Annoying creationists [Archive] - Page 18

kleinman

22nd May 2007, 10:53 AM

Kleinman, You haven't addressed this issue. Please explain why anyone would believe anything you say? And remember, we've found you woefully ignorant of, well, about everything.
What issue are you talking about? You make a long post with no coherent explanation to what point you are trying to make. I’ll try to sort through your post and try to figure out what you are trying to say, if for nothing more than to try to stop your whining for a while.
I think this paper wouldn't have been accepted if that was the case:
Carvajal-Rodriguez A, Crandall KA, Posada D. "Recombination favors the evolution of drug resistance in HIV-1 during antiretroviral therapy." Infect Genet Evol. 2007 Feb 12; [Epub ahead of print]
I can't access the paper yet, but from the abstract: Using computer simulations we show that the effect of recombination on the evolution of drug resistance depends strongly on the intensity of selection, as well as on the viral population size. Under the high selection pressure expected during antiretroviral therapy, the strength of the Hill-Robertson effect increases and recombination favors the evolution of resistance under a wide range of population sizes, independently of the sign of the epistatic interaction. Our results suggest that recombination plays an important role in the evolution of drug resistance in HIV-1 under various realistic scenariosSeems like evolution has a mathematical basis after all.
Certainly evolution has a mathematical basis. If you studied ev you would understand this. Do you think that recombination overcomes the effect that multiple selection pressures slow evolution? If you do, then why is combination therapy used to treat HIV? Why have all the citations to the treatment of HIV call for combination therapy? Despite HIV’s ability to do recombination, multiple selection pressures still slows the evolution of drug resistance in this virus.
Unfortunately, you've been using HIV viruses as proof of why evolution is impossible. I show a study where they demonstrate how multiple selection pressures won't HALT HIV evolution, and now you claim that I can't extrapolate this truth to anything else.
Joobz, combination therapy for the treatment of HIV is only one of the many examples of how multiple selection pressures slow evolution. HIV is one of the most extreme cases of evolution because it has a very small genome length, high reproductive rate and large populations with high mutation rates. HIV also does recombination. Despite all these evolutionary advantages, as few as three selective pressures are sufficient to slow the evolution of resistance of this virus profoundly and prevent AIDS. Just because you are pessimistic that resistance still occurs, I have confidence in intelligent biochemical designers who will make molecules that will halt the evolution of the virus completely.
This isn't an "adjustment of a theory". This is intellectual dishonesty.
We have been discussing how multiple pressures doesn't stop evolution using HIV as an example. I give evidence that states mathematically that this isn't the case. And now you claim that it doesn't apply.
This is the worst form of professional behavior.
Don’t blame your failure to understand the mathematics of mutation and selection on me. You are responsible for your own ignorance. If you want to see an example of how multiple selection pressures stops evolution read this link http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219)

Joobz, multiple selection pressures slow and ultimately stops evolution. If you study ev, you would understand this. If you read Delphi’s reference to Wikipedia and the fitness landscape you would understand this. If you read any of the citations I have made that discuss this topic you would know this. Instead you prefer to live in ignorance and denial of the mathematical and real fact that multiple selection pressures slow and ultimately stop evolution. Since you believe otherwise, give us one real example where multiple selection pressures accelerate evolution. Post your proof and stop whining.

Here are a couple more examples of how multiple selection pressures slow evolution. The second example in the post is interesting because it pertains to the evolution of resistance in cancer cells.

http://jac.oxfordjournals.org/cgi/content/full/52/1/11 (http://jac.oxfordjournals.org/cgi/content/full/52/1/11)
Since many bacterial species have two intracellular targets for the fluoroquinolones (DNA gyrase and DNA topoisomerase IV), these agents have been investigated for dual targeting.58 Several new compounds (moxifloxacin, gatifloxacin, gemifloxacin and clinafloxacin) approach the dual target situation with S. pneumoniae, as judged (i) by very low mutation frequencies,59 (ii) by decreased susceptibility of both gyrA and parC resistance mutants (clinafloxacin),59 and (iii) by a diminished plateau (inflection point) in plots of mutant recovery versus fluoroquinolone concentration (moxifloxacin).24 Thus dual targeting appears to be a good approach for refining compounds to restrict resistance.
In this case, a single drug acts as two selection pressures.
According to these ideas, restricting the development of resistance requires that antimicrobial concentrations at the site of infection be kept above MPC. If that cannot be done for a given agent–pathogen combination, the agent should be used as part of a combination therapy involving agents with different targets. Such an approach is likely to be required for plasmid-borne resistance.
If you don’t have a drug that can act at multiple targets, use combinations to prevent the slow the evolution of resistance.

Here is a nice example of how multiple drug therapy slows the evolution of resistance with cancer therapy.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1863594 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1863594)
Single agent therapy is unlikely to be successful for very long because the emergence of resistant strains of tumor cells is almost the rule in such circumstances. Only combination therapy using different types of drugs that attack a target at different sites on a molecule or attack other key molecules can prevent resistance in most cases.

More quotes which substantiates what ev shows, what the Wikipedia reference to fitness landscape shows us, that is multiple selection pressures slow evolution.

joobz

22nd May 2007, 11:10 AM

What issue are you talking about?
Let me remind you. Here's a summary of what that post shows:
I don't know. I thought the change from
"HIV is proof evolution is impossible" to
"HIV is not representative of evolution"
was a very humorous transition.
Ooh, yes!

* claps hands *

And look at the reason he gives.

It undergoes recombination!

:dl:

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

Did you get that folks?

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

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

You see, Kleinman, like you said before. google is watching. You may wish to play a bizarre game of missdirection, but we have proof of what you really are. Feel free to keep on posting more papers showing what everyone knows. You have yet to show one single bit of evidence that macroevolution doesn't occur.

Dr Adequate

22nd May 2007, 11:38 AM

You have, rather than repeating it again, I’ll show you how to do it using ev. Start by using Dr Schneider’s baseline case that he used in his publication. Then use his suggestion that he published to vary genome length, mutation rates, population, selection etc. and if you systemically tabulate the generations for convergence as you vary these parameters, you will find that the dominant parameters in the model are the genome length and the number of selection pressures. That is the analysis that you have missed.

If you practice medicine for any length of time, you will find that faith has a major impact. The terminology used is placebo/nocebo effect. When you are practicing law, does it matter what you and your clients are putting your faith in?

Where is Unnamed to defend his selection scheme? What happens to the data when using Unnamed’s selection scheme and you set two of the three weight factors to zero? What are the real examples that you can give us that demonstrate Unnamed’s selection scheme? This is why I disregard what you have posted. In contrast, the data I post is from Dr Schneider’s peer reviewed and published model of mutation and selection and I have posted 15-20 real examples of this mathematical behavior shown by ev.

I am, I’m still looking for a plumber to clean the clog pipes in your brainwashed cultist evolutionist minds. Then perhaps you will understand the mathematics that ev demonstrates and the numerous real examples of this mathematics that I have posted.

The only dead end in this discussion is the one for the theory of evolution. Once you comprehend that the emergence of a trait occurs by evolution and that is slowed by the introduction of more selection pressures you to will realize that the theory of evolution is a dead end. Huge populations won’t rescue your theory but at least you now realize that recombination and natural selection can and does reduce the number of alleles and thus the amount of information in the gene pool. You really need to study ev, you will learn something about the mathematics of mutation and selection.

Tell that to the editors of Wikipedia:

Paul, would you give us an example of a selection pressure that increases replication?

Stop whining Sesame Street dropout. I just posted the Wikipedia definition for selection pressure. I had already posted the definitions used in Genetics in Medicine, by Thompson and Thompson. So, Sesame Street dropout, when are you going to point out the error in the equation from the link you posted that computes selection pressures and then to explain the equation from your link? Once you learn how to count, everything I say will make sense to you.

I’m not uncomfortable with any question asked in this thread, pussycat. Do you think I should feel bad when mathematics and reality show the theory of evolution to be untrue? The answer to your question is Matthew 25:23.

Joobz, not only have you failed to refute my hypothesis, I have given you a real case where multiple selection pressures stops evolution. I will continue to present new references that show that multiple selection pressures slow and ultimately stop evolution. This is what ev shows and this is what reality shows. This is how the mathematics of mutation and selection works. You are still in the running to be the last evolutionist to understand how the mathematics of mutation and selection works. If you don’t want to win this race of denial and ignorance, study ev.

Here are a couple of more references which show that combination selection pressures slow evolution (and in one case appears to reverse evolution of drug resistance).

http://www.bioone.org/perlserv/?request=get-document&doi=10.1603%2F0022-2585(2003)040%5B0985%3AEFSOIR%5D2.0.CO%3B2 (http://www.bioone.org/perlserv/?request=get-document&doi=10.1603%2F0022-2585(2003)040%5B0985%3AEFSOIR%5D2.0.CO%3B2)

I added the highlighting.

http://www.ucsf.edu/synapse/content/51007/bacteria.html (http://www.ucsf.edu/synapse/content/51007/bacteria.html)

This link is particularly interesting since it appears that the evolution of drug resistance can be reversed.
Of course your brainwashed and prejudiced evolutionist’s mind remembers things differently. Now if you can only recall your mathematical training that was required of you in order to obtain your degree in alchemical engineering, we can free you from your unscientific bias.

Po’ old joobz can’t understand the link so I have to spell it out for him.
http://www.ucsf.edu/synapse/content/51007/bacteria.html (http://www.ucsf.edu/synapse/content/51007/bacteria.html)

I added the highlighting.

The use of ciprofloxacin on doxycycline resistant bacteria resulted in the selection of doxycyline sensitive bacteria reversing the evolution of doxycyline resistance.

Understand rubberband?
What intellectual dishonesty? I’ve simply taken an evolutionist written, peer reviewed and published model of mutation and selection and done a parametric study with the model that shows with realistic genome lengths the model takes huge numbers of generations to evolve only a small number of loci. The number of generations is so huge that it shows the theory of evolution is impossible by this mechanism. I have also shown that the reason this model takes huge numbers of generations to converge in the three selection conditions. When you eliminate two of the three selection conditions, you can evolve the remaining selection condition very rapidly. I have then shown numerous real examples of this mathematical behavior including one example where evolution is actually stopped. The only thing you have shown in this thread is that you have no mathematical competence or understanding of the mathematics of mutation and selection, but that is nothing unusual for you. Despite your training and PhD in alchemical engineering, you have no idea how ribose can form nonenzymatically yet you believe abiogenesis is true.

It seems joobz just gave us a serving of kjkent1’s red herring, your post so far has been loaded with whine as well.

Of course you don’t understand the mathematics of mutation and selection. You try to cover your ignorance by calling this gibberish.

This author has yet to learn that extinction does occur. Perhaps you and he need to read this link http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219) where multiple selection pressures can and do stop the evolution of resistance.
Little gator, you have a few problems with your conclusion here. The first problem for you is that the author of this program disagrees with you and his analysis has been peer reviewed and published. The second problem for you is that even if the selection process is not totally realistic, it simulates a real selection process mathematically close enough that there are numerous real examples of this mathematical behavior. The third problem for you is there are no external environmental forces that would change the mathematical fact that multiple selection pressures slow the evolutionary process. Your objection is overruled.

Yes, it is mostly speculation except the results from ev that closely matches the numerous real examples of mutation and selection (which are not limited to random point mutations) and Delphi’s Wikipedia reference to fitness landscape which nicely explains the results from ev. Objection overruled.

Does your faith in your string cheese theory of evolution cause your hormones to change?

Why kjkent1, I am doing my calling, I’m disposing of the theory of evolution.

You haven’t paid attention to what Unnamed has said:

That is the last we heard from Unnamed.

Let’s see, Dr Schneider’s is unrealistic and Unnamed’s selection process outperforms it. Does that make Unnamed’s selection process really unrealistic?

What Dr Schneider’s algorithm properly models is the mathematics of multiple selection conditions and how this slows the evolutionary process. This is the mathematical reality of the mutation and selection process. I have presented numerous real examples of this mathematical fact and will present to more examples at the end of this post.

Are you talking about the brainwashed, mathematically challenge, cultist evolutionists who are racing to win the race to be the last evolutionist to understand the mathematics of mutation and selection? I’m still waiting for Dr Richard to point out the error in the equation from the link that he posted.

We are seeking a professional gardener who can do something with the evolutionary landscape but alas, you can’t do much with a dead theory.

You read Matthew 26:23, not Matthew 25:23.

In the context of this thread, you evolutionists really have trouble with numbers.

Since Mr Scott was so kind to give me the opportunity to clarify my post, I return the kindness to you Taffer. Explain to us how recombination and selection increases variation in the population and does not decrease it. If you want, you can also explain to us how resistance emerges without evolution.

More articles on combination therapy for slowing evolution.

http://www.journals.uchicago.edu/JID/journal/issues/v192n7/34874/34874.html (http://www.journals.uchicago.edu/JID/journal/issues/v192n7/34874/34874.html)

http://www.hivandhepatitis.com/2006icr/16aids/docs/082106_e.html (http://www.hivandhepatitis.com/2006icr/16aids/docs/082106_e.html)

More real examples of multiple selection pressures demonstrating the mathematics of ev that multiple selection conditions slow the evolutionary process (including one example where it stops the evolutionary process). Can’t any of you evolutionists use google and find one example of multiple selection conditions accelerating evolution?

Joobz apparently hasn’t noticed that I have stated microevolution occurs. It is macroevolution which doesn’t occur. The reason macroevolution does not occur is that multiple selection pressures slow and ultimately stop the evolutionary process. Joobz can’t find an example where multiple selection conditions accelerate evolution because there isn’t an example of this.

The only way to explain this is that you are ignorant of the mathematics of mutation and selection and you can not tell the difference. This is why you have trouble understanding the logic of this discussion. You are certainly working hard to win the race to be the last evolutionist to understand the mathematics of mutation and selection.

Are you still trying to get the monkey role in the next Scopes trial?

Your construction of an argument by Dr Schneider of what I am saying ev shows….is a fabrication on your part little gator. Let’s look at what he said precisely.

If Dr Schneider thinks that varying the mutation rate will overcome the effect of multiple selection pressures, he could easily add this to ev and prove his point.

If Dr Schneider thinks that these mechanisms will overcome the effect of multiple selection pressures, he should add any or all of these features to ev and prove his point.
You left this part of his quote out little gator.

You can find Dr Schneider’s link at http://www.ncbi.nlm.nih.gov/books/bv.fcgi?call=&rid=mono_001.TOC&depth=2. You should look at the link. If this is Dr Schneider’s idea of divergence, he chose a very strange way of showing this. This link to ABC transporter genes is a listing of all the diseases associated with these genes. Why are there diseases to ABC transporter genes? Mutations to these genes cause the genes to become poor or nonfunctional. His link is an example of stabilizing selection pressures, not divergence.

Now if you want to quote Dr Schneider, do it like this:
Dr Schneider said the following in response to a critique of ev written by Royal Truman. This quote is taken from Dr Schneider’s web site at:
http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/truman/

And Dr Schneider said the following:
http://www.lecb.ncifcrf.gov/~toms/paper/ev/blog-ev.html
The following are Dr Schneider’s responses to a critique of his paper Evolution of biological information by Dr Stephen E Jones.

The following is a response Dr Schneider made to a statement made by David Berlinski.

This lame legal attempt at refuting a mathematical finding won’t cut it.

How many paper’s and statements from scientists that state that multiple selection pressures slow evolution do you need? Well, I have two more quotes that state this for this post. You can see them below.

I’m chicken? Other than Paul and Delphi who reveal his identity, all you evolutionists hide behind pseudonyms. You evolutionists are the cowards. If your ideas are so good, put your real name behind them.

You are wrong on several points here but we see an example of how a cowardly bigot operates. One wonders how lawyers ever get bad reputations.

Let’s see if Paul or Dr Schneider embraces Unnamed’s selection process since it has no connection with reality.

I have mathematical proof and numerous real examples that the theory of evolution is unreal. Do you have mathematical proof that God is unreal? We all would like to see this.

Are you Dr Schneider’s lawyer? If you are, you are chasing an ambulance with a dead theory in it.

Ev demonstrates a simple mathematical fact. That fact is that multiple selection pressures profoundly slow the evolutionary process. Wikipedia describes this fact nicely in the fitness landscape topic. I have and will continue to post more links of real examples of the phenomenon. Only brainwashed, cultist evolutionists will fail to acknowledge this mathematical and real fact.

We are seeking professionals, a plumber to clear the clogged pipes evolutionists suffer from and a landscaper who perhaps can do something with the evolutionary landscape. There is little hope for the latter since the theory of evolution is a dead tree.

Do you mean like your basic genetics that recombination and natural selection can not result in the loss of alleles? Perhaps you are talking about how multiple selection pressures accelerates evolution? Would you give us a citation which shows that multiple selection pressures accelerate evolution? These citations I present show that multiple selection pressures slow and ultimately stops evolution. This is what ev shows, this is what reality shows. I have more citations below.

Isn’t it enough that a bad scientific theory be refuted?

What you said was:

If you read the entire Wikipedia quote on “selection pressure” you would have seen the following line which I highlighted.

Selection pressures remove the un-fittest. Selection pressures only inhibit replication, they do not enhance replication.

I don’t believe you are correct in this point Paul. Consider the following example. You have a Petri dish with bacteria in it. Some of the bacteria are sensitive to an antibiotic and others are resistant. Initially you have no antibiotic in the dish an all bacteria are reproducing at the same rate. You then place the antibiotic into the dish and select out all the sensitive bacteria. The sensitive bacteria are inhibited from reproducing. The resistant bacteria do not reproduce at a higher rate (unless you want to say that the nutrient supply that the sensitive bacteria no longer can use is now available to the resistant bacteria).

This little side bar discussion on selection pressures does not override the fact that ev shows that multiple selection pressures slow evolution and there are numerous real examples of this mathematical fact.

More links to combination selection pressures slowing evolution.

http://www.bact.wisc.edu/themicrobialworld/bactresanti.html (http://www.bact.wisc.edu/themicrobialworld/bactresanti.html)

http://content.healthaffairs.org/cgi/content/abstract/25/2/325 (http://content.healthaffairs.org/cgi/content/abstract/25/2/325)

What issue are you talking about? You make a long post with no coherent explanation to what point you are trying to make. I’ll try to sort through your post and try to figure out what you are trying to say, if for nothing more than to try to stop your whining for a while.

Certainly evolution has a mathematical basis. If you studied ev you would understand this. Do you think that recombination overcomes the effect that multiple selection pressures slow evolution? If you do, then why is combination therapy used to treat HIV? Why have all the citations to the treatment of HIV call for combination therapy? Despite HIV’s ability to do recombination, multiple selection pressures still slows the evolution of drug resistance in this virus.

Joobz, combination therapy for the treatment of HIV is only one of the many examples of how multiple selection pressures slow evolution. HIV is one of the most extreme cases of evolution because it has a very small genome length, high reproductive rate and large populations with high mutation rates. HIV also does recombination. Despite all these evolutionary advantages, as few as three selective pressures are sufficient to slow the evolution of resistance of this virus profoundly and prevent AIDS. Just because you are pessimistic that resistance still occurs, I have confidence in intelligent biochemical designers who will make molecules that will halt the evolution of the virus completely.

Don’t blame your failure to understand the mathematics of mutation and selection on me. You are responsible for your own ignorance. If you want to see an example of how multiple selection pressures stops evolution read this link http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219)

Joobz, multiple selection pressures slow and ultimately stops evolution. If you study ev, you would understand this. If you read Delphi’s reference to Wikipedia and the fitness landscape you would understand this. If you read any of the citations I have made that discuss this topic you would know this. Instead you prefer to live in ignorance and denial of the mathematical and real fact that multiple selection pressures slow and ultimately stop evolution. Since you believe otherwise, give us one real example where multiple selection pressures accelerate evolution. Post your proof and stop whining.

Here are a couple more examples of how multiple selection pressures slow evolution. The second example in the post is interesting because it pertains to the evolution of resistance in cancer cells.

http://jac.oxfordjournals.org/cgi/content/full/52/1/11 (http://jac.oxfordjournals.org/cgi/content/full/52/1/11)

In this case, a single drug acts as two selection pressures.

If you don’t have a drug that can act at multiple targets, use combinations to prevent the slow the evolution of resistance.

Here is a nice example of how multiple drug therapy slows the evolution of resistance with cancer therapy.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1863594 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1863594)

More quotes which substantiates what ev shows, what the Wikipedia reference to fitness landscape shows us, that is multiple selection pressures slow evolution. No new lies.

No math.

No surprise.

However, I notice that "rubberband" is this week's magic word. I'm betting it won't make reality disappear any more than your ravings about cheese, alchemy, gators, herrings or all the other crazy crap you come out with.

Is this really all you've got?

kleinman

22nd May 2007, 12:00 PM

And here we are folks back to our horserace to find out who will be the last evolutionist to understand the mathematics of mutation and selection. Adebz and joobz are running tale to tale. Joobz surges into the lead by posting the same old gif but here comes Adebz as he stamps his hoof three times and whinnies “its lies, lies, its all lies”. Stay tuned folks as we wait to find out who is the evolutionist with the most ignorance of the mathematics of mutation and selection.

joobz

22nd May 2007, 01:04 PM

its lies, lies, its all lies.
You're right. What you say are lies. I'm gald we agree.

kleinman

22nd May 2007, 01:32 PM

its lies, lies, its all lies.You're right. What you say are lies. I'm gald we agree.
And the James Randi Educational Forum clown fish surges into the lead as the last evolutionist to understand the mathematics of mutation and selection with his clever retort. This clown fish certainly has an impressive amount of ignorance. He is showing himself to be a real champion of ignorance.

Dr Schneider has again posted on his ev blog. He seems to be relieved that an evolutionist still thinks his ev model is worthwhile. Here is his quote from http://www-lmmb.ncifcrf.gov/~toms/paper/ev/blog-ev.html (http://www-lmmb.ncifcrf.gov/~toms/paper/ev/blog-ev.html)
2007 May 21. Molecular Biology and the New Creationism? by Sahotra Sarkar on January 02nd 2006 cites this work (reference 13).
Here is a quote from the link which cites Dr Schneider’s work, this quote is taken from http://www.medbioworld.com/postgenomics_blog/?p=16#more-16 (http://www.medbioworld.com/postgenomics_blog/?p=16#more-16)
The creationists’ cause is inadvertently aided by some older information theorists who have also expressed bewilderment over the evolution of information. It is high time that we had sustained discussion of the utility of informational metaphors in biology (on which there is considerable skepticism 12) as well as the evolution of information (on which there is already some good work 13).
Reference 13 is to Dr Schneider’s Evolution of Biological Information paper published in Nucleic Acids Research. I’m glad to see that not all evolutionists have discredited your work Dr Schneider. Even if all evolutionists abandon your model Dr Schneider, I’m with you.

kjkent1

22nd May 2007, 01:41 PM

Are you still trying to get the monkey role in the next Scopes trial?No, I'll leave the role to you, you little knuckle dragger you!Your construction of an argument by Dr Schneider of what I am saying ev shows….is a fabrication on your part little gator. Let’s look at what he said precisely.Nah, let's look at the huge post that you were emotionally induced to author when I quoted Schneider correcting your errors.

That's your hot button -- it's not about evolution or creation. It's about kleinman's little ego being bruised by a highly respected Ph.D researcher, and kleinman being unable to do much of anything in response, except expectorate into this forum.If Dr Schneider thinks that varying the mutation rate will overcome the effect of multiple selection pressures, he could easily add this to ev and prove his point.If kleinman really believed he could prove Schneider wrong, then kleinman would add this to ev and prove his point.If Dr Schneider thinks that these mechanisms will overcome the effect of multiple selection pressures, he should add any or all of these features to ev and prove his point.Ditto, my previous response.How many paper’s and statements from scientists that state that multiple selection pressures slow evolution do you need?One valid one would do it -- so far none of your cites support your argument.I’m chicken? Other than Paul and Delphi who reveal his identity, all you evolutionists hide behind pseudonyms. You evolutionists are the cowards. If your ideas are so good, put your real name behind them.The risk of my identifying myself outweighs any possible benefit. There are too many nutcases out there who might want to physically or reputationally injure someone who routinely makes a fool out of a religious zealot such as yourself.You are wrong on several points here but we see an example of how a cowardly bigot operates. One wonders how lawyers ever get bad reputations.Am I? Well, being as you've already identified yourself, and you say you're not a coward, then feel free to post your C.V. for everyone to evaluate.Let’s see if Paul or Dr Schneider embraces Unnamed’s selection process since it has no connection with reality.I thought Paul already did embrace Unnamed's selection process as being a reasonable substitute for Schneider's original. As far as Schneider's concerned, he hasn't posted here in propria persona, so I have no comment.I have mathematical proof and numerous real examples that the theory of evolution is unreal. Do you have mathematical proof that God is unreal? We all would like to see this.You have no such proof that evolution is unreal, because your claims are based on ev, and ev does not model the entire landscape of real-world evolutionary behaviors. So, what you really have, is a vivid imagination and a bone to pick with Schneider that you just can't extract from your throat, except by railing to the gods of the internet. Well, be mine guest, littleman.Are you Dr Schneider’s lawyer? If you are, you are chasing an ambulance with a dead theory in it.Am I Schneider's attorney? Why, are you getting paranoid? If I am Schneider's counsel, and you cross the line into malicious defamation against him, then you'll find out my ID when you're served the summons and complaint -- it'll appear in the top left corner of the cover page.Ev demonstrates a simple mathematical fact. That fact is that multiple selection pressures profoundly slow the evolutionary process. Wikipedia describes this fact nicely in the fitness landscape topic. I have and will continue to post more links of real examples of the phenomenon. Only brainwashed, cultist evolutionists will fail to acknowledge this mathematical and real fact.Dreamer.We are seeking professionals, a plumber to clear the clogged pipes evolutionists suffer from and a landscaper who perhaps can do something with the evolutionary landscape. There is little hope for the latter since the theory of evolution is a dead tree.Beats a dead cross, any day.

joobz

22nd May 2007, 01:49 PM

[more inane nonsense]
what happened to the mathematical proof of the arc you were going to give us?
http://forums.randi.org/showthread.php?t=82190

Or was that just another lie?

I know, I know. You have so many, why would one more make a difference? eh?

kleinman

22nd May 2007, 02:25 PM

what happened to the mathematical proof of the arc you were going to give us?
And the clown fish continues to flop toward the lead as the evolutionist with the most ignorance of the mathematics of mutation and selection. Clown fish is really giving an impressive performance of ignorance.

But wait a minute folks a new horse has decided to enter the race. It is little gator. This is one ambulance chaser that is loaded with ignorance. We have a real horse race.

Let’s take a break from our horse race and have a word from out sponsor, multiple selection pressures.

Are you tired of waiting for evolution to occur; well we have the perfect solution for you. It is single selection pressures. It is mathematically proven and tested in real life. You won’t get birds from reptiles but you will get something for your mutation. So send for yours today.*

A portion of the profits is designated for the society to prevent ignorance of the mathematics of mutation and selection among evolutionists.
Now back to our horse race.

joobz

22nd May 2007, 02:29 PM

And the clown fish continues to flop toward the lead as the evolutionist with the most ignorance of the mathematics of mutation and selection. Clown fish is really giving an impressive performance of ignorance.

This is nowhere near an answer to the question I asked.

let's try again:

what happened to the mathematical proof of the arc you were going to give us?
http://forums.randi.org/showthread.php?t=82190 (http://forums.randi.org/showthread.php?t=82190)

Or was that just another lie?

kleinman

22nd May 2007, 03:08 PM

And clown fish blubbers:
This is nowhere near an answer to the question I asked.
Clown fish continues to flop to the lead as the evolutionist with the most ignorance of the mathematics of mutation and selection. What a performance clown fish. How deep does your ignorance go? Folks, we may have a record setter here. Who would believe that a clown fish could be so ignorant, but there you have it.

joobz

22nd May 2007, 03:14 PM

And clown fish blubbers:

Clown fish continues to flop to the lead as the evolutionist with the most ignorance of the mathematics of mutation and selection. What a performance clown fish. How deep does your ignorance go? Folks, we may have a record setter here. Who would believe that a clown fish could be so ignorant, but there you have it.
This is nowhere near an answer to the question I asked.

let's try again:

what happened to the mathematical proof of the arc you were going to give us?
http://forums.randi.org/showthread.php?t=82190 (http://forums.randi.org/showthread.php?t=82190)

Or was that just another lie?

Paul C. Anagnostopoulos

22nd May 2007, 04:13 PM

kleinman

22nd May 2007, 05:47 PM

I don’t believe you are correct in this point Paul. Consider the following example. You have a Petri dish with bacteria in it. Some of the bacteria are sensitive to an antibiotic and others are resistant. Initially you have no antibiotic in the dish an all bacteria are reproducing at the same rate. You then place the antibiotic into the dish and select out all the sensitive bacteria. The sensitive bacteria are inhibited from reproducing. The resistant bacteria do not reproduce at a higher rate (unless you want to say that the nutrient supply that the sensitive bacteria no longer can use is now available to the resistant bacteria).Yeah, I want to say that. And it's even possible that something you add to the petri dish might make some bacteria reproduce faster.
If that something you add to the Petri dish is nutrients, then the less efficient users of the nutrients will still be selected against. I understand what you are saying. If you do something that makes the environment more hospitable to creatures, creatures that would not otherwise survive to reproduce are able to reproduce. What you are doing is making a more diverse population. When you then stress this population, you reduce the diversity of the population. Only those creatures which can withstand the selection pressure are able to reproduce.
If selection only ever selects against existing organisms and reduces their rate of reproduction, I'm fairly certain that, taken over a long period, there would be no organisms left at all.
Selection can only select against existing organisms. Only those organisms fit enough to withstand that selection pressure are able to reproduce. There are people who hold the view that things are running down. This is in contradiction to the evolutionist view that mutation and selection simply makes life forms better and better. I find it interesting that drug resistant microbes often time are not as good reproducers as the wild form of the microbe when not subjected to the antimicrobial selection pressure.
Selection pressures remove the un-fittest. Selection pressures only inhibit replication, they do not enhance replication.And so the term "positive selection pressure" exists for what reason?
That is terminology that was introduced into this discussion by Dr Richard’s citation.
Thus a Ka/Ks = 1 value indicates neutral selection. Ordinarily Ka/Ks is « 1, indicating negative selection against amino acid mutations (far fewer observed than expected under a neutral model). Ka/Ks > 1 is referred to as positive selection (i.e. amino acid mutations increase reproductive fitness) and is observed in rare cases where new evolutionary challenges create strong pressure for rapid evolution of a protein (e.g. immune system genes like MHC that are involved in recognizing pathogenic antigens).
The terminology “positive selection pressure” is speaking to individual loci which evolve to a directed selection pressure. Note that many loci can evolve due to a directed selection pressure. A particular drug may cause 60-70 amino acid substitutions (positive selection pressures) to the HIV virus. This is what Dr Richard tried to argue that there are numerous selection pressures on HIV. This is equivalent to saying that the three selection condition in ev lead to 96 bases having “positive selection pressure” or 32 amino acid substitutions. This leads to the discussion of how to quantify selection pressures. The Ka/Ks ratio only partially quantifies this property of selection pressures. It gives a measure of how many amino acid substitutions are required to evolve a genome to a particular selection pressure. It does not give a measure of the lethality of the selection pressure.

Dr Adequate

22nd May 2007, 06:02 PM

So kleinman hasn't thought of any new lies or posted any math.

Wow, who'd have thought it?

kleinman

22nd May 2007, 06:21 PM

So kleinman hasn't thought of any new lies or posted any math.
Folks, back to the horserace. Adebz after falling behind for a moment now rushes to the front of those evolutionists who are completely ignorant of the mathematics of mutation and selection. He passes clown fish and ambulance chaser to again take the lead. What a race, what a race!

Now a word from our sponsor, multiple selection pressures slow and ultimately stop evolution.

More citations how multiple selection pressures slow evolution.

The following case concern drug resistance with cytomegalovirus and the article can be found at http://jcm.asm.org/cgi/content/full/43/1/208 (http://jcm.asm.org/cgi/content/full/43/1/208)
Infection with cytomegalovirus (CMV) remains a significant cause of morbidity and mortality among hematopoietic cell transplant (HCT) recipients. We describe two pediatric HCT recipients who developed persistent and severe drug-resistant CMV infections. CMV resistance to foscarnet and ganciclovir was detected after only 6 and 11 weeks of therapy, respectively. Viral pol mutations associated with drug resistance in these patients included T838A (a novel mutation) and D588N, which were shown by marker transfer to confer foscarnet and multidrug resistance, respectively. Each of these mutations significantly reduced in vitro replication of CMV, suggesting that they may decrease viral fitness. This finding was further supported by the disappearance of mutations upon withdrawal of antiviral pressure in one patient. Novel antivirals or combination therapy may be required for the treatment of drug-resistant CMV in HCT recipients and perhaps in other severely immunocompromised patients.
Here is another reference to combination therapy for malaria and can be found at http://www.malariajournal.com/content/3/1/2 (http://www.malariajournal.com/content/3/1/2)
The effect is extremely dependent on the size of infection. As an example, if a human is inoculated with a drug-sensitive clone and there are 10^11 parasites in the host and the mutation rate to the drug resistant form is 10^-8, then there will be a sub-population of 10^3 resistant parasites. Following drug treatment, the sensitive forms will be eliminated and the sub-population of 10^3 resistant forms will expand to dominate the infection. Needless to say, if the mutation rate to resistance is 10^-8, then infection sizes of less than ten thousand would rarely contain the appropriate mutation. Current antimalarial drug deployment strategies utilise this effect by using drugs in combination. If mutation rates to resistance are 10^-8 for each drug in a two-drug mixture, then even an infection of 10^12 individual malaria parasites is highly unlikely (a probability of 0.0001) to simultaneous contain a spontaneous drug-resistant mutation in each gene.

joobz

22nd May 2007, 06:22 PM

If that something you add to the Petri dish is nutrients, then the less efficient users of the nutrients will still be selected against. I understand what you are saying. If you do something that makes the environment more hospitable to creatures, creatures that would not otherwise survive to reproduce are able to reproduce. What you are doing is making a more diverse population. When you then stress this population, you reduce the diversity of the population. Only those creatures which can withstand the selection pressure are able to reproduce.

And what if the nutrient is something that only a certain population can take advantage of due to mutation in metabolic enzymes? Seems to me, you are enhancing the selection of one creature over the other.

But this is beside the point:
et's try again:

what happened to the mathematical proof of the arc you were going to give us?
http://forums.randi.org/showthread.php?t=82190 (http://forums.randi.org/showthread.php?t=82190)

Or was that just another lie?

kleinman

22nd May 2007, 07:06 PM

If that something you add to the Petri dish is nutrients, then the less efficient users of the nutrients will still be selected against. I understand what you are saying. If you do something that makes the environment more hospitable to creatures, creatures that would not otherwise survive to reproduce are able to reproduce. What you are doing is making a more diverse population. When you then stress this population, you reduce the diversity of the population. Only those creatures which can withstand the selection pressure are able to reproduce.And what if the nutrient is something that only a certain population can take advantage of due to mutation in metabolic enzymes? Seems to me, you are enhancing the selection of one creature over the other.
Why that’s how you get the evolution of clown fish out of sea slugs. Now don’t get to distracted clown fish, you do want to win the race to be the last evolutionist to understand the mathematics of mutation and selection.

joobz

22nd May 2007, 07:10 PM

Why that’s how you get the evolution of clown fish out of sea slugs.
This is nowhere near an answer to the question I asked. I realize the answer to that question completely destroys your entire premise. But when has that stopped you from repeating the lies?

Well, lets go back to the previous question I asked:

what happened to the mathematical proof of the arc you were going to give us?
http://forums.randi.org/showthread.php?t=82190 (http://forums.randi.org/showthread.php?t=82190)

So this was another lie?

kleinman

22nd May 2007, 07:22 PM

Why that’s how you get the evolution of clown fish out of sea slugs.This is nowhere near an answer to the question I asked. I realize the answer to that question completely destroys your entire premise. But when has that stopped you from repeating the lies?
Poor unhappy clown fish didn’t get the answer to his question. You just put your hope in winning the horserace to be the last evolutionist to understand the mathematics of mutation and selection. You are working so hard to win this honor. It would be a shame for such ignorance to go unrewarded so you keep working at it.

joobz

22nd May 2007, 07:29 PM

kleinman

22nd May 2007, 07:57 PM

Poor unhappy clown fish didn’t get the answer to his question. You just put your hope in winning the horserace...SO you admit you lied again? And you admit you won't answer honest questions? you admit your entire posts are just a foolish game proving your inability to think and reason?
Clown fish asks an honest question? I can’t resist it any more. That’s a good fish story.
http://forums.randi.org/images/smilies/doglaugh.gif

joobz

22nd May 2007, 08:10 PM

Clown fish asks an honest question? I can’t resist it any more. That’s a good fish story.
http://forums.randi.org/images/smilies/doglaugh.gif (http://forums.randi.org/images/smilies/doglaugh.gif)

This is nowhere near an answer to the question I asked.
Let's try again:
So you admit you lied? You admit you won't answer HONEST questions?

Taffer

22nd May 2007, 08:20 PM

kleinman

22nd May 2007, 08:27 PM

Kleinman, your links do not show that evolution has slowed. If you understood genetics you would know that. What is funny is you claim that I do not understand genetics because I "do not understand that recombination does not increase information in the population, and only results in the loss of alleles". This is funny becuase it is utter rubbish, and I know this because I understand genetics.
And here comes Taffer emerging on the outside. Folks, we have a four way race at this point for the last evolutionist to understand the mathematics of mutation and selection. The thrills, the chills, what will this race evolve into?

Taffer

22nd May 2007, 08:30 PM

And so the term "positive selection pressure" exists for what reason?

~~ Paul

In all fairness, Paul, he is actually correct when he says this. Which is funny, because it was I who told him this as he used to go on about "positive selection pressures not stabilizing selection pressures".

This is a common misunderstanding. If we look at the model I have many pages ago, we model the change in allele frequency based on the selection coefficient acting on the less fit allele. And this selection coefficient is a relative coefficient, with the most fit allele having a selection coefficient of 0 (and thus a fitness of 1). He is quite right, selection causes those who are less fit to contribute fewer genes to the next generation. If selection "chose" other alleles to increase in frequency, then it would be a directional force, which it is not. It is "blind", as it were. Thus, some alleles increase in frequency as a result of the less fit alleles decreasing in frequency.

The terms "positive selection" and "stabilizing selection", etc, are used to describe situations, not distinct forms of selection. This is kind of hard to explain, but think of it as "positive selection" describing the result of selection against other alleles then the one we are looking at. Thus, the most fit allele undergoes "positive selection", which is a synonym for "does not undergo selection, and thus increases in frequency".

The key thing is that 'fitness' is a relative concept (except "absolute fitness", which is fairly arbitrary and not used in any model I've ever seen). If there were only one allele, or two alleles of equal fitness, then they would not increase or decrease in allele frequency. But as soon as one allele becomes less fit, it will decrease in frequency ("negative selection") and the other will increase in frequency as a result ("positive selection"). Similarly, if you have only one allele, and all new alleles are less fit, then it will generally not change in allele frequency (it will also probably be already in a high frequency).

I hope that makes sense... :o

Taffer

22nd May 2007, 08:31 PM

Kleinman, you are not fooling anyone. Everyone (but you, it seems) can see what I've already stated.

Go away and learn some genetics, and then we'll have something to discuss.

Mr. Scott

22nd May 2007, 09:02 PM

You know, science has done an awfully good job at finding the truth in areas like physics, astronomy, medicine, and technology, because science is an evidence-based system.

My understanding is that when evidence is the guide, evolution comes to the forefront as the most likely explanation for the origin of species.

However, the creationists, instead of relying on evidence, use the Bible as their guide. They dismiss the mountain of consistent evidence for evolution and instead find their version of reality in an ancient book written by authors who seemed to know no more than the common man of several thousand years ago.

Now, with the system of science and evidence we have, that has been so fruitful in so many areas, if creationism were true, one would think that at least someone would come to the conclusion that life, genes, and species must have come about through some type of divine intervention.

I don't know of one single person who, following the physical evidence alone, has reached the creationist conclusion. Instead of following physical evidence, it seems, to the man, creationists all have an axe to grind -- shoring up their dogma and holy book.

Is there a single person who, studying the physical evidence only, and without the need to promote an ancient religion, concluded that life must have arose from divine intervention? Anyone?

BPScooter

23rd May 2007, 01:29 AM

Wow, I need to go take a shower after reading this thread again.

What can I say. Kleinman, you stung me as a lurker, with your insults. Go learn the math, go read the Wikipedia page. Well, on its face, your argument of "impossibility of phenomenon proven by model" seriously insults my understanding of words like 'proof' or 'ignorance' or 'impossible.' Not to mention that these models are, after all, only human creations with specific constraints.

I'm way more interested in your (Dr. Adequate wouldn't call it rhetoric!) use of metaphor and such to further a conviction. Come on, man, "little gator" and "last horse in the race" reveal more about your strategy than your more lengthy verbiage.

Most appalling to me is a usage of us v. them. "You evolutionists" implies to me that you have a chip on your shoulder (metaphor) and an axe to grind. What is it?

In the 100+ pages of this thread, have you proposed a testable, falsifiable, Popperian hypothesis that constitutes your "shoulder?" Rather than say It's Mathematically Impossible and You're Ignorant, what have you really said here?

Is it simply that God must have Done It? Forgive us Evolutionists if we don't simply take that, and ask a few more questions. If enough questions are asked and answered, maybe the God part of it becomes quite small to some analyst's points of view.

