Annoying creationists

[articulett]

Watching video ... turning annoying sound off ...

"For the sake of argument and simplicity, let's define information on DNA as a sequence that tells us something about the environment."

This guy is clever!

~~ Paul

Wouldn't the world be so much better if old creationists spent their time catching up on new information instead of rehashing the same old argument in an everlasting quest to keep their intelligent designer alive? If they put just half the energy they spend defending their "belief" into actually learning something, think how smart they could be. But alas, religion has a vested interest in keeping the faith alive--and that means keeping the faithful ignorant and running about proffering reasons to believe so they never have to utilize their brain power with the question that maybe they've been deluding themselves...

Anyhow, the guy has several good video--I figured that with such talent and intelligence he must be a JREF member...

Is there any known remedy for breaking creationist thinking? It seems so intractable...I'm not sure anything works...I think all the evidence in the world could be staring kleinman in the face and he'd just claim that nothing was there...

It would be interesting hearing what worked for former "intelligent design proponents"--

[joobz]

I’m not sure why all you evolutionarians want to credit me with Dr Schneider’s peer reviewed and published mathematical model of random point mutation and natural selection but I don’t take credit for his work. The first video says creationists claim that information can’t come about by random processes. I have never made that claim. In fact I say that Dr Schneider’s ev computer simulation correctly models how information comes about by random point mutations and natural selection and it comes about profoundly slowly if there is more than one selection pressure. That’s how the mathematics of mutation and selection works. They also say that creationists never define what information is. That is also incorrect. Early in this thread the issue was discussed and information is mathematically equal to the negative of entropy. The derivation of this mathematical relationship can be found in the text Equilibrium Statistical Mechanics by Andrews. This is mathematically the same as Shannon’s information theory.

I don’t know how old you have to be not to learn something new but I only started studying the mathematics of mutation and selection a little over a year ago and the mathematical behavior of this process is nothing like evolutionarians allege. It was only after I studied Dr Schneider’s model that it became apparent why it converged so slowly and it was the multiple selection conditions which slowed the convergence of the model. It then became abundantly clear why combination therapy is used to treat HIV and slow or prevent the evolution of resistant viruses, and why combination therapy is used to treat TB and why combination therapy is used to treat malaria and why combination herbicides are used and why combination chemotherapy is used to treat cancer and why combination rodenticides are uses… This is how the mutation and selection process works. Single selection pressures can evolve rapidly, each additional selection pressure slows the evolutionary process (unless you are cheese wiz and you think multiple selection pressures accelerate evolution but he has yet to post a single example of this).

You call that good music? Is mental frustration anything like annoying? I am really, really sorry that I have mentally frustrated you with the mathematical and real facts of how mutation and selection works. Oh, oh, that’s the second lie I’ve told on this thread, the first one was when I told Delphi that he didn’t contradict himself in order to get the name of the paper he published in Science.

Why jimbob, you are correct, 7 million generations is not actually a very long time for a bacterium. How many bacterium do you know of that has a genome length of 16,384. Why don’t you run the 32k genome length and see how many generations you get? What is the shortest genome length for any free living life form?

If you read the entire thread, you will find the answer to what is the shortest genome length of a free living creature. Population is a user definable parameter in the model. The mutation rate is a user definable parameter in the model.

I don’t know how many people have pointed out that ev is only a model. Ask cheese wiz, he likes to count how many times things have been said. With respects to antibiotic resistance only having evolved over the last 60 years, that’s and interesting question since I would have to think that the penicillium mold was producing penicillin for more than 60 years. Anyway, it still doesn’t change the mathematical fact that multiple selection pressures slow and ultimately stop evolution. That’s what ev shows and that is what reality shows.

It seems that you evolutionarians didn’t like the Stephen Hawking video on youtube.

I think you are wrong here lita’ gator. There is a difference between spurious binding outside the genome and spurious binding in the gene. Let’s see if you can guess what it is.

Now lita’ gator, there is a difference between hardware and software. Where have you been anyway, I hardly ever get a chance to discuss the string cheese theory of evolution any more except cheese wiz has come up with a gif of comparable quality where he says that multiple selection pressures accelerates evolution. Were waiting for cheese wiz to post a real example of his fantasy world, excuse me, alternative universe.

That’s the point Paul, single selection pressures evolve much more rapidly than multiple selection pressures. That what ev shows, that is what the Delphi’s Wikipedia reference to the fitness landscape shows and that is what the numerous real examples I have been posting of mutation and selection shows. That’s what your model of mutation and selection shows Paul.

That’s a good question, how many selection pressures did it take to transform a reptile into a bird? Let’s consider HIV since it is the best example of evolution by mutation and selection and probably has the most data available. What are the populations, reproduction rates and mutation rates? How many selection pressures is the virus being subjected to? We know that people with the virus can survive years on appropriate combination therapy despite the high reproductive rate of the virus, huge populations, high mutation rate and as can’t brain has pointed out, the virus does recombination.

If you want to talk about slow, we can talk about the convergence of ev with an e coli size genome, do you want to use that as a baseline?

Hey, I wonder if I can add that music to this thread, you know how I enjoy annoying evolutionarians.

That’s not going to fly, information has a precise mathematical definition even if Dr Schneider dropped a sign on his web site definition.

He may be clever but he is not correct. I’ve agreed with you and Dr Schneider since the beginning of this discussion that random mutation and selection can lead to the increase in information in a genome. What you have not come to grips with is that this process is profoundly slow, too slow to support your theory of evolution. Why does your model show this process is so slow? It is the multiple selection conditions which slows the evolutionary process. Here is another real example of how multiple selection pressures slow evolution.

http://clinicaltrials.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pctr.0010015 (http://clinicaltrials.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pctr.0010015)

Now you evolutionarians all have a good weekend and don’t believe everything you see on the tube. I’ll be back next week posting more examples of how multiple selection pressures slow and ultimately stop evolution.
lots of words...none of it worth reading or commenting on.

You are simply wrong.

[kjkent1]

I think you are wrong here lita’ gator. There is a difference between spurious binding outside the genome and spurious binding in the gene. Let’s see if you can guess what it is.Immaterial. What matters is that ev's selection pressures do not model the entire landscape of evolutionary actualities, and in the case of a frame shift, this apparently caused a gene to appear and digest nylon, where that capability didn't previously exist. Such a change is not contemplated by the ev model, therefore your contention that ev proves macroevolution mathematically impossible is quite simply false.Now lita’ gator, there is a difference between hardware and software. Where have you been anyway, I hardly ever get a chance to discuss the string cheese theory of evolution any more except cheese wiz has come up with a gif of comparable quality where he says that multiple selection pressures accelerates evolution. Were waiting for cheese wiz to post a real example of his fantasy world, excuse me, alternative universe.The thread is boring, Alan. I like to learn relevant information re evolution. You rarely present anything relevant, so there's no reason for me to respond.

I know you believe that your posts are relevant, but they're not. Get help.

[joobz]

Wouldn't the world be so much better if old creationists spent their time catching up on new information instead of rehashing the same old argument in an everlasting quest to keep their intelligent designer alive? If they put just half the energy they spend defending their "belief" into actually learning something, think how smart they could be. But alas, religion has a vested interest in keeping the faith alive--and that means keeping the faithful ignorant and running about proffering reasons to believe so they never have to utilize their brain power with the question that maybe they've been deluding themselves...

Anyhow, the guy has several good video--I figured that with such talent and intelligence he must be a JREF member...

Is there any known remedy for breaking creationist thinking? It seems so intractable...I'm not sure anything works...I think all the evidence in the world could be staring kleinman in the face and he'd just claim that nothing was there...

It would be interesting hearing what worked for former "intelligent design proponents"--

The problem is that it requires an entire rewiring of someone's logic. The first chink is to have them come to terms with the fact that there faith may have factual errors in it.

Since this is typically taken as a "test of their faith", it is highly unlikely they will even contemplate this notion.

The funny part of this whole game is that if something did come to light that disproved all current views on how speciation occured, then science would adopt a new model without a second glance.

Do you think for a moment if there was a historical find that conclusively disproved Jesus' divinity, that all of christian religions would admit it?

[articulett]

The problem is that it requires an entire rewiring of someone's logic. The first chink is to have them come to terms with the fact that there faith may have factual errors in it.

Since this is typically taken as a "test of their faith", it is highly unlikely they will even contemplate this notion.

The funny part of this whole game is that if something did come to light that disproved all current views on how speciation occured, then science would adopt a new model without a second glance.

Do you think for a moment if there was a historical find that conclusively disproved Jesus' divinity, that all of christian religions would admit it?

Nope. Some guru would call it a test from satan and they would just proclaim their beliefs louder as in "when prophecy fails" http://www.whenprophecyfails.org/

You'd think that the end-of-the world cults would have all the reasons in the world to stop believing when the world didn't end on the day prophecied, but alas...

I've been over at the thread about the creationist museum using science to teach "anti science" bigotry and bible stories as fact-- and someone suggested it was child abuse... and when you see how intractable it can be in a long time believer like kleinman--I have to concur. You can make someone so faith-blind that all the evidence in the world can't shed the smallest bit of light in--that's... brain damage. And yet they bleat on and on defending the meme virus with complete agnosia.

A pity.

[Dr Adequate]

Not the massive evolutionary changes that exist only in your imagination. Mutation and selection is a profoundly slow process. Put two or more selective pressures on any population and it slows down the evolutionary process.

Ok lazy can’t brain; I’ll repost some of the data so you can get an idea how many generations it take to accumulate information. The following series is for a population of 64, mutation rate=1/G, gamma=16, site width=6, weight width=5
Genome length\generations to Rs>=Rf
256 \ 675
512 \ 2,925
1024 \ 10,108
2048 \ 35,486
4096 \ 162,892
8192 \ 710,152
16384 \ 6,894,433 (Perfect Creature)
Can’t brain, why don’t you run the G=32k for this series?

Sure cheese wiz is squirming. He has taken a mathematically ridiculous position that has no basis in reality. He has no real examples of his gif and his view is contradicted by ev, the Wikipedia reference to the fitness landscape and numerous real examples of how mutation and selection works. If you think cheese wiz’s silly gif is true, why don’t you post a real example of his nonsense?

So not only do you not understand the mathematics of mutation and selection, you don’t understand what an avatar is. Here’s what Wikipedia has to say about avatars.
http://en.wikipedia.org/wiki/Avatar_(virtual_reality) (http://en.wikipedia.org/wiki/Avatar_(virtual_reality))

Any problem with that definition can’t brain?

Oh dear, have I annoyed an evolutionarian. Delphi, study Dr Schneider’s ev model and associated publications a bit. He has nicely documented his model. If you will do a parametric study with his model, you will get some understanding of the mutation/selection process. What you will find is that the rate of information acquisition by the mutation/selection process strongly dependent on the genome length, the model is less dependent on mutation rate and population but is strongly dominated by the number of selection conditions. In fact, the number of selection conditions in ev can prevent ev from evolving at all.

Hey, tell me, how long did it take you to make the skateboarding video?

Delphi, your feelings aren’t serving you well and mathematics is not serving your theory of evolution well either.

No real examples of your ridiculous proposal that multiple selection pressures accelerate evolution?

http://img514.imageshack.us/img514/3974/genegraphhx4.jpg

http://forums.randi.org/images/smilies/doglaugh.gif
Hey Dr Schneider, cheese wiz has something to tell the oncologists at the National Cancer Institute. Care to sign on?

Now for those of you who want to understand how the mathematics of mutation and selection works, understand that multiple selection pressures slow and ultimately stop the evolutionary process. Here is another publication that demonstrates this effect.

http://asmcourse.ivic.ve/articulos/Hastings-2004.pdf (http://asmcourse.ivic.ve/articulos/Hastings-2004.pdf)

See how simple it is cheese wiz? Make a postulate that multiple selection pressures slows evolution, prove it mathematically with a peer reviewed and published mathematical model of mutation and selection and then post a real example of this postulate (or is that greater than 50 real examples of the postulate).


Delphi, I have done the parametric studies with ev and it shows how the mathematics of mutation and selection works. I have reposted a series for clown fish can’t brain which demonstrates how mutation and selection works as you lengthen the genome in ev. What you see is that as you lengthen the genome, the number of generations required for the acquisition of the same amount of information increases at an exponential rate. That is a starting for you to understand the mathematics of mutation and selection.

Don’t be silly Delphi. Mutation and selection can not be written as a direct algebraic equation. It is a complex relationship of multiple parameters. That is what the ev computer model does. These variables only have functional relationships that can not be expressed in closed form algebraic format. That doesn’t mean that you can’t map these variables, which is what a parametric study of Dr Schneider’s model does. If you want a direct equation form for the mathematics of mutation and selection it would look as follows.
f(G,γ,sw,nsc,n,mr,…) = 0
where,
G=genome length
γ =number of binding sites
sw=site width
nsc=number of selection conditions
n=population
mr=mutation rate
… and so on
Delphi, you know well that the above functional equation can be mapped and described. That is what the fitness landscape is all about. When you map the above functional equation, you will find out which variables dominate the mathematics of this system. Dr Schneider’s model describes very well how mutation and selection works. In particular, the number of selection conditions dominates the model and this is seen in reality as shown in the numerous citations I have posted and will continue to post. I wonder how many of these citations I can find? This thread may go on for hundreds of more pages.

Delphi, must you use so many asterisks? There are so many sensitive evolutionarians reading this thread that may be offended by such blatant keystrokes.

Now can’t brain, can’t see.

Now I do appreciate your reference to HIV recombination because it shows that multiple selection pressures slow the evolution of resistance despite HIV does recombination, huge populations, high reproductive rate, high mutation rate and short genome length. Every possible beneficial condition for evolution of this virus is still slowed by multiple selection conditions. Hmm, I wonder what variable dominates the mathematics of mutation and selection (and recombination)?

I have critiqued cheese wiz’s gif, don’t you recall?
http://forums.randi.org/images/smilies/doglaugh.gif
Now I will give you and cheese wiz a hint on how to search for a real example of his gif, use the following search terms “+selection”, “-mutation”, “+recombination”.

Choose whatever avatar you want clown fish can’t brain.

Now for those of you interested in how mutation and selection actually works, here is another citation written by people who must solve a real problem of evolution not the fantasies put forth by the dim bulbs of evolutionism.

http://www-wds.worldbank.org/external/default/WDSContentServer/IW3P/IB/2005/07/20/000016406_20050720164750/Rendered/INDEX/wps3670.txt (http://www-wds.worldbank.org/external/default/WDSContentServer/IW3P/IB/2005/07/20/000016406_20050720164750/Rendered/INDEX/wps3670.txt)



What I think is that you have no understanding of functional equations (or of grammar or of spelling or of the mathematics of mutation and selection…).

The following series is for a population of 64, mutation rate=1/G, gamma=16, site width=6, weight width=5
Genome length\generations to Rs>=Rf
256 \ 675
512 \ 2,925
1024 \ 10,108
2048 \ 35,486
4096 \ 162,892
8192 \ 710,152
16384 \ 6,894,433 (Perfect Creature)
Can’t brain, do I have to paint you a picture or perhaps post a gif. This series shows the effects of genome length on the rate of information acquisition in ev. Can’t brain can’t see this?

Somebody has to be the iconoclast to the false belief system of evolutionism.

The only dance I’m doing is on the grave of evolutionism. You want my advice on your choice of avatars? I don’t think you need it; you do just fine in representing yourself clown fish can’t brain.

It doesn’t mean accelerate evolution either which your partner in fantasy cheese wiz thinks that multiple selection pressures does.

I noticed you haven’t posted any real examples of cheese wiz’s silly gif yet, I gave you a hint, to you want me to paint you a picture or perhaps post a gif?


Oh, is that what you want me to show brain washed and biased evolutionarian? I understand how much work it takes to reverse the highly ingrained evolutionarian mind set so I will repeat that data for you.
Let’s use the final point in the above series (G=16,384) to demonstrate how quickly any one of the three selection conditions evolve. The following data from ev shows the number of generations necessary to evolve to zero mistakes for one of the selection conditions when the other weights for the other selection conditions are set to zero.
missed site\spurious binding within gene\spurious binding outside gene
1 \ 223 \ 223
So the ev model goes from requiring almost 7 million generations for evolving out mistakes for all three simultaneous selection conditions to taking only at most 223 generations for each selection condition alone. This effect is seen in reality as shown by the numerous citations I have and will continue to post. Still can’t see can’t brain?


I wondered if you would reenter the discussion on this point. It doesn’t matter what function evolves from a selection condition. The only requirement is that mutations are selected to give the most fit creatures, that is unless you are arguing that there is a goal for evolution.

Now whether ev will evolve the selection conditions simultaneously and sequentially and still give the same function I leave to you to either disprove my contention or verify my argument. I like having a little mystery in this debate. It makes it more interesting. I will instead continue to post real examples of mutation and selection which show that the greater the number of selection conditions, the slower evolution goes. There is something about reality which makes all these speculations moot.


Can’t brain, what natural selection does is choose for the best reproducing creature. Dr Schneider’s selection conditions are contrived but still capture the mathematical behavior of mutation and selection process. Each one of the selection conditions in his model affects the fitness to reproduce just as if you use three drug therapy to treat HIV. Each drug has effect on the fitness to reproduce of the virus. Single selection conditions in ev allow for rapid evolution to that one selection condition just as monotherapy of HIV allows for rapid evolution of resistance to that drug. Imposing all three selection conditions in ev markedly slows evolution to these three selection conditions in the same way combination therapy slows the evolution of resistance to the three drugs despite HIV’s ability to do recombination. That is how the mutation selection process works.

Hey, you evolutionarians make a reptile into a bird; maybe it’s closer to making a pig into a football.

You mean like this one which shows again that multiple selection pressures slow and ultimately stop evolution?

http://www.ajtmh.org/cgi/reprint/71/2_suppl/187.pdf (http://www.ajtmh.org/cgi/reprint/71/2_suppl/187.pdf)



I’m not sure why all you evolutionarians want to credit me with Dr Schneider’s peer reviewed and published mathematical model of random point mutation and natural selection but I don’t take credit for his work. The first video says creationists claim that information can’t come about by random processes. I have never made that claim. In fact I say that Dr Schneider’s ev computer simulation correctly models how information comes about by random point mutations and natural selection and it comes about profoundly slowly if there is more than one selection pressure. That’s how the mathematics of mutation and selection works. They also say that creationists never define what information is. That is also incorrect. Early in this thread the issue was discussed and information is mathematically equal to the negative of entropy. The derivation of this mathematical relationship can be found in the text Equilibrium Statistical Mechanics by Andrews. This is mathematically the same as Shannon’s information theory.

I don’t know how old you have to be not to learn something new but I only started studying the mathematics of mutation and selection a little over a year ago and the mathematical behavior of this process is nothing like evolutionarians allege. It was only after I studied Dr Schneider’s model that it became apparent why it converged so slowly and it was the multiple selection conditions which slowed the convergence of the model. It then became abundantly clear why combination therapy is used to treat HIV and slow or prevent the evolution of resistant viruses, and why combination therapy is used to treat TB and why combination therapy is used to treat malaria and why combination herbicides are used and why combination chemotherapy is used to treat cancer and why combination rodenticides are uses… This is how the mutation and selection process works. Single selection pressures can evolve rapidly, each additional selection pressure slows the evolutionary process (unless you are cheese wiz and you think multiple selection pressures accelerate evolution but he has yet to post a single example of this).

You call that good music? Is mental frustration anything like annoying? I am really, really sorry that I have mentally frustrated you with the mathematical and real facts of how mutation and selection works. Oh, oh, that’s the second lie I’ve told on this thread, the first one was when I told Delphi that he didn’t contradict himself in order to get the name of the paper he published in Science.

Why jimbob, you are correct, 7 million generations is not actually a very long time for a bacterium. How many bacterium do you know of that has a genome length of 16,384. Why don’t you run the 32k genome length and see how many generations you get? What is the shortest genome length for any free living life form?

If you read the entire thread, you will find the answer to what is the shortest genome length of a free living creature. Population is a user definable parameter in the model. The mutation rate is a user definable parameter in the model.

I don’t know how many people have pointed out that ev is only a model. Ask cheese wiz, he likes to count how many times things have been said. With respects to antibiotic resistance only having evolved over the last 60 years, that’s and interesting question since I would have to think that the penicillium mold was producing penicillin for more than 60 years. Anyway, it still doesn’t change the mathematical fact that multiple selection pressures slow and ultimately stop evolution. That’s what ev shows and that is what reality shows.

It seems that you evolutionarians didn’t like the Stephen Hawking video on youtube.

I think you are wrong here lita’ gator. There is a difference between spurious binding outside the genome and spurious binding in the gene. Let’s see if you can guess what it is.

Now lita’ gator, there is a difference between hardware and software. Where have you been anyway, I hardly ever get a chance to discuss the string cheese theory of evolution any more except cheese wiz has come up with a gif of comparable quality where he says that multiple selection pressures accelerates evolution. Were waiting for cheese wiz to post a real example of his fantasy world, excuse me, alternative universe.

That’s the point Paul, single selection pressures evolve much more rapidly than multiple selection pressures. That what ev shows, that is what the Delphi’s Wikipedia reference to the fitness landscape shows and that is what the numerous real examples I have been posting of mutation and selection shows. That’s what your model of mutation and selection shows Paul.

That’s a good question, how many selection pressures did it take to transform a reptile into a bird? Let’s consider HIV since it is the best example of evolution by mutation and selection and probably has the most data available. What are the populations, reproduction rates and mutation rates? How many selection pressures is the virus being subjected to? We know that people with the virus can survive years on appropriate combination therapy despite the high reproductive rate of the virus, huge populations, high mutation rate and as can’t brain has pointed out, the virus does recombination.

If you want to talk about slow, we can talk about the convergence of ev with an e coli size genome, do you want to use that as a baseline?

Hey, I wonder if I can add that music to this thread, you know how I enjoy annoying evolutionarians.

That’s not going to fly, information has a precise mathematical definition even if Dr Schneider dropped a sign on his web site definition.

He may be clever but he is not correct. I’ve agreed with you and Dr Schneider since the beginning of this discussion that random mutation and selection can lead to the increase in information in a genome. What you have not come to grips with is that this process is profoundly slow, too slow to support your theory of evolution. Why does your model show this process is so slow? It is the multiple selection conditions which slows the evolutionary process. Here is another real example of how multiple selection pressures slow evolution.

http://clinicaltrials.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pctr.0010015 (http://clinicaltrials.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pctr.0010015)

Now you evolutionarians all have a good weekend and don’t believe everything you see on the tube. I’ll be back next week posting more examples of how multiple selection pressures slow and ultimately stop evolution. I've only skim-read it, but this would appear to be more of the same old crap. Perhaps you could save us the trouble of reading though it all by highlighting any new lies or magic words in some appropriate colored font.

Tell me, did it take you long to type?

[Paul C. Anagnostopoulos]

Perhaps you could save us the trouble of reading though it all by highlighting any new lies or magic words in some appropriate colored font.
I recommend mauve or taupe.

~~ Paul

[UnrepentantSinner]

This was posted by a TE on Christianforums and I thought I'd share it here.

I didn't realize that reporting on ICR's pretend-science projects now constituted "slander". I'll have to file it away in my creationist-to-English dictionary.

ad hominem: any unflattering evaluation of a creationist. "That dirty, evil, lying Nazi evolutionist said I was ignorant when I said that there are no transitional fossils. He should be banned for ad hominem!"

arrogance: coming to conclusions that don't explicitly mention God.

closed-minded: the state of mind which precludes one from treating creationism as being equal to conventional science. "Their refusal to teach creationism alongside evolution is just closed-minded!"

Darwinism: a supposed scientific theory that is in fact a cult based on the writings of Charles Darwin. It is responsible for most of the evils of the 20th century, such as Nazism, communism, tolerance, gay rights, birth control, and school shootings.

evidence: see Scriptural Quotations

humility: believing that God created the Earth just for humans and that the rest of the universe is merely an afterthought.

intolerant: insisting that science come to conclusions based on facts instead of fitting the facts to a pre-determined conclusion. "is science such a closed-minded, elitest, intolerant group that there is only one way to do anything? their way?"

religion: anything that's not Christianity. "Evolution is just a secular religion for atheists!"

science: an evil conspiracy to drive God out of public life, as opposed to true science.

slander: accurately reporting on a creationist organization's activities.

true science: anything that confirms a creationist's beliefs. "True science will never contradict a literal reading of the Genesis account."

Word of God: a creationist's interpretation of the Bible.

[kleinman]

Watching video ... turning annoying sound off ...…the guy has several good video…
Hey articulett, what happens when you put the mushy soft theory of evolution to music? Answer, you have a musical farce. What happens when you put the mushy soft theory of evolution to mathematics? Answer, you have a mathematical farce. Don’t worry, we’ll show you what the mathematics of mutation and selection really shows, I have a few more citations of how it really works below.
lots of words...none of it worth reading or commenting on.
Ev, a peer reviewed and published model of mutation and selection which you neither study nor understand and huge numbers of peer reviewed and published examples of how mutation and selection actually works which you don’t read, can’t brain you are the quintessential example of evolutionarian thinking.
You are simply wrong.
Oh yes, and your gross speculations about cooperative chemistry and abiogenesis are nothing short of a brilliant example of evolutionarian science when compared to all the peer reviewed and published examples of how mutation and selection actually works.
I think you are wrong here lita’ gator. There is a difference between spurious binding outside the genome and spurious binding in the gene. Let’s see if you can guess what it is. Immaterial. What matters is that ev's selection pressures do not model the entire landscape of evolutionary actualities, and in the case of a frame shift, this apparently caused a gene to appear and digest nylon, where that capability didn't previously exist. Such a change is not contemplated by the ev model, therefore your contention that ev proves macroevolution mathematically impossible is quite simply false.
All the posted citations of real examples of mutation and selection include the entire evolutionary landscape. HIV does recombination, frame shifts, stutters, insertion deletions and insertions yet still shows that combination selection pressures slow evolution profoundly with only three selection pressures. Ev shows the same with its three selection conditions. Perhaps you want to join the cheese wiz camp and argue that multiple selection pressures accelerate evolution?
Now lita’ gator, there is a difference between hardware and software. Where have you been anyway, I hardly ever get a chance to discuss the string cheese theory of evolution any more except cheese wiz has come up with a gif of comparable quality where he says that multiple selection pressures accelerates evolution. Were waiting for cheese wiz to post a real example of his fantasy world, excuse me, alternative universe.The thread is boring, Alan. I like to learn relevant information re evolution. You rarely present anything relevant, so there's no reason for me to respond.
Let’s talk about the string cheese theory of evolution, that’s interesting.
I've only skim-read it, but this would appear to be more of the same old crap.
It must be part skim cheese wiz we are seeing here, so let’s read the great a gifted cheese wiz’s post in detail.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
The red line shows generations to achieve fixation of n alleles acted on by n selection pressures, the n+1th selection pressure being introduced only after the nth allele is fixed.

The blue line shows generations to achieve fixation of n alleles acted on by n selection pressures simultaneously.

All other features and parameters of the two models are identical. The model is designed so that the relative advantage of n+1 new genes over n (when selection is acting) is the same for all n, i.e. each new allele carries the same advantage.

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
http://forums.randi.org/images/smilies/doglaugh.gif
Cheese wiz, could you show a real example of your silly gif?
Perhaps you could save us the trouble of reading though it all by highlighting any new lies or magic words in some appropriate colored font.I recommend mauve or taupe.
Hey Paul, are you going to embrace cheese wiz’s gif where he contends that multiple selection pressures accelerate evolution? Notice how many real examples cheese wiz has posted of his gif?
This was posted by a TE on Christianforums and I thought I'd share it here.
What’s the matter Un-ner, don’t you have anything to say about the mathematics of mutation and selection? Well, here are a couple of more real examples of how mutation and selection really works, that is multiple selection pressures slow and ultimately stop evolution.

The following two quotes are found at http://www.chemweb.com/journals?type=issue&jid=09298673&iid=14002 (http://www.chemweb.com/journals?type=issue&jid=09298673&iid=14002)

This first reference is for Dr Schneider and the gang over at the National Cancer Institute.
Possible Effects of Early Treatments of Hsp90 Inhibitors on Preventing the Evolution of Drug Resistance to Other Anti-Cancer Drugs (http://www.bentham-direct.org/pages/content.php?CMC/2007/00000014/00000002/0009C.SGM) by Li Xiao, Parsa Rasouli, Douglas Ruden (pp. 223-232).
Hsp90 is a chaperone that is critically important for both cancer progression and tumor survival. Hsp90 is an exciting target for anti-cancer drugs because most of the proteins that interact with Hsp90 are known to be in the cell cycle, signaling and chromatin-remodeling pathways. Recent work in fungi has shown that reduction of Hsp90 activity dramatically increases the efficacy of many fungicides. Furthermore, in studies on the evolution of drug resistance in fungi, it has been shown that high levels of Hsp90 increase the rate of the development of fungicide resistance, whereby low levels of Hsp90 decrease the rate of fungicide resistance. Similarly, in humans and mammalian models, Hsp90 inhibitors have been shown to act additively or synergistically with many other cancer therapies for killing both solid tumors and leukemias. Also, several recent studies have shown that Hsp90 inhibitors potentiate the activity of drugs in cancer cells lines that are otherwise resistant to the drug. However, during the evolution of drug resistance in cancer cells, it has not yet been determined whether early exposure to Hsp90 inhibitors slows the rate of developing resistance to other anti-cancer drugs, as would be expected from the fungal studies. In this review, we summarize the effects of the Hsp90 inhibitors geldanamycin and its derivatives with other anti-cancer drugs on killing cancer cells. We also discuss other basic science and clinical studies that need to be done to determine the optimum exposure regimens for Hsp90 inhibitor treatments to maximize its cancer-killing activities, and to minimize the evolution of resistance to other anti-cancer drugs.

Virostatics: A New Class of Anti-HIV Drugs (http://www.bentham-direct.org/pages/content.php?CMC/2007/00000014/00000002/0010C.SGM) by F. Lori, A. Foli, L.M. Kelly, J. Lisziewicz (pp. 233-241).
In this review we discuss the features of a new class of antiretroviral combinations, namely “Virostatics”. Virostatics are characterized by the combination of a drug directly inhibiting virus production (viro), and another drug indirectly inhibiting the virus by reducing cellular proliferation (static). In particular, we will focus on the combination of hydroxyurea and didanosine against HIV-1. Hydroxyurea and didanosine synergize to control viral replication and present with a favorable resistance profile, suppressing several resistant quasi-species. Because virostatics target essential cellular proteins, they exert an immune modulating activity and reduce viral targets (CD4 T cells), possibly with limited immunosuppressive effects. Importantly, a dose-finding clinical study has shown that decreasing the dose of hydroxyurea not only diminishes toxicity but also increases antiviral potency. Therefore, the combination of hydroxyurea and didanosine strikes a balance between viral suppression, drug-related toxicity and viral escape, and could have a role both in induction and maintenance therapy. In this review we would like to appraise what is known about hydroxyurea and didanosine and specifically address the major advantages, i.e. novel mechanism of action leading to a new class of drugs and resistance profile providing durability, as well as the major criticisms of this combination, i.e. toxicity and reasons for prescribing a perceived immune suppressant to immune compromised patients.
See how easy it is cheese wiz?

[kjkent1]

All the posted citations of real examples of mutation and selection include the entire evolutionary landscape. HIV does recombination, frame shifts, stutters, insertion deletions and insertions yet still shows that combination selection pressures slow evolution profoundly with only three selection pressures. Ev shows the same with its three selection conditions.Once again -- irrelevant and immaterial. We have conclusive proof of a bacteria that underwent a frame shift which resulted in its obtaining the ability to digest nylon. This type of error is not modeled by EV. Thus it is outside the scope of your parametric analysis, because that analysis is entirely dependent upon EV.

It may have been be a different story were the bacteria to not exist, because then all of your cites to articles discussing the effect of multiple selective pressures would not be subject to the empircal evidence of the bacteria's existence. But, as the new bacteria and its predecessors exist, and the new bacteria appeared during a a very short time span, there are only two possibilities:

1. The bacteria evolved;
2. A designer created the bacteria.

As there is no scientific evidence of an alien or supernatural force recently acting upon the Earth, #1 is therefore proven true -- and said proof falsifies your theory.

Evolution may not be a perfect storm of smooth gradualism, but unexpected things happen to biological organisms all the time, and the result is that they change. And, if those changes provide a selective advantage in the status quo environment, then the changed organisms survive and reproduce.

Get over it, Alan. Evolution is not only mathematically possible -- it's just plain true.

[kleinman]

All the posted citations of real examples of mutation and selection include the entire evolutionary landscape. HIV does recombination, frame shifts, stutters, insertion deletions and insertions yet still shows that combination selection pressures slow evolution profoundly with only three selection pressures. Ev shows the same with its three selection conditions.Once again -- irrelevant and immaterial. We have conclusive proof of a bacteria that underwent a frame shift which resulted in its obtaining the ability to digest nylon. This type of error is not modeled by EV. Thus it is outside the scope of your parametric analysis, because that analysis is entirely dependent upon EV.
I see, you think that frame shifts is the crucial mechanism for evolution which will overcome the mathematical and real fact that multiple selection pressures slow and ultimately stop evolution. That should be easy enough for you to incorporate into ev and prove that this overcomes this mathematical and real fact that multiple selection pressures slow evolution even though the evolution of HIV, TB, malaria, weeds, cancer cells, agricultural pests and all microorganisms and large creatures cited in these many references are slowed in their evolution when additional selection pressures are applied to them. It will be interesting to see you prove this.
It may have been be a different story were the bacteria to not exist, because then all of your cites to articles discussing the effect of multiple selective pressures would not be subject to the empircal evidence of the bacteria's existence. But, as the new bacteria and its predecessors exist, and the new bacteria appeared during a a very short time span, there are only two possibilities:
Really, the predecessors to bacteria exist?
1. The bacteria evolved;
Certainly bacteria evolve, but they remain bacteria. Just because a polymerase can mutate to digest a xenopolymer does not explain the evolution of reptiles to birds. It is this type of hyperextrapolation and extreme speculation that forms the foundation to the theory of evolution. The mathematics of mutation and selection and real examples of this process tells an entirely different story.
2. A designer created the bacteria.
It is clear that evolution didn’t do it. There is no mathematical basis to explain how it happened.
As there is no scientific evidence of an alien or supernatural force recently acting upon the Earth, #1 is therefore proven true -- and said proof falsifies your theory.
Look for the evidence lita’ gator, you will find it.
Evolution may not be a perfect storm of smooth gradualism, but unexpected things happen to biological organisms all the time, and the result is that they change. And, if those changes provide a selective advantage in the status quo environment, then the changed organisms survive and reproduce.
The theory of evolution doesn’t even qualify as a tempest in a teapot. If fact it only serves as a corrupt framework for viewing reality. Why do you think you evolutionarians are having so much trouble comprehending the results from ev and the numerous real examples of what ev shows? The theory of evolution leads to a perversion of the interpretation of reality. The problem of antimicrobial resistance, pesticide and herbicide resistance and cancer cell resistance to chemotherapies is much easier to understand if you discard the false theory of evolution. Evolutionarians stand in the way of advancement of science in order to maintain their belief system. Especially when you have evolutionarians like cheese wiz who posts silly gifs where he claims multiple selection pressures accelerate evolution. I happen to agree with articulett that religion should not be taught in school, including the religion of evolutionism. It is one of the most dangerous and corrupt religions of the past century.
Get over it, Alan. Evolution is not only mathematically possible -- it's just plain true.
It may be true in one of your 10^500 alternative universes but not in this one, mutation and selection doesn’t work properly for your theory. It is mathematically impossible; ev shows this and numerous real examples of how mutation and selection works shows this.

[kjkent1]

I see, you think that frame shifts is the crucial mechanism for evolution which will overcome the mathematical and real fact that multiple selection pressures slow and ultimately stop evolution. That should be easy enough for you to incorporate into ev and prove that this overcomes this mathematical and real fact that multiple selection pressures slow evolution even though the evolution of HIV, TB, malaria, weeds, cancer cells, agricultural pests and all microorganisms and large creatures cited in these many references are slowed in their evolution when additional selection pressures are applied to them. It will be interesting to see you prove this.Irrelevant and immaterial. You are misquoting me so as to erect a strawman. I didn't say that frame shift is "the crucial mechanism for evolution." I said that the frame shift caused the bacteria to be able to digest nylon, and that is a substantial change to the organism's capability. Suppose humans were able to do similarly -- that would be quite a metabolic change from the status quo.

Regardless, ev is not set up to deal with external selection pressures, and only bases fitness upon internal pressure (missing and spurious bindings).

A missed and/or spurious binding in ev does not equate to some external environmental pressure. Suppose you have two completely evolved ev genomes of identical length. Each one is equally fit for its external environment, because there "is" no external environment in ev. A completely evolved ev genome, no matter what its order, exhibits no organic behavior which would make it more or less fit to survive.

It just has no missing or spurious bindings. But, in the real world, such an organism might be completely unfit for its environment, which an organism which was alive but less perfect in terms of missing and spurious bindings, might be far more fit for its external environment, and far more likely to propagate its genes to a new generation.

In the real world, one "perfect" ev genome may be capable of digesting some simple sugars, while some other may be capable of digesting crude oil.

In an environment devoid of sugar and full of oil, one would survive while the other would perish, and visa versa.

Is it any wonder that ev doesn't evolve fast enough? Ev uses only two very simple selective pressures appropriate to an extremely primitive organism. Ev mutations have no external manifestation and no external environment exists to select for or against such manifestations, even were they to be externally exhibited.

Your theory is based on an algorithm designed to demonstrate simple information gain -- and the algorithm works. Extrapolating this to include complex multicellular organisms who must interact with a complex environment is frivolous.

Now, this is where you jump in and defend Schneider's statements about how ev demonstrates the workings of evolution, so that you can use that strawman to make your theory seem impossible to defeat.

Nevertheless, your theory is entirely defeated, by a little bacteria that eats nylon.

You ought to be ashamed of yourself for continuing to rain out this nonsensical blather. Get a life.

[kleinman]

I see, you think that frame shifts is the crucial mechanism for evolution which will overcome the mathematical and real fact that multiple selection pressures slow and ultimately stop evolution. That should be easy enough for you to incorporate into ev and prove that this overcomes this mathematical and real fact that multiple selection pressures slow evolution even though the evolution of HIV, TB, malaria, weeds, cancer cells, agricultural pests and all microorganisms and large creatures cited in these many references are slowed in their evolution when additional selection pressures are applied to them. It will be interesting to see you prove this.Irrelevant and immaterial. You are misquoting me so as to erect a strawman. I didn't say that frame shift is "the crucial mechanism for evolution." I said that the frame shift caused the bacteria to be able to digest nylon, and that is a substantial change to the organism's capability. Suppose humans were able to do similarly -- that would be quite a metabolic change from the status quo.
A polymerase evolves to a polymerase and a bacterium evolves to a bacterium. That’s what your example shows. That’s what mutation and selection is capable of doing.
Regardless, ev is not set up to deal with external selection pressures, and only bases fitness upon internal pressure (missing and spurious bindings).
Ev is not set up to deal with external selection pressures, what are you talking about? A selection pressure is something that affects the fitness of a population to reproduce, that is what ev simulates.
A missed and/or spurious binding in ev does not equate to some external environmental pressure. Suppose you have two completely evolved ev genomes of identical length. Each one is equally fit for its external environment, because there "is" no external environment in ev. A completely evolved ev genome, no matter what its order, exhibits no organic behavior which would make it more or less fit to survive.
I have always realized that ev is an idealized model of mutation and selection and that Dr Schneider’s selection condition is contrived. Despite this, the model still properly simulates the mathematics of mutation and selection. Dr Schneider’s selection condition can be seen as an environmental change that requires increased recognition of the binding sites in order for the creatures to survive but it doesn’t matter with respects to the behavior of the mathematical model. Dr Schneider’s model still properly captures the essentials of the mutation and selection process.
It just has no missing or spurious bindings. But, in the real world, such an organism might be completely unfit for its environment, which an organism which was alive but less perfect in terms of missing and spurious bindings, might be far more fit for its external environment, and far more likely to propagate its genes to a new generation.
Spurious binding in the nonbinding site region represents a way of handling neutral versus harmful mutations in that region. If the mutation in the nonbinding site region gives rise to a recognizable binding site it is considered a harmful mutation and weighs against that creature in the selection process. If the mutation in the nonbinding site region does not give rise to a recognizable binding site, it doesn’t affect the selection of that creature. It can be argued that mutations in the nonbinding site region of the genome may be far more harmful if the nonbinding portion of the genome was a full functional genetic sequence. So what if this model doesn’t represent a total functional genome in a real living creature? It doesn’t alter the underlying mathematics of the mutation/selection process.
In the real world, one "perfect" ev genome may be capable of digesting some simple sugars, while some other may be capable of digesting crude oil.
I see, if a mathematical model doesn’t simulate the entire universe, it is invalid. You can not simulate a portion of reality? You are demonstrating your lack of knowledge and experience how computer simulations are used.
Is it any wonder that ev doesn't evolve fast enough? Ev uses only two very simple selective pressures appropriate to an extremely primitive organism. Ev mutations have no external manifestation and no external environment exists to select for or against such manifestations, even were they to be externally exhibited.
You are correct here, as you complicate the model and try to more accurately simulate the real world, the rate of evolution will slow down even more so in the simulation. By the way, there are three distinct selection pressures in ev. There is a difference between spurious binding in the nonbinding site region and spurious binding in the gene. Do you know what that difference is?
Your theory is based on an algorithm designed to demonstrate simple information gain -- and the algorithm works. Extrapolating this to include complex multicellular organisms who must interact with a complex environment is frivolous.
What you still don’t understand about the mathematics of mutation and selection is that as you complicate the system, the evolutionary process slows down. This is most clearly seen by what happens with additional selection pressures. This is why the theory of evolution is mathematically impossible. I agree that expanding the model to complex multicellular organisms is frivolous. If you can carry out the evolution of the binding sites with all these simplifying assumptions, you will never be able to do it with a complex multicellular organism.
Now, this is where you jump in and defend Schneider's statements about how ev demonstrates the workings of evolution, so that you can use that strawman to make your theory seem impossible to defeat.
What’s wrong with using Dr Schneider’s own public comments about his peer reviewed and published mathematical model? If I am misinterpreting what Dr Schneider is saying, he has more than enough ways to correct me, including a huge tax payer financed web site. Dr Schneider has defended his model for years in a very vocal manner. Why do you think you barely hear a whisper from him now?
Nevertheless, your theory is entirely defeated, by a little bacteria that eats nylon.
A polymerase evolving to a polymerase and a bacterium evolving to a bacterium hardly defeats what ev shows and the numerous real examples of what it shows. Perhaps in one of your 10^500 alternative universes a polymerase mutating in order to be able to digest nylon fills in the gap between reptile and bird but multiple selection pressures slowing evolution really messes up this fantasy of yours.
You ought to be ashamed of yourself for continuing to rain out this nonsensical blather. Get a life.
The only rain I am making is a little mathematical scientific analysis on the evolutionarian day parade. Sorry to mess up your little religious holiday.

