Annoying creationists

[rocketdodger]

What studies have you posted?
See post #5993 on the previous page of the thread.

We all know you are being purposefully ignorant, so I will make it so simple even you can't deny understanding what I say.

[rocketdodger]

Answer the question rocketdodger; that if someone with HIV who could not mount a humoral immune response against the virus was given therapy, would the virus evolve more slowly against that therapy than a person who could mount a humoral immune response against the given the same therapy?

No. As the studies you cite show, certain combinations of selection pressures profoundly slow the evolution of populations they affect. WTF does this have to do with my question about the validity of the studies I cited?

And while you are thinking about the question, here is another example of how mutation and selection actually works.

Right back at you genius:

"Resistance emerges as a result of selection and then disemination of spontaneous mutant parasites with reduced drug susceptibility. Combination therapy is considered as the main strategy to control antimalarial drug resistance."

Why would antimalarial drug resistance be a problem, Kleinman, if the evolution of it happened too slow to matter?

[kjkent1]

You are the whiney coward. Why don’t you post under your real name so we can google search on your name and find out all about you? Of course we know plenty about you already. You are a greedy ambulance chaser who is totally ignorant of the mathematics of mutation and selection.You said "intellectual" coward. If you want me to stop referring to you in that fashion, then stop refusing to directly address contrary evidence.

I've presented evidence that varying the selective pressure weights in ev causes three pressure to converge faster in some instances.

Unless you can explain why, then you're theory is demonstrated false.

You have presented evidence which shows that a single overwhelming pressure renders natural pressures insignificant, but still existent. All of your quoted papers show this, because none of those experiments protected the pathogen from all other pressures other than the one(s) to which the organism is subjected.

This proves that a single intense pressure can and does completely overcome your sorting problem.

Now, Alan -- let's read something more intelligent from you as a response, than just:

"Sorry, it's impossible, therefore you're wrong."

You should consider getting a tattoo on your forehead with that phrase.

ROFLMAO!

[kleinman]

You are such a dodo rocketdodger.
Two examples, right out of your own citations, that evolution occurs rapidly in the natural world. Care to argue with that? Many, many, many more (judging by how many of your citations I can crawl through and use against you) on the way...
http://www.omafra.gov.on.ca/english/...5/vg1105a4.htm (http://www.omafra.gov.on.ca/english/crops/hort/news/vegnews/2005/vg1105a4.htm)
Resistance to pesticides can develop very quickly.
The quote that rocketdodger ignores from the citation.
Resistance to pesticides can develop very quickly. Do not use the same chemical repeatedly unless used in rotation with a different chemical or in combination with other chemicals having a different mode of action. Compounds within a chemical group usually share a common target site within the pest and mode of action. When a pest develops resistance to a chemical due to a mutation, there is a risk that the resistance will also result in cross-resistance to all the other compounds in the same sub-group. A pest population may develop cross resistance to closely related chemicals if a common detoxification mechanism exists, even in the absence of a selection pressure against individual compounds. Multiple resistance occurs through selective pressure on separate detoxification mechanisms for unrelated pesticides. In some species-specific cases, resistance develops due to an increased ability to metabolize toxins. Where these metabolic resistance mechanisms are not linked to a specific site of action, resistance to several different chemical families or mode of action can occur. Both metabolic and multiple resistant create serious challenges to the success of integrated resistance management strategies.
And
http://www.lshtm.ac.uk/people/roper.cally (http://www.lshtm.ac.uk/people/roper.cally)
and I am working on the problem of antimalarial drug resistance in Africa. The emergence and spread of drug resistance is a major threat to effective malaria treatment
and the part of the citation which rocketdodger ignores:
In my research group, Cally Roper Lab, we investigate the molecular genetic basis of drug resistance using population genetic approaches. We aim to determine which factors are most important in determining the rate of emergence and rate of spread of resistance. Our work includes the evaluation of combination therapy and its potential for slowing resistance evolution, and evaluating the selective pressure applied by intermittent preventive treatment. We are mapping the dispersal of resistance mutations in Africa.
Sure resistance can occur quickly, when you have single selection pressures, both these citations explicitly say that combination selection pressures slow the evolution of resistance. Now why don’t you go through the hundreds of citations I have posted and see if you can make a single point because so far you have no point.
Answer the question rocketdodger; that if someone with HIV who could not mount a humoral immune response against the virus was given therapy, would the virus evolve more slowly against that therapy than a person who could mount a humoral immune response against the given the same therapy?No. As the studies you cite show, certain combinations of selection pressures profoundly slow the evolution of populations they affect. WTF does this have to do with my question about the validity of the studies I cited?
Because the studies you cited show that evolution occurs much more quickly with single selection pressures (single drug therapy) than with combination therapy. So answer the question, if someone with HIV who could not mount a humoral immune response against the virus was given therapy, would the virus evolve more slowly against that therapy than a person who could mount a humoral immune response against the given same therapy?
And while you are thinking about the question, here is another example of how mutation and selection actually works. Right back at you genius: Resistance emerges as a result of selection and then disemination of spontaneous mutant parasites with reduced drug susceptibility. Combination therapy is considered as the main strategy to control antimalarial drug resistance."
I don’t even have to repost the quote, you ignore that combination therapy is the strategy from slowing or stopping the evolution of resistance. If you want rapid evolution of resistance, use monotherapy. So answer the question, if someone with HIV who could not mount a humoral immune response against the virus was given therapy, would the virus evolve more slowly against that therapy than a person who could mount a humoral immune response against the given same therapy?
Why would antimalarial drug resistance be a problem, Kleinman, if the evolution of it happened too slow to matter?
The point is rocketwhomissesthetarget is that the use of monotherapy has led to rapid evolution of resistance of these drugs. That’s why combination therapy is now the considered the standard of care in order to avoid selection of resistant parasites. Now are you going to answer the question, if someone with HIV who could not mount a humoral immune response against the virus was given therapy, would the virus evolve more slowly against that therapy than a person who could mount a humoral immune response against the given same therapy?
You are the whiney coward. Why don’t you post under your real name so we can google search on your name and find out all about you? Of course we know plenty about you already. You are a greedy ambulance chaser who is totally ignorant of the mathematics of mutation and selection.You said "intellectual" coward. If you want me to stop referring to you in that fashion, then stop refusing to directly address contrary evidence.
I would never mistake you as an “intellectual”. You seem to think you understand how strong and weak selection pressures work, post your data and explain to us how they work. While you are not posting your data or giving us your explanation, here is another real example of how mutation and selection actually works.
http://www.anopheles.org/showabstract.php?pmid=2571247 (http://www.anopheles.org/showabstract.php?pmid=2571247)
Blood induced Plasmodium berghei infection in Swiss mice was exposed during successive passages to mefloquine alone or mefloquine in combination with dapsone or primaquine or erythromycin, and the level of resistance to mefloquine in four sub-lines was compared at ED90 level. Treatment with mefloquine alone resulted in a 201.14 fold increase in resistance after 21 passages. Use of drug combination (mefloquine + dapsone) delayed the acquisition of resistance as shown by a marginal increase of ED90 by 5.76 fold after 34 passages. Similarly, there was a 17.84 fold increase of resistance after 32 passages involving exposure to mefloquine-primaquine and a 112.28 fold increase after exposure to melfoquine-erythromycin combination for 31 passages. The study emphasizes that rational drug combinations should be developed to protect the melfoquine against the emergence of resistance in P. falciparum cases.

[joobz]

yawn.
Horribly wrong assumptions in the Kleinman theory:
1.) Mutation rate remains constant
2.) Mutation rate is known
3.) Number of selection pressures for all species for all time in all areas is known
4.) Number of selection pressures is constant
5.) Selection pressure magnitude is constant and equal for all pressures
6.) Point mutations are the only mutation/adaptation mechanism
7.) defining selection pressure is unimportant
8.) slow equals stop
9.) Mutation is non-random


/prediction: Kleinman will pretend that these assumptions aren't relavent to his theory, but all his references clearly indicate otherwise.

[rocketdodger]

The point is rocketwhomissesthetarget is that the use of monotherapy has led to rapid evolution of resistance of these drugs.

So you agree that rapid evolution exists in nature (where by "nature" I mean "not in a controlled environment"). Thank you. Why has it taken 150 pages of rubbish for you to reach this conclusion?


Now are you going to answer the question, if someone with HIV who could not mount a humoral immune response against the virus was given therapy, would the virus evolve more slowly against that therapy than a person who could mount a humoral immune response against the given same therapy?

I did answer, in the first paragraph of my very last post. Read what I wrote if you are interested (but I know you are not).


While you are not posting your data or giving us your explanation, here is another real example of how mutation and selection actually works.

That study confirms that evolution can occur rapidly in nature. Why do you keep posting studies that are PREDICATED on the fact that evolution can occur rapidly? Every single study you cite, Kleinman, only solidifies the fact that evolution is fast enough to get results.

[kleinman]

/prediction: Kleinman will pretend that these assumptions aren't relavent to his theory, but all his references clearly indicate otherwise.
First, joobz doesn’t make predictions, he makes speculations, second, joobz doesn’t read his own citations let alone citations posted by others. Joobz thinks just if a citation has the word “environment” in it, they are talking about the weather. Here’s another citation for you not to read joobz.
http://www.anopheles.org/showabstract.php?pmid=15667718 (http://www.anopheles.org/showabstract.php?pmid=15667718)
When the larvae of Anopheles stephensi, a malaria vector, were selected with deltamethrin for 40 successive generations, there was a 60-fold increase in larval resistance to deltamethrin but no increase in the resistance of the adult mosquitoes. This result, and the observation that deltamethrin selection of adults for 40 generations resulted in only a six-fold increase in adult resistance to deltamethrin, indicated some stage specificity. When F(24) deltamethrin-resistant larvae were selected with 1:5 deltamethrin-piperonyl butoxide (deltamethrin-PBO), instead of deltamethrin alone, for 16 generations, the level of resistance to deltamethrin in the F(40) larvae was reduced by 6%-21%. Similarly, selection with deltamethrin-PBO of adults of the parental strain for 20 generations reduced the speed of the development of resistance to deltamethrin, compared with that seen using selection with deltamethrin alone. Deltamethrin selection appears to select initially a monooxygenase-based mechanism. When the monooxygenase-based mechanism is blocked, by treatment with PBO, selection of a kdr-type mechanism is accelerated, as is evident from increased cross-resistance to 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT) in the adults selected with deltamethrin-PBO. The implications of these results are discussed in terms of the management of the larval and adult stages of An. stephensi .
Sorry the title of this article doesn’t have the word “environment” in it joobz, but it does have the word “spectrum”, you probably thing they are talking about colors.
The point is rocketwhomissesthetarget is that the use of monotherapy has led to rapid evolution of resistance of these drugs.So you agree that rapid evolution exists in nature (where by "nature" I mean "not in a controlled environment"). Thank you. Why has it taken 150 pages of rubbish for you to reach this conclusion?
How would you know what is written in the 150 pages of this thread? The only way you can get rapid evolution of any gene is with a single selection pressure, of course, feel free to post a citation which says otherwise. And now are you going to answer the question, if someone with HIV who could not mount a humoral immune response against the virus was given therapy, would the virus evolve more slowly against that therapy than a person who could mount a humoral immune response against the given same therapy?

[rocketdodger]

The only way you can get rapid evolution of any gene is with a single selection pressure, of course, feel free to post a citation which says otherwise.

IT IS IMPOSSIBLE TO EXERT ONLY A SINGLE SELECTION PRESSURE ON A POPULATION.




And now are you going to answer the question, if someone with HIV who could not mount a humoral immune response against the virus was given therapy, would the virus evolve more slowly against that therapy than a person who could mount a humoral immune response against the given same therapy?

In post #6006 I told you that I answered that question already in post #6002, which means this is the second time I have told you I already answered it. Because you are not smart enough to navigate this thread accordingly, I will paste it here to make it simple for you:

"No. As the studies you cite show, certain combinations of selection pressures profoundly slow the evolution of populations they affect."

Here is what your last citation has to say about the rapidity of evolution in nature:

http://www.anopheles.org/showabstract.php?pmid=15667718

" ... were selected with deltamethrin for 40 successive generations, there was a 60-fold increase in larval resistance to deltamethrin . . . deltamethrin selection of adults for 40 generations resulted in only a six-fold increase in adult resistance to deltamethrin . . ."

A 60-fold increase in only 40 generations, Kleinman? That seems to be pretty rapid to me.

[joobz]

First, joobz doesn’t make predictions, [snip repeated nonsense]
Excellent. I predicted correctly!

Do I win anything?

[kleinman]

The only way you can get rapid evolution of any gene is with a single selection pressure, of course, feel free to post a citation which says otherwise.IT IS IMPOSSIBLE TO EXERT ONLY A SINGLE SELECTION PRESSURE ON A POPULATION.
You are correct rocketdodger! That is why the theory of evolution is mathematically impossible.
And now are you going to answer the question, if someone with HIV who could not mount a humoral immune response against the virus was given therapy, would the virus evolve more slowly against that therapy than a person who could mount a humoral immune response against the given same therapy?In post #6006 I told you that I answered that question already in post #6002, which means this is the second time I have told you I already answered it. Because you are not smart enough to navigate this thread accordingly, I will paste it here to make it simple for you:In post #6006 I told you that I answered that question already in post #6002, which means this is the second time I have told you I already answered it. Because you are not smart enough to navigate this thread accordingly, I will paste it here to make it simple for you:

"No. As the studies you cite show, certain combinations of selection pressures profoundly slow the evolution of populations they affect."
I know you are trying to squirm out of answering the question.
Here is what your last citation has to say about the rapidity of evolution in nature:
http://www.anopheles.org/showabstract.php?pmid=15667718 (http://www.anopheles.org/showabstract.php?pmid=15667718)
... were selected with deltamethrin for 40 successive generations, there was a 60-fold increase in larval resistance to deltamethrin . . . deltamethrin selection of adults for 40 generations resulted in only a six-fold increase in adult resistance to deltamethrin . . .A 60-fold increase in only 40 generations, Kleinman? That seems to be pretty rapid to me.
Of course when you are applying a single selection pressure to a population, mutation and selection can evolve rapidly to that single selection pressure. If you had run any cases with ev you would see this exact same effect. But then you missed this part of the quote.
When F(24) deltamethrin-resistant larvae were selected with 1:5 deltamethrin-piperonyl butoxide (deltamethrin-PBO), instead of deltamethrin alone, for 16 generations, the level of resistance to deltamethrin in the F(40) larvae was reduced by 6%-21%. Similarly, selection with deltamethrin-PBO of adults of the parental strain for 20 generations reduced the speed of the development of resistance to deltamethrin, compared with that seen using selection with deltamethrin alone.
The combination of deltamethrin and PBO slows the evolution of resistance when compared to deltamethrin alone, there’s a lesson here if you want to learn it rocketdodger.
First, joobz doesn’t make predictions, [snip repeated nonsense][snip everything joobz says is nonsense especially about mutation and selection and abiogenesis]
At least you’re smart enough to admit that you don’t make predictions, you only make speculations.

Here’s another citation for joobz and rocketthatmissesthetarget.
http://www.anopheles.org/showabstract.php?pmid=17092790 (http://www.anopheles.org/showabstract.php?pmid=17092790)
Throughout the tropical world antimalarial drug resistance is increasing, particularly in the potentially lethal malaria parasite Plasmodium falciparum. In some parts of Southeast Asia, parasites which are resistant to chloroquine, pyrimethamine-sulfadoxine, and mefloquine are prevalent. The characteristics of a drug that make it vulnerable to the development of resistance are a long terminal elimination half-life, a shallow concentration-effect relationship, and that one or two base-pair mutations confer a marked reduction in susceptibility. The development of resistance can be delayed or prevented by drug combinations. The artemisinin derivatives are the most potent of all antimalarial drugs. They reduce the infecting parasite biomass by approximately 10 000-fold per asexual life cycle. There are good arguments for combining, de novo, an artemisinin derivative with all newly introduced antimalarial drugs.
Hey joobz, these authors seem to think they can stop the evolution of resistance. You better contact them and tell them slow doesn’t mean stop.

[kjkent1]

You are correct rocketdodger! That is why the theory of evolution is mathematically impossible.ROFLMAO! You've done it again, Alan. If it's impossible, then how do you explain the fact that every one of your quoted papers begins with a "single" pressure, and produces rapid resistance?

That would be impossible, because as you've just said, a single selective pressure is impossible.

Of course, the answer is obvious to an open-minded person: intensity of selection pressure accounts for why evolution in nature occurs. For the closed-minded creationist, however, the answer is simply that intensity cannot have any effect, because that would make evolution by mutation and selection possible.

But, it can't be possible, says the creatonist -- evolution must be impossible -- otherwise, when I die, I may go nowhere, and I'm afraid of the dark. Mommy, save me -- the boogyman is in the closet!

[kleinman]

You are correct rocketdodger! That is why the theory of evolution is mathematically impossible.ROFLMAO! You've done it again, Alan. If it's impossible, then how do you explain the fact that every one of your quoted papers begins with a "single" pressure, and produces rapid resistance?
Because that’s the way mutation and selection works.
That would be impossible, because as you've just said, a single selective pressure is impossible.
You are correct kjkent1, that’s why the theory of evolution is mathematically impossible.
Of course, the answer is obvious to an open-minded person: intensity of selection pressure accounts for why evolution in nature occurs. For the closed-minded creationist, however, the answer is simply that intensity cannot have any effect, because that would make evolution by mutation and selection possible.
Now I understand how your theory of evolution works, a little weather change here, a little breeze there and reptiles evolve feathers and wings. It is all so obvious, how could I have missed this?
But, it can't be possible, says the creatonist -- evolution must be impossible -- otherwise, when I die, I may go nowhere, and I'm afraid of the dark. Mommy, save me -- the boogyman is in the closet!
Hey kjkent1, I heard there are lots of golf courses in hell, just no clubs or balls.

[joobz]

At least you’re smart enough to admit that you don’t make predictions, you only make speculations.Too bad I can't say the same. You haven't offered any reason for anyone to label you as smart, or even smart enough regarding anything related to evolution.

Here’s another citation for joobz and rocketthatmissesthetarget.
http://www.anopheles.org/showabstract.php?pmid=17092790 (http://www.anopheles.org/showabstract.php?pmid=17092790)

Hey joobz, these authors seem to think they can stop the evolution of resistance. You better contact them and tell them slow doesn’t mean stop.
See what I mean.

[kleinman]

At least you’re smart enough to admit that you don’t make predictions, you only make speculations.Too bad I can't say the same. You haven't offered any reason for anyone to label you as smart, or even smart enough regarding anything related to evolution.
I realize this; the theory of evolution is only understandable to speculators and extrapolators. Do you think that some day you would teach me how to speculate and extrapolate? How’s the weather in your rainforest? Do you see evolution accelerating as the earth’s plates are moving?

One thing I have learned from you is that if there is enough free energy, anything is possible.
http://forums.randi.org/images/smilies/doglaugh.gif

[joobz]

One thing I have learned from you is that if there is enough free energy, anything is possible.

I see were back to this nonsense?

Dr. Alan Kleinman, Have you stopped killing your patients?

[balrog666]

P.S. What is the goal of each side of this nearly 6000-post thread?


It's a study in abnormal psychology. Shhhh - several Ph.D.'s are being created here.

[Paul C. Anagnostopoulos]

Perhaps if you ask yourself the question, why does ev converge when Rfrequency < Rcapacity? Then perhaps you would understand that the fitness landscape is finally getting small enough with isoclines that allow for convergence to perfect creature local optima. Another way to get an easier to traverse fitness landscape is to reduce down the selection pressures to one and then the Rcapacity issue disappears. That is a real phenomenon.
The Rcapacity issue disappears because Rcapacity is irrelevant when you're not trying to evolve a creature that distinguishes binding sites from other positions on the genome.


Every example of convergence with ev is easy to explain. A local optimum is found by the model. You are hung up on the fact that ev stops converging to perfect creature local optima when Rcapacity > Rfrequency. Why you would think that ev should behave in a linear manner shows your lack of experience with non-linear mathematics.
Say what? I don't think Ev should behave in a linear manner. I think it should be prevented from converging when Rcapacity > Rfrequency.


The rationale for this was that benzyl benzoate and 5% tea tree oil were consistently the topical scabicides that killed scabies mites the quickest in our earlier in vitro studies [7].
What does this have to do with evolution?


Are you claiming that benzyl benzoate alone and 5% tea tree oil alone are both fatal to scabies? If so, why would these authors subject their patient to the distressing effects of the combination?
No, I'm asking what killing mites has to do with evolution.

~~ Paul

[Paul C. Anagnostopoulos]

ROFLMAO! You've done it again, Alan. If it's impossible, then how do you explain the fact that every one of your quoted papers begins with a "single" pressure, and produces rapid resistance?

Because that’s the way mutation and selection works.

That would be impossible, because as you've just said, a single selective pressure is impossible.

You are correct kjkent1, that’s why the theory of evolution is mathematically impossible.
Is it just me, or :crazy:?

~~ Paul

[kleinman]

One thing I have learned from you is that if there is enough free energy, anything is possible.I see were back to this nonsense?
This is one of my favorite of your quotes.
I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.
http://forums.randi.org/images/smilies/doglaugh.gif
Dr. Alan Kleinman, Have you stopped killing your patients?
Come on into the office and find out but you had better make an appointment, we are very busy.
http://forums.randi.org/images/smilies/doglaugh.gif
P.S. What is the goal of each side of this nearly 6000-post thread?It's a study in abnormal psychology. Shhhh - several Ph.D.'s are being created here.
Now that’s a good one, someone running around calling himself balrog666 is going to tell us what is normal and abnormal.
Perhaps if you ask yourself the question, why does ev converge when Rfrequency < Rcapacity? Then perhaps you would understand that the fitness landscape is finally getting small enough with isoclines that allow for convergence to perfect creature local optima. Another way to get an easier to traverse fitness landscape is to reduce down the selection pressures to one and then the Rcapacity issue disappears. That is a real phenomenon.The Rcapacity issue disappears because Rcapacity is irrelevant when you're not trying to evolve a creature that distinguishes binding sites from other positions on the genome.
You really like clinging to this issue. When are you going to learn that optimization problems have domains of convergence?
Every example of convergence with ev is easy to explain. A local optimum is found by the model. You are hung up on the fact that ev stops converging to perfect creature local optima when Rcapacity > Rfrequency. Why you would think that ev should behave in a linear manner shows your lack of experience with non-linear mathematics.Say what? I don't think Ev should behave in a linear manner. I think it should be prevented from converging when Rcapacity > Rfrequency.
Paul, it’s all about the shape of the fitness landscape and the starting point for the search for a local optimum. Map out the fitness landscape and you will know exactly why ev stops converging. You only have to computer 4^G points.
The rationale for this was that benzyl benzoate and 5% tea tree oil were consistently the topical scabicides that killed scabies mites the quickest in our earlier in vitro studies [7].What does this have to do with evolution?
Aren’t they killing scabies with selection pressures? Isn’t that what ev does? For that matter, they are using combination selection pressures.
Are you claiming that benzyl benzoate alone and 5% tea tree oil alone are both fatal to scabies? If so, why would these authors subject their patient to the distressing effects of the combination?No, I'm asking what killing mites has to do with evolution.
They are trying to evolve perfect scabies.

[kleinman]

Is it just me, or http://forums.randi.org/images/smilies/crazyeyes.gif?
It’s just you Paul.

[joobz]

This is one of my favorite of your quotes.
I'm sure you love it. It's completely correct in regards to what it was refering to.




Come on into the office and find out but you had better make an appointment, we are very busy.
Not sure what this means. or how it relates to your half-brained theory.

But continue to dance for us. It's funny watching you derail your own foolish thread.

[kjkent1]

It’s just you Paul.No, Alan it's just "you." You make a jackass out of yourself over and over by not recognizing the substantial flaws in your logic.

Apparently you don't want anyone to take you seriously. If you did, then you would take your opponent's seriously.

Do you ever discuss your theories with the other doctors in your clinic, or other collegues whom you respect?

Do you respect anyone, Alan, or are you simply so superior to every other human on Earth that only you can expound on what is or is not "true?"

Think about it. Your theory is wrong. If it wasn't, others would agree with you. But, no one does -- no one.

Not ONE person on planet Earth agrees with your theory.

If I were arguing a legal theory, and I couldn't find a single human being who would agree with me, I damn certain wouldn't bring that theory into a courtroom, because that would be a loooooooooser.

[rocketdodger]

You are correct rocketdodger! That is why the theory of evolution is mathematically impossible.

Then how do pathogens/rodents/weeds evolve resistance to drugs/poisons/herbicides?

I know you are trying to squirm out of answering the question.

You quoted my answer immediately above this statement in your post, you human paraquat.

Yet, here it is for you to ignore, like the de-evolved monkey you are, once again:

"No. As the studies you cite show, certain combinations of selection pressures profoundly slow the evolution of populations they affect."


Here’s another citation for joobz and rocketthatmissesthetarget.
http://www.anopheles.org/showabstract.php?pmid=17092790


Here is the first half of the first sentence in the abstract: "Throughout the tropical world antimalarial drug resistance is increasing"

Contrast this with Kleinman's latest absurdity: "You are correct rocketdodger! That is why the theory of evolution is mathematically impossible."
...which, of course, is totally the opposite of his earlier statement:
The point is rocketwhomissesthetarget is that the use of monotherapy has led to rapid evolution of resistance of these drugs.

Does anybody have info on this Kleinman tool? I would like to put a face with the stupidity I am seeing here.

[rocketdodger]

It’s just you Paul.

Well... actually... no, Kleinman, Paul is not the only person who thinks you are clueless.

[Deetee]

The theory of evolution is mathematically impossible.
Once upon a time people thought it was mathematically impossible for bumble bees to fly.
Their theories were wrong, just like yours.

[Belz...]

All the more reason not to separate the posts, you need to learn how mutation and selection actually works.

I STILL skip to the answers to my posts, Klein. It's just more work for no reason.

This discussion is not about your faith system

You're the creationist and you call MY opinion faith-based ?

:id:

In order to be faith-based, it would have to be unsupported by evidence. EVEN if you were correct about what you've been saying here, and I were wrong, it still wouldn't make it faith-based. You clearly don't understand what these words mean.

It’s easy to understand Belz; all you have to do is read what he means, not what he writes.

Perhaps, but don't do it like Kleinman does, because he is obviously incapable of doing that.

I apologise to all the OTHER posters if I've been terribly unclear.

The goal in this thread is the same as it was in the beginning of this discussion; to show that ev demonstrates that the theory of evolution is mathematically impossible and that real empirical examples of mutation and selection demonstrates what ev shows. Here are some more citations which show that combination selection pressures profoundly slow the evolutionary process.

Fine. Get a real scientist in here -- you know, those you say agree with you -- because it's obvious you are incapable of making your case.

[Belz...]

Kleinman's goal is to show that evolution happens too slow to actually work in the natural world, using, get this, data from experiments designed to find ways of slowing the rapid evolution that can occur in the natural world.

That's the best summary of a thread I've ever seen.

[Belz...]

http://http://forums.randi.org/showpost.php?p=3062923&postcount=5981

Still waiting, Klein.

[Belz...]

Woah, woah. Wait a minute...

You say:

The point is rocketwhomissesthetarget is that the use of monotherapy has led to rapid evolution of resistance of these drugs.

Bolding mine. So, rapid evolution IS possible, since it happened.

But then,

The only way you can get rapid evolution of any gene is with a single selection pressure, of course, feel free to post a citation which says otherwise.

Okay... so there ARE instances of a single selection pressure, since rapid evolution DID happen, by your admission.

And lastly...

IT IS IMPOSSIBLE TO EXERT ONLY A SINGLE SELECTION PRESSURE ON A POPULATION.

You are correct rocketdodger! That is why the theory of evolution is mathematically impossible.

Huh ? How is it impossible if YOU ADMIT IT HAPPENS ?

You have seriously shot yourself in the foot now, Kleinman.

[Belz...]

Because that’s the way mutation and selection works.

You are a walking paradox, Klein.

Now I understand how your theory of evolution works, a little weather change here, a little breeze there and reptiles evolve feathers and wings. It is all so obvious, how could I have missed this?

Don't forget the planet-busting meteors...

Now that’s a good one, someone running around calling himself balrog666 is going to tell us what is normal and abnormal.

Ad hominem.

It’s just you Paul.

No, it's not. Everybody's called you on this one. You are contradicting yourself, quite blatantly, in fact. It's been quite a show, but now we have clear proof that you have nothing. You will simply say anything -- anything -- to continue refusing to accept facts. Yours is a religious view, not a scientific one.

Good luck.

[Paul C. Anagnostopoulos]

You really like clinging to this issue. When are you going to learn that optimization problems have domains of convergence?
As soon as you learn that there are reasons why there are domains of convergence. In the case we are talking about, the reason is Rcapacity.

Do you treat everything in life as an amorphous mystery?


Aren’t they killing scabies with selection pressures? Isn’t that what ev does? For that matter, they are using combination selection pressures.
No, they are killing scabies with poisons. Killing them. Like dead. With weapons. Like you might stomp on a spider.


They are trying to evolve perfect scabies.
They are?

~~ Paul

[LibraryLady]

Tone it down, folks.

“Attack the argument, not the arguer." Having your opinion, claim or argument challenged, doubted or dismissed is not attacking the arguer.

[kleinman]

This is one of my favorite of your quotes.I'm sure you love it. It's completely correct in regards to what it was refering to.
It’s so correct, let’s read it again.
I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.
Joobz, you are correct, it is complete speculation.
Apparently you don't want anyone to take you seriously. If you did, then you would take your opponent's seriously.
Oh, I take you seriously; I think your string cheese theory of evolution is seriously funny. How many alternative universes are there kjkent1, 10^500? How many of these alternative universes have you visited? Next time you visit one of your alternative universes, send us a postcard, post mark the Twilight Zone.
You are correct rocketdodger! That is why the theory of evolution is mathematically impossible.Then how do pathogens/rodents/weeds evolve resistance to drugs/poisons/herbicides?
Why should I answer your questions? You don’t answer my questions. I think we should call you questiondodger instead of rocketdodger. Just to show you that I am not a questiondodger, I’ll answer your question.

Pathogens/rodents/weeds evolve resistance to drugs/poisons/herbicides in the same way that HIV evolves resistance in the presence of a weak humoral immune response. The greater the number of selection pressures, the more difficult for these populations to adapt to these selection pressures.
It’s just you Paul.Well... actually... no, Kleinman, Paul is not the only person who thinks you are clueless.
Oh no questiondodger, I have plenty of clues, both mathematical and empirical, check below, I’ll post more clues for you.
The theory of evolution is mathematically impossible.Once upon a time people thought it was mathematically impossible for bumble bees to fly. Their theories were wrong, just like yours.
You got it wrong Deetee, it’s Dr Schneider’s model which shows this, not my model and surprise, surprise, what his model shows is backed up by empirical evidence.

Now Deetee, once upon a time people thought that life arose from a primordial soup and evolved into everything we see today, your theory are wrong, the mathematics and empirical evidence of how mutation and selection works proves this.
All the more reason not to separate the posts, you need to learn how mutation and selection actually works.I STILL skip to the answers to my posts, Klein. It's just more work for no reason.
No wonder you have no idea how mutation and selection works. You are still trying to figure out the difference between atheist and agnostic. Have you figured out the difference between evolve and beggaminases?
You really like clinging to this issue. When are you going to learn that optimization problems have domains of convergence?As soon as you learn that there are reasons why there are domains of convergence. In the case we are talking about, the reason is Rcapacity.

Do you treat everything in life as an amorphous mystery?
Paul, the mystery is gone from how mutation and selection actually works, it is simply an optimization problem and the more conditions being optimized, the more difficult to find a local optimum. It is obvious why there are domains of convergence; I’ll repost my little ascii drawings which shows what determines which local optima and the domains of convergence.
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.................................................. ......
.............................C.................... ......
.................................................. ......
.................................................. ......
.................................................. ......
.................................................. ......
.................................................. .....
...........A...................................... ......
.................................................. ......
........D......................................... ......
...................E.............................. ......
.................B................................ ......
.................................................. ......
.................................................. ......
.................................................. ......
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A member of the population at point D will be selected over a member at point E because member D has fewer mistakes on the fitness landscape than does member E. This occurs despite that member D is on a trajectory to optimum A which is a lower optimum than member E which is on a trajectory to optimum C (the perfect creature optimum). Ev will always converge on a local optimum; it just may not be a perfect creature optimum. It isn’t Rcapacity that prevents convergence on a perfect creature optimum; it is the complexity of the fitness landscape and the existence of other local optimums that prevents ev from finding a trajectory to a perfect creature optimum every time.
And
-----------------------------------------------------------------------------------------------------
.................................................. ......
.............................D.................... ......
.................................................. ......
.................................................. ......
.................................................. ......
.................................................. ......
.................................................. ......
...........B...................................... ......
................................................F. ......
.................................................. ......
.................................................. ......
.................C................................ ......
....A......................................E...... ...G..
.................................................. ......
.................................................. ......
-----------------------------------------------------------------------------------------------------
In optimization problems, there are limits to which optima will be located depending on the initial starting point for the search. In the above figure, local optimum B will be found if you start your search between points A and C. Local optimum D will be found in your search starts between points C and E. Local optimum F will be found if you search is started between points E and G. The “perfect creature” optimum will only be found (D) when the search is started between points C and E. It has nothing to do with the information content of binding sites. This is a fundamental principle of optimization problems.

Paul it’s not Rcapacity or beggaminases. Ev will always converge to a local optima, even when Rfrequency > Rcapacity.
Aren’t they killing scabies with selection pressures? Isn’t that what ev does? For that matter, they are using combination selection pressures. No, they are killing scabies with poisons. Killing them. Like dead. With weapons. Like you might stomp on a spider.
Selection pressures do that to populations.
They are trying to evolve perfect scabies.They are?
Isn’t that what evolution is supposed to do?

Chillzero and Librarylady are both moderators.
http://forums.randi.org/showpost.php?p=3044651&postcount=5894 (http://forums.randi.org/showpost.php?p=3044651&postcount=5894)
And
http://forums.randi.org/showpost.php?p=3065762&postcount=6032 (http://forums.randi.org/showpost.php?p=3065762&postcount=6032)
Seems some of the moderators on this site are suffering from some despotism. Let’s see if they can come up with a coherent counterargument to the hypothesis that combination selection pressures profoundly slow the evolutionary process. Here are some clues for the moderators and questiondodgers to ponder.
http://www.anopheles.org/showabstract.php?pmid=10212909 (http://www.anopheles.org/showabstract.php?pmid=10212909)
Antimalarial combinations make therapeutic sense. As we have few antimalarial drugs and even fewer in development, and as the malaria parasite shows a remarkable ability to develop resistance, all possible measures should be taken to protect those drugs that we do have available. Although in experimental animals combinations have been shown unequivocally to delay the onset of resistance, this has not yet been proved formally in human malaria. Yet formal proof is extremely difficult to obtain. However, there is sufficient circumstantial evidence to suggest that resistance can be delayed. As there are no counter arguments and the stakes are high, it seems reasonable that an artemisinin derivative should be combined with all slow acting antimalarial drugs. Those drugs with a particularly vulnerable profile, in which a single or double point mutation confers high level resistance, should not be deployed alone and should always be combined with an artemisinin derivative.
http://www.anopheles.org/showabstract.php?pmid=12803854 (http://www.anopheles.org/showabstract.php?pmid=12803854)
The influence of combinations containing the blood schizontocides chloroquine (CQ) or mefloquine (MEF), together with the 8-aminoquinolines (8AQ) primaquine (PQ) or the new, long-acting compound, tafenoquine (TAF), on the rate of selection of resistance to the individual compounds was examined using the asexual, intra-erythrocytic stages in rodent malaria models. The two main procedures used were a 'serial technique' (ST) and the '2%- relapse technique' (2%RT). The ST provided evidence for the contention that a combination with PQ slowed the selection of resistance to CQ or MEF; it has been shown previously that synergism exists between CQ and either PQ or TAF in rodent malaria. Data obtained with the 2%RT, and three parasite lines derived from Plasmodium berghei N (the 238B line), P. chabaudi ASS (the 238C line) or P. yoelii ssp. NS (the 238Y line), indicated that resistance to TAF used alone is acquired rapidly under drug pressure and that this resistance is stable when selection pressure is removed. In the 2%RT, resistance to CQ developed when another line of P. chabaudi (AS15) was exposed to that compound alone, although more slowly than the development of resistance to TAF in the 238C line. However, treatment of a TC line of P. chabaudi, developed in a 2%RT using a combination of CQ with TAF, led to little resistance to either compound. A totally unforeseen phenomenon was the appearance of a high level of resistance to CQ in the 238C line of P. chabaudi that had been exposed only to TAF; this was not observed with the 238B or 238Y lines. Attention has been refocused recently on the use of 8AQ for prophylaxis in man. It remains to be determined if resistance in the asexual intra-erythrocytic forms is carried over to the other stages of the malarial life-cycle, especially the hepatic, pre-erythrocytic schizonts. The implications of the present results for the possible clinical deployment of 8AQ in the future are discussed. It is concluded that, whereas use of an 8AQ alone carries a high risk of selecting resistance, combinations containing 8AQ may have a place in the protection of blood schizontocides that are to be deployed in endemic areas. Furthermore, the inherent gametocytocidal action of the 8AQ should promote the reduction of transmission.
http://www.anopheles.org/showabstract.php?pmid=10697872 (http://www.anopheles.org/showabstract.php?pmid=10697872)
Resistance to antimalarial drugs arises when spontaneously occurring mutants with gene mutations or amplifications which confer reduced drug susceptibility are selected, and are then transmitted. Simultaneous use of two or more antimalarials with different modes of action and which therefore do not share the same resistance mechanisms will reduce the chance of selection, because the chance of a resistant mutant surviving is the product of the parasite mutation rates for the individual drugs, multiplied by the number of parasites in an infection that are exposed to the drugs. The artemisinin derivatives are very active antimalarials, which produce large reductions in parasite biomass per asexual cycle, and reduce malaria transmissibility. To date no resistance to these drugs has been reported. These drugs therefore make particularly effective combination partners. This suggests that antimalarial drugs should not be used alone in treatment, but always in combination, as in the treatment of tuberculosis or HIV, and that the combination should include artemisinin or one of its derivatives.
http://www.anopheles.org/showabstract.php?pmid=12641911 (http://www.anopheles.org/showabstract.php?pmid=12641911)
Antimalarial drug resistance emerges de novo predominantly in areas of low malaria transmission. Because of the logarithmic distribution of parasite numbers in human malaria infections, inadequately treated high biomass infections are a major source of de novo antimalarial resistance, whereas use of antimalarial prophylaxis provides a low resistance selection risk. Slowly eliminated antimalarials encourage resistance largely by providing a selective filter for resistant parasites acquired from others, and not by selecting resistance de novo. The de novo emergence of resistance can be prevented by use of antimalarial combinations. Artemisinin derivative combinations are particularly effective. Ensuring adequate treatment of the relatively few heavily infected patients would slow the emergence of resistance.
Joobz, here are some other authors who don’t seem to understand slow does not equal stop. You better contact them and give them your speculations.

Now I hate to disappoint you evolutionists (my goal is to annoy you with the facts of how mutation and selection actually works) but I have something else which I must attend to and will not be back until next week. I’m sure you will find something interesting to discuss about the mathematics of mutation and selection and the empirical evidence which supports this mathematics. Until then, may all your selection pressures be weak selection pressures.

[rocketdodger]

Why should I answer your questions? You don’t answer my questions. I think we should call you questiondodger instead of rocketdodger. Just to show you that I am not a questiondodger, I’ll answer your question.

I did answer your question, the same question, three times -- in posts #6002, #6006, and #6023. Yet, you insist I have not, trying to rally any idiots who browse this forum to your case. Guess what, Kleinman -- it isn't happening. People who come here (well, not all of them, obviously) can read. They see what is going on. If you were vomiting this nonsense at your local church, and had tough guys to throw out people like me when we called your hand, maybe your misinformation tactics would work. But not here.