Dr Adequate

23rd May 2007, 01:52 AM

Folks, back to the horserace. Adebz after falling behind for a moment now rushes to the front of those evolutionists who are completely ignorant of the mathematics of mutation and selection. He passes clown fish and ambulance chaser to again take the lead. What a race, what a race!

Now a word from our sponsor, multiple selection pressures slow and ultimately stop evolution.

More citations how multiple selection pressures slow evolution.

The following case concern drug resistance with cytomegalovirus and the article can be found at http://jcm.asm.org/cgi/content/full/43/1/208 (http://jcm.asm.org/cgi/content/full/43/1/208)

Here is another reference to combination therapy for malaria and can be found at http://www.malariajournal.com/content/3/1/2 (http://www.malariajournal.com/content/3/1/2)

Why that’s how you get the evolution of clown fish out of sea slugs. Now don’t get to distracted clown fish, you do want to win the race to be the last evolutionist to understand the mathematics of mutation and selection.
Poor unhappy clown fish didn’t get the answer to his question. You just put your hope in winning the horserace to be the last evolutionist to understand the mathematics of mutation and selection. You are working so hard to win this honor. It would be a shame for such ignorance to go unrewarded so you keep working at it.

Clown fish asks an honest question? I can’t resist it any more. That’s a good fish story.
http://forums.randi.org/images/smilies/doglaugh.gif
And here comes Taffer emerging on the outside. Folks, we have a four way race at this point for the last evolutionist to understand the mathematics of mutation and selection. The thrills, the chills, what will this race evolve into? No new lies, no math. Consists mainly of petulant whining about the people he's lying to. Gibberish quotient up slightly.

Dr Adequate

23rd May 2007, 06:32 AM

Aside from annoying Dr. Adequate, what is your main purpose for doing this thread? That's like asking a Tourette's sufferer the purpose of his tics, or someone with OCD what the purpose of his rituals are.

Do you realise that kleinman has told Lie #5 no less than fifty-two times in the past six weeks or so --- to an audience composed entirely of people who know he's lying?

This is not the sort of behavior which has a purpose.

Paul C. Anagnostopoulos

23rd May 2007, 07:09 AM

This is a common misunderstanding. If we look at the model I have many pages ago, we model the change in allele frequency based on the selection coefficient acting on the less fit allele. And this selection coefficient is a relative coefficient, with the most fit allele having a selection coefficient of 0 (and thus a fitness of 1). He is quite right, selection causes those who are less fit to contribute fewer genes to the next generation. If selection "chose" other alleles to increase in frequency, then it would be a directional force, which it is not. It is "blind", as it were. Thus, some alleles increase in frequency as a result of the less fit alleles decreasing in frequency.
But what he said was that "selection pressures inhibit replication." I believe he means something different from what you're saying.

Let's think about this. Wiki's description of selection pressure is bogus:

"Evolutionary pressure or selection pressure can be formalized as an external pressure applied to a process, thereby pushing that process in a distinct direction."

And its description of selection is tilted in the wrong direction:

"In the context of evolution, certain traits or alleles of a species may be subject to selection. Under selection, individuals with advantageous or "adaptive" traits tend to be more successful than their peers reproductively--meaning they contribute more offspring to the succeeding generation than others do."

Back to Kleinman's question:

Paul, would you give us an example of a selection pressure that increases replication?
A fair question. So what do we say if a situation actually increases the replication rate of some organisms relative to the status quo? It seems misleading to say that the status-quo organisms were selected against, rather than saying that the higher-replication organisms were selected for, although it is technically correct.

But as soon as one allele becomes less fit, it will decrease in frequency ("negative selection") and the other will increase in frequency as a result ("positive selection").

So I believe it is still incorrect for Kleinman to say:

Selection pressures remove the un-fittest. Selection pressures only inhibit replication, they do not enhance replication.
which is why I asked about the term "positive selection pressure." What he really wants to say is:

Selection removes the unfittest. Selection situations can slow or accelerate replication of certain phenotypes, then selection removes the slower-replicating organisms.

Is that correct? Is the term "selection situation" used in genetics? Would "environmental pressures" be better?

~~ Paul

Paul C. Anagnostopoulos

23rd May 2007, 07:23 AM

Taffer

23rd May 2007, 07:30 AM

To answer this backwards:

Is that correct? Is the term "selection situation" used in genetics?

Well, no, it isn't. You will almost always hear people talk about "positive selection" or one trait being "selected for", even by professionals.

I think I understand this. In particular, I understand the selection coefficient. But even though selection does not choose alleles to increase in frequency, a selection situation can.

Basically, yes. The key point I was making is that for selection to "select for" a particular trait, it must have some pre-determined trait "in mind". But selection is blind.

Although, I guess in all fairness we could say that "increased reproduction" could be a pre-determined trait. Dunno, I'll have to think on that.

So Wiki's description of selection pressure is bogus:

"Evolutionary pressure or selection pressure can be formalized as an external pressure applied to a process, thereby pushing that process in a distinct direction."

This actually isn't bad. It doesn't specify that the pressure is directional, only that the result is directional. In other words, the pressure can be negative for one trait and thus you have a positive result for another.

And its description of selection is tilted in the wrong direction:

"In the context of evolution, certain traits or alleles of a species may be subject to selection. Under selection, individuals with advantageous or "adaptive" traits tend to be more successful than their peers reproductively--meaning they contribute more offspring to the succeeding generation than others do."

No, this is actually correct. The fittest traits produce more offspring then those with lower fitness traits. I'll come back to this.

Back to Kleinman's question:

A fair question. So what do we say if a situation actually increases the replication rate of some organisms relative to the status quo? It seems misleading to say that the status-quo organisms were selected against, rather than saying that the higher-replication organisms were selected for, although it is technically correct.

According to the model, the fittest allele has no selection applied to it. If a new allele arises which is more fit, it becomes the new fittest allele.

So I believe it is still incorrect for Kleinman to say:

which is why I asked about the term "positive selection pressure." What he really wants to say is:

Selection removes the unfittest. Selection situations can slow or accelerate replication of certain phenotypes, then selection removes the slower-replicating organisms.

~~ Paul

Yes, you have it.

But this can get very muddled. It depends strongly upon what we are talking about. If we are saying "those with fitter alleles produce more offspring for the next generation on average then those with less fit alleles", we aren't talking about selection per se, but the "result" of selection.

To make an example, consider an ecosystem in which there is only enough resources to support 100 organisms. If we consider the most fit individual, they will be slightly more able to use those resources to produce offspring. The least fit individual will be slightly less able to use those resources. Thus, over time, the most fit individual's alleles will proliferate throughout the population. But the key to what we're discussing is "does selection drive the increase or decrease" in allele frequency?

Y'know, this has actually made me think. I might be wrong about this. I know that, according to population genetic models, selection is considered a 'negative force', as the most fit allele has a fitness of 1. However, this may just be a mathematical description, as it were.

Thinking on it more, perhaps a better way to describe selection is not as a force but as a phenomenon. We observe that, in a population, those with more favourable traits contribute more genes to the next generation, on average, then those with less favourable traits. Perhaps it is best not to say that "selection is negative", or "selection acts against those with less favourable traits". Perhaps we should say instead that "selection happens", and that it doesn't really 'exist', per se, but is simply a description of the phenomenon we observe.

This really has got me thinking, Paul. When get a chance I will go to one of my supervisors (one is a population geneticist) and talk to him about this. Until I can clarify, I will retract my correction.

Allow me to also correct myself. I am now thinking that "selection is a description of an observed phenomenon" is a better way to describe selection, then as a force.

Taffer

23rd May 2007, 07:32 AM

If you look for definitions of selection pressure on the Net, you'll find that it is used to mean the selection coefficient, but also to mean the environmental situation/pressure causing the selection. This is one source of our confusion.

~~ Paul

Yes, I do believe you are correct. As a selection coefficient, it most certainly is entirely negative. But as an environmental situation, I'm not so sure. An environmental pressure cannot be positive, as that would suggest predetermined 'guided' pressure.

As you say, there is some confusion. :o

kjkent1

23rd May 2007, 07:48 AM

And here comes Taffer emerging on the outside. Folks, we have a four way race at this point for the last evolutionist to understand the mathematics of mutation and selection. The thrills, the chills, what will this race evolve into?I think that there's some room at the gate for a few more horses. So, as you are prone to indirectly casting dispersions at string theorist and professor of physics at Stanford University, Leonard Susskind, Ph.D (http://en.wikipedia.org/wiki/Leonard_Susskind), and as you have repeatedly mentioned that you need a plumber to deal with the bad pipes of evolution, and as Dr. Susskind was indeed a plumber prior to becoming one of the world's leading theoretical physicists, I suggest that it's entirely fair that you add him to the race of those too ignorant to understand the mathematics of mutation and selection.

Also, let's not forget to add geneticist Francis Collins (http://en.wikipedia.org/wiki/Francis_Collins), director of the National Human Genome Institute, and a theist -- but also an evolutionist.

I think that while you continue to post your host of irrelevant citations about drug therapy, I will try to seek out more "horsepower" to add to to the list of names who would likely find your conclusion re the impossibility of evolution silly and perhaps even disordered.

After all, there's no reason to argue about the science, until you provide the changes to ev necessary to support your theory.

So, as long as you're content to argue strawmen, I'll be content to appeal to authority.

Oh, and of course, let's not forget that Thomas D. Schnedier, Ph.D. (http://www.lecb.ncifcrf.gov/~toms/schneider.html), the author of the ev program from which you derive your remarkable theory of impossible evolution, is also in the race to see who will be the last person to understand the mathematics of mutation and evolution.

I've got to tell ya, Alan -- this is already a rather intimidating list of "horses" who would firmly oppose you. Of course, you could be Albert Einstein reincarnate. But, if you were, I would have expected to see you write more than a few equations in this thread to demonstrate that evolution by any conceivable mutation and selection method is impossible.

It certainly would save us all (you included) a whole lot of time, were you to put your money where your mouth is and formally lay out the theory. Hell, if you actually did that, then perhaps you and Dr. Adequate would actually have something to argue about.

As it is now, this has become really boring.

Hey, I just had a thought, Alan -- you should ask some of your scientific colleagues who support your position to start posting here. It would make things so much more of a...ahem, pardon my irony...a "horse race!"

kleinman

23rd May 2007, 08:12 AM

Kleinman, you are not fooling anyone. Everyone (but you, it seems) can see what I've already stated.
Silly Taffer, I’m not trying to fool anyone. I’m showing you what an evolutionist written, peer reviewed and published mathematical model of random point mutation reveals. What it reveals is that multiple selection pressures slow and ultimately stop evolution. I have presented dozens of real examples of this phenomenon and will continue to present more. This is why the theory of evolution is mathematically impossible.
Go away and learn some genetics, and then we'll have something to discuss.And so the term "positive selection pressure" exists for what reason?In all fairness, Paul, he is actually correct when he says this. Which is funny, because it was I who told him this as he used to go on about "positive selection pressures not stabilizing selection pressures".
Taffer, I’m also correct on the mathematics of mutation and selection. (And you have taught me nothing about selection pressures.)
You know, science has done an awfully good job at finding the truth in areas like physics, astronomy, medicine, and technology, because science is an evidence-based system.
I have no problem with the evidence, I do have a problem with the way evolutionists interpret the evidence.
My understanding is that when evidence is the guide, evolution comes to the forefront as the most likely explanation for the origin of species.
Well, we have an evolutionist written, peer reviewed and published model of random point mutation and natural selection that shows that multiple selection pressures slow and ultimately stops evolution. I have cited dozens of references which give evidence of this mathematical fact and will continue to post more (see below).
However, the creationists, instead of relying on evidence, use the Bible as their guide. They dismiss the mountain of consistent evidence for evolution and instead find their version of reality in an ancient book written by authors who seemed to know no more than the common man of several thousand years ago.
So what if I use the Bible as my guide. My Bible tells me to seek the truth. What you call a mountain of consistent evidence for evolution are concocted interpretations of the evidence that has no mathematical basis. What I am doing is using your own mathematical model and showing you what it reveals and presenting real examples of what this model reveals. It is you who is in denial of what the evidence is really saying. This is what happens when you brainwash naïve children with a bad scientific hypothesis. You lose the ability to recognize your prejudices and biases and the result is you misinterpret the evidence.
Now, with the system of science and evidence we have, that has been so fruitful in so many areas, if creationism were true, one would think that at least someone would come to the conclusion that life, genes, and species must have come about through some type of divine intervention.
There is more than enough evidence that there was an intelligent hand in our creation. You are just in denial of this evidence. If you saw the slightest sign of structure in the SETI observations of radio signals, you would be the first to say there was intelligence out there. Yet with all the complex genetic structure that we are now aware of, you refuse to see any sign of an intelligent origin of these structures. Well, we have a mathematical model of mutation and selection that shows that multiple selection pressures interfere with the formation of these structures. It is your theory of evolution that has no mathematical or scientific basis. That is what the mathematics shows, that is what the evidence shows.
I don't know of one single person who, following the physical evidence alone, has reached the creationist conclusion. Instead of following physical evidence, it seems, to the man, creationists all have an axe to grind -- shoring up their dogma and holy book.
If you didn’t hang out with your brainwashed cultist evolutionists, you would hear the proper interpretation of the evidence. The ev mathematical model gives us a clue how to follow the physical evidence and that physical evidence shows that your theory is mathematically impossible. I have no axe to grind, I simply think that the theory of evolution is wrong and I’m showing you why. A bad theory when shown wrong interferes with scientific investigation when adherents to that theory twist the evidence to try to fit it to their belief system.
Is there a single person who, studying the physical evidence only, and without the need to promote an ancient religion, concluded that life must have arose from divine intervention? Anyone?
Abiogenesis has no scientific basis. No evidence, no experiments that show how it happened. It is just another belief system.
What can I say. Kleinman, you stung me as a lurker, with your insults. Go learn the math, go read the Wikipedia page. Well, on its face, your argument of "impossibility of phenomenon proven by model" seriously insults my understanding of words like 'proof' or 'ignorance' or 'impossible.' Not to mention that these models are, after all, only human creations with specific constraints.
Don’t forget the dozens of real examples of this mathematics of ev and Wikipedia page, more real examples of this mathematics of ev and Wikipedia page are posted below which show that multiple selection pressures slow and ultimately stop evolution.
I'm way more interested in your (Dr. Adequate wouldn't call it rhetoric!) use of metaphor and such to further a conviction. Come on, man, "little gator" and "last horse in the race" reveal more about your strategy than your more lengthy verbiage.
You evolutionist are a bunch of thin skinned crybabies. You can dish it out but can’t take it. You go running home to your mother whining that the bad old creationist is picking on me.
Most appalling to me is a usage of us v. them. "You evolutionists" implies to me that you have a chip on your shoulder (metaphor) and an axe to grind. What is it?
It’s very simple BPScooter, the theory of evolution is a dumb theory that has no mathematical basis and requires contrived interpretation of the evidence to be propped up. Dr Schneider had to use a contrived interpretation of the single case that he published from his mathematical model to prop up the theory. When a thorough analysis of his model is done, it shows that multiple selection pressures slow then ultimately stop evolution. What’s the problem with a little competition, an us v. them game? Dr Schneider interprets his model one way, I interpret it another way. Which interpretation is supported by the evidence? The only problem for you evolutionists is that you need to find the ball park before you can see the goalposts.
In the 100+ pages of this thread, have you proposed a testable, falsifiable, Popperian hypothesis that constitutes your "shoulder?" Rather than say It's Mathematically Impossible and You're Ignorant, what have you really said here?
I can’t help it if your evolutionist brainwashing makes you slow to understand the mathematics of mutation and selection. The fact is that multiple selection pressures slow and ultimately stop evolution. Multiple selection pressures interfere with ability of a creature to evolve to these selection pressures. Unless you are going to propose that a single selection pressure evolve reptiles into birds, how do you explain multiple selection pressures bring about such huge numbers of genetic changes required to make such a transformation. Multiple selection pressures interfere with each other preventing evolution. This is what the mathematics shows, this is what the real examples of mutation and selection shows.
Is it simply that God must have Done It? Forgive us Evolutionists if we don't simply take that, and ask a few more questions. If enough questions are asked and answered, maybe the God part of it becomes quite small to some analyst's points of view.
I’m simply showing that evolution didn’t do it.
Aside from annoying Dr. Adequate, what is your main purpose for doing this thread?
If I had no other reason than annoying Adebz, that would be enough. Where else would I get the opportunity to annoy a PhD in amathematics with some mathematics?
Selection pressures remove the un-fittest. Selection pressures only inhibit replication, they do not enhance replication.which is why I asked about the term "positive selection pressure." What he really wants to say is:
Paul, I’m here to say what I really want to say. Don’t get confused by terminology. You have directional selection pressures and stabilizing selection pressures. In ev, the selection conditions are initially directional until the selection conditions are met. Then they become stabilizing selection pressures. Turn off selection in the model after the selection conditions are met and the binding sites revert to random.

As I promised earlier in this post, here are more references to multiple selection pressures slowing evolution. This is what ev shows, this is what the Wikipedia reference to fitness landscape shows and this is why the theory of evolution is mathematically impossible. In addition, these examples are not limited to random point mutations. These examples include recombination and there is no limitation on the type of mutation that may occur. Do you understand this little gator, the ambulance chaser?

http://www.touchbriefings.com/pdf/886/lth041_negredo.pdf (http://www.touchbriefings.com/pdf/886/lth041_negredo.pdf)
The main objective of antiretroviral drug resistance testing in clinical practice is to improve the outcome of therapy by helping to choose the most effective combination regimens.
and
Other factors related to the evolution of drug resistance concerned or associated with antiretroviral therapy, such as inadequate drug prescription, drug–drug interactions, previous sequential monotherapy or pre-existing resistance.
I added the highlighting for you Taffer.

http://www.malariajournal.com/content/5/1/48 (http://www.malariajournal.com/content/5/1/48)
This improved understanding of the evolution of drug resistance has come from a relatively simple situation. Until recently, the number of antimalaria drugs in common use was small: chloroquine and sulfadoxine-pyrimethamine in Africa and the Americas, with mefloquine and more recently, mefloquine-artesunate in Southeast Asia[13]. As chloroquine and sulfadoxine-pyrimethamine have lost their efficacy, combination drugs have been strongly endorsed as the most effective next step [14].

http://www.mja.com.au/public/issues/186_04_190207/sas10773_fm.html (http://www.mja.com.au/public/issues/186_04_190207/sas10773_fm.html)
Despite the emergence of multidrug-resistant strains of hepatitis B virus (HBV) and previous success with combination therapy for other chronic viral infections, we are still using sequential monotherapy for chronic HBV infection.

Here is another example of combination therapy used for the treatment of cancer, the reference can be found at http://www.dissectmedicine.com/resistance (http://www.dissectmedicine.com/resistance)
"Long-term endocrine therapy with either aromatase inhibitors (AIs) or tamoxifen may lead to endocrine resistance and disease progression. Recent years have seen advances in our understanding of the complex biological mechanisms associated with resistance. Growth factor signaling pathways appear to be upregulated in hormone-resistant tumours and interact with oestrogen-receptor (ER) signaling, which remains functional even after long-term endocrine deprivation. Signaling through the human epidermal and insulin-like growth-factor receptor (HER and IGFR, respectively) pathways may promote ligand-independent ER gene transcription and stimulate growth factor signaling. Therapeutic agents that inhibit these signal transduction pathways, when combined with AIs, may offer breast cancer patients new hope for more robust, longer-term remissions. Preliminary data from phase II studies of combination therapies are encouraging. There is a large programme of ongoing randomised, controlled trials, the results of which should pave the way for integrating combination therapies into clinical practice. To identify which patients will respond best to particular combinations of treatments, biomarkers and gene expression profiles are being investigated as predictors of sensitivity or resistance. In time, breast cancer treatment will become truly individualised because physicians will be able to match patients with a variety of disease phenotypes to optimal combination therapies." British Journal of Cancer (2006) 95, 661-666.

Paul C. Anagnostopoulos

23rd May 2007, 08:29 AM

Basically, yes. The key point I was making is that for selection to "select for" a particular trait, it must have some pre-determined trait "in mind". But selection is blind.
Why do you say that? Selection "selects against" the least fit organisms, and "selects for" the most fit organisms. Either both terms are tainted with teleology, or neither are.

This actually isn't bad. It doesn't specify that the pressure is directional, only that the result is directional. In other words, the pressure can be negative for one trait and thus you have a positive result for another.
Agreed, although the distinction between the pressure being directional and the result being directional doesn't really matter in general conversation.

Thinking on it more, perhaps a better way to describe selection is not as a force but as a phenomenon. We observe that, in a population, those with more favourable traits contribute more genes to the next generation, on average, then those with less favourable traits. Perhaps it is best not to say that "selection is negative", or "selection acts against those with less favourable traits". Perhaps we should say instead that "selection happens", and that it doesn't really 'exist', per se, but is simply a description of the phenomenon we observe.
If we're going to be careful, then I agree we have to go with something like this. This is like trying to define random. :D

I just want to make sure that Kleinman doesn't think that all environmental pressures necessarily result in overall lower reproduction rates.

~~ Paul

Paul C. Anagnostopoulos

23rd May 2007, 08:31 AM

joobz

23rd May 2007, 08:36 AM

I just want to make sure that Kleinman doesn't think that all environmental pressures necessarily result in overall lower reproduction rates.

~~ Paul
This is a rather silly wish. Kleinman has no desire to listen or pay attention to facts that refute his case.

Someone who can go from
"HIV proves evolution is impossible"
to
"HIV doesn't count because of recombination"
to
"HIV proves evolution is impossible"
obviously has no problem with intellectual dishonesty.

joobz

23rd May 2007, 08:49 AM

I have cited dozens of references which give evidence of this mathematical fact and will continue to post more (see below). and you are a fool if you actually believe this.

If you didn’t hang out with your brainwashed cultist evolutionists, you would hear the proper interpretation of the evidence. Cultists??? Like a cult that worships an entity described in a book written thousands of years ago that has all the truths of our world and that none of those "truths" are questionable because that would be a punishment worthy of eternal torment?

Yeah, science and evolutionary theory is just like that.:rolleyes:

It’s very simple BPScooter, the theory of evolution is a dumb theory that has no mathematical basis and requires contrived interpretation of the evidence to be propped up.
what is the mathematical basis for your ID theory then?
If you believe that you've fully squashed evolution through "maths", go ahead and use the same "maths" to prove your case.

kleinman

23rd May 2007, 09:01 AM

There is more than enough evidence that there was an intelligent hand in our creation. You are just in denial of this evidence. If you saw the slightest sign of structure in the SETI observations of radio signals, you would be the first to say there was intelligence out there.Such as the periodic signals coming from pulsars?
The presence of harmonics in many physical systems (perhaps all physical systems) can be construed as a sign of intelligence. Who would have the power to create a pulsar?
I just want to make sure that Kleinman doesn't think that all environmental pressures necessarily result in overall lower reproduction rates.This is a rather silly wish. Kleinman has no desire to listen or pay attention to facts that refute his case.
Clown fish, all directional selection pressures result in overall lower reproductive fitness to that population subjected to the selection pressure. Once that directional selection pressure is met, the selection pressure becomes stabilizing, increasing the frequency of that genetic phenotype and reducing the diversity of the population. If you understood that mathematics of mutation and selection this would be apparent to you. But what can you expect from a clown fish?

Dr Adequate

23rd May 2007, 09:09 AM

The presence of harmonics in many physical systems (perhaps all physical systems) can be construed as a sign of intelligence. Who would have the power to create a pulsar? That was funny, thanks.

Dr Adequate

23rd May 2007, 09:11 AM

Silly Taffer, I’m not trying to fool anyone. I’m showing you what an evolutionist written, peer reviewed and published mathematical model of random point mutation reveals. What it reveals is that multiple selection pressures slow and ultimately stop evolution. I have presented dozens of real examples of this phenomenon and will continue to present more. This is why the theory of evolution is mathematically impossible.

Taffer, I’m also correct on the mathematics of mutation and selection. (And you have taught me nothing about selection pressures.)

I have no problem with the evidence, I do have a problem with the way evolutionists interpret the evidence.

Well, we have an evolutionist written, peer reviewed and published model of random point mutation and natural selection that shows that multiple selection pressures slow and ultimately stops evolution. I have cited dozens of references which give evidence of this mathematical fact and will continue to post more (see below).

So what if I use the Bible as my guide. My Bible tells me to seek the truth. What you call a mountain of consistent evidence for evolution are concocted interpretations of the evidence that has no mathematical basis. What I am doing is using your own mathematical model and showing you what it reveals and presenting real examples of what this model reveals. It is you who is in denial of what the evidence is really saying. This is what happens when you brainwash naïve children with a bad scientific hypothesis. You lose the ability to recognize your prejudices and biases and the result is you misinterpret the evidence.

There is more than enough evidence that there was an intelligent hand in our creation. You are just in denial of this evidence. If you saw the slightest sign of structure in the SETI observations of radio signals, you would be the first to say there was intelligence out there. Yet with all the complex genetic structure that we are now aware of, you refuse to see any sign of an intelligent origin of these structures. Well, we have a mathematical model of mutation and selection that shows that multiple selection pressures interfere with the formation of these structures. It is your theory of evolution that has no mathematical or scientific basis. That is what the mathematics shows, that is what the evidence shows.

If you didn’t hang out with your brainwashed cultist evolutionists, you would hear the proper interpretation of the evidence. The ev mathematical model gives us a clue how to follow the physical evidence and that physical evidence shows that your theory is mathematically impossible. I have no axe to grind, I simply think that the theory of evolution is wrong and I’m showing you why. A bad theory when shown wrong interferes with scientific investigation when adherents to that theory twist the evidence to try to fit it to their belief system.

Abiogenesis has no scientific basis. No evidence, no experiments that show how it happened. It is just another belief system.

Don’t forget the dozens of real examples of this mathematics of ev and Wikipedia page, more real examples of this mathematics of ev and Wikipedia page are posted below which show that multiple selection pressures slow and ultimately stop evolution.

You evolutionist are a bunch of thin skinned crybabies. You can dish it out but can’t take it. You go running home to your mother whining that the bad old creationist is picking on me.

It’s very simple BPScooter, the theory of evolution is a dumb theory that has no mathematical basis and requires contrived interpretation of the evidence to be propped up. Dr Schneider had to use a contrived interpretation of the single case that he published from his mathematical model to prop up the theory. When a thorough analysis of his model is done, it shows that multiple selection pressures slow then ultimately stop evolution. What’s the problem with a little competition, an us v. them game? Dr Schneider interprets his model one way, I interpret it another way. Which interpretation is supported by the evidence? The only problem for you evolutionists is that you need to find the ball park before you can see the goalposts.

I can’t help it if your evolutionist brainwashing makes you slow to understand the mathematics of mutation and selection. The fact is that multiple selection pressures slow and ultimately stop evolution. Multiple selection pressures interfere with ability of a creature to evolve to these selection pressures. Unless you are going to propose that a single selection pressure evolve reptiles into birds, how do you explain multiple selection pressures bring about such huge numbers of genetic changes required to make such a transformation. Multiple selection pressures interfere with each other preventing evolution. This is what the mathematics shows, this is what the real examples of mutation and selection shows.

I’m simply showing that evolution didn’t do it.

If I had no other reason than annoying Adebz, that would be enough. Where else would I get the opportunity to annoy a PhD in amathematics with some mathematics?

Paul, I’m here to say what I really want to say. Don’t get confused by terminology. You have directional selection pressures and stabilizing selection pressures. In ev, the selection conditions are initially directional until the selection conditions are met. Then they become stabilizing selection pressures. Turn off selection in the model after the selection conditions are met and the binding sites revert to random.

As I promised earlier in this post, here are more references to multiple selection pressures slowing evolution. This is what ev shows, this is what the Wikipedia reference to fitness landscape shows and this is why the theory of evolution is mathematically impossible. In addition, these examples are not limited to random point mutations. These examples include recombination and there is no limitation on the type of mutation that may occur. Do you understand this little gator, the ambulance chaser?

http://www.touchbriefings.com/pdf/886/lth041_negredo.pdf (http://www.touchbriefings.com/pdf/886/lth041_negredo.pdf)

and

I added the highlighting for you Taffer.

http://www.malariajournal.com/content/5/1/48 (http://www.malariajournal.com/content/5/1/48)

http://www.mja.com.au/public/issues/186_04_190207/sas10773_fm.html (http://www.mja.com.au/public/issues/186_04_190207/sas10773_fm.html)

Here is another example of combination therapy used for the treatment of cancer, the reference can be found at http://www.dissectmedicine.com/resistance (http://www.dissectmedicine.com/resistance)
Same old lies, no math.

You've now told Lie #5 fifty-three times --- number of people deceived: zero.

Taffer

23rd May 2007, 09:20 AM

Taffer

23rd May 2007, 09:25 AM

Why do you say that? Selection "selects against" the least fit organisms, and "selects for" the most fit organisms. Either both terms are tainted with teleology, or neither are.

Yes, I am beginning to see that this is correct. As I was saying, it kind of depends on how you are viewing selection: a mathematical definition or a naturalistic description. I was inclining towards the former, while letting it taint my view of the latter.

Agreed, although the distinction between the pressure being directional and the result being directional doesn't really matter in general conversation.

Very true. It only comes into play when we are talking with a creationist, IMHO.

If we're going to be careful, then I agree we have to go with something like this. This is like trying to define random. :D

At least we don't have mijo. :rolleyes:

I just want to make sure that Kleinman doesn't think that all environmental pressures necessarily result in overall lower reproduction rates.

~~ Paul

Agreed. The model considers selection to be negative. In nature, we see the phenomenon of selection acting both ways. One environmental change drives up some alleles and down others. Depending on our definitions and intentions, we can say it "selects for" and "selects against". Perhaps it is better to say that selection isn't directional, but the environment is?

joobz

23rd May 2007, 09:45 AM

The presence of harmonics in many physical systems (perhaps all physical systems) can be construed as a sign of intelligence. Who would have the power to create a pulsar?

I think you accidentally cranked up the stupid on your lie generator again.

kleinman

23rd May 2007, 10:01 AM

Kleinman, I no longer have any interest in discussing this with you. I could point out for every citation you make why it doesn't say what you think it does, but you will continue to ignore it. I will participate in this thread only in the things which are actually interesting.
You would point it out if you could. You tried to by saying that emergence of resistance has nothing to do with evolution but many of these citations explicitly say that it does, many in the titles of their paper. So ignore these facts of life in the way mutation and selection works. Dr Schneider’s model describes these facts of life mathematically and these examples demonstrate this mathematical fact that multiple selection pressures slow and ultimately stop evolution. Hiding your head under the blanket does not make these facts go away.
I just want to make sure that Kleinman doesn't think that all environmental pressures necessarily result in overall lower reproduction rates.Agreed. The model considers selection to be negative. In nature, we see the phenomenon of selection acting both ways. One environmental change drives up some alleles and down others. Depending on our definitions and intentions, we can say it "selects for" and "selects against". Perhaps it is better to say that selection isn't directional, but the environment is?
Ok kids; let’s watch while these evolutionists try to contrive a “positive selection pressure” that will somehow accelerate evolution. Paul, I would really like to see you put a “positive selection pressure” into ev. This is going to be fun to watch. You evolutionists can really twist and squirm.
The presence of harmonics in many physical systems (perhaps all physical systems) can be construed as a sign of intelligence. Who would have the power to create a pulsar?I think you accidentally cranked up the stupid on your lie generator again.
Somebody rang clown fish’s bell and he is back in the race to prove his ignorance of the mathematics of mutation and selection. It also appears that alchemical engineers are taught nothing of resonance in their training. What can you expect from a brainwashed cultist evolutionist alchemical engineer?

Paul C. Anagnostopoulos

23rd May 2007, 11:03 AM

The presence of harmonics in many physical systems (perhaps all physical systems) can be construed as a sign of intelligence.
Or a sign of rotation.

~~ Paul

Dr Adequate

23rd May 2007, 11:50 AM

You would point it out if you could. You tried to by saying that emergence of resistance has nothing to do with evolution but many of these citations explicitly say that it does, many in the titles of their paper. So ignore these facts of life in the way mutation and selection works. Dr Schneider’s model describes these facts of life mathematically and these examples demonstrate this mathematical fact that multiple selection pressures slow and ultimately stop evolution. Hiding your head under the blanket does not make these facts go away.

Ok kids; let’s watch while these evolutionists try to contrive a “positive selection pressure” that will somehow accelerate evolution. Paul, I would really like to see you put a “positive selection pressure” into ev. This is going to be fun to watch. You evolutionists can really twist and squirm.

Somebody rang clown fish’s bell and he is back in the race to prove his ignorance of the mathematics of mutation and selection. It also appears that alchemical engineers are taught nothing of resonance in their training. What can you expect from a brainwashed cultist evolutionist alchemical engineer? Lies, hysteria and magic words --- but no math.

kleinman

23rd May 2007, 11:51 AM

The presence of harmonics in many physical systems (perhaps all physical systems) can be construed as a sign of intelligence.Or a sign of rotation.
Paul, I’m going to concede this point to you. You still didn’t answer the question where pulsars have come from.

joobz

23rd May 2007, 12:14 PM

You still didn’t answer the question where pulsars have come from.
Yup, you definitely turned the stupid gain up from foolish to blathering idiot.

kleinman

23rd May 2007, 12:41 PM

Envision a system of millions of forming and destructive chemical reactions. Now, envision that intermediates of there reactions associate through non-covalent means and that this complex becomes protected against the destructive reactive pathway, perhaps by a reversible precipitation. These new complexes result in a localized increased of new chemical species. These chemical species then progress in a new series of reaction... that is what I mean through cooperative means. I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.
This is what a clown fish’s explanation for abiogenesis is. The following are real examples of how multiple selection pressures slow and ultimately stop evolution. These examples demonstrate the mathematical result from a peer reviewed and published model of mutation and natural selection, not the raw, baseless speculation of a clown fish alchemical engineer. Clown fish thinks “anything is possible” constitutes a scientific proof. For a brainwashed cultist evolutionist, this may work, but for anyone who knows how to count, they will realize what it is, silly speculation (the basis for the theory of evolution).

http://www.mitpressjournals.org/doi/abs/10.1162/106454698568431 (http://www.mitpressjournals.org/doi/abs/10.1162/106454698568431)
An understanding of antiviral drug resistance is important in the design of effective drugs. Comprehensive features of the interaction between drug designs and resistance mutations are difficult to study experimentally because of the very large numbers of drugs and mutants involved. We describe a computational framework for studying antiviral drug resistance. Data on HIV-1 protease are used to derive an approximate model that predicts interaction of a wide range of mutant forms of the protease with a broad class of protease inhibitors. An algorithm based on competitive coevolution is used to find highly resistant mutant forms of the protease, and effective inhibitors against such mutants, in the context of the model. We use this method to characterize general features of inhibitors that are effective in overcoming resistance, and to study related issues of selection pathways, cross-resistance, and combination therapies.

http://www.imbim.uu.se/forskning/swedbergresearch.html (http://www.imbim.uu.se/forskning/swedbergresearch.html)
Several antimalarial drugs act on the folate metabolism affecting synthesis of DNA precursors, especially dTTP. Examples are Fansidar, which is a combination of pyrimethamine and sulfadoxine, and LapDap, which is a combination of chlorproguanil and dapsone. We still do not know exactly how these compounds interfere with the folate pathways, which include both de novo synthesis and salvage of folates from the host. To be an efficient antimalarial, a drug or drug combination should act on both pathways.

joobz

23rd May 2007, 01:23 PM

[/color]
This is what a clown fish’s explanation for abiogenesis is. The following are real examples of how multiple selection pressures slow and ultimately stop evolution. These examples demonstrate the mathematical result from a peer reviewed and published model of mutation and natural selection, not the raw, baseless speculation of a clown fish alchemical engineer. Clown fish thinks “anything is possible” constitutes a scientific proof. For a brainwashed cultist evolutionist, this may work, but for anyone who knows how to count, they will realize what it is, silly speculation (the basis for the theory of evolution).

look at that. more nonsense and I've noticed you've been dodging all questions.

what happened to the mathematical proof of the arc you were going to give us?
http://forums.randi.org/showthread.php?t=82190 (http://forums.randi.org/showthread.php?t=82190)

So this was another lie?

kleinman

23rd May 2007, 05:57 PM

look at that. more nonsense and I've noticed you've been dodging all questions.
And clown fish flops back to the lead as the evolutionist with the greatest ignorance of the mathematics of mutation and selection. What a flop this fish is.

And now a word from out sponsor, ev which shows that multiple selection pressures slows and ultimately stops evolution. Here are two testimonials from satisfied customers:

Mr Farmer, how do you slow the evolution of resistant weeds, tell us in your own words:

http://www.cropscience.org.au/icsc2004/symposia/2/5/1401_powles.htm (http://www.cropscience.org.au/icsc2004/symposia/2/5/1401_powles.htm)
It is clear that herbicides remain the most efficient technology for large-scale weed control, worldwide. However, the continued increase in evolved herbicide resistance in prominent weed species must lead to change in the way herbicides are used. As there is a paucity of new herbicide modes of action being commercialised there is an imperative to maximize the longevity of the available herbicide resource. To do this requires more pro-active herbicide usage than has been the case until now. Herbicide resistance management strategies need to be implemented that aim to maximise herbicide longevity in farming systems. Maximising the diversity of crops and weed control tools employed is essential for sustainable crop weed management. In the future, bio-economic and population genetics simulation models will assist more sustainable herbicide usage. Careful crop and herbicide rotation together with herbicide sequences and mixtures will be required. Equally, non-herbicide agronomic and biological techniques will be employed to reduce herbicide reliance thereby helping to ensure greater longevity of the precious herbicide resource.
Thank you Mr Farmer for telling us that herbicide mixtures and other combination selection pressures slows the evolution of resistant strains of weeds. Dr Conservationist, tell us you own words what causes the decline of species.

http://www.conservationmedicine.org/papers/Kilpatrick/Kilpatrick_2006_BiolCons.pdf (http://www.conservationmedicine.org/papers/Kilpatrick/Kilpatrick_2006_BiolCons.pdf)
In some cases it is the combination of multiple stressors that lead to the decline of species or groups of species; e.g., amphibians by nematodes (Johnson et al., 1999), increased UV radiation and pollutants (Hatch and Blaustein, 2003; Beebee and Griffiths, 2005), and disease (Collins and Storfer, 2003; Daszak et al., 2003). Conserving endangered species and facilitating their recovery is one the main environmental challenges of the 21st century. Unfortunately, history has shown that in most cases permanent removal of stressors has not been possible and species often need to be
managed indefinitely to ensure their persistence; of the 1263 species listed under the Endangered Species Act of the United States less than 2% have been de-listed (US Fish and Wildlfe Service, 2004).
Thank you Dr Conservationist for telling us that combinations of stressors, which is selection pressures lead to the decline of species.

Multiple selection pressures slow evolution and ultimately lead to extinction. Ev shows this, reality shows this.

Paul C. Anagnostopoulos

23rd May 2007, 06:06 PM

kleinman

23rd May 2007, 06:33 PM

Multiple selection pressures slow evolution and ultimately lead to extinction.So you are saying that all species have gone extinct. I thought that's what you were saying. Now I'm confident you're living in an alternate universe.
I’m not saying that all species have gone extinct. Paul, remember you said:
If selection only ever selects against existing organisms and reduces their rate of reproduction, I'm fairly certain that, taken over a long period, there would be no organisms left at all.
What your own computer model says is that multiple selection pressures slow and ultimately stop evolution. I’m posting numerous citations that show this. These real examples are not limited to random point mutations and natural selection yet they show exactly what your model shows and what Delphi’s Wikipedia reference to fitness landscape explains. What is so strange is that you evolutionists think that mutation and selection somehow worked differently at the time when you say reptiles evolved into birds.

It is little gator, the ambulance chaser that lives in an alternative universe and I’m starting to think that rest of you evolutionists are there with him. Otherwise, why would you be in denial of the mathematics of mutation and selection that your own computer model shows and the numerous real examples of this mathematics?

Paul C. Anagnostopoulos

23rd May 2007, 06:40 PM

I’m not saying that all species have gone extinct.
How would "multiple selection pressures slow evolution and ultimately lead to extinction" not result in a complete lack of species?

~~ Paul

kleinman

23rd May 2007, 06:51 PM

I’m not saying that all species have gone extinct.How would "multiple selection pressures slow evolution and ultimately lead to extinction" not result in a complete lack of species?
That’s an interesting question. Do you think that there are more new species appearing every day or more species going extinct every day? By the way, it is your model which shows that multiple selection pressures slow and ultimately stops evolution and it is the numerous real examples of microevolution which show this as well. How do you get to macroevolution with this type of mathematical fact and numerous real examples of this mathematical fact?

Taffer

23rd May 2007, 07:05 PM

There is more evidence that evolution happened then there is evidence that we landed on the moon.

kleinman

23rd May 2007, 07:41 PM

There is more evidence that evolution happened then there is evidence that we landed on the moon.
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?

joobz

23rd May 2007, 07:48 PM

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?
Is the mathematical evidence of Noah's ark anything like your proof against evolution? nonexistant.

http://forums.randi.org/showthread.php?t=82190 (http://forums.randi.org/showthread.php?t=82190)

Yup, that seems to be the case.

Mr. Scott

23rd May 2007, 11:49 PM

Dr. A., I think we can declare this a "new lie" worthy of assigning it a lie number on our list of Kleinlies. May I suggest #9? Thanks!

I’m not uncomfortable with any question asked in this thread

what is your main purpose for doing this thread?

That reason is none of your business

Isn’t it enough that a bad scientific theory be refuted?

