Annoying creationists [Archive] - Page 19

kleinman

4th June 2007, 09:25 PM

I’m not like evolutionists. I saw the results from the ev model which shows that multiple selection pressures slow evolution and looked to see if empiric data fit the model. The data fits over and over.Nope you aren't like, evolutionists. You like to ignore data. You like to ignore points that refute your entire premise. You saw what you can have ev show and thought you could lie to us about it. I've noticed you stopped claiming population doesn't matter. I wonder why that is? Remember that little foolishness that you use to carry on about? I Do.
Clown fish, do you want to talk more about population and the effects on the mutation and selection process. That is one more example of how you and other evolutionist don’t understand the mathematics of mutation and selection. If you did, you would understand that huge populations don’t give a marked increase in the rates of evolution.
The mathematics is consistent including the concept of the fitness landscape.Of course it is. What is inconsistent is your understanding of either of these two issues. Oh well. BTW, I hope you understand this sentence is a rather amatuerish thing to say.
Oh yes, you clarified the principle of the fitness landscape when you told us that local optimums don’t come to a point like the top of your head.
Clown fish, feel free to post your real example of this mathematics. You can’t do it because that is not how mutation works mathematically and that is not how mutation and selection works in the real world. It works the way Dr Schneider’s ev model shows.With all asumptions built into the model, yes ev is a fine model.. But show me where evolution stops? When is it?You haven't presented any stopped evolution. Interesting...
Clown fish, you don’t have a real example which shows that multiple selection pressures can accelerate evolution. I have posted a case were evolution has stopped. Look back at the citations I have posted, there is at least one case in which evolution has stopped. There are many other cases where evolution has stopped, its called extinction. If you have trouble finding the case, don’t worry, I’ll point it out for you. Just like I pointed out the error in Dr Richard’s equation which you so astutely discovered after it was pointed out to you. You are a very smart clown fish.
Paul and I ran cases that give estimates of these values. It certainly isn’t the 1 bit of information per 11 generation estimate that Dr Schneider obtained with his 256 base genome case. Why don’t you run some cases with ev and make your own estimates?Yawn. It's your job to figure out too slow. We have tens of thousands of years, even millions, and we see adaptation in a mere decade. You have some really hard proofs to make to say slow=stop.
Now don’t be a lazy clown fish, you need to work for your worm.
And while you are doing that, you can ponder what is the selection pressure that evolves a gene de novo, what were the components of the DNA replicase system doing before DNA could be replicated, what is the selection pressure that would evolve a reptile into a bird,… Ah look a gap! Do you feel comfortable there? You are welcome to it.
Still can’t count, can you clown fish. These are gaps, not a gap.
The large colored type is for the benefit of Taffer and clown fish so they can see the real evidence that multiple selection pressures slow and ultimately stop evolution.Funny, I didn't see anything in that quote that said STOP. Interesting.. Can you explain when slow becomes stop? I still haven't seen any math that you presented to explain this little game.
Look carefully little clown fish, if you can’t find it (which is always), I’ll point it out to you.
Kleinman, you are either willfully ignorant, truly stupid or a liar. Which is it?
When it comes to the theory of evolution by mutation and selection, it is none of the above. Some day you may learn the mathematics of mutation and selection, you will then understand that your theory is mathematically impossible and then you will understand the numerous citations which demonstrate this mathematical fact. Poor little clown fish, your theory is a flop.

Here’s another example that shows that multiple selection pressures slow evolution. This is just for you little clown fish.

http://journal.paho.org/?a_ID=335 (http://journal.paho.org/?a_ID=335)
Suboptimal treatment regimens, such as monotherapy or dual therapy, treatment with poor-quality antiretroviral drugs, suboptimal dosing, and poor absorption, may increase the rate at which viral resistance evolves among treated individuals

kjkent1

4th June 2007, 10:50 PM

Sure you can have alteration in the invariant region of the hemoglobin gene. The problem is that it gives a molecule that does not have the proper conformation to function as hemoglobin.That's only a problem if the only possible oxygen transport mechanism for a carbon-based life form is hemoglobin. However, if some other mechanism had evolved first, then the invariance that you see as problematic is no longer at issue -- it's irrelevant.

But, because you believe that hemoglobin was designed by God, you view the fact that any variation on that design, destroys its functionality, as proof of the divine nature of hemoglobin.

This is the predicament of a mindset which assumes only one possible truth, and then attempts to engineer all descendant knowledge as subject to that one truth.

Once you give up that mindset and accept the reality that the universe is the product of an ocean of cascading accidents, which sometimes coalesce as channels of temporal order, everything becomes clear.

Hemoglobin is not a requirement of universe design -- it's an accident -- one which may have been more probable than other alternatives, but not necessarily so. And, if something else had appeared first, then we would be arguing over the invariance present in that something else. But, we're not, because hemoglobin appeared first, so that's what we're arguing over.

I'd still like to see you actually do the math on my question -- it would be a pleasant diversion from so much wasted typing from both sides of the aisle.

Taffer

4th June 2007, 11:33 PM

And look, when I provide a refutation of his claim, I am simply ignored. No surprises there.

I am over with this thread. For real this time. Honest.

joobz

5th June 2007, 05:20 AM

And look, when I provide a refutation of his claim, I am simply ignored. No surprises there.

I am over with this thread. For real this time. Honest.
ALl he does is insult or ignore. presenting anything remotely mathematical and logical is beyond his abilities.

joobz

5th June 2007, 05:32 AM

Clown fish, do you want to talk more about population and the effects on the mutation and selection process. That is one more example of how you and other evolutionist don’t understand the mathematics of mutation and selection. If you did, you would understand that huge populations don’t give a marked increase in the rates of evolution.really? waht is marked? Your accurate use of language is very impressive. :rolleyes: You prove yourself a liar again.

Increaseing pop. in ev decreases the time til perfect creature. Simple.

Oh yes, you clarified the principle of the fitness landscape when you told us that local optimums don’t come to a point like the top of your head.Sorry Kleinman, the thread exists and my point still exists. It is you who ignores it. Pretends it doesn't demonstrate your lies and your willfull ignorance. I know better, and so does everyone here. We find you laughable.

Clown fish, you don’t have a real example which shows that multiple selection pressures can accelerate evolution. I don't need to. WHen has this ever been a requirement? YOU need to show where evolution stops. All evidence shows that evolution is only slowed. (or kills off all the population). BUt if the stress doesn't kill all the population, evolution will occur. Don't cry, Kleinman, you can still believe what you want. It just doesn't have any real effect on reality.
I have posted a case were evolution has stopped.???No you haven't.
Look back at the citations I have posted, there is at least one case in which evolution has stopped. There are many other cases where evolution has stopped, its called extinction. By your argument, multiple pressures result in extinction, since we are all under millions of pressures we will be extinct? some theory. NAstradamus would love you.

If you have trouble finding the case, don’t worry, I’ll point it out for you. Just like I pointed out the error in Dr Richard’s equation which you so astutely discovered after it was pointed out to you. You are a very smart clown fish.

Now don’t be a lazy clown fish, you need to work for your worm.

Still can’t count, can you clown fish. These are gaps, not a gap.

Look carefully little clown fish, if you can’t find it (which is always), I’ll point it out to you.

When it comes to the theory of evolution by mutation and selection, it is none of the above. Some day you may learn the mathematics of mutation and selection, you will then understand that your theory is mathematically impossible and then you will understand the numerous citations which demonstrate this mathematical fact. Poor little clown fish, your theory is a flop.

Here’s another example that shows that multiple selection pressures slow evolution. This is just for you little clown fish.

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

Still have nothing to present? No Math, no actual evidence.
I must assume now that that you are willfullly ignorant liar.

Dr Adequate

5th June 2007, 05:59 AM

No new lies in here, and no math.

He appears to be working on a lie about horseshoe crabs, but evidently it's not finished yet, 'cos he doesn't actually tell the lie. And here it comes:

Meadmaker, you are the one who is proposing that local optimums do not exist. Evolutionists say that the horseshoe crabs have not changed in a quarter of a billion years. I’m sure you evolutionists can speculate that humans evolved from horseshoe crabs and that some horseshoe crabs decided not to make the trek on the fitness landscape.

That was a stupid lie, wasn't it? Not quite as stupid as, say, Lie #5, but pretty darn moronic.

Apart from that, kleinman doesn't seem to have come up with any new lies or magic words, and of course he hasn't done any math.

Dr Adequate

5th June 2007, 06:19 AM

Kleinman, you are either willfully ignorant, truly stupid or a liar. Which is it? The evidence suggests that he's all three.

kleinman

5th June 2007, 09:14 AM

And look, when I provide a refutation of his claim, I am simply ignored. No surprises there.
What refutation? You claim you have a mathematical model that shows that multiple selection pressures evolve more rapidly than single selection pressures. We are all waiting for you to post a single real example of your self evident mathematics.
I am over with this thread. For real this time. Honest.
It’s the combination selection pressures, its driving you evolutionists to extinction. Here are two more selection pressures.
And here it comes:
This is another example of combination selection pressures which slows the evolution or resistant cancer cells. This example is for Dr Schneider and the gang over at the National Cancer Institute. This reference can be found at http://dimacs.rutgers.edu/Workshops/TumorModeling/abstracts.html (http://dimacs.rutgers.edu/Workshops/TumorModeling/abstracts.html)
The genetic instability of tumor cells renders them the ability to rapidly become resistant to many chemotherapies. As a result, there is great interest in selecting combination chemotherapeutic regimens that will overcome resistance and exert synergistic therapeutic activity.

This example is for Taffer on his favorite topic of the evolution of resistance to combination therapy of the HIV virus. Notice how even when resistance has evolved, the combination selection pressures still has benefit for the patient. This abstract can be found at http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=17413693&dopt=Abstract (http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=17413693&dopt=Abstract)
Even patients with extensive resistance to the failing regimen were still receiving benefit from treatment.

joobz

5th June 2007, 10:00 AM

The evidence suggests that he's all three.
I think you are right. Only someone with all three characteristics would continue to quote from studies that clearly refute his entire premise.
http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=17413 693&dopt=Abstract (http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=17413693&dopt=Abstract)
In patients kept on the same virologically failing cART regimen for a median of 6 months, there was considerable accumulation of drug resistance mutations, particularly in patients with initial low level of resistance to the failing regimen. Randomized comparisons of maintenance treatment strategies while awaiting a new suppressive therapy to become available are warranted.

Kleinman=typical, unintelligent intelligent designer: have a theory and look at data supporting it, ignore all evidence that shows the contrary.

What's really funny is that even highly intelligently designed drug treatment strategies can't stop evolution, the most we hope for is a delay in resistance development.

Meadmaker

5th June 2007, 11:28 AM

kjkent1

5th June 2007, 11:29 AM

I think you are right. Only someone with all three characteristics would continue to quote from studies that clearly refute his entire premise.
http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=17413 693&dopt=Abstract (http://www.ncbi.nlm.nih.gov/entrez/queryd.fcgi?cmd=Retrieve&db=PubMed&list_uids=17413693&dopt=Abstract)

Kleinman=typical, unintelligent intelligent designer: have a theory and look at data supporting it, ignore all evidence that shows the contrary.

What's really funny is that even highly intelligently designed drug treatment strategies can't stop evolution, the most we hope for is a delay in resistance development.We're all wasting our time. This is a game for kleinman that he uses to keep himself from cracking up during his night shift in Clovis. He's not interested in an objective search for truth. He's just interested in being annoying.

kleinman, you've finally succeeded in boring me to the point where I'm satisfied to put you on "ignore." Good luck to you and your mission.

Paul C. Anagnostopoulos

5th June 2007, 03:50 PM

Why Paul, you are correct, I haven’t modified ev to apply the selection processes sequentially. I’ll let you have that privilege. Then you can post the model on the internet so everyone can test out the concept. I do have an idea though about which will occur more quickly, sequential or simultaneous selection pressures. We have numerous real examples of which compare the different scenarios and sequential selection pressures evolve far more rapidly than simultaneous selection pressures. So Paul, you are wrong on your second point.
My earlier analysis indicates that Ev already does apply the selection sequentially and cumulatively. So apply them sequentially and cumulatively is unlikely to result in much of a speedup.

~~ Paul

Paul C. Anagnostopoulos

5th June 2007, 03:59 PM

The link to the Dembski paper:

http://web.ecs.baylor.edu/faculty/ma.../ev/index.html
This should be interesting.

~~ Paul

Taffer

5th June 2007, 04:28 PM

Paul C. Anagnostopoulos

6th June 2007, 06:54 AM

Dr Adequate

6th June 2007, 06:56 AM

Kleinman, when you understand what I stated earlier (which you have ignored more then once, now), that evolution is not the emergence of a specific trait, then you will understand why you are wrong. Evolution is the change in allele frequencies over time. The alleles have to exist for this to happen. Well, that's one way of looking at it I guess, but the appearance of a new allele through mutation does in fact change the allele frequencies.

Now, when I did my computer model of simultaneous as opposed to selection pressures, I started the populations off with none of the beneficial alleles, simulated random mutation and selection, and took the "rate of evolution" to be fixations per generation.

How kleinman thinks the rate of evolution should be defined is shrouded in the dense fogs of his brain.

Meadmaker

6th June 2007, 09:40 AM

I read over Dembski's paper once quickly, and now I am reading it more carefully.

My first reaction is that his thesis is essentially correct, although entirely uninteresting.

He has made some mistakes:

At the beginning of section 1.1, he states that Ev's standard model has 131 nucleotides that serve as potential binding sites. He does not realize that every position on the chromosome is evaluated as a binding site. That is 256 nucleotides in the standard model.

In the third paragraph on page 4, he determines what the endogenous information is. He decides to use the bit string target from his search structure in figure 1. This is 131 bits, although it should be 256. However, I see no reason why a more compact representation of the binding site positions can't be used. In particular, the bit string varies in length directly with the size of the chromosome. A table of binding site positions would vary as the product of the number of binding sites and the log of the chromosome size, which increases much more slowly with the size of the chromosome.

On page 5, Dembski compares the efficiencies of random search with Ev's search. He uses a mean value for the number of queries needed for the random search, but only a single value for the number of queries in Ev's search. He should have run Ev's standard model many times with different random seeds and calculated the mean. Also, a population of 64 is entirely arbitrary, yet directly affects his query calculation for Ev. I cut the population from 64 to 16 and ended up with half as many queries. Then I increased it to 256 and ended up with three times as many queries. Finally, why the number of queries is interesting at all I do not know.

~~ Paul

I think, but I'm not certain, that his point is that some people are looking to various evolutionary algorithms as some amazing way of discovering new stuff. He's pointing out that if your goal is to find something, ev, and in general other genetic algorithms, are a lousy way to do it.

Of course, his real point is to get published in a reputable journal so he can gain legitimacy.

What I found interesting was the general implication that ev didn't really discover anything, but just used hidden information contained in the structure of the perceptron. Well, duh. Yes, evolution, and all algorithms based on it, "find" things by being influenced by their environment. The penguind "discovered" that flightless waterfowl who could stand still for very long periods of time were well suited for life on ice floes. Yes, they stole the information that it was very cold from their environment.

Paul C. Anagnostopoulos

6th June 2007, 09:47 AM

I think, but I'm not certain, that his point is that some people are looking to various evolutionary algorithms as some amazing way of discovering new stuff. He's pointing out that if your goal is to find something, ev, and in general other genetic algorithms, are a lousy way to do it.
Perhaps, but he should focus on genetic algorithms if he wants to make that claim. Ev is a simulation of a piece of the real world, and no one is claiming that the real world is efficient. Certainly the number of queries is irrelevant to a system with 10^24 organisms.

What I found interesting was the general implication that ev didn't really discover anything, but just used hidden information contained in the structure of the perceptron. Well, duh. Yes, evolution, and all algorithms based on it, "find" things by being influenced by their environment. The penguind "discovered" that flightless waterfowl who could stand still for very long periods of time were well suited for life on ice floes. Yes, they stole the information that it was very cold from their environment.
Bingo! There is no way to evolve anything from an information-free environment, except if you are interested in truly, utterly, completely random things.

Say, Meadmaker, were you able to find a date for that paper anywhere?

~~ Paul

kleinman

6th June 2007, 10:03 AM

I have to give some credit to kleinman for staying on message. He's got a mantra and he's sticking to it. Multiple selection pressures prevent evolution from happening, and ev demonstrates this quite nicely, according to him. And it's backed up by studies, most of which deal with drug resistance in the face of combination therapies.
You mean you aren’t going to whine that I keep moving the goalposts? That’s been one of the main arguments that evolutionists are trying to make against what the mathematics of ev shows and the real examples of this mathematics.

I agree that most of the studies presented concerns combination therapies for infectious diseases but there are many examples from other scientific disciplines including oncology (which Dr Schneider should be interested in since he works at the National Cancer Institute), agriculture (the effects for herbicides), pest control (the effects of rodenticides) and from the study of ecology.
My own response to that is that multiple selection pressures may be more likely to destroy a local population, and that will indeed prevent evolution, but saying that it "slows" or "stops" evolution is too much of a reach. Meanwhile, ev is a nice little model that shows practically nothing, except demonstrating that supervised learning really works, slowly. Perceptrons weren't very good models for brain cells, and they aren't good models of evolution. (That's not a knock on ev. It does exactly what it says it does. I'm just saying that there's a limit to what it can do.)
If you are going to take this viewpoint, you are in direct contradiction to Gould’s hypothesis of punctuated equilibrium.

If you think that Perceptrons are not a good model for the theory of evolution, you should tell the editors of Nucleic Acids Research because they felt Dr Schneider’s model was worthy to be published. I happen to agree with you Dr Schneider’s approximation of the selection process by using his weight matrix is a contrivance but this contrivance give more rapid accumulation of information than would be obtained with a more realistic mathematical approximation. A more realistic approximation would evaluate each individual mutation to whether it improves fitness or not. I believe this would be a slower process than Dr Schneider’s Perceptron. Dr Schneider’s model brackets the solution to this problem; it gives the best possible case for the mutation and selection process. After all, it does give very rapid information gains for extremely short genomes.
Kleinman also says that it has been mathematically proven that evolution is impossible, but none of us have noticed the proof. There have been some examples of long ev runs, and there have been some discussion of local optima. As for the ev runs, it's all well and good, but as I noted above, I don't think ev is a great simulation of evolution. As for the "local optima", if you want to call it a mathematical proof, you will have to either give the formula for the function which has the local optimum, or find some way to graph some empirical data and show them. That hasn't been done, nor do I think it can be done. To the extent that the concept makes sense, I don't think any species is at a true local optimum, because I think that there is some change that could be made that would improve breeding success and transmission. However, I must admit that the horseshoe crab was a good example of a species that must be somewhere near a "local optimum".
If you think that ev is not a great simulation for evolution, write a selection process that speeds up the rate of information gain. You continue to miss the fact that ev accumulates information very rapidly for short genomes. It is the longer genomes and the multiple selection conditions that confound the trek to a local optimum in the fitness landscape. Ev does an excellent job in simulating these effects and this is what reality shows. If multiple selection pressures could accelerate evolution, I’m sure you evolutionists would post examples of this.
In short, it's an interesting message, but the math is pretty much conceptual. It doesn't amount to proof.
It is a message based on a peer reviewed and published computer simulation of random point mutation and natural selection. I told Dr Schneider last year than once evolutionist realize what his model really shows, his model would be discredited by evolutionists. You are just another evolutionist on this ever growing list. I find it interesting that a computer simulation that has been criticized for years by IDers is now being criticized by evolutionists. I happen to believe that Dr Schneider has made a plausible model of the mutation and selection process and that it demonstrates the way mutation and selection actually works as I have been citing. When will you post an example of multiple selection pressures accelerating evolution?
Kleinman, Anything to add to your position?
Of course, I will continue to post examples of multiple selection pressures slowing and ultimately stopping evolution.
We're all wasting our time. This is a game for kleinman that he uses to keep himself from cracking up during his night shift in Clovis. He's not interested in an objective search for truth. He's just interested in being annoying.
Lita’ gator, your data is out of date. I am cracking up, with laughter, as I post objective evidence of multiple selection pressures slowing and ultimately stopping evolution. Annoying evolutionists is icing on the cake.
kleinman, you've finally succeeded in boring me to the point where I'm satisfied to put you on "ignore." Good luck to you and your mission.
You evolutionists always say this kind of stuff. This isn’t the first time you’ve said this. Taffer said the same thing a few posts ago and he is already posting again a couple of posts down. What do you think you are doing? Do you think that you can take the ball home and the game is over? You evolutionists can be so silly. Just because you can’t even see the goalposts you think the game doesn’t go on?
Why Paul, you are correct, I haven’t modified ev to apply the selection processes sequentially. I’ll let you have that privilege. Then you can post the model on the internet so everyone can test out the concept. I do have an idea though about which will occur more quickly, sequential or simultaneous selection pressures. We have numerous real examples of which compare the different scenarios and sequential selection pressures evolve far more rapidly than simultaneous selection pressures. So Paul, you are wrong on your second point.My earlier analysis indicates that Ev already does apply the selection sequentially and cumulatively. So apply them sequentially and cumulatively is unlikely to result in much of a speedup.
What you are seeing is the dominance of spurious binding errors initially and then once binding errors are reduced then the model locks into a local optimum which doesn’t allow the selection conditions to completely evolve. You may think it is unlikely that allowing the selection conditions to evolve sequentially will change this behavior of the model, I don’t mind letting this issue hang out in the breeze. Evolutionists are abandoning ev in droves anyway.
The link to the Dembski paper:This should be interesting.
I notice the link doesn’t work but I downloaded the paper yesterday and this paper is very critical of how Dr Schneider used ev.
Evolution is the change in allele frequencies over time. The alleles have to exist for this to happen.
Does this mean you finally understand that there is no way to evolve a gene de novo?
Gah, someone stop me! It's like I'm a sucker for punishment or something.
Somebody stop Taffer before he posts again. My suggestion to you Taffer is to go home and sort your sock drawer and ponder why you are getting a graduate degree in a mathematically impossible theory. This has proven to be very therapeutic for Delphi.

Here are more citations which show that multiple selection pressures slow and ultimately stop evolution.

http://www.annclinlabsci.org/cgi/content/abstract/32/4/406 (http://www.annclinlabsci.org/cgi/content/abstract/32/4/406)
In recent years, resistance testing has become an important tool in optimizing the combination therapy for treating HIV infected individuals. The identification of resistance mutations has allowed physicians to select the antiviral agents with maximum therapeutic benefic and minimum toxic side effects.

http://www.inspection.gc.ca/english/plaveg/bio/resist/disdoce.shtml (http://www.inspection.gc.ca/english/plaveg/bio/resist/disdoce.shtml)
There is a need to develop broadleaf combinations or mixtures to control glyphosate and multiple HT volunteers pre-seed. For example, 2,4-D, MCPA, bromoxynil and a low residual sulfonylurea like tribenuron methyl in combination with glyphosate would provide broad-spectrum pre-seed weed control including volunteer glyphosate HT canola. In some situations amitrole and paraquat could provide effective pre-seed control and resistance management for volunteer HT canola.
And
Herbicide mixtures to manage volunteers and reduce selection pressure could be a requirement for future HT crop releases.
Taffer, notice how I use font size and color to help you see the point in these posts that multiple selection pressures slow evolution? And Meadmaker, notice how one of these references is to infectious diseases and the other to agriculture?

Paul C. Anagnostopoulos

6th June 2007, 10:09 AM

Here are some interesting PowerPoint presentations by Robert J. Marks II, the coauthor of the Dembski paper:

http://web.ecs.baylor.edu/faculty/marks/Marks/ChristainFacultyNetwork/index_apologetics.htm

~~ Paul

Dr Adequate

6th June 2007, 10:17 AM

I notice that kleinman's usual screaming, twitching, raving, lying and babbling has now been supplemented by the use of colored fonts.

I always wondered how people got this way.

Dr Adequate

6th June 2007, 10:27 AM

You mean you aren’t going to whine that I keep moving the goalposts? That’s been one of the main arguments that evolutionists are trying to make against what the mathematics of ev shows and the real examples of this mathematics.

I agree that most of the studies presented concerns combination therapies for infectious diseases but there are many examples from other scientific disciplines including oncology (which Dr Schneider should be interested in since he works at the National Cancer Institute), agriculture (the effects for herbicides), pest control (the effects of rodenticides) and from the study of ecology.

If you are going to take this viewpoint, you are in direct contradiction to Gould’s hypothesis of punctuated equilibrium.

If you think that Perceptrons are not a good model for the theory of evolution, you should tell the editors of Nucleic Acids Research because they felt Dr Schneider’s model was worthy to be published. I happen to agree with you Dr Schneider’s approximation of the selection process by using his weight matrix is a contrivance but this contrivance give more rapid accumulation of information than would be obtained with a more realistic mathematical approximation. A more realistic approximation would evaluate each individual mutation to whether it improves fitness or not. I believe this would be a slower process than Dr Schneider’s Perceptron. Dr Schneider’s model brackets the solution to this problem; it gives the best possible case for the mutation and selection process. After all, it does give very rapid information gains for extremely short genomes.

If you think that ev is not a great simulation for evolution, write a selection process that speeds up the rate of information gain. You continue to miss the fact that ev accumulates information very rapidly for short genomes. It is the longer genomes and the multiple selection conditions that confound the trek to a local optimum in the fitness landscape. Ev does an excellent job in simulating these effects and this is what reality shows. If multiple selection pressures could accelerate evolution, I’m sure you evolutionists would post examples of this.

It is a message based on a peer reviewed and published computer simulation of random point mutation and natural selection. I told Dr Schneider last year than once evolutionist realize what his model really shows, his model would be discredited by evolutionists. You are just another evolutionist on this ever growing list. I find it interesting that a computer simulation that has been criticized for years by IDers is now being criticized by evolutionists. I happen to believe that Dr Schneider has made a plausible model of the mutation and selection process and that it demonstrates the way mutation and selection actually works as I have been citing. When will you post an example of multiple selection pressures accelerating evolution?

Of course, I will continue to post examples of multiple selection pressures slowing and ultimately stopping evolution.

Lita’ gator, your data is out of date. I am cracking up, with laughter, as I post objective evidence of multiple selection pressures slowing and ultimately stopping evolution. Annoying evolutionists is icing on the cake.

You evolutionists always say this kind of stuff. This isn’t the first time you’ve said this. Taffer said the same thing a few posts ago and he is already posting again a couple of posts down. What do you think you are doing? Do you think that you can take the ball home and the game is over? You evolutionists can be so silly. Just because you can’t even see the goalposts you think the game doesn’t go on?

What you are seeing is the dominance of spurious binding errors initially and then once binding errors are reduced then the model locks into a local optimum which doesn’t allow the selection conditions to completely evolve. You may think it is unlikely that allowing the selection conditions to evolve sequentially will change this behavior of the model, I don’t mind letting this issue hang out in the breeze. Evolutionists are abandoning ev in droves anyway.

I notice the link doesn’t work but I downloaded the paper yesterday and this paper is very critical of how Dr Schneider used ev.

Does this mean you finally understand that there is no way to evolve a gene de novo?

Somebody stop Taffer before he posts again. My suggestion to you Taffer is to go home and sort your sock drawer and ponder why you are getting a graduate degree in a mathematically impossible theory. This has proven to be very therapeutic for Delphi.

Here are more citations which show that multiple selection pressures slow and ultimately stop evolution.

http://www.annclinlabsci.org/cgi/content/abstract/32/4/406 (http://www.annclinlabsci.org/cgi/content/abstract/32/4/406)

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

And

Taffer, notice how I use font size and color to help you see the point in these posts that multiple selection pressures slow evolution? And Meadmaker, notice how one of these references is to infectious diseases and the other to agriculture? You're talking crap, we know you're talking crap, you know you're talking crap, you know we know you're talking crap, we know you know you're talking crap, and we know you know we know you're talking crap. What we don't know is why you're talking crap when you know we know you're talking crap. Why are you talking crap?

kleinman

6th June 2007, 11:27 AM

You're talking crap, …
Now cheese wiz, you know I use more gentility when talking about the theory of evolution. I prefer to use the word compost when speaking of the theory of evolution. For example, the mathematics of ev is turning the theory of evolution into a pile of steaming decomposing compost.

joobz

6th June 2007, 01:01 PM

You mean you aren’t going to whine that I keep moving the goalposts?
Really, you don't move the goals?

For clarity, I have summarized the key points of this conversation. I think we have a new lie here.

If you studied ev, you would understand this. If you examined the real cases of combination therapy for the treatment of HIV, combination therapy for the treatment of TB, combination pesticides, combination herbicides, combination rodenticides, you would see real examples of what ev demonstrates and what the fitness landscape requires. Mutation and selection can not and does not do what evolutionists allege, it is mathematically impossible.

It is the number of directional selection pressures and genome length which dominate the mathematics of mutation and selection. There is no reason to believe that frame shift mutations, translocations, duplications or any other way of scrambling a genome is going to change the underlying mathematics of mutation and selection.

This is your concrete basis for not worring about it?

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 scenarios
Seems like evolution has a mathematical basis after all.

So how does this work with HIV? Here is a quote from an article located at http://www.cdc.gov/ncidod/eid/vol3no3/burke.htm

Human immunodeficiency virus (HIV)-1, like all retroviruses, is "diploid." Each viral particle contains two RNA strands of positive polarity, each full length and potentially able to replicate (1). No other virus families, RNA or DNA, are diploid. Typically both RNA strands in a retroviral particle derive from the same parent provirus. However, if an infected cell simultaneously harbors two different proviruses, one RNA transcript from each provirus can be encapsidated into a single "heterozygous" virion. When this virion subsequently infects a new cell, the reverse transcriptase may jump back and forth between the two RNA templates so that the newly synthesized retroviral DNA sequence is recombinant between that of the two parents (2). All subsequent progeny virions will be of this recombinant genotype. HIV-1 strains with chimeric genomes thought to have arisen through homologous recombination have recently been discovered in nature (3).
This is a property unique to the retroviruses, are you trying to generalize this phenomenon to the entire theory of evolution? This appears like a baseless extrapolation.

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.

No it doesn’t, it only shows that you know how to make a baseless extrapolation.

I see, when evolutionists adjust their theory, this is scientific research, when I adjust my theory, I’m moving the goal posts.
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.

How sad for you, the facts just won't go away...BTW, none of those papers mention stopped evolution. I wonder why?

kleinman

6th June 2007, 02:28 PM

Really, you don't move the goals?
Meadmaker doesn’t seem to think so; he realizes I keep this thread on topic. Unlike your posts which flop around like a clown fish out of water. Now if you could post a citation which shows that multiple selection pressures accelerate evolution that would be on topic. Alas, I think it is more likely that you will describe how ribose can be formed nonenzymatically in the primordial soup.

joobz

6th June 2007, 02:47 PM

Meadmaker doesn’t seem to think so; he realizes I keep this thread on topic. Unlike your posts which flop around like a clown fish out of water. :D :D You mistake his politeness for acceptance of your position. It is blatantly obvious you have switched tactics several times throughout this thread.

what part of ...

For clarity, I have summarized the key points of this conversation. I think we have a new lie here.

If you studied ev, you would understand this. If you examined the real cases of combination therapy for the treatment of HIV, combination therapy for the treatment of TB, combination pesticides, combination herbicides, combination rodenticides, you would see real examples of what ev demonstrates and what the fitness landscape requires. Mutation and selection can not and does not do what evolutionists allege, it is mathematically impossible.

It is the number of directional selection pressures and genome length which dominate the mathematics of mutation and selection. There is no reason to believe that frame shift mutations, translocations, duplications or any other way of scrambling a genome is going to change the underlying mathematics of mutation and selection.

This is your concrete basis for not worring about it?

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 scenarios
Seems like evolution has a mathematical basis after all.

So how does this work with HIV? Here is a quote from an article located at http://www.cdc.gov/ncidod/eid/vol3no3/burke.htm

Human immunodeficiency virus (HIV)-1, like all retroviruses, is "diploid." Each viral particle contains two RNA strands of positive polarity, each full length and potentially able to replicate (1). No other virus families, RNA or DNA, are diploid. Typically both RNA strands in a retroviral particle derive from the same parent provirus. However, if an infected cell simultaneously harbors two different proviruses, one RNA transcript from each provirus can be encapsidated into a single "heterozygous" virion. When this virion subsequently infects a new cell, the reverse transcriptase may jump back and forth between the two RNA templates so that the newly synthesized retroviral DNA sequence is recombinant between that of the two parents (2). All subsequent progeny virions will be of this recombinant genotype. HIV-1 strains with chimeric genomes thought to have arisen through homologous recombination have recently been discovered in nature (3).
This is a property unique to the retroviruses, are you trying to generalize this phenomenon to the entire theory of evolution? This appears like a baseless extrapolation.

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.

No it doesn’t, it only shows that you know how to make a baseless extrapolation.

I see, when evolutionists adjust their theory, this is scientific research, when I adjust my theory, I’m moving the goal posts.
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.

do you not understand. You are a liar. This is only one demonstration (out of many) of your intellectual dishonesty. The fact that you go back to HIV as example of stopped evolution is another.

kleinman

6th June 2007, 03:32 PM

Meadmaker doesn’t seem to think so; he realizes I keep this thread on topic. Unlike your posts which flop around like a clown fish out of water.You mistake his politeness for acceptance of your position. It is blatantly obvious you have switched tactics several times throughout this thread.
Obviously, clown fish does not know how to post a citation which supports his position that multiple selection pressures accelerate evolution, probably because he doesn’t have any. So let see if clown fish can take instruction. Here is another citation which shows that multiple selection pressure slow evolution.

http://www.people.fas.harvard.edu/~beerenw/Altmann2007.pdf (http://www.people.fas.harvard.edu/~beerenw/Altmann2007.pdf)
Combining drugs from different classes can slow down the emergence of resistant variants substantially, because mutants that are resistant to all components are unlikely to pre-exist, and new variants need to generate several escape mutations while retaining the ability of effective replication.
See how simple it is clown fish, why don’t you flop one out on your next post that supports your mathematically and scientifically baseless thinking. Hey Taffer, how do you think resistance emerges?

Meadmaker

6th June 2007, 03:51 PM

You mean you aren’t going to whine that I keep moving the goalposts?

I can't speak for the first 100 pages of the thread, but lately your goalposts have been positively rigid.