So here’s another example citation of how multiple selection pressures slow and ultimately stop evolution.

http://www6.lexisnexis.com/publisher/EndUser?Action=UserDisplayFullDocument&orgId=1809&topicId=26923&docId=l:623811163&start=23 (http://www6.lexisnexis.com/publisher/EndUser?Action=UserDisplayFullDocument&orgId=1809&topicId=26923&docId=l:623811163&start=23)
To avoid the selection of these genetic variants by exposure to the drug during therapy, it is vital that a combination of different TB drugs is administered together since the odds of a single bacterium simultaneously carrying mutations that are able to confer resistance to two or more drugs are extremely slim (much less than one in a trillion).
Isn’t that interesting, combination selection pressures slow the selection of resistant strains of TB.

[Paul C. Anagnostopoulos]

A missed and/or spurious binding in ev does not equate to some external environmental pressure. Suppose you have two completely evolved ev genomes of identical length. Each one is equally fit for its external environment, because there "is" no external environment in ev. A completely evolved ev genome, no matter what its order, exhibits no organic behavior which would make it more or less fit to survive.
I think we need to be careful here. One could argue that there is an external pressure in Ev, namely the external pressure that causes creatures with more accurate bindings to survive better than those with less accurate bindings. The only reason this doesn't seem like an external pressure is that Ev does not draw any analogy to a typical environmental/chemical mechanism for this pressure. It's a black box pressure, if you will. It just "magically" selects creatures with better binding. But it is external to the chemistry of the creatures.


Is it any wonder that ev doesn't evolve fast enough? Ev uses only two very simple selective pressures appropriate to an extremely primitive organism. Ev mutations have no external manifestation and no external environment exists to select for or against such manifestations, even were they to be externally exhibited.
Again, one can say that the mechanism that is selecting creatures in Ev is the external environment. But what is not happening is any (gradual) change in the external environment, manifesting in changes in the selection pressures, and therefore in a continuing evolution of the creatures. For example, at no time is nylon introduced into the environment. :D

~~ Paul

[Paul C. Anagnostopoulos]

I see, if a mathematical model doesn’t simulate the entire universe, it is invalid.
You forgot to finish that sentence:

I see, if a mathematical model doesn’t simulate the entire universe, it is invalid to draw sweeping conclusions about the entire universe.

~~ Paul

[kleinman]

I see, if a mathematical model doesn’t simulate the entire universe, it is invalid.You forgot to finish that sentence:
Nope, I didn’t forget to finish this sentence.
I see, if a mathematical model doesn’t simulate the entire universe, it is invalid to draw sweeping conclusions about the entire universe.
This is your sentence, not mine. I am drawing a very narrow conclusion from the results of ev and what it represents in reality. The conclusion that I am drawing is that ev shows that the rate of information acquisition based on random point mutation and selection is such a profoundly slow process that the theory of evolution is mathematically impossible. The reason why this process is profoundly slow in ev is the multiple selection conditions which slow the acquisition of information, in particular as you lengthen the genome in the model. I am backing up this conclusion with numerous real examples which demonstrate the mathematical behavior which ev shows. Now if you want to add other mechanisms of mutations and recombination to the model and expect a different result, we would all be interested in seeing this.

[joobz]

Nope, I didn’t forget to finish this sentence.

This is your sentence, not mine. I am drawing a very narrow conclusion...
this is blatantly not true and therefore invalidates the rest of your jibberish.

In other words, you're wrong...again.

[kleinman]

Nope, I didn’t forget to finish this sentence.

This is your sentence, not mine. I am drawing a very narrow conclusion...this is blatantly not true and therefore invalidates the rest of your jibberish.
Can’t brain, I keep forgetting that you have explained the origin of life with your narrow and precise cooperative chemistry hypothesis. Who could debate your air tight logic?
In other words, you're wrong...again.
Can’t brain, since you are a supporter of cheese wiz’s gif, when are you going to post an example where multiple selection pressures accelerate evolution?

[articulett]

I just want to interject that I think it's cute when they get peeved and use big red fonts--like that makes it even more valid or something. Precious.

[joobz]

Can’t brain, I keep forgetting that you have explained the origin of life with your narrow and precise cooperative chemistry hypothesis. Who could debate your air tight logic?
Obviously, you. You can't debate it. My critique of your entire argument is sound. It is why you use non sequitors and ad homs.

[kleinman]

I just want to interject that I think it's cute when they get peeved and use big red fonts--like that makes it even more valid or something. Precious.
Wait a minute; you are supposed to be annoyed by these large red fonts. That’s ok, I’m glad you find these large red fonts precious. Now if you mathematically challenged evolutionarians learn how mutation and selection behaves mathematically, you then would understand what the large red font is illustrating. By the way, I am not peeved; however you almost succeeded in annoying me with the sound tracks from those silly youtube videos. You would have succeeded if I had not quickly hit the mute button on my computer. Did you really think that was good music? There’s no telling for the tastes of evolutionarians.
Can’t brain, I keep forgetting that you have explained the origin of life with your narrow and precise cooperative chemistry hypothesis. Who could debate your air tight logic?Obviously, you. You can't debate it. My critique of your entire argument is sound. It is why you use non sequitors and ad homs.
Can’t brain, your cooperative chemistry hypothesis has the impact of lita’ gator’s string cheese theory.

Here is another citation where they have figured out that combination selection pressures slow evolution. Again, this demonstrates the mathematics of ev and shows how mutation and selection works and that is multiple selection pressures slow and ultimately stop evolution.
http://doctor.medscape.com/viewarticle/420664 (http://doctor.medscape.com/viewarticle/420664)
Dr. Daniel Kuritzkes of the University of Colorado began his plenary presentation[1] by commenting on the incremental benefits we have seen over the evolution of antiretroviral therapy, from modest survival improvements with monotherapy to the current era of combination therapy. Success is now measured by the proportions of patients achieving plasma viral load suppression and by the number of years to viral rebound. This has been accompanied by dramatic falls in the number of clinical events amongst people with established HIV infection and declines in vertical transmission. However, these advances have not been without costs in terms of toxicity, regimen complexity, resistance, quality of life, and financial burdens on society. Clearly, there is still a need for new drugs to help manage these problems. Many questions remain, including when to start, what to start, the role of resistance testing, definitions of drug failure, and the management of metabolic and fat redistribution problems. As many of these subjects have been addressed during the conference, Dr Kuritzkes chose to discuss three other issues: viral reservoirs, treatment interruptions, and discordant CD4+/viral load responses.
I dedicate the large red font above to articulett.

[Paul C. Anagnostopoulos]

The conclusion that I am drawing is that ev shows that the rate of information acquisition based on random point mutation and selection is such a profoundly slow process that the theory of evolution is mathematically impossible.
You're saying that this is not a sweeping conclusion about the entire universe? Precious.

~~ Paul

[kleinman]

The conclusion that I am drawing is that ev shows that the rate of information acquisition based on random point mutation and selection is such a profoundly slow process that the theory of evolution is mathematically impossible.You're saying that this is not a sweeping conclusion about the entire universe? Precious.
Oh no Paul, it’s a precious little conclusion about how mutation and selection works. You know what mutation and selection is; it’s the cornerstone mechanism for how the theory of evolution works. Are you going to propose that evolution works by some other mechanism? What I really like about this precious little conclusion from the results of ev is how it explains all these citations I have been posting. I guess you can say my conclusion encompasses the entire universe of evolutionism which is rapidly shrinking.

[Paul C. Anagnostopoulos]

Oh no Paul, it’s a precious little conclusion about how mutation and selection works. You know what mutation and selection is; it’s the cornerstone mechanism for how the theory of evolution works. Are you going to propose that evolution works by some other mechanism?
You know, Alan, I think I've been reasonably polite to you over the months, but you really are whacked. Here you challenge me to say whether "mutation and selection" are sufficient, but in your previous post to me you were talking about "random point mutation and selection."

The goalposts have become uprooted and are spinning about like a couple of spastic wrestlers covered in oil.

~~ Paul

[kleinman]

Oh no Paul, it’s a precious little conclusion about how mutation and selection works. You know what mutation and selection is; it’s the cornerstone mechanism for how the theory of evolution works. Are you going to propose that evolution works by some other mechanism?You know, Alan, I think I've been reasonably polite to you over the months, but you really are whacked. Here you challenge me to say whether "mutation and selection" are sufficient, but in your previous post to me you were talking about "random point mutation and election."
Paul, if you think the other forms of mutations are going to change the results that ev is showing, that is combination selection pressures slow and ultimately stop evolution then you are in complete denial of all these citations I have been posting. None of these citations that I have been posting are limited to random point mutations and still multiple selection pressures slow evolution. Recombination does not stop this effect with HIV and that is by far the most favorable case of mutation and selection with it’s high mutation rate, large populations and reproductive rate. Yet multiple selection pressures slow the evolution of resistance. This effect is seen in multiple areas of science, medicine and agriculture. Dr Schneider’s model got the mathematics of mutation and selection correct and it shows how rapidly the rate of information acquisition declines with increasing genome length and more importantly with increasing number of selection conditions. Dr Schneider simply did not do a complete analysis of his model, if he had, he would have seen why it takes so long for it to converge with realistic genomes. This is why the theory of evolution is mathematically impossible.
The goalposts have become uprooted and are spinning about like a couple of spastic wrestlers covered in oil.
Stop whining Paul, it’s not becoming for a moderator on the James Randi educational forum. It’s been a while since I posted the goalposts, so for you Paul, here they are again.
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*░░░░░░░░░This is what ev shows.░░░░░░░░░*
*░░░░░░░This is what reality shows.░░░░░░*
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After:

It’s been a while since I posted the goalposts, so for you Paul, here they are again.
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*░░░░░░░░░This is what ev shows.░░░░░░░░░*
*░░░░░░░This is what reality shows.░░░░░░*
******************************************

Time for another round of beer. While we are laughing about your goalpost move and its denial, we can read the following proof that humans and chimps diverged from a common ancestor (http://www.dailykos.com/story/2005/4/7/7723/67027).

A quote from that in red for the Kleinophiles:
Well, it so happens humans and chimpanzees, have seven, count'em, seven, of the exact same viral base pairs sequences, each roughly one-thousand or so pairs long, and each in several hundred respective locations in their respective genomes. We know how that can happen; chimps and humans shared a common ancestor. We can also estimate how long those viral fragments have been there because there are slight, random changes to the sequence over time. The molecular clock on the shared ERVs works out to about 5-8 million years.

[joobz]

Can’t brain, your cooperative chemistry hypothesis has the impact of lita’ gator’s string cheese theory.
ad hom and non sequitor...lovely.

[joobz]

Time for another round of beer.
that's classic.
:D

[Dr Adequate]

Stop whining Paul, it’s not becoming for a moderator on the James Randi educational forum. If you are genuinely too stupid to tell "whining" from mockery, I guess that explains some of your grosser social handicaps.

It’s been a while since I posted the goalposts,. Yes, it's been a while since you posted this, isn't it:

The goal post for evolution is the transformation of a gene from some initial function to a new and completely different function and the evolution of a gene from the beginning.

Remember how we kicked your arse over that one? It was most amusing.

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*░░░░░░░░░This is what ev shows.░░░░░░░░░*
*░░░░░░░This is what reality shows.░░░░░░*
****************************************** So, we've proved you wrong about that, too. I guess we win.

Was there anything else you wanted to discuss?

[cyborg]

Do you think projection explains why kleinman thinks we are all as stupid as he is?

[Dr Adequate]

Hey articulett, what happens when you put the mushy soft theory of evolution to music? Answer, you have a musical farce. What happens when you put the mushy soft theory of evolution to mathematics? Answer, you have a mathematical farce. Don’t worry, we’ll show you what the mathematics of mutation and selection really shows, I have a few more citations of how it really works below.

Ev, a peer reviewed and published model of mutation and selection which you neither study nor understand and huge numbers of peer reviewed and published examples of how mutation and selection actually works which you don’t read, can’t brain you are the quintessential example of evolutionarian thinking.

Oh yes, and your gross speculations about cooperative chemistry and abiogenesis are nothing short of a brilliant example of evolutionarian science when compared to all the peer reviewed and published examples of how mutation and selection actually works.

All the posted citations of real examples of mutation and selection include the entire evolutionary landscape. HIV does recombination, frame shifts, stutters, insertion deletions and insertions yet still shows that combination selection pressures slow evolution profoundly with only three selection pressures. Ev shows the same with its three selection conditions. Perhaps you want to join the cheese wiz camp and argue that multiple selection pressures accelerate evolution?

Let’s talk about the string cheese theory of evolution, that’s interesting.

It must be part skim cheese wiz we are seeing here, so let’s read the great a gifted cheese wiz’s post in detail.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg

http://forums.randi.org/images/smilies/doglaugh.gif


Hey Paul, are you going to embrace cheese wiz’s gif where he contends that multiple selection pressures accelerate evolution? Notice how many real examples cheese wiz has posted of his gif?

What’s the matter Un-ner, don’t you have anything to say about the mathematics of mutation and selection? Well, here are a couple of more real examples of how mutation and selection really works, that is multiple selection pressures slow and ultimately stop evolution.

The following two quotes are found at http://www.chemweb.com/journals?type=issue&jid=09298673&iid=14002 (http://www.chemweb.com/journals?type=issue&jid=09298673&iid=14002)

This first reference is for Dr Schneider and the gang over at the National Cancer Institute.
Possible Effects of Early Treatments of Hsp90 Inhibitors on Preventing the Evolution of Drug Resistance to Other Anti-Cancer Drugs (http://www.bentham-direct.org/pages/content.php?CMC/2007/00000014/00000002/0009C.SGM) by Li Xiao, Parsa Rasouli, Douglas Ruden (pp. 223-232).


Virostatics: A New Class of Anti-HIV Drugs (http://www.bentham-direct.org/pages/content.php?CMC/2007/00000014/00000002/0010C.SGM) by F. Lori, A. Foli, L.M. Kelly, J. Lisziewicz (pp. 233-241).

See how easy it is cheese wiz?


I see, you think that frame shifts is the crucial mechanism for evolution which will overcome the mathematical and real fact that multiple selection pressures slow and ultimately stop evolution. That should be easy enough for you to incorporate into ev and prove that this overcomes this mathematical and real fact that multiple selection pressures slow evolution even though the evolution of HIV, TB, malaria, weeds, cancer cells, agricultural pests and all microorganisms and large creatures cited in these many references are slowed in their evolution when additional selection pressures are applied to them. It will be interesting to see you prove this.

Really, the predecessors to bacteria exist?

Certainly bacteria evolve, but they remain bacteria. Just because a polymerase can mutate to digest a xenopolymer does not explain the evolution of reptiles to birds. It is this type of hyperextrapolation and extreme speculation that forms the foundation to the theory of evolution. The mathematics of mutation and selection and real examples of this process tells an entirely different story.

It is clear that evolution didn’t do it. There is no mathematical basis to explain how it happened.

Look for the evidence lita’ gator, you will find it.

The theory of evolution doesn’t even qualify as a tempest in a teapot. If fact it only serves as a corrupt framework for viewing reality. Why do you think you evolutionarians are having so much trouble comprehending the results from ev and the numerous real examples of what ev shows? The theory of evolution leads to a perversion of the interpretation of reality. The problem of antimicrobial resistance, pesticide and herbicide resistance and cancer cell resistance to chemotherapies is much easier to understand if you discard the false theory of evolution. Evolutionarians stand in the way of advancement of science in order to maintain their belief system. Especially when you have evolutionarians like cheese wiz who posts silly gifs where he claims multiple selection pressures accelerate evolution. I happen to agree with articulett that religion should not be taught in school, including the religion of evolutionism. It is one of the most dangerous and corrupt religions of the past century.

It may be true in one of your 10^500 alternative universes but not in this one, mutation and selection doesn’t work properly for your theory. It is mathematically impossible; ev shows this and numerous real examples of how mutation and selection works shows this.


A polymerase evolves to a polymerase and a bacterium evolves to a bacterium. That’s what your example shows. That’s what mutation and selection is capable of doing.

Ev is not set up to deal with external selection pressures, what are you talking about? A selection pressure is something that affects the fitness of a population to reproduce, that is what ev simulates.

I have always realized that ev is an idealized model of mutation and selection and that Dr Schneider’s selection condition is contrived. Despite this, the model still properly simulates the mathematics of mutation and selection. Dr Schneider’s selection condition can be seen as an environmental change that requires increased recognition of the binding sites in order for the creatures to survive but it doesn’t matter with respects to the behavior of the mathematical model. Dr Schneider’s model still properly captures the essentials of the mutation and selection process.

Spurious binding in the nonbinding site region represents a way of handling neutral versus harmful mutations in that region. If the mutation in the nonbinding site region gives rise to a recognizable binding site it is considered a harmful mutation and weighs against that creature in the selection process. If the mutation in the nonbinding site region does not give rise to a recognizable binding site, it doesn’t affect the selection of that creature. It can be argued that mutations in the nonbinding site region of the genome may be far more harmful if the nonbinding portion of the genome was a full functional genetic sequence. So what if this model doesn’t represent a total functional genome in a real living creature? It doesn’t alter the underlying mathematics of the mutation/selection process.

I see, if a mathematical model doesn’t simulate the entire universe, it is invalid. You can not simulate a portion of reality? You are demonstrating your lack of knowledge and experience how computer simulations are used.

You are correct here, as you complicate the model and try to more accurately simulate the real world, the rate of evolution will slow down even more so in the simulation. By the way, there are three distinct selection pressures in ev. There is a difference between spurious binding in the nonbinding site region and spurious binding in the gene. Do you know what that difference is?

What you still don’t understand about the mathematics of mutation and selection is that as you complicate the system, the evolutionary process slows down. This is most clearly seen by what happens with additional selection pressures. This is why the theory of evolution is mathematically impossible. I agree that expanding the model to complex multicellular organisms is frivolous. If you can carry out the evolution of the binding sites with all these simplifying assumptions, you will never be able to do it with a complex multicellular organism.

What’s wrong with using Dr Schneider’s own public comments about his peer reviewed and published mathematical model? If I am misinterpreting what Dr Schneider is saying, he has more than enough ways to correct me, including a huge tax payer financed web site. Dr Schneider has defended his model for years in a very vocal manner. Why do you think you barely hear a whisper from him now?

A polymerase evolving to a polymerase and a bacterium evolving to a bacterium hardly defeats what ev shows and the numerous real examples of what it shows. Perhaps in one of your 10^500 alternative universes a polymerase mutating in order to be able to digest nylon fills in the gap between reptile and bird but multiple selection pressures slowing evolution really messes up this fantasy of yours.

The only rain I am making is a little mathematical scientific analysis on the evolutionarian day parade. Sorry to mess up your little religious holiday.

So here’s another example citation of how multiple selection pressures slow and ultimately stop evolution.

http://www6.lexisnexis.com/publisher/EndUser?Action=UserDisplayFullDocument&orgId=1809&topicId=26923&docId=l:623811163&start=23 (http://www6.lexisnexis.com/publisher/EndUser?Action=UserDisplayFullDocument&orgId=1809&topicId=26923&docId=l:623811163&start=23)

Isn’t that interesting, combination selection pressures slow the selection of resistant strains of TB.


Nope, I didn’t forget to finish this sentence.

This is your sentence, not mine. I am drawing a very narrow conclusion from the results of ev and what it represents in reality. The conclusion that I am drawing is that ev shows that the rate of information acquisition based on random point mutation and selection is such a profoundly slow process that the theory of evolution is mathematically impossible. The reason why this process is profoundly slow in ev is the multiple selection conditions which slow the acquisition of information, in particular as you lengthen the genome in the model. I am backing up this conclusion with numerous real examples which demonstrate the mathematical behavior which ev shows. Now if you want to add other mechanisms of mutations and recombination to the model and expect a different result, we would all be interested in seeing this.


Can’t brain, I keep forgetting that you have explained the origin of life with your narrow and precise cooperative chemistry hypothesis. Who could debate your air tight logic?

Can’t brain, since you are a supporter of cheese wiz’s gif, when are you going to post an example where multiple selection pressures accelerate evolution?


Wait a minute; you are supposed to be annoyed by these large red fonts. That’s ok, I’m glad you find these large red fonts precious. Now if you mathematically challenged evolutionarians learn how mutation and selection behaves mathematically, you then would understand what the large red font is illustrating. By the way, I am not peeved; however you almost succeeded in annoying me with the sound tracks from those silly youtube videos. You would have succeeded if I had not quickly hit the mute button on my computer. Did you really think that was good music? There’s no telling for the tastes of evolutionarians.

Can’t brain, your cooperative chemistry hypothesis has the impact of lita’ gator’s string cheese theory.

Here is another citation where they have figured out that combination selection pressures slow evolution. Again, this demonstrates the mathematics of ev and shows how mutation and selection works and that is multiple selection pressures slow and ultimately stop evolution.
http://doctor.medscape.com/viewarticle/420664 (http://doctor.medscape.com/viewarticle/420664)

I dedicate the large red font above to articulett.


Oh no Paul, it’s a precious little conclusion about how mutation and selection works. You know what mutation and selection is; it’s the cornerstone mechanism for how the theory of evolution works. Are you going to propose that evolution works by some other mechanism? What I really like about this precious little conclusion from the results of ev is how it explains all these citations I have been posting. I guess you can say my conclusion encompasses the entire universe of evolutionism which is rapidly shrinking.

So, a quick summary:

You haven't thought of any new lies.

You haven't done any math.

You haven't found any scientific paper which supports your loonytunes fantasies.

You still don't know how combination therapy works.

You have no criticism of my model.

You have no counterexample to my model.

You are still screaming gibberish at reality as though that would make it go away.

You are a liar and a fool.

[kjkent1]

Do you think projection explains why kleinman thinks we are all as stupid as he is?No. Corn mash and fuel oil.

[BPScooter]

Kleinman said in 4773:
You know what mutation and selection is; it’s the cornerstone mechanism for how the theory of evolution works.

Kleinman, if you have a readily understandable alternative, write it up and publish it. Really. Or at least establish a researchable part of it with "YOUR NAME ON IT"

Your attitude and verbiage strikes one as being defensive, rather than offensive. Defending the future while also offending the past. Put up with Darwin or refute him. Please? How does anything you say *explain* anything?

I'm not trying to be an ass, really. What is your alternate theory, that is testable, that is so rampantly better than Evolution (an overall view) by Natural Selection (a process)??? What is the Kleinmannian theory of Why it all Appears to have Happened????

I will put seventeen question marks by this. If it will help.

[articulett]

Kleinman said in 4773:
You know what mutation and selection is; it’s the cornerstone mechanism for how the theory of evolution works.

Kleinman, if you have a readily understandable alternative, write it up and publish it. Really. Or at least establish a researchable part of it with "YOUR NAME ON IT"

Your attitude and verbiage strikes one as being defensive, rather than offensive. Defending the future while also offending the past. Put up with Darwin or refute him. Please? How does anything you say *explain* anything?

I'm not trying to be an ass, really. What is your alternate theory, that is testable, that is so rampantly better than Evolution (an overall view) by Natural Selection (a process)??? What is the Kleinmannian theory of Why it all Appears to have Happened????

I will put seventeen question marks by this. If it will help.

Oooh....goody....now at last, we'll know. That Darwin dude sure had me fooled--especially with that Vitamins C pseudogene thing... cuz Darwin he didn't even know there were such things as genes really. Never saw one. So I'm guessing Kleinmannian theory will have a good explanation for that one, and I am just dying to find out what it is. And didn't you think the banding pattern with the great Ape chromosomes next to ours was a sure sign that we were on the right path. How could we have been lead astray so easily?
And the chromosome 2 fusion--that was sly.

[Anacoluthon64]

It may be more apt to refer to the alternative theory, should it ever present itself, as "kleinmanesque." At the risk of pointing out what has perhaps been raised elsewhere, the translation of "kleinman" from quasi-German is especially relevant in this context.

'Luthon64

[Kotatsu]

It may be more apt to refer to the alternative theory, should it ever present itself, as "kleinmanesque." At the risk of pointing out what has perhaps been raised elsewhere, the translation of "kleinman" from quasi-German is especially relevant in this context.

A previous instar of his rambling was named "KOMPOSTE", but I can't remember what it was an abbreviation of. As much of his arguments have undergone no visible metamorphosis since then, I propose that the name KOMPOSTE, or some variation thereof, could still be used.

EDIT:
Back in post 1374, I found the complete name to be "Kleinman's Own Mindless Pretentions Of Smashing the Theory of Evolution".

[articulett]

Thanks...
man, I just drop in for an instant, and I learn so much...
And good sleuthing Kotatsu--it's nice to have someone keep tabs of acronym meanings so that we stay up on the etymology of words should they gain wide spread recognition.

[Kotatsu]

Thanks...
man, I just drop in for an instant, and I learn so much...
And good sleuthing Kotatsu--it's nice to have someone keep tabs of acronym meanings so that we stay up on the etymology of words should they gain wide spread recognition.

You will notice that there is a certain amount of ego-inflating in reviving that term, as I was the one who initially distilled it from some previous incarnations of Mercutio's doing, which didn't form real words, though.

I am frankly amazed that anyone still has the stamina to read through Kleinman's posts. There's so much silliness going on it'd be enough to keep all of Sub-Saharan Africa with silly for generations to come.

[BPScooter]

I just posted 100 ago, and came back. 100 silly Africas with 200 silly sprinklers would only get to the edge of Conrad's deepest and darkest river stream with the wealth of intrigue and wonder here in this possibly deranged mind. You all have come downriver with canoes intact. I'm not about to go anywhere near it, apologies to all. Just let me know about TAM events on the west coast.

[Dr Adequate]

It may be more apt to refer to the alternative theory, should it ever present itself, as "kleinmanesque." "Kleinmania."

[Dr Adequate]

I am frankly amazed that anyone still has the stamina to read through Kleinman's posts. I'm not sure that anyone does. To speak for myself, I just skim through it looking for his latest lie. Of course I don't read all his gibberish --- who'd be bothered?

[joobz]

I am frankly amazed that anyone still has the stamina to read through Kleinman's posts. There's so much silliness going on it'd be enough to keep all of Sub-Saharan Africa with silly for generations to come.
I merely skim and throw a few bones toward Kleinman in the hopes that he'll be entertaining. Unfortunately, he has become tiresome and even more raving.

It's like watching a Robin Williams standup routine. It was super funny when I first saw him(When I was 12), but now seeing his tired shtick is a bit sad and depressing.

[Paul C. Anagnostopoulos]

I am frankly amazed that anyone still has the stamina to read through Kleinman's posts. There's so much silliness going on it'd be enough to keep all of Sub-Saharan Africa with silly for generations to come.
I just look for certain keywords. However, with statements like the following, this technique is becoming more difficult.

"Can’t brain, your cooperative chemistry hypothesis has the impact of lita’ gator’s string cheese theory."


~~ Paul

[Paul C. Anagnostopoulos]

:hit:

I have to laugh at the way we all just tried to justify sticking around in this sick **** of a thread. I love you guys!

~~ Paul

[Kotatsu]

It's like watching a Robin Williams standup routine. It was super funny when I first saw him(When I was 12), but now seeing his tired shtick is a bit sad and depressing.

I was thinking more along the lines of his posts being so many whale carcasses. You are repulsed by them, they stink, and the simple act of looking on them seem to be enough for them to fall apart into some sort of undefinable goo. But still, you just can't stop yourself from licking on the next one as well, just in case that one is made of licorice.

Not that we have many whales where I live.

I have to laugh at the way we all just tried to justify sticking around in this sick **** of a thread. I love you guys!

You should all get "I survived the Kleinman thread!" t-shirts. I think pink is a suitable colour.

[Myriad]

I was thinking more along the lines of his posts being so many whale carcasses. You are repulsed by them, they stink, and the simple act of looking on them seem to be enough for them to fall apart into some sort of undefinable goo. But still, you just can't stop yourself from licking on the next one as well, just in case that one is made of licorice.

Not that we have many whales where I live.


Post by Kleinman attempting to pretend that you were really comparing the theory of evolution to a dead whale carcass in 3, 2, 1...

Respectfully,
Myriad

[kleinman]

Time for another round of beer. While we are laughing about your goalpost move and its denial, we can read the following proof that humans and chimps diverged from a common ancestor.
Pussycat, perhaps your theory of evolution is a little more believable after you have had a few rounds of beer. However, your gross extrapolations and speculations about some genetic similarities between humans and chimps do not override the mathematical and empirical facts that multiple selection pressures slows and ultimately stop evolution. It might be viewed that you are trying to change the topic of this thread away from the mathematics of mutation and selection. You wouldn’t move the goalposts would you pussycat?
It’s been a while since I posted the goalposts,.Yes, it's been a while since you posted this, isn't it:
But it hasn’t been a while since I posted your silly gif and you continue to fail to post a single real example of your amathematics.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
The red line shows generations to achieve fixation of n alleles acted on by n selection pressures, the n+1th selection pressure being introduced only after the nth allele is fixed.

The blue line shows generations to achieve fixation of n alleles acted on by n selection pressures simultaneously.

All other features and parameters of the two models are identical. The model is designed so that the relative advantage of n+1 new genes over n (when selection is acting) is the same for all n, i.e. each new allele carries the same advantage.

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
http://forums.randi.org/images/smilies/doglaugh.gif
Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution cheese wiz?
Do you think projection explains why kleinman thinks we are all as stupid as he is?
Cyborg, I don’t think you evolutionarians are stupid, I think you are brainwashed. I’ll just continue to give you examples of how mutation and selection actually works and hope the facts will work their way through all the cruft in your mathematically illogical theory.
You know what mutation and selection is; it’s the cornerstone mechanism for how the theory of evolution works.
And ev show how this mechanism works mathematically and reality confirms what ev shows. What does ev show, ev shows that multiple selection pressures slow and ultimately stop evolution.
Kleinman, if you have a readily understandable alternative, write it up and publish it. Really. Or at least establish a researchable part of it with "YOUR NAME ON IT"
Right now I’m establishing how mutation and selection actually works for the benefit of you evolutionarians. I’m establishing this using a peer reviewed and published model of random point mutations and natural selection and posting real examples of what this model shows.
Your attitude and verbiage strikes one as being defensive, rather than offensive. Defending the future while also offending the past. Put up with Darwin or refute him. Please? How does anything you say *explain* anything?
I guess you could say that I’m being defensive. I’ve put forth a hypothesis based on the results of a peer reviewed and published model of mutation and selection which show that multiple selection pressures slow and ultimately stop evolution. I am now defending it with numerous citations which demonstrate this mathematical fact, I have a couple more which I am posting below.
I'm not trying to be an ass, really. What is your alternate theory, that is testable, that is so rampantly better than Evolution (an overall view) by Natural Selection (a process)??? What is the Kleinmannian theory of Why it all Appears to have Happened????
BPS, I don’t take what you are doing as being an ass. Look at the title of the thread if you want to know how I think we came into being, but I’m not here to debate this issue, I’m here to discuss the mathematics of mutation and selection and examine the empirical evidence of this phenomenon.
I will put seventeen question marks by this. If it will help.
Once you evolutionarians acknowledge how mutation and selection actually works, we can go on to other questions.
It may be more apt to refer to the alternative theory, should it ever present itself, as "kleinmanesque." At the risk of pointing out what has perhaps been raised elsewhere, the translation of "kleinman" from quasi-German is especially relevant in this context.
Why is it that you evolutionarians want to discuss an alternative theory? Isn’t it enough that we discuss the mathematics of mutation and selection? This is an issue that has important scientific, medical and agricultural repercussions. It also demonstrates how a flawed theory distorts the perceptions of its adherents in their interpretation of reality. The belief system surrounding the theory becomes more important than what the mathematical facts show and the empirical evidence which substantiates these mathematical facts. The theory of evolution has become our era’s version of the flat earth hypothesis.
Back in post 1374, I found the complete name to be "Kleinman's Own Mindless Pretentions Of Smashing the Theory of Evolution".
Oh Kotatsu, this is not mindless pretentions of smashing the theory of evolution, I am using an evolutionist written and peer reviewed model of random point mutations to smash the theory of evolution. Why should I do this? I do this because the theory is wrong and interferes with the understanding of the real behavior of mutation and selection. I proper understanding of mutation and selection will aid in the treatment of diseases, cancer and a variety of other societal problems. Evolutionism interferes with the proper understanding of the phenomenon of mutation and selection.
I am frankly amazed that anyone still has the stamina to read through Kleinman's posts. There's so much silliness going on it'd be enough to keep all of Sub-Saharan Africa with silly for generations to come.I merely skim and throw a few bones toward Kleinman in the hopes that he'll be entertaining. Unfortunately, he has become tiresome and even more raving.
Hey kids, I’m just warming up. I’ve only posted about 60-70 citations of how mutation and selection actually works. I have only about 1.7 million hits to go through on my search for references. Can’t brain, you and Paul better take some power naps.
I am frankly amazed that anyone still has the stamina to read through Kleinman's posts. There's so much silliness going on it'd be enough to keep all of Sub-Saharan Africa with silly for generations to come.I just look for certain keywords. However, with statements like the following, this technique is becoming more difficult.
Those keywords obviously don’t include, “combination”, “selection”, “evolution”, “resistance”. If they did, you would get some understanding of how mutation and selection actually works. But that’s ok Paul, I’m doing the literature search for you and posting the results so you evolutionarians can learn how mutation and selection actually works.
"Can’t brain, your cooperative chemistry hypothesis has the impact of lita’ gator’s string cheese theory."
If you buy this Paul then you probably buy cheese wiz’s silly gif. What I find interesting is that you don’t buy what your own model shows even though there is a huge amount of empirical evidence to confirm this result.
I have to laugh at the way we all just tried to justify sticking around in this sick **** of a thread. I love you guys!
There you go again Paul; I love it when you evolutionarians use asterisks.
I was thinking more along the lines of his posts being so many whale carcasses. You are repulsed by them, they stink, and the simple act of looking on them seem to be enough for them to fall apart into some sort of undefinable goo. But still, you just can't stop yourself from licking on the next one as well, just in case that one is made of licorice.

Not that we have many whales where I live.Post by Kleinman attempting to pretend that you were really comparing the theory of evolution to a dead whale carcass in 3, 2, 1...
Myriad, the theory of evolution is a dead whale carcass, you don’t have to giggle, oops jiggle the weight matrix in ev to find this out. Just set two of the three selections conditions to zero in the model and you will see what accelerates evolution.

For those of you who are interested in how mutation and selection actually works, here are a couple more citations which reveal the facts. The first one is for Dr Schneider and the rest his cohort at the National Cancer Institute.

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. Traditional analysis of drug combination effects on cells is based on a number of assumptions and idealizations. A more rational mechanistic modeling approach may accelerate the search for effective drug combinations that are tailored to individual responses. The chemotherapeutic drugs, carmustine and etoposide, each nominally induces G2 phase arrest and, secondarily, apoptosis. Despite this similarity in mechanism, we found that the pharmacodynamic responses to these agents is dramatically different on human glioma cell lines. We have developed a cell cycle structured model of chemotherapeutic activity based on the dynamic transitions of cells along the phases of the cell cycle. We show that our mathematical model is able to explain the shapes of the dose response curves of multiple cell lines to these agents. We are able to predict with the model the effects of drug combinations, taking into account variable dose and timing regimens, to determine the most effective strategy. Using this model, we are able to explain several non-intuitive experimental observations involving combinations of chemotherapeutic drugs on glioma-derived cell lines.

http://clinicaltrials.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pctr.0010039 (http://clinicaltrials.plosjournals.org/perlserv/?request=get-document&doi=10.1371/journal.pctr.0010039)
Drug combinations have the potential to protect the two partner drugs against selection of resistant strains, thus delaying the emergence of drug-resistant organisms. Combinations may allow dosage reduction of each drug in the combination, reduce the overall toxicity while maintaining good efficacy. Combinations may also allow for a simpler administration, improving the feasibility of treatment in Africa's isolated health facilities, most of which have logistic and staffing limitations.
Hey articulett, isn’t that large red type precious? Isn’t the fact multiple selection pressures slow and ultimately stop evolution precious? When will you evolutionarians learn this mathematical and empirically verified fact?

[joobz]

However, your gross extrapolations and speculations about some genetic similarities between humans and chimps do not override the mathematical and empirical facts that multiple selection pressures slows and ultimately stop evolution.
Actually, it does over ride it, because your model is nonsense. Reality trumps nonsense.

It might be viewed that you are trying to change the topic of this thread away from the mathematics of mutation and selection. You wouldn’t move the goalposts would you pussycat?
Your sentence contains nested wrongs.
changing topics isn't the same as "moving goal posts". Presenting evidence of evolution is not changing topics.


Changing topics would be me asking, "What happened to your mathematical proof of Noah's Arc?"

Moving goal posts would be:
evolution = new genes
evolution = multiple selection pressures
evolution = multiple directional selection presssures
evoltuion = multiple directional selection pressures, recombination doesn't count..stop presenting evidence against me, [fingers in ears] LA LA LA LA I'm Not LISTENING!!!

[Anacoluthon64]

It also demonstrates how a flawed theory distorts the perceptions of its adherents in their interpretation of reality. The belief system surrounding the theory becomes more important than what the mathematical facts show and the empirical evidence which substantiates these mathematical facts.;) :D :rolleyes:

I met an engineer with a Ph.D. once who asked me what the symbol "∫" meant in a solution I derived for a relatively simple problem in compressible fluid flow. Yup, there are some strange things in this world.

'Luthon64

[kleinman]

However, your gross extrapolations and speculations about some genetic similarities between humans and chimps do not override the mathematical and empirical facts that multiple selection pressures slows and ultimately stop evolution.Actually, it does over ride it, because your model is nonsense. Reality trumps nonsense.
Can’t brain, you’ve made an error here. Ev is not my computer model, it is Dr Schneider’s peer reviewed and published model of random point mutation and natural selection. However you are correct, reality trumps nonsense. That is why I can post dozens of citations that show that multiple selection pressures slow and ultimately stop evolution while you and cheese wiz have posted a grand total of zero citations which show that multiple selection pressures accelerate evolution. Your evidence of how you contend mutation and selection works is nonexistent, but you do have cheese wiz’s silly gif.

[joobz]

Can’t brain, you’ve made an error here. Ev is not my computer model, it is Dr Schneider’s peer reviewed and published model of random point mutation and natural selection.
I love how easy it is to get you to make stupid statements. I wasn't refering to Ev, I was talking about YOUR model, the one you haven't presented. The one that says "Multiple selection pressures prevents all evolution from occuring regardless of mutation and adaptation mechanisms". Ev doesn't make such nonsensical claims. It was made by REAL scientists, who actually have RESPECT for themselves and reality.



However you are correct, reality trumps nonsense.
Yes, it does. Yes, it does.

[kleinman]

Can’t brain, you’ve made an error here. Ev is not my computer model, it is Dr Schneider’s peer reviewed and published model of random point mutation and natural selection.I love how easy it is to get you to make stupid statements. I wasn't talking about EV, I was talking about YOUR model, the one you haven't presented. The one that says "Multiple selection pressures prevents all evolution from occuring regardless of mutation and adaptation mechanisms".
Don’t be silly can’t brain, I don’t need to write a model, Dr Schneider got the mathematics of mutation and selection correct and it shows that with just three selection conditions the model stops converging even with unrealistically short genomes.
However you are correct, reality trumps nonsense.Yes, it does. Doesn't it?
Yes and here is an example how your brainwashed evolutionarian thinking interferes with the advancement of science.

Here’s an example were monotherapy leads to quick evolution of resistance to medications.
http://pubs.ama-assn.org/media/2007j/0403.dtl (http://pubs.ama-assn.org/media/2007j/0403.dtl)
“The report by Hatakeyama et al raises more questions than it answers, including questions about viral evolution, biological fitness, and transmissibility. But some facts are strikingly clear. Influenza B mutants with reduced sensitivity to neuraminidase inhibitors are circulating, and these viruses can cause infections with no difference in duration of symptoms, level of viral shedding, or clinical outcome. Contrary to what had been hoped until now, some resistant variants are vigorous pathogens. Whether these viruses arise by spontaneous mutation or through drug selection, or whether they are transmitted within families or acquired from the community, the resistant variants may be here to stay. In light of the recent observation that oseltamivir may be less effective against influenza B than against influenza A, an important concern is whether suboptimal dosing for these viruses will lead to increased selection of viruses with high-level resistance.”

“Influenza viruses evolve rapidly and nimbly, which compels ongoing investigation of antiviral therapies that use alternative mechanisms of action and target different points in the viral life cycle. The emergence of drug-resistant influenza B should draw attention to the importance of continual monitoring of strains over time and to the need for frequent rethinking of policies for use of antiviral drugs. While the news about resistance is not good and certainly calls into question some of the current assumptions about drug-resistant viruses, an effective response to this news can help contend with the new challenges of influenza.”

Monotherapy of influenza is giving rapid evolution of resistance of the virus to these drugs. This is how mutation and selection works. You dim bulbs of evolutionism deny this reality and slow the advancement of science.

[joobz]

Don’t be silly can’t brain, I don’t need to write a model,wrong.
Actually, you do need to write a model. Ev doesn't do what you say it does, no matter how many times you chant.

[kleinman]

Don’t be silly can’t brain, I don’t need to write a model,wrong.
Well can’t brain, we’ll see how far I get posting real examples of mutation and selection which shows that multiple selection pressures slow and ultimately stop evolution. We’ll see how long you dim bulbs of evolutionism can deny this mathematical and empirical fact.
Actually, you do need to write a model. Ev doesn't do what you say it does, no matter how many times you chant.
So let’s see, you a supporter of cheese wiz’s silly gif have absolutely zero real examples of what you contend, that is multiple selection pressures accelerate evolution and I have posted 60-70 real examples of what I contend, that is multiple selection pressures slow and ultimately stop evolution. What does ev show and what does cheese wiz’s silly gif show? Ev models the mathematical reality of mutation and selection, cheese wiz’s gif, is nonsense. Can’t brain, post a real example of cheese wiz’s gif and prove otherwise. I don’t expect you to post anything like this soon. You all might as well make yourselves comfortable as I continue to post more real examples of how mutation and selection actually works.