If I had no other reason than annoying Adebz, that would be enough. Where else would I get the opportunity to annoy a PhD in amathematics with some mathematics?

Mr. Scott

24th May 2007, 12:02 AM

Mr. Scott

24th May 2007, 12:31 AM

What I am doing is using your own mathematical model and showing you what it reveals and presenting real examples of what this model reveals.

You are not using that mathematical model. You are misusing it, as has been pointed out to you literally dozens of times in this thread. This is, IIRC, your lie #1 which you repeat daily. I cannot for the life of me understand why the lord will say "well done, good and faithful servant" (Matthew 25:23) for such an appalingly dishonest claim (Exodus 20:16) and its vain repetition. You've accomplished nothing here except to make creationists look ever more stupid and hateful.

Which reminds me: How do you justify, to Christ, the hatefulness you exhibit so generously in this thread? (Luke 6:27-31)

kleinman

24th May 2007, 07:54 AM

The presence of harmonics in many physical systems (perhaps all physical systems) can be construed as a sign of intelligence.Surely, you must allow your assertions to be subjected to the same demands for mathematical foundation that you make of evolutionists. Please present your mathematical model that proves "the presence of harmonics in many physical systems" is impossible except through divine intervention.
This is not as difficult as you might imagine. If you subscribe to the principle of “cause and effect”, the cause for the universe is nothing short of divine.
What I am doing is using your own mathematical model and showing you what it reveals and presenting real examples of what this model reveals.You are not using that mathematical model. You are misusing it, as has been pointed out to you literally dozens of times in this thread. This is, IIRC, your lie #1 which you repeat daily. I cannot for the life of me understand why the lord will say "well done, good and faithful servant" (Matthew 25:23) for such an appalingly dishonest claim (Exodus 20:16) and its vain repetition. You've accomplished nothing here except to make creationists look ever more stupid and hateful.
I love it when you evolutionists claim that I am misusing Dr Schneider’s computer model. All that I have done is what he called for in his publication on his model. Here, let me remind you what he said in his peer reviewed and published paper.
Variations of the program could be used to investigate how population size, genome length, number of sites, size of recognition regions, mutation rate, selective pressure, overlapping sites and other factors affect the evolution.
So I did as Dr Schneider suggested for me to do both in private communications and what he suggests to others in his peer reviewed and published paper on the model. I have then reported to the results of these studies to the wise and educated scientists on the James Randi Educational Forum. If you do as Dr Schneider suggests, you find that I am not violating Exodus 20:16. In fact, this study reveals an important principle of the mutation and selection process that has many applications in real life including the treatment of cancer. After all, Dr Schneider is employed by the main institution in the United States dedicated to the eradication of cancer and if he had followed his own suggestion and did a more complete investigation of his model, he would have verified mathematically what oncologists have discovered empirically, that is multiple selection pressures slow the evolution of cancer cells. Instead, he selected a total unrealistic case from his model to suggest the evolution of humans. This is how the theory of evolution has warped the interpretation of evidence that is presented. Evolutionists twist data any way you can in an effort to fit it into the evolutionist belief system. This is the violation of Exodus 20:16.
Which reminds me: How do you justify, to Christ, the hatefulness you exhibit so generously in this thread? (Luke 6:27-31)
You think you know my mind? If you want to understand my mind a little, read Proverbs 27:5-6. By the way, are these Bible verses you are quoting some of the lies your parents told you?

Here are more real examples of what Dr Schneider’s ev model reveals when a more thorough study of the model is done, that is multiple selection pressures slow and ultimately stop evolution.

http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=453423 (http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=453423)
The Global Program for the Elimination of Lymphatic Filariasis (GPELF) intends to achieve its aims through yearly mass treatments with albendazole (ABZ) combined with ivermectin (IVM) or diethylcarbamazine (DEC). The use of ABZ and IVM separately to combat parasites of veterinary importance has, on many occasions, resulted in widespread drug resistance. In order to help predict the spread of potential ABZ resistance alleles through a population of Wuchereria bancrofti, we have developed a mathematical model that incorporates population genetics into EPIFIL, a model which examines the transmission dynamics of the parasite. Our model considers the effect of the combined treatments on the frequency of a recessive allele, which confers ABZ resistance. The model predicts that after 10 yearly treatments with ALB and DEC, 85% coverage and an initial resistance allele frequency of 5%, the frequency of the resistance genotype will increase from 0·25 to 12·7%. If non-random mating is assumed, the initial genotype frequency will be 2·34% and will increase to 62·7%. ABZ and IVM combination treatment may lead to weaker selection for this genotype. Treatment coverage, initial allele frequencies and number of treatments also affect the rate of selection.

http://www.freepatentsonline.com/20050148523.html (http://www.freepatentsonline.com/20050148523.html)
A method of treating HIV infection in a human patient wherein the infecting HIV strain has become resistant to atazanavir, the method comprising administration of a therapeutically effective amount of a combination of atazanavir or a pharmaceutically acceptable salt thereof, and at least one other HIV protease inhibitor.A method for enhancing the effectiveness of a second HIV protease inhibitor in treating HIV infection in a human patient whose HIV strain has become resistant to atazanavir or a pharmaceutically acceptable salt thereof, comprising administering to said human patient an amount of atazanavir or a pharmaceutically acceptable salt thereof effective in maintaining the resistant strain, in combination with the second HIV protease inhibitor.The resistance to atazanavir in the human is manifested by the existence of the signature mutation consisting of I50L mutation in the HIV protease.

joobz

24th May 2007, 09:09 AM

kjkent1

24th May 2007, 09:22 AM

I have then reported to the results of these studies to the wise and educated scientists on the James Randi Educational Forum.To a person, all of the "wise and educated scientists" here have made numerous suggestions as to why your findings are wrong, and what you might do to prove your theory. As you have dismissed all of these suggestions out of hand, one wonders why you would refer to the scientists here as "wise and educated?" Sarcasm? Cynicism?

If so, then you are not following your Master's will, because you are entirely closed to the possibility that you are capable of error. Were this not true, then you would have long ago, sought to reprogram ev so as to test your hypotheses about the impossibility of evolution. As you have not, you are intentionally blinding yourself to the possibility that you may be wrong, and therefore for you to state continuously and unequivocally that others are deluded, brainwashed, etc., is the work of a corrupt heart. You cast stones against those you view as heretical, before evaluating all of the facts.

You have intentionally bottled yourself up in this single thread on the web, where you can hear only the sound of your own voice screaming in the wind.

Until you engage others with the same respect you demand of yourself, you will garner no respect from others.

You have sown the wind. You know the rest.

Dr Richard

24th May 2007, 09:46 AM

Here are more real examples of what Dr Schneider’s ev model reveals when a more thorough study of the model is done, that is multiple selection pressures slow and ultimately stop evolution.

http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=453423 (http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=453423)

http://www.freepatentsonline.com/20050148523.html (http://www.freepatentsonline.com/20050148523.html)

Although it pains me to keep this poor thread alive, sometimes I just can't help myself. From kleinman's first link:

The model predicts that after 10 yearly treatments with ALB and DEC, 85% coverage and an initial resistance allele frequency of 5%, the frequency of the resistance genotype will increase from 0·25 to 12·7%. If non-random mating is assumed, the initial genotype frequency will be 2·34% and will increase to 62·7%

Evolution is stopped how?

And the second link...

is a patent application!

Is that sound kleinman scrabbling at the bottom of the barrel? Or has his macro generator gone into meltdown?

Paul C. Anagnostopoulos

24th May 2007, 10:48 AM

kleinman

24th May 2007, 10:50 AM

This is not as difficult as you might imagine. If you subscribe to the principle of “cause and effect”, the cause for the universe is nothing short of divine.Oh, I see: My pure speculation (and I called it such) for abiogenesis is unacceptable because I have no immediate evidence that it is what happened.
Oh clown fish, how astute of you to catch this flaw in my logic. I am speculation about the cause of the universe. However, I am not speculating about the mathematics of mutation and selection. I am using a peer reviewed and published model of random point mutation and natural selection which shows that multiple selection pressures slow and ultimately stop evolution. And I am citing large numbers of peer reviewed publications that show this same effect occurs in reality. I must complement you on how well you are doing in this horserace to be the last evolutionist to understand the mathematics of mutation and selection. You are displaying true winning form in this area.
I have then reported to the results of these studies to the wise and educated scientists on the James Randi Educational Forum.To a person, all of the "wise and educated scientists" here have made numerous suggestions as to why your findings are wrong, and what you might do to prove your theory. As you have dismissed all of these suggestions out of hand, one wonders why you would refer to the scientists here as "wise and educated?" Sarcasm? Cynicism?
Me be sarcastic? Me be cynical? I am shocked at such an accusation. I dismiss all of the suggestions by the wise and educated scientists from the James Randi Educational Forum out of hand because I have presented large numbers of citations which show that what I assert (multiple selection pressures slow and ultimately stop evolution) is true while evolutionists have yet to present a single case which shows the multiple selection pressures accelerate evolution. Would it make you feel better if I called the evolutionists who post on this thread “brainwashed cultists”?
If so, then you are not following your Master's will, because you are entirely closed to the possibility that you are capable of error. Were this not true, then you would have long ago, sought to reprogram ev so as to test your hypotheses about the impossibility of evolution. As you have not, you are intentionally blinding yourself to the possibility that you may be wrong, and therefore for you to state continuously and unequivocally that others are deluded, brainwashed, etc., is the work of a corrupt heart. You cast stones against those you view as heretical, before evaluating all of the facts.
Little gator, tell me what the Master’s will is for you? How do you know it is not the Master’s will for you to reprogram ev?

When people call themselves scientists and are presented with the results from a computer simulation of one of their peer reviewed adherent to their theory that completely contradicts their theory and those results is backed by large amounts of empirical and reproducible evidence and completely deny those results then what other conclusion can you come to about these people? By the way, I haven’t called evolutionists delusional, but your description may have application.
You have intentionally bottled yourself up in this single thread on the web, where you can hear only the sound of your own voice screaming in the wind.
Just think of this as standing in the gap. With respects to hearing the sound of my own voice on this thread, as of this post, I have posted 702 times on this forum, not all on this thread. There have been over 4,000 posts on this thread alone. I listen to the other voices on this thread (though it is rare that I agree with these voices).
Until you engage others with the same respect you demand of yourself, you will garner no respect from others.
I haven’t demanded respect from any of the posters. I would rather hear a heated argument with honest expression of your opinions rather than hypocritical flattery. My honest opinion of the theory of evolution is that it is a dumb theory without a mathematical basis and I am showing you why with a peer reviewed mathematical model written by one of your own and large amounts of empirical evidence which supports my assertion. Present your case if you have one or you are better off pleading guilty and throwing your client to the mercy of the court.
You have sown the wind. You know the rest.
If you believe that verse, do you believe Genesis 1:1?
Here are more real examples of what Dr Schneider’s ev model reveals when a more thorough study of the model is done, that is multiple selection pressures slow and ultimately stop evolution.

http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=453423 (http://journals.cambridge.org/action/displayAbstract?fromPage=online&aid=453423)

http://www.freepatentsonline.com/20050148523.html (http://www.freepatentsonline.com/20050148523.html)Although it pains me to keep this poor thread alive, sometimes I just can't help myself. From kleinman's first link:
I appreciate your support to keep this thread alive, so let’s consider what was said in the first link.
The model predicts that after 10 yearly treatments with ALB and DEC, 85% coverage and an initial resistance allele frequency of 5%, the frequency of the resistance genotype will increase from 0·25 to 12·7%. If non-random mating is assumed, the initial genotype frequency will be 2·34% and will increase to 62·7%Evolution is stopped how?
This example only shows the slowing of evolution and how monotherapy (single selection pressure) leads to resistance more quickly than combination therapy (multiple selection pressures). You missed the following when you selected from the full quote.
The use of ABZ and IVM separately to combat parasites of veterinary importance has, on many occasions, resulted in widespread drug resistance.
And the second link...

is a patent application!

Is that sound kleinman scrabbling at the bottom of the barrel? Or has his macro generator gone into meltdown?

Oh, you only accept peer review publications? Well, here’s a couple more that show that multiple selection pressures slow and ultimately stop evolution.

http://evonet.sdsc.edu/evoscisociety/eb_meeting_societal_needs.htm (http://evonet.sdsc.edu/evoscisociety/eb_meeting_societal_needs.htm)
Agricultural entomologists trained in evolutionary genetics 31, 53 are contributing to efforts to delay or prevent the evolution of resistance, such as rotational use of different control measures and judicious combination of chemical with nonchemical controls.

http://content.nejm.org/cgi/content/extract/350/10/1023?ck=nck (http://content.nejm.org/cgi/content/extract/350/10/1023?ck=nck)
The use of combinations of antiretroviral drugs has proven remarkably effective in controlling the progression of human immunodeficiency virus (HIV) disease and prolonging survival,1 but these benefits can be compromised by the development of drug resistance.2,3 Resistance is the consequence of mutations that emerge in the viral proteins targeted by antiretroviral agents.

Dr Richard, the only thing melting down here is the theory of evolution. By the way, have you found the error in the equation from the link you posted previously? Dr Richard, are you trying to enter the horserace to be the last evolutionist to understand the mathematics of mutation and selection?

kleinman

24th May 2007, 11:08 AM

That’s an interesting question. Do you think that there are more new species appearing every day or more species going extinct every day?I have no idea, but it doesn't matter. If everything is going to go extinct, it will indeed be selection pressures that do the trick. It does not follow, however, that the mere existence of multiple pressures of any sort is enough to eliminate all species. If that were the case, no species would have every arisen in the first place.

Oops. I think I just fell into a trap.
It is not my intention to trap you. It is my intention to debate the merits of the theory of evolution. Most selection pressures are stabilizing selection pressures. These stabilizing selection pressures eliminate creatures that have mutations that damage essential genes. These types of selection pressures favor the optimum and eliminate the phenodeviants. Only directional selection pressures select toward a new optimum and once that optimum is attained, this selection pressure becomes a stabilizing selection pressure. This is what is demonstrated with ev when the model is initially started, the selection conditions are directional. Once the new optimum is attained the selection pressures become stabilizing. Once that state is attained in ev, if you turn off selection, the evolved state for those conditions disappears. It is also the directional selection pressures that reduce the reproductive fitness of creatures.

joobz

24th May 2007, 11:16 AM

Oh clown fish, how astute of you to catch this flaw in my logic.
It wasn't very hard. You have a knack for the illogical and inane.

kleinman

24th May 2007, 04:28 PM

Oh clown fish, how astute of you to catch this flaw in my logic.It wasn't very hard. You have a knack for the illogical and inane.
Too bad you don’t have a knack for the mathematics of mutation and selection; otherwise you would understand these next two citations.

http://www.stanford.edu/~siegelr/philhsu.htm (http://www.stanford.edu/~siegelr/philhsu.htm)
Protease inhibitors are the latest addition to the arsenal of drugs designed to combat the HIV virus. Preliminary studies show that combination therapy with reverse transcriptase inhibitors have resulted in decrease of viral load to undetectable levels.1 The FDA, encouraged by these early studies, approved protease inhibitors in late 1995 after an accelerated approval process.2 The popular media has portrayed protease inhibitors as the cure for HIV infection and AIDS. However, the medical community remains reservedly optimistic about protease inhibitors because studies have also shown that despite early potent antiviral effects, HIV eventually develops resistance to protease inhibitors.1 This review will attempt to explain the mechanism by which HIV gains resistance and the potential limits to HIV's mutability as elucidated by recent scientific literature.
And
Protease inhibitor therapy has been shown to decrease viral load substantially, but in the long run, it has not been shown to maintain its antiviral potency. However, this does not mean that protease inhibitor therapy is a lost cause. Recent research suggests that HIV gains resistance at substantial cost to protease functionality and that increased selective pressure from more protease inhibitors may lead to less virulent strains of HIV. Therefore, more funding should be given to new and more potent protease inhibitor development.

In addition, the appearance of cleavage site mutations and the possibility that these mutations might be a rate limiting step in the evolution of resistance give hope that HIV has only a limited amount of options left for resistance mutation. Research should focus on ways to inhibit the mutated cleavage sites. If cleavage site mutations are a rate limiting step in resistance development, simultaneous inhibition of cleavage site and protease could be very effective; HIV would have to mutate at both the protease and the cleavage site simultaneously to develop resistance.

http://www.medscape.com/viewarticle/512015_4 (http://www.medscape.com/viewarticle/512015_4)
Predicting the degree of resistance and its clinical relevance of any set of mutations to a specific antiretroviral agent, or combination therapy, is complicated by several factors, including the potential for interactions within and between drug classes.[8,26,27] Therefore we augmented our analyses of antiretroviral susceptibility based on a genotypic rule-based algorithm, with predicted phenotypic results. Because the degree of reduced susceptibility correlated with diminished clinical response is not well defined for most antiretroviral agents, we assessed several available cut-offs.[28] In all cases our analyses were consistent with the genotype rule-based results.

Current treatment guidelines recommend switching patients to at least 2 active antiretroviral agents at the earliest evidence of detectable viremia related to decreased drug susceptibility.[1,5] This approach is appealing if a new regimen is available, well tolerated, and succeeds in limiting HIV replication to undetectable levels, thereby minimizing the probability of acquiring additional resistance. The aggressiveness with which to approach virologic failure, however, must be balanced by the risks associated with exposing patients to additional antiretroviral agents. Our findings demonstrate a relatively slow rate of resistance evolution in patients with HIV-1 subtype B, especially among individuals with multiple mutations, who have stable HIV RNA levels in plasma over time, and who maintain HIV RNA levels <1000 copies/mL. These data suggest that maintaining specific patients on a failing regimen results in relatively slow resistance evolution with limited reduction in antiretroviral drug susceptibility. However, this must be tempered by the specific regimen and prior resistance profile of the patient, because acquiring even a single mutation may cause resistance to all NNRTIs and the M184V mutation leads to resistance to lamivudine and emtricitabine.

Many patients maintained on an incompletely suppressive regimen continue to derive immunologic, virologic, and clinical benefit, possibly due to the reduced replication capacity of mutant HIV variants, enhanced HIV-specific immune responses, and residual drug activity.[3,6,29,30] Therefore, delaying switching of suboptimal regimens may be indicated in some patients. However, patients with HIV-1, with limited resistance, especially those with plasma HIV RNA >1000 copies/mL, are at risk for emergence of increasingly resistant virus. Further studies monitoring resistance evolution over time are needed, and combined analyses across observational clinical cohorts would strengthen our initial observations.

Dr Richard, if you are concerned about me running low on citations that substantiate my contention that multiple selection pressures slow and ultimately stop evolution, the google search I am using to draw from for these articles has more than a million hits. I’m going to be posting these articles for a long time. You might as well sit back, relax and make yourself comfortable; this thread is just getting started. Of course, if you or any evolutionist can find a citation that shows that multiple selection pressures accelerate evolution, we would all be interested in seeing that link.

Paul C. Anagnostopoulos

24th May 2007, 06:02 PM

It is not my intention to trap you. It is my intention to debate the merits of the theory of evolution.
Whew, I didn't fall into the trap I suspected I had.

Most selection pressures are stabilizing selection pressures. These stabilizing selection pressures eliminate creatures that have mutations that damage essential genes. These types of selection pressures favor the optimum and eliminate the phenodeviants. Only directional selection pressures select toward a new optimum and once that optimum is attained, this selection pressure becomes a stabilizing selection pressure. This is what is demonstrated with ev when the model is initially started, the selection conditions are directional. Once the new optimum is attained the selection pressures become stabilizing. Once that state is attained in ev, if you turn off selection, the evolved state for those conditions disappears. It is also the directional selection pressures that reduce the reproductive fitness of creatures.
Then why did you say "multiple selection pressures slow evolution and ultimately lead to extinction"?

~~ Paul

joobz

24th May 2007, 07:04 PM

Too bad you don’t have a knack for the mathematics of mutation and selection; otherwise you would understand these next two citations.

But the truth is I do have a knack for it. That's why I'm not at all fooled by your complete missrepresentation of the papers you're citing.

You keep claiming math, but you've failed time and again to say how long is too long. You're showing things over a course of years, when life has had millions of years. You're using a micrometer and claiming that the sear's tower is too tall.

kleinman

24th May 2007, 07:14 PM

It is not my intention to trap you. It is my intention to debate the merits of the theory of evolution.Whew, I didn't fall into the trap I suspected I had.
But you did touch on an important principle which is whether mutation and selection when you said this:
If everything is going to go extinct, it will indeed be selection pressures that do the trick. It does not follow, however, that the mere existence of multiple pressures of any sort is enough to eliminate all species. If that were the case, no species would have every arisen in the first place.
Each time you add an additional selection pressure to a species, you impair its reproductive fitness more so and make it more difficult to evolve to each of the individual selection pressures. This is what ev shows and this is what all these citations I’ve been posting show.
Most selection pressures are stabilizing selection pressures. These stabilizing selection pressures eliminate creatures that have mutations that damage essential genes. These types of selection pressures favor the optimum and eliminate the phenodeviants. Only directional selection pressures select toward a new optimum and once that optimum is attained, this selection pressure becomes a stabilizing selection pressure. This is what is demonstrated with ev when the model is initially started, the selection conditions are directional. Once the new optimum is attained the selection pressures become stabilizing. Once that state is attained in ev, if you turn off selection, the evolved state for those conditions disappears. It is also the directional selection pressures that reduce the reproductive fitness of creatures.Then why did you say "multiple selection pressures slow evolution and ultimately lead to extinction"?
I should be more precise in my wording. It is multiple directional selection pressures which slow evolution and ultimately lead to extinction. Stabilizing selection pressures have less effect but still have impact. One of the citations I posted previously http://www.nature.com/nature/journal/v446/n7136/abs/nature05685.html (http://www.nature.com/nature/journal/v446/n7136/abs/nature05685.html) shows that e coli bacteria that is resistant to a particular antibiotic (doxycycline) can still have difficulty navigating the fitness landscape to an new optimum when another antibiotic (selection pressure) is introduced at the same time.

The point here is that you need directional selection pressures to evolve new life forms. Stabilizing selection pressures increase the frequency of those adapted genes in the gene pool and reduce diversity of the life forms. The mathematical problem for your theory is that more directional selection pressures you put on a population the more difficult it is for the population to evolve to a new optimum on the fitness landscape. If the population can not evolve to a new optimum, it goes extinct.

Consider this, in these citations I have been posting, as few as 2 or 3 selection pressures applied simultaneously impair the ability of the population to adapt to these selection pressures when if applied sequentially, the population easily adapts one at a time. What kind of directional selection pressure can you put on a reptile that would evolve it into a bird? The genetic optimums on the fitness landscape for each of these life forms are so far removed from each other, what kind of path could be taken that would transform the huge number of genes involved?

Think about it and you can tell me how this is done next week. And remember our soldiers who bleed for our right to have this type of conversation.

Dr Adequate

25th May 2007, 04:42 AM

So, kleinman hasn't thought of any new lies or done any math.

Dr Adequate

25th May 2007, 04:55 AM

Hey, the following thread titles just lined up:

Annoying creationists
Charlatanry
Human race in danger of being stupided to death.

I think the FSM is trying to tell us something.

Cuddles

25th May 2007, 05:12 AM

Paul C. Anagnostopoulos

25th May 2007, 06:10 AM

Hey, the following thread titles just lined up:
And they still do! It's a sign, I tell you!

~~ Paul

joobz

25th May 2007, 07:26 AM

I should be more precise in my wording. It is multiple directional selection pressures which slow evolution and ultimately lead to extinction. Stabilizing selection pressures have less effect but still have impact.
and stablizing pressures are stabilizing typically becuase a creature has adapted to that "directional" pressure.

The point here is that you need directional selection pressures to evolve new life forms. Stabilizing selection pressures increase the frequency of those adapted genes in the gene pool and reduce diversity of the life forms. The mathematical problem for your theory is that more directional selection pressures you put on a population the more difficult it is for the population to evolve to a new optimum on the fitness landscape. If the population can not evolve to a new optimum, it goes extinct.

Consider this, in these citations I have been posting, as few as 2 or 3 selection pressures applied simultaneously impair the ability of the population to adapt to these selection pressures when if applied sequentially, the population easily adapts one at a time.
We've already established that:
1.) You haven't been able to define what 2 or 3 selection pressures mean. Considering that a single insult like heat shock can result in a multitude of stresses. But you still use "more" as some acceptable mathematical measure
2.) even with these multiple pressures (values you select), we see adaptation take palce. Resistance develops. In our short span of observational time, we see resistance develop. This KILLS your entire hypothesis.

If I start walking west from New York, will you claim that I will never reach the west coast? the landscape is rough in parts, but there are paths across.

For your sake and the sake of the soldiers that have allowed us to have this discussion, stop squandering it on lies and foolishness. It is very disrespectful to them.

Dr Richard

25th May 2007, 09:02 AM

This example only shows the slowing of evolution and how monotherapy (single selection pressure) leads to resistance more quickly than combination therapy (multiple selection pressures). You missed the following when you selected from the full quote.

You missed the point that two selection pressures cause increased resistance.

You continually misunderstand the following point:

If one or more sufficient "selection presures" are applied to a single generation of a population such that the resulting surviving population is too small to allow evolutionary adaptation before the population becomes extinct, then evolution is halted.

There is nothing magical about the number of selection pressures. One can do it, 3 can do it, 3 million can do it. To prove your theory, you need to demonstrate that not only was this the case for the dodo, it also applies to every living species today. I await your proof with interest....

Oh, you only accept peer review publications? Well, here’s a couple more that show that multiple selection pressures slow and ultimately stop evolution.

You are suprised that a patent application is not acceptable? Really? Your scientific background betrays you...

Dr Richard, the only thing melting down here is the theory of evolution. By the way, have you found the error in the equation from the link you posted previously?

I avoided mentioning this to spare your blushes. But you keep on repeating it. There is not a single error in the equation you posted. Go back and try again, in the meantime an F for arithmetic.

Dr Richard, are you trying to enter the horserace to be the last evolutionist to understand the mathematics of mutation and selection?

I presume you are trying to be the first creationist to understand the mathematics of mutation and natural selection? Let me know when you are at the starting line by answering the following questions:

1. How many "directional" selection pressures do you think act on the HIV virus when it infects an untreated patient?

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

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

Dr Adequate

26th May 2007, 05:00 AM

And remember our soldiers who bleed for our right to have this type of conversation. So far as I'm aware, the insurgents in Iraq aren't fighting against your right to babble about cheese. And as most of them are religious nutjobs, they probably approve of fellow-whackos like you telling stupid lies about evolution.

(Kleinman statistic: he's made 64 posts involving cheese. That's more often than he's told Lie #5. I guess he realises which is the stronger argument.)

Paul C. Anagnostopoulos

26th May 2007, 08:53 AM

I tell ya, Kleinman is a mole for the Wisconsin cheese lobby.

Eat Cheese or Die!

~~ Paul

kleinman

27th May 2007, 08:07 AM

It's interesting the threads that get the most activity. A quick look shows the following as some of the longest threads:

Bigfoot.
Creationism.
Jews destroying the World Trade Centre with Mega-Death-Ray-Space-Beams, possibly with the help of elves.
Buzz Lightyear.

I wonder if Kleinman realises just how it makes his argument look when the best comparisons are Buzz and Christophera.
Cuddles, this is how you are trying to make argument look. Since your own evolutionary math shows your theory to be mathematically impossible and I am now posting dozens of citations of real examples why the theory is mathematically impossible, you are left with these types of arguments to try to refute my contentions.
I should be more precise in my wording. It is multiple directional selection pressures which slow evolution and ultimately lead to extinction. Stabilizing selection pressures have less effect but still have impact.and stablizing pressures are stabilizing typically becuase a creature has adapted to that "directional" pressure.
Is clown fish ready to describe the directional selection pressures that evolve genes de novo?
This example only shows the slowing of evolution and how monotherapy (single selection pressure) leads to resistance more quickly than combination therapy (multiple selection pressures). You missed the following when you selected from the full quote.You missed the point that two selection pressures cause increased resistance.
And you missed the point that when the selection pressures are applied sequentially, the resistance is evolved much more quickly than when the selection pressures are applied simultaneously. This is what is shown with the mathematics of ev shows and this is what the citations being posted shows.
If one or more sufficient "selection presures" are applied to a single generation of a population such that the resulting surviving population is too small to allow evolutionary adaptation before the population becomes extinct, then evolution is halted.
The size of population does not matter when the selection pressure(s) are “sufficient”. You will always have extinction with “sufficient” selection pressure(s). The ev model does not allow for extinction, therefore the selection pressures(s) are never “sufficient” to cause extinction of the population no matter how small the population is. This is the best of all possible scenarios to try to prove your theory and you still have the problem that multiple selection pressures slow and ultimately stop the evolutionary process even without the possibility of extinction.
There is nothing magical about the number of selection pressures. One can do it, 3 can do it, 3 million can do it. To prove your theory, you need to demonstrate that not only was this the case for the dodo, it also applies to every living species today. I await your proof with interest....
I agree with you that there is nothing magical about 3 or 3 million selection pressures. But there is something mathematical about 3 or 3 million selection pressures and that mathematics is the greater the number of selection pressures, the slower and more difficult the process to navigate the fitness landscape to a new optimum. Ev shows this and the numerous citations posted show this. In addition, the more selection pressures you have, the greater the reduction in reproductive fitness and the more likely the population will go extinct.
Oh, you only accept peer review publications? Well, here’s a couple more that show that multiple selection pressures slow and ultimately stop evolution.You are suprised that a patent application is not acceptable? Really? Your scientific background betrays you...
I think a patent application is not acceptable in this argument only if it is not true but since this application is true, I gave it as a citation. If this makes you sad, content yourself with the numerous other citations from Nature, NEJM, JAMA, …
Dr Richard, the only thing melting down here is the theory of evolution. By the way, have you found the error in the equation from the link you posted previously?I avoided mentioning this to spare your blushes. But you keep on repeating it. There is not a single error in the equation you posted. Go back and try again, in the meantime an F for arithmetic.
So let’s post the equation again and let me give you a hint.
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1669717&blobname=gkl855e1.jpg
Look at the last term in the denominator of the right side of the equation. And then explain to us the meaning of this equation from your link.
Dr Richard, are you trying to enter the horserace to be the last evolutionist to understand the mathematics of mutation and selection?I presume you are trying to be the first creationist to understand the mathematics of mutation and natural selection? Let me know when you are at the starting line by answering the following questions:
I don’t know if I am the first creationist to understand the mathematics of mutation and selection but I now do understand that multiple selection pressures slow and ultimately stop the evolutionary process. Now when will you understand this mathematical fact?
1. How many "directional" selection pressures do you think act on the HIV virus when it infects an untreated patient?
Now don’t confuse your terminology here. I count each drug used in the therapy of HIV as an additional directional selection pressure. Some drugs affect more loci than others and some drugs have greater “sufficiency” than others. In the untreated patient, the number of directional selection pressures depends on the immune competency of the patient such as the number of different and quantity of antibodies the patient’s immune system can direct toward the virus. This number must be very low and of low sufficiency since so few people with the virus survive for long without treatment.
2. If one base pair mutation is a microevolutionary event, how many base pair mutations to make a macroevolutionary event? 2? 10? 100?
None of the base pair events with HIV are create any new gene function. Proteases remain proteases, reverse transcriptases remain reverse transcriptases.
3. (for old time's sake) What is your definition of macroevolution again? (NB random lists of things you think it is are not acceptable)
Let’s start with this, macroevolution is the evolution of reptiles to birds, and this doesn’t happen. With your help, we can firm up this definition.
I tell ya, Kleinman is a mole for the Wisconsin cheese lobby.

Eat Cheese or Die!
I think the theory of evolution is starting to smell like limburger.

Dr Richard, here are some more citations that show that multiple selection pressures slow and ultimately stop evolution. I hope the first citation is from a source that you find acceptable.

http://www.journals.royalsoc.ac.uk/content/kljr3bmug6kxqppu/ (http://www.journals.royalsoc.ac.uk/content/kljr3bmug6kxqppu/)
Antimarial drug resistance develops when spontaneously occurring parasite mutants with reduced susceptibility are selected, and are then transmitted. Drugs for which a single point mutation confers a marked reduction in susceptibility are particularly vulnerable. Low clearance and a shallow concentration–effect relationship increase the chance of selection. Use of combinations of antimalarials that do not share the same resistance mechanisms will reduce the chance of selection because the chance of a resistant mutant surviving is the product of the per parasite mutation rates for the individual drugs, multiplied by the number of parasites in an infection that are exposed to the drugs. Artemisinin derivatives are particularly effective combination partners because (i) they are very active antimalarials, producing up to 10 000-fold reductions in parasite biomass per asexual cycle; (ii) they reduce malaria transmissibility; and (iii) no resistance to these drugs has been reported yet. There are good arguments for no longer using antimalarial drugs alone in treatment, and instead always using a combination with artemisinin or one of its derivatives.

http://www.annals.org/cgi/content/short/128/11/951 (http://www.annals.org/cgi/content/short/128/11/951)
First, using drugs that require the virus to undergo multiple mutations to achieve high-level resistance maximizes the efficacy of the drug for the existing viral population and minimizes the probability of breakthrough. In this respect, a drug to which resistance develops after only a single amino acid substitution is expected to be more vulnerable to resistance than an equipotent drug that requires the virus to undergo multiple mutations to achieve the same degree of resistance.

Second, the need for multiple mutations can be increased further by combining different drugs that inhibit independent targets. Three distinct therapeutic classes of drugs with nonoverlapping sets of resistance determinants exist: protease inhibitors, nucleoside inhibitors, and non-nucleoside reverse transcriptase inhibitors. There is no evidence that mutations compromising the effects of members of one class will reduce the utility of members of any other class. This is one of the most important benefits of divergent combination therapy: When many simultaneous mutations are required, the probability of preexisting resistance in a therapy-naive patient becomes negligible and the effect of the drug combination is maximized.

Paul C. Anagnostopoulos

27th May 2007, 09:07 AM

joobz

27th May 2007, 10:00 AM

Is clown fish ready to describe the directional selection pressures that evolve genes de novo??? are you ready to define what the heck macroevolution is?

1.) You haven't been able to define what 2 or 3 selection pressures mean. Considering that a single insult like heat shock can result in a multitude of stresses. But you still use "more" as some acceptable mathematical measure
2.) even with these multiple pressures (values you select), we see adaptation take palce. Resistance develops. In our short span of observational time, we see resistance develop. This KILLS your entire hypothesis.

So let’s post the equation again and let me give you a hint.
http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1669717&blobname=gkl855e1.jpg
Look at the last term in the denominator of the right side of the equation. And then explain to us the meaning of this equation from your link.
Kleinman, you are trying very hard to demonstrate your knowledge and ability with math. But pointing out an obviously missing subscript (which anyone reading the equation can see and understand what it should be) isn't going to impress anyone.

In fact, it simply reinforces the obvious fact that your handle of math is more in form than function. Otherwise, even you wouldn't continually use such inexact comparisons(more, less, too slow...) and stick with actual values.

But, then, if you did that, you would have to accept the fact that your whole argument falls to bits.

Yahzi

27th May 2007, 10:37 AM

We would all like to hear a clear, concise, non-cryptic Bible lesson from you.
Are you serious? People actually read Klienman's posts?

I just come here to see what witty things Dr. Adequate and Joobz have to say.

Meadmaker

27th May 2007, 08:14 PM

Is clown fish ready to describe the directional selection pressures that evolve genes de novo

Pardon a latecomer's comments, because I have only skimmed the last few pages. If this has already been addressed, sorry for doing so again.*

I would hope that Clown Fish would not do such a thing, because I would hope that he, and everyone else reading this thread, would know that selection pressures can't evolve genes de novo. Selection can't create. It merely selects. In order to be selected, it must already exist.

Only the random mutations can create new genes. (Biologists: Begging your pardon if there is some other way to produce a new gene other than through mutation. Either way, it's the random part of the process that makes new stuff.) Most of those new genes are neutral or detrimental to the host organism, but if one of them provides a new function, it will appear increasingly more frequently in subsequent generations, as it is selected for continuance.

It just seems that there's a misconception in this thread that somehow mutations arise in response to some sort of selection pressure. If that is what anyone meant, that can't be the case. The mutations just exist.

In the case of bacteria and antibiotics, there is some variation in the DNA sequences in a population of bacteria. Some of that population is resistant to an antibiotic. When that population is hit with an antibiotic for the first time, most will die, but a few will live. If they manage to divide and grow, then the next time you hit the population with the same antibiotic, very few will die. We say that the strain has developed resistance, but really, the individual bugs had developed resistance even before being hit with an antibiotic. The new strain is the descendants of the bugs that survived when the antibiotic hit them.

And of course, applying two new sorts of brand new selection pressures will indeed make it more likely that you will kill everything you are "pressuring", for exactly the reason cited in the article. The probability that an existing organism will have two different mutations that make it less susceptible to two previously unencountered selection pressures is indeed quite small.

But what's the point? Sure, new and novel selection pressures can make species go extinct. Also, if a species has to evolve or die, it usually "chooses" die. Evolution is so slow that rapid adpatation to novel pressures doesn't work so well. Fortunately, there aren't all that many novel pressures to deal with. Somewhere in the last three billion years, a lot of things have happened, and our ancestors survived. The new things are really just variations on an old theme, mostly.

ETA:* Of course, all of this has been addressed before somewhere. The evolution vs. creationism topic has been around since Darwin, and it migrated onto bulletin boards as soon as someone invented them.

Taffer

27th May 2007, 09:58 PM

Pardon a latecomer's comments, because I have only skimmed the last few pages. If this has already been addressed, sorry for doing so again.*

I would hope that Clown Fish would not do such a thing, because I would hope that he, and everyone else reading this thread, would know that selection pressures can't evolve genes de novo. Selection can't create. It merely selects. In order to be selected, it must already exist.

Only the random mutations can create new genes. (Biologists: Begging your pardon if there is some other way to produce a new gene other than through mutation. Either way, it's the random part of the process that makes new stuff.) Most of those new genes are neutral or detrimental to the host organism, but if one of them provides a new function, it will appear increasingly more frequently in subsequent generations, as it is selected for continuance.

It just seems that there's a misconception in this thread that somehow mutations arise in response to some sort of selection pressure. If that is what anyone meant, that can't be the case. The mutations just exist.

In the case of bacteria and antibiotics, there is some variation in the DNA sequences in a population of bacteria. Some of that population is resistant to an antibiotic. When that population is hit with an antibiotic for the first time, most will die, but a few will live. If they manage to divide and grow, then the next time you hit the population with the same antibiotic, very few will die. We say that the strain has developed resistance, but really, the individual bugs had developed resistance even before being hit with an antibiotic. The new strain is the descendants of the bugs that survived when the antibiotic hit them.

And of course, applying two new sorts of brand new selection pressures will indeed make it more likely that you will kill everything you are "pressuring", for exactly the reason cited in the article. The probability that an existing organism will have two different mutations that make it less susceptible to two previously unencountered selection pressures is indeed quite small.

But what's the point? Sure, new and novel selection pressures can make species go extinct. Also, if a species has to evolve or die, it usually "chooses" die. Evolution is so slow that rapid adpatation to novel pressures doesn't work so well. Fortunately, there aren't all that many novel pressures to deal with. Somewhere in the last three billion years, a lot of things have happened, and our ancestors survived. The new things are really just variations on an old theme, mostly.

ETA:* Of course, all of this has been addressed before somewhere. The evolution vs. creationism topic has been around since Darwin, and it migrated onto bulletin boards as soon as someone invented them.

The misconception is on the part of kleinman.

kleinman

27th May 2007, 10:20 PM

And you missed the point that when the selection pressures are applied sequentially, the resistance is evolved much more quickly than when the selection pressures are applied simultaneously. This is what is shown with the mathematics of ev shows and this is what the citations being posted shows.Dr. Adequate, we need a new lie number here, I think.
Paul, you don’t need a new number, you need a new theory. If you think that modifying ev to do selection sequentially will show something different than the dozens of citations presented that show that sequential selection pressures evolve much more quickly than simultaneous selection pressures, modify ev and show me wrong. Here’s the goalpost for you Mr Rcapacity. You did a case with G=16,384, all other parameters the same as Dr Schneider’s published case at obtained the number of generations for perfect creature=6,894,433. The number of generations to evolve the binding sites alone was a single generation, to evolve no spurious binding sites in the gene alone is 223 generations and to evolve no spurious binding outside the gene again was 223 generations. We have numerous real examples that show that sequential selection pressures evolve more quickly. So show us that ev shows us differently, otherwise you need to do some work on parsing sentences Mr Rcapacity. This type of stupid defense of your dumb theory will get you nowhere. Of course that is what you evolutionists have done for years with your mathematically deficient theory.
Have you modified Evj so that it can apply the selection criteria sequentially instead of all at once? If so, could you present the results of those experiments?
No I have not silly Mr Rcapacity. I have presented numerous real examples of this effect. I also have not claimed that I have done this with ev but again, if you think ev will show differently, modify your model and show otherwise.
In particular, I'd be interested in the experiments where the selections are applied sequentially as follows:
1. Evolve a creature that does not match anywhere on the genome.
2. Then evolve a creature that matches at the binding sites, without still applying the selection against matching anywhere else.
It would be easy for you to do. Loop your individual selection conditions. Set the weight for spurious binding to 1 and for binding sites to 0 and evolve the population to that condition. Then set that weight condition for binding sites to 1 and continue program execution until that condition is satisfied. See if ev surprises us with a different result than what we see in reality. If you really want to get fancy, use all three of your weigh factors and see whether it makes a difference in the sequence of the selection conditions.
I just come here to see what witty things Dr. Adequate and Joobz have to say.
You evolutionists really need to do some work on your arithmetic. Adebz = ¼ wit, joobequate=1/4 wit. Adebz + joobequate = ½ wit.
Pardon a latecomer's comments, because I have only skimmed the last few pages. If this has already been addressed, sorry for doing so again.*

I would hope that Clown Fish would not do such a thing, because I would hope that he, and everyone else reading this thread, would know that selection pressures can't evolve genes de novo. Selection can't create. It merely selects. In order to be selected, it must already exist.
Meadmaker, if you had read the entire thread, you would have seen the following argument in one of my earlier posts.