Of course, I will continue to post examples of multiple selection pressures slowing and ultimately stopping evolution.

I don't know why, though. We all understand that combination treatments (of bacteria, parasites, weeds, whatever) are more effective and less likely to produce resistant strains. More examples won't make that point any better than the ones you have already made. To get further, though, you will have to do better explaining how that "slows", or even more difficult "stops" evolution.

joobz

6th June 2007, 04:15 PM

Obviously, clown fish does not know how to post a citation which supports his position that multiple selection pressures accelerate evolution, ....[snip]
You utter baffoon. While you continue to strawman, realize that NO ONE HERE thinks that's my position. I have never said that is my position. MY position is that Multiple selection pressures (what ever that means) doesn't stop evolution.
SLOW does not equal STOP.
You are again being wholly dishonest.

joobz

6th June 2007, 04:34 PM

I can't speak for the first 100 pages of the thread, but lately your goalposts have been positively rigid.
Since you have been here, yes. But he has set varied ones.

He's play the macro vs. micro evolution game
1.) de novo gene formation is macro evolution (discounted by evidence)
2.) Speciation is macro evolution (provided evidence)
he then changed definitions of speciation...

ev proves evolution is too slow using "realistic mutation rates" (data was given to show mutation rate highly variable throughout time and not a good assumption)

ev proves evolution is too slow because population size doesn't matter (This was also discounted by ev runs)

Multiple selection pressures prove evolution is too slow (this one was rapidly discounted by resisistance data)

Multiple "directional" selection pressures prove evolution is too slow: this one makes absolutely no sense and he has held a double fisted grip to the poor reality.

kleinman

6th June 2007, 05:19 PM

You mean you aren’t going to whine that I keep moving the goalposts?I can't speak for the first 100 pages of the thread, but lately your goalposts have been positively rigid.
I’ll make it easy for you, read my first post on the Evolutionisdead forum located at http://www.evolutionisdead.com/forum/viewtopic.php?t=348&sid=05cba3e6ad1c6a1ee1c550b01ee8815d (http://www.evolutionisdead.com/forum/viewtopic.php?t=348&sid=05cba3e6ad1c6a1ee1c550b01ee8815d) .This was my first public statement about ev. The only thing that has been added to the original hypothesis is the reason why ev evolves information so slowly and of course that is the multiple selection conditions in combination with large genome lengths.
Of course, I will continue to post examples of multiple selection pressures slowing and ultimately stopping evolution.I don't know why, though. We all understand that combination treatments (of bacteria, parasites, weeds, whatever) are more effective and less likely to produce resistant strains. More examples won't make that point any better than the ones you have already made. To get further, though, you will have to do better explaining how that "slows", or even more difficult "stops" evolution.
I’m going to continue to post citations so you will have to pardon my redundancy to you; however there are many that don’t accept what ev is showing and what reality is showing. That said, it is very straight forward to understand why multiple selection pressures slow evolution. Mutation and selection is a sorting process. If you are sorting a database and have a single primary key, it is relatively easy and fast to do the sort. If you add additional keys to the database, the sorting process becomes more complex. Now consider while doing the sort of the database, you randomly change characters in the different fields of the database, it becomes easy to see why this process would become profoundly slow. Add to this that the sorting conditions are changing with time and it becomes absurdly difficult to do the sort. It is clear that selection pressures are what stops evolution, we call this extinction. A single overwhelming selection pressure can cause extinction, this is easy to see. What is more difficult to see is how combinations of less overwhelming selection pressures can cause extinction but there are examples of this. The particular example of using a bacterium which produces 4 cytotoxins to suppress mosquito larvae is an example. Despite decades of usage of this mosquito control technique, resistance to all four of the toxins can only be achieved using genetically modified bacteria that produce fewer toxins. From an ecological point of view, it is easy to see how several different selection pressures can lead to the extinction of a species. Reduce the habitat, reduce the food supply a little, chemically alter the water supply to make it slightly toxic and so on and you can drive a species to extinction where any single selection pressure would not cause extinction. Each additional selection pressure slows the creatures’ ability to adapt to the pressures especially if the creature must depend on mutation and selection to adapt. This is what the mathematics of ev shows and this is what reality shows. There is/are no selection pressure(s) that would drive a reptile to evolve into a bird. Reptiles are highly efficient creatures that would have to make a huge trek on the fitness landscape to make the transformation into birds. This type of transformation can only occur in the minds of evolutionists and writers on the SciFi channel. Mutation and selection does not work this way. Ev shows this and the dozens of citations posted shows this.
Obviously, clown fish does not know how to post a citation which supports his position that multiple selection pressures accelerate evolution,While you continue to strawman, realize that NO ONE HERE thinks that's my position. I have never said that is my position. MY position is that Multiple selection pressures (what ever that means) doesn't stop evolution.
Poor clown fish, he has never heard of extinction but at least now this flopping fish acknowledges that multiple selection pressures slow evolution. Here’s a worm for you for finally figuring this out. You are such a smart clown fish; you must have been at the top of your school.

joobz

6th June 2007, 06:16 PM

I’ll make it easy for you, read my first post on the Evolutionisdead forum located at http://www.evolutionisdead.com/forum/viewtopic.php?t=348&sid=05cba3e6ad1c6a1ee1c550b01ee8815d (http://www.evolutionisdead.com/forum/viewtopic.php?t=348&sid=05cba3e6ad1c6a1ee1c550b01ee8815d) .This was my first public statement about ev. The only thing that has been added to the original hypothesis is the reason why ev evolves information so slowly and of course that is the multiple selection conditions in combination with large genome lengths.Don't forget the hundereds of posts that discounted your ENTIRE theory. Oh well. You'll continue to be delusional.

I’m going to continue to post citationsbecause you have no argument, and simply wish to present an entirely silly and moronic theory.
so you will have to pardon my redundancy because you are a pathological liar?

Poor clown fish, he has never heard of extinction but at least now this flopping fish acknowledges that multiple selection pressures slow evolution. Here’s a worm for you for finally figuring this out. You are such a smart clown fish; you must have been at the top of your school.microevolution exists, but "macroevolution" doesn't. Macroevolution doesn't exist becuase things go extinct before it can happen. Yet species have existed for millions of years and species exist today that didn't exist millions of years ago... Hmmm, something in your logic is missing....I wonder what that is...

Oh I know, your completely delusional.

Mr. Scott

6th June 2007, 06:41 PM

Is this why you hate God and now have a reason to hate physicians?

Wow, how did you pull that from your deluded imagination? Suggesting I hate God is like suggesting I hate Darth Vader. How does one hate a fictional character?

I have nothing but admiration for physicians who expertly use scientific principles and practices to heal. A physician who ignores evidence when it conflicts with "faith?" Sure, my feeling towards them is very much like hate. I'd never go to a doctor who discounted evidence-based medical knowledge merely because he felt it conflicted with a phrase cherry-picked from an ancient holy book.

Sorry if anyone thinks this post is off-topic, but the title of the thread is "Annoying Creationists," after all.

Carry on...

kleinman

6th June 2007, 07:11 PM

I’ll make it easy for you, read my first post on the Evolutionisdead forum located at http://www.evolutionisdead.com/forum/viewtopic.php?t=348&sid=05cba3e6ad1c6a1ee1c550b01e e8815d .This was my first public statement about ev. The only thing that has been added to the original hypothesis is the reason why ev evolves information so slowly and of course that is the multiple selection conditions in combination with large genome lengths.Don't forget the hundereds of posts that discounted your ENTIRE theory. Oh well. You'll continue to be delusional.
That explains why your arguments are so weak; you got them at a discount store.
I’m going to continue to post citations.because you have no argument, and simply wish to present an entirely silly and moronic theory.
I understand you now, you have an argument that you can not support with citations, which should convince brainwashed evolutionists around the world. You like to tell fish stories, don’t you clown fish.
so you will have to pardon my redundancybecause you are a pathological liar?
Oh no little clown fish, I have to post numerous citations for brainwashed evolutionists like you and its working, you have finally understood that multiple selection pressures slow evolution.
Poor clown fish, he has never heard of extinction but at least now this flopping fish acknowledges that multiple selection pressures slow evolution. Here’s a worm for you for finally figuring this out. You are such a smart clown fish; you must have been at the top of your school.microevolution exists, but "macroevolution" doesn't. Macroevolution doesn't exist becuase things go extinct before it can happen. Yet species have existed for millions of years and species exist today that didn't exist millions of years ago... Hmmm, something in your logic is missing....I wonder what that is...
You wouldn’t let a little gap in a theory mean that you should throw out the whole theory, would you little clown fish? There’s nothing missing in my hypothesis that a little cooperative chemistry would solve.
Oh I know, your completely delusional.
At least I have citations to support my delusions, you only have whining and flopping around to support yours. So here are a couple more citations that show multiple selection pressures slow and ultimately stop evolution. Now I want you all to realize that clown fish believes that multiple selection pressures slow evolution but he does not believe that multiple selection pressure stops evolution (yet).

http://www.ecologyandsociety.org/vol3/iss2/art12/ (http://www.ecologyandsociety.org/vol3/iss2/art12/)
Protease inhibitors of HIV prevent infected cells from producing infectious virus. The overall dynamics are very similar to the case of reverse transcriptase inhibitors, because the infectious virus particles present initially decay very rapidly. Combination of reverse transcriptase and protease inhibitors has led to tremendous success in HIV therapy.

Essentially, all of these drugs, if used as single antiviral therapy, lead to the emergence of resistant virus mutants. The pattern is often similar. Initially, there is a decay in virus abundance, but after some time, the virus resurges. The decisive treatment breakthrough was to combine several drugs at once. For about 2 years, this combination therapy has proved to be a tremendous success. In many patients, virus abundance in the blood decays below detection limit within weeks of treatment and can remain undetectable for years.

http://www.globalforumhealth.org/filesupld/interventions/Interventions%20Anex%201.pdf (http://www.globalforumhealth.org/filesupld/interventions/Interventions%20Anex%201.pdf)
Antimicrobial exposure inevitably exerts a selection pressure on the pathogen being actively treated, as well as commensal organisms, 80% to 90% of which are currently non-culturable (Wilson & Blitchington, 1996; Langendijk et al 1995). Therefore, its potential to act as a reservoir for antimicrobial resistance genes may be immense. As the “normal” commensal flora acts to inhibit the attachment and multiplication of pathogenic micro-organisms by various mechanisms, its disturbance may also facilitate colonization with exogenously acquired pathogens. Consequently, the aim of antimicrobial therapy must be to destroy the pathogen rapidly and efficiently, while producing the least amount of “collateral” damage. This can be achieved by giving careful consideration to the agent employed, its spectrum of activity, method of administration, penetration to the site of infection, magnitude of dose, frequency of administration, duration of therapy, and the use of agents in combination, such as in TB and HIV therapy.
Now clown fish, you check at your local discount store and see if you can get some more discount posts. Perhaps you can find a discount citation that shows that selection pressures don’t cause extinction.
Is this why you hate God and now have a reason to hate physicians?Wow, how did you pull that from your deluded imagination? Suggesting I hate God is like suggesting I hate Darth Vader. How does one hate a fictional character?
How long did you have to think about this response pussycat?
I have nothing but admiration for physicians who expertly use scientific principles and practices to heal. A physician who ignores evidence when it conflicts with "faith?" Sure, my feeling towards them is very much like hate. I'd never go to a doctor who discounted evidence-based medical knowledge merely because he felt it conflicted with a phrase cherry-picked from an ancient holy book.
Why pussycat, the evidence shows that multiple selection pressures slow and ultimately stop evolution. That’s also what ev shows. So the evidence and the mathematics show that the rust age theory of evolution is wrong. Isn’t that interesting, it is also in agreement with an ancient holy book.
Sorry if anyone thinks this post is off-topic, but the title of the thread is "Annoying Creationists," after all.

Carry on...
It doesn’t bother me at all pussycat, feel free to come to this thread and cough up a fur ball whenever you need.

In the meantime, you evolutionists work on your posts and I’ll continue to post citations next week that show that multiple selection pressures slow and ultimately stop evolution. For those of you new this thread, this is what the ev computer simulation of mutation and selection shows and this is what reality shows. You all have a good week end.

joobz

6th June 2007, 07:38 PM

Oh no little clown fish, I have to post numerous citations for brainwashed evolutionists like you and its working,
:D It's really funny watching you make a complete fool of yourself. Please, continue presenting more citations that demonstrate that evolution occurs. Why don't you also claim that they prove mushroom gravy will reverse global warming. There's about as much evidence of that in those citations as in your mathematically retarded theory.

joobz

6th June 2007, 07:53 PM

Dr Adequate

6th June 2007, 09:40 PM

Now cheese wiz, you know I use more gentility when talking about the theory of evolution. I prefer to use the word compost when speaking of the theory of evolution. For example, the mathematics of ev is turning the theory of evolution into a pile of steaming decomposing compost.

Meadmaker doesn’t seem to think so; he realizes I keep this thread on topic. Unlike your posts which flop around like a clown fish out of water. Now if you could post a citation which shows that multiple selection pressures accelerate evolution that would be on topic. Alas, I think it is more likely that you will describe how ribose can be formed nonenzymatically in the primordial soup.
Obviously, clown fish does not know how to post a citation which supports his position that multiple selection pressures accelerate evolution, probably because he doesn’t have any. So let see if clown fish can take instruction. Here is another citation which shows that multiple selection pressure slow evolution.

http://www.people.fas.harvard.edu/~beerenw/Altmann2007.pdf (http://www.people.fas.harvard.edu/~beerenw/Altmann2007.pdf)

See how simple it is clown fish, why don’t you flop one out on your next post that supports your mathematically and scientifically baseless thinking. Hey Taffer, how do you think resistance emerges?

I’ll make it easy for you, read my first post on the Evolutionisdead forum located at http://www.evolutionisdead.com/forum/viewtopic.php?t=348&sid=05cba3e6ad1c6a1ee1c550b01ee8815d (http://www.evolutionisdead.com/forum/viewtopic.php?t=348&sid=05cba3e6ad1c6a1ee1c550b01ee8815d) .This was my first public statement about ev. The only thing that has been added to the original hypothesis is the reason why ev evolves information so slowly and of course that is the multiple selection conditions in combination with large genome lengths.

I’m going to continue to post citations so you will have to pardon my redundancy to you; however there are many that don’t accept what ev is showing and what reality is showing. That said, it is very straight forward to understand why multiple selection pressures slow evolution. Mutation and selection is a sorting process. If you are sorting a database and have a single primary key, it is relatively easy and fast to do the sort. If you add additional keys to the database, the sorting process becomes more complex. Now consider while doing the sort of the database, you randomly change characters in the different fields of the database, it becomes easy to see why this process would become profoundly slow. Add to this that the sorting conditions are changing with time and it becomes absurdly difficult to do the sort. It is clear that selection pressures are what stops evolution, we call this extinction. A single overwhelming selection pressure can cause extinction, this is easy to see. What is more difficult to see is how combinations of less overwhelming selection pressures can cause extinction but there are examples of this. The particular example of using a bacterium which produces 4 cytotoxins to suppress mosquito larvae is an example. Despite decades of usage of this mosquito control technique, resistance to all four of the toxins can only be achieved using genetically modified bacteria that produce fewer toxins. From an ecological point of view, it is easy to see how several different selection pressures can lead to the extinction of a species. Reduce the habitat, reduce the food supply a little, chemically alter the water supply to make it slightly toxic and so on and you can drive a species to extinction where any single selection pressure would not cause extinction. Each additional selection pressure slows the creatures’ ability to adapt to the pressures especially if the creature must depend on mutation and selection to adapt. This is what the mathematics of ev shows and this is what reality shows. There is/are no selection pressure(s) that would drive a reptile to evolve into a bird. Reptiles are highly efficient creatures that would have to make a huge trek on the fitness landscape to make the transformation into birds. This type of transformation can only occur in the minds of evolutionists and writers on the SciFi channel. Mutation and selection does not work this way. Ev shows this and the dozens of citations posted shows this.

Poor clown fish, he has never heard of extinction but at least now this flopping fish acknowledges that multiple selection pressures slow evolution. Here’s a worm for you for finally figuring this out. You are such a smart clown fish; you must have been at the top of your school.

That explains why your arguments are so weak; you got them at a discount store.

I understand you now, you have an argument that you can not support with citations, which should convince brainwashed evolutionists around the world. You like to tell fish stories, don’t you clown fish.

Oh no little clown fish, I have to post numerous citations for brainwashed evolutionists like you and its working, you have finally understood that multiple selection pressures slow evolution.

You wouldn’t let a little gap in a theory mean that you should throw out the whole theory, would you little clown fish? There’s nothing missing in my hypothesis that a little cooperative chemistry would solve.

At least I have citations to support my delusions, you only have whining and flopping around to support yours. So here are a couple more citations that show multiple selection pressures slow and ultimately stop evolution. Now I want you all to realize that clown fish believes that multiple selection pressures slow evolution but he does not believe that multiple selection pressure stops evolution (yet).

http://www.ecologyandsociety.org/vol3/iss2/art12/ (http://www.ecologyandsociety.org/vol3/iss2/art12/)

http://www.globalforumhealth.org/filesupld/interventions/Interventions%20Anex%201.pdf (http://www.globalforumhealth.org/filesupld/interventions/Interventions%20Anex%201.pdf)

Now clown fish, you check at your local discount store and see if you can get some more discount posts. Perhaps you can find a discount citation that shows that selection pressures don’t cause extinction.

How long did you have to think about this response pussycat?

Why pussycat, the evidence shows that multiple selection pressures slow and ultimately stop evolution. That’s also what ev shows. So the evidence and the mathematics show that the rust age theory of evolution is wrong. Isn’t that interesting, it is also in agreement with an ancient holy book.

It doesn’t bother me at all pussycat, feel free to come to this thread and cough up a fur ball whenever you need.

In the meantime, you evolutionists work on your posts and I’ll continue to post citations next week that show that multiple selection pressures slow and ultimately stop evolution. For those of you new this thread, this is what the ev computer simulation of mutation and selection shows and this is what reality shows. You all have a good week end. I think the only new lie here is where you pretended that joobz had "never heard of extinction".

Apart from that, you haven't thought up any new lies, you haven't recited any new pathetic magic words, and of course you have done no math.

Dr Adequate

6th June 2007, 09:52 PM

I should like to ask kleinman again the question that he is too frightened to answer:

You're talking crap, we know you're talking crap, you know you're talking crap, you know we know you're talking crap, we know you know you're talking crap, and we know you know we know you're talking crap. What we don't know is why you're talking crap when you know we know you're talking crap. Why are you talking crap?

Dr Adequate

6th June 2007, 10:25 PM

I have to give some credit to kleinman for staying on message. He's got a mantra and he's sticking to it. Multiple selection pressures prevent evolution from happening, and ev demonstrates this quite nicely, according to him. No, actually, from what I can discover from google it seems that he's only been whining out this crap about "multiple selection pressures" for the last couple of months, whereas he's been exposing himself as a liar on this thread since last November,

It just seems like the dullwitted bore has been gabbling out this gibberish about "multiple selection pressures" forever. In fact, this is some new garbage that he's made up in his crazy little head many months after he started posting.

Taffer

6th June 2007, 11:46 PM

Oh good, kleinman has ignored my refutation of his sources. What a surprise. :rolleyes:

I think I shall go away now.

Taffer

6th June 2007, 11:50 PM

Well, that's one way of looking at it I guess, but the appearance of a new allele through mutation does in fact change the allele frequencies.

An allele frequency cannot change until it exists. I would not classify a frequency change from q=0 to q>0 as a change in allele frequency, because that would suggest knowledge of the allele before hand (i.e. we knew what the allele was, and were judging it to be 0).

I guess this all comes down to your definitions, though. Even if you include all possible alleles, the rate at which they arise (the rate of mutation), is completely independant of any selection pressures.

Now, when I did my computer model of simultaneous as opposed to selection pressures, I started the populations off with none of the beneficial alleles, simulated random mutation and selection, and took the "rate of evolution" to be fixations per generation.

That is a good way of looking at it. It all boils down to the rate at which the allele frequencies change over time.

If you include mutation in your "rate of evolution", at each locus this would basically be an added constant. And if we look at the equations (as you've posted a few pages back), we see that this is so. What's funny, though, is that kleinman thinks that "mutation" and "recombination" are two completely different things. Really, they're just two different mechanisms of developing variation in a population.

How kleinman thinks the rate of evolution should be defined is shrouded in the dense fogs of his brain.

Many things are shrouded in a dense fog in his brain.

Mr. Scott

7th June 2007, 06:17 AM

To "Wow, how did you pull that from your deluded imagination? Suggesting I hate God is like suggesting I hate Darth Vader. How does one hate a fictional character?" Kleinman responded:

How long did you have to think about this response pussycat?

About one minute, the last 59 seconds of which I needed to pick a fictional character. I didn't read the "Annoying Creationists" thread while I was involved in the funeral arrangements for my stepfather. I actually have a life beyond posting on JREF. A pause in my posting history should never be construed as indicating I've been temporarily stumped by a remark from an opponent. Indeed, debating science with the emotionally disturbed has a very low priority in my daily life.

Dr. Kleinman, why do you hate Thor and his Hammer?

Paul C. Anagnostopoulos

7th June 2007, 06:22 AM

Dr. Kleinman, why do you hate Thor and his Hammer?
Well now, a hammer is just plain silly!

~~ Paul

Mr. Scott

7th June 2007, 06:33 AM

Well now, a hammer is just plain silly!

~~ Paul

Paul, why do you hate Thor and not His hammer?

Taffer

7th June 2007, 06:38 AM

Dr. Kleinman, why do you hate Thor and his Hammer?

How can anyone dislike Mjölnir?

Mr. Scott

7th June 2007, 07:09 AM

I'm curious about one thing, Dr. Kleinman.

You've argued that three selection pressures slow or stop evolution. You've cited articles about triple drug therapy that, to the best of my observation, never characterized their function as slowing or stopping evolution.

Is this hypothesis that triple therapy retards evolution your personal one or did you pick it up from someone else? Where did this idea of "three selection pressures slow or stop evolution" originate?

Paul C. Anagnostopoulos

7th June 2007, 10:29 AM

Where did this idea of "three selection pressures slow or stop evolution" originate?
A bit further back in this thread, I believe.

~~ Paul

Mr. Scott

7th June 2007, 02:37 PM

To:

Where did this idea of "three selection pressures slow or stop evolution" originate?

A bit further back in this thread, I believe.

~~ Paul

Are you suggeting Kleinman made it up while posting in this thread?

Or, perhaps it was a discovery he made from running Ev?

I'm really wondering if this is a novel discovery made by Kleinman himself, or if he picked it up from someone else.

Paul C. Anagnostopoulos

7th June 2007, 05:21 PM

Are you suggeting Kleinman made it up while posting in this thread?

Or, perhaps it was a discovery he made from running Ev?

I'm really wondering if this is a novel discovery made by Kleinman himself, or if he picked it up from someone else.
I think it is something he derived from hours of Ev-watching.

~~ Paul

Dr Adequate

7th June 2007, 07:40 PM

whiteyonthemoon

8th June 2007, 12:06 AM

I'll agree with Kleinman. If an entire species is suddenly exposed to three new toxins, unrelated in physiological action and at high concentration, it will soon be extinct.

What planet is this supposed to have happened on?

Mr. Scott

8th June 2007, 07:30 AM

I found this wonderful description of chromosome duplication and interspecies mating that powerfully explains their great importance in evolution. It's from the book "The Tree: A Natural History of What Trees Are, How They Live, and Why They Matter" by Colin Tudge (Crown Publishers, New York, (c) 2005,2006). The quote is from page 13-14 and is reproduced here under the "fair use" portion of the copyright law.

...there is the extremely important phenomenon of polyploidy. Genes, as everyone knows these days, are aligned along chromosomes. Every kind of organism has its characteristic number and arrangements of chromosomes. Eggs and sperm (or the appropriate cells in ovules and pollen) contain only one set of chromosomes, and are said to be “haploid.” When they fuse in the act of fertilization, the resulting embryo has two sets of chromosomes and then is said to be “diploid.” Most organisms (at least the most familiar kinds) are diploid: for example, human beings have fourty-six chromosomes – twenty-three acquired by the egg of the mother and twenty-three acquired from the sperm of the father. Chimpanzees have fourty-eight chromosomes, twenty-four from each parent.

Sometimes, however, apparently spontaneously, the chromosome number will double. (The chromosomes divide in the normal way they do in preparation for cell division, but then the cell fails to divide.) Thus the diploid cell becomes tetraploid, with four sets of chromosomes. This does not apparently happen much in animals (or not, at least, in mammals), but it is extremely common in plants. The newly formed tetraploid organism can breed successfully with other tetraploids of its kind, but it cannot usually breed successfully with either of its parents. So it forms an instant new species. Many plants in nature turn out to be tetraploid, and many tetraploids have been produced in cultivation. The common potatoes in Europe are tetraploid derivatives of diploid potatoes that grow wild (and are cultivated) in the Andes. Many trees, wild and cultivated, are tetraploid. Sometimes the chromosomes of the tetraploid plant double again and produce octoploids. These octoploids form a new, discrete species – generally unable to interbreed with the tetraploid parents who gave rise to them. “Polyploid” is the general term that describes any organism with more than two sets of chromosomes. Sometimes the complications become too much even for the plants and they end up with an odd number of chromosomes (some having been lost among all the cell divisions and matings). Plants with anomalous numbers of chromosomes are said to be “aneuploid.” Aneuploidy in animals generally leads to various degrees of disorder; aneuploid animals usually die, and if they live they tend to be compromised at least to some extent. But many plants put up with aneuploidy. Sugarcane is aneuploid; but that doesn’t stop it from being an extremely vigorous, major crop.

There is one further complication. As we have noted, diploid organisms that are of different species sometimes mate to produce fully viable offspring (as the eastern and western species of Platanus evidently did). But usually such crosses fail, and often this is because the chromosomes of the two parents are incompatible. The two different sets of chromosomes might be able to support body cells that work well enough (as in the mule). But even if cells with two different kinds of chromosomes succeed this far, they will not necessarily produce sound gametes (eggs and sperm or ovules and pollen), because this requires close cooperation between the chromosomes.

Yet if a hybrid organism doubles its chromosomes, it often can produce viable gametes. So we find diploid parents of different species mating to produce diploid hybrid offspring that are sterile; but the hybrids then double their chromosomes and become tetraploid – and the hybrid tetraploids are fertile. This happens a lot among plants, and has produced many, many new plant species, both in the wild and in cultivation.

I figure such aggressive functions that produce new species, though observed in nature, are unfortunately not modeled in Ev. Therefore, unless a mathematical proof is supplied that discounts the importance to evolution of the above, Ev cannot be relied on to prove evolution is too slow to have happened the way evolutionists claim.

http://forums.randi.org/imagehosting/673646695ace1c309.jpg

joobz

8th June 2007, 09:42 AM

Therefore, unless a mathematical proof is supplied that discounts the importance to evolution of the above, Ev cannot be relied on to prove evolution is too slow to have happened the way evolutionists claim.
Oh My god, you mean that a mathematical model with inherent assumptions and approximations and doesn't account for all known processes can't be used to disprove the existance of the real system?

Man, I was this close to proving that shear thickening fluids (corn starch in water) are impossible because the terminal velocity equation can't explain them.

Paul C. Anagnostopoulos

8th June 2007, 10:41 AM

Oh My god, you mean that a mathematical model with inherent assumptions and approximations and doesn't account for all known processes can't be used to disprove the existance of the real system?
To a rough approximation, yes.

~~ Paul

delphi_ote

8th June 2007, 10:47 PM

I tried to catch up on this thread. The result was roughly this:
http://i71.photobucket.com/albums/i133/delphi_ote/look2crys.gif

jimbob

9th June 2007, 04:56 AM

How can anyone dislike Mjölnir?

Maybe one is a Giant?

Paul C. Anagnostopoulos

9th June 2007, 06:54 AM

I tried to catch up on this thread.
Nothing has happened. You were already caught up.

~~ Paul

Taffer

9th June 2007, 07:35 AM

Maybe one is a Giant?

Good point. :D

kleinman

10th June 2007, 08:21 AM

Oh no, it looks like selection pressure isn't the only thing that controls emergence!?!?

Simosen Et. al. "The Genesis and Spread of Reassortant Human Influenza A/H3N2 Viruses Conferring Adamantane Resistance." mol. biol. ev. 2007More generally, these findings illustrate that drug selection pressure is not the sole factor determining the evolution and maintenance of drug resistance in human pathogens. How can this be? Kleinman says evolution is impossible and Kleinman is really smart, so....
Let’s post the entire abstract which is found at http://mbe.oxfordjournals.org/cgi/content/abstract/msm103v1 (http://mbe.oxfordjournals.org/cgi/content/abstract/msm103v1)
A dramatic rise in the frequency of resistance to adamantane drugs by influenza A (H3N2) viruses has occurred in recent years – from 2% to 90% in multiple countries worldwide – and associated with a single S31N amino acid replacement in the viral matrix M2 protein. To explore the emergence and spread of these adamantane resistant viruses we performed a phylogenetic analysis of recently sampled complete A/H3N2 genome sequences. Strikingly, all adamantane resistant viruses belonged to a single lineage (the ‘N-lineage’) characterized by 17 amino acid replacements across the viral genome. Further, our analysis revealed that the genesis of the N-lineage was due to a 4+4 segment reassortment event involving two distinct lineages of influenza A/H3N2 virus. A subsequent study of hemagglutinin HA1 sequences suggested that the N-lineage was circulating widely in Asia during 2005, and then dominated the Northern hemisphere 2005-2006 season in Japan and the USA. Given the infrequent use of adamantane drugs in many countries, as well as the decades of use in the US associated with little drug resistance, we propose that the globally increasing frequency of adamantane resistance is more likely attributable to its interaction with fitness-enhancing mutations at other genomic sites rather than to direct drug selection pressure. This implies that adamantanes may not be useful for treatment and prophylaxis against influenza viruses in the long term. More generally, these findings illustrate that drug selection pressure is not the sole factor determining the evolution and maintenance of drug resistance in human pathogens.
Poor clown fish, you had been doing so well up to now. You have just proven that you can’t count up to one. This abstract discusses a single selection pressure and if you think there are other mechanisms besides drug selection pressures which evolve and maintain drug resistance in human pathogens somehow overcomes the effect that multiple selection pressures which slow and ultimately stop evolution, post the proof. In the meantime, join Dr Richard in remedial Sesame Street and learn how to count.
Oh good, kleinman has ignored my refutation of his sources. What a surprise.
Stamping your foot and whining does not qualify as a refutation of the citations I have been posting (and will continue to post) which shows that multiple selection pressures slow and ultimately stop evolution. Post a citation which shows that multiple selection pressures accelerate evolution.
I think I shall go away now.
Honest?
Dr. Kleinman, why do you hate Thor and his Hammer?Well now, a hammer is just plain silly!
It’s more like ev the hammer, I like using ev to hammer the theory of evolution into oblivion.
I'm curious about one thing, Dr. Kleinman.
You know what curiosity did to the pussycat, don’t you?
You've argued that three selection pressures slow or stop evolution. You've cited articles about triple drug therapy that, to the best of my observation, never characterized their function as slowing or stopping evolution.
It is multiple selection pressures not just three selection pressures which slow and ultimately stop evolution. Extinction stops evolution.
Is this hypothesis that triple therapy retards evolution your personal one or did you pick it up from someone else? Where did this idea of "three selection pressures slow or stop evolution" originate?
We can thank ev and Dr Schneider for this hypothesis. This is what ev shows.
Or, perhaps it was a discovery he made from running Ev?
You got it pussycat. It’s interesting the things you can learn from a computer simulation when you do more than a superficial analysis.
I think it is something he derived from hours of Ev-watching.
I prefer to call this studying ev, ev-watching sounds to much like TV-watching. That’s what evolutionists do; you watch the SciFi channel and gather you “proof” for your theory.
I'll agree with Kleinman. If an entire species is suddenly exposed to three new toxins, unrelated in physiological action and at high concentration, it will soon be extinct.

What planet is this supposed to have happened on?
How many planets do you know where life exists? Have you heard something recently from SETI?
I figure such aggressive functions that produce new species, though observed in nature, are unfortunately not modeled in Ev. Therefore, unless a mathematical proof is supplied that discounts the importance to evolution of the above, Ev cannot be relied on to prove evolution is too slow to have happened the way evolutionists claim.
Hey Paul, polyploidy solves your problem in ev! Pussycat, where did the original genes to be duplicated come from?
I tried to catch up on this thread. The result was roughly this:
Did you finally organize your sock drawer?
I tried to catch up on this thread.Nothing has happened. You were already caught up.
It’s easy to catch up with Paul; he spends all his time in reverse gear.

Delphi, here are some more examples of how multiple selection pressures slow and ultimately stop evolution. I have to highlight the text in a large font, in red so Taffer can see. By the way, thank you again for your Wikipedia reference to the fitness landscape. Perhaps you can post an example where multiple selection pressures accelerate evolution?
http://www.crcsalinity.com.au/newsletter/sea/articles/SEA_2102.html (http://www.crcsalinity.com.au/newsletter/sea/articles/SEA_2102.html)
In this paper we discuss the case of the evolution in weed species of resistance to glyphosate, a valuable and widely used broad-spectrum non-selective herbicide first developed by Monsanto in the early 1970s.
and
The authors conclude that “The use of glyphosate in combination with other low risk herbicides for weed control with RR cotton provides an opportunity to significantly reduce the risk of off-site herbicide contamination in Australian cotton production”

http://www.aegis.com/factshts/tpc/guide/ (http://www.aegis.com/factshts/tpc/guide/)
Based on what is known about HIV's error-prone replication process (see above), we can assume that all patients have at least a few subpopulations of HIV that are resistant to individual drugs. However, these strains are often too limited in number and strength to compete with wild-type virus, and they stand a good chance of being killed off by initiating combination antiretroviral therapy. After all, the purpose of combination therapy is to serve as a multipronged attack on such strains.