[Paul C. Anagnostopoulos]

So let’s see, you a supporter of cheese wiz’s silly gif have absolutely zero real examples of what you contend, that is multiple selection pressures accelerate evolution and I have posted 60-70 real examples of what I contend, that is multiple selection pressures slow and ultimately stop evolution. What does ev show and what does cheese wiz’s silly gif show? Ev models the mathematical reality of mutation and selection, cheese wiz’s gif, is nonsense. Can’t brain, post a real example of cheese wiz’s gif and prove otherwise. I don’t expect you to post anything like this soon. You all might as well make yourselves comfortable as I continue to post more real examples of how mutation and selection actually works.
Pretend, for a moment, that you haven't read this entire thread. Now read that statement from Kleinman in vacuo.

~~ Paul

[cyborg]

A mad-man and his macro executor. Tsk.

[kjkent1]

How evolution actually works:

http://www.biomedcentral.com/1471-2148/7/28

[kleinman]

So let’s see, you a supporter of cheese wiz’s silly gif have absolutely zero real examples of what you contend, that is multiple selection pressures accelerate evolution and I have posted 60-70 real examples of what I contend, that is multiple selection pressures slow and ultimately stop evolution. What does ev show and what does cheese wiz’s silly gif show? Ev models the mathematical reality of mutation and selection, cheese wiz’s gif, is nonsense. Can’t brain, post a real example of cheese wiz’s gif and prove otherwise. I don’t expect you to post anything like this soon. You all might as well make yourselves comfortable as I continue to post more real examples of how mutation and selection actually works.Pretend, for a moment, that you haven't read this entire thread. Now read that statement from Kleinman in vacuo.
That’s what you evolutionarians like to do, pretend. But that’s not what is happening here. The evolutionism cult has been engaged in false teaching of how mutation and selection works for years in the evolutionism indoctrination system. Your own computer model shows how mutation and selection actually works but you have gone into denial about this mathematical fact. And as I said above, I will continue to post real examples of this mathematical fact, including my most recent example which shows the influenza virus is developing resistance to the drugs used in monotherapy to treat this infection. Paul, do you have any idea how many people die from influenza every year? If you want to solve real problems of mutation and selection, don’t try to do it with the evolutionarian interpretation of how mutation and selection works.

Now Paul, why don’t you tell us your view of cheese wiz’s gif where he claims multiple selection pressures accelerate evolution. Don’t worry, you can still hop on your bicycle with the six reverse gears and no forward gears and the seat that faces backwards.

[joobz]

Well can’t brain, we’ll see how far I get posting real examples of mutation and selection which shows that multiple selection pressures slow and ultimately stop evolution.
Wrong, you haven't been doing this.
We’ll see how long you dim bulbs of evolutionism can deny this mathematical and empirical fact.wrong, again. All we are denying is your lies.

So let’s see, you a supporter of cheese wiz’s silly gif have absolutely zero real examples of what you contend,
meaningless phrase
that is multiple selection pressures accelerate evolution and I have posted 60-70 real examples of what I contend,
wrong
that is multiple selection pressures slow and ultimately stop evolution.
wrong. slow doesn't equal stop.
What does ev show and what does cheese wiz’s silly gif show?
That you don't know math.
Ev models the mathematical reality of mutation and selection, cheese wiz’s gif, is nonsense. prove it.
Can’t brain, post a real example of cheese wiz’s gif and prove otherwise. I don’t expect you to post anything like this soon. You all might as well make yourselves comfortable as I continue to post more real examples of how mutation and selection actually works.I'm very comfortable watching you blather.
Please, continue...

[joobz]

That’s what you evolutionarians like to do, pretend. But that’s not what is happening here. The evolutionism cult has been engaged in false teaching of how mutation and selection works for years in the evolutionism indoctrination system. Your own computer model shows how mutation and selection actually works but you have gone into denial about this mathematical fact. And as I said above, I will continue to post real examples of this mathematical fact, including my most recent example which shows the influenza virus is developing resistance to the drugs used in monotherapy to treat this infection. Paul, do you have any idea how many people die from influenza every year? If you want to solve real problems of mutation and selection, don’t try to do it with the evolutionarian interpretation of how mutation and selection works.

Now Paul, why don’t you tell us your view of cheese wiz’s gif where he claims multiple selection pressures accelerate evolution. Don’t worry, you can still hop on your bicycle with the six reverse gears and no forward gears and the seat that faces backwards.
Are you preaching now? Tell us, Brother Kleinman, Testify!

[kleinman]

That’s what you evolutionarians like to do, pretend. But that’s not what is happening here. The evolutionism cult has been engaged in false teaching of how mutation and selection works for years in the evolutionism indoctrination system. Your own computer model shows how mutation and selection actually works but you have gone into denial about this mathematical fact. And as I said above, I will continue to post real examples of this mathematical fact, including my most recent example which shows the influenza virus is developing resistance to the drugs used in monotherapy to treat this infection. Paul, do you have any idea how many people die from influenza every year? If you want to solve real problems of mutation and selection, don’t try to do it with the evolutionarian interpretation of how mutation and selection works.

Now Paul, why don’t you tell us your view of cheese wiz’s gif where he claims multiple selection pressures accelerate evolution. Don’t worry, you can still hop on your bicycle with the six reverse gears and no forward gears and the seat that faces backwards.Are you preaching now? Tell us, Brother Kleinman, Testify!
Why can’t brain, I have been testifying and will continue to do so. Your understanding of influenza is about as good as your understanding of abiogenesis. Make sure you tell researchers trying to combat influenza not to use combination therapy, after all, according to you, multiple selection pressures accelerate evolution.

I do enjoy quoting from real examples of how mutation and selection works. No speculation, no extrapolation, just hard empirical data which demonstrates the mathematical results from a peer reviewed and published mathematical model of mutation and selection.

[Paul C. Anagnostopoulos]

Now Paul, why don’t you tell us your view of cheese wiz’s gif where he claims multiple selection pressures accelerate evolution.
Alan, d00d, I don't even know who cheese wiz is.

~~ Paul

[articulett]

:hit:

I have to laugh at the way we all just tried to justify sticking around in this sick **** of a thread. I love you guys!

~~ Paul

Paul, you should be canonized for skeptic sainthood for running all of Kleimnan's math problems.

I find I really enjoy the woo bashing--both as a participant and an observer...it's so sweet of their "intelligent designer" to send them to us, don't you think? It allows me to contain a good deal of eye-rolling and acidic barbs directed at the woos who inhabit my actual reality. (Which is a possible lifesaver in my case--I am a small unarmed woman).

But the best part is the way they never change their viewpoint...just like the diviners and other woos that take the MDC. They blame everybody and everything except the very thing that is at the root of all their failures--themselves.

I must make a confession...sometimes I cut and paste bits to show my students to see if they can "spot the logical fallacy'-- creationists are the champions of it--gotta love the goalpost moving too.

(And speaking of whale carcases, Kokatsu-- http://www.youtube.com/watch?v=AtVSzU20ZGk
It's an oldie, but a goodie. Nothing like an exploding whale to make you glad that you weren't there.)

[kleinman]

Now Paul, why don’t you tell us your view of cheese wiz’s gif where he claims multiple selection pressures accelerate evolution.Alan, d00d, I don't even know who cheese wiz is.
Sure you do, I’ll even repost his ridiculous gif and claims again. You may better know him as the imaginary superhero who thinks ev will converge in zero generations with an infinite population. Here is cheese wiz’s hypothesis.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
The red line shows generations to achieve fixation of n alleles acted on by n selection pressures, the n+1th selection pressure being introduced only after the nth allele is fixed.

The blue line shows generations to achieve fixation of n alleles acted on by n selection pressures simultaneously.

All other features and parameters of the two models are identical. The model is designed so that the relative advantage of n+1 new genes over n (when selection is acting) is the same for all n, i.e. each new allele carries the same advantage.

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
http://forums.randi.org/images/smilies/doglaugh.gif
I highlighted his proposal in red type. You know how precious red type is.

[joobz]

Sure you do, I’ll even repost his ridiculous gif and claims again. You may better know him as the imaginary superhero who thinks ev will converge in zero generations with an infinite population. I don't know that person. I do not think he exists. Afterall, everyone here (who isn't a malfunctioning nincompoop) KNOWS that as population goes to infinity, the number of generations ev takes to converage APPROACHES ZERO.

[cyborg]

It's obvious to anyone who understands the concept of infinity that any genome of any length of any configuration one can imagine can be plucked from an infinite pool of random genomes in one step.

Unfortunately kleinman can't brain this.

[articulett]

I highlighted his proposal in red type. You know how precious red type is.[/SIZE][/FONT]

Thanks, sweetie. I love the emoticon abuse too.

[joobz]

It's obvious to anyone who understands the concept of infinity that any genome of any length of any configuration one can imagine can be plucked from an infinite pool of random genomes in one step.

Unfortunately kleinman can't brain this.
He also can't brain asymptotes.
Yup, he sure has the dumb.

[kleinman]

Sure you do, I’ll even repost his ridiculous gif and claims again. You may better know him as the imaginary superhero who thinks ev will converge in zero generations with an infinite population.I don't know that person. I do not think he exists. Afterall, everyone here (who isn't a malfunctioning nincompoop) KNOWS that as population goes to infinity, the number of generations ev takes to converage APPROACHES ZERO.
You evolutionarians spend a lot of time at infinity, what happens to the rate of information acquisition when you have an infinite number of selection pressures.
http://forums.randi.org/images/smilies/doglaugh.gif
It's obvious to anyone who understands the concept of infinity that any genome of any length of any configuration one can imagine can be plucked from an infinite pool of random genomes in one step.
Ah yes, the infinite cruft theory of evolution, it explains everything.
Unfortunately kleinman can't brain this.
I can brain that the theory of evolution by mutation and selection is infinitely dumb, it’s mathematically impossible. Multiple selection pressures slow and ultimately stop evolution. That’s what ev shows and that is what reality shows.
I highlighted his proposal in red type. You know how precious red type is.Thanks, sweetie. I love the emoticon abuse too.
Articulett, I only abuse evolutionist computer simulations by revealing what they really show. What evolutionist computer simulations really show is that multiple selection pressures slow and ultimately stop evolution and you know what, that’s what happens in reality. That’s how mutation and selection really works. Reality can be so abusive.
It's obvious to anyone who understands the concept of infinity that any genome of any length of any configuration one can imagine can be plucked from an infinite pool of random genomes in one step.

Unfortunately kleinman can't brain this.He also can't brain asymptotes.
Yup, he sure has the dumb.
Can’t brain, I do not lay claim to your avatar, it describes yourself so well. Here’s what is dumb, you evolutionarians think that multiple selection pressures accelerates evolution when reality shows this:

http://mct.aacrjournals.org/cgi/content/abstract/6/2/655 (http://mct.aacrjournals.org/cgi/content/abstract/6/2/655)
Chronic myelogenous leukemia is caused by the Bcr-Abl hybrid gene that encodes the p210Bcr-Abl chimeric oncoprotein. Although it reduces the total body burden of leukemia cells, the use of imatinib mesylate as a single agent may be accompanied by the evolution of resistance due mainly to the acquisition of point mutations. Imatinib has been combined with drugs that inhibit both the active and the inactive states of the p210Bcr-Abl kinase. These combinations have reduced but not completely eliminated the rate at which point mutations are acquired in the p210Bcr-Abl kinase. Thus, it is important to identify additional new inhibitors of the p210Bcr-Abl kinase. One possible method to prevent evolution of resistance is to simultaneously use multiple kinase inhibitors each with a different mechanism of action. To identify such a new class of inhibitors that could suppress the growth of chronic myelogenous leukemia cells and prevent the evolution of cells that are resistant to imatinib, we screened two low-complexity libraries of compounds based on planar and linear scaffolds. These libraries were screened using a cell-based assay for molecules that suppress p210Bcr-Abl–dependent cell growth. The application of this method resulted in the isolation of two new classes of drugs, both of which inhibited imatinib-resistant cells in the low micromolar range. Some of these drugs were potent inhibitors not only of Abl tyrosine kinase but also of the Src, Lyn, and Fyn tyrosine kinases. [Mol Cancer Ther 2007;6(2):655–66]
This citation again is dedicated to Dr Schneider and his legion at the National Cancer Institute. Dr Schneider, your computer simulation shows this, you got your model right.

[Paul C. Anagnostopoulos]

This citation again is dedicated to Dr Schneider and his legion at the National Cancer Institute. Dr Schneider, your computer simulation shows this, you got your model right.
Checking for hidden code that models p210Bcr-Abl kinase and its inhibitors ... boy, it's well hidden.

~~ Paul

[kleinman]

This citation again is dedicated to Dr Schneider and his legion at the National Cancer Institute. Dr Schneider, your computer simulation shows this, you got your model right.Checking for hidden code that models p210Bcr-Abl kinase and its inhibitors ... boy, it's well hidden.
Let me decode this mystery for you Paul.
http://mct.aacrjournals.org/cgi/content/abstract/6/2/655 (http://mct.aacrjournals.org/cgi/content/abstract/6/2/655)
Chronic myelogenous leukemia is caused by the Bcr-Abl hybrid gene that encodes the p210Bcr-Abl chimeric oncoprotein. Although it reduces the total body burden of leukemia cells, the use of imatinib mesylate as a single agent may be accompanied by the evolution of resistance due mainly to the acquisition of point mutations. Imatinib has been combined with drugs that inhibit both the active and the inactive states of the p210Bcr-Abl kinase. These combinations have reduced but not completely eliminated the rate at which point mutations are acquired in the p210Bcr-Abl kinase. Thus, it is important to identify additional new inhibitors of the p210Bcr-Abl kinase. One possible method to prevent evolution of resistance is to simultaneously use multiple kinase inhibitors each with a different mechanism of action. To identify such a new class of inhibitors that could suppress the growth of chronic myelogenous leukemia cells and prevent the evolution of cells that are resistant to imatinib, we screened two low-complexity libraries of compounds based on planar and linear scaffolds. These libraries were screened using a cell-based assay for molecules that suppress p210Bcr-Abl–dependent cell growth. The application of this method resulted in the isolation of two new classes of drugs, both of which inhibited imatinib-resistant cells in the low micromolar range. Some of these drugs were potent inhibitors not only of Abl tyrosine kinase but also of the Src, Lyn, and Fyn tyrosine kinases. [Mol Cancer Ther 2007;6(2):655–66]
Imatinib mesylate as a single agent may be accompanied by the evolution of resistance is an example of monotherapy leading to rapid evolution of resistance to the drug. (This is in red text in the citation.) Precious isn’t it articulett?
Imatinib has been combined with drugs that inhibit both the active and the inactive states of the p210Bcr-Abl kinase. These combinations have slowed the evolution of resistance but not completely. (This is in blue text in the citation.)
One possible method to prevent evolution of resistance is to simultaneously use multiple kinase inhibitors each with a different mechanism of action. (This is in green text in the citation) and demonstrates the strategy for stopping of evolution.
These oncologists definitely understand how mutation and selection works and it’s not like what you evolutionarians allege.

[joobz]

Let me decode this mystery for you Paul.
http://mct.aacrjournals.org/cgi/content/abstract/6/2/655 (http://mct.aacrjournals.org/cgi/content/abstract/6/2/655)

Imatinib mesylate as a single agent may be accompanied by the evolution of resistance is an example of monotherapy leading to rapid evolution of resistance to the drug. (This is in red text in the citation.) Precious isn’t it articulett?
Imatinib has been combined with drugs that inhibit both the active and the inactive states of the p210Bcr-Abl kinase. These combinations have slowed the evolution of resistance but not completely. (This is in blue text in the citation.)
One possible method to prevent evolution of resistance is to simultaneously use multiple kinase inhibitors each with a different mechanism of action. (This is in green text in the citation) and demonstrates the strategy for stopping of evolution.
These oncologists definitely understand how mutation and selection works and it’s not like what you evolutionarians allege.
the amazing technicolor foolpost.

Your use of color reminds me that you can't polish a turd. No matter what color your font is, you're still wrong.

Thanks for this
These combinations have reduced but not completely eliminated

Not eliminated.... I wonder what that means??? hmmm..


Think of it (i know it's hard for you). Even with the multiple selection pressures that they used, they couldn't eliminate the evolutionary forces. An intelligently designed therapy couldn't stop evolution. rather poetic, don't you think?


Chew on this one: If we can't halt evolution (over a matter of years) by purposefully selecting the most difficult pressures, what hope do you have that elements in the wild can do it?

[kleinman]

Let me decode this mystery for you Paul.
http://mct.aacrjournals.org/cgi/content/abstract/6/2/655 (http://mct.aacrjournals.org/cgi/content/abstract/6/2/655)

Imatinib mesylate as a single agent may be accompanied by the evolution of resistance is an example of monotherapy leading to rapid evolution of resistance to the drug. (This is in red text in the citation.) Precious isn’t it articulett?
Imatinib has been combined with drugs that inhibit both the active and the inactive states of the p210Bcr-Abl kinase. These combinations have slowed the evolution of resistance but not completely. (This is in blue text in the citation.)
One possible method to prevent evolution of resistance is to simultaneously use multiple kinase inhibitors each with a different mechanism of action. (This is in green text in the citation) and demonstrates the strategy for stopping of evolution.
These oncologists definitely understand how mutation and selection works and it’s not like what you evolutionarians allege.the amazing technicolor foolpost.
Yes, only a fool can’t understand it.
These combinations have reduced but not completely eliminatedNot eliminated.... I wonder what that means??? hmmm..
Once again can’t brain proves he can’t read. If he could, he would have seen the sentence in green:
One possible method to prevent evolution of resistance is to simultaneously use multiple kinase inhibitors each with a different mechanism of action.
Think of it (i know it's hard for you). Even with the multiple selection pressures that they used, they couldn't eliminate the evolutionary forces. An intelligently designed therapy couldn't stop evolution. rather poetic, don't you think?
Can’t brain’s sloppy reading of the citation match his sloppy understanding of mutation and selection. Can’t brain, you are not poetic, you have no mathematical or scientific skills but you are very good at choosing your avatars.
Chew on this one: If we can't halt evolution (over a matter of years) by purposefully selecting the most difficult pressures, what hope do you have that elements in the wild can do it?
If you were correct, we should stop wasting money on the National Cancer Institute, but of course you are not correct. Can’t brain, perhaps you are color blind?

[joobz]

Yes, only a fool can’t understand it.
This sentence is not a response to my comment. Are you responding to voices in your head?

Once again can’t brain proves he can’t read. If he could, he would have seen the sentence in green: I saw that, but it was moot. They didn't show that. The only data present was that emergence couldn't be stopped. Which completely and totally without a shadow of any doubt, proves you are wrong.

Can’t brain’s sloppy reading of the citation match his sloppy understanding of mutation and selection. Can’t brain, you are not poetic, you have no mathematical or scientific skills but you are very good at choosing your avatars.This doesn't follow logically from my comment. You didn't state why I was wrong. I'll state my point again, because it is quite simple and perhaps you'll get it this time. So think hard...

Think of it (i know it's hard for you). Even with the multiple selection pressures that they used, they couldn't eliminate the evolutionary forces. An intelligently designed therapy couldn't stop evolution. rather poetic, don't you think?

If you were correct, we should stop wasting money on the National Cancer Institute, but of course you are not correct. Can’t brain, perhaps you are color blind?
This again doesn't follow my statement. Are you commenting on the voices in your head? Because, if you are, the voices are utter retards. No one hear is advocating such nonsense as abandoning cancer therapy. That would be stupid and moronic.

I said, quite simply
If we can't halt evolution (over a matter of years) by purposefully selecting the most difficult pressures, what hope do you have that elements in the wild can do it?
This statement cuts at the heart of your argument. Even when we try, we haven't stopped the evolutionary process. We may be able to one day, but that takes design. Since there isn't "something" at every spot throughout our world designing multiple selection pressures to stop evolution, we are left to assume that evolution can occur in the wild.

[HawkeyeMD]

Pretend, for a moment, that you haven't read this entire thread. Now read that statement from Kleinman in vacuo.

~~ Paul

Ow.

Brain went all 'splodey there. You should post a warning first.

:monconfused:

[Mr. Scott]

How evolution actually works:

http://www.biomedcentral.com/1471-2148/7/28

Oooh! That's a good one! Let me quote it in big red letters for the blind Kleinman:

Molecular clock dating suggests that gene exchange may continue for more than 3 million years after speciation. In addition, one species, H. heurippa, appears to have formed as a result of hybrid speciation.

[Anacoluthon64]

Sure you do, I’ll even repost his ridiculous gif and claims again. … Here is cheese wiz’s hypothesis. http://img514.imageshack.us/img514/3974/genegraphhx4.jpg The red line shows generations to achieve fixation of n alleles acted on by n selection pressures, the n+1th selection pressure being introduced only after the nth allele is fixed.
The blue line shows generations to achieve fixation of n alleles acted on by n selection pressures simultaneously.

All other features and parameters of the two models are identical. The model is designed so that the relative advantage of n+1 new genes over n (when selection is acting) is the same for all n, i.e. each new allele carries the same advantage.

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures. I highlighted his proposal in red type.Are you saying that "cheese wiz" (whoever that might be) is wrong about the graph showing an increased rate of fixations per generation of the blue over the red line? Because the graph plainly does show exactly that for the stated assumptions. The fact that n is discrete doesn't change the fact that (dn/dG)blue ≥ (dn/dG)red.

Or maybe you are saying the graph is simply wrong — a fabrication perhaps, or too limited, or too simplistic. If so, it would be good of you to pull out the Real Thing™ for everyone's edification.

I note also that my earlier anecdote about the engineering Ph.D. who was unfamiliar with the symbol "∫" was passed over in silence. The point – somewhat cryptic perhaps – of it is that those who use mathematical models don't necessarily understand them fully, even though it is reasonable to expect otherwise. The GIGO beastie is relentlessly vigilant for a chance to bite you on the nose.

'Luthon64

[Kotatsu]

Oh Kotatsu,

Just like last time I was active in this thread, I don't get any "humourous" nickname based on my avatar. It's unfair. It's favouritism, I say! Booooo!

this is not mindless pretentions of smashing the theory of evolution, I am using an evolutionist written and peer reviewed model of random point mutations to smash the theory of evolution. Why should I do this? I do this because the theory is wrong and interferes with the understanding of the real behavior of mutation and selection.

What's the real behaviour of mutation and selection, then? "It ain't doing s**t" is not really an explanation...

I proper understanding of mutation and selection will aid in the treatment of diseases, cancer and a variety of other societal problems. Evolutionism interferes with the proper understanding of the phenomenon of mutation and selection.

In what way? Would the results of all those numerous papers be much different if the evolution had never been discovered? How would they differ?

Myriad, the theory of evolution is a dead whale carcass,

Incidentally, people down the hall here at my university works with various annelids and stuff which have evolved to live on whale falls (whale carcasses at the bottom of the sea).

[cyborg]

What's the real behaviour of mutation and selection, then? "It ain't doing s**t" is not really an explanation...

God Makes It So.

Therefore You Must Pray To God For Good Genetic Changes Or He Will Punish You.

[Kotatsu]

So let’s see, you a supporter of cheese wiz’s silly gif have absolutely zero real examples of what you contend, that is multiple selection pressures accelerate evolution

Okay, a simple search provided, among other, no doubt interesting, things, the following articles. I will read them more thoroughly this afternoon, but for the moment, I will content myself with summarising the abstracts below (If I have misunderstood them, please feel free to correct me). It will be noted that it doesn't say explicitly that the rate of evolution has increased with increasing amounts of selection pressures in the studies cited below. However --- and this is more pertinent --- they show that even when the amount of selection pressures increase, evolution certainly does not "ultimately stop".

The examples below are written in no special order.

Lowell (1987) Evolution 41(3), pp 638-650:
Tropical limpets were compared to temperate ones. The tropical ones were subject to more and partly different selection pressures (in the form of a more diverse array of predators with different techniques for getting at the gooey inside of the limpet) than the temperate ones, and were found to show more variable shell structures. The magnitude of these variations, we are told, "were correlated with the degree of exposure to this additional selection pressure", which is claimed to be "as predicted".

Fullard (1988) Experientia 44, pp 423-428:
A comparison is made between the ears of moths. The"best frequency" for these to be tuned in to is determined primarily by predation of frequency-matched bats. However, there are also allotonic moths (1) that provide an additional selection pressure. Moths in areas where both types of bats live need to have ears that aid in escaping both types. Consequently, some Neotropical moths have specialized "external hearing aids [that] provide a mechanical means of obtaining this sensitivity". In other words, at least some moths that have this extra type of predator pressure are more derived (i.e., "more evolved") than those who have not. Again, evolution certainly has not "ultimately stop[ed]" by addition of selection pressures.

Martínez and Levinton (1996) Evolution 50(3), pp 1339-1343 and therein cited papers:
Upon exposure to several heavy metals, the oligochaete Limnodrilus hoffmeisteri resulted in more tolerant offspring. In other words, increasing the selection pressures acting on the population by at least one did not cause the evolution of the population to "stop".

Mopper (1996) Trends in Ecology and Evolution 11(6), pp 235-238 mentions the following:
Populations of the phytophagous soapberry bug switched hosts to plants introduced to America, and were thus subjected to new selection pressures of these new hosts, which were added to the ones already present (i.e., predation and so on). If this had "slowed and ultimately stopped" evolution, the bugs would neither have been able to utilize these new host plants due to its morphological differences from the old host plants, nor would it have been able to adapt to the biochemical defences of this new host. In reality, however, it took less than 50 years for the bugs to adapt to these new plants, and to change its beak lengths to fit more accurately to the new hosts.

How's that for a start, Kleinman? Like you, I've only skimmed the surface of the available litterature, but in all these examples, introduction of additional selection pressures did not "slow and ultimately stop" evolution, but lead the history of tehse respective animals in new directions. Especially interesting would be the last example, as host switching in parasitic animals may lead to sympatric speciation.

---
(1) Though the difference between syntonic and allotonic is lost on me until I've read the whole article, and possible some others.

[Dr Adequate]

Pretend, for a moment, that you haven't read this entire thread. Now read that statement from Kleinman in vacuo. Hmm ...

Hebephrenic Schizophrenia

A form of schizophrenia in which affective changes are prominent, delusions and hallucinations fleeting and fragmentary, behaviour irresponsible and unpredictable, and mannerisms common. The mood is shallow and inappropriate and often accompanied by giggling or self-satisfied, self-absorbed smiling, or by a lofty manner, grimaces, mannerisms, pranks, hypochondriacal complaints, and reiterated phrases. Thought is disorganized and speech rambling and incoherent. There is a tendency to remain solitary, and behaviour seems empty of purpose and feeling. This form of schizphrenia usually starts between the ages of 15 and 25 years and tends to have a poor prognosis because of the rapid development of "negative" symptoms, particularly flattening of affect and loss of volition.

In addition, disturbances of affect and volition, and thought disorder are usually prominent. Hallucinations and delusions may be present but are not usually prominent. Drive and determination are lost and goals abandoned, so that the patient's behaviour becomes characteristically aimless and empty of purpose. A superficial and manneristic preoccupation with religion, philosophy, and other abstract themes may add to the listener's difficulty in following the train of thought.

[Anacoluthon64]

I'm not sure, though, that "flattening of affect and loss of volition" and "[d]rive and determination [being] lost and goals abandoned" really apply. It seems that the opposite may be more accurate.

'Luthon64

[Dr Adequate]

He's abandoned lots of goals. But he always takes the goalposts with him.

No, seriously, I take it that his beef with science is the "superficial and manneristic preoccupation" with "abstract themes".

[delphi_ote]

Don’t be silly Delphi. Mutation and selection can not be written as a direct algebraic equation. It is a complex relationship of multiple parameters. That is what the ev computer model does. These variables only have functional relationships that can not be expressed in closed form algebraic format.
Are you trying to say that it's mathematically impossible to express your proof that evolution is mathematically impossible in mathematical notation? I would've thought a closed cycle of contradictions that tight would make even you uncomfortable...

[Anacoluthon64]

Apologies, but I've only recently reacquired access to the forum (and who knows how long it'll last?), so I haven't had the time to catch up properly on several months' worth of thread.

Science is a hard taskmaster, and the sooner its detractors heed this, the better. It requires discipline, rigour and dedication if "abstract themes" are to be meaningfully penetrated, notwithstanding the deceitful attempts at devaluation thereof by postmodernists and deconstructionists and such. Mud-slinging is no substitute for cogency.

Sermon over.

'Luthon64

[kleinman]

Yes, only a fool can’t understand it.This sentence is not a response to my comment. Are you responding to voices in your head?
I am not responding to voices in my head, I am responding to the mathematical results shown by ev and the numerous real examples of this mathematics. This is in contrast to the strange speculations and extrapolations that you evolutionarians engage in. Your concept of inorganic chemicals spontaneously forming life by cooperative chemistry is bizarre and illogical.
Once again can’t brain proves he can’t read. If he could, he would have seen the sentence in green:I saw that, but it was moot. They didn't show that. The only data present was that emergence couldn't be stopped. Which completely and totally without a shadow of any doubt, proves you are wrong.
The data already shows that multiple selection pressures slow the evolution of resistance of cancer cells to chemotherapy. This is in contrast to yours and cheese wiz’s strange speculation that multiple selection pressures accelerate evolution. Do you want to produce a single real example of your strange speculation?
Can’t brain’s sloppy reading of the citation match his sloppy understanding of mutation and selection. Can’t brain, you are not poetic, you have no mathematical or scientific skills but you are very good at choosing your avatars.This doesn't follow logically from my comment. You didn't state why I was wrong. I'll state my point again, because it is quite simple and perhaps you'll get it this time. So think hard...
Certainly it does, the authors state the following:
Although it reduces the total body burden of leukemia cells, the use of imatinib mesylate as a single agent may be accompanied by the evolution of resistance due mainly to the acquisition of point mutations. Imatinib has been combined with drugs that inhibit both the active and the inactive states of the p210Bcr-Abl kinase. These combinations have reduced but not completely eliminated the rate at which point mutations are acquired in the p210Bcr-Abl kinase. Thus, it is important to identify additional new inhibitors of the p210Bcr-Abl kinase. One possible method to prevent evolution of resistance is to simultaneously use multiple kinase inhibitors each with a different mechanism of action.
Their logic is simple, imatinib mesylate used alone may be accompanied by the evolution of resistance (red text), when imatinib is combined with other drugs, these combination reduce the evolution of resistance (blue text) and their conclusion is that additional drugs will prevent the evolution of resistance (green text). Simple isn’t it can’t brain.
If we can't halt evolution (over a matter of years) by purposefully selecting the most difficult pressures, what hope do you have that elements in the wild can do it? This statement cuts at the heart of your argument. Even when we try, we haven't stopped the evolutionary process. We may be able to one day, but that takes design. Since there isn't "something" at every spot throughout our world designing multiple selection pressures to stop evolution, we are left to assume that evolution can occur in the wild.
Can’t brain must be talking about the “wild” selection pressures that all cooperate to accelerate evolution, you all know the ones he is talking about, they are the ones that he can’t give a real example of. This is the strange and bizarre type of speculation that evolutionarians must engage in. They think that somehow environmental selection pressures will behave differently mathematically than human applied selection pressures. Can’t brain thinks that chemistry cooperates to create life out of inorganic molecules and selection pressures cooperate to evolve birds from reptiles. Too bad he doesn’t have any mathematical or empirical basis to show this. The way mutation and selection actually works is that single selection pressures evolve most rapidly while additional selection pressures slow down the process profoundly. This is shown mathematically with ev and empirically with numerous examples of mutation and selection.
How evolution actually works:

http://www.biomedcentral.com/1471-2148/7/28 (http://www.biomedcentral.com/1471-2148/7/28) Oooh! That's a good one! Let me quote it in big red letters for the blind Kleinman:
Now I see pussycat, hybridization is the new secret mechanism that overcomes the mathematical and empirical fact that multiple selection pressures slow and ultimately stop evolution. What strange and bizarre speculations you evolutionarians engage in.
Sure you do, I’ll even repost his ridiculous gif and claims again. … Here is cheese wiz’s hypothesis...Are you saying that "cheese wiz" (whoever that might be) is wrong about the graph showing an increased rate of fixations per generation of the blue over the red line? Because the graph plainly does show exactly that for the stated assumptions. The fact that n is discrete doesn't change the fact that (dn/dG)blue ≥ (dn/dG)red.
You can check out cheese wiz’s original post on page 105, post number 4163. Cheese wiz’s gif has no basis in reality; neither he nor any other evolutionarian can give a real example of this silly drawing. So what if the slope of one curve is greater than the slope of another curve when he has no real examples. Perhaps you would give us a real example of cheese wiz’s nonsensical analysis?
Or maybe you are saying the graph is simply wrong — a fabrication perhaps, or too limited, or too simplistic. If so, it would be good of you to pull out the Real Thing™ for everyone's edification.
What I am saying is that if cheese wiz says his analysis which shows that multiple selection pressures accelerate evolution, give us a real example of this analysis. I have shown how mutation and selection in ev accelerates with the reduction of the number of selection conditions and have posted numerous real examples of this phenomenon (and will continue to post examples of this-see below). The contrast is clear, cheese wiz says multiple selection pressures accelerates evolution, I say that multiple selection pressures slow and ultimately stop evolution. Cheese wiz has posted zero real examples of his gif, I have posted numerous real examples of what ev shows.
I note also that my earlier anecdote about the engineering Ph.D. who was unfamiliar with the symbol "∫" was passed over in silence. The point – somewhat cryptic perhaps – of it is that those who use mathematical models don't necessarily understand them fully, even though it is reasonable to expect otherwise. The GIGO beastie is relentlessly vigilant for a chance to bite you on the nose.
Oh, Anacoluthon64, another evolutionarian who has posted no results from ev (and probably run no cases) is now going to interpret ev for all of us. Here’s how evolutionarian logic works with ev, the fewer cases you run with the model the greater your expertise in interpreting the results. What impressive mathematical and scientific skills you demonstrate Anacoluthon64.
Oh Kotatsu, Just like last time I was active in this thread, I don't get any "humourous" nickname based on my avatar. It's unfair. It's favouritism, I say! Booooo!
Now what are you whining about? Do you feel neglected?
this is not mindless pretentions of smashing the theory of evolution, I am using an evolutionist written and peer reviewed model of random point mutations to smash the theory of evolution. Why should I do this? I do this because the theory is wrong and interferes with the understanding of the real behavior of mutation and selection.What's the real behaviour of mutation and selection, then? "It ain't doing s**t" is not really an explanation...
Here come the asterisks again. The real behavior of mutation and selection is that multiple selection conditions slow and ultimately stop evolution. That is what ev shows mathematically and that is what the numerous examples of mutation and selection that I have been citing is showing empirically. Now if you believe that multiple selection pressures accelerate evolution, would you post a real example of this?
I proper understanding of mutation and selection will aid in the treatment of diseases, cancer and a variety of other societal problems. Evolutionism interferes with the proper understanding of the phenomenon of mutation and selection.In what way? Would the results of all those numerous papers be much different if the evolution had never been discovered? How would they differ?
It is obvious now how mutation and selection works. It is clear now that anyone involved in treating infectious diseases, treating cancer, involved in agriculture and many other scientific disciplines that creatures can evolve to single selection pressures much more quickly than multiple selection pressures. Evolutionarians take the phenomenon of mutation and selection and extrapolate and speculate this phenomenon to the evolution of birds from reptiles. The mathematics and empirical data of mutation and selection shows something entirely different than these gross evolutionarian speculations and extrapolations. The brainwashing that evolutionarians have received is so thorough that they continue to attempt to argue that multiple selection pressures accelerate evolution despite the mathematical and empirical evidence to the contrary.
Myriad, the theory of evolution is a dead whale carcass,Incidentally, people down the hall here at my university works with various annelids and stuff which have evolved to live on whale falls (whale carcasses at the bottom of the sea).
Is that your attempt to explain how mutation and selection actually works?
So let’s see, you a supporter of cheese wiz’s silly gif have absolutely zero real examples of what you contend, that is multiple selection pressures accelerate evolution Okay, a simple search provided, among other, no doubt interesting, things, the following articles. I will read them more thoroughly this afternoon, but for the moment, I will content myself with summarising the abstracts below (If I have misunderstood them, please feel free to correct me). It will be noted that it doesn't say explicitly that the rate of evolution has increased with increasing amounts of selection pressures in the studies cited below. However --- and this is more pertinent --- they show that even when the amount of selection pressures increase, evolution certainly does not "ultimately stop".
Finally, an evolutionarian who is going to try to show examples of multiple selection pressures accelerating evolution.
Lowell (1987) Evolution 41(3), pp 638-650:
Tropical limpets were compared to temperate ones. The tropical ones were subject to more and partly different selection pressures (in the form of a more diverse array of predators with different techniques for getting at the gooey inside of the limpet) than the temperate ones, and were found to show more variable shell structures. The magnitude of these variations, we are told, "were correlated with the degree of exposure to this additional selection pressure", which is claimed to be "as predicted".
This is typical of the mushy soft science of the theory of evolution. What are the selection pressures that the limpets are subjected too and what are the genetic changes that you propose occurred. How do you differentiate these changes in limpet by recombination and selection versus mutation and selection? This example is more analogous to dog breeding (recombination and selection) than mutation and selection.
Fullard (1988) Experientia 44, pp 423-428:
A comparison is made between the ears of moths. The"best frequency" for these to be tuned in to is determined primarily by predation of frequency-matched bats. However, there are also allotonic moths (1) that provide an additional selection pressure. Moths in areas where both types of bats live need to have ears that aid in escaping both types. Consequently, some Neotropical moths have specialized "external hearing aids [that] provide a mechanical means of obtaining this sensitivity". In other words, at least some moths that have this extra type of predator pressure are more derived (i.e., "more evolved") than those who have not. Again, evolution certainly has not "ultimately stop[ed]" by addition of selection pressures.
If you want dogs with better hearing, breed those animals with the best hearing. This is another example of recombination and selection. Where are the multiple selection pressures which accelerate evolution?
Martínez and Levinton (1996) Evolution 50(3), pp 1339-1343 and therein cited papers:
Upon exposure to several heavy metals, the oligochaete Limnodrilus hoffmeisteri resulted in more tolerant offspring. In other words, increasing the selection pressures acting on the population by at least one did not cause the evolution of the population to "stop".
Don’t give it to us in your words; post the authors statements which show that multiple selection pressures accelerate evolution. What happens when the heavy metal exposure is performed sequentially versus simultaneous exposure to the heavy metals?
Mopper (1996) Trends in Ecology and Evolution 11(6), pp 235-238 mentions the following:
Populations of the phytophagous soapberry bug switched hosts to plants introduced to America, and were thus subjected to new selection pressures of these new hosts, which were added to the ones already present (i.e., predation and so on). If this had "slowed and ultimately stopped" evolution, the bugs would neither have been able to utilize these new host plants due to its morphological differences from the old host plants, nor would it have been able to adapt to the biochemical defences of this new host. In reality, however, it took less than 50 years for the bugs to adapt to these new plants, and to change its beak lengths to fit more accurately to the new hosts.
Again you post in your own words an example of recombination and natural selection. These bugs have beaks? I thought bugs had proboses. No matter, if you want to lengthen the beak or proboscis on a creature rapidly, do it by recombination and natural selection. Let the creatures with the longest beaks or proboses breed and you will rapidly get offspring with longer beaks or proboses.
How's that for a start, Kleinman? Like you, I've only skimmed the surface of the available litterature, but in all these examples, introduction of additional selection pressures did not "slow and ultimately stop" evolution, but lead the history of tehse respective animals in new directions. Especially interesting would be the last example, as host switching in parasitic animals may lead to sympatric speciation.
It’s a really slow start, you give examples of recombination and selection, not mutation and selection and you fail to define the selection pressures and genetic changes that occur. But, you have done nothing to be ashamed of, Stephen Gould made the same error when he postulated the hypothesis of punctuated equilibrium. Gould confused mutation and selection with recombination and natural selection. If you apply recombination and natural selection to Gould’s hypothesis, you get your mathematics right, but if you try to apply mutation and natural selection to the hypothesis, it is mathematically impossible.
He's abandoned lots of goals. But he always takes the goalposts with him.
Hey cheese wiz, maybe you can do a better job than Kotatsu and show us some real examples of your contention that multiple selection pressures accelerate evolution. He tried to use examples of recombination and natural selection; would you show us an example where this occurs with mutation and selection?
Don’t be silly Delphi. Mutation and selection can not be written as a direct algebraic equation. It is a complex relationship of multiple parameters. That is what the ev computer model does. These variables only have functional relationships that can not be expressed in closed form algebraic format.Are you trying to say that it's mathematically impossible to express your proof that evolution is mathematically impossible in mathematical notation? I would've thought a closed cycle of contradictions that tight would make even you uncomfortable...
Again, Delphi, you are being very silly. Most real physical problems can only be expressed in functional notation. You don’t have a closed form algebraic expression that describes the function. In fact, every real mathematical scientific problem that I have worked on ultimately comes down to solving a functional equation which can not be expressed algebraically. We know there is a functional relationship between the variables that is expressed by a complex mathematical interaction of the variable. Dr Schneider’s computer model is an example of this complex mathematical interaction. The way you analyze such a mathematical interaction is you map out the function. The way you map out the function is to choose values for the variables and in Dr Schneider’s model this maps out to a number of generations for convergence of the model. If you are systematic in your analysis, you can map out the function and understand how the function behaves. The way to do this with ev is to systematically vary genome length, mutation rate, population, gamma, site width, selection conditions and so on. This was suggested by Dr Schneider in his publication on ev. Do this and you will understand the mathematics of mutation and selection. There is nothing contradictory about this type of analysis. In fact this analysis gives an accurate prediction of how mutation and selection works in reality as attested to by the numerous citations I have and will continue to post. It also verifies your Wikipedia reference to the fitness landscape.
Science is a hard taskmaster, and the sooner its detractors heed this, the better. It requires discipline, rigour and dedication if "abstract themes" are to be meaningfully penetrated, notwithstanding the deceitful attempts at devaluation thereof by postmodernists and deconstructionists and such. Mud-slinging is no substitute for cogency.
Well let’s see if we can put a little hard mathematical science into the theory of evolution before it completely disappears into the mushy mud.