A gene is to evolve. The first base in the sequence for the gene is laid down on the genome. One base codes for nothing so there is nothing for natural selection to act upon. A second base added by random chance is laid down in the sequence. Still nothing to code for, natural selection can not act on this sequence. A third base in the sequence is laid down. You now have enough bases to form a codon for a single amino acid. A single amino acid has no functional use so there is still nothing for natural selection to act upon. So bases must be added randomly until you have a long enough sequence of bases to produce a functional polypeptide and then natural selection can act. Adding bases randomly yield probabilities so infinitesimally small that evolution is mathematically impossible.
And of course, applying two new sorts of brand new selection pressures will indeed make it more likely that you will kill everything you are "pressuring", for exactly the reason cited in the article. The probability that an existing organism will have two different mutations that make it less susceptible to two previously unencountered selection pressures is indeed quite small.

But what's the point? Sure, new and novel selection pressures can make species go extinct. Also, if a species has to evolve or die, it usually "chooses" die. Evolution is so slow that rapid adpatation to novel pressures doesn't work so well. Fortunately, there aren't all that many novel pressures to deal with. Somewhere in the last three billion years, a lot of things have happened, and our ancestors survived. The new things are really just variations on an old theme, mostly.
The point is that with out selection, how do you propose original genes evolved? Without selection pressures, how do you propose that life forms transform from one to another. “a lot of things have happened” does not constitute a scientific proof for how life forms evolved. You sound like an adherent to Cyborg’s cruft theory of evolution. It seems Taffer is as well, but what can you expect of someone who is ignorant of the mathematics of mutation and selection.

Taffer

27th May 2007, 10:25 PM

"A gene is to evolve" means nothing, by the way kleinman. Perhaps you'd like to post your definition of "gene"?

kjkent1

27th May 2007, 11:21 PM

Meadmaker, if you had read the entire thread, you would have seen the following argument in one of my earlier posts.

A gene is to evolve. The first base in the sequence for the gene is laid down on the genome. One base codes for nothing so there is nothing for natural selection to act upon. A second base added by random chance is laid down in the sequence. Still nothing to code for, natural selection can not act on this sequence. A third base in the sequence is laid down. You now have enough bases to form a codon for a single amino acid. A single amino acid has no functional use so there is still nothing for natural selection to act upon. So bases must be added randomly until you have a long enough sequence of bases to produce a functional polypeptide and then natural selection can act. Adding bases randomly yield probabilities so infinitesimally small that evolution is mathematically impossible.PS. Meadmaker, had you been following along, you would also have been shown the disingenuousness of kleinman's above conclusion.

kleinman insists that a gene de novo cannot evolve from scratch, because no selection mechanism can operate on the bases until they are capable of doing something worth selecting against. Yet, he simultaneously argues that the software program ev is an accurate model of evolutionary behavior, even though ev selects from scratch against organisms with missing or spurious chemical binding sites.

Furthermore, kleinman insists that ev accurately demonstrates that multiple selective pressures slow and ultimately halt the evolutionary process, however, he rejects the condition where all evolutionary pressures in ev are turned off, because the result is instantaneous abiogenesis from a random genome.

Thus, kleinman's argument is wholly illogical, based on his own selective method, which seeks to reinforce his personal theistic belief system, by ignoring whatever evidence defeats his beliefs, while simultaneously emphasizing whatever evidence supports those beliefs.

In short, kleinman's as nutty as a peanut butter cup. So, if you're allergic, then caveat emptor.

Meadmaker

28th May 2007, 12:15 AM

In short, kleinman's as nutty as a peanut butter cup. [/FONT]So, if you're allergic, then caveat emptor.

I'm blessed with a non-allergic immune system, I guess.

It's been so long since I discussed things with an honest to goodness creationist that I'm curious what the state of the art is today.

Meadmaker

28th May 2007, 12:31 AM

A gene is to evolve. The first base in the sequence for the gene is laid down on the genome....So bases must be added randomly until you have a long enough sequence of bases to produce a functional polypeptide and then natural selection can act. Adding bases randomly yield probabilities so infinitesimally small that evolution is mathematically impossible.

I would think there would be some other mechanism by which DNA gets swapped around, and chunks of one sort of DNA gets mixed and matched with other sorts of DNA.

Are you sure one at a time addition of amino acids or base pairs is the only way?

The point is that with out selection, how do you propose original genes evolved?

Certainly not by selection. Selection can only "select" things that exist. I would think mutation creates the new genes.

Without selection pressures, how do you propose that life forms transform from one to another.

Selection is indeed the driver for that. When a random DNA change is useful, it survives. (Well, it's more likely to survive. It might still die.) Make enough changes, and the descendants of the original can't breed with each other, because some mutated and some didn't. Throwing some of them onto an island helps.

“a lot of things have happened” does not constitute a scientific proof for how life forms evolved.

If you want "scientific proof" read a journal article. This is an internet forum. I do the best I can.

Paul C. Anagnostopoulos

28th May 2007, 06:38 AM

No I have not silly Mr Rcapacity. I have presented numerous real examples of this effect. I also have not claimed that I have done this with ev but again, if you think ev will show differently, modify your model and show otherwise.
I didn't think so, which is why this is a lie:

And you missed the point that when the selection pressures are applied sequentially, the resistance is evolved much more quickly than when the selection pressures are applied simultaneously. This is what is shown with the mathematics of ev shows ...

It would be easy for you to do. Loop your individual selection conditions. Set the weight for spurious binding to 1 and for binding sites to 0 and evolve the population to that condition. Then set that weight condition for binding sites to 1 and continue program execution until that condition is satisfied. See if ev surprises us with a different result than what we see in reality. If you really want to get fancy, use all three of your weigh factors and see whether it makes a difference in the sequence of the selection conditions.
I don't need to do this, because it is patently obvious that my suggested sequence will not work at all:

Evolve a creature that does not match anywhere on the genome.
Then evolve a creature that matches at the binding sites, without still applying the selection against matching anywhere else.

If you don't continue to apply the selection against spurious bindings, then step 2 will simply evolve a creature that matches everywhere. A perfect creature cannot evolve unless both selections are applied at the same time. Whatever you evolve with single selections, either alone or sequentially, is not the same function, so comparisons of generations do not mean anything.

The right way to look at this may be that Ev only applies one selection pressure, period. In which case it is useless as a tool to promote your multiple selection pressure thingie.

~~ Paul

joobz

28th May 2007, 07:44 AM

It's been so long since I discussed things with an honest to goodness creationist that I'm curious what the state of the art is today.
Honest??? Hardly. Kleinman has a viscoelastic theory on truth and reason. He sticks with amorphous definitions that can shift and stretch to suit his needs. He loves to use phrase like "too slow", multiple selection pressures..., things that have no inherent numerical system. He then claims that these terms are mathematically sound and calls it proof against evolution.

to get caught up to speed check
1.) Dr. Adequate's Kleinman FAQ (http://forums.randi.org/showthread.php?p=2533858#post2533858)

and

2.) My Discourse with him (http://forums.randi.org/showpost.php?p=2591274&postcount=4079) that demonstrates perfectly his inability to remain honest AND remain a creationist.

He must lie to keep his faith and he does so with gusto.

kleinman

28th May 2007, 09:55 AM

I noticed this post on another thread.
It boils down to this canard which is kleinman's mantra: So, the question is... Can you provide an example of a random mutation that is known to increase the information content of the genome?No problem, and this is why kleinman is so universally reviled; when faced with this example, he ignores it.

Chromosomes recombine at conception; two haploid gametes meet and form a diploid zygote. If a site on one chromosome of one gamete has mutated, is the chromosome of the zygote more or less complex? Clearly, if the mutation site is the locus of a protein template, then a novel protein will be expressed. Therefore, in these cases, mutation adds information, from a purely biochemical point of view.
I am not sure whether Schneibster is ignorant or inattentive. If he read my original post on the Evolutionisdead forum, he would have seen the following:
Information theory has been used as evidence of evolution. At the invitation of Dr. Tom Schneider, the author of ev, a computer program which simulates the gain of evolutionary information by genetic systems by a series of random mutations to a genome and natural selection, I examined the behavior of this computer model. Both the publication which describes the ev model and an online version evj (ev java) program are accessible on the internet through URL:

http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/ev.html (http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/ev.html)

In my examination of the behavior of the evj program, the following data was obtained using 1 mutation per generation and a population of 64:

Genome Length Binding Sites on Genome Generations to Complete Evolutionary Process
256 16 1000
512 32 3100
1024 64 7000
2048 128 17,000
4096 256 42,000
8192 512 170,000

The exponential growth rate of the number of generations to complete an evolutionary process with respects to the genome length presents itself despite what mutation rate or population size is set.

Dr. Schneider in his paper, “Evolution of biological information” published in Nucleic Acid Research and available online through the above URL, states that the transition from a random to fully evolved system is “rapid, demonstrating that information gain can occur by punctuated equilibrium.”

This rapid gain of information only occurs with unrealistically small genomes and as genome length is increased, the number of generations necessary to complete the evolutionary process increases at an exponential rate.

The significance of this mathematical behavior in the ev program demonstrates the huge number of generations necessary for any real genome to theoretically evolve by a random mutation/natural selection process. The number of generations needed to complete a single evolutionary step for a bacterium reproducing every 20 minutes with genome length of 5,000,000 base pairs exceeds the age of the earth. For a genome the length of a human, approximately 3,000,000,000 base pairs in length, his program demonstrates that the 1,000,000 generations which evolutionists propose separate us from our closest related primate relative could not occur by a random mutation/natural selection process.
Not only do I think that the mutation and selection process can accumulate information, I think that Dr Schneider’s algorithm properly simulates the mathematics of this phenomenon. My point is that this process is so profoundly slow that it shows the theory of evolution is mathematically impossible. The reason the mutation and selection process is so profoundly slow is that multiple selection pressures confound the evolutionary process. This is what ev shows and this is what reality shows. Throw in a few other problems for your theory like how do you evolve a gene de novo and the hypothesis of irreducible complexity (what were the components of the DNA replicase system doing before DNA could be replicated?) and you can conclude that “evolution didn’t do it”.

"A gene is to evolve" means nothing, by the way kleinman. Perhaps you'd like to post your definition of "gene"?
Taffer, a “gene” is whatever you want it to be and you have no explanation of how they appear de novo (at least no explanation that has any scientific or mathematical basis).
A gene is to evolve. The first base in the sequence for the gene is laid down on the genome. One base codes for nothing so there is nothing for natural selection to act upon. A second base added by random chance is laid down in the sequence. Still nothing to code for, natural selection can not act on this sequence. A third base in the sequence is laid down. You now have enough bases to form a codon for a single amino acid. A single amino acid has no functional use so there is still nothing for natural selection to act upon. So bases must be added randomly until you have a long enough sequence of bases to produce a functional polypeptide and then natural selection can act. Adding bases randomly yield probabilities so infinitesimally small that evolution is mathematically impossible.PS. Meadmaker, had you been following along, you would also have been shown the disingenuousness of kleinman's above conclusion.
Meadmaker, it is my pleasure to introduce you to lita’ gator the ambulance chaser.
kleinman insists that a gene de novo cannot evolve from scratch, because no selection mechanism can operate on the bases until they are capable of doing something worth selecting against. Yet, he simultaneously argues that the software program ev is an accurate model of evolutionary behavior, even though ev selects from scratch against organisms with missing or spurious chemical binding sites.
Meadmaker, if you and lita’ gator read back in the thread, you will find that Paul Anagnostopoulos, Dr Schneider’s coworker has pointed out that ev does not model the de novo evolution of either binding sites or genes.
Furthermore, kleinman insists that ev accurately demonstrates that multiple selective pressures slow and ultimately halt the evolutionary process, however, he rejects the condition where all evolutionary pressures in ev are turned off, because the result is instantaneous abiogenesis from a random genome.
Lita’ gator can be a bit dramatic at times. He gives me too much credit here. It is the dozens of citations which show that multiple selection pressures slow and ultimately stop evolution that need to be given the credit that substantiate the results from ev. His contention that turning off selection in ev results in instantaneous abiogenesis carries as much mathematical and scientific weight as his string cheese theory of evolution. Did you know there are 10^500 alternative universes?
Thus, kleinman's argument is wholly illogical, based on his own selective method, which seeks to reinforce his personal theistic belief system, by ignoring whatever evidence defeats his beliefs, while simultaneously emphasizing whatever evidence supports those beliefs.
Lita’ gator likes to serve whine with his string cheese theory.
In short, kleinman's as nutty as a peanut butter cup. So, if you're allergic, then caveat emptor.
Is that smooth or chunky?
A gene is to evolve. The first base in the sequence for the gene is laid down on the genome....So bases must be added randomly until you have a long enough sequence of bases to produce a functional polypeptide and then natural selection can act. Adding bases randomly yield probabilities so infinitesimally small that evolution is mathematically impossible.I would think there would be some other mechanism by which DNA gets swapped around, and chunks of one sort of DNA gets mixed and matched with other sorts of DNA.

Are you sure one at a time addition of amino acids or base pairs is the only way?
So are you swapping around these chunks of DNA with or without selection and are there any other chemicals in your primordial alphabet soup that combine with DNA. And perhaps you can answer the following question which the James Randi Education Forum resident PhD in alchemical engineering can not answer. How do you form ribose nonenzymatically?
The point is that with out selection, how do you propose original genes evolved?Certainly not by selection. Selection can only "select" things that exist. I would think mutation creates the new genes.
Hey Paul, here’s an evolutionist who thinks that abiogenesis occurs without selection. What do you think of that mathematical possibility? Ok Meadmaker, let’s assume that somehow you can form ribose nonenzymatically and that DNA bases can somehow form in the primordial alphabet soup. And this primordial soup of DNA bases can somehow combine to form the hundreds of genes required to make the simplest life form. How do you replicate these genes without the proteins that make up the DNA replicase system?
Without selection pressures, how do you propose that life forms transform from one to another.Selection is indeed the driver for that. When a random DNA change is useful, it survives. (Well, it's more likely to survive. It might still die.) Make enough changes, and the descendants of the original can't breed with each other, because some mutated and some didn't. Throwing some of them onto an island helps.
Sure it makes sense. Dr Schneider mathematically modeled this phenomenon. And guess what, the process is so profoundly slow that you don’t have enough time (generations) for the theory of evolution to be mathematically possible.
“a lot of things have happened” does not constitute a scientific proof for how life forms evolved.If you want "scientific proof" read a journal article. This is an internet forum. I do the best I can.
I do read journal articles, thousands of them and I’m posting numerous citations that show that multiple selection pressures slow and ultimately stop evolution. This is what the ev, the mathematical model of random point mutations and natural selection shows. At the end of this post, I give more real examples of the phenomenon. Now if you can find a journal article that shows that multiple selection pressures accelerate evolution, you would be making a contribution to your cause. So far, no evolutionist has been able to do this. Perhaps you will be the first.
No I have not silly Mr Rcapacity. I have presented numerous real examples of this effect. I also have not claimed that I have done this with ev but again, if you think ev will show differently, modify your model and show otherwise.I didn't think so, which is why this is a lie:And you missed the point that when the selection pressures are applied sequentially, the resistance is evolved much more quickly than when the selection pressures are applied simultaneously. This is what is shown with the mathematics of ev shows ...
I don't need to do this, because it is patently obvious that applying the selection pressures individually evolves each of these selection conditions at least tens of thousands of times faster than evolving all three selection conditions simultaneously and that is on a case with G=16384, an extremely short genome. This is why combination treatment of HIV is such a relevant example since its genome length is comparable.
It would be easy for you to do. Loop your individual selection conditions. Set the weight for spurious binding to 1 and for binding sites to 0 and evolve the population to that condition. Then set that weight condition for binding sites to 1 and continue program execution until that condition is satisfied. See if ev surprises us with a different result than what we see in reality. If you really want to get fancy, use all three of your weigh factors and see whether it makes a difference in the sequence of the selection conditions.I don't need to do this, because it is patently obvious that my suggested sequence will not work at all:

Evolve a creature that does not match anywhere on the genome.
Then evolve a creature that matches at the binding sites, without still applying the selection against matching anywhere else.If you don't continue to apply the selection against spurious bindings, then step 2 will simply evolve a creature that matches everywhere. A perfect creature cannot evolve unless both selections are applied at the same time. Whatever you evolve with single selections, either alone or sequentially, is not the same function, so comparisons of generations do not mean anything.
Paul, that’s exactly how directional selection pressures work. They drive evolution of genomes to a new optimum and then become stabilizing pressures that increase the frequency of those optimum sequences. Both you and Dr Schneider have said that ev can and does evolve to more than one perfect creature. So what if applying the selection pressures sequentially evolve to a different perfect creature than when evolving to simultaneous selection pressures. You are trying to make a distinction that does not exist. The only function for evolution is to improve reproductive fitness to selection pressures. There is no other function.
The right way to look at this may be that Ev only applies one selection pressure, period. In which case it is useless as a tool to promote your multiple selection pressure thingie.
Then why do you have three weight factors for the different selection conditions? You are trying to split a hair in order to make a point. The selection of particular sequences at the binding sites and prevention of these sequences at nonbinding sites are different selection conditions. You are squirming again. You are so cute when you squirm. You really like my multiple selection thingie, don’t you?
It's been so long since I discussed things with an honest to goodness creationist that I'm curious what the state of the art is today.Honest??? Hardly. Kleinman has a viscoelastic theory on truth and reason. He sticks with amorphous definitions that can shift and stretch to suit his needs. He loves to use phrase like "too slow", multiple selection pressures..., things that have no inherent numerical system. He then claims that these terms are mathematically sound and calls it proof against evolution.
Meadmaker, meet clown fish, clown fish is the resident James Randi Educational Forum PhD in alchemical engineering. His proof for abiogenesis is let’s all get along chemistry.

Here are more examples of multiple selection pressures slowing evolution. http://www.bentham.org/cdt/contabs/cdt3-4.htm (http://www.bentham.org/cdt/contabs/cdt3-4.htm) has a couple of different examples; the first should be of interest to Dr Schneider since he works at the National Cancer Institute.
Recent preclinical and clinical studies have addressed the resistance problem by using combinations of different drugs that target TS, or by combining TS-targeting and non-TS-targeting drugs.
And
Distinctive cellular responses to targeting of specific TS mRNA regions provide exciting therapeutic opportunities. Antisense ODN treatment to modulate TS activity, in combination with TS-targeting chemotherapeutic drugs, has the potential to be an effective anti-tumor therapy.

Protozoan parasites are responsible for important diseases that threaten the lives of nearly one-quarter of the human population world-wide. Among them, leishmaniasis has become the second cause of death, mainly due to the emergence of parasite resistance to conventional drugs. P-glycoprotein (Pgp)-like transporters overexpression is a very efficient mechanism to reduce the intracellular accumulation of many drugs in cancer cells and parasitic protozoans including Plasmodium and Leishmania, thus conferring a multidrug resistance (MDR) phenotype. Therefore, there is a great clinical interest in developing inhibitors of these transporters to overcome such a resistance. Pgps are active pumps belonging to the ATPbinding cassette (ABC) superfamily of proteins, and consist of two homologous halves, each containing a transmembrane domain (TMD) involved in drug efflux, and a cytosolic nucleotide-binding domain (NBD) responsible for ATP binding and hydrolysis. Most conventional cancer MDR modulators interact with the drug-binding sites on the TMDs of Pgps, but they are also usually transported and the required concentrations for a permanent inhibition produce subsequent side effects that hamper their clinical use. Besides, they only poorly modulate the resistance in protozoan parasites. We review here a rational strategy developed to overcome the MDR phenotype in Leishmania, consisting in: i) the selection of an MDR Leishmania tropica line that overexpresses a Pgp-like transporter; ii) the use of their cytosolic NBDs as new pharmacological targets; iii) the search of new natural compounds that revert the MDR phenotype in Leishmania by binding to the TMDs; iv) the combination of subdoses of the above selected modulators directed to both targets in the transporter, NBDs and TMDs, to accumulate their reversal effects while diminishing their toxicity. In this way, we have reverted the MDR phenotype in Leishmania, including the resistance to the most promising new antileishmania agents, the alkyl-lysophospholipids. This approach might be extrapolated to be used in other eukaryotic cells.

The following article talks about the management of potato blight and can be found at http://www.k-state.edu/pdecology/MundtGarrett2002.pdf (http://www.k-state.edu/pdecology/MundtGarrett2002.pdf) .
Integration of practices often provided better disease control than using either practice singly. In two of three cases, the effect of combining management practices was greater than that predicted by a multiplicative relationship. Clearly, it is possible to attain substantial epidemiological synergism by combining disease practices.

joobz

28th May 2007, 10:10 AM

I noticed this post on another thread.

I am not sure whether Schneibster is ignorant or inattentive. If he read my original post on the Evolutionisdead forum, he would have seen the following:

Not only do I think that the mutation and selection process can accumulate information, I think that Dr Schneider’s algorithm properly simulates the mathematics of this phenomenon. My point is that this process is so profoundly slow that it shows the theory of evolution is mathematically impossible. The reason the mutation and selection process is so profoundly slow is that multiple selection pressures confound the evolutionary process. This is what ev shows and this is what reality shows. Throw in a few other problems for your theory like how do you evolve a gene de novo and the hypothesis of irreducible complexity (what were the components of the DNA replicase system doing before DNA could be replicated?) and you can conclude that “evolution didn’t do it”.

Taffer, a “gene” is whatever you want it to be and you have no explanation of how they appear de novo (at least no explanation that has any scientific or mathematical basis).

Meadmaker, it is my pleasure to introduce you to lita’ gator the ambulance chaser.

Meadmaker, if you and lita’ gator read back in the thread, you will find that Paul Anagnostopoulos, Dr Schneider’s coworker has pointed out that ev does not model the de novo evolution of either binding sites or genes.

Lita’ gator can be a bit dramatic at times. He gives me too much credit here. It is the dozens of citations which show that multiple selection pressures slow and ultimately stop evolution that need to be given the credit that substantiate the results from ev. His contention that turning off selection in ev results in instantaneous abiogenesis carries as much mathematical and scientific weight as his string cheese theory of evolution. Did you know there are 10^500 alternative universes?

Lita’ gator likes to serve whine with his string cheese theory.

Is that smooth or chunky?

So are you swapping around these chunks of DNA with or without selection and are there any other chemicals in your primordial alphabet soup that combine with DNA. And perhaps you can answer the following question which the James Randi Education Forum resident PhD in alchemical engineering can not answer. How do you form ribose nonenzymatically?

Hey Paul, here’s an evolutionist who thinks that abiogenesis occurs without selection. What do you think of that mathematical possibility? Ok Meadmaker, let’s assume that somehow you can form ribose nonenzymatically and that DNA bases can somehow form in the primordial alphabet soup. And this primordial soup of DNA bases can somehow combine to form the hundreds of genes required to make the simplest life form. How do you replicate these genes without the proteins that make up the DNA replicase system?

Sure it makes sense. Dr Schneider mathematically modeled this phenomenon. And guess what, the process is so profoundly slow that you don’t have enough time (generations) for the theory of evolution to be mathematically possible.

I do read journal articles, thousands of them and I’m posting numerous citations that show that multiple selection pressures slow and ultimately stop evolution. This is what the ev, the mathematical model of random point mutations and natural selection shows. At the end of this post, I give more real examples of the phenomenon. Now if you can find a journal article that shows that multiple selection pressures accelerate evolution, you would be making a contribution to your cause. So far, no evolutionist has been able to do this. Perhaps you will be the first.

I don't need to do this, because it is patently obvious that applying the selection pressures individually evolves each of these selection conditions at least tens of thousands of times faster than evolving all three selection conditions simultaneously and that is on a case with G=16384, an extremely short genome. This is why combination treatment of HIV is such a relevant example since its genome length is comparable.

Paul, that’s exactly how directional selection pressures work. They drive evolution of genomes to a new optimum and then become stabilizing pressures that increase the frequency of those optimum sequences. Both you and Dr Schneider have said that ev can and does evolve to more than one perfect creature. So what if applying the selection pressures sequentially evolve to a different perfect creature than when evolving to simultaneous selection pressures. You are trying to make a distinction that does not exist. The only function for evolution is to improve reproductive fitness to selection pressures. There is no other function.

Then why do you have three weight factors for the different selection conditions? You are trying to split a hair in order to make a point. The selection of particular sequences at the binding sites and prevention of these sequences at nonbinding sites are different selection conditions. You are squirming again. You are so cute when you squirm. You really like my multiple selection thingie, don’t you?

Meadmaker, meet clown fish, clown fish is the resident James Randi Educational Forum PhD in alchemical engineering. His proof for abiogenesis is let’s all get along chemistry.

Here are more examples of multiple selection pressures slowing evolution. http://www.bentham.org/cdt/contabs/cdt3-4.htm (http://www.bentham.org/cdt/contabs/cdt3-4.htm) has a couple of different examples; the first should be of interest to Dr Schneider since he works at the National Cancer Institute.

And

The following article talks about the management of potato blight and can be found at http://www.k-state.edu/pdecology/MundtGarrett2002.pdf (http://www.k-state.edu/pdecology/MundtGarrett2002.pdf) .

ANd welcome back to the completely irrelevant. I'm still waiting for a mathematical proof that you've claimed all along. I see you still gobbling along about ev, but we've already addressed that 100+pages ago. Don't you have any math to backup your claim. Indeed, do you have ANY example where evolution can occur in short times, but stops for long?

In other words, can you show me that a person can't ever walk across the united states.

kleinman

28th May 2007, 10:35 AM

ANd welcome back to the completely irrelevant… In other words, can you show me that a person can't ever walk across the united states.
Welcome to clown fish's world.

Taffer

28th May 2007, 11:10 AM

Meadmaker

28th May 2007, 11:13 AM

My point is that this process is so profoundly slow that it shows the theory of evolution is mathematically impossible.

"Mathematically impossible" is a pretty strong statement. I know other people have brought this up, but it's worth reiterating. If you want to say that something is "mathematically impossible", you'll have to show some math somewhere.

Evolution is very, very, slow. On the other hand, we've got lots and lots of time. If you want to say that we definitely have enough time, or definitely do not have enough time, you have to get away from the qualitative "very slow" characterization, and move to something quantitative.

So are you swapping around these chunks of DNA with or without selection

The swapping happens without selection. Selection then acts on the results of the swapping.

How do you form ribose nonenzymatically?

Good question. I assume that in broader terms you are getting at the whole problem of abiogenesis. The answer is, no one knows.

Hey Paul, here’s an evolutionist who thinks that abiogenesis occurs without selection.

Sort of. What I'm saying is that the molecular combinations occur, then are selected. It isn't a single step process, though. It's not like you perform the Miller-Urey experiment and pull out DNA. There must be some intermediate steps in there, and selection does occur at each step. What I am saying is that selection doesn't form the compounds. Selection, well, selects the compounds that were formed.

How do you replicate these genes without the proteins that make up the DNA replicase system?

That's a very good question, and no one knows the answer. I'm willing to bet that there's more than one Nobel Prize between now and the time anyone comes up with a good answer.

Now if you can find a journal article that shows that multiple selection pressures accelerate evolution, you would be making a contribution to your cause. So far, no evolutionist has been able to do this. Perhaps you will be the first.

Not likely. First, I would have to know what it means to "accelerate evolution".

Taffer

28th May 2007, 11:20 AM

Paul C. Anagnostopoulos

28th May 2007, 11:41 AM

Paul, that’s exactly how directional selection pressures work. They drive evolution of genomes to a new optimum and then become stabilizing pressures that increase the frequency of those optimum sequences. Both you and Dr Schneider have said that ev can and does evolve to more than one perfect creature. So what if applying the selection pressures sequentially evolve to a different perfect creature than when evolving to simultaneous selection pressures. You are trying to make a distinction that does not exist. The only function for evolution is to improve reproductive fitness to selection pressures. There is no other function.
Ah, you don't want me to apply the various selections in Evj sequentially. Instead you want me to ... So what the hell are you claiming regarding simultaneous pressures vs. sequential ones? Please state your claim, making sure to use the adjectives directional and stabilizing as appropriate.

To answer your "so what," it makes no sense to compare timespans when you are talking about the evolution of different functions. It's not just a different creature, their genes perform different functions.

Then why do you have three weight factors for the different selection conditions? You are trying to split a hair in order to make a point. The selection of particular sequences at the binding sites and prevention of these sequences at nonbinding sites are different selection conditions. You are squirming again. You are so cute when you squirm. You really like my multiple selection thingie, don’t you?
I added the three mistake point settings at the request of another creationist. I certainly didn't think I was suddenly splitting one pressure into three, so the mere existence of these settings does not dictate how we should think about the number of selection pressures in Evj. I have no idea how to think about the number of pressures in Evj. In fact,

Trying to divide the complexity of the real world into discrete selection pressures is surely a fool's errand.

~~ Paul

kleinman

28th May 2007, 01:03 PM

Kleinman, with all due respect, do you really want to argue that I do not know the definition of a gene? When, not only is that what my under graduate degree is in, but also my graduate degree?
You are the one who wants to argue on this point. I said use whatever definition you want.
Seriously, get a grip. It's ok to be wrong sometimes.
Of course I’m wrong sometimes but not on the mathematics of mutation and selection. And what this mathematics shows is that multiple selection pressures slow and ultimately stop evolution. This is what the mathematics of ev shows and this is what the dozens of citations I have posted and reality shows. This mathematical fact has a grip on the theory of evolution and the theory is strangled.
My point is that this process is so profoundly slow that it shows the theory of evolution is mathematically impossible."Mathematically impossible" is a pretty strong statement. I know other people have brought this up, but it's worth reiterating. If you want to say that something is "mathematically impossible", you'll have to show some math somewhere.
Dr Schneider has published the math for this assertion. If you want to see the parametric studies of his mathematical model, read this thread and the related thread on the Evolutionisdead forum located at http://www.evolutionisdead.com/forum/viewtopic.php?t=348&sid=4cd482e2f69ce35e3cd81119e1a3c32d (http://www.evolutionisdead.com/forum/viewtopic.php?t=348&sid=4cd482e2f69ce35e3cd81119e1a3c32d) . Once you do your homework, you will understand the math upon which my assertion is made.
Evolution is very, very, slow. On the other hand, we've got lots and lots of time. If you want to say that we definitely have enough time, or definitely do not have enough time, you have to get away from the qualitative "very slow" characterization, and move to something quantitative.
The problem for you theory is that you don’t have enough time. The reason why you don’t have enough time is that multiple selection pressures confound the evolutionary process. Perhaps you would like to tell us what the selection pressure was that evolved reptiles into birds?
So are you swapping around these chunks of DNA with or without selection The swapping happens without selection. Selection then acts on the results of the swapping.
Study the ev model and what it shows mathematically and the numerous citations of real examples of this mathematics I have and will continue to post. What you will find is despite the mechanism of rearrangement of the genome, multiple selection pressures profoundly slow the evolutionary process. Mutation and selection is much more limited in reality than what you evolutionists allege. You certainly can not evolve birds from reptiles.
How do you form ribose nonenzymatically?Good question. I assume that in broader terms you are getting at the whole problem of abiogenesis. The answer is, no one knows.
The reason why no one knows is that the nonenzymatic formation of ribose is a very complex organic chemistry problem that requires a tightly controlled laboratory environment. Even if you do form ribose nonenzymatically, it is an unstable molecule that has a short half life. You don’t have this molecule sitting around for millions of years waiting to form DNA or RNA bases to form from them. It doesn’t remain stable for thousands of even hundreds of years. It only can stay around for a few years. Not much time to form bases by random chemical process.
Hey Paul, here’s an evolutionist who thinks that abiogenesis occurs without selection.Sort of. What I'm saying is that the molecular combinations occur, then are selected. It isn't a single step process, though. It's not like you perform the Miller-Urey experiment and pull out DNA. There must be some intermediate steps in there, and selection does occur at each step. What I am saying is that selection doesn't form the compounds. Selection, well, selects the compounds that were formed.
Care to describe these selection processes to us. We would all like to know what they are. Or our we going to get another description of the gap theory?
How do you replicate these genes without the proteins that make up the DNA replicase system?That's a very good question, and no one knows the answer. I'm willing to bet that there's more than one Nobel Prize between now and the time anyone comes up with a good answer.
You find one gap after another in your theories of abiogenesis and evolution. If you ignore mathematics, chemistry and physics, you might find some soft and mushy arguments for your theory but include these scientific disciplines in the discussion and you find these theories have no mathematical or scientific basis.
Now if you can find a journal article that shows that multiple selection pressures accelerate evolution, you would be making a contribution to your cause. So far, no evolutionist has been able to do this. Perhaps you will be the first.Not likely. First, I would have to know what it means to "accelerate evolution".
“Accelerate evolution” means to take fewer generations to evolve or adapt to selection pressures when applied simultaneously than when applied sequentially.
What's funny, Meadmaker, is that both Dr. A and myself have given mathematical proofs which show that increased selection speeds up evolution. In my case, it "didn't count" to kleinman because it modelled "recombination and selection not mutation and selection", which is obviously utter rubbish.
Are you talking about Adebz’s example of gif and awe? That was funny. If you think that increased selection speeds up evolution, give us a real example of the gif Adebz posted. If I recall, Adebz didn’t post the genome length, population, mutation rate…, just a gif. Dr Schneider’s model includes all these parameters. And I have posted numerous citations that show Dr Schneider modeled mutation and selection properly. In addition, I never said that recombination doesn’t count, what I have said is that recombination without error can not increase information in the gene pool and that recombination with selection can cause the loss of alleles (and thus the loss of information) from the gene pool. Recombination of the HIV virus does not prevent the slowing of the evolution of this virus when multiple selection pressures are applied simultaneously. This is why combination therapy is used to treat this virus. It slows the evolution of resistant strains despite recombination, the large populations of viruses, the larger reproduction rates and high mutation rates. If you understood the mathematics of mutation and selection, this would make sense to you.
Paul, that’s exactly how directional selection pressures work. They drive evolution of genomes to a new optimum and then become stabilizing pressures that increase the frequency of those optimum sequences. Both you and Dr Schneider have said that ev can and does evolve to more than one perfect creature. So what if applying the selection pressures sequentially evolve to a different perfect creature than when evolving to simultaneous selection pressures. You are trying to make a distinction that does not exist. The only function for evolution is to improve reproductive fitness to selection pressures. There is no other function.Ah, you don't want me to apply the various selections in Evj sequentially. Instead you want me to ... So what the hell are you claiming regarding simultaneous pressures vs. sequential ones? Please state your claim, making sure to use the adjectives directional and stabilizing as appropriate.
Paul, you still don’t understand what you own model shows. The way your model is set up now, you have three simultaneous directional selection pressures. You can set any of these selection pressures to zero using your weight factors. If you set any or all of the selection condition weight factors to non-zero values, the model will attempt to evolve to these selection conditions. If you turn off selection in the model, any of the evolutionary progress the model has made will be lost over time. If you try to model sequential evolution of the directional selection pressures, any evolution progress for previous selection conditions will be lost if you set those conditions to zero. You need to maintain the previous directional selection pressures as stabilizing selection pressures, otherwise you will. In order to model what ev is showing with simultaneous selection pressures using sequential selection pressures, you need to start the model with a single directional selection pressure such as selection against spurious binding in the nonbinding site region of the genome. Allow that condition to evolve a population that satisfies that selection condition. Do not turn off that selection condition that selects against spurious binding sites in the nonbinding site region of the genome. Leave that selection condition on as a stabilizing selection pressure. Then introduce the second directional selection pressure, the condition that selects against spurious binding in the gene. Allow that direction selection pressure to evolve that condition for the population. Leave the second directional condition on as a stabilizing selection pressure and then introduce the third selection condition, the locating of binding sites at their proper locations. Allow this third directional condition to evolve. When this third condition evolves, the selection pressure changes from a directional to a stabilizing selection pressure and you have perfect creatures that are analogous to what you have now with the three simultaneous directional/stabilizing selection pressures.
To answer your "so what," it makes no sense to compare timespans when you are talking about the evolution of different functions. It's not just a different creature, their genes perform different functions.
If you do the selection as I describe above, you will have the same function.
Then why do you have three weight factors for the different selection conditions? You are trying to split a hair in order to make a point. The selection of particular sequences at the binding sites and prevention of these sequences at nonbinding sites are different selection conditions. You are squirming again. You are so cute when you squirm. You really like my multiple selection thingie, don’t you?I added the three mistake point settings at the request of another creationist. I certainly didn't think I was suddenly splitting one pressure into three, so the mere existence of these settings does not dictate how we should think about the number of selection pressures in Evj. I have no idea how to think about the number of pressures in Evj. In fact,
Each of the three selection conditions in ev do a unique thing to the genome, eliminating spurious binding in the nonbinding site region, eliminating spurious binding in the gene and insuring that binding site appear where they should. It is natural to see each of these conditions as individual selection pressures because each does something on different parts of the genome.
Trying to divide the complexity of the real world into discrete selection pressures is surely a fool's errand.
Well then you have a lot of fools trying to stop the evolution of drug resistance in microbes, stopping the evolution of resistance in parasites, stopping the evolution of resistance to herbicides, stopping the evolution of resistance to pesticides, stopping the evolution of resistance to rodenticides, stopping the evolution of resistance of cancer cells,…, all by using multiple discrete selection pressures.

joobz

28th May 2007, 01:09 PM

Welcome to clown fish's world.
What's wrong, kleinman? Do you recognize that the comparison is dead on, so you'd rather use derision than realization?

joobz

28th May 2007, 01:12 PM

joobz

28th May 2007, 01:19 PM

Of course I’m wrong sometimes but not on the mathematics of mutation and selection.I find it quite funny how wrong you can be about being wrong.

tsig

28th May 2007, 02:32 PM

Meadmaker

28th May 2007, 02:40 PM

The problem for you theory is that you don’t have enough time.

How much time do I need?

Care to describe these selection processes to us. We would all like to know what they are.

I would if I could, but someone else is going to get that Nobel Prize.

“Accelerate evolution” means to take fewer generations to evolve or adapt to selection pressures when applied simultaneously than when applied sequentially.

Again, this seems like the cart is before the horse. A "selection pressure" is something that could kill an organism (more accurately, prevent it from reproducing. Unless it's important, I'm going to refer to evolution and natural selection as if the issue is organisms living and dying. I know it's not true, but it's close enough.) When the selection pressure comes along, the organism has one generation to adapt. i.e. if it hasn't already adapted, it's toast. The overall population has a bit more time than that, because once the organism survives, it will pass on its genes to its descendants, and the population of organisms will "evolve" to be like the original mutant. Either way, there's one generation involved in the adaptation. The organism lives, or dies. If it lives, it passes on the genes.

kleinman

28th May 2007, 03:52 PM

What's funny, Meadmaker, is that both Dr. A and myself have given mathematical proofs which show that increased selection speeds up evolution. In my case, it "didn't count" to kleinman because it modelled "recombination and selection not mutation and selection", which is obviously utter rubbish.Don't forget Delphi's brief yet accurate example of multiple pressures running faster than 1 single pressure.
Clown fish, you are hilarious, Delphi has withdrawn to organize his sock drawer and try to figure out what he is going to do with a Masters degree in a field without a mathematical and scientific basis.
Of course I’m wrong sometimes but not on the mathematics of mutation and selection.I find it quite funny how wrong you can be about being wrong.
Oh, I know. I am overwhelmed by the number of citations of real cases that verify the mathematics that Adebz, Taffer and Delphi have shown while I have present only 25-30 citations of real cases that verify the mathematics shown by ev. How could I be so wrong that multiple selection pressures really accelerate evolution? Oh the shame, the shame.