Dr Adequate

10th June 2007, 08:51 AM

delphi_ote

10th June 2007, 08:53 AM

Mr. Scott

10th June 2007, 11:23 AM

Let’s post the entire abstract which is found at http://mbe.oxfordjournals.org/cgi/content/abstract/msm103v1 (http://mbe.oxfordjournals.org/cgi/content/abstract/msm103v1)

Poor clown fish, you had been doing so well up to now. You have just proven that you can’t count up to one. This abstract discusses a single selection pressure and if you think there are other mechanisms besides drug selection pressures which evolve and maintain drug resistance in human pathogens somehow overcomes the effect that multiple selection pressures which slow and ultimately stop evolution, post the proof. In the meantime, join Dr Richard in remedial Sesame Street and learn how to count.

Stamping your foot and whining does not qualify as a refutation of the citations I have been posting (and will continue to post) which shows that multiple selection pressures slow and ultimately stop evolution. Post a citation which shows that multiple selection pressures accelerate evolution.

Honest?

It’s more like ev the hammer, I like using ev to hammer the theory of evolution into oblivion.

You know what curiosity did to the pussycat, don’t you?

It is multiple selection pressures not just three selection pressures which slow and ultimately stop evolution. Extinction stops evolution.

We can thank ev and Dr Schneider for this hypothesis. This is what ev shows.

You got it pussycat. It’s interesting the things you can learn from a computer simulation when you do more than a superficial analysis.

I prefer to call this studying ev, ev-watching sounds to much like TV-watching. That’s what evolutionists do; you watch the SciFi channel and gather you “proof” for your theory.

How many planets do you know where life exists? Have you heard something recently from SETI?

Hey Paul, polyploidy solves your problem in ev! Pussycat, where did the original genes to be duplicated come from?

Did you finally organize your sock drawer?

It’s easy to catch up with Paul; he spends all his time in reverse gear.

Delphi, here are some more examples of how multiple selection pressures slow and ultimately stop evolution. I have to highlight the text in a large font, in red so Taffer can see. By the way, thank you again for your Wikipedia reference to the fitness landscape. Perhaps you can post an example where multiple selection pressures accelerate evolution?
http://www.crcsalinity.com.au/newsletter/sea/articles/SEA_2102.html (http://www.crcsalinity.com.au/newsletter/sea/articles/SEA_2102.html)

and

http://www.aegis.com/factshts/tpc/guide/ (http://www.aegis.com/factshts/tpc/guide/)

I laugh every time you move the goal post. You’ve said no new species ever evolved, and when I point out how they do, you ask how the ancestor of the new species could have evolved. I think that in the face of every solid refutation of every creationist claim you make, you’ll move the goalposts again and I’ll just laugh at your intellectual dishonesty.

Dr. Kleinman, I don't see support for your hypothesis that multiple selection pressures slow or stop evolution anywhere in the articles you site. Any kind of multi-prong attack on any problem will likely be better than a single prong attack. The objective in all these cases is to increase the likelihood of extinction, not to slow or stop evolution.

For example...

...a parasite colony size may take one week to adapt to resist a particular targeted toxin. If you were to apply one toxin the first week, one the next week, and another the third, the colony will have just enough time to adapt to each toxin. That would be a total of three weeks to adapt to three toxins.

Now, if all three toxins are applied at once in the first week, and the colony needs three weeks to adapt to those toxins, then the colony could very easily become extinct in the first week, and it would have nothing at all to do with a hypothetical slowing of evolution. Evolution could move ahead at the same exact cumulative speed.

With multiple selection pressures, what occurs is cumulative selection pressure increases, while the rate of adaptation remains the same. Additionally, with a colony markedly reduced in size by toxins of cumulative effect, the chance of the right adaptation occurring for any of the toxins is thus markedly reduced, and the probability of extinction is therefore markedly increased, without any need for the hypothesis of evolutionary retardation.

At no point in the process of multiple selection pressures is the hypothesis of slowing evolution required to explain the increased likelihood of extinction.

Add to that the principle of using multiple toxins with an additive effect on the parasite without additive side effects on the patient, and we have yet another explanation for the effectiveness of multi-prong therapy that has nothing at all to do with slowing down or stopping evolution.

And, as has been pointed out by others in this thread, colonies of species seldom face multiple selection pressures of near-extinction intensity simultaneously. When they do, and a species becomes extinct, then an environmental niche is opened that another species can quickly adapt to fill, thus resulting, for the opportunistic species, acceleration of evolution that tidily offsets the loss from the extinct species. Ultimately the cumulative rate of evolution remains constant.

Dr. Kleinman, your use of big red fonts is not helping to prove your point. Your name-calling is not helping. Your citing irrelevant articles is not helping. Your misuse of the Ev simulation is not helping. Your dishonest is not helping. Your ludicrous statements about "dancing on the grave of evolution" merely indicate you know the shallowness of your scientific arguments and reveal your insecurity about your position. The appeal to emotion is the last futile vestige of defiance of a warrior who knows deep down he's lost the battle.

The death of the theory of evolution was predicted to be imminent virtually the day Darwin first disclosed it. It's survived a century and a half and in fact grown, been embellished, been perfected, and been confirmed by an ever growing mountain of evidence.

Dr. Kleinman, you're through. You've got nothing.

joobz

10th June 2007, 11:26 AM

kleinman

10th June 2007, 06:41 PM

Delphi, here are some more examples of how multiple selection pressures slow and ultimately stop evolution.Here are some examples which completely disprove your theory.
http://i71.photobucket.com/albums/i133/delphi_ote/504181586_6822bf2eba_o.gif
Adebz the cheese wiz has tried the gif and awe strategy, it doesn’t work. Now a quote from a 50 year old Nobel prize lecture shows how long the concept that multiple selection pressures slow evolution has been around, that has paints a picture for your theory of evolution and it is all black. That said, now that you have figured out that your theory of evolution is mathematically impossible, you do have a career as a stop action film maker. You have successfully used this technique to prove that humans can evolve into skateboards.
At no point in the process of multiple selection pressures is the hypothesis of slowing evolution required to explain the increased likelihood of extinction.
Pussycat, quoting yourself in large red type does not reinforce your point. It just shows you have no point other than your own. Just what do you think causes extinction?
what part of "drug selection pressure is not the sole factor" did you not understand it. whether it is one or more than one.
Silly clown fish, you still don’t understand that no matter what type of genetic changes, mutations, recombination or factors you might want to propose, multiple selection pressures slow the process of evolution. And with sufficient selection pressure, you have extinction; after all, that is what selection pressures do.
I'm still waiting for your proof of slow equals stop.
Silly clown fish, at least one of my citations shows this. Let’s see if you can find it. You were so successful at finding the error in the equation from Dr Richard’s citation after it was shown to you; perhaps you can find this citation as successfully. Anyway, ev already shows that the acquisition of information becomes so profoundly slow that the theory of evolution is mathematically impossible and the reason why the acquisition of information is so profoundly slow is the multiple selection pressures. Some day you might come to understand the mathematics of mutation and selection and your confusion will lift.

You evolutionists still haven’t given a single citation which shows that multiple selection pressures accelerate evolution. At least Delphi has presented proof that humans can evolve into skateboards. I have to use primitive ascii art to make my case.

http://gateway.nlm.nih.gov/MeetingAbstracts/102225407.html (http://gateway.nlm.nih.gov/MeetingAbstracts/102225407.html)
The combined antiviral effects of indinavir and RT inhibitors dramatically suppressed the emergence of resistance to these agents, in a bi-directional fashion, relative to the rates observed during inhibition of the protease or RT alone. This suggests that the durability of viral inhibition can be increased by combining indinavir with one or more inhibitors of the reverse transcriptase, suppressing the viral replication that drives the evolution of resistance.

Here is an interesting link from the Nobel Prize lecture given in 1958 by Edward Tatum. Why evolutionists did not understand the significance what was said almost 50 years ago can only be attributed to the bias that is indoctrinated into them by their training.
http://nobelprize.org/nobel_prizes/medicine/laureates/1958/tatum-lecture.html (http://nobelprize.org/nobel_prizes/medicine/laureates/1958/tatum-lecture.html)
In microbiology the roles of mutation and selection in evolution are coming to be better understood through the use of bacterial cultures of mutant strains. In more immediately practical ways, mutation has proven of primary importance in the improvement of yields of important antibiotics - such as in the classic example of penicillin, the yield of which has gone up from around 40 units per ml of culture shortly after its discovery by Fleming to approximately 4,000, as the result of a long series of successive experimentally produced mutational steps. On the other side of the coin, the mutational origin of antibiotic-resistant micro-organisms is of definite medical significance. The therapeutic use of massive doses of antibiotics to reduce the numbers of bacteria which by mutation could develop resistance, is a direct consequence of the application of genetic concepts. Similarly, so is the increasing use of combined antibiotic therapy, resistance to both of which would require the simultaneous mutation of two independent characters.

As an important example of the application of these same concepts of microbial genetics to mammalian cells, we may cite the probable mutational origin of resistance to chemotherapeutic agents in leukemic cells 44, and the increasing and effective simultaneous use of two or more chemotherapeutic agents in the treatment of this disease.
Notice pussycat that I use large red type when quoting others so you can see the point that they are making.

Dr Adequate

10th June 2007, 06:45 PM

http://i71.photobucket.com/albums/i133/delphi_ote/504181586_6822bf2eba_o.gif
Adebz the cheese wiz has tried the gif and awe strategy, it doesn’t work. Now a quote from a 50 year old Nobel prize lecture shows how long the concept that multiple selection pressures slow evolution has been around, that has paints a picture for your theory of evolution and it is all black. That said, now that you have figured out that your theory of evolution is mathematically impossible, you do have a career as a stop action film maker. You have successfully used this technique to prove that humans can evolve into skateboards.

Pussycat, quoting yourself in large red type does not reinforce your point. It just shows you have no point other than your own. Just what do you think causes extinction?

Silly clown fish, you still don’t understand that no matter what type of genetic changes, mutations, recombination or factors you might want to propose, multiple selection pressures slow the process of evolution. And with sufficient selection pressure, you have extinction; after all, that is what selection pressures do.

Silly clown fish, at least one of my citations shows this. Let’s see if you can find it. You were so successful at finding the error in the equation from Dr Richard’s citation after it was shown to you; perhaps you can find this citation as successfully. Anyway, ev already shows that the acquisition of information becomes so profoundly slow that the theory of evolution is mathematically impossible and the reason why the acquisition of information is so profoundly slow is the multiple selection pressures. Some day you might come to understand the mathematics of mutation and selection and your confusion will lift.

You evolutionists still haven’t given a single citation which shows that multiple selection pressures accelerate evolution. At least Delphi has presented proof that humans can evolve into skateboards. I have to use primitive ascii art to make my case.

http://gateway.nlm.nih.gov/MeetingAbstracts/102225407.html (http://gateway.nlm.nih.gov/MeetingAbstracts/102225407.html)

Here is an interesting link from the Nobel Prize lecture given in 1958 by Edward Tatum. Why evolutionists did not understand the significance what was said almost 50 years ago can only be attributed to the bias that is indoctrinated into them by their training.
http://nobelprize.org/nobel_prizes/medicine/laureates/1958/tatum-lecture.html (http://nobelprize.org/nobel_prizes/medicine/laureates/1958/tatum-lecture.html)

Notice pussycat that I use large red type when quoting others so you can see the point that they are making. So, you've got no new lies, no new magic words, and no math?

Ah well. I liked the bit where you used bright red letters to highlight a Nobel Prize winner (evolutionist, natch) without noticing that he's directly contradicting one of your favorite lies. And then whine that evolutionists didn't understand what he was saying.

That was quite funny, though still not as funny as Lie #5.

joobz

10th June 2007, 07:17 PM

Silly clown fish, you still don’t understand that no matter what type of genetic changes, mutations, recombination or factors you might want to propose, multiple selection pressures slow the process of evolution. And with sufficient selection pressure, you have extinction; after all, that is what selection pressures do.
It seems you are rather slow. Let's retry. If any of these words are too big, break them down into smaller bits til you can understand it.

Simosen Et. al. "The Genesis and Spread of Reassortant Human Influenza A/H3N2 Viruses Conferring Adamantane Resistance." mol. biol. ev. 2007

More generally, these findings illustrate that drug selection pressure is not the sole factor determining the evolution and maintenance of drug resistance in human pathogens.

selection pressure = what ev models.
not sole factor in evolution = ev doesn't model all of evolution.

therefore, your crap about "evolution is too slow becuase my imaginary math based upon ev says so" is crap.

Meadmaker

10th June 2007, 07:37 PM

Here are some examples which completely disprove your theory.
:)

kleinman

10th June 2007, 07:54 PM

It seems you are rather slow. Let's retry. If any of these words are too big, break them down into smaller bits til you can understand it.

Simosen Et. al. "The Genesis and Spread of Reassortant Human Influenza A/H3N2 Viruses Conferring Adamantane Resistance." mol. biol. ev. 2007More generally, these findings illustrate that drug selection pressure is not the sole factor determining the evolution and maintenance of drug resistance in human pathogens.selection pressure = what ev models.
not sole factor in evolution = ev doesn't model all of evolution.
So silly clown fish first argues that recombination of HIV will overcome the effect of multiple selection pressures slow the evolution of resistant strains but dozens of citations prove otherwise. Now clown fish tries to argue that some vague factors will overcome this effect. So what if ev only models random point mutations? All the real cases posted here are not limited to random point mutations and they all show that multiple selection pressures slow evolution. Clown fish you are grasping at strawmen. Now if you were a really clever clown fish, you would tell Paul what these other factors are that would accelerate the acquisition of information in ev. Alas, since you are not a really clever clown fish, you can’t. The reason why you can’t is that it is not the type of mutation or other factors that alter genomes which affect the rate of information acquisition; it is the number of selection pressures and the length of the genome which dominates the mathematics of ev. Once again clown fish, you flop.
Here are some examples which completely disprove your theory.http://forums.randi.org/images/smilies/smile.gif
Meadmaker, I have to agree that Delpi’s human skateboard video is amusing. It certainly represents a valid career change for him from the theory of evolution.

Dr Adequate

10th June 2007, 11:04 PM

So silly clown fish first argues that recombination of HIV will overcome the effect of multiple selection pressures slow the evolution of resistant strains but dozens of citations prove otherwise. Now clown fish tries to argue that some vague factors will overcome this effect. So what if ev only models random point mutations? All the real cases posted here are not limited to random point mutations and they all show that multiple selection pressures slow evolution. Clown fish you are grasping at strawmen. Now if you were a really clever clown fish, you would tell Paul what these other factors are that would accelerate the acquisition of information in ev. Alas, since you are not a really clever clown fish, you can’t. The reason why you can’t is that it is not the type of mutation or other factors that alter genomes which affect the rate of information acquisition; it is the number of selection pressures and the length of the genome which dominates the mathematics of ev. Once again clown fish, you flop.

Meadmaker, I have to agree that Delpi’s human skateboard video is amusing. It certainly represents a valid career change for him from the theory of evolution. The number of magic words in this post is getting close to the number of actual lies.

Let me know if saying the words "clown fish" over and over change reality, won't you?

joobz

11th June 2007, 06:51 AM

So silly clown fish first argues that recombination of HIV will overcome the effect of multiple selection pressures slow the evolution of resistant strains but dozens of citations prove otherwise. The demonstration of HIV recombination was not just proof against your flawed theory, but also proof of your lieing hypocritical nature. Why would I abandon it?
Now clown fish tries to argue that some vague factors will overcome this effect. So what if ev only models random point mutations? Are you really asking this question? I mean, you've said some really retarded things, but this one is probably one of the most inane.

All the real cases posted here are not limited to random point mutations and they all show that multiple selection pressures slow evolution. no they don't. They show that you can skateboard on a person.
Clown fish you are grasping at strawmen. you know what strawmen are, correct? A strawman is taking an obviously weak argument (presumably held by your opponent) and refuting that argument, with hopes that it will tear down your opponents real arguments. Hmm, considering you have ignored my points, Taffer's arguments, Dr. Scott's, Delphi's, Dr. Adequate's model, and many others, yet hold to your rediculous (and already refuted claim).....If you want to know what a strawman is, look at yourself. Now if you were a really clever clown fish, you would tell Paul what these other factors are that would accelerate the acquisition of information in ev. Alas, since you are not a really clever clown fish, you can’t. The reason why you can’t is that it is not the type of mutation or other factors that alter genomes which affect the rate of information acquisition; it is the number of selection pressures and the length of the genome which dominates the mathematics of ev. Once again clown fish, you flop.bwa ha ha ha ha ha

I take my previous statement back, THAT is the most retardedly inane thing you have said. Wow, two in one post. Keep this up, and you stand a great shot of being the biggest twit in the world! I have faith in you.

Paul C. Anagnostopoulos

11th June 2007, 05:39 PM

The reason why you can’t is that it is not the type of mutation or other factors that alter genomes which affect the rate of information acquisition; it is the number of selection pressures and the length of the genome which dominates the mathematics of ev.
Why do you keep spewing this lie, Alan? You have not run any Ev models where the selection pressures are applied sequentially and cumulatively. You're just making up this crap as you go along.

~~ Paul

Dr Adequate

11th June 2007, 06:39 PM

You're just making up this crap as you go along. Ah yes ... creationism.

Next you'll be complaining about the lavatory habits of bears.

kleinman

13th June 2007, 09:01 AM

Let me know if saying the words "clown fish" over and over change reality, won't you?
I certainly will cheese wiz. I’ll also let you know that your silly gifs don’t change reality either. I’ll do this by position citations which show how mutation and selection actually works and it works as ev shows, that is multiple selection pressures slow and ultimately stops evolution.
So silly clown fish first argues that recombination of HIV will overcome the effect of multiple selection pressures slow the evolution of resistant strains but dozens of citations prove otherwise.The demonstration of HIV recombination was not just proof against your flawed theory, but also proof of your lieing hypocritical nature. Why would I abandon it?
You should abandon it because you are wrong. Are you advocating the return to monotherapy for the treatment of HIV because the virus is able to do recombination? That sounds like your fishy type of logic.
The reason why you can’t is that it is not the type of mutation or other factors that alter genomes which affect the rate of information acquisition; it is the number of selection pressures and the length of the genome which dominates the mathematics of ev.Why do you keep spewing this lie, Alan? You have not run any Ev models where the selection pressures are applied sequentially and cumulatively. You're just making up this crap as you go along.
Paul, you are again sinking into denial. Your own computer model shows that single selection pressures evolve extremely rapidly, this calculation has already been done with your model and I have posted dozens of citations of real examples of how sequential application of selection pressures allows for much more rapid evolution than if the selection pressures are applied simultaneously.

In fact, here are some more real examples of how multiple selection pressures slow and ultimately stop evolution.

http://www.mdlinx.com/IDLinx/news.cfm?subspec_id=125 (http://www.mdlinx.com/IDLinx/news.cfm?subspec_id=125)
Conclusions: Resistant HCV isolates are selected rapidly during therapy with the highly active protease inhibitor telaprevir. Combination therapy with pegylated interferon-alfa or other direct antiviral drugs seem mandatory to avoid developing resistance

http://www.nature.com/nature/journal/v446/n7136/abs/nature05685.html (http://www.nature.com/nature/journal/v446/n7136/abs/nature05685.html)
Multidrug combinations are increasingly important in combating the spread of antibiotic-resistance in bacterial pathogens 1, 2, 3. On a broader scale, such combinations are also important in understanding microbial ecology and evolution 4, 5. Although the effects of multidrug combinations on bacterial growth have been studied extensively, relatively little is known about their impact on the differential selection between sensitive and resistant bacterial populations 1, 6, 7.Normally, the presence of a drug confers an advantage on its resistant mutants in competition with the sensitive wild-type population1. Here we show, by using a direct competition assay between doxycycline-resistant and doxycycline-sensitive Escherichia coli, that this differential selection can be inverted in a hyper-antagonistic class of drug combinations. Used in such a combination, a drug can render the combined treatment selective against the drug's own resistance allele. Further, this inversion of selection seems largely insensitive to the underlying resistance mechanism and occurs, at sublethal concentrations, while maintaining inhibition of the wild type. These seemingly paradoxical results can be rationalized in terms of a simple geometric argument. Our findings demonstrate a previously unappreciated feature of the fitness landscape for the evolution of resistance and point to a trade-off between the effect of drug interactions on absolute potency and the relative competitive selection that they impose on emerging resistant populations.
There is an arithmetic lesson here for you brainwashed evolutionists. All you have to do is set aside your false belief system in order to understand it.

kjkent1

13th June 2007, 10:11 AM

joobz

13th June 2007, 10:30 AM

You should abandon it because you are wrong. Are you advocating the return to monotherapy for the treatment of HIV because the virus is able to do recombination? That sounds like your fishy type of logic.
Show me where I ever said we should abandon combination therapy. Show me where I advocated using monotherapy over combination therapy? Please quote the exact post I said this. You can't, because I never did, you moron.

The reference I showed demonstrated that even under your multiple selection pressures, resistance can still emerge. You claimed it "didn't count" because HIV was using recombination and that is, well, a rather dumb thing to say.

The burden of proof was on you to show it was impossible and you've failed. No one would ever question the idea that too strong of pressure would halt all of evolution by causing extinction. I could use a single pressure of 1000ºC, does that mean we only need 1 pressure to halt evolution???!?!?. You can see why we find your entire theory contemptably moronic. It isn't interesting or even novel.

The only way you can use this line of reasoning is to show that at all moments throughout history the environmental conditions were too great to expect this to occur. Please, go step for step across each epoch and explain how this is the case. We need details. Evolution occurs over a rather broad range, so we'll need many details about how it is impossible at all locations and all moments in earth history. Be specific.

kleinman

13th June 2007, 11:10 AM

http://www.nature.com/nature/journal/v446/n7136/abs/nature05685.html (http://www.nature.com/nature/journal/v446/n7136/abs/nature05685.html)

There is an arithmetic lesson here for you brainwashed evolutionists. All you have to do is set aside your false belief system in order to understand it.Alan, you have finally said something interesting, again.
Wait a minute, I’m not trying to be interesting, I’m trying to annoy evolutionists. I feel like I have failed in my mission when you say something like this.
When you suggested that ev demonstrates that random point mutation alone may be too slow to permit observed evolution to take place in the time available, that called for a rational response. And, the response was (and is) simply that ev does not model the entire evolutionary landscape, because it lacks the other scientifically observed mutational mechanisms, and ev's selection mechanism considers only missing and spurious bindings in the genome, whereas in nature, there are other environmental influences, such as having one's planet struck by a large meteor.
You are correct; ev demonstrates that random point mutations and natural selection is too slow a process for the theory of evolution to be true. It is the numerous citations I have and will continue to post which show that the other mechanisms of mutations do not change the mathematical fact which ev shows. I would now like to suggest that ev is the meteor which has struck the theory of evolution. The only thing remaining of the theory of evolution is a gigantic crater where once the theory resided. Now if you would like to try and fill this crater with real examples where multiple selection pressures accelerate evolution, feel free to start doing this now.
And, now, your latest post actually provides some real evidence of how a "hyper-antagonistic class of drug combinations" can inhibit the allele-resistance of a bacteria strain. The counterargument is, however, trivially simple: what is the probability in nature that a nexus of "hyper-antagonistic" selective pressures will occur so as to prevent further evolution to occur?
Lita’ gator, that is the point of this entire thread, all selection pressures are antagonistic, that is what the mathematics of ev shows, that is what all the citations I have posted shows, that is what the Wikipedia reference to fitness landscape shows. Some selection pressures are more antagonistic than others but all selection pressures interfere with the mutation and selection process of other selection pressures. Do you care to show an example where this is not true?
Considering the fact, that in your cited example, the issue random chance has been replaced by a known intelligent designer, undertaking a completely deterministic process, the obvious answer is: zero -- this never happens with "natural selection," because if it did, the selection wouldn't be natural, anymore -- now would it?
If you think “natural selection” works differently when intelligent designers are not involved, give us an example where multiple selection pressures accelerates evolution in “nature”.
Alan, you doth protest too much, using far too little proof. You have raised the claim that evolution can be shown to be mathematically impossible via a rigorous mathematical proof. But, you refuse to show that proof. Instead, you fall back on Schneider already did the math (which he didn't, because ev doesn't model the entire evolutionary landscape), and your empirical evidence of how intelligently designed drugs tend to prevent bacterial/viral resistance from occurring.
So, let’s see, I use the results of a peer reviewed and published mathematical model of random point mutations and natural selection, and numerous real examples of what the mathematics of this model shows from the fields of infectious diseases, parasitology, agriculture, oncology, ecology,… and that is not enough for you. If you evolutionists think that other mechanisms of mutation will change the mathematical facts that ev reveals, you evolutionists need to prove your case. I have already shown that your case collapses based on random point mutations alone. Paul and Dr Schneider will not add other mechanisms of genome alteration to ev because they know that I will co-opt the results. It already galls them that I use ev to batter the theory of evolution. Sadly, they are more concerned about their beloved but false theory than the mathematical and scientific explanation of how mutation and selection actually works. I will wait until they finally figure out that they have been betrayed by their own theory which has misled them into a false belief system.
What the latter evidence proves is merely that if a man builds a gun and points it at an enemy with sufficient antagonism, that enemy will be rendered extinct. A similarly antagonistic agent in nature will render biological organisms extinct, as well. So, congratulations, doctor -- you have proved that extinction can occur in laboratory conditions.
Lita’ gator, news flash, extinction occurs outside the laboratory as well. That’s what selection pressures do.
That is really hot info. "I'll alert the media." -- John Gielgud, as Hobson, "Arthur," Orion Pictures Corporation (1981).
Lita’ gator cites from a 25 year old movie and thinks that will change the mathematical facts which ev shows. The evolutionists’ favorite source of information appears to be the movie industry, in particular, the SciFi channel. I’ll stick with sources like medical journals, scientific agricultural journal, Nobel prize lectures,…
You should abandon it because you are wrong. Are you advocating the return to monotherapy for the treatment of HIV because the virus is able to do recombination? That sounds like your fishy type of logic.Show me where I ever said we should abandon combination therapy. Show me where I advocated using monotherapy over combination therapy? Please quote the exact post I said this. You can't, because I never did, you moron.
So clown fish thinks that recombination does not overcome the effect of multiple selection pressures and does advocate the use of combination therapy, you are a smart fish.

joobz

13th June 2007, 11:29 AM

I’m trying to annoy evolutionists. ....Sorry, your lies and antics are amusing, not annoying.

So clown fish thinks that recombination does not overcome the effect of multiple selection pressures and does advocate the use of combination therapy, you are a smart fish.I see you are having a reading comprehension problem. Let me speak in short sentences for you:

Recombination helps to overcome multiple selection pressures.
Evolution still happens.
Multidrug therapy is better than monotherapy.
Multidrug therapy isn't perfect.

If you are having trouble, sound out each word aloud. Sometimes, hearing the words can aide in you learning them. If you have any questions, I'm sure many of the grownups around you will be willing to help. But avoid talking to strangers and make sure the people who pick you up know your secret word.

kleinman

13th June 2007, 11:55 AM

So clown fish thinks that recombination does not overcome the effect of multiple selection pressures and does advocate the use of combination therapy, you are a smart fish.I see you are having a reading comprehension problem. Let me speak in short sentences for you:
It is better for grammatically challenged clown fish speak in short sentences.
Recombination helps to overcome multiple selection pressures.
Really, recombination helps to overcome multiple selection pressures? Clown fish thinks there will never be a cure for HIV. How pessimistic clown fish are.
Evolution still happens.
Do you care to describe the selection pressure that evolved reptiles into birds? You can describe that right after you describe how ribose forms nonenzymatically.
Multidrug therapy is better than monotherapy.
Why is that clown fish?
Multidrug therapy isn't perfect.
It certainly works better than monotherapy; do you want to hazard a guess why?
If you are having trouble, sound out each word aloud. Sometimes, hearing the words can aide in you learning them. If you have any questions, I'm sure many of the grownups around you will be willing to help. But avoid talking to strangers and make sure the people who pick you up know your secret word.
Since clown fish has been so kind to give us a lecture in grammar, I will return the favor and give him a lesson in arithmetic. Clown fish, 1+1=2, however, don’t tell any evolutionists, we are trying to keep it a secret from them.

joobz

13th June 2007, 12:55 PM

kleinman

13th June 2007, 01:37 PM

Really, recombination helps to overcome multiple selection pressures? Clown fish thinks there will never be a cure for HIV. How pessimistic clown fish are.You would prefer to live in a fantasy world where you can cure anything with gum drops and lollipops? Sorry, I'd rather think that medical research adapt to reality and wishful thinking. Remember, we also thought we had tb licked as well. Interesting to see how nature fights back.
Oh no clown fish, I prefer to live in the real world where multiple selection pressures slow and ultimately stop evolution. That’s what medical research is showing, that is what the numerous citations I have posted shows. Of course, all zero of your citations that you have posted that show that multiple selection pressure accelerate evolution makes for an overwhelming argument on your part.
Do you care to describe the selection pressure that evolved reptiles into birds? You can describe that right after you describe how ribose forms nonenzymatically.Do you care to show us that at all moments throughout history the environmental conditions posed too great a selection pressure for evolution to occur. Please, go step for step across each epoch and explain how this is the case. We need details. Evolution occurs over a rather broad range, so we'll need many details about how it is impossible at all locations and all moments in earth history. Be specific.
Why certainly clown fish, we can do this, start with the mathematics of ev which shows that multiple selection pressures stops evolution. Then we can move on to the numerous real examples that I have posted, including a 50 year old Nobel lecture which shows that multiple selection pressures slow evolution. So where does your description start. It doesn’t start with any mathematical model and it finishes without any real examples of you hypothesis. You obviously live in a fantasy world of gum drops and lollipops, not of mathematics and real empirical evidence. Clown fish, you are a very slow learner of the mathematics of mutation and selection.
Why is that clown fish?it delays emergence. Note that delay doesn't equal stop.
So nobody gets cured from any diseases. They only develop resistant strains of the bacteria or viruses. So how long do multiple selection delay emergence of resistance? Do multiple selection pressures delay evolution at all?
It certainly works better than monotherapy; do you want to hazard a guess why?already addressed.
Really, you addressed this? If you have then why don’t you give us a real example where multiple selection pressures accelerate evolution?
Since clown fish has been so kind to give us a lecture in grammar, I will return the favor and give him a lesson in arithmetic. Clown fish, 1+1=2, however, don’t tell any evolutionists, we are trying to keep it a secret from them.This is rather a blatheringly pointless and nonsensical comment. You are now officially dumber for having typed it.
Why certainly there is a point to teach you how to add 1+1=2. My argument has a mathematical basis derived from a peer reviewed and published mathematical model of random point mutations and natural selection and the results of this model are supported by numerous real examples of this mathematics, and your argument clown fish? Your argument is nothing more than a fish story which gets longer and longer every time you tell it.

joobz

13th June 2007, 02:17 PM

jimbob

13th June 2007, 02:26 PM

How do multiple selection pressures stop evolution?

Assuming the mutations occur independently of each other, the worst that can happen is for the rate of evolution is reduced by the probability of acquiring the correct mutation squared.

With sexual reproduction, this is vastly increased.

Having an increased tolleence of one drug will improve the overall chances of survival, providing some bacteria/viruses survive.

Evolution is only stopped if there are no survivors.

Mercutio

13th June 2007, 02:56 PM

I could use a single pressure of 1000ºC, does that mean we only need 1 pressure to halt evolution???!?!?.

Oh, good, finally some common ground! Perhaps when Kleinman said "eventually" (as in "slows and eventually stops"), he means "when the sun goes supernova."

You see, I'm right, as I can show,
Selection pressures all must slow
The changing of genetic codes--
'Twill stop just as the sun explodes!

So, thanks to time, and thanks to fission,
I might--just might--complete my mission:
Convincing skeptics in this thread
(Or posting till they all are dead).

And just for fun and pure delight, dears,
I'll move the goalposts ten more light years.

Dr Adequate

13th June 2007, 04:37 PM

fish
fish
fish
fish
fish
fish
fish
fish
fish
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fish
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fish
fish
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fish
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fish
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fish
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fish
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fish
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fish
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fish
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fish
fish

Conclusion: creationist morons cannot make reality go away by repeating the word "fish".

Dr Adequate

13th June 2007, 04:41 PM

[SIZE=3Then we can move on to the numerous real examples that I have posted, including a 50 year old Nobel lecture which shows that multiple selection pressures slow evolution.[/SIZE] You are a liar, kleinman. The lecture does not show that, does it, kleinman? The lecturer doesn't say that, does he, kleinman? You can't find a single scientist who does say that, can you, kleinman? The Nobel Laureate also directly contradicts your lie about the irrelevance of population size, doesn't he, kleinman? Why are you such a liar, kleinman?

kjkent1

13th June 2007, 05:36 PM

Wait a minute, I’m not trying to be interesting, I’m trying to annoy evolutionists. I feel like I have failed in my mission when you say something like this.You haven't failed in your mission -- however, you have failed in your emission.You are correct; ev demonstrates that random point mutations and natural selection is too slow a process for the theory of evolution to be true.Strawman alert. Please don't misrepresent my statement so as to imply that I said something that I did not say. I said that random point mutations and ev's natural selection mechanism may be too slow to permit evolution in the time available. You're the only one saying that this proves that the entire theory of evolution is falsified. You're also the only one who is making the unwarranted leap to a conclusion which does not follow logically from the available evidence.Lita’ gator, that is the point of this entire thread, all selection pressures are antagonistic, that is what the mathematics of ev shows, that is what all the citations I have posted shows, that is what the Wikipedia reference to fitness landscape shows. Some selection pressures are more antagonistic than others but all selection pressures interfere with the mutation and selection process of other selection pressures. Do you care to show an example where this is not true?Certainly -- just look in the mirror. The creature who is staring back at you is the product of a fusion of two preexisting genes which continue to appear as discrete entities in your primate relatives. This evolutionary change was not prevented by selective pressure. And, so we are here to argue about it today.If you think “natural selection” works differently when intelligent designers are not involved, give us an example where multiple selection pressures accelerates evolution in “nature”Selection does not accelerate anything. Mutation creates change and selection refines the change to fit the average environment over the time period that the mutation manages to survive and reproduce within that environment. Accellerating evolution requires more mutations per generation, but not so many as to render the host organism inert.So, let’s see, I use the results of a peer reviewed and published mathematical model of random point mutations and natural selection, and numerous real examples of what the mathematics of this model shows from the fields of infectious diseases, parasitology, agriculture, oncology, ecology,… and that is not enough for you.It shouldn't be enough for you, either, Alan. The question you should ask yourself is: why is it enough for you? Could it be that your personal belief system interferes with your ability to logically analyze the facts? I think it does. So does most everyone else on this thread.