Here’s another citation which shows how mutation and selection actually works and that multiple selection pressure slows evolution.
http://www.fghp.org/monitor/pdf/HTM070416.pdf (http://www.fghp.org/monitor/pdf/HTM070416.pdf)
“The rapid evolution of bacterial drug resistance and the alarming slowdown in development of new antibiotics is spurring attention towards multidrug treatments, ”say Remy Chait and colleagues of Harvard Medical School in an article published in Nature this week. But mixing drugs can have odd effects: the combinations can be synergistic, additive, or antagonistic. In certain ‘hyper-antagonistic’ cases, the mixture can prove even less effective than either drug alone; this is called suppression. In general, resistance to one of the drugs in a combination gives the resistant bacteria an advantage, so they outgrow those that are sensitive to the drug. But, Chait et al. theorised that in suppressive cases, resistance to one of the drugs might actually be a disadvantage to bacteria. Although resistance would diminish the effects of one of the medicines, it might also remove the suppression, making the drug combination more effective against resistant bacteria than sensitive ones.

[Paul C. Anagnostopoulos]

Now I see pussycat, hybridization is the new secret mechanism that overcomes the mathematical and empirical fact that multiple selection pressures slow and ultimately stop evolution.
Alan, you gotta stop saying this. If multiple pressures slow and stop evolution, then evolution would never have gotten started to begin with, since there are always multiple pressures. If it had never gotten started to begin with, then there would be no chance for it to be slowed and stopped. Your argument shoots itself in the foot from the get-go.

~~ Paul

[Paul C. Anagnostopoulos]

Here’s another citation which shows how mutation and selection actually works and that multiple selection pressure slows evolution.


... But mixing drugs can have odd effects: the combinations can be synergistic, additive, or antagonistic. In certain ‘hyper-antagonistic’ cases, the mixture can prove even less effective than either drug alone; this is called suppression.

Is it just me?

~~ Paul

[joobz]

I am not responding to voices in my head, I am responding to the mathematical results shown by ev and the numerous real examples of this mathematics. This is in contrast to the strange speculations and extrapolations that you evolutionarians engage in. Your concept of inorganic chemicals spontaneously forming life by cooperative chemistry is bizarre and illogical.

The data already shows that multiple selection pressures slow the evolution of resistance of cancer cells to chemotherapy. This is in contrast to yours and cheese wiz’s strange speculation that multiple selection pressures accelerate evolution. Do you want to produce a single real example of your strange speculation?

Certainly it does, the authors state the following:

Their logic is simple, imatinib mesylate used alone may be accompanied by the evolution of resistance (red text), when imatinib is combined with other drugs, these combination reduce the evolution of resistance (blue text) and their conclusion is that additional drugs will prevent the evolution of resistance (green text). Simple isn’t it can’t brain.

Can’t brain must be talking about the “wild” selection pressures that all cooperate to accelerate evolution, you all know the ones he is talking about, they are the ones that he can’t give a real example of. This is the strange and bizarre type of speculation that evolutionarians must engage in. They think that somehow environmental selection pressures will behave differently mathematically than human applied selection pressures. Can’t brain thinks that chemistry cooperates to create life out of inorganic molecules and selection pressures cooperate to evolve birds from reptiles. Too bad he doesn’t have any mathematical or empirical basis to show this. The way mutation and selection actually works is that single selection pressures evolve most rapidly while additional selection pressures slow down the process profoundly. This is shown mathematically with ev and empirically with numerous examples of mutation and selection.

Now I see pussycat, hybridization is the new secret mechanism that overcomes the mathematical and empirical fact that multiple selection pressures slow and ultimately stop evolution. What strange and bizarre speculations you evolutionarians engage in.

You can check out cheese wiz’s original post on page 105, post number 4163. Cheese wiz’s gif has no basis in reality; neither he nor any other evolutionarian can give a real example of this silly drawing. So what if the slope of one curve is greater than the slope of another curve when he has no real examples. Perhaps you would give us a real example of cheese wiz’s nonsensical analysis?

What I am saying is that if cheese wiz says his analysis which shows that multiple selection pressures accelerate evolution, give us a real example of this analysis. I have shown how mutation and selection in ev accelerates with the reduction of the number of selection conditions and have posted numerous real examples of this phenomenon (and will continue to post examples of this-see below). The contrast is clear, cheese wiz says multiple selection pressures accelerates evolution, I say that multiple selection pressures slow and ultimately stop evolution. Cheese wiz has posted zero real examples of his gif, I have posted numerous real examples of what ev shows.

Oh, Anacoluthon64, another evolutionarian who has posted no results from ev (and probably run no cases) is now going to interpret ev for all of us. Here’s how evolutionarian logic works with ev, the fewer cases you run with the model the greater your expertise in interpreting the results. What impressive mathematical and scientific skills you demonstrate Anacoluthon64.

Now what are you whining about? Do you feel neglected?

Here come the asterisks again. The real behavior of mutation and selection is that multiple selection conditions slow and ultimately stop evolution. That is what ev shows mathematically and that is what the numerous examples of mutation and selection that I have been citing is showing empirically. Now if you believe that multiple selection pressures accelerate evolution, would you post a real example of this?

It is obvious now how mutation and selection works. It is clear now that anyone involved in treating infectious diseases, treating cancer, involved in agriculture and many other scientific disciplines that creatures can evolve to single selection pressures much more quickly than multiple selection pressures. Evolutionarians take the phenomenon of mutation and selection and extrapolate and speculate this phenomenon to the evolution of birds from reptiles. The mathematics and empirical data of mutation and selection shows something entirely different than these gross evolutionarian speculations and extrapolations. The brainwashing that evolutionarians have received is so thorough that they continue to attempt to argue that multiple selection pressures accelerate evolution despite the mathematical and empirical evidence to the contrary.

Is that your attempt to explain how mutation and selection actually works?

Finally, an evolutionarian who is going to try to show examples of multiple selection pressures accelerating evolution.

This is typical of the mushy soft science of the theory of evolution. What are the selection pressures that the limpets are subjected too and what are the genetic changes that you propose occurred. How do you differentiate these changes in limpet by recombination and selection versus mutation and selection? This example is more analogous to dog breeding (recombination and selection) than mutation and selection.

If you want dogs with better hearing, breed those animals with the best hearing. This is another example of recombination and selection. Where are the multiple selection pressures which accelerate evolution?

Don’t give it to us in your words; post the authors statements which show that multiple selection pressures accelerate evolution. What happens when the heavy metal exposure is performed sequentially versus simultaneous exposure to the heavy metals?

Again you post in your own words an example of recombination and natural selection. These bugs have beaks? I thought bugs had proboses. No matter, if you want to lengthen the beak or proboscis on a creature rapidly, do it by recombination and natural selection. Let the creatures with the longest beaks or proboses breed and you will rapidly get offspring with longer beaks or proboses.

It’s a really slow start, you give examples of recombination and selection, not mutation and selection and you fail to define the selection pressures and genetic changes that occur. But, you have done nothing to be ashamed of, Stephen Gould made the same error when he postulated the hypothesis of punctuated equilibrium. Gould confused mutation and selection with recombination and natural selection. If you apply recombination and natural selection to Gould’s hypothesis, you get your mathematics right, but if you try to apply mutation and natural selection to the hypothesis, it is mathematically impossible.

Hey cheese wiz, maybe you can do a better job than Kotatsu and show us some real examples of your contention that multiple selection pressures accelerate evolution. He tried to use examples of recombination and natural selection; would you show us an example where this occurs with mutation and selection?

Again, Delphi, you are being very silly. Most real physical problems can only be expressed in functional notation. You don’t have a closed form algebraic expression that describes the function. In fact, every real mathematical scientific problem that I have worked on ultimately comes down to solving a functional equation which can not be expressed algebraically. We know there is a functional relationship between the variables that is expressed by a complex mathematical interaction of the variable. Dr Schneider’s computer model is an example of this complex mathematical interaction. The way you analyze such a mathematical interaction is you map out the function. The way you map out the function is to choose values for the variables and in Dr Schneider’s model this maps out to a number of generations for convergence of the model. If you are systematic in your analysis, you can map out the function and understand how the function behaves. The way to do this with ev is to systematically vary genome length, mutation rate, population, gamma, site width, selection conditions and so on. This was suggested by Dr Schneider in his publication on ev. Do this and you will understand the mathematics of mutation and selection. There is nothing contradictory about this type of analysis. In fact this analysis gives an accurate prediction of how mutation and selection works in reality as attested to by the numerous citations I have and will continue to post. It also verifies your Wikipedia reference to the fitness landscape.

Well let’s see if we can put a little hard mathematical science into the theory of evolution before it completely disappears into the mushy mud.

Here’s another citation which shows how mutation and selection actually works and that multiple selection pressure slows evolution.
http://www.fghp.org/monitor/pdf/HTM070416.pdf
IN all of this rambling incoherence, You failed to address this simple point:

If we can't halt evolution (over a matter of years) by purposefully selecting the most difficult pressures, what hope do you have that elements in the wild can do it?

This statement cuts at the heart of your argument. Even when we try, we haven't stopped the evolutionary process. We may be able to one day, but that takes design. Since there isn't "something" at every spot throughout our world designing multiple selection pressures to stop evolution, we are left to assume that evolution can occur in the wild.

[kleinman]

Now I see pussycat, hybridization is the new secret mechanism that overcomes the mathematical and empirical fact that multiple selection pressures slow and ultimately stop evolution.Alan, you gotta stop saying this. If multiple pressures slow and stop evolution, then evolution would never have gotten started to begin with, since there are always multiple pressures. If it had never gotten started to begin with, then there would be no chance for it to be slowed and stopped. Your argument shoots itself in the foot from the get-go.
Why should I stop saying this? Single selection pressures can accomplish microevolutionary processes. You contend that macroevolution is simply the summation of microevolutionary processes. However, we see in reality that multiple selection pressures slow the processes profoundly and ev shows that it stops the process entirely. Just because microevolutionary processes occur, multiple selection pressures stop the transformation of these microevolutionary processes into macroevolutionary changes. Just because a bacterium can evolve resistance to an antibiotic, you can’t reasonably extrapolate this process to reptiles evolving into birds. It is mathematically impossible.
Here’s another citation which shows how mutation and selection actually works and that multiple selection pressure slows evolution.... But mixing drugs can have odd effects: the combinations can be synergistic, additive, or antagonistic. In certain ‘hyper-antagonistic’ cases, the mixture can prove even less effective than either drug alone; this is called suppression.Is it just me?
It’s good to see you are reading my citations. I thought I’d throw some red meat to you evolutionarians; you’ve been acting like pussycats for so long.

So what does this statement have to say about mutation and selection? Not much. I can recall from my infectious disease lectures many years ago that it was not recommended to mix bacteriostatic and bacteriocidal antibiotics because the action of one would interfere with the action of the other. For example using a beta-lactam antibiotic which interferes with the assembly of the cell wall of bacteria (which occurs during reproduction of the bacteria) and are considered a bacteriocidal drugs would not work well in the presence of a bacteriostatic drug which interferes with protein synthesis of the bacteria and prevents bacterial reproduction without killing the bacteria. In this case, the beta-lactam drug is not exerting a selection pressure because the bacteria are not allowed to reproduce by the bacteriostatic drug which will confuse the situation a little for evolutionarians. These “odd” effects will become more understandable when the drugs being considered are determined or are not determined to be exerting selection pressures and how they affect the path the bacterial population must make on the fitness landscape. Of course, Paul, you can try to draw the conclusion from this post that multiple selection pressures accelerate evolution but then you would be in disagreement with your own computer model.
If we can't halt evolution (over a matter of years) by purposefully selecting the most difficult pressures, what hope do you have that elements in the wild can do it?
Can’t brain makes two erroneous assumptions here. The first is that can’t brain thinks that extinction does not occur and the second is that can’t brain thinks that environmental selection pressures will work different mathematically than human induced selection pressures. Can’t brain, I appreciate you combining your errors into a single sentence; it makes it much more efficient to respond.

[Belz...]

I can brain that the theory of evolution by mutation and selection is infinitely dumb, it’s mathematically impossible.

Well, it's a good thing you discovered that, otherwise all those brainy scientists around the world would have continued to be completely wrong about the best-supported scientific theory in existence.

[Belz...]

Please, Klein, stick to regular fonts.

[Anacoluthon64]

Cheese wiz’s gif has no basis in reality; neither he nor any other evolutionarian can give a real example of this silly drawing.

…

What I am saying is that if cheese wiz says his analysis which shows that multiple selection pressures accelerate evolution, give us a real example of this analysis.

…

I have shown how mutation and selection in ev accelerates with the reduction of the number of selection conditions…Before tackling the issue of a real example, you've a prior difficulty. If the graph in question was arrived at from data points calculated using the same ev program (a point the posts aren't clear on), then the results directly contradict those you claim, and it seems obvious that at least one of the result sets was produced by deficient simulations, possibly bad input. This case can readily be sorted out by stating the relevant numbers and configurations used in each instance. If different simulators were used, then this situation too can be examined and resolved – it would just take more effort. Oozing slurs is, however, a non-starter.


Oh, Anacoluthon64, another evolutionarian who has posted no results from ev (and probably run no cases) is now going to interpret ev for all of us. Here’s how evolutionarian logic works with ev, the fewer cases you run with the model the greater your expertise in interpreting the results. What impressive mathematical and scientific skills you demonstrate Anacoluthon64.As for my "now going to interpret ev for all of us," I make no such pretensions. I'm much more interested in how the same or a functionally equivalent simulator can yield contradictory results.

And here's how kleinmanian argument appears to work: manufacture ridicule and concoct unwarranted inferences – the more, the deliriously merrier – and then stretch them past their sell-by date. It is becoming clear why you're consistently met with much disputatious contumely: you court it.

'Luthon64

[kjkent1]

Now I see pussycat, hybridization is the new secret mechanism that overcomes the mathematical and empirical fact that multiple selection pressures slow and ultimately stop evolution. What strange and bizarre speculations you evolutionarians engage in.I've yet to see you provide any peer-reviewed evidence to contradict my citation (http://www.biomedcentral.com/1471-2148/7/28 (http://www.biomedcentral.com/1471-2148/7/28)). And, as hybridization isn't modeled in ev, you have no mathmatics to contradict it, either.

So, stop with the juvenile ad hominems and let's see you disprove the above cite, because, if you can't -- you theory is screwed.

[kleinman]

Cheese wiz’s gif has no basis in reality; neither he nor any other evolutionarian can give a real example of this silly drawing.Before tackling the issue of a real example, you've a prior difficulty. If the graph in question was arrived at from data points calculated using the same ev program (a point the posts aren't clear on), then the results directly contradict those you claim, and it seems obvious that at least one of the result sets was produced by deficient simulations, possibly bad input. This case can readily be sorted out by stating the relevant numbers and configurations used in each instance. If different simulators were used, then this situation too can be examined and resolved – it would just take more effort. Oozing slurs is, however, a non-starter.
If cheese wiz derived this curve from ev, have him list the parameters he used to derive the figure, but I wouldn’t hold my breath waiting for this data. What’s the matter with a little ooze isn’t that where evolutionarians contend life arose spontaneously?
Oh, Anacoluthon64, another evolutionarian who has posted no results from ev (and probably run no cases) is now going to interpret ev for all of us. Here’s how evolutionarian logic works with ev, the fewer cases you run with the model the greater your expertise in interpreting the results. What impressive mathematical and scientific skills you demonstrate Anacoluthon64.As for my "now going to interpret ev for all of us," I make no such pretensions. I'm much more interested in how the same or a functionally equivalent simulator can yield contradictory results.
This discussion has been going on for more than a year and no evolutionarian has presented any equivalent simulator to mutation and selection. Ev is the only peer reviewed and published simulator of mutation and selection that has been discussed on this thread. Surprise us all with another simulator, especially one which shows that multiple selection pressures accelerate evolution.
And here's how kleinmanian argument appears to work: manufacture ridicule and concoct unwarranted inferences – the more, the deliriously merrier – and then stretch them past their sell-by date. It is becoming clear why you're consistently met with much disputatious contumely: you court it.
Well now isn’t that a surprise, a thin skinned crybaby evolutionarian has decided to post on this thread. I don’t need to concoct unwarranted inferences, I have a peer reviewed and published model of random point mutation and natural selection which shows that multiple selection pressures slow and ultimately stop evolution. In addition, I am posting numerous references which demonstrate this mathematical fact. Here’s another example for you to ponder while you try to think of the next thing to whine about.

http://cohesion.rice.edu/Engineering/bioe/emplibrary/Physics_Today_Jan07.pdf (http://cohesion.rice.edu/Engineering/bioe/emplibrary/Physics_Today_Jan07.pdf)
At the molecular level, what are the likely escape mutants that lead to new viral strains or new antibiotic-resistant bacteria? To be specific, I’ll consider viruses. The immune system recognizes regions of viral proteins, and it develops the ability to clear the virus from the body based on that recognition. If not completely eradicated from the human(and possibly animal) population, the surviving virus will tend to accumulate mutations in the region of the genetic sequence that codes for those recognizable protein pieces and thus avoid immune recognition. Predicting which mutations are likely in the surviving virus could allow vaccination against potential future strains—the escape mutants—and more effective control of the virus in the population. Similarly, the ability to predict at the molecular level which changes may lead to resistance against a drug can aid in the design of improved drugs or suggest optimal combinations of existing drugs to mitigate the evolution of resistance and eradicate the pathogen.
It seems everyone but you evolutionarians realize that multiple selection pressures slow evolution.

[joobz]

Can’t brain makes two erroneous assumptions here. The first is that can’t brain thinks that extinction does not occur and the second is that can’t brain thinks that environmental selection pressures will work different mathematically than human induced selection pressures. Can’t brain, I appreciate you combining your errors into a single sentence; it makes it much more efficient to respond.
Oh goody, you tried to actually critique my argument. Let me patt you on the head...

Unfortunately.
1.) I assume no such thing as extinction is impossible. Extinction is an issue about the severity of cummulative effects. Not the number of effects. This is a very important point, not all pressures are created equal. Designed cummulative pressures exerted simultaneously to force extinction is not a model for natural selection in the wild. It is a narrow subset of reality.
2.) Your second point," thinks that environmental selection pressures will work different mathematically" is stupid. I claim no such thing.

Which leads us back to my previous point:
If we can't halt evolution (over a matter of years) by purposefully selecting the most difficult pressures, what hope do you have that elements in the wild can do it?

This statement cuts at the heart of your argument. Even when we try, we haven't stopped the evolutionary process. We may be able to one day, but that takes design. Since there isn't "something" at every spot throughout our world designing multiple selection pressures to stop evolution, we are left to assume that evolution can occur in the wild.

[joobz]

thank you for your red text
Similarly, the ability to predict at the molecular level which changes may lead to resistance against a drug can aid in the design of improved drugs or suggest optimal combinations of existing drugs to mitigate the evolution of resistance and eradicate the pathogen.
Do you think that there is something out in the forests, seas, air, caves.... that is going arround selecting the "optimal combinations" to "halt evolution"?

If we can't halt evolution (over a matter of years) by purposefully selecting the most difficult pressures, what hope do you have that elements in the wild can do it?

This statement cuts at the heart of your argument. Even when we try, we haven't stopped the evolutionary process. We may be able to one day, but that takes design. Since there isn't "something" at every spot throughout our world designing multiple selection pressures to stop evolution, we are left to assume that evolution can occur in the wild.

[kleinman]

I can brain that the theory of evolution by mutation and selection is infinitely dumb, it’s mathematically impossible.Well, it's a good thing you discovered that, otherwise all those brainy scientists around the world would have continued to be completely wrong about the best-supported scientific theory in existence.
Well, I will admit that the theory of evolution is the best-supported scientific theory since the flat earth hypothesis but you might get some argument from those who think the laws of thermodynamics have a bit more of empirical support.
Please, Klein, stick to regular fonts.
Just be thankful I’m not using old English fonts, Paul had trouble reading that font.

[kjkent1]

Is it just me?

~~ PaulWith due respect, you allow Kleinman to control this thread. If you don't force him to argue rationally, then he will rely on his ridiculous talismen and the thread will just wander aimlessly.

I suppose you can consider the thread a charitable contribution to the scientific community, because "but for" this public outlet, Kleinman might go "postal."

[kleinman]

Can’t brain makes two erroneous assumptions here. The first is that can’t brain thinks that extinction does not occur and the second is that can’t brain thinks that environmental selection pressures will work different mathematically than human induced selection pressures. Can’t brain, I appreciate you combining your errors into a single sentence; it makes it much more efficient to respond.1.) I assume no such thing as extinction is impossible. Extinction is an issue about the severity of cummulative effects. Not the number of effects. This is a very important point, not all pressures are created equal. Designed cummulative pressures exerted simultaneously to force extinction is not a model for natural selection in the wild. It is a narrow subset of reality.
And then can’t brain says this:
Which leads us back to my previous point:
If we can't halt evolution (over a matter of years) by purposefully selecting the most difficult pressures, what hope do you have that elements in the wild can do it?
So can’t brain says extinction can occur but evolution doesn’t stop when extinction occurs. Well, evolution for that population certainly stops, doesn’t it can’t brain.
Then can’t brain says this:
2.) Your second point," thinks that environmental selection pressures will work different mathematically" is stupid. I claim no such thing.
Can’t brain, I’ve posted more than 60 real examples of mutation and selection which show that multiple selection pressures slow evolution. Why don’t you post a real example where multiple environmental selection pressures accelerate evolution?
Similarly, the ability to predict at the molecular level which changes may lead to resistance against a drug can aid in the design of improved drugs or suggest optimal combinations of existing drugs to mitigate the evolution of resistance and eradicate the pathogen.Do you think that there is something out in the forests, seas, air, caves.... that is going arround selecting the "optimal combinations" to "halt evolution"?
Can’t brain, if it is a selection pressure, it impairs the fitness of the population to reproduce. Just because a drug has selective action against one population of bacteria does not mean it has selection action against another population of bacteria. If you have two different selection pressures that affect two different genetic systems it requires that simultaneous mutations to occur in the two different genetic systems in order to evolve to these selection pressures. It doesn’t matter whether these are human applied selection pressures or environmentally applied selection pressures. In order to evolve all the genetic systems required to transform a reptile into a bird requires multiple different selection pressures on these genetic systems. This is mathematically impossible.
If we can't halt evolution (over a matter of years) by purposefully selecting the most difficult pressures, what hope do you have that elements in the wild can do it?
Somewhere in your mathematically challenged imagination, you see all these selection pressures (which are impairing the ability of the population to reproduce) magically transforming reptiles into birds. It doesn’t matter whether the selection pressures are “wild” or human induced, when you have multiple selection pressures they interfere with each other from enabling the population to adapt to these selection pressures. Mutation and selection is simply too slow a process to accomplish what you envision in your imagination. Mutation and selection does not work like you see it in your dreams. If you studied ev and examined the numerous real examples of mutation and selection that I have been presenting, you would understand this mathematical and empirical fact of how mutation and selection actually works.

[kleinman]

With due respect, you allow Kleinman to control this thread. If you don't force him to argue rationally, then he will rely on his ridiculous talismen and the thread will just wander aimlessly.
Let’s all talk about lita’ gators 10^500 alternative universes, that rational. Lita’ gator would make a good censor in a dictatorial regime.

What lita’ gator doesn’t realize is that I was invited by Paul to discuss this issue on this forum, who invited you to discuss your string cheese theory of evolution.

[joobz]

And then can’t brain says this:

So can’t brain says extinction can occur but evolution doesn’t stop when extinction occurs. Well, evolution for that population certainly stops, doesn’t it can’t brain.
Then can’t brain says this:

Can’t brain, I’ve posted more than 60 real examples of mutation and selection which show that multiple selection pressures slow evolution. Why don’t you post a real example where multiple environmental selection pressures accelerate evolution?

Can’t brain, if it is a selection pressure, it impairs the fitness of the population to reproduce. Just because a drug has selective action against one population of bacteria does not mean it has selection action against another population of bacteria. If you have two different selection pressures that affect two different genetic systems it requires that simultaneous mutations to occur in the two different genetic systems in order to evolve to these selection pressures. It doesn’t matter whether these are human applied selection pressures or environmentally applied selection pressures. In order to evolve all the genetic systems required to transform a reptile into a bird requires multiple different selection pressures on these genetic systems. This is mathematically impossible.

Somewhere in your mathematically challenged imagination, you see all these selection pressures (which are impairing the ability of the population to reproduce) magically transforming reptiles into birds. It doesn’t matter whether the selection pressures are “wild” or human induced, when you have multiple selection pressures they interfere with each other from enabling the population to adapt to these selection pressures. Mutation and selection is simply too slow a process to accomplish what you envision in your imagination. Mutation and selection does not work like you see it in your dreams. If you studied ev and examined the numerous real examples of mutation and selection that I have been presenting, you would understand this mathematical and empirical fact of how mutation and selection actually works.
Since life is not extinct and we are all in the presence of continual multiple selection pressures, than this theory must be wrong.

However, let's consider all of the data you have presented:
If we can't halt evolution (over a matter of years) by purposefully selecting the most difficult pressures, what hope do you have that elements in the wild can do it?

This statement cuts at the heart of your argument. Even when we try, we haven't stopped the evolutionary process. We may be able to one day, but that takes design. Since there isn't "something" at every spot throughout our world designing multiple selection pressures to stop evolution, we are left to assume that evolution can occur in the wild.

[kleinman]

Since life is not extinct and we are all in the presence of continual multiple selection pressures, than this theory must be wrong.
Wrong conclusion can’t brain, mutation and selection is far too slow to accomplish what you allege, and why is mutation and selection such a slow process, multiple selection pressures slow the process. That’s what the mathematics of mutation and selection shows and that is what the empirical evidence shows. Now if you can show a real example of multiple selection pressures accelerating evolution, then you would have an argument.
However, let's consider all of the data you have presented:
If we can't halt evolution (over a matter of years) by purposefully selecting the most difficult pressures, what hope do you have that elements in the wild can do it?
Ok, can’t brain, tell us what the selection pressure(s) is/are that would transform a reptile into a bird. By the way, I posted a citation where evolution has been halted for about 20 years by multiple selection pressures and resistance to these selection pressures are seen only in the lab by subjecting the target pest to fewer selection pressures in a sequential manner. Do you remember that citation?
This statement cuts at the heart of your argument. Even when we try, we haven't stopped the evolutionary process. We may be able to one day, but that takes design. Since there isn't "something" at every spot throughout our world designing multiple selection pressures to stop evolution, we are left to assume that evolution can occur in the wild.
Can’t brain, tell us how many selection pressures it takes to transform a reptile into a bird?

[joobz]

Wrong conclusion can’t brain, mutation and selection is far too slow to accomplish what you allege, and why is mutation and selection such a slow process, multiple selection pressures slow the process. That’s what the mathematics of mutation and selection shows and that is what the empirical evidence shows. Now if you can show a real example of multiple selection pressures accelerating evolution, then you would have an argument.

Ok, can’t brain, tell us what the selection pressure(s) is/are that would transform a reptile into a bird. By the way, I posted a citation where evolution has been halted for about 20 years by multiple selection pressures and resistance to these selection pressures are seen only in the lab by subjecting the target pest to fewer selection pressures in a sequential manner. Do you remember that citation?

Can’t brain, tell us how many selection pressures it takes to transform a reptile into a bird?
Evolutionary theory explains quite nicely what all evidence has shown. And 20 years isn't a very long time compared to a millions that this process has been working on. Regardless, evolutionary theory predicts that some situations will result in a halted/arrested evolutionary form. Nothing really suprising.

What we are discussing is your Multiple selection pressure theory which predicts the stopping of ALL of evolution:

If we can't halt evolution (over a matter of years) by purposefully selecting the most difficult pressures, what hope do you have that elements in the wild can do it?

This statement cuts at the heart of your argument. Even when we try, we haven't stopped the evolutionary process. We may be able to one day, but that takes design. Since there isn't "something" at every spot throughout our world designing multiple selection pressures to stop evolution, we are left to assume that evolution can occur in the wild.

[kjkent1]

Let’s all talk about lita’ gators 10^500 alternative universes that rational. Lita’ gator would make a good censor in a dictatorial regime.

What lita’ gator doesn’t realize is that I was invited by Paul to discuss this issue on this forum, who invited you to discuss your string cheese theory of evolution.1. What's irrational about string theory Alan? Lots of very credible and well-respected scientist find the theory worthy of considerable resource investment. Who are you, sitting in your office at Clovis, Ca. Urgent Care, to proclaim string theory irrational?
2. While you may have invited Paul to discuss ev here, Paul is nevertheless the forum moderator, so he controls what appears on the thread. Thus, my comments with regard to him reigning you in are entirely appropriate.
3. You are not discussing ev in isolation anymore, and you haven't for a long time. You are posting a string of citations to papers that discuss methods of preventing the spread of disease by means of multiple artificial suppressive therapies, and you are suggesting that this proves that natural evolution cannot take place because natural selective pressures are equally hostile to life as are the artificial therapies.

The trivially simple response to your theory is that whenever a natural environment is as hostile to an organism as is your various cited multiple artificial therapies, the result is that the organism goes extinct, unless it happens to avoid extinction via some unexpected evolved advantage. Which, in case you haven't noticed, is EXACTLY what occurs in all of your cited studies. Despite the fact that there are so many different therapies proposed for HIV, HIV consistently escapes our artificial selection traps and survives to infect again.

This utterly disproves your theory. Unfortunately, you refuse to recognize how profoundly you blind yourself to the obvious in order to maintain your belief in your personal superiority over others.

4. As for my being a dictatorial censor, reality is that nowhere on Earth does there exist a place where rational debate takes place absent any rules. Thus, your insistence on complete freedom of expression is just another proof of your own irrationality.

[Belz...]

It seems everyone but you evolutionarians realize that multiple selection pressures slow evolution.

Actually, no, they don't.

Well, I will admit that the theory of evolution is the best-supported scientific theory since the flat earth hypothesis

Wow. That's a very mature answer.

but you might get some argument from those who think the laws of thermodynamics have a bit more of empirical support.

The laws of thermodynamics are not a scientific theory. They are fact.

Just be thankful I’m not using old English fonts, Paul had trouble reading that font.

"Just be thankful ?" Don't you want to be easier to read ?

mutation and selection is far too slow to accomplish what you allege

Evidence ? I think you just WANT it to be too slow because you have a religious agenda.

Can’t brain, tell us how many selection pressures it takes to transform a reptile into a bird?

That you even asked this question shows how little you know of evolution. How can you hope to claim better understanding than all the world's biologists if you don't know the first thing about the theory ?

[kleinman]

Evolutionary theory explains quite nicely what all evidence has shown. And 20 years isn't a very long time compared to a millions that this process has been working on. Regardless, evolutionary theory predicts that some situations will result in a halted/arrested evolutionary form. Nothing really suprising.
You are demonstrating the mathematical deficiency of the evolutionarian theory. Most of these citations that I have posted concern the evolution of microbes by mutation and selection (and in some cases recombination). These examples have huge populations, extremely rapid reproduction rates, and in the case of HIV, very high mutation rates and much shorter genomes than either reptiles or birds. When you are talking about the delay in evolution of HIV, you are talking about millions if not billions of generations to accomplish the evolution of only a small number of loci. When you talk about the evolution of reptiles to birds, you don’t have the huge number of generations necessary to accomplish this massive genetic transformation. Reptiles don’t reproduce at rates anywhere near those of the HIV virus. How many billions of generations do you think reptiles have lived on earth? Use your best evolutionarian numbers. Then look at the differences in reptile and bird genomes and try to do the bookkeeping to accomplish the transformation of reptiles to birds. You can’t do it, it is mathematically impossible.
If we can't halt evolution (over a matter of years) by purposefully selecting the most difficult pressures, what hope do you have that elements in the wild can do it?
I have already posted an example where evolution has been stopped for years. It is commonly stopped for years in people suffering from HIV which is the most extreme case of mutation and selection (and recombination) with its high mutation rate, huge populations, high reproductive rate and short genome. So much for your proposal that evolution can’t be stopped, evolution is commonly stopped by using multiple selection pressures.
This statement cuts at the heart of your argument. Even when we try, we haven't stopped the evolutionary process. We may be able to one day, but that takes design. Since there isn't "something" at every spot throughout our world designing multiple selection pressures to stop evolution, we are left to assume that evolution can occur in the wild.
In your dreams can’t brain. You can’t extrapolate from the reality of how evolution works by mutation and selection with microbes which shows that multiple selection pressures slow and ultimately stop the process to reptiles which evolve into birds. You have too large a genome, too few numbers of generations, insufficient reproductive rates and too small populations to accomplish the transformation. If that is not enough, you have no selection pressures that would accomplish such a transformation. You theory is suitable for the Scifi channel but not for hard mathematical science.
As for my being a dictatorial censor, reality is that nowhere on Earth does there exist a place where rational debate takes place absent any rules. Thus, your insistence on complete freedom of expression is just another proof of your own irrationality.
Since when was your string cheese theory of evolution rational debate? I think you should continue to make your case for this brilliant piece of logic. Why don’t you post some evidence of your 10^500 alternative universes?
It seems everyone but you evolutionarians realize that multiple selection pressures slow evolution.Actually, no, they don't.
Well then, those who don’t should look at all the empirical evidence how multiple selection pressures slow evolution. This is why combination therapy is used to treat HIV, this is why combination therapy is used to treat TB, this is why combination therapy should have been used to treat Gonorrhea, this is why combination therapy should have been used to treat MRSA, this is why combination therapy is being used to treat Malaria, this is why combination therapy should be used to treat influenza, this is why combination therapy is used to treat cancer…
Well, I will admit that the theory of evolution is the best-supported scientific theory since the flat earth hypothesis Wow. That's a very mature answer.
It’s clear that the mathematics of mutation and selection and the empirical evidence of mutation and selection doesn’t support the mushy soft theory of evolution.
but you might get some argument from those who think the laws of thermodynamics have a bit more of empirical support.The laws of thermodynamics are not a scientific theory. They are fact.
Wrong Belz, the laws of thermodynamics may be very useful for predicting the behavior of things but it is still theory. It just happens to be a much better theory than the theory of evolution.
Just be thankful I’m not using old English fonts, Paul had trouble reading that font. "Just be thankful ?" Don't you want to be easier to read ?
A couple of posts back, can’t brain thanked me for using the red text, I guess you just can’t make everyone happy.
mutation and selection is far too slow to accomplish what you allege.Evidence ? I think you just WANT it to be too slow because you have a religious agenda.
It doesn’t matter whether I have a religious agenda or not. Unless mathematics works different for you and I, it doesn’t matter. The reason why I say mutation and selection works so slowly is based on the evolutionist written, peer reviewed and published mathematical model of mutation and selection. Try the model out yourself and see what it shows. You can then ask yourself why is the convergence of the model so slow? You will find out that it converges so slowly because of the multiple selection conditions used in the model. This phenomenon is seen empirically as shown by the numerous citations I have posted and will continue to post.
Can’t brain, tell us how many selection pressures it takes to transform a reptile into a bird? That you even asked this question shows how little you know of evolution. How can you hope to claim better understanding than all the world's biologists if you don't know the first thing about the theory ?
I assure you that I know something about the mathematic of mutation and selection, I studied the evolutionist written a peer reviewed model of the process. If you understood the ev model, you would ask the same question. What is the selection pressure that would turn a reptile into a bird? It is really a dumb notion that has overtaken the field of biology.

[Paul C. Anagnostopoulos]

Why should I stop saying this?
I just explained why:

Alan, you gotta stop saying this. If multiple pressures slow and stop evolution, then evolution would never have gotten started to begin with, since there are always multiple pressures. If it had never gotten started to begin with, then there would be no chance for it to be slowed and stopped. Your argument shoots itself in the foot from the get-go.

~~ Paul

[joobz]

You are demonstrating the mathematical deficiency of the evolutionarian theory. Most of these citations that I have posted concern the evolution of microbes by mutation and selection (and in some cases recombination). These examples have huge populations, extremely rapid reproduction rates, and in the case of HIV, very high mutation rates and much shorter genomes than either reptiles or birds. When you are talking about the delay in evolution of HIV, you are talking about millions if not billions of generations to accomplish the evolution of only a small number of loci. When you talk about the evolution of reptiles to birds, you don’t have the huge number of generations necessary to accomplish this massive genetic transformation. Reptiles don’t reproduce at rates anywhere near those of the HIV virus. How many billions of generations do you think reptiles have lived on earth? Use your best evolutionarian numbers. Then look at the differences in reptile and bird genomes and try to do the bookkeeping to accomplish the transformation of reptiles to birds. You can’t do it, it is mathematically impossible.

I have already posted an example where evolution has been stopped for years. It is commonly stopped for years in people suffering from HIV which is the most extreme case of mutation and selection (and recombination) with its high mutation rate, huge populations, high reproductive rate and short genome. So much for your proposal that evolution can’t be stopped, evolution is commonly stopped by using multiple selection pressures.

In your dreams can’t brain. You can’t extrapolate from the reality of how evolution works by mutation and selection with microbes which shows that multiple selection pressures slow and ultimately stop the process to reptiles which evolve into birds. You have too large a genome, too few numbers of generations, insufficient reproductive rates and too small populations to accomplish the transformation. If that is not enough, you have no selection pressures that would accomplish such a transformation. You theory is suitable for the Scifi channel but not for hard mathematical science.

Since when was your string cheese theory of evolution rational debate? I think you should continue to make your case for this brilliant piece of logic. Why don’t you post some evidence of your 10^500 alternative universes?

Well then, those who don’t should look at all the empirical evidence how multiple selection pressures slow evolution. This is why combination therapy is used to treat HIV, this is why combination therapy is used to treat TB, this is why combination therapy should have been used to treat Gonorrhea, this is why combination therapy should have been used to treat MRSA, this is why combination therapy is being used to treat Malaria, this is why combination therapy should be used to treat influenza, this is why combination therapy is used to treat cancer…

It’s clear that the mathematics of mutation and selection and the empirical evidence of mutation and selection doesn’t support the mushy soft theory of evolution.

Wrong Belz, the laws of thermodynamics may be very useful for predicting the behavior of things but it is still theory. It just happens to be a much better theory than the theory of evolution.

A couple of posts back, can’t brain thanked me for using the red text, I guess you just can’t make everyone happy.

It doesn’t matter whether I have a religious agenda or not. Unless mathematics works different for you and I, it doesn’t matter. The reason why I say mutation and selection works so slowly is based on the evolutionist written, peer reviewed and published mathematical model of mutation and selection. Try the model out yourself and see what it shows. You can then ask yourself why is the convergence of the model so slow? You will find out that it converges so slowly because of the multiple selection conditions used in the model. This phenomenon is seen empirically as shown by the numerous citations I have posted and will continue to post.

I assure you that I know something about the mathematic of mutation and selection, I studied the evolutionist written a peer reviewed model of the process. If you understood the ev model, you would ask the same question. What is the selection pressure that would turn a reptile into a bird? It is really a dumb notion that has overtaken the field of biology.

you have only presented data that shows under very specific conditions, emergence can be slowed. This is nothing new or unsuprising. Indeed, it all leads to the following question:

If we can't halt evolution (over a matter of years) by purposefully selecting the most difficult pressures, what hope do you have that elements in the wild can do it?

This statement cuts at the heart of your argument. Even when we try, we haven't stopped the evolutionary process. We may be able to one day, but that takes design. Since there isn't "something" at every spot throughout our world designing multiple selection pressures to stop evolution, we are left to assume that evolution can occur in the wild.

[Paul C. Anagnostopoulos]

With due respect, you allow Kleinman to control this thread. If you don't force him to argue rationally, then he will rely on his ridiculous talismen and the thread will just wander aimlessly.
I've long since given up hoping for a rational argument. But see my previous post.

~~ Paul

[kjkent1]

I've long since given up hoping for a rational argument. But see my previous post.

~~ PaulYeah. Kleinman insists that no one but he understands genetics, biology, taxonomy, mathematics, religion, physics, engineering, etc.

I wonder if it's ever occurred to Alan, than not one single person here buys into his analysis. And, not a single other creationist has appeared here in all this time to defend Kleinman's conclusions.

So what we have is on one side: Kleinman. And, on the other: everybody else.

The conclusion of this circumstantial evidence is inescapable (cue Twilight Zone theme music).

[Kotatsu]

Now what are you whining about? Do you feel neglected?

Yes. However, if it is because I've not been very active in this thread for a while, I can accept it. For now.

Here come the asterisks again.

Yeah, you're not really worth risking suspension for...

Is that your attempt to explain how mutation and selection actually works?

If this is my entry ticket to Nickname Land, then my answer is yes. Yes, despite what it looks like, I do attempt to explain how mutation and selection actually works by not mentioning either term.

Finally, an evolutionarian who is going to try to show examples of multiple selection pressures accelerating evolution.

Not at all, which will be clear as you continue reading through this post.

This is typical of the mushy soft science of the theory of evolution. What are the selection pressures that the limpets are subjected too and what are the genetic changes that you propose occurred. How do you differentiate these changes in limpet by recombination and selection versus mutation and selection? This example is more analogous to dog breeding (recombination and selection) than mutation and selection.

Except that it doesn't involve any breeding.

Also, the selection pressures relevant to the study I cited involve:
- Predation by crabs
- Predation by birds that try to pry the limpet shells open
- Predation by birds that try to open the limpet shells by lateral crushing.

It is the last pressure that differs between the populations.

I do not differentiate between those "changes in limpet by recombination and selection versus mutation and selection", since doing so serves no practical purpose with regards to what I actually contend. As you make this mistake repeatedly throughout your post, you will find several more detail justifications below.

If you want dogs with better hearing, breed those animals with the best hearing. This is another example of recombination and selection. Where are the multiple selection pressures which accelerate evolution?

Indeed, all of these examples involve recombination and selection. Why is that a problem? Both are phenomena that occur in natural populations, and which "evolutionarians" have repeatedly claimed to have an influence on whether or not evolution occurs, and, if it does, at what speed this happens. I can see no reason except idiocy to disqualify these examples because they do not fit a certain narrow subset of the possibilities we may utilize to explain evolution.

The multiple selection pressures relevant to the study is the presence or absence of allotonic moths which catch their prey using another method than the frequency-matched bats. When both kinds of bats are present, moths, in order to survive, will need to look out for different kinds of predators. In at least some places, this has been accomplished by the evolution of what the authors described as an "external hearing aid". Thus, addition of another selection pressure did not slow evolution down, but rather resulted in a more derived structure, which is usually seen as evidence for the continuance of evolution.

Don’t give it to us in your words; post the authors statements which show that multiple selection pressures accelerate evolution. What happens when the heavy metal exposure is performed sequentially versus simultaneous exposure to the heavy metals?