Pathogens/rodents/weeds evolve resistance to drugs/poisons/herbicides in the same way that HIV evolves resistance in the presence of a weak humoral immune response. The greater the number of selection pressures, the more difficult for these populations to adapt to these selection pressures.

So evolution is possible again?

The only way I can account for your series of posts, Kleinman, is that you are in fact a group of bible-study children experimenting with the wonders of the internet, and you all are taking turns making posts. Otherwise, one would notice at least a little consistency between them.

Oh no questiondodger, I have plenty of clues, both mathematical and empirical, check below, I’ll post more clues for you.

Thank you for posting more evidence that shows evolution occurs rapidly in nature. Here are the relevant statements from the abstracts:

http://www.anopheles.org/showabstract.php?pmid=10212909

". . . and as the malaria parasite shows a remarkable ability to develop resistance. . ."

http://www.anopheles.org/showabstract.php?pmid=10697872

" . . . whereas use of an 8AQ alone carries a high risk of selecting resistance . . ."

http://www.anopheles.org/showabstract.php?pmid=10697872

"Resistance to antimalarial drugs arises when spontaneously occurring mutants with gene mutations or amplifications which confer reduced drug susceptibility are selected, and are then transmitted."

http://www.anopheles.org/showabstract.php?pmid=12641911

"Antimalarial drug resistance emerges de novo predominantly in areas of low malaria transmission."

[Belz...]

No wonder you have no idea how mutation and selection works. You are still trying to figure out the difference between atheist and agnostic. Have you figured out the difference between evolve and beggaminases?

There's so much vitriol there it's hard to know where to start.

First of all, the fact that I'm focusing on your responses to MY posts means that my posts won't get steadily longer and clog the thread.

Second, I know quite well the difference between atheist and agnostic, and there's been a recent thread about just that distinction. That you lump the two together is no concern of mine.

Third, the term "beggiminases" was an invention by me SPECIFICALLY to avoid using the loaded word "evolve" while not talking about selection. You should remember this, and obviously, since it was invented to distinguish it from "evolve" I pretty much have to know that they are different.

Please learn to read.

[Belz...]

The only way I can account for your series of posts, Kleinman, is that you are in fact a group of bible-study children experimenting with the wonders of the internet, and you all are taking turns making posts. Otherwise, one would notice at least a little consistency between them.

Ouch.

[kjkent1]

Another day, another post from kleinman clearly showing that his proofs prove how evolution works (assuming that we concede that this is all there is to it, which I, for one, do not). To wit:

resistance to TAF used alone is acquired rapidly under drug pressure and that this resistance is stable when selection pressure is removed.

So, based on the above, the target organism was under no selective pressure prior to the introduction of the toxin, because it was stable after removal of the toxin. And, once exposed to a single overwhelmingly intense pressure, the organism evolved resistance -- exactly as would occur in a natural environment, where an organism was stable and suddenly exposed to a single overwhelmingly intense selective pressure.

Nice proof, Alan. Demonstrates how evolution works in natue and that it's quite possible.

Thanks!!!

ROFLMAO!

[rocketdodger]

Now I hate to disappoint you evolutionists (my goal is to annoy you with the facts of how mutation and selection actually works) but I have something else which I must attend to and will not be back until next week. I’m sure you will find something interesting to discuss about the mathematics of mutation and selection and the empirical evidence which supports this mathematics. Until then, may all your selection pressures be weak selection pressures.[/SIZE][/FONT]

We all agree with each other, so if we discuss anything, it will be how badly you just got whipped in the last few pages of this thread.

If you ever come back, you will just get whipped again. I have half a mind to do the same over in those stupid "evolution is dead" forums, but luckally for you the large backlog of games I need to play and porn I need to dl is where I would rather spend my time.

[Belz...]

my goal is to annoy you with the facts of how mutation and selection actually works

Oh, you annoy us, allright. But not with facts.

[Belz...]

We all agree with each other, so if we discuss anything, it will be how badly you just got whipped in the last few pages of this thread.

If you ever come back, you will just get whipped again. I have half a mind to do the same over in those stupid "evolution is dead" forums, but luckally for you the large backlog of games I need to play and porn I need to dl is where I would rather spend my time.

An interesting choice of words...

[rocketdodger]

An interesting choice of words...

I am a man of many needs...

[Paul C. Anagnostopoulos]

So I just read in the newspaper that there is now a staph bacterium resistant to methicillin and also a bacterium that causes ear infections resistant to every approved antibiotic for children. If I understand correctly, this is due to the fact that those bacteria were facing only one selection pressure. Have I got that right?

~~ Paul

[Belz...]

Yep. No selection pressures here. Nothing to see. Move along.

[circuit_bent]

Now urban music is ganging up on Darwin.

http://www.youtube.com/watch?v=siBCajh2g5E&mode=related&search=

Check out 0:41.

WARNING : song fades out on trumpet wah-wahing.

WARNING : bloody annoying chorus

WARNING : urban music

[Shalamar]

As best as I can tell from reading far too many pages on this thread, Klienman has a large number of assumptions on Evolution (That are false), and all he has 'proven' thus far is that Evolution can not be mathematically proven. Too many variables, and many of those are unknown.

Am I right?

[Belz...]

Silence, you mathematically-challenged evolutionarianist!!

[Shalamar]

Silence, you mathematically-challenged evolutionarianist!!

I'll take that as a.. yes. :p

[delphi_ote]

... he has 'proven' claimed thus far is that Evolution can not be mathematically proven. Too many variables, and many of those are unknown.
There. That's much more accurate. :D

[Belz...]

Hey! Delphi. Long time no see.

[delphi_ote]

Hey! Delphi. Long time no see.
Being a grad student is t3h buzy! It's good to see you, Belz.

If you'll excuse me, I have to go work on scripts to generate a list of the homologous genes between various insect species (which obviously won't work of course, because insects are under more than one selection pressure.)

[Shalamar]

There. That's much more accurate. :D

To be fair, he's claimed that Evolution is impossible, because his math disproves it.

I stated the other way around.. more or less. :)

[delphi_ote]

To be fair, he's claimed that Evolution is impossible, because his math disproves it.
Yes, but he never shows his work! It's a claim (which I find dubious given a lack of supporting evidence) that this math even exists, whatever it does or does not prove. :D

[Shalamar]

Yes, but he never shows his work! It's a claim (which I find dubious given a lack of supporting evidence) that this math even exists, whatever it does or does not prove. :D

It seems that he BELIEVES with all his heart and soul that evolution is false, that he has the proof that it can not exist. He's latched onto this simulation (which is limited in scope) to 'prove his point'.

It just seems that Evolution is far too complex, far too.. immense.. to be tackled mathematically.

[rocketdodger]

It seems that he BELIEVES with all his heart and soul that evolution is false, that he has the proof that it can not exist. He's latched onto this simulation (which is limited in scope) to 'prove his point'.


At first I was also that forgiving. Now, after arguing with him, I know better. He hasn't latched on to anything. He doesn't even understand the simulation, look at his argument with Paul. He doesn't understand the studies he cites. And saddest of all, he actually doesn't even understand the extremely simple process that is evolution.


It just seems that Evolution is far too complex, far too.. immense.. to be tackled mathematically.

Right now, yes. Not for long. Just need better computers so I can play games ... err... I mean run more realistic simulations...

[Shalamar]

Right now, yes. Not for long. Just need better computers so I can play games ... err... I mean run more realistic simulations...


Hey! I've played Sim-Earth.. That proves Evolution.. Or.. disproves it.. or.. something. But it was a simulation.. right?

;)

[Belz...]

Being a grad student is t3h buzy! It's good to see you, Belz.

If you'll excuse me, I have to go work on scripts to generate a list of the homologous genes between various insect species (which obviously won't work of course, because insects are under more than one selection pressure.)

:D

[Belz...]

Hey! I've played Sim-Earth.. That proves Evolution.. Or.. disproves it.. or.. something. But it was a simulation.. right?

;)

Sim Earth !!! And who HASN'T made dinosaurs into intelligent, space-faring creatures ?

[Paul C. Anagnostopoulos]

If you'll excuse me, I have to go work on scripts to generate a list of the homologous genes between various insect species (which obviously won't work of course, because insects are under more than one selection pressure.)
Yup, it's a fool's errand, my friend.

~~ Paul

[Soapy Sam]

I think "an errand" might be something illogical that happens in the sort of mathematics that can prove evolution has not happened.

[Paul C. Anagnostopoulos]

Let's define errand as the event where god magically intervenes to tweak genes so that macroevolution can occur.

~~ Paul

[kleinman]

Did you evolutionists make any progress this past week in understanding the mathematical and empirical facts of how mutation and selection actually works or are you still trying to support your mathematically and empirically impossible theory with speculations, extrapolations and denial? Let’s find out, we’ll start with the rocketwhomissesthetarget who also demonstrates skill as questiondodger.
Why should I answer your questions? You don’t answer my questions. I think we should call you questiondodger instead of rocketdodger. Just to show you that I am not a questiondodger, I’ll answer your question.I did answer your question, the same question, three times -- in posts #6002, #6006, and #6023. Yet, you insist I have not, trying to rally any idiots who browse this forum to your case. Guess what, Kleinman -- it isn't happening. People who come here (well, not all of them, obviously) can read. They see what is going on. If you were vomiting this nonsense at your local church, and had tough guys to throw out people like me when we called your hand, maybe your misinformation tactics would work. But not here.
Let’s see, the question I asked questiondodger is, if someone with HIV who could not mount a humoral immune response against the virus was given therapy, would the virus evolve more slowly against that therapy than a person who could mount a humoral immune response against the given same therapy? What’s the problem questiondodger, is it to difficult a question to answer?
Pathogens/rodents/weeds evolve resistance to drugs/poisons/herbicides in the same way that HIV evolves resistance in the presence of a weak humoral immune response. The greater the number of selection pressures, the more difficult for these populations to adapt to these selection pressures.So evolution is possible again?

The only way I can account for your series of posts, Kleinman, is that you are in fact a group of bible-study children experimenting with the wonders of the internet, and you all are taking turns making posts. Otherwise, one would notice at least a little consistency between them.
Sure questiondodger, evolution is possible, microevolution. Now if you can show how these microevolutionary processes can be added together to produce macroevolution without using speculations, irrational extrapolations and denial of how mutation and selection actually works, that would be a miracle.
Oh no questiondodger, I have plenty of clues, both mathematical and empirical, check below, I’ll post more clues for you. Thank you for posting more evidence that shows evolution occurs rapidly in nature. Here are the relevant statements from the abstracts:
Now questiondodger is going to try to make points by taking sentence fragments or perhaps a single sentence from these citations in order to go into denial of how mutation and selection actually works. So let’s see these sentence fragments.
http://www.anopheles.org/showabstract.php?pmid=10212909 (http://www.anopheles.org/showabstract.php?pmid=10212909)
. . . and as the malaria parasite shows a remarkable ability to develop resistance. . .
Here’s the part of the abstract questiondodger forgets to post.
Although in experimental animals combinations have been shown unequivocally to delay the onset of resistance, this has not yet been proved formally in human malaria. Yet formal proof is extremely difficult to obtain. However, there is sufficient circumstantial evidence to suggest that resistance can be delayed. As there are no counter arguments and the stakes are high, it seems reasonable that an artemisinin derivative should be combined with all slow acting antimalarial drugs. Those drugs with a particularly vulnerable profile, in which a single or double point mutation confers high level resistance, should not be deployed alone and should always be combined with an artemisinin derivative.[/quote]
What’s this questiondodger? Combination selection pressures slow the ability of the malaria parasite to evolve resistance.
http://www.anopheles.org/showabstract.php?pmid=10697872 (http://www.anopheles.org/showabstract.php?pmid=10697872)
Actually the reference should be http://www.anopheles.org/showabstract.php?pmid=12803854 (http://www.anopheles.org/showabstract.php?pmid=12803854)
. . . whereas use of an 8AQ alone carries a high risk of selecting resistance . . .
The implications of the present results for the possible clinical deployment of 8AQ in the future are discussed. It is concluded that, whereas use of an 8AQ alone carries a high risk of selecting resistance, combinations containing 8AQ may have a place in the protection of blood schizontocides that are to be deployed in endemic areas. Furthermore, the inherent gametocytocidal action of the 8AQ should promote the reduction of transmission.
What’s this questiondodger? Combination selection pressures slow the ability of the malaria parasite to evolve resistance.
http://www.anopheles.org/showabstract.php?pmid=10697872 (http://www.anopheles.org/showabstract.php?pmid=10697872)
Resistance to antimalarial drugs arises when spontaneously occurring mutants with gene mutations or amplifications which confer reduced drug susceptibility are selected, and are then transmitted.
Resistance to antimalarial drugs arises when spontaneously occurring mutants with gene mutations or amplifications which confer reduced drug susceptibility are selected, and are then transmitted. Simultaneous use of two or more antimalarials with different modes of action and which therefore do not share the same resistance mechanisms will reduce the chance of selection, because the chance of a resistant mutant surviving is the product of the parasite mutation rates for the individual drugs, multiplied by the number of parasites in an infection that are exposed to the drugs.
What’s this questiondodger? Combination selection pressures slow the ability of the malaria parasite to evolve resistance.
http://www.anopheles.org/showabstract.php?pmid=12641911 (http://www.anopheles.org/showabstract.php?pmid=12641911)
Antimalarial drug resistance emerges de novo predominantly in areas of low malaria transmission.
The de novo emergence of resistance can be prevented by use of antimalarial combinations.[/quote]
What’s this questiondodger? Combination selection pressures slow the ability of the malaria parasite to evolve resistance.
So when are you going to answer this question, questiondodger, if someone with HIV who could not mount a humoral immune response against the virus was given therapy, would the virus evolve more slowly against that therapy than a person who could mount a humoral immune response against the given same therapy?
No wonder you have no idea how mutation and selection works. You are still trying to figure out the difference between atheist and agnostic. Have you figured out the difference between evolve and beggaminases?There's so much vitriol there it's hard to know where to start.
I’m not angry at all with you Belz, I’m having fun.
First of all, the fact that I'm focusing on your responses to MY posts means that my posts won't get steadily longer and clog the thread.
How thoughtless of me to clog this thread with mathematical and empirical facts of how mutation and selection actually works.
Second, I know quite well the difference between atheist and agnostic, and there's been a recent thread about just that distinction. That you lump the two together is no concern of mine.
You understand the difference once rcronk explained the difference to you. The only thing I am doing is giving the theory of evolution a some lumps.
Third, the term "beggiminases" was an invention by me SPECIFICALLY to avoid using the loaded word "evolve" while not talking about selection. You should remember this, and obviously, since it was invented to distinguish it from "evolve" I pretty much have to know that they are different.
The theory of evolution is also an invention of you evolutionists, mutation and selection doesn’t work the right way for your invention to work.
Another day, another post from kleinman clearly showing that his proofs prove how evolution works (assuming that we concede that this is all there is to it, which I, for one, do not). To wit:
Kjkent1 shows a lack of creativity and takes up questiondodger’s strategy of posting sentence fragments in order to try to make a point.
resistance to TAF used alone is acquired rapidly under drug pressure and that this resistance is stable when selection pressure is removed.
I like clogging up the thread with the mathematical and empirical facts of how mutation and selection actually works, so let’s repost the portion the kjkent1 left out of the citation.
Data obtained with the 2%RT, and three parasite lines derived from Plasmodium berghei N (the 238B line), P. chabaudi ASS (the 238C line) or P. yoelii ssp. NS (the 238Y line), indicated that resistance to TAF used alone is acquired rapidly under drug pressure and that this resistance is stable when selection pressure is removed. In the 2%RT, resistance to CQ developed when another line of P. chabaudi (AS15) was exposed to that compound alone, although more slowly than the development of resistance to TAF in the 238C line. However, treatment of a TC line of P. chabaudi, developed in a 2%RT using a combination of CQ with TAF, led to little resistance to either compound.
What’s this kjkent1? Combinations of CQ with TAF led to little resistance to either compound. You should also know this kjkent1 that ev shows the same thing. Any of the three selection conditions evolve very rapidly when applied alone, only when the selection pressures are applied simultaneously does the evolutionary process slow profoundly.
So I just read in the newspaper that there is now a staph bacterium resistant to methicillin and also a bacterium that causes ear infections resistant to every approved antibiotic for children. If I understand correctly, this is due to the fact that those bacteria were facing only one selection pressure. Have I got that right?
It also works that way for gonorrhea, malaria, TB, HIV, weeds,… If you want to accelerate the evolutionary process, use selection pressures one at a time. You should understand Paul, your own computer model shows the same thing.
As best as I can tell from reading far too many pages on this thread, Klienman has a large number of assumptions on Evolution (That are false), and all he has 'proven' thus far is that Evolution can not be mathematically proven. Too many variables, and many of those are unknown.

Am I right?
Nope Shalamar, I’m posting the results from Dr Tom Schneider’s (head of computational molecular biology at the National Cancer Institute) peer reviewed and published computer simulation of random point mutations and natural selection which shows that combination selection pressures evolve far, far more slowly than single selection pressures and I am also posting hundreds of empirical examples of mutation and selection which shows the same thing. Evolution by mutation and selection is profoundly slowed when you have more than a single selection pressure. This effect can be understood if you realize that mutation and selection is simply an optimization problem. When you try to optimize by more than a single optimization condition, this process becomes profoundly slow.
Silence, you mathematically-challenged evolutionarianist!!
Once again you have it backwards Belz, I am not the one trying to silence anyone, it is you evolutionarianists who are trying to silence people. I think evolution should be taught in school, especially how mutation and selection actually works, then this nonsense of common descent will be discarded.
... he has 'proven' claimed thus far is that Evolution can not be mathematically proven. Too many variables, and many of those are unknown.There. That's much more accurate.
On no Delphi, I don’t claim there are too many variables and many are unknown, that’s what you evolutionists do in order to try to support your mathematically impossible theory.
Hey! Delphi. Long time no see. Being a grad student is t3h buzy! It's good to see you, Belz.

If you'll excuse me, I have to go work on scripts to generate a list of the homologous genes between various insect species (which obviously won't work of course, because insects are under more than one selection pressure.)
Don’t believe him Belz; Delphi has been out sorting his sock drawer and making stop action human skateboard films.

Delphi, Dr Richard tried this argument before. Why don’t you explain to us why humans and chimpanzees have identical insulin yet don’t have identical preproinsulin despite evolutionists allege we evolved from a common ancestor?
To be fair, he's claimed that Evolution is impossible, because his math disproves it.Yes, but he never shows his work! It's a claim (which I find dubious given a lack of supporting evidence) that this math even exists, whatever it does or does not prove.
Delphi, it is true that I haven’t shown my work. I don’t have to. I show the results from Dr Schneider’s peer reviewed and published model of mutation and selection and then I post hundreds of real examples of mutation and selection which substantiates the results from Dr Schneider’s computer simulation. In case you have forgotten, what Dr Schneider’s model shows is that combination selection pressures profoundly slow the evolutionary process.

In addition Delphi, I have your Wikipedia reference to the fitness landscape. Do you remember what your own citation shows? So Delphi, you are correct, I have not shown my math. I have shown you your own math and hundreds of empirical examples which substantiate this mathematics and what your mathematics show is that combination selection pressures profoundly slow the evolutionary process. By the way Delphi, did you ever get your sock drawer sorted?
If you'll excuse me, I have to go work on scripts to generate a list of the homologous genes between various insect species (which obviously won't work of course, because insects are under more than one selection pressure.)Yup, it's a fool's errand, my friend.
I don’t think it’s a fool’s errand to find out that insects evolve into insects. Now if Delphi tries to show that reptiles evolve into birds, that’s another story.

So, another week has gone by and you evolutionists still don’t understand how mutation and selection actually works. Let’s try posting a couple more citations which show how the process actually works empirically.
http://www.anopheles.org/showabstract.php?pmid=10723521 (http://www.anopheles.org/showabstract.php?pmid=10723521)
The search for combinations of antimalarial drugs that will impede the selection of drug resistance, especially in Plasmodium falciparum, is currently focused on the use of a member of the artemisinin family, with a short half-life, in association with a relatively long-acting blood schizontocide. Experiments with such 'third-generation' combinations, in mice infected either with chloroquine-sensitive P. berghei or P. chabaudi, or chloroquine-resistant P. yoelii ssp. NS, have produced interesting results. The data collected, using the '2% relapse technique' (2%RT), indicate that a combination of artemisinin with mefloquine can impede to a significant degree, although by no means completely, the selection of resistance to both compounds in P. berghei and in P. yoelii ssp. NS. Similarly, a combination of artesunate with pyronaridine impedes the selection of resistance to these compounds in P. berghei. Parallels are drawn between observations with such combinations in man and in the rodent models which, it is argued, once again demonstrate their value in predicting the protective value of using different types of antimalarials together. Evidence is presented that resistance to single compounds may emerge more rapidly when a high dose is employed in the 2%RT than a lower dose. It is noted also that the rate at which resistance to pyronaridine is selected by a given dose varies with the species of rodent Plasmodium, and the relevance of this to the malarial parasites of human is discussed.
http://www.anopheles.org/showabstract.php?pmid=10365399 (http://www.anopheles.org/showabstract.php?pmid=10365399)
Antimarial drug resistance develops when spontaneously occurring parasite mutants with reduced susceptibility are selected, and are then transmitted. Drugs for which a single point mutation confers a marked reduction in susceptibility are particularly vulnerable. Low clearance and a shallow concentration-effect relationship increase the chance of selection. Use of combinations of antimalarials that do not share the same resistance mechanisms will reduce the chance of selection because the chance of a resistant mutant surviving is the product of the per parasite mutation rates for the individual drugs, multiplied by the number of parasites in an infection that are exposed to the drugs. Artemisinin derivatives are particularly effective combination partners because (i) they are very active antimalarials, producing up to 10,000-fold reductions in parasite biomass per asexual cycle; (ii) they reduce malaria transmissibility; and (iii) no resistance to these drugs has been reported yet. There are good arguments for no longer using antimalarial drugs alone in treatment, and instead always using a combination with artemisinin or one of its derivatives.
I really seem to be clogging up this thread with the facts of how mutation and selection actually works.

[rocketdodger]

Kleinman, when I think of you I am reminded of that scene from "SpaceBalls" where dark helmet is trying to slash lonestar, but lonestar is holding him at arms length, and as a result dark helmet does nothing but swipe at the air for twenty seconds or so.

[kleinman]

Kleinman, when I think of you I am reminded of that scene from "SpaceBalls" where dark helmet is trying to slash lonestar, but lonestar is holding him at arms length, and as a result dark helmet does nothing but swipe at the air for twenty seconds or so.
Now questiondodger, I know you evolutionists like to use the Scifi Channel as a source of evidence for your theory. Let’s see, the Star Wars bar room scene is proof of panspermia and diversity of life.

Aren’t you going to take any of my recent citations and prove that populations can evolve far more rapidly to single selection conditions than to multiple selection conditions?

[Shalamar]

I'm interested in seeing your math that evolution is impossible. All of it.

And, oh, not based on the model. If your math is based on the model, then all that shows is that the model is wrong. Not evolution.

[kleinman]

I'm interested in seeing your math that evolution is impossible. All of it.

And, oh, not based on the model. If your math is based on the model, then all that shows is that the model is wrong. Not evolution.
First of all, it is not my mathematics, it is Dr Schneider’s peer reviewed and published model of random point mutation and natural selection. Second, the data has already been posted on this thread. Third, the results of the model are substantiated by hundreds of real empirical examples of mutation and selection which have been measured and repeated by numerous scientists in numerous different fields of science. The mathematics and empirical evidence is not wrong, it is your theory of evolution by mutation and selection which is wrong. Mutation and selection simply does not work the way you evolutionists allege.

If you have trouble reading the thread, I’ll repost what you need to know in order to understand how mutation and selection actually works.

[rocketdodger]

Aren’t you going to take any of my recent citations and prove that populations can evolve far more rapidly to single selection conditions than to multiple selection conditions?

As soon as you come up with a consistent definition of "single selection conditions" and "multiple selection conditions" I will be happy to.

Since, however, you have demonstrated that you are utterly incapable of doing so, as your definition of every term you use is radically changed on a per-post basis, it doesn't look like I will have much proving to do in the foreseeable future.

Arguing with you is like trying to converse with yoshi, except that yoshi is cute.

[Belz...]

I’m not angry at all with you Belz, I’m having fun.

Ah! Is that what you're doing ? You're certainly not debating, that's for sure.

How thoughtless of me to clog this thread with mathematical and empirical facts of how mutation and selection actually works.

Here, Kleinman forgets, once again, what was the point of the discussion. Once more he shows he is incapable of following a train of thought.

If he had bothered to check, he would've known what I was talking about. But it's much more "fun" to just take words in the opponent's sentence and construct a non-answer to that. Pwned, I guess.

You understand the difference once rcronk explained the difference to you.

Since you do not know what is occuring in my head, I find it presumptuous of you to claim that you do.

The theory of evolution is also an invention of you evolutionists, mutation and selection doesn’t work the right way for your invention to work.

For the second time in four sentences adressed to me, Kleinman AGAIN forgets what we were talking about.

Is there no end to this ? Find out on the next exciting episode of "Annoying Kleinman."

[Belz...]

Once again you have it backwards Belz, I am not the one trying to silence anyone, it is you evolutionarianists who are trying to silence people.

Kleinman is attempting, here, to invoke the Galileo syndrome. In other words, since all his attempts to show us wrong have failed, he's trying to claim that only he can see the light and that, in time, he'll be proven right.

I can't wait for THAT second coming, let me tell you that.

I think evolution should be taught in school, especially how mutation and selection actually works, then this nonsense of common descent will be discarded.

Sure, Klein. Whatever makes you sleep.

Don’t believe him Belz; Delphi has been out sorting his sock drawer and making stop action human skateboard films.

Silly scientists and their silly evidences.

[Belz...]

First of all, it is not my mathematics, it is Dr Schneider’s peer reviewed and published model of random point mutation and natural selection.

Again, it's your interpretation that's in question, but I fully expect you to dodge this one as well.

[Shalamar]

First of all, it is not my mathematics, it is Dr Schneider’s peer reviewed and published model of random point mutation and natural selection. Second, the data has already been posted on this thread. Third, the results of the model are substantiated by hundreds of real empirical examples of mutation and selection which have been measured and repeated by numerous scientists in numerous different fields of science. The mathematics and empirical evidence is not wrong, it is your theory of evolution by mutation and selection which is wrong. Mutation and selection simply does not work the way you evolutionists allege.

If you have trouble reading the thread, I’ll repost what you need to know in order to understand how mutation and selection actually works.

Hmm... So that would be a 'no'?

My understanding on Science is that if something is proven to be wrong, it will be corrected. As far as I can see, you are the only one making the claim that the Theory of Evolution is wrong. If you are so certain, why not publish your findings? Science is not about upholding current views, but about testing what is known, to find what is unknown. So, if you find out all is wrong, point it out, and correct it, wouldn't that be a wonderful thing? Nobel prize in Biology, perhaps.

Or am I wrong?

[kleinman]

First of all, it is not my mathematics, it is Dr Schneider’s peer reviewed and published model of random point mutation and natural selection. Second, the data has already been posted on this thread. Third, the results of the model are substantiated by hundreds of real empirical examples of mutation and selection which have been measured and repeated by numerous scientists in numerous different fields of science. The mathematics and empirical evidence is not wrong, it is your theory of evolution by mutation and selection which is wrong. Mutation and selection simply does not work the way you evolutionists allege.

If you have trouble reading the thread, I’ll repost what you need to know in order to understand how mutation and selection actually works.Hmm... So that would be a 'no'?
Wrong, that would be a “yes”, where do you want me to start? Do you want me to teach you how Dr Schneider’s computer model works first?
My understanding on Science is that if something is proven to be wrong, it will be corrected. As far as I can see, you are the only one making the claim that the Theory of Evolution is wrong. If you are so certain, why not publish your findings? Science is not about upholding current views, but about testing what is known, to find what is unknown. So, if you find out all is wrong, point it out, and correct it, wouldn't that be a wonderful thing? Nobel prize in Biology, perhaps.

Or am I wrong?
I am posting my findings here on the James Randi Educational Forum at the invitation of moderator Paul Anagnostopoulos, the programmer for Dr Schneider’s online version of the ev computer simulation. If you study this computer simulation and the hundreds of empirical examples of mutation and selection which I have posted, you can understand how the mutation and selection phenomenon actually works. There is nothing to be corrected in the theory of evolution by mutation and selection. Common descent is impossible by this mechanism, mutation and selection simply doesn’t work that way.
Aren’t you going to take any of my recent citations and prove that populations can evolve far more rapidly to single selection conditions than to multiple selection conditions?As soon as you come up with a consistent definition of "single selection conditions" and "multiple selection conditions" I will be happy to.
Hey, this is your theory of evolution by mutation and selection. If you can’t figure out what a selection condition is, don’t blame me.

Let’s see if we can clear up your confusion by starting with a more general question for you to consider. Do you think that mutation and selection proceeds more rapidly with more or fewer selection conditions?
Since, however, you have demonstrated that you are utterly incapable of doing so, as your definition of every term you use is radically changed on a per-post basis, it doesn't look like I will have much proving to do in the foreseeable future.

Arguing with you is like trying to converse with yoshi, except that yoshi is cute.
Oh, I’m not trying to be cute; don’t you know what the title of this thread is?

I must admit, my task is very easy when I post the mathematical and empirical facts of how mutation and selection actually works.
I’m not angry at all with you Belz, I’m having fun.Ah! Is that what you're doing ? You're certainly not debating, that's for sure.
That is true; I’m waiting for you evolutionists to post a real argument. It’s hard to have a debate when the other side has no mathematical or empirical evidence to support your contentions. As soon as you do, we’ll start the debate.
How thoughtless of me to clog this thread with mathematical and empirical facts of how mutation and selection actually works.Here, Kleinman forgets, once again, what was the point of the discussion. Once more he shows he is incapable of following a train of thought.

If he had bothered to check, he would've known what I was talking about. But it's much more "fun" to just take words in the opponent's sentence and construct a non-answer to that. Pwned, I guess.
That’s right; the point of this discussion is the theory of evolution by beggaminases. Sorry I have drifted off topic.
You understand the difference once rcronk explained the difference to you.Since you do not know what is occuring in my head, I find it presumptuous of you to claim that you do.
Once again you are correct, even though you write down things, they have nothing to do with what is occurring in your head.
The theory of evolution is also an invention of you evolutionists, mutation and selection doesn’t work the right way for your invention to work.For the second time in four sentences adressed to me, Kleinman AGAIN forgets what we were talking about.

Is there no end to this ? Find out on the next exciting episode of "Annoying Kleinman."
This is going to continue on for a while as long as I can find more empirical examples of how mutation and selection actually works. If I come across a citation for beggaminases, I’ll be sure to post that as well.
Once again you have it backwards Belz, I am not the one trying to silence anyone, it is you evolutionarianists who are trying to silence people.Kleinman is attempting, here, to invoke the Galileo syndrome. In other words, since all his attempts to show us wrong have failed, he's trying to claim that only he can see the light and that, in time, he'll be proven right.

I can't wait for THAT second coming, let me tell you that.
Now Belz, don’t confuse your failure to understand how mutation and selection actually works as the explanation is wrong.
I think evolution should be taught in school, especially how mutation and selection actually works, then this nonsense of common descent will be discarded.Sure, Klein. Whatever makes you sleep.
You wouldn’t be suggesting that I should be silenced, would you?
Don’t believe him Belz; Delphi has been out sorting his sock drawer and making stop action human skateboard films.Silly scientists and their silly evidences.
Strange but true Belz, read the thread and find out.
First of all, it is not my mathematics, it is Dr Schneider’s peer reviewed and published model of random point mutation and natural selection.Again, it's your interpretation that's in question, but I fully expect you to dodge this one as well.
Again Belz, strange but true, my interpretation is substantiated by hundreds of real empirical examples of how mutation and selection works. Here’s another example for you to consider.
http://www.jci.org/cgi/reprint/113/8/1084.pdf (http://www.jci.org/cgi/reprint/113/8/1084.pdf)
Malaria, the most prevalent and most pernicious parasitic disease of humans, is estimated to kill between one and two million people, mainly children, each year. Resistance has emerged to all classes of antimalarial drugs except the artemisinins and is responsible for a recent increase in malaria-related mortality, particularly in Africa. The de novo emergence of resistance can be prevented by the use of antimalarial drug combinations. Artemisinin derivative combinations are particularly effective, since they act rapidly and are well tolerated and highly effective. Widespread use of these drugs could roll back malaria.
Isn’t that interesting? Another example which shows that evolution of resistance is profoundly slowed by combination selection pressures.

[rocketdodger]

If you can’t figure out what a selection condition is, don’t blame me.

Everyone can see, Kleinman, that you actively avoid defining the terms you use. And we all know why you refuse -- because as soon as you give us a definition you end up contradicting yourself.

If you disagree, then simply give us your definition of "single selection conditions" and "multiple selection conditions."

[Belz...]

I am posting my findings here on the James Randi Educational Forum at the invitation of moderator Paul Anagnostopoulos, the programmer for Dr Schneider’s online version of the ev computer simulation.

And yet he disagrees with you on the interpretation of those results. Care to explain that ?

If you study this computer simulation and the hundreds of empirical examples of mutation and selection which I have posted, you can understand how the mutation and selection phenomenon actually works.

Considering how you use circular reasoning to support your contention, I don't think we'll understand it in the sense that we'll agree with you...

There is nothing to be corrected in the theory of evolution by mutation and selection. Common descent is impossible by this mechanism, mutation and selection simply doesn’t work that way.

Indeed, it doesn't.

That is true; I’m waiting for you evolutionists to post a real argument.

First off, I'm not an "evolutionist" or an "evolutionarian" or whatever definition you invent.

Second, it's YOUR claim. It's only been proven in your head.

It’s hard to have a debate when the other side has no mathematical or empirical evidence to support your contentions.

It does. You just refuse to accept it.

That’s right; the point of this discussion is the theory of evolution by beggaminases. Sorry I have drifted off topic.

Here, Kleinman forgets the definition of the term "beggaminases", which is basically the variation of a gene through mutation but independent of selection pressures.

Once again you are correct, even though you write down things, they have nothing to do with what is occurring in your head.

Since you do not know what is occuring in my head, I find it presumptuous of you to claim that you do.

This is going to continue on for a while as long as I can find more empirical examples of how mutation and selection actually works.

You mean, your ONE and ONLY example of how adding more selection pressures can slow down evolution ? You haven't yet shown how evolution works, and your examples are limited to variations on the same theme. Also, you've been shown time and time again how and why you're wrong.

I refuse to accept that you haven't seen this. You are being willfully obtuse.

Now Belz, don’t confuse your failure to understand how mutation and selection actually works as the explanation is wrong.

Funny, I was thinking the exact opposite.

You wouldn’t be suggesting that I should be silenced, would you?

What ?

Strange but true Belz, read the thread and find out.

I've been there pretty much since the beggining, remember ?

Yet, no evidence. You're the one who's claiming that all the other scientists are wrong. Did I say "other" ? Pfah! Like YOU'RE a scientist.

Again, it's your interpretation that's in question, but I fully expect you to dodge this one as well.

Again Belz, strange but true

Wow. You ADMIT you're dodging the question ?

Isn’t that interesting? Another example which shows that evolution of resistance is profoundly slowed by combination selection pressures.

It's a good thing, Klein, that REAL scientists always take ALL the data into account, not just the examples they like.

[kleinman]

If you can’t figure out what a selection condition is, don’t blame me.Everyone can see, Kleinman, that you actively avoid defining the terms you use. And we all know why you refuse -- because as soon as you give us a definition you end up contradicting yourself.

If you disagree, then simply give us your definition of "single selection conditions" and "multiple selection conditions."
It’s clear that you haven’t read this thread because this discussion has occurred previously but since you are having trouble understanding this particular part of the topic; it would be worthwhile to discuss it again.

Let’s start with this basic principle. A selection pressure is a stress put on a population which impairs some or all individuals in the population’s ability to reproduce.
I am posting my findings here on the James Randi Educational Forum at the invitation of moderator Paul Anagnostopoulos, the programmer for Dr Schneider’s online version of the ev computer simulation.And yet he disagrees with you on the interpretation of those results. Care to explain that ?
Belz, I can’t explain what is going on in Paul’s head but I can tell you what Paul has done. Several years ago before this discussion started, Paul argued that ev represented reality. Since this discussion has started, Paul has backpedaled from this position numerous times. Perhaps you should ask Paul why he has backpedaled so many times on his view of what ev shows. Ask Paul what ev represents now.
If you study this computer simulation and the hundreds of empirical examples of mutation and selection which I have posted, you can understand how the mutation and selection phenomenon actually works.Considering how you use circular reasoning to support your contention, I don't think we'll understand it in the sense that we'll agree with you...
Considering that the reasoning is that the mathematics supports the empirical evidence supports the mathematics, I don’t mind that kind of circular reasoning. Your reasoning goes no where.
That is true; I’m waiting for you evolutionists to post a real argument.First off, I'm not an "evolutionist" or an "evolutionarian" or whatever definition you invent.

Second, it's YOUR claim. It's only been proven in your head.
Well Belz, I put my thoughts down on this topic in this thread and those thoughts are supported by the mathematics of mutation and selection which is supported by the empirical evidence of how mutation and selection actually works which is supported by the mathematics. Some kind of circular reasoning this is, isn’t it?
It’s hard to have a debate when the other side has no mathematical or empirical evidence to support your contentions.It does. You just refuse to accept it.
Oh no Belz, I accept the fact that the evolutionist view has no mathematics or empirical evidence of how mutation and selection works to support your contentions. It makes for a very unfair debate. However, it does not bother me to show why the theory of evolution is mathematically impossible..
That’s right; the point of this discussion is the theory of evolution by beggaminases. Sorry I have drifted off topic.Here, Kleinman forgets the definition of the term "beggaminases", which is basically the variation of a gene through mutation but independent of selection pressures.
So are you saying that reptiles beggaminases into birds?
Once again you are correct, even though you write down things, they have nothing to do with what is occurring in your head.Since you do not know what is occuring in my head, I find it presumptuous of you to claim that you do.
We already know that we have to read what you mean to say, not what you write.
This is going to continue on for a while as long as I can find more empirical examples of how mutation and selection actually works.You mean, your ONE and ONLY example of how adding more selection pressures can slow down evolution ? You haven't yet shown how evolution works, and your examples are limited to variations on the same theme. Also, you've been shown time and time again how and why you're wrong.

I refuse to accept that you haven't seen this. You are being willfully obtuse.
No Belz, as long as I continue to find more examples of how mutation and selection actually work, I will continue to post these examples. Since combination selection pressures profoundly slow the evolutionary process, I believe there will be more citations published which show this on an ongoing basis and therefore there is no end to this thread in sight.
Now Belz, don’t confuse your failure to understand how mutation and selection actually works as the explanation is wrong.Funny, I was thinking the exact opposite.
So what is your circular reasoning? There is no mathematical evidence which supports common descent by mutation and selection and there is no empirical evidence to support this mathematical finding?
Strange but true Belz, read the thread and find out. I've been there pretty much since the beggining, remember ?

Yet, no evidence. You're the one who's claiming that all the other scientists are wrong. Did I say "other" ? Pfah! Like YOU'RE a scientist.
Pretty much in the beginning there was Belz and Belz was without form, but Belz beggaminases and he has stayed that way.
Again, it's your interpretation that's in question, but I fully expect you to dodge this one as well.Again Belz, strange but trueWow. You ADMIT you're dodging the question ?
Really, I’m dodging your question? I post mathematical and empirical evidence of my interpretation of how mutation and selection actually works and you post beggaminases. Belz, you are beggaminasesing the question.
Isn’t that interesting? Another example which shows that evolution of resistance is profoundly slowed by combination selection pressures.It's a good thing, Klein, that REAL scientists always take ALL the data into account, not just the examples they like.
Where is all this real data which supports your viewpoint of how mutation and selection actually works, either mathematical or empirical?

[rocketdodger]

Let’s start with this basic principle. A selection pressure is a stress put on a population which impairs some or all individuals in the population’s ability to reproduce.