If I were confronted by a room full of well-educated people who thought I was loony, I would undertake to examine myself to discover why. You should consider similar action, if your goal is to remain a scientist, because you are not being objective in your analyses.If you evolutionists think that other mechanisms of mutation will change the mathematical facts that ev reveals, you evolutionists need to prove your case. I have already shown that your case collapses based on random point mutations alone. Paul and Dr Schneider will not add other mechanisms of genome alteration to ev because they know that I will co-opt the results. It already galls them that I use ev to batter the theory of evolution. Sadly, they are more concerned about their beloved but false theory than the mathematical and scientific explanation of how mutation and selection actually works. I will wait until they finally figure out that they have been betrayed by their own theory which has misled them into a false belief system.Your stated perception of reality is entirely imaginary. No one but you believes that you have proved your case. That should give you pause -- instead, you take it as proof that you are correct. If my horse crosses the finish line last and everyone in the stands says so, except for me, I won't be able to collect any winnings at the ticket window.

And, you cannot take your imaginary win to the bank.Lita’ gator, news flash, extinction occurs outside the laboratory as well. That’s what selection pressures do.Duh -- really?Lita’ gator cites from a 25 year old movie and thinks that will change the mathematical facts which ev shows. The evolutionists’ favorite source of information appears to be the movie industry, in particular, the SciFi channel. I’ll stick with sources like medical journals, scientific agricultural journal, Nobel prize lectures.That's pretty funny. You quote from a 3,000 year old dead sea scroll and think that it will change the course of scientific research. I'll stick with my funny movie. At least there's a negative proving that the quoted scene actually occurred. Not so with Genesis.

UnrepentantSinner

14th June 2007, 07:42 AM

I'm sorry to tangent from all the math and navel gazing (I'm still at an utter loss as to how crunching numbers makes Turkana Boy, Tiktaalik, ERVs or human chromosome 2 go away) but I received an interesting e-mail from NCSE today and had to share it with people interested in the Creationism v. evolution debate.
---------------------------------------

From the National Center for Science Education:

Dear Friends of NCSE,

Project Steve breaks the 800 barrier. Plus: a belated addendum to
last week's discussion of the global expansion of creationism, and a
problem with a few copies of the latest issue of Reports of the NCSE.

PROJECT STEVE: N > 800

With the addition of Steve Russell on April 24, 2007, NCSE's Project
Steve attained its 800th signatory. A tongue-in-cheek parody of a
long-standing creationist tradition of amassing lists of "scientists
who doubt evolution" or "scientists who dissent from Darwinism,"
Project Steve mocks such lists by restricting its signatories to
scientists whose first name is Steve (or a cognate, such as Stephanie,
Esteban, Istvan, Stefano, or even Tapani -- the Finnish equivalent).
About 1% of the United States population possesses such a first name,
so each signatory represents about 100 potential signatories. ("Steve"
was selected in honor of the late Stephen Jay Gould, a Supporter of
NCSE and a dauntless defender of evolution education.)

Although the idea of Project Steve is frivolous, the statement is
serious. It reads, "Evolution is a vital, well-supported, unifying
principle of the biological sciences, and the scientific evidence is
overwhelmingly in favor of the idea that all living things share a
common ancestry. Although there are legitimate debates about the
patterns and processes of evolution, there is no serious scientific
doubt that evolution occurred or that natural selection is a major
mechanism in its occurrence. It is scientifically inappropriate and
pedagogically irresponsible for creationist pseudoscience, including
but not limited to 'intelligent design,' to be introduced into the
science curricula of our nation's public schools."

Highlights from the history of Project Steve include the original
press release, Glenn Branch and Skip Evans's description of the
project for Geotimes, the announcement that Steven W. Hawking was
Steve #300, the announcement (on St. Stephen's Day!) of Steve #400,
the publication of a front-page story on Project Steve in a leading
Canadian newspaper, the announcement of Steve #600, and the
announcement of Steve #700. And, of course, Project Steve proved to be
scientifically fruitful in its own right. "The Morphology of Steve,"
by Eugenie C. Scott, Glenn Branch, Nick Matzke, and several hundred
Steves, appeared in the prestigious Annals of Improbable Research; the
paper provided "the first scientific analysis of the sex, geographic
location, and body size of scientists named Steve."

For information about Project Steve, visit:
http://www.ncseweb. org/resources/ articles/ 3541_project_ steve_2_16_ 2003.asp

For the various highlights, visit:
http://www.ncseweb. org/resources/ articles/ 4023_the_ press_release_ 2_16_2003. asp
http://www.geotimes .org/may03/ column.html
http://www.ncseweb. org/resources/ news/2003/ ZZ/751_hawking_ is_steve_ 300_4_21_ 2003.asp
http://www.ncseweb. org/resources/ news/2003/ ZZ/244_project_ steve_update_ 12_26_2003. asp
http://www.ncseweb. org/resources/ news/2005/ ZZ/154_project_ steve_in_ ottawa_2_ 24_2005.asp
http://www.ncseweb. org/resources/ news/2005/ ZZ/657_project_ steve_n__ 600_9_16_ 2005.asp
http://www.ncseweb. org/resources/ news/2006/ ZZ/634_announcin g_the_ncse_ 700_club_ 2_16_2006. asp

And for "The Morphology of Steve" (PDF), visit:
http://www.improb. com/airchives/ paperair/ volume10/ v10i4/morph- steve-10- 4.pdf

CREATIONISM GOING GLOBAL -- ADDENDUM

In the April 20, 2007, update's description of The Economist's article
on creationism' s global expansion, a somewhat misleading passage from
the article was quoted. The Economist referred to attempts of "school
boards in other parts of America to mandate curbs on the teaching of
evolution." Such attempts are rare, although informal pressures to
curtail the teaching of evolution are unfortunately common, as the
National Science Teachers Association noted in 2005. In the recent
past, most formal antievolution policies, proposed or implemented,
have instead either required or allowed a form of creationism to be
taught alongside evolution or attempted to instill scientifically
unwarranted doubts about evolution by, for example, describing it as
"just a theory." In the Kitzmiller disclaimer, both strategies were
visible.

For the story in The Economist, visit:
http://www.economis t.com/world/ displaystory. cfm?story_ id=9036706

For the NSTA's press release about its survey, visit:
http://www.nsta. org/pressroom& news_story_ ID=50377

For NCSE's previous story, supplemented with the foregoing addendum,
visit:
http://www.ncseweb. org/resources/ news/2007/ XX/394_creationi sm_going_ global_4_ 20_2007.asp

OOPS: RNCSE 26:4

A few copies of Reports of the NCSE, volume 26, number 4 -- with the
mudskipper on the cover -- were miscollated by the printer. Please
check your copy to make sure that all 48 pages appear in order and
with no repetitions. If you have a faulty copy, please let NCSE know,
ideally by e-mailing oops@ncseweb. org with your name and address, and
we will send you a replacement copy staightaway. And if you don't
subscribe to Reports --what are you waiting for?

For subscriptions to Reports of the NCSE, visit:
http://www.ncseweb. org/membership. asp

Thanks for reading! And as always, be sure to consult NCSE's web
site: http://www.ncseweb. org
where you can always find the latest news on evolution education and
threats to it.

kleinman

14th June 2007, 09:18 AM

Oh no clown fish, I prefer to live in the real world where multiple selection pressures slow and ultimately stop evolution. That’s what medical research is showing, that is what the numerous citations I have posted shows.They show it slows emergence within a population, not your moronic pet theory.
Clown fish tries Taffer’s argument that emergence of resistance doesn’t occur by mutation and selection and therefore emergence of resistance is not evolution. Once again, your semantic argument collapses before mathematical and empirical facts.
Of course, all zero of your citations that you have posted that show that multiple selection pressure accelerate evolution makes for an overwhelming argument on your part.you are debating arguments I've never made. That is something a moron does, are you a moron?
Clown fish needs another lesson in mathematics, 0+0=0. You still have zero citations to support your argument. Of course you know 0 about the mathematics of mutation and selection as well.
Why certainly clown fish, we can do this, start with the mathematics of ev which shows that multiple selection pressures stops evolution. Then we can move on to the numerous real examples that I have posted, including a 50 year old Nobel lecture which shows that multiple selection pressures slow evolution.so what was the world like 5 billion years ago? What were the conditions at every point throughout the globe? What were the caves like? the beaches? the land masses? The chemical content of all of those points? Can you show me that at no point throughout any time in history, none of them had the ability to be within the rather large parameter space that allows evolution? We need a detailed, point for point explanation. All you've offered is hand waving and poor extrapolations based off of unrealistic conditions.
Why clown fish, you know what the world was like 5 billion years ago, it was filled with gum drops and lollipops all working together with cooperative chemistry to make alchemical engineers.
So where does your description start. It doesn’t start with any mathematical model and it finishes without any real examples of you hypothesis. You obviously live in a fantasy world of gum drops and lollipops, not of mathematics and real empirical evidence. Clown fish, you are a very slow learner of the mathematics of mutation and selection.Actually, it starts with the fossil record and ends with molecular biology. and uses math to explain much along the way.
Too bad Dr Schneider’s mathematical model of mutation and selection doesn’t fit your brainwashed collage that you call the theory of evolution, and too bad that there is a huge amount of empirical data which shows that Dr Schneider’s mathematical model of mutation and selection is correct.
So nobody gets cured from any diseases. They only develop resistant strains of the bacteria or viruses. So how long do multiple selection delay emergence of resistance? Do multiple selection pressures delay evolution at all?Yup, you just said something more stupid than your previously stupid comments. When did I say nobody gets cured?
Oh no clown fish, stupid is the theory of evolution and stupider is the concept of abiogenesis. No mathematics, no science to these ideas but plenty of denial, extrapolation and speculation.
Really, you addressed this? If you have then why don’t you give us a real example where multiple selection pressures accelerate evolution? ohh, I see your going for the moron trifecta. Unfortuantely, this one doesn't count because you already made this completely irrelavent comment.
Again, clown fish shows us that 0+0=0, the number of citations he has posted that supports his hypothesis. Evolution is like the Eveready bunny, it gets there eventually, to bad ev doesn’t show this.
Why certainly there is a point to teach you how to add 1+1=2. My argument has a mathematical basis derived from a peer reviewed and published mathematical model of random point mutations and natural selection and the results of this model are supported by numerous real examples of this mathematics, and your argument clown fish? Your argument is nothing more than a fish story which gets longer and longer every time you tell it.THERE YOU GO! The Moron trifecta has been acheived. Good job. I knew you could do it.

Now, would you care to start posting real math and real examples of your points instead of moronic inferences and foolish nonmath that you keep using.
Don’t worry Dr Schneider; I support your mathematics even if clown fish don’t. And clown fish, don’t you worry, I’ll continue to post real examples of this mathematics. I have two more examples below, just for you and all the other clown fish.
How do multiple selection pressures stop evolution?
The first way multiple selection pressures stop evolution is by extinction. The second way multiple selection pressures stop evolution without extinction occurs when a local optimum is achieved on the fitness landscape which prevents evolution of the population away from that local optimum.
Assuming the mutations occur independently of each other, the worst that can happen is for the rate of evolution is reduced by the probability of acquiring the correct mutation squared.
That is not what the mathematics of ev shows and that is not what the real examples of mutation and selection show. Additional selection pressures slow the process much more than what you allege here.
With sexual reproduction, this is vastly increased.
Clown fish as tried to allege this by noting that HIV does recombination with crossing over. Still, combination therapy with three effective drugs (3 selection pressures) profoundly slows the emergence of resistant HIV. Recombination does not overcome the effect of multiple selection pressures even for the short genome HIV virus with its large populations, high reproductive rate and high mutation rate. This is the best case for evolution and it still is interfered with when you have combination selection pressures.
Having an increased tolleence of one drug will improve the overall chances of survival, providing some bacteria/viruses survive.
However, if the microbe is at a local optimum on the fitness landscape and the multiple selection pressures limit the number of pathways to the next higher local optimum, the multiple selection pressures act as stabilizing pressures preventing evolution to another local optimum.
Evolution is only stopped if there are no survivors.
Not so, if a population is at a local optimum on the fitness landscape and there is no pathway which doesn’t require the population to go to lower fitness point on the fitness landscape, the population will be stuck at that local optimum. Any direction the population moves on the fitness landscape would take it to a lower fitness state and there for, the population would be selected back to that local optimum.
You see, I'm right, as I can show,
Selection pressures all must slow
The changing of genetic codes--
'Twill stop just as the sun explodes!

So, thanks to time, and thanks to fission,
I might--just might--complete my mission:
Convincing skeptics in this thread
(Or posting till they all are dead).

And just for fun and pure delight, dears,
I'll move the goalposts ten more light years.
Multiple selection pressures, that’s what slows,
the evolution of genetic codes.

The only thing that this does show,
Is that the theory of evolution does explode.

There are no moving goal posts on this thread,
There’s only mathematics showing the theory of evolution is dead.
fish…
Does the theory of evolution smell more like limburger cheese or dead fish?

And now for a couple more citations which show that multiple selection pressures slow and ultimately stop evolution.

http://www.natap.org/2006/AASLD/AASLD_17.htm (http://www.natap.org/2006/AASLD/AASLD_17.htm)
Brief Summary: Tara Keiffer from Vertex presented an oral talk at AASLD on VX-950 drug resistance and how to prevent resistance. She presented an analysis of patients who received VX950 in a 14-day study. The goal of this sub-study analysis was to identify VX950 resistant variants (mutations) and the kinetics of their emergence (selection) in patients dosed with VX950 or VX950+Pegasys. They used a highly sensitive clonal method to characterize the mutations (viral variants), and they also did a phenotypic analysis. VX-950 has demonstrated a rapid & profound viral load reduction; drug resistance mutations can emerge when VX950 is given alone (as monotherapy), as sequence changes (mutations) in the HCV genome occur spontaneously & frequently as a natural result of the high levels of replication of the HCV virus-pre-existing mutations are likely present at a low level prior to drug treatment; but, resistant HIV and wild-type HCV (non-resistant virus) were suppressed & became undetectable with Pegasys added in combination therapy. With continued use of Pegasys+Ribavirin, after VX950 was stopped in the short-term study of VX950, wild-type & resistant HCV were suppressed & became or remained undetectable.

Telaprevir, also known as VX-950, is an oral HCV protease inhibitor, which has been previously shown in study to reduce HCV RNA by 4.4 logs as monotherapy and by 5.5 logs in combination with peginterferon in patients with HCV genotype 1.

In early studies there has been some patients whose viral load rebounded on VX950 monotherapy. I have reported from EASL in the Spring 2006 where Vertex reported this information on the development of resistance mutations: low-level resistance (< 25-fold increase in 50% inhibitory concentration): V36M/A, T54A, R155K/T, A156S; high-level resistance (> 50-fold increase in 50% inhibitory concentration): A156V/T, V36M/A + R155K/T, V36M/A + A156V/T

Tara Keiffer from Vertex, reported on a sub-study at AASLD an analysis to display the emergence & kinetics of VX950 HCV protease mutations when dosed with VX950 alone or in combination with Pegasys. Using sensitive methods to identify & characterize resistant variants she showed that although VX-950 produces dramatic HCV RNA suppression over 14-day course of treatment either alone or in combination with peginterferon alfa-2a, viruses with VX950 resistance mutations emerged as wild-type virus was cleared. Keiffer, however, reported that subsequent peginterferon alfa-2a/ribavirin therapy suppressed VX950 resistant virus to undetectable levels.

http://www.journals.uchicago.edu/cgi-bin/resolve?JID990624PDF (http://www.journals.uchicago.edu/cgi-bin/resolve?JID990624PDF)
We suggest that the risk of emergence of nucleoside-analogue resistance will be reduced by initial use of potent drug combinations, rather than sequential therapy, as has been illustrated for human immunodeficiency virus–infected patients. [15]

joobz

14th June 2007, 10:14 AM

Clown fish tries Taffer’s argument that emergence of resistance doesn’t occur by mutation and selection and therefore emergence of resistance is not evolution. Once again, your semantic argument collapses before mathematical and empirical facts.

Clown fish needs another lesson in mathematics, 0+0=0. You still have zero citations to support your argument. Of course you know 0 about the mathematics of mutation and selection as well.

Why clown fish, you know what the world was like 5 billion years ago, it was filled with gum drops and lollipops all working together with cooperative chemistry to make alchemical engineers.

Too bad Dr Schneider’s mathematical model of mutation and selection doesn’t fit your brainwashed collage that you call the theory of evolution, and too bad that there is a huge amount of empirical data which shows that Dr Schneider’s mathematical model of mutation and selection is correct.

Oh no clown fish, stupid is the theory of evolution and stupider is the concept of abiogenesis. No mathematics, no science to these ideas but plenty of denial, extrapolation and speculation.

Again, clown fish shows us that 0+0=0, the number of citations he has posted that supports his hypothesis. Evolution is like the Eveready bunny, it gets there eventually, to bad ev doesn’t show this.

Don’t worry Dr Schneider; I support your mathematics even if clown fish don’t. And clown fish, don’t you worry, I’ll continue to post real examples of this mathematics. I have two more examples below, just for you and all the other clown fish.

The first way multiple selection pressures stop evolution is by extinction. The second way multiple selection pressures stop evolution without extinction occurs when a local optimum is achieved on the fitness landscape which prevents evolution of the population away from that local optimum.

That is not what the mathematics of ev shows and that is not what the real examples of mutation and selection show. Additional selection pressures slow the process much more than what you allege here.

Clown fish as tried to allege this by noting that HIV does recombination with crossing over. Still, combination therapy with three effective drugs (3 selection pressures) profoundly slows the emergence of resistant HIV. Recombination does not overcome the effect of multiple selection pressures even for the short genome HIV virus with its large populations, high reproductive rate and high mutation rate. This is the best case for evolution and it still is interfered with when you have combination selection pressures.

However, if the microbe is at a local optimum on the fitness landscape and the multiple selection pressures limit the number of pathways to the next higher local optimum, the multiple selection pressures act as stabilizing pressures preventing evolution to another local optimum.

Not so, if a population is at a local optimum on the fitness landscape and there is no pathway which doesn’t require the population to go to lower fitness point on the fitness landscape, the population will be stuck at that local optimum. Any direction the population moves on the fitness landscape would take it to a lower fitness state and there for, the population would be selected back to that local optimum.

Multiple selection pressures, that’s what slows,
the evolution of genetic codes.

The only thing that this does show,
Is that the theory of evolution does explode.

There are no moving goal posts on this thread,
There’s only mathematics showing the theory of evolution is dead.

Does the theory of evolution smell more like limburger cheese or dead fish?

And now for a couple more citations which show that multiple selection pressures slow and ultimately stop evolution.

http://www.natap.org/2006/AASLD/AASLD_17.htm (http://www.natap.org/2006/AASLD/AASLD_17.htm)

http://www.journals.uchicago.edu/cgi-bin/resolve?JID990624PDF (http://www.journals.uchicago.edu/cgi-bin/resolve?JID990624PDF)

Oh, look at all those non sequitors. It's like they're congregating together. hmm, Is it non sequitor mating season already?

Dr Adequate

14th June 2007, 10:30 AM

Clown fish tries Taffer’s argument that emergence of resistance doesn’t occur by mutation and selection and therefore emergence of resistance is not evolution. Once again, your semantic argument collapses before mathematical and empirical facts.

Clown fish needs another lesson in mathematics, 0+0=0. You still have zero citations to support your argument. Of course you know 0 about the mathematics of mutation and selection as well.

Why clown fish, you know what the world was like 5 billion years ago, it was filled with gum drops and lollipops all working together with cooperative chemistry to make alchemical engineers.

Too bad Dr Schneider’s mathematical model of mutation and selection doesn’t fit your brainwashed collage that you call the theory of evolution, and too bad that there is a huge amount of empirical data which shows that Dr Schneider’s mathematical model of mutation and selection is correct.

Oh no clown fish, stupid is the theory of evolution and stupider is the concept of abiogenesis. No mathematics, no science to these ideas but plenty of denial, extrapolation and speculation.

Again, clown fish shows us that 0+0=0, the number of citations he has posted that supports his hypothesis. Evolution is like the Eveready bunny, it gets there eventually, to bad ev doesn’t show this.

Don’t worry Dr Schneider; I support your mathematics even if clown fish don’t. And clown fish, don’t you worry, I’ll continue to post real examples of this mathematics. I have two more examples below, just for you and all the other clown fish.

The first way multiple selection pressures stop evolution is by extinction. The second way multiple selection pressures stop evolution without extinction occurs when a local optimum is achieved on the fitness landscape which prevents evolution of the population away from that local optimum.

That is not what the mathematics of ev shows and that is not what the real examples of mutation and selection show. Additional selection pressures slow the process much more than what you allege here.

Clown fish as tried to allege this by noting that HIV does recombination with crossing over. Still, combination therapy with three effective drugs (3 selection pressures) profoundly slows the emergence of resistant HIV. Recombination does not overcome the effect of multiple selection pressures even for the short genome HIV virus with its large populations, high reproductive rate and high mutation rate. This is the best case for evolution and it still is interfered with when you have combination selection pressures.

However, if the microbe is at a local optimum on the fitness landscape and the multiple selection pressures limit the number of pathways to the next higher local optimum, the multiple selection pressures act as stabilizing pressures preventing evolution to another local optimum.

Not so, if a population is at a local optimum on the fitness landscape and there is no pathway which doesn’t require the population to go to lower fitness point on the fitness landscape, the population will be stuck at that local optimum. Any direction the population moves on the fitness landscape would take it to a lower fitness state and there for, the population would be selected back to that local optimum.

Multiple selection pressures, that’s what slows,
the evolution of genetic codes.

The only thing that this does show,
Is that the theory of evolution does explode.

There are no moving goal posts on this thread,
There’s only mathematics showing the theory of evolution is dead.

Does the theory of evolution smell more like limburger cheese or dead fish?

And now for a couple more citations which show that multiple selection pressures slow and ultimately stop evolution.

http://www.natap.org/2006/AASLD/AASLD_17.htm (http://www.natap.org/2006/AASLD/AASLD_17.htm)

http://www.journals.uchicago.edu/cgi-bin/resolve?JID990624PDF (http://www.journals.uchicago.edu/cgi-bin/resolve?JID990624PDF)
No new lies, and twenty-three occurences of the word "fish".

Mad people are funny.

kleinman

14th June 2007, 10:37 AM

Oh, look at all those non sequitors. It's like they're congregating together. hmm, Is it non sequitor mating season already?
Let’s see if we can make it sequitor so that clown fish will understand this.

Ev, the peer reviewed and published model of random point mutation and natural selection shows that mutation and selection is a profoundly slow process. Why does ev show the mutation and selection process profoundly slow? Clown fish, it is because of multiple selection conditions which make this process profoundly slow. And are there real examples of multiple selection pressures profoundly slowing the evolutionary process. Yes clown fish, there are numerous real examples of this. I’ve posted dozens of citations which demonstrate the mathematical fact that ev shows.

Perhaps in your dreams clown fish you see multiple selection pressures accelerating the evolutionary process along with seeing images of lollipops and gumdrops. That’s the only place you see this, you certainly don’t see it in reality. If you did, you would post the citations.

Clown fish, your incompetence in the mathematics of mutation and selection is truly evolutionary.

Dr Adequate

14th June 2007, 10:54 AM

Let’s see if we can make it sequitor so that clown fish will understand this.

Ev, the peer reviewed and published model of random point mutation and natural selection shows that mutation and selection is a profoundly slow process. Why does ev show the mutation and selection process profoundly slow? Clown fish, it is because of multiple selection conditions which make this process profoundly slow. And are there real examples of multiple selection pressures profoundly slowing the evolutionary process. Yes clown fish, there are numerous real examples of this. I’ve posted dozens of citations which demonstrate the mathematical fact that ev shows.

Perhaps in your dreams clown fish you see multiple selection pressures accelerating the evolutionary process along with seeing images of lollipops and gumdrops. That’s the only place you see this, you certainly don’t see it in reality. If you did, you would post the citations.

Clown fish, your incompetence in the mathematics of mutation and selection is truly evolutionary. You know we all know you're lying, right?

I notice that "lollipops" and "gumdrops" have joined your assortment of magic words.

Do you have some sort of eating disorder?

joobz

14th June 2007, 10:58 AM

Let’s see if we can make it sequitor so that clown fish will understand this.
hmmmm, go on.

Ev, the peer reviewed and published model of random point mutation and natural selection shows that mutation and selection is a profoundly slow process. Profoundly? wow, what a precise, mathematical term. (btw, ev doesn't show that)
Why does ev show the mutation and selection process profoundly slow? Clown fish, it is because of multiple selection conditions which make this process profoundly slow. there is that word again, profoundly. I wonder. Does that mean it takes weeks? months? years? decades? Centuries? thousands of years? tens of thousands of years? hundreds of thousands of years? millions of years? All of which, there is time for. We have 8 orders of magnitude in time scale that allows for this to happen.

That's quite a huge time duration. So again, What does profoundly mean exactly...and remember, we're being mathematical here. ;)

And are there real examples of multiple selection pressures profoundly slowing the evolutionary process. Yes clown fish, there are numerous real examples of this. I’ve posted dozens of citations which demonstrate the mathematical fact that ev shows.Oh you mean all those citations that have no bearing on your claims?

Perhaps in your dreams clown fish you see multiple selection pressures accelerating the evolutionary process along with seeing images of lollipops and gumdrops. That’s the only place you see this, you certainly don’t see it in reality. If you did, you would post the citations.excellent. Again you argue against something I never said.

Clown fish, your incompetence in the mathematics of mutation and selection is truly evolutionary.
What does this mean? I feel you are tring to be insulting, but it don't know let me see if I can translate:
"Joobz, your inability to understand my lies and nonmath increases based upon environmental adaptations."

Wow, thank you. I do find myself understanding you less and less as time goes on.

the question is, if there were multiple copies of you, would my ability to understand you decrease at a faster rate or slower rate?

kleinman

14th June 2007, 11:29 AM

Ev, the peer reviewed and published model of random point mutation and natural selection shows that mutation and selection is a profoundly slow process.Profoundly? wow, what a precise, mathematical term. (btw, ev doesn't show that)
If clown fish weren’t so inattentive, you would have seen Paul’s estimate of 200,000,000 million generations to evolve only 96 loci on a 100k genome. It gets worse for longer genomes, the evolutionary process slows on longer genomes.
Why does ev show the mutation and selection process profoundly slow? Clown fish, it is because of multiple selection conditions which make this process profoundly slow.there is that word again, profoundly. I wonder. Does that mean it takes weeks? months? years? decades? Centuries? thousands of years? tens of thousands of years? hundreds of thousands of years? millions of years? All of which, there is time for. We have 8 orders of magnitude in time scale that allows for this to happen.
Seems like a lot of time to an evolutionist who has no idea how the mathematics of mutation and selection works. Well, according to evolutionist numbers, you have 500,000 generations to evolve 35,000,000 base substitutions on a 3gig genome to get from primate precursor to humans and chimps. You have no selection pressures to do this and you have no mathematics to support this even if you did have the selection pressures.
That's quite a huge time duration. So again, What does profoundly mean exactly...and remember, we're being mathematical here.
It is far more time than even your extravagant speculation allows for. Evolution by mutation and selection is far too slow to accomplish what your dreams allege.
And are there real examples of multiple selection pressures profoundly slowing the evolutionary process. Yes clown fish, there are numerous real examples of this. I’ve posted dozens of citations which demonstrate the mathematical fact that ev shows.Oh you mean all those citations that have no bearing on your claims?
These citations have no bearing only to those who have no understanding of the mathematics of mutation and selection. So I can understand why these citations don’t seem to have any bearing to you.
Perhaps in your dreams clown fish you see multiple selection pressures accelerating the evolutionary process along with seeing images of lollipops and gumdrops. That’s the only place you see this, you certainly don’t see it in reality. If you did, you would post the citations.excellent. Again you argue against something I never said.
Oh, so clown fish finally acknowledges that multiple selection pressures slow the evolutionary process?
Clown fish, your incompetence in the mathematics of mutation and selection is truly evolutionary.What does this mean? I feel you are tring to be insulting, but it don't know let me see if I can translate:
"Joobz, your inability to understand my lies and nonmath increases based upon environmental adaptations."
Bad translation clown fish, a better translation would be; clown fish doesn’t understand ev and what it shows and clown fish doesn’t understand the real examples of what ev shows. The question is whether this is ignorance or denial on the part of clown fish, I think it is both.
Wow, thank you. I do find myself understanding you less and less as time goes on.
Let’s start with the basics clown fish, 1+1=2.
the question is, if there were multiple copies of you, would my ability to understand you decrease at a faster rate or slower rate?
Clown fish, your inability to understand what is said here is based on your ignorance and denial of what the mathematics of mutation and selection shows and the numerous real examples of this mathematics.

Dr Adequate

14th June 2007, 11:38 AM

Seems like a lot of time to an evolutionist who has no idea how the mathematics of mutation and selection works. Well, according to evolutionist numbers, you have 500,000 generations to evolve 35,000,000 base substitutions on a 3gig genome to get from primate precursor to humans and chimps. You have no selection pressures to do this and you have no mathematics to support this even if you did have the selection pressures. But this is a lie. We showed you the math, remember? And you said it must be wrong, and it turned out you'd got the length of the human genome wrong by a factor of ten, remember? And then when you realised this, you again said that the math must be wrong, remember? And it turned out you'd forgotten that the human genome was diploid, remember? And then you started raving about cheese, remember? And now you're lying about it as though telling lies would magically make the facts go away, aren't you?

Oh, so clown fish finally acknowledges that multiple selection pressures slow the evolutionary process?. But this is a lie. He said no such thing. We can all see that he said no such thing. Why do you tell lies when you know you're going to be caught? Isn't that completely frickin' stupid? You know, the sort of thing an insane halfwitted liar would do?

It is far more time than even your extravagant speculation allows for. Evolution by mutation and selection is far too slow to accomplish what your dreams allege.

These citations have no bearing only to those who have no understanding of the mathematics of mutation and selection. So I can understand why these citations don’t seem to have any bearing to you. You keep talking about "mathematics". Why? You never do any.

1+1=2. Kleinman said something true about mathematics. Well, arithmetic, anyway. Actual mathematics is beyond the poor chap.

Still, it is true. I expect the Four Horsemen of the Apocalypse any minute now.

Lensman

14th June 2007, 11:50 AM

Check this out:

Sinfest today (http://sinfest.net/comikaze/comics/2007-06-14.gif)

Dr Adequate

14th June 2007, 12:00 PM

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Number of posts in which kleinman talks about "mathematics": 294.

Number of posts in which kleinman offers any mathematical reasoning to support his halfwitted fantasies: 0.

To some of us, mathematics is an intellectual discipline. To kleinman, it seems that it's just another magic word by repetition of which he intends to abolish reality.

kleinman

14th June 2007, 12:40 PM

mathematics…Number of posts in which kleinman talks about "mathematics": 294.
Now cheese wiz, don’t forget the number of posts where I cite real examples which demonstrates the mathematics of ev. What the mathematics of ev shows is that multiple selection pressures slow and ultimately stops evolution. Here are two more examples of this mathematics.

http://focus.hms.harvard.edu/2007/042007/systems_biology.shtml (http://focus.hms.harvard.edu/2007/042007/systems_biology.shtml)
Combining two different antibiotics has long been used as a way to prevent resistance.

http://www.genetics.org/cgi/reprint/163/4/1237.pdf (http://www.genetics.org/cgi/reprint/163/4/1237.pdf)
In addition to predicting the ways in which specific enzymes can evolve the ability to confer resistance to different antibiotics, pharmaceutical companies could also use this method to test the effectiveness of using different antibiotic combinations to inhibit the evolution of resistance. For example, while it is clear that selection for resistance to cefepime indirectly selects TEM alleles that confer high levels of resistance to aztreonam and ceftazadime, it is possible that the TEM enzymes are not capable of conferring high levels of resistance to cefepime and cefotaxime at the same time. Combination of those two antibiotics may increase the time required for resistance to those antibiotics to evolve.

joobz

14th June 2007, 12:45 PM

Bad translation clown fish, a better translation would be; clown fish doesn’t understand ev and what it shows and clown fish doesn’t understand the real examples of what ev shows. You find the need to translate your own writings now? So you admit you post utter gibberish?

Clown fish, your inability to understand what is said here is based on your ignorance and denial of what the mathematics of mutation and selection shows and the numerous real examples of this mathematics.
translation:
"Joobz, your inability to understand my lies and foolish meanderings is based on your refusal to accept magical words like "fish", "mathematical" and "profoundly". Watermelon hate hopscotch demure."
I'm not quite certain what you mean by that last bit. The Kleinman to reality translator isn't perfected yet.

joobz

14th June 2007, 01:01 PM

kleinman

14th June 2007, 01:15 PM

http://focus.hms.harvard.edu/2007/042007/systems_biology.shtml (http://focus.hms.harvard.edu/2007/042007/systems_biology.shtml)
As expected, the resistant strain out-competed the susceptible one when the two drugs were synergistic, but when one drug suppressed the other, there was less selection for resistance overall, and Chait found a region of drug concentration at which the resistant strain lost the battle.You know what you call each of those events? hmmm? Here's a hint it starts with a "ev" and ends with a "olution"...
Silly clown fish, some combinations of selection pressures slow evolution more than others. Are you going to try to argue this is an example of multiple selection pressures accelerating evolution? Let’s see you try to twist the words to do this.

joobz

14th June 2007, 01:25 PM

http://focus.hms.harvard.edu/2007/042007/systems_biology.shtml (http://focus.hms.harvard.edu/2007/042007/systems_biology.shtml)

Silly clown fish, some combinations of selection pressures slow evolution more than others. Are you going to try to argue this is an example of multiple selection pressures accelerating evolution? Let’s see you try to twist the words to do this.
Yeah!! I knew you'd write something foolish and idiotic. You never dissappoint. All that quote shows is that the change in population varies with concentration and drug combination. And yet you make a comment about rate again.

delphi_ote

14th June 2007, 04:02 PM

:eek:
You mean drug interactions and their effects on bacterial drug resistance are more complicated than kleinman depicts them?! Say it isn't so! I'm shocked, I tell you. Shocked!