You have failed to note my initial statements to the effect that:
1) I have so far only read the abstracts and skimmed the rest;
2) These examples do not necessarily state that the rate of evolution is accelerated, but show that it at least does not slow down and "ultimately stop".
My contention is not necessarily that Dr. Adequate is correct when he claims that evolution is accelerated when more selection pressures are added, but rather that you are wrong when you claim that it is decelerated and, in particular, when you claim that it will ultimately stop. If or when I find papers claiming that acceleration has occurred, this contention may change.

Again you post in your own words an example of recombination and natural selection. These bugs have beaks? I thought bugs had proboses. No matter, if you want to lengthen the beak or proboscis on a creature rapidly, do it by recombination and natural selection. Let the creatures with the longest beaks or proboses breed and you will rapidly get offspring with longer beaks or proboses.

The usage of the term "beak" for these structures comes from the article; it is not my invention. Presumably this is established terminology among entomologists working with, at least, these kinds of bugs. I do not pretend to know enough about the morphology of these bugs to use another term.

And, again, I feel quite certain that recombination and selection is involved. In this, you are correct. However, the point is moot. I dispute your statement that multiple selection pressures slow and ultimately stop evolution. If addition of selection pressures don't show this, I see no reason to discard these studies because of the mode with which the variation selected on came to be.

It’s a really slow start, you give examples of recombination and selection, not mutation and selection and you fail to define the selection pressures and genetic changes that occur. But, you have done nothing to be ashamed of, Stephen Gould made the same error when he postulated the hypothesis of punctuated equilibrium. Gould confused mutation and selection with recombination and natural selection. If you apply recombination and natural selection to Gould’s hypothesis, you get your mathematics right, but if you try to apply mutation and natural selection to the hypothesis, it is mathematically impossible.

I thought we were discussing the real world, in which evolution utilizes not only (random point) mutation, but a vast array of different methods, including recombination. Do you have a basis for disqualifying these studies apart from peevishness?

If addition of selection pressures does not slow and ultimately stop evolution, even though --- and this should not be interpreted as an admission that you are correct in your assertion --- mutation and selection as implemented in ev shows this to be the most likely outcome, this is testimony only of that ev is not an adequate model of all the ways in which evolution may work.

This was pointed out to you over 100 pages ago as well.

A question:
Will you allow as counter-examples for your claim that multiple selection pressures will slow and ultimately stop evolution only those where it can be show (by some means) that random point mutation was the only mechanism operating on the evolution of the organism at the time?

[Kotatsu]

Can’t brain, I appreciate you combining your errors into a single sentence; it makes it much more efficient to respond.

Sadly, though, the usefulness of your response stays the same.

[Kotatsu]

Ok, can’t brain, tell us what the selection pressure(s) is/are that would transform a reptile into a bird.

I trust you will not protest too much if someone else responds (and maybe this has already happened, because I seem to recall this is not the first time you have asked this), but off the top of my head, I could think of several, including (note that these are not necessarily pressures that did "transform a reptile into a bird", but rather ones which could):

1. Intense predation at ground-level inviting the reptile into trees, where flight would be an aid in locomotion and escape from arboreal predators. this also includes pressures for aiding in the escape of ground-bound reptiles from ground-bound predators;
2. Intense competition for food at ground-level, inviting reptile to adopt an tree-based life where, again, flight could be useful;
3. This is especially true if the reptile eats mainly insects, which could already fly;
4. Intense competition for nest spaces at ground level, inviting reptiles to take to the trees, between which it may be easier to fly than to jump;
5. Utilization of nest sites at less accessible areas while remaining essentially ground-bound;
6. The need for an easy mode of locomotion at tree-to-tree level regardless of if the reptile is tree-bound or not;
7. Escape from parasitism by attempting not to mix with potentially infected populations at ground-level;
8. Thermoregulatory pressures, including climate change and annual or spatial variations in temperature;
9. Sexual selection by females prejudiced for colourful displays, leading to enlargement of scales, which would expand the area usable for these displays;
10. Development of feathers as an aid to seeming bigger in courtship fights (this may overlap with 8 above);
11. Utilization of fish as a food source in areas of water bodies not accessible from land;
12. "Arms race" with food sources which develop harder and harder shells or covers, inducing the need for a beak;
13. "Arms race" with other individuals resulting in a more beak-like structures used in courtship fights or displays;
14. "Arms race" with prey hiding in for example hollow areas in the bark of trees, requiring a beak or beak-like structure to extract them;
15. Potentially greater success at escaping from a predator by having a cover of non-edible structures around your body (i.e., the predator bites you but only get a mouthful of feathers);
16. Greater efficiency of keeping an even temperature for eggs and nestlings;
17. Greater efficiency of balancing when hunting.

From the mundane to the fanciful, these are some of the pressures that, alone or in any combination, could "transform" (by which at least I mean evolve) reptiles into birds.

[Kotatsu]

I have already posted an example where evolution has been stopped for years.

English isn't my first language (as some of you may have gathered), but if something is stopped, and then starts up again after a while, isn't this called "slowed" or "delayed" rather than "stopped"?

[Kotatsu]

I wonder if it's ever occurred to Alan, than not one single person here buys into his analysis. And, not a single other creationist has appeared here in all this time to defend Kleinman's conclusions.

So what we have is on one side: Kleinman. And, on the other: everybody else.


What about Hammegk? I can't really remember what he was talking about when he participated in this thread, but I don't think Id say he was on our side.

[Herzblut]

Yeah. Kleinman insists that no one but he understands genetics, biology, taxonomy, mathematics, religion, physics, engineering, etc.

I wonder if it's ever occurred to Alan, than not one single person here buys into his analysis. And, not a single other creationist has appeared here in all this time to defend Kleinman's conclusions.

So what we have is on one side: Kleinman. And, on the other: everybody else.

Sorry to jump in.

But that is why I wonder how this kind of thread could grow out of proportion.

I mean, any creator based theory is non-scientific per se. Also, evolution research
is progressed outside of Internet forums like this one. Legitimate criticism is taken
care of in the labs, illegitimate rubbish is ignored.

Thus, from a science perspective there is not much need for putting excessive efforts
into such a painful discussion. What purpose does is serve? Education? For whom?

Herzblut

[Apathia]

What about Hammegk? I can't really remember what he was talking about when he participated in this thread, but I don't think Id say he was on our side.

Hammy was always on his own side. His comments in this thread showed a very poor understanding of Natural Selection, but that may have been for drama's sake.

BTW, Dr. Klienman has more than fulfilled the purpose he stated in his first post in this thread.

Originally Posted by Paul
Sometimes these annoying creationists just piss me off:

One of the reasons Paul says this is that he believes when I quote him, I twist his words, so a figure I may as well start twisting.

He has certainly played the role of the "Annoying Creationist."
it has passed beyond the realm of the peer testing of ideas to a circus of insults.

This is the most sucessful trolling thread I've seen on these boards.

[Paul C. Anagnostopoulos]

Thus, from a science perspective there is not much need for putting excessive efforts into such a painful discussion. What purpose does is serve? Education? For whom?
I've learned a lot from this thread and I think others would agree. I have received PMs from evolution newbies telling me that they have learned much about evolution.

I think you had to be here all along. :D


This is the most sucessful trolling thread I've seen on these boards.
I believe a troll is someone who posts inflammatory messages about sensitive topics with no intention of discussing them. Kleinman has every intention of discussing this topic, as the length of this thread demonstrates. I do not believe Kleinman is a troll.

~~ Paul

[joobz]

Sorry to jump in.

But that is why I wonder how this kind of thread could grow out of proportion.

I mean, any creator based theory is non-scientific per se. Also, evolution research
is progressed outside of Internet forums like this one. Legitimate criticism is taken
care of in the labs, illegitimate rubbish is ignored.

Thus, from a science perspective there is not much need for putting excessive efforts
into such a painful discussion. What purpose does is serve? Education? For whom?

Herzblut
Actually, I found this a great place to cut my teeth as it were.
Kleinman makes an easy punching bag.

[CapelDodger]

Kleinman makes an easy punching bag.

At 122 one-sided pages it surely earns an endorsement as "unbreakable".

[joobz]

At 122 one-sided pages it surely earns an endorsement as "unbreakable".
True..
Let me rephrase, a punching bag that doesn't lose his stuffing.

[Mr. Scott]

I got it!

Dr. Kleinman is arguing about evolution to get his mind off the malpractice lawsuit (publicly posted on the Internet) filed against him by Dennis Powell. The summary judgement granted to Kleinman was reversed May 23, 2007. Later the very day of that disappointing ruling against him, Dr. Kleinman posted:


Too bad that so called evidence doesn’t have any mathematical basis and the mathematics of mutation and selection says that macroevolution can not happen. And there are numerous real examples of this mathematics. What the theory of evolution has is a collection of twisted and concocted interpretations of the evidence. Dr Schneider’s ev model shows how mutation and selection really works and it doesn’t evolve reptiles into birds. Maybe something new will emerge from the theory of evolution that will change this mathematical fact that multiple selection pressures slow and ultimately stops evolution, but I doubt it. Taffer, why don’t you give us a real example of multiple selection pressures accelerating evolution?

The Internet sure is a good place to vent rage. I wonder if Dr. Kleinman uses clinic computers to run Ev simulations and submit his annoying creationist macros to the forum.

[cyborg]

Well I can't say I'm surprised - it certainly only serves to make kleinman an even more pathetic character than he already is.

[kleinman]

Hey, I forgot to wish you all a happy and joyous Fourth of July!
Why should I stop saying this?I just explained why:

Alan, you gotta stop saying this. If multiple pressures slow and stop evolution, then evolution would never have gotten started to begin with, since there are always multiple pressures. If it had never gotten started to begin with, then there would be no chance for it to be slowed and stopped. Your argument shoots itself in the foot from the get-go.
Your right Paul, evolution never started it all, of course neither did abiogenesis.
you have only presented data that shows under very specific conditions, emergence can be slowed. This is nothing new or unsuprising. Indeed, it all leads to the following question:
Ev does not model special or unique conditions and the citations I have posted cover wide areas of science and medicine.
If we can't halt evolution (over a matter of years) by purposefully selecting the most difficult pressures, what hope do you have that elements in the wild can do it?
Can’t brain, the point you are missing is that even if evolution isn’t completely stopped, it is slowed so profoundly that it makes the theory of evolution mathematically impossible.
This statement cuts at the heart of your argument. Even when we try, we haven't stopped the evolutionary process. We may be able to one day, but that takes design. Since there isn't "something" at every spot throughout our world designing multiple selection pressures to stop evolution, we are left to assume that evolution can occur in the wild.
The only thing cut to the heart is the fundamental premise of the theory of evolution. Mutation and selection can’t do it, evolution didn’t do it.
With due respect, you allow Kleinman to control this thread. If you don't force him to argue rationally, then he will rely on his ridiculous talismen and the thread will just wander aimlessly.
I've long since given up hoping for a rational argument. But see my previous post.
Come on Paul, let’s have a discussion about lita’ gator’s 10^500 alternative universes, isn’t that rational?
I wonder if it's ever occurred to Alan, than not one single person here buys into his analysis. And, not a single other creationist has appeared here in all this time to defend Kleinman's conclusions.
It’s a lonely life being an iconoclast but somebody has to do it. Hey, where are all your defenders to your 10^500 alternative universes?
Now what are you whining about? Do you feel neglected?Yes. However, if it is because I've not been very active in this thread for a while, I can accept it. For now.
I’ll try to pay more attention to you, we don’t want anyone’s feeling hurt on this thread.
Here come the asterisks again.Yeah, you're not really worth risking suspension for...
Whatever you do, do not use the forbidden punctuation marks.
Is that your attempt to explain how mutation and selection actually works?If this is my entry ticket to Nickname Land, then my answer is yes. Yes, despite what it looks like, I do attempt to explain how mutation and selection actually works by not mentioning either term.
Not yet, if it’s any help, cheese wiz earn his nickname by making an entire post with the word cheese.
Finally, an evolutionarian who is going to try to show examples of multiple selection pressures accelerating evolution.Not at all, which will be clear as you continue reading through this post.
You evolutionarians are always clear, except when you are not which is most of the time. That’s what happens when you try to fit reality to a mathematically impossible theory.
This is typical of the mushy soft science of the theory of evolution. What are the selection pressures that the limpets are subjected too and what are the genetic changes that you propose occurred. How do you differentiate these changes in limpet by recombination and selection versus mutation and selection? This example is more analogous to dog breeding (recombination and selection) than mutation and selection.Except that it doesn't involve any breeding.
However limpets reproduce sexually and you have recombination and selection. Isn’t population genetics your area? If it is, you should know that the Hardy-Weinberg equilibrium is shifted by selection.
Also, the selection pressures relevant to the study I cited involve:
- Predation by crabs
- Predation by birds that try to pry the limpet shells open
- Predation by birds that try to open the limpet shells by lateral crushing.

It is the last pressure that differs between the populations.
If you think that the limpet population is going to respond rapidly to these selection pressures by mutation and selection rather than recombination and selection, you don’t understand how slowly mutation and selection occurs.
I do not differentiate between those "changes in limpet by recombination and selection versus mutation and selection", since doing so serves no practical purpose with regards to what I actually contend. As you make this mistake repeatedly throughout your post, you will find several more detail justifications below.
There is a huge difference between recombination and selection and mutation and selection. In the former case you are selecting alleles in the later case you selecting mutations.
If you want dogs with better hearing, breed those animals with the best hearing. This is another example of recombination and selection. Where are the multiple selection pressures which accelerate evolution?Indeed, all of these examples involve recombination and selection. Why is that a problem? Both are phenomena that occur in natural populations, and which "evolutionarians" have repeatedly claimed to have an influence on whether or not evolution occurs, and, if it does, at what speed this happens. I can see no reason except idiocy to disqualify these examples because they do not fit a certain narrow subset of the possibilities we may utilize to explain evolution.
Are you proposing that reptiles evolved to birds by recombination and selection? Recombination without error can not increase information in the gene pool while recombination with selection can cause the loss of information (alleles) from the gene pool. You need errors in order to increase information in the gene pool and ev shows this process to be profoundly slow. However, you can change the morphology of the limpet population very quickly by recombination and selection. This is what Gould’s postulate for punctuated equilibrium is all about. If you get a couple of limpets that have beneficial characteristics and they happen to breed and improve on those characteristics, you get the improvement in a single generation. This can happen very quickly with a small subpopulation.
The multiple selection pressures relevant to the study is the presence or absence of allotonic moths which catch their prey using another method than the frequency-matched bats. When both kinds of bats are present, moths, in order to survive, will need to look out for different kinds of predators. In at least some places, this has been accomplished by the evolution of what the authors described as an "external hearing aid". Thus, addition of another selection pressure did not slow evolution down, but rather resulted in a more derived structure, which is usually seen as evidence for the continuance of evolution.
This is such a contorted story, how can you tell what is occurring by mutation and selection and what is occurring by recombination and selection?
Don’t give it to us in your words; post the authors statements which show that multiple selection pressures accelerate evolution. What happens when the heavy metal exposure is performed sequentially versus simultaneous exposure to the heavy metals?You have failed to note my initial statements to the effect that:
1) I have so far only read the abstracts and skimmed the rest;
2) These examples do not necessarily state that the rate of evolution is accelerated, but show that it at least does not slow down and "ultimately stop".
My contention is not necessarily that Dr. Adequate is correct when he claims that evolution is accelerated when more selection pressures are added, but rather that you are wrong when you claim that it is decelerated and, in particular, when you claim that it will ultimately stop. If or when I find papers claiming that acceleration has occurred, this contention may change.
If you are talking about recombination and selection, you might be able to get more rapid microevolutionary changes such as selecting for longer legs and longer fur simultaneously but you can’t carry that over to random mutation and natural selection. This is a big problem you evolutionarians have, you think the mathematics of mutation and selection is the same as the mathematics of recombination and selection. It isn’t, one is selecting for mutations and the other is selecting for alleles. In addition, you are still having a hard time understanding that recombination without error can not increase information in the gene pool (it can not create new alleles) and recombination with selection can cause the loss of information (alleles) from the gene pool. Without errors in the construction of a gene, there is no possible way to increase information in the gene pool. This is what ev is modeling for random point mutations and selection and it is a profoundly slow process. It takes huge numbers of generations to accumulate the information and if you impose extra selection pressures, it slows the process down. This is exactly what we see in all the citations I have been posting (including the HIV example which includes recombination).
Again you post in your own words an example of recombination and natural selection. These bugs have beaks? I thought bugs had proboses. No matter, if you want to lengthen the beak or proboscis on a creature rapidly, do it by recombination and natural selection. Let the creatures with the longest beaks or proboses breed and you will rapidly get offspring with longer beaks or proboses. The usage of the term "beak" for these structures comes from the article; it is not my invention. Presumably this is established terminology among entomologists working with, at least, these kinds of bugs. I do not pretend to know enough about the morphology of these bugs to use another term.
ok
And, again, I feel quite certain that recombination and selection is involved. In this, you are correct. However, the point is moot. I dispute your statement that multiple selection pressures slow and ultimately stop evolution. If addition of selection pressures don't show this, I see no reason to discard these studies because of the mode with which the variation selected on came to be.
You need errors and selection to increase information in the gene pool. I think you are going to back yourself into a corner if you are going to content that recombination and selection is how reptiles evolved into birds.
It’s a really slow start, you give examples of recombination and selection, not mutation and selection and you fail to define the selection pressures and genetic changes that occur. But, you have done nothing to be ashamed of, Stephen Gould made the same error when he postulated the hypothesis of punctuated equilibrium. Gould confused mutation and selection with recombination and natural selection. If you apply recombination and natural selection to Gould’s hypothesis, you get your mathematics right, but if you try to apply mutation and natural selection to the hypothesis, it is mathematically impossible.I thought we were discussing the real world, in which evolution utilizes not only (random point) mutation, but a vast array of different methods, including recombination. Do you have a basis for disqualifying these studies apart from peevishness?
Ok, tell us how recombination increases information in the gene pool?
If addition of selection pressures does not slow and ultimately stop evolution, even though --- and this should not be interpreted as an admission that you are correct in your assertion --- mutation and selection as implemented in ev shows this to be the most likely outcome, this is testimony only of that ev is not an adequate model of all the ways in which evolution may work.
Then why has it been so easy to find numerous examples of how multiple selection pressures slow evolution? Even the evolution of HIV with recombination is slowed by multiple selection pressures. You need to work on being able to distinguish between mutation and selection and recombination and selection. The former is a very slow process for increasing information in the gene pool and the later is a very rapid process that can change the morphology of a population in a small number of generations. The former requires large populations with high reproductive rates to accumulate information and the later can accomplish large morphological changes with a small population in a relatively few generations.
This was pointed out to you over 100 pages ago as well.
The only thing you are pointing out here is that you can’t tell the difference between mutation and selection and recombination and selection.
A question:
Will you allow as counter-examples for your claim that multiple selection pressures will slow and ultimately stop evolution only those where it can be show (by some means) that random point mutation was the only mechanism operating on the evolution of the organism at the time?
I’m not a moderator on this thread, say what ever you want. If you want to say limpets evolve to limpets and moths evolve to moths, I’m not sure what your point is. If you are going to contend that recombination increases information in the gene pool, I’m going to ask you how.
Ok, can’t brain, tell us what the selection pressure(s) is/are that would transform a reptile into a bird.I trust you will not protest too much if someone else responds (and maybe this has already happened, because I seem to recall this is not the first time you have asked this), but off the top of my head, I could think of several, including (note that these are not necessarily pressures that did "transform a reptile into a bird", but rather ones which could):
Why is this an off limits question to you evolutionarians?
1. Intense predation at ground-level inviting the reptile into trees, where flight would be an aid in locomotion and escape from arboreal predators. this also includes pressures for aiding in the escape of ground-bound reptiles from ground-bound predators;
2. Intense competition for food at ground-level, inviting reptile to adopt an tree-based life where, again, flight could be useful;
3. This is especially true if the reptile eats mainly insects, which could already fly;
4. Intense competition for nest spaces at ground level, inviting reptiles to take to the trees, between which it may be easier to fly than to jump;
5. Utilization of nest sites at less accessible areas while remaining essentially ground-bound;
6. The need for an easy mode of locomotion at tree-to-tree level regardless of if the reptile is tree-bound or not;
7. Escape from parasitism by attempting not to mix with potentially infected populations at ground-level;
8. Thermoregulatory pressures, including climate change and annual or spatial variations in temperature;
9. Sexual selection by females prejudiced for colourful displays, leading to enlargement of scales, which would expand the area usable for these displays;
10. Development of feathers as an aid to seeming bigger in courtship fights (this may overlap with 8 above);
11. Utilization of fish as a food source in areas of water bodies not accessible from land;
12. "Arms race" with food sources which develop harder and harder shells or covers, inducing the need for a beak;
13. "Arms race" with other individuals resulting in a more beak-like structures used in courtship fights or displays;
14. "Arms race" with prey hiding in for example hollow areas in the bark of trees, requiring a beak or beak-like structure to extract them;
15. Potentially greater success at escaping from a predator by having a cover of non-edible structures around your body (i.e., the predator bites you but only get a mouthful of feathers);
16. Greater efficiency of keeping an even temperature for eggs and nestlings;
17. Greater efficiency of balancing when hunting.
This is all a very nice list but you have a bookkeeping problem. How do you account for the huge number of genetic differences between reptiles and birds? Are you going to suggest that recombination accounts for these differences? If not, then you are left with mutation and selection and this is a profoundly slow process where multiple selection pressures interfere with the process. This is why I think you should study ev to get a sense how slow the mutation and selection process actual is. It also would help you to make sense of why multiple selection pressures is so useful in the treatment of diseases and cancer for preventing the evolution of resistant strains. Learn to distinguish between recombination and selection and mutation and selection. They work differently.
From the mundane to the fanciful, these are some of the pressures that, alone or in any combination, could "transform" (by which at least I mean evolve) reptiles into birds.
Or more reasonably would explain why a reptile would climb in a tree, or migrate, or breed with another reptile that has beneficial traits, but to grow feathers, beak and wings is a strange extrapolation in the face of the huge genetic differences between the two animals.
I have already posted an example where evolution has been stopped for years. English isn't my first language (as some of you may have gathered), but if something is stopped, and then starts up again after a while, isn't this called "slowed" or "delayed" rather than "stopped"?
Your English is fine, your understanding of the mathematics of mutation and selection needs work, can’t brain tries to make the same argument. The problem for adherents to the theory of evolution is that multiple selection pressures so profoundly slow the rate of information acquisition by mutation and selection that it makes the theory mathematically impossible.
But that is why I wonder how this kind of thread could grow out of proportion.
Just what is the proper proportion for this thread?
Thus, from a science perspective there is not much need for putting excessive efforts
into such a painful discussion. What purpose does is serve? Education? For whom?
Maybe evolutionarians just enjoy pain. Now from a mathematical and scientific perspective, see the citation below which shows that multiple selection pressures slow evolution.
BTW, Dr. Klienman has more than fulfilled the purpose he stated in his first post in this thread.
You evolutionarians do get annoyed by mathematics, especially when it is backed up by empirical evidence.
He has certainly played the role of the "Annoying Creationist."
it has passed beyond the realm of the peer testing of ideas to a circus of insults.
You evolutionarians are so stuck in your doctrine that anyone who dare challenge it is making an insult, so stop whining and look at what the mathematics is showing and the numerous real examples of this mathematics.
This is the most sucessful trolling thread I've seen on these boards.I believe a troll is someone who posts inflammatory messages about sensitive topics with no intention of discussing them. Kleinman has every intention of discussing this topic, as the length of this thread demonstrates. I do not believe Kleinman is a troll.
Yehren from the Evolutionisdead forum called me a beast, I told him to stay away from the entrance to my cave.

Now for those of you interested in how mutation and selection really works, here is another citation which shows this (again, this example is for the gang at the NCI):
http://www.haematologica.org/eha10/edu/pdf/08.2.pdf (http://www.haematologica.org/eha10/edu/pdf/08.2.pdf)
Thus, if a cell-based approach is used, known resistance mechanisms can be studied in detail and novel mechanisms of resistance can be identified for different targets using investigational compounds and clinically used drugs. This or similar screening approaches will provide data that can be translated into combination and sequential treatment strategies for a variety of rational drug targets in hematology and oncology. Specific patterns of resistance mutations can be predicted prior to their identification in patients, and critical serum concentrations can be defined that must be achieved in the clinic in order to minimize the emergence of resistance.

[joobz]

Thus, if a cell-based approach is used, known resistance mechanisms can be studied in detail and novel mechanisms of resistance can be identified for different targets using investigational compounds and clinically used drugs. This or similar screening approaches will provide data that can be translated into combination and sequential treatment strategies for a variety of rational drug targets in hematology and oncology. Specific patterns of resistance mutations can be predicted prior to their identification in patients, and critical serum concentrations can be defined that must be achieved in the clinic in order to minimize the emergence of resistance.


Do you think that there is something out in the forests, seas, air, caves.... that is going around using "cell based approaches" to "identify targets" to design pressures for selecting the "optimal combinations" to "halt evolution"?

If we can't halt evolution (over a matter of years) by purposefully selecting the most difficult pressures, what hope do you have that elements in the wild can do it?

This statement cuts at the heart of your argument. Even when we try, we haven't stopped the evolutionary process. We may be able to one day, but that takes design. Since there isn't "something" at every spot throughout our world designing multiple selection pressures to stop evolution, we are left to assume that evolution can occur in the wild.

[Apathia]

a troll is someone who posts inflammatory messages about sensitive topics with no intention of discussing them. Kleinman has every intention of discussing this topic, as the length of this thread demonstrates. I do not believe Kleinman is a troll.

~~ Paul

I recant. I wish this were a trolling thread instaed of being a serious debacle.

Kleinman wrote:
You evolutionarians are so stuck in your doctrine that anyone who dare challenge it is making an insult,

I never took your objections to the Theory of Evolution as insulting. The circus of insults I spoke of is being carried out on both sides of the aisle.
I apologise for adding another clown (myself) to the act.

[delphi_ote]

Again, Delphi, you are being very silly. Most real physical problems can only be expressed in functional notation. You don’t have a closed form algebraic expression that describes the function. In fact, every real mathematical scientific problem that I have worked on ultimately comes down to solving a functional equation which can not be expressed algebraically.
A simple "yes" would've sufficed. Or perhaps you weren't aware that mathematical proofs involving "functional equations" are not only possible, they're common. Routine, even. Necessary. A fundamental concept in many branches of mathematics. In fact, some functions (http://en.wikipedia.org/wiki/Ackermann_function) only exist because they're useful in formal proofs.

Cut the crap. Either you have a mathematical proof that evolution is mathematically impossible or you don't. Show your work or shut up.

[delphi_ote]

Is it just me?
No. Some of the rest of us in this thread are also literate.


Sadly, one of us has some obvious difficulties in that area...

[trvlr2]

Sorry to jump in.

But that is why I wonder how this kind of thread could grow out of proportion.

I mean, any creator based theory is non-scientific per se. Also, evolution research
is progressed outside of Internet forums like this one. Legitimate criticism is taken
care of in the labs, illegitimate rubbish is ignored.

Thus, from a science perspective there is not much need for putting excessive efforts
into such a painful discussion. What purpose does is serve? Education? For whom?

Herzblut



Herzblut, I wonder about the purpose ,also.
I believe it may be that some members are trying to teach a pig to fly, or, at least, to sing.

[kjkent1]

CoIt’s a lonely life being an iconoclast but somebody has to do it. Hey, where are all your defenders to your 10^500 alternative universes?I offered Dr. Susskind's theory as a means of explainng the appearance of randomness in a potentially deterministic universe. Certainly, if there is a separate universe to house the resulting future of every possible outcome, that would explain a great deal about how God may interact in the world.

If you had any sort of inquiring disposition, this sort of theory would be worthy of your interest. It would even empower a divine creator to permit randomness to his creations and yet simultaneously permit the creator the power to remain in control of all possibilities.

Instead, you ridicule the theory -- which, to me, makes you seem extraordinarily dull.

Tell me, Alan -- as a self-professed "iconoclast," do you put your money where your mouth is? That is, when a patient presents in your office with what appears to be a bacterial infection, do you follow the standard protocol, or do you prescribe a regimen of multiple antibiotics so as to slow down and ultimately halt the evolution of the bacteria?

[Kotatsu]

If you think that the limpet population is going to respond rapidly to these selection pressures by mutation and selection rather than recombination and selection, you don’t understand how slowly mutation and selection occurs.

As you make this observation several times throughout your response, I will start off by saying that for the purposes of my claim, there is no need to differentiate between variation stemming from mutation and that coming from recombination. My claim is, again, that added selection pressures do not "slow and ultimately stop" evolution, but that it's business as usual, and that it may even lead to the evolution of more derived structures. To do so, I assume all mechanisms and methods of evolution to be more or less constant in their presence or absence in the history of a certain organism, and see what happens when the load of selection pressures is increased. In all cases I have cited so far, this did not "slow and ultimately stop" evolution. This is contrary to, perhaps even the opposite of, your claim and your understanding of the 70+ examples you have posted.

Are you proposing that reptiles evolved to birds by recombination and selection?

No. In the section you quote, I am proposing that an added selection pressure in the form of a additional kind of predator using a slightly different mode of hunting in at least some cases lead to the development of more derived structures in the prey organism to directly counter these novel hunting methods.

Recombination without error can not increase information in the gene pool while recombination with selection can cause the loss of information (alleles) from the gene pool. You need errors in order to increase information in the gene pool and ev shows this process to be profoundly slow.

But in the real world, as opposed to in ev (as I understand it), these errors are not limited to random point mutation, which you seem to be exclusively focused on. Other methods for introducing an error in a genome exist, but you consistently overlook or disregard these.

This is such a contorted story, how can you tell what is occurring by mutation and selection and what is occurring by recombination and selection?

You have not yet provided me with sufficient reason to make this distinction at all with regards to what I am actually claiming (see above). Present a reasonable argument for why the origin of the variation is important which, if dismissed, would ruin my claim, and I might address it. Making the distinction between variation due to mutation and variation due to recombination for the sake of making a distinction seems a useless exercise to me.

This is a big problem you evolutionarians have, you think the mathematics of mutation and selection is the same as the mathematics of recombination and selection. It isn’t, one is selecting for mutations and the other is selecting for alleles. In addition, you are still having a hard time understanding that recombination without error can not increase information in the gene pool (it can not create new alleles) and recombination with selection can cause the loss of information (alleles) from the gene pool. Without errors in the construction of a gene, there is no possible way to increase information in the gene pool. This is what ev is modeling for random point mutations and selection and it is a profoundly slow process. It takes huge numbers of generations to accumulate the information and if you impose extra selection pressures, it slows the process down. This is exactly what we see in all the citations I have been posting (including the HIV example which includes recombination).

Again, I do not at this point feel that it would make any difference where the variation selected on comes from. And the speed of mutation in ev is irrelevant, as it is forced to limit itself to some kinds of mutations, and not all the ones which can happen to real organisms.

While certainly the use of, say, three antigens would cause a substantial portion of a germ population to diminish, I believe --- and this sort of thing has never interested me, so I may be wrong, and my choice of words is probably not optimal, but I hope you will understand anyway --- that the small percentage which do survive this multi-pressure treatment --- and in many of your cases there is such a percentage --- at least some do so because they are resistant to all the chemicals used in the treatment. This means (and here I enter the realm of speculation entirely), that the germs surviving at the end of the treatment have evolved resistance to three chemicals in the same amount of time that a germ population exposed to only one chemical would evolve resistance only to that one (in a simplistic world where we consider evolution only in terms of the resistance to man-made drugs). In essence, if I am correct in my speculation, you have disproved your own claim.

You need errors and selection to increase information in the gene pool. I think you are going to back yourself into a corner if you are going to content that recombination and selection is how reptiles evolved into birds.

I feel quite safe in claiming that recombination and selection surely must have played a part, but that it would hardly be the only factor influencing this step in evolution.

Ok, tell us how recombination increases information in the gene pool?

This is not an answer to my question. Why are only random point mutations interesting when it comes to determining how added selection pressures affect the rate of evolution?

I’m not a moderator on this thread, say what ever you want. If you want to say limpets evolve to limpets and moths evolve to moths, I’m not sure what your point is. If you are going to contend that recombination increases information in the gene pool, I’m going to ask you how.

My point is that evolution does not "slow and ultimately stop" when additional selection pressures are introduced in all real-world examples. Whether or not the limpets and moths evolve into something different from limpets and moths is not interesting. There is nothing in the theory of evolution, to my knowledge, that states that an organism has to evolve into something else after a certain amount of time. Further, the moths have evolved into moths with a different kind of ear. Depending on the arbitrariness of current classification of moths, this could very well mean that these moths have evolved from one genus, subfamily or even family to another, which is a substantial (but arbitrary) difference.

Why is this an off limits question to you evolutionarians?

I can speak for no one except myself when I say that this is because I have not particularly studied this for quite some time, and thus cannot state with any degree of certainty what evidence shows, without looking at relevant literature. Had I done so, the list may or may not have been substantially altered to reflect contemporary hypotheses.

This is all a very nice list but you have a bookkeeping problem. How do you account for the huge number of genetic differences between reptiles and birds? Are you going to suggest that recombination accounts for these differences? If not, then you are left with mutation and selection and this is a profoundly slow process where multiple selection pressures interfere with the process.

As should now be evident, I do not believe that multiple selection pressures interfere with the process in the same way that you do. Further, I would like to draw your attention to the fact that several of the items listed above are connected with sexual selection, which may very well be a reasonable inclusion in the problem (as many birds show sexual selection). This, I understand, is not modelled by ev, and ev is thus an insufficient basis oto stand on when dismissing evolutionary histories involving sexual selection.

Or more reasonably would explain why a reptile would climb in a tree, or migrate, or breed with another reptile that has beneficial traits, but to grow feathers, beak and wings is a strange extrapolation in the face of the huge genetic differences between the two animals.

Certainly not. I believe that a combination of the selection pressures listed above which would favour for instance a greater surface area for gliding between trees would favour the development of wing-like structures. Several unrelated arboreal animals use different methods to increase this gliding area; some of them have developed flights. Gliding structures include extensions of the skin of the sides, enlargement of feet, and protruding structures from the sides of the body. That one group should have developed feathers --- perhaps initially for another purpose --- and then adapted these structures for flight does not seem unreasonable.

Your English is fine, your understanding of the mathematics of mutation and selection needs work, can’t brain tries to make the same argument. The problem for adherents to the theory of evolution is that multiple selection pressures so profoundly slow the rate of information acquisition by mutation and selection that it makes the theory mathematically impossible.

This seems to be more of a problem for you than for anyone who actually understands what he's talking about.

If I am late in responding to you over the next few days, it is not due to cowardice, but because I am going to Würzburg to visit a friend for a few days. While I am there, I will also take time to visit the Senckenberg museum where they have casts of, among other things, Microraptor and Caudipteryx, both of which are dinosaurs with feathers. Hopefully, there will be information of some sort there that will help me to better understand the evolution of reptiles into birds. Until then, wish you all a nice weekend and Monday.

[Anacoluthon64]

This thread itself gives an allegorically near-perfect counterexample to kleinman's thesis: if increased selection pressures really did inhibit evolutionary rates, this thread would have died a long time ago.

'Luthon64

[Belz...]

When you are talking about the delay in evolution of HIV, you are talking about millions if not billions of generations to accomplish the evolution of only a small number of loci.

We're talking about barely-alive viruses, now ?

Then look at the differences in reptile and bird genomes and try to do the bookkeeping to accomplish the transformation of reptiles to birds. You can’t do it, it is mathematically impossible.

Ah! Good. Show it, mathematically.

Well then, those who don’t should look at all the empirical evidence how multiple selection pressures slow evolution.

And how come NO scientist has discovered this while spending a lifetime trying to understand the process ? Why have YOU spotted it ? What are YOUR qualifications ?

This is why combination therapy is used to treat HIV, this is why combination therapy is used to treat TB, this is why combination therapy should have been used to treat Gonorrhea, this is why combination therapy should have been used to treat MRSA, this is why combination therapy is being used to treat Malaria, this is why combination therapy should be used to treat influenza, this is why combination therapy is used to treat cancer…

Do you have a point ?

It’s clear that the mathematics of mutation and selection and the empirical evidence of mutation and selection doesn’t support the mushy soft theory of evolution.

Mushy soft ? EVERYTHING supports the theory. You rant about how pressures SLOW evolution, but that actually doesn't make any sense. If there were NO environmental pressures, then mutations could go either way with no selection at all. How would that "evolve" ?

Wrong Belz, the laws of thermodynamics may be very useful for predicting the behavior of things but it is still theory.

Really ?

Name one example of the laws of thermodynamics being violated ?

What would you consider a fact, if a proven-true, always-right theory isn't fact ?

It just happens to be a much better theory than the theory of evolution.

Your statements of opinions are known, and useless without proof.

A couple of posts back, can’t brain thanked me for using the red text, I guess you just can’t make everyone happy.

You should stop calling other people names. It's against forum rules.

He was being sarcastic about the red text.

It doesn’t matter whether I have a religious agenda or not.

Yes it does, because belief clouds reason.

Unless mathematics works different for you and I, it doesn’t matter.

It doesn't work different, but people can interpret it differently.

The reason why I say mutation and selection works so slowly is based on the evolutionist written, peer reviewed and published mathematical model of mutation and selection. Try the model out yourself and see what it shows.

Again, why are you the only one saying this ?

I assure you that I know something about the mathematic of mutation and selection, I studied the evolutionist written a peer reviewed model of the process.

Studied with a religious agenda. Do you have a diploma in molecular biology ?

If you understood the ev model, you would ask the same question. What is the selection pressure that would turn a reptile into a bird? It is really a dumb notion that has overtaken the field of biology.

That's a strawman. No one ever said a reptile could turn into a bird.

[Belz...]

What about Hammegk? I can't really remember what he was talking about when he participated in this thread, but I don't think Id say he was on our side.

Hammegk is on NOBODY's side.

[Belz...]

Your right Paul, evolution never started it all, of course neither did abiogenesis.

How do you explain the various breeds of dog ?

Can’t brain

Reported.

the point you are missing is that even if evolution isn’t completely stopped, it is slowed so profoundly that it makes the theory of evolution mathematically impossible.

I don't think that means what you think it means.

[krazyKemist]

So the strongest proof against evolution is a computer simulation ? I mean come on...:rolleyes:

Similarly, the ability to predict at the molecular level which changes may lead to resistance against a drug can aid in the design of improved drugs or suggest optimal combinations of existing drugs to mitigate the evolution of resistance and eradicate the pathogen.

That is correct, but only very partly. As someone who works on drug design, I can tell you there are very tight limits to doing this... We can guess what point mutations will do with some degree of accuracy (and even that is highly debatable), but what about deletions ? Additions ? Those will change the complete sequence of amino acids in the mutated protein downwards !!! Can you predict its new structure ? Its new function ??? Suppose another gene is cut off, but still has its primer (the part that allows it to be expressed), and the shortened version happens to have less selectivity but is still functional, on new substrates ? And what about the pathogen getting a complete resistance gene in the form of a plasmid ?

And how exactly the theory of evolution is hindering cancer research ? I'd like to know, as it happens to be my field of research.

the Kemist

[Mr. Scott]

It just occurred to me how useful good knowledge of the evolution of human anatomy would be to a doctor in making their various diagnoses, and having incorrect ideas about the origin of species could increase the chances of misdiagnoses.

An example that comes to mind is the human spine.

On the one hand, a doctor could believe that the human kind was created by God with all the details of the spine appropriate for efficient and safe erect bipedal activities -- a rational assumption for a creationist.

On the other hand, an evolutionist doctor would understand the weaknesses naturally due to the vestiges of the quadrapedal posture of human ancestors.

A creationist doctor would have to learn the specific details of all the weaknesses of the human spine, and could develop no intuition about how evolution from quadruped to biped could give a doctor good diagnostic leads.

So if Dr. Kleinman had been an evolutionist instead of a creationist, he may have more promptly diagnosed Mr. Powell's herniated nucleas pulposis at T8-9. Instead, Dr. Kleinman gave Mr. Powell pain medication and muscle relaxant. Now he is being sued for malpractice.

I assert that creationist belief can cripple a doctor's understanding of human anatomy enough to increase their chances of defending themselves against malpractice suits.

In conclusion, I offer this google find, with a quote in large red text, attesting to the weakness of the human spine due to recent bipedal evolution and the importance of making evolution a basic science in medical school:

Medicine Needs Evolution (http://www.sciencemag.org/cgi/content/summary/311/5764/1071)


Although anatomy, physiology, biochemistry, and embryology are recognized as basic sciences for medicine, evolutionary biology is not. Future clinicians are generally not taught evolutionary explanations for why our bodies are vulnerable to certain kinds of failure....

Evolution is also the origin of apparent anatomical anomalies such as the vulnerabilities of the lower back...

[Making evolution a basic science in medicine] will help clinicians and biomedical researchers understand that both the human body and its pathogens are not perfectly designed machines but evolving biological systems shaped by selection under the constraints of tradeoffs that produce specific compromises and vulnerabilities. Powerful insights from evolutionary biology generate new questions whose answers will help improve human health.


...and avoid malpractice suits.

[joobz]

I do not think it does any of us a service to attack Kleinman on such a personal level. His own foolishness is enough to prove to everyone his non-existant intellectual academic worth. But there is no reason to allow this to translate into him being a bad doctor or a horrible person. Who we are on the net is hardly an indication of who we are in real life.

Besides, even though he admits to his identity, doesn't incorporating more personal information into this thread constitute a violation of forum policy?

In truth, this thread should have been moved to abandon all hope months ago. As one of the primary Kleinman antagonists, I take responsibilty for allowing it to progress for so long. For that, I apologize. It does not serve JREF in any positive way.

