our results have several clinical implications and suggest that antiviral response to famciclovir is independent of viral genotypes, the emergence of famciclovir-resistant strains is associated with a complex variability of the RT, and sequential antiviral therapy may allow the rapid selection of resistant strains. On the basis of these results and those obtained in lamivudine-treated patients, the selection of resistant mutants is expected to occur with any nucleoside analogue therapy. The capacity of new antiviral strategies based on combinations of inhibitors to prevent the emergence of resistant viral strains needs to be further evaluated in animal models and clinical trials.

Rocketdodger, this citation as well as the hundreds of other citations which I have posted show how mutation and selection sorting process works in real life. There are no examples of a population evolving to simultaneous selection pressures more rapidly than when the selection pressures are applied sequentially. The concept that mutations can be sorted more rapidly with simultaneous selection (sorting) conditions is mathematically irrational and illogical.

 

[rocketdodger]

Rocketdodger, you are wrong about this, there is one thing more that you have to add to your description. How does this mutation and selection process work mathematically and empirically?

Did you even read my post? Obviously not, because I made it very clear exactly how mutation and selection works mathematically -- mutations affect the chances their carriers have of passing them on to the next generation. It is that simple Kleinman.

Again rocketdodger, you are wrong about this, the environment does the sort.

No. The environment is an inanimate object. How you think it could possibly sort anything is beyond me.

The individuals who have the best fitness in given environment are able to reproduce; this is not determined by the individuals themselves.

So you contend that a race track sorts the field, rather than the drivers? The environment determines which individuals have the most relative fitness, but the individuals themselves do the reproducing or the dying.

Rocketdodger, mutation and selection is not somewhat analogous to sorting, it is exactly analogous.

Except for the two differences I pointed out, of course. Selection happens in O(1) time. Sorting can't happen faster than O(nlogn) time.

And the rate can be measured by the number of generations required to evolve a given number of loci for a given size genome, population, mutation rate and number of selection conditions. If read the earlier portions of this thread, you will see that was what was done with ev.

Yes. The important point is that the average rate is more important than the instantaneous rate, which you seem to agree with.

You are missing an important point. The way selection pressures affect the population is by changing the frequency of particular sequences of bases. That’s how a population finds a trajectory on the fitness landscape to a new local optimum.

The notion of a "fitness landscape" and "local optimum" are non-existent in reality. They are simply ideas used in models to help explain certain concepts. You don't even understand them to begin with, so why do you bring them up?

What exactlly is a "local optimum" in the context of a "fitness landscape?"

That’s pretty much how the sort works rocketdodger. When you plug in the numbers like Dr Schneider did, you can watch how this process works mathematically.

Except that Schneider's program is an extremely limited model that is only supposed to show the ability of populations to evolve control mechanisms for their genomes. I still don't know how you are applying it to mutation and selection in general. As Paul says, it doesn't even really include the ability to use truly different selective pressures at once.

That’s not correct rocketdodger. Every mutation has affect on the process but not nearly as much as the number of selection conditions.

What does this have to do with what I wrote?

You can run the numbers in Dr Schneider’s model. To evolve all three selection conditions simultaneously for a 16k genome takes more than 5,000,000 generations while each of the individual selection pressures when applied singly only take at most 100 generations. Your hunch is wrong.

We will see.