Dr Adequate

14th June 2007, 06:08 PM

It is better for grammatically challenged clown fish speak in short sentences. I believe that you want the word "to" in that sentence.

The gibberish which you wish to recite should read: "It is better for grammatically challenged clown fish to speak in short sentences."

I realise that you are a halfwit, but surely basic English grammar is not beyond you.

Anyway, you were lying to us about how joobz is "grammatically challenged". Do go on, this is most amusing,

kleinman

14th June 2007, 06:12 PM

Silly clown fish, some combinations of selection pressures slow evolution more than others. Are you going to try to argue this is an example of multiple selection pressures accelerating evolution? Let’s see you try to twist the words to do this.Yeah!! I knew you'd write something foolish and idiotic. You never dissappoint. All that quote shows is that the change in population varies with concentration and drug combination. And yet you make a comment about rate again.
That’s what selection pressures do to populations, they drive them down silly clown fish. In your static mind you can’t see that there is a rate associated with evolution and that rate is really slow. And why is the rate of evolution slow by mutation and selection? It is really slow because multiple selection pressures confound the evolutionary process. That’s what the mathematics of ev shows and that is what the numerous citations I have posted show including the one you have just flopped out a comment on.
You mean drug interactions and their effects on bacterial drug resistance are more complicated than kleinman depicts them?! Say it isn't so! I'm shocked, I tell you. Shocked!
Delphi, I’m surprised you took enough time off your skateboard to make post a comment. Certainly the mathematics is more complicated than what ev simulates, however Dr Schneider modeled the essential variables to properly capture the mathematics of mutation and selection. And the overriding properties of evolution by mutation and selection are that the greater the number of selection pressures, the slower evolution proceeds and the longer the genome, the slower evolution proceeds. There may be finer points to the evolutionary process where drug resistance can be made to devolve by applying combination selection pressures. Do you want to propose the theory of devolution? So you all seem to be annoyed by my posting of citations which show that multiple selection pressures slow and ultimately stop evolution, here are two more.

http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowFulltext&ArtikelNr=95155&ProduktNr=224031 (http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowFulltext&ArtikelNr=95155&ProduktNr=224031)
Objective: Ribavirin and interferon combination therapy is more effective than interferon monotherapy in patients with chronic hepatitis C virus (HCV) infection. To test the hypothesis that ribavirin induces nucleotide substitutions in the viral genome and reduces viral load by forcing it into error catastrophe in the combination therapy, we investigated the molecular evolution of HCV quasispecies in 3 patients who received combination therapy and 2 patients who received interferon monotherapy. Methods: The quasispecies were analyzed before and after therapy by sequencing at least 8 clones in five regions of the HCV genome; 5' untranslated region, EI, E2, NS5A and NS5B. Results: Marked genetic drift was observed in the NS5A and NS5B regions in patients treated with combination therapy. However, genetic distances between clones obtained after therapy were closer than those obtained before therapy. Conclusion: Our results suggest that the combination therapy modified HCV quasispecies, but that this did not reflect the induction of error catastrophe by ribavirin. Modification of quasispecies by this therapy requires further investigation in a larger number of patients to elucidate the possible mechanism of viral resistance against the combination therapy.

http://jcm.asm.org/cgi/reprint/43/1/208.pdf (http://jcm.asm.org/cgi/reprint/43/1/208.pdf)
The clinical settings in which combination anti-CMV therapy should be used remain to be established. The observation of attenuated growth in viruses with resistant genotypes (such as the T838A and D588N pol mutations seen here) may help to explain the reported superior clinical efficacy of combination therapy compared with single-agent anti-CMV therapy (21), even when one of the agents appears to have lost its activity against CMV (29). Maintaining therapy with the drug to which resistance has developed could be beneficial if the drug selects for growth-impaired genotypes.

Dr Adequate

14th June 2007, 06:23 PM

:eek:
You mean drug interactions and their effects on bacterial drug resistance are more complicated than kleinman depicts them?! Say it isn't so! I'm shocked, I tell you. Shocked! You think that kleinman might be a teensy bit dishonest?

Who would have thought that he might be a stupid dirty liar droning out witless lies over and over to an audience who know that he is a stupid crawling filthy liar?

We'd never have guessed, unless by some wild coincidence we'd heard him bleat out his moronic pathetic soiled dirty stinking filthy lies like the degraded halfwitted degenerate sordid putrid stinking liar that he is.

Oh, look, we have.

Dr Adequate

14th June 2007, 06:26 PM

That’s what selection pressures do to populations, they drive them down silly clown fish. In your static mind you can’t see that there is a rate associated with evolution and that rate is really slow. And why is the rate of evolution slow by mutation and selection? It is really slow because multiple selection pressures confound the evolutionary process. That’s what the mathematics of ev shows and that is what the numerous citations I have posted show including the one you have just flopped out a comment on.

Delphi, I’m surprised you took enough time off your skateboard to make post a comment. Certainly the mathematics is more complicated than what ev simulates, however Dr Schneider modeled the essential variables to properly capture the mathematics of mutation and selection. And the overriding properties of evolution by mutation and selection are that the greater the number of selection pressures, the slower evolution proceeds and the longer the genome, the slower evolution proceeds. There may be finer points to the evolutionary process where drug resistance can be made to devolve by applying combination selection pressures. Do you want to propose the theory of devolution? So you all seem to be annoyed by my posting of citations which show that multiple selection pressures slow and ultimately stop evolution, here are two more.

http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowFulltext&ArtikelNr=95155&ProduktNr=224031 (http://content.karger.com/ProdukteDB/produkte.asp?Aktion=ShowFulltext&ArtikelNr=95155&ProduktNr=224031)

http://jcm.asm.org/cgi/reprint/43/1/208.pdf (http://jcm.asm.org/cgi/reprint/43/1/208.pdf)
No new lies then?

Not only are you crap at biology, you're crap at lying about biology.

You are a failed liar.

kleinman

14th June 2007, 06:43 PM

Not only are you crap at biology, you're crap at lying about biology.
Poor cheese wiz, his gif and awe attempt at showing multiple selection pressures accelerates evolution is a complete failure. Not only does he have no real examples of his gif, he demonstrates that he has a PhD in amathematics. I do enjoy posting citations which demonstrate the mathematics of ev. It is so effective at annoying cheese wiz. Anyone care for some cheese wiz and whine? Now you mathematically deprived evolutionists all have a good weekend, I’ll be back next week with more citations that show that multiple selection pressures slow and ultimately stop evolution. In case you didn’t know this, the mathematics of ev shows this.

joobz

14th June 2007, 07:03 PM

Dr Adequate

14th June 2007, 07:44 PM

Poor cheese wiz, his gif and awe attempt at showing multiple selection pressures accelerates evolution is a complete failure. Not only does he have no real examples of his gif, he demonstrates that he has a PhD in amathematics. I do enjoy posting citations which demonstrate the mathematics of ev. It is so effective at annoying cheese wiz. Anyone care for some cheese wiz and whine? Now you mathematically deprived evolutionists all have a good weekend, I’ll be back next week with more citations that show that multiple selection pressures slow and ultimately stop evolution. In case you didn’t know this, the mathematics of ev shows this. So, you don't have any new lies?

As I said, not only are you crap at biology, you're also crap at lying about biology.

I notice that you have once again recited the magic word "cheese", and once again, it has not changed reality: you are still crap at lying about biology.

Kleinman, you are crap at lying about biology. You have not deceived anyone. Not one single person. If you are insane enough to think you have, please point out one person (other than yourself) who has been deceived by your halfwitted lies.

Dr Adequate

14th June 2007, 07:49 PM

Poor cheese wiz, his gif and awe attempt at showing multiple selection pressures accelerates evolution is a complete failure. Not only does he have no real examples of his gif, he demonstrates that he has a PhD in amathematics. There are a lot of stupid magic words here. "Cheeze wiz"; "gif and awe"; "amathematics". We've all seen you trying to make reality go away by reciting magic words. You failed. You are an idiot. You do not have magical powers.

I think I terrify you more than anyone on this thread.

In real life, which is kind of different from the crazy imaginary world in your head, I have a PhD in mathematics, and this scares you so ****less that you have to lie about it over and over, doesn't it?

Dr Adequate

14th June 2007, 07:54 PM

Latest kleinman statistic: he has made 78 posts involving the word "cheese", And reality still hasn't vanished and been replaced by his halfwitted fantasies.

Mercutio

14th June 2007, 09:34 PM

Multiple selection pressures, that’s what slows,
the evolution of genetic codes.
The only thing that this does show,
Is that the theory of evolution does explode.
There are no moving goal posts on this thread,
There’s only mathematics showing the theory of evolution is dead.

Your grasp of mathematics, logic, and evolutionary theory is matched by your grasp of meter and rhyme. I begin to suspect that you are actually a parody. No one is that bad at poetry, even if they might be at evolution.

Dr Adequate

15th June 2007, 07:37 AM

Is there no beginning to his talents?

jimbob

15th June 2007, 11:04 AM

This is as good thread as any to post this link:

http://www.b3ta.com/challenge/creationism/

Is this thread derailable?

Dr Adequate

15th June 2007, 11:51 AM

I like it.

http://www.b3tards.com/u/21ab3a0ca48f542bebe6/creationism.gif

jimbob

15th June 2007, 03:54 PM

How about this one?
http://www.pepperzone.org/images/b3ta/creation.gif

delphi_ote

16th June 2007, 11:21 PM

Delphi, I’m surprised you took enough time off your skateboard to make post a comment.
Poor kleinman. Are the damn crazy kids riding all over your lawn and disproving your favorite fairy tale with scientific evidence again?

Mr. Scott

17th June 2007, 07:30 AM

Do you care to describe the selection pressure that evolved reptiles into birds?

Start with a pterodactyl-like dino. The pressure is: those that fly better eat better and escape predators better. So, scales that became more feathery were an advantage in flying, and after many, many small improvements to feathers, birds came into their own.

The evidence that birds and dinosaurs are related keeps piling up, and evidence against it doesn't.

Here's a link to a good article with other links with the evidence that birds evolved from dinosaurs.

Then, there was a recent discovery of soft tissue inside dinosaur bones that support their relation to birds. Here's a bit of an article about it from the Chicago Tribune (http://www.accessmylibrary.com/premium/0286/0286-8298682.html)

The science team that previously announced the discovery of surviving soft tissue in the fossilized thighbone of a Tyrannosaurus rex has determined the dinosaur was a young female and she had been producing eggs when she died.

The team detected microscopic evidence of a specialized reproductive tissue, known as medullary bone, which is found in modern birds. The first such discovery in any dinosaur, it strengthens the link between dinosaurs and living birds

Gargoyle

17th June 2007, 07:51 AM

Wow... This thread is a classic! Still going after all this time. :jaw-dropp
I love the circular arguments of the "creationistas"!!

:cheerleader5
5000 GET! GO GO GO!

Mr. Scott

17th June 2007, 10:39 AM

Here's a link to a good article with other links with the evidence that birds evolved from dinosaurs.

Link to article. (http://hometown.aol.com/darwinpage/dinobirds.htm)

Quote from article:There is a massive body of published evidence for the evolution of birds. Unfortunately, most of it is not available on the Internet, at least not without expensive subscriptions to a wide variety of science journals. For the average person access to many science journals is difficult unless one has available a university or museum library. I give below links to numerous websites containing relevant articles.

Here's a nice article about how scales evolved into feathers: In a first, Keck researchers show how feathers evolved (http://www.usc.edu/uscnews/stories/8456.html)

This quote is also a dilly:Feathers and scales are both made of keratin. As with reptilian scales, feathers begin their development from a follicle. A single point mutation will change the scales of a chicken into feathers.

Dr Adequate

17th June 2007, 12:01 PM

Start with a pterodactyl-like dino. Or if the Oxymoron Shop is fresh out of them, you could just use a coelurosaur.

jimbob

17th June 2007, 12:24 PM

In a similar vein to my previous posts (I am taking the thread title as an instruction)

http://intelligentdesignr.org.uk/

Thanks to Vbloke at badscience.net

I especially liked the many typos

Mr. Scott

17th June 2007, 07:02 PM

Or if the Oxymoron Shop is fresh out of them, you could just use a coelurosaur.

Do I need to fill in every gap for you evolutionists? God obviously turned a pterodactyl-like dino into a coelurosaur and back again. I win!

Thanks for the adequetizing. :D

BTW: The question posed was "What selection pressures evolve birds from reptiles" which I answered with an example more easily digestible for a creationist.

Oh, before I forget: cheese, cheese-wiz, string cheese, gif and awe, clown fish, amathematical.

Schneibster

17th June 2007, 07:13 PM

In a similar vein to my previous posts (I am taking the thread title as an instruction)

http://intelligentdesignr.org.uk/

Thanks to Vbloke at badscience.net

I especially liked the many typosHamsterma was good. I also enjoyed hypr-bunnies from a highr dimension.

Mr. Scott

17th June 2007, 07:35 PM

Hamsterma was good. I also enjoyed hypr-bunnies from a highr dimension.

My favorite is "Unlessenable complicatedness" from Evidence for intelligent designr (http://intelligentdesignr.org.uk/evidence.html)

Foster Zygote

18th June 2007, 09:45 AM

I believe that you want the word "to" in that sentence.

The gibberish which you wish to recite should read: "It is better for grammatically challenged clown fish to speak in short sentences."

I realise that you are a halfwit, but surely basic English grammar is not beyond you.

Anyway, you were lying to us about how joobz is "grammatically challenged". Do go on, this is most amusing,

Oh, the delicious irony of committing a grammatic error in a post critical of another's grammar.

Foster Zygote

18th June 2007, 09:56 AM

Do I need to fill in every gap for you evolutionists? God obviously turned a pterodactyl-like dino into a coelurosaur and back again. I win!

Thanks for the adequetizing. :D

BTW: The question posed was "What selection pressures evolve birds from reptiles" which I answered with an example more easily digestible for a creationist.

Oh, before I forget: cheese, cheese-wiz, string cheese, gif and awe, clown fish, amathematical.

Not to dispute your main point, but pterosaurs, like the marine reptiles of the time, were not actually dinosaurs. They were an evolutionary "dead end" and are not the ancestors of birds. Current theory is that feathers first evolved in theropods as insulation.

Mr. Scott

18th June 2007, 10:29 AM

Not to dispute your main point, but pterosaurs, like the marine reptiles of the time, were not actually dinosaurs. They were an evolutionary "dead end" and are not the ancestors of birds. Current theory is that feathers first evolved in theropods as insulation.

...which touches on a point that might be missed in this thread. A random mutation can offer an advantage that is not related to a selection pressure. We keep thinking of point mutations of microbes so they can survive an antibiotic, as if it was some kind of cause and effect. How about a mutation that simply makes an altered organism that can then evolve in its own way to fill a niche?

We have to dismiss the implication in Kleinman's posts that a "pressure" causes a point mutation out of determination to resist that pressure. It's his creationist heart subtly altering the slant of evolutionary theory. Sometimes, no "pressure" is necessary. A feathered dinosaur may just do well in a previously unoccupied niche, no?

cyborg

18th June 2007, 01:12 PM

We keep thinking of point mutations of microbes so they can survive an antibiotic, as if it was some kind of cause and effect.

No, that would be kleinman who is insisting that the mutation itself must be selected, not the result of that mutation.

A priori selection is design. A posteriori selection is evolution.

Kleinman's creationist viewpoint requires that a priori selection is the only type that can allow for certain variations in genomic structure. Since he clearly cannot argue that an a posteriori selection of a mutation would in any way result in a different outcome than an a priori selection (since it would be the same mutation for the same organism in the same environment) he is left arguing that there must be some key mutations which a posteriori selection would never allow propagation thereof and as such must be inserted a priori by a designer - namely an omnipotent god.

He does this by insisting that any particular mutation he selects is crucial, presents the trivially obvious fact that particular mutation is unlikely and then concludes that it wouldn't have happened unless someone made it happen.

As the rest of us realise that no particular mutation is crucial, necessary or intended the fact that the particular genetic landscape happens to stand as it is has no bearing on the mechanism as to how it got here. Kleinman either cannot or will not acknowledge this.

Alareth

18th June 2007, 04:01 PM

There was an engineer I saw on TV one time that was studing the designs of animal species and trying to adapt them to machines.

His philosophy was, "Nature already tried everything and all that is left are the experiments that worked."

joobz

18th June 2007, 08:56 PM

His philosophy was, "Nature already tried everything and all that is left are the experiments that worked."
Yeah. it's an easy mistake to make. At least in his instance, it's a faulty premise that doesn't detract from the goal of his research. Biomimetics is a very interesting area of engineering research.

kleinman

19th June 2007, 07:05 AM

Poor cheese wiz, his gif and awe attempt at showing multiple selection pressures accelerates evolution is a complete failure.
what does this mean? Are you referring to the model of multiple pressures that you never bothered to address? Instead of making this UNSUBSTANTIATED ASSERTION, present exactly what parts of his model are flawed.
My apologies for not addressing to cheese wiz’s silly gif, here is an appropriate response:
http://forums.randi.org/images/smilies/doglaugh.gif
Exactly what part of cheese wiz’s silly gif is flawed, the part which shows that multiple selection pressures accelerates evolution. Of course, a couple of lines on a gif is enough to convince any brainwashed evolutionarian that his theory is true.
Not only does he have no real examples of his gif, he demonstrates that he has a PhD in amathematics. I do enjoy posting citations which demonstrate the mathematics of ev.ev shows the de novo evolution of a gene from single point mutation alone is possible. Since you have presented citations demonstrating this claim, you further proved evolution. Thank you for ending your foolishness.\
Well little clown fish, you must know something that Paul doesn’t know because Paul doesn’t claim that ev models the de novo evolution of binding sites let alone the de novo evolution of a gene. Fear not little clown fish, I’ll keep posting real examples of how mutation and selection actually works so that the mathematics of ev will some day become apparent to you then the light will finally turn on for you dim bulbs.
As I said, not only are you crap at biology, you're also crap at lying about biology.
Now cheese wiz, you know that I enjoy annoying you with the truth and the truth is that multiple selection pressures slow and ultimately stop evolution. However, do not stop posting your gifs, especially those which show that multiple selection pressures accelerate evolution. We enjoy reading your citations of real examples of this phenomenon that you have described with your pretty picture. How many citations have you posted so far that shows that multiple selection pressures accelerate evolution, there have been so many I seem to have lost count. On the other hand I have had to toil at my keyboard, sweat dripping from my brow, and I have found only about 50 real examples of multiple selection pressures slowing and ultimately stopping evolution including a 1958 Nobel Prize lecture. Cheese wiz, your skills at amathematics are a wonder to behold.
Multiple selection pressures, that’s what slows,
the evolution of genetic codes.
The only thing that this does show,
Is that the theory of evolution does explode.
There are no moving goal posts on this thread,
There’s only mathematics showing the theory of evolution is dead.Your grasp of mathematics, logic, and evolutionary theory is matched by your grasp of meter and rhyme. I begin to suspect that you are actually a parody. No one is that bad at poetry, even if they might be at evolution.
Alas, if the theory of evolution were a rose,
It would smell like limburger under your nose.
Delphi, I’m surprised you took enough time off your skateboard to make post a comment.Poor kleinman. Are the damn crazy kids riding all over your lawn and disproving your favorite fairy tale with scientific evidence again?
I don’t have a lawn Delphi but I do have the Wikipedia reference to the fitness landscape thanks to you. I’m not sure what scientific evidence you are talking about which shows that multiple selection pressures accelerate evolution. Along with fitness landscape, I have ev and about 50 real examples which show that multiple selection pressures slow and ultimately stops evolution. Doesn’t your experience with your sock drawer convince you of this mathematical fact?
Do you care to describe the selection pressure that evolved reptiles into birds?Start with a pterodactyl-like dino. The pressure is: those that fly better eat better and escape predators better. So, scales that became more feathery were an advantage in flying, and after many, many small improvements to feathers, birds came into their own.
Now pussy cat, that’s an interesting speculation which should give warm and tingly feelings to evolutionists far and wide. Too bad the mathematics of mutation and selection doesn’t support this possibility.
The evidence that birds and dinosaurs are related keeps piling up, and evidence against it doesn't.
Only the evidence of how mutation and selection works mathematically as shown by ev and Delphi’s reference to the fitness landscape and the 50 or so citations which show empirically how mutation and selection works piles up against your speculations but don’t let this stop you evolutionists from developing your mathematically deficient science fiction.
I love the circular arguments of the "creationistas"!!
This circular argument presented here is a noose that strangulates the theory of evolution. Where do you want the remains of the theory buried?
Hamsterma was good. I also enjoyed hypr-bunnies from a highr dimension.
Well Schneibster, aren’t you going to complain that I’m trying to drive a wedge between the physical and biological sciences? Or are you another one of the dim evolutionist bulbs who is having trouble understanding what the mathematics of ev is shows, that is multiple selection pressures slow and ultimately stop evolution. Perhaps you want to argue that cheese wiz’s gif that shows that multiple selection pressures accelerate evolution is correct? Perhaps you will give us a real example of cheese wiz’s silly gif where multiple selection pressures accelerate evolution? You evolutionists are really having trouble with this mathematics of mutation and selection.
Not to dispute your main point, but pterosaurs, like the marine reptiles of the time, were not actually dinosaurs. They were an evolutionary "dead end" and are not the ancestors of birds. Current theory is that feathers first evolved in theropods as insulation.
If abiogenesis had occurred based on silicon rather than carbon then fiberglass insulation would have evolved.
We keep thinking of point mutations of microbes so they can survive an antibiotic, as if it was some kind of cause and effect.No, that would be kleinman who is insisting that the mutation itself must be selected, not the result of that mutation.
Viva la cruft!
There was an engineer I saw on TV one time that was studing the designs of animal species and trying to adapt them to machines.

His philosophy was, "Nature already tried everything and all that is left are the experiments that worked."
That’s the problem with you evolutionists. You expect TV to provide you with the proof for your theory. Next time try something other than the SciFi channel, in fact instead of looking at TV, look at ev.

Here’s a couple of more examples of how mutation and selection actually works, you remember what ev shows don’t you, multiple selection pressures slow and ultimately stop evolution.

http://www.medscape.com/viewarticle/424503_6 (http://www.medscape.com/viewarticle/424503_6)
While we await the results of studies that will help define the best time to alter therapy, the guiding principle for selecting a new combination remains to switch as many drugs as possible, preferably including new drugs from two or more different classes of agents. Dr. Lawrence illustrated this point by discussing ACTG 364, a rollover study for patients who participated in ACTG 175 (the study that compared zidovudine monotherapy versus ddI monotherapy and ZDV + ddI and ZDV + ddC) then received a second nucleoside RTI regimen in ACTG 302/303 (a rollover study of ACTG 175)[12]. Thus, patients in ACTG 364 had experience with at least two nucleoside reverse transcriptase inhibitors, but were NNRTI and PI naive. Patients were assigned to efavirenz (600 mg qd), nelfinavir (750 mg q8h), or a combination of the two drugs, in combination with two nucleoside RTIs (ideally those ones that the patient had not experienced). After 24 weeks of study, a greater proportion of patients on the four drug combination had viral loads less than 500 copies/mL than patients receiving triple therapy with either efavirenz or nelfinavir.

https://www.mja.com.au/public/issues/186_04_190207/sas10773_fm.html (https://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.
and
Studies of combination therapy to date have used traditional endpoints — short-term reduction of HBV DNA levels and HBeAg seroconversion — rather than evolution of resistance.
and
There is now an emerging body of data suggesting that combination therapy can decrease antiviral resistance in HBV infection, the endpoint likely to be of greatest long-term importance, and, rather than adding or replacing an antiviral agent after resistance develops, it is likely to be more effective in treatment-naïve patients.
Ev shows how mutation and selection actually works. Delphi’s reference to Wikipedia and the fitness landscape supports this mathematical fact and I will continue to post real examples of this mathematical fact that multiple selection pressures slow and ultimately stop evolution.

joobz

19th June 2007, 07:27 AM

My apologies for not addressing to cheese wiz’s silly gif, here is an appropriate response:
http://forums.randi.org/images/smilies/doglaugh.gif
Exactly what part of cheese wiz’s silly gif is flawed, the part which shows that multiple selection pressures accelerates evolution. Of course, a couple of lines on a gif is enough to convince any brainwashed evolutionarian that his theory is true.
\
Well little clown fish, you must know something that Paul doesn’t know because Paul doesn’t claim that ev models the de novo evolution of binding sites let alone the de novo evolution of a gene. Fear not little clown fish, I’ll keep posting real examples of how mutation and selection actually works so that the mathematics of ev will some day become apparent to you then the light will finally turn on for you dim bulbs.

Now cheese wiz, you know that I enjoy annoying you with the truth and the truth is that multiple selection pressures slow and ultimately stop evolution. However, do not stop posting your gifs, especially those which show that multiple selection pressures accelerate evolution. We enjoy reading your citations of real examples of this phenomenon that you have described with your pretty picture. How many citations have you posted so far that shows that multiple selection pressures accelerate evolution, there have been so many I seem to have lost count. On the other hand I have had to toil at my keyboard, sweat dripping from my brow, and I have found only about 50 real examples of multiple selection pressures slowing and ultimately stopping evolution including a 1958 Nobel Prize lecture. Cheese wiz, your skills at amathematics are a wonder to behold.

Alas, if the theory of evolution were a rose,
It would smell like limburger under your nose.

I don’t have a lawn Delphi but I do have the Wikipedia reference to the fitness landscape thanks to you. I’m not sure what scientific evidence you are talking about which shows that multiple selection pressures accelerate evolution. Along with fitness landscape, I have ev and about 50 real examples which show that multiple selection pressures slow and ultimately stops evolution. Doesn’t your experience with your sock drawer convince you of this mathematical fact?

Now pussy cat, that’s an interesting speculation which should give warm and tingly feelings to evolutionists far and wide. Too bad the mathematics of mutation and selection doesn’t support this possibility.

Only the evidence of how mutation and selection works mathematically as shown by ev and Delphi’s reference to the fitness landscape and the 50 or so citations which show empirically how mutation and selection works piles up against your speculations but don’t let this stop you evolutionists from developing your mathematically deficient science fiction.

This circular argument presented here is a noose that strangulates the theory of evolution. Where do you want the remains of the theory buried?

Well Schneibster, aren’t you going to complain that I’m trying to drive a wedge between the physical and biological sciences? Or are you another one of the dim evolutionist bulbs who is having trouble understanding what the mathematics of ev is shows, that is multiple selection pressures slow and ultimately stop evolution. Perhaps you want to argue that cheese wiz’s gif that shows that multiple selection pressures accelerate evolution is correct? Perhaps you will give us a real example of cheese wiz’s silly gif where multiple selection pressures accelerate evolution? You evolutionists are really having trouble with this mathematics of mutation and selection.

If abiogenesis had occurred based on silicon rather than carbon then fiberglass insulation would have evolved.

Viva la cruft!

That’s the problem with you evolutionists. You expect TV to provide you with the proof for your theory. Next time try something other than the SciFi channel, in fact instead of looking at TV, look at ev.

Here’s a couple of more examples of how mutation and selection actually works, you remember what ev shows don’t you, multiple selection pressures slow and ultimately stop evolution.

http://www.medscape.com/viewarticle/424503_6 (http://www.medscape.com/viewarticle/424503_6)

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

and

and

Ev shows how mutation and selection actually works. Delphi’s reference to Wikipedia and the fitness landscape supports this mathematical fact and I will continue to post real examples of this mathematical fact that multiple selection pressures slow and ultimately stop evolution.
What you've just said is one of the most insanely idiotic things I have ever heard. At no point in your rambling, incoherent response were you even close to anything that could be considered a rational thought. Everyone in this room is now dumber for having listened to it. I award you no points, and may God have mercy on your soul.

kleinman

19th June 2007, 07:50 AM

What you've just said is one of the most insanely idiotic things I have ever heard. At no point in your rambling, incoherent response were you even close to anything that could be considered a rational thought. Everyone in this room is now dumber for having listened to it. I award you no points, and may God have mercy on your soul.
Clown fish, just what kind of mathematics did they teach you when you were trained as an alchemical engineer? You obviously have no experience in the mathematics of optimization otherwise you would understand that the greater the number of optimization conditions you have, the slower the process is. You obviously have no experience in the mathematics of database sorting otherwise you would understand that the greater the number of sorting conditions, the slower the process is. And you obviously have no experience or understanding of the mathematics mutation and selection otherwise you would know that the greater the number of selection conditions, the slower the evolutionary process proceeds. You do have experience in alchemical engineering; you do know how to turn inorganic matter into life (well except you have no idea how to generate ribose nonenzymatically). What a fish story you tell clown fish. Now don’t you worry, I’ll continue to post citations which show that multiple selection pressures slow and ultimately stop the evolutionary process. Then some day you will understand the mathematics of mutation and selection. Until then, tell us more fish stories (or are they reptile evolving to bird stories) about the theory of evolution.

rcronk

19th June 2007, 10:07 AM

joobz

19th June 2007, 10:35 AM

Clown fish, just what kind of mathematics did they teach you when you were trained as an alchemical engineer? You obviously have no experience in the mathematics of optimization otherwise you would understand that the greater the number of optimization conditions you have, the slower the process is. You obviously have no experience in the mathematics of database sorting otherwise you would understand that the greater the number of sorting conditions, the slower the process is. And you obviously have no experience or understanding of the mathematics mutation and selection otherwise you would know that the greater the number of selection conditions, the slower the evolutionary process proceeds. You do have experience in alchemical engineering; you do know how to turn inorganic matter into life (well except you have no idea how to generate ribose nonenzymatically). What a fish story you tell clown fish. Now don’t you worry, I’ll continue to post citations which show that multiple selection pressures slow and ultimately stop the evolutionary process. Then some day you will understand the mathematics of mutation and selection. Until then, tell us more fish stories (or are they reptile evolving to bird stories) about the theory of evolution.
please tell me you aren't confusing code optimization times with actual real life times again. You know when things happen in reality, there isn't some big computer that's crunching numbers to calculate the physics of everything occuring, right? We aren't in some big game of Quake that will start to lag if there are multiple projectiles wizzing arroung at the same time. You know this, right?

We are still waiting for your point for point proof that evolution can't occur. PLEASE show me exactly how at every place on this earth for the past 5 billion years, conditions existed that resulted in too strong of selection conditions and would result in extinction rather than evolution.

joobz

19th June 2007, 10:39 AM

rcronk

19th June 2007, 10:49 AM

Ok - that looks like a possible "I'll put down my weapon if the other guy does" vote. Does "the other guy (Kleinman)" agree?

Myriad

19th June 2007, 11:42 AM

A momentous milestone for this discussion has passed unnoticed. June 13th was the first anniversary of the original thread at the evolutionisdead forums. (http://www.evolutionisdead.com/forum/viewtopic.php?t=348)

Reading portions of that thread and early parts of this one, it's clear that the quality of the discussion has declined. For my own part, I decided to cease addressing Dr. Kleinman directly late last November, for the reasons I explained in the (currently) next-to-last post in the evolutionisdead thread. (You can link to here (http://www.evolutionisdead.com/forum/viewtopic.php?t=348&start=450) and scroll down, but be warned that because of evolutionisdead's practice of deleting posts, their database is internally inconsistent and links often malfunction.) I reproduce the relevant portion here:

Alan, I see no reason to accept your halfhearted and self-servingly misdirected apology. (It is not "splitting hairs" to point out that you accused me of lying and demanded apologies when I was actually telling the truth.) Sure, your excuse of having misread the post means you're not a deliberate baldfaced liar. But it also means you are something that, for discourse purposes, is worse: a careless reader.

It's unfortunate. I'd rather speak to a baldfaced liar. In that dialog there's hope. A liar usually cares about the information he's lying about (or else, why would he bother to lie?). A liar can be confronted with evidence of his lies, and might possibly feel some shame. A liar might be convinced that lying is wrong, that telling the truth would be better.

But for a careless reader -- and I see you as careless in every sense of the word; in the sense of sloppy and error-prone, but also in the sense that you literally do not care about what others write -- is a hopeless case. If a reader doesn't care enough to actually read what one writes, then what can more writing accomplish?...

(The "apology" referred to precedes that post, and was also posted by Dr. Kleinman here in this thread (http://forums.randi.org/showthread.php?postid=2129598#post2129598).)

I have considered, in honor of the discussion's first birthday (soon it will be walking and talking, and it's long overdue for weaning), resuming actual dialog. But at present there are no points under discussion worth addressing. We'll see what develops.

Also, rcronk, your complaint is groundless in one respect. While the topic of the original eid thread was the ev program, the original topic of this thread was ways in which creationists are annoying. Dr. Kleinman volunteered to provide examples. The ensuing discussion of the science -- interesting as it might have been, for a while -- was, technically, off-topic.

Respectfully,
Myriad

Dr Adequate

19th June 2007, 11:58 AM

My apologies for not addressing to cheese wiz’s silly gif, here is an appropriate response:
http://forums.randi.org/images/smilies/doglaugh.gif
Exactly what part of cheese wiz’s silly gif is flawed, the part which shows that multiple selection pressures accelerates evolution. Of course, a couple of lines on a gif is enough to convince any brainwashed evolutionarian that his theory is true.
\
Well little clown fish, you must know something that Paul doesn’t know because Paul doesn’t claim that ev models the de novo evolution of binding sites let alone the de novo evolution of a gene. Fear not little clown fish, I’ll keep posting real examples of how mutation and selection actually works so that the mathematics of ev will some day become apparent to you then the light will finally turn on for you dim bulbs.

Now cheese wiz, you know that I enjoy annoying you with the truth and the truth is that multiple selection pressures slow and ultimately stop evolution. However, do not stop posting your gifs, especially those which show that multiple selection pressures accelerate evolution. We enjoy reading your citations of real examples of this phenomenon that you have described with your pretty picture. How many citations have you posted so far that shows that multiple selection pressures accelerate evolution, there have been so many I seem to have lost count. On the other hand I have had to toil at my keyboard, sweat dripping from my brow, and I have found only about 50 real examples of multiple selection pressures slowing and ultimately stopping evolution including a 1958 Nobel Prize lecture. Cheese wiz, your skills at amathematics are a wonder to behold.

Alas, if the theory of evolution were a rose,
It would smell like limburger under your nose.