Clown fish flops back into the lead as the last evolutionist to understand the mathematics of mutation and selection.
What's funny, Meadmaker, is that both Dr. A and myself have given mathematical proofs which show that increased selection speeds up evolution. In my case, it "didn't count" to kleinman because it modelled "recombination and selection not mutation and selection", which is obviously utter rubbish.K'man found a simple computer model of evolution and played with the parameters enough until he could get a timeline that did not match reality.
I like the way Dr Schneider responded to this type of argument.
A good simulation does not attempt to simulate everything; only the essential components are modeled. For the issue at hand, the form of the genetic code is not relevant; information measured by Shannon's method is more general than that.
Oh yes tsig, I played with the parameters, I made them more realistic and my, my, what did it show?
He then used this result to say evolution is wrong.
Yes, this result and 25-30 citations of real examples that show that result is correct and the theory of evolution is mathematically impossible.
When you and Paul, et al. to improve his understanding he became increasingly abusive and arrogant
Tsig, are talking about Taffer’s so called mathematics which he has no real examples that verify his results. Well tsig, you have just added you name to the long list of whining, thin skinned crybaby evolutionists. Do you want to add your name to the list of evolutionists who can’t post a real example of where multiple selection pressures accelerate evolution? It’s easy to join that list, simply do nothing.
His name should be Klien bottle for he has only one side.
It is a fitting place for the ashes of the cremated theory of evolution.
The problem for you theory is that you don’t have enough time.How much time do I need?
If you do the reading I suggested, you would have some idea for the answer to this question. To give you a starting point, consider that Dr Schneider made an estimate based on the rate of accumulation of information on a 256 base genome with a mutation rate of 1 mutation per 256 bases per generation and got an estimate of 1 billion years to evolve a human genome. If you put a realistic mutation rate of 1 mutation per 1 million bases per generation and his estimate goes to 4 trillion years. If you use a realistic genome length, that number goes, let’s say, astronomical.
Care to describe these selection processes to us. We would all like to know what they are.I would if I could, but someone else is going to get that Nobel Prize.
I think this one is going to be the NoNobel Prize.
“Accelerate evolution” means to take fewer generations to evolve or adapt to selection pressures when applied simultaneously than when applied sequentially.Again, this seems like the cart is before the horse. A "selection pressure" is something that could kill an organism (more accurately, prevent it from reproducing. Unless it's important, I'm going to refer to evolution and natural selection as if the issue is organisms living and dying. I know it's not true, but it's close enough.) When the selection pressure comes along, the organism has one generation to adapt. i.e. if it hasn't already adapted, it's toast. The overall population has a bit more time than that, because once the organism survives, it will pass on its genes to its descendants, and the population of organisms will "evolve" to be like the original mutant. Either way, there's one generation involved in the adaptation. The organism lives, or dies. If it lives, it passes on the genes.
Meadmaker, you are demonstrating some understanding here. When you apply mathematical bookkeeping to the concept that you describe, you get some interesting results. Dr Schneider did this. His model is on the internet and you can find it at http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/evj/evjava/index.html (http://www.ccrnp.ncifcrf.gov/~toms/paper/ev/evj/evjava/index.html) . Go back and read this thread and the associated thread on the Evolutionisdead forum and then duplicate the parametric studies Paul and I have done and you can learn about the mathematics of mutation and selection and why it shows that the theory of evolution is mathematically impossible.

tsig

28th May 2007, 05:07 PM

"Well tsig, you have just added you name to the long list of whining, thin skinned crybaby evolutionists."

Reported.

Is that whining, thin-skinned and crying enough for you!

kleinman

28th May 2007, 05:45 PM

Well tsig, you have just added you name to the long list of whining, thin skinned crybaby evolutionists.Is that whining, thin-skinned and crying enough for you!
No, I can tell you are a rookie. Let me instruct you on how the professional evolutionist does it. First, you need to learn the vocabulary. There are key words such as “strawman”, “meaningless”, “irrelevant”, “misleading”, and a favorite on this thread is “moving goalposts”. So an example sentence might go like this: Your conclusion is meaningless and irrelevant because the strawman you put up is misleading and you just moved the goalposts. Make sure you use large fonts, bold face and colored fonts may be used as well but should be color coordinated with your avatar. Once you master the introduction to the whining thin-skinned evolutionist, we will teach you the skill of posting a gif or jpeg which has been mastered by Adebz and is called the gif and awe strategy. Whatever you do, do not learn the mathematics of mutation and selection, otherwise you will run home and immediately start sorting your sock drawer.

Enough of this serious stuff, now on to some lighter topics such as citations which show that multiple selection pressures slow and ultimately stop evolution.

The following reference concerns the treatment of parasitic infections in livestock and is located at http://www.csiro.au/proprietaryDocuments/dobson_barnes.pdf (http://www.csiro.au/proprietaryDocuments/dobson_barnes.pdf) .
2.4. Drug Combinations: Computer modelling has shown that the best way to inhibit the development of drug resistance is by the simultaneous applications of drugs (i.e. the use of combinations or mixtures) [3,12].

http://jama.ama-assn.org/cgi/content/abstract/286/2/196 (http://jama.ama-assn.org/cgi/content/abstract/286/2/196)
Based on the samples that could be amplified, low-level viremia in children and adults receiving HAART with prolonged suppression of viremia to less than 50 copies/mL of HIV-1 RNA may result primarily from archival, pre-HAART virus, reflecting earlier treatment conditions, and does not appear to require development of new, HAART-selected mutations reflecting partial resistance to therapy. Low-level viremia below 50 copies/mL may represent less of a concern regarding impending drug failure of current HAART regimens. However, the archival drug-resistant virus may be relevant regarding future treatment strategies.

Paul C. Anagnostopoulos

28th May 2007, 06:11 PM

joobz

28th May 2007, 06:17 PM

Meadmaker, I think you are starting to get the point at what I was stating earlier.

The most is play a game of trying to guess how Kleinman will respond

the choices are

1.) A Non-sequitor ad hom
2.) A non-sequitor referal back to ev and some potential maths he may have
3.) Non-sequitor quotes from articles that he claims to support his case, of which he has never been definitive on.

Long shots are
1.) Honesty
2.) Humility
3.) anything remotely considered intelligent (1st law = natural selection, that one will never get old)

Meadmaker

28th May 2007, 06:18 PM

Kleinman,

Be careful how you interpret your papers. Here's a quote from the one from csiro.au:

Computer modelling has shown that the best way to inhibit the development of
drug resistance is by the simultaneous applications of drugs (i.e. the use of combinations or mixtures)
[3,12].WARNING, this strategy will fail if all animals are treated and then placed on uncontaminated
pasture such as crop stubble, that is, pastures with no refugia. Under these circumstances there is a high
risk of rapid selection for resistance to all drugs used in the combination because only the worms that
survive drug treatment become the founders of the next generation. For example, we modelled Ostertagia
circumcincta populations in a Mediterranean climate (hot dry summers and wet winters). Selection for
resistance was examined for a single treatment with a macrocyclic lactone (ML) when moving the flock to
crop stubble. This imposed intense selection for drug resistance, resulting in up to a 10-fold increase in
ML-R allele frequency from a single treatment.

In other words, if you don't kill all of them, the survivors will be resistant to both. In that sense, it "speeds up" evolution.

tsig

28th May 2007, 06:19 PM

No, I can tell you are a rookie. Let me instruct you on how the professional evolutionist does it. First, you need to learn the vocabulary. There are key words such as “strawman”, “meaningless”, “irrelevant”, “misleading”, and a favorite on this thread is “moving goalposts”. So an example sentence might go like this: Your conclusion is meaningless and irrelevant because the strawman you put up is misleading and you just moved the goalposts. Make sure you use large fonts, bold face and colored fonts may be used as well but should be color coordinated with your avatar. Once you master the introduction to the whining thin-skinned evolutionist, we will teach you the skill of posting a gif or jpeg which has been mastered by Adebz and is called the gif and awe strategy. Whatever you do, do not learn the mathematics of mutation and selection, otherwise you will run home and immediately start sorting your sock drawer.

A rookie?

You are a large-fount loving, no-sense of color poultroon.

You reduce the average IQ in any room you enter.

You do not move the goalposts but refuse to acknowledge the rules of the game.

My socks have no holes

joobz

28th May 2007, 06:27 PM

"Well tsig, you have just added you name to the long list of whining, thin skinned crybaby evolutionists."

Reported.

Is that whining, thin-skinned and crying enough for you!
tsiq, don't get too bothered by kleinman. We've demonstrated several times over his inability to present any facts that refute evolution. All he has are lies and insults.
Yahzi said it best long ago, (to paraphrase), "He is a madman in a cardboard box throwing rocks at the mansion, evolution, being errected by scientists."

So kick back and relax, and watch him make a fool of himself multiple times over.

Meadmaker

28th May 2007, 06:40 PM

Meadmaker, you are demonstrating some understanding here.

Flattery will get you nowhere. (I'm not that kind of girl.)

Speaking of flattery, I think you flatter the modellers of evolution you have encountered by giving credence to any specific predictions made by their models about such things as time scales.

The authors can correct me if I'm wrong, but I think the state of the art of these models is best described as "conceptual", meaning they illustrate certain concepts and share certain properties with what is presumed to be real evolution, but they don't accurately model real reproduction, the formation of germ cells, the recomination of DNA in an embryo, or the various ways in which a gene might mutate and/or change its function.

I'm sure they are fine models, but I wouldn't take seriously any time scale predictions made by them.

tsig

28th May 2007, 06:41 PM

tsiq, don't get too bothered by kleinman. We've demonstrated several times over his inability to present any facts that refute evolution. All he has are lies and insults.
Yahzi said it best long ago, (to paraphrase), "He is a madman in a cardboard box throwing rocks at the mansion, evolution, being errected by scientists."

So kick back and relax, and watch him make a fool of himself multiple times over.

The mods have again and again told us not to respond to lies and insults but report them.'

I have done so and await the results.

tsig

28th May 2007, 06:48 PM

Flattery will get you nowhere. (I'm not that kind of girl.)

Speaking of flattery, I think you flatter the modellers of evolution you have encountered by giving credence to any specific predictions made by their models about such things as time scales.

The authors can correct me if I'm wrong, but I think the state of the art of these models is best described as "conceptual", meaning they illustrate certain concepts and share certain properties with what is presumed to be real evolution, but they don't accurately model real reproduction, the formation of germ cells, the recomination of DNA in an embryo, or the various ways in which a gene might mutate and/or change its function.

I'm sure they are fine models, but I wouldn't take seriously any time scale predictions made by them.

You make the best mead.

Is that enough flattery?

shazuga

28th May 2007, 07:02 PM

The Evolution is not dead!!!

Until now the theory was incomplete...

See:
COMPLETING THE WORKS OF DARWIN... (http://lexuniversalis.blogspot.com/2007/05/completing-works-of-darwin.html)

NATURAL SELECTION, EVOLUTION and CREATIVE INTELLIGENCE (http://lexuniversalis.blogspot.com/2007/05/natural-selection-evolution-and.html)

THE EVOLUTION OF THE HUMAN MINDS (http://lexuniversalis.blogspot.com/2007/05/evolution-of-human-minds.html)

:D

Meadmaker

28th May 2007, 07:10 PM

You make the best mead.

Is that enough flattery?

For what?

Just in case there were any misconceptions, before you answer, you should know that I am not only not that kind of girl, I'm not any kind of girl. I'm a 45 year old male. (And married.) (To a woman.)

And to be honest, I haven't made mead in a few years.:( Someday, I'll get back to it.

Dr Adequate

28th May 2007, 07:13 PM

So, kleinman still hasn't done any math, he hasn't thought of any new lies, and my simulation of multiple selection pressures still sends him into fits of incoherent screaming twitching hysteria. Good-oh.

Dr Adequate

28th May 2007, 07:23 PM

I played with the parameters, I made them more realistic ... This is a stupid lie, which we have refuted. We all know you're lying.

Yes, this result and 25-30 citations of real examples that show that result is correct and the theory of evolution is mathematically impossible. This is a stupid lie, which we have refuted. We all know you're lying.

And what this mathematics shows is that multiple selection pressures slow and ultimately stop evolution. This is a stupid lie, which we have refuted. We all know you're lying.

This is what the mathematics of ev shows and this is what the dozens of citations I have posted and reality shows. This is a stupid lie, which we have refuted. We all know you're lying.

Dr Schneider has published the math for this assertion. This is a stupid lie, which we have refuted. We all know you're lying.

The reason why you don’t have enough time is that multiple selection pressures confound the evolutionary process. This is a stupid lie, which we have refuted. We all know you're lying.

tsig

28th May 2007, 07:30 PM

For what?

Just in case there were any misconceptions, before you answer, you should know that I am not only not that kind of girl, I'm not any kind of girl. I'm a 45 year old male. (And married.) (To a woman.)

And to be honest, I haven't made mead in a few years.:( Someday, I'll get back to it.

When you say" I'm not that kind of girl", well...

We're equal I haven't drank mead in a few years.

kleinman

28th May 2007, 07:30 PM

In order to model what ev is showing with simultaneous selection pressures using sequential selection pressures, you need to start the model with a single directional selection pressure such as selection against spurious binding in the nonbinding site region of the genome. Allow that condition to evolve a population that satisfies that selection condition. Do not turn off that selection condition that selects against spurious binding sites in the nonbinding site region of the genome. Leave that selection condition on as a stabilizing selection pressure. Then introduce the second directional selection pressure, the condition that selects against spurious binding in the gene. Allow that direction selection pressure to evolve that condition for the population. Leave the second directional condition on as a stabilizing selection pressure and then introduce the third selection condition, the locating of binding sites at their proper locations. Allow this third directional condition to evolve. When this third condition evolves, the selection pressure changes from a directional to a stabilizing selection pressure and you have perfect creatures that are analogous to what you have now with the three simultaneous directional/stabilizing selection pressures.Ah, I get it. But you haven't done this, yet you are claiming that a perfect creature will evolve more quickly, that the mathematics shows this, and that the real world follows suit.
I never said I have done this. If ev models the real world as the numerous citations are showing, evolving the selection conditions in ev sequentially should happen much more quickly than evolving the selection conditions simultaneously as you do now in the model. Here’s a chance to prove me wrong.
Here's the thing. If you watch the standard model (genome size 256) generation by generation, you see that all the spurious bindings are gone within 30 generations. The rest of the time is required to evolve the gene to match the binding sites. Essentially, your scenario is already happening: The spurious bindings are selected against first, then the binding site bindings are selected for.
Spurious binding sites in the nonbinding site region represent most of the mistakes in the model and should dominate the selection process. The question is, what happens when you use much large genomes than the standard model. Will the selection conditions evolve rapidly if they are applied sequentially when the evolution process becomes extremely slow when the selection conditions are applied simultaneously?
Let's see how long it takes to reach 16 mistakes with normal mistake points, and also how long it takes to reach 0 mistakes when the missed site mistake points are set to zero. In both cases, it's the time required to evolve a creature with no spurious bindings. I've used a genome size of 2048 with 16 binding sites:
What happens with a genome length such that Rfrequency < 2 * binding site width?
Well then you have a lot of fools trying to stop the evolution of drug resistance in microbes, stopping the evolution of resistance in parasites, stopping the evolution of resistance to herbicides, stopping the evolution of resistance to pesticides, stopping the evolution of resistance to rodenticides, stopping the evolution of resistance of cancer cells,…, all by using multiple discrete selection pressures.But not making any claims about the degree to which they have discretized the selection pressures. In Ev, is the pressure to avoid spurious bindings within the gene really a separate pressure from the one to avoid spurious bindings outside the gene? Why not divide the spurious bindings within the gene into those in the weight matrix vs. those in the threshold? It's arbitrary.
Yes, avoiding spurious binding sites inside and outside the gene are different selection pressures. You can examine the mathematics of selection by dividing up the genome into any number of regions and defining binding sites in the odd numbered regions as spurious and the even number regions not spurious. It is up to the programmer to define a selection condition and then the model tries to evolve to satisfy the selection condition(s). I think we both agree that ev is an idealized mathematical model of the random point mutation and selection process. The lesson that this model teaches is that multiple simultaneous selection pressures slows the evolutionary process profoundly. If you make a slight modification to the model such that the selection pressures are applied sequentially such that each condition evolves to an optimum in the population before the next selection pressure is applied, I think you will see your Rcapacity concept disappear. An easy way to modify the model would be to put a conditional statement in the generation loop. Set two of the three selection weights to zero. Once the population evolves (the entire population satisfies the selection condition) to the first selection condition, set one of the remaining two selection condition weights to one while maintaining the first weight factor at one. When these two conditions are satisfied for the population, set the third weight factor to one keeping the other two weight factors at one. You will then have the same “functionality” as when you apply all the selection conditions simultaneously. If the number of generations to converge the selection conditions for the sequential version v. the simultaneous version is much smaller, you will have the answer or at least a better understanding of the mathematics of mutation and selection.
The most is play a game of trying to guess how Kleinman will respond
You don’t need to guess at clown fish’s response, it will be one of complete ignorance of the mathematic of mutation and selection. You are so dependable clown fish.
Be careful how you interpret your papers. Here's a quote from the one from csiro.au:Computer modelling has shown that the best way to inhibit the development of drug resistance is by the simultaneous applications of drugs (i.e. the use of combinations or mixtures) [3,12].WARNING, this strategy will fail if all animals are treated and then placed on uncontaminated pasture such as crop stubble, that is, pastures with no refugia. Under these circumstances there is a high risk of rapid selection for resistance to all drugs used in the combination because only the worms that survive drug treatment become the founders of the next generation. For example, we modelled Ostertagia circumcincta populations in a Mediterranean climate (hot dry summers and wet winters). Selection for resistance was examined for a single treatment with a macrocyclic lactone (ML) when moving the flock to crop stubble. This imposed intense selection for drug resistance, resulting in up to a 10-fold increase in ML-R allele frequency from a single treatment.In other words, if you don't kill all of them, the survivors will be resistant to both. In that sense, it "speeds up" evolution.
I commend you for reading the link but think you need to read the link more closely. When I first read this link, I did not understand what they were doing. In particular, I did not understand the word refugia.
refugia-An area that has escaped ecological changes occurring elsewhere and so provides a suitable habitat for relict species.
Well what is a “relict” species?
relict-2. Something that has survived; a remnant.
The second definition for “relict” is the appropriate definition for our purposes.
So what is being said here from this link? If you partially treat your population of parasites and withdraw treatment by placing your flock in an untreated pasture, the remaining parasites population will no longer have selection pressure and repopulation will be by the selected parasites (the relict). They authors then do an example with a single selection pressure and show how you can rapidly achieve resistance to that single chemical. This is not an example of multiple selection pressures accelerating evolution.
A rookie?
Pardon me, you are not a rookie, you are a rookie with a thesaurus and no knowledge of the mathematics of mutation and selection. You an example of a truly well rounded evolutionist.

Here’s another real example of the mathematics of mutation and selection.

http://jvi.asm.org/cgi/content/abstract/74/19/9328 (http://jvi.asm.org/cgi/content/abstract/74/19/9328)
We studied the combined anti-human immunodeficiency virus type 1 (HIV-1) effects of a derivative of stroma-derived factor 1 (SDF-1), Met-SDF-1, and a modified form of RANTES, aminooxypentane (AOP)-RANTES. The antiviral agents were tested singly or in combination at 95 and 99% virus inhibitory concentrations. Clinical R5 and X4 HIV-1 isolates were used. AOP-RANTES inhibited R5 but not X4 viruses, whereas Met-SDF-1 had the opposite effect. Combinations of these compounds inhibited mixed infections with R5 and X4 viruses (95 to 99%), whereas single drugs were less inhibitory (32 to 61%). Combinations of R5 and X4 inhibitors are promising and deserve further evaluation.
I wonder how long you evolutionists will dwell in your ignorance of the mathematics of mutation and selection. I only have about 1,039,950 hits left in my google search to go through.

tsig

28th May 2007, 07:50 PM

Pardon me, you are not a rookie, you are a rookie with a thesaurus and no knowledge of the mathematics of mutation and selection. You an example of a truly well rounded evolutionist.

And you are a example of a truly well rounded wheel of swiss cheese.

Full of holes.

tsig

28th May 2007, 07:59 PM

I never said I have done this. If ev models the real world as the numerous citations are showing, evolving the selection conditions in ev sequentially should happen much more quickly than evolving the selection conditions simultaneously as you do now in the model. Here’s a chance to prove me wrong.

Spurious binding sites in the nonbinding site region represent most of the mistakes in the model and should dominate the selection process. The question is, what happens when you use much large genomes than the standard model. Will the selection conditions evolve rapidly if they are applied sequentially when the evolution process becomes extremely slow when the selection conditions are applied simultaneously?

What happens with a genome length such that Rfrequency < 2 * binding site width?

Yes, avoiding spurious binding sites inside and outside the gene are different selection pressures. You can examine the mathematics of selection by dividing up the genome into any number of regions and defining binding sites in the odd numbered regions as spurious and the even number regions not spurious. It is up to the programmer to define a selection condition and then the model tries to evolve to satisfy the selection condition(s). I think we both agree that ev is an idealized mathematical model of the random point mutation and selection process. The lesson that this model teaches is that multiple simultaneous selection pressures slows the evolutionary process profoundly. If you make a slight modification to the model such that the selection pressures are applied sequentially such that each condition evolves to an optimum in the population before the next selection pressure is applied, I think you will see your Rcapacity concept disappear. An easy way to modify the model would be to put a conditional statement in the generation loop. Set two of the three selection weights to zero. Once the population evolves (the entire population satisfies the selection condition) to the first selection condition, set one of the remaining two selection condition weights to one while maintaining the first weight factor at one. When these two conditions are satisfied for the population, set the third weight factor to one keeping the other two weight factors at one. You will then have the same “functionality” as when you apply all the selection conditions simultaneously. If the number of generations to converge the selection conditions for the sequential version v. the simultaneous version is much smaller, you will have the answer or at least a better understanding of the mathematics of mutation and selection.

You don’t need to guess at clown fish’s response, it will be one of complete ignorance of the mathematic of mutation and selection. You are so dependable clown fish.

I commend you for reading the link but think you need to read the link more closely. When I first read this link, I did not understand what they were doing. In particular, I did not understand the word refugia.

Well what is a “relict” species?

The second definition for “relict” is the appropriate definition for our purposes.
So what is being said here from this link? If you partially treat your population of parasites and withdraw treatment by placing your flock in an untreated pasture, the remaining parasites population will no longer have selection pressure and repopulation will be by the selected parasites (the relict). They authors then do an example with a single selection pressure and show how you can rapidly achieve resistance to that single chemical. This is not an example of multiple selection pressures accelerating evolution.

Pardon me, you are not a rookie, you are a rookie with a thesaurus and no knowledge of the mathematics of mutation and selection. You an example of a truly well rounded evolutionist.

Here’s another real example of the mathematics of mutation and selection.

http://jvi.asm.org/cgi/content/abstract/74/19/9328 (http://jvi.asm.org/cgi/content/abstract/74/19/9328)

I wonder how long you evolutionists will dwell in your ignorance of the mathematics of mutation and selection. I only have about 1,039,950 hits left in my google search to go through.

I will dwell in the house of the lord forever

For his rod and his staff

compell me

dominate me

joobz

28th May 2007, 08:09 PM

You don’t need to guess at clown fish’s response, it will be one of complete ignorance of the mathematic of mutation and selection. You are so dependable clown fish.

Excellent. Option 1 and 2. Non-sequitor ad homs and referals to magical math. Hav eyou presented any that hasn't been found wanting?

Or will you continue to awe us with your ability to notice typos in equations and generate probabilities greater than 1?

kleinman

28th May 2007, 08:20 PM

Or will you continue to awe us with your ability to notice typos in equations and generate probabilities greater than 1?
Very good clown fish, I thought I was going to have to underline, bold face, and change the color and font of that term in the equation for you evolutionists to find the error. I only had to tell you it was the last term in the denominator of the right hand side of the equation and you found the error with my obscure hint. You give clown fish a good name. Now that you found the typo error in the equation, do you want to explain the equation to us since Dr Richard doesn’t seem able to do it? It must be too technical for Dr Richard.

tsig

28th May 2007, 08:36 PM

Meadmaker

28th May 2007, 08:49 PM

So what is being said here from this link? If you partially treat your population of parasites and withdraw treatment by placing your flock in an untreated pasture, the remaining parasites population will no longer have selection pressure and repopulation will be by the selected parasites (the relict).

That is not what the link says. The link says that if you fully treat your flock, and then put your sheep in a pasture that was previously unused (i.e. "no refugia". For those not following the links, "refugia" are piles of sheep manure that might have worms in them.) the only parasites that will survive will be ones who were resistant to all drugs in the initial treatment, and when the sheep are reinfected, as they inevitably will be, they will be reinfected with totally immune bugs.

The authors recommend that you make sure this doesn't happen by leaving 1-2% of the sheep untreated. That way, the parasites that reinfect the sheep will be primarily from the untreated sheep, and so will not be immune to the drugs in the cocktail.

Here's how they summarized the findings:

Using combinations does not reduce
this risk, but using combinations and leaving a small proportion of the flock untreated can greatly reduce
the risk. Leaving the small proportion of the flock untreated was the key to making sure you didn't select bugs that were immune to everything you threw at them the first time.

joobz

28th May 2007, 09:07 PM

Very good clown fish, I thought I was going to have to underline, bold face, and change the color and font of that term in the equation for you evolutionists to find the error. I only had to tell you it was the last term in the denominator of the right hand side of the equation and you found the error with my obscure hint. You give clown fish a good name. Now that you found the typo error in the equation, do you want to explain the equation to us since Dr Richard doesn’t seem able to do it? It must be too technical for Dr Richard.
Wow, you actually believe you are doing something smart by finding an omitted subscript, one that is blatantly obvious to anyone who knows math. Dr. Richard didn't notice anything wrong with the equation, because nothing is wrong with the equation. The symbolic logical interpretation that the equation represents. He's not wasting his time with silly games of "find the typo".

Let me refer back to my original point:
Kleinman, you are trying very hard to demonstrate your knowledge and ability with math. But pointing out an obviously missing subscript (which anyone reading the equation can see and understand what it should be) isn't going to impress anyone.

In fact, it simply reinforces the obvious fact that your handle of math is more in form than function. Otherwise, even you wouldn't continually use such inexact comparisons(more, less, too slow...) and stick with actual values.

But, then, if you did that, you would have to accept the fact that your whole argument falls to bits.

Would you critique Einstein for his notation's dropping of the summation symbol?

Taffer

28th May 2007, 10:48 PM

Hi Taffer.

I have followed this whole thread and here is my understanding of it.

K'man found a simple computer model of evolution and played with the parameters enough until he could get a timeline that did not match reality.

He then used this result to say evolution is wrong.

When you and Paul, et al. to improve his understanding he became increasingly abusive and arrogant

His name should be Klien bottle for he has only one side.

:D

Kleinman,

Be careful how you interpret your papers. Here's a quote from the one from csiro.au:

In other words, if you don't kill all of them, the survivors will be resistant to both. In that sense, it "speeds up" evolution.

He does this constantly.

Oh, and Kleinman? I'm talking specifically of the formula I gave which is a mathematical model for selection, which shows that increased selection pressure increases the rate of evolution. Do you care to comment on it? Or do you continue to think it doesn't cound because "It models recombination and selection".

Also, your assertion that "recombination cannot increase information in a genome" is a load of bollocks. Just FYI, so that you don't make a (bigger) fool of yourself in the future by saying that around geneticists.

kjkent1

28th May 2007, 10:57 PM

Meadmaker, if you and lita’ gator read back in the thread, you will find that Paul Anagnostopoulos, Dr Schneider’s coworker has pointed out that ev does not model the de novo evolution of either binding sites or genes.So, like I said, whenever kleinman can use Paul, or any other evidence or authority, as a means to avoid admitting that kleinman's argument is wholly inconsistent, he will do just that. And, when he can't, then he will claim that the same authority or evidence is wrong and that kleinman is correct.

The truth, however, is much simpler. Ev is designed to demonstrate information gain using random "point" mutation and a selection mechanism that operates only on organisms with missing and/or spurious binding sites. Thus, ev does not model the entire evolutionary landscape of possibilities, and it must necessarily follow that whatever ev demonstrates, cannot possibly be used to prove that evolution is mathematically impossible.

All of which demonstrates that kleinman's arguments are intentionally disingenuous, because he knows all of the above is true, but prefers to argue it anyway, because it supports his personal theistic beliefs.

Lita’ gator can be a bit dramatic at times. He gives me too much credit here. It is the dozens of citations which show that multiple selection pressures slow and ultimately stop evolution that need to be given the credit that substantiate the results from ev. His contention that turning off selection in ev results in instantaneous abiogenesis carries as much mathematical and scientific weight as his string cheese theory of evolution. Did you know there are 10^500 alternative universes?kleinman now gives me too much credit. The cheese theory that kleinman refers to is the work of Leonard Susskind, Ph.D., professor of physics at Stanford University. Susskind is well-known as a supporter of a version of string theory which posits many alternative universes as a reasonable explanation for why this universe seems so "anthropically" suited to the existence of carbon-based organic life forms. And, as the supporting math is likely way over kleinman's head, he prefers to make fun of Susskind's theory, rather than actually try to argue against it.

Regardless, I don't need string theory to ruin kleinman's whole day. All I need to is state the obvious -- which is that kleinman has not produced a single piece of evidence which proves evolution impossible. The best he may have done is demonstrate that evolution using only the mechanisms modeled by ev may be too slow by themselves to account for the present state of organic life.

To which, the entire crowd of posters here, uniformily shrugs their collective shoulders with an indifferent "So what?" Ev shows Shannon information gain from a random start using some scientifically established behaviors of DNA -- which demonstrates that evolution is possible without intelligent direction.

And, that is all that ev needs to prove, because ev demonstrates that God is not required -- which, of course is the thing that kleinman hates most -- because it threatens his persona belief system.

Lita’ gator likes to serve whine with his string cheese theory.While kleinman hopes to get a job writing material for cruise ship comedians -- but, as you can see, it's a lost cause.

Is that smooth or chunky?The routine content of your underwear is none of my concern, Alan.

Meadmaker

29th May 2007, 04:46 AM

The cheese theory that kleinman refers to is the work of Leonard Susskind, Ph.D., professor of physics at Stanford University. Susskind is well-known as a supporter of a version of string theory which posits many alternative universes as a reasonable explanation for why this universe seems so "anthropically" suited to the existence of carbon-based organic life forms.

I was guessing that's what it was. I'm not such a big fan of "many worlds" interpretations, but then again, any attempt to explain quantum mechanics just gets weird. My explanation is that the universe is broken. When the celestial repairman shows up, the electrons will go through one slit at a time, like they are supposed to.

Dr Adequate

29th May 2007, 06:08 AM

I thought I was going to have to underline, bold face, and change the color and font of that term in the equation for you evolutionists to find the error. You mean the error I pointed out over two weeks and two hundred posts back?

Dr Richard has given several references containing several equations.

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

---

Now that you found the typo error in the equation, do you want to explain the equation to us ... Hey, halfwit, why don't you read the frickin' article?

Paul C. Anagnostopoulos

29th May 2007, 07:01 AM

What happens with a genome length such that Rfrequency < 2 * binding site width?
I'm not sure what you're asking. In the experiments I ran, Rfrequency = 7.0 and Rcapacity = 12.0.

The lesson that this model teaches is that multiple simultaneous selection pressures slows the evolutionary process profoundly.
It might teach us that lesson if you would do the math.

An easy way to modify the model would be to put a conditional statement in the generation loop. Set two of the three selection weights to zero. Once the population evolves (the entire population satisfies the selection condition) to the first selection condition, set one of the remaining two selection condition weights to one while maintaining the first weight factor at one. When these two conditions are satisfied for the population, set the third weight factor to one keeping the other two weight factors at one. You will then have the same “functionality” as when you apply all the selection conditions simultaneously. If the number of generations to converge the selection conditions for the sequential version v. the simultaneous version is much smaller, you will have the answer or at least a better understanding of the mathematics of mutation and selection.
Yes, I agree, it would be interesting if you would make these modifications. Why is it that you present me with an unsupported criticism of Ev and then expect me to do the work to lend support to your criticism?

You know, I would be perfectly happy to stipulate that in the real world, with two discrete selection pressures, some scenarios result in "faster" evolution when both are present together, and other scenarios result in faster evolution when they are applied sequentially.* It depends on so many factors that I doubt there is a universal rule.

~~ Paul

* So nice of Mother Nature to apply them sequentially, ain't it?

Mr. Scott

29th May 2007, 07:55 AM

Are you serious? People actually read Klienman's posts?

I just come here to see what witty things Dr. Adequate and Joobz have to say.

Well, I was seriously encouraging Kleinman to share with us, but of course, I should only speak for myself. Dr. Adequate and Joobz have the burden of read Dr. Kleinman's posts to come up with their witty things. Unpleasant, but worth it.

Mr. Scott

29th May 2007, 08:23 AM

You think you know my mind? If you want to understand my mind a little, read Proverbs 27:5-6. By the way, are these Bible verses you are quoting some of the lies your parents told you?

I anticipated you would make a remark like that, so I went into the family archive.

Below is a photo of my grandfather, a pastor at a Baptist church. I possess his theology diploma and his bible. He believed that God planted dinosaur fossils to confuse us. As a small child, I would listen to lively debates at family gatherings between him and my father, an atheist, about creationism and evolutionary science.

My parents lied to me about Santa and the Tooth Fairy. My grandparents told me lies they unfortunately believed about the origin of life. The quote in my sig refers to more profound truths one has to see the movie to understand.

You still haven't explained to us, Dr. Alan Kleinman, how the gratuitous meanness you express in this thread is in accord with the teachings of Christ.

http://forums.randi.org/imagehosting/6736465c34dcb742f.jpg

Complexity

29th May 2007, 09:21 AM

What a waste of bits.

kleinman

29th May 2007, 10:18 AM

Meadmaker, you said the following with respects to this link http://www.csiro.au/proprietaryDocuments/dobson_barnes.pdf (http://www.csiro.au/proprietaryDocuments/dobson_barnes.pdf) and the following quote I used from this link.
2.4. Drug Combinations: Computer modelling has shown that the best way to inhibit the development of drug resistance is by the simultaneous applications of drugs (i.e. the use of combinations or mixtures) [3,12].
In other words, if you don't kill all of them, the survivors will be resistant to both. In that sense, it "speeds up" evolution.
It is you who misinterpret the results of this article. The following quotes are from the article.
that resistance to two drugs will develop at much the same rate regardless of the drug rotation strategy adopted [3]. Interestingly, treating with two effective drugs at the same time will substantially delay selection to both [3, 12].
The rate of resistance when monotherapy of two different antihelmintic drugs is used does not depend on the timing of uses of the drugs but if you use two drugs simultaneously (combination therapy), you delay resistance in both.
The strategy of leaving a few animals untreated to preserve susceptible worms has some risk associated with it, in relation to worm control, but can delay selection for resistance [3].
This strategy only works if susceptible worms dominate the population. Clearly, resistance doesn’t develop if you don’t use the drug.

You now quote the following:
Here's how they summarized the findings:Using combinations does not reduce this risk, but using combinations and leaving a small proportion of the flock untreated can greatly reduce the risk.
You left off the preceding sentence, the entire statement is:
The important message is that treating sheep when there is no refugia is a very high-risk strategy. Using combinations does not reduce this risk, but using combinations and leaving a small proportion of the flock untreated can greatly reduce the risk.
Ranchers when they treat their sheep do not treat the entire environment, they only treat their sheep. If they treat their sheep and then put their sheep in an environment that is dominated by resistant parasites, their next attempt at treatment will be against already selected parasites. If you are going to treat parasites, better to treat susceptible parasites.

The point here is that if you had the finances to treat the entire environment (or the sheep alone), use combination therapy. It delays the onset of resistance when compared to using monotherapy sequentially. If you don’t have the finances to treat the entire environment, try to insure when your animals get reinfected that they be reinfected with susceptible parasites. It is not as you claim:
In other words, if you don't kill all of them, the survivors will be resistant to both. In that sense, it "speeds up" evolution.
Very good clown fish, I thought I was going to have to underline, bold face, and change the color and font of that term in the equation for you evolutionists to find the error. I only had to tell you it was the last term in the denominator of the right hand side of the equation and you found the error with my obscure hint. You give clown fish a good name. Now that you found the typo error in the equation, do you want to explain the equation to us since Dr Richard doesn’t seem able to do it? It must be too technical for Dr Richard.Wow, you actually believe you are doing something smart by finding an omitted subscript, one that is blatantly obvious to anyone who knows math. Dr. Richard didn't notice anything wrong with the equation, because nothing is wrong with the equation. The symbolic logical interpretation that the equation represents. He's not wasting his time with silly games of "find the typo".
Oh no clown fish, I don’t think I’m smart by finding the typo error. I found the typo error because I took the time to study the equation and learn what the equation means and what is being calculated with this equation. Since neither you nor Dr Richard have studied the equation and do not understand what the equation is calculating, neither of you could find the typo error in the equation. This is just another example that neither of you understand the mathematics of mutation and selection.
Oh, and Kleinman? I'm talking specifically of the formula I gave which is a mathematical model for selection, which shows that increased selection pressure increases the rate of evolution. Do you care to comment on it? Or do you continue to think it doesn't cound because "It models recombination and selection".
Why don’t you repost the part of you model that talk about genome length, population, mutation rate…?
Meadmaker, if you and lita’ gator read back in the thread, you will find that Paul Anagnostopoulos, Dr Schneider’s coworker has pointed out that ev does not model the de novo evolution of either binding sites or genes.So, like I said, whenever kleinman can use Paul, or any other evidence or authority, as a means to avoid admitting that kleinman's argument is wholly inconsistent, he will do just that. And, when he can't, then he will claim that the same authority or evidence is wrong and that kleinman is correct.
So when you use your string cheese theory; that is an example of scientific consistency? I like the way you cite your authorities. Speaking of cheese, tsig thinks I’m a swiss cheese round. Do you see the swiss cheese tire tracks as I drive back and forth over the dead theory of evolution? The theory of evolution smells like limburger, don’t you think its time to bury it?
The truth, however, is much simpler. Ev is designed to demonstrate information gain using random "point" mutation and a selection mechanism that operates only on organisms with missing and/or spurious binding sites. Thus, ev does not model the entire evolutionary landscape of possibilities, and it must necessarily follow that whatever ev demonstrates, cannot possibly be used to prove that evolution is mathematically impossible.
Again I quote Dr Schneider:
A good simulation does not attempt to simulate everything; only the essential components are modeled. For the issue at hand, the form of the genetic code is not relevant; information measured by Shannon's method is more general than that.
What Dr Schneider’s model simulates is the effects of combination selection conditions and natural selection. What happens to the evolution of binding sites as you increase genome length is demonstrated with the evolution of any sequence of bases to other selection conditions. What is demonstrated is that multiple selection conditions slow and ultimately stops evolution. This effect is more profound on longer genomes. I have posted dozens of citations that demonstrate this effect. Now how many citations have evolutionists posted that show that multiple selection pressures accelerate evolution? Zero.
All of which demonstrates that kleinman's arguments are intentionally disingenuous, because he knows all of the above is true, but prefers to argue it anyway, because it supports his personal theistic beliefs.
Lita’ gator, the ambulance chaser calls my arguments disingenuous!
Lita’ gator can be a bit dramatic at times. He gives me too much credit here. It is the dozens of citations which show that multiple selection pressures slow and ultimately stop evolution that need to be given the credit that substantiate the results from ev. His contention that turning off selection in ev results in instantaneous abiogenesis carries as much mathematical and scientific weight as his string cheese theory of evolution. Did you know there are 10^500 alternative universes?kleinman now gives me too much credit. The cheese theory that kleinman refers to is the work of Leonard Susskind, Ph.D., professor of physics at Stanford University. Susskind is well-known as a supporter of a version of string theory which posits many alternative universes as a reasonable explanation for why this universe seems so "anthropically" suited to the existence of carbon-based organic life forms. And, as the supporting math is likely way over kleinman's head, he prefers to make fun of Susskind's theory, rather than actually try to argue against it.
So, like I said, whenever lita’ gator can use Leonard Susskind, PhD, or any other evidence or authority, as a means to avoid admitting that lita’ gator's argument is wholly inconsistent, he will do just that. And, when he can't, then he will claim that the same authority or evidence is wrong and that lita’ gator is correct.
Regardless, I don't need string theory to ruin kleinman's whole day. All I need to is state the obvious -- which is that kleinman has not produced a single piece of evidence which proves evolution impossible. The best he may have done is demonstrate that evolution using only the mechanisms modeled by ev may be too slow by themselves to account for the present state of organic life.
Lita’ gator, you are correct, I haven’t presented a “single” piece of evidence, I have presented dozens of citations that demonstrate what ev shows mathematically, that is that multiple selection pressures slow and ultimately stop evolution. The examples shown in these citations are not limited to random point mutations. These are real life examples of mutation of any possible form, recombination and natural selection. Yet they all demonstrate that multiple selection pressures profoundly slow evolution and ultimately stop the process.
To which, the entire crowd of posters here, uniformily shrugs their collective shoulders with an indifferent "So what?" Ev shows Shannon information gain from a random start using some scientifically established behaviors of DNA -- which demonstrates that evolution is possible without intelligent direction.
Listen lita’ gator, it takes time to teach brainwashed evolutionists the mathematics of mutation and selection. And the evolution you talk about is microevolution lita’ gator, microevolution.
And, that is all that ev needs to prove, because ev demonstrates that God is not required -- which, of course is the thing that kleinman hates most -- because it threatens his persona belief system.
Another evolutionist who doesn’t understand the mathematics of mutation and selection, well lita’ gator, what ev shows is the “evolution didn’t do it”.
Lita’ gator likes to serve whine with his string cheese theory.While kleinman hopes to get a job writing material for cruise ship comedians -- but, as you can see, it's a lost cause.
The theory of evolution does remind me of the Titanic. Did you hear the one about the guy who got a job leading tours at the natural history museum? He was leading a tour when he came to a dinosaur skeleton, he said:
Tour guide leader: “This dinosaur skeleton is one million and six years old.”
Man in the crowd: “One million and six years old! How do you know this dinosaur skeleton is one million and six years old?”
Tour guide leader” “I came to work here six years ago and the skeleton was a million years old then.”
What happens with a genome length such that Rfrequency < 2 * binding site width?I'm not sure what you're asking. In the experiments I ran, Rfrequency = 7.0 and Rcapacity = 12.0.
If you run ev with selection pressures applied sequentially, I believe your Rcapacity issue will disappear and you will end up with a population that has the same “functionality” as when you apply the selection pressures simultaneously. The difference will be that it will take far fewer generations for the “functionality” to evolve when the selection pressures are applied sequentially then when applied simultaneously.
The lesson that this model teaches is that multiple simultaneous selection pressures slows the evolutionary process profoundly.It might teach us that lesson if you would do the math.
Dr Schneider has already done the math and put it into a well written program. You have done a good job it making an online version of this program that enables anyone who wishes to understand the mathematics of mutation and selection. You think the Rcapacity issue prevents ev from evolving all the selection conditions when the genome length becomes too long. I have shown that all the selection conditions will evolve individually no matter how long the genome (up to the limits of my computer). I have also posted dozens of citations that demonstrate this effect. Apply the selection conditions in ev sequentially and see whether your Rcapacity concept still holds.
An easy way to modify the model would be to put a conditional statement in the generation loop. Set two of the three selection weights to zero. Once the population evolves (the entire population satisfies the selection condition) to the first selection condition, set one of the remaining two selection condition weights to one while maintaining the first weight factor at one. When these two conditions are satisfied for the population, set the third weight factor to one keeping the other two weight factors at one. You will then have the same “functionality” as when you apply all the selection conditions simultaneously. If the number of generations to converge the selection conditions for the sequential version v. the simultaneous version is much smaller, you will have the answer or at least a better understanding of the mathematics of mutation and selection.Yes, I agree, it would be interesting if you would make these modifications. Why is it that you present me with an unsupported criticism of Ev and then expect me to do the work to lend support to your criticism?
Your fellow evolutionists already think that the results from ev and ev itself is my mathematics. I’ll let you do this because it is your program. You evolutionists like to say that your theory is scientifically based but you refuse to go were the evidence leads when you realize it will contradict your theory. I don’t criticize ev, in fact I am one of the few who say that Dr Schneider got the model correct. The only thing that I have criticized you and Dr Schneider about is extrapolating the results of a 256 base genome to the evolution of a human genome. It is evolutionists who are discrediting the model, but when you do a parametric study with the model, it properly depicts what happens with multiple selection pressures. And what it shows is that multiple selection pressures slow evolution. I’ll keep posting real examples of this phenomenon. This massive amount of empirical evidence that shows that sequential selection pressures evolve much more quickly than simultaneous selection pressures has important scientific impact, especially with the treatment of cancer. The question is, is it more important for Dr Schneider, an employee of the National Cancer Institute to try to support the theory of evolution with his mathematics or explain mathematically how more effective treatments for cancer should be developed.
You know, I would be perfectly happy to stipulate that in the real world, with two discrete selection pressures, some scenarios result in "faster" evolution when both are present together, and other scenarios result in faster evolution when they are applied sequentially.* It depends on so many factors that I doubt there is a universal rule.
Why don’t you give us a scenario where two discrete selection pressures result in “faster” evolution when both are presented together?
* So nice of Mother Nature to apply them sequentially, ain't it?
We can file this concept with your mother nature idea that the primordial soup consisted of rapidly reproducing tiny genome creatures. What was that selection pressure that led to the evolution of hemoglobin again?
My parents lied to me about Santa and the Tooth Fairy. My grandparents told me lies they unfortunately believed about the origin of life. The quote in my sig refers to more profound truths one has to see the movie to understand.
Why do you harbor so much bitterness against your family?
You still haven't explained to us, Dr. Alan Kleinman, how the gratuitous meanness you express in this thread is in accord with the teachings of Christ.
You know, I had to sew a gapping laceration on a child’s face a couple of weeks ago. In order to do this, I had to restrain the child and stick needles multiple times into the child. If you asked the child, I’m sure the child would say that I showed gratuitous meanness, but when the stitches were taken out last week, the laceration looked much better. Why do you believe in the teachings of Christ when Christ believes the Genesis story?