[kleinman]

Do you think that there is something out in the forests, seas, air, caves.... that is going around using "cell based approaches" to "identify targets" to design pressures for selecting the "optimal combinations" to "halt evolution"?
If they are selection pressures they are targeting a particular gene or genes. For example the penicillium mold produces penicillin which targets bacterial cell wall formation. However, even more generalized environmental stresses on life forms target particular genes. Take Delphi’s speculation that temperature change in the environment is what drove the evolution of reptiles to birds. Temperature changes in the environment will target large numbers of enzyme systems which are extremely temperature sensitive. What is called for is that all these temperature sensitive systems will be affected simultaneously and must evolve simultaneously. Random mutations do not cooperate to evolve all these genes simultaneously. Then consider what happens with the mathematical behavior of ev. If you think that the selection conditions that Dr Schneider designed for the model are optimized to stop evolution then perhaps he should redesign the selection conditions and show how evolution can occur with simultaneous selection conditions. Lastly on this point, read the citations carefully which show that multiple selection pressures slow the evolution of resistance. The condition that multiple selection pressures slow evolution by mutation and selection is that the selection pressures target different enzyme systems. Now if those enzyme systems are related in such a way that the selection pressures work synergistically, you potentially drive the fitness of that life form to zero. Even if you don’t drive the fitness to zero, you impair the fitness of the life form while at the same time making it more difficult for mutation and selection to get the correct combinations of random mutations to overcome these selection pressures. This is what ev is showing mathematically and this is what these real examples of mutation and selection show.
If we can't halt evolution (over a matter of years) by purposefully selecting the most difficult pressures, what hope do you have that elements in the wild can do it?
Again, you miss the point, ev demonstrates how slow the process becomes with only three selection conditions and I doubt Dr Schneider chose his selection conditions to stop evolution but mathematically that is what his model shows. The behavior of ev with genome lengths near to that of HIV shows how many generations it takes to accomplish the evolution of only 100 loci. HIV and other microbes are the only life forms that have the populations and reproduction rates to accomplish this type of evolution. Now can’t brain, if you think there are multiple selection pressures which cooperate and allow evolution by mutation and selection to proceed rapidly, tell us what those selection pressures are.
This statement cuts at the heart of your argument. Even when we try, we haven't stopped the evolutionary process. We may be able to one day, but that takes design. Since there isn't "something" at every spot throughout our world designing multiple selection pressures to stop evolution, we are left to assume that evolution can occur in the wild.
Can’t brain, you’ve neither shown this mathematically or empirically. The only thing that has happened here is the heart of the theory of evolution, mutation and selection, has been cut out with a mathematical scalpel and is buried under a mountain of empirical evidence.
You evolutionarians are so stuck in your doctrine that anyone who dare challenge it is making an insult,I never took your objections to the Theory of Evolution as insulting. The circus of insults I spoke of is being carried out on both sides of the aisle.
I apologise for adding another clown (myself) to the act.
Don’t worry about it.
Again, Delphi, you are being very silly. Most real physical problems can only be expressed in functional notation. You don’t have a closed form algebraic expression that describes the function. In fact, every real mathematical scientific problem that I have worked on ultimately comes down to solving a functional equation which can not be expressed algebraically.A simple "yes" would've sufficed. Or perhaps you weren't aware that mathematical proofs involving "functional equations" are not only possible, they're common. Routine, even. Necessary. A fundamental concept in many branches of mathematics. In fact, some functions only exist because they're useful in formal proofs.
I’ll leave the formal proof to you. I will confess that my engineering background emphasized applied mathematics at the expense of formal proofs. That said, from the applied mathematical point of view, ev shows that multiple selection conditions is what slows the acquisition of information by mutation and selection in the model. This is consistent with your Wikipedia reference to fitness landscape and this is consistent with the empirical evidence. Do a formal mathematical proof and prove otherwise.
Cut the crap. Either you have a mathematical proof that evolution is mathematically impossible or you don't. Show your work or shut up.
Why do evolutionarians whine so much? For the time being, you will have to content yourself with the results ev, your own Wikipedia reference to fitness landscape and the numerous citations that I have and will continue to post (see below). The formal mathematical proof will come since so many areas of science and medicine are demonstrating this real mathematical fact of mutation and selection that multiple selection pressures slow and ultimately stop evolution.
Is it just me?No. Some of the rest of us in this thread are also literate. Sadly, one of us has some obvious difficulties in that area...
Now Delphi, just because you are having trouble organizing the socks in your sock drawer, don’t get mad at me, but it is alright to get annoyed, especially by the applied mathematical results from ev and all the empirical evidence which shows that multiple selection pressures slow and ultimately stop evolution.
If you think that the limpet population is going to respond rapidly to these selection pressures by mutation and selection rather than recombination and selection, you don’t understand how slowly mutation and selection occurs.As you make this observation several times throughout your response, I will start off by saying that for the purposes of my claim, there is no need to differentiate between variation stemming from mutation and that coming from recombination. My claim is, again, that added selection pressures do not "slow and ultimately stop" evolution, but that it's business as usual, and that it may even lead to the evolution of more derived structures. To do so, I assume all mechanisms and methods of evolution to be more or less constant in their presence or absence in the history of a certain organism, and see what happens when the load of selection pressures is increased. In all cases I have cited so far, this did not "slow and ultimately stop" evolution. This is contrary to, perhaps even the opposite of, your claim and your understanding of the 70+ examples you have posted.
Your assumption that there is no need to differentiate between variation stemming from mutation and recombination shows a fundamental misunderstanding of the two phenomena. In fact there is strong evidence that recombination and selection is not a random phenomenon. Hardy-Weinberg equilibrium is maintained only if there is random mating.
Are you proposing that reptiles evolved to birds by recombination and selection?No. In the section you quote, I am proposing that an added selection pressure in the form of a additional kind of predator using a slightly different mode of hunting in at least some cases lead to the development of more derived structures in the prey organism to directly counter these novel hunting methods.
If the population can not adapt by recombination and selection (or some behavior change such as migration) then the added selection pressure of an additional kind of predator using a slightly different mode of hunting will only under very rare instances be adapted to by mutation and selection. The mutation and selection process is many orders of magnitude slower than recombination and selection for adapting to selection pressures. Why is it that the vast majority of examples of adaptation by mutation and selection is seen in microbes with their huge populations, rapid reproduction times and short genomes?
Recombination without error can not increase information in the gene pool while recombination with selection can cause the loss of information (alleles) from the gene pool. You need errors in order to increase information in the gene pool and ev shows this process to be profoundly slow. But in the real world, as opposed to in ev (as I understand it), these errors are not limited to random point mutation, which you seem to be exclusively focused on. Other methods for introducing an error in a genome exist, but you consistently overlook or disregard these.
I remind you that the empirical examples that I post are not limited random point mutations. In fact, the HIV example includes random recombination yet the evolution of drug resistance for this virus is still markedly slowed by three drug combinations. None of the empirical examples that I have and continue to present are limited to random point mutation yet all show slowing of evolution to multiple selection pressures. Study and learn the mathematics of ev and this will make more sense to you.
This is such a contorted story, how can you tell what is occurring by mutation and selection and what is occurring by recombination and selection?You have not yet provided me with sufficient reason to make this distinction at all with regards to what I am actually claiming (see above). Present a reasonable argument for why the origin of the variation is important which, if dismissed, would ruin my claim, and I might address it. Making the distinction between variation due to mutation and variation due to recombination for the sake of making a distinction seems a useless exercise to me.
I am not arguing that variation does not occur, what I am arguing is that variation by recombination and selection is a very rapid process but does not have the capability of adding information to the gene pool and that variation by mutation and selection is a profoundly slow process for adding information to the gene pool. We have real empirical examples of how rapidly variation can occur in a population by recombination and selection and we have real examples of how slowly variation can occur in a population by mutation and selection. The process for the later case occurs most rapidly when there is only a single selection pressure; each addition selection pressure profoundly slows the process of evolution.
This is a big problem you evolutionarians have, you think the mathematics of mutation and selection is the same as the mathematics of recombination and selection. It isn’t, one is selecting for mutations and the other is selecting for alleles. In addition, you are still having a hard time understanding that recombination without error can not increase information in the gene pool (it can not create new alleles) and recombination with selection can cause the loss of information (alleles) from the gene pool. Without errors in the construction of a gene, there is no possible way to increase information in the gene pool. This is what ev is modeling for random point mutations and selection and it is a profoundly slow process. It takes huge numbers of generations to accumulate the information and if you impose extra selection pressures, it slows the process down. This is exactly what we see in all the citations I have been posting (including the HIV example which includes recombination).Again, I do not at this point feel that it would make any difference where the variation selected on comes from. And the speed of mutation in ev is irrelevant, as it is forced to limit itself to some kinds of mutations, and not all the ones which can happen to real organisms.
I understand your feelings and this is one of the reasons why I think indoctrination into evolutionism introduces a bias into the interpretation of reality and thus is a theory which is harmful to science. It is my hope that the hard mathematical facts which ev demonstrates and the empirical evidence of these facts will move you to investigate.
While certainly the use of, say, three antigens would cause a substantial portion of a germ population to diminish, I believe --- and this sort of thing has never interested me, so I may be wrong, and my choice of words is probably not optimal, but I hope you will understand anyway --- that the small percentage which do survive this multi-pressure treatment --- and in many of your cases there is such a percentage --- at least some do so because they are resistant to all the chemicals used in the treatment. This means (and here I enter the realm of speculation entirely), that the germs surviving at the end of the treatment have evolved resistance to three chemicals in the same amount of time that a germ population exposed to only one chemical would evolve resistance only to that one (in a simplistic world where we consider evolution only in terms of the resistance to man-made drugs). In essence, if I am correct in my speculation, you have disproved your own claim.
I think you need to look up the word “antigen”, I suspect you meant to use the word “antibiotic”. Now, it may be possible that treating a population of microbes with three drugs may yield a small population that is resistant to all three drugs; however, the point is that it is much more difficult for a population to evolve resistance to three drugs simultaneously than to the same three drugs when applied sequentially. You may have a few bacteria in a population which is already resistant to all three drugs and when these selection pressures are applied, the only bacteria left are the resistant members. This is why monotherapy is discouraged for the treatment of HIV because mutation and selection can quickly evolve resistance to that single drug. You don’t want to introduce into the population of microbes members who are already resistant to drugs you want to use in combination therapy.
You need errors and selection to increase information in the gene pool. I think you are going to back yourself into a corner if you are going to content that recombination and selection is how reptiles evolved into birds.I feel quite safe in claiming that recombination and selection surely must have played a part, but that it would hardly be the only factor influencing this step in evolution.
The intense breeding of dogs in the past 10,000 years has led to large morphological differences in the species but they are still all homologous. You need errors to transform reptiles to birds and ev shows this to be mathematically impossible (for random point mutations).
Ok, tell us how recombination increases information in the gene pool? This is not an answer to my question. Why are only random point mutations interesting when it comes to determining how added selection pressures affect the rate of evolution?
According to the Hardy-Weinberg law, random recombination can not even change the frequency of alleles in a population, let alone increase the information in the gene pool. The reason why random point mutations are the most important and most interesting form of mutations is that they are the most common and least destructive form of mutation. Insertion/deletions cause frame shifts which are almost always lethal, other forms of mutations are more rare and usually are not beneficial.
I’m not a moderator on this thread, say what ever you want. If you want to say limpets evolve to limpets and moths evolve to moths, I’m not sure what your point is. If you are going to contend that recombination increases information in the gene pool, I’m going to ask you how.My point is that evolution does not "slow and ultimately stop" when additional selection pressures are introduced in all real-world examples. Whether or not the limpets and moths evolve into something different from limpets and moths is not interesting. There is nothing in the theory of evolution, to my knowledge, that states that an organism has to evolve into something else after a certain amount of time. Further, the moths have evolved into moths with a different kind of ear. Depending on the arbitrariness of current classification of moths, this could very well mean that these moths have evolved from one genus, subfamily or even family to another, which is a substantial (but arbitrary) difference.
A population may be able to adapt to multiple selection pressures quickly by recombination but this is not a random process. When it comes to a population adapting by random mutation and natural selection then you see the effect of multiple selection pressures slowing the process.
Why is this an off limits question to you evolutionarians?I can speak for no one except myself when I say that this is because I have not particularly studied this for quite some time, and thus cannot state with any degree of certainty what evidence shows, without looking at relevant literature. Had I done so, the list may or may not have been substantially altered to reflect contemporary hypotheses.
When I ask the question, what is/are the selection pressures which would transform a reptile into a bird, at least you try to pose an argument. However, many evolutionarians respond that if I knew something about evolution, I would never ask the question. Science is the study of cause and effect. If evolutionarians can not define the cause which would transform a reptile into a bird, they are abandoning scientific reasoning. If you are going to argue that a predator chasing a reptile into the tree is the stimulus for the reptile to grow wings, the more obvious counter argument is that recombination and selection would select for a population with longer legs which would be achieved quickly. The number of genetic changes needed to evolve wings by mutation and selection would take massive numbers of generations. It’s a mathematical impossibility.
This is all a very nice list but you have a bookkeeping problem. How do you account for the huge number of genetic differences between reptiles and birds? Are you going to suggest that recombination accounts for these differences? If not, then you are left with mutation and selection and this is a profoundly slow process where multiple selection pressures interfere with the process.As should now be evident, I do not believe that multiple selection pressures interfere with the process in the same way that you do. Further, I would like to draw your attention to the fact that several of the items listed above are connected with sexual selection, which may very well be a reasonable inclusion in the problem (as many birds show sexual selection). This, I understand, is not modelled by ev, and ev is thus an insufficient basis oto stand on when dismissing evolutionary histories involving sexual selection.
Again, you confuse variation by recombination and selection and variation by mutation and selection. The former can achieve large morphological changes in the population in a very short time while the later requires huge numbers of generations to achieve much smaller changes.
Or more reasonably would explain why a reptile would climb in a tree, or migrate, or breed with another reptile that has beneficial traits, but to grow feathers, beak and wings is a strange extrapolation in the face of the huge genetic differences between the two animals. Certainly not. I believe that a combination of the selection pressures listed above which would favour for instance a greater surface area for gliding between trees would favour the development of wing-like structures. Several unrelated arboreal animals use different methods to increase this gliding area; some of them have developed flights. Gliding structures include extensions of the skin of the sides, enlargement of feet, and protruding structures from the sides of the body. That one group should have developed feathers --- perhaps initially for another purpose --- and then adapted these structures for flight does not seem unreasonable.
It is these kinds of vague imaginations of arms transforming into wings and scales transforming into feathers which makes the theory of evolution only suitable for the Scifi channel. It is hard mathematical analysis like what is seen with ev which explains how mutation and selection actually works. Then the empirical evidence can be examined to see whether the results of this mathematical analysis has any validity and we find it does.
Your English is fine, your understanding of the mathematics of mutation and selection needs work, can’t brain tries to make the same argument. The problem for adherents to the theory of evolution is that multiple selection pressures so profoundly slow the rate of information acquisition by mutation and selection that it makes the theory mathematically impossible. This seems to be more of a problem for you than for anyone who actually understands what he's talking about.
It should be of importance for you because if you are interested in describing variation in populations, doing this without mathematical tools leaves you at a marked disadvantage.
If I am late in responding to you over the next few days, it is not due to cowardice, but because I am going to Würzburg to visit a friend for a few days. While I am there, I will also take time to visit the Senckenberg museum where they have casts of, among other things, Microraptor and Caudipteryx, both of which are dinosaurs with feathers. Hopefully, there will be information of some sort there that will help me to better understand the evolution of reptiles into birds. Until then, wish you all a nice weekend and Monday.
There are plenty of people who have different interpretations of these fossils. This is why I prefer to stick with a mathematically based argument. If you are going to argue that mutation and selection is the driving force for the theory of evolution, you need to account for this mathematically and ev shows you can’t.
This thread itself gives an allegorically near-perfect counterexample to kleinman's thesis: if increased selection pressures really did inhibit evolutionary rates, this thread would have died a long time ago.
If you are arguing that this thread is an example of mutation and selection, you are inaccurate in your analysis. If anything, the mathematics of ev and the numerous empirical examples of this mathematics are stabilizing selection pressures for my argument.
When you are talking about the delay in evolution of HIV, you are talking about millions if not billions of generations to accomplish the evolution of only a small number of loci. We're talking about barely-alive viruses, now ?
HIV is the quintessential example of how mutation and selection works (and random recombination and selection as well).
Then look at the differences in reptile and bird genomes and try to do the bookkeeping to accomplish the transformation of reptiles to birds. You can’t do it, it is mathematically impossible.Ah! Good. Show it, mathematically.
It’s simple Belz, compare the genomes of the two and count the differences between the two genomes.
Well then, those who don’t should look at all the empirical evidence how multiple selection pressures slow evolution.And how come NO scientist has discovered this while spending a lifetime trying to understand the process ? Why have YOU spotted it ? What are YOUR qualifications ?
Scientists have known this for years; I posted a 1958 Nobel laureate lecture where this effect was acknowledged. My qualifications are already posted on this thread.
This is why combination therapy is used to treat HIV, this is why combination therapy is used to treat TB, this is why combination therapy should have been used to treat Gonorrhea, this is why combination therapy should have been used to treat MRSA, this is why combination therapy is being used to treat Malaria, this is why combination therapy should be used to treat influenza, this is why combination therapy is used to treat cancer… Do you have a point ?
Certainly I have a point, and that point is that evolution by mutation and selection is slowed and ultimately stopped as you increase the number of selection pressures.
It’s clear that the mathematics of mutation and selection and the empirical evidence of mutation and selection doesn’t support the mushy soft theory of evolution. Mushy soft ? EVERYTHING supports the theory. You rant about how pressures SLOW evolution, but that actually doesn't make any sense. If there were NO environmental pressures, then mutations could go either way with no selection at all. How would that "evolve" ?
EVERYTHING except the mathematics of random point mutations and natural selection as shown by the peer reviewed and published ev computer model of this phenomenon and the numerous empirical examples that demonstrate the mathematics of this phenomenon.
Wrong Belz, the laws of thermodynamics may be very useful for predicting the behavior of things but it is still theory.Really ?

Name one example of the laws of thermodynamics being violated ?

What would you consider a fact, if a proven-true, always-right theory isn't fact ?
You are demonstrating a lack of knowledge of the history of the laws of thermodynamics. Consider the 1st law, conservation of energy. A century ago, this law would have been violated when considering nuclear reactions because the mass/energy relationship was not understood. The 1st law had to be modified to take this effect into account. The original hypothesis had to be modified. Just because the 1st law of thermodynamics is a very good and useful hypothesis does not mean that it will need further modifications in the future.
It just happens to be a much better theory than the theory of evolution.Your statements of opinions are known, and useless without proof.
I’m using the peer reviewed and published mathematical model of random point mutations and natural selection which shows that multiple selection pressures slow and ultimately stop evolution. I am supporting this contention with numerous empirical examples which demonstrates this mathematics. (See below for another example).
A couple of posts back, can’t brain thanked me for using the red text, I guess you just can’t make everyone happy. You should stop calling other people names. It's against forum rules.

He was being sarcastic about the red text.
That’s what is written on his avatar. Here’s the Wikipedia definition for “avatar”.
http://en.wikipedia.org/wiki/Avatar_(virtual_reality) (http://en.wikipedia.org/wiki/Avatar_%28virtual_reality%29)
An avatar (abbreviations include AV, ava, avie, avy, avi, avvie, and avvy) is an Internet user's representation of himself or herself, whether in the form of a three-dimensional model used in computer games, [1] a two-dimensional icon (picture) used on Internet forums and other communities, [2][3] or a text construct found on early systems such as MUDs. The term "avatar" can also refer to the personality connected with the screen name, or handle, of an Internet user.[4]
Is there a problem on this forum referencing people by their avatar?
It doesn’t matter whether I have a religious agenda or not.Yes it does, because belief clouds reason.
I agree with you, a belief in evolutionism clouds reason. You evolutionarians certainly seem to be having trouble with the mathematics of mutation and selection.
Unless mathematics works different for you and I, it doesn’t matter.It doesn't work different, but people can interpret it differently.
That’s true, however with mathematics; you can trace back to the underlying assumptions and look for empirically evidence that verifies the interpretations. For example, I am taking the mathematics of ev and arguing that multiple selection pressures slow evolution by mutation and selection. Anyone can duplicate my mathematics and obtain identical results. I then take my hypothesis and show real examples which demonstrate this mathematics. I’m still waiting for you evolutionarians to show the mathematics that multiple selection pressures accelerate evolution and give some real examples of this mathematics.
The reason why I say mutation and selection works so slowly is based on the evolutionist written, peer reviewed and published mathematical model of mutation and selection. Try the model out yourself and see what it shows.Again, why are you the only one saying this ?
I don’t know, perhaps it’s the bias that has been put into evolutionarians by their years of indoctrination in the belief system. However, this is a mathematical and real fact that is seen in many areas of science and medicine.
I assure you that I know something about the mathematic of mutation and selection, I studied the evolutionist written a peer reviewed model of the process.Studied with a religious agenda. Do you have a diploma in molecular biology ?
I see, evolutionarians have no agenda; let’s see where the mathematics and empirical evidence leads us. My academic credentials are posted on this thread but what difference do the credentials make if what I propose is true?
If you understood the ev model, you would ask the same question. What is the selection pressure that would turn a reptile into a bird? It is really a dumb notion that has overtaken the field of biology.That's a strawman. No one ever said a reptile could turn into a bird.
Belz, you need to get a new playbook, the strawman argument does not work on this thread. This thread is about the mathematics of mutation and selection as shown by the ev computer model. What this model shows is that multiple selection pressures slow and ultimately stop evolution. I have and will continue to post citations which demonstrates this mathematical fact.
Your right Paul, evolution never started it all, of course neither did abiogenesis.How do you explain the various breeds of dog ?
Common Belz, let’s play hardball, not softball. The rapid changes in the canine population were achieved by recombination and selection. However, all these breeds are still homologous. If you read Stephen Gould’s hypothesis of punctuated equilibrium and replaced “mutation and selection” with “recombination and selection” you will get a reasonable hypothesis. You can accomplish what Gould proposes with small population in short periods of time with recombination and selection but it is mathematically impossible to do what he proposes with mutation and selection.
the point you are missing is that even if evolution isn’t completely stopped, it is slowed so profoundly that it makes the theory of evolution mathematically impossible. I don't think that means what you think it means.
Study the mathematics of mutation and selection as demonstrated by the ev computer model and the numerous real examples that I have and will continue to post and you will see that I mean what I say.
So the strongest proof against evolution is a computer simulation ? I mean come on...
It’s a peer reviewed and publish computer simulation of random point mutations and natural selection which shows that multiple selection slow the evolutionary process, and I have posted numerous citations which demonstrate this fact.
Similarly, the ability to predict at the molecular level which changes may lead to resistance against a drug can aid in the design of improved drugs or suggest optimal combinations of existing drugs to mitigate the evolution of resistance and eradicate the pathogen.That is correct, but only very partly. As someone who works on drug design, I can tell you there are very tight limits to doing this... We can guess what point mutations will do with some degree of accuracy (and even that is highly debatable), but what about deletions ? Additions ? Those will change the complete sequence of amino acids in the mutated protein downwards !!! Can you predict its new structure ? Its new function ??? Suppose another gene is cut off, but still has its primer (the part that allows it to be expressed), and the shortened version happens to have less selectivity but is still functional, on new substrates ? And what about the pathogen getting a complete resistance gene in the form of a plasmid ?
The point to that citation was that combination of existing drugs can mitigate (slow) the evolution of resistance. That’s what the mathematics of the ev computer simulation of random point mutations and natural selection shows.
And how exactly the theory of evolution is hindering cancer research ? I'd like to know, as it happens to be my field of research.
If you study the mathematics of mutation and selection you will find that multiple selection pressures slow the evolution of resistance. The ingrained indoctrination of evolutionism impairs the comprehension of this mathematical and empirical fact. If you want to slow the evolution of resistance to a particular cancer therapy, don’t use the drug as monotherapy, use it in combination with a drug that targets a different genetic system. I have posted many articles which attest to this fact. Analogous examples of this phenomenon are seen in multiple areas of science and medicine. In fact, here is an example from the field of infectious diseases that demonstrates this phenomenon where multiple selection pressures slow and ultimately stop evolution and where monotherapy allows for rapid evolution to that selection pressure.

http://www.annalsnyas.org/cgi/content/abstract/918/1/9?ck=nck (http://www.annalsnyas.org/cgi/content/abstract/918/1/9?ck=nck)
Large-cohort studies in North America, Europe, and Thailand have shown that zidovudine/azidothymidine (AZT) monotherapy, given at the late stages of pregnancy, is of proven benefit in reducing mother-to-infant HIV transmission by 51% to 68%. AZT monotherapy will not be of long-term benefit for mothers because no single drug can counteract viral infection; benefits to babies will be short-lived if HIV-1 is acquired through breastfeeding after birth. Unfortunately, ongoing mutation of HIV under conditions of drug pressure allows for the evolution and selection of AZT-resistant viruses. Emergence of AZT-resistant variants in pregnant mothers (7-29%) and their infected offspring (5-21%) has been described in several studies. Drug resistance arises more frequently in those mothers who received AZT therapy before pregnancy. Recent advances in combination chemotherapy may provide alternative strategies in prevention of vertical transmission and drug resistance.Genotypic screening of the HIV-1 isolated from pregnant mothers may provide rational modifications in antiretroviral (ARV) strategies to circumvent vertical HIV transmission. This may be of advantage for resource-rich nations but not for underdeveloped nations with limited access to ARVs. Public health programs are vital to have an impact on the tragic pandemic of pediatric AIDS.

Do not continue to change other members' names on quotes. Additionally, please make proper use of the quote and multiquote functions when creating such long posts, referring to so many other posts. If you need help with this, it can be found in the forum help section, tutorials, such as here:
http://forums.randi.org/showthread.php?t=85266.

[Belz...]

HIV is the quintessential example of how mutation and selection works

Why is it "quintessential" ? It's just one example.

It’s simple Belz, compare the genomes of the two and count the differences between the two genomes.

No, no, no, no. You said it was impossible MATHEMATICALLY. Please present mathematical proof to support that statement.

Scientists have known this for years; I posted a 1958 Nobel laureate lecture where this effect was acknowledged. My qualifications are already posted on this thread.

Out of 123 pages, why don't you simply repeat them; same for the 1958 lecture.

Certainly I have a point, and that point is that evolution by mutation and selection is slowed and ultimately stopped as you increase the number of selection pressures.

Which doesn't make sense in the light of things that we CAN see evolve.

EVERYTHING except the mathematics of random point mutations and natural selection as shown by the peer reviewed and published ev computer model of this phenomenon and the numerous empirical examples that demonstrate the mathematics of this phenomenon.

So there's ONE exception ?

You are demonstrating a lack of knowledge of the history of the laws of thermodynamics. Consider the 1st law, conservation of energy. A century ago, this law would have been violated when considering nuclear reactions because the mass/energy relationship was not understood.

But the law was NEVER violated, was it ?

The 1st law had to be modified to take this effect into account.

Actually, the law remained unchanged.

That’s what is written on his avatar. Here’s the Wikipedia definition for “avatar”.

It's not his username, and it's clear you're using it as an insult.

Don't play dumb.

I’m still waiting for you evolutionarians to show the mathematics that multiple selection pressures accelerate evolution and give some real examples of this mathematics.

You first, claimant.

I don’t know, perhaps it’s the bias that has been put into evolutionarians by their years of indoctrination in the belief system.

There is no belief system, Chap. It's called evidence. I have no emotional involvement in either possibility. If someone proves special creation, then so be it.

I see, evolutionarians have no agenda

Nice dodge. Do you have an agenda or not ? You seemed to hint that yes, you did.

Belz, you need to get a new playbook, the strawman argument does not work on this thread.

If you claim that someone says something when they don't then that is a strawman and that is a fallacy.

No one ever said a reptile could turn into a bird.

The rapid changes in the canine population were achieved by recombination and selection.

Thank you. The very core of evolution.

However, all these breeds are still homologous.

A poodle isn't very homologous with a wolf. Plus they won't breed, and therefore could be said to be different species.

Study the mathematics of mutation and selection as demonstrated by the ev computer model and the numerous real examples that I have and will continue to post and you will see that I mean what I say.

Not my burden.

[kjkent1]

Insertion/deletions cause frame shifts which are almost always lethal, other forms of mutations are more rare and usually are not beneficial.I think your hypothesis re the impossibility of macro-evolutionary change is a roiling pile of feces. And, your quote above explains why:

1. We have empirical evidence of frame shifts that are not lethal and which have caused substantial evolutionary change.

2. We have empirical evidence of "other forms of mutations" which have caused substantial evolutionary change.

3. None of these mutational forces are modeled in ev, therefore ev is not a suitable model from which to proclaim that evolution is impossible, even if there were no empirical evidence demonstrating the fact that other than random-point mutation causes substantial evolutionary charge.

So, all of your cited evidence of multi-therapeutic selective suppression, and references to ev's random-point mutations means bupkis, because we have observed evidence of evolution from the very sources of change which you claim cannot produce the change that they have actually produced.

Your entire argument comes down to one thing: you believe that changes are divine intervention rather than random accidents.

Well, that's great, and you're entitled to your belief. But, as a scientist, you can't assert God as the solution. All you can assert is the random accidents.

The mathematics of evolution, via ev, show information gain is possible by the most finely grained process: random-point mutation and natural selection based on nothing more than missing and spurious chemical bindings.

Considering the very minimal process requirements necessary to cause evolutionary change in ev, it's little wonder that real life has managed to accomplish what it has in the time available.

Nothing you've presented in this forum poses the slightest problem for evolutionary theory, Alan -- nothing.

[kleinman]

HIV is the quintessential example of how mutation and selection works.Why is it "quintessential" ? It's just one example.
HIV is the quintessential example of how mutation and selection works for several reasons. HIV has a very short genome length. Ev shows that the shorter the genome the more rapid the acquisition of information by mutation and selection. HIV has a very high mutation rate because there is no error checking proteins. Ev shows that within limits, the mutation rate affects the rate of information acquisition in approximately linear fashion. HIV has huge populations and high reproduction rates. Ev shows that huge populations accelerate the rate of information acquisition. In addition HIV does recombination. This is the most commonly mentioned feature missing from ev that evolutionists allege will make the theory of evolution possible. Despite all these beneficial conditions, three drug therapy marked slows the evolution of resistance in this virus. This is exactly what ev shows. When any two of the three selection conditions are set to zero in ev, the third selection condition evolves rapidly. In the same way, attempts to use monotherapy with HIV allows for very rapid evolution of resistance to this single drug. This is why this approach for treatment of HIV has been abandoned as shown by the many citations on this topic.
It’s simple Belz, compare the genomes of the two and count the differences between the two genomes.No, no, no, no. You said it was impossible MATHEMATICALLY. Please present mathematical proof to support that statement.
Fair enough, let’s try to do the computation. Let’s start with trying to compare the genome sizes of existing birds and reptiles. The following link lists the weights of genomes of reptiles and birds.
http://www.genomesize.com/index.php (http://www.genomesize.com/index.php)
For reptiles, the range of sizes are,
Smallest reptile genome size: 1.05pg, Chalcides mionecton, Skink
Largest reptile genome size: 5.44pg, Testudo graeca, Greek tortoise
Mean for reptiles: 2.25pg ± 0.04
For birds, the range of sizes are,
Smallest bird genome size: 0.97pg, Phasianus colchicus, Common pheasant
Largest bird genome size: 2.16pg, Struthio camelus, Ostrich
Mean for birds: 1.45pg ± 0.01
You start with a average genome size for reptile 25% larger than birds yet birds are supposed to be more advanced than reptiles. Where do you want to go next in the calculation?
Scientists have known this for years; I posted a 1958 Nobel laureate lecture where this effect was acknowledged. My qualifications are already posted on this thread. Out of 123 pages, why don't you simply repeat them; same for the 1958 lecture.
It’s enough that you know my name and that you know that my qualifications are posted on this thread. Show some initiative and read the thread and learn something about the mathematics of mutation and selection. So as not to be too coy, I will repost the reference and quote from the 1958 Nobel Prize l
This link is from the Nobel Prize lecture given in 1958 by Edward Tatum.
http://nobelprize.org/nobel_prizes/medicine/laureates/1958/tatum-lecture.html (http://nobelprize.org/nobel_prizes/medicine/laureates/1958/tatum-lecture.html)
In microbiology the roles of mutation and selection in evolution are coming to be better understood through the use of bacterial cultures of mutant strains. In more immediately practical ways, mutation has proven of primary importance in the improvement of yields of important antibiotics - such as in the classic example of penicillin, the yield of which has gone up from around 40 units per ml of culture shortly after its discovery by Fleming to approximately 4,000, as the result of a long series of successive experimentally produced mutational steps. On the other side of the coin, the mutational origin of antibiotic-resistant micro-organisms is of definite medical significance. The therapeutic use of massive doses of antibiotics to reduce the numbers of bacteria which by mutation could develop resistance, is a direct consequence of the application of genetic concepts. Similarly, so is the increasing use of combined antibiotic therapy, resistance to both of which would require the simultaneous mutation of two independent characters.

As an important example of the application of these same concepts of microbial genetics to mammalian cells, we may cite the probable mutational origin of resistance to chemotherapeutic agents in leukemic cells 44, and the increasing and effective simultaneous use of two or more chemotherapeutic agents in the treatment of this disease.
Edward Tatum recognized 50 years ago that combination selection pressures slows the evolution of resistance of bacteria to combination antibiotics and cancer cells to combination chemotherapeutic agents. This is a mathematical fact demonstrated by the ev computer model and more than 50 citations which I have posted. This is how the mathematics of mutation works and this is demonstrated by the empirical evidence. The greater the number of selection pressures, the slower evolution proceeds. This is why the theory of evolution is mathematically impossible.

I apologize for not answering all your questions but we can pick up next week where we left off. Until then, study the thread and learn the mathematics of mutation and selection.

[kjkent1]

So may words to say so little. Your logic would be perfect if not for the existence of HIV itself, apparently the result of all those "other" mutational forms that you find "almost lethal" or "rarely beneficial."

On the other hand, what's not particularly beneficial to humans seems to be quite beneficial to to the humble HIV.

[delphi_ote]

I’ll leave the formal proof to you. I will confess that my engineering background emphasized applied mathematics at the expense of formal proofs.
You could've just said you don't have a proof that it is mathematically possible. That really would've saved a lot of time. Now if we could just get you to stop repeating that it's mathematically impossible despite having no evidence to back up your claim, we might get somewhere.

[Belz...]

You start with a average genome size for reptile 25% larger than birds yet birds are supposed to be more advanced than reptiles.

Irrelevant. Anyone with a modicrum of understanding of evolution knows that it's a strawman. Why aren't there anti-evolutionists with actual knowledge of the theory ?

Who ever said birds are more "advanced" ?

Where do you want to go next in the calculation?

"Next" ? I want you to present MATHEMATICAL proof, as you have claimed you have, to support your statements.

It’s enough that you know my name and that you know that my qualifications are posted on this thread. Show some initiative and read the thread and learn something about the mathematics of mutation and selection.

It would have been much, much faster to type your name and specialty. Instead you go about and write a whole paragraph telling me to look for it. Fine, then. I'll just assume you are unwilling to divulge that information.

Edward Tatum recognized 50 years ago that combination selection pressures slows the evolution of resistance of bacteria to combination antibiotics and cancer cells to combination chemotherapeutic agents.

Well, he doesn't say that, per se, in the article you linked, but even if it did, I don't think we're talking about the same thing. The way I understand it, and people can correct me if I'm wrong, they're trying to cull bacteria population by the use of antibiotics in order to slow down their evolution, not because of environmental pressures, but because of low populations.

The greater the number of selection pressures, the slower evolution proceeds.

Unfortunately that makes no logical sense. More difficult environments will either kill off every living beings or quickly leave only those "fit" for that environment. Wouldn't that kind of accelerate the process ?

This is why the theory of evolution is mathematically impossible.

Even assuming that your premise is correct, this isn't true if the number of pressures is relatively low.

I’ll leave the formal proof to you. I will confess that my engineering background emphasized applied mathematics at the expense of formal proofs.

Good, good. Engineering. Not biology.

[cyborg]

You start with a average genome size for reptile 25% larger than birds yet birds are supposed to be more advanced than reptiles.

Hmm, kleinman also thinks that better programs are longer.

Your ignorance knows no bounds kleinman. I suggest you hand that engineering degree back - how the **** you earned it is beyond me.

[krazyKemist]

It’s a peer reviewed and publish computer simulation of random point mutations and natural selection which shows that multiple selection slow the evolutionary process, and I have posted numerous citations which demonstrate this fact.


And there's your problem... Point mutation isn't the only type of mutation. You forgot truncation, addition, deletion, copy, gene transfer from plasmids and viruses... A host of things that we know happen in nature... The problem of physicists and mathematicians is that they think they know biology and genetics... That's why they think they know better than a host of biologists that work in the field. There is a reason the theory of evolution is accepted by mainstream biologists, and that reason is that it is confirmed by empirical observation, which physicists and mathematicians, absorbed in theory, have not made...

While I respect the abilities of theoricians, I have observed a lot of condescention of them for people working in the life sciences, where observation is the most important aspect :( .

And a word of advice on simulations : don't rely on them too much. If they were always right, costs of developping new drugs would have crashed... Just find your magic molecule with computer time, make it, and voilà ! But that's not the case, obviously. Lots of costly labwork still going on...

The point to that citation was that combination of existing drugs can mitigate (slow) the evolution of resistance. That’s what the mathematics of the ev computer simulation of random point mutations and natural selection shows.

The whole process of antibiotics/chemotherapy resistance is well understood from the point of view of evolution. That is why doctors will seek to eliminate, ie, to put so much pressure on the population, before it has time to adapt and produce new offspring. That demands excessive pressure, either single or multiple, but the key word here is excessive. In other words, a high concentration, to kill as many as you can in the shortest time possible. If on the contrary, you use doses that are too low, chances of adaptation are much higher, even if you use multiple drugs. In the case of antibiotics, the theory of evolution explains why somebody who ingest antibiotics continually will be affected by resistant bacteria, thanks to transfer of genetic material from plasmids, developped by his own friendly bacteria in the gastrointestinal tract. And if that person ingested several antibiotics continually, the infection will be resistant to all of them !

If you study the mathematics of mutation and selection you will find that multiple selection pressures slow the evolution of resistance. The ingrained indoctrination of evolutionism impairs the comprehension of this mathematical and empirical fact. If you want to slow the evolution of resistance to a particular cancer therapy, don’t use the drug as monotherapy, use it in combination with a drug that targets a different genetic system. I have posted many articles which attest to this fact. Analogous examples of this phenomenon are seen in multiple areas of science and medicine. In fact, here is an example from the field of infectious diseases that demonstrates this phenomenon where multiple selection pressures slow and ultimately stop evolution and where monotherapy allows for rapid evolution to that selection pressure.

As I explained, drug combinations are not forbidden by the theory of evolution. We understand that from the standpoint of evolution, excessive pressure (either multiple or single) has a higher chance of resulting in extinction (death of the entire population). I think you do not understand that evolution allows indeed for extinction. It has happened a lot of times in the past (sometimes massively), and will continue to happen.

Drug combinations are used all the time (in chemo, antibiotics, antivirals, ect.), and the reason for not combining is not because we fear something will evolve faster but because drug combinations also mean a combination of side-effects and toxicity. In cancer therapy, the reason not to administer second or thrid line chemo agents at the same time as first line ones is because they are much more toxic... They will be used only as a last resort, in case of lack of response. Remember, the goal of this therapy is to prolong life...

the Kemist

[Belz...]

Nice post, Kemist. What's your field ?

[krazyKemist]

Nice post, Kemist. What's your field ?

Medicinal chemistry/drug design applied to cancer hormonal therapy. That means I do some organic chemistry, some enzyme assays, and some nice computer modeling of enzyme-drug interactions... Kind of a combined field.

the Kemist

[Belz...]

So in a way, you're exactly what's needed against Klein's arguments !

[kjkent1]

Medicinal chemistry/drug design applied to cancer hormonal therapy. That means I do some organic chemistry, some enzyme assays, and some nice computer modeling of enzyme-drug interactions... Kind of a combined field.

the KemistThis should be fun. Your adversary is Dr. Alan Kleinman, Ph.D., licensed as both a mechanical engineer and a medical doctor, by the State of California. So, it's a veritable certainty that he will shortly be explaining to you why you don't know what you're talking about...

...as he does with everyone else here at randi.org.

PS. He never posts on Friday or Saturday.

[Belz...]

Medical doctor in what ? Bleeding by leeches ?

[kjkent1]

Medical doctor in what ? Bleeding by leeches ?Now, we must give the good doctor his due. He seems to know why he believes as he does. I just don't think he is particularly interested in any opposing evidence -- except to immediately discredit it.

[Paul C. Anagnostopoulos]

Your right Paul, evolution never started it all, of course neither did abiogenesis.
Then your argument in this thread is a complete sham.

~~ Paul

[krazyKemist]

This should be fun. Your adversary is Dr. Alan Kleinman, Ph.D., licensed as both a mechanical engineer and a medical doctor, by the State of California. So, it's a veritable certainty that he will shortly be explaining to you why you don't know what you're talking about...

...as he does with everyone else here at randi.org.

PS. He never posts on Friday or Saturday.

This guy's a MD ? :jaw-dropp. Well, I've seen perfectly good MD/PhDs turn to homeopathy, one good chemist become a raelian, and Linus Pauling did prescribe vitamin C as a panacea, so I shouldn't be surprised anymore... But still... Makes you wonder, doesn't it ?

the Kemist

[Dr Adequate]

You start with a average genome size for reptile 25% larger than birds yet birds are supposed to be more advanced than reptiles. Where do you want to go next in the calculation? Cheers, that made me chuckle.

Before you got into such a tizzy about the theory of evolution, why didn't you find out what it is? You will find it awfully hard to refute a theory of which you are ignorant.

[Dr Adequate]

This week's kleinman statistics.

Amount of mathematics done by kleinman this week: 0. (Running total: 0.)

Amount of evidence produced for kleinman's delusions this week: 0. (Running total: 0.)

Number of people kleinman has convinced with his stupid lies this week: 0. (Running total: 0.)

Occurences of the word "cheese" in kleinman's posts this week: 59.

[trvlr2]

Dr. Adequate-really mind numbing stats! Certainly glad someone is keeping score!

What I am most curious about:
1. How many here would be the first to cross a bridge that Kleinman built?
2. How many would let Kleinman treat their child's skinned knee?

Just askin'.

[Mr. Scott]

This guy's a MD ? :jaw-dropp. Well, I've seen perfectly good MD/PhDs turn to homeopathy, one good chemist become a raelian, and Linus Pauling did prescribe vitamin C as a panacea, so I shouldn't be surprised anymore... But still... Makes you wonder, doesn't it ?

the Kemist

Since the topic of this thread is "Annoying Creationists" I feel comfortable discussing the one posting in this thread. Dr. Kleinman is a contract physician at a 24 hour urgent care clinic. He is currently defending himself in a malpractice suit, which I suspect is so unpleasant for him that lashing out against evolution is how he's coping with the stress.

Annoying, isn't it?