I don’t have a lawn Delphi but I do have the Wikipedia reference to the fitness landscape thanks to you. I’m not sure what scientific evidence you are talking about which shows that multiple selection pressures accelerate evolution. Along with fitness landscape, I have ev and about 50 real examples which show that multiple selection pressures slow and ultimately stops evolution. Doesn’t your experience with your sock drawer convince you of this mathematical fact?

Now pussy cat, that’s an interesting speculation which should give warm and tingly feelings to evolutionists far and wide. Too bad the mathematics of mutation and selection doesn’t support this possibility.

Only the evidence of how mutation and selection works mathematically as shown by ev and Delphi’s reference to the fitness landscape and the 50 or so citations which show empirically how mutation and selection works piles up against your speculations but don’t let this stop you evolutionists from developing your mathematically deficient science fiction.

This circular argument presented here is a noose that strangulates the theory of evolution. Where do you want the remains of the theory buried?

Well Schneibster, aren’t you going to complain that I’m trying to drive a wedge between the physical and biological sciences? Or are you another one of the dim evolutionist bulbs who is having trouble understanding what the mathematics of ev is shows, that is multiple selection pressures slow and ultimately stop evolution. Perhaps you want to argue that cheese wiz’s gif that shows that multiple selection pressures accelerate evolution is correct? Perhaps you will give us a real example of cheese wiz’s silly gif where multiple selection pressures accelerate evolution? You evolutionists are really having trouble with this mathematics of mutation and selection.

If abiogenesis had occurred based on silicon rather than carbon then fiberglass insulation would have evolved.

Viva la cruft!

That’s the problem with you evolutionists. You expect TV to provide you with the proof for your theory. Next time try something other than the SciFi channel, in fact instead of looking at TV, look at ev.

Here’s a couple of more examples of how mutation and selection actually works, you remember what ev shows don’t you, multiple selection pressures slow and ultimately stop evolution.

http://www.medscape.com/viewarticle/424503_6 (http://www.medscape.com/viewarticle/424503_6)

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

and

and

Ev shows how mutation and selection actually works. Delphi’s reference to Wikipedia and the fitness landscape supports this mathematical fact and I will continue to post real examples of this mathematical fact that multiple selection pressures slow and ultimately stop evolution.

Clown fish, just what kind of mathematics did they teach you when you were trained as an alchemical engineer? You obviously have no experience in the mathematics of optimization otherwise you would understand that the greater the number of optimization conditions you have, the slower the process is. You obviously have no experience in the mathematics of database sorting otherwise you would understand that the greater the number of sorting conditions, the slower the process is. And you obviously have no experience or understanding of the mathematics mutation and selection otherwise you would know that the greater the number of selection conditions, the slower the evolutionary process proceeds. You do have experience in alchemical engineering; you do know how to turn inorganic matter into life (well except you have no idea how to generate ribose nonenzymatically). What a fish story you tell clown fish. Now don’t you worry, I’ll continue to post citations which show that multiple selection pressures slow and ultimately stop the evolutionary process. Then some day you will understand the mathematics of mutation and selection. Until then, tell us more fish stories (or are they reptile evolving to bird stories) about the theory of evolution. Summary.

No new magic words.

No math.

One new lie: "That’s the problem with you evolutionists. You expect TV to provide you with the proof for your theory."

That was a stupid lie, 'cos the people you're lying about are also the people you're lying to.

Why do you tell lies when you're certain to be caught? Is it just from sheer hatred of the truth --- like a psychopath, in an idle moment, might pause to pull the wings off a fly?

Dr Adequate

19th June 2007, 12:06 PM

I plead with everyone involved in this debate to please drop the sarcasm and personal attacks, and get back to discussing the results of the ev program and how, through skeptical rational sincere debate, we can improve the program to better match the reality it is trying to model so we can all learn something together and do something useful with our time.

Just a thought. Take it or leave it. It's been several months since kleinman has said anything about ev except reciting the same old lies about the results already obtained. I supplied him with some new data from a different simulation, but it showed the opposite of what he thinks, so he started screaming magic words.

We seem to have reached an impasse. He babbles nonsense about cheese, we laugh at him. Unless he says something that is not (a) complete gibberish (b) a blunder we've already corrected, then I don't see how we can move forward.

cyborg

19th June 2007, 12:07 PM

The basic problem with any sort of pretence of a real discussion is quite simply that kleinman isn't interested in whether or not evolution is true; he is content to merely know that he finds it contradicts his bronze-age belief system and that is adequate enough.

The rest is just floundering around to convince himself that he's the one basing this on the evidence and we're the one's rejecting the evidence; classic projection. Since it's got nothing to actually do with us or anything we say not there really isn't much point is bothering talking to him.

delphi_ote

19th June 2007, 03:45 PM

Since it's got nothing to actually do with us or anything we say not there really isn't much point is bothering talking to him.
That's because we've all had a conversation that progressed as new evidence has come to light, but the discussion has clearly gone over Kleinman's head. We've left him in the dust about 50 pages ago. He's been literally repeating exactly the same thing for the past 30 pages or so (complete with lame attempts at humor!) Aside from picking up a little catch phrase here or there, he hasn't learned anything in this thread.

It's fun to point out the more interesting contradictions in his thinking. When a new topic of interest comes up, I'll dive right in. For now, though, it's the same old crap, so I'm content to post amusing animated GIFS I found on t3h int4rw3bz to keep you entertained:
http://i71.photobucket.com/albums/i133/delphi_ote/1180079940845.gif

rcronk

19th June 2007, 04:55 PM

Fair enough - carry on with whatever the thread goal is then.

Mercutio

19th June 2007, 07:30 PM

Alas, if the theory of evolution were a rose,
It would smell like limburger under your nose.

xXxxXxxXxXxXxX (or xXxxXxxXxXXxxX)
xxXxXxxXxxX

Either way, 6 feet, then 4.

Your limburger smells better than your feet.

rcronk-- I may be wrong, but it may be that you are more sympathetic to Kleinman's views than many here are. (This is a compliment--from me, at least, it is.) If you have been following this thread, and the previous, perhaps you could act as a proxy Kleinman; that is, since he has (in the considered opinion of many here) abandoned his arguments in favor of ad homs and gibberish, perhaps you could attempt to salvage the remnants of any relevant argument he once had, and present it. You could do so here, or in a new thread dedicated to that purpose.

It is my belief that any and all of Kleinman's points have been answered. But I am willing to entertain the notion that I am wrong. If you can present his view better than he can (and I doubt very much you could do worse--I know this sounds wrong, but I honestly do not mean to be challenging or insulting you; I am quite serious, and take you at your word), then you will learn more from presenting that view than from waiting for Kleinman to do so.

delphi_ote

19th June 2007, 08:15 PM

Fair enough - carry on with whatever the thread goal is then.
We can have fun and be entertaining, you know.

kleinman

20th June 2007, 08:28 AM

I've followed this thread all the way back to mid-2006 when kleinman and Paul were discussing the results of the ev program (over on the "evolution is dead" forum) and going back and forth trying to figure out the results it was putting out. For me it was an educational and enlightening thread for about the first third of it.

It has since degenerated into ad hominem attacks and been transplanted here to JREF and has only become worse.
Rcronk, evolutionists can’t discuss the results of ev, it completely contradicts their belief system. So what do evolutionists do when their theory is contradicted by their own mathematical model and there is a huge amount of empirical data which supports the results of this model? They resort do ad hominem attacks. I myself will continue to post empirical evidence which supports the results of ev.
I plead with everyone involved in this debate to please drop the sarcasm and personal attacks, and get back to discussing the results of the ev program and how, through skeptical rational sincere debate, we can improve the program to better match the reality it is trying to model so we can all learn something together and do something useful with our time.
Again, rcronk what you don’t realize is that there is nothing that is going to change the mathematical reality that multiple selection pressures profoundly slow evolution in ev. In addition, increasing the genome length also slows the evolutionary process in ev and increasing population has a decreasing rate of accelerating evolution in the ev model. This again contradicts a common misconception that evolutionist hold, which is that huge populations markedly accelerate evolution.
Just a thought. Take it or leave it.
It’s not a bad thought but don’t place your hope on evolutionists abiding by it. They have no mathematics or empirical evidence to support their theory of evolution by mutation and selection so they argue with what they have.
Clown fish, just what kind of mathematics did they teach you when you were trained as an alchemical engineer? You obviously have no experience in the mathematics of optimization otherwise you would understand that the greater the number of optimization conditions you have, the slower the process is. You obviously have no experience in the mathematics of database sorting otherwise you would understand that the greater the number of sorting conditions, the slower the process is. And you obviously have no experience or understanding of the mathematics mutation and selection otherwise you would know that the greater the number of selection conditions, the slower the evolutionary process proceeds. You do have experience in alchemical engineering; you do know how to turn inorganic matter into life (well except you have no idea how to generate ribose nonenzymatically). What a fish story you tell clown fish. Now don’t you worry, I’ll continue to post citations which show that multiple selection pressures slow and ultimately stop the evolutionary process. Then some day you will understand the mathematics of mutation and selection. Until then, tell us more fish stories (or are they reptile evolving to bird stories) about the theory of evolution.please tell me you aren't confusing code optimization times with actual real life times again. You know when things happen in reality, there isn't some big computer that's crunching numbers to calculate the physics of everything occuring, right? We aren't in some big game of Quake that will start to lag if there are multiple projectiles wizzing arroung at the same time. You know this, right?
Clown fish, a generation in ev corresponds to a generation in the real situation. Dr Schneider knows this, Paul knows this, some day you may understand this.
We are still waiting for your point for point proof that evolution can't occur. PLEASE show me exactly how at every place on this earth for the past 5 billion years, conditions existed that resulted in too strong of selection conditions and would result in extinction rather than evolution.
Do you want me to prove to you that extinction actually occurs? Stop acting like a dodo.
A momentous milestone for this discussion has passed unnoticed. June 13th was the first anniversary of the original thread at the evolutionisdead forums.
Those were the good old days. Remember when I set the goal posts at ev shows the theory of evolution is mathematically impossible. Now the goal posts have moved to that ev shows the theory of evolution is mathematically impossible.
Reading portions of that thread and early parts of this one, it's clear that the quality of the discussion has declined. For my own part, I decided to cease addressing Dr. Kleinman directly late last November, for the reasons I explained in the (currently) next-to-last post in the evolutionisdead thread. (You can link to here and scroll down, but be warned that because of evolutionisdead's practice of deleting posts, their database is internally inconsistent and links often malfunction.) I reproduce the relevant portion here:
Why don’t you repost your speculations that by giggling, oops jiggling, the threshold in ev will make the model converge more rapidly? You almost got it correct. If you giggle, oops jiggle, the weights for the selection conditions to zero for any two of the three selection conditions, the remaining selection condition converges thousands of times faster than all three selection conditions. You would then understand that it is the multiple selection conditions which stop ev from converging as you increase the genome length.
I have considered, in honor of the discussion's first birthday (soon it will be walking and talking, and it's long overdue for weaning), resuming actual dialog. But at present there are no points under discussion worth addressing. We'll see what develops.
Myriad, the key to the complexity of the mutation and selection process is the number of selection conditions. You have experience with ev, set any two of the three weight factors to zero and see what happens to the rate of evolution of the remaining selection condition. When you do that, the numerous citations I have and continue to post which show that multiple selection pressures slow and ultimately stop evolution will make sense to you.
Also, rcronk, your complaint is groundless in one respect. While the topic of the original eid thread was the ev program, the original topic of this thread was ways in which creationists are annoying. Dr. Kleinman volunteered to provide examples. The ensuing discussion of the science -- interesting as it might have been, for a while -- was, technically, off-topic.
Myriad, the main difference between the eid thread and this thread is that it is now apparent that the reason the rate of evolution slows profoundly in ev as you increase the genome length in the model is the multiple selection conditions. This is consistent with Delphi’s Wikipedia reference to fitness landscape and the numerous real examples of multiple selection pressures that I have and continue to cite. What ev does is converge on a local optimum and because of the three selection conditions can not traverse the fitness landscape to a global optimum.

Now perhaps you want to support cheese wiz’s silly gif which shows that multiple selection pressures accelerate evolution. You could spice up this thread with a real example of cheese wiz’s amathematical nonsense. Cheese wiz has already posted zero real examples of his art work; you could try to double his number. In the meantime, I will continue to bore you all with more citations of how mutation and selection actually works.
The basic problem with any sort of pretence of a real discussion is quite simply that kleinman isn't interested in whether or not evolution is true; he is content to merely know that he finds it contradicts his bronze-age belief system and that is adequate enough.
Now cyborg, stop whining just because you don’t have any mathematics or empirical evidence to support your rust age theory, we’ll keep on going here until you finally understand how mutation and selection really works.
The rest is just floundering around to convince himself that he's the one basing this on the evidence and we're the one's rejecting the evidence; classic projection. Since it's got nothing to actually do with us or anything we say not there really isn't much point is bothering talking to him.
Oh yes, I enjoy floundering around with a peer reviewed and published model of mutation and selection which shows that multiple selection pressures slow and ultimately stop evolution and then posting real examples of this mathematics. However, I do find your cruft theory of evolution most interesting.
That's because we've all had a conversation that progressed as new evidence has come to light, but the discussion has clearly gone over Kleinman's head. We've left him in the dust about 50 pages ago. He's been literally repeating exactly the same thing for the past 30 pages or so (complete with lame attempts at humor!) Aside from picking up a little catch phrase here or there, he hasn't learned anything in this thread.
I assure you Delphi, your Wikipedia reference to the fitness landscape did not go over my head and I appreciate very much bringing this to our attention. It makes for a very nice package, ev, the fitness landscape and numerous real examples of how mutation and selection actually works. The only thing left in the dust is your decomposing theory of evolution.
rcronk-- I may be wrong, but it may be that you are more sympathetic to Kleinman's views than many here are. (This is a compliment--from me, at least, it is.) If you have been following this thread, and the previous, perhaps you could act as a proxy Kleinman; that is, since he has (in the considered opinion of many here) abandoned his arguments in favor of ad homs and gibberish, perhaps you could attempt to salvage the remnants of any relevant argument he once had, and present it. You could do so here, or in a new thread dedicated to that purpose.
Mercutio, I don’t need sympathy for my arguments, I’m presenting hard mathematical results from ev which shows that multiple selection pressures slow and ultimately stop evolution. Delphi’s Wikipedia reference to fitness landscape and the numerous citations which I have posted support this contention. You can believe in evolutionism but it doesn’t have any mathematical or scientific basis.
It is my belief that any and all of Kleinman's points have been answered. But I am willing to entertain the notion that I am wrong. If you can present his view better than he can (and I doubt very much you could do worse--I know this sounds wrong, but I honestly do not mean to be challenging or insulting you; I am quite serious, and take you at your word), then you will learn more from presenting that view than from waiting for Kleinman to do so.
Oh yes Mercutio, cheese wiz has posted zero references which show that multiple selection pressures accelerate evolution, clown fish has no idea how ribose could have formed nonenzymatically in the primordial soup and no one has offered an explanation what the components of the DNA replicase system were doing before DNA could be replicated. On the other hand, I am using an evolutionist written, peer reviewed and published model of mutation and selection which shows that multiple selection conditions profoundly slows the evolutionary process. This is totally consistent with the concept of the fitness landscape and a huge and growing body of empirical scientific evidence.
Fair enough - carry on with whatever the thread goal is then.We can have fun and be entertaining, you know.
Don’t forget that annoying an evolutionist can be fun as well. Hey Delphi, sober up and get your sock drawer sorted.

While Delphi works on his new career as stop action filmmaker here’s a couple more citations which show that multiple selection pressures slow and ultimately stop evolution.

http://www.malariajournal.com/content/5/1/48 (http://www.malariajournal.com/content/5/1/48)
Whenever drug treatment is required to control a pathogen, selection of drug resistance is inevitable [1]. The huge size of pathogen populations and their short generation times guarantee the outcome. Plasmodium falciparum is a prime example. In humans, an acute infection can produce a population as high as 1011 haploid parasites, so that mutations have ample scope to occur [2]. In the obligate sexual cycle, reassortment and recombination can "reshuffle the deck" for rapid evolution of new resistant genotypes in each generation. Thus, favoured combinations of genes can arise fairly quickly, even if more than one mutant gene is required for resistance. These sets of genes can, of course, also be separated during the sexual cycle but under the strong selection that drugs can exert, even a multigenic, resistant genotype may become fixed in a population.

The impact of this strong selection has been revealed at many different levels. Most important, as the use of chloroquine increased, drug resistance evolved in parasite populations and childhood mortality from malaria increased, even as all-cause mortality in children decreased [3-5]. The sequence of the P. falciparum genome has recently been published [6] and this has made it possible to trace the ancestry of highly drug-resistant parasites. These studies show that parasites resistant to chloroquine and sulfadoxine-pyrimethamine have arisen relatively rarely, but they have spread widely from a few initial foci in "selective sweeps" of the parasite population [7-11]. This new view affects many of the assumptions that underlie models of the speed at which resistance evolves [12] and inform practical decisions about changes in drug policy. Parasites without borders make it absolutely essential that the emergence of drug resistant populations be "tracked" worldwide; a resistant parasite that arises in Southeast Asia may travel rapidly to East Africa.

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]. In response to this emphasis, many different combination drugs, most containing an artemisinin derivative are being used in various countries, especially in East Africa (Figure 1. Many of these combinations have shown excellent initial efficacy in drug trials [13], but only mefloquine/artesunate has a long enough history to allow a strong prediction of the useful therapeutic life of these combinations [15]. It is particularly important to establish a baseline for effectiveness of new drugs and combinations so that any subsequent changes can be seen. This complex situation underlines the importance of regional surveillance of drug use, efficacy and effectiveness as these new combinations are tried in a variety of demographic and ecological settings. What has worked well for a long time in Thailand may not be so long lived in Tanzania [16]!

Appropriately, the gold standard for drug efficacy has been the outcome of clinical treatment. When patients are treated with the drug, do they recover? The substantial expense and logistical difficulty to change the recommended drug treatment have led most countries to rely on a large increase in clinical treatment failure before initiating a change [17]. Systematic studies have shown repeatedly that assessment in vitro of drug efficacy in local parasite isolates can give an early warning of rising drug resistance in vivo [18-20]. In addition, when molecular correlates of drug resistance are known, the prevalence of resistant alleles can also give early warning of evolving resistance in the parasite population [21-23]. In all three approaches, the temporal and geographic patterns of resistance are most informative. When the in vitro tolerance of parasites to a drug is rising or when the prevalence or the geographic range of resistant alleles is increasing, clinical drug failure is likely to increase as well. Figure 2 shows a small example of the linkage among the three parameters. In this data set, the increase in the in vitro IC50 values and the increased prevalence of the triple mutant allele of P. falciparum dhfr preceded by several years the increase in sulfadoxine-pyrimethamine treatment failure among young children in Coastal Kenya. Similar studies will be needed to determine whether the lags between these parameters observed in Kilifi will be similar in other sites or for other drugs, but it is clear that the in vitro increase in IC50 values and the increase in the molecular marker can provide an early warning of the onset of clinical treatment failure. The community will need similar data sets in many different settings for all of the drugs in use to manage effectively the current drugs and any novel drugs that are introduced in the future.

http://www.retroconference.org/2007/Abstracts/30238.htm (http://www.retroconference.org/2007/Abstracts/30238.htm)
Background: HIV drug resistance is thought to have at least 2 origins: pre-existing resistant mutants at a low frequency that are selected by therapy; and suboptimal therapy that permits replication, evolution, and selection of resistant mutants. Studying the mechanisms and anatomic origins of HIV drug resistance in humans is constrained by limited blood or tissue sampling and ethical restrictions on therapy. Here we examined the impact of short-course efavirenz (EFV) monotherapy on the evolution of drug resistance in a macaque model of ART.
and
Conclusions: Combination therapy with TDF+FTC+EFV was effective in suppressing RT-SHIV replication in macaques. Brief exposure to EFV monotherapy resulted in selection of NNRTI-resistant variants in 2 of 3 animals and early failure of triple drug therapy in 1 of 3 animals. The effect of interruption and re-initiation of therapy on the selection of resistance is being determined. This new animal model of ART has the flexibility to address many key questions about the selection, tissue origins and persistence of drug resistance that cannot be answered in human studies.

Stitch

20th June 2007, 10:02 AM

Lots of large red text

Well, that tells me all I need to know.

kleinman

20th June 2007, 10:19 AM

Lots of large red textWell, that tells me all I need to know.
It’s all about advertising Stitch; I want you evolutionists to see the billboard. I hope it is leaving you in stitches; after all, it is leaving the theory of evolution in tatters.

It’s good to see Dr Schneider advertising his ev model again. His latest advertisement can be found at: http://www-lmmb.ncifcrf.gov/~toms/paper/ev/blog-ev.html (http://www-lmmb.ncifcrf.gov/~toms/paper/ev/blog-ev.html)
2007 Jun 10. How Evolution Causes an Increase in Information Part II a Youtube video.
This video is located at http://www.youtube.com/watch?v=i9u50wKDb_4 (http://www.youtube.com/watch?v=i9u50wKDb_4)

This video is a replay of his year 2000 Nucleic Acid Research paper Ev: Evolution of Biological Information. He still is working with his 256 base case so don’t worry, we will tell you the rest of the story in lots of large red text when you use larger genomes in the model. However, it is useful if you want to try to understand the mathematics of information theory and how it contributes to the understanding of mutation and selection.

Dr Schneider, I’m glad you are still supporting your model despite the large number of evolutionists who are discrediting your work including your own programmer Paul Anagnostopoulos. I think your model has captured the essentials of mutation and selection and shows why the theory of evolution is mathematically impossible. Multiple selection conditions slow down and ultimately stop the acquisition of information in your model Dr Schneider. The same effect is seen in the treatment of cancers, multiple drug therapy slows the evolution of cancers resistant to the drugs. You might be interested in that since you work at the National Cancer Institute.

joobz

20th June 2007, 11:01 AM

rcronk

20th June 2007, 11:05 AM

Hmm - I'm trying to stay above the argument and just take a look at the information available. I apologize - I only read the first half of the thread over on evolutionisdead and the last couple of pages on JREF so I have missed much of the debate - I couldn't bring myself to read the other 100+ pages if they were just personal attacks gone awry.

So, could someone summarize what the conclusions are so far. Kleinman is saying that the ev program was showing that evolution was mathematically impossible and what is the response to that so far? Hopefully we can keep things simple and directed and squeeze a little usefulness out of this thread before we get back to entertainment. And I'd like to hear the answer from a non-kleinman to be fair.

kleinman

20th June 2007, 12:00 PM

You obviously have no experience in the mathematics of optimization otherwise you would understand that the greater the number of optimization conditions you have, the slower the process is.
And
You obviously have no experience in the mathematics of database sorting otherwise you would understand that the greater the number of sorting conditions, the slower the process is.
And
Clown fish, a generation in ev corresponds to a generation in the real situation. Dr Schneider knows this, Paul knows this, some day you may understand this.YEAH! Three sentences that have absolutely no bearing on eachother or what the initial point. Evolution isn't a database sort nor is it a computational optimization algorthim.
Clown fish, you are correct! Mutation and selection is a much worse situation mathematically than optimization or database sorting. With mutation and selection you have random changes occurring to your ensemble of information and a single fatal mutation can cause the loss of information. Not only does mutation and selection do sorting, it must also accumulate information, system optimization and database sorting do not have to accumulate information. Understand rubberband?
Hmm - I'm trying to stay above the argument and just take a look at the information available. I apologize - I only read the first half of the thread over on evolutionisdead and the last couple of pages on JREF so I have missed much of the debate - I couldn't bring myself to read the other 100+ pages if they were just personal attacks gone awry.
Don’t let a little name calling distract you from the mathematical facts which ev shows and that the numerous citations I have and will continue to post demonstrate. When the evolutionist whining gets to loud, just remember, that’s what the “Page Down” button is for.
So, could someone summarize what the conclusions are so far. Kleinman is saying that the ev program was showing that evolution was mathematically impossible and what is the response to that so far? Hopefully we can keep things simple and directed and squeeze a little usefulness out of this thread before we get back to entertainment. And I'd like to hear the answer from a non-kleinman to be fair.
You evolutionists want some help with this one? Here are some phrases you can incorporate into your denial of what the mathematics of ev shows, “Kleinman abuses computer models”, “it’s a strawman”, “ev only models 0.1% of the evolutionary landscape”, “it’s irrelevant”, and for cheese wiz, “it’s lies, lies, all lies”.

Now rcronk, it’s not only what ev shows, it’s what Delphi’s Wikipedia reference to the fitness landscape shows and it is what the numerous citations of real examples of mutation and selection shows which is that multiple selection pressures slow and ultimately stop evolution. Of course cheese wiz has posted a gif which he claims shows that multiple selection pressures accelerate evolution, too bad he doesn’t have any real examples of this twisted brainwashed logic.

rcronk

20th June 2007, 12:21 PM

homer

20th June 2007, 12:45 PM

Yes it's all too clear .There has not been time for the evolution of an intelligence capable of designing the universe .

kleinman

20th June 2007, 12:49 PM

I'm looking for a specific detailed answer to Kleinman's assertions about ev from someone other than kleinman - no offense kleinman, I just think it's only fair for you to assert your side and for someone else to assert theirs.
No offense taken. Evolutionists have had plenty of opportunity to assert their side on this thread. I have posted about 750 times on this thread and evolutionists have posted almost 4,000 times on this thread and I think it is likely they will continue to try to assert their viewpoint. If you read this thread and the related thread on the Evolutionisdead forum completely, you can ferret out this viewpoint. The same arguments get recycled over and over.
I want to turn this into a logical debate where perhaps we could learn something about evolution and the ev program. Once we've learned something, everyone else can go back to the entertainment portion of the thread.
There you go Paul, clown fish and cheese wiz, the call is out for you to make a logical argument. Tell us logically how you overcome the mathematical fact that multiple selection pressures slow and ultimately stop evolution.

kleinman

20th June 2007, 12:52 PM

Yes it's all too clear .There has not been time for the evolution of an intelligence capable of designing the universe .
Doh!

joobz

20th June 2007, 01:09 PM

homer

20th June 2007, 01:25 PM

Originally Posted by homer
Yes it's all too clear .There has not been time for the evolution of an intelligence capable of designing the universe .

Doh!
Evolution explains how we got here . How do you think we got here ?

kleinman

20th June 2007, 01:31 PM

I'm looking for a specific detailed answer to Kleinman's assertions about ev from someone other than kleinman - no offense kleinman, I just think it's only fair for you to assert your side and for someone else to assert theirs.

I want to turn this into a logical debate where perhaps we could learn something about evolution and the ev program. Once we've learned something, everyone else can go back to the entertainment portion of the thread.A great place to start is the Kleinman FAQ in Dr. Adequate's sig.

It's rather old, but as Dr. A has said, there has been no knew lies, so really no reason to update it yet.
Clown fish, rcronk is not looking for fish stories or cheese wiz’s whining, he is looking for a logical argument. Let me give you another example of a citation which shows the multiple selection pressures slow evolution:

http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15766932 (http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15766932)
The 2362 strain of Bacillus sphaericus (Bs) Neide is a highly mosquitocidal bacterium used in commercial bacterial larvicides primarily to control mosquitoes of the genus Culex. Unfortunately, Bs is at high risk for selecting resistance in mosquito populations, because its binary toxin apparently only binds to a single receptor type on midgut microvilli. A potential key strategy for delaying resistance to insecticidal proteins is to use mixtures of toxins that act at different targets within the insect, especially mixtures that interact synergistically. We tested this hypothesis for delaying the phenotypic expression of resistance by exposing Culex quinquefasciatus Say larvae to Bs alone or in combination with Cyt1A from Bacillus thuringiensis subsp. israelensis. Two laboratory lines of Cx. quinquefasciatus, one sensitive to Bs and the other containing Bs resistance alleles, were subjected to intensive selection pressure for 20 generations with either Bs 2362 or a 3:1 mixture of Bs 2362+Cyt1A. At the end of the study, the sensitive line had evolved >1000-fold resistance when selected with Bs alone, whereas the parallel line selected with Bs+Cyt1A exhibited only low resistance toward this mixture (RR95, 1.4). Similar results were observed in the lines containing Bs resistance alleles. Both lines selected with Bs+Cyt1A exhibited substantial resistance to Bs in the absence of Cyt1A. Although selection with Bs+Cyt1A did not prevent the underlying evolution of resistance to Bs, these results suggest that a mixture of Bs with other endotoxins, particularly one like Bs+Cyt1A in which the components interact synergistically, will provide longer lasting and more effective mosquito control than Bs alone.

That’s how you make a logical argument. You make a hypothesis such as multiple selection pressures slow and ultimately stop the evolutionary process, you demonstrate it mathematically and then you show empirical evidence for the hypothesis. So clown fish, when are you going to show us an example of multiple selection pressures accelerating evolution? Have you got that in cheese wiz’s “Kleinman FAQ”? When it comes to the mathematics of mutation and selection, you evolutionarians are really a collection of dim bulbs.

kleinman

20th June 2007, 01:37 PM

Evolution explains how we got here . How do you think we got here ?
Homer, read the thread.

rcronk

20th June 2007, 01:40 PM

A great place to start is the Kleinman FAQ (http://forums.randi.org/showthread.php?p=2533858#post2533858) in Dr. Adequate's sig.

It's rather old, but as Dr. A has said, there has been no knew lies, so really no reason to update it yet.

Thanks. With regard to the ev program, Dr. A said:

The mistake Kleinman has made, or one of them, is to take a realistic value for p (the probability of a point mutation for a given base) but not for n (the population). This gives a totally unrealistic value for the probability that a given substition will occur in the gene pool per generation, which is given by:

q = 1 - (1 - p/3)n

If, for example, we take a realistic value for p of 10-8, then for a measly million organisms, q is 0.3%. For a lousy billion, it's 96.4%.

If we use a more realistic order of magnitude for the bacteria, say something like the 1014 present in a single human gut, then my calculator isn't accurate enough to tell us the difference between q and 1.

Schneider is forced by practical constraints to take n to be small, and has compensated for this by using an unrealistic value for p to give himself a realistic value for q. This is eminently sensible, since it is the amount of variation within the gene pool, rather than the variation between individuals per generation, that determines the rate of evolution.

Kleinman, on the other hand, has chosen his numbers so that the value for q is wildly unrealistic; this is why his estimate of the time the process would take is also wildly unrealistic.

So, Kleinman, Dr. A asserted that you chose an unrealistic value for n (the population). Dr. A asserts that Schneider is forced by practical restraints to take n to be small, compensating for this by using an unrealistic value for p. Dr. A states that using an unrealistic value for n is not valid but using an unrealistic value for p is sensible and valid.

Summary of assertions:

1. Dr. A asserts that Kleinman is purposefully using an unrealistic value for n to get the results he wants.

2. Dr. A asserts that the ev computer model cannot practically model reality so some numbers are fudged to make it practical but that the fudging is ok and should not affect the accuracy of the outcome.

Is this correct?

joobz

20th June 2007, 01:40 PM

Clown fish, you are correct! Mutation and selection is a much worse situation mathematically than optimization or database sorting. With mutation and selection you have random changes occurring to your ensemble of information and a single fatal mutation can cause the loss of information. Not only does mutation and selection do sorting, it must also accumulate information, system optimization and database sorting do not have to accumulate information. Understand rubberband?

no

kleinman

20th June 2007, 02:32 PM

So, Kleinman, Dr. A asserted that you chose an unrealistic value for n (the population). Dr. A asserts that Schneider is forced by practical restraints to take n to be small, compensating for this by using an unrealistic value for p. Dr. A states that using an unrealistic value for n is not valid but using an unrealistic value for p is sensible and valid.
So cheese wiz makes an assertion about ev? It must be all zero of the cases he has run vs the hundreds of cases that I have run including a case with n=10^6 that makes him such an expert on ev. What ev shows with increasing population is that the rate of decrease in the generations for evolution drops markedly with increasing population. The reason this happens is that increasing population increases the probability of a beneficial mutation at a particular loci at less than additive amounts. In fact, the once you reach populations of 10^5, the slope for the generations for convergence/population curve is approaching zero. Increasing population does very little to accelerate the acquisition of information once you have reached this population. I have posted 4 different series with G=256, 512, 1024 and 2048 which show this with populations ranging between 64 and 10^6 (the memory limitations of my computer).
Dr. A asserts that Kleinman is purposefully using an unrealistic value for n to get the results he wants.
Simple enough, let cheese wiz run any cases he wants and prove whatever point he wants with ev. All the results which I have obtained can be easily duplicated by anyone interested in running ev except for a few large population cases which I ran using Dr Schneider’s Pascal version of ev because of memory limitations for the Java version of ev. These cases can be duplicated with a little effort but anyone wanting to do this can do this.
Dr. A asserts that the ev computer model cannot practically model reality so some numbers are fudged to make it practical but that the fudging is ok and should not affect the accuracy of the outcome.
Just what numbers does cheese wiz think are being fudged in ev. Cheese wiz’s assertions are in direct contradiction to what the author of this peer reviewed and published model has said about ev. Here is an example of Dr Schneider has said about ev:
The following quotes were taken from Dr Schneider’s blog web page: http://www.lecb.ncifcrf.gov/~toms/paper/ev/blog-ev.html (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.

"Schneider's paper is misleadingly titled: "Evolution of biological information". But it is just a *computer* simulation. No actual *biological* materials (e.g. genomes of nucleic acids, proteins, etc) were used, nor does Schneider propose that his simulation be tested with *real* genomes or proteins Actual biological materials were used to determine the original hypothesis. Read the literature: Schneider1986

It only becomes *real* biological information and random mutation and natural selection, when the simulation is tested in the *real* world, using *real* DNA, proteins, with *real* mutations and a *real* environment does the selecting. It is significant that Schneider does not propose this, presumably because he knows it wouldn't work.You are very bad at reading my mind, I have considered doing this experiment. Given the right conditions, it WILL WORK. Do you have th gumption to do the experiment yourself? That's the way real science works! FURTHERMORE, if you read the literature, you will recognize that related experiments have been repeatedly done for 20 years. Look up SELEX.

In the rest of the paper he uses the single word "selection". I take this as a tacit admission that his model is not a simulation of *real* biological natural selection. No. A rose is a rose by any other name. Selection is selection whether it be natural (generally meaning the environment of earth), breeding (by humans usually, though perhaps some ants select their fungi), SELEX or in a computer simulation. Of COURSE it is a simulation of natural selection! The paper would not be relevant to biology and would not have been published in a major scientific journal if it were not!