So a population under a "single selection pressure" has only one such stress affecting it?

[kleinman]

Let’s start with this basic principle. A selection pressure is a stress put on a population which impairs some or all individuals in the population’s ability to reproduce.So a population under a "single selection pressure" has only one such stress affecting it?
Rocketdodger, before I answer your question, answer this question. Does a greater number of selection pressures accelerate evolution or slow the evolutionary process when compared to a smaller number of selection pressures?

[rocketdodger]

Rocketdodger, before I answer your question, answer this question. Does a greater number of selection pressures accelerate evolution or slow the evolutionary process when compared to a smaller number of selection pressures?

Since I am asking you to define what a "single selection pressure" means, how should I know what you mean when you say "a greater number or selection pressures" versus "a smaller number of selection pressures" ???

Sure I will answer your question -- I don't know, because you haven't provided me with enough information.

Try again.

[kjkent1]

Another day, another post from kleinman clearly showing that his proofs prove how evolution works (assuming that we concede that this is all there is to it, which I, for one, do not). To wit: resistance to TAF used alone is acquired rapidly under drug pressure and that this resistance is stable when selection pressure is removed.
Kjkent1 shows a lack of creativity and takes up questiondodger’s strategy of posting sentence fragments in order to try to make a point.

I like clogging up the thread with the mathematical and empirical facts of how mutation and selection actually works, so let’s repost the portion the kjkent1 left out of the citation.

Originally Posted by the part of the quote that kjkent1 neglects to post :

Data obtained with the 2%RT, and three parasite lines derived from Plasmodium berghei N (the 238B line), P. chabaudi ASS (the 238C line) or P. yoelii ssp. NS (the 238Y line), indicated that resistance to TAF used alone is acquired rapidly under drug pressure and that this resistance is stable when selection pressure is removed. In the 2%RT, resistance to CQ developed when another line of P. chabaudi (AS15) was exposed to that compound alone, although more slowly than the development of resistance to TAF in the 238C line. However, treatment of a TC line of P. chabaudi, developed in a 2%RT using a combination of CQ with TAF, led to little resistance to either compound.

What’s this kjkent1? Combinations of CQ with TAF led to little resistance to either compound. You should also know this kjkent1 that ev shows the same thing. Any of the three selection conditions evolve very rapidly when applied alone, only when the selection pressures are applied simultaneously does the evolutionary process slow profoundly.Gee, Alan, you're terrific at avoiding the point rather than addressing it.

And, the point is that all organisms are under many selective pressures, throughout their existence. That's what keeps them stable. It's only when a single, overwhelming pressure is applied that the organism evolves.

This is precisely what your posts show, and precisely what you allege.

Your problem is that you focus on what happens when multiple severe pressures are applied -- evolution slows -- because it appears to support your theory that evolution is impossible. What you continually miss is that it's the relative intensity of pressures that slows evolution. This is demonstrated in ev: if you set each of the three selective pressures to the same number -- be it 1 or 100, evolution is slow. It's only when you change the weights relative to each other that evolution speeds up.

And, just as you claim, evolution is fastest when there is a huge disparity in selective weight: the fastest performance occurs with one weight set to any number and the others set to zero (an infinitely large difference).

But, suppose that the difference is 1,000,000 to one, rather than the maximum difference available in ev of 100 to 1. You know that mathematically, you can create a ratio between selective intensities sufficiently large so that for all practical purposes the difference is near infinite (limit of a function).

And the result is the same, as demonstrated by each of your posts. Given any organism in a stable environment, with many selective pressures applied, but not of overwhelming strength, no evolution occurs. But, apply one overwhelming pressure and suddenly we see a change.

This sort of thing happens in nature all the time.

Congrats, Alan. You've proven your own theory wrong.

ROFLMAO!

[kleinman]

Rocketdodger, before I answer your question, answer this question. Does a greater number of selection pressures accelerate evolution or slow the evolutionary process when compared to a smaller number of selection pressures?Since I am asking you to define what a "single selection pressure" means, how should I know what you mean when you say "a greater number or selection pressures" versus "a smaller number of selection pressures" ???

Sure I will answer your question -- I don't know, because you haven't provided me with enough information.

Try again.
Fair enough. The question you are asking is important to understand if you want to precisely describe the mutation and selection process. Actually there are at least two definitions for the concept of selection pressure. One definition was raised in the discussions with Dr Richard and a citation he presented where they are quantifying the changes in HIV when subjected to therapy. In their terminology, a selection pressure is counted as a change at a single locus in the viral genome. I would term this type of description as the microscopic definition for a selection pressure. The other definition which I have been using is the macroscopic definition for a selection pressure. In this particular application of the term, a drug or toxin targeted at a particular gene would be a single selection pressure. Actually, to get a more accurate description of what a selection pressure is, you have to take into account both concepts. In some cases, a single drug may actually target two or more genes such as the quinolone antibiotics which if the concentrations are sufficient will act on two genetic pathways while disinfectants chemically react with large numbers of proteins and would therefore put selection pressures on many genetic systems simultaneously. Ultimately, if you want to get a grasp on how selection pressures act at the genetic level, you need to consider at least these two definitions of selection pressures.


Rocketdodger, what I think you don’t understand yet is that the mutation and selection process is simply an optimization process. The ability for a population to optimize against multiple strong selection pressures simultaneously is profoundly difficult. This is demonstrated by the many citations I have been and will continue to post. Anticipating your question about strong selection pressures, these are pressures which strongly affect the fitness of a population to reproduce. Populations which can not adapt to strong selection pressures are likely to face extinction. On the other hand, weak selection pressures don’t have a large affect on the fitness of a population to reproduce and therefore don’t change the frequency of particular sequences of genes by much. The question you should consider is whether multiple simultaneous weak selection pressures can be optimized by a population. I say no because of the results from ev. Ev’s selection conditions can not drive the population to extinction so they are weak selection conditions yet ev has a very difficult time sorting beneficial and detrimental mutations on all but the tiniest genomes.

There is more to say about selection pressures such as whether they are directional or stabilizing, the intensity of the selection pressure but as an adaptation mechanism, the mutation and selection process can only occur rapidly when only a single genetic target occurs. The greater the number of genetic targets for this process, the far more difficult it is for this process to optimize the mutations in order for the population to adapt to the stresses. This is why the concept of common descent is mathematically impossible by mutation and selection.
And, the point is that all organisms are under many selective pressures, throughout their existence. That's what keeps them stable. It's only when a single, overwhelming pressure is applied that the organism evolves. … And the result is the same, as demonstrated by each of your posts. Given any organism in a stable environment, with many selective pressures applied, but not of overwhelming strength, no evolution occurs. But, apply one overwhelming pressure and suddenly we see a change. And the result is the same, as demonstrated by each of your posts. Given any organism in a stable environment, with many selective pressures applied, but not of overwhelming strength, no evolution occurs. But, apply one overwhelming pressure and suddenly we see a change. … This sort of thing happens in nature all the time.

Congrats, Alan. You've proven your own theory wrong.
You are starting to understand how mutation and selection works but you are still missing the crucial point, if the overwhelming selection pressure targets only a single gene and the population is able to reproduce quickly enough despite the selection pressure, then you can get adaptation. Where the mutation and selection process is crippled occurs when you have more than a single overwhelming selection pressure. Then the ability of the population to adapt to these multiple overwhelming selection pressures by mutation and selection is markedly hindered. That’s the mathematical and empirical story of how mutation and selection actually works.

[Paul C. Anagnostopoulos]

Belz, I can’t explain what is going on in Paul’s head but I can tell you what Paul has done. Several years ago before this discussion started, Paul argued that ev represented reality. Since this discussion has started, Paul has backpedaled from this position numerous times. Perhaps you should ask Paul why he has backpedaled so many times on his view of what ev shows. Ask Paul what ev represents now.
If I have backpedaled from that position, it is simply over the degree to which Ev represents reality. From day one, of course, I argued that it only represents a tiny fraction of real life. I knew that because I programmed it, don't you know.

The problem for you is this: The more I might backpedal, the weaker your argument becomes.

~~ Paul

[Paul C. Anagnostopoulos]

You are starting to understand how mutation and selection works but you are still missing the crucial point, if the overwhelming selection pressure targets only a single gene and the population is able to reproduce quickly enough despite the selection pressure, then you can get adaptation. Where the mutation and selection process is crippled occurs when you have more than a single overwhelming selection pressure. Then the ability of the population to adapt to these multiple overwhelming selection pressures by mutation and selection is markedly hindered. That’s the mathematical and empirical story of how mutation and selection actually works.
Your argument has turned into philosophical gobbledygook, Alan. Now you have "overwhelming" selection pressures; pressures targeting only a single gene; reproduction speed; adaptation vs. evolution; crippling; multiple overwhelming selection pressures; marked hindrance. You appear to be saying the following:

If a bunch of selection pressures are rigged or happen to work out just right, they can significantly increase the time it takes an organism to adapt to them, or possibly cause extinction.

If that is what you're saying, I'll stipulate to it.

~~ Paul

[kleinman]

Belz, I can’t explain what is going on in Paul’s head but I can tell you what Paul has done. Several years ago before this discussion started, Paul argued that ev represented reality. Since this discussion has started, Paul has backpedaled from this position numerous times. Perhaps you should ask Paul why he has backpedaled so many times on his view of what ev shows. Ask Paul what ev represents now.If I have backpedaled from that position, it is simply over the degree to which Ev represents reality. From day one, of course, I argued that it only represents a tiny fraction of real life. I knew that because I programmed it, don't you know.
I think it is good to remind the readers that you said this about ev.
http://forums.randi.org/showthread.php?t=48008&page=6 (http://forums.randi.org/showthread.php?t=48008&page=6) ?
There are plenty of examples of A-life evolving. I think Ev rankles the IDers because it is a model of actual life, and also because Schneider is fairly good at advertising it.
Now Paul, ev doesn’t rankle me at all, in fact I think that Dr Schneider properly captured the mathematical behavior of the mutation and selection process in his model.
The problem for you is this: The more I might backpedal, the weaker your argument becomes.
It’s not a problem for me at all. Say whatever you want about ev. I’ll defend the validity of the model even if you, Dr Schneider and the peer review editors at Nucleic Acids Research abandon the model. The reason why I’ll defend the model is that I think that Dr Schneider did get the essential features correct in the model. It properly shows what happens to the mathematical behavior of the mutation and selection process when you have multiple selection pressures acting simultaneously. My argument is not dependent on your endorsement of ev. It is kind of silly when you do backpedal because your model doesn’t fit your world view especially when there are so many empirical examples which fit the mathematical behavior of ev.

[Paul C. Anagnostopoulos]

So first you claim that I've backpedaled and quote me from awhile ago as evidence that I've done so:

I think it is good to remind the readers that you said this about ev.


I think Ev rankles the IDers because it is a model of actual life, ...
Then you say this:

The reason why I’ll defend the model is that I think that Dr Schneider did get the essential features correct in the model.
Apparently, that's what I was saying, too.

Then, to get even whackier, you try to claim that I've backpedaled because I realize---oh, horror---that Ev disproves the theory of evolution. You do this even though I've argued precisely the opposite.

It is kind of silly when you do backpedal because your model doesn’t fit your world view especially when there are so many empirical examples which fit the mathematical behavior of ev.
Alan, you're arguing with your own arse.

~~ Paul

[kleinman]

You are starting to understand how mutation and selection works but you are still missing the crucial point, if the overwhelming selection pressure targets only a single gene and the population is able to reproduce quickly enough despite the selection pressure, then you can get adaptation. Where the mutation and selection process is crippled occurs when you have more than a single overwhelming selection pressure. Then the ability of the population to adapt to these multiple overwhelming selection pressures by mutation and selection is markedly hindered. That’s the mathematical and empirical story of how mutation and selection actually works.Your argument has turned into philosophical gobbledygook, Alan. Now you have "overwhelming" selection pressures; pressures targeting only a single gene; reproduction speed; adaptation vs. evolution; crippling; multiple overwhelming selection pressures; marked hindrance. You appear to be saying the following:
Somewhere along the line you have to find terminology to describe the mathematical behavior of the problem.
If a bunch of selection pressures are rigged or happen to work out just right, they can significantly increase the time it takes an organism to adapt to them, or possibly cause extinction.
I used strikethough to properly describe what I am saying. Did Dr Schneider choose his selection pressures to significantly increase the time it takes to evolve the binding sites? What selection pressures will work together in order to accelerate the evolutionary process? Paul, as soon as you try to sort mutations for two or more different genes, this confounds the mutation and selection process. There are no selection conditions that “cooperate” with each other.
If that is what you're saying, I'll stipulate to it.
It’s not what I’m saying, what I am saying is what ev shows and the hundreds of real examples of mutation and selection show and that is that combination selection pressures profoundly slow the evolutionary process by mutation and selection.

[kleinman]

So first you claim that I've backpedaled and quote me from awhile ago as evidence that I've done so:
Paul, it is obvious you have backpedaled on your description of what ev shows.
Then you say this:The reason why I’ll defend the model is that I think that Dr Schneider did get the essential features correct in the model.Apparently, that's what I was saying, too.

Then, to get even whackier, you try to claim that I've backpedaled because I realize---oh, horror---that Ev disproves the theory of evolution. You do this even though I've argued precisely the opposite.
Paul, you have argued Rcapacity, you have argued that setting two of the three selection conditions to zero is not valid and you have missed the obvious finding that the number of selection conditions dominates the mathematical behavior of the mutation selection process. You can squirm around all you want but that is how the mathematics of mutation and selection works and this is easily demonstrated empirically. You are now trying to claim that somehow selection pressures cooperate with each other in order for things to evolve that’s what is whacky. You have no mathematical or empirical evidence for your bizarre speculation.
It is kind of silly when you do backpedal because your model doesn’t fit your world view especially when there are so many empirical examples which fit the mathematical behavior of ev.Alan, you're arguing with your own arse.
When it comes to your theory of evolution, your arse is in a sling, use your head and get it out of there and stop practice your bizarre speculations to try to defend your mathematically impossible theory. It makes you look like you should be carrying on a discussion on a paranormal thread.

[Belz...]

Belz, I can’t explain what is going on in Paul’s head

Well, that's funny because you seem to claim to know what's going on in mine...

but I can tell you what Paul has done. Several years ago before this discussion started, Paul argued that ev represented reality. Since this discussion has started, Paul has backpedaled from this position numerous times.

Well, you see it's like this: if you look at a caricature, you will say that it represents the person that was used as a model. But if some nutter comes along and says the person looks EXACTLY like that, you can bet your bible that you will back down from saying it "represents" him.

Considering that the reasoning is that the mathematics supports the empirical evidence supports the mathematics, I don’t mind that kind of circular reasoning. Your reasoning goes no where.

Klein makes a huge mistake, here, folks. He doesn't know what circular reasoning means, because nobody who knows what it means wants to be accused of it. Being right for the wrong reason is never a good thing.

But of course, Klein isn't right.

He also makes the mistake of saying that MY reasoning goes nowhere, as though it was somehow worse than circular reasoning. Circular reasoning goes nowhere, either.

Well Belz, I put my thoughts down on this topic in this thread and those thoughts are supported by the mathematics of mutation and selection which is supported by the empirical evidence of how mutation and selection actually works which is supported by the mathematics. Some kind of circular reasoning this is, isn’t it?

Well, yeah, actually. It is.

Oh no Belz, I accept the fact that the evolutionist view has no mathematics or empirical evidence of how mutation and selection works to support your contentions.

You know, Klein, just because you can pick a single word in someone else's sentence -- in this case, "accept" -- doesn't mean that whatever clever retort you can come up with has anything to do with the opponent's point.

Take this, for example:

It makes for a very unfair debate.

Indeed, it's very unfair for you to be pitted against people who know so much more than you do.

Or this:

However, it does not bother me to show why the theory of evolution is mathematically impossible.

I understand. You're saying that YOUR version of the theory of evolution is mathematically impossible.

So are you saying that reptiles beggaminases into birds?

Nope. I never said that.

I said they evolved into birds. But don't take my word for it.

http://forums.randi.org/imagehosting/thum_608047022eae7e563.jpg (http://forums.randi.org/vbimghost.php?do=displayimg&imgid=8609)

We already know that we have to read what you mean to say, not what you write.

Since you do not know what is occuring in my head, I find it presumptuous of you to claim that you do.

No Belz, as long as I continue to find more examples of how mutation and selection actually work, I will continue to post these examples.

Make that: as long as you find more examples of virus evolution being slowed down by a process nobody here disagrees slows down evolution, you'll keep posting them.

Since combination selection pressures profoundly slow the evolutionary process, I believe there will be more citations published which show this on an ongoing basis and therefore there is no end to this thread in sight.

The thread was over the first time you posted in it. You've lost, black knight.

So what is your circular reasoning? There is no mathematical evidence which supports common descent by mutation and selection and there is no empirical evidence to support this mathematical finding?

You really don't know what "circular reasoning" means, do you ?

Pretty much in the beginning there was Belz and Belz was without form, but Belz beggaminases and he has stayed that way.

Sure, Klein. Whatever helps you feel better about yourself.

Really, I’m dodging your question?

You admitted so.

I post mathematical and empirical evidence of my interpretation of how mutation and selection actually works and you post beggaminases. Belz, you are beggaminasesing the question.

Thank you. That's the single best thing you've ever said to me.

You haven't forgotten what "beggaminases" means, have you ?

Where is all this real data which supports your viewpoint of how mutation and selection actually works, either mathematical or empirical?

You keep posting it over and over. I can't believe you haven't noticed it.

[Belz...]

The ability for a population to optimize against multiple strong selection pressures simultaneously is profoundly difficult.

Precisely what other people have been telling you.

I'll take the addition of "strong" in your definition to be an admission of defeat. You are retreating.

[Belz...]

I’ll defend the validity of the model even if you, Dr Schneider and the peer review editors at Nucleic Acids Research abandon the model. [/SIZE][/FONT]

Dear readers, I do believe we've hit the bottom of Kleinman's ocean.

He doesn't care if the model if accepted or not. He doesn't care if its creators say it's flawed. He WANTS the model to be true, and no matter of fact will stop him.

[Belz...]

There are no selection conditions that “cooperate” with each other.

Really ?

[Paul C. Anagnostopoulos]

I used strikethough to properly describe what I am saying.
I see no strikethrough.


Did Dr Schneider choose his selection pressures to significantly increase the time it takes to evolve the binding sites?
Significantly increase the time over what? The unrelated situation where Rfrequency and Rcapacity are irrelevant?


Paul, you have argued Rcapacity, you have argued that setting two of the three selection conditions to zero is not valid
I didn't say it was invalid. Pay attention. I said that it is meaningless to compare the model where Rfrequency and Rsequence matter with the model where they do not.

You are now trying to claim that somehow selection pressures cooperate with each other in order for things to evolve that’s what is whacky.
Where did I claim that?

~~ Paul

[kleinman]

Belz, I can’t explain what is going on in Paul’s headWell, that's funny because you seem to claim to know what's going on in mine...
Yes, it’s beggaminases.
but I can tell you what Paul has done. Several years ago before this discussion started, Paul argued that ev represented reality. Since this discussion has started, Paul has backpedaled from this position numerous times.Well, you see it's like this: if you look at a caricature, you will say that it represents the person that was used as a model. But if some nutter comes along and says the person looks EXACTLY like that, you can bet your bible that you will back down from saying it "represents" him.
Is that what’s going on in your head?
The ability for a population to optimize against multiple strong selection pressures simultaneously is profoundly difficult.Precisely what other people have been telling you.

I'll take the addition of "strong" in your definition to be an admission of defeat. You are retreating.
So, are you going to claim that multiple weak selection pressures evolve rapidly? Or do you mean to say that multiple weak selection pressures beggaminases quickly?
I’ll defend the validity of the model even if you, Dr Schneider and the peer review editors at Nucleic Acids Research abandon the model. Dear readers, I do believe we've hit the bottom of Kleinman's ocean.

He doesn't care if the model if accepted or not. He doesn't care if its creators say it's flawed. He WANTS the model to be true, and no matter of fact will stop him.
Oh, has Dr Schneider denied the validity of his model? Have the peer review editors at Nucleic Acids Research published a retraction about ev? Belz, they aren’t going to do that, the mathematics is correct. I do believe we’ve hit the bottom of the primordial soup.
There are no selection conditions that “cooperate” with each other.Really ?
Really Belz there are no cooperative selection pressures, except maybe those going around in your head along with the beggaminases.
I used strikethrough to properly describe what I am saying.I see no strikethrough.
Sorry, the quick post feature did not take the strikethrough font. I’ll repost it here.
If a bunch of selection pressures are rigged or happen to work out just right, they can significantly increase the time it takes an organism to adapt to them, or possibly cause extinction.
And here is what I really am saying:
A bunch of selection pressures significantly increase the time it takes an organism to adapt to them, or possibly cause extinction.
Did Dr Schneider choose his selection pressures to significantly increase the time it takes to evolve the binding sites?Significantly increase the time over what? The unrelated situation where Rfrequency and Rcapacity are irrelevant?
Paul, you have a big blind spot here. Dr Schneider has designed three selection conditions to evolve particular sequences of bases. It takes huge numbers of generations to satisfy all three conditions simultaneously while any one of the selection conditions can be evolved in trivially small numbers of generations even when ev shows no sign of converging the longer genome lengths using all three selection conditions. If you want to argue against the obvious, be my guest. We already know how much you enjoy painting yourself into a corner. I’ll supply you with as much paint as you want; your choice of colors.
Paul, you have argued Rcapacity, you have argued that setting two of the three selection conditions to zero is not validI didn't say it was invalid. Pay attention. I said that it is meaningless to compare the model where Rfrequency and Rsequence matter with the model where they do not.
Then why don’t you tell us again what is the basis of selection for ev? Didn’t you say that Rfrequency and Rsequence have nothing to do with selection in the model? Let’s give your actual quote.
The problem with using Rs > Rf as the test, rather than the perfect creature, is that there is no selection pressure to reach Rs > Rf. There is only pressure to reach a perfect creature. There is no Rs > Rf selection pressure in nature, either.
The selection in ev is dependent on matches of the weight matrix with particular sequences of bases. In particular areas of the genome, matches give mistakes and in other areas of the genome, the lack of matches gives mistakes. Any one of the selection conditions can be easily satisfied in a tiny number of generations; it is only when ev tries to evolve all three selection conditions simultaneously that the process becomes profoundly slow. And guess what Paul, mutation and selection works that way in reality.
You are now trying to claim that somehow selection pressures cooperate with each other in order for things to evolve that’s what is whacky.Where did I claim that?
You claimed that when you tried to state what I was claiming.
If a bunch of selection pressures are rigged or happen to work out just right, they can significantly increase the time it takes an organism to adapt to them, or possibly cause extinction.
And then you said:
If that is what you're saying, I'll stipulate to it.
Selection pressures don’t have to be rigged to significantly increase the time it takes an organism to adapt to them. All this shows that you still have a fundamental misunderstanding of how the mathematics of mutation and selection actually works and what the empirical evidence which substantiates this mathematics. Whether they are weak or strong selection pressures, when applied simultaneously, combination selection pressures interfere with a populations’ ability to sort beneficial and detrimental mutations. That is the mathematical and empirical fact of how mutation and selection actually works. So let’s have another empirical example of this mathematical fact.
http://frac.info/frac/publication/anhang/FRAC_Mono1_2007_100dpi.pdf (http://frac.info/frac/publication/anhang/FRAC_Mono1_2007_100dpi.pdf)
The approaches taken for different groups of fungicides will be discussed later, but first let us consider briefly the range of use strategies for resistance management that are available. Although they are discussed individually, the integrated use of combinations of different strategies is feasible, beneficial, and often implemented.

1. Do not use the product exclusively Apply it as a mixture with one or more fungicides of a different type, or as one component in a rotation or alternation of different fungicide treatments. The ‘companion’ or ‘partner’ compounds applied in either of these ways will dilute the selection pressure exerted by the at-risk fungicide and inhibit the growth of any resistant biotypes that arise. The companion compound can be a multi-site compound known to have a low risk of inducing resistance. Alternatively, it can be a single-site fungicide that is known not to be related to its partner by cross-resistance or (in the absence of known resistance) by a similar mode of action. Use of a mixture of two single-site fungicides must carry some element of risk of selecting dual-resistant strains. However, the chances of two mutations occurring simultaneously will be very small compared to that of a single mutation (e.g. 10^-18 instead of 10^-9). Consecutive development of double resistance could occur, but would seem much less likely to develop than if the two components were used separately and repeatedly. This type of strategy is widely recommended by industry and also by advisory bodies. The use of formulated (‘pre-packed’) mixtures of two different fungicides has often been favoured by manufacturers. If an at-risk fungicide is not sold alone, then use of the mixture is the only use option open to the farmer and implementation of the strategy is ensured.

[Belz...]

Is that what’s going on in your head?

Are you ever going to answer what anyone says, you dullard ?

So, are you going to claim that multiple weak selection pressures evolve rapidly? Or do you mean to say that multiple weak selection pressures beggaminases quickly?

No, I'm saying that...

Never mind, you didn't read it the other times it's been mentioned. Why should I bother ?

Oh, has Dr Schneider denied the validity of his model? Have the peer review editors at Nucleic Acids Research published a retraction about ev?

Goddammit, Klein. Follow the damn conversation! If you can't even remember what was said this morning, then there's no hope for you.

Really Belz there are no cooperative selection pressures, except maybe those going around in your head along with the beggaminases.

Beggaminases is a verb, Klein. Pay attention.

[kleinman]

Is that what’s going on in your head?Are you ever going to answer what anyone says, you dullard ?
Oh my, an evolutionist resorts to name calling.
Really Belz there are no cooperative selection pressures, except maybe those going around in your head along with the beggaminases.Beggaminases is a verb, Klein. Pay attention.
I beggaminases your pardon.

[Shalamar]

I'm trying to understand. So how Valid is this model in relation to the actual process of evolution?

Models are all well and good, and can be used for understanding certain aspects of what it models, but its not perfect. And can not be. One can study the model, but ALSO study the actual processes. Perhaps use different and additional models. And as far as I can tell only ONE PERSON is claiming that the model disproves evolution, and thus, Creationism MUST be true.

[rocketdodger]

You still haven't addressed my last post Kleinman. I wonder why...

[rocketdodger]

So, are you going to claim that multiple weak selection pressures evolve rapidly?

We claim that a single strong selection pressure combined with multiple weak selection pressures can lead to rapid evolution.

Despite your best efforts to sidestep around agreeing with this claim (since it completely refutes your theory), the sum of your posts states that you in fact do agree with it.

Of course you will reply with some nonsense about "directional" and "stabilizing" pressures, totally failing to realize that all your statements do nothing but solidify the above claim.

[Belz...]

Oh my, an evolutionist resorts to name calling.

1) Am I not an evolutionist. I don't even know what it's supposed to mean.
2) Why wouldn't you expect a certain subset of the set of human beings to use name calling ?
3) Weren't YOU the one repeatedly calling us "mathematically-challenged evolutionarians" and isn't that name-calling ?

And I notice you continue to avoid answering my points when the going gets tough.

I beggaminases your pardon.

Okay. That was funny.

[Belz...]

We claim that a single strong selection pressure combined with multiple weak selection pressures can lead to rapid evolution.

Despite your best efforts to sidestep around agreeing with this claim (since it completely refutes your theory), the sum of your posts states that you in fact do agree with it.

Of course you will reply with some nonsense about "directional" and "stabilizing" pressures, totally failing to realize that all your statements do nothing but solidify the above claim.

That's the one thing that binds anti-evolution people together.

They say evolution is silly, impossible, blasphemous, etc., but when put to the test, they actually agree with all the elements that make up the theory of evolution. They just don't like the conclusion.

[kleinman]

So, are you going to claim that multiple weak selection pressures evolve rapidly?We claim that a single strong selection pressure combined with multiple weak selection pressures can lead to rapid evolution.

Despite your best efforts to sidestep around agreeing with this claim (since it completely refutes your theory), the sum of your posts states that you in fact do agree with it.

Of course you will reply with some nonsense about "directional" and "stabilizing" pressures, totally failing to realize that all your statements do nothing but solidify the above claim.
If you think that a single strong selection pressure combined with multiple weak selection pressures accelerates evolution, post a real example of this and don’t forget to identify the genes evolved and the mutations that give the improved fitness.
Oh my, an evolutionist resorts to name calling.1) Am I not an evolutionist. I don't even know what it's supposed to mean.
2) Why wouldn't you expect a certain subset of the set of human beings to use name calling ?
3) Weren't YOU the one repeatedly calling us "mathematically-challenged evolutionarians" and isn't that name-calling ?

And I notice you continue to avoid answering my points when the going gets tough.
Now calling you an evolutionist is name calling. If I call you a beggaminasesarian, is that name calling?

What points do you have? Are you talking about your evolutionist Rorschach test?
I'm trying to understand. So how Valid is this model in relation to the actual process of evolution?

Models are all well and good, and can be used for understanding certain aspects of what it models, but its not perfect. And can not be. One can study the model, but ALSO study the actual processes. Perhaps use different and additional models. And as far as I can tell only ONE PERSON is claiming that the model disproves evolution, and thus, Creationism MUST be true.
Shalamar, you are asking the right question. How valid is ev in simulating the mutation and selection process? No evolutionist questioned the validity of ev until I posted data from the model that contradicts the theory of evolution. Is what Dr Schneider published from his model valid and shows mathematically how the theory of evolution works or what I have posted and shows that the theory of evolution is mathematically impossible?

The answer to these conflicting interpretations can be found in the mathematical behavior of the mutation and selection process. What is the mathematical behavior of the mutation and selection process? This type of mathematical behavior is found in many areas of science and mathematics. The mutation and selection process mathematically is an optimization or sorting problem. It is a process of sorting beneficial and detrimental mutations based on optimizing particular conditions. You can think of this geometrically as a population moving on a surface based on fitness to reproduce. This surface is called a fitness landscape. Higher points on the surface represent point of greater fitness to reproduce. It is this property of fitness to reproduce which drives the mutation and selection process.

Dr Schneider’s model is based on three selection conditions. One condition is that if a binding site is not located where it should be found, it is counted as a mistake. The second condition is if a binding site is found in the gene area it is counted as a mistake. And the third selection condition is if a binding site is found in the nonbinding site region of the genome, it is considered a mistake. The half of the population of genomes which has the fewest number of mistakes is allowed to reproduce each generation in order to produce a population with the fewest number of mistakes.

If you study the behavior of the ev model, you will find some interesting properties several of which contradict evolutionist speculations. I’ll only discuss the most important property in this post.

If you take the ev model and Dr Schneider’s published case and increase the genome length, you will find that the number of generations to converge the three selection conditions becomes huge. This is a fundamental property of optimization problems. As you increase the size of the search space for your optimum solution, the process becomes profoundly slower but this is not the main reason why convergence becomes so slow. It is the multiple selection conditions which slows the process so profoundly. This can easily be verified by running ev with two of the three selection pressures set to zero. The remaining selection pressure can be satisfied in trivially small numbers of generations. So, not only does the search space size increase by 4^G, the irregularity of the search space is much greater with multiple selection conditions. It is vastly easier for the mutation and selection process to find an optimum on a fitness landscape with only a single selection pressure than a complex fitness landscape with multiple selection conditions. The population has a much greater difficulty finding a trajectory on the fitness landscape to satisfy all three selection conditions simultaneously.

Now, you should ask if this mathematical behavior of the mutation and selection process is reflected in reality. The answer to this question is an emphatic yes. I have posted hundreds of empirical examples of the mutation and selection process which show that combination selection pressures profoundly slow the evolutionary process by mutation and selection. This observation is seen in infectious diseases (HIV, HBV, HCV, TB, Malaria, Leprosy…), oncology, agriculture (pesticides, herbicides, insecticides…) and other scientific disciplines as well.

Mutation and selection is a mathematically and empirically understandable phenomenon. It simply does not do what evolutionists allege. Mutation and selection can transform a single gene subject to a single selection pressure relatively easily, especially if only a single mutation is required to adapt to the single selection pressure. However, evolution by mutation and selection becomes a profoundly slow process when multiple selection pressures are applied to a population which requires the transformation of multiple different genes simultaneously. The ability to find a trajectory on this complex fitness landscape becomes a profoundly slow process. This is why the concept of common descent by mutation and selection is mathematically impossible. The concept of the transformation of reptiles into birds is a mathematically and empirically irrational concept. You don’t have the selection conditions that would do this and if you did, the process would be so profoundly slow; you don’t have enough generations to carry out the transformation.

The story which the ev model tells is that combination selection pressures profoundly slow the evolutionary process by mutation and selection. The empirical data substantiates this finding. Here are a couple of these empirical examples.
http://gateway.nlm.nih.gov/MeetingAbstracts/102225407.html (http://gateway.nlm.nih.gov/MeetingAbstracts/102225407.html)
Objective: To investigate the effects of combination therapy with the HIV-1 protease inhibitor CRIXIVAN (indinavir, IDV) and reverse transcriptase (RT) inhibitors ZDV and/or ddI on the emergence of drug-resistant HIV-1 variants in a clinical setting. Methods: We followed the emergence of resistance mutations in circulating viral RNAs over 24 weeks from patients receiving either IDV (600 mg q6h) vs ZDV (200 mg tid) vs IDV + ZDV (Protocol 019), or IDV (600 mg q6h) vs ZDV (200 mg tid) + ddI (200 mg bid) vs IDV + ZDV + ddI (Protocol 020). Serum viral RNAs were amplified by multiple independent RT-PCR reactions, molecularly cloned, and the DNA sequenced. The appearance of resistance mutations in the protease or RT was scored by measuring substitutions from baseline among the key amino acid residues correlated with IDV, ZDV, or ddI resistance. Results: In Protocol 019, a highly statistically significant reduction in the incidence of ZDV resistance mutations (p is less than 0.001) was observed in patients receiving a combination of IDV + ZDV (mutations in 1 of 22 patients) relative to those receiving ZDV monotherapy (11 of 17 patients). Although not statistically significant (p is less than 0.104), there was also a trend toward reduced emergence of IDV resistance in patients treated with IDV + ZDV (4 of 22 patients) relative to those on IDV monotherapy (9 of 21 patients). In Protocol 020, patients receiving a triple combination of IDV + ZDV + ddI experienced a highly significant reduction (p is less than 0.001) in ZDV or ddI resistance mutations (0 of 20 patients) relative to those receiving ZDV + ddI (10 of 16 patients). Similarly, patients on triple therapy showed a highly significant reduction (p=0.003) in IDV resistance mutations (2 of 20 patients) relative to those on IDV alone (13 of 24 patients). Conclusions: The accumulation of mutations conferring resistance to antiviral drugs requires viral replication in the presence of the inhibitor(s). Thus, the emergence of resistance to these antivirals should be reduced when viral replication is effectively suppressed. The combined antiviral effects of indinavir and RT inhibitors dramatically suppressed the emergence of resistance to these agents, in a bi-directional fashion, relative to the rates observed during inhibition of the protease or RT alone. This suggests that the durability of viral inhibition can be increased by combining indinavir with one or more inhibitors of the reverse transcriptase, suppressing the viral replication that drives the evolution of resistance.
http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=17591026&dopt=AbstractPlus (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=17591026&dopt=AbstractPlus)
BACKGROUND: The clinical management of H5N1 influenza virus infection in humans remains unclear. Combination chemotherapy with drugs that target different viral proteins might be more effective than monotherapy. METHODS: BALB/c mice were treated by oral gavage for 5 days with amantadine (1.5, 15 or 30 mg/kg/day) and oseltamivir (1 or 10 mg/kg/day) separately or in combination. Mice were challenged 24 h after initiation of treatment with 10 mouse 50% lethal doses of either amantadine-sensitive (having S31 in the M2 protein) or amantadine-resistant (having N31 in the M2 protein) recombinant A/Vietnam/1203/04 (H5N1) virus. RESULTS: Combination treatment with amantadine (15 or 30 mg/kg/day) and oseltamivir (10 mg/kg/day) provided greater protection (60% and 90%, respectively) against lethal infection with amantadine-sensitive H5N1 virus than did monotherapy. Moreover, spread of the virus to the brain was prevented by both combination regimens. The efficacy of the drug combinations against amantadine-resistant H5N1 virus was comparable to that of oseltamivir alone. Oseltamivir produced a dose-dependent effect against both recombinant H5N1 viruses (P < 0.05) but did not provide complete protection against lethal infection. Importantly, no mutations in the HA, NA and M2 proteins were detected when the two drugs were used in combination. CONCLUSIONS: Combination chemotherapy provided a survival advantage over single-agent treatment of mice inoculated with neurotropic H5N1 influenza virus. This strategy might be an option for the control of pandemic influenza viruses that are sensitive to amantadine. Combinations that include other drugs should be explored.
http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=8595505&dopt=AbstractPlus&holding=f1000%2Cf1000m%2Cisrctn (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&list_uids=8595505&dopt=AbstractPlus&holding=f1000%2Cf1000m%2Cisrctn)
Mounting scientific evidence suggests that viral replication and evolution of diversification, with the resulting emergence of variants including drug-resistant strains, is responsible for the gradual destruction of the immune system and is the mechanism of disease progression in HIV-infected patients. Monotherapy does not give long-term suppression of viral replication and evolution, and combination therapy is viewed as a potentially more effective long-term approach based on increased and more durable suppression of HIV replication. Because of the large number of drugs that could be used in combination therapy regimens, it is important to investigate, in clinical studies, only those combinations likely to be most effective. In vitro studies are therefore critical in the selection of such combinations. Resistance mutations to many antiretroviral agents have been documented and their patterns of emergence elucidated. A number of studies have since demonstrated the phenomenon of cross-resistance, in which resistant virus emerging under the selective pressure of one therapy is also cross-resistant to a second antiviral agent. This information can be used to avoid combining agents to which cross-resistance can occur. Suppression or "phenotypic reversal" of zidovudine resistance by the lamivudine-resistance mutation at codon 184 has been demonstrated in in vitro studies. It is encouraging that this finding has led to the clinical evaluation of these two agents with promising results. Moreover, in vitro scientific data are critical in facilitating the identification of potentially effective combination therapies.
Shalamar, ev shows how mutation and selection works mathematically and these types of example show how it works empirically. Of course this doesn’t include the beggaminases affect.

[kjkent1]

Alan, your two quotes below, from the same post, create a profound conflict:


Actually, there are at least two definitions for the concept of selection pressure. One definition was raised in the discussions with Dr Richard and a citation he presented where they are quantifying the changes in HIV when subjected to therapy. In their terminology, a selection pressure is counted as a change at a single locus in the viral genome. I would term this type of description as the microscopic definition for a selection pressure. The other definition which I have been using is the macroscopic definition for a selection pressure. In this particular application of the term, a drug or toxin targeted at a particular gene would be a single selection pressure. Actually, to get a more accurate description of what a selection pressure is, you have to take into account both concepts. In some cases, a single drug may actually target two or more genes such as the quinolone antibiotics which if the concentrations are sufficient will act on two genetic pathways while disinfectants chemically react with large numbers of proteins and would therefore put selection pressures on many genetic systems simultaneously. Ultimately, if you want to get a grasp on how selection pressures act at the genetic level, you need to consider at least these two definitions of selection pressures.

You are starting to understand how mutation and selection works but you are still missing the crucial point, if the overwhelming selection pressure targets only a single gene and the population is able to reproduce quickly enough despite the selection pressure, then you can get adaptation. Where the mutation and selection process is crippled occurs when you have more than a single overwhelming selection pressure. Then the ability of the population to adapt to these multiple overwhelming selection pressures by mutation and selection is markedly hindered. That’s the mathematical and empirical story of how mutation and selection actually works.

So, here's the conflicting issue:

A single selection pressure which affects multiple genetic pathways does not appear to create a sorting problem in the same manner as multiple selection pressures, each of which affects only a single genetic pathway.

Based on ev, the insertion of multiple mutations into a genome while maintaining only one selective pressure/weight, does not negatively affect evolutionary speed.