Here are a couple more citations that show that multiple selection pressures slow evolution.

http://homepages.ed.ac.uk/eang09/research.html (http://homepages.ed.ac.uk/eang09/research.html)
The development of combination antiretroviral therapy was an immense breakthrough in HIV treatment, turning a previously lethal infection into a chronic treatable condition. In the absence of a vaccine, combination therapy is the only way HIV infection can be controlled, but there are two major problems, side effects due to toxicity and the development of resistance. Almost all drug failure is associated with antiretroviral resistance, which for some drugs (eg 3TC monotherapy) can arise within days (Frost et al. 2000). Combination therapy extends the period of efficacy greatly, but resistance still appears in a majority of patients.

http://www.ajtmh.org/cgi/content/full/71/2_suppl/179 (http://www.ajtmh.org/cgi/content/full/71/2_suppl/179)
Increasing resistance of Plasmodium falciparum malaria to antimalarial drugs is posing a major threat to the global effort to "Roll Back Malaria". Chloroquine and sulfadoxine-pyrimethamine (SP) are being rendered increasingly ineffective, resulting in increasing morbidity, mortality, and economic and social costs. One strategy advocated for delaying the development of resistance to the remaining armory of effective drugs is the wide-scale deployment of artemisinin-based combination therapy. However, the cost of these combinations are higher than most of the currently used monotherapies and alternative non-artemisinin-based combinations.

tsig

29th May 2007, 10:26 AM

I was guessing that's what it was. I'm not such a big fan of "many worlds" interpretations, but then again, any attempt to explain quantum mechanics just gets weird. My explanation is that the universe is broken. When the celestial repairman shows up, the electrons will go through one slit at a time, like they are supposed to.

We don't have to explain the universe, just live in it.

tsig

29th May 2007, 10:30 AM

Meadmaker, you said the following with respects to this link http://www.csiro.au/proprietaryDocuments/dobson_barnes.pdf (http://www.csiro.au/proprietaryDocuments/dobson_barnes.pdf) and the following quote I used from this link.

It is you who misinterpret the results of this article. The following quotes are from the article.

The rate of resistance when monotherapy of two different antihelmintic drugs is used does not depend on the timing of uses of the drugs but if you use two drugs simultaneously (combination therapy), you delay resistance in both.

This strategy only works if susceptible worms dominate the population. Clearly, resistance doesn’t develop if you don’t use the drug.

You now quote the following:

You left off the preceding sentence, the entire statement is:

Ranchers when they treat their sheep do not treat the entire environment, they only treat their sheep. If they treat their sheep and then put their sheep in an environment that is dominated by resistant parasites, their next attempt at treatment will be against already selected parasites. If you are going to treat parasites, better to treat susceptible parasites.

The point here is that if you had the finances to treat the entire environment (or the sheep alone), use combination therapy. It delays the onset of resistance when compared to using monotherapy sequentially. If you don’t have the finances to treat the entire environment, try to insure when your animals get reinfected that they be reinfected with susceptible parasites. It is not as you claim:

Oh no clown fish, I don’t think I’m smart by finding the typo error. I found the typo error because I took the time to study the equation and learn what the equation means and what is being calculated with this equation. Since neither you nor Dr Richard have studied the equation and do not understand what the equation is calculating, neither of you could find the typo error in the equation. This is just another example that neither of you understand the mathematics of mutation and selection.

Why don’t you repost the part of you model that talk about genome length, population, mutation rate…?

So when you use your string cheese theory; that is an example of scientific consistency? I like the way you cite your authorities. Speaking of cheese, tsig thinks I’m a swiss cheese round. Do you see the swiss cheese tire tracks as I drive back and forth over the dead theory of evolution? The theory of evolution smells like limburger, don’t you think its time to bury it?

Again I quote Dr Schneider:

What Dr Schneider’s model simulates is the effects of combination selection conditions and natural selection. What happens to the evolution of binding sites as you increase genome length is demonstrated with the evolution of any sequence of bases to other selection conditions. What is demonstrated is that multiple selection conditions slow and ultimately stops evolution. This effect is more profound on longer genomes. I have posted dozens of citations that demonstrate this effect. Now how many citations have evolutionists posted that show that multiple selection pressures accelerate evolution? Zero.

Lita’ gator, the ambulance chaser calls my arguments disingenuous!

Lita’ gator, you are correct, I haven’t presented a “single” piece of evidence, I have presented dozens of citations that demonstrate what ev shows mathematically, that is that multiple selection pressures slow and ultimately stop evolution. The examples shown in these citations are not limited to random point mutations. These are real life examples of mutation of any possible form, recombination and natural selection. Yet they all demonstrate that multiple selection pressures profoundly slow evolution and ultimately stop the process.

Listen lita’ gator, it takes time to teach brainwashed evolutionists the mathematics of mutation and selection. And the evolution you talk about is microevolution lita’ gator, microevolution.

Another evolutionist who doesn’t understand the mathematics of mutation and selection, well lita’ gator, what ev shows is the “evolution didn’t do it”.

The theory of evolution does remind me of the Titanic. Did you hear the one about the guy who got a job leading tours at the natural history museum? He was leading a tour when he came to a dinosaur skeleton, he said:
Tour guide leader: “This dinosaur skeleton is one million and six years old.”
Man in the crowd: “One million and six years old! How do you know this dinosaur skeleton is one million and six years old?”
Tour guide leader” “I came to work here six years ago and the skeleton was a million years old then.”

If you run ev with selection pressures applied sequentially, I believe your Rcapacity issue will disappear and you will end up with a population that has the same “functionality” as when you apply the selection pressures simultaneously. The difference will be that it will take far fewer generations for the “functionality” to evolve when the selection pressures are applied sequentially then when applied simultaneously.

Dr Schneider has already done the math and put it into a well written program. You have done a good job it making an online version of this program that enables anyone who wishes to understand the mathematics of mutation and selection. You think the Rcapacity issue prevents ev from evolving all the selection conditions when the genome length becomes too long. I have shown that all the selection conditions will evolve individually no matter how long the genome (up to the limits of my computer). I have also posted dozens of citations that demonstrate this effect. Apply the selection conditions in ev sequentially and see whether your Rcapacity concept still holds.

Your fellow evolutionists already think that the results from ev and ev itself is my mathematics. I’ll let you do this because it is your program. You evolutionists like to say that your theory is scientifically based but you refuse to go were the evidence leads when you realize it will contradict your theory. I don’t criticize ev, in fact I am one of the few who say that Dr Schneider got the model correct. The only thing that I have criticized you and Dr Schneider about is extrapolating the results of a 256 base genome to the evolution of a human genome. It is evolutionists who are discrediting the model, but when you do a parametric study with the model, it properly depicts what happens with multiple selection pressures. And what it shows is that multiple selection pressures slow evolution. I’ll keep posting real examples of this phenomenon. This massive amount of empirical evidence that shows that sequential selection pressures evolve much more quickly than simultaneous selection pressures has important scientific impact, especially with the treatment of cancer. The question is, is it more important for Dr Schneider, an employee of the National Cancer Institute to try to support the theory of evolution with his mathematics or explain mathematically how more effective treatments for cancer should be developed.

Why don’t you give us a scenario where two discrete selection pressures result in “faster” evolution when both are presented together?

We can file this concept with your mother nature idea that the primordial soup consisted of rapidly reproducing tiny genome creatures. What was that selection pressure that led to the evolution of hemoglobin again?

Why do you harbor so much bitterness against your family?

You know, I had to sew a gapping laceration on a child’s face a couple of weeks ago. In order to do this, I had to restrain the child and stick needles multiple times into the child. If you asked the child, I’m sure the child would say that I showed gratuitous meanness, but when the stitches were taken out last week, the laceration looked much better. Why do you believe in the teachings of Christ when Christ believes the Genesis story?

Here are a couple more citations that show that multiple selection pressures slow evolution.

http://homepages.ed.ac.uk/eang09/research.html (http://homepages.ed.ac.uk/eang09/research.html)

http://www.ajtmh.org/cgi/content/full/71/2_suppl/179 (http://www.ajtmh.org/cgi/content/full/71/2_suppl/179)

This is the way we cut and paste

cut and paste cut and paste

This is the way we cut and paste

And waste the JREF bandwith

Taffer

29th May 2007, 10:51 AM

joobz

29th May 2007, 10:57 AM

The rate of resistance when monotherapy of two different antihelmintic drugs is used does not depend on the timing of uses of the drugs Why do you say this?
but if you use two drugs simultaneously (combination therapy), you delay resistance in both.resistance is delayed but not stopped. You still haven't shown how evolution is prevented from going too far..?

The point here is that if you had the finances to treat the entire environment (or the sheep alone), use combination therapy. It delays the onset of resistance when compared to using monotherapy sequentially. But you will eventually have problems because resistance develops. All you have presented substantiates the theory of evolution. I thank you for your efforts in demonstrating this.

Oh no clown fish, I don’t think I’m smart by finding the typo error. I found the typo error because I took the time to study the equation and learn what the equation means and what is being calculated with this equation. Since neither you nor Dr Richard have studied the equation and do not understand what the equation is calculating, neither of you could find the typo error in the equation. This is just another example that neither of you understand the mathematics of mutation and selection.
??? back to delusional gibberish again?

Refresh our memories, when will you start presenting your mathematical proof against evolution? (Or proof for Noah's ark)? We've been waiting, and haven't seen anything remotely like a mathematical proof from you.
Why don’t you repost the part of you model that talk about genome length, population, mutation rate…?

kleinman

29th May 2007, 10:58 AM

And waste the JREF bandwith

When an evolutionist can not mount an argument against a mathematical and empirical scientific proof, they can always fall back on the tried and true technique of censorship. If my post is a waste of JREF bandwidth, why do you repost it?

On a different point, recombination of HIV and the evolution of drug resistance, here are two articles which pose two different viewpoints.

Here is an interesting article that proposes that recombination of HIV may actually slow evolution of drug resistance. This article can be found at http://www.ethlife.ethz.ch/e/articles/sciencelife/hivrekombination.html (http://www.ethlife.ethz.ch/e/articles/sciencelife/hivrekombination.html)
The immune deficiency syndrome, AIDS is a huge health problem worldwide – and will remain so for some time to come. One reason lies in the HI-viruses' ability to become resistant to specific drugs. Until now, scientists have supposed that the recombination of different viruses plays an important role here. But researchers at ETH now show that the recombination can in fact slow down the build-up of resistance and that it advances it under certain specific conditions. This throws light on the question of why sexuality exists.
and
So what are the possible consequences of this model for the ETH research team? Sebastian Bonhoeffer points to two aspects, the first of which is medical. If gene variants that are antagonistic to one another exist, then the build-up of resistance to a combination of drugs that favours such genes would be slowed down by recombination. What is missing from the picture is information on how strongly certain mutations in the HIV genome act synergistically or antagonistically on one another. Bonhoeffer now wants to turn his attention to this question using HI-virus data sequences, which he has in abundance.

However, such an analysis is not only relevant from a medical point of view. Bonhoeffer comes to his second point. It is highly possible that the results of such an investigation could also deliver insights into a far more fundamental question; why on earth does recombination exist? Because, as Bonhoeffer's model shows, in many cases this process has unfavourable consequences for HI-viruses. From an evolutionary point of view, it must be presumed that, under certain circumstances, the acquisition of recombination is advantageous. If these circumstances can be identified in the case of the HI-viruses then conclusions might be drawn on the reason – or reasons – for recombination in higher-order beings. Even though sexual reproduction and concomitant recombination is widespread, the advantages of sex as a means of reproduction is still one of biology's better kept secrets – despite numerous theories.

Here is an article that says the opposite and can be found at http://vir.sgmjournals.org/cgi/content/full/86/11/3109 (http://vir.sgmjournals.org/cgi/content/full/86/11/3109) .
It has been previously shown that the majority of human immunodeficiency virus type 1 (HIV-1)-infected splenocytes can harbour multiple, divergent proviruses with a copy number ranging from one to eight. This implies that, besides point mutations, recombination should be considered as an important mechanism in the evolution of HIV within an infected host. To explore in detail the possible contributions of multi-infection and recombination to HIV evolution, the effects of major microscopic parameters of HIV replication (i.e. the point-mutation rate, the crossover number, the recombination rate and the provirus copy number) on macroscopic characteristics (such as the Hamming distance and the abundance of n-point mutants) have been simulated in silico. Simulations predict that multiple provirus copies per infected cell and recombination act in synergy to speed up the development of sequence diversity. Point mutations can be fixed for some time without fitness selection. The time needed for the selection of multiple mutations with increased fitness is highly variable, supporting the view that stochastic processes may contribute substantially to the kinetics of HIV variation in vivo.

Dr Adequate

29th May 2007, 01:03 PM

Meadmaker, you said the following with respects to this link http://www.csiro.au/proprietaryDocuments/dobson_barnes.pdf (http://www.csiro.au/proprietaryDocuments/dobson_barnes.pdf) and the following quote I used from this link.

It is you who misinterpret the results of this article. The following quotes are from the article.

The rate of resistance when monotherapy of two different antihelmintic drugs is used does not depend on the timing of uses of the drugs but if you use two drugs simultaneously (combination therapy), you delay resistance in both.

This strategy only works if susceptible worms dominate the population. Clearly, resistance doesn’t develop if you don’t use the drug.

You now quote the following:

You left off the preceding sentence, the entire statement is:

Ranchers when they treat their sheep do not treat the entire environment, they only treat their sheep. If they treat their sheep and then put their sheep in an environment that is dominated by resistant parasites, their next attempt at treatment will be against already selected parasites. If you are going to treat parasites, better to treat susceptible parasites.

The point here is that if you had the finances to treat the entire environment (or the sheep alone), use combination therapy. It delays the onset of resistance when compared to using monotherapy sequentially. If you don’t have the finances to treat the entire environment, try to insure when your animals get reinfected that they be reinfected with susceptible parasites. It is not as you claim:

Oh no clown fish, I don’t think I’m smart by finding the typo error. I found the typo error because I took the time to study the equation and learn what the equation means and what is being calculated with this equation. Since neither you nor Dr Richard have studied the equation and do not understand what the equation is calculating, neither of you could find the typo error in the equation. This is just another example that neither of you understand the mathematics of mutation and selection.

Why don’t you repost the part of you model that talk about genome length, population, mutation rate…?

So when you use your string cheese theory; that is an example of scientific consistency? I like the way you cite your authorities. Speaking of cheese, tsig thinks I’m a swiss cheese round. Do you see the swiss cheese tire tracks as I drive back and forth over the dead theory of evolution? The theory of evolution smells like limburger, don’t you think its time to bury it?

Again I quote Dr Schneider:

What Dr Schneider’s model simulates is the effects of combination selection conditions and natural selection. What happens to the evolution of binding sites as you increase genome length is demonstrated with the evolution of any sequence of bases to other selection conditions. What is demonstrated is that multiple selection conditions slow and ultimately stops evolution. This effect is more profound on longer genomes. I have posted dozens of citations that demonstrate this effect. Now how many citations have evolutionists posted that show that multiple selection pressures accelerate evolution? Zero.

Lita’ gator, the ambulance chaser calls my arguments disingenuous!

Lita’ gator, you are correct, I haven’t presented a “single” piece of evidence, I have presented dozens of citations that demonstrate what ev shows mathematically, that is that multiple selection pressures slow and ultimately stop evolution. The examples shown in these citations are not limited to random point mutations. These are real life examples of mutation of any possible form, recombination and natural selection. Yet they all demonstrate that multiple selection pressures profoundly slow evolution and ultimately stop the process.

Listen lita’ gator, it takes time to teach brainwashed evolutionists the mathematics of mutation and selection. And the evolution you talk about is microevolution lita’ gator, microevolution.

Another evolutionist who doesn’t understand the mathematics of mutation and selection, well lita’ gator, what ev shows is the “evolution didn’t do it”.

The theory of evolution does remind me of the Titanic. Did you hear the one about the guy who got a job leading tours at the natural history museum? He was leading a tour when he came to a dinosaur skeleton, he said:
Tour guide leader: “This dinosaur skeleton is one million and six years old.”
Man in the crowd: “One million and six years old! How do you know this dinosaur skeleton is one million and six years old?”
Tour guide leader” “I came to work here six years ago and the skeleton was a million years old then.”

If you run ev with selection pressures applied sequentially, I believe your Rcapacity issue will disappear and you will end up with a population that has the same “functionality” as when you apply the selection pressures simultaneously. The difference will be that it will take far fewer generations for the “functionality” to evolve when the selection pressures are applied sequentially then when applied simultaneously.

Dr Schneider has already done the math and put it into a well written program. You have done a good job it making an online version of this program that enables anyone who wishes to understand the mathematics of mutation and selection. You think the Rcapacity issue prevents ev from evolving all the selection conditions when the genome length becomes too long. I have shown that all the selection conditions will evolve individually no matter how long the genome (up to the limits of my computer). I have also posted dozens of citations that demonstrate this effect. Apply the selection conditions in ev sequentially and see whether your Rcapacity concept still holds.

Your fellow evolutionists already think that the results from ev and ev itself is my mathematics. I’ll let you do this because it is your program. You evolutionists like to say that your theory is scientifically based but you refuse to go were the evidence leads when you realize it will contradict your theory. I don’t criticize ev, in fact I am one of the few who say that Dr Schneider got the model correct. The only thing that I have criticized you and Dr Schneider about is extrapolating the results of a 256 base genome to the evolution of a human genome. It is evolutionists who are discrediting the model, but when you do a parametric study with the model, it properly depicts what happens with multiple selection pressures. And what it shows is that multiple selection pressures slow evolution. I’ll keep posting real examples of this phenomenon. This massive amount of empirical evidence that shows that sequential selection pressures evolve much more quickly than simultaneous selection pressures has important scientific impact, especially with the treatment of cancer. The question is, is it more important for Dr Schneider, an employee of the National Cancer Institute to try to support the theory of evolution with his mathematics or explain mathematically how more effective treatments for cancer should be developed.

Why don’t you give us a scenario where two discrete selection pressures result in “faster” evolution when both are presented together?

We can file this concept with your mother nature idea that the primordial soup consisted of rapidly reproducing tiny genome creatures. What was that selection pressure that led to the evolution of hemoglobin again?

Why do you harbor so much bitterness against your family?

You know, I had to sew a gapping laceration on a child’s face a couple of weeks ago. In order to do this, I had to restrain the child and stick needles multiple times into the child. If you asked the child, I’m sure the child would say that I showed gratuitous meanness, but when the stitches were taken out last week, the laceration looked much better. Why do you believe in the teachings of Christ when Christ believes the Genesis story?

Here are a couple more citations that show that multiple selection pressures slow evolution.

http://homepages.ed.ac.uk/eang09/research.html (http://homepages.ed.ac.uk/eang09/research.html)

http://www.ajtmh.org/cgi/content/full/71/2_suppl/179 (http://www.ajtmh.org/cgi/content/full/71/2_suppl/179)
So, you still don't understand combination therapy; you're still pretending to "understand the mathematics of mutation and selection" without posting any math; and you're still babbling about cheese, which believe me is no substitute.

Dr Adequate

29th May 2007, 01:11 PM

Kleinman, genome length has nothing to do with the rate of evolution. I posted a model for evolution, which clearly shows that increased selection pressures speed up evolution. Are you going to comment? When he could scream gibberish about cheese?

As for my model, he can shriek and drool schizophrenic gibble-gabble about "gif and awe".

And eventually either reality will disappear as a result of his magical incantations; or he'll realise that his ravings don't confer godlike supernatural powers on him; or he'll die as deluded as he lived: eventualities which I have listed in increasing order of likelihood.

kleinman

29th May 2007, 01:57 PM

Kleinman, genome length has nothing to do with the rate of evolution. I posted a model for evolution, which clearly shows that increased selection pressures speed up evolution. Are you going to comment?
Hey Paul, what do you think? Does genome length have any affect on the rate of evolution in ev?

So Taffer, what parameters do you think affect the rate of evolution? And Taffer, could you give a real example of what your model simulates. I have given dozens of citations of what ev simulates. Could you give us a single real example of your model? Pretty please?

kjkent1

29th May 2007, 01:59 PM

joobz

29th May 2007, 02:29 PM

I have given dozens of citations of what ev simulates.
Um, no. you haven't.

kleinman

29th May 2007, 02:39 PM

When an evolutionist can not mount an argument against a mathematical and empirical scientific proof, they can always fall back on the tried and true technique of censorship.Alan, if you ever actually want to engage in a reasonable debate, I'm sure anyone of the other posters here would be happy to accommodate you.
Lita’ gator, who would have thought that so many evolutionists would get so upset about a little arithmetic problem. What do you want me to say, 2+2=5 and then evolutionists will accommodate me, no thank you.
But, you'll have to lower the rhetoric, because when you say something like "evolution is mathematically impossible," you immediately demonstrate that you have no interest in any conversation approaching reasonableness.
Have I hurt the feelings of all you poor sensitive evolutionists? I am so sorry. So why don’t you brainwashed evolutionists go back and finish Sesame Street and learn how to count and then you would know that your theory is mathematically impossible. And why don’t you leave children alone so they can learn how to count? I left off the adjective “cultist” when I described “brainwashed evolutionists” does that lower the rhetoric enough?
I have given dozens of citations of what ev simulates.Um, no. you haven't.
Um, none that a mathematically challenged clown fish would understand, clown fish, you are doing well in the race to be the last evolutionist on this thread to understand the mathematics of mutation and selection. What I need to do for you clown fish is look for references in Highlights magazine. Perhaps you will understand those references.

joobz

29th May 2007, 03:05 PM

Um, none that a mathematically challenged clown fish would understand, clown fish, Who do you hope to fool with this? You know full well I see through your trite descriptions and lack of mathematical prowress. Indeed, you still seem to believe that running simulations = maths.

What I need to do for you clown fish is look for references in Highlights magazine. Perhaps you will understand those references.
No, I'd rather reference the great fool*'s list of accomplishments
1.) Setting the First law of thermodynamics = natural selection.
2.) Confuse thermodynamics with kinetics
3.) Having probabilities in excess of 1.
4.) Confusing the number of truck routes in the description of the evolutionary landscape with the number of selection pressures
5.) Providing a mathematical defense of Noah's ark (Oh wait, we're still waiting for him to make good on this promise)
6.) Setting slower(a term which is relative and has no inherent numerical value) = never (an absolute).
7.) Randomly setting HIV as an example of evolution being impossible or (not representative of evolution, scince a new paper shows mathematically how it can evolve rapidly to multiple selection pressures)
8.) Ignore math models which refute his claim because to address them would be to admit defeat.

*For purposes of this discussion, great fool=Kleinman.

kjkent1

29th May 2007, 03:36 PM

Paul C. Anagnostopoulos

29th May 2007, 03:39 PM

If you run ev with selection pressures applied sequentially, I believe your Rcapacity issue will disappear and you will end up with a population that has the same “functionality” as when you apply the selection pressures simultaneously. The difference will be that it will take far fewer generations for the “functionality” to evolve when the selection pressures are applied sequentially then when applied simultaneously.
Oh, you mean Rfrequency > Rcapacity. Let's try that:

Genome size, site width, generations to 16 mistakes

4096, 3, 1
8192, 4, 50
16384, 4, 135

So, as before, the selection against spurious bindings happens fairly quickly. The pressures are effectively applied in order, yet the Rcapacity issue remains. I'm up to 20,000 generations on that last case and there are still 16 mistakes.

Even if I modified Evj to apply the selection against spurious bindings, followed by the selection for binding sites, why do you think the Rcapacity problem would disappear? How does applying the pressures sequentially defeat the problem that there are not enough bits in the binding sites to contain a unique code?

Why don’t you give us a scenario where two discrete selection pressures result in “faster” evolution when both are presented together?
Someone else will have to do this. Do you have a case in nature where the pressures were applied in parallel in one location and sequentially in another, otherwise identical, location, so we can compare the speed of adaptation?

~~ Paul

Paul C. Anagnostopoulos

29th May 2007, 03:46 PM

Hey Paul, what do you think? Does genome length have any affect on the rate of evolution in ev?
What is the "rate of evolution"?

~~ Paul

Meadmaker

29th May 2007, 03:57 PM

The point here is that if you had the finances to treat the entire environment (or the sheep alone), use combination therapy. It delays the onset of resistance when compared to using monotherapy sequentially. If you don’t have the finances to treat the entire environment, try to insure when your animals get reinfected that they be reinfected with susceptible parasites. It is not as you claim:

Actually, this isn't what it says at all, because the farmers do have the option to treat the entire environment. They can do so by moving the sheep to a new field, i.e. a field with no refugia. If you treat all the sheep, and move them into a fresh field, then all the parasites in the sheep are now resistant, and there are no parasites in the field. As parasites grow in the sheep, they will be resistant parasites.

So, it is important not to treat the entire environment. If you do that, your animals will be reinfected with only non-susceptible parasites. A better strategy will be to make sure that either the environment, or the sheep, remain with a low level infection, so that the reinfection occurs with susceptible parasites.

However, that's probably enough discussion of sheep manure.

The sheep paper discussed a situation where the parasitic organisms were widely present and had already mutated at various rates to be immune to certain drugs. The paper was discussing how to prevent the spread of resistant organisms through the population. Other papers you post deal with a different situation. They deal with the situation in which there are no known resistances already in the population. There, combination therapy is much more effective than individual therapy because there is a chance that the combination therapy will not encounter any organisms that are immune to both drugs.

Evolution does indeed "slow down", because all the organisms exposed are now dead. It's a good strategy. If you tried sequential therapy, a few might live, and then establish a population. Among this new population, most would be resistant to the first drug. Some of them would also mutate to develop resistance to the second drug. Now there's a problem, because the survivors of the second drug treatment would be immune to both. If you hit them with both at the same time, you might be able to kill them all.

(More to come)

Meadmaker

29th May 2007, 04:51 PM

All this talk about drug combination therapy is interesting, but I don't think it really addresses the question. It deals with the spread of existing genes through a population. That's an interesting field of study, but does it really address the question of whether evolution is possible? It seems to me that most creationists are not all that worried about how genes spread through populations, but rather in the creation of genes and the organisms that carry them.

You (kleinman) have said it is "mathematically impossible" for evolution to occur. I have a problem with that statement. It seems to me that the only way you could make that statement is by examining a model of evolution, calculating the time required, or at least the minimum time required, and showing that it is greater than or equal to the amount of time available. If there's not enough time, evolution could not happen.

However, I think you would agree with me that the models we have of evolution are so sparse, missing so much detail, that we can't make any such calculation. You referenced ev and some calculations, but do you really think that model is good enough to use for time scale calculations? I don't think so. I don't think any existing model of evolution is sufficiently accurate for such calculations.

Those of us who believe in evolution have an additional tool available to us. We can look at clues from paleontology and see how long real evolutionary transformations take, and we can compare organisms who are presumed to have common ancestors and use studies of their DNA and/or anatomy to make some estimates. However, if you don't believe that the fossils represent "real evolution", you're stuck. You have no experimental data, and you have no decent theoretical data. In the absence of such data, how can you make an estimate to say how long the process would take?

kleinman

29th May 2007, 08:11 PM

Lita’ gator, who would have thought that so many evolutionists would get so upset about a little arithmetic problem. What do you want me to say, 2+2=5 and then evolutionists will accommodate me, no thank you.No, but you could say, "In my opinion, evolution is mathematically improbable, because ___ (fill in the blank)," and you would probably get a more reasonable conversation.
You are so diplomatic. Let’s put it this way. The mathematics of ev and numerous real examples of this mathematics show that the theory of evolution is mathematically impossible because multiple selection pressures slow and ultimately stop the evolutionary process. Do you think that would make it through the security counsel at the UN?
Have I hurt the feelings of all you poor sensitive evolutionists? I am so sorry. So why don’t you brainwashed evolutionists go back and finish Sesame Street and learn how to count and then you would know that your theory is mathematically impossible. And why don’t you leave children alone so they can learn how to count? I left off the adjective “cultist” when I described “brainwashed evolutionists” does that lower the rhetoric enough?No. It just makes you look like someone in need of anger-management training.
Ok, I promise not to kick any puppies or misinformed evolutionists.
Prior to selection taking place during the first generation of any ev program run, are the creatures created by the program genetically viable (i.e., can they survive in their environment long enough to reproduce)?
Is this your idea of a reasonable question? I’ll still answer it anyway. At no time do the genetic sequences used in ev represent genetically viable creatures, either before the first run or at any time through a run. What ev is an idealize simulation of random point mutation and natural selection. Half the creatures are mathematically viable before each evolutionary step because that is the way Dr Schneider designed the model. What Dr Schneider’s model simulates is the evolution of portions of the genome to specific selection conditions. What you can do with a model like this is examine the behavior of mutation and selection mathematically and what this model shows is that multiple selection pressures is the cause for slow convergence of the model. Now, the question you should ask is this a real phenomenon or is this due some peculiarity in the model? I have several reasons why I believe this is a real phenomenon. The first reason is Delphi’s reference to the fitness landscape on Wikipedia which discusses why it becomes more and more difficult for evolution to occur as you add selection pressures. The next reason is that there are numerous real examples of this mathematical phenomenon. Start with the use of combination therapy of HIV, combination antibiotics, combination pesticides, combination anti-malarial treatments, combination herbicides, combination cancer treatments… Another reason is that evolutionists, including Paul and Myriad have not been able to provide a reasonable selection condition that accelerates the rate of convergence. The only thing that accelerates convergence in ev is reducing the number of selection conditions. Before you jump on this sentence and say Unnamed’s selection condition proves otherwise, let’s see whether Paul and Dr Schneider say this represents a realistic selection condition and let’s see this model up on the web so we can all study the behavior of Unnamed’s selection condition.
If you run ev with selection pressures applied sequentially, I believe your Rcapacity issue will disappear and you will end up with a population that has the same “functionality” as when you apply the selection pressures simultaneously. The difference will be that it will take far fewer generations for the “functionality” to evolve when the selection pressures are applied sequentially then when applied simultaneously.Oh, you mean Rfrequency > Rcapacity. Let's try that:

Genome size, site width, generations to 16 mistakes

4096, 3, 1
8192, 4, 50
16384, 4, 135

So, as before, the selection against spurious bindings happens fairly quickly. The pressures are effectively applied in order, yet the Rcapacity issue remains. I'm up to 20,000 generations on that last case and there are still 16 mistakes.
The reason why spurious binding dominates selection initially is that most of the mistakes are spurious binding mistakes. You can see this by starting the program with only a single none zero weight factor.
For your G=16384, site width=4, you get the following numbers.
Selection condition/Best creature mistakes/Worst creature mistakes/Gens to 0 mistakes
Missed binding sites/1/14/104
Spurious in gene/2/48/14
Spurious outside gene/1235/15432/114
It is clear that the vast majority of mistakes are due to spurious binding initially. Even so, all three selection condition will converge quickly when applied singly.
Even if I modified Evj to apply the selection against spurious bindings, followed by the selection for binding sites, why do you think the Rcapacity problem would disappear? How does applying the pressures sequentially defeat the problem that there are not enough bits in the binding sites to contain a unique code?
I don’t think the failure to converge with the three simultaneous selection condition is due to insufficient bits in the binding site. I think the problem is that the fitness landscape is too complex with the three selection conditions applied simultaneously. The model gets stuck at a suboptimal point on the fitness landscape. It takes more than a single beneficial mutation occurring on a given creature to in a given generation to get off of this suboptimal point. It is clear that when the selection conditions are applied one at a time, ev can easily converge that selection condition. This is analogous to using monotherapy with HIV v. combination therapy, or any of the other numerous examples where combined selection pressures slow evolution.
Why don’t you give us a scenario where two discrete selection pressures result in “faster” evolution when both are presented together?Someone else will have to do this. Do you have a case in nature where the pressures were applied in parallel in one location and sequentially in another, otherwise identical, location, so we can compare the speed of adaptation?
That’s what all the citations that have been posting is all about. There is a huge amount of empirical evidence that combined selection pressures slow and ultimately stops evolution. Here is a particularly good example of this located at http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219)
In this case, a bacterium which produces 4 toxins is used to control mosquito larvae. There is virtually no resistance seen to this bacterium in the 30 years of its use. However, in the laboratory, genetically reengineered bacterium which produce one, two or three of the toxins can yield resistant larvae and very quickly.
Hey Paul, what do you think? Does genome length have any affect on the rate of evolution in ev?What is the "rate of evolution"?
Now don’t be cute Paul, you know it is the rate of information acquisition per generation.
The point here is that if you had the finances to treat the entire environment (or the sheep alone), use combination therapy. It delays the onset of resistance when compared to using monotherapy sequentially. If you don’t have the finances to treat the entire environment, try to insure when your animals get reinfected that they be reinfected with susceptible parasites. It is not as you claim:Actually, this isn't what it says at all, because the farmers do have the option to treat the entire environment. They can do so by moving the sheep to a new field, i.e. a field with no refugia. If you treat all the sheep, and move them into a fresh field, then all the parasites in the sheep are now resistant, and there are no parasites in the field. As parasites grow in the sheep, they will be resistant parasites.
I think you are wrong here Meadmaker. If you move treated sheep into a field with no parasites, you will be populating that field with worms that have survived treatment. The next year, your sheep will be re-infected by already selected parasites.
So, it is important not to treat the entire environment. If you do that, your animals will be reinfected with only non-susceptible parasites. A better strategy will be to make sure that either the environment, or the sheep, remain with a low level infection, so that the reinfection occurs with susceptible parasites.
If farmers could treat the entire environment economically with chemicals that cause extinction of the parasites, I believe they would do it.
The sheep paper discussed a situation where the parasitic organisms were widely present and had already mutated at various rates to be immune to certain drugs. The paper was discussing how to prevent the spread of resistant organisms through the population. Other papers you post deal with a different situation. They deal with the situation in which there are no known resistances already in the population. There, combination therapy is much more effective than individual therapy because there is a chance that the combination therapy will not encounter any organisms that are immune to both drugs.
The use of combination therapy will slow evolution of resistant organisms in either already selected organisms or organism that have not been selected. This is the lesson that is being learned as shown in the numerous citations I have presented. Monotherapy has led to the selection for multiple drug resistant MRSA, HIV, TB, Gonorrhea, weeds, malaria, rodents,… This is what the mathematics of ev shows as well. If you want to evolve resistance to a selection pressure quickly, don’t use more than a single selection pressure.
Evolution does indeed "slow down", because all the organisms exposed are now dead. It's a good strategy. If you tried sequential therapy, a few might live, and then establish a population. Among this new population, most would be resistant to the first drug. Some of them would also mutate to develop resistance to the second drug. Now there's a problem, because the survivors of the second drug treatment would be immune to both. If you hit them with both at the same time, you might be able to kill them all.
Now you are starting to understand. Multiple selection pressures reduce reproductive fitness in multiple ways and require multiple mutations to occur simultaneously in order to adapt to those selection pressures. If have only a single selection pressure, you have less reduction of reproductive fitness and require fewer mutations in order to adapt. It is much easier for organisms to evolve to a single selection pressure.
All this talk about drug combination therapy is interesting, but I don't think it really addresses the question. It deals with the spread of existing genes through a population. That's an interesting field of study, but does it really address the question of whether evolution is possible? It seems to me that most creationists are not all that worried about how genes spread through populations, but rather in the creation of genes and the organisms that carry them.
Unless a population can evolve resistance to multiple selection pressures, there will be no spread of existing genes through a population. HIV has the ability to do recombination yet multiple selection pressures still slow the evolution of resistance to multiple drugs.
You (kleinman) have said it is "mathematically impossible" for evolution to occur. I have a problem with that statement. It seems to me that the only way you could make that statement is by examining a model of evolution, calculating the time required, or at least the minimum time required, and showing that it is greater than or equal to the amount of time available. If there's not enough time, evolution could not happen.
That’s not quite accurate. I have said that the theory of evolution is mathematically impossible. Ev shows how slow the mutation and selection process is. To evolve 96 loci on a genome length of 16,384 takes almost 7,000,000 generations. The only life forms that can achieve this kind of reproduction rate are HIV and other viruses. When you get to genome lengths approaching free living organisms, this number approaches and exceeds hundreds of millions or billions of generations. Genomes the size of humans would take astronomically large numbers of generations to evolve binding sites in ev. Mutation and selection is a profoundly slow process, too slow to support the theory of evolution.
However, I think you would agree with me that the models we have of evolution are so sparse, missing so much detail, that we can't make any such calculation. You referenced ev and some calculations, but do you really think that model is good enough to use for time scale calculations? I don't think so. I don't think any existing model of evolution is sufficiently accurate for such calculations.
I do agree with you. Ev is a sparse model and includes only random point mutations. The question is does ev demonstrate a real phenomenon that multiple selection pressures slow and ultimately stop evolution. I believe that is a real phenomenon and I have posted numerous citations which demonstrates what ev shows mathematically.
Those of us who believe in evolution have an additional tool available to us. We can look at clues from paleontology and see how long real evolutionary transformations take, and we can compare organisms who are presumed to have common ancestors and use studies of their DNA and/or anatomy to make some estimates. However, if you don't believe that the fossils represent "real evolution", you're stuck. You have no experimental data, and you have no decent theoretical data. In the absence of such data, how can you make an estimate to say how long the process would take?
You are going to have a lot of trouble accounting for the millions of differences between humans and chimpanzees genomes by mutation and selection and that’s just in the homologous portions of the genome. And according to evolutionists, you only have about 500,000-1,000,000 generations to account for these differences and relatively small populations for most of this time to work with.

Here are two more citations which show that combination selection pressures slow the evolution of resistance.
http://www.annalsnyas.org/cgi/content/abstract/918/1/9 (http://www.annalsnyas.org/cgi/content/abstract/918/1/9)
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.

http://www.aiedrp.org/pdfpubs/Nunag2006_26.pdf (http://www.aiedrp.org/pdfpubs/Nunag2006_26.pdf)
HIV drug resistance is both a major consequence and cause of HIV treatment failure (Hirsch et al., 1998, 2000, 2003). The prevalence of acquired drug resistance (although emerging less frequently with the availability of better regimens and with patients not previously exposed to nucleosides only) is remarkably high in patients not fully suppressed on potent combination therapy (Richman et al., 2004).

Meadmaker

29th May 2007, 09:25 PM

Taffer

29th May 2007, 11:11 PM

Hey Paul, what do you think? Does genome length have any affect on the rate of evolution in ev?