Schneider lets slip that there is another unrealistic element in his (and indeed all) computer simulations in that it (they) "does not correlate with time": So? Run the program slower if you want. Make one generation per 20 minutes to match rapid bacterial growth. THIS WILL NOT CHANGE THE FINIAL RESULT!

Well, when Schneider's simulation is actually tested with *real* "life" (e.g. a bacterium), and under *real* mutation and natural selection it gains information, then, and only then, would "creationists" be favourably impressed. But if they are like me, they would already be impressed (but unfavourably) that Schneider does not mention in his paper that his simulation should now be so tested in the *real* "biological" world.1. The simulation was of phenomena in the "real" world.
2. Dr. Jones is invited yet again to do an experiment.

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

Where attempts to replicate Darwinian evolution on the computer have been successful, they have not used classical Darwinian principles, and where they have used such principles, they have not been successful. The ev program disproves this statement since it uses classical Darwinian principles and was successful.
And Dr Schneider said the following about his model:
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.
I believe that Dr Schneider’s model properly captures the essentials of the mathematics of mutation and selection. It is an idealized model but if cheese wiz thinks the numbers are being fudged, he can try and prove it, any one can, the model is public domain.
Is this correct?
Rcronk, run the model yourself and see whether I have fudged anything. Cheese wiz is wrong about these assertions and he is wrong about his assertion that multiple selection pressures accelerate evolution.
Clown fish, you are correct! Mutation and selection is a much worse situation mathematically than optimization or database sorting. With mutation and selection you have random changes occurring to your ensemble of information and a single fatal mutation can cause the loss of information. Not only does mutation and selection do sorting, it must also accumulate information, system optimization and database sorting do not have to accumulate information. Understand rubberband?no
Let’s see if I can make it simple enough so even a clown fish can understand it. Let’s say you start with a shuffled deck of cards and the sorting condition is to arrange the cards by clubs, diamonds, hearts and spades. It will take a particular amount of time to do the sort. Now let’s say you start with a shuffled deck of cards and you not only have to sort by clubs, diamonds, hearts and spades, you must sort by A,2,…Q,K as well. The extra condition makes the sorting process go slower. Now imagine that you start with a shuffled deck that is missing a few cards and has duplicates of other cards and periodically you replace cards randomly. You still must sort by clubs, diamonds, hearts and spades but you don’t get a complete deck until you have successfully taken out the duplicates and replaced them with the missing cards. This is a far slower and more difficult process than simply doing the sort.

joobz

20th June 2007, 02:42 PM

Let’s see if I can make it simple enough so even a clown fish can understand it. Let’s say you start with a shuffled deck of cards and the sorting condition is to arrange the cards by clubs, diamonds, hearts and spades. It will take a particular amount of time to do the sort. Now let’s say you start with a shuffled deck of cards and you not only have to sort by clubs, diamonds, hearts and spades, you must sort by A,2,…Q,K as well. The extra condition makes the sorting process go slower. Now imagine that you start with a shuffled deck that is missing a few cards and has duplicates of other cards and periodically you replace cards randomly. You still must sort by clubs, diamonds, hearts and spades but you don’t get a complete deck until you have successfully taken out the duplicates and replaced them with the missing cards. This is a far slower and more difficult process than simply doing the sort.
no.
sorting a deck of cards is not at all a model of evolution.
a sorted deck of cards has 1 predetermined and ultimate final goal. there is NO predetermined goal in evolution. It's the difference between walking a mile to the groceryand walking a mile away.

kleinman

20th June 2007, 03:03 PM

no.
sorting a deck of cards is not at all a model of evolution.
a sorted deck of cards has 1 predetermined and ultimate final goal. there is NO predetermined goal in evolution. It's the difference between walking a mile to the groceryand walking a mile away.
Clown fish, you are demonstrating a fundamental flaw of logic here. Evolution by mutation and selection does have a goal, that goal is the fitness of the population to reproduce. What ev, Delphi’s Wikipedia reference to the fitness landscape and the numerous citations I have posted which show real examples of evolution by mutation and selection with the goal of achieving the most fit population to the selection pressures all demonstrate why evolution by mutation and selection is limited. Multiple selection pressures confound the process. That is how the mathematics of mutation and selection works.

joobz

20th June 2007, 03:15 PM

kleinman

20th June 2007, 03:28 PM

Clown fish, you are demonstrating a fundamental flaw of logic here. Evolution by mutation and selection does have a goal, that goal is the fitness of the population to reproduce. What ev, Delphi’s Wikipedia reference to the fitness landscape and the numerous citations I have posted which show real examples of evolution by mutation and selection with the goal of achieving the most fit population to the selection pressures all demonstrate why evolution by mutation and selection is limited. Multiple selection pressures confound the process. That is how the mathematics of mutation and selection works.no.
fitness isn't a goal, it's a result. Or do you claim that a falling object's goal is a lower altitude?
Whether you want to call fitness the goal or result, it is what drives the mutation and selection process. If the mutation leads to a better reproducing phenotype, the frequency of that genotype increases in the population. This is the cause and effect phenomenon that drives evolution and Dr Schneider properly modeled this phenomenon. Fitness is the cause, selection is the effect. Fitness is the driving force for evolution. Gravity is the cause and the falling object is the effect.

joobz

20th June 2007, 03:49 PM

kleinman

20th June 2007, 04:28 PM

Whether you want to call fitness the goal or result, it is what drives the mutation and selection process. If the mutation leads to a better reproducing phenotype, the frequency of that genotype increases in the population. This is the cause and effect phenomenon that drives evolution and Dr Schneider properly modeled this phenomenon. Fitness is the cause, selection is the effect. Fitness is the driving force for evolution. Gravity is the cause and the falling object is the effect.You originally stated that fitness is the goal, and now say fitness is the cause. fitness's own effect is fitness. Effectively, you are saying evolution is it's own end. This is true and you just talked yourself away from your initial argument.
This entire thread is about the theory of evolution by mutation and selection. Ev models this phenomenon. The fitness to reproduce is the driving force for evolution. This is the consequence, goal or result of the selection process. This is how the sequences of bases are modified in a population (as well as recombination). Optimum fitness to reproduce is the end point according to the theory of evolution. What ev and the Wikipedia reference to fitness landscape and the numerous real examples of mutation and selection show that the mutation and selection process in order to achieve the most fit population is a very limited phenomenon. It is a profoundly slow mechanism for acquiring information in a gene pool and works most rapidly if there is only a single directed selection pressure. As soon as you introduce additional selection pressures, you confound the ability of the population to traverse the fitness landscape to a new local optimum. This is what happens to the mathematics of fitness to reproduce and mutation/selection (cause and effect) process for evolution.
You claimed that a shuffled deck = evolution.
it doesn't. There is no reason to presume that an ordered deck is the only fit organized form. If there was only 1 available geneotype for survival, extinction would occur. this isn't a model of reality. Sorry.
No need to be sorry, you are simply confused about the mathematics of mutation and selection. I’ll continue to post examples of how multiple selection pressures slow and ultimately stop the evolutionary process and as I do this, perhaps you will begin to understand why the mathematics of mutation and selection undermines the theory of evolution. Multiple selection pressures confound the ability of a population to adapt by mutation and selection. This is why you can’t achieve the huge number of genetic changes required to transform a reptile to a bird or a human from a primate precursor. Multiple selection pressures don’t work in harmony to evolve new species. Multiple selection pressures interfere with each other as the population tries to traverse the fitness landscape to a new local optimum.

Dr Adequate

20th June 2007, 04:47 PM

joobz

20th June 2007, 06:17 PM

This entire thread is about the theory of evolution by mutation and selection. Ev models this phenomenon. The fitness to reproduce is the driving force for evolution. This is the consequence, goal or result of the selection process. This is how the sequences of bases are modified in a population (as well as recombination). Optimum fitness to reproduce is the end point according to the theory of evolution. What ev and the Wikipedia reference to fitness landscape and the numerous real examples of mutation and selection show that the mutation and selection process in order to achieve the most fit population is a very limited phenomenon. It is a profoundly slow mechanism for acquiring information in a gene pool and works most rapidly if there is only a single directed selection pressure. As soon as you introduce additional selection pressures, you confound the ability of the population to traverse the fitness landscape to a new local optimum. This is what happens to the mathematics of fitness to reproduce and mutation/selection (cause and effect) process for evolution.

No need to be sorry, you are simply confused about the mathematics of mutation and selection. I’ll continue to post examples of how multiple selection pressures slow and ultimately stop the evolutionary process and as I do this, perhaps you will begin to understand why the mathematics of mutation and selection undermines the theory of evolution. Multiple selection pressures confound the ability of a population to adapt by mutation and selection. This is why you can’t achieve the huge number of genetic changes required to transform a reptile to a bird or a human from a primate precursor. Multiple selection pressures don’t work in harmony to evolve new species. Multiple selection pressures interfere with each other as the population tries to traverse the fitness landscape to a new local optimum.
nope, you're wrong.

kleinman

20th June 2007, 07:02 PM

1. Dr. A asserts that Kleinman is purposefully using an unrealistic value for n to get the results he wants.

2. Dr. A asserts that the ev computer model cannot practically model reality so some numbers are fudged to make it practical but that the fudging is ok and should not affect the accuracy of the outcome.

Is this correct?I'm not certain that his mistake was "purposeful" originally. Apart from that, yes.
What I did “purposeful” with ev was a systematic parametric study with the model including varying genome length systematically, populations systematic, mutation rates systematically, number of binding sites systematically, and site width and examined how each parameter affect the rate of information acquisition. Each of these parameters exhibit particular affects on the rate of evolution (information acquisition). Population does not affect the rate of evolution the way cheese wiz alleges. If he took the time out to run the model he would understand this but instead he makes assertion based in ignorance. Huge populations do not have the marked affect on the rate of evolution as cheese wiz alleges.

Note that apart from anything else, it is a trivial consequence of the Law of Large Numbers that as the population size tends to infinity, the number of generations to produce the "perfect organism" tends to 0 (as ev counts it).
Cheese wiz is misapplying the Law of Large Numbers. The probability of getting a beneficial mutation at the proper location somewhere in a large population approach 1 very quickly as population is increased. Further increases in population give smaller and smaller increases to this probability and this effect is demonstrated by ev. The largest effects of increasing the rate of evolution is seen with first 7 or 8 doubling of population (starting with a population of 64) with the greatest effect seen in first 3 or 4 doubling of population. Ev appears to be approaching asymptotes at much larger values than 0 with much smaller populations than infinity as cheese wiz is speculating.

Kleinman has been told this. His response, as you can see from his blatherings above (message #4665) is to reply that the population-generations curve which I claim is tending asymptotically to the population axis is not doing so linearly, and that its slope aproaches 0, both of which must be true if I'm right. We've explained this to him too.
I have data from ev which is showing different than what cheese wiz is wizzing. I also have real examples of multiple selection pressures which slow and ultimately stop evolution. Now cheese wiz posted a gif where he claims that multiple selection pressures accelerate evolution. Cheese wiz, where are your real examples of your gif?

You will notice that kleinman's snippets of quotations from Dr Schneider in message #4665 have nothing to do with this question: not one of them refers to the effect of population size in any way.
It is abundantly clear that Dr Schneider believes his simulation models reality. Dr Schneider still supports the validity of his model and so do I. Ev gives plausible simulations of the effects of genome length, population sizes and multiple selection pressures and the genome length and multiple selection pressures dominate the simulation. Population size demonstrates a second order affect. If cheese wiz did a parametric study with ev, he would realize these mathematical facts.

In the meantime, I will continue to post real examples of the mathematics which ev demonstrates, many of which deal with huge populations and reproduction rates seen with viruses and bacteria and are not limited to random point mutation and often include recombination yet multiple selection pressures still succeed in slowing and ultimately stopping evolution.

http://www3.interscience.wiley.com/cgi-bin/abstract/112607405/ABSTRACT?CRETRY=1&SRETRY=0 (http://www3.interscience.wiley.com/cgi-bin/abstract/112607405/ABSTRACT?CRETRY=1&SRETRY=0)
The following possible methods of minimising the risks of resistance are considered: (a) adjustment of the dosage and frequency of spraying so that resistance genes are effectively recessive; (b) detection and eradication of new foci of resistance before they have a chance to spread; (c) spraying a mosaic of unrelated insecticides with the intention that immigrants from one sector of the mosaic to another will dilute the frequency of resistance genes; (d) re-introduction of susceptibility genes into the progeny of wild females by the release of heterozygous males with resistance genes translocated on to their Y chromosome so that they are protected from insecticidal killing but will pass susceptibility to their female progeny; (e) replacement of a resistant by a susceptible population by means of a negatively heterotic system such as bidirectional cytoplasmic incompatibility. A plausible case can be made for each of these methods based on theoretical models and appropriate assumptions. However, an assessment of whether any of them will really beof any value depends on the answers to certain questions in the field. Therefore field projects have been initiated on Anopheles culicifacies in Sri Lanka and Pakistan, Culex quinquefasciatus in Tanzania and Anopheles arabiensis in Sudan. The results so far are summarized.

http://www.dcp2.org/pubs/DCP/55/Section/8167 (http://www.dcp2.org/pubs/DCP/55/Section/8167)
Some interventions, such as the use of drug combinations, reduce the likelihood that resistance will emerge, whereas other interventions, such as improvements in drug prescribing and patient compliance with dosing, reduce the likelihood that a resistant pathogen will survive and proliferate.
and
The appropriate choice of drug treatment is an important step in delaying the evolution of drug resistance. Drug combinations that include drugs with different targets were first used in the treatment of tuberculosis and have now become routine practice in the treatment of cancer and HIV/AIDS. Combinations of artemisinin and its derivatives with other antimalarials, notably mefloquine, have accelerated recoveries, increased cure rates, and reduced transmissibility. In the refugee camps on the western border of Thailand, where most of the recent studies with artemisinin combinations have been conducted, the use of combinations delayed the development of resistance and reduced the incidence of disease (Nosten and others 2000). The rationale behind drug combinations is that, if resistance results from spontaneous genetic mutations, the chance that a parasite will emerge that is simultaneously resistant to two drugs with unrelated modes of action (that is, drug targets) is the mathematical product of the individual parasite mutation frequencies multiplied by the total number of parasites exposed to the drugs (White 1998, 1999). Combinations, therefore, reduce enormously the probability that a resistant mutant will arise. Sequential deployment of the drugs is much less effective, because it does not exploit the multiplicative reduction in selection risk.
and
In the context of antibiotics, combinations have typically been used to broaden the spectrum of antimicrobial coverage rather than to reduce the likelihood of the emergence of resistance. With the development of new penicillins and cephalosporins with broader spectra of activity a decade ago, most serious infections have been treated with monotherapy. The use of combination therapy to preserve new classes of antibiotics from the emergence of resistance at a societal level may be rational, but it has not been implemented because of cost concerns and the potential for enhanced toxicity associated with the use of more agents than necessary to effect a cure in an individual patient.

Dr Adequate

21st June 2007, 12:10 AM

What I did “purposeful” with ev was a systematic parametric study with the model including varying genome length systematically, populations systematic, mutation rates systematically, number of binding sites systematically, and site width and examined how each parameter affect the rate of information acquisition. Each of these parameters exhibit particular affects on the rate of evolution (information acquisition). Population does not affect the rate of evolution the way cheese wiz alleges. If he took the time out to run the model he would understand this but instead he makes assertion based in ignorance. Huge populations do not have the marked affect on the rate of evolution as cheese wiz alleges.

Cheese wiz is misapplying the Law of Large Numbers. The probability of getting a beneficial mutation at the proper location somewhere in a large population approach 1 very quickly as population is increased. Further increases in population give smaller and smaller increases to this probability and this effect is demonstrated by ev. The largest effects of increasing the rate of evolution is seen with first 7 or 8 doubling of population (starting with a population of 64) with the greatest effect seen in first 3 or 4 doubling of population. Ev appears to be approaching asymptotes at much larger values than 0 with much smaller populations than infinity as cheese wiz is speculating.

I have data from ev which is showing different than what cheese wiz is wizzing. I also have real examples of multiple selection pressures which slow and ultimately stop evolution. Now cheese wiz posted a gif where he claims that multiple selection pressures accelerate evolution. Cheese wiz, where are your real examples of your gif?

It is abundantly clear that Dr Schneider believes his simulation models reality. Dr Schneider still supports the validity of his model and so do I. Ev gives plausible simulations of the effects of genome length, population sizes and multiple selection pressures and the genome length and multiple selection pressures dominate the simulation. Population size demonstrates a second order affect. If cheese wiz did a parametric study with ev, he would realize these mathematical facts.

In the meantime, I will continue to post real examples of the mathematics which ev demonstrates, many of which deal with huge populations and reproduction rates seen with viruses and bacteria and are not limited to random point mutation and often include recombination yet multiple selection pressures still succeed in slowing and ultimately stopping evolution.

http://www3.interscience.wiley.com/cgi-bin/abstract/112607405/ABSTRACT?CRETRY=1&SRETRY=0 (http://www3.interscience.wiley.com/cgi-bin/abstract/112607405/ABSTRACT?CRETRY=1&SRETRY=0)

http://www.dcp2.org/pubs/DCP/55/Section/8167 (http://www.dcp2.org/pubs/DCP/55/Section/8167)

and

and
I think the only new lie here is where kleinman says "Cheese wiz is misapplying the Law of Large Numbers."

"Cheese wiz" is his magical word for me, and obviously I have not misapplied the Law of Large Numbers, as kleinman would know if he was not innumerate.

kleinman

21st June 2007, 08:23 AM

"Cheese wiz" is his magical word for me, and obviously I have not misapplied the Law of Large Numbers, as kleinman would know if he was not innumerate.
Cheese wiz is not the magical word for you; it is what comes out of you when you open your mouth. So let’s see how you misapply the Law of Large Numbers:
The Law of Large Numbers is the statement that the number of times with which a chance event has occurred, divided by the number of trials made, will tend more and more closely to approximate the actual probability of that event as the number of trials gets larger. For example, if we toss a fair coin repeatedly, the proportion of the tosses which have come up heads will tend to get closer and closer to 50% the more tosses we have made.
and
The law of large numbers is the basis of statistical sampling. Suppose, for example, we wish to know what proportion of the population likes mustard. It would be impractical to ask them all, so instead we ask a randomly chosen sample of them. If our sample is truly random, then the law of large numbers gives us confidence that as the sample size becomes large, so the proportion of pro-mustard votes we get from the people we've polled will better and better approximate the actual probability that a randomly selected member of the population is pro-mustard; and this actual proability is, of course, equal to the proportion of people in the population who like mustard.
From this cheese wiz draws the conclusion that the number of generations for convergence of ev goes to zero with infinite population. I think it is more likely that the probability of a beneficial mutation occurring at a particular loci equals 1 but let’s say that cheese wiz is correct. Let’s see if cheese wiz can tell us how quickly the generations for convergence approaches 0. Does a genome length, G=10^9 and a population of n=10^6 give a value for generations for convergence less than 1? Does a G=17,000 and n=10^12 give a value generations for convergence less than 1? Since cheese wiz has no idea of what realistic values of G and n will give a generations for convergence less than 1 and the largest population case run with ev has a n=10^6 and G=10^3 and still requires over 400 generations to converge, we must look at real examples such as HIV, HBV and various bacterial and parasitic infections, all which show that evolution of these huge population cases still are suppressed by multiple selection pressures. Cheese wiz, you know what multiple selection pressures are; they are the things you say in your silly gif that accelerate evolution. If you ever come back from infinity and see what happens in reality, you will see that multiple selection pressures slow and ultimately stop evolution. That is what ev shows, that is what Delphi’s Wikipedia reference to the fitness landscape shows and that is what reality shows. In fact, here are two more real examples of multiple selection pressures slowing evolution (and where monotherapy allows for more rapid evolution of drug resistance). These examples deal with populations of billions and billions. You still don’t have evolution in 0 generations do you cheese wiz? Multiple selection pressures still slow evolution. Now if you could give us a single reference where multiple selection pressures accelerate evolution like you show in your silly gif, there would be more than cheese wiz coming out of your mouth.

http://newsarchive.asm.org/jan01/feature3.asp (http://newsarchive.asm.org/jan01/feature3.asp)
Conceptually, a combination treatment regimen containing two or more drugs of different classes should require at least two resistance mutations for the pathogen to grow. Because the simultaneous development of two such mutations could be expected only in a bacterial population of much greater size than is normally present within any individual, combination therapy with two distinct antibiotic types provides a way to reduce mutant selection using moderate concentrations of compounds that may individually have very high MPCs.

The best examples of combination therapy are found with tuberculosis. Because the standard agents used for treating patients with this disease cannot be dosed at concentrations that exceed the respective MPCs of these drugs, resistance readily arises when any of the agents is used in monotherapy. Dual-drug and often multidrug therapies thus are used routinely to reduce the number of treatment failures. Currently cases of drug resistance developing among tuberculosis patients are generally associated with the failure of patients to comply fully with therapy regimens. In effect, sporadic compliance creates the equivalent of repeated monotherapy punctuated by periods of bacterial population expansion. To assure patient compliance, a major effort has been placed on directly observed therapy (DOT), which significantly lowers the incidence of resistance-associated treatment failure.

http://www.3dgenoscience.com/molecular_modeling/halfon_aucopy2.pdf (http://www.3dgenoscience.com/molecular_modeling/halfon_aucopy2.pdf)

Development of hepatitis B virus (HBV)-resistant strains following nucleos(t)ide analogue treatment is a major concern. The A181V mutation within the reverse transcriptase (RT) of HBV has been shown to be associated with HBV resistance to adefovir dipivoxil (ADV), and its level of sensitivity to other nucleos(t)ide analogues is an important issue. This article reports two cases of chronically HBV infected patients who developed rtA181V HBV mutants following lamivudine (LAM) monotherapy. This was subsequently associated with virological breakthrough under LAM monotherapy or LAM/ADV bi-therapy, which were rescued by tenofovir disoproxil fumarate treatment. These observations suggest that rtA181V mutation may unusually emerge under LAM monotherapy, and may be associated with cross resistance to LAM and ADV, but remains sensitive to tenofovir disoproxil fumarate. Moreover, they highlight that HBV sequence analysis is an essential tool to optimize therapeutic management of HBV chronic infection in clinical practice in order to choose the appropriate nucleos(t)ide analogues.

joobz

21st June 2007, 08:51 AM

From this cheese wiz draws the conclusion that the number of generations for convergence of ev goes to zero with infinite population. as ev counts it, yes. Dr. Adequate accurately and correctly states this.

I think it is more likely that the probability of a beneficial mutation occurring at a particular loci equals 1 but let’s say that cheese wiz is correct. um....no. This sentence makes absolutely no sense.
[Masque of the red text]Nope, you still haven't shown how evolution is impossible.

kleinman

21st June 2007, 09:41 AM

From this cheese wiz draws the conclusion that the number of generations for convergence of ev goes to zero with infinite population.as ev counts it, yes. Dr. Adequate accurately and correctly states this.
So clown fish and cheese wiz, two evolutionarian clones who have not run a single case from ev can predict how ev will behave with infinite populations. Well silly clown fish, this type of behavior is not seen in reality with HIV, HBV and other examples with huge populations so whatever conclusion cheese wiz draws with infinite populations has no bearing on evolution in reality. Multiple selection pressures always slows down and ultimately stops evolution.
I think it is more likely that the probability of a beneficial mutation occurring at a particular loci equals 1 but let’s say that cheese wiz is correct.um....no. This sentence makes absolutely no sense.
Do you want me to translate it to clown fishian? Let’s see if you can comprehend this. It makes no difference what happens mathematically with infinite populations. Paul reported previously of a microbe that has a population of 10^28. According to cheese wiz’s silly logic this creature should be the most evolutionarily advanced because it takes the least number of generations to evolve due to its huge population. The only thing you two have proved is that you have no understanding of the mathematics of mutation and selection. The dominant mathematical parameters in this system are the genome length and number of selection pressures. Population has only a second order effect on the mathematical behavior of the model. Increase the genome length in ev and the model stops converging unless you reduce the number of selection conditions. You two are a couple of dim bulbs when it comes to the mathematics of mutation and selection.
[Masque of the red text]Nope, you still haven't shown how evolution is impossible.
Somebody turn on the light for this dim bulb. Multiple selection pressure interferes with the evolutionary process. This is shown mathematically with ev, this is explained with Delphi’s Wikipedia reference to fitness landscape and this shown by dozens of citations of real examples of mutation and selection. There is no selection pressure that transforms a reptile to a bird, if you propose that this transformation is done by a combination of selection pressures, it is mathematically impossible. That is how the mathematics of mutation and selection works. Some day perhaps you and cheese wiz will return from infinity and come to understand how mutation and selection works in reality.

joobz

21st June 2007, 10:15 AM

So clown fish and cheese wiz, two evolutionarian clones who have not run a single case from ev can predict how ev will behave with infinite populations. you know this is a lie, why do you say it? It only further demonstates the fact you are a raving loon. Do you enjoy being a raving loon?

Well silly clown fish, this type of behavior is not seen in reality with HIV, HBV and other examples with huge populations so whatever conclusion cheese wiz draws with infinite populations has no bearing on evolution in reality. Multiple selection pressures always slows down and ultimately stops evolution. Too much is wrong with these sentences to even bother addressing them, again.

Do you want me to translate it to clown fishian? oh, please do.

Let’s see if you can comprehend this. It makes no difference what happens mathematically with infinite populations. Paul reported previously of a microbe that has a population of 10^28. According to cheese wiz’s silly logic this creature should be the most evolutionarily advanced because it takes the least number of generations to evolve due to its huge population. The only thing you two have proved is that you have no understanding of the mathematics of mutation and selection. The dominant mathematical parameters in this system are the genome length and number of selection pressures. Population has only a second order effect on the mathematical behavior of the model. Increase the genome length in ev and the model stops converging unless you reduce the number of selection conditions. You two are a couple of dim bulbs when it comes to the mathematics of mutation and selection. wow, that's a lot of words. Let me summarize
1.) large/infinite populations are not relavent
2.) Bacteria should be the most evolutionarily advanced
3.) Dr. A. and I do not understand your maths
4.) Dominant variables are genome length and number of selection pressures
5.) Population has a second order effect on the model
6.) Increase in genome length stops convergence with large number of selection presures.

Allow me to address this
1.) Wrong
2.) Wrong
3.) True, We have no clue what kind of math you use
4.) they are important, but you haven't shown any ev run with multiple selection pressures. this is a simple lie.
5.) Your use of second-order is undefined and is foolish if you mean to say population is bounded.
6.) This is a lie. You have not presented or shown this in ev. It is especially untrue considering your ignorance of population effects.

Now, that was supposed to be a translation of this sentence.

I think it is more likely that the probability of a beneficial mutation occurring at a particular loci equals 1 but let’s say that cheese wiz is correct.
Allow me to translate what this says: "I think that [an infinite population] will have a 100% chance of having a beneficial mutation at 1 location."

This is just plain dumb. Not to mention that your "explantion" of what you said is completely unrelated to any of this gobbleygook.

At infinite population, the likelyhood of a single member of that population having the exact right sequence being selected for is 100%. The xext step mutation in the model is immaterial. We do not need worry about if the next mutation will be beneficial, because our model is done. At the zero generation point we acheived our goal.

What you said makes no sense. Moreover, you were not even capable of explaining why you think what you said makes sense. If you can't understand your lunacy, how are we supposed to?

cyborg

21st June 2007, 10:20 AM

I see kleinman is using the 'advancement' equivocates with 'genomes exhibiting phenotypes I consider advancement according to my favoured bronze-age mythology' fallacy.

That's a new lie.

kleinman

21st June 2007, 10:53 AM

So clown fish and cheese wiz, two evolutionarian clones who have not run a single case from ev can predict how ev will behave with infinite populations.you know this is a lie, why do you say it? It only further demonstates the fact you are a raving loon. Do you enjoy being a raving loon?
Well silly clown fish, then post your results and prove your point. Since the only point you have is on top of your head, you have already prove this. Why don’t you continue to argue that evolution has no goal and prove your ignorance of the theory? Did you see SciFi American from earlier this month? There’s an article in there where they are abandoning the RNA world and returning to the old Miller experiment and amino acids as the next dumb ass attempt at explaining abiogenesis. You can stick with your dumb ass explanation of cooperative chemistry. Do you want me to remind the readers of your dumb ass explanation? Sure, here it is:
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.
Well clown fish, you have no mathematics and no empirical evidence. We have a peer reviewed and published model of evolution by random point mutation and natural selection. The results from this model (none of which you have posted) show that multiple selection pressures slow and ultimately stop evolution and we have numerous examples of empirical evidence of this mathematical behavior. You have dumb ass speculation. You are certainly qualified as an alchemical engineer.
At infinite population, the likelyhood of a single member of that population having the exact right sequence being selected for is 100%. The xext step mutation in the model is immaterial. We do not need worry about if the next mutation will be beneficial, because our model is done. At the zero generation point we acheived our goal.
There are no infinite populations and now you have a goal? Clown fish, you aren’t moving the goalposts are you? Clown fish, you are such a dim bulb when it comes to the mathematics of mutation and selection. When are you going to post an example of multiple selection pressures accelerating evolution?
I see kleinman is using the 'advancement' equivocates with 'genomes exhibiting phenotypes I consider advancement according to my favoured bronze-age mythology' fallacy.
Hey cyborg, clown fish is an adherent to the cruft theory of evolution. He thinks evolution has no goal as well. I guess you evolutionarians have forgotten that the fitness to reproduce is what drives the selection process. Do you want to post an example where multiple selection pressures accelerate evolution? Then perhaps you could prove your rust-age mythology.

Dr Adequate

21st June 2007, 12:04 PM

So clown fish and cheese wiz, two evolutionarian clones who have not run a single case from ev can predict how ev will behave with infinite populations. I don't know about joobz, but I can, because the question's trivial: obviously the number of generations required will be 0. Moreover, as the population size tends to infinity, the generations required tends to 0, which is what I actually said, you halfwitted liar.

Well silly clown fish, this type of behavior is not seen in reality with HIV, HBV and other examples with huge populations so whatever conclusion cheese wiz draws with infinite populations has no bearing on evolution in reality. But this is a stupid lie: reality and your own figures from ev show that generations to completion decreases as population size increases.

Multiple selection pressures always slows down and ultimately stops evolution. I am at a loss to know why you should tell this lie here. You're meant to be lying about population size, remember?

Do you want me to translate it to clown fishian? Let’s see if you can comprehend this. It makes no difference what happens mathematically with infinite populations. I think I see your problem. You don't know what "tends to infinity" means, right?

According to cheese wiz’s silly logic this creature should be the most evolutionarily advanced because it takes the least number of generations to evolve due to its huge population. But this is a stupid lie: obviously I have said no such thing.

The only thing you two have proved is that you have no understanding of the mathematics of mutation and selection. The dominant mathematical parameters in this system are the genome length and number of selection pressures. Population has only a second order effect on the mathematical behavior of the model. Increase the genome length in ev and the model stops converging unless you reduce the number of selection conditions. You two are a couple of dim bulbs when it comes to the mathematics of mutation and selection. You know everyone knows you're lying, right?

Somebody turn on the light for this dim bulb. Multiple selection pressure interferes with the evolutionary process. This is shown mathematically with ev, this is explained with Delphi’s Wikipedia reference to fitness landscape and this shown by dozens of citations of real examples of mutation and selection. There is no selection pressure that transforms a reptile to a bird, if you propose that this transformation is done by a combination of selection pressures, it is mathematically impossible. That is how the mathematics of mutation and selection works. Some day perhaps you and cheese wiz will return from infinity and come to understand how mutation and selection works in reality. You know everyone knows you're lying, right?

Cheese wiz is not the magical word for you; it is what comes out of you when you open your mouth. And yet, you halfwitted liar, you use the term to address me, do you not? It's your magical phrase for me, not for my statements, isn't it?

We can all see you're lying.

So let’s see how you misapply the Law of Large Numbers:

From this cheese wiz draws the conclusion that the number of generations for convergence of ev goes to zero with infinite population. Of course I draw that conclusion, because it is trivially true, as you would know if you were not innumerate. Hence, you are lying when you pretend that I have "misapplied" the Law of Large Numbers.

---

I notice that "dim bulb" is the new magical incantation for this week. Let us know if it changes reality, won't you?

Dr Adequate

21st June 2007, 12:13 PM

Well silly clown fish, then post your results and prove your point. Since the only point you have is on top of your head, you have already prove this. Why don’t you continue to argue that evolution has no goal and prove your ignorance of the theory? Did you see SciFi American from earlier this month? There’s an article in there where they are abandoning the RNA world and returning to the old Miller experiment and amino acids as the next dumb ass attempt at explaining abiogenesis. You can stick with your dumb ass explanation of cooperative chemistry. Do you want me to remind the readers of your dumb ass explanation? Sure, here it is:

Well clown fish, you have no mathematics and no empirical evidence. We have a peer reviewed and published model of evolution by random point mutation and natural selection. The results from this model (none of which you have posted) show that multiple selection pressures slow and ultimately stop evolution and we have numerous examples of empirical evidence of this mathematical behavior. You have dumb ass speculation. You are certainly qualified as an alchemical engineer.

There are no infinite populations and now you have a goal? Clown fish, you aren’t moving the goalposts are you? Clown fish, you are such a dim bulb when it comes to the mathematics of mutation and selection. When are you going to post an example of multiple selection pressures accelerating evolution?

Hey cyborg, clown fish is an adherent to the cruft theory of evolution. He thinks evolution has no goal as well. I guess you evolutionarians have forgotten that the fitness to reproduce is what drives the selection process. Do you want to post an example where multiple selection pressures accelerate evolution? Then perhaps you could prove your rust-age mythology. And thus you propose to overturn biology?