So, if you accept ev, then you must allow for the very real possibility that an overwhelming selective pressure can sort for multiple pathways without slowing the evolutionary process.

Which creates a Grand Canyon sized chasm in your theory.

[rocketdodger]

If you think that a single strong selection pressure combined with multiple weak selection pressures accelerates evolution, post a real example of this and don’t forget to identify the genes evolved and the mutations that give the improved fitness.

I know now that you are jesting us, Kleinman, and that this whole thread is a farce. You cannot be stupid enough to seriously question the above because it is exactly what you have been arguing for this whole time.


Replace

"a single strong selection pressure combined with multiple weak selection pressures accelerates evolution"

with

"a single strong <directional> selection pressure combined with multiple weak <stabilizing> selection pressures accelerates evolution"

DOES THAT SOUND FAMILIAR?

[Belz...]

Now calling you an evolutionist is name calling.

Of all the dishonest slime I've seen...

Did you not see the "mathematically-challenged" part of what I said ?

You're playing dumb, Klein. But I know you're not that dumb.

If I call you a beggaminasesarian, is that name calling?

I'm sure you don't even remember what the term means, anymore.

What points do you have? Are you talking about your evolutionist Rorschach test?

Are you talking about Archaeopteryx, again ?

Are those teeth in its mouth, Klein ?

And I notice you continue to avoid answering my points when the going gets tough.

[kleinman]

If you think that a single strong selection pressure combined with multiple weak selection pressures accelerates evolution, post a real example of this and don’t forget to identify the genes evolved and the mutations that give the improved fitness.I know now that you are jesting us, Kleinman, and that this whole thread is a farce. You cannot be stupid enough to seriously question the above because it is exactly what you have been arguing for this whole time.
Rocketdodger, that’s not what I am arguing. What these examples which I am posting show is that only the single strong pressures evolve quickly. These single strong selection pressures do nothing to accelerate the evolution of weak selection pressures. In fact, the weak selection pressures do little to influence the trajectory which the strong selection pressure pushes the population along on the fitness landscape unless to slow the evolution of this single strong condition. This is why I raised the question which you have refused to answer. If a person with HIV can not mount a humoral response against the virus, will that person have a better response to RT and PI treatment than someone who can mount a humoral response against the virus? A humoral response will, weak as it may be, apply additional selection pressure against the virus which in turn will further slow the evolution of the virus against the pharmacological selection pressures. Weak or strong selection pressures interfere with a populations’ ability to respond against these pressures resulting in a slowing of the evolutionary process when these multiple pressures are applied simultaneously.
Now calling you an evolutionist is name calling.Of all the dishonest slime I've seen...
Now wait just a minute, didn’t abiogenesis occur in the primordial slime? Are you an abiogeneholic?
Did you not see the "mathematically-challenged" part of what I said ?
Yes I did Belz, but I have been censored for using that terminology. It appears to be too insensitive of a description for you graduates of Mathishard University. You beggaminasesarians think you can describe mutation and selection without mathematics. That’s a good technique for writing mythology but not very good if you are claiming scientific method. Don’t worry Belz, you evolutionarians, abiogeneholics and beggaminasesarians can always find work on the SciFi channel.

[rocketdodger]

What these examples which I am posting show is that only the single strong pressures evolve quickly.
YES!

These single strong selection pressures do nothing to accelerate the evolution of weak selection pressures.
YES!

In fact, the weak selection pressures do little to influence the trajectory which the strong selection pressure pushes the population along on the fitness landscape unless to slow the evolution of this single strong condition.
YES!

So ... if there is a strong selection pressure and multiple weak selection pressures, rapid evolution to alleviate the strong pressure can occur? I don't know why it took you 150 pages to agree to this, considering it is the driving force behind all the studies you cite.

Yet, these are cases where 1) there are multiple selection pressures (a single strong and many weak) and 2) evolution proceeds fairly quickly. Doesn't that violate your theory that combination selection pressures always slow evolution, Kleinman?


This is why I raised the question which you have refused to answer.
No. I answered it four times already. You are either illiterate, stupid, or purposefully trying to mislead readers with childish debate tactics. Which one is it, Kleinman? I will answer your question again, for the fifth time, but I predict you will try to pull the same stunt.

If a person with HIV can not mount a humoral response against the virus, will that person have a better response to RT and PI treatment than someone who can mount a humoral response against the virus?

NO, BECAUSE AS YOUR STUDIES SHOW CERTAIN COMBINATIONS OF PRESSURES CAN SLOW EVOLUTION.

[kleinman]

So ... if there is a strong selection pressure and multiple weak selection pressures, rapid evolution to alleviate the strong pressure can occur? I don't know why it took you 150 pages to agree to this, considering it is the driving force behind all the studies you cite.
The point you continue to miss is that weak selection pressures don’t help the evolution of the strong selection pressures. At best, they don’t interfere sufficiently to markedly slow or stop the evolutionary process. As soon as you have additional selection pressures of sufficient strength, they interfere with each others movement of the population on the fitness landscape, that’s the point of the studies cited.

If a person with HIV can not mount a humoral response against the virus, will that person have a better response to RT and PI treatment than someone who can mount a humoral response against the virus?NO, BECAUSE AS YOUR STUDIES SHOW CERTAIN COMBINATIONS OF PRESSURES CAN SLOW EVOLUTION.
Rocketdodger, perhaps you want to try to take up joobz and Paul’s banner and argue that selection pressures somehow cooperate with each other to accelerate the evolutionary process? Show us examples of combination selection pressures which do not slow evolution.

If you don’t want to take on that question, perhaps you would like to explain to us how a gene evolves de novo?

[rocketdodger]

The point you continue to miss is that weak selection pressures don’t help the evolution of the strong selection pressures.

No, I am not missing that point, because I have never said anything, or even implied anything, to the contrary. You are simply, once again, using a cheap debate tactic -- inserting obvious facts and trying to make it seem like we claim otherwise, in the hopes that it will make us look stupid. That only works with idiots, Kleinman.


At best, they don’t interfere sufficiently to markedly slow or stop the evolutionary process.
As soon as you have additional selection pressures of sufficient strength, they interfere with each others movement of the population on the fitness landscape, that’s the point of the studies cited.

If you believe that, then wtf was the point to this entire thread? This is exactly what we have been trying to tell you. Well... I am glad we are done with all of that...

Rocketdodger, perhaps you want to try to take up joobz and Paul’s banner and argue that selection pressures somehow cooperate with each other to accelerate the evolutionary process?

Here is another cheap debate tactic -- once on the retreat (as evidenced by Kleinman's above admission) try to change the topic as fast as possible!

Guess what Kleinman -- I won't bite. I don't wish to discuss joobz and Paul's banner right now. Fail. Try again.

Show us examples of combination selection pressures which do not slow evolution.

Human pathogenic bacteria evolving resistance to penicillin.

HIV evolving resistance to drugs used against it.

Weeds evolving resistance to herbicides.

etc.

etc.

etc.


If you don’t want to take on that question, perhaps you would like to explain to us how a gene evolves de novo?

Another attempt at diverting everyone's attention to the gaping flaw in your argument that I am exposing -- I don't care about de novo evolution, I don't even really know wtf it means. Fail. Try again.

[kleinman]

The point you continue to miss is that weak selection pressures don’t help the evolution of the strong selection pressures.No, I am not missing that point, because I have never said anything, or even implied anything, to the contrary. You are simply, once again, using a cheap debate tactic -- inserting obvious facts and trying to make it seem like we claim otherwise, in the hopes that it will make us look stupid. That only works with idiots, Kleinman.
No tricks here, nothing up my sleeves, just plain old mathematics and empirical evidence which substantiates the mathematics.
At best, they don’t interfere sufficiently to markedly slow or stop the evolutionary process. As soon as you have additional selection pressures of sufficient strength, they interfere with each others movement of the population on the fitness landscape, that’s the point of the studies cited.If you believe that, then wtf was the point to this entire thread? This is exactly what we have been trying to tell you. Well... I am glad we are done with all of that...
Rocketdodger, didn’t you notice the title of the thread, I’m here to annoy evolutionists with the mathematical and empirical evidence of how mutation and selection actually works. Annoying evolutionists with the mathematical and empirical facts of how mutation and selection actually works is an ongoing project.
Rocketdodger, perhaps you want to try to take up joobz and Paul’s banner and argue that selection pressures somehow cooperate with each other to accelerate the evolutionary process?Here is another cheap debate tactic -- once on the retreat (as evidenced by Kleinman's above admission) try to change the topic as fast as possible!

Guess what Kleinman -- I won't bite. I don't wish to discuss joobz and Paul's banner right now. Fail. Try again.
The only thing I admit is that you understand enough about mutation and selection to not take up this challenge since it is both mathematically and empirically impossible. Selection pressures to do not cooperate. Mutation and selection simply does not work that way. Don’t confuse low budget with cheap.
Show us examples of combination selection pressures which do not slow evolution.Human pathogenic bacteria evolving resistance to penicillin. HIV evolving resistance to drugs used against it. Weeds evolving resistance to herbicides. etc. etc. etc.
Rocketdodger, you and Adequate need to go on tour and tell infectious disease experts, farmers, etc. etc. etc., that combination selection pressures do not slow the evolutionary process. Oh, that’s right, you say only certain combinations of selection pressures slow the evolutionary process, all the rest of the selection pressures are hard at work turning reptiles into birds.
If you don’t want to take on that question, perhaps you would like to explain to us how a gene evolves de novo?Another attempt at diverting everyone's attention to the gaping flaw in your argument that I am exposing -- I don't care about de novo evolution, I don't even really know wtf it means. Fail. Try again.
What? Genes have to come from somewhere. De novo means from the beginning. How do genes initially appear? What is the mutation and selection process that bring about a gene that does not exist?

Anyway, the only gaping flaw is the one in the theory of evolution by mutation and selection, this hole in the theory is of Titanic proportions.

[Mr. Scott]

Dr. Kleinman,

You keep propping up that strawman about reptiles turning into birds, but I don't think you've answered without evasion a comment I posed earlier.

The idea that reptiles evolved into birds in tiny steps over millions of years poses no problem at all for evolutionists. Birds have scales on their legs and feet that are quite a bit like reptile's. I've learned that a single point mutation will cause the scales on bird feet to develop as feathers. One single point mutation. It's also been found that soft tissue collagen in dinosaur bones closely matches modern bird's and little else. My question is: How do you account for the massive amount of DNA and fossil records that consistently support Darwin's theory of evolution? Why did god create life that looked exactly as if it had evolved with him? Why would he design bird DNA so that a single point mutation turns a bird's scales to feathers?

[rocketdodger]

Rocketdodger, didn’t you notice the title of the thread, I’m here to annoy evolutionists with the mathematical and empirical evidence of how mutation and selection actually works. Annoying evolutionists with the mathematical and empirical facts of how mutation and selection actually works is an ongoing project.

TRANSLATION: "I have no good response to your statement rocketdodger, so instead I will try to cut my losses with humor."

I actually don't need to reply to anything else. You have demonstrated, just now, that you either a) are an idiot or b) take none of this seriously. In either case, the only reason we are here now is to toy with you. Have fun wasting your time looking for more references "Dr."

[kleinman]

Rocketdodger, didn’t you notice the title of the thread, I’m here to annoy evolutionists with the mathematical and empirical evidence of how mutation and selection actually works. Annoying evolutionists with the mathematical and empirical facts of how mutation and selection actually works is an ongoing project.TRANSLATION: "I have no good response to your statement rocketdodger, so instead I will try to cut my losses with humor."
I think what I have and will continue to say about mutation and selection doesn’t need translation. They are mathematically and empirically clear. If you want to think that somehow only some combinations of selection pressures slow the evolutionary process while others don’t that’s fine, it just doesn’t have any mathematical or empirical basis.
I actually don't need to reply to anything else. You have demonstrated, just now, that you either a) are an idiot or b) take none of this seriously. In either case, the only reason we are here now is to toy with you. Have fun wasting your time looking for more references "Dr."
So far, the only responses you have given are mathematically and empirically baseless. You try to claim that the citations posted show that combination selection pressures do not slow evolution. You have qualified yourself for both a) and b). I do have fun looking for references which show how mutation and selection actually works. It’s not a waste of time correcting the strange interpretation that evolutionists have put on this phenomenon. It’s too important to leave the description of this phenomenon to evolutionists like you. If fact, here are a couple more citations for you to consider.
http://jcm.asm.org/cgi/reprint/43/1/208.pdf (http://jcm.asm.org/cgi/reprint/43/1/208.pdf)
Infection with cytomegalovirus (CMV) remains a significant cause of morbidity and mortality among hematopoietic cell transplant (HCT) recipients. We describe two pediatric HCT recipients who developed persistent and severe drug-resistant CMV infections. CMV resistance to foscarnet and ganciclovir was detected after only 6 and 11 weeks of therapy, respectively. Viral pol mutations associated with drug resistance in these patients included T838A (a novel mutation) and D588N, which were shown by marker transfer to confer foscarnet and multidrug resistance, respectively. Each of these mutations significantly reduced in vitro replication of CMV, suggesting that they may decrease viral fitness. This finding was further supported by the disappearance of mutations upon withdrawal of antiviral pressure in one patient. Novel antivirals or combination therapy may be required for the treatment of drug-resistant CMV in HCT recipients and perhaps in other severely immunocompromised patients.
And
The clinical settings in which combination anti-CMV therapy should be used remain to be established. The observation of attenuated growth in viruses with resistant genotypes (such as the T838A and D588N pol mutations seen here) may help to explain the reported superior clinical efficacy of combination therapy compared with single-agent anti-CMV therapy (21), even when one of the agents appears to have lost its activity against CMV (29). Maintaining therapy with the drug to which resistance has developed could be beneficial if the drug selects for growth-impaired genotypes. Novel antivirals with different mechanisms of action, when they become available, may provide another option for the treatment of resistant CMV.
http://www3.interscience.wiley.com/cgi-bin/abstract/112773693/ABSTRACT?CRETRY=1&SRETRY=0 (http://www3.interscience.wiley.com/cgi-bin/abstract/112773693/ABSTRACT?CRETRY=1&SRETRY=0)
Multi-drug resistant hepatitis B virus (HBV) has been reported in hepatitis B patients who received sequential antiviral therapy. In vitro studies showed that HBV constructs with mutations resistant to lamivudine and adefovir have marked reduction in sensitivity to combination of lamivudine and adefovir, whereas constructs with mutations resistant to either drug remain sensitive to the other drug. We conducted this study to determine whether mutations conferring resistance to multiple antiviral agents co-locate on the same HBV genome in vivo and to describe the evolution of these mutations. Sera from six patients who had been found to have multi-drug resistant HBV mutations to lamivudine + adefovir, lamivudine + hepatitis B immunoglobulin (HBIG), or lamivudine + entecavir on direct sequencing were cloned after nested polymerase chain reaction (PCR). Analysis of 215 clones from 11 samples with multi-drug resistant mutations on direct sequencing showed that 183 (85%) clones had mutations to both therapies on the same genome; 31 clones had lamivudine-resistant mutants only. Clonal analysis of serial samples from three patients showed progressive evolution from all clones with lamivudine-resistant HBV mutations only to mixtures of clones that have multi-drug resistant mutations and clones that have lamivudine-resistant HBV mutations only, and ultimately all clones having multi-drug resistant HBV mutations. In conclusion, mutations conferring resistance to multiple antiviral agents co-locate on the same viral genome, suggesting that combination therapy directed against mutants resistant to each treatment may not be adequate in suppressing multi-drug resistant HBV. De novo combination therapy may prevent the emergence of multi-drug resistant mutants. (HEPATOLOGY 2006;44:703-712.)
http://www.springerlink.com/content/8370414px3523672/ (http://www.springerlink.com/content/8370414px3523672/)
Abstract The treatment of chronic hepatitis C is currently based on the pegylated interferon alpha and ribavirin combination. Despite this treatment, a significant number of patients still fail to eradicate the virus. The mechanisms underlying this failure are unknown, but indirect evidence suggests that chronic infection is associated with phenomena that protect hepatitis C virus (HCV) from the antiviral action of interferon alpha and hinder the clearance of infected cells. Viral factors responsible for true "HCV resistance" probably play a partial role. Numerous new HCV drugs are currently at the developmental stage. It is foreseeable that specific HCV inhibitors will select resistant viral variants. As a result, combination therapy will probably become the standard of care in chronic hepatitis C.
http://jac.oxfordjournals.org/cgi/content/full/55/4/413 (http://jac.oxfordjournals.org/cgi/content/full/55/4/413)
The clinical goals of HIV treatment are optimally accomplished through consistent high-level adherence to highly active antiretroviral therapy (HAART) and durable suppression of the viral load. However, as a result of the need for lifelong therapy and HIV's prodigious replication rate and error-prone reverse transcriptase, varying amounts of antiretroviral drug resistance are common in treated individuals. Medication adherence is linked to the development of drug resistance, although not by a simple linear relationship. Recent studies have suggested that extensive drug resistance is not a major determinant of HIV disease progression and death. Rather, failure to access care and discontinuation of or non-adherence with therapy are arguably the most important factors associated with HIV disease progression in the HAART era. Other data indicate that continued therapy in the setting of extensive drug resistance and the inability to achieve viral suppression can provide continued clinical benefit. Such benefit may be mediated, at least partially, by reductions in viral fitness associated with drug resistance mutations.
And
The data above were obtained during a period of rapid change in the treatment of HIV-infected individuals, including the introduction of a large number of drugs and growing expertise among clinicians, and therefore cannot be extrapolated to the future. However, an argument can be made that HIV-infected individuals who are entering care currently will be less likely to acquire as much drug resistance (or least to acquire it as rapidly) as those treated in the 1990s because of the exclusive use of combination drug therapy.1 Many HIV-infected individuals who were in care throughout the 1990s were sequentially exposed to NRTI monotherapy, dual therapy, and finally to PI and NNRTI—essentially a boot camp for HIV drug resistance.
There you go rocketdodger, let’s see you twist these citations to say that combination therapy doesn’t profoundly slow the evolutionary process by mutation and selection. Oh, that’s right, only some combination selection pressures profoundly slow the evolutionary process, others accelerate the process, don’t they rocketdodger? Hey rocketdodger, you want to know something else, I had fun finding these citations.

[rocketdodger]

Kleinman's obstacle:

a) All of the studies cited are predicated on the documented existence of the rapid evolution of resistance to human drugs/poisons/herbicides in many populations.

b) The conditions that lead to this rapid evolution are best characterized by a dominant selective pressure (the drug/poison/herbicide) against the pre-existing background of numerous relatively weaker selective pressures.

c) This directly contradicts Kleinman's claim that multiple selective pressures always slow the evolutionary process, or more formally, his claim that any evolutionary rate (in any direction) under n selective pressures will be greater than the rate (in any direction) under n + 1 pressures.

d) In all the cited cases, we have a group of n pressures, under which evolution is relatively slow, to which we add a single dominant pressure (the drug/poison/herbicide) and the result is rapid evolution of resistance.

Kleinman's solutions or "how to pound a square peg into a round hole":

a) Claim that even though the studies explicitly detail the evolution of resistance that they in fact do not.
a) Claim that even though this evolution occurs inside of a human lifetime that it in fact is not "rapid."
a) Claim that all of these populations would have in fact developed the resistances in the absence of drugs/poisons/herbicides.

b) Claim that all naturally occuring populations are in fact never under any selective pressures at all.
b) Claim that all naturally occuring populations are completely stationary at a local optimum at all times.
b) Claim that all naturally occuring populations are only under the influence of stabilizing selective pressures.
b) Claim that all weak selective pressures must be stabilizing selective pressures.

c/d) Claim that any existing group of multiple selective pressures must in fact be stabilizing selective pressures.
c/d) Claim that any selective pressure added to an existing group must be a directional selective pressure, even if it is a stabilizing selective pressure.
c/d) Claim that the case of a single relatively strong selective pressure combined with multiple weak selective pressures is impossible in reality, despite the fact that it is the base case for the very argument Kleinman uses and one can find mention of it in every single abstract Kleinman has posted in this thread.

[Belz...]

Now wait just a minute, didn’t abiogenesis occur in the primordial slime?

Are you trying to be clever again and failing miserably ?

Are you an abiogeneholic?

Well, coming from someone who believes a mythical god waved his hand after an eternity of boredom and created a universe for who-knows-what reason, magically, violating all the known laws of physics, and created humans even knowing they'd piss him off and he'd have to create an eternal hell for them, I'll take that as a compliment.

Yes I did Belz, but I have been censored for using that terminology.

Good, so you admit to calling others names. Oh my, an creationist resorts to name calling.

You beggaminasesarians think you can describe mutation and selection without mathematics.

There's that straw army, again. I never said you can. I said that mathematics don't always translate into reality. Again, think of a 5411984-dimensional object. Possible in math, not so in reality.

That’s a good technique for writing mythology but not very good if you are claiming scientific method.

Well, coming from someone who believes a mythical god waved his hand after an eternity of boredom and created a universe for who-knows-what reason, magically, violating all the known laws of physics, and created humans even knowing they'd piss him off and he'd have to create an eternal hell for them, I'll take that as a compliment.

Don’t worry Belz, you evolutionarians, abiogeneholics and beggaminasesarians can always find work on the SciFi channel.

It's already better than working at answersingenesis.com.

[Belz...]

The point you continue to miss is that weak selection pressures don’t help the evolution of the strong selection pressures. At best, they don’t interfere sufficiently to markedly slow or stop the evolutionary process.

Yes, that is precisely what we're saying.

The strong one makes the weak ones less relevant.

Think "meteor".

As soon as you have additional selection pressures of sufficient strength, they interfere with each others movement of the population on the fitness landscape, that’s the point of the studies cited.

And how can you be sure of the relative strength of the various pressures, eh ?

Annoying evolutionists with the mathematical and empirical facts of how mutation and selection actually works is an ongoing project.

That's called trolling. If you really believed what you say, you'd be doing something to change the scientific community's opinion on this subject. But you'd rather bask in the attention you're getting on an internet forum.

Despicable.

Selection pressures to do not cooperate.


http://forums.randi.org/imagehosting/thum_608045fd3d3d0d455.jpg (http://forums.randi.org/vbimghost.php?do=displayimg&imgid=4646)

[Belz...]

Rocketdodger, you and Adequate need to go on tour and tell infectious disease experts, farmers, etc. etc. etc., that combination selection pressures do not slow the evolutionary process.

What's funny is how you http://forums.randi.org/imagehosting/608045fd3950b30f8.gif (http://forums.randi.org/vbimghost.php?do=displayimg&imgid=4645) the topic once Rocketdodger answers your question with examples.

Oh, that’s right, you say only certain combinations of selection pressures slow the evolutionary process, all the rest of the selection pressures are hard at work turning reptiles into birds

Are those teeth, Klein ?

http://forums.randi.org/imagehosting/thum_608047022eae7e563.jpg (http://forums.randi.org/vbimghost.php?do=displayimg&imgid=8609)

What? Genes have to come from somewhere. De novo means from the beginning. How do genes initially appear? What is the mutation and selection process that bring about a gene that does not exist?

Read a book.

I think what I have and will continue to say about mutation and selection doesn’t need translation.

And you're about to be the only person who'll post in this thread.

Why ? You've already lost.

[Belz...]

Why did god create life that looked exactly as if it had evolved with him?

Because he's a sick prankster who enjoys ******* with our minds. ;)

[Belz...]

a) Claim that even though the studies explicitly detail the evolution of resistance that they in fact do not.
a) Claim that even though this evolution occurs inside of a human lifetime that it in fact is not "rapid."
a) Claim that all of these populations would have in fact developed the resistances in the absence of drugs/poisons/herbicides.

b) Claim that all naturally occuring populations are in fact never under any selective pressures at all.
b) Claim that all naturally occuring populations are completely stationary at a local optimum at all times.
b) Claim that all naturally occuring populations are only under the influence of stabilizing selective pressures.
b) Claim that all weak selective pressures must be stabilizing selective pressures.

c/d) Claim that any existing group of multiple selective pressures must in fact be stabilizing selective pressures.
c/d) Claim that any selective pressure added to an existing group must be a directional selective pressure, even if it is a stabilizing selective pressure.
c/d) Claim that the case of a single relatively strong selective pressure combined with multiple weak selective pressures is impossible in reality, despite the fact that it is the base case for the very argument Kleinman uses and one can find mention of it in every single abstract Kleinman has posted in this thread.

I'd like to use Occam's razor on those assumptions, please.

I'm reminded of other such cop-outs.

a) claim that, somehow, same cures same
b) claim that, somehow, dilution increases potency
c) claim that, somehow, water 'memorises' other molecules
d) claim that, perhaps, physics aren't well understood enough
e) claim that, of course, the cited patients aren't deluded

Ugh.

[Paul C. Anagnostopoulos]

Paul, you have a big blind spot here. Dr Schneider has designed three selection conditions to evolve particular sequences of bases. It takes huge numbers of generations to satisfy all three conditions simultaneously while any one of the selection conditions can be evolved in trivially small numbers of generations even when ev shows no sign of converging the longer genome lengths using all three selection conditions. If you want to argue against the obvious, be my guest.
What's obvious is that you refuse to acknowledge that different functions are evolving when the selection conditions are taken in different combinations.

Also, you do realize that the idea that there are three selection conditions came long after Schneider wrote the original Ev, right?

Then why don’t you tell us again what is the basis of selection for ev? Didn’t you say that Rfrequency and Rsequence have nothing to do with selection in the model? Let’s give your actual quote.

The problem with using Rs > Rf as the test, rather than the perfect creature, is that there is no selection pressure to reach Rs > Rf. There is only pressure to reach a perfect creature. There is no Rs > Rf selection pressure in nature, either.
The selection in ev is dependent on matches of the weight matrix with particular sequences of bases. In particular areas of the genome, matches give mistakes and in other areas of the genome, the lack of matches gives mistakes. Any one of the selection conditions can be easily satisfied in a tiny number of generations; it is only when ev tries to evolve all three selection conditions simultaneously that the process becomes profoundly slow. And guess what Paul, mutation and selection works that way in reality.
What does this have to do with the fact that you are comparing the evolution of two different functions when you adjust the selection conditions?

~~ Paul

[Paul C. Anagnostopoulos]

Dr Schneider’s model is based on three selection conditions. One condition is that if a binding site is not located where it should be found, it is counted as a mistake. The second condition is if a binding site is found in the gene area it is counted as a mistake. And the third selection condition is if a binding site is found in the nonbinding site region of the genome, it is considered a mistake.
Shalamar, this division of the pressures into three types is entirely arbitrary, and was done long after Schneider wrote the first version of Ev. It was done is response to a criticism that Ev's selection process was too rigid.


If you take the ev model and Dr Schneider’s published case and increase the genome length, you will find that the number of generations to converge the three selection conditions becomes huge. This is a fundamental property of optimization problems. As you increase the size of the search space for your optimum solution, the process becomes profoundly slower but this is not the main reason why convergence becomes so slow. It is the multiple selection conditions which slows the process so profoundly. This can easily be verified by running ev with two of the three selection pressures set to zero. The remaining selection pressure can be satisfied in trivially small numbers of generations.
Note, Shalamar, that when you run a model with only one of the three selection conditions active, you are not evolving the same function as when all three conditions are active. Comparing the number of generations between the two models seems a bit dicey.


This suggests that the durability of viral inhibition can be increased by combining indinavir with one or more inhibitors of the reverse transcriptase, suppressing the viral replication that drives the evolution of resistance.
Note, Shalamar, that this experiment involves introducing specific chemicals with known effects on the virus. As I said above:

If a bunch of selection pressures are rigged or happen to work out just right, they can significantly increase the time it takes an organism to adapt to them, or possibly cause extinction.

~~ Paul

[Paul C. Anagnostopoulos]

Rocketdodger, perhaps you want to try to take up joobz and Paul’s banner and argue that selection pressures somehow cooperate with each other to accelerate the evolutionary process?
Where did I say this? Please quote the post where I make this claim. That must mean that I've also claimed that the 3-pressure model evolves faster than the 1-pressure model, but I don't think I have.

~~ Paul

[kleinman]

Kleinman's obstacle:
At least I have a mathematical and empirical ladder which overcomes my obstacles. What do you have to overcome your obstacles, irrational extrapolation and speculation?
a) All of the studies cited are predicated on the documented existence of the rapid evolution of resistance to human drugs/poisons/herbicides in many populations.
Get it right rocketdodger, which is rapid evolution of resistance to single human drugs/poisons/herbicides in every example cited. When more than single drugs/poisons/herbicides are used, the ability of the population to evolve resistance to all drugs/poisons/herbicides simultaneously is markedly hindered.
b) The conditions that lead to this rapid evolution are best characterized by a dominant selective pressure (the drug/poison/herbicide) against the pre-existing background of numerous relatively weaker selective pressures.
That’s correct and rocketdodger’s obstacle here is to show that the presence of the weaker selection pressures somehow help lead to this rapid evolution of a single dominant selective pressure. The mathematical and empirical evidence show that the weaker selection pressures do not help speed up the evolution of dominant or any other selection pressures. Each selection pressure is pushing the population on a particular trajectory on the fitness landscape. Eliminating weaker selection pressures as done with in vitro experiments shows that these dominant single selection pressures evolve more quickly. There is no way that adding more selection conditions speeds up the sort for beneficial and detrimental mutations.
c) This directly contradicts Kleinman's claim that multiple selective pressures always slow the evolutionary process, or more formally, his claim that any evolutionary rate (in any direction) under n selective pressures will be greater than the rate (in any direction) under n + 1 pressures.
Rocketdodger could draw this conclusion if a) and b) were true, but they aren’t.
d) In all the cited cases, we have a group of n pressures, under which evolution is relatively slow, to which we add a single dominant pressure (the drug/poison/herbicide) and the result is rapid evolution of resistance.
Rocketdodger could make this argument if all n + 1 conditions were evolving simultaneously, but they are not. Only the single dominant selection condition is evolving with some background noise from the weaker selection conditions which slow the population in evolving this single dominant selection condition.
Kleinman's solutions or "how to pound a square peg into a round hole":
Oh no rocketdodger, I am pounding the theory of evolution into a six foot hole.
Now wait just a minute, didn’t abiogenesis occur in the primordial slime?Are you trying to be clever again and failing miserably ?
Life is like that, we must learn to overcome our failings, when are you evolutionists going to realize you have a failed theory.
Are you an abiogeneholic?Well, coming from someone who believes a mythical god waved his hand after an eternity of boredom and created a universe for who-knows-what reason, magically, violating all the known laws of physics, and created humans even knowing they'd piss him off and he'd have to create an eternal hell for them, I'll take that as a compliment.
This is coming from someone who calls himself the “fiend god”.
Yes I did Belz, but I have been censored for using that terminology.Good, so you admit to calling others names. Oh my, an creationist resorts to name calling.
Yes Belz, I confess I called you evolutionists “mathematically challenged”, I apologize to all you non-evolutionists who are “mathematically challenged”. Perhaps we can design a twelve step program for you evolutionists to overcome your deficiency? Oh no, that will never work, you have to be able to count to twelve.
You beggaminasesarians think you can describe mutation and selection without mathematics.There's that straw army, again. I never said you can. I said that mathematics don't always translate into reality. Again, think of a 5411984-dimensional object. Possible in math, not so in reality.
Don’t forget to include Dr Schneider and the peer reviewers at Nucleic Acids Research in that army. You are correct about a 5411984-dimensional object. Possible in math, not so in reality. Just as evolving a 5411984-selection condition fitness landscape, not possible in math, not so in reality. Look at what it takes to evolve a 3-selection condition fitness landscape. Mutation and selection is a profoundly slow sorting mechanism when you have more than a single selection condition.
As soon as you have additional selection pressures of sufficient strength, they interfere with each others movement of the population on the fitness landscape, that’s the point of the studies cited.And how can you be sure of the relative strength of the various pressures, eh ?
You can be sure of the strength of the various pressures when they are zero, see what happens in ev when you set two of the three selection conditions to zero. Also, many of the citations posted are examples of in vitro mutation and selection processes where these weaker selection pressures are eliminated and the strong selection condition evolves more quickly under these conditions.
Annoying evolutionists with the mathematical and empirical facts of how mutation and selection actually works is an ongoing project.That's called trolling. If you really believed what you say, you'd be doing something to change the scientific community's opinion on this subject. But you'd rather bask in the attention you're getting on an internet forum.

Despicable.
Now what is wrong with using the James Randi Educational forum to change the scientific community’s opinion on this subject? You wouldn’t be using this thread to advertise “Current avatar from jaestudio.com”. How disgracefully capitalistic!
Paul, you have a big blind spot here. Dr Schneider has designed three selection conditions to evolve particular sequences of bases. It takes huge numbers of generations to satisfy all three conditions simultaneously while any one of the selection conditions can be evolved in trivially small numbers of generations even when ev shows no sign of converging the longer genome lengths using all three selection conditions. If you want to argue against the obvious, be my guest.What's obvious is that you refuse to acknowledge that different functions are evolving when the selection conditions are taken in different combinations.

Also, you do realize that the idea that there are three selection conditions came long after Schneider wrote the original Ev, right?
Paul, you keep trying to call the evolution of particular sequences of bases a function. These selection conditions are simply based on matches with the weigh matrix. In some cases the matches are considered errors and in other cases the lack of matches are considered errors. There is no function being evolved in this sorting problem.

Lot’s of thing have come along since Dr Schneider wrote the original ev and they show how the mutation and selection process actually works.
Then why don’t you tell us again what is the basis of selection for ev? Didn’t you say that Rfrequency and Rsequence have nothing to do with selection in the model? Let’s give your actual quote.The problem with using Rs > Rf as the test, rather than the perfect creature, is that there is no selection pressure to reach Rs > Rf. There is only pressure to reach a perfect creature. There is no Rs > Rf selection pressure in nature, either.The selection in ev is dependent on matches of the weight matrix with particular sequences of bases. In particular areas of the genome, matches give mistakes and in other areas of the genome, the lack of matches gives mistakes. Any one of the selection conditions can be easily satisfied in a tiny number of generations; it is only when ev tries to evolve all three selection conditions simultaneously that the process becomes profoundly slow. And guess what Paul, mutation and selection works that way in reality.What does this have to do with the fact that you are comparing the evolution of two different functions when you adjust the selection conditions?
Paul, ev is not evolving any kind of function. Ev is a sorting algorithm based on matches with a weight matrix. What ev shows is that sorting on a single condition is much easier than sorting on three conditions.
Dr Schneider’s model is based on three selection conditions. One condition is that if a binding site is not located where it should be found, it is counted as a mistake. The second condition is if a binding site is found in the gene area it is counted as a mistake. And the third selection condition is if a binding site is found in the nonbinding site region of the genome, it is considered a mistake.Shalamar, this division of the pressures into three types is entirely arbitrary, and was done long after Schneider wrote the first version of Ev. It was done is response to a criticism that Ev's selection process was too rigid.
Paul, you made this “arbitrary” division. Make some other arbitrary division and see if you can change the behavior of this sorting algorithm. I wonder if you will ever acknowledge that your “arbitrary” division show exactly how the mutation and selection process works?
If you take the ev model and Dr Schneider’s published case and increase the genome length, you will find that the number of generations to converge the three selection conditions becomes huge. This is a fundamental property of optimization problems. As you increase the size of the search space for your optimum solution, the process becomes profoundly slower but this is not the main reason why convergence becomes so slow. It is the multiple selection conditions which slows the process so profoundly. This can easily be verified by running ev with two of the three selection pressures set to zero. The remaining selection pressure can be satisfied in trivially small numbers of generations.Note, Shalamar, that when you run a model with only one of the three selection conditions active, you are not evolving the same function as when all three conditions are active. Comparing the number of generations between the two models seems a bit dicey.
Note, Shalamar, Paul is trying to say that ev evolves some type of function, it does not. Ev is simply a sorting algorithm that works much more quickly when sorting on a single selection condition then when trying to sort on all three selection conditions simultaneously. Note something else Shalamar, the empirical evidence of mutation and selection shows the same thing, read the hundreds of citations posted which shows the mathematical behavior of mutation and selection is substantiated by the real behavior of mutation and selection.
This suggests that the durability of viral inhibition can be increased by combining indinavir with one or more inhibitors of the reverse transcriptase, suppressing the viral replication that drives the evolution of resistance.Note, Shalamar, that this experiment involves introducing specific chemicals with known effects on the virus. As I said above:

If a bunch of selection pressures are rigged or happen to work out just right, they can significantly increase the time it takes an organism to adapt to them, or possibly cause extinction.
Note, Shalamar, Paul’s own computer model must have been rigged because it shows the same behavior.
Rocketdodger, perhaps you want to try to take up joobz and Paul’s banner and argue that selection pressures somehow cooperate with each other to accelerate the evolutionary process?Where did I say this? Please quote the post where I make this claim. That must mean that I've also claimed that the 3-pressure model evolves faster than the 1-pressure model, but I don't think I have.
Paul, do you think that only “rigged” selection pressures interfere with the mutation and selection sorting process?

Since Paul is still having difficulty coming to grips with what his own mathematical is showing, let’s review this citation in more detail.
http://jac.oxfordjournals.org/cgi/content/full/55/4/413 (http://jac.oxfordjournals.org/cgi/content/full/55/4/413)
The clinical goals of HIV treatment are optimally accomplished through consistent high-level adherence to highly active antiretroviral therapy (HAART) and durable suppression of the viral load. However, as a result of the need for lifelong therapy and HIV's prodigious replication rate and error-prone reverse transcriptase, varying amounts of antiretroviral drug resistance are common in treated individuals. Medication adherence is linked to the development of drug resistance, although not by a simple linear relationship. Recent studies have suggested that extensive drug resistance is not a major determinant of HIV disease progression and death. Rather, failure to access care and discontinuation of or non-adherence with therapy are arguably the most important factors associated with HIV disease progression in the HAART era. Other data indicate that continued therapy in the setting of extensive drug resistance and the inability to achieve viral suppression can provide continued clinical benefit. Such benefit may be mediated, at least partially, by reductions in viral fitness associated with drug resistance mutations.
And
The data above were obtained during a period of rapid change in the treatment of HIV-infected individuals, including the introduction of a large number of drugs and growing expertise among clinicians, and therefore cannot be extrapolated to the future. However, an argument can be made that HIV-infected individuals who are entering care currently will be less likely to acquire as much drug resistance (or least to acquire it as rapidly) as those treated in the 1990s because of the exclusive use of combination drug therapy.1 Many HIV-infected individuals who were in care throughout the 1990s were sequentially exposed to NRTI monotherapy, dual therapy, and finally to PI and NNRTI—essentially a boot camp for HIV drug resistance.
Note that this author understands empirically how the mutation and selection process works. When initial attempts at treatment of HIV were initiated in the 1990s sequential monotherapy was initially tried which quickly failed, then dual therapy was used which was a little more successful then finally PI and NNRTI therapy was used. This process led to the rapid evolution of resistant viruses until triple therapy was initiated.

This pattern is seen over and over in numerous examples of mutation and selection. Whether it is the evolution of multi-drug resistant Gonorrhea, TB, MRSA, Malaria, weeds, insects…, it is far easier for a population to evolve resistance against a single selection pressure than multiple selection pressures simultaneously. This is the mathematical and empirical fact of how the mutation and selection sorting problem works.

[Darat]

...snip..

This pattern is seen over and over in numerous examples of mutation and selection. Whether it is the evolution of multi-drug resistant Gonorrhea, TB, MRSA, Malaria, weeds, insects…, it is far easier for a population to evolve resistance against a single selection pressure than multiple selection pressures simultaneously. This is the mathematical and empirical fact of how the mutation and selection sorting problem works.

All of the above examples of evolution have occurred in environments where there were simultaneous multiple selection pressures.

[kleinman]

...snip..