[juninho]

Fair enough, let’s try to do the computation. Let’s start with trying to compare the genome sizes of existing birds and reptiles. The following link lists the weights of genomes of reptiles and birds.

Hmmmm.

However, your protestations are a load of arse. By your reckoning you are suggesting that a whisk fern (Psilotum nudum) is more evolved (advanced) than humans.

Base pairs

Humans - 3.3 x 10 power 9
Psilotum nudum - 2.5 x 10 power 11

Or rice is more advanced than pufferfish

Pufferfish - 3.42 x 10 power 8
Rice 3.9 x 10 power 8

Oh and this little snippet - some amphibians contain 30 times as much DNA as we do. Hail the croaky overlords.

[krazyKemist]

Hmmmm.

Oh and this little snippet - some amphibians contain 30 times as much DNA as we do. Hail the croaky overlords.

Hail !

(well, you never know... :D )

the Kemist

[delphi_ote]

Hail !

(well, you never know... :D )
Pascal's Wager for Anura, huh? And what if Diptera turn out to be our true overlords? You'll have a lot of explaining to do!

[krazyKemist]

Pascal's Wager for Anura, huh? And what if Diptera turn out to be our true overlords? You'll have a lot of explaining to do!

I'm safe, the frogs will eat 'em all out !!! :D

Diptera may survive all of us though. But in that case, none of us will be here to hail them...

the Kemist

[BPScooter]

Halleluja, amen. This thread may be dead. Selection pressure applied to me may yet allow me to taunt K the way that he taunts. I will only do it in three or four brackets, at some future time. Like this: [[{{neener neener neener}}]] or something.

[kleinman]

It appears you mathematically challenged evolutionarians are still having trouble with the mathematics of mutation and selection, I’m back to help you out of your intellectual morass.
I’ll leave the formal proof to you. I will confess that my engineering background emphasized applied mathematics at the expense of formal proofs.You could've just said you don't have a proof that it is mathematically possible. That really would've saved a lot of time. Now if we could just get you to stop repeating that it's mathematically impossible despite having no evidence to back up your claim, we might get somewhere.
Why Delphi, we thought that you sorting your sock drawer would be enough proof for you. The more different color socks you have the more difficult to sort your sock drawer. If you don’t like that, you can reread your own reference to the Wikipedia and the fitness landscape. You slow moes of evolutionism are having a hard time recognizing that evolution by mutation and selection is simply a sorting problem of beneficial and detrimental mutations and the more sorting conditions imposed, the more difficult and the slower the sort proceeds. This type of mathematical behavior is seen all over in science whether it is system optimization, database sorting or any other iterative mathematical problems. And Delphi, if you look below, you will see more evidence of how evolution by mutation and selection actually works.
You start with a average genome size for reptile 25% larger than birds yet birds are supposed to be more advanced than reptiles.Irrelevant. Anyone with a modicrum of understanding of evolution knows that it's a strawman. Why aren't there anti-evolutionists with actual knowledge of the theory ?
I see, it doesn’t matter what size a genome is, it has no effect on the mathematics of mutation and selection. You evolutionarians need to study your own computer models; you might learn something about the mathematics of mutation and selection.
It’s a peer reviewed and publish computer simulation of random point mutations and natural selection which shows that multiple selection slow the evolutionary process, and I have posted numerous citations which demonstrate this fact.And there's your problem... Point mutation isn't the only type of mutation. You forgot truncation, addition, deletion, copy, gene transfer from plasmids and viruses... A host of things that we know happen in nature... The problem of physicists and mathematicians is that they think they know biology and genetics... That's why they think they know better than a host of biologists that work in the field. There is a reason the theory of evolution is accepted by mainstream biologists, and that reason is that it is confirmed by empirical observation, which physicists and mathematicians, absorbed in theory, have not made...

While I respect the abilities of theoricians, I have observed a lot of condescention of them for people working in the life sciences, where observation is the most important aspect .

And a word of advice on simulations : don't rely on them too much. If they were always right, costs of developping new drugs would have crashed... Just find your magic molecule with computer time, make it, and voilà ! But that's not the case, obviously. Lots of costly labwork still going on...
For those of you who just drop in and don’t bother reading the thread, the numerous real examples of mutation and selection I have been posting are not limited to random point mutations and natural selection and they still show that combination selection pressures slow evolution. If you are going to join the ranks of mathematically challenged evolutionarians and claim that other forms of mutations or recombination will somehow magically overcome the effect that multiple selection pressure causes to the evolutionary process, simply study the real case of how HIV evolves when subjected to multiple selection pressures. krazykemist, you better learn this mathematical fact of life if you are developing drugs whose effectiveness is dependant on mutation and selection.
The point to that citation was that combination of existing drugs can mitigate (slow) the evolution of resistance. That’s what the mathematics of the ev computer simulation of random point mutations and natural selection shows.The whole process of antibiotics/chemotherapy resistance is well understood from the point of view of evolution. That is why doctors will seek to eliminate, ie, to put so much pressure on the population, before it has time to adapt and produce new offspring. That demands excessive pressure, either single or multiple, but the key word here is excessive. In other words, a high concentration, to kill as many as you can in the shortest time possible. If on the contrary, you use doses that are too low, chances of adaptation are much higher, even if you use multiple drugs. In the case of antibiotics, the theory of evolution explains why somebody who ingest antibiotics continually will be affected by resistant bacteria, thanks to transfer of genetic material from plasmids, developped by his own friendly bacteria in the gastrointestinal tract. And if that person ingested several antibiotics continually, the infection will be resistant to all of them !
Really, the evolution of antibiotic/chemotherapy evolution is well understood? Do you think this process of evolution is any different from other evolutionary processes?
Your right Paul, evolution never started it all, of course neither did abiogenesis.Then your argument in this thread is a complete sham.
I see Paul; you are one of joobz’s cooperative chemistry adherents to abiogenesis. Are you also and adherent to joobz’s cooperative selection pressures theory of evolution? Why don’t you rewrite ev and get the selection conditions to cooperate so that it will evolve more quickly?
This week's kleinman statistics.

Amount of mathematics done by kleinman this week: 0. (Running total: 0.)

Amount of evidence produced for kleinman's delusions this week: 0. (Running total: 0.)

Number of people kleinman has convinced with his stupid lies this week: 0. (Running total: 0.)

Occurences of the word "cheese" in kleinman's posts this week: 59.
Too bad the James Randi forum PhD in amathematics is not so good at counting mutations. Let’s review the PhD in amathematics gif of mutation and selection:
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.
http://forums.randi.org/images/smilies/doglaugh.gif
Total number of real examples that show the multiple selection pressures accelerate evolution this week = 0. Total number or real examples the PhD in amathematics has posted = 0. You are really building up the evidence there.
Halleluja, amen. This thread may be dead. Selection pressure applied to me may yet allow me to taunt K the way that he taunts. I will only do it in three or four brackets, at some future time. Like this: [[{{neener neener neener}}]] or something.
Now don’t be silly BPScooter, the only thing dead on this thread is the dumb theory of evolution. Cause of death; hyperextrapolation, speculationitis, denialophilia, and sciencea amathematica.

Here’s another example of how evolution by mutation and selection works as shown by the ev computer simulation, that is multiple selection pressures slow and ultimately stops evolution.
http://www.thebody.com/content/art39095.html (http://www.thebody.com/content/art39095.html)
This year's Resistance Workshop featured three oral presentations on the activity and mechanisms of drug resistance associated with anti-HCV polymerase inhibitors. Investigators from Merck & Co. presented an important proof of concept study, which showed that two chimpanzees receiving the novel nucleoside polymerase inhibitor MK-0608 had 2- to 3-log reductions in virus levels after a single intravenous dose, and up to a 5-log reduction after seven days of therapy [Abstract 5].24 Whether or not this compound will be found to be useful for treating human HCV infection will not be known for a few years. Several days following the discontinuation of MK-0608, investigators detected a mixture of wild-type and mutant virus at a position in the enzyme associated with HCV resistance. Nonetheless, this study suggests that we may soon be seeing more potent polymerase inhibitors with activity rivaling that of the HCV protease inhibitors.

Isabel Najera (Roche Pharmaceuticals) and Akhter Molla (Abbott Laboratories) [Abstracts 3 and 4, respectively]25,26 each described data on the in vitro activity and in vitro selection of mutations associated with resistance to nonnucleoside polymerase activity. Najera described the activity of two nonnucleoside polymerase inhibitors -- one that binds to the polymerase thumb region and the other to the palm region. During in vitro passage with each drug alone, mutations developed in the region of the molecule that was targeted by the inhibitor, as well as secondary mutations for the palm site inhibitor. During in vitro passage with both inhibitors, both thumb and palm site mutations emerged allowing the virus to develop resistance to both drugs. Molla described a new highly active polymerase inhibitor to which virus resistance developed rapidly during in vitro passage but which was highly synergistic when used in combination with interferon (IFN).

Taken together, these and previous studies of new small molecule inhibitors of HCV suggest that although some inhibitors will be highly potent, most will have a low genetic barrier to resistance. If these drugs are used as monotherapy agents, the rapid development of resistance appears to be inevitable. This resistance may be more rapid than that observed for HIV-1, as it is estimated that HCV is replicating at a level that is 2 to 3 logs higher than HIV-1 (i.e., the production of about 1 trillion virions per day), and because it appears that even within tissue culture there may be more heterogeneous genotypes than observed with HIV-1.

[Belz...]

Why hasn't this thread evolved yet ?

[cyborg]

You need a magical stone in order to evolve some types of thread.

[Anacoluthon64]

Why Delphi, we thought that you sorting your sock drawer would be enough proof for you. The more different color socks you have the more difficult to sort your sock drawer. If you don’t like that, you can reread your own reference to the Wikipedia and the fitness landscape. You slow moes of evolutionism are having a hard time recognizing that evolution by mutation and selection is simply a sorting problem of beneficial and detrimental mutations and the more sorting conditions imposed, the more difficult and the slower the sort proceeds.That would be true in an environment where processing is choked by being limited to procedural/sequential "execution." With the right sorting algorithm on a massively parallel platform (such as occurs in natural selection), it's largely irrelevant.

'Luthon64

[kleinman]

Why hasn't this thread evolved yet ?
Belz, this thread is about bookkeeping. It is based on Dr Schneider’s ev computer simulation which models the bookkeeping of random point mutations and natural selection. What that model shows is that random point mutation and natural selection is a profoundly slow way of accumulating information, too slow for the theory of evolution to be mathematically possible. The only thing that has evolved in this thread is that we now know that the reason this model accumulates information so slowly is the three selection conditions in the model. Set any two of the three conditions to zero and the model rapidly can evolve the third condition. This is how mutation and selection works mathematically and this is how mutation and selection works in reality. The more selection conditions imposed on a population, the more difficult and slower the sorting process for beneficial and detrimental mutations becomes. Someday, this mathematical and real fact of life will soak through the barren dry ground of pseudo-scientific evolutionarian thinking.
You need a magical stone in order to evolve some types of thread.
No magical stone needed here master of cruft; you just need a little mathematics to understand how mutation and selection works. I find it interesting that it was accountants who brought down Al Capone and it is accounting which has brought down the mythical theory of evolution.
Why Delphi, we thought that you sorting your sock drawer would be enough proof for you. The more different color socks you have the more difficult to sort your sock drawer. If you don’t like that, you can reread your own reference to the Wikipedia and the fitness landscape. You slow moes of evolutionism are having a hard time recognizing that evolution by mutation and selection is simply a sorting problem of beneficial and detrimental mutations and the more sorting conditions imposed, the more difficult and the slower the sort proceeds.That would be true in an environment where processing is choked by being limited to procedural/sequential "execution." With the right sorting algorithm on a massively parallel platform (such as occurs in natural selection), it's largely irrelevant.
Anacoluthon64, you aren’t paying attention to the real examples of mutation and selection posted here. The previous citation that discusses HCV reports the production of a trillion virons per day. What kind of “massively parallel platform” do you want to speculate into existence? There is no such thing, well; maybe there is one, right next to the imaginary primordial soup. But don’t let me discourage you from discussing this “massively parallel platform” that has no mathematical or physical evidence of its existence. We can file your discussion right next to kjkent1’s string cheese theory of evolution.

[krazyKemist]

For those of you who just drop in and don’t bother reading the thread, the numerous real examples of mutation and selection I have been posting are not limited to random point mutations and natural selection and they still show that combination selection pressures slow evolution. If you are going to join the ranks of mathematically challenged evolutionarians and claim that other forms of mutations or recombination will somehow magically overcome the effect that multiple selection pressure causes to the evolutionary process, simply study the real case of how HIV evolves when subjected to multiple selection pressures. krazykemist, you better learn this mathematical fact of life if you are developing drugs whose effectiveness is dependant on mutation and selection.

There... See what I mean ? Total condescention... Please don't try to use the "if you dont see this, you must be stupid" technique :( ... It is highly unpleasant and works only on those who have some level of vanity, which I, and most people here, don't have. As to reading this entire 120 plus pages tread, I think, from the sample I've read, that it will be a pointless, boring, waste of time ponctuated with insulting comments. I may be "mathematically challenged", but I can still make out, however dim I am, that as a population decreases, the chances for the "winning gene(s)" to be drawn get lower...

The fact that you call a computer simulation an "empirical fact" makes me think you have a serious understanding problem of what an empirical fact actually is. Mathematical models and computer simulations are tools designed to test theories. They are only as good as their power of prediction of observable, empirical facts.

But I'm also inclined to think that you do understand that a simulation is a numerical extrapolation of a model (which may be wrong on several aspects), and that you may be blinded, not by faith (after all, evolution is no proof against god), but by a desire to see man as the specially created "child of god", and that you dislike having common ancestry with apes, however distant... Vanity makes men do very odd and sometimes horrible things...

As for HIV, I invite you to read about it. It really has an unsual, fascinating biology, which explains why it cannot be eradicated, even with severe pressure from multiple antivirals...

Really, the evolution of antibiotic/chemotherapy evolution is well understood? Do you think this process of evolution is any different from other evolutionary processes?


A lot of things are being understood about chemotherapy resistance. Some specific mutations are now known which help predict how a patient will respond to specific agents. Pharmacogenetics is a developping field still in its infancy, which will definitely help increase the success rates of many treatments. But I have serious doubts as to how your model will contribute to the advancement of anything except your own religious beliefs. As I already told, biology is a very observation-oriented science. Dogmas have very short lifetimes in biology. As an example, you should know that the discovery of HIV as the causative agent of AIDS broke one such dogmas (retroviruses were thought unable to cause serious illnesses).

the Kemist

[Mr. Scott]

I figured the medically challenged on this thread would find this article on the evolution of the human spine helpful to diagnose back problems:

Are your back problems caused by evolution? (http://valleynews.com/TheValley/Stories/Health/Advice/Story~299563.aspx)

The spine was originally designed to work more as a flexible suspension bridge than as a support column, as it does now. There is a balance between flexibility and stability of the spine. When we have a more flexible spine, we are potentially losing stability. As it becomes more stable, some flexibility can be lost because there is a complex interplay between joints and discs. The more freedom we have to bend, rotate and move to the side, the more potential there is for areas of weakness that can be injured. Problems with our spines may be linked closely to our evolution and heritage

[Anacoluthon64]

Anacoluthon64, you aren’t paying attention to the real examples of mutation and selection posted here. The previous citation that discusses HCV reports the production of a trillion virons per day. What kind of “massively parallel platform” do you want to speculate into existence?Why, the one that consists of large numbers of organisms (whether of the same type or not) competing for the same or overlapping resources, of course. No speculation necessary.


We can file your discussion right next to kjkent1’s string cheese theory of evolution.… where it will not intrude on kleinman's bizarre faculties of comprehension.

'Luthon64

[kleinman]

For those of you who just drop in and don’t bother reading the thread, the numerous real examples of mutation and selection I have been posting are not limited to random point mutations and natural selection and they still show that combination selection pressures slow evolution. If you are going to join the ranks of mathematically challenged evolutionarians and claim that other forms of mutations or recombination will somehow magically overcome the effect that multiple selection pressure causes to the evolutionary process, simply study the real case of how HIV evolves when subjected to multiple selection pressures. krazykemist, you better learn this mathematical fact of life if you are developing drugs whose effectiveness is dependant on mutation and selection.There... See what I mean ? Total condescention... Please don't try to use the "if you dont see this, you must be stupid" technique ... It is highly unpleasant and works only on those who have some level of vanity, which I, and most people here, don't have. As to reading this entire 120 plus pages tread, I think, from the sample I've read, that it will be a pointless, boring, waste of time ponctuated with insulting comments. I may be "mathematically challenged", but I can still make out, however dim I am, that as a population decreases, the chances for the "winning gene(s)" to be drawn get lower...
If you are interested in learning about the mathematics of mutation and selection, study the ev model. Without looking at the model or the results obtained from the model a have drawn conclusions about the model. The model shows something about the affects of population on the rate of evolution (accumulation of information) as well as the affects of genome size, mutation rate, number of selection pressures as well as a variety of other parameters. If you read the thread, you will find the data posted, if you take Dr Schneider’s model and do a parametric study, you can generate the identical data. When you do either, you will get some understanding how mutation and selection behaves mathematically. When you do this, you understand the dozens of citations I have posted which show that multiple selection pressures slow evolution. So before you jump to your conclusions, either study the thread and the data posted in it or study the model, or better do both.
The fact that you call a computer simulation an "empirical fact" makes me think you have a serious understanding problem of what an empirical fact actually is. Mathematical models and computer simulations are tools designed to test theories. They are only as good as their power of prediction of observable, empirical facts.
Another inattentive evolutionist posts on this thread. The computer simulation shows the mathematical behavior, the numerous real examples cited in this thread demonstrate empirically the mathematical fact. What the ev model shows about the effects of number selection pressures and the rate of evolution is demonstrated over and over in reality. What the computer model demonstrates mathematically is the greater the number of selection pressures, the slow evolution proceeds. I have cited more than 50 real examples of this with respects to combination therapy of HIV, combination therapy of HCV, combination therapy of TB, combination therapy of Malaria, combination therapy of mosquito larvae, combination therapy of cancer cells, combination use of herbicides on weeds, combination rodenticides… Every one of these examples shows that combination selection pressures slow the ability of the population to evolve resistance to these selection pressures. This is what ev shows mathematically and these numerous citation show the empirical evidence. This is an obvious finding if you understand the mathematics of sorting and optimization. The more conditions upon which you are sorting or optimizing, the slower the process becomes. Mutation and selection is a sorting process of beneficial and detrimental mutations. As you increase the number of selection conditions this process becomes profoundly slows, too slow for the theory of evolution to be mathematically possible. Ev accurately simulates the mutation and selection process, so study the model if you want to understand how this phenomenon actually works and it is not like the silly extrapolations that evolutionarians like to make.
But I'm also inclined to think that you do understand that a simulation is a numerical extrapolation of a model (which may be wrong on several aspects), and that you may be blinded, not by faith (after all, evolution is no proof against god), but by a desire to see man as the specially created "child of god", and that you dislike having common ancestry with apes, however distant... Vanity makes men do very odd and sometimes horrible things...
I have decades of experience both in writing and using complex computer simulations of nonlinear systems and I know how to evaluate the behavior of such models. I made my claims about ev after running hundreds of cases with the model. It is your vanity that leads you to draw conclusions about ev without running a single case.
As for HIV, I invite you to read about it. It really has an unsual, fascinating biology, which explains why it cannot be eradicated, even with severe pressure from multiple antivirals...
Really, you are so sure about this conclusion? I remember when people like you made similar claims about the virus and disease only 15-20 years when they said there would be no treatment at all. In just a short period of time treatments have been developed which length lives of those with HIV by decades, of course with evolutionarians like you who don’t understand how mutation and selection actually works, eradication of the virus will take decades longer than it really needs to.
Really, the evolution of antibiotic/chemotherapy evolution is well understood? Do you think this process of evolution is any different from other evolutionary processes? A lot of things are being understood about chemotherapy resistance. Some specific mutations are now known which help predict how a patient will respond to specific agents. Pharmacogenetics is a developping field still in its infancy, which will definitely help increase the success rates of many treatments. But I have serious doubts as to how your model will contribute to the advancement of anything except your own religious beliefs. As I already told, biology is a very observation-oriented science. Dogmas have very short lifetimes in biology. As an example, you should know that the discovery of HIV as the causative agent of AIDS broke one such dogmas (retroviruses were thought unable to cause serious illnesses).
That all fine, now if you just learn how mutation and selection works mathematically as shown by ev and that the results of this model are verified over and over by empirical evidence then you would discard the pseudo-scientific dogma of evolutionism. This pseudo-scientific dogma biases its adherents to the interpretation of reality so severely that they can’t comprehend the obvious mathematical fact of how mutation and selection actually works. By the way, the model isn’t mine, it is the peer reviewed and published model of mutation and selection written by the head of computational molecular biology at the National Cancer Institute and was published in the Oxford University Press journal Nucleic Acids Research. Of course you would have known this if you had read the thread.

[Belz...]

Belz, this thread is about bookkeeping.

Looks more like book thumping to me.

What that model shows is that random point mutation and natural selection is a profoundly slow way of accumulating information

Yeah. But when you start figuring out that hundreds of millions of years come into play...

too slow for the theory of evolution to be mathematically possible.

So you keep claiming.

The more selection conditions imposed on a population, the more difficult and slower the sorting process for beneficial and detrimental mutations becomes.

That makes no sense whatsoever, and is not supported by the document you linked to.

Someday, this mathematical and real fact of life will soak through the barren dry ground of pseudo-scientific evolutionarian thinking.

Is that an argument from future possibilities ? Seems pretty vacuous to me.

[kleinman]

Belz, this thread is about bookkeeping.Looks more like book thumping to me.
You’ve gotten so used to the mushy soft theory of evolution when you are fed a hard mathematical scientific meal, your teeth break.
What that model shows is that random point mutation and natural selection is a profoundly slow way of accumulating informationYeah. But when you start figuring out that hundreds of millions of years come into play...
It isn’t enough time Belz, consider that when dealing with HCV, you are dealing with a trillion reproductions per day yet combination selection pressures still profoundly slow the evolution of resistance to the multiple drugs. This is the mathematical fact of life you evolutionarians have to come to grips with.
too slow for the theory of evolution to be mathematically possible.
So you keep claiming.
And showing mathematically with ev and giving citations of real examples of this mathematics. Ev shows how the mathematics of mutation and selection actually works.
The more selection conditions imposed on a population, the more difficult and slower the sorting process for beneficial and detrimental mutations becomes.That makes no sense whatsoever, and is not supported by the document you linked to.
Post the portion of the document that doesn’t make sense to you. The mathematics of ev makes total sense. If you understand mutation and selection as a sorting process of beneficial and detrimental mutations, increasing the number of selection condition slows the process down. These citations demonstrate real examples of this phenomenon. You have spent so much time drowning in the doctrine of evolutionism, this obvious mathematical situation confuses you.
Someday, this mathematical and real fact of life will soak through the barren dry ground of pseudo-scientific evolutionarian thinking.Is that an argument from future possibilities ? Seems pretty vacuous to me.
This is not at all an argument from future possibilities. This argument concerns real problems of today such as drug resistant microbes, herbicide resistant weeds, chemotherapy resistant cancers… The empty explanations offered up by evolutionism for how mutation and selection works misses the obvious mathematical and real examples of how this phenomenon actually works. This is why the mathematically impossible theory of evolution blocks real advances in science and medicine.

[krazyKemist]

If you are interested in learning about the mathematics of mutation and selection, study the ev model. Without looking at the model or the results obtained from the model a have drawn conclusions about the model. The model shows something about the affects of population on the rate of evolution (accumulation of information) as well as the affects of genome size, mutation rate, number of selection pressures as well as a variety of other parameters. If you read the thread, you will find the data posted, if you take Dr Schneider’s model and do a parametric study, you can generate the identical data. When you do either, you will get some understanding how mutation and selection behaves mathematically. When you do this, you understand the dozens of citations I have posted which show that multiple selection pressures slow evolution. So before you jump to your conclusions, either study the thread and the data posted in it or study the model, or better do both.


But don't you see that this is pointless ? I'm sure that a "mathematically challenged evolutionarian" already answered the citations for you ! Everything can be interpreted both ways !

What drew me to this discussion is the fact that you use a computer simulation as an empirical fact to declare that evolution could not have happened ! Don't you see the sheer size of the assumption you're making to declare that ? You are assuming we know everything of the process of evolution ! Everything ! I've yet to meet a biologist who is so sure of himself ! We're just beginning to understand the role of viruses in evolution ! We're just discovering funny little beasts called ERVs in the human genome ! The only fact that can be deduced with certainty from your simulations is that this model of evolution does not work, whomever designed it !

Surely you understand how approximation can lead to aberrant behavior in any iterative process ? That if you ignore a fact that you may think is insignificant, huge errors will result ?

I have decades of experience both in writing and using complex computer simulations of nonlinear systems and I know how to evaluate the behavior of such models. I made my claims about ev after running hundreds of cases with the model. It is your vanity that leads you to draw conclusions about ev without running a single case.

Sigh... Ok then. What about assuming one knows all of the processes life ?

Really, you are so sure about this conclusion? I remember when people like you made similar claims about the virus and disease only 15-20 years when they said there would be no treatment at all. In just a short period of time treatments have been developed which length lives of those with HIV by decades, of course with evolutionarians like you who don’t understand how mutation and selection actually works, eradication of the virus will take decades longer than it really needs to.

Please... Do you actually know anything at all about HIV biology ? About how the virus does not seem to be lytic ? About how it hides in the lymphatic system ? Do you even have the tiniest idea of how little is known about the immune system ? You think you will solve everybody's problems with a computer simulation ? And you call me vain :boggled: ?

Don't you see that the things you supposedly want to apply in clinical research are already being done without any need for your model ? HIV positive patients are already given multiple drugs despite the "indoctrination" of biologists and MDs with evolution ! It does not eradicate the virus ! (You may ask yourself why :confused: ?) Work is done on several targets in cancer therapy ! Synergy between drugs is looked for in a host of clinical trials on any type of disease !

That all fine, now if you just learn how mutation and selection works mathematically as shown by ev and that the results of this model are verified over and over by empirical evidence then you would discard the pseudo-scientific dogma of evolutionism. This pseudo-scientific dogma biases its adherents to the interpretation of reality so severely that they can’t comprehend the obvious mathematical fact of how mutation and selection actually works. By the way, the model isn’t mine, it is the peer reviewed and published model of mutation and selection written by the head of computational molecular biology at the National Cancer Institute and was published in the Oxford University Press journal Nucleic Acids Research. Of course you would have known this if you had read the thread.

Whoever designed the model is irrelevant. Nobody knows everything there is to life. If we did, things like HIV and cancer would be trivial to us. This is like saying that the big bang can't have happened because there isn't enough mass in the universe. The mathematics are perfect, but, oops, you may have forgotten some dark matter.

I think it is useful however to run such simulations. As you point out, the NCI model does not work. We've got some "dark matter" missing. Hints to that effect are provided when you consider the influence of viruses on the evolution of life (a thing that is not readily done by most biologists since viruses are not considered alive). The things we're missing may well prove to be of enormous importance. But we will never find out these things if we just give up on evolution based on a faulty model...

the Kemist

[Belz...]

You’ve gotten so used to the mushy soft theory of evolution when you are fed a hard mathematical scientific meal, your teeth break.

That's nice. Only I don't care for your rhetoric. You have only claims, no evidence. Your meal is just air. And I don't need teeth for that.

It isn’t enough time Belz, consider that when dealing with HCV, you are dealing with a trillion reproductions per day yet combination selection pressures still profoundly slow the evolution of resistance to the multiple drugs. This is the mathematical fact of life you evolutionarians have to come to grips with.

That's not what the document says. Read again.

Post the portion of the document that doesn’t make sense to you.

The doc's not a problem. Your interpretation of it is.

The mathematics of ev makes total sense.

Yeah, because you think it agrees with you.

If you understand mutation and selection as a sorting process of beneficial and detrimental mutations, increasing the number of selection condition slows the process down.

Again, that doesn't make sense whatsoever. If there are MORE selection pressures, it will INCREASE the rate at which selection is made.

These citations demonstrate real examples of this phenomenon. You have spent so much time drowning in the doctrine of evolutionism, this obvious mathematical situation confuses you.

I don't spend time with evolutionism at all, much like I don't spend time thinking about gravity or entropy.

This is not at all an argument from future possibilities.

Yes, it is. You said you'd be vindicated one day. That's NOT an argument.

This argument concerns real problems of today such as drug resistant microbes, herbicide resistant weeds, chemotherapy resistant cancers… The empty explanations offered up by evolutionism for how mutation and selection works misses the obvious mathematical and real examples of how this phenomenon actually works.

If that were the case, MORE use of antibiotics would result in LESS resistance, not more.

This is why the mathematically impossible theory of evolution blocks real advances in science and medicine

Mathematics < Reality.

[delphi_ote]

It appears you mathematically challenged evolutionarians are still having trouble with the mathematics of mutation and selection, I’m back to help you out of your intellectual morass.
You still haven't post a formal proof of your claim, kleinman. How can you say we're mathematically challenged when you haven't brought mathematics to bear once during this entire conversation?

Would any of your mathematics teachers have accepted "it's impossible" on an exam without a formal proof? Stop wasting everyone's time. If you know that evolution is mathematically impossible, you should be able to write a formal mathematical proof.

[kleinman]

If you are interested in learning about the mathematics of mutation and selection, study the ev model. Without looking at the model or the results obtained from the model a have drawn conclusions about the model. The model shows something about the affects of population on the rate of evolution (accumulation of information) as well as the affects of genome size, mutation rate, number of selection pressures as well as a variety of other parameters. If you read the thread, you will find the data posted, if you take Dr Schneider’s model and do a parametric study, you can generate the identical data. When you do either, you will get some understanding how mutation and selection behaves mathematically. When you do this, you understand the dozens of citations I have posted which show that multiple selection pressures slow evolution. So before you jump to your conclusions, either study the thread and the data posted in it or study the model, or better do both.But don't you see that this is pointless ? I'm sure that a "mathematically challenged evolutionarian" already answered the citations for you ! Everything can be interpreted both ways !
Don’t be silly. Ev shows that multiple selection conditions slow and ultimately stop the evolutionary process and I have posted over 50 citations which demonstrate this fact (see below for another citation that demonstrates this fact empirically). The basic argument that evolutionarians (including you) is that ev doesn’t include all the mechanisms of mutation and recombination. However, in the real examples posted all forms of mutations and recombination occur yet these real examples still demonstrate that multiple selection pressures slow the evolutionary process. It doesn’t matter what mechanism you want to include in the mutation and selection process (including recombination), they all demonstrate that multiple selection conditions slow the evolutionary process.
What drew me to this discussion is the fact that you use a computer simulation as an empirical fact to declare that evolution could not have happened ! Don't you see the sheer size of the assumption you're making to declare that ? You are assuming we know everything of the process of evolution ! Everything ! I've yet to meet a biologist who is so sure of himself ! We're just beginning to understand the role of viruses in evolution ! We're just discovering funny little beasts called ERVs in the human genome ! The only fact that can be deduced with certainty from your simulations is that this model of evolution does not work, whomever designed it !
Incorrect krazyKemist, I used Dr Schneider’s computer simulation to establish a mathematical fact, that is that multiple selection conditions profoundly slow the evolutionary process. I then looked in the literature to see whether there was any empirical data to substantiate this mathematical fact and what do we find? There is empirical data from numerous areas of science and medicine that demonstrates the mathematical fact the ev shows. Multiple selection conditions slow evolution. That’s what the mathematics shows and that’s what the empirical data shows. You should really learn the mathematics of mutation and selection.
Surely you understand how approximation can lead to aberrant behavior in any iterative process ? That if you ignore a fact that you may think is insignificant, huge errors will result ?
Perhaps you want to take Adequate’s position that multiple selection pressures accelerate evolution, which would be aberrant. So what type of aberrant behavior do you want to attribute to ev, a computer model which you have yet to do a single case?
I have decades of experience both in writing and using complex computer simulations of nonlinear systems and I know how to evaluate the behavior of such models. I made my claims about ev after running hundreds of cases with the model. It is your vanity that leads you to draw conclusions about ev without running a single case.Sigh... Ok then. What about assuming one knows all of the processes life ?
Oh, I am not assuming I know all the processes of life, I am saying that mutation and selection does not behave either mathematically or empirically the way evolutionarians allege. It is evolutionarians who assume that mutation and selection can explain all the processes of life. Well, the mathematics and empirical evidence says that evolution by mutation and selection slows profoundly when you have multiple selection conditions.
Really, you are so sure about this conclusion? I remember when people like you made similar claims about the virus and disease only 15-20 years when they said there would be no treatment at all. In just a short period of time treatments have been developed which length lives of those with HIV by decades, of course with evolutionarians like you who don’t understand how mutation and selection actually works, eradication of the virus will take decades longer than it really needs to. Please... Do you actually know anything at all about HIV biology ? About how the virus does not seem to be lytic ? About how it hides in the lymphatic system ? Do you even have the tiniest idea of how little is known about the immune system ? You think you will solve everybody's problems with a computer simulation ? And you call me vain ?
I’ll tell you what I do know about HIV, combination therapy slow the evolution of the virus profoundly despite it doesn’t seem to be lytic, that it hides in the lymphatic system, that it does recombination,… That’s exactly what ev shows, combination selection pressures slow evolution. I don’t call you vain; I call you uninformed of the mathematics of mutation and selection.
Don't you see that the things you supposedly want to apply in clinical research are already being done without any need for your model ? HIV positive patients are already given multiple drugs despite the "indoctrination" of biologists and MDs with evolution ! It does not eradicate the virus ! (You may ask yourself why ?) Work is done on several targets in cancer therapy ! Synergy between drugs is looked for in a host of clinical trials on any type of disease !
Of course reality trumps the silly theory of evolution. Clinician and scientist who must deal with real problems of mutation and selection realize that multiple selection pressures slow evolution. I posted for you a 50 year old Nobel laureate speech which attests to this fact. Why don’t evolutionarians teach this empirical fact? It is not taught because it interferes with the evolutionarian belief system. Instead evolutionarians concoct ridiculous stories that reptile transform into birds by mutation and selection when the empirical data and now the mathematics say something totally to the contrary.
That all fine, now if you just learn how mutation and selection works mathematically as shown by ev and that the results of this model are verified over and over by empirical evidence then you would discard the pseudo-scientific dogma of evolutionism. This pseudo-scientific dogma biases its adherents to the interpretation of reality so severely that they can’t comprehend the obvious mathematical fact of how mutation and selection actually works. By the way, the model isn’t mine, it is the peer reviewed and published model of mutation and selection written by the head of computational molecular biology at the National Cancer Institute and was published in the Oxford University Press journal Nucleic Acids Research. Of course you would have known this if you had read the thread.Whoever designed the model is irrelevant. Nobody knows everything there is to life. If we did, things like HIV and cancer would be trivial to us. This is like saying that the big bang can't have happened because there isn't enough mass in the universe. The mathematics are perfect, but, oops, you may have forgotten some dark matter.
Dr Schneider, I don’t think you are irrelevant. KrazyKemist, join the ranks of evolutionarians in denial of the mathematics and empirical evidence how mutation and selection works.
I think it is useful however to run such simulations. As you point out, the NCI model does not work. We've got some "dark matter" missing. Hints to that effect are provided when you consider the influence of viruses on the evolution of life (a thing that is not readily done by most biologists since viruses are not considered alive). The things we're missing may well prove to be of enormous importance. But we will never find out these things if we just give up on evolution based on a faulty model...
Dr Schneider’s model works just fine, it very accurately predicts what happens with multiple selection conditions, however if you want to add “dark matter” to the model, we would all be interested in seeing these results. Hey Paul, does the java language have “dark matter” routines? KrazyKemist, the problem is not with Dr Schneider’s model, the problem is with the theory of evolution by mutation and selection. Until it registers with you that mutation and selection is simply a sorting process of beneficial and detrimental mutations and that as you increase the number of selection conditions, the sorting process becomes slower and slower, you will never understand how mutation and selection actually works.
You’ve gotten so used to the mushy soft theory of evolution when you are fed a hard mathematical scientific meal, your teeth break.That's nice. Only I don't care for your rhetoric. You have only claims, no evidence. Your meal is just air. And I don't need teeth for that.
A little air, a little mathematics, a little empirical evidence, do you want some little dentures?
It isn’t enough time Belz, consider that when dealing with HCV, you are dealing with a trillion reproductions per day yet combination selection pressures still profoundly slow the evolution of resistance to the multiple drugs. This is the mathematical fact of life you evolutionarians have to come to grips with.That's not what the document says. Read again.
Oh, are you going to take the position that multiple selection pressures accelerate evolution?
Post the portion of the document that doesn’t make sense to you.The doc's not a problem. Your interpretation of it is.
So what is your interpretation? Since you are having trouble understanding that citation, I’ll give you another citation below which shows that multiple selection pressures slow evolution.
The mathematics of ev makes total sense.Yeah, because you think it agrees with you.
It also agrees with the empirical data.
If you understand mutation and selection as a sorting process of beneficial and detrimental mutations, increasing the number of selection condition slows the process down.Again, that doesn't make sense whatsoever. If there are MORE selection pressures, it will INCREASE the rate at which selection is made.
I understand this is what the evolutionarian dogma is but it is not mathematically or empirically true.
These citations demonstrate real examples of this phenomenon. You have spent so much time drowning in the doctrine of evolutionism, this obvious mathematical situation confuses you.I don't spend time with evolutionism at all, much like I don't spend time thinking about gravity or entropy.
Well Belz, if you want to understand how mutation and selection actually works you need to spend time studying the phenomenon and it doesn’t work the way you were taught by the evolutionarian creed. Scientists and clinicians who have to deal with real problems of mutation and selection are learning this lesson.
This is not at all an argument from future possibilities.Yes, it is. You said you'd be vindicated one day. That's NOT an argument.
That’s interesting; I don’t recall using the word “vindicated” at all in this discussion. The phenomenon of mutation and selection is a now present problem in medicine, agriculture, pest control… The empirical evidence shows that multiple selection pressures slow evolution. This is shown by the ev computer simulation as well.
This argument concerns real problems of today such as drug resistant microbes, herbicide resistant weeds, chemotherapy resistant cancers… The empty explanations offered up by evolutionism for how mutation and selection works misses the obvious mathematical and real examples of how this phenomenon actually works.If that were the case, MORE use of antibiotics would result in LESS resistance, not more.
Don’t get monotherapy and combination therapy confused.
This is why the mathematically impossible theory of evolution blocks real advances in science and medicine Mathematics < Reality.
Therefore, I will continue to post real examples of mutation and selection for you.
It appears you mathematically challenged evolutionarians are still having trouble with the mathematics of mutation and selection, I’m back to help you out of your intellectual morass.You still haven't post a formal proof of your claim, kleinman. How can you say we're mathematically challenged when you haven't brought mathematics to bear once during this entire conversation?
So you don’t think a parametric study of the ev computer model constitutes a mathematical study? This is standard practice for studying a complex computer model in order to understand the mathematical behavior of the model. I understand this is a bit esoteric for an evolutionarian but that is how you do it. Dr Schneider suggested to me personally that I do the study and he suggested this to everyone in his publication on ev. I’ll continue to post empirical examples of this mathematical behavior and you can periodically whine that I am not doing a formal mathematical proof. Do you have any more skateboarding videos?
Would any of your mathematics teachers have accepted "it's impossible" on an exam without a formal proof? Stop wasting everyone's time. If you know that evolution is mathematically impossible, you should be able to write a formal mathematical proof.
There are many examples of computer simulations of scientific problems that do not have formal proofs yet the results are accepted because of empirical testing. Perhaps you want to present to us a formal proof that the theory of evolution is mathematically true? Now come on Delphi, we are all waiting for you to present the formal mathematical proof for your theory. Alas, I only have a peer reviewed and published model of random point mutation and natural selection and numerous real examples of how mutation and selection actually works, that is multiple selection pressures slow and ultimately stop evolution. Never mind the mathematical model that shows that multiple selection pressures accelerate evolution, give us one real example where multiple selection pressures accelerate evolution.

The following example of how mutation and selection actually works is for you Delphi, perhaps if the weeds do gene duplication they can overcome the affect of multiple selection pressures.

http://www.blackwell-synergy.com/doi/abs/10.1046/j.1365-3180.2003.00355.x?journalCode=wre (http://www.blackwell-synergy.com/doi/abs/10.1046/j.1365-3180.2003.00355.x?journalCode=wre)
A simulation study was conducted to examine the effect of pattern of herbicide use on development of resistance to two herbicides with different modes of action in finite weed populations. The effects of the size of the treatment area (analogous to initial weed population), germination fraction and degree of self-pollination in the weed were investigated. The results indicate that the probability of developing resistance to one or both herbicides decreases as the size of the area/initial population decreases. For treatment areas of 100 ha or less with an initial weed seedbank of 100 seeds m2 and initial frequencies of the resistance genes of 106, development of resistance to both herbicides (double-resistance) is uncommon within 50 years for all types of weeds if both herbicides are used in all years (used in combination). If herbicides are used in alternate years (rotated) double-resistance almost always occurs in 100 ha areas but is uncommon in areas of 1 ha or less. The results suggest that adoption of practices that limit movement of weeds in conjunction with using herbicides in combination rather than in rotation can substantially delay development of herbicide resistance
You all have a good weekend and we can continue this discussion next week.

[Dr Adequate]

It appears you mathematically challenged evolutionarians are still having trouble with the mathematics of mutation and selection, I’m back to help you out of your intellectual morass.

Why Delphi, we thought that you sorting your sock drawer would be enough proof for you. The more different color socks you have the more difficult to sort your sock drawer. If you don’t like that, you can reread your own reference to the Wikipedia and the fitness landscape. You slow moes of evolutionism are having a hard time recognizing that evolution by mutation and selection is simply a sorting problem of beneficial and detrimental mutations and the more sorting conditions imposed, the more difficult and the slower the sort proceeds. This type of mathematical behavior is seen all over in science whether it is system optimization, database sorting or any other iterative mathematical problems. And Delphi, if you look below, you will see more evidence of how evolution by mutation and selection actually works.

I see, it doesn’t matter what size a genome is, it has no effect on the mathematics of mutation and selection. You evolutionarians need to study your own computer models; you might learn something about the mathematics of mutation and selection.