No, kleinman, the genome length effects the rate of emergence of pre-determined traits. Not evolution. Genome length also affects how many mutations will occur each generation, and thus effect the possibility of the emergence of a pre-determined trait (such as binding site recognition, or resistance to an antimicrobial), but not the rate of evolution.

So Taffer, what parameters do you think affect the rate of evolution? And Taffer, could you give a real example of what your model simulates. I have given dozens of citations of what ev simulates. Could you give us a single real example of your model? Pretty please?

It models reality, kleinman.

And what parameters affect the rate of evolution? S, the selection coefficient, and the allele frequency.

kjkent1

30th May 2007, 12:34 AM

Is this your idea of a reasonable question?Yes, it is, because it's sufficiently restrictive to permit a judge or jury to digest the answer.I’ll still answer it anyway.I'll be the judge of that.At no time do the genetic sequences used in ev represent genetically viable creatures, either before the first run or at any time through a run.So you contend that ev accurately models reality even though the creatures it models are inviable throughout the program's operation. You appear to be the only person here who doesn not recognize the rather spectacular contradiction here. The rest of the gang is satisfied that ev demonstrates how information gain in a disordered system can occur through an evolutionary process. Even Schneider himself recognizes that ev does not model "polymerase slippage, illegitimate recombination, transposons, insertion sequences, tetraploidization, and Robertsonain translations." Regardless, you insist, without any mathematical proof, that none of these processes will have any effect on the performance of ev -- while you simultaneously insist that ev is a correct mathematical model.
Do you understand yet why people here view you as disingenuous?What ev is an idealize simulation of random point mutation and natural selection. Half the creatures are mathematically viable before each evolutionary step because that is the way Dr Schneider designed the model. What Dr Schneider’s model simulates is the evolution of portions of the genome to specific selection conditions. What you can do with a model like this is examine the behavior of mutation and selection mathematically and what this model shows is that multiple selection pressures is the cause for slow convergence of the model.But, as I have just explained, ev does not show all of the known evolutionary processes, yet you insist that it is completely accurate for all possible real-world conditions. Now, the question you should ask is this a real phenomenon or is this due some peculiarity in the model?Yes, do go on.I have several reasons why I believe this is a real phenomenon. The first reason is Delphi’s reference to the fitness landscape on Wikipedia which discusses why it becomes more and more difficult for evolution to occur as you add selection pressures.Show us the math -- otherwise, your position is merely philosophy.The next reason is that there are numerous real examples of this mathematical phenomenon.I have yet to read one in all of your posts.Start with the use of combination therapy of HIV, combination antibiotics, combination pesticides, combination anti-malarial treatments, combination herbicides, combination cancer treatments.How come it's only multiple human developed artificial selective methods that slow and halt evolution. Why doesn't natural selective methods already present in the environment, when combined with the first artificial selective method administered via human therapy, immediately prevent anti-bacterial/fungal/etc. resistance from occuring?

Until you can address this concern, none of your citations have any merit, other than to show that if you create a bunch of toxins all of which are designed to kill a specific organism, the result is likely that you will succeed.Another reason is that evolutionists, including Paul and Myriad have not been able to provide a reasonable selection condition that accelerates the rate of convergence. The only thing that accelerates convergence in ev is reducing the number of selection conditions. Before you jump on this sentence and say Unnamed’s selection condition proves otherwise, let’s see whether Paul and Dr Schneider say this represents a realistic selection condition and let’s see this model up on the web so we can all study the behavior of Unnamed’s selection condition.All of the code is readily available. All you need do is learn how to write software, or, alternatively pay someone to do it for you.

PS. By raising Unnamed's selection method as a legitimate issue, you've impliedly conceded that you don't really know whether or not some other selection method may improve ev's performance. Thus, your statement that "the theory of evolution is mathematically impossible," is really just your unsupported opinion, because you haven't excluded all of the mathematical possibilities.

joobz

30th May 2007, 07:32 AM

PS. By raising Unnamed's selection method as a legitimate issue, you've impliedly conceded that you don't really know whether or not some other selection method may improve ev's performance. Thus, your statement that "the theory of evolution is mathematically impossible," is really just your unsupported opinion, because you haven't excluded all of the mathematical possibilities.
This is just one of the many chinks in his Kleinman's paper mache armor.

It still isn't know that the navier-stoke's equations, which describes all fluid mechanics, is continuous under all conditions. meaning, are there cases where the equation breaks down and fails to model fluid flow or that fluid behavior is more bizarre than we would imagine. there's actually million dollar challenge made to answer this question.

However, let's say for argument, that there are domains where Navier-stoke's equations fail. This wouldn't mean that all the planes would fall from the sky, that ships would fail to sail, that fluid in pipes would instantly freeze and stop moving.

This is the silliness that kleinman has presented all of us. He thinks proving that a math model in some conditions demonstrate failure to evolve will unravel all of the theory, all of reality.

As I said before, he's using a micrometer to measure the Sear's tower. He wishes we would all instantly forget that he hasn't offered a single explanation as to what "too slow" is (numerically). without this value and without any concrete explanation as to why he thinks this rate is valid(and he knows as much of the world 1-5billion years ago as I do), his whole idea is just that much more absurd.

tsig

30th May 2007, 08:24 AM

When an evolutionist can not mount an argument against a mathematical and empirical scientific proof, they can always fall back on the tried and true technique of censorship. If my post is a waste of JREF bandwidth, why do you repost it?

On a different point, recombination of HIV and the evolution of drug resistance, here are two articles which pose two different viewpoints.

Here is an interesting article that proposes that recombination of HIV may actually slow evolution of drug resistance. This article can be found at http://www.ethlife.ethz.ch/e/articles/sciencelife/hivrekombination.html (http://www.ethlife.ethz.ch/e/articles/sciencelife/hivrekombination.html)

and

Here is an article that says the opposite and can be found at http://vir.sgmjournals.org/cgi/content/full/86/11/3109 (http://vir.sgmjournals.org/cgi/content/full/86/11/3109) .

Hope you have help with all that formatting.

So much

No content

Cuddles

30th May 2007, 08:50 AM

Cuddles, this is how you are trying to make argument look. Since your own evolutionary math shows your theory to be mathematically impossible and I am now posting dozens of citations of real examples why the theory is mathematically impossible, you are left with these types of arguments to try to refute my contentions.

Please show an example of my "evolutionary maths". Please state what you think my theory is. Please give an example where I have ever used maths in relation to evolution. Or should I just assume that this is yet another of your many lies?

I am not trying to make your argument look like anything. It does that perfectly well all by itself. I am just pointing out that the only other threads on this forum that proceed in a similar way to yours involve people that are, quite simply, bat**** insane.

kleinman

30th May 2007, 10:17 AM

It is clear that the vast majority of mistakes are due to spurious binding initially. Even so, all three selection condition will converge quickly when applied singly....I don’t think the failure to converge with the three simultaneous selection condition is due to insufficient bits in the binding site. I think the problem is that the fitness landscape is too complex with the three selection conditions applied simultaneously. The model gets stuck at a suboptimal point on the fitness landscape. It takes more than a single beneficial mutation occurring on a given creature to in a given generation to get off of this suboptimal point. It is clear that when the selection conditions are applied one at a time, ev can easily converge that selection condition. This is analogous to using monotherapy with HIV v. combination therapy, or any of the other numerous examples where combined selection pressures slow evolution.One of my problems with ev as an evolutionary model is this talk of "convergence". Real life doesn't "converge". It diverges. If real evolution were aiming at a target, that target would never be reached. The actual evolutionary path taken by an organism and its descendants is far too random to "converge" on anything. Real evolution takes life in all sorts of different directions simultaneously, but that's hard to model on a computer with a finite hard disk.
If you hold to the view that directional selection pressures drive the mutation selection process to a new optimum and that when reaching that new optimum is considered the point of convergence, you will understand this talk of “convergence”. I think it is arguable whether real life converges or diverges. Stabilizing selection pressures prevent divergence. The only divergence you can obtain is that divergence that either has no effect on or improves reproductive fitness. Selection prevents the evolutionary path from being random. Any random step in the path must improve reproductive fitness or is selected against until the evolutionary path leads to a local optimum. Ev demonstrates what happens when evolution takes all sorts of different directions simultaneously. When the genome length is too long in ev, ev converges on a local optimum that prevents the evolution of fully functioning binding sites. Increasing the number of selection pressures and the size of the genome only makes the mathematics of ev more difficult for the theory of evolution. If you can’t evolve the simple selection conditions that ev simulates on small genomes, how do you evolve the much more complex selection conditions on much longer genomes? You can’t.
I think the authors of ev would agree that their model is very limited, and primarily meant to show that random mutation and selection can lead to an increase in information. One of the differences between real life and ev is that in real life, a suboptimal point is just fine, really. As long as you are living and breeding, suboptimal is ok.
You are taking up lita’ gator’s and Paul’s argument, however this is not the position that Dr Schneider and the peer review editors at Nucleic Acids Research have taken who published the results from ev. My view toward ev is it is a limited model but does simulate a crucial principle of mutation and selection properly, that principle is that multiple selection pressures slow and ultimately stop the evolutionary process.

Your contention that a suboptimal point is fine as long as you are living and breeding is ok with me. In fact you can argue that nothing has evolved to the “perfect” optimum. However, if you take this view, how do you explain the evolution of reptiles to birds? Reptiles certainly are at a functional suboptimal state. How do you explain the profound divergence required to take reptiles from their functional suboptimal state through millions of genetic changes to another functional suboptimal state? It is a mathematical incomprehensible concept. You don’t have the selection conditions and if you did, the multiple selection conditions would confound the evolutionary process.
Also, in real life, where do these selection pressures come from? Populations of organisms remain relatively stable for long periods of time. Once in a while there's an asteroid. That's a case of sudden and intense "selection pressure", and what happens? Lots of organisms die. However, except for that, where do these selection pressures come from? They come from other real life.
Try to describe the selection pressure that would transform a reptile into a bird.
If life were not constantly changing, there would be no new "selection pressures". Organisms don't have to adapt very much, and when they do, it's because some other organism adapted and started causing trouble. Maybe a food source grew spines, or maybe a new predator moved into the neighborhood. Then, a lot of organisms will die, and suddenly the funny looking guy with the thick lips or spindly legs is a lot more appealing, what with the fact that there aren't so many potential mates around, and a lot of them look so skinny.
This is a nice story but you extrapolate the mutation and selection process far beyond what it can really do. Do you think it was spines on a food source or one organism caused trouble for another organism caused reptiles to evolve into birds? That’s a story suitable for the SciFi channel. The mathematics of mutation and selection tells a totally different story. That story is that the mutation and selection process is profoundly slow. And why is it profoundly slow? Because multiple selection pressures slow the evolutionary process, I have posted numerous real examples of this and post two more examples of this below.
I think you are wrong here Meadmaker. If you move treated sheep into a field with no parasites, you will be populating that field with worms that have survived treatment. The next year, your sheep will be re-infected by already selected parasites.Right. If that's not what I said, it is what I meant.

So, isn't that the same thing as "accelerating evolution"? In one step, using the combined treatment, you produced immunity to two drugs. It would have taken you two steps if you had supplied the two drugs sequentially.
You can still get immunity to two drugs by using inadequate treatment or if the selection pressures are not sufficient to cause extinction. The creatures can attain a functional suboptimal state. This is demonstrated with noncompliance with HIV treatment. However, if you use two drugs sequentially, you will obtain resistance much more quickly than when using those two drugs simultaneously.
If farmers could treat the entire environment economically with chemicals that cause extinction of the parasites, I believe they would do it.Agreed. And in that case evolution would stop, because all the "evolvers" would be dead, and you are much more likely to achieve that condition with combination therapy (two selection pressures). However, if, instead of causing the extinction of the parasites, you instead caused the near extinction of the parasites, evolution would have accelerated, because the survivors would be resistant to multiple selection pressures.
Again, you miss the point. If farmers used only single drug treatment, parasites will attain resistance more quickly to that drug than if multiple drug treatment is used. This is especially true if the sheep are re-infected with worms that have already faced the selection pressure previously. You can design a situation where you accelerate the evolution of resistance to either single or multi-drug selection pressures but all other factors being equal, you will obtain resistance more quickly to single drugs than drugs used in combinations. That is the lesson from this citation.
Now you are starting to understand. Multiple selection pressures reduce reproductive fitness in multiple ways and require multiple mutations to occur simultaneously in order to adapt to those selection pressures. If have only a single selection pressure, you have less reduction of reproductive fitness and require fewer mutations in order to adapt.Here's where I think you have an error. Organisms don't adapt. They live, or they die. Multiple selection pressures make them more likely to die. They don't adapt to the selection pressures. By the time the "selection" is on them, it's too late. Their genes are set. Where adaptation comes in is that random mutations occur, and it may so happen that a random mutation occurs that makes an organism more likely to survive than its cousin. If it does, then those genes will be found more frequently in the next generation.
I think an argument can be made that organisms do adapt, for example, they migrate if temperatures are not appropriate for their lifestyle but I think I understand the point you are trying to make. It is populations which adapt in the evolutionary sense.
It's not like in ev where there's some sort of target.
Here I think you are wrong. Directional selection pressures do have a target. That target is genetic sequences that give a local optimal reproductive fitness.
We talk of species adapting to pressures, but that's not a genuine real behavior of a species. It's more of a metaphor. An organism will have a number of slightly differing offspring. One of those is more likely to live than the others. The organism doesn't know that it just adapted. It didn't have offspring in response to the selection pressure.
That viewpoint is fine with me and that is the concept that Dr Schneider has applied in his ev simulation.
Ev shows how slow the mutation and selection process is.You are being awfully generous to ev.
Why shouldn’t I be? I think that Dr Schneider properly modeled the mutation and selection process and so does he. So do the editors of the peer reviewed journal Nucleic Acids Research.
You are going to have a lot of trouble accounting for the millions of differences between humans and chimpanzees genomes by mutation and selectionWell, yeah. As every paper seems to say at the end of it, "More research is necessary." Implicit in this statement is usually, "More funding is necessary.", but that's another story.
Dr Schneider has done research and it shows why the theory of evolution is mathematically impossible. I guess there is no funding available for this.
(My guess is that there aren't actually millions of differences, but that is pure speculation on my part.)
You are going to have a hard time supporting your speculation with facts. Both the human and chimpanzee genomes have been sequenced and these millions of differences are obtained by comparing the two genomes.
Hey Paul, what do you think? Does genome length have any affect on the rate of evolution in ev?No, kleinman, the genome length effects the rate of emergence of pre-determined traits. Not evolution. Genome length also affects how many mutations will occur each generation, and thus effect the possibility of the emergence of a pre-determined trait (such as binding site recognition, or resistance to an antimicrobial), but not the rate of evolution.
Pre-determined traits, what is that? So these “pre-determined” traits emerge and don’t evolve. You really need to study ev, you need some lessons on mutation and selection.
So Taffer, what parameters do you think affect the rate of evolution? And Taffer, could you give a real example of what your model simulates. I have given dozens of citations of what ev simulates. Could you give us a single real example of your model? Pretty please?It models reality, kleinman.

And what parameters affect the rate of evolution? S, the selection coefficient, and the allele frequency.
If it models reality, give us a single example of this, pretty please?
At no time do the genetic sequences used in ev represent genetically viable creatures, either before the first run or at any time through a run.So you contend that ev accurately models reality even though the creatures it models are inviable throughout the program's operation. You appear to be the only person here who doesn not recognize the rather spectacular contradiction here. The rest of the gang is satisfied that ev demonstrates how information gain in a disordered system can occur through an evolutionary process. Even Schneider himself recognizes that ev does not model "polymerase slippage, illegitimate recombination, transposons, insertion sequences, tetraploidization, and Robertsonain translations." Regardless, you insist, without any mathematical proof, that none of these processes will have any effect on the performance of ev -- while you simultaneously insist that ev is a correct mathematical model.
Do you understand yet why people here view you as disingenuous?
The numerous citations I have posted are not limited to random point mutations. These examples include recombination in many cases and are not limited to the type of mutation that occurs yet they demonstrate exactly what ev is showing. It is not the type of mutation or recombination that limits evolution, it is the mathematical fact that multiple selection pressures slow and ultimately stops evolution despite recombination or the type of mutation.

I can help if people find me disingenuous because they are ignorant of the mathematic of mutation and selection. I’ll just have to continue explaining the results of ev and give real examples of this result.
What ev is an idealize simulation of random point mutation and natural selection. Half the creatures are mathematically viable before each evolutionary step because that is the way Dr Schneider designed the model. What Dr Schneider’s model simulates is the evolution of portions of the genome to specific selection conditions. What you can do with a model like this is examine the behavior of mutation and selection mathematically and what this model shows is that multiple selection pressures is the cause for slow convergence of the model.But, as I have just explained, ev does not show all of the known evolutionary processes, yet you insist that it is completely accurate for all possible real-world conditions.
Ev is accurate for describing what multiple selection pressures do to the evolutionary process. If you evolutionists think that other mechanisms of mutations and recombination will somehow change this mathematical fact, modify ev and prove it. Reality already shows that recombination and these other mechanism of mutation don’t change the fact that multiple selection pressures slow and ultimately stop evolution, but don’t let this stop you evolutionists from trying to prove otherwise. I think its fun watching you try but at some point you will have to acknowledge this mathematical fact (at least if you still want to claim you are scientists, of course you are a lita’ gator, not a scientist).
I have several reasons why I believe this is a real phenomenon. The first reason is Delphi’s reference to the fitness landscape on Wikipedia which discusses why it becomes more and more difficult for evolution to occur as you add selection pressures.Show us the math -- otherwise, your position is merely philosophy.
Did I forget to mention Dr Schneider’s mathematics and his ev program which applies this mathematics? Pardon me.
The next reason is that there are numerous real examples of this mathematical phenomenon.I have yet to read one in all of your posts.
Well read further down in this post, I have two more real examples of multiple selection pressures slowing evolution.
Start with the use of combination therapy of HIV, combination antibiotics, combination pesticides, combination anti-malarial treatments, combination herbicides, combination cancer treatments.How come it's only multiple human developed artificial selective methods that slow and halt evolution. Why doesn't natural selective methods already present in the environment, when combined with the first artificial selective method administered via human therapy, immediately prevent anti-bacterial/fungal/etc. resistance from occuring?

Until you can address this concern, none of your citations have any merit, other than to show that if you create a bunch of toxins all of which are designed to kill a specific organism, the result is likely that you will succeed.
Now that’s a surprise to me, I didn’t know that Penicillin was human developed. The reason why we observe the effect of human applied selection pressures is because we look to see the consequences of our actions. I previously posted a citation from ecologists who discussed extinction and the effects of multiple selection pressures. The same effect that is seen by human applied selection pressures are seen when the pressures arise from other sources. And that affect is that multiple selection pressures slow and ultimately stop evolution.
Another reason is that evolutionists, including Paul and Myriad have not been able to provide a reasonable selection condition that accelerates the rate of convergence. The only thing that accelerates convergence in ev is reducing the number of selection conditions. Before you jump on this sentence and say Unnamed’s selection condition proves otherwise, let’s see whether Paul and Dr Schneider say this represents a realistic selection condition and let’s see this model up on the web so we can all study the behavior of Unnamed’s selection condition.All of the code is readily available. All you need do is learn how to write software, or, alternatively pay someone to do it for you.
I already know how to write software, so far we have one lita’ gator who thinks that Unnamed’s selection condition models reality. If Paul and Dr Schneider embrace and accept Unnamed’s selection scheme represents reality, then I’ll put the effort in to verify the scheme. I don’t think they will accept Unnamed’s algorithm because it has no basis in reality. But don’t let this stop you from making this argument, after all, you are a lita’ gator.
PS. By raising Unnamed's selection method as a legitimate issue, you've impliedly conceded that you don't really know whether or not some other selection method may improve ev's performance. Thus, your statement that "the theory of evolution is mathematically impossible," is really just your unsupported opinion, because you haven't excluded all of the mathematical possibilities.
PPS You think that the string cheese theory is a legitimate issue, that doesn’t make it true. Perhaps you want to post a citation of a real example of Unnamed’s selection process or better yet, post a real example of the string cheese theory and choosing toppings on a pizza is not an example of natural selection.
PS. By raising Unnamed's selection method as a legitimate issue, you've impliedly conceded that you don't really know whether or not some other selection method may improve ev's performance. Thus, your statement that "the theory of evolution is mathematically impossible," is really just your unsupported opinion, because you haven't excluded all of the mathematical possibilities.This is just one of the many chinks in his Kleinman's paper mache armor.
Clown fish, thank you for reminding me to put on my full armor.
Cuddles, this is how you are trying to make argument look. Since your own evolutionary math shows your theory to be mathematically impossible and I am now posting dozens of citations of real examples why the theory is mathematically impossible, you are left with these types of arguments to try to refute my contentions.Please show an example of my "evolutionary maths". Please state what you think my theory is. Please give an example where I have ever used maths in relation to evolution. Or should I just assume that this is yet another of your many lies?
Cuddles, where have you been? This entire thread is based on the evolutionist written and peer reviewed mathematical model ev and Delphi added on the mathematics of the fitness landscape that is so nicely described on Wikipedia. Are you discrediting the mathematics of your own theory?
I am not trying to make your argument look like anything. It does that perfectly well all by itself. I am just pointing out that the only other threads on this forum that proceed in a similar way to yours involve people that are, quite simply, bat**** insane.
Of course this sounds insane to someone who has succumbed to evolutionist programming. These kinds of facts are not included in your programming and don’t fit your prejudice and bias, but ponder this fact, multiple selection pressures slow and ultimately stop evolution. Ev, an evolutionist written computer model of mutation and selection shows this and numerous real examples of this phenomenon show this. If fact, here are a couple more examples of this. It seems everyone knows this except evolutionists.

http://www.who.int/infectious-disease-report/2000/ch5.htm (http://www.who.int/infectious-disease-report/2000/ch5.htm)
Drug combinations have long been recognised as critical in combating multi drug-resistant malaria.
And
It wasn't until the 1950s that effective treatment for leprosy was introduced into vulnerable populations. By the 70s, the organism had launched a major counter-offensive and had effectively disarmed and rendered obsolete the sulpha drug dapsone. By the 1980s, two drugs – rifampicin and clofazamine – cleared the way for viable treatment alternatives. The organism developed resistance to all three drugs when prescribed singly but in combination with dapsone, these new medications effectively trounced the leprosy bacilli and led the way to cure and – researchers hope – elimination by 2005. Wiser for the experience, scientists are holding back three alternative drugs in the event that resistance recurs. The only outstanding issue however is cost. Fortunately, a solution involving the private and public sectors working in tandem with corporate interests means patients need wait no longer. Blister packs containing multi-drug therapies are now being distributed to patients free of charge. Thanks to WHO-sponsored research grants, Nippon Foundation funds, and donations of medication from the Swiss pharmaceutical Novartis, leprosy is on the way out.

http://www.nyas.org/ebriefreps/main.asp?intSubsectionID=5103 (http://www.nyas.org/ebriefreps/main.asp?intSubsectionID=5103)
"In the history of malaria disease, we lost all the single drugs by drug resistance."
and
For example, the best current treatments for malaria are clearly artemisinin-based combination therapies, or ACTs, which were develop in the early 1990s. These drugs exploit the effectiveness of artemisinin, to which resistance has not yet developed, but combine it with older antibiotics to sustain this effectiveness.

Dr Adequate

30th May 2007, 10:27 AM

If you hold to the view that directional selection pressures drive the mutation selection process to a new optimum and that when reaching that new optimum is considered the point of convergence, you will understand this talk of “convergence”. I think it is arguable whether real life converges or diverges. Stabilizing selection pressures prevent divergence. The only divergence you can obtain is that divergence that either has no effect on or improves reproductive fitness. Selection prevents the evolutionary path from being random. Any random step in the path must improve reproductive fitness or is selected against until the evolutionary path leads to a local optimum. Ev demonstrates what happens when evolution takes all sorts of different directions simultaneously. When the genome length is too long in ev, ev converges on a local optimum that prevents the evolution of fully functioning binding sites. Increasing the number of selection pressures and the size of the genome only makes the mathematics of ev more difficult for the theory of evolution. If you can’t evolve the simple selection conditions that ev simulates on small genomes, how do you evolve the much more complex selection conditions on much longer genomes? You can’t.

You are taking up lita’ gator’s and Paul’s argument, however this is not the position that Dr Schneider and the peer review editors at Nucleic Acids Research have taken who published the results from ev. My view toward ev is it is a limited model but does simulate a crucial principle of mutation and selection properly, that principle is that multiple selection pressures slow and ultimately stop the evolutionary process.

Your contention that a suboptimal point is fine as long as you are living and breeding is ok with me. In fact you can argue that nothing has evolved to the “perfect” optimum. However, if you take this view, how do you explain the evolution of reptiles to birds? Reptiles certainly are at a functional suboptimal state. How do you explain the profound divergence required to take reptiles from their functional suboptimal state through millions of genetic changes to another functional suboptimal state? It is a mathematical incomprehensible concept. You don’t have the selection conditions and if you did, the multiple selection conditions would confound the evolutionary process.

Try to describe the selection pressure that would transform a reptile into a bird.

This is a nice story but you extrapolate the mutation and selection process far beyond what it can really do. Do you think it was spines on a food source or one organism caused trouble for another organism caused reptiles to evolve into birds? That’s a story suitable for the SciFi channel. The mathematics of mutation and selection tells a totally different story. That story is that the mutation and selection process is profoundly slow. And why is it profoundly slow? Because multiple selection pressures slow the evolutionary process, I have posted numerous real examples of this and post two more examples of this below.

You can still get immunity to two drugs by using inadequate treatment or if the selection pressures are not sufficient to cause extinction. The creatures can attain a functional suboptimal state. This is demonstrated with noncompliance with HIV treatment. However, if you use two drugs sequentially, you will obtain resistance much more quickly than when using those two drugs simultaneously.

Again, you miss the point. If farmers used only single drug treatment, parasites will attain resistance more quickly to that drug than if multiple drug treatment is used. This is especially true if the sheep are re-infected with worms that have already faced the selection pressure previously. You can design a situation where you accelerate the evolution of resistance to either single or multi-drug selection pressures but all other factors being equal, you will obtain resistance more quickly to single drugs than drugs used in combinations. That is the lesson from this citation.

I think an argument can be made that organisms do adapt, for example, they migrate if temperatures are not appropriate for their lifestyle but I think I understand the point you are trying to make. It is populations which adapt in the evolutionary sense.

Here I think you are wrong. Directional selection pressures do have a target. That target is genetic sequences that give a local optimal reproductive fitness.

That viewpoint is fine with me and that is the concept that Dr Schneider has applied in his ev simulation.

Why shouldn’t I be? I think that Dr Schneider properly modeled the mutation and selection process and so does he. So do the editors of the peer reviewed journal Nucleic Acids Research.

Dr Schneider has done research and it shows why the theory of evolution is mathematically impossible. I guess there is no funding available for this.

You are going to have a hard time supporting your speculation with facts. Both the human and chimpanzee genomes have been sequenced and these millions of differences are obtained by comparing the two genomes.

Pre-determined traits, what is that? So these “pre-determined” traits emerge and don’t evolve. You really need to study ev, you need some lessons on mutation and selection.

If it models reality, give us a single example of this, pretty please?

The numerous citations I have posted are not limited to random point mutations. These examples include recombination in many cases and are not limited to the type of mutation that occurs yet they demonstrate exactly what ev is showing. It is not the type of mutation or recombination that limits evolution, it is the mathematical fact that multiple selection pressures slow and ultimately stops evolution despite recombination or the type of mutation.

I can help if people find me disingenuous because they are ignorant of the mathematic of mutation and selection. I’ll just have to continue explaining the results of ev and give real examples of this result.

Ev is accurate for describing what multiple selection pressures do to the evolutionary process. If you evolutionists think that other mechanisms of mutations and recombination will somehow change this mathematical fact, modify ev and prove it. Reality already shows that recombination and these other mechanism of mutation don’t change the fact that multiple selection pressures slow and ultimately stop evolution, but don’t let this stop you evolutionists from trying to prove otherwise. I think its fun watching you try but at some point you will have to acknowledge this mathematical fact (at least if you still want to claim you are scientists, of course you are a lita’ gator, not a scientist).

Did I forget to mention Dr Schneider’s mathematics and his ev program which applies this mathematics? Pardon me.

Well read further down in this post, I have two more real examples of multiple selection pressures slowing evolution.

Now that’s a surprise to me, I didn’t know that Penicillin was human developed. The reason why we observe the effect of human applied selection pressures is because we look to see the consequences of our actions. I previously posted a citation from ecologists who discussed extinction and the effects of multiple selection pressures. The same effect that is seen by human applied selection pressures are seen when the pressures arise from other sources. And that affect is that multiple selection pressures slow and ultimately stop evolution.

I already know how to write software, so far we have one lita’ gator who thinks that Unnamed’s selection condition models reality. If Paul and Dr Schneider embrace and accept Unnamed’s selection scheme represents reality, then I’ll put the effort in to verify the scheme. I don’t think they will accept Unnamed’s algorithm because it has no basis in reality. But don’t let this stop you from making this argument, after all, you are a lita’ gator.

PPS You think that the string cheese theory is a legitimate issue, that doesn’t make it true. Perhaps you want to post a citation of a real example of Unnamed’s selection process or better yet, post a real example of the string cheese theory and choosing toppings on a pizza is not an example of natural selection.

Clown fish, thank you for reminding me to put on my full armor.

Cuddles, where have you been? This entire thread is based on the evolutionist written and peer reviewed mathematical model ev and Delphi added on the mathematics of the fitness landscape that is so nicely described on Wikipedia. Are you discrediting the mathematics of your own theory?

Of course this sounds insane to someone who has succumbed to evolutionist programming. These kinds of facts are not included in your programming and don’t fit your prejudice and bias, but ponder this fact, multiple selection pressures slow and ultimately stop evolution. Ev, an evolutionist written computer model of mutation and selection shows this and numerous real examples of this phenomenon show this. If fact, here are a couple more examples of this. It seems everyone knows this except evolutionists.

http://www.who.int/infectious-disease-report/2000/ch5.htm (http://www.who.int/infectious-disease-report/2000/ch5.htm)

And

http://www.nyas.org/ebriefreps/main.asp?intSubsectionID=5103 (http://www.nyas.org/ebriefreps/main.asp?intSubsectionID=5103)

and
Same old lies, no math.

Dr Adequate

30th May 2007, 10:34 AM

You are going to have a lot of trouble accounting for the millions of differences between humans and chimpanzees genomes by mutation and selection We've already done so, remember? And we showed you a peer-reviewed paper which contained the math, remember? And you said the math was wrong, remember? And you'd got the number of base pairs in the human genome wrong by a factor of ten, remember? And then you said the math was wrong again, remember? And then it turned out that you'd forgotten that the human genome was diploid, remember? And then you ran off blubbering and whining about cheese, remember?

Even if your sick little mind has buried the trauma of these events, we remember. So there's no use lying to us about it.

Meadmaker

30th May 2007, 11:01 AM

Taffer

30th May 2007, 11:03 AM

Like I said, kleinman, it models reality. It is a well developed model. If you don't think it models reality, then give us an example of where it doesn't. At this stage, the model I gave is about as proven as you can get.

Oh, and you wanted a model. Several have been given. Now, are you going to reply to the model?

joobz

30th May 2007, 11:10 AM

In fact you can argue that nothing has evolved to the “perfect” optimum. However, if you take this view, how do you explain the evolution of reptiles to birds? Do you really think this is an intelligent thing to say? the fact that evolution has no predetermined goal makes this entire comment pure gibberish with a dash of delusional nutjob.

It is a mathematical incomprehensible concept. Just like quantum tunneling? it can't be!!!!!

Why shouldn’t I be? I think that Dr Schneider properly modeled the mutation and selection process and so does he. So do the editors of the peer reviewed journal Nucleic Acids Research.There we go! BOING!!!! the elastic theory snaps back.

Sorry, Meadmaker, You got as much out of kleinman as you can expect before he snaps back to his "appeal to authority" starting point.
Fromt this point on, you will either go through the game again, where he repeats all of his already defunct claims or he'll start to use "clever" insults leveled against your avatar or screen name. But he will NEVER acknowledge the truth that refutes his delusion.

Clown fish, thank you for reminding me to put on my full armor.
Yes, your tinfoil hat is a sight to behold.

kjkent1

30th May 2007, 02:02 PM

Now that’s a surprise to me, I didn’t know that Penicillin was human developed. The reason why we observe the effect of human applied selection pressures is because we look to see the consequences of our actions. I previously posted a citation from ecologists who discussed extinction and the effects of multiple selection pressures. The same effect that is seen by human applied selection pressures are seen when the pressures arise from other sources. And that affect is that multiple selection pressures slow and ultimately stop evolution.Restrain your sarcasm and you may learn something.

Suppose, you have a bacteria which has never encountered penicillin, so there is no resistance to the toxin. However, the bacteria constantly encounters all sorts of other environmental selective pressures which it must either resist or succumb. If your conclusion that multiple selective pressures halts evolution were accurate, then no bacteria would survive the multiple selective pressures routinely placed upon it by its environment. But, bacteria exists, so there must be more to the process.

The reasonable conclusion is that multiple pressures which remain stable over long periods of time, will indeed stabilize an organism's genome, because the organism will not need to change because no new pressures are introduced.

Then, when a toxin like penicillin is introduced into the bacterial environment, the bacteria must develop resistance or succumb. If you introduce multiple toxins simultaneously, especially toxins specifically designed to attack different systems in the bacteria, the bacteria's ability to resist is clearly overwhelmed and it has greater difficulty developing resistance to all of the toxins.

However, eventually, one of two things must happen. Either the bacteria mutates a successful resistance to all of the new environmental toxins, and is radically evolved, or, the bacterial population dies off and disappears.

So, while I would agree with you that combination therapies will be more difficult for the bacteria to overcome, it should be obvious, that if the bacteria manages to survive long enough to finally succeed in developing resistance to those combination therapies, then the slow down which was observed is rendered instantly void, and the organism will suddenly appear to have radically evolved.

Which is exactly what happens. The combination therapies created a bottleneck through which a sufficiently evolved bacteria could not easily escape, but when one finally does, the result is much more evolved than it would have otherwise been.

And we already have a name for this process: punctuated equilibrium. So, what you're describing matches precisely with what is already observed in the fossil record.

PPS You think that the string cheese theory is a legitimate issue, that doesn’t make it true. Perhaps you want to post a citation of a real example of Unnamed’s selection process or better yet, post a real example of the string cheese theory and choosing toppings on a pizza is not an example of natural selection.String theory, at its base is little more than a means of explaining randomness through determinism.

If all possibilities actually occur, but in different universes, then randomness is but an illusion relative to the observer who has access only to observations in his/her own universe.

String theory explains reality via math -- and it's funny that you find it so absurd, because that's exactly what you constantly attempt to do via ev.

I think that string theory is, to quote you, "a plausible explanation" for the anthropic nature of the universe. I don't think that it's the only possible explanation -- whereas with regards to evolution, you find the results of ev to be the only possible explanation, and thus evolution must be mathematically impossible.

But, until you stop willfully excluding evolutionary processes which would cause dramatic change from your experiments and thought processes, you will never know for certain.

kleinman

30th May 2007, 03:07 PM

If you hold to the view that directional selection pressures drive the mutation selection process to a new optimum and that when reaching that new optimum is considered the point of convergence, you will understand this talk of “convergence”.So, what? If we're at an optimum, does that mean evolution stops at that point? It's stabilized? I don't see how that could happen. How could you prevent it? DNA will mutate. Those mutations will affect function. The change in function will affect survival and breeding success. How can you stop it?
When an organism is at its local optimum, any mutation will reduce its reproductive fitness and therefore will be selected out. Stabilizing selection pressures favor those phenotypes at the local optimum and increase the frequency of their genotypes. Yes there is evolution and that evolution reduces the diversity of the population.
The only divergence you can obtain is that divergence that either has no effect on or improves reproductive fitness.Sure. It seems like there's plenty of room for improvement in pretty much any organism. That's plenty of possible divergence.
Stabilizing selection pressures prevent divergence and directional selection pressures interfere with the evolutionary process. That is what the mathematics show and that is what real examples of evolution show.
However, if you take this view, how do you explain the evolution of reptiles to birds? Reptiles certainly are at a functional suboptimal state. How do you explain the profound divergence required to take reptiles from their functional suboptimal state through millions of genetic changes to another functional suboptimal state?Obviously, every step along the way was a different functional suboptimal state.
That’s a nice speculation for the SciFi channel but has no mathematical or scientific basis. Why don’t you describe the selection pressure(s) that transform a reptile into a bird?
This is a nice story but you extrapolate the mutation and selection process far beyond what it can really do. Do you think it was spines on a food source or one organism caused trouble for another organism caused reptiles to evolve into birds?I don't know what caused reptiles to evolve into birds, and I don't think "caused" is the proper term, anyway. Somewhere along the line, a reptile grew scales that were slightly longer than the old scales. There was no "cause" for why their scales were longer, but they were. It worked out. The organism didn't die. It bred, and you had long scaled reptiles running about. By a couple of changes down the road, those scales were called "feathers". The prevailing belief is that these longer, lighter, scales kept those dinosaurs warmer than the regular scales. Is that right? I don't know.
Again, a nice story for the SciFi channel, however science describes the principles of “cause” and effect. You want to say there was and effect but no cause. The mathematics is not there to support your speculations. In fact, the mathematics contradicts your speculations. What makes a point on the fitness landscape a local optimum is that any deviation from that optimum reduces reproductive fitness and that creature will be selected out. You talk about populations moving from one local optimum to the next like a child stepping from stone to stone when crossing a creek. The problem with this concept is the mathematics demonstrates you will be continually stepping into the creek and be washed away.
That story is that the mutation and selection process is profoundly slow.But the history of the Earth is profoundly long. You may think it takes you a long time to walk to the corner chemist's, but that's peanuts compared to the age of the Earth.
4 billion years is peanuts for the mathematics of mutation and selection. Trillions of years are not enough. Adebz, don’t you have a number larger than trillions?
Which one's longer? The amount of time required, or the amount of time available? I don't know how to compute the amount of time required, and I don't think anyone else does either. It appears to me that it happened, so that gives me some basis for speculation on how long it took, but if you reject that idea, then your stuck with "I don't see how it happened, so I don't believe it."
Study this thread and ev and you will get a sense of how many generations it takes to evolve a few loci on a 100k genome. Even for generation times for bacteria, you get millions of years to evolve less than 100 loci on this small genome.
Far be it from me to discourage skepticism, but if you go farther and say, "I don't see how it happened, therefore it couldn't have happened." then you have made an error.
Meadmaker, I haven’t said I don’t see how it happened, I have said that ev shows that the theory of evolution is mathematically impossible because multiple selection pressures profoundly slow the evolutionary process. I have then posted numerous citations that demonstrate the mathematics that ev shows.
Again, you miss the point. If farmers used only single drug treatment, parasites will attain resistance more quickly to that drug than if multiple drug treatment is used.You can't get faster than one step. If you kill everything, you've slowed down the development of resistance. If you kill almost everything, you've speeded it up.
Sure you have for a single selection pressure, but when you have combination selection pressures, you slow down the process. That is the point. That is the lesson from the numerous citations I’m posting.
Here I think you are wrong. Directional selection pressures do have a target. That target is genetic sequences that give a local optimal reproductive fitness.But they don't have "a" target. They have any target that leads to any stable situation.
That’s fine, you can have more than a single genetic sequence that will give a variety of different local optimums but achieving those optimums are more difficult when you have multiple selection pressures. Ev has more than a single “perfect creature”.
You are going to have a hard time supporting your speculation with facts. Both the human and chimpanzee genomes have been sequenced and these millions of differences are obtained by comparing the two genomes.There are millions of differences in base pairs, but there are millions of differences between different humans as well. The number of differences between two humans is only 1/10 as much between a human and a chimp.
Well, the 35 million base pair differences already reported between human and chimpanzee genomes is not my number, the is the number reported by those sequencing the genomes.
Hmmm. Perhaps that means that only 60000 years were required for the divergence of humans and chimps.
You evolutionists really like to speculate and then call it science.
Like I said, kleinman, it models reality. It is a well developed model. If you don't think it models reality, then give us an example of where it doesn't. At this stage, the model I gave is about as proven as you can get.
Let’s see what you said about your model.
What's funny, Meadmaker, is that both Dr. A and myself have given mathematical proofs which show that increased selection speeds up evolution. In my case, it "didn't count" to kleinman because it modelled "recombination and selection not mutation and selection", which is obviously utter rubbish.
So you have presented a model of recombination and natural selection and you propose that it accelerates evolution. You don’t want to give a real example of your model and you don’t understand the difference between mutation and selection and recombination and selection. On the other hand, I have given dozens of citations that show what ev models. If you think your model describes reality, post your citations of real examples. In the meantime, I will continue to post citations of real examples that demonstrate the mathematics of ev.
Now that’s a surprise to me, I didn’t know that Penicillin was human developed. The reason why we observe the effect of human applied selection pressures is because we look to see the consequences of our actions. I previously posted a citation from ecologists who discussed extinction and the effects of multiple selection pressures. The same effect that is seen by human applied selection pressures are seen when the pressures arise from other sources. And that affect is that multiple selection pressures slow and ultimately stop evolution.Restrain your sarcasm and you may learn something.
Hey, you tried to allege that human applied selection pressures are somehow different than natural selection pressures. If you look into this issue a little you will find that many antibiotics are derived from natural sources, so are herbicides, so are many of the other chemicals used to control biology in our environment. There is no difference in the mathematics of human caused selection pressures and other sources of selection pressures.
Suppose, you have a bacteria which has never encountered penicillin, so there is no resistance to the toxin. However, the bacteria constantly encounters all sorts of other environmental selective pressures which it must either resist or succumb. If your conclusion that multiple selective pressures halts evolution were accurate, then no bacteria would survive the multiple selective pressures routinely placed upon it by its environment. But, bacteria exists, so there must be more to the process.
The point is that most selection pressures are stabilizing. Bacteria exist but it is not because evolution did it.
The reasonable conclusion is that multiple pressures which remain stable over long periods of time, will indeed stabilize an organism's genome, because the organism will not need to change because no new pressures are introduced.
Give that man a cigar.
Then, when a toxin like penicillin is introduced into the bacterial environment, the bacteria must develop resistance or succumb. If you introduce multiple toxins simultaneously, especially toxins specifically designed to attack different systems in the bacteria, the bacteria's ability to resist is clearly overwhelmed and it has greater difficulty developing resistance to all of the toxins.
Somebody light that cigar.
However, eventually, one of two things must happen. Either the bacteria mutates a successful resistance to all of the new environmental toxins, and is radically evolved, or, the bacterial population dies off and disappears.
Somebody open the window so kjkent1 can smoke his cigar.
So, while I would agree with you that combination therapies will be more difficult for the bacteria to overcome, it should be obvious, that if the bacteria manages to survive long enough to finally succeed in developing resistance to those combination therapies, then the slow down which was observed is rendered instantly void, and the organism will suddenly appear to have radically evolved.
You should give up smoking; it’s not good for you. Bacteria which have evolved resistance to antibiotics have not radically evolved. Now a reptile transforming into a bird; that you can call radically evolved.
Which is exactly what happens. The combination therapies created a bottleneck through which a sufficiently evolved bacteria could not easily escape, but when one finally does, the result is much more evolved than it would have otherwise been.
So what does that bottleneck look like that a reptile squirts through and comes out a bird?
And we already have a name for this process: punctuated equilibrium. So, what you're describing matches precisely with what is already observed in the fossil record.
Stephen Gould said a couple things which are mathematically inconsistent with mutation and selection. The first is that punctuated equilibrium occurs with small sub-populations and occurs over short periods of time. Both of these work against the mathematics of mutation and selection. Mutation and selection slows with small populations and requires a lot of time to accomplish anything. Now if you want to apply Gould’s concept of punctuated equilibrium to recombination and natural selection that makes some sense.
PPS You think that the string cheese theory is a legitimate issue, that doesn’t make it true. Perhaps you want to post a citation of a real example of Unnamed’s selection process or better yet, post a real example of the string cheese theory and choosing toppings on a pizza is not an example of natural selection.String theory, at its base is little more than a means of explaining randomness through determinism.
That’s fine; if you think it explains evolution, give us a real example.
If all possibilities actually occur, but in different universes, then randomness is but an illusion relative to the observer who has access only to observations in his/her own universe.
Do you really believe that all possibilities actually occur?
String theory explains reality via math -- and it's funny that you find it so absurd, because that's exactly what you constantly attempt to do via ev.
If a premise for string theory is that all possibilities actually occur, I would have trouble with this theory from this first assumption. There are some things that have an infinitesimally small mathematical possibility but they don’t occur.
I think that string theory is, to quote you, "a plausible explanation" for the anthropic nature of the universe. I don't think that it's the only possible explanation -- whereas with regards to evolution, you find the results of ev to be the only possible explanation, and thus evolution must be mathematically impossible.
Hey, whatever turns your crank. This type of think has no place in the training of children and neither does the theory of evolution. After all, the theory of evolution is mathematically impossible everywhere except in one of your 10^500 alternative universes.
But, until you stop willfully excluding evolutionary processes which would cause dramatic change from your experiments and thought processes, you will never know for certain.
None of the real examples that I have cited exclude any evolutionary process. If you think any of these processes will change the mathematical fact that ev reveals that multiple selection pressures slow and ultimately stop evolution, add the feature to ev and prove me wrong.

joobz

30th May 2007, 03:25 PM

That’s a nice speculation for the SciFi channel but has no mathematical or scientific basis. Why don’t you describe the selection pressure(s) that transform a reptile into a bird?