This pattern is seen over and over in numerous examples of mutation and selection. Whether it is the evolution of multi-drug resistant Gonorrhea, TB, MRSA, Malaria, weeds, insects…, it is far easier for a population to evolve resistance against a single selection pressure than multiple selection pressures simultaneously. This is the mathematical and empirical fact of how the mutation and selection sorting problem works.All of the above examples of evolution have occurred in environments where there were simultaneous multiple selection pressures.
Darat, consider what happens with weak selection pressures. If they are stabilizing pressures such as those which prevent genetic sequences from diverging too far so that the enzymes produced no longer function, these types of selection pressures do not move a population on a trajectory on the fitness landscape, they are keeping the population at that local optimum. If they are directional selection pressures but weak, they do not affect the fitness of the population or change the frequency of particular genetic sequences by much. For example, let’s say the temperature which a population is subjected to is not the optimum temperature for the fitness of the population. Less fit individuals are selected out but as a whole, most individuals still can survive and reproduce. In order for this population to evolve, numerous temperature dependent enzymes must evolve simultaneously to sequences which function optimally at that temperature.

Now, subject this slightly less fit population to a single strong selection pressure. The thermal stress the population is subjected to does not help the population to evolve against this single strong selection pressure, in fact it hinders the population when compared to a population evolving against this same selection pressure but in a thermally optimum environment.

Selection pressures whether weak or strong do not help each other in the mutation and selection sorting process. The ability of a population to evolve against a single strong selection pressure in the presence of weak pressures doesn’t mean that the weak pressures are helping the population to evolve against the strong pressure. It only means that there are enough resources in the environment for the population to endure the weak selection pressures while still evolving against the single strong selection pressure.

[Belz...]

Life is like that, we must learn to overcome our failings, when are you evolutionists going to realize you have a failed theory.

You know, Klein, when I'm telling you that you are FAILING at being clever, the very LAST thing you should do is to take that and try to sound clever, again.

This is coming from someone who calls himself the “fiend god”.

Yes, it is. And contrary to popular belief, I don't really think I'm the lord of Hell. You see, that's because I don't believe in any of that crap. I just like monster stories.

Unlike you, I can distinguish between fantasy and reality.

Yes Belz, I confess I called you evolutionists “mathematically challenged”, I apologize to all you non-evolutionists who are “mathematically challenged”. Perhaps we can design a twelve step program for you evolutionists to overcome your deficiency? Oh no, that will never work, you have to be able to count to twelve.

Well we already know YOU can't count passed two, because then that would profoundly slow your brain process.

Don’t forget to include Dr Schneider and the peer reviewers at Nucleic Acids Research in that army.

Are you STILL battling that old strawman ? I said NOT ALWAYS. Not NEVER.

You're either the densest man in the universe after Christophera, or you're being cruelly obtuse. I can see you still claiming that science will vindicate you on your deathbed.

You are correct about a 5411984-dimensional object. Possible in math, not so in reality. Just as evolving a 5411984-selection condition fitness landscape, not possible in math, not so in reality.

How can you, with a straight face (I assume), make an analogy between something that is true in mathematics but not in reality, and something that you claim is false BOTH in mathematics and in reality ? Or are you just trying to pick words form my sentences and sounding clever, again ?

Klein, you are NOT sounding clever. Not one bit.

Look at what it takes to evolve a 3-selection condition fitness landscape.

What relative strengths are we talking about, now, Klein ?

You can be sure of the strength of the various pressures when they are zero, see what happens in ev when you set two of the three selection conditions to zero.

Why the hell would I want to do that ? When is a selection pressure both extant and equal to zero ? That doesn't even make sense. I asked you a very real question and now you're back to talking about ev. I asked you how can you know what the relative strengths of selection pressures are, say, for dinosaurs evolving into birds over millions of years ? I certainly don't know what pressures were present before the big rock hit.

Now what is wrong with using the James Randi Educational forum to change the scientific community’s opinion on this subject?

"Why is it that complaining on the GameFaqs forums hasn't changed anything about the way they make video games ?"

How disgracefully capitalistic!

I don't think anyone found that one clever, except you, Klein.

[rocketdodger]

The ability of a population to evolve against a single strong selection pressure in the presence of weak pressures doesn’t mean that the weak pressures are helping the population to evolve against the strong pressure.

Not once, in this entire thread, has anyone claimed such a thing.

You have repeatedly, however, tried to put those words into our mouths, in order to prevent yourself from looking like a fool. Too late.

You claimed "combination selection pressures profoundly slow evolution." We have shown you, over and over, examples of combination selection pressures under which evolution is not profoundly slowed. Your above statement admits that you understand this is possible:
The ability of a population to evolve against a single strong selection pressure in the presence of weak pressures . . .

If you want to wiggle words around and claim that " a single strong selection pressure in the presence of weak pressures " is NOT in fact a combination, but something else, then you will have to re-write every English dictionary on Earth.

[Paul C. Anagnostopoulos]

Paul, you keep trying to call the evolution of particular sequences of bases a function. These selection conditions are simply based on matches with the weigh matrix. In some cases the matches are considered errors and in other cases the lack of matches are considered errors. There is no function being evolved in this sorting problem.
Who cares if I call it a function, Alan? The gene performs a function: It matches the binding sites and no other sites. The point is that the function performed when all three selections are active is not the same function performed when only one is active.


Lot’s of thing have come along since Dr Schneider wrote the original ev and they show how the mutation and selection process actually works.
Nonetheless, you're still wrong when you say:

Dr Schneider has designed three selection conditions to evolve particular sequences of bases.


Paul, ev is not evolving any kind of function. Ev is a sorting algorithm based on matches with a weight matrix. What ev shows is that sorting on a single condition is much easier than sorting on three conditions.
Okay, then you are comparing two different sorting situations. :rolleyes:


Paul, you made this “arbitrary” division. Make some other arbitrary division and see if you can change the behavior of this sorting algorithm.
I didn't say I could. I'm simply correcting your erroneous statements.


Note, Shalamar, Paul is trying to say that ev evolves some type of function, it does not.
Certainly it does. Perhaps you have a strange definition of function in mind?


Note, Shalamar, Paul’s own computer model must have been rigged because it shows the same behavior.
And yet you still use it as the fundamental component of your argument.


Paul, do you think that only “rigged” selection pressures interfere with the mutation and selection sorting process?
No, that's why I said:

If a bunch of selection pressures are rigged or happen to work out just right, they can significantly increase the time it takes an organism to adapt to them, or possibly cause extinction.

But meanwhile, you didn't quote the post where I supposedly said that selection pressures somehow cooperate with each other to accelerate the evolutionary process. Could you quote that post, please?

~~ Paul

[kleinman]

Life is like that, we must learn to overcome our failings, when are you evolutionists going to realize you have a failed theory.You know, Klein, when I'm telling you that you are FAILING at being clever, the very LAST thing you should do is to take that and try to sound clever, again.
If at first you don’t succeed, try, try again.
This is coming from someone who calls himself the “fiend god”.Yes, it is. And contrary to popular belief, I don't really think I'm the lord of Hell. You see, that's because I don't believe in any of that crap. I just like monster stories.

Unlike you, I can distinguish between fantasy and reality.
We all live by faith Belz, the difference is in what you put your faith in.
Yes Belz, I confess I called you evolutionists “mathematically challenged”, I apologize to all you non-evolutionists who are “mathematically challenged”. Perhaps we can design a twelve step program for you evolutionists to overcome your deficiency? Oh no, that will never work, you have to be able to count to twelve. Well we already know YOU can't count passed two, because then that would profoundly slow your brain process.
Doesn’t that say something about how weak your theory is?
Don’t forget to include Dr Schneider and the peer reviewers at Nucleic Acids Research in that army.Are you STILL battling that old strawman ? I said NOT ALWAYS. Not NEVER.

You're either the densest man in the universe after Christophera, or you're being cruelly obtuse. I can see you still claiming that science will vindicate you on your deathbed.
I doubt I will be thinking about this topic on my deathbed, what will you be thinking about on your deathbed?
You are correct about a 5411984-dimensional object. Possible in math, not so in reality. Just as evolving a 5411984-selection condition fitness landscape, not possible in math, not so in reality.How can you, with a straight face (I assume), make an analogy between something that is true in mathematics but not in reality, and something that you claim is false BOTH in mathematics and in reality ? Or are you just trying to pick words form my sentences and sounding clever, again ?

Klein, you are NOT sounding clever. Not one bit.
But is it annoying?
Look at what it takes to evolve a 3-selection condition fitness landscape.What relative strengths are we talking about, now, Klein ?
What difference do the strengths of selection pressures have in the mutation and selection sorting process?
You can be sure of the strength of the various pressures when they are zero, see what happens in ev when you set two of the three selection conditions to zero.Why the hell would I want to do that ? When is a selection pressure both extant and equal to zero ? That doesn't even make sense. I asked you a very real question and now you're back to talking about ev. I asked you how can you know what the relative strengths of selection pressures are, say, for dinosaurs evolving into birds over millions of years ? I certainly don't know what pressures were present before the big rock hit.
No selection pressures, no evolution.
Now what is wrong with using the James Randi Educational forum to change the scientific community’s opinion on this subject?"Why is it that complaining on the GameFaqs forums hasn't changed anything about the way they make video games ?"
I’m not complaining, are you complaining?
How disgracefully capitalistic!I don't think anyone found that one clever, except you, Klein.
But was it annoying?
The ability of a population to evolve against a single strong selection pressure in the presence of weak pressures doesn’t mean that the weak pressures are helping the population to evolve against the strong pressure.Not once, in this entire thread, has anyone claimed such a thing.
So, what’s the problem?
You have repeatedly, however, tried to put those words into our mouths, in order to prevent yourself from looking like a fool. Too late.
I don’t have to put anything in your mouths.
You claimed "combination selection pressures profoundly slow evolution." We have shown you, over and over, examples of combination selection pressures under which evolution is not profoundly slowed. Your above statement admits that you understand this is possible:
Perhaps in your mathematically challenged mind you think this is true but you can’t twist the mathematical and empirical facts of how mutation and selection actually works. n + 1 selection conditions do not evolve faster than n selection conditions.
The ability of a population to evolve against a single strong selection pressure in the presence of weak pressures . . . If you want to wiggle words around and claim that " a single strong selection pressure in the presence of weak pressures " is NOT in fact a combination, but something else, then you will have to re-write every English dictionary on Earth.
It seems that rocketdodger is having trouble with words, perhaps if I repost a figure of what a population does on a fitness landscape would help clarify his confused thinking.
http://www.pnas.org/cgi/content/full/104/34/13711 (http://www.pnas.org/cgi/content/full/104/34/13711)
http://www.pnas.org/content/vol104/issue34/images/medium/zpq0310771490005.gif
Fig. 5. A schematic view of fitness landscapes and evolution under fixed goal and MVG. (a) A typical trajectory under fixed goal evolution. The population tends to spend long periods on local maxima or plateaus. (b) A typical trajectory under MVG. Dashed arrows represent goal switches. An effectively continuous positive gradient on the alternating fitness landscapes leads to an area where global maxima exist in close proximity for both goals.
The top image shows the trajectory that the population takes on the fitness landscape to get to the global optimum for goal 1. The second and third images show the trajectory the population takes when the goals are switched back and forth from goals 1 and 2. The bottom image shows the trajectory the population takes to achieve both goals sequentially. Now if goals 1 and 2 are applied simultaneously, you have two different selection conditions pushing the population on two different trajectories. Selection condition 1 is trying to push the population to the global optimum 1 and selection condition 2 is trying to push the population to global optimum 2. A step that would be advantageous for one condition is disadvantageous for the other condition which confounds both selection conditions in their search for their new optimums. This is why combined selection pressures confound the evolutionary process. This is the same reason ev becomes very slow converging for longer genomes.
Paul, you keep trying to call the evolution of particular sequences of bases a function. These selection conditions are simply based on matches with the weigh matrix. In some cases the matches are considered errors and in other cases the lack of matches are considered errors. There is no function being evolved in this sorting problem.Who cares if I call it a function, Alan? The gene performs a function: It matches the binding sites and no other sites. The point is that the function performed when all three selections are active is not the same function performed when only one is active.
You can squirm all you want. What you call a function is simply no sequences in the nonbinding site region of the genome that match the weight matrix, no sequences in the gene that match the weight matrix and sequences at the binding site which do match the weight matrix. Any one of the three conditions can be satisfied very quickly. It is only when you try to satisfy all three conditions simultaneously that the sorting process becomes profoundly slow. This is analogous to what happens in the real world when populations are subjected to simultaneous selection pressures.
Lot’s of thing have come along since Dr Schneider wrote the original ev and they show how the mutation and selection process actually works.Nonetheless, you're still wrong when you say:Dr Schneider has designed three selection conditions to evolve particular sequences of bases.

Paul, ev is not evolving any kind of function. Ev is a sorting algorithm based on matches with a weight matrix. What ev shows is that sorting on a single condition is much easier than sorting on three conditions.Okay, then you are comparing two different sorting situations.
Of course sorting on one selection condition with three selection conditions is comparing two different sorting conditions. In one case (single selection condition) it is very easy to sort based on this single condition, while in the other case (three selection conditions) it is far more difficult to carry out the sort. This occurs even when any of the three single sorting conditions are very easy to sort on when done singly but when doing the sort simultaneously; it becomes a profoundly slow sorting process. And that’s the way the mutation and selection sorting process works.
Paul, you made this “arbitrary” division. Make some other arbitrary division and see if you can change the behavior of this sorting algorithm.I didn't say I could. I'm simply correcting your erroneous statements.
The error in this discussion is yours when you say that only rigged simultaneous selection conditions slow the mutation and selection sorting process.
Note, Shalamar, Paul is trying to say that ev evolves some type of function, it does not.Certainly it does. Perhaps you have a strange definition of function in mind?
Paul, you’re the one who is telling us that a sorting algorithm somehow produces function. I told you I would give you whatever color paint you wanted to paint yourself into a corner.
Note, Shalamar, Paul’s own computer model must have been rigged because it shows the same behavior.And yet you still use it as the fundamental component of your argument.
I sure do because I know that combination selection pressures don’t have to be rigged to interfere with the evolution by mutation and selection. What ev shows is what is seen empirically.
Paul, do you think that only “rigged” selection pressures interfere with the mutation and selection sorting process?No, that's why I said:

If a bunch of selection pressures are rigged or happen to work out just right, they can significantly increase the time it takes an organism to adapt to them, or possibly cause extinction.

But meanwhile, you didn't quote the post where I supposedly said that selection pressures somehow cooperate with each other to accelerate the evolutionary process. Could you quote that post, please?
Here’s what you said Paul.
If a bunch of selection pressures are rigged or happen to work out just right, they can significantly increase the time it takes an organism to adapt to them, or possibly cause extinction.
And then you said:
If that is what you're saying, I'll stipulate to it.
So Paul, you think that only rigged selection pressures slow down the evolutionary process. What do selection pressures that aren’t rigged do and don’t forget to give us a mathematical example of this sorting process or a real empirical example of the process.

[rocketdodger]

Perhaps in your mathematically challenged mind you think this is true but you can’t twist the mathematical and empirical facts of how mutation and selection actually works. n + 1 selection conditions do not evolve faster than n selection conditions.

Try to understand the following documented observations, Kleinman:

1) Bacteria in people before penicillin is used -- n selective pressures, slow or nonexistent evolution of penicillin resistance.

2) Bacteria in people after penicillin is used -- n + 1 selective pressures, rapid evolution of penicillin resistance.

What about this common scenario (so common, I might add, that it is illustrated in every single study you cite) don't you get?

I predict the following nonsensical responses from Kleinman:

a) How do you know the bacteria were under n selective pressures?
b) I said "selection condition," which is not the same as "selective pressure."
c) How do you know the evolution was rapid?
d) How do you know the evolution of penicillin resistance was caused by the penicillin pressure?
e) Show me evidence that bacteria have evolved resistance to penicillin.

[rocketdodger]

Is everyone having fun on the Kleinman bible study merry-go-round? Weee!

The ability of a population to evolve against a single strong selection pressure in the presence of weak pressures doesn’t mean that the weak pressures are helping the population to evolve against the strong pressure. It only means that there are enough resources in the environment for the population to endure the weak selection pressures while still evolving against the single strong selection pressure.


Perhaps in your mathematically challenged mind you think this is true but you can’t twist the mathematical and empirical facts of how mutation and selection actually works. n + 1 selection conditions do not evolve faster than n selection conditions.

US: "Here is a good example of rapid evolution under multiple selective pressures."

KLEINMAN: "Yes that is an example of rapid evolution under multiple selective pressures."

US: "So you admit that rapid evolution can occur under multiple selective pressures?"

KLEINMAN: "No, it is impossible. Show me evidence of rapid evolution under multiple selective pressures."

[Belz...]

If at first you don’t succeed, try, try again.

In your case, you should give up, right away.

We all live by faith Belz, the difference is in what you put your faith in.

That's solipsist nonsense. Not all of us live by faith, theist.

Doesn’t that say something about how weak your theory is?

Actually, it was a comment about yours. But I'm not surprised my point was lost on you.

I doubt I will be thinking about this topic on my deathbed, what will you be thinking about on your deathbed?

Finding a way to make "Mein leiben" my last words.

But is it annoying?

Yes, but not because I'm an "evolutionist". Because I'm a rationalist and I find your form of arguing childish. At best.

What difference do the strengths of selection pressures have in the mutation and selection sorting process?

:jaw-dropp

No selection pressures, no evolution.

Not quite. But I agree that it wouldn't be very ...

Wait a minute, Klein. Didn't you just contradict yourself ? No selection pressures, no evolution. Multiple selection pressures, no evolution ?

I’m not complaining, are you complaining?

Zip! Again, Klein misses the point. How old are you, anyway ?

[kleinman]

Perhaps in your mathematically challenged mind you think this is true but you can’t twist the mathematical and empirical facts of how mutation and selection actually works. n + 1 selection conditions do not evolve faster than n selection conditions.1) Bacteria in people before penicillin is used -- n selective pressures, slow or nonexistent evolution of penicillin resistance.
Why should penicillin resistance evolve when there is no selection pressure for this transformation? Why don’t you tell us what these n selection pressures are that bacteria are being subjected to?
2) Bacteria in people after penicillin is used -- n + 1 selective pressures, rapid evolution of penicillin resistance.
So, bacteria evolve resistance to penicillin, what are the other n evolutionary transformations that the bacteria population do?
The ability of a population to evolve against a single strong selection pressure in the presence of weak pressures doesn’t mean that the weak pressures are helping the population to evolve against the strong pressure. It only means that there are enough resources in the environment for the population to endure the weak selection pressures while still evolving against the single strong selection pressure.
And
Perhaps in your mathematically challenged mind you think this is true but you can’t twist the mathematical and empirical facts of how mutation and selection actually works. n + 1 selection conditions do not evolve faster than n selection conditions.US: "Here is a good example of rapid evolution under multiple selective pressures."
Rocketdodger, only one selection condition is evolving on the background of n weak selection conditions which are not evolving anywhere. These n weak selection conditions only serve to slow the evolution of the one strong selection condition. The weak selection conditions only interfere with the sorting of mutations for the strong selection condition.

Now, if you superimpose a second strong selection condition to the sorting process, it profoundly slows the sorting process for both strong selection conditions because in this case, each strong selection condition is pushing the population on two different trajectories, again with a background of weak selection conditions interfering with the sorting process of both strong selection conditions.

Rocketdodger, you have a basic misunderstanding how sorting or optimization processes work. The more conditions you try to sort or optimize by, the more difficult the process becomes. It is more difficult to sort by n+1 conditions than by n conditions. That is a mathematical and empirical fact of life. It doesn’t matter whether your selection conditions are weak or strong.

We can go around on this topic as long as you want, you will still be wrong about the mathematics of sorting. You can not sort by n+1 conditions more quickly than by n conditions.
No selection pressures, no evolution.Not quite. But I agree that it wouldn't be very ...
Oh, that’s right, genomes also beggaminases.

[rocketdodger]

Did I predict correctly, or what? What are these responses even supposed to mean, Kleinman?

Why should penicillin resistance evolve when there is no selection pressure for this transformation?

It shouldn't evolve at all, that is the whole point of that observation -- that penicillin resistance doesn't usually evolve in the absence of penicillin. Congratulations on being denser than depleted uranium.

Why don’t you tell us what these n selection pressures are that bacteria are being subjected to?

I don't know what the n pressures are, they are different for every population, thats why I said "n" -- it is a variable that stands for "whatever pressures happened to be affecting the population." Congratulations on being denser than depleted uranium.


So, bacteria evolve resistance to penicillin, what are the other n evolutionary transformations that the bacteria population do?

I didn't say "n evolutionary transformations," I said "n selective pressures." Congratulations on being denser than depleted uranium.

Rocketdodger, only one selection condition is evolving on the background of n weak selection conditions which are not evolving anywhere.

Which means a) evolution is happening and b) there is more than one selective pressure at work. Seriously, how can you be so dense?


The more conditions you try to sort or optimize by, the more difficult the process becomes. It is more difficult to sort by n+1 conditions than by n conditions. That is a mathematical and empirical fact of life. It doesn’t matter whether your selection conditions are weak or strong.

Unless your goal is to just sort or optimize as best you can, instead of fully, in which case the number of conditions is irrelevant. And since nature just does the best it can, this is what we see in evolution -- nature sorts by the strongest conditions and ignores the rest, effectively.

You can not sort by n+1 conditions more quickly than by n conditions.

Yes you are correct -- too bad fully sorting against all selective pressures has nothing to do with how fast a population evolves!

All that needs to happen for evolution to occur is progress sorting against the strongest pressure. All of your examples show this, penicllin resistance included.

[kleinman]

Did I predict correctly, or what? What are these responses even supposed to mean, Kleinman?
Rocketdodger, you may be able to predict what I’m going to say but that is the limit of your predictive abilities. If you think that you can sort mutations for n+1 selection conditions more rapidly than for n selection conditions, then you know nothing about how mutation and selection works. Neither the mathematics of mutation and selection nor the empirical data for mutation and selection works that way.

[rocketdodger]

Rocketdodger, you may be able to predict what I’m going to say but that is the limit of your predictive abilities. If you think that you can sort mutations for n+1 selection conditions more rapidly than for n selection conditions, then you know nothing about how mutation and selection works. Neither the mathematics of mutation and selection nor the empirical data for mutation and selection works that way.

Kleinman, you may be copy and paste citations but that is the limit of your analytical abilities. If you think that evolution requires fully sorting mutations against all selective pressures affecting a population, then you know nothing about how mutation and selection works. Neither the mathematics of mutation and selection nor the empirical data for mutation and selection works that way.

[kleinman]

Rocketdodger, you may be able to predict what I’m going to say but that is the limit of your predictive abilities. If you think that you can sort mutations for n+1 selection conditions more rapidly than for n selection conditions, then you know nothing about how mutation and selection works. Neither the mathematics of mutation and selection nor the empirical data for mutation and selection works that way.Kleinman, you may be copy and paste citations but that is the limit of your analytical abilities. If you think that evolution requires fully sorting mutations against all selective pressures affecting a population, then you know nothing about how mutation and selection works. Neither the mathematics of mutation and selection nor the empirical data for mutation and selection works that way.
The reason why I can copy and paste citations is that I understand how mutation and selection actually works, now rocketdodger joins Adequate and argues that n +1 selection conditions sort mutations more quickly than n selection conditions.
http://forums.randi.org/images/smilies/doglaugh.gif

[rocketdodger]

The reason why I can copy and paste citations is that I understand how mutation and selection actually works, now rocketdodger joins Adequate and argues that n +1 selection conditions sort mutations more quickly than n selection conditions.
http://forums.randi.org/images/smilies/doglaugh.gif

The reason why I can actually make sense of the citations is that I understand how mutation and selection actually works, now Kleinman joins the bible study kiddies and argues that n +1 selective pressures always slows evolution compared to n selective pressures.

[joobz]

I see that Kleinman has still failed to explain or justify ANY of his model's assumptions. I'm not shocked. You can't justify them, they are wrong.

Horribly wrong assumptions in the Kleinman theory:
1.) Mutation rate remains constant
2.) Mutation rate is known
3.) Number of selection pressures for all species for all time in all areas is known
4.) Number of selection pressures is constant
5.) Selection pressure magnitude is constant and equal for all pressures
6.) Point mutations are the only mutation/adaptation mechanism
7.) defining selection pressure is unimportant
8.) slow equals stop
9.) Mutation is non-random

[kleinman]

The reason why I can copy and paste citations is that I understand how mutation and selection actually works, now rocketdodger joins Adequate and argues that n +1 selection conditions sort mutations more quickly than n selection conditions.The reason why I can actually make sense of the citations is that I understand how mutation and selection actually works, now Kleinman joins the bible study kiddies and argues that n +1 selective pressures always slows evolution compared to n selective pressures.
Rocketdodger, if you could make any sense of mutation and selection, you wouldn’t be arguing that n+1 selection pressures evolve more quickly than n selection pressures.
I see that Kleinman has still failed to explain or justify ANY of his model's assumptions. I'm not shocked. You can't justify them, they are wrong.
Here’s the author of cooperative chemistry for abiogenesis and cooperative selection pressures for evolution who not only admits his science is based on speculation but also admits he knows nothing about evolution.
If there was a "sticky" thread on drug delivery, biomaterials or polymer chemistry, I'd be there instantly. But evolution isn't my field.
He is also wrong about whose model it is, it is not my model, it’s Dr Schneider’s model.

Since you know nothing about the mathematics of mutation and selection and your knowledge of abiogenesis is based on raw speculation, tell us all you know about Madagascar rainforests and plate tectonics accelerates evolution. Better yet, tell us how this article you cited has anything to do with the weather.
http://www.pnas.org/cgi/content/full/104/34/13711 (http://www.pnas.org/cgi/content/full/104/34/13711) Varying environments can speed up evolution.

For those of you who want to learn something about the mathematics of mutation and selection, consider the following citation. This paper takes a different approach to the way combination selection pressures slow and ultimately stops evolution.
http://www.journals.royalsoc.ac.uk/content/lc1kmcw0hee4m3rl/ (http://www.journals.royalsoc.ac.uk/content/lc1kmcw0hee4m3rl/)
Viruses, bacteria, eukaryotic parasites, cancer cells, agricultural pests and other inconvenient animates have an unfortunate tendency to escape from selection pressures that are meant to control them. Chemotherapy, anti-viral drugs or antibiotics fail because their targets do not hold still, but evolve resistance. A major problem in developing vaccines is that microbes evolve and escape from immune responses. The fundamental question is the following: if a genetically diverse population of replicating organisms is challenged with a selection pressure that has the potential to eradicate it, what is the probability that this population will produce escape mutants? Here, we use multi-type branching processes to describe the accumulation of mutants in independent lineages. We calculate escape dynamics for arbitrary mutation networks and fitness landscapes. Our theory shows how to estimate the probability of success or failure of biomedical intervention, such as drug treatment and vaccination, against rapidly evolving organisms.
And a particular example of the combination is shown here.
In HIV therapy, single point mutations confer resistance to non-nucleoside reverse transcriptase inhibitors, while resistance to protease inhibitors or nucleoside/nucleotide reverse transcriptase inhibitors usually evolves gradually by accumulation of multiple mutations (Larder & Kemp 1989; Nowak & May 2000; Condra et al. 1995; Martinez-Picado et al. 2000; Casado et al. 2001; Richman 2001). Consider a particular combination therapy for which n = 3 point mutations are required for resistance. The wild-type is denoted by 000, whereas the escape mutant is given by 111. In the best possible scenario, wild-type and all intermediate mutants cannot replicate during therapy, R = 0, and all mutants have minimum fitness prior to therapy, w = 0. In this case, the critical virus population
size is given by N∗ = 9 × 10^12. This assumes that the mutations have to occur in a particular order, otherwise N∗ = 3 × 10^12. Patients with a virus load below N∗ will not
evolve resistance. If, by contrast, the mutants have only a 10% selective disadvantage compared with wild-type prior to therapy, w = 0.9, then N∗ = 3 × 10^10. If the intermediate mutants, 001 and 011, have a 1% selective disadvantage (R = 0.99) and the 011 mutant has a basic reproductive ratio of R = 0.9, then N∗ = 4 × 10^8. For comparison, a perfect intervention (R = 0, w = 0) that requires only n = 2 point mutations has a critical population size of N∗ = 6 × 10^8. Figure 3 gives further examples and also
shows how the risk of escape is distributed between the evolution of escape mutants following intervention and the pre-existence of escape mutants. The success of anti-HIV
therapy crucially depends on: (i) the minimum number of point mutations required for escape; (ii) the virus load in the patient; (iii) the residual replication of wild-type and intermediate mutants during therapy; and (iv) the selective pressure against relevant mutations prior to treatment. Our calculation quantifies the individual contributions of these four factors and thus allows us to estimate the probabilities of success of particular interventions.

[rocketdodger]

Rocketdodger, if you could make any sense of mutation and selection, you wouldn’t be arguing that n+1 selection pressures evolve more quickly than n selection pressures.

Kleinman, if you could make any sense of mutation and selection, you wouldn’t be arguing that n+1 selection pressures always evolve more slowly than n selection pressures.

[kleinman]

Rocketdodger, if you could make any sense of mutation and selection, you wouldn’t be arguing that n+1 selection pressures evolve more quickly than n selection pressures.Kleinman, if you could make any sense of mutation and selection, you wouldn’t be arguing that n+1 selection pressures always evolve more slowly than n selection pressures.

http://forums.randi.org/showpost.php?p=3007230&postcount=5718 (http://forums.randi.org/showpost.php?p=3007230&postcount=5718)
I am eager to participate in this discussion but I don't know the mathematical details of the topic, only general ideas. Paul, is there a good introductory source (assuming I am fluent in mathematics) where I can learn what this equation you guys are talking about represents? All this Rseq~ and Rfreq~ stuff is lost on me.

[geo_flux]

Hi all, this is my first post so apologies for any mistakes i make. I'll admit right at the start that i havent read the entire 150 pages of this thread, so my question might have already been answered. if it has please let me know and i'll search back to try and find it.
This is a question for Kleinman-
When there is a huge amount of physical evidence to support the theory of evolution (fossil record, DNA record, vestigal limbs, lab experiments, etc) compared to a limited computer simulation which can be taken to contradict evolution, isn't it more reasonable to assume the computer simulation isn't accurate enough than that all the physical evidence is wrong?

By definition a computer simulation can never be completely accurate. nobody knows exactly how evolution works on a genetic level so any model can only be based on incomplete data. anything based on incomplete and unproven data can never be assumed to give completely accurate results.

Again, sorry if this has already been answered and a big HI to everyone at JREF.

[rocketdodger]

Ahh a typical Kleinman strategy -- instead of addressing the pertinent statements I made in post #6131, vomit completely unrelated rubbish into the thread like a squid releasing an ink cloud to cover its retreat.

You are right, Kleinman, not understanding what the variables in the ev program correspond to does disqualify me from making my own arguments about the ev program -- too bad not a single post of mine has made any type of reference to it.

Fail. Try again. Care to tell us how bacteria developing resistance to penicillin is an example of profoundly slowed evolution?

[joobz]

Ahh, nothing new.

[kleinman]

When there is a huge amount of physical evidence to support the theory of evolution (fossil record, DNA record, vestigal limbs, lab experiments, etc) compared to a limited computer simulation which can be taken to contradict evolution, isn't it more reasonable to assume the computer simulation isn't accurate enough than that all the physical evidence is wrong?
Hi geo_flux. Are you ready to enter the not so lost world of mutation and selection?

There are plenty of other threads, blogs, web sites which discuss these other issues which you raise here. The discussion on this thread is about the mathematics of mutation and selection and the empirical evidence which supports these mathematical results. The central mathematical model in this discussion is the ev computer simulation written by Dr Tom Schneider who is head of computational molecular biology at the National Cancer Institute. Dr Schneider published his results from a case from his computer simulation in the Oxford University Press journal, Nucleic Acids Research. The results from this model and hundreds of empirical examples which substantiates these results show that the theory of evolution by mutation and selection is mathematically impossible.
By definition a computer simulation can never be completely accurate. nobody knows exactly how evolution works on a genetic level so any model can only be based on incomplete data. anything based on incomplete and unproven data can never be assumed to give completely accurate results.
It is true that any computer model can never perfectly model reality. The question is whether Dr Schneider’s model properly captures the essential features of the mutation and selection process and is there physical/empirical evidence which substantiates these mathematical findings. The answers to these questions are yes and yes.
Again, sorry if this has already been answered and a big HI to everyone at JREF
They have but I don’t mind going over it again. Let’s start with the fundamental hypothesis.

Dr Schneider’s computer simulation of the evolution of binding sites by random point mutations and natural selection takes huge numbers of generations to carry out this evolutionary process on any genome length for a free living creature, far too many generations for the theory of evolution to be mathematically possible. The reason why this evolutionary process takes such profoundly huge numbers of generations is that the model uses three selection conditions. If you run the model with two of the three selection conditions set to zero, the remaining selection condition evolves in trivial small number of generations. It is the sorting of mutations to multiple selection conditions which profoundly slows the evolutionary process. Only single selection conditions can evolve rapidly. Multiple simultaneous selection conditions profoundly slow the evolutionary process.

This mathematical finding is reflected by hundreds of empirical examples of mutation and selection, all of which show that multiple simultaneous selection pressures profoundly slow the evolutionary process. These findings are seen in the fields of virology, bacteriology, parasitology, oncology, agriculture and other fields as well. In addition there are other mathematical models which show what Dr Schneider’s model shows that simultaneous selection pressures slow the evolutionary process by mutation and selection.

These findings are more easily understood if you realize that evolution by mutation and selection is simply and optimization problem. If you have only a single optimization condition, it is much easier both mathematically and empirically to find a local optimum. When you have additional optimization conditions (selection conditions), the trajectory to these different optima are confounded by the different optimization conditions.

The prime empirical example of this is the evolution of the HIV virus when subjected either to monotherapy or combination therapy. The virus population easily evolves resistance to monotherapy but combination therapy stymies the viral population in its search on the fitness landscape for a new local optimum.

I hope this give you an introduction to this discussion.

[rocketdodger]

They have but I don’t mind going over it again. Let’s start with the fundamental hypothesis

Yes, geo, Kleinman's argument. Let me sum it up for you:

1) Many organisms we don't like quickly evolve resistances to our methods of killing them.

2) Studies show that if we use more than one method at once, they have a much harder time evolving resistance.

3) Thus evolution is impossible, despite the fact that the truth of premise 1) depends on evolution being possible.

[geo_flux]

Hi Kleinman, thanks for the response.
so in summary your saying that multiple evolution pressures slow evolution?
but from looking through this thread it seems like othe posters have linked many examples of where this hasn't happened.
wouldnt it be more accurate to say that multiple pressures have the potential to slow evolution in some instances?
looking at all the other evidence to support evolution would suggest that there must be more to the story than this simulation suggests.

[joobz]

Hi Kleinman, thanks for the response.
so in summary your saying that multiple evolution pressures slow evolution?
but from looking through this thread it seems like othe posters have linked many examples of where this hasn't happened.
wouldnt it be more accurate to say that multiple pressures have the potential to slow evolution in some instances?
looking at all the other evidence to support evolution would suggest that there must be more to the story than this simulation suggests.
Hi Geo. Kleinman's main problem is that his theory has inherent assumptions that are not justified. Indeed, they can't be justified becuase they are false. As a result, nothing he says is relevant.

We generally just post here waiting for him to say something new and funny.

For your reference,
Horribly wrong assumptions in the Kleinman theory:
1.) Mutation rate remains constant
2.) Mutation rate is known
3.) Number of selection pressures for all species for all time in all areas is known
4.) Number of selection pressures is constant
5.) Selection pressure magnitude is constant and equal for all pressures
6.) Point mutations are the only mutation/adaptation mechanism
7.) defining selection pressure is unimportant
8.) slow equals stop
9.) Mutation is non-random

[geo_flux]

Hi Joobz, thanks for the list of unknowns and variables that are built into the model Kleinman is referring to.
it really does demonstrate how limited the model is.

Does Kleinman believe that these factors are not important to the outcome of the simulation or that the list is wrong in some way?

"For your reference,
Horribly wrong assumptions in the Kleinman theory:
1.) Mutation rate remains constant
2.) Mutation rate is known
3.) Number of selection pressures for all species for all time in all areas is known
4.) Number of selection pressures is constant
5.) Selection pressure magnitude is constant and equal for all pressures
6.) Point mutations are the only mutation/adaptation mechanism
7.) defining selection pressure is unimportant
8.) slow equals stop
9.) Mutation is non-random[/QUOTE]" - Joobz

[kleinman]

so in summary your saying that multiple evolution pressures slow evolution?
but from looking through this thread it seems like othe posters have linked many examples of where this hasn't happened.
wouldnt it be more accurate to say that multiple pressures have the potential to slow evolution in some instances?
looking at all the other evidence to support evolution would suggest that there must be more to the story than this simulation suggests.
No one has posted any citations which show that multiple selection pressures accelerate the evolutionary process. Evolutionists have posted citations but none clearly identify the selection pressures, target genes for the selection pressures or mutations required in order for the evolutionary process to occur.

Here’s another citation which show how evolution by mutation and selection actually works.
http://www.ajtmh.org/cgi/content/full/71/2_suppl/179 (http://www.ajtmh.org/cgi/content/full/71/2_suppl/179)
Reducing the future burden of resistance requires that effective antimalarial drugs continue to be available in the future and requires the continuous search for and development of potential new antimalarial drugs31,32 (http://www.mmv.org). However, the complete drug development process can take 10–15 years, making it imperative that the currently available drugs are deployed in a way most likely to maximize their lifespan by decreasing the likelihood that resistance will develop. The key strategy put forward to do this is to use available drugs in combination to prevent the emergence and spread of resistance.
and
Because it is difficult to control antimalarial drug resistance once it has emerged, there is a need for strategies that prevent the rare event of initial emergence. Combinations of drugs which have different molecular targets delay the emergence of resistance. However, malaria control programs may be reluctant to adopt this strategy because until resistance emerges, there is no evident benefit to the more expensive combination treatment.
and
Artemisinins taken on their own as monotherapy must be taken for seven days for radical cure. However, adherence to seven-day regimens is extremely low and a three-day regimen is generally regarded as the maximum because most people discontinue treatment when they feel better usually after a couple of days, and this can result in late recrudescences with monotherapy. Used in combination with another effective drug, a three-day course is sufficient and better adhered to and has the important advantage of protecting these valuable drugs.38
and
There is an increasing body of field evidence supporting the theoretical basis for ACTs, principally from the Thailand-Myanmar border and more recently from South Africa. In an area on the Thailand-Myanmar border, the widespread deployment of ACT was associated with a decreased incidence in malaria,39 sustained effectiveness of the combination for more than 10 years, and an increase in mefloquine sensitivity in vitro.40 These results were obtained despite artesunate being added to mefloquine when resistance to the latter was already widespread, a less than ideal scenario in terms of delaying antimalarial resistance. In Kwa-Zulu-Natal in South Africa, the combined effect of switching from SP to the fixed combination of artemether-lumefantrine and residual spraying with DDT was associated with a decrease in cases of 78% and an increase in cure rate of 87% (Barnes K, unpublished data).
and
Resistance to antimalarial drugs is resulting in avoidable morbidity, mortality, and financial losses. Urgent measures are needed now to reduce the current and future burden of disease. There is little justification for the continued use of ineffective drugs because effective drugs are currently available. The decisions of which drug regimen to change to, and how to implement the change in a way that maximizes potential benefit, are more difficult, but delaying a decision to switch because of these difficulties can only result in increased morbidity and mortality. Furthermore, delaying a switch to ACTs potentially puts at risk one of the key advantages of this strategy, which is to delay the emergence of resistance. The longer the decision is delayed, the more entrenched will become the unregulated use of the artemisinins and partner drugs as monotherapies. Partly because of the uncertainties, there is still significant reluctance to take action amongst potential funders and some national governments, both of whose commitment is essential for the success of any change in policy.
Geo_flux, not only do multiple selection pressures have the potential to slow the evolutionary process, they always do this.
Hi Noobz, thanks for the list of unknowns and variables that are built into the model Kleinman is referring to.
it really does demonstrate how limited the model is.
Geo_flux, I would watch how you spell joobz, he gets very upset if you misspell his name.

joobz like to refer to Dr Schneider’s model as my model but what joobz forgets is that the empirical examples are not limited in any way yet the still show that combination selection pressures profoundly slow the evolutionary process. For example HIV does recombination, and is not limited to point mutations. The mutation rate is not fixed or constant. In fact HIV does insertions and deletions; here is an example of this.
http://lib.bioinfo.pl/auth:Boucher,CA (http://lib.bioinfo.pl/auth:Boucher,CA)
Here is an example of a 15 base insertion in HIV, an example that point mutations are not the only mechanism.
HIV-1 isolates harbouring an insertion in the beta3-beta4 loop of reverse transcriptase (RT) confer high-level resistance to nucleoside analogues. We have identified a novel 5-amino-acid insertion (KGSNR amino acids 66-70) in a patient on prolonged nucleoside combination therapy (didanosine and stavudine) and investigated which factors were responsible for its outgrowth. Remarkably, only small fold increases in drug resistance to nucleoside analogues were observed compared to wild type. The insertion variant displayed a reduced replicative capacity in the absence of inhibitor, but had a slight replicative advantage in the presence of zidovudine, didanosine or stavudine, resulting in the selection and persistence of this insertion in vivo. Mathematical analyses of longitudinal samples indicated a 2% in vivo fitness advantage for the insertion variant compared to the initial viral population. The novel RT insertion variant conferring low levels of resistance was able to evolve towards a high-level resistant replication-competent variant.
The dominant variable in the mutation and selection process is the number of selection conditions, not the mutation rate, type of mutation, recombination or any of the issues raised in joobz list. If they were, he would post either a mathematical or empirical example which demonstrates this. In fact joobz can only speculate about this.