You sad little man.

joobz

21st June 2007, 12:25 PM

Well silly clown fish, then post your results and prove your point. Since the only point you have is on top of your head, you have already prove this. Why don’t you continue to argue that evolution has no goal and prove your ignorance of the theory? Did you see SciFi American from earlier this month? There’s an article in there where they are abandoning the RNA world and returning to the old Miller experiment and amino acids as the next dumb ass attempt at explaining abiogenesis. You can stick with your dumb ass explanation of cooperative chemistry. Do you want me to remind the readers of your dumb ass explanation? Sure, here it is:

Well clown fish, you have no mathematics and no empirical evidence. We have a peer reviewed and published model of evolution by random point mutation and natural selection. The results from this model (none of which you have posted) show that multiple selection pressures slow and ultimately stop evolution and we have numerous examples of empirical evidence of this mathematical behavior. You have dumb ass speculation. You are certainly qualified as an alchemical engineer.

There are no infinite populations and now you have a goal? Clown fish, you aren’t moving the goalposts are you? Clown fish, you are such a dim bulb when it comes to the mathematics of mutation and selection. When are you going to post an example of multiple selection pressures accelerating evolution?

Hey cyborg, clown fish is an adherent to the cruft theory of evolution. He thinks evolution has no goal as well. I guess you evolutionarians have forgotten that the fitness to reproduce is what drives the selection process. Do you want to post an example where multiple selection pressures accelerate evolution? Then perhaps you could prove your rust-age mythology.
Wow, you are having a very hard time remaining coherent. You jump from simulation talk to abiogenesis to random point mutation to multiple selection pressures to infinite populations to goalposts to bulbs....
But in none of that, did you actually come anywhere close to forming a logical thought.

You have yet to prove that you even understand the ramblings you make. My simple question for you to clarify your own sentence demonstrates this.

kleinman

21st June 2007, 12:50 PM

And thus you propose to overturn biology?
It is time to review what cheese wiz, PhD in amathematics, view of biology is, in particular his “proof” of multiple selection pressures accelerating evolution.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
The red line shows generations to achieve fixation of n alleles acted on by n selection pressures, the n+1th selection pressure being introduced only after the nth allele is fixed.

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

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

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
http://forums.randi.org/images/smilies/doglaugh.gif
Now that you have magically produced this gif that shows that multiple selection pressures accelerate evolution, perhaps you could magically produce some real examples of your amathematical model.
You sad little man.
Oh I know cheese wiz. I have cited only about 50 real examples that demonstrate the mathematics of ev and how mutation and selection actually works and am completely overwhelmed by all zero of your examples that demonstrates how your dumb gif works. Perhaps if I post a couple more examples that will cheer me up? I think it will, my favorite little annoyee.

http://www.bioone.org/perlserv/?request=get-document&issn=0015-4040&volume=89&issue=02&page=117 (http://www.bioone.org/perlserv/?request=get-document&issn=0015-4040&volume=89&issue=02&page=117)
These reduced-risk insecticides offer a wide range of pest management options available to vegetable growers and should be used wisely or in rotation with one another to minimize selection for resistance to any one given material.

http://www.malariajournal.com/content/6/1/9 (http://www.malariajournal.com/content/6/1/9)
Combination therapy would also be advantageous if the required set of mutations was initially absent in the population, so that selection could not start to act.
I do enjoy posting real examples of how mutation and selection works to shed some light on the dim bulbs of evolutionism. Some day cheese wiz you will understand that multiple selection pressures slow evolution, it does not accelerate evolution. Of course, there is always the possibility that you live in one of kjkent1’s alternative universes. Cheese wiz, I think I hear your mother calling you, “earth to cheese wiz, earth to cheese wiz, time to come home and take your nap, you can be an imaginary superhero later”.

cyborg

21st June 2007, 02:48 PM

I guess you evolutionarians have forgotten that the fitness to reproduce is what drives the selection process.

Oh right kleinman! Stupid me! That's for edumacating me.

And the goal of rain is to put out fires right? About time we fired those lazy firemen and let your god decide what does and does not burn; what, what?

joobz

21st June 2007, 02:57 PM

It is time to review what cheese wiz, PhD in amathematics, view of biology is, in particular his “proof” of multiple selection pressures accelerating evolution.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg

http://forums.randi.org/images/smilies/doglaugh.gif
Now that you have magically produced this gif that shows that multiple selection pressures accelerate evolution, perhaps you could magically produce some real examples of your amathematical model.

Oh I know cheese wiz. I have cited only about 50 real examples that demonstrate the mathematics of ev and how mutation and selection actually works and am completely overwhelmed by all zero of your examples that demonstrates how your dumb gif works. Perhaps if I post a couple more examples that will cheer me up? I think it will, my favorite little annoyee.

http://www.bioone.org/perlserv/?request=get-document&issn=0015-4040&volume=89&issue=02&page=117

http://www.malariajournal.com/content/6/1/9

I do enjoy posting real examples of how mutation and selection works to shed some light on the dim bulbs of evolutionism. Some day cheese wiz you will understand that multiple selection pressures slow evolution, it does not accelerate evolution. Of course, there is always the possibility that you live in one of kjkent1’s alternative universes. Cheese wiz, I think I hear your mother calling you, “earth to cheese wiz, earth to cheese wiz, time to come home and take your nap, you can be an imaginary superhero later”.
You now go from a poor analysis to Dr.A's model to a lie about examples to more examples which do not support anything you claim. Yup, you sure are making headway in proving nothing.

kleinman

21st June 2007, 03:14 PM

You now go from a poor analysis to Dr.A's model to a lie about examples to more examples which do not support anything you claim. Yup, you sure are making headway in proving nothing.
Well clown fish, here’s your big opportunity to explain cheese wiz’s gif and give us some examples of multiple selection pressures accelerating evolution. We all want to hear this fish story. Let’s see if you can prove that you’re more than just another dim bulb of evolutionism. I doubt I’ll need to get out the sun glasses for this tale. I’ll tell you what, if you tell a good story, we’ll get you a worm, great and wise professor of alchemical engineering and explainer of abiogenesis.
http://forums.randi.org/images/smilies/doglaugh.gif

delphi_ote

21st June 2007, 04:37 PM

Oh right kleinman! Stupid me! That's for edumacating me.

And the goal of rain is to put out fires right? About time we fired those lazy firemen and let your god decide what does and does not burn; what, what?
Or it is the goal of gravity to make a ball roll down a hill?

The fitness landscape is called a landscape for a reason. Natural selection acting on the population is analogous to gravity acting on a ball. Just like the ball rolls to the lowest point when acted on by gravity, the population evolves to the fittest point when acted on by natural selection. The analogy isn't perfect, of course. The fitness landscape would have a huge number of dimensions and would constantly shift if we could actually calculate it for a real critter.

kleinman

21st June 2007, 05:25 PM

And the goal of rain is to put out fires right? About time we fired those lazy firemen and let your god decide what does and does not burn; what, what?Or it is the goal of gravity to make a ball roll down a hill?
Now don’t be silly Delphi, we are talking about cause and effect relationships which can be measures and modeled so as to predict how these systems will behave, whether it is the effects of gravity on a mass or fitness of a population to reproduce subject to mutation and selection. It so happens that Dr Schneider has written a plausible model of the later phenomenon and this model makes some interesting predictions of the behavior of mutation and selection acted on by reproductive fitness.
The fitness landscape is called a landscape for a reason. Natural selection acting on the population is analogous to gravity acting on a ball. Just like the ball rolls to the lowest point when acted on by gravity, the population evolves to the fittest point when acted on by natural selection. The analogy isn't perfect, of course. The fitness landscape would have a huge number of dimensions and would constantly shift if we could actually calculate it for a real critter.
Delphi, did I ever thank you for raising the issue of fitness landscape. It really clarified my understanding on the mutation and selection process. Your description of the fitness landscape here is a good one. I’m glad to see you took time off from sorting your sock drawer and skateboarding to give us this description. You should also point out that when a population is at a local optimum and subjected to a single new selection pressure, it is much easier for that population to evolve (traverse the fitness landscape) to a new local optimum than if the population is subjected to multiple selection pressures simultaneously.

So we have ev, the peer reviewed and published mathematical model of random point mutations and natural selection which predicts that multiple selection pressures slow the evolutionary process profoundly, we have your Wikipedia reference which shows that multiple selection pressures slow the ability of a population to traverse the fitness landscape and we have numerous real examples (which are not limited to random point mutations and include recombination in many cases) of this phenomenon. Now perhaps you want to support cheese wiz’s gif which shows that multiple selection pressures accelerate evolution. If you do, would you give us a real example where multiple selection pressures accelerate evolution?

So Delphi, what is the selection pressure that evolves a reptile into a bird? Do you think that feathers grew on reptiles for insulation? Do you think any of these feathered reptiles had feathers coming out of their armpits? I don’t want to get too down on these evolutionarian ideas but it sound pretty bird brained.

Back to reality, here are a couple more citations which show that multiple selection pressures slow evolution. Seems everybody knows this but you evolutionarians. Ev shows this, Delphi’s Wikipedia reference to the fitness landscape shows this and an ever growing collection of scientific papers report this. You dim bulbs of evolutionism need a new myth to put your faith in.

https://content.nejm.org/cgi/content/extract/350/10/1023?ck=nck (https://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. In the United States, as many as 50 percent of patients receiving antiretroviral therapy are infected with viruses that express resistance to at least one of the available antiretroviral drugs. 4 Consequently, the transmission of drug-resistant strains is also a growing concern. 5,6,7

http://www-wds.worldbank.org/external/default/WDSContentServer/IW3P/IB/2005/07/20/000016406_20050720164750/Rendered/INDEX/wps3670.txt (http://www-wds.worldbank.org/external/default/WDSContentServer/IW3P/IB/2005/07/20/000016406_20050720164750/Rendered/INDEX/wps3670.txt)
This study finds that a subsidy to ACTs is likely to slow the rate of emergence of resistance to artemisinin and partner drugs, even if such a subsidy were to increase the use of ACTs significantly. This conclusion is robust to alternative assumptions regarding the responsiveness of demand to the lower price for ACTs and a wide range of epidemiological and economic parameters. However, the simulation results show that a subsidy for two or more ACT combinations is likely to be much more cost-effective than a subsidy to a single ACT. The only consideration is that the drugs used as partners to artemisinin be unrelated to each other and to artemisinin in mechanism of action and in genetic bases of resistance, so that a single mutation cannot encode resistance to both components. Such a subsidy program for ACTs, administered globally, that reduces reliance on any single combination, and discourages monotherapy, not only of artemisinin but of any effective antimalarial that could potentially be used as partner drug with artemisinin, is likely to be effective (and cost-effective) both in buying time for ACTs and in saving lives.

You evolutionarians have a good weekend. I’ll post more citations next week which show that multiple selection pressures slow and ultimately stop evolution.

Dr Adequate

21st June 2007, 06:10 PM

Now don’t be silly Delphi, we are talking about cause and effect relationships which can be measures and modeled so as to predict how these systems will behave, whether it is the effects of gravity on a mass or fitness of a population to reproduce subject to mutation and selection. It so happens that Dr Schneider has written a plausible model of the later phenomenon and this model makes some interesting predictions of the behavior of mutation and selection acted on by reproductive fitness.

Delphi, did I ever thank you for raising the issue of fitness landscape. It really clarified my understanding on the mutation and selection process. Your description of the fitness landscape here is a good one. I’m glad to see you took time off from sorting your sock drawer and skateboarding to give us this description. You should also point out that when a population is at a local optimum and subjected to a single new selection pressure, it is much easier for that population to evolve (traverse the fitness landscape) to a new local optimum than if the population is subjected to multiple selection pressures simultaneously.

So we have ev, the peer reviewed and published mathematical model of random point mutations and natural selection which predicts that multiple selection pressures slow the evolutionary process profoundly, we have your Wikipedia reference which shows that multiple selection pressures slow the ability of a population to traverse the fitness landscape and we have numerous real examples (which are not limited to random point mutations and include recombination in many cases) of this phenomenon. Now perhaps you want to support cheese wiz’s gif which shows that multiple selection pressures accelerate evolution. If you do, would you give us a real example where multiple selection pressures accelerate evolution?

So Delphi, what is the selection pressure that evolves a reptile into a bird? Do you think that feathers grew on reptiles for insulation? Do you think any of these feathered reptiles had feathers coming out of their armpits? I don’t want to get too down on these evolutionarian ideas but it sound pretty bird brained.

Back to reality, here are a couple more citations which show that multiple selection pressures slow evolution. Seems everybody knows this but you evolutionarians. Ev shows this, Delphi’s Wikipedia reference to the fitness landscape shows this and an ever growing collection of scientific papers report this. You dim bulbs of evolutionism need a new myth to put your faith in.

https://content.nejm.org/cgi/content/extract/350/10/1023?ck=nck (https://content.nejm.org/cgi/content/extract/350/10/1023?ck=nck)

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

You evolutionarians have a good weekend. I’ll post more citations next week which show that multiple selection pressures slow and ultimately stop evolution. None of the lies in this post have convinced us in the past. What makes you think that they will convince us now?

Are you mentally ill?

Dr Adequate

21st June 2007, 06:25 PM

You evolutionarians have a good weekend. What, you're crawling off already?

But you've only said "cheese" sixty-two times this week!

If you said it a few more times, maybe reality would crumble and be replaced by your delusional fantasy world.

Dr Adequate

21st June 2007, 06:28 PM

It is time to review what cheese wiz, PhD in amathematics, view of biology is, in particular his “proof” of multiple selection pressures accelerating evolution.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg

http://forums.randi.org/images/smilies/doglaugh.gif
Now that you have magically produced this gif that shows that multiple selection pressures accelerate evolution, perhaps you could magically produce some real examples of your amathematical model.

Oh I know cheese wiz. I have cited only about 50 real examples that demonstrate the mathematics of ev and how mutation and selection actually works and am completely overwhelmed by all zero of your examples that demonstrates how your dumb gif works. Perhaps if I post a couple more examples that will cheer me up? I think it will, my favorite little annoyee.

http://www.bioone.org/perlserv/?request=get-document&issn=0015-4040&volume=89&issue=02&page=117 (http://www.bioone.org/perlserv/?request=get-document&issn=0015-4040&volume=89&issue=02&page=117)

http://www.malariajournal.com/content/6/1/9 (http://www.malariajournal.com/content/6/1/9)

I do enjoy posting real examples of how mutation and selection works to shed some light on the dim bulbs of evolutionism. Some day cheese wiz you will understand that multiple selection pressures slow evolution, it does not accelerate evolution. Of course, there is always the possibility that you live in one of kjkent1’s alternative universes. Cheese wiz, I think I hear your mother calling you, “earth to cheese wiz, earth to cheese wiz, time to come home and take your nap, you can be an imaginary superhero later”. To summarise:

(1) You have no criticism of my model.

(2) You yourself have made no attempt to model the situation about which you keep lying.

(3) You do say "cheese" a lot, don't you?

Paul C. Anagnostopoulos

21st June 2007, 06:36 PM

Whether you want to call fitness the goal or result, it is what drives the mutation and selection process.
Zing! Sproing! Fwoop!

Dodgeball, anyone?

~~ Paul

joobz

21st June 2007, 06:40 PM

Well clown fish, here’s your big opportunity to explain cheese wiz’s gif and give us some examples of multiple selection pressures accelerating evolution. We all want to hear this fish story. Let’s see if you can prove that you’re more than just another dim bulb of evolutionism. I doubt I’ll need to get out the sun glasses for this tale. I’ll tell you what, if you tell a good story, we’ll get you a worm, great and wise professor of alchemical engineering and explainer of abiogenesis.
http://forums.randi.org/images/smilies/doglaugh.gif
Are you finally admitting you didn't understand what was shown? Are you going to admit that you didn't understand Delphi's code?

Now, will you start to explain how at every moment throughout the history of the earth, that at every location on this earth, conditions were such that only extinction would occur? We are waiting for this detailed account.

Here's some food for thought. Your whole claim is that evolution is too slow. WHo would have thought that reality would say otherwise?

Wicker T, Yahiaoui N, Keller B. " Illegitimate recombination is a major evolutionary mechanism for initiating size variation in plant resistance genes."
Plant J. 2007 Jun 15;
We found that illegitimate recombination (IR) is the major mechanism that generates quasi-random duplications within the LRR domain. These initial duplications are required as seeds for subsequent unequal crossing-over events which cause the observed rapid increase or decrease in LRR repeat numbers.

Joos B, Fischer M, Schweizer A, Kuster H, Boni J, Wong JK, Weber R, Trkola A, Gunthard HF. Positive In Vivo Selection of the HIV-1 Envelope Protein gp120 Occurs at Surface-Exposed Regions.
J Infect Dis. 2007 Jul 15;196(2):313-20.
The rapid evolution of human immunodeficiency virus (HIV) envelope represents a major challenge to vaccine and drug development,
Hua Q, Joyce AR, Palsson BO, Fong SS. "Metabolic characterization of Escherichia coli adapted to growth on lactate.
Appl Environ Microbiol. 2007 May 18; "

Despite different evolutionary trajectories among parallel evolved populations, most improvements were obtained within the first 250 generations of evolution and were generally characterized by a significant increase in pathway capacity.

Hmm, look at that. 250 generations regardless of the starting point? Evolution is too slow, eh?

cyborg

21st June 2007, 06:52 PM

Dodgeball, anyone?

When kleinman dodges it's into another ball - his statement is still wrong of course, he's just adjusted what is wrong about it.

delphi_ote

21st June 2007, 10:01 PM

So Delphi, what is the selection pressure that evolves a reptile into a bird?
In your strawman version of evolution, I guess a cold day comes along and a crocodile lays a chicken egg. Since you're not actually interested in learning anything, you can go ahead and stop reading here. While you're at it, post a lame joke about this paragraph.

In reality, it's obvious that flight and endothermy are both very useful adaptations in a world where other critters have already crowded the readily available niches. There are a lot of good hypotheses as to just what sequence of events caused birds to evolve (http://en.wikipedia.org/wiki/Origin_of_birds), but it doesn't seem like there's a consensus yet. Based on the fossil record, the fact that it happened is now (http://en.wikipedia.org/wiki/Pedopenna) fairly (http://en.wikipedia.org/wiki/Dilong_paradoxus) obvious (http://en.wikipedia.org/wiki/Shuvuuia).

Dr Adequate

21st June 2007, 10:38 PM

Based on the fossil record, the fact that it happened is now (http://en.wikipedia.org/wiki/Pedopenna) fairly (http://en.wikipedia.org/wiki/Dilong_paradoxus) obvious (http://en.wikipedia.org/wiki/Shuvuuia). Kleinman doesn't understand obvious things, they make his brain all hurty.

Schneibster

22nd June 2007, 03:33 AM

Of course I draw that conclusion, because it is trivially true, as you would know if you were not innumerate. Awesome! A New Word: innumerate, as in, mathematically illiterate. Nice, I'll keep this one in my back pocket for a good occasion.

delphi_ote

22nd June 2007, 05:12 AM

Kleinman doesn't understand obvious things, they make his brain all hurty.
That's why I gave him permission to stop reading after the first paragraph. If he continues after my warning, I can't be held accountable for what happens. It's a bit like There's A Monster at the End of this Book.

Paul C. Anagnostopoulos

22nd June 2007, 05:25 AM

Awesome! A New Word: innumerate, as in, mathematically illiterate. Nice, I'll keep this one in my back pocket for a good occasion.
Dude, where you been, man? The word innumerate has been around since 1959 or so. It's really handy!

http://www.amazon.com/Innumeracy-Mathematical-Illiteracy-Its-Consequences/dp/0809058405/ref=pd_bbs_sr_1/105-0978227-1146007?ie=UTF8&s=books&qid=1182511436&sr=8-1

~~ Paul

jimbob

22nd June 2007, 10:04 AM

Awesome! A New Word: innumerate, as in, mathematically illiterate. Nice, I'll keep this one in my back pocket for a good occasion.

Whatr about "demiglot" for his linguistic abilities, and "demimath" for his grasp of a wide range of subjects; I know it is generous, but I think it gets the point across. (I can't think of an opposite of "Rennaiscence man", mabe a "neo-paleolithic philosophy"?)

mijopaalmc

22nd June 2007, 10:18 AM

Whatr about "demiglot" for his linguistic abilities, and "demimath" for his grasp of a wide range of subjects; I know it is generous, but I think it gets the point across. (I can't think of an opposite of "Rennaiscence man", mabe a "neo-paleolithic philosophy"?)

I think "dilettante" is just fine.

Mercutio

23rd June 2007, 05:03 AM

(I can't think of an opposite of "Rennaiscence man", mabe a "neo-paleolithic philosophy"?)

The Geico cavemen use the phrase "it's so easy, Kleinman can understand it."

jimbob

23rd June 2007, 03:48 PM

Maybe "Remortance" man (damn my paltry classical education, I am trying for the literal translation of "redeath" as opposed to "rebirth")

jimbob

24th June 2007, 08:42 AM

The Geico cavemen use the phrase "it's so easy, Kleinman can understand it."

Surly shome mishtake? Nothing's that simple.

Mercutio

24th June 2007, 09:51 AM

Surly shome mishtake? Nothing's that simple.
An honest misunderstanding, actually; the cavemen thought Kleinman was only mythological.

kleinman

25th June 2007, 08:59 AM

Are you mentally ill?
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
The red line shows generations to achieve fixation of n alleles acted on by n selection pressures, the n+1th selection pressure being introduced only after the nth allele is fixed.

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

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

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
http://forums.randi.org/images/smilies/doglaugh.gif
(1) You have no criticism of my model.
You have no real examples of your model oh great PhD of gifematics.
(2) You yourself have made no attempt to model the situation about which you keep lying.
I don’t have to, Dr Schneider has already done it and his model is peer reviewed and published dim bulb of evolutionism.
(3) You do say "cheese" a lot, don't you?
I’m fondue the word since the dead theory of evolution smells like limburger.

Now folks, if cheese wiz’s gif was correct, we need to contact all the infectious disease experts treating HIV and TB and tell them that combination therapy accelerates the evolution of resistance and we need to contact parasitologists and warn them that combination therapy will accelerate the evolution of resistant malaria and we need to warn agricultural experts that combination herbicides will accelerate the evolution of resistant weeds and pesticide experts and oncologists and ecologists and…

Cheese wiz’s silly gif and his silly conclusion he draws from it has no mathematical or empirical scientific basis. He is completely ignorant of the mathematics of mutation and selection and the mathematics of fitness landscape. However, he is a gifmeister.
Whether you want to call fitness the goal or result, it is what drives the mutation and selection process.Zing! Sproing! Fwoop!

Dodgeball, anyone?
Now what are you whining about Paul? Do you want to tell us what ev represents again on the evolutionary landscape?
Well clown fish, here’s your big opportunity to explain cheese wiz’s gif and give us some examples of multiple selection pressures accelerating evolution. We all want to hear this fish story. Let’s see if you can prove that you’re more than just another dim bulb of evolutionism. I doubt I’ll need to get out the sun glasses for this tale. I’ll tell you what, if you tell a good story, we’ll get you a worm, great and wise professor of alchemical engineering and explainer of abiogenesis.
http://forums.randi.org/images/smilies/doglaugh.gif (http://forums.randi.org/images/smilies/doglaugh.gif) Are you finally admitting you didn't understand what was shown? Are you going to admit that you didn't understand Delphi's code?
Certainly I understand cheese wiz’s claims. He is claiming that multiple selection pressures evolve more quickly than single selection pressures. I am overwhelmed by the empirical evidence of his silly gif. He doubled the number of citations of real examples of his gif this weekend. His number of citations of real examples of his gif is now up to zero. You evolutionarians really know how to make your scientific skills shine.

I yes, Delphi’s secret code of evolutionism, his Rosetta stone is only understood by high priests of the evolutionarian faith and clown fish.
Now, will you start to explain how at every moment throughout the history of the earth, that at every location on this earth, conditions were such that only extinction would occur? We are waiting for this detailed account.
Sure I’ll start the explanation for you clown fish. Let’s start with what we know now. We know now that multiple selection pressures slow and ultimately stop evolution silly Dodo. However, long ago in a place far away, multiple selection pressures accelerated evolution and inorganic chemicals cooperated to make life, those were the good ole days.
Here's some food for thought. Your whole claim is that evolution is too slow. WHo would have thought that reality would say otherwise?
No worm for you yet clown fish, you have to give us examples where multiple selection pressures accelerate evolution.
Wicker T, Yahiaoui N, Keller B. " Illegitimate recombination is a major evolutionary mechanism for initiating size variation in plant resistance genes."
Plant J. 2007 Jun 15;We found that illegitimate recombination (IR) is the major mechanism that generates quasi-random duplications within the LRR domain. These initial duplications are required as seeds for subsequent unequal crossing-over events which cause the observed rapid increase or decrease in LRR repeat numbers.
So what? Combination herbicides still slows the evolution of resistant weeds, perhaps you want to give us an example where illegitimate recombination overcomes the effect of multiple selection pressures, then you can get your worm.
Joos B, Fischer M, Schweizer A, Kuster H, Boni J, Wong JK, Weber R, Trkola A, Gunthard HF. Positive In Vivo Selection of the HIV-1 Envelope Protein gp120 Occurs at Surface-Exposed Regions.
J Infect Dis. 2007 Jul 15;196(2):313-20.The rapid evolution of human immunodeficiency virus (HIV) envelope represents a major challenge to vaccine and drug development,
Again, so what? Multiple selection pressures still slows the evolution of the HIV virus. Just because people are having difficulty developing a vaccine for HIV (and for the influenza virus and many other infectious agents) doesn’t change the mathematical and empirical facts that multiple selection pressures slow and ultimately stop evolution.
Hua Q, Joyce AR, Palsson BO, Fong SS. "Metabolic characterization of Escherichia coli adapted to growth on lactate.
Appl Environ Microbiol. 2007 May 18; "Despite different evolutionary trajectories among parallel evolved populations, most improvements were obtained within the first 250 generations of evolution and were generally characterized by a significant increase in pathway capacity.
So what^3? None of these citations address the mathematical and empirical facts that multiple selection pressures slow and ultimately stop evolution.
Hmm, look at that. 250 generations regardless of the starting point? Evolution is too slow, eh?
Well that explains why we see new species every 250 generations. However clown fish, that is not enough to get your worm.
Dodgeball, anyone?When kleinman dodges it's into another ball - his statement is still wrong of course, he's just adjusted what is wrong about it.
Now cyborg, I would never dodge your cruft theory of evolution, in fact I embrace it with open arms. I consider it a mozzarella ball of a theory. (That one’s for you cheese wiz.)
So Delphi, what is the selection pressure that evolves a reptile into a bird?In your strawman version of evolution, I guess a cold day comes along and a crocodile lays a chicken egg. Since you're not actually interested in learning anything, you can go ahead and stop reading here. While you're at it, post a lame joke about this paragraph.
Oh no, not the strawman argument, anything but that, help me, help me, I’ve been strawmanned. Sure I’m interested in learning things. You (and Wikipedia) taught me about the fitness landscape. Now are you evolutionarians ready to learn anything about the mathematics of mutation and selection?
In reality, it's obvious that flight and endothermy are both very useful adaptations in a world where other critters have already crowded the readily available niches. There are a lot of good hypotheses as to just what sequence of events caused birds to evolve, but it doesn't seem like there's a consensus yet. Based on the fossil record, the fact that it happened is now fairly obvious.
Too bad that mutation and selection can’t accomplish any of these things. Mutation and selection does not work this way. Mutation and selection is far too slow a process to do any of what you allege here. It is mathematically impossible. The books don’t balance. Ev shows this, your reference to the fitness landscape shows this and the empirical data shows this. Multiple selection pressures confound the evolutionary process. This is why it takes hundreds of millions and billions of generations to evolve only a 100 loci on a bacterial size genome. The mathematics only gets worse on the huge genomes of complex life forms. Your theory is mathematically impossible.

Gould proposed the concept of punctuated equilibrium to account for the lack of transitional forms in the fossil record. The evolutionarian version of a Rorschach test for the interpretation of fossils as transitional form does not overcome the mathematical fact the multiple selection pressures slow and ultimately stop evolution. This is what ev shows, this is what the fitness landscape shows and this is what the empirical data shows. Delphi, your theory is mathematically impossible.

Since you dim bulbs of evolutionism are having difficulty understanding the mathematics of mutation and selection, I now post more empirical examples that demonstrate that multiple selection pressures slow and ultimately stop evolution.

http://www.malariaconsortium.org/data/files/pages/act_6.pdf (http://www.malariaconsortium.org/data/files/pages/act_6.pdf)
Antifolate drug resistance (i. e. pyrimethamine means that new combinations are urgently needed particularly because addition of a single drug to an already failing regimen is rarely effective for very long.

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.

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.

Now, I feel like I’m being a bit unfair, ganging up on you poor helpless evolutionarians so I’ve decided to help you find citations which support your belief system that multiple selection pressures accelerate evolution. You may use the search engine of your choice.

For Paul, your key words for your search are, “crapola”, “goalposts”, “evolutionary landscape” and “Zing! Sproing! Fwoop!”.

For cheese wiz, “red line”, “blue line”, “gif”. “jpeg”, “cheese”, “FAQ”.

For clown fish, “cooperative chemistry”, “speculation”, “anything is possible”, “fish story”.

For Delphi, “skateboard”, “stop action photography”, “sock drawer”, “job.com”

For evolutionarians in general, “denial”, “speculation”, “extrapolation”, “any web site that engages in mushy soft mathematically deficient science”

So you evolutionarians don’t whine that I haven’t tried to help you find citations which show that multiple selection pressures accelerate evolution.

joobz

25th June 2007, 09:41 AM

So what?
It proves that evolution happens

Again, so what?
It proves evolution happens

So what^3?
It proves that evolution happens
None of these citations address the mathematical and empirical facts that multiple selection pressures slow and ultimately stop evolution.
wrong.

kleinman

25th June 2007, 10:21 AM

So what? ^3It proves that evolution happens ^3
Clown fish, you will never get your worm this way. Of course evolution happens, microevolution. The reason why macroevolution can not happen is that it is mathematically impossible. Multiple selection pressures interfere with each other and slows then ultimately stops evolution. That is what ev shows, that is what the Wikipedia reference to fitness landscape shows and that is what reality shows.
None of these citations address the mathematical and empirical facts that multiple selection pressures slow and ultimately stop evolution.wrong.
Your answer may convince devout and brainwashed evolutionarians but it will not convince others. Until you can show an example where multiple selection pressures accelerate evolution your theory is without a mathematical or empirical basis, unless you are convinced by cheese wiz’s silly gif.
http://forums.randi.org/images/smilies/doglaugh.gif
As it stands now, the only empirical evidence of how mutation and selection behaves is that it slows down and ultimately stops the greater the number of selection pressures. That is a mathematical and empirical fact silly clown fish. You and the other dim bulbs of evolutionism have to come to grips with this fact. That is why the theory of evolution is mathematically impossible.

joobz

25th June 2007, 12:01 PM

Clown fish, you will never get your worm this way. Of course evolution happens, microevolution. yup, evolution occurs.
The reason why macroevolution can not happen is that it is mathematically impossible.
Nope. we proved this wrong with each any every redefinition of macroevolution. see the Kleinman faq for more details. Sorry, evolution occurs (whether you want to call it macro or micro).

Multiple selection pressures interfere with each other and slows then ultimately stops evolution.
This sentence has no meaning.

That is what ev shows, that is what the Wikipedia reference to fitness landscape shows and that is what reality shows.
This sentence refers to the sentence that holds no meaning. therefore, this sentence also holds no meaning.

Your answer may convince devout and brainwashed evolutionarians but it will not convince others.
This sentence holds only ad homs and has no connection with reality. Not suprising, considering it follows two sentences of yours which were devoid of meaning.
Until you can show an example where multiple selection pressures accelerate evolution your theory is without a mathematical or empirical basis, unless you are convinced by cheese wiz’s silly gif.
Definition of false diachotomy.

As it stands now, the only empirical evidence of how mutation and selection behaves is that it slows down and ultimately stops the greater the number of selection pressures.
Nope, this has not been what you have shown.
All evidence you have shown points to the existence of evolution.

That is a mathematical and empirical fact silly clown fish.
nope.
You and the other dim bulbs of evolutionism have to come to grips with this fact. That is why the theory of evolution is mathematically impossible.
nope.

some more papers that prove evolution occurs and is mathematically possible.

Ethan O. Perlstein et al., "Quantifying fitness distributions and phenotypic relationships in recombinant yeast populations" (2007) PNAS V 104, 10553-10558

Alfredo Villasante, José P. Abad, and María Méndez-Lago,"Centromeres were derived from telomeres during the evolution of the eukaryotic chromosome" PNAS 2007 104: 10542-10547

Rajkumar Sasidharan and Cyrus Chothia "The selection of acceptable protein mutations" PNAS 2007 104: 10080-10085

Hans Zauner and Ralf J. Sommer "Evolution of robustness in the signaling network of Pristionchus vulva development" PNAS 2007 104: 10086-10091

Matthew P. Heinicke, William E. Duellman, and S. Blair Hedges "Major Caribbean and Central American frog faunas originated by ancient oceanic dispersal" PNAS 2007 104: 10092-10097

And this last one I found particularly juicy, considering your distain toward my cooperative chemistry speculation:

Justin A. Bradford and Ken A. Dill, "Stochastic innovation as a mechanism by which catalysts might self-assemble into chemical reaction networks" PNAS 2007 104: 10098-10103

We develop a computer model for how two different chemical catalysts in solution, A and B, could be driven to form AB complexes, based on the concentration gradients of a substrate or product that they share in common. If A's product is B's substrate, B will be attracted to A, mediated by a common resource that is not otherwise plentiful in the environment. By this simple physicochemical mechanism, chemical reactions could spontaneously associate to become chained together in solution. According to the model, such catalyst self-association processes may resemble other processes of "stochastic innovation," such as Darwinian evolution in biology, that involve a search among options, a selection among those options, and then a lock-in of that selection. Like Darwinian processes, this simple chemical process exhibits cooperation, competition, innovation, and a preference for consistency. This model may be useful for understanding organizational processes in prebiotic chemistry and for developing new kinds of self-organization in chemically reacting systems.

see that bolded text there? hmm, which one of our theories has a basis in reality, your's or mine?
I'll give you a hint, It's not your's.

kleinman

25th June 2007, 01:12 PM

Clown fish, you will never get your worm this way. Of course evolution happens, microevolution.yup, evolution occurs.
However, not the mythical evolutionary notions that you evolutionarians propose, that is mathematically impossible.
The reason why macroevolution can not happen is that it is mathematically impossible.Nope. we proved this wrong with each any every redefinition of macroevolution. see