Again, a nice story for the SciFi channel, however science describes the principles of “cause” and effect. You want to say there was and effect but no cause. The mathematics is not there to support your speculations. In fact, the mathematics contradicts your speculations. What makes a point on the fitness landscape a local optimum is that any deviation from that optimum reduces reproductive fitness and that creature will be selected out. You talk about populations moving from one local optimum to the next like a child stepping from stone to stone when crossing a creek. The problem with this concept is the mathematics demonstrates you will be continually stepping into the creek and be washed away.

4 billion years is peanuts for the mathematics of mutation and selection. Trillions of years are not enough. Adebz, don’t you have a number larger than trillions?

Study this thread and ev and you will get a sense of how many generations it takes to evolve a few loci on a 100k genome. Even for generation times for bacteria, you get millions of years to evolve less than 100 loci on this small genome.

Meadmaker, I haven’t said I don’t see how it happened, I have said that ev shows that the theory of evolution is mathematically impossible because multiple selection pressures profoundly slow the evolutionary process. I have then posted numerous citations that demonstrate the mathematics that ev shows.

Sure you have for a single selection pressure, but when you have combination selection pressures, you slow down the process. That is the point. That is the lesson from the numerous citations I’m posting.

That’s fine, you can have more than a single genetic sequence that will give a variety of different local optimums but achieving those optimums are more difficult when you have multiple selection pressures. Ev has more than a single “perfect creature”.

Well, the 35 million base pair differences already reported between human and chimpanzee genomes is not my number, the is the number reported by those sequencing the genomes.

You evolutionists really like to speculate and then call it science.

Wow, I feel almost prophetic.
There we go! BOING!!!! the elastic theory snaps back.

Sorry, Meadmaker, You got as much out of kleinman as you can expect before he snaps back to his "appeal to authority" starting point.
Fromt this point on, you will either go through the game again, where he repeats all of his already defunct claims or he'll start to use "clever" insults leveled against your avatar or screen name. But he will NEVER acknowledge the truth that refutes his delusion.

Meadmaker

30th May 2007, 04:52 PM

kjkent1

30th May 2007, 05:41 PM

You should give up smoking; it’s not good for you. Bacteria which have evolved resistance to antibiotics have not radically evolved.Haven't they? I'd say that a bacteria that eats nylon is a pretty radical change. So is a bacteria that eats your flesh while you're still alive. Your perspective is that no bacteria today has radically evolved into a herring. But, between three billion years ago and today, one may well have. You cannot exclude this probability until you have at least modeled all of the known mutational devices and and selective pressures.Now a reptile transforming into a bird; that you can call radically evolved.You're being unreasonable again. Exposing a reptile to penicillin will not evolve it into a bird withing a 10-day course of treatment. However, an accidental mutation which produces a flap of skin underneath both of a reptile's front legs, may well begin that process.So what does that bottleneck look like that a reptile squirts through and comes out a bird?Use your imagination. I could very easily come up with small morphological mutations which would take a reptile and transform it into a bird over time. Not really that difficult at all.Stephen Gould said a couple things which are mathematically inconsistent with mutation and selection. The first is that punctuated equilibrium occurs with small sub-populations and occurs over short periods of time. Both of these work against the mathematics of mutation and selection.Ev's model provids only for gradual changes. As I have repeatedly stated, by modelling the more expansive mutational mechanisms, you will get more expansive and radical morphologic changes in the organism, which will then gradually stabilize, as exhibited when Rseq -> Rfreq.Mutation and selection slows with small populations and requires a lot of time to accomplish anything.For gradual change, yes, for radical changes, no.Now if you want to apply Gould’s concept of punctuated equilibrium to recombination and natural selection that makes some sense.Why stop with recombination -- why not add all the other known mutational mechanisms?Do you really believe that all possibilities actually occur?As I've also repeatedly stated, I don't "believe" anything. Evertt's "many worlds" interpretation of quantum uncertainty is consistent with Susskind's string theory. If all possibilities (constrained by the limits of the observed wave function) do actually occur, but in other universes, then that would explain why what you view as impossible, is not only possible, but absolutely true.

The difference between you and me, is that I'm open to the possibility, and you're not.If a premise for string theory is that all possibilities actually occur, I would have trouble with this theory from this first assumption. There are some things that have an infinitesimally small mathematical possibility but they don’t occur.I think you mean "infinitessibally small mathematical 'probability.'"

At any given moment, the sands on a beach are configured in an arrangement, the odds of which are so infinitessimally small, that one would have to agree that the configuration is mathematically impossible. But, the beach is there, nonetheless, and every moment of every day, that beach changes its configuration to another arrangment of infintessimally small probability.

Incredibly unlikely things happen all the time. Sometimes the sands arrange themselves in the shape of a face. And, no one complains that this is mathematically impossible.

But, if DNA does it, then suddenly you have a problem of faith, and that makes all the difference.Hey, whatever turns your crank. This type of think has no place in the training of children and neither does the theory of evolution. After all, the theory of evolution is mathematically impossible everywhere except in one of your 10^500 alternative universes.[/quote[What children are taught is a political issue, not a scientific one. It has no relevance in this dabate -- and frankly, if you want to go there, you're gonna get slaughtered, because I'm the expert in that area -- at least around these parts.None of the real examples that I have cited exclude any evolutionary process.False. They all exclude the most important evolutionary process of all -- time. Your examples all take place in the blink of an eye, as compared to what is required for evolution to take place.[quote]If you think any of these processes will change the mathematical fact that ev reveals that multiple selection pressures slow and ultimately stop evolution, add the feature to ev and prove me wrong.I don't need to prove you wrong. You need to prove you right. That's how it works in science (and law). Proving a negative is not enough and never has been. You must set forth affirmative evidence to support your position, or you can never accomplish anything more than skepticizm.

Meadmaker

30th May 2007, 07:14 PM

Why don’t you describe the selection pressure(s) that transform a reptile into a bird?

Because selection pressures don't transform anything. Selection pressures transform living organisms into dead ones.

Random mutations transform species. If those random mutations are not so severe that the mutant organisms are able to survive, there is a new suboptimal functional organism on the block. If that mutation actually helps, then that new suboptimal organism will actually grow more common. If its descendants mutate again, after a few times they won't be able to, or maybe willing to, mate with the original unmutated descendants of the same organism.

Selection pressures can hasten the process by which populations of animals are transformed. If you kill off all organisms except ones that have specific traits, then those traits are suddenly much more common than they were in the original population.

But, you might ask why I don't describe the combinations of mutations and selection pressures that developed birds from their reptilian ancestors. Of course, you know the answer to that. It's because I don't know. All I know is that I can compare the anatomy of birds and reptiles, and the fossils of long dead creatures with similarities to both, and note that there are an awful lot of common features. One explanation is that they got those common features from common ancestors, but each then evolved in different directions from there.

Any other explanations?

In fact, the mathematics contradicts your speculations. What makes a point on the fitness landscape a local optimum is that any deviation from that optimum reduces reproductive fitness and that creature will be selected out.

Perhaps you can give an example of a creature that is at a local optimum, and maybe describe the fitness landscape around it?

My son seems a lot like me, but not exactly. Did he devolve from a local optimum? Or had we not quite reached it and he's a bit closer than the rest of us?

The problem with this concept is the mathematics demonstrates you will be continually stepping into the creek and be washed away.

Perhaps you can post an example of the mathematics of local optima as applied to evolution?

Meadmaker, I haven’t said I don’t see how it happened, I have said that ev shows that the theory of evolution is mathematically impossible because multiple selection pressures profoundly slow the evolutionary process.

So, if we could just get a population of organisms that had no significant selection pressure (or only one), we could see them evolve?

Sure you have for a single selection pressure, but when you have combination selection pressures, you slow down the process.

I haven't read every link you posted, nor do I intend to, but I have skimmed some of them, and read a couple with more attention. One key feature of the ones I've read is that all of them talk about the possibility that the process will be slowed down, but not stopped. In the case of the HIV studies, they noted that resistant strains do develop, even in the case of multi drug therapies. I haven't seen any paper you cited say that evolution was stopped.

So, was it slowed down enough? In this case, no, because they all talk about developing resistance even in the face of the combination therapies, and we are talking about a time period that is less than the lifetime of a single individual. Just imagine what you could do if you had a million years for this.

Well, the 35 million base pair differences already reported between human and chimpanzee genomes is not my number, the is the number reported by those sequencing the genomes.

Yes. And 3 million base pair differences is the number reported between two humans.

On the other hand, I have given dozens of citations that show what ev models.

We don't have the authors of all those papers here, but I'm willing to bet that none of them think it shows what you think it shows. Either you are onto something very, very big that a lot of people have overlooked, or you might be making an extrapolation from a not very accurate model.

kleinman

30th May 2007, 09:00 PM

Sorry, Meadmaker, You got as much out of kleinman as you can expect before he snaps back to his "appeal to authority" starting point.But I can't resist the odds. Besides, it's always good to know what the "other side" is saying. I find that often, both sides of this debate mischaracterize the other.
Which authority is clown fish talking about, it must be ev.
On the rare occasion I discuss things with creationists, I encourage them to read about evolution in books written by evolutionists. As I'm sure you know, a lot of them only read their own fundamentalists writings. I might as well get the creationist line from a creationist once in a while.
Where do you think I learned about ev, comic books? Now if you evolutionists would read about ev and work with the model, you would learn something about mutation and selection.
You should give up smoking; it’s not good for you. Bacteria which have evolved resistance to antibiotics have not radically evolved.Haven't they? I'd say that a bacteria that eats nylon is a pretty radical change. So is a bacteria that eats your flesh while you're still alive. Your perspective is that no bacteria today has radically evolved into a herring. But, between three billion years ago and today, one may well have. You cannot exclude this probability until you have at least modeled all of the known mutational devices and and selective pressures.
A bacterium that eats nylon is not so radical if that capability is transmitted by a plasmid. Flesh eating bacteria are not so radical either when you consider all infectious agents in humans use us as a food source. A bacterium evolving into a red herring, that is only probable with string cheese.
Now a reptile transforming into a bird; that you can call radically evolved.You're being unreasonable again. Exposing a reptile to penicillin will not evolve it into a bird withing a 10-day course of treatment. However, an accidental mutation which produces a flap of skin underneath both of a reptile's front legs, may well begin that process.
Oh yes, the suboptimal reptile is going to evolve huge anatomical changes including skeletal changes, feathers, wings, beak… all to become a suboptimal bird. Yes I agree with you, it would take more than a 10 day course of penicillin.
So what does that bottleneck look like that a reptile squirts through and comes out a bird?Use your imagination. I could very easily come up with small morphological mutations which would take a reptile and transform it into a bird over time. Not really that difficult at all.
You must be talking about one of Delphi’s bottles.
Stephen Gould said a couple things which are mathematically inconsistent with mutation and selection. The first is that punctuated equilibrium occurs with small sub-populations and occurs over short periods of time. Both of these work against the mathematics of mutation and selection.Ev's model provids only for gradual changes. As I have repeatedly stated, by modelling the more expansive mutational mechanisms, you will get more expansive and radical morphologic changes in the organism, which will then gradually stabilize, as exhibited when Rseq -> Rfreq.
Dr Schneider seems to disagree with you; he says that ev shows rapid gains of information. All the expansive mutational mechanisms are available in the citations I have been posting and they still demonstrate that multiple selection pressures slow and ultimately stop evolution.
Mutation and selection slows with small populations and requires a lot of time to accomplish anything.For gradual change, yes, for radical changes, no.
Sorry to tell you this, the mathematics of mutation and selection contradicts what you have just alleged.
Now if you want to apply Gould’s concept of punctuated equilibrium to recombination and natural selection that makes some sense.Why stop with recombination -- why not add all the other known mutational mechanisms?
So you think that sexual recombination is a form of mutation? You can get rapid and large morphological changes by recombination and natural selection with small populations. You can not do this with mutation and selection. This is why Gould’s concept of punctuated equilibrium is only applicable to recombination and natural selection not mutation and natural selection.
Do you really believe that all possibilities actually occur?As I've also repeatedly stated, I don't "believe" anything. Evertt's "many worlds" interpretation of quantum uncertainty is consistent with Susskind's string theory. If all possibilities (constrained by the limits of the observed wave function) do actually occur, but in other universes, then that would explain why what you view as impossible, is not only possible, but absolutely true.

The difference between you and me, is that I'm open to the possibility, and you're not.
Do you think it is possible that I can be nice to an evolutionist?
If a premise for string theory is that all possibilities actually occur, I would have trouble with this theory from this first assumption. There are some things that have an infinitesimally small mathematical possibility but they don’t occur.I think you mean "infinitessibally small mathematical 'probability.'"
I think you meant infinitesimally small mathematical probability.
At any given moment, the sands on a beach are configured in an arrangement, the odds of which are so infinitessimally small, that one would have to agree that the configuration is mathematically impossible. But, the beach is there, nonetheless, and every moment of every day, that beach changes its configuration to another arrangment of infintessimally small probability.
This is a common mistake that evolutionists try to argue. The configuration of the sands on the beach at any moment represents a single ensemble out of a huge number of possible ensembles. Now if a hurricane sweeps through and the sand blows around and returns to the same ensemble, that would be an infinitely small probability, but I’m sure you evolutionists think it is possible.
Incredibly unlikely things happen all the time. Sometimes the sands arrange themselves in the shape of a face. And, no one complains that this is mathematically impossible.
Ah, I see, erosion can occasionally make something that appears recognizable so abiogenesis occurs.
But, if DNA does it, then suddenly you have a problem of faith, and that makes all the difference.Hey, whatever turns your crank. This type of thing has no place in the training of children and neither does the theory of evolution. After all, the theory of evolution is mathematically impossible everywhere except in one of your 10^500 alternative universes.What children are taught is a political issue, not a scientific one. It has no relevance in this dabate -- and frankly, if you want to go there, you're gonna get slaughtered, because I'm the expert in that area -- at least around these parts.
Hey, I have no problem with teaching children that multiple selection pressures slow and ultimately stop the evolutionary process. I even think there is a place for teaching about ev as long as the full story is told. What I object to is the concocted extrapolations that evolutionists have convinced themselves as being true being taught to children who don’t have the capability to counter such stories. Evolutionists realize they have to indoctrinate children because it is much more difficult to convince adults of these wild imaginations that evolutionists have.
None of the real examples that I have cited exclude any evolutionary process.False. They all exclude the most important evolutionary process of all -- time. Your examples all take place in the blink of an eye, as compared to what is required for evolution to take place.
There is more than enough time to demonstrate that a single selection pressure evolve more rapidly than multiple selection pressures. This fact is known my many scientists in many different fields. Since the longest duration for any of the citations I have posted is 30 years, you have to fall back on mathematical models to see whether time will overcome the effect of multiple selection pressures. Ev demonstrates that you will never have enough time.
If you think any of these processes will change the mathematical fact that ev reveals that multiple selection pressures slow and ultimately stop evolution, add the feature to ev and prove me wrong.I don't need to prove you wrong. You need to prove you right. That's how it works in science (and law). Proving a negative is not enough and never has been. You must set forth affirmative evidence to support your position, or you can never accomplish anything more than skepticizm.
Ok, here are two more citations that show that multiple selection pressures slow evolution at the end of this post.
Why don’t you describe the selection pressure(s) that transform a reptile into a bird?Because selection pressures don't transform anything. Selection pressures transform living organisms into dead ones.
Then what do you propose is the cause and effect mechanism that transforms reptiles into birds.
Random mutations transform species. If those random mutations are not so severe that the mutant organisms are able to survive, there is a new suboptimal functional organism on the block. If that mutation actually helps, then that new suboptimal organism will actually grow more common. If its descendants mutate again, after a few times they won't be able to, or maybe willing to, mate with the original unmutated descendants of the same organism.
The problem you have with this argument is that stabilizing selection pressures select against the mutants ultimately and reduce diversity. A beneficial mutation only exists if a directional selection pressure selects for this mutation. Study ev, this is the mathematics of what you are trying to describe.
Selection pressures can hasten the process by which populations of animals are transformed. If you kill off all organisms except ones that have specific traits, then those traits are suddenly much more common than they were in the original population.
Selection pressures are the only way you can transform populations. Stabilizing selection pressures reduce the diversity of the population and directional selection pressures drive the population to a new local optimum.
But, you might ask why I don't describe the combinations of mutations and selection pressures that developed birds from their reptilian ancestors. Of course, you know the answer to that. It's because I don't know. All I know is that I can compare the anatomy of birds and reptiles, and the fossils of long dead creatures with similarities to both, and note that there are an awful lot of common features. One explanation is that they got those common features from common ancestors, but each then evolved in different directions from there.
Birds have different skeletons than reptiles, they need to in order to support the loads of the flight muscles, you have beaks, wings, feathers,… You extrapolate the similarities of these creatures beyond scientific reason. When you get beyond the gross anatomical differences between reptiles and birds and try to reconcile the genetic differences you enter into the realm of mathematical impossibility. You have no way to account for the huge number of genetic differences.
Any other explanations?
Was there an explanation imbedded in what you just wrote? All I saw was speculations and extrapolations. Now the mathematics of ev which show that multiple selection pressures slow and ultimately stop evolution and the numerous citations I have posted of real examples of this mathematical fact, that is an explanation.
In fact, the mathematics contradicts your speculations. What makes a point on the fitness landscape a local optimum is that any deviation from that optimum reduces reproductive fitness and that creature will be selected out.Perhaps you can give an example of a creature that is at a local optimum, and maybe describe the fitness landscape around it?
I’ve given dozens of these already. Let’s take the example of HIV. Before the advent of HIV drugs, the wild virus was at a local optimum. Once therapies were developed and monotherapy was instituted, there was brief improvement for the patient but resistance of the virus to this monotherapy quickly evolved. That is a new local optimum for the virus was achieved due to the monotherapy selection pressure. When this was recognized, combination therapy was instituted. This made the fitness landscape much more difficult for the virus to traverse to a new local optimum. You can think of the fitness landscape as a multi-dimensional surface with peaks and valleys. When a virus is at a local optimum, any change in the genome reduces reproductive fitness. If that reduction in reproductive fitness is not as severe as to stop reproduction, the virus may be able to find another local optimum by further mutations but with multiple selection pressures, this excursion becomes very difficult for the virus. There is something else that is interesting about HIV that has evolved resistance to drugs. These viruses can not reproduce as quickly as the wild virus does in an environment without selection pressures.
My son seems a lot like me, but not exactly. Did he devolve from a local optimum? Or had we not quite reached it and he's a bit closer than the rest of us?
Now don’t confuse recombination and natural selection with mutation and natural selection. And you are demonstrating one of the big problems with the theory of evolution, eugenics.
The problem with this concept is the mathematics demonstrates you will be continually stepping into the creek and be washed away.Perhaps you can post an example of the mathematics of local optima as applied to evolution?
Mull over that example that I have described above. If you have trouble understanding it, I will give you another example.
Meadmaker, I haven’t said I don’t see how it happened, I have said that ev shows that the theory of evolution is mathematically impossible because multiple selection pressures profoundly slow the evolutionary process.So, if we could just get a population of organisms that had no significant selection pressure (or only one), we could see them evolve?
There are always have selection pressures, most of them are stabilizing selection pressures. You can see a stabilizing selection pressures in action when you have a mutation to a crucial gene which makes the gene nonfunctional and causes the death of that creature. Stabilizing selection pressures maintain the status quo of the population. If you have a supportive enough environment that suboptimal creatures can survive then you will get some diversity in the population but as soon as something changes in the environment, only the most fit will survive and diversity is reduced. The citations I have been posting describe directional selection pressures (those pressures which drive a population to a new local optimum). For example antibiotics are directional selection pressures. When a bacterium evolves resistance to that antibiotic, you have just seen evolution in action. If you use combination antibiotics you slow the ability of the bacterium to evolve to those two selection pressures.
Sure you have for a single selection pressure, but when you have combination selection pressures, you slow down the process.I haven't read every link you posted, nor do I intend to, but I have skimmed some of them, and read a couple with more attention. One key feature of the ones I've read is that all of them talk about the possibility that the process will be slowed down, but not stopped. In the case of the HIV studies, they noted that resistant strains do develop, even in the case of multi drug therapies. I haven't seen any paper you cited say that evolution was stopped.
Read this article http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219 (http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219)
. This bacterium has been used to kill mosquito larvae for more than thirty years. The bacterium produces four cytotoxins. In the laboratory these bacteria have been genetically reengineered to produce one, two or three cytotoxins in which case the larvae can quickly evolve resistance when exposed to the toxins in fewer numbers.
So, was it slowed down enough? In this case, no, because they all talk about developing resistance even in the face of the combination therapies, and we are talking about a time period that is less than the lifetime of a single individual. Just imagine what you could do if you had a million years for this.
HIV is a very short genome with a very high mutation rate, reproduction rate and population size plus it does recombination. It represents the best of all cases for evolution, yet it still is suppressed by multiple selection pressures. When you get to longer genomes, smaller mutation rates, smaller reproduction rates and population sizes, this process becomes much, much slower. This is what the mathematics that ev demonstrates.
Well, the 35 million base pair differences already reported between human and chimpanzee genomes is not my number, the is the number reported by those sequencing the genomes.Yes. And 3 million base pair differences is the number reported between two humans.
Those 35 million base pair differences are in the homologous portions of the genome. It wouldn’t surprise me if this number goes up.
On the other hand, I have given dozens of citations that show what ev models.We don't have the authors of all those papers here, but I'm willing to bet that none of them think it shows what you think it shows. Either you are onto something very, very big that a lot of people have overlooked, or you might be making an extrapolation from a not very accurate model.
It wouldn’t bother me to have these authors weigh in. I don’t think people have ignored the fact that multiple selection pressures slow evolution. What I think people haven’t considered is that all selection pressures generally work this way. This is why I keep asking evolutionists like Taffer to give us a real example where multiple selection pressures accelerate evolution. I have come across one example where there may be a slight acceleration of evolution when two selection pressures v. a single selection pressure are applied but I am still studying the paper. I’ll post that link tomorrow, until then, her are two more papers which show that combination selection pressures slow evolution.

http://www.ctu.mrc.ac.uk/penta/abcpath.pdf (http://www.ctu.mrc.ac.uk/penta/abcpath.pdf)
Abacavir (ABC) selects for four mutations (K65R, L74V, Y115F and M184V) in HIV-1 reverse transcriptase (RT), both in vitro and during monotherapy in vivo. The aim of this analysis was to compare the selection of these and other nucleoside reverse transcriptase inhibitor (NRTI)-associated mutations by ABC-containing therapies in the presence and absence of concurrent lamivudine (3TC) and/or zidovudine (ZDV) and to assess the effect of these mutations on phenotypic susceptibility to the NRTIs.
and
The results of this study demonstrate that ZDV is useful as a resistance modulator, at least in combination with ABC, effectively reducing the incidence of selection forK65R and L74V. This may increase the likelihood that agents such as ddI, TDF and others affected by these two mutations will remain efficacious in second-line regimens. The relevance of these findings to combinations including NRTIs other than ABC, 3TC and ZDV remains to be elucidated.

http://cancerres.aacrjournals.org/cgi/reprint/22/11_Part_1/1290.pdf (http://cancerres.aacrjournals.org/cgi/reprint/22/11_Part_1/1290.pdf)
The possible application to chemotherapy of factors affecting the regulatory systems of cells has been considered. The extensive coordinate changes in intracellular enzyme concentrations which result from exposure to compounds interfering with the normal regulatory mechanisms suggest the possibility of combination therapy based upon the selective induction of quantitative changes in enzymatic activities. Such approaches would appear to be useful in circumventing two major problems of chemotherapy: finding sufficient metabolic differences between host and parasite to provide targets for selective drug toxicity, and preventing the eventual development of drug resistance.

It is concluded that a combination of two compounds affecting the same metabolic pathway, one producing feedback inhibition and the other effective through lethal synthesis, will show an enhanced differential toxicity greater than that from either drug alone. Similarly, pairs of compounds in which one member produces enzyme repression and the other is active through lethal synthesis should produce collateral sensitivity and thus prevent the development of drug-resistant populations.

Meadmaker

30th May 2007, 09:46 PM

I’ve given dozens of these already. Let’s take the example of HIV. Before the advent of HIV drugs, the wild virus was at a local optimum. ....

Local optimum...? Optimum of what?

What I was getting at is that if you want to talk about local optima, you have to have a function with an optimum. What's the function? "Fitness" is not a function. It's a noun. It's a word.

In ev, you do indeed have local optima because someone has contrived a fitness function for the purposes of modelling. What function is at a local optimum for a coconut? When I say "what function", I really mean a function. Something with parameters that renders a value. Something you could graph. You talk about evolution being "mathematically impossible", but where's the math?

It is my contention that every organism has a genetic code that could experience a mutation that would increase the probability that its genes will be passed on to future generations. Do you dispute that?

Now don’t confuse recombination and natural selection with mutation and natural selection.

I'm just asking whether me or my kid is closer to the local optimum.

And you are demonstrating one of the big problems with the theory of evolution, eugenics.

I'm not following. Why is eugenics a problem for the theory of evolution?

Meadmaker

30th May 2007, 09:51 PM

Read this article [URL="http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219"]

Here's the title:

"Cyt1A of Bacillus thuringiensis Delays Evolution of Resistance to Cry11A in the Mosquito Culex quinquefasciatus"

I wonder why they said "delays" instead of "stops".

kjkent1

30th May 2007, 11:08 PM

A bacterium that eats nylon is not so radical if that capability is transmitted by a plasmid. Flesh eating bacteria are not so radical either when you consider all infectious agents in humans use us as a food source. A bacterium evolving into a red herring, that is only probable with string cheese.I think it's more like a bacterium that eats nylon is not so radical as long as it doesn't defeat kleinman's argument, by demonstrating that a positive evolutionary change can arise despite the existence of stabilizing selective pressures.

Oh yes, the suboptimal reptile is going to evolve huge anatomical changes including skeletal changes, feathers, wings, beak… all to become a suboptimal bird. Yes I agree with you, it would take more than a 10 day course of penicillin.Appeal to incredulity is boring. You apparently can't refute the analysis. If the reptile gets a flap of skin under its arms, and it can use it to provide lift so as to better jump from one branch of a tree to another, then that reptile is no longer suboptimal in an environment with tree branches. The mutation will reproduce, and we are one step closer to a bird than we were prior to the mutation.

Dr Schneider seems to disagree with you; he says that ev shows rapid gains of information. All the expansive mutational mechanisms are available in the citations I have been posting and they still demonstrate that multiple selection pressures slow and ultimately stop evolution.Although I respect Dr. Schneider, I'm really not interested in the dicta contained his paper. It's his finding that matters -- nothing else. The ev experiment proves Shannon information gain from a random start using evolutionary mechanisms. And, because it does, it proves that God is not the only possible creative force for life in this universe. What follows is that you cannot rationally claim that evolution is mathematically impossible, unless you first exclude every possible means of evolutionary information gain. And, as you refuse to do the work -- you lose to the incumbant theory: evolution.

Sorry to tell you this, the mathematics of mutation and selection contradicts what you have just alleged.Modify ev and prove it. Until you do, you're spouting philosophy, not science.

So you think that sexual recombination is a form of mutation? You can get rapid and large morphological changes by recombination and natural selection with small populations. You can not do this with mutation and selection.In your "unsupported" opinion. Until you modify ev and show that none of the evolutionary mechanisms not currently modeled, will improve ev's performance, you have no support for your conclusion -- and therefore, you lose.This is why Gould’s concept of punctuated equilibrium is only applicable to recombination and natural selection not mutation and natural selection.Any time you want to provide proof for the above speculation, we will all be here waiting.Do you think it is possible that I can be nice to an evolutionist?Only your therapist knows for sure.This is a common mistake that evolutionists try to argue. The configuration of the sands on the beach at any moment represents a single ensemble out of a huge number of possible ensembles. Now if a hurricane sweeps through and the sand blows around and returns to the same ensemble, that would be an infinitely small probability, but I’m sure you evolutionists think it is possible.This is a common mistake that creationists try to argue. They believe that the universe is front loaded by God, therefore evolution must lead to some final, predictable outcome. But, the beach doesn't need to ever return to the same ensemble -- and DNA didn't need to be in a particular configuration at any point in the evolutionary process. From the moment that there was a configuration which could evolve via replication, it did -- without any particular destination in mind -- exactly like the beach.Ah, I see, erosion can occasionally make something that appears recognizable so abiogenesis occurs.That's an interesting comment -- and it's probably exactly what happened. One, incredibly improbable accident produced a molecule that could replicate. There was no particular reason why it had to happen, but it did. And, the result is evolution.Hey, I have no problem with teaching children that multiple selection pressures slow and ultimately stop the evolutionary process. I even think there is a place for teaching about ev as long as the full story is told. What I object to is the concocted extrapolations that evolutionists have convinced themselves as being true being taught to children who don’t have the capability to counter such stories. Evolutionists realize they have to indoctrinate children because it is much more difficult to convince adults of these wild imaginations that evolutionists have.You can take evolution out of the science classroom, but you can't put Christianity in, because that violates the 1st Amendment. Under the "Lemon" test, any goverment action that (1) promotes a particular religious sect, (2) prefers one religious sect to another, or (3) creates an unnecessary entanglement between religion and goernment, is prohibited.So, what you will end up with is a classroom with a biology teacher who will answer every question re the existence of life with "I can't talk about that subject." And, if that's what you want, then that's okay with me.

God is unprovable, scientifically, therefore nothing that you disprove re evolution, makes the discussion of God fair game in a biology class. Of course, you can get a Christian President to overweight the U.S. Supreme Court, and have the Lemon test overturned. But, until you do, you're stuck with my legal analysis, above.

Which is why I said that this subject is really nothing but politics. It has no place in a science discussion, any more than does a religious discussion.There is more than enough time to demonstrate that a single selection pressure evolve more rapidly than multiple selection pressures. This fact is known my many scientists in many different fields. Since the longest duration for any of the citations I have posted is 30 years, you have to fall back on mathematical models to see whether time will overcome the effect of multiple selection pressures. Ev demonstrates that you will never have enough time.This issue that you've raised is completely irrelevant. One large mutational accident gets past all of your complaints.

You know who David Tammet (http://en.wikipedia.org/wiki/Daniel_Tammet) is? He's not just a smart guy. He's a major evolutionary accident. And, if his genes get into the general population, all of the stanardized tests will suddenly be skewed by a group of humans who will have a huge competative advantage over the rest of us mere mortals.

Tammet is evolution in action -- and there's simply no denying it.

Mr. Scott

31st May 2007, 12:43 AM

You know, I had to sew a gapping laceration on a child’s face a couple of weeks ago. In order to do this, I had to restrain the child and stick needles multiple times into the child. If you asked the child, I’m sure the child would say that I showed gratuitous meanness, but when the stitches were taken out last week, the laceration looked much better. Why do you believe in the teachings of Christ when Christ believes the Genesis story

I never said I believed in the teachings of Christ. You said you believed in them, and I was pointing out your hypocrisy.

So, you called the child a whining cry-baby, called him diminuitive names and ridiculed him in various other ways while he suffered? Do you see evolutionists as injured children you need to restrain and mend? Are your nuts so big you could only fit one at a time into an MRI? It's bullies like you who, because they believe God is on their side...

The great benefit of your participation here is to inspire so many evolutionists to make so many vivid and articulate arguments for evolution. For this, you deserve back-handed thanks.

I've found a reference for a new species appearing in our lifetime (a plant in this case) and will type it in when I have time. Right now, I'm helping out with the funeral arrangements for my stepfather, who's cancer evolved too quickly to be stopped by the triple therapy administered by some of the world's finest physicians in one of the world's finest cancer hospitals.

Taffer

31st May 2007, 12:59 AM

No, kleinman, it is you who said it modeled only "recombination and and selection". It is me that explained that that is a meaningless concept. It models the change in alleles over time. This is evolution.

I'm sorry, but I think it's perfectly clear that you do not understand basic evolutionary theory. Especially given the fact that you are convinced there is a difference between "recombination and selection" and "mutation and selection". There is no difference, because they are not different things, kleinman. There is only "variaton and selection". Get this through your thick head.

So are you going to respond to my model?

And for the record, I don't have to provide any "real examples". Why? Because the model is so well supported it is taken to be fact. You are making the claim that a theory is false. Provide counter evidence.

Also for the record, not a single citation you have provided has given counter evidence.

Dr Adequate

31st May 2007, 04:48 AM

When an organism is at its local optimum, any mutation will reduce its reproductive fitness and therefore will be selected out. Stabilizing selection pressures favor those phenotypes at the local optimum and increase the frequency of their genotypes. Yes there is evolution and that evolution reduces the diversity of the population.

Stabilizing selection pressures prevent divergence and directional selection pressures interfere with the evolutionary process. That is what the mathematics show and that is what real examples of evolution show.

That’s a nice speculation for the SciFi channel but has no mathematical or scientific basis. Why don’t you describe the selection pressure(s) that transform a reptile into a bird?

Again, a nice story for the SciFi channel, however science describes the principles of “cause” and effect. You want to say there was and effect but no cause. The mathematics is not there to support your speculations. In fact, the mathematics contradicts your speculations. What makes a point on the fitness landscape a local optimum is that any deviation from that optimum reduces reproductive fitness and that creature will be selected out. You talk about populations moving from one local optimum to the next like a child stepping from stone to stone when crossing a creek. The problem with this concept is the mathematics demonstrates you will be continually stepping into the creek and be washed away.

4 billion years is peanuts for the mathematics of mutation and selection. Trillions of years are not enough. Adebz, don’t you have a number larger than trillions?

Study this thread and ev and you will get a sense of how many generations it takes to evolve a few loci on a 100k genome. Even for generation times for bacteria, you get millions of years to evolve less than 100 loci on this small genome.

Meadmaker, I haven’t said I don’t see how it happened, I have said that ev shows that the theory of evolution is mathematically impossible because multiple selection pressures profoundly slow the evolutionary process. I have then posted numerous citations that demonstrate the mathematics that ev shows.

Sure you have for a single selection pressure, but when you have combination selection pressures, you slow down the process. That is the point. That is the lesson from the numerous citations I’m posting.

That’s fine, you can have more than a single genetic sequence that will give a variety of different local optimums but achieving those optimums are more difficult when you have multiple selection pressures. Ev has more than a single “perfect creature”.

Well, the 35 million base pair differences already reported between human and chimpanzee genomes is not my number, the is the number reported by those sequencing the genomes.

You evolutionists really like to speculate and then call it science.

Let’s see what you said about your model.

So you have presented a model of recombination and natural selection and you propose that it accelerates evolution. You don’t want to give a real example of your model and you don’t understand the difference between mutation and selection and recombination and selection. On the other hand, I have given dozens of citations that show what ev models. If you think your model describes reality, post your citations of real examples. In the meantime, I will continue to post citations of real examples that demonstrate the mathematics of ev.

Hey, you tried to allege that human applied selection pressures are somehow different than natural selection pressures. If you look into this issue a little you will find that many antibiotics are derived from natural sources, so are herbicides, so are many of the other chemicals used to control biology in our environment. There is no difference in the mathematics of human caused selection pressures and other sources of selection pressures.

The point is that most selection pressures are stabilizing. Bacteria exist but it is not because evolution did it.

Give that man a cigar.

Somebody light that cigar.

Somebody open the window so kjkent1 can smoke his cigar.

You should give up smoking; it’s not good for you. Bacteria which have evolved resistance to antibiotics have not radically evolved. Now a reptile transforming into a bird; that you can call radically evolved.

So what does that bottleneck look like that a reptile squirts through and comes out a bird?

Stephen Gould said a couple things which are mathematically inconsistent with mutation and selection. The first is that punctuated equilibrium occurs with small sub-populations and occurs over short periods of time. Both of these work against the mathematics of mutation and selection. Mutation and selection slows with small populations and requires a lot of time to accomplish anything. Now if you want to apply Gould’s concept of punctuated equilibrium to recombination and natural selection that makes some sense.

That’s fine; if you think it explains evolution, give us a real example.

Do you really believe that all possibilities actually occur?

If a premise for string theory is that all possibilities actually occur, I would have trouble with this theory from this first assumption. There are some things that have an infinitesimally small mathematical possibility but they don’t occur.

Hey, whatever turns your crank. This type of think has no place in the training of children and neither does the theory of evolution. After all, the theory of evolution is mathematically impossible everywhere except in one of your 10^500 alternative universes.

None of the real examples that I have cited exclude any evolutionary process. If you think any of these processes will change the mathematical fact that ev reveals that multiple selection pressures slow and ultimately stop evolution, add the feature to ev and prove me wrong.

Which authority is clown fish talking about, it must be ev.

Where do you think I learned about ev, comic books? Now if you evolutionists would read about ev and work with the model, you would learn something about mutation and selection.

A bacterium that eats nylon is not so radical if that capability is transmitted by a plasmid. Flesh eating bacteria are not so radical either when you consider all infectious agents in humans use us as a food source. A bacterium evolving into a red herring, that is only probable with string cheese.

Oh yes, the suboptimal reptile is going to evolve huge anatomical changes including skeletal changes, feathers, wings, beak… all to become a suboptimal bird. Yes I agree with you, it would take more than a 10 day course of penicillin.

You must be talking about one of Delphi’s bottles.

Dr Schneider seems to disagree with you; he says that ev shows rapid gains of information. All the expansive mutational mechanisms are available in the citations I have been posting and they still demonstrate that multiple selection pressures slow and ultimately stop evolution.

Sorry to tell you this, the mathematics of mutation and selection contradicts what you have just alleged.

So you think that sexual recombination is a form of mutation? You can get rapid and large morphological chan