[kjkent1]

For those of you who want to learn something about the mathematics of mutation and selection, consider the following citation. This paper takes a different approach to the way combination selection pressures slow and ultimately stops evolution.
http://www.journals.royalsoc.ac.uk/content/lc1kmcw0hee4m3rl/
How droll...

An important quote from the same article, that kleinman clearly missed:

"There are some limitations to our approach. The theory is based on multi-type branching processes that describe the accumulation of mutations in independent lineages. Therefore, we cannot describe recombination, horizontal gene transfer or frequency-dependent fitness. All of these phenomena can be important in certain situations of escape dynamics."

Mighty kleinman has struck out -- again.

[joobz]

Geo_flux, I would watch how you spell joobz, he gets very upset if you misspell his name.When did I get upset? From what I remember, others asked you to correct your error.

joobz like to refer to Dr Schneider’s model as my model but what joobz forgets is that the empirical examples are not limited in any way yet the still show that combination selection pressures profoundly slow the evolutionary process. For example HIV does recombination, and is not limited to point mutations. The mutation rate is not fixed or constant. In fact HIV does insertions and deletions; here is an example of this.
http://lib.bioinfo.pl/auth:Boucher,CA (http://lib.bioinfo.pl/auth:Boucher,CA)
Here is an example of a 15 base insertion in HIV, an example that point mutations are not the only mechanism.Yes, of course. How silly of me for thinking that 15 years of data CAN'T be extrapolated 100,000+years. :rolleyes:

The dominant variable in the mutation and selection process is the number of selection conditions, not the mutation rate, type of mutation, recombination or any of the issues raised in joobz list. If they were, he would post either a mathematical or empirical example which demonstrates this. In fact joobz can only speculate about this.
Yes, because rate of mutation is completely unimportant when talking kinetics. :rolleyes:

And Rocketdodger has done a nice job explaining why magnitude is highly important.

I do not need to speculate on your model. You've done enough yourself. I'm simply asking you to justify it. All you need to do is change reality. That shouldn't be too hard.

[geo_flux]

I do not need to speculate on your model. You've done enough yourself. I'm simply asking you to justify it. All you need to do is change reality. That shouldn't be too hard.

LOL, i think that summarises my thoughts perfectly.

The scientific interpretation of the physical reality around us overwhelmingly supports the theory of evolution. Either all of the physical evidence is wrong or the conclusions reached by Kleinman from this model is wrong.

If i was a betting man i would put my money on the physical evidence.

[kleinman]

I do not need to speculate on your model. You've done enough yourself. I'm simply asking you to justify it. All you need to do is change reality. That shouldn't be too hard.
Joobz, it’s Dr Schneider’s model, didn’t you know that?

I don’t have to change reality; you just have to learn how to recognize it.
http://www.absw.org.uk/Briefings/insecticide_resistance.htm (http://www.absw.org.uk/Briefings/insecticide_resistance.htm)
Using high doses of insecticide should maximise kill of heterozygotes and this strategy was popular among theorists in the 1970s. But to be really effective, the dose was too high to be acceptable on either environmental or cost grounds. Another drawback was that uniform coverage of the crop was not assured. The high dose strategy could be revived though with transgenic plants if it is possible to maintain a high level of expression of the toxin gene. The other strategy is pyramiding which involves creating trangenic plants with genes for two different toxins. Insects resistant to one will be killed by the other, and vice versa. This provides a double hit strategy for seeing off heterozygotes and discouraging the spread of resistance genes. It also parallels the successful use of combination drug therapy in leprosy, TB and HIV/AIDS.
http://72.14.253.104/search?q=cache:fh1zDOBmpQMJ:eebweb.arizona.edu/courses/ecol409_509/lectures/lecture20.ppt+combination+selection+evolution+resi stance&hl=en&ct=clnk&cd=297&gl=us (http://72.14.253.104/search?q=cache:fh1zDOBmpQMJ:eebweb.arizona.edu/courses/ecol409_509/lectures/lecture20.ppt+combination+selection+evolution+resi stance&hl=en&ct=clnk&cd=297&gl=us)
With its high mutation rate, small genome, and large population size, HIV is highly likely to generate resistance mutations (as we’ve seen with AZT)

What was needed was a way to increase the number of mutations that must arise in a virion’s genome to render it resistant to the drug

The key breakthrough was to use combination therapy, cocktails of multiple drugs acting together which are not only very effective, but which delay evolution of resistance

The following example is more implicit but still shows that multiple selection pressures slow evolution of resistance, this example is found at http://www.ann-clinmicrob.com/content/5/1/25 (http://www.ann-clinmicrob.com/content/5/1/25)
in this study the checkerboard analysis showed that amikacin in combination with cephalothin or dicloxacillin was synergistic against most of the resistant strains of S. aureus and coagulase-negative Staphylococcus. Vancomycin in combination with a beta-lactam (cephalothin or imipenem) showed additivity. An indifferent effect predominated for the combination vancomycin plus amikacin. Even though a synergistic effect is expected when using a beta-lactam plus amikacin combination, it is possible that the effect cannot be clinically achievable. Careful selection of antimicrobial combinations and initial MICs are mandatory for future evaluations.
http://homes.esat.kuleuven.be/~bioiuser/symbiosys_new/index.php?option=events&task=detail&eid=344 (http://homes.esat.kuleuven.be/~bioiuser/symbiosys_new/index.php?option=events&task=detail&eid=344)
Evolution of drug resistance is a major cause for treatment of HIV infected patients with combination therapy.
http://www.bmj.com/cgi/content/full/325/7374/1221?etoc (http://www.bmj.com/cgi/content/full/325/7374/1221?etoc)
Artemisin combinations may delay and possibly reverse the development of drug resistance through a variety of mechanisms.
http://journal.paho.org/?a_ID=335 (http://journal.paho.org/?a_ID=335)
Suboptimal treatment regimens, such as monotherapy or dual therapy, treatment with poor-quality antiretroviral drugs, suboptimal dosing, and poor absorption, may increase the rate at which viral resistance evolves among treated individuals
http://dimacs.rutgers.edu/Workshops/TumorModeling/abstracts.html (http://dimacs.rutgers.edu/Workshops/TumorModeling/abstracts.html)
The genetic instability of tumor cells renders them the ability to rapidly become resistant to many chemotherapies. As a result, there is great interest in selecting combination chemotherapeutic regimens that will overcome resistance and exert synergistic therapeutic activity.
http://www.inspection.gc.ca/english/plaveg/bio/resist/disdoce.shtml (http://www.inspection.gc.ca/english/plaveg/bio/resist/disdoce.shtml)
There is a need to develop broadleaf combinations or mixtures to control glyphosate and multiple HT volunteers pre-seed. For example, 2,4-D, MCPA, bromoxynil and a low residual sulfonylurea like tribenuron methyl in combination with glyphosate would provide broad-spectrum pre-seed weed control including volunteer glyphosate HT canola. In some situations amitrole and paraquat could provide effective pre-seed control and resistance management for volunteer HT canola.
And
Herbicide mixtures to manage volunteers and reduce selection pressure could be a requirement for future HT crop releases.
There’s reality for you joobz, now if you could only find a single citation which supports your speculations.

[geo_flux]

Hi Kleinman, All those seemingly cherry picked quotes all seem to say that infections can be fought better by using multiple lines of attack.

I seriously doubt anyone would question assertion but i fail to see how that can be categorically applied as the only driver in terms of evolution.

That just seems a little bit to simplistic to me.

[kleinman]

Hi Kleinman, All those seemingly cherry picked quotes all seem to say that infections can be fought better by using multiple lines of attack.

I seriously doubt anyone would question assertion but i fail to see how that can be categorically applied as the only driver in terms of evolution.

That just seems a little bit to simplistic to me.
There are lots of cherries on this tree. Certainly when you apply multiple selection pressures on a population it compounds the reduction in fitness of the population but when these selection pressures target more than a single gene, it becomes much more difficult for the mutation and selection process to sort beneficial and detrimental mutations. That is what Dr Schneider’s computer simulation shows and that is what the empirical data shows. It is the number of selection pressures that profoundly slows the evolutionary process by mutation and selection. It’s just that simple. That’s what the mathematics shows and that’s what the empirical data shows.

[joobz]

Joobz, it’s Dr Schneider’s model, didn’t you know that?Really? When did he start talking about multiple selection pressures?

I don’t have to change reality; you just have to learn how to recognize it.
http://www.absw.org.uk/Briefings/insecticide_resistance.htm (http://www.absw.org.uk/Briefings/insecticide_resistance.htm)

http://72.14.253.104/search?q=cache:fh1zDOBmpQMJ:eebweb.arizona.edu/courses/ecol409_509/lectures/lecture20.ppt+combination+selection+evolution+resi stance&hl=en&ct=clnk&cd=297&gl=us (http://72.14.253.104/search?q=cache:fh1zDOBmpQMJ:eebweb.arizona.edu/courses/ecol409_509/lectures/lecture20.ppt+combination+selection+evolution+resi stance&hl=en&ct=clnk&cd=297&gl=us)


The following example is more implicit but still shows that multiple selection pressures slow evolution of resistance, this example is found at http://www.ann-clinmicrob.com/content/5/1/25 (http://www.ann-clinmicrob.com/content/5/1/25)

http://homes.esat.kuleuven.be/~bioiuser/symbiosys_new/index.php?option=events&task=detail&eid=344 (http://homes.esat.kuleuven.be/~bioiuser/symbiosys_new/index.php?option=events&task=detail&eid=344)

http://www.bmj.com/cgi/content/full/325/7374/1221?etoc (http://www.bmj.com/cgi/content/full/325/7374/1221?etoc)

http://journal.paho.org/?a_ID=335 (http://journal.paho.org/?a_ID=335)

http://dimacs.rutgers.edu/Workshops/TumorModeling/abstracts.html (http://dimacs.rutgers.edu/Workshops/TumorModeling/abstracts.html)

http://www.inspection.gc.ca/english/plaveg/bio/resist/disdoce.shtml (http://www.inspection.gc.ca/english/plaveg/bio/resist/disdoce.shtml)

And

There’s reality for you joobz, now if you could only find a single citation which supports your speculations.
Yup. that is reality allright, which has nothing at all to do with what you claim.
You forgot your silly assumption #8, which NONE of those references claim. only you.

[geo_flux]

That’s what the mathematics shows and that’s what the empirical data shows.

but the physical reality shows otherwise.

Simulations are good, maths is great, but physical reality is king. :D

[Mr. Scott]

The concept of the transformation of reptiles into birds is a mathematically and empirically irrational concept. You don’t have the selection conditions that would do this and if you did, the process would be so profoundly slow; you don’t have enough generations to carry out the transformation.

Dr. Kleinman,

You keep propping up that strawman about reptiles turning into birds, but I don't think you've answered without evasion my comments on this topic.

The idea that reptiles evolved into birds in tiny steps over millions of years poses no problem at all for evolutionists. Birds have scales on their legs and feet that are quite a bit like reptile's. I've learned that a single point mutation will cause the scales on bird feet to develop as feathers. One single point mutation. Soft tissue collagen has been found in dinosaur bones that closely matches modern bird's and little else. My questions are: How do you account for the massive amount of DNA and fossil records that consistently support Darwin's theory of evolution? Why did god create life that looked exactly as if it had evolved without him? Why would he design bird DNA so that a single point mutation turns a bird's scales into feathers?

[rocketdodger]

We are all still waiting for Kleinman to explain how, if evolution is impossible, bacteria evolve resistance to penicillin. Or how weeds evolve resistance to herbicides. Or how HIV evolves resistance to treatments.

I have a feeling we will be waiting for a very long time indeed. Probably because we don't understand the mathematical and empirical facts of evolution. Which is impossible, by the way -- evolution is impossible, did I say that yet?

[Shalamar]

Besides. Reptiles did not turn into Birds.. DINOSAURS did. Dinosaurs aren't reptiles.

[Mr. Scott]

We are all still waiting for Kleinman to explain how, if evolution is impossible, bacteria evolve resistance to penicillin. Or how weeds evolve resistance to herbicides. Or how HIV evolves resistance to treatments.

Bacteria evolve resistance by point mutation that results from their emotional response to a pressure. They squint, grimmace, strain, and wish really hard to make their DNA change to produce resistance. Remarkably, they can do this with two pressures at once, but three? That's the magic number. All the wishing the bacteria can muster just won't change three nucleotides at the same time, and the microbe dies from the effort. God has given bacteria exactly two duplicate mechanisms they use to will themselves point mutations in response to selection pressures. This, you silly evolutionarians, is how the mathematics of mutation and natural selection work.
;)

[Kotatsu]

I've learned that a single point mutation will cause the scales on bird feet to develop as feathers. One single point mutation. Why would he design bird DNA so that a single point mutation turns a bird's scales into feathers?

This interests me You wouldn't happen to have a reference to this?

[Belz...]

Not quite. But I agree that it wouldn't be very ...

Oh, that’s right, genomes also beggaminases.

Oh, no, Klein. You're not getting away this easily.

What I said was this:

No selection pressures, no evolution.

Not quite. But I agree that it wouldn't be very ...

Wait a minute, Klein. Didn't you just contradict yourself ? No selection pressures, no evolution. Multiple selection pressures, no evolution ?

Now, why you chose to ignore the second part of what I wrote seems quite clear.

Of course, if you wanted to dodge the question, you would've done a better job if what you answered actually had anything to do with what I said.

Of course, completely evading the question and not answering might've been a better idea, too. I mean, you did ignore all my other points, so far, and only answered with insults or "clever" retorts.

What I'm saying is that you claim that

1) No pressures, no evolution
2) Multiple pressures, no evolution
3) One pressure, it's a stabilising pressure, ergo no evolution

So, what you're saying, basically, is that your opinion that evolution is mathematically impossible has nothing to do with selection pressures ?

[Belz...]

No one has posted any citations which show that multiple selection pressures accelerate the evolutionary process.

Don't be modest, Klein. Yourself have posted, how do you put it, hundreds of examples of how mutation and selection actually work.

Kleinman, you've done a beautiful job of proving your own theory wrong.

The reason why I can copy and paste citations is that I understand how mutation and selection actually works

CTRL-C doesn't work if you don't understand the text you're copying ?

[Belz...]

Hi Kleinman, All those seemingly cherry picked quotes all seem to say that infections can be fought better by using multiple lines of attack.

I seriously doubt anyone would question assertion but i fail to see how that can be categorically applied as the only driver in terms of evolution.

That just seems a little bit to simplistic to me.

Hi, Geo. Welcome to the forum.

As you may have read already, and as Rocketdodger has already put it, Kleinman's own cherry-picked (he doesn't know what the term means, by the way) examples PROVE his point wrong, because their very existence shows that evolution happens, sometimes blindingly fast.

Poor Kleinman should've stayed in the pond and out of the deep waters.

[Belz...]

This interests me You wouldn't happen to have a reference to this?

I second that.

[Paul C. Anagnostopoulos]

So Paul, you think that only rigged selection pressures slow down the evolutionary process.
Let me post what I said one more time, with emphasis:

If a bunch of selection pressures are rigged or happen to work out just right, they can significantly increase the time it takes an organism to adapt to them, or possibly cause extinction.
And then, interestingly enough, I added:

If that is what you're saying, I'll stipulate to it.
If that is not what you're saying, then just say so and I'll retract my summary of what you are saying. I'm simply trying to understand you. I am not making any claims about how things actually work.

~~ Paul

[Kotatsu]

So, what you're saying, basically, is that your opinion that evolution is mathematically impossible has nothing to do with selection pressures ?

Well, it certainly doesn't seem to be connected with any other part of reality, so why should selection pressures be an exception?

[Paul C. Anagnostopoulos]

Why should penicillin resistance evolve when there is no selection pressure for this transformation? Why don’t you tell us what these n selection pressures are that bacteria are being subjected to?
Surely you're joking, Mr. Kleynman.

~~ Paul

[Paul C. Anagnostopoulos]

Let's see ...

The key strategy put forward to do this is to use available drugs in combination to prevent the emergence and spread of resistance.

Combinations of drugs which have different molecular targets delay the emergence of resistance.

Used in combination with another effective drug, a three-day course is sufficient and better adhered to and has the important advantage of protecting these valuable drugs.
Now, these would be examples of targeted toxins being introduced. So perhaps this is what you're saying, Alan:

If a bunch of selection pressures are rigged, they can significantly increase the time it takes an organism to adapt to them, or possibly cause extinction.

Have I got that right now?

~~ Paul

[Mr. Scott]

This interests me You wouldn't happen to have a reference to this?

I found the original link I learned this from, but now the link is dead. It's http://hometown.aol.com/darwinpage/dinobirds.htm and here's the quote:
A single point mutation will change the scales of a chicken into feathers.

While googling for it I found this really cool paper about dinosaur/bird evolution:
http://www.talkreason.org/articles/coulter3.cfm
Structurally, feathers are essentially frayed scales. Just how closely feathers and "scales" are related has also been noted by French paleontologist Philippe Taquet (1994, 197): "This is so true that if you inject retinoic acid under the skin of the feet on chicken embryos, they'll grow feathers there where normally there are scales." For the technically minded, Zou & Niswander (1996), Crowe & Niswander (1998) and Widelitz et al. (2000) examine the signaling paths that transform scutellae into feather filaments and buds. For meringue, Menon & Menon (2000, 551) recently noted that "retinoids are increasingly being implicated in morphogenesis, homeobox gene transcription, etc."
The specialized form of β-keratin in feathers (f-keratin) differs slightly in having a repeated tripeptide. See Molloy et al. (1982), Koltunow et al. (1986), Presland et al. (1989) and Whitbread et al. (1991) on relevant keratin genes and their expression -- with Gregg et al. (1984) suggesting "feather-like keratin genes may have evolved from a scale keratin gene by a single deletion event."

A remark there on "hen's teeth:"
By some curious coincidence, modern birds still retain the genetic mechanisms for making teeth, as evidenced by Kollar & Fisher (1980), Chen et al. (2000), Narayanan et al. (2001) and Mitsiadis et al. (2003).

[Belz...]

Why should penicillin resistance evolve when there is no selection pressure for this transformation?

Precisely. Add pressures, quicken evolution.

[Belz...]

Just a thought: has anyone argued that mutations can create their own selection pressures ?

Does that make sense, or am I just making stuff up ?

ETA: And by that, I mean that the action of some new or altered genes may create new selection pressures that will hasten the emergence of something else, assumine the altered gene is passed on.

[Belz...]

Well, it certainly doesn't seem to be connected with any other part of reality, so why should selection pressures be an exception?

:D

[Shalamar]

So... Is Kleinman arguing that mutation and evolution ONLY occur with selection pressures? There have been recorded mutations that basically created a new species for no real apparent reason.

[rocketdodger]

Just a thought: has anyone argued that mutations can create their own selection pressures ?

Does that make sense, or am I just making stuff up ?

ETA: And by that, I mean that the action of some new or altered genes may create new selection pressures that will hasten the emergence of something else, assumine the altered gene is passed on.

I did, earlier, when I suggested populations exerting their own pressures on themselves.

Kleinman wouldn't have any of it, and since I am too lazy to crawl the archives looking for documented examples... so I just let it drop.

It would be hard to show, however, that if such cases exist (and I think they do) they can't also be described in terms of external selective pressures. So I think maybe the idea is just a convenience and not actually a separate case.

[rocketdodger]

So... Is Kleinman arguing that mutation and evolution ONLY occur with selection pressures? There have been recorded mutations that basically created a new species for no real apparent reason.

Yes. Even more absurd, he claims that it can only happen when there is one and only one selective pressure, which makes no sense at all, because there is never such a thing as only a single selective pressure.

He has, on occaision, for the duration of a post or two, admitted that he means "single strong pressure with a background of multiple weak pressures," which is a step in the right direction, but he always reverts to his nonsense mantra soon thereafter.

Very little progress is being made here, except in making Kleinman look like a fool.

[Mr. Scott]

Just a thought: has anyone argued that mutations can create their own selection pressures ?

Yes, I think it can. A mutation that lets an individual reproduce more readily than its non-mutated bretheren puts a pressure on the bretheren what can lead them to become extinct if resources are limited. For example, the evolution of color vision will help an herbivore spot ripe fruit quickly, putting a selection pressure on color-blind individuals leading to their extinction through starvation if there is a limited supply of said fruit.

Ergo an advantageous mutation is almost inevitably a selection pressure against unmutated individuals. You could even view bacterial resistance to penicillin in this light.

[Belz...]

Very little progress is being made here, except in making Kleinman look like a fool.

Hopefully, this annoys him, as well.

[Belz...]

Yes, I think it can. A mutation that lets an individual reproduce more readily than its non-mutated bretheren puts a pressure on the bretheren what can lead them to become extinct if resources are limited. For example, the evolution of color vision will help an herbivore spot ripe fruit quickly, putting a selection pressure on color-blind individuals leading to their extinction through starvation if there is a limited supply of said fruit.

I would even speculate that, within the same individual, a certain mutation/disability that is not crippling might put a selection pressure on the individual and its offsprings to evolve a way around it.

If that's true, then duplicated genes might actually beggaminase faster this way.

[kleinman]

Joobz, it’s Dr Schneider’s model, didn’t you know that?Really? When did he start talking about multiple selection pressures?
Why don’t you ask him because that’s why his sorting algorithm converges so slowly for all but the tiniest genome lengths? You do understand that mutation and selection is a sorting problem based on the optimization of the selection conditions or is mathematics not your field as well.
There’s reality for you joobz, now if you could only find a single citation which supports your speculations.Yup. that is reality allright, which has nothing at all to do with what you claim. You forgot your silly assumption #8, which NONE of those references claim. only you.
You must be one of those evolutionists that claim that infectious diseases and cancers can never me cured, they will always evolve resistance. Oh, but I forgot, evolution is not your field. You aren’t a mathematician and evolution is not your field but you claim you know everything about mutation and selection. As long as there is enough free energy, anything is possible.
That’s what the mathematics shows and that’s what the empirical data shows.but the physical reality shows otherwise.

Simulations are good, maths is great, but physical reality is king.
You have not physical reality which shows mutation and selection can transform reptile into birds. The physical reality of how mutation and selection actually works is demonstrated in the hundreds of citations posted which accurately measure the process. These empirical examples of mutation and selection demonstrate exactly what the mathematics show, that is the mutation and selection sorting process is profoundly slowed when you have more than a single selection condition. Until you understand that mutation and selection is nothing more than a sorting process of beneficial and detrimental mutations based on the optimization of selection conditions you will not understand that optimizing on multiple different selection conditions becomes a profoundly slow process. You will have to ignore the simulation, mathematics and reality which all demonstrate this fact.
The concept of the transformation of reptiles into birds is a mathematically and empirically irrational concept. You don’t have the selection conditions that would do this and if you did, the process would be so profoundly slow; you don’t have enough generations to carry out the transformation.Dr. Kleinman,

You keep propping up that strawman about reptiles turning into birds, but I don't think you've answered without evasion my comments on this topic.

The idea that reptiles evolved into birds in tiny steps over millions of years poses no problem at all for evolutionists. Birds have scales on their legs and feet that are quite a bit like reptile's. I've learned that a single point mutation will cause the scales on bird feet to develop as feathers. One single point mutation. Soft tissue collagen has been found in dinosaur bones that closely matches modern bird's and little else. My questions are: How do you account for the massive amount of DNA and fossil records that consistently support Darwin's theory of evolution? Why did god create life that looked exactly as if it had evolved without him? Why would he design bird DNA so that a single point mutation turns a bird's scales into feathers?
Mr Scott,

You keep propping up you theory of evolution with strange speculations and extrapolations.

The idea that reptiles evolved into birds in tiny steps over millions of years should pose problems for evolutions when the mechanism of mutation and selection can transform only a tiny number of genes at once. The mutation and selection process is confounded when more than a single gene is transformed at a time. The fact that feathers can be made to grow on a bird should not surprise anyone since their genetic code contains the sequences required to do such a thing. Ask God why He would make life like this. Ask yourself why you would make such strange interpretation of the physical evidence when the mathematics of mutation and selection and the physical evidence which substantiates this mathematics says exactly the opposite.
We are all still waiting for Kleinman to explain how, if evolution is impossible, bacteria evolve resistance to penicillin. Or how weeds evolve resistance to herbicides. Or how HIV evolves resistance to treatments.
Oh no rocketdodger, I didn’t say evolution was impossible. What I said was the theory of evolution was mathematically and empirically impossible; you can’t get common descent by the mutation and selection process.

The way bacteria evolve resistance against antibiotics and weeds evolve resistance against herbicides occurs most easily one selection pressure at a time. Add additional selection pressures and the process become profoundly slower. If you want to argue that reptiles evolved into birds, tell us what the selection conditions are that would evolve one gene at a time.
I have a feeling we will be waiting for a very long time indeed. Probably because we don't understand the mathematical and empirical facts of evolution. Which is impossible, by the way -- evolution is impossible, did I say that yet?
We all know that you don’t understand the mathematics of mutation and selection but we are working to get you to understand it. In the meantime, we will continue to post examples of how the process actually works and you can continue to argue that n+1 selection conditions will sort mutations faster than n selection conditions.
Besides. Reptiles did not turn into Birds.. DINOSAURS did. Dinosaurs aren't reptiles.
Oh, that’s right, we all saw Jurassic Park, that’s how science works --- in Hollywood.
Not quite. But I agree that it wouldn't be very ...Oh, that’s right, genomes also beggaminases.Oh, no, Klein. You're not getting away this easily.

What I said was this:
Now the plot thickens:
No selection pressures, no evolution.Not quite. But I agree that it wouldn't be very ...

Wait a minute, Klein. Didn't you just contradict yourself ? No selection pressures, no evolution. Multiple selection pressures, no evolution ?Now, why you chose to ignore the second part of what I wrote seems quite clear.
Belz is still mystified how mutation and selection actually works. You need selection pressure if something is to evolve but the behavior of the mutation and selection process does not behave linearly with increasing number of selection pressures. Doubling the number of selection pressures does not double the rate of evolution. The first selection pressure is the easiest for a population to evolve to. Each additional selection pressure slows the process much more so. So Belz, no selection pressures, no evolution, one selection pressure, the easiest for the population to evolve to, additional selection pressures confound the sorting process for beneficial and detrimental mutations. That’s how the mathematics works and that’s how reality works.
No one has posted any citations which show that multiple selection pressures accelerate the evolutionary process.Don't be modest, Klein. Yourself have posted, how do you put it, hundreds of examples of how mutation and selection actually work.

Kleinman, you've done a beautiful job of proving your own theory wrong.
Belz, you’ve gotten me so confused, I can’t remember what my theory is. Could you help me out, now don’t be fiendish.
The reason why I can copy and paste citations is that I understand how mutation and selection actually worksCTRL-C doesn't work if you don't understand the text you're copying ?
Belz, don’t you realize that I am using the CTRL-X key on the theory of evolution.
Poor Kleinman should've stayed in the pond and out of the deep waters.
Come on Belz; let’s take a dip in the primordial soup. Just watch out for the replicators.
This interests me You wouldn't happen to have a reference to this?I second that.
Yea, Mr Scott, give us a reference which proves that feathers can grow on birds.
So Paul, you think that only rigged selection pressures slow down the evolutionary process.Let me post what I said one more time, with emphasis:If a bunch of selection pressures are rigged or happen to work out just right, they can significantly increase the time it takes an organism to adapt to them, or possibly cause extinction. And then, interestingly enough, I added: If that is what you're saying, I'll stipulate to it. If that is not what you're saying, then just say so and I'll retract my summary of what you are saying. I'm simply trying to understand you. I am not making any claims about how things actually work.
That’s all right Paul, until you, Dr Schneider and I started this discussion over a year ago, I didn’t understand how mutation and selection actually worked. Once you realize that evolution by mutation and selection is simply a sorting problem based on the optimization of selection conditions, it becomes obvious that the greater the number of sorting conditions the slower the process works. Both you and Dr Schneider have done an excellent job in modeling this very complex problem.
Why should penicillin resistance evolve when there is no selection pressure for this transformation? Why don’t you tell us what these n selection pressures are that bacteria are being subjected to?Surely you're joking, Mr. Kleynman.
Me joke? Surely you’re joking Mr. Anagangangangnoendtothisnameopopop… ah, forget it.
Let's see ...The key strategy put forward to do this is to use available drugs in combination to prevent the emergence and spread of resistance.

Combinations of drugs which have different molecular targets delay the emergence of resistance.

Used in combination with another effective drug, a three-day course is sufficient and better adhered to and has the important advantage of protecting these valuable drugs.Now, these would be examples of targeted toxins being introduced. So perhaps this is what you're saying, Alan:

If a bunch of selection pressures are rigged, they can significantly increase the time it takes an organism to adapt to them, or possibly cause extinction.

Have I got that right now?
You are getting closer. The reason why these examples use targeted toxins (targeted selection pressures) is that disinfectants (multiple targeted toxins) generally react with the host as well. If antimicrobial agents could be designed that target multiple different genes simultaneously, these agents would be much less likely to select for resistance. The point is, these strong selection pressures demonstrate exactly how the mutation and selection process works. The reason why bacteria don’t evolve resistance to disinfectants is that these toxins put strong selection pressure on too many genetic targets simultaneously. Any strong selection pressure targets one or more genetic systems. Now the question you should ask is whether weak selection pressures will sort mutations any faster than strong selection pressures.
Why should penicillin resistance evolve when there is no selection pressure for this transformation?Precisely. Add pressures, quicken evolution.
Add a single strong selection pressure, quicken evolution; add additional selection pressures, slow evolution profoundly.
Just a thought: has anyone argued that mutations can create their own selection pressures ?
Sure they do Belz, consider what happens what a lethal mutation does to a functioning gene. These are called stabilizing selection pressures.
So... Is Kleinman arguing that mutation and evolution ONLY occur with selection pressures? There have been recorded mutations that basically created a new species for no real apparent reason.
Shalamar, I do read this thread, you can ask me directly. What I am arguing is that the mutation and selection process is profoundly slow when you have more than a single selection pressure. If you are going to argue that evolution occurs without selection, you should look at the probabilities of forming even the most simple protein or genetic sequence by the random addition of mers.
Very little progress is being made here, except in making Kleinman look like a fool.Hopefully, this annoys him, as well.
That’s true, rocketdodger started out knowing nothing of the mathematics of mutation and selection and has made no progress. If he is making me look like a fool, it is not with his mathematical prowess.

Sorry Belz, you are putting your hopes in the wrong thing but it is nice to know that I am annoying you with the mathematical and empirical facts of how mutation and selection actually works. I can see why you want to talk about your evolutionist Rorschach tests.

What would one of my posts be without a couple of citations which show how mutation and selection actually works?
http://jac.oxfordjournals.org/cgi/reprint/dki042v1.pdf (http://jac.oxfordjournals.org/cgi/reprint/dki042v1.pdf)
The clinical goals of HIV treatment are optimally accomplished through consistent high-level adherence to highly active antiretroviral therapy (HAART) and durable suppression of the viral load. However, as a result of the need for lifelong therapy and HIV’s prodigious replication rate and error-prone reverse transcriptase, varying amounts of antiretroviral drug resistance are common in treated individuals. Medication adherence is linked to the development of drug resistance, although not by a simple linear relationship. Recent studies have suggested that extensive drug resistance is not a major determinant of HIV disease progression and death. Rather, failure to access care and discontinuation of or non-adherence with therapy are arguably the most important factors associated with HIV disease progression in the HAART era. Other data indicate that continued therapy in the setting of extensive drug resistance and the inability to achieve viral suppression can provide continued clinical benefit. Such benefit may be mediated, at least partially, by reductions in viral fitness associated with drug resistance mutations.
If you don’t maintain the combination selection pressures, evolution proceeds.
http://www.pasteur.fr/applications/euroconf/hygiene/hygiene-abs.html (http://www.pasteur.fr/applications/euroconf/hygiene/hygiene-abs.html)
The continuous evolution of bacterial resistance to antimicrobial agents is a major threat for the coming years. Indeed, there are now cases where the penicillin resistance of Streptococcus pneumoniae has reached a level that ends in that some patients with penicillin resistant S. pneumoniae meningitis are very difficult to treat (1). Other examples of human infections for which the therapeutic arsenal is quasi evanescent include infections caused by multiresistant strains of Mycobacterium tuberculosis (2), glycopeptide-resistant Enterococcus (3), and Staphylococcus aureus multiresistant strains with decreased susceptibility to glycopeptides (4). Some gram-negative bacterial species causing community acquired infections, such as Yersinia pestis (5) or nosocomial infections, such as Pseudomonas aeruginosa (6), are also sometimes resistant to all available antibiotics. This evolution is by no means a new phenomenon. To the contrary, it was suspected very early in the development of antibiotics. Indeed, in a famous and premonitory interview, Alexander Flemming himself suggested that the development of resistance to penicillin of S. pneumoniae could become a major threat. Also, the development of resistance was observed very early after the introduction of antibiotics in human medicine, for instance against S. aureus or M. tuberculosis. However, neither the medical community nor the general public did developed too much concern about the development of bacterial resistance to antibiotics since the pharmaceutical industry discovered and regularly put on the market new drugs with increased antibacterial activity which restored the therapeutic balance. However, during the last decade, the rises in the rates of resistance to antimicrobial agents together with the scarcity of new antibiotics have resulted in a critical situation. This situation is often referred to as "window of vulnerability" during which an outbreak of infections due to a bacterial strain resistant to all available agents and with high epidemic and pathogenic potentials can occur. Even more, what we know of the continuous evolution of bacteria towards resistance since antibiotics have began to be used suggests strongly that the occurrence of such an event is only a matter of time, would everything be equal elsewhere. This talk will try to review the possible interventions that we have at hand to interfere with this process. The means that we have at hand to control bacterial resistance are limited to interventions on what we currently understand of the selection, multiplication and spread of bacterial resistance.
And
Can we influence the evolution of bacterial resistance ? They are a number of ways to influence the evolution of bacterial resistance. First we can try to prevent the selection of resistant mutants. This can be first achieved by using combination therapy. The best example of such a strategy is the prevention of selection of resistant in tuberculosis.
http://www.utm.utoronto.ca/~anders38/anderson2005.pdf (http://www.utm.utoronto.ca/~anders38/anderson2005.pdf)
Managing antifungal-drug resistance Given what is already known about the fitness landscape for antifungal-drug resistance, how might the evolution of resistance be channelled in a less damaging direction? There are three main possibilities, including combination therapy, which is already in use. Combination therapy uses two different antifungal drugs, simultaneously or in succession. The degree of interaction between the drugs that affect the fungus is commonly measured by the fractional inhibitory concentration index, which is determined by deploying both drugs in a checkerboard pattern in 96-well plates. Here, the effects might be categorized as synergism, indifference (that is, independence or absence of interaction) or antagonism42. The interactive effect of the drugs on the fungus can also be evaluated in time-kill studies. Beyond the immediate effects on the growth of the fungal pathogen, combination therapy might impede the evolution of resistance in two fundamental ways. First, where the combination of drugs has a greater inhibitory or killing effect on the fungus than either agent separately, the pathogen population size will be further reduced. Second, the overall rate of resistance to both agents will ideally approach zero, as the probability of simultaneously overcoming two different types of inhibition is the product of the probabilities of developing resistance to either agent when used on its own. An extreme example of using combination therapy to prevent resistance is flucytosine, which is only used in combination with other drugs because a high rate of resistance results when this drug is used alone. An intriguing interaction occurs between certain immunosuppressive agents, such as cyclosporine and FK506, and azole drugs, which have the potential for combination therapy. In Candida spp. and Saccharomyces spp., the immunosuppressive drugs inhibit the calcineurin pathway, which is an important component of the general response to stress. The calcineurin response is necessary for the fungal pathogen to maintain viability when azole drugs are present in the cell and are bound to their target protein, Erg11p (lanosterol 14α-demethylase).In combination with fluconazole, the combined effect on the pathogen is synergistic and results in loss of viability in the pathogen43–45, essentially because the tolerance response is curtailed. For the interference with calcineurin function to be exploited in combination with other antifungal drugs, however, it will ultimately be necessary to have antifungal molecules that distinguish the fungal calcineurin from the host calcineurin, to avoid modification of the host immune response. Similarly, the molecular chaperone Hsp90 (heat shock protein)is necessary for the general stress response, and a therapeutic antifungal anti-Hsp90 antibody that inhibits this chaperone is currently being tested in clinical trials46. In practice, the usefulness of combination therapy in treating fungal infections is mixed42, 47–49. Each potential drug combination requires in vitro tests, experiments with animal models, clinical trials and careful consideration of costs and benefits. Along with these direct effects on the pathogen, the patterns of resistance should also be evaluated.
Once again, combination selection pressures are shown to slow the evolutionary process by mutation and selection. That is the mathematical fact and that is the empirical fact.

[Shalamar]

Oh, that’s right, we all saw Jurassic Park, that’s how science works --- in Hollywood.

Errrrr. I see. Dinosaurs may be related to reptiles, but they are their own class of critter. Bone structure alone shows them to be vastly different. Reptiles are slung low to the ground with wide spacing legs. Dinosuars were upright, with legs under the bodies, not to the side. It is also theorized that dinosaurs due to their size, were warm blooded, and had hollow bones.

Birds fit the structure of dinosaurs. Upright bodies, warm blooded, and hollow bones.

There is also fossil evidence of dinosaurs with feathers, or evidence that the creature had feathers.

Jurrasic Park was a Movie, and should not be taken as pure science. They got a lot wrong. But it doesn't mean that they were ALL wrong. Velociraptors were, after all, about 3 -4 feet tall, and likely feathered.

Shalamar, I do read this thread, you can ask me directly. What I am arguing is that the mutation and selection process is profoundly slow when you have more than a single selection pressure. If you are going to argue that evolution occurs without selection, you should look at the probabilities of forming even the most simple protein or genetic sequence by the random addition of mers.

Others in this thread seem to know, and understand better than you do. You are basing your hypothesis on a model. A model is not reality. If anything your 'proofs' have shown that either your math is wrong, or the model is flawed. You also seem to be the only one arguing that Evolution is wrong, and thus Creationism must be true.

Mutations happen a great deal. Not all cause selection pressures. However, selection pressures don't cause mutations. They just enable mutations to become more or less prevalent. Some mutations don't do anything at all, and others may cause the creature to die before anything happens.

There are those that can say this better than I. I'm not a biologist, or a mathematician. I'm a lay person. I do understand the basic principles of Evolution, but not the true nitty gritty.

That said, there is a GREAT deal of evolution available. And far better than a model that seeks to create a 'perfect' or 'optimized' organism.