For those of you who just drop in and don’t bother reading the thread, the numerous real examples of mutation and selection I have been posting are not limited to random point mutations and natural selection and they still show that combination selection pressures slow evolution. If you are going to join the ranks of mathematically challenged evolutionarians and claim that other forms of mutations or recombination will somehow magically overcome the effect that multiple selection pressure causes to the evolutionary process, simply study the real case of how HIV evolves when subjected to multiple selection pressures. krazykemist, you better learn this mathematical fact of life if you are developing drugs whose effectiveness is dependant on mutation and selection.

Really, the evolution of antibiotic/chemotherapy evolution is well understood? Do you think this process of evolution is any different from other evolutionary processes?

I see Paul; you are one of joobz’s cooperative chemistry adherents to abiogenesis. Are you also and adherent to joobz’s cooperative selection pressures theory of evolution? Why don’t you rewrite ev and get the selection conditions to cooperate so that it will evolve more quickly?

Too bad the James Randi forum PhD in amathematics is not so good at counting mutations. Let’s review the PhD in amathematics gif of mutation and selection:

http://forums.randi.org/images/smilies/doglaugh.gif
Total number of real examples that show the multiple selection pressures accelerate evolution this week = 0. Total number or real examples the PhD in amathematics has posted = 0. You are really building up the evidence there.

Now don’t be silly BPScooter, the only thing dead on this thread is the dumb theory of evolution. Cause of death; hyperextrapolation, speculationitis, denialophilia, and sciencea amathematica.

Here’s another example of how evolution by mutation and selection works as shown by the ev computer simulation, that is multiple selection pressures slow and ultimately stops evolution.
http://www.thebody.com/content/art39095.html (http://www.thebody.com/content/art39095.html)

Belz, this thread is about bookkeeping. It is based on Dr Schneider’s ev computer simulation which models the bookkeeping of random point mutations and natural selection. What that model shows is that random point mutation and natural selection is a profoundly slow way of accumulating information, too slow for the theory of evolution to be mathematically possible. The only thing that has evolved in this thread is that we now know that the reason this model accumulates information so slowly is the three selection conditions in the model. Set any two of the three conditions to zero and the model rapidly can evolve the third condition. This is how mutation and selection works mathematically and this is how mutation and selection works in reality. The more selection conditions imposed on a population, the more difficult and slower the sorting process for beneficial and detrimental mutations becomes. Someday, this mathematical and real fact of life will soak through the barren dry ground of pseudo-scientific evolutionarian thinking.

No magical stone needed here master of cruft; you just need a little mathematics to understand how mutation and selection works. I find it interesting that it was accountants who brought down Al Capone and it is accounting which has brought down the mythical theory of evolution.

Anacoluthon64, you aren’t paying attention to the real examples of mutation and selection posted here. The previous citation that discusses HCV reports the production of a trillion virons per day. What kind of “massively parallel platform” do you want to speculate into existence? There is no such thing, well; maybe there is one, right next to the imaginary primordial soup. But don’t let me discourage you from discussing this “massively parallel platform” that has no mathematical or physical evidence of its existence. We can file your discussion right next to kjkent1’s string cheese theory of evolution.
If you are interested in learning about the mathematics of mutation and selection, study the ev model. Without looking at the model or the results obtained from the model a have drawn conclusions about the model. The model shows something about the affects of population on the rate of evolution (accumulation of information) as well as the affects of genome size, mutation rate, number of selection pressures as well as a variety of other parameters. If you read the thread, you will find the data posted, if you take Dr Schneider’s model and do a parametric study, you can generate the identical data. When you do either, you will get some understanding how mutation and selection behaves mathematically. When you do this, you understand the dozens of citations I have posted which show that multiple selection pressures slow evolution. So before you jump to your conclusions, either study the thread and the data posted in it or study the model, or better do both.

Another inattentive evolutionist posts on this thread. The computer simulation shows the mathematical behavior, the numerous real examples cited in this thread demonstrate empirically the mathematical fact. What the ev model shows about the effects of number selection pressures and the rate of evolution is demonstrated over and over in reality. What the computer model demonstrates mathematically is the greater the number of selection pressures, the slow evolution proceeds. I have cited more than 50 real examples of this with respects to combination therapy of HIV, combination therapy of HCV, combination therapy of TB, combination therapy of Malaria, combination therapy of mosquito larvae, combination therapy of cancer cells, combination use of herbicides on weeds, combination rodenticides… Every one of these examples shows that combination selection pressures slow the ability of the population to evolve resistance to these selection pressures. This is what ev shows mathematically and these numerous citation show the empirical evidence. This is an obvious finding if you understand the mathematics of sorting and optimization. The more conditions upon which you are sorting or optimizing, the slower the process becomes. Mutation and selection is a sorting process of beneficial and detrimental mutations. As you increase the number of selection conditions this process becomes profoundly slows, too slow for the theory of evolution to be mathematically possible. Ev accurately simulates the mutation and selection process, so study the model if you want to understand how this phenomenon actually works and it is not like the silly extrapolations that evolutionarians like to make.

I have decades of experience both in writing and using complex computer simulations of nonlinear systems and I know how to evaluate the behavior of such models. I made my claims about ev after running hundreds of cases with the model. It is your vanity that leads you to draw conclusions about ev without running a single case.

Really, you are so sure about this conclusion? I remember when people like you made similar claims about the virus and disease only 15-20 years when they said there would be no treatment at all. In just a short period of time treatments have been developed which length lives of those with HIV by decades, of course with evolutionarians like you who don’t understand how mutation and selection actually works, eradication of the virus will take decades longer than it really needs to.

That all fine, now if you just learn how mutation and selection works mathematically as shown by ev and that the results of this model are verified over and over by empirical evidence then you would discard the pseudo-scientific dogma of evolutionism. This pseudo-scientific dogma biases its adherents to the interpretation of reality so severely that they can’t comprehend the obvious mathematical fact of how mutation and selection actually works. By the way, the model isn’t mine, it is the peer reviewed and published model of mutation and selection written by the head of computational molecular biology at the National Cancer Institute and was published in the Oxford University Press journal Nucleic Acids Research. Of course you would have known this if you had read the thread.
Don’t be silly. Ev shows that multiple selection conditions slow and ultimately stop the evolutionary process and I have posted over 50 citations which demonstrate this fact (see below for another citation that demonstrates this fact empirically). The basic argument that evolutionarians (including you) is that ev doesn’t include all the mechanisms of mutation and recombination. However, in the real examples posted all forms of mutations and recombination occur yet these real examples still demonstrate that multiple selection pressures slow the evolutionary process. It doesn’t matter what mechanism you want to include in the mutation and selection process (including recombination), they all demonstrate that multiple selection conditions slow the evolutionary process.

Incorrect krazyKemist, I used Dr Schneider’s computer simulation to establish a mathematical fact, that is that multiple selection conditions profoundly slow the evolutionary process. I then looked in the literature to see whether there was any empirical data to substantiate this mathematical fact and what do we find? There is empirical data from numerous areas of science and medicine that demonstrates the mathematical fact the ev shows. Multiple selection conditions slow evolution. That’s what the mathematics shows and that’s what the empirical data shows. You should really learn the mathematics of mutation and selection.

Perhaps you want to take Adequate’s position that multiple selection pressures accelerate evolution, which would be aberrant. So what type of aberrant behavior do you want to attribute to ev, a computer model which you have yet to do a single case?

Oh, I am not assuming I know all the processes of life, I am saying that mutation and selection does not behave either mathematically or empirically the way evolutionarians allege. It is evolutionarians who assume that mutation and selection can explain all the processes of life. Well, the mathematics and empirical evidence says that evolution by mutation and selection slows profoundly when you have multiple selection conditions.

I’ll tell you what I do know about HIV, combination therapy slow the evolution of the virus profoundly despite it doesn’t seem to be lytic, that it hides in the lymphatic system, that it does recombination,… That’s exactly what ev shows, combination selection pressures slow evolution. I don’t call you vain; I call you uninformed of the mathematics of mutation and selection.

Of course reality trumps the silly theory of evolution. Clinician and scientist who must deal with real problems of mutation and selection realize that multiple selection pressures slow evolution. I posted for you a 50 year old Nobel laureate speech which attests to this fact. Why don’t evolutionarians teach this empirical fact? It is not taught because it interferes with the evolutionarian belief system. Instead evolutionarians concoct ridiculous stories that reptile transform into birds by mutation and selection when the empirical data and now the mathematics say something totally to the contrary.

Dr Schneider, I don’t think you are irrelevant. KrazyKemist, join the ranks of evolutionarians in denial of the mathematics and empirical evidence how mutation and selection works.

Dr Schneider’s model works just fine, it very accurately predicts what happens with multiple selection conditions, however if you want to add “dark matter” to the model, we would all be interested in seeing these results. Hey Paul, does the java language have “dark matter” routines? KrazyKemist, the problem is not with Dr Schneider’s model, the problem is with the theory of evolution by mutation and selection. Until it registers with you that mutation and selection is simply a sorting process of beneficial and detrimental mutations and that as you increase the number of selection conditions, the sorting process becomes slower and slower, you will never understand how mutation and selection actually works.

A little air, a little mathematics, a little empirical evidence, do you want some little dentures?

Oh, are you going to take the position that multiple selection pressures accelerate evolution?

So what is your interpretation? Since you are having trouble understanding that citation, I’ll give you another citation below which shows that multiple selection pressures slow evolution.

It also agrees with the empirical data.

I understand this is what the evolutionarian dogma is but it is not mathematically or empirically true.

Well Belz, if you want to understand how mutation and selection actually works you need to spend time studying the phenomenon and it doesn’t work the way you were taught by the evolutionarian creed. Scientists and clinicians who have to deal with real problems of mutation and selection are learning this lesson.

That’s interesting; I don’t recall using the word “vindicated” at all in this discussion. The phenomenon of mutation and selection is a now present problem in medicine, agriculture, pest control… The empirical evidence shows that multiple selection pressures slow evolution. This is shown by the ev computer simulation as well.

Don’t get monotherapy and combination therapy confused.

Therefore, I will continue to post real examples of mutation and selection for you.

So you don’t think a parametric study of the ev computer model constitutes a mathematical study? This is standard practice for studying a complex computer model in order to understand the mathematical behavior of the model. I understand this is a bit esoteric for an evolutionarian but that is how you do it. Dr Schneider suggested to me personally that I do the study and he suggested this to everyone in his publication on ev. I’ll continue to post empirical examples of this mathematical behavior and you can periodically whine that I am not doing a formal mathematical proof. Do you have any more skateboarding videos?

There are many examples of computer simulations of scientific problems that do not have formal proofs yet the results are accepted because of empirical testing. Perhaps you want to present to us a formal proof that the theory of evolution is mathematically true? Now come on Delphi, we are all waiting for you to present the formal mathematical proof for your theory. Alas, I only have a peer reviewed and published model of random point mutation and natural selection and numerous real examples of how mutation and selection actually works, that is multiple selection pressures slow and ultimately stop evolution. Never mind the mathematical model that shows that multiple selection pressures accelerate evolution, give us one real example where multiple selection pressures accelerate evolution.

The following example of how mutation and selection actually works is for you Delphi, perhaps if the weeds do gene duplication they can overcome the affect of multiple selection pressures.

http://www.blackwell-synergy.com/doi/abs/10.1046/j.1365-3180.2003.00355.x?journalCode=wre (http://www.blackwell-synergy.com/doi/abs/10.1046/j.1365-3180.2003.00355.x?journalCode=wre)

You all have a good weekend and we can continue this discussion next week. You still whining on?

Only I couldn't help noticing, as I skimmed through your turgid drivel, that this is the same halfwitted crap that failed to deceive anyone the last hundred times you parrotted it. There's the lie about Wikipedia, there's the lie about Dr Schneider, there's the lie about "mathematics", there's your halfwitted pretence to have evidence for your views, there's the lie about combination therapy, there's the "slows and ultimately stops" lie, and there's your continuing delusion that you are anything more then an amusing nutter.

This isn't fooling anyone, you realise.

See if you can think of any new lies over the weekend, there's a good creationist.

[kjkent1]

The basic argument that evolutionarians (including you) is that ev doesn’t include all the mechanisms of mutation and recombination. However, in the real examples posted all forms of mutations and recombination occur yet these real examples still demonstrate that multiple selection pressures slow the evolutionary process. It doesn’t matter what mechanism you want to include in the mutation and selection process (including recombination), they all demonstrate that multiple selection conditions slow the evolutionary process.This statement is provably false, as demonstrated by the quote from your latest referenced citation:For treatment areas of 100 ha or less with an initial weed seedbank of 100 seeds m2 and initial frequencies of the resistance genes of 106, development of resistance to both herbicides (double-resistance) is uncommon within 50 years for all types of weeds if both herbicides are used in all years (used in combination). If herbicides are used in alternate years (rotated) double-resistance almost always occurs in 100 ha areas but is uncommon in areas of 1 ha or less. The results suggest that adoption of practices that limit movement of weeds in conjunction with using herbicides in combination rather than in rotation can substantially delay development of herbicide resistance.Note the words "uncommon" and "delay" above. These words mean that evolved resistance is slowed in some, but not all cases. Thus there are cases exist wherein your hypothesis does not hold. And, for those cases, you need an explanation for the exception that comports with your theory -- otherwise your theory is is falsified.

If you were a rationale fellow, you would at least suspect that in the cases where your theory doesn't hold, that some other evolutionary mechanism may be responsible.

But, instead, you treat the exceptions as if they don't exist, maintain that you have proved evolution impossible, and thus by elimination, that God exists.

God will not subordinate His power to anyone (not even Dr. Alan Kleinman), whether directly or by inference, because to do so renders God less than almighty.

Your temerity is only bounded by your disingenuousness.

[Belz...]

Ev shows that multiple selection conditions slow and ultimately stop the evolutionary process and I have posted over 50 citations which demonstrate this fact

Have you, now ?

The basic argument that evolutionarians (including you) is that ev doesn’t include all the mechanisms of mutation and recombination.

I smell burning straw.

However, in the real examples posted all forms of mutations and recombination occur yet these real examples still demonstrate that multiple selection pressures slow the evolutionary process.

Well, the first article you linked to didn't. So what OTHER source do you have ?

Of course reality trumps the silly theory of evolution.

Nonsense. You can see evolution at work every day. So clearly, life forms evolve. The question is, how ?

Of course we ALSO have a very good theory to answer that.

So, do you deny the theory, or the event ?

A little air, a little mathematics, a little empirical evidence, do you want some little dentures?

You keep SAYING that you have mathematics and empirical evidence.

SHOW IT.

Oh, are you going to take the position that multiple selection pressures accelerate evolution?

I'm taking the position that no one claims what you say but you.

So what is your interpretation?

Are we going to play this game ? I say it's your interpretation of the article and you retort by saying that that's my interpretation ? Grow up.

Since you are having trouble understanding that citation, I’ll give you another citation below which shows that multiple selection pressures slow evolution.

I'm not having trouble with it at all. Seems quite clear to me.

It also agrees with the empirical data.

It's hard to say because you haven't presented either.

I understand this is what the evolutionarian dogma

Dogma ? Do you think I go to some sort of evolution church every Sunday and get indoctrinated ? How exactly have I been indoctrinated ? No, better yet, just stick with evidence instead of rhetoric, and we'll do fine.

is but it is not mathematically or empirically true.

"Or" ? Which is it ?

Well Belz, if you want to understand how mutation and selection actually works you need to spend time studying the phenomenon and it doesn’t work the way you were taught by the evolutionarian creed.

Haven't you been paying attention to my post ? I said:

I don't spend time with evolutionism at all, much like I don't spend time thinking about gravity or entropy.

I know enough about the theory to know how it works, but I don't spend my free time obsessing about it the way you seem to think I do. I spend my time doing other things, and I let the scientists obsess with it.

Scientists and clinicians who have to deal with real problems of mutation and selection are learning this lesson.

So far, only you seem to have these "real" problems.

That’s interesting; I don’t recall using the word “vindicated” at all in this discussion.

Perhaps you should look up the word "paraphrase", then.

The phenomenon of mutation and selection is a now present problem in medicine, agriculture, pest control… The empirical evidence shows that multiple selection pressures slow evolution.

Read it again.

Don’t get monotherapy and combination therapy confused.

I must have hit something...

I will continue to post real examples of mutation and selection for you.

I don't think that word means what you think it means. "Continue" implies that you've started.

[krazyKemist]

(Long tired sigh) I'm sorry Dr. Kleinman, but I don't think you really understand my objections. And the reasons I'm not inclined to look in detail in the model. You see, I'm a chemist. I do have some maths background, enough to understand thermodynamics and chemical kinetics and equilibrium, but I can't pretend to understand the complete maths of computational models and what can be wrong (or right!) with them. I'm certain other people here are much more qualified than me to do this. The type of simulation I do involves modeling of molecules and finding energy minimums. Funnily one of the way to do this involves a skimpy little algorithm called the "genetic (or evolutionary) algorithm". But, don't worry, I won't state that it proves evolution is right.

I used to be quite condescendingly amused at the way biochemists write chemical compounds as little triangles and packmans. And to find biology in general quite whooly. Until I got into medicinal research that is. Then I began to understand the type of problems biologists face, and how they cope with them.

Don’t be silly. Ev shows that multiple selection conditions slow and ultimately stop the evolutionary process and I have posted over 50 citations which demonstrate this fact (see below for another citation that demonstrates this fact empirically). The basic argument that evolutionarians (including you) is that ev doesn’t include all the mechanisms of mutation and recombination. However, in the real examples posted all forms of mutations and recombination occur yet these real examples still demonstrate that multiple selection pressures slow the evolutionary process. It doesn’t matter what mechanism you want to include in the mutation and selection process (including recombination), they all demonstrate that multiple selection conditions slow the evolutionary process.

I'm sorry again to repeat what I just said, but all these examples could be interpreted in both the creationist or evolutionist view. There are other explanations to them. So they can't constitute a proof of what you say.

Incorrect krazyKemist, I used Dr Schneider’s computer simulation to establish a mathematical fact, that is that multiple selection conditions profoundly slow the evolutionary process. I then looked in the literature to see whether there was any empirical data to substantiate this mathematical fact and what do we find? There is empirical data from numerous areas of science and medicine that demonstrates the mathematical fact the ev shows. Multiple selection conditions slow evolution. That’s what the mathematics shows and that’s what the empirical data shows. You should really learn the mathematics of mutation and selection.

Not really, Dr. Kleinman. You looked into litterature and interpreted what you found, plus your simulations, as proof of your creationist point of view. And now you are trying to have people believe that clinical research is somehow being affected by this, to turn other people to this view.

I don't spend time contemplating the theory of evolution Dr. Kleinman, and neither do other clinical researchers. Nobody bases protocols on the idea that "multiple selection pressures slow/accelerate evolution". They are based simply on what works, if it is toxic, is it better than the old drug, is there synergy between these drugs, ect. Nowhere does the theory of evolution intervenes.

Perhaps you want to take Adequate’s position that multiple selection pressures accelerate evolution, which would be aberrant. So what type of aberrant behavior do you want to attribute to ev, a computer model which you have yet to do a single case?

I don't take anyone's view. I just say that you are a tad fast to conclude from your model. If evolution is dogma, Dr. Kleinman, surely you know that you need to present overwhelming proof ?

Oh, I am not assuming I know all the processes of life, I am saying that mutation and selection does not behave either mathematically or empirically the way evolutionarians allege. It is evolutionarians who assume that mutation and selection can explain all the processes of life. Well, the mathematics and empirical evidence says that evolution by mutation and selection slows profoundly when you have multiple selection conditions.

No? Please Dr. Kleinman... If you are a specialist of iterative processes and simulation (as I am assuming), then don't you know that something you don't know about may make your simulations go wrong ? I just use computer simulations for molecular modeling and I'm quite aware of this fact...

I’ll tell you what I do know about HIV, combination therapy slow the evolution of the virus profoundly despite it doesn’t seem to be lytic, that it hides in the lymphatic system, that it does recombination,… That’s exactly what ev shows, combination selection pressures slow evolution. I don’t call you vain; I call you uninformed of the mathematics of mutation and selection.

You did call me vain, Dr. Kleinman. I recognize that you may have felt that I was calling you vain, but that is not the case. I was simply saying that creationism is more flattering to mankind than evolution is. You did say that "people like me" slowed down HIV research and cancer research. Do you think it's the first time I, or anyone else in this field, face such critics ? From people whom have never in their lives touched a petry dish ?

And indeed multiple pressures are applied to HIV, Dr. Kleinman, and you seem to think it slows its evolution. Well and good. But then why doesn't die (if viruses are alive, silly me ;) ) ? How is this model of yours helping then ? Aren't there other facts then that could explain this ? Facts from the biology of the virus ?

Of course reality trumps the silly theory of evolution. Clinician and scientist who must deal with real problems of mutation and selection realize that multiple selection pressures slow evolution. I posted for you a 50 year old Nobel laureate speech which attests to this fact. Why don’t evolutionarians teach this empirical fact? It is not taught because it interferes with the evolutionarian belief system. Instead evolutionarians concoct ridiculous stories that reptile transform into birds by mutation and selection when the empirical data and now the mathematics say something totally to the contrary.

Dr. Kleinman, I'm not very impressed by what Nobel laureates have to say on any and every subject. Remember when I said that Linus Pauling, an excellent chemist and Nobel laureate, prescribed megadoses of vitamin C as a cure for cancer ? I still respect Pauling's chemistry, but I can tell you that if I get cancer, I definitely won't be using his treatment...

And, once again, cancer research has little or nothing to do with evolutionary theory, or the way birds or reptiles evolved. If you have a concrete example of how cancer research may be affected by this, please do post it. It may help us understand your worries.

Dr Schneider, I don’t think you are irrelevant. KrazyKemist, join the ranks of evolutionarians in denial of the mathematics and empirical evidence how mutation and selection works.

I never said that Dr. Schneider is irrelevant. I just said that the identity of the conceptor is irrelevant to this discussion. Credentials do not give someone knowledge about everything and anything. Biology and especially virology are extremely "hot" fields. Everything there moves very fast. Its pretty easy to get obsolete.

Dr Schneider’s model works just fine, it very accurately predicts what happens with multiple selection conditions, however if you want to add “dark matter” to the model, we would all be interested in seeing these results. Hey Paul, does the java language have “dark matter” routines? KrazyKemist, the problem is not with Dr Schneider’s model, the problem is with the theory of evolution by mutation and selection. Until it registers with you that mutation and selection is simply a sorting process of beneficial and detrimental mutations and that as you increase the number of selection conditions, the sorting process becomes slower and slower, you will never understand how mutation and selection actually works.

According to your interpretation. Given the model represents the totality of evolutionary processes. I've already expressed why that is a huge given.

Your scoffing at the problem of dark matter is interesting. I used "dark matter" as an analogy of what we don't know about a given field. You do seem to think there's nothing we don't know then. How can you be so sure ? Inspiration from God ;) ?

There are several example in science of things that went quite differently from what we predicted because of something we didn't take into account. Take the evaluation of the human genome to 100 000 genes, when the actual genome has only about 30 000. Or this silly thing that was done in my place, introducing japanese bettles as predators to a pest (ecological pesticide, if you will), telling ourselves that they would die come winter. But oops, they hid in warm houses, and now we're stuck with them.

A good week-end to you too.

the Kemist

[sphenisc]

( From people whom have never in their lives touched a petry dish ?


Petri dish. From Julius Richard Petri, it's an easy one to koch up. ;)

[Dr Adequate]

Please Dr. Kleinman... If you are a specialist of iterative processes and simulation (as I am assuming), then don't you know that something you don't know about may make your simulations go wrong ? No, he's not a specialist in any of the subjects he's discussing, and no, the idea that there are things he doesn't know (basic math, biology, what the theory of evolution is, that sort of thing) appears never to have occurred to the poor chap.

If you want to know where he screwed up with ev, follow the link in my sig, which also contains rebuttals of many of his other amusing opinions.

Dr. Kleinman, I'm not very impressed by what Nobel laureates have to say on any and every subject. Actually, kleinman's just lying about what the Nobel Laureate said. I ought to add that to the FAQ, but I only update it occasionally 'cos it's so rare for him to think up a new lie. For a confirmed fantasist, he's strangely unimaginative.

[Belz...]

Dang, Kemist. Didn't have to say it 3 times!! ;)

[krazyKemist]

Dang, Kemist. Didn't have to say it 3 times!! ;)

Sorry :blush: !

Something went seriously wrong on my end, I guess... The 2 other posts were not there when I finished !

Petri dish. From Julius Richard PetriWP, it's an easy one to koch up.

Oops, my mistake. You might add packman = pacman too. Never been good at spelyng.

the Kemist

[krazyKemist]

I might add that we use 96-wells reaction plates for intact cell assays, but you gotta admit petri dish sounded cooler.

the Kemist

[Kotatsu]

If they are selection pressures they are targeting a particular gene or genes. For example the penicillium mold produces penicillin which targets bacterial cell wall formation. However, even more generalized environmental stresses on life forms target particular genes. Take Delphi’s speculation that temperature change in the environment is what drove the evolution of reptiles to birds. Temperature changes in the environment will target large numbers of enzyme systems which are extremely temperature sensitive. What is called for is that all these temperature sensitive systems will be affected simultaneously and must evolve simultaneously. Random mutations do not cooperate to evolve all these genes simultaneously.

Let me stop your silly-fest here by pointing out that unlike in ev, most reptiles and birds do have sex. The necessary random point mutations --- if we are forced to limit ourselves to discussing that mode of variation-initiation --- need therefore not occur in the same individual.

Your assumption that there is no need to differentiate between variation stemming from mutation and recombination shows a fundamental misunderstanding of the two phenomena. In fact there is strong evidence that recombination and selection is not a random phenomenon. Hardy-Weinberg equilibrium is maintained only if there is random mating.

Not at all. The mutations may occur by God pouring ice cream into the cells for all I care. The important part is not how the variation occurs, but how selection works. If increased numbers selection pressures, regardless of the origin of variation, slows and ultimately stops evolution, then you have a case. If it does not, you do not. It is really not interesting for my argument how the variation originates, as long as it does. And this seems not to be disputed by anyone, at least not in this thread.

If the population can not adapt by recombination and selection (or some behavior change such as migration) then the added selection pressure of an additional kind of predator using a slightly different mode of hunting will only under very rare instances be adapted to by mutation and selection.

Certainly. I am not proposing that it always causes the evolution of new structures. If it did, extinction may have been less common. However, it is sufficient that it does occasionally yield a more derived organism for your claim that added selection pressures will slow and ultimately stop evolution to be revealed as flawed.

The mutation and selection process is many orders of magnitude slower than recombination and selection for adapting to selection pressures. Why is it that the vast majority of examples of adaptation by mutation and selection is seen in microbes with their huge populations, rapid reproduction times and short genomes?

Even though this has no bearing on my argument, a guess would be that there is simply more money involved in the research on microbes which may be of economical or health-related interest than on larger organisms. Also, the larger organisms may be less easy to subject to variations in single selection pressures, as so many affect them, making the study of the effects of variations in selection pressures less easy to study efficiently. It may also be more expensive exactly because the larger organisms generally have longer generation times, need more space, and require more complex environments which may be harder to reproduce in the lab.

I remind you that the empirical examples that I post are not limited random point mutations. In fact, the HIV example includes random recombination yet the evolution of drug resistance for this virus is still markedly slowed by three drug combinations. None of the empirical examples that I have and continue to present are limited to random point mutation yet all show slowing of evolution to multiple selection pressures. Study and learn the mathematics of ev and this will make more sense to you.

Then I take it you agree that ev is not actually a good model, as it models only random point mutations? Good, then we can move away from the failures or successes of ev and focus entirely on the real world.

I am not arguing that variation does not occur, what I am arguing is that variation by recombination and selection is a very rapid process but does not have the capability of adding information to the gene pool and that variation by mutation and selection is a profoundly slow process for adding information to the gene pool. We have real empirical examples of how rapidly variation can occur in a population by recombination and selection and we have real examples of how slowly variation can occur in a population by mutation and selection. The process for the later case occurs most rapidly when there is only a single selection pressure; each addition selection pressure profoundly slows the process of evolution.

And I argue, again, that as long as there is variation over time, it does not matter how this variation came to be. Variation from both these sources as well as many others occur at the same time between generations. The selection pressures are largely independent of how the variation originates, and this origin is therefore not interesting.

I understand your feelings and this is one of the reasons why I think indoctrination into evolutionism introduces a bias into the interpretation of reality and thus is a theory which is harmful to science. It is my hope that the hard mathematical facts which ev demonstrates and the empirical evidence of these facts will move you to investigate.

An as soon as you exchange your normal modus operandi of insults, lying and subterfuge for actually presenting a coherent explanation, mathematical proof, or similar, the points you raise may actually do so. Behaving like a ten-year-old in calling people names, wilfully misunderstanding what they say to make them look ridiculous, and call any protests "whining" profits no one. It makes you look silly, makes people take you less serious, and, ultimately, stops all interest in you and your claims, except for intellectual scavengers.

I think you need to look up the word “antigen”, I suspect you meant to use the word “antibiotic”. Now, it may be possible that treating a population of microbes with three drugs may yield a small population that is resistant to all three drugs; however, the point is that it is much more difficult for a population to evolve resistance to three drugs simultaneously than to the same three drugs when applied sequentially. You may have a few bacteria in a population which is already resistant to all three drugs and when these selection pressures are applied, the only bacteria left are the resistant members. This is why monotherapy is discouraged for the treatment of HIV because mutation and selection can quickly evolve resistance to that single drug. You don’t want to introduce into the population of microbes members who are already resistant to drugs you want to use in combination therapy.

But in these therapy tests, the selection pressure (i.e., the antibiotic) is basically an on-off switch, isn't it? Either the germ is resistant to it, and then it survives, or it is not, and then it dies. There is, ideally, no state in between those to in which even non-resistant germs may survive to a lesser degree? If so, this situation is not a parallel to the situation outside the lab, where not all selection pressures need to be of the on-off variety.

The intense breeding of dogs in the past 10,000 years has led to large morphological differences in the species but they are still all homologous. You need errors to transform reptiles to birds and ev shows this to be mathematically impossible (for random point mutations).

And thus, again, what ev shows and does not show becomes irrelevant, as it does not consider all kinds of mutations which we see in real life. I think your case would be stronger if you just abandoned this strange clinging to ev all the time.

Further, 10,000 years is more or less a sneeze into the cosmos. It would be more amazing if non-homologous structures had evolved in that short space of time. Especially considering that the basic uses of dogs are more or less homogeneous, and thus do not generally provide an impetus for any great range of variation to occur.

According to the Hardy-Weinberg law, random recombination can not even change the frequency of alleles in a population, let alone increase the information in the gene pool. The reason why random point mutations are the most important and most interesting form of mutations is that they are the most common and least destructive form of mutation. Insertion/deletions cause frame shifts which are almost always lethal, other forms of mutations are more rare and usually are not beneficial.

I will concede that that is a valid answer, though not a satisfactory one. While I can agree with what you say, it still doesn't tell me why adding selection pressures would only have an effect on the variation coming from random point mutation.

A population may be able to adapt to multiple selection pressures quickly by recombination but this is not a random process. When it comes to a population adapting by random mutation and natural selection then you see the effect of multiple selection pressures slowing the process.

And yet, we also see that when a holistic approach is taken, including origins of variation other than random point mutation, evolution is not slowed by added selection pressures. A case in point is the limpets, for instance. An added for a predation did not slow or stop evolution of its shell structures. This example alone may be sufficient to dismiss all your protestations and your insistence to look only at random point mutations.

Further, I have not said that selection is a purely random process, and I do not believe it is (depending on how "random" is defined, of course).

When I ask the question, what is/are the selection pressures which would transform a reptile into a bird, at least you try to pose an argument. However, many evolutionarians respond that if I knew something about evolution, I would never ask the question. Science is the study of cause and effect. If evolutionarians can not define the cause which would transform a reptile into a bird, they are abandoning scientific reasoning. If you are going to argue that a predator chasing a reptile into the tree is the stimulus for the reptile to grow wings, the more obvious counter argument is that recombination and selection would select for a population with longer legs which would be achieved quickly. The number of genetic changes needed to evolve wings by mutation and selection would take massive numbers of generations.

Your question, though, is not necessarily an honest one. In any event which has taken place before recorded history, there is bound to be a degree of (qualified) guess work, regardless of how highly scientific standards are cherished. While the standard answer you have received is not a good one, it does have some truth in it. Isolating single --- or even multiple --- selection pressures resulting in events that took place hundreds of millions or years ago. Your question implies the need for an absoluteness of certainty which cannot be achieved.

And, to continue, I believe that if most predators are ground-bound, adopting an arboreal life style would still be a valid option. It does not have to be the most obvious or the best one, because there are no such requirements in the theory of evolution. It is sufficient that it happened at least once, and that the results of this events were to some extent fortuitous.

It’s a mathematical impossibility.

Show this in one or a set of formulae. I am not a math expert, but I understand that there are several others here --- some even participating in this very thread --- who are, and who could test your formulae.

Again, you confuse variation by recombination and selection and variation by mutation and selection. The former can achieve large morphological changes in the population in a very short time while the later requires huge numbers of generations to achieve much smaller changes.

And again, I state that this confusion is neither a confusion, nor really pertinent. The predator does not care if the prey species sudden increased success in getting away is due to random point mutations, polyploidy, or sexual selection.

It is these kinds of vague imaginations of arms transforming into wings and scales transforming into feathers which makes the theory of evolution only suitable for the Scifi channel. It is hard mathematical analysis like what is seen with ev which explains how mutation and selection actually works. Then the empirical evidence can be examined to see whether the results of this mathematical analysis has any validity and we find it does.

I would hesitate to call it "vague imaginations", given the great fossil material showing exactly the transitions you refer to.

There are plenty of people who have different interpretations of these fossils. This is why I prefer to stick with a mathematically based argument.

Or, at least, claiming you are.

If you are going to argue that mutation and selection is the driving force for the theory of evolution, you need to account for this mathematically and ev shows you can’t.

No, ev shows that you can't if you arbitrarily deprive yourself of large parts of the spectrum of different ways to achieve changes. That is not the same thing.


---

I would like to apologise in advance for any silliness this message may contain. I was visiting a friend in Würzburg until yesterday lunch, and have had a lovely 22-hour trip back home now, containing spending the night awake at Stanstead and then walking for 40 minutes from the airport to the bus stop as I didn't have any cash left. I am therefore incredibly tired, and may have forgot to think before I answered.

[Kotatsu]

You start with a average genome size for reptile 25% larger than birds yet birds are supposed to be more advanced than reptiles. Where do you want to go next in the calculation?

I would like to draw your attention to my post count, yours, and the concept of "junk DNA".

[articulett]

I would like to draw your attention to my post count, yours, and the concept of "junk DNA".

What an excellent analogy!

Too bad he's impervious.

Just wanted to let you know that there is someone in the cyberworld enjoying the repartee.

[Belz...]

Show this in one or a set of formulae. I am not a math expert, but I understand that there are several others here --- some even participating in this very thread --- who are, and who could test your formulae.

You're wasting your time. If he HAD any mathematical proof he'd have presented it, by now.

All he has is his interpretation of a piece of cherry-picked paragraph.

Excellent post, by the way.

[Belz...]

I would like to draw your attention to my post count, yours, and the concept of "junk DNA".

Hopefully my own bloated post count, in relation to our mutual join dates, won't be construed as being part of the same analogy.

[Kotatsu]

What an excellent analogy!
Too bad he's impervious.
Just wanted to let you know that there is someone in the cyberworld enjoying the repartee.
and,
Excellent post, by the way.

Hooray for praise! Hooray for me!

You're wasting your time. If he HAD any mathematical proof he'd have presented it, by now.
All he has is his interpretation of a piece of cherry-picked paragraph.

Yeah, I know... But I do believe it bears repeating. I mean, everything else in this thread is repeated over and over again.

It sometimes seems to me as if Kleinman uses the number of times something has been said as evidence of it being true. If that's how he works, then we should exploit it.

Hopefully my own bloated post count, in relation to our mutual join dates, won't be construed as being part of the same analogy.

Like all analogies, it can be stretched only so far. Though if you are a regular of the Politics subforum, I cannot guarantee that the analogy does not still hold.

[Dr Adequate]

Belz, this thread is about bookkeeping. But without actual numbers, 'cos they make your little brain all hurty.

[BPScooter]

Hey, man, thanks for not discouraging us from discussing things like "massively parallel platforms." Really kind of you.

And also thanks for implying that each and every one of us fall into your neat categories of "amathematicians" and such, that's a nifty name-call.

Do indeed continue to call us out, as a group, and make snappy insulting names up for all of us. That will surely make your case, I'm surprised I didn't get it the first time, but now I'm totally convinced that your case is iron-clad. Persistence does pay off.

[Belz...]

Like all analogies, it can be stretched only so far. Though if you are a regular of the Politics subforum, I cannot guarantee that the analogy does not still hold.

I don't go to Politics often. The "critical" part of "critical thinking" seems somewhat ineffective, there.

[Kotatsu]

I don't go to Politics often. The "critical" part of "critical thinking" seems somewhat ineffective, there.

[obvious joke alert]
During my infrequent visits there, I have often found the "thinking" part leaving something to be desired as well.
[/obvious joke]

[Belz...]

Maybe it's not the folk, but the forum itself, that crates this effect...

[BPScooter]

Well, all I want to say at the moment is that when I said "your case" and 'iron clad" my tongue was in my own personal cheek. Yes, just the British English term: cheeky.

[kleinman]

You evolutionarians still are having a hard time understanding how mutation and selection actually works. I’m back to correct your tangled pseudo-intellectual belief system. Let’s start with Adequate.
This isn't fooling anyone, you realise.
Do you mean the results I have presented from Dr Schneider’s peer reviewed and published model of mutation and selection or the numerous citations of empirical examples of this mathematics which show that combination selection pressures slow evolution? Let’s look again at your analysis of how mutation and selection works.
Adequate’s multiple selection pressure gif from pg 105
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
The red line shows generations to achieve fixation of n alleles acted on by n selection pressures, the n+1th selection pressure being introduced only after the nth allele is fixed.

The blue line shows generations to achieve fixation of n alleles acted on by n selection pressures simultaneously.

All other features and parameters of the two models are identical. The model is designed so that the relative advantage of n+1 new genes over n (when selection is acting) is the same for all n, i.e. each new allele carries the same advantage.

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
http://forums.randi.org/images/smilies/doglaugh.gif
Could you give us a real example of your silly gif which shows that multiple selection pressures accelerate evolution cheese wiz?
Now we come to kjkent1 who thinks that he can parse his way out of irrational view of how mutation and selection actually works.
http://www.blackwell-synergy.com/doi/abs/10.1046/j.1365-3180.2003.00355.x?journalCode=wre (http://www.blackwell-synergy.com/doi/abs/10.1046/j.1365-3180.2003.00355.x?journalCode=wre)
A simulation study was conducted to examine the effect of pattern of herbicide use on development of resistance to two herbicides with different modes of action in finite weed populations. The effects of the size of the treatment area (analogous to initial weed population), germination fraction and degree of self-pollination in the weed were investigated. The results indicate that the probability of developing resistance to one or both herbicides decreases as the size of the area/initial population decreases. For treatment areas of 100 ha or less with an initial weed seedbank of 100 seeds m2 and initial frequencies of the resistance genes of 106, development of resistance to both herbicides (double-resistance) is uncommon within 50 years for all types of weeds if both herbicides are used in all years (used in combination). If herbicides are used in alternate years (rotated) double-resistance almost always occurs in 100 ha areas but is uncommon in areas of 1 ha or less. The results suggest that adoption of practices that limit movement of weeds in conjunction with using herbicides in combination rather than in rotation can substantially delay development of herbicide resistance
Note the words "uncommon" and "delay" above. These words mean that evolved resistance is slowed in some, but not all cases. Thus there are cases exist wherein your hypothesis does not hold. And, for those cases, you need an explanation for the exception that comports with your theory -- otherwise your theory is is falsified.
Kjkent1, if you read the entire sentence, you will see that combination herbicides make it uncommon for resistance to evolve in 50 years where as alternating monotherapy, resistance almost always occurs in the larger acreages. The last sentence in the quote above clearly states that combination herbicides are more effective than monotherapy herbicides used in rotation. Is that the best argument that you evolutionarians can raise by parsing sentences?
Ev shows that multiple selection conditions slow and ultimately stop the evolutionary process and I have posted over 50 citations which demonstrate this fact.Have you, now ?
Certainly have.
The basic argument that evolutionarians (including you) is that ev doesn’t include all the mechanisms of mutation and recombination.I smell burning straw.
That smell is the decomposing remains of the theory of evolution. It produces quite a stink. Of course, now that we know how mutation and selection actually works, science can finally start advancing again, none of this silly mythology that evolutionarians put forward.
However, in the real examples posted all forms of mutations and recombination occur yet these real examples still demonstrate that multiple selection pressures slow the evolutionary process.Well, the first article you linked to didn't. So what OTHER source do you have ?
If you are too lazy to go back and read the numerous citations I have posted (I even highlighted these posts with large red type), it doesn’t matter, I have many more citations to post so just keep reading. At least kjkent1 parses these citations trying to make a point; you don’t even do as much. All these citations show empirically what ev shows mathematically, that is multiple selection pressures slow evolution.
Of course reality trumps the silly theory of evolution.Nonsense. You can see evolution at work every day. So clearly, life forms evolve. The question is, how ?
Certainly we see evolution at work, single selection pressures evolve relatively quickly while additional selection pressures slow down the process profoundly. This is what ev shows and this is what reality shows. You don’t have the selection pressures and you don’t have the time to evolve birds from reptiles. This is the mythological fantasy that evolutionarians extrapolate. It is a mathematical impossibility.
You keep SAYING that you have mathematics and empirical evidence.

SHOW IT.
I have posted the results from ev multiple times and the numerous citations are there for anyone who wants to read them. I’ll continue to post more citations for you since you are having a hard time understanding how mutation and selection actually works.
Oh, are you going to take the position that multiple selection pressures accelerate evolution?I'm taking the position that no one claims what you say but you.
And I have the mathematical and empirical evidence to back up my contention. I’m still waiting for you evolutionarians to post a single example of multiple selection pressures accelerating evolution, but alas I believe this will be a long wait.
I understand this is what the evolutionarian dogmaDogma ? Do you think I go to some sort of evolution church every Sunday and get indoctrinated ? How exactly have I been indoctrinated ? No, better yet, just stick with evidence instead of rhetoric, and we'll do fine.
You evolutionarians are more faithful to your dogma than many other religious fanatics. You think you have a scientific basis to your belief system but put a little mathematics to your allegations and we find out how mutation and s