[rocketdodger]

Oh no rocketdodger, I didn’t say evolution was impossible. What I said was the theory of evolution was mathematically and empirically impossible; you can’t get common descent by the mutation and selection process.

Ahh I see what you are saying, evolution is mathematically and empirically impossible, but evolution is not impossible. That makes much more sense, thank you for clearing that up.

And you are right, you can't get common descent by the mutation and selection process, thats why bacteria that have evolved resistances are not descended from bacteria without resistances, they just pop into the world like antimatter. You are very sharp, I must admit, to have seen this when others have not. Bravo.

If you want to argue that reptiles evolved into birds, tell us what the selection conditions are that would evolve one gene at a time.

Why don't you tell us the environmental conditions that would lead to a bird popping into existence out of nowhere, since that seems to be your contention.

After you have done so, lets see whose idea is more absurd.


and you can continue to argue that n+1 selection conditions will sort mutations faster than n selection conditions.

I never claimed such a thing. I claimed that n + 1 selective pressures can lead to faster evolution than n pressures, depending on what the pressures are.

If this was not true, then bacteria would not evolve resistance to penicillin. Are you claiming that bacteria don't evolve resistance to penicillin, Kleinman?

[kleinman]

Oh, that’s right, we all saw Jurassic Park, that’s how science works --- in Hollywood.Errrrr. I see. Dinosaurs may be related to reptiles, but they are their own class of critter. Bone structure alone shows them to be vastly different. Reptiles are slung low to the ground with wide spacing legs. Dinosuars were upright, with legs under the bodies, not to the side. It is also theorized that dinosaurs due to their size, were warm blooded, and had hollow bones.

Birds fit the structure of dinosaurs. Upright bodies, warm blooded, and hollow bones.

There is also fossil evidence of dinosaurs with feathers, or evidence that the creature had feathers.

Jurrasic Park was a Movie, and should not be taken as pure science. They got a lot wrong. But it doesn't mean that they were ALL wrong. Velociraptors were, after all, about 3 -4 feet tall, and likely feathered.
You can give a course in comparative anatomy and birds may have some reptileopomorphism but to extrapolate that they descended from one another has no scientific or mathematical basis. Mutation and selection simply doesn’t work that way. Thank you for telling me that Jurassic Park is not science. I’ll return the favor to you and tell you the theory of evolution by mutation and selection is not science. The mathematical and empirical evidence of mutation and selection contradicts the theory.
Shalamar, I do read this thread, you can ask me directly. What I am arguing is that the mutation and selection process is profoundly slow when you have more than a single selection pressure. If you are going to argue that evolution occurs without selection, you should look at the probabilities of forming even the most simple protein or genetic sequence by the random addition of mers.Others in this thread seem to know, and understand better than you do. You are basing your hypothesis on a model. A model is not reality. If anything your 'proofs' have shown that either your math is wrong, or the model is flawed. You also seem to be the only one arguing that Evolution is wrong, and thus Creationism must be true.
I’m not basing my hypothesis on any old model. This is a model written by an ardent evolutionist who is head of computational molecular biology at the National Cancer Institute and this model was peer reviewed and published by the Oxford University Press Journal Nucleic Acids Research. In addition, my hypothesis is not based solely on Dr Schneider’s model; it is based on hundreds of real examples of precisely measured mutation and selection processes. Neither Dr Schneider’s math nor is his model wrong. It properly demonstrates the behavior of the mutation and selection process when multiple selection conditions are applied and when only a single selection condition is applied. And what it shows is the sorting of mutations is much, much faster when only a single selection condition is applied than when evolving all three selection conditions simultaneously.

Shalamar, have you looked at Dr Schneider’s model? Why don’t you look at the model and see if you can find an error in his model or his mathematics?
Mutations happen a great deal. Not all cause selection pressures. However, selection pressures don't cause mutations. They just enable mutations to become more or less prevalent. Some mutations don't do anything at all, and others may cause the creature to die before anything happens.
What you have just said is the basis for Dr Schneider’s model. What his model shows is that sorting mutations becomes profoundly slow when you have multiple selection conditions. Read the citations which I have and will continue to post. They show the same thing as Dr Schneider’s model. That is the mathematical and empirical reality of how mutation and selection works.
There are those that can say this better than I. I'm not a biologist, or a mathematician. I'm a lay person. I do understand the basic principles of Evolution, but not the true nitty gritty.
Well Shalamar, I am both a mathematician and a biologist (before you evolutionists start screaming that I am not a biologist, I have a BS degree in advanced biological sciences as well as my other advanced degrees) and I’ll try to explain this to you so a lay person can understand how mutation and selection works.

Mutation and selection is a sorting problem. Beneficial and detrimental mutations are sorted based on selection conditions. What the mathematical and empirical evidence shows is the sorting process only works quickly with a single selection condition. If you have multiple selection conditions, the sorting process is profoundly slowed. Here is an example of sorting which you might understand. Take the telephone book. If you are to sort by the names in the phone book, that is fairly simple. However, if I ask you to not only sort by name but by address and phone number simultaneously, this becomes a much more difficult sorting process. Compared to the mutation and selection process, this sorting of the telephone book is trivial when compared to the sorting that mutation and selection must do to evolve against multiple selection conditions simultaneously. This is why combination therapy works at profoundly slowing and in some cases stopping the evolutionary process by mutation and selection for treatment of infectious diseases, cancer, weeds…
That said, there is a GREAT deal of evolution available. And far better than a model that seeks to create a 'perfect' or 'optimized' organism.
There is a great deal of microevolutionary processes occurring but none which add up to an explanation for common descent. Mutation and selection simply doesn’t work that way.
Oh no rocketdodger, I didn’t say evolution was impossible. What I said was the theory of evolution was mathematically and empirically impossible; you can’t get common descent by the mutation and selection process.Ahh I see what you are saying, evolution is mathematically and empirically impossible, but evolution is not impossible. That makes much more sense, thank you for clearing that up.

And you are right, you can't get common descent by the mutation and selection process, thats why bacteria that have evolved resistances are not descended from bacteria without resistances, they just pop into the world like antimatter. You are very sharp, I must admit, to have seen this when others have not. Bravo.
If you want to call bacteria evolving to bacteria as an example of common descent, I’ll accept your terminology but if you are going to argue that bacteria evolved into humans, no sale.
If you want to argue that reptiles evolved into birds, tell us what the selection conditions are that would evolve one gene at a time.Why don't you tell us the environmental conditions that would lead to a bird popping into existence out of nowhere, since that seems to be your contention.

After you have done so, lets see whose idea is more absurd.
Can’t you read the title of this thread? So you would rather believe in a mathematically and empirically impossible theory. Now that’s absurd.
and you can continue to argue that n+1 selection conditions will sort mutations faster than n selection conditions.I never claimed such a thing. I claimed that n + 1 selective pressures can lead to faster evolution than n pressures, depending on what the pressures are.

If this was not true, then bacteria would not evolve resistance to penicillin. Are you claiming that bacteria don't evolve resistance to penicillin, Kleinman?
Oh, a little slipping and sliding in your argument. Tell us what those n+1 selective pressures are that can lead to faster evolution than n selective pressures?

Bacteria evolve resistance to penicillin because of the selection pressure of this bacterial toxin. Put a second selection pressure on the bacteria and it slows the ability of the bacterial population to evolve to both selection pressures simultaneously. That’s how mutation and selection works mathematically and that’s how mutation and selection works empirically.

[Belz...]

Belz is still mystified how mutation and selection actually works. You need selection pressure if something is to evolve

Well, actually you need a selection pressure in order to drive evolution in a certain direction. Without selection pressures, a situation that never happens, any and all mutations would be viable, which is nonsense. I don't know why you even brought it up.

I wonder who's mystified about how mutation and selection works.

Doubling the number of selection pressures does not double the rate of evolution. The first selection pressure is the easiest for a population to evolve to. Each additional selection pressure slows the process much more so.

Aside from the fact that you're taking out of your ass, the simple fact is that the relative strengths of the pressures is also important. Again, think "meteor". If the weaker selection pressures becomes irrelevant, the fact that they're there doesn't really matter, anymore (hence the term "irrelevant"). Of course, it's debatable that there was ever two identically strong selection pressures before we started to try to stop viral evolution...

Each additional selection pressure slows the process much more so.

For no apparent reason...

So Belz, no selection pressures, no evolution, one selection pressure, the easiest for the population to evolve to, additional selection pressures confound the sorting process for beneficial and detrimental mutations. That’s how the mathematics works and that’s how reality works.

That's great, Klein. 0 < 1 > 2.

Belz, you’ve gotten me so confused, I can’t remember what my theory is. Could you help me out, now don’t be fiendish.

Your theory is that multiple selection pressures profoundly slow evolution, making it impossible, which is why your examples, which prove that evolution exists -- because why the hell would we want to slow down the evolution of viruses if they don't evolve in the first place ?

Belz, don’t you realize that I am using the CTRL-X key on the theory of evolution.

There is no such thing as a CTRL-X key. It's a combination of keys. Which means it profoundly slows down your attempts at typing it.

Yea, Mr Scott, give us a reference which proves that feathers can grow on birds.

On scales. Didn't you even read it ?

Add a single strong selection pressure, quicken evolution; add additional selection pressures, slow evolution profoundly.

Even if those pressures are relatively very, very weak ?

Sorry Belz, you are putting your hopes in the wrong thing but it is nice to know that I am annoying you with the mathematical and empirical facts of how mutation and selection actually works.

Only in your mind, Klein. You're annoying me because you're too dense to understand why your own arguments defeat your conclusion.

[Belz...]

Why don't you tell us the environmental conditions that would lead to a bird popping into existence out of nowhere, since that seems to be your contention.

What I find funny is that creationists sometimes use the first law of thermodynamics as proof that God created the universe. Oh, the irony.

If this was not true, then bacteria would not evolve resistance to penicillin. Are you claiming that bacteria don't evolve resistance to penicillin, Kleinman?

Of course they do! But they're only affected by a single selection pressure. Somehow.

[kleinman]

Belz is still mystified how mutation and selection actually works. You need selection pressure if something is to evolveWell, actually you need a selection pressure in order to drive evolution in a certain direction. Without selection pressures, a situation that never happens, any and all mutations would be viable, which is nonsense. I don't know why you even brought it up.

I wonder who's mystified about how mutation and selection works.
You don’t have that quite right Belz. Even in the absence of directional selection pressures you always have stabilizing selection pressures. A member of a population can have a fatal mutation and is selected out despite every other gene in his genome is perfectly functional.

Belz, if you study the mathematics of mutation and selection, it takes the mystery out of the process.
Doubling the number of selection pressures does not double the rate of evolution. The first selection pressure is the easiest for a population to evolve to. Each additional selection pressure slows the process much more so.Aside from the fact that you're taking out of your ass, the simple fact is that the relative strengths of the pressures is also important. Again, think "meteor". If the weaker selection pressures becomes irrelevant, the fact that they're there doesn't really matter, anymore (hence the term "irrelevant"). Of course, it's debatable that there was ever two identically strong selection pressures before we started to try to stop viral evolution...
Why don’t you explain to us in your mathematically challenged mind how the strengths of selection pressures affect the sorting process of beneficial and detrimental mutations?

[joobz]

You must be one of those evolutionists that claim that infectious diseases and cancers can never me cured, they will always evolve resistance. You aren't one of those doctors who thinks that there's no such thing as antibiotic-resistant bacteria, are you?


Oh, but I forgot, evolution is not your field. You aren’t a mathematician and evolution is not your field but you claim you know everything about mutation and selection. As long as there is enough free energy, anything is possible.Why don't you explain how any of those sentences are related to anything that is being discussed here.

[rocketdodger]

Here is an example of sorting which you might understand. Take the telephone book. If you are to sort by the names in the phone book, that is fairly simple. However, if I ask you to not only sort by name but by address and phone number simultaneously, this becomes a much more difficult sorting process.

Unless you tell him that sorting by name is 1000 times as important as sorting by address and phone number, in which case he will surely worry about the names and ignore the addresses and phone numbers.

Which is exactly what happens in nature when a strong pressure combined with other weaker ones.


So you would rather believe in a mathematically and empirically impossible theory. Now that’s absurd.

I never claimed that humans descend from bacteria. Or that birds descend from reptiles. I frankly don't really care about that stuff, never said I did. You keep trying to bring it up to draw attention away from the fact that we have shown you documented examples of multiple selective pressures that lead to rapid evolution.


Oh, a little slipping and sliding in your argument. Tell us what those n+1 selective pressures are that can lead to faster evolution than n selective pressures?

Oh, I dunno, how about for the n pressures we have (with bacteria)

{weak pressure, weak pressure, ... , weak pressure} = n pressures and no evolution

{weak pressure, weak pressure, ... , weak pressure, very strong pressure} = n + 1 pressures and rapid evolution.

In the words of Biff Tanner, HELLO, MCFLY.

Bacteria evolve resistance to penicillin because of the selection pressure of this bacterial toxin.

Which shows that evolution can occur rapidly under multiple selective pressures, if the difference in magnitudes between the strongest pressure and all the rest is sufficient.


Put a second selection pressure on the bacteria and it slows the ability of the bacterial population to evolve to both selection pressures simultaneously.

Which shows that evolution can be profoundly slowed under multiple selective pressures, if the magnitude of the strongest pressures are similar.

Put those two together, and a sane person will conclude that multiple selective pressures may or may not slow evolution.

[rocketdodger]

Even in the absence of directional selection pressures you always have stabilizing selection pressures.

Now you claim populations are always under the effects of multiple selective pressures? That would mean, according to your theory, that any additional pressures would only slow evolution. So how do bacteria evolve resistance to pencillin?

Why don’t you explain to us in your mathematically challenged mind how the strengths of selection pressures affect the sorting process of beneficial and detrimental mutations?

What difference do the strengths of selection pressures have in the mutation and selection sorting process?


Its funny you say such things, given that you have already explained it yourself:

Rocketdodger, only one selection condition is evolving on the background of n weak selection conditions which are not evolving anywhere. These n weak selection conditions only serve to slow the evolution of the one strong selection condition. The weak selection conditions only interfere with the sorting of mutations for the strong selection condition.

Does anyone know if this Kleinman guy really is a "doctor?" Does anyone have a link to a site with info about him? I would really like to see a picture of him so I have a face to associate with this stupidity.

[kleinman]

You must be one of those evolutionists that claim that infectious diseases and cancers can never me cured, they will always evolve resistance.You aren't one of those doctors who thinks that there's no such thing as antibiotic-resistant bacteria, are you?
Of course not joobz, I know there is such thing as antibiotic-resistant bacteria and if listen to the mathematically baseless bizarre speculations that you evolutionist put forth of how mutation and selection works, there will be plenty more resistant bacteria.
Oh, but I forgot, evolution is not your field. You aren’t a mathematician and evolution is not your field but you claim you know everything about mutation and selection. As long as there is enough free energy, anything is possible.Why don't you explain how any of those sentences are related to anything that is being discussed here.
That’s easy to explain, science is not supposed to be based on ignorant speculation and that is the basis of your argument in this discussion. If you think that I am making this up about you, recall you own words.
Envision a system of millions of forming and destructive chemical reactions. Now, envision that intermediates of there reactions associate through non-covalent means and that this complex becomes protected against the destructive reactive pathway, perhaps by a reversible precipitation. These new complexes result in a localized increased of new chemical species. These chemical species then progress in a new series of reaction... that is what I mean through cooperative means. I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.
and
If there was a "sticky" thread on drug delivery, biomaterials or polymer chemistry, I'd be there instantly. But evolution isn't my field.
Joobz, you have a PhD and are a professor of chemical engineering. If you want to engage in a discussion with me about the mathematics of mutation and selection and the empirical evidence which supports this mathematics, do it with scientific rigor, not the sloppy ignorant speculations you are using because what I am presenting doesn’t agree with your belief system. Until then, I’ll call you out for your use of sloppy ignorant speculations.
Put a second selection pressure on the bacteria and it slows the ability of the bacterial population to evolve to both selection pressures simultaneously.Which shows that evolution can be profoundly slowed under multiple selective pressures, if the magnitude of the strongest pressures are similar.

Put those two together, and a sane person will conclude that multiple selective pressures may or may not slow evolution.
What a sane person who understands the mathematics of mutation and selection would conclude is there are no cooperative selection pressures weak or strong. Every selection pressure interferes with the evolution of the other selection pressures.

Rocketdodger, which population of bacteria will evolve resistance to penicillin more quickly, a population in vitro which is not subject to a patient’s immune system and all weak selection pressures reduced to a minimum or a population in vivo that is subject to a patient’s immune system and numerous other weak selection pressures?

[rocketdodger]

What a sane person who understands the mathematics of mutation and selection would conclude is there are no cooperative selection pressures weak or strong. Every selection pressure interferes with the evolution of the other selection pressures.

Assuming this is true, so what? It only means "combination selective pressures slow evolution," not 'profoundly slow.'

You have already admitted that relatively weak pressures do not interfere with a relatively strong pressure sufficiently to slow evolution much at all -- that is why bacteria evolve resistance to penicillin. If you mean "profoundly" to mean "not much at all" then yes your theory is spot on. Pure brilliance.


Rocketdodger, which population of bacteria will evolve resistance to penicillin more quickly, a population in vitro which is not subject to a patient’s immune system and all weak selection pressures reduced to a minimum or a population in vivo that is subject to a patient’s immune system and numerous other weak selection pressures?

Probably the one in vitro. Which is still under multiple selective pressures, as you admit here with the phrase "weak selection pressures reduced to a minimum." So now you are claiming that evolution can be rapid under multiple selection pressures, as long as all but one of them are relatively weak. Given that you just claimed the strength of selection pressures is irrelevant in a previous post, I don't see how you arrived at this (correct) conclusion.

[kleinman]

What a sane person who understands the mathematics of mutation and selection would conclude is there are no cooperative selection pressures weak or strong. Every selection pressure interferes with the evolution of the other selection pressures.Assuming this is true, so what? It only means "combination selective pressures slow evolution," not 'profoundly slow.'

You have already admitted that relatively weak pressures do not interfere with a relatively strong pressure sufficiently to slow evolution much at all -- that is why bacteria evolve resistance to penicillin. If you mean "profoundly" to mean "not much at all" then yes your theory is spot on. Pure brilliance.
Rocketdodger, if you studied ev, you would realize that “combination selection pressures profoundly slow evolution,” not ‘slow’. Weak selection pressures may not profoundly slow the evolution of a single strong selection pressure but they do slow the evolutionary process.
Rocketdodger, which population of bacteria will evolve resistance to penicillin more quickly, a population in vitro which is not subject to a patient’s immune system and all weak selection pressures reduced to a minimum or a population in vivo that is subject to a patient’s immune system and numerous other weak selection pressures?Probably the one in vitro. Which is still under multiple selective pressures, as you admit here with the phrase "weak selection pressures reduced to a minimum." So now you are claiming that evolution can be rapid under multiple selection pressures, as long as all but one of them are relatively weak. Given that you just claimed the strength of selection pressures is irrelevant in a previous post, I don't see how you arrived at this (correct) conclusion.
Now you are starting to get a little understanding of the mutation and selection process except you still need to understand only the strong selection pressure is evolving in these situations on a background of weak selection pressures that only serve to slow the evolutionary process for that single strong selection pressure. As soon as you add a second strong selection pressure it becomes profoundly more difficult for the population to evolve to both strong selection pressures simultaneously. In addition any weak selection pressures the populations are subject to only make it more difficult for the population to evolve to the two strong selection pressures. Each selection pressure adds an additional sorting condition for the mutation and selection process confounding the population finding a trajectory to a new local optimum.

I have not said that weak selection pressures are irrelevant; I have said that weak selection pressures do not have a marked effect on a population finding a trajectory to a new fitness local optimum for a single strong selection pressure but what effect they do have is to slow the search for that trajectory. Each selection pressure has its own trajectory to a new local optimum, each competing with the other. This effect is most pronounced when you have two or more strong selection pressures each pushing the population in their own particular directions on the fitness landscape.

Here is another empirical example of how this mathematical behavior plays out in reality.
http://hbvadvocate.org/news/NewsUpdates_pdf/2.2_Conference_Reports/EASL_2002_Agenda/Section4/zoulim.pdf (http://hbvadvocate.org/news/NewsUpdates_pdf/2.2_Conference_Reports/EASL_2002_Agenda/Section4/zoulim.pdf)
HBV resistance to lamivudine is a frequent and significant therapeutical problem. With the results of clinical trials and independent studies, clinicians have now a better knowledge of the incidence of drug resistance and its clinical consequence. There are still many clinical questions to be answered regarding the predictive factors of lamivudine resistance development and of the severity associated with viral resistance. New drugs are being evaluated in experimental models and clinical trials. Among them, Adefovir dipivoxil is the more advanced in clinical development and represents a very promising inhibitor that has been assessed in phase III trials and should be registered soon. It has an interesting antiviral profile with i) a potent activity against lamivudine resistant strains which is useful as a rescue treatment of lamivudine resistance, ii) and the absence of selection of drug resistant strains up to 3 years of therapy. As new progress has been made, we have now not only the capacity to control lamivudine resistance but also many tools to detect and prevent treatment failure. In this view, it will be important to determine the best strategy to prevent drug resistance using combinations of nucleoside analogs such as lamivudine, adefovir, and others, with immunostimulatory approaches based on pegylated interferon alfa, new therapeutic vaccines or others.
This is what combination selection pressures do in reality.

[joobz]

That’s easy to explain, science is not supposed to be based on ignorant speculation and that is the basis of your argument in this discussion. If you think that I am making this up about you, recall you own words.
Nope. Your assumptions are wrong. That isn't speculative. It's reality.
Joobz, you have a PhD and are a professor of chemical engineering. If you want to engage in a discussion with me about the mathematics of mutation and selection and the empirical evidence which supports this mathematics, do it with scientific rigor, not the sloppy ignorant speculations you are using because what I am presenting doesn’t agree with your belief system. Until then, I’ll call you out for your use of sloppy ignorant speculations.
Too bad that you are the least qualified to do so. I have been very explicit and accurate in my critique of YOUR theory. Your theory has been dead for over a year. You have nothing new to offer.

[kleinman]

That’s easy to explain, science is not supposed to be based on ignorant speculation and that is the basis of your argument in this discussion. If you think that I am making this up about you, recall you own wordsNope. Your assumptions are wrong. That isn't speculative. It's reality.
You try to tell people that Dr Schneider’s computer model is mine then you try to tell people your ignorant speculations are mine. If you had any evidence for your ignorant speculations you would have posted it long ago. Oh yes, you have posted a citation, you believe that Madagascar rainforests and plate tectonics accelerated the mutation and selection process. Let’s remind the readers of this.
If there was a "sticky" thread on drug delivery, biomaterials or polymer chemistry, I'd be there instantly. But evolution isn't my field.
So your field is chemical engineering, lets hear your view of chemistry and abiogenesis.
Envision a system of millions of forming and destructive chemical reactions. Now, envision that intermediates of there reactions associate through non-covalent means and that this complex becomes protected against the destructive reactive pathway, perhaps by a reversible precipitation. These new complexes result in a localized increased of new chemical species. These chemical species then progress in a new series of reaction... that is what I mean through cooperative means. I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?

Now joobz, let’s post another citation which supports the hypothesis that combination selection pressures profoundly slow and can stop the evolutionary process.
http://qjmed.oxfordjournals.org/cgi/reprint/91/9/593.pdf (http://qjmed.oxfordjournals.org/cgi/reprint/91/9/593.pdf)
I have attempted to highlight the recent significant and impressive advances in the treatment of chronic viral hepatitis. Profound inhibition of viral replication is associated with normalization of serum transminases and with a favourable evolution of liver histology. For many patients, treatment of short duration can achieve sustained inhibition of viral replication. Attention needs to be focused on (a) the development of combination therapy for prolonged inhibition of HBV replication without the emergence of resistance, and (b) improved protocols for the treatment of HCV-infected patients with advanced disease and unfavourable virological characteristics.
Joobz, you better contact these authors and tell them that you can’t stop evolution but you can change lead into gold by letting the sun shine on it long enough.
http://forums.randi.org/images/smilies/doglaugh.gif

[rocketdodger]

Rocketdodger, if you studied ev, you would realize that “combination selection pressures profoundly slow evolution,” not ‘slow’. Weak selection pressures may not profoundly slow the evolution of a single strong selection pressure but they do slow the evolutionary process.

These two statements perfectly illustrate the nonsense of your arguments in this thread Kleinman.

In the first, you say multiple selective pressures profoundly slow evolution.

In the second, you say multiple selective pressures may not profoundly slow, but rather simply slow evolution.

So you claim that multiple selective pressures profoundly slow evolution, but may not profoundly slow evolution? I honestly think you don't even know what you are saying anymore.

For the record, I would have no problem with your claim if you changed the wording to "combination selective pressures of similar strengths profoundly slow evolution," but for some reason (probably you being stubborn) you just refuse.

[kleinman]

Rocketdodger, if you studied ev, you would realize that “combination selection pressures profoundly slow evolution,” not ‘slow’. Weak selection pressures may not profoundly slow the evolution of a single strong selection pressure but they do slow the evolutionary process.These two statements perfectly illustrate the nonsense of your arguments in this thread Kleinman.
If you understood the mathematics of mutation and selection, these statements would make sense to you but this will have to wait for a little while. While you try to figure out the mathematics of mutation and selection, I have a few more citations which show how mutation and selection works empirically.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1692562 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1692562)
Antimarial drug resistance develops when spontaneously occurring parasite mutants with reduced susceptibility are selected, and are then transmitted. Drugs for which a single point mutation confers a marked reduction in susceptibility are particularly vulnerable. Low clearance and a shallow concentration-effect relationship increase the chance of selection. Use of combinations of antimalarials that do not share the same resistance mechanisms will reduce the chance of selection because the chance of a resistant mutant surviving is the product of the per parasite mutation rates for the individual drugs, multiplied by the number of parasites in an infection that are exposed to the drugs. Artemisinin derivatives are particularly effective combination partners because (i) they are very active antimalarials, producing up to 10,000-fold reductions in parasite biomass per asexual cycle; (ii) they reduce malaria transmissibility; and (iii) no resistance to these drugs has been reported yet. There are good arguments for no longer using antimalarial drugs alone in treatment, and instead always using a combination with artemisinin or one of its derivatives.
http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&dopt=AbstractPlus&list_uids=10697872 (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=PubMed&dopt=AbstractPlus&list_uids=10697872)
Resistance to antimalarial drugs arises when spontaneously occurring mutants with gene mutations or amplifications which confer reduced drug susceptibility are selected, and are then transmitted. Simultaneous use of two or more antimalarials with different modes of action and which therefore do not share the same resistance mechanisms will reduce the chance of selection, because the chance of a resistant mutant surviving is the product of the parasite mutation rates for the individual drugs, multiplied by the number of parasites in an infection that are exposed to the drugs. The artemisinin derivatives are very active antimalarials, which produce large reductions in parasite biomass per asexual cycle, and reduce malaria transmissibility. To date no resistance to these drugs has been reported. These drugs therefore make particularly effective combination partners. This suggests that antimalarial drugs should not be used alone in treatment, but always in combination, as in the treatment of tuberculosis or HIV, and that the combination should include artemisinin or one of its derivatives.
http://clincancerres.aacrjournals.org/cgi/content/abstract/7/8/2168 (http://clincancerres.aacrjournals.org/cgi/content/abstract/7/8/2168)
The concept of combining chemotherapeutic agents to increase cytotoxic efficacy has evolved greatly over the past several years. The rationale for combination chemotherapy has centered, in the past, on attacking different biochemical targets, overcoming drug resistance in heterogeneous tumors, and by taking advantage of tumor growth kinetics with increasing the dose-density of combination chemotherapy. The overall goal was to improve clinical efficacy with acceptable clinical toxicity. With our increased understanding of the cell cycle and the impact chemotherapeutic agents have on the cell cycle, it is increasingly apparent that this physiology can create drug resistance, thereby reducing combination chemotherapeutic efficacy. This is particularly relevant with the advent of cell cycle-specific inhibitors but also has relevance for the action of standard chemotherapeutic agents currently in clinical practice. This cell cycle-mediated resistance may be overcome by a greater understanding of chemotherapeutic cell cycle effects and by appropriate sequencing and scheduling of agents in combination chemotherapy. In this review, we have elected to illustrate the evolving concept of cell cycle-mediated drug resistance with novel drug combinations that include the taxanes, camptothecins, and fluorouracil. This review indicates that as our understanding of the cell cycle grows, our ability to appropriately sequence chemotherapy to overcome cell cycle-mediated drug resistance can have a great impact on our therapeutic approach in the treatment of human cancers.
You all have a good week end and may your selection pressures be weak and few in number.

[Shalamar]

Got it Kleinman does allow for 'micro evolution', but discounts Speciation or 'Macro Evolution'.

Scary that he claims to be a Biologist. At least I know where he stands now. No point debating him. I don't have the skills to do so, and I can't refute his math. Despite the fact that Evolution on a grand scale exists, and that mutations, and speciation has occurred without his mandatory selection pressures.

[geo_flux]

i think its interesting what happens when we apply Kleinman's logic to other computer models.

There are plenty of computer models around designed to simulate and forecast weather, some using extremely powerful super computers. None of these models can completely model the behaviour inside a hurricane or predict where they will strike. So therefore hurricanes don't exist!

If a computer model can't accurately simulate and predict a hurricane then its obvious that hurricanes are a lie, it couldnt possible mean that the computer models are lacking.

No wonder George W was so slow to react to Katrina! (sorry to drag bad taste and politics into this, couldn't resist)

[joobz]

You try to tell people that Dr Schneider’s computer model is mine then you try to tell people your ignorant speculations are mine. If you had any evidence for your ignorant speculations you would have posted it long ago. Oh yes, you have posted a citation, you believe that Madagascar rainforests and plate tectonics accelerated the mutation and selection process. Let’s remind the readers of this.

So your field is chemical engineering, lets hear your view of chemistry and abiogenesis.
[/color]
http://forums.randi.org/images/smilies/doglaugh.gif
Joobz, if the sun shines on lead long enough does it turn into gold?

Now joobz, let’s post another citation which supports the hypothesis that combination selection pressures profoundly slow and can stop the evolutionary process.
http://qjmed.oxfordjournals.org/cgi/reprint/91/9/593.pdf (http://qjmed.oxfordjournals.org/cgi/reprint/91/9/593.pdf)

Joobz, you better contact these authors and tell them that you can’t stop evolution but you can change lead into gold by letting the sun shine on it long enough.
http://forums.randi.org/images/smilies/doglaugh.gif
you're funny.
inconsequential, but funny.

had any luck with your assumptions?
nope.
Oh well.

[kjkent1]

i think its interesting what happens when we apply Kleinman's logic to other computer models.The concept of kleinman logic is roughly the same as that of jumbo shrimp.

[rocketdodger]

No point debating him. I don't have the skills to do so, and I can't refute his math.

Wrong, and wrong. All you need to debate him is common sense, and he has no math to refute. Join the fun!

[Kotatsu]

I found the original link I learned this from, but now the link is dead. It's http://hometown.aol.com/darwinpage/dinobirds.htm and here's the quote:


While googling for it I found this really cool paper about dinosaur/bird evolution:
http://www.talkreason.org/articles/coulter3.cfm

A remark there on "hen's teeth:"

This sounds amazing! I will look at this after the bloody journal club I have to go to soon. Many thanks! I have almost two decimetres of papers on dinosaur-bird evolution (most of which is sadly unread), and the sites you linked to seemt o be able to add to that considerably.

[Kotatsu]

Just a thought: has anyone argued that mutations can create their own selection pressures ?

Does that make sense, or am I just making stuff up ?

ETA: And by that, I mean that the action of some new or altered genes may create new selection pressures that will hasten the emergence of something else, assumine the altered gene is passed on.

I'm not really sure if I follow you entirely, but does the paper I posted earlier (when Hammegk was still in the thread) with the hybridisation between Brassica species in any way similar to what you are thinking of? The new sequences caused by recombination when these hybrids were formed caused the offspring to evolve extremely quickly over just a few generations, and expressing these changes in half a dozen phenotypic characters. It's been some time since I went over that paper last, so I don't remember the details much, but I could check it for you, if you want (or send you a link to or a copy of the paper if you prefer to check for yourself).

[Kotatsu]

You have not physical reality which shows mutation and selection can transform reptile into birds.

As has been pointed out to you before, dinosaurs, not any generic reptile, are thought to have evolved into birds. As I just mentioned, I have almost two decimetres of articles describing this process, as well as descriptions and (originally) colour plates showing the various feathered dinosaur fossils that have been found, primarily in China.

The idea that reptiles evolved into birds in tiny steps over millions of years should pose problems for evolutions when the mechanism of mutation and selection can transform only a tiny number of genes at once.

What is the mechanism that at least theoretically stops all genes in a e.g. a sperm to mutate and then get transmitted to the next generation?

you can’t get common descent by the mutation and selection process.

Of course you can. Look in more or less any phylogenetic paper and you will get exactly that. For instance, I have in front of me a sort of technical meta-study which uses the data of two previously published studies to study a certain aspect of Bayesian inference and gene trees vs. species trees. It displays a partly well resolved tree of the genus Macaca which --- ignoring the branches with low probability --- shows quite nicely that the genus is descended from the same ancestor (1). This tree is based on genes which differ due to mutations, and --- so the authors assure me, and I know little of Macaques, so I cannot dispute it --- corresponds strongly with the geographical distribution of the species.

Yea, Mr Scott, give us a reference which proves that feathers can grow on birds.

And now that he has kindly provided you (and me!) with more references than I'd care to shake a stick at, what will you do? Ignore it, dismiss it or obfuscate matters by your usual c&p routine?

---
(1) A caveat: only one outgroup taxon is used, but the authors claim the tree is the same as that of the original study, in which six outgroup taxa were used. I haven't read the original paper, though. The paper, the maths of which I don't claim to understand, is Liu and Pearl (2007), Syst. Biol. 56 (3), 504-514.

[Belz...]

You need selection pressure if something is to evolve

Well, actually you need a selection pressure in order to drive evolution in a certain direction. Without selection pressures, a situation that never happens, any and all mutations would be viable, which is nonsense. I don't know why you even brought it up.

You don’t have that quite right Belz. Even in the absence of directional selection pressures you always have stabilizing selection pressures. A member of a population can have a fatal mutation and is selected out despite every other gene in his genome is perfectly functional.

That's true, but that's not what you were saying, Klein. Again, moving the goalposts. What you said WAS:

You need selection pressure if something is to evolve

Where does it say "directional" ?

You're lying, again.

Belz, if you study the mathematics of mutation and selection, it takes the mystery out of the process.

Yes indeed. So why don't you ?

Why don’t you explain to us in your mathematically challenged mind

Reported.

how the strengths of selection pressures affect the sorting process of beneficial and detrimental mutations?

You mean, you need it explained to you AGAIN ?

[Belz...]

Rocketdodger, which population of bacteria will evolve resistance to penicillin more quickly, a population in vitro which is not subject to a patient’s immune system and all weak selection pressures reduced to a minimum or a population in vivo that is subject to a patient’s immune system and numerous other weak selection pressures?

Bacteria evolve resistance to penicillin because of the selection pressure of this bacterial toxin.

So, basically, you're admitting that evolution CAN be hastened by a strong selection pressure when other pressures are relatively weak ?

Why the hell are you arguing with us, then ?

Rocketdodger, if you studied ev, you would realize that “combination selection pressures profoundly slow evolution,” not ‘slow’. Weak selection pressures may not profoundly slow the evolution of a single strong selection pressure but they do slow the evolutionary process.

You're just chock-full of contradictions, aren't you ?

...except you still need to understand only the strong selection pressure is evolving in these situations on a background of weak selection pressures that only serve to slow the evolutionary process for that single strong selection pressure.

That makes no sense at all, and it sounds suspiciously like someone who's trying to desperatly save face after badly losing an argument.

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

And this is especially telling of how much you understand...

[Belz...]

I'm not really sure if I follow you entirely, but does the paper I posted earlier (when Hammegk was still in the thread) with the hybridisation between Brassica species in any way similar to what you are thinking of?

I was just speculating about selection pressures internal to an individual.

The concept of kleinman logic is roughly the same as that of jumbo shrimp.

http://forums.randi.org/imagehosting/thum_60804721d5d0eb899.jpg (http://forums.randi.org/vbimghost.php?do=displayimg&imgid=8937)

[Dr Adequate]

Has he thought of any new lies?

[Dr Adequate]

The reason why I can copy and paste citations is that I understand how mutation and selection actually works, now rocketdodger joins Adequate and argues that n +1 selection conditions sort mutations more quickly than n selection conditions. I notice that you're now too frightened of my results to tell people what I have actually argued.

You used to quote my actual posts on this subject over and over, until you realised what a bloody fool you were making of yourself.

Poor little man.

[Dr Adequate]

Let's do it again. I guess most of you will have seen this, but for the newbies, this is what kleinman is whining and lying about.

http://img514.imageshack.us/img514/3974/genegraphhx4.jpg

Here's the description I posted of the graph.

The red line shows generations to achieve fixation of n alleles acted on by n selection pressures, the n+1th selection pressure being introduced only after the nth allele is fixed.

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

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

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.

It is, of course, this last statement which kleinman is attempting to conceal behind his crude, stupid mis-statement of my results.

And here is my layman's explanation of why my result must be true, specially adapted for the use of drooling retards and kleinman.

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

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

Now, consider the following two options:

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

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

Which method do you think would be faster?

NOTE FOR COMPLETE MORONS, I.E. KLEINMAN: the fact that both methods take longer the more animals there are on the list does not somehow magically mean that the first method is better.

It is interesting to note that kleinman has never had the guts to respond to this little parable, although I've repeated it several times for his edification, which suggests that I have in fact, made it simple enough for him to realise that I'm right and he's wrong.

[Kotatsu]

I was just speculating about selection pressures internal to an individual.

Then maybe that paper is relevant after all? The original mutation wasn't a point mutation, but rather a cross-over event between genomes from two different species, but the resulting hybrid genome --- influenced heavily, if I recall correctly, by that of the mitochondria --- did put a lot of pressure on itself, which lead to an extremely rapid evolution.

[T'ai Chi]

Arguing against intelligent designers from a computer program is poor logic since it takes an intelligent designer to write a computer program.

Yup.

[CFLarsen]

Arguing against intelligent designers from a computer program is poor logic since it takes an intelligent designer to write a computer program.

Yup.

....yes, T'ai Chi.

That's the idea.

[delphi_ote]

Yup.
I'm going to just go ahead and assume this nasty bit of arrogance tacked on to the end of your incoherent post is your answer to the obvious question: "I guess you're not getting enough attention in all the other threads you start but never respond to, so now you're trolling this thread, too?"

[Dr Adequate]

Arguing against intelligent designers from a computer program is poor logic since it takes an intelligent designer to write a computer program. As you come up with this witless crap every coupla months or so, could I refer you to the last time I refuted this pile of crud?

http://fstdt.com/winace/pics/broken_record.jpg

By the way, are you hammegk's kid brother?

[rocketdodger]

Arguing against intelligent designers from a computer program is poor logic since it takes an intelligent designer to write a computer program.

Yup.

Yup.

Specifically, intelligent human designers, who are a product of evolution, to write a computer program. Which means you are implying evolved beings created evolution...

Of course, you have heard this before, and you know it effectively counters your argument, but you try and try again hoping that someone new won't know about it yet.

[rocketdodger]

Has he thought of any new lies?

Not so much lies as utter stupidity, including:

-Asking me to list exactly which n pressures a population of bacteria is under, including the mutations/alleles/genes they "target?" before I can show that adding penicillin, the n + 1 pressure, spurs the rapid evolution of penicillin resistance.

-Claiming that penicillin resistance might have evolved, in every species that exhibits it, in the absence of penicillin.

-Claiming that every population that has ever evolved resistances to chemicals was completely stationary at a "local optimum" prior to the introduction of the chemical.

-Claiming that stabilizing selective pressures are not selective pressures.

-Claiming that the magnitude of a selective pressure is irrelevant.

-Claiming that "a single strong pressure and multiple weak pressures" are in fact not "multiple pressures."

-Asking me to post references to studies that show populations can evolve resistances to chemicals, despite every study he cites being predicated on such a phenomenon.

[T'ai Chi]

Specifically, intelligent human designers, who are a product of evolution, to write a computer program. Which means you are implying evolved beings created evolution...


Well wouldn't it strike you as interesting that a single cell is more complex than any C+ program?

It probably wouldn't.

[Mercutio]

The cell has spent more time compiling.

[rocketdodger]

Well wouldn't it strike you as interesting that a single cell is more complex than any C+ program?

It probably wouldn't.

I take it you mean "eukaryotic cell." And you are right, it would not "strike" me as interesting because, being as I nearly completed a B.S. in molecular biology prior to completing my B.S. in computer science, I already knew that.

And what is your point? Are you suggesting that since a (eukaryotic) cell is more complex than anything humans have designed, then the "designers" behind I.D. must be more advanced than we are now? In the words of one of my favorite popular phenomena, ORLY? Thank you for the insult of assuming I am dense enough to not realize this is a central assumption underlying all of I.D., and feeling the need to set the record straight. Guess what -- I already know, and it doesn't change validity or potency of the counter-argument.

But, as I said before, you already know this, because people have used this counter-argument against you, successfully, numerous times before.

[delphi_ote]

Well wouldn't it strike you as interesting that a single cell is more complex than any C++ program?
Ah, but is this actually true? Is Windows less complex than e. coli? I guess you'd have to define complexity in some precise way, which I suspect you won't do. In fact, I predict you'll ignore this post altogether, because I'm discussing something substantive, and you usually flee to another thread as soon as anyone actually gets down to brass tacks.

[Belz...]

Then maybe that paper is relevant after all? The original mutation wasn't a point mutation, but rather a cross-over event between genomes from two different species, but the resulting hybrid genome --- influenced heavily, if I recall correctly, by that of the mitochondria --- did put a lot of pressure on itself, which lead to an extremely rapid evolution.

Thanks, Kotatsu.

Arguing against intelligent designers from a computer program is poor logic since it takes an intelligent designer to write a computer program.

Well, isn't that post interesting ?

Well wouldn't it strike you as interesting that a single cell is more complex than any C+ program?

Ah! That's better...

[Mercutio]

Ah, but is this actually true? Is Windows less complex than e. coli? I guess you'd have to define complexity in some precise way, which I suspect you won't do. In fact, I predict you'll ignore this post altogether, because I'm discussing something substantive, and you usually flee to another thread as soon as anyone actually gets down to brass tacks.
Hmm...seems to me that any C+ program presupposes the presence of a human programmer, yes? (Actually, it presupposes the existence of an entire civilization advanced enough to have developed computers.) So that, in order to evaluate the complexity of a "simple" program compared to a single cell, one must bear in mind the complexity of the assumptions inherent in the "simple" program.

Rather like the simplicity of "goddiddit" as an explanation. It's just one simple step...presupposing the existence of a god somehow powerful and/or complex enough to take that one simple step.

I begin to wonder if TC isn't Dawkins in Socratic form, feeding us easy questions that demonstrate the elegant simplicity and power of the Theory of Evolution.

[Paul C. Anagnostopoulos]

Arguing against intelligent designers from a computer program is poor logic since it takes an intelligent designer to write a computer program.
Are you saying that the existence of computer models is evidence of intelligent design, or is there a logical relationship there?


Well wouldn't it strike you as interesting that a single cell is more complex than any C+ program?
Wow, yeah, and consider the complexity of the entire universe and stuff.

~~ Paul

[Apathia]

:bcake:

:hb:

An amazing year!

[kleinman]

Any of you evolutionists finally understand the mathematics of mutation and selection and the vast amount of empirical evidence which supports this mathematics? Let’s find out.
Got it Kleinman does allow for 'micro evolution', but discounts Speciation or 'Macro Evolution'.

Scary that he claims to be a Biologist. At least I know where he stands now. No point debating him. I don't have the skills to do so, and I can't refute his math. Despite the fact that Evolution on a grand scale exists, and that mutations, and speciation has occurred without his mandatory selection pressures.
Shalamar, Halloween is coming up, so what are you going to dress up as, a scientist? Shalamar, do you have any idea what the probabilities are for the formation of even the simplest sequence of amino acids for a protein or sequence of bases for a gene are without selection? So we start this week with Shalamar having no idea of the mathematics of mutation and selection. So where do we go from here on the fitness landscape? Ah yes, Geo_flux.
There are plenty of computer models around designed to simulate and forecast weather, some using extremely powerful super computers. None of these models can completely model the behaviour inside a hurricane or predict where they will strike. So therefore hurricanes don't exist!

If a computer model can't accurately simulate and predict a hurricane then its obvious that hurricanes are a lie, it couldnt possible mean that the computer models are lacking.

No wonder George W was so slow to react to Katrina! (sorry to drag bad taste and politics into this, couldn't resist)
Geo_flux, at least these computer models which simulate and forecast weather give some general indication the direction a hurricane will take based on a variety of variables. The mathematical models of mutation and selection point in the exact opposite direction for this process that you evolutionists allege and so does the empirical data of mutation and selection which shows the same behavior as the mathematical models.

I see, George W was the only politician that was slow to react to Katrina. Years of neglect of the levees and building homes below sea level had nothing to do with this disaster. George W, why did you let these people do this? The depths of your political thinking match the depths of your scientific thinking.
… Joobz, you better contact these authors and tell them that you can’t stop evolution but you can change lead into gold by letting the sun shine on it long enough. …you're funny.
inconsequential, but funny.

had any luck with your assumptions?
nope.
joobz, I do address your silly speculations, I did address your slow does not equal stop speculation with this citation. Of course you can argue that with enough free energy, anything can evolve.
i think its interesting what happens when we apply Kleinman's logic to other computer models.The concept of kleinman logic is roughly the same as that of jumbo shrimp.
How about evolutionist mathematics? Hey kjkent1, would you like some primordial soup with your jumbo shrimp. It’s mmm, mmm good!
No point debating him. I don't have the skills to do so, and I can't refute his math.Wrong, and wrong. All you need to debate him is common sense, and he has no math to refute. Join the fun!
Shalamar, rocketdodger is correct, it is Dr Schneider’s mathematics which you would have to refute and hundreds of real examples of this mathematics. We are all waiting for rocketdodger to demonstrate some common sense. You must have infinite patience to engage in this discussion.
…A remark there on "hen's teeth:This sounds amazing! I will look at this after the bloody journal club I have to go to soon. Many thanks! I have almost two decimetres of papers on dinosaur-bird evolution (most of which is sadly unread), and the sites you linked to seemt o be able to add to that considerably.
I must admit that I have fallen behind on my Marvel comics reading as well since mutation and selection doesn’t work that way. Kotatsu, since it mathematically impossible for mutation and selection to do such a transformation, how do dinosaurs transform into birds? Wait a minute, this has happened. Big Bird turned into Barney on Sesame Street.
You have not physical reality which shows mutation and selection can transform reptile into birds.As has been pointed out to you before, dinosaurs, not any generic reptile, are thought to have evolved into birds. As I just mentioned, I have almost two decimetres of articles describing this process, as well as descriptions and (originally) colour plates showing the various feathered dinosaur fossils that have been found, primarily in China.
I realize this is what you think has happened but we know how mutation and selection actually works and it can’t do what you are thinking.
The idea that reptiles evolved into birds in tiny steps over millions of years should pose problems for evolutions when the mechanism of mutation and selection can transform only a tiny number of genes at once.What is the mechanism that at least theoretically stops all genes in a e.g. a sperm to mutate and then get transmitted to the next generation?
That mechanism is random mutations and natural selection. This sorting process is profoundly slowed when more than a single gene is being transformed at a time. In addition, we are still waiting for you tell us what that selection pressure is that would transform reptiles or dinosaurs into birds. So not only do you lack any selection pressure that would do this, you can only transform a single gene at a time with the mutation and selection process.
you can’t get common descent by the mutation and selection process.Of course you can. Look in more or less any phylogenetic paper and you will get exactly that. For instance, I have in front of me a sort of technical meta-study which uses the data of two previously published studies to study a certain aspect of Bayesian inference and gene trees vs. species trees. It displays a partly well resolved tree of the genus Macaca which --- ignoring the branches with low probability --- shows quite nicely that the genus is descended from the same ancestor (1). This tree is based on genes which differ due to mutations, and --- so the authors assure me, and I know little of Macaques, so I cannot dispute it --- corresponds strongly with the geographical distribution of the species.
Kotatsu, the underlying mathematics of mutation and selection and the empirical evidence which supports this mathematics refutes the conclusions you try to draw from you phylogenetics pictures. Mutation and selection is a profoundly slow process for more than the transformation of a single gene and you don’t have the selection pressures which would accomplish the huge transformations you allege for common descent.
Yea, Mr Scott, give us a reference which proves that feathers can grow on birds.And now that he has kindly provided you (and me!) with more references than I'd care to shake a stick at, what will you do? Ignore it, dismiss it or obfuscate matters by your usual c&p routine?
There it is folks; the theory of evolution must be true because Mr Scott has shown that feathers can grow on birds. That must be the kind of common sense that rocketdodger is talking about. Kotatsu, I admit that feathers do grow on birds, I will not ignore this.
Rocketdodger, which population of bacteria will evolve resistance to penicillin more quickly, a population in vitro which is not subject to a patient’s immune system and all weak selection pressures reduced to a minimum or a population in vivo that is subject to a patient’s immune system and numerous other weak selection pressures?

Bacteria evolve resistance to penicillin because of the selection pressure of this bacterial toxin.So, basically, you're admitting that evolution CAN be hastened by a strong selection pressure when other pressures are relatively weak ?

Why the hell are you arguing with us, then ?
Belz, those weak selection pressures slow the evolution of the strong selection pressure. What I am arguing is that combination selection pressures slow the evolutionary process, oh yes, I’m also here to annoy you with the mathematical and empirical facts of how mutation and selection actually works.
Rocketdodger, if you studied ev, you would realize that “combination selection pressures profoundly slow evolution,” not ‘slow’. Weak selection pressures may not profoundly slow the evolution of a single strong selection pressure but they do slow the evolutionary process.You're just chock-full of contradictions, aren't you ?
No Belz, you are chock-full of confusion of how mutation and selection works. Weak selection pressures don’t accelerate the evolution of a strong selection pressure, which is why I gave rocketdodger the example of evolving resistance to penicillin in vivo and in vitro. Rockdodger understands that the resistance to penicillin will evolve in vitro more quickly because of fewer weak selection pressures on the bacterial population. Each selection pressure imposes a trajectory on the fitness landscape interfering with the trajectories for the other selection pressures.
The reason why I can copy and paste citations is that I understand how mutation and selection actually works, now rocketdodger joins Adequate and argues that n +1 selection conditions sort mutations more quickly than n selection conditions.I notice that you're now too frightened of my results to tell people what I have actually argued.

You used to quote my actual posts on this subject over and over, until you realised what a bloody fool you were making of yourself.

Poor little man.
Adequate has results?
http://forums.randi.org/images/smilies/doglaugh.gif
Here’s one of Adequate’s posts where he admits to the truth of his understanding of the mathematics of mutation and selection.
If there was a "sticky" thread on drug delivery, biomaterials or polymer chemistry, I'd be there instantly. But evolution isn't my field.And I, sir, am a mathematician, and I may be the greatest expert in the UK on certain aspects of non-associative algebras, and on absolutely nothing else ... oh, certain aspects of neoclassical economics ... uses of geometry in design ... OK, there are lots of things I'm an expert on ... none of which are relevant to our great struggle between truth and bullcrap.

But when I put together an article summarising the present state of scientific knowledge for popular consumption, emphasising the skeptical point of view, the only requirements placed on me are that I should be honest, diligent, consciencious, and clear.

If you don't think that you can do that, then you shouldn't write about anything at all, even when arguing with whackjobs. If you can, then your articles may be of interest to thousands of people.

In which case, why waste your time on nutters?

Your call.
So Adequate, none of your mathematical skills are relevant to the mathematics of mutation and selection? You can’t recognize a sorting/optimization problem? You can’t recognize an iterative problem when you see one? You are either incompetent in your field or a whackjob. But I don’t mind wasting a little of my time on you, it will be instructive to others who are interested in learning how the mutation and selection process actually works, both mathematically and empirically.
Let's do it again. I guess most of you wll have seen this, but for the newbies, this is what kleinman is whining and lying about.
I need neither to whine nor lie about Adequate’s wacky graph. Adequate has already admitted that he knows nothing about the mathematics of mutation and selection and that he has no empirical evidence of his silly gif.

Here’s a little common sense for you rocketdodger. If you increase the number of sorting condition in a mathematical problem, the process does not speed up, it slows down but Adequate is such a nutter, he thinks it does speed up. This is why Adequate can find no empirical evidence of his silly graph. On the other hand, Dr Schneider’s ev model shows that combination selection pressures profoundly slow the evolutionary process and there are hundreds of empirical examples of this mathematical fact.

So Adequate wants me to critique his silly graph, here it is. I like the colors, red, white and blue but his concept is completely irrational and illogical, additional selection pressures do not accelerate the evolutionary process. What’s your PhD in Adequate, irrationematics?
Yup.I'm going to just go ahead and assume this nasty bit of arrogance tacked on to the end of your incoherent post is your answer to the obvious question: "I guess you're not getting enough attention in all the other threads you start but never respond to, so now you're trolling this thread, too?"
Delphi, when are you going to tell us how a temperature change transforms a reptile population into a bird population? Or is this just another of your arrogant and incoherent ideas. Delphi, you understand something about the mutation and selection process, otherwise you wouldn’t have brought into the discussion the concept of the fitness landscape. How long will you deny how mutation and selection actually works?
The cell has spent more time compiling.
Mutation and selection wasn’t the compiler that created this executable.
Well wouldn't it strike you as interesting that a single cell is more complex than any C++ program?Ah, but is this actually true? Is Windows less complex than e. coli? I guess you'd have to define complexity in some precise way, which I suspect you won't do. In fact, I predict you'll ignore this post altogether, because I'm discussing something substantive, and you usually flee to another thread as soon as anyone actually gets down to brass tacks.
Delphi, do you think that Windows came about by mutation and selection? Delphi, explain to us how any gene can evolve de novo by mutation and selection. I can tell you how the Hello World program originated.
Arguing against intelligent designers from a computer program is poor logic since it takes an intelligent designer to write a computer program.Are you saying that the existence of computer models is evidence of intelligent design, or is there a logical relationship there?
Paul, the argument is whether mutation and selection can produce and transform the wide variety of different life forms that we see. Your own computer model shows why your theory of evolution is mathematically impossible. It takes something more than mutation and selection to generate and make the life forms that we observe.
Well wouldn't it strike you as interesting that a single cell is more complex than any C+ program?Wow, yeah, and consider the complexity of the entire universe and stuff.
Yet you still cling to the theory of evolution even though your own mathematical model contradicts this world view. Perhaps a couple more examples of how mutation and selection actually works will bring you back to your senses.
http://www.sciencemag.org/cgi/content/summary/298/5591/74 (http://www.sciencemag.org/cgi/content/summary/298/5591/74)
The arrival of chloroquine resistance in malaria parasites ended the reign of the best and most affordable antimalarial drug ever. The resurgence of malaria in developing countries, particularly in sub-Saharan Africa, is nothing short of a humanitarian disaster. In this Perspective, Hastings and colleagues explore new findings (Sidhu et al.) that reveal how chloroquine resistance evolved. The new work may shed light on appropriate antimalarial drug combinations that do not exhibit cross-resistance, in this way delaying the emergence of resistance to new frontline drugs.

http://www.bioline.org.br/request?jp06094 (http://www.bioline.org.br/request?jp06094)
The growing problem of drug resistance has greatly complicated the treatment for falciparum malaria. Whereas chloroquine and sulfadoxine/pyrimethamine could once cure most infections, this is no longer true and requires examination of alternative regimens. Not all treatment failures are drug resistant and other issues such as expired antimalarials and patient compliance need to be considered. Continuation of a failing treatment policy after drug resistance is established suppresses infections rather than curing them, leading to increased transmission of malaria, promotion of epidemics and loss of public confidence in malaria control programs. Antifolate drug resistance (i.e. pyrimethamine) means that new combinations are urgently needed particularly because addition of a single drug to an already failing regimen is rarely effective for very long. Atovaquone/proguanil and mefloquine have been used against multiple drug resistant falciparum malaria with resistance to each having been documented soon after drug introduction. Drug combinations delay further transmission of resistant parasites by increasing cure rates and inhibiting formation of gametocytes. Most currently recommended drug combinations for falciparum malaria are variants of artemisinin combination therapy where a rapidly acting artemisinin compound is combined with a longer half-life drug of a different class. Artemisinins used include dihydroartemisinin, artesunate, artemether and companion drugs include mefloquine, amodiaquine, sulfadoxine/pyrimethamine, lumefantrine, piperaquine, pyronaridine, chlorproguanil/dapsone. The standard of care must be to cure malaria by killing the last parasite. Combination antimalarial treatment is vital not only to the successful treatment of individual patients but also for public health control of malaria.
Once again, more empirical example which shows that combination selection pressures profoundly slow the evolutionary process. The theory of evolution is mathematically and empirically impossible. It is an irrational and illogical theory.

[joobz]

Here’s one of Adequate’s posts where he admits to the truth of his understanding of the mathematics of mutation and selection.


So Adequate, none of your mathematical skills are relevant to the mathematics of mutation and selection? You can’t recognize a sorting/optimization problem? You can’t recognize an iterative problem when you see one? You are either incompetent in your field or a whackjob. But I don’t mind wasting a little of my time on you, it will be instructive to others who are interested in learning how the mutation and selection process actually works, both mathematically and empirically.

I need neither to whine nor lie about Adequate’s wacky graph. Adequate has already admitted that he knows nothing about the mathematics of mutation and selection and that he has no empirical evidence of his silly gif.

Yeah! A new example of your reading comprehension diffiuculties.

Do you honestly believe that anyone would interpret that conversation as Dr. A saying he didn't understand evolution or that he isn't qualified to comment on evolution? Or that I am not qualified to see your argument as nonsense?

The conversation was really why we spend time goofing on you. It is more related to the fact that your arguments are so mundane that they don't require a significant level of expertise in the field and that they don't really deserve any more time. Except that it's fun watching you say silly stupid things, such as the quoted comment above.

[rocketdodger]

1) You claim that nobody besides you understands the underlying mathematics of mutation and selection. The only evidence you have for this is apparently the fact that you repeat it over and over. You have not given us a single derivation, solid understanding, or even proper use of an equation or concept this entire thread.

2) You claim that additional sorting conditions "slow down" sorting/optimization problems. You have not presented any formal arguments showing us why this would be true. On the contrary, you have done nothing but make personal attacks against Adequate when he demonstrates otherwise.

3) You claim that mutation and selection is simply a sorting/optimization problem. You have not presented any formal arguments to show that this is true.

If you understood the mechanisms behind mutation and selection, Kleinman, then you would be able to present formal arguments to back up your claims.

Since you do not, we can assume you either do not in fact understand those mechanisms or that you realize any formal arguments developed from those mechanisms would refute your theory.

Instead, you rely on the behavior of bombarding us with random citations featuring arbitrarily highlighted sentences in the hopes that it makes you look smarter than a cumquat -- it has not had this effect.

[Mr. Scott]

There it is folks; the theory of evolution must be true because Mr Scott has shown that feathers can grow on birds. That must be the kind of common sense that rocketdodger is talking about. Kotatsu, I admit that feathers do grow on birds, I will not ignore this

The usual dodge via ridicule and strawman argument. I see you ignored my mention that bird DNA includes the genetic mechanism for making teeth.

The key to understanding the creationist mind is to tune in to where they dodge or outright ignore points they can't refute. Kleinman is a textbook example of this psychological syndrome confirmation bias (http://www.psychsystems.net/lab/06_Westen_fmri.pdf). He offers skeptics a tremendous benefit in stimulating conversation supporting evolution and to study the psychology of creationists.

When mathematical models and extrapolations from experimental results don't match reality, we must identify the problems with the models and extrapolations, not the problems with reality. There is a mountain of evidence that evolution happened pretty much as Darwin said. The Ev simulation is simply not comprehensive enough to be used to disprove evolution, and extrapolations from antibiotic synergy cannot either.

We can identify the creationists' achilles heels by taking note of their evasions and apparent deafness to arguments that disprove the ID hypothesis. This phenomenon was exemplified spectacularly in the Dover PA trial when proof was presented that humans and the great apes had a common ancestor. The creationists' response was dumbstruck silence.

I found this video presentation by a Christian evolutionist explaining that event. I await Dr. Kleinman's refutation.

zi8FfMBYCkk

[Kotatsu]

I must admit that I have fallen behind on my Marvel comics reading as well since mutation and selection doesn’t work that way. Kotatsu, since it mathematically impossible for mutation and selection to do such a transformation, how do dinosaurs transform into birds? Wait a minute, this has happened. Big Bird turned into Barney on Sesame Street.

I assume these are references to American popular culture, but they are quite meaningless to me. Sorry.

However, to answer your question, the transition between dinosaurs and birds was accomplished by the same mechanisms as all other evolution: mutations of various sorts and selection of various sorts.

That mechanism is random mutations and natural selection. This sorting process is profoundly slowed when more than a single gene is being transformed at a time.

I realise this is an inconsequential tangent, and most likely will not be satisfactorily addressed, but do you hold that its is entirely impossible for a sperm to contain mutations in every single gene compared to the genome of the father? If so, what mechanism in the cell prevents this from happening at least occasionally by sheer coincidence? I know there are several control mechanisms, but as mutations can happen in even very conservative regions, there must be occasions when these control mechanisms are somehow not enough.

In addition, we are still waiting for you tell us what that selection pressure is that would transform reptiles or dinosaurs into birds. So not only do you lack any selection pressure that would do this, you can only transform a single gene at a time with the mutation and selection process.

I have already provided you with a list precisely of that, which you have so far chosen to misinterpret and mock. In the vain hope that this time you might actually read it and try to understand it, I refer you to that list again. It can easily be found by clicking on my screen name and select the option "Find more posts by Kotatsu".

Kotatsu, the underlying mathematics of mutation and selection and the empirical evidence which supports this mathematics refutes the conclusions you try to draw from you phylogenetics pictures. Mutation and selection is a profoundly slow process for more than the transformation of a single gene and you don’t have the selection pressures which would accomplish the huge transformations you allege for common descent.

Then perhaps you would be so kind to explain to me exactly what it is we see in a phylogenetic tree? Why do the data sets almost invariably form nested hierarchies and show that the ingroup taxa, at least, appear to be the result of common descent modified step by step over time? Chose any tree you like, and explain this to me. I am a systematicist and an aspiring taxonomist, and surely you would not be so cruel as to not explain this to me, would you? Just imagine if you are correct --- which, by the way, you are not --- would you deprive me of the exact knowledge which you allegedly possess --- but which, for some reason, you have hitherto smugly chosen to keep to yourself --- that would convince me that the arguments and data needed to convert to your view are within my own field?

And, while you are at it, could you perhaps finally answer Belz' question about what that Archaeopteryx actually is? This has been bugging me for some time. As you can so summarily dismiss the fossils we claim are forms transitional between dinosaurs and birds, I am sure you have a better explanation of what they really are than an "evolutionary [R]orschach test".

There it is folks; the theory of evolution must be true because Mr Scott has shown that feathers can grow on birds. That must be the kind of common sense that rocketdodger is talking about. Kotatsu, I admit that feathers do grow on birds, I will not ignore this.

That is not the important thing that MrScott showed us, Kleinman. The important thing was that it takes only one mutation to change scales into feathers. Does this fact mean nothing to you, more than yet another way to behave in what I can only assume is a deliberately buffoonish way? To me, it means that your arguments are lessened enormously with regard to the dinosaur-bird evolution. If one mutation is all it takes, then I would think it odd if no dinosaurs ever evolved feathers. And once you have feathers --- remember that the dinosaurs thought ancestral to birds were largely arboreal --- all the other morphological differences between dinosaurs and birds seem inconsequential, for the groundwork --- making feathers out of scales --- have already been laid, and the rest are just consequences of this.

[Kotatsu]

I hate to blow my own horn (or do I?), but it struck me as remarkable how similar this:

Any of you evolutionists finally understand the mathematics of mutation and selection and the vast amount of empirical evidence which supports this mathematics? Let’s find out.

Delphi, when are you going to tell us how a temperature change transforms a reptile population into a bird population?

Delphi, explain to us how any gene can evolve de novo by mutation and selection.

Your own computer model shows why your theory of evolution is mathematically impossible.

Perhaps a couple more examples of how mutation and selection actually works will bring you back to your senses.

Once again, more empirical example which shows that combination selection pressures profoundly slow the evolutionary process. The theory of evolution is mathematically and empirically impossible. It is an irrational and illogical theory.

is to this:

http://forums.randi.org/showthread.php?postid=3097753#post3097753

I don't know if I should be proud or not, though.

[kjkent1]

The usual dodge via ridicule and strawman argument. I see you ignored my mention that bird DNA includes the genetic mechanism for making teeth.

The key to understanding the creationist mind is to tune in to where they dodge or outright ignore points they can't refute. Kleinman is a textbook example of this psychological syndrome confirmation bias (http://www.psychsystems.net/lab/06_Westen_fmri.pdf). He offers skeptics a tremendous benefit in stimulating conversation supporting evolution and studying the psychology of creationists.

When mathematical models and extrapolations from experimental results don't match reality, we must identify the problems with the models and extrapolations, not the problems with reality. There is a mountain of evidence that evolution happened pretty much as Darwin said. The Ev simulation is simply not comprehensive enough to be used to disprove evolution, and extrapolations from antibiotic synergy cannot either.

We can identify the creationists' achilles heels by taking note of their evasions and apparent deafness to arguments that disprove the ID hypothesis. This phenomenon was exemplified spectacularly in the Dover PA trial when proof was presented that humans and the great apes had a common ancestor. The creationists' response was dumbstruck silence.

I found this video presentation by a Christian evolutionist explaining that event. I await Dr. Kleinman's refutation.

zi8FfMBYCkkThis evidence, which is well known to everyone here, including kleinman, really should halt the debate, at least with respect to the idea that Adam and Eve and a rib were involved in the establishment of homo sapiens.

It doesn't necessarily refute the existence of an intelligent designer, because that designer could certainly have fused the two chimp chromosomes to form the #2 human chromosome. But, it does make one wonder about the sophistication of the designer, because he /she/it didn't design the #2 chromosome with telomeres on the end, like all the others. Instead, the evidence shows telomeres exactly where they would be predicted to be found were two preexisting chromosomes to be fused: in the middle of the new chromosome.

So, maybe we had an alien visitor 4.5 million years ago, and it did a little genetic engineering. Now, this begs the question of where the alien came from -- which is why evolution is a much more plausible conclusion.

Not to kleinman, of course -- but, to everyone without a "cross" to bear.

[rocketdodger]

So, maybe we had an alien visitor 4.5 million years ago, and it did a little genetic engineering. Now, this begs the question of where the alien came from -- which is why evolution is a much more plausible conclusion.



Can you imagine how awesome it would be if we found conclusive evidence for such a thing?

[Mr. Scott]

It doesn't necessarily refute the existence of an intelligent designer, because that designer could certainly have fused the two chimp chromosomes to form the #2 human chromosome. But, it does make one wonder about the sophistication of the designer, because he /she/it didn't design the #2 chromosome with telomeres on the end, like all the others. Instead, the evidence shows telomeres exactly where they would be predicted to be found were two preexisting chromosomes to be fused: in the middle of the new chromosome.

What I realize is this event -- fusing two chromosomes of a great ape to produce a proto-human -- was, for all intents and purposes, an ape mother giving birth to a human child, not too unlike when the first bird came out of a dinosaur egg (probably a dino with fluffy scales via a single mutation). The assertion that these events never happened has been thought a key creationist strawman. I bet fused chromosome baby #1 looked a bit weird and had difficulty attracting mates, and may have been banished for being "different" leading to their separate evolution into us. It's also tempting to speculate that the fusion was somehow an advantageous mutation.

[rocketdodger]

I bet fused chromosome baby #1 looked a bit weird and had difficulty attracting mates, and may have been banished for being "different" leading to their separate evolution into us. It's also tempting to speculate that the fusion was somehow an advantageous mutation.

If the fusion wasn't advantageous, it couldn't have been too much of the opposite, either, or else we wouldn't be around today.

[Paul C. Anagnostopoulos]

It doesn't necessarily refute the existence of an intelligent designer, because that designer could certainly have fused the two chimp chromosomes to form the #2 human chromosome. But, it does make one wonder about the sophistication of the designer, because he /she/it didn't design the #2 chromosome with telomeres on the end, like all the others. Instead, the evidence shows telomeres exactly where they would be predicted to be found were two preexisting chromosomes to be fused: in the middle of the new chromosome.
And why in the name of all that is holy would the designer do endogenous retroviruses?

http://www.dailykos.com/story/2005/4/7/7723/67027

~~ Paul

[delphi_ote]

Delphi, when are you going to tell us how a temperature change transforms a reptile population into a bird population? Or is this just another of your arrogant and incoherent ideas.
Do you have an entire planet I can use as a laboratory and a few hundred million years to wait around? I can't promise the exact results you want, but I could give it a try.
How long will you deny how mutation and selection actually works?
How do they "actually works", kleinman?
Delphi, explain to us how any gene can evolve de novo by mutation and selection.
This has been explained to you again and again... :mad:

[T'ai Chi]

And why in the name of all that is holy would the designer do endogenous retroviruses?

http://www.dailykos.com/story/2005/4/7/7723/67027

~~ Paul

Well, now's your chance to explain in complete detail, how random mutations and selection did it, starting from non-life to the endogenous retroviruses.

Be sure to not leave out any steps. Since you are the one claiming a scientific path for this, should be easy to provide all the steps, and not make any scientistic jumps that require your faith to fill.

[joobz]

Do you have an entire planet I can use as a laboratory and a few hundred million years to wait around? I can't promise the exact results you want, but I could give it a try.

How do they "actually works", kleinman?

This has been explained to you again and again... :mad:
Remember when Kleinman didn't understand how your quick simple code could demonstrate that multiple selection pressures could indeed be faster than 1 huge one.

Good times, good times.

[rocketdodger]

Be sure to not leave out any steps. Since you are the one claiming a scientific path for this, should be easy to provide all the steps, and not make any scientistic jumps that require your faith to fill.

And since you seem to be incapable of understanding that the magnitude of a leap of faith is of prime importance, why don't you try jumping out the window instead of taking the stairs next time?

[joobz]

Well, now's your chance to explain in complete detail, how random mutations and selection did it, starting from non-life to the endogenous retroviruses.

Be sure to not leave out any steps. Since you are the one claiming a scientific path for this, should be easy to provide all the steps, and not make any scientistic jumps that require your faith to fill.
Please prove that this post is done by a human. Be sure to include a detailed description of all muscular movements, hormone releases, neuronal firings, and a description of the cognitive networks invloved.

Don't leave out a single cell or molecule.

[Myriad]

Happy birthday to the thread!

Once your baby has turned a year old, it seems that she begins to develop at a more rapid rate. It feels like only yesterday she was staring up at you lovingly while drinking from her bottle. Was it only a few months ago when she stunned everybody by saying “mama” for the first time?...
...
If you thought she liked getting attention before, wait until she starts loving to be the center of attention. She will make her presence known and be sure that everybody in the room is paying attention to her and only her. She will love to have others dote on her and clap for her as she shows everyone a new trick or a new dance move. Granted, she will not only want attention for all the cute little things she does that make you laugh and smile; she will probably not care what kind of attention she gets at this point, even if it means throwing her plate off the high chair to make sure you are looking at her. When children are this age, many parents wonder if they have started to create a monster, but as long as you are firm and show your child that you will not tolerate her being naughty in order to gain attention, she will eventually cool down this behavior.
...
Whereas she might have been able to sleep most of the night in her room by herself, she may start to become scared of the dark. You may want to invest in a small nightlight for her room or keep the closet light on with the door closed, so some light comes into the room.
...
Meanwhile, there will be some things, like playing with certain toys, that will make her frustrated and angry, especially if she cannot figure them out. Temper tantrums will start to rear their ugly heads around the fourteenth month, so be prepared.
...
You will want to keep a close eye on your child during this time because she will soon become mesmerized by tiny things, including small rocks, coins and insects. She will pick things up off the floor and stare at them (or put them in her mouth, if you don’t watch her).


Source: http://www.essortment.com/family/yourbabyssecon_sihi.htm.

Repsectfully,
Myriad

[delphi_ote]

Remember when Kleinman didn't understand how your quick simple code could demonstrate that multiple selection pressures could indeed be faster than 1 huge one.

Good times, good times.
Ah, yes. Those were the good old days. I was so young and naive, in the prime of my life. You were a dashing businessman full of bravado. We were ready to take on the world! Er... wait. Maybe I'm thinking of something else.

But yes, those were the halcyon days when I imagined that, perhaps, Kleinman might actually read and think about the things we typed. Despite all the very intelligent posts the community has made to help nudge him toward the truth, he still clings to roughly the same set of nonsense he did when we all entered this thread. These things have been demonstrated without ambiguity over and over again for a year, and he still gets it wrong.

[Paul C. Anagnostopoulos]

Well, now's your chance to explain in complete detail, how random mutations and selection did it, starting from non-life to the endogenous retroviruses.

Be sure to not leave out any steps. Since you are the one claiming a scientific path for this, should be easy to provide all the steps, and not make any scientistic jumps that require your faith to fill.
That's the stupidest thing you've said since the last time you said it. You are, for consistency, rejecting all of the science, since not every question has been answered in its entirety, right?

And, to an even greater degree, you are rejecting the goddidit hypothesis, since not a single question has been answered by it, right? Or does it get cut some slack just because you say it's faith-based?

And, as Joobz noted, you are rejecting pretty much everything else, right?

~~ Paul

[T'ai Chi]

You are, for consistency, rejecting all of the science, since not every question has been answered in its entirety, right?


Well, if I get emotional like you, the same could be said about you rejecting everything, of course. You are not clear on how the entire universe works, yet you extrapolate, via an intelligently designed computer program, that there can't be an intelligent designer(s).


And, to an even greater degree, you are rejecting the goddidit hypothesis, since not a single question has been answered by it, right?


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


And, as Joobz noted, you are rejecting pretty much everything else, right?


Well, I am rejecting your argument, but that is such a small thing. You are the one claiming a naturalistic pathway for all. You assume that, fine. But natural stuff can be shown. Unless you're making a time + chance = magic argument, which are fairly common, even without the supernaturalism.

[Mercutio]

Well, I am rejecting your argument, but that is such a small thing. You are the one claiming a naturalistic pathway for all. You assume that, fine. But natural stuff can be shown. Unless you're making a time + chance = magic argument, which are fairly common, even without the supernaturalism.

Re: the bit in blue...that is, of course, a strawman. Closer to the truth, we are looking for explanations. So far, when we have found explanations, they have been naturalistic. As you say, natural stuff can be shown. What you are suggesting is that we should consider supernaturalism--but of course, when we have found explanations, they have uniformly not been supernatural.

You have asked for a complete explanation. So far, of course, no one can give this to you. But thus far all of the puzzle pieces are consistent with a naturalistic explanation, and none support a supernatural explanation. As you said earlier, the seemingly simpler computer program (or "goddiddit") presupposes an incredibly complex substrate, far more complex than the seemingly complex single cell.

So, of course, your task is to provide positive evidence for your view. You have not, thus far, nor can you. And the fact that you have to resort to misrepresentation of the naturalist position in order to attempt to take potshots at it, is telling; frankly, if you had an argument that applied to the real stance, I suspect you would have presented it.

[kjkent1]

Re: the bit in blue...that is, of course, a strawman. Closer to the truth, we are looking for explanations. So far, when we have found explanations, they have been naturalistic. As you say, natural stuff can be shown. What you are suggesting is that we should consider supernaturalism--but of course, when we have found explanations, they have uniformly not been supernatural.

You have asked for a complete explanation. So far, of course, no one can give this to you. But thus far all of the puzzle pieces are consistent with a naturalistic explanation, and none support a supernatural explanation. As you said earlier, the seemingly simpler computer program (or "goddiddit") presupposes an incredibly complex substrate, far more complex than the seemingly complex single cell.

So, of course, your task is to provide positive evidence for your view. You have not, thus far, nor can you. And the fact that you have to resort to misrepresentation of the naturalist position in order to attempt to take potshots at it, is telling; frankly, if you had an argument that applied to the real stance, I suspect you would have presented it.What the person who seeks to use probability to eliminate abiogenesis and evolution as a possibility misses, is the fact that no matter how minute the probability a natural explanation being correct may be, that probability is infinitely greater than the probability that a supernatural diety is responsible for creation.

Because, of course, the science of probability is naturalistic, and as the diety is unmeasurable by any natural means -- therefore the probability of the diety's existence, is zero.

[Apathia]

You ignorant evolutionarians with your fused chromosomes and retroviruses in the genome, you haven't read the Bible!
If you had, you'd know how the designer works. Take Eve for example, God made her from parts of Adam! And what did he make Adam of? You guessed it: clay and various parts taken from the beasts.
Ah the grandure if the Human body, cobbled together from ape and pig parts!
And the Designer didn't use a computer. :D

[Mercutio]

What the person who seeks to use probability to eliminate abiogenesis and evolution as a possibility misses, is the fact that no matter how minute the probability a natural explanation being correct may be, that probability is infinitely greater than the probability that a supernatural diety is responsible for creation.

Because, of course, the science of probability is naturalistic, and as the diety is unmeasurable by any natural means -- therefore the probability of the diety's existence, is zero.
Well... to use, I think, Dawkins's word, there could be a perinormal explanation, rather than a paranormal one. That is, there may be an explanation that involves a natural phenomenon of which we are currently unaware.

As TC implied in a different thread, we cannot reasonably claim to know all of the laws of nature at present; indeed, as such laws are descriptive, and our ability to measure increases constantly, we can expect minor or even major revisions to our accepted laws. The trick is, TC implies that this renders any scientific explanation incomplete (which it is) and therefor dismissable (which it is not) and on a par with non-naturalistic explanations (which it most certainly not).

Any new law, or reformation of an old law, must not only accurately describe/predict a previously unexplained phenomenon, but it must also be able to predict the same things that the law that it is replacing did. Newton's laws are still good enough to use for the vast majority of situations, even though Einstein's encompass them and more.

Bottom line is, even though we cannot claim to have any absolute perfect understanding of natural laws, this in no way invalidates the observations we have built our current laws on. The phenomena do, so far, have naturalistic explanations, and no amount of sniping at strawman versions of science can influence that. The world waits for the first positive evidence for even a perinormal explanation...let alone a paranormal one.

Kleinman, of course, tries the same technique--potshots at a strawman version of evolution, to make up for a lack of positive evidence for what he inaccurately sees as the only possible alternative. If this is the best they can do, Darwin's ghost can rest easy this Halloween.

[Mr. Scott]

And why in the name of all that is holy would the designer do endogenous retroviruses?

http://www.dailykos.com/story/2005/4/7/7723/67027

~~ Paul


When Alan first responded to this he brushed it off as a "coincidence" that human and chimp genomes had the same viral insertions in the same places, so I wanted to calculate the probability of this coincidence. I just did a rough back-of-the-envelope estimate. Someone correct my math if there is a serious problem:

Number of nucleotides in the human and chimp genomes: 3 billion (3*10^9)

Number of endogenous retroviruses (ERVs) in the human and chimp genomes in identical positions: 7

Chance of 1 ERV appearing in identical positions independently in chimp and human: One in three billion.

Chance of 7 ERVs appearing in identical positions independently: One in three billion to the seventh power.

Probability chimps and humas share a common ancestor, going just by the seven ERV insertions, is about 99.99999999999999999999999999999999999999999999999 999999999999999999% (65 nines after the decimal place) It's true! :D

Figures are approximate, and further "coincidences" in the genomes make the probabilities for common ancestry even higher.

If I made a gross error in my calculations someone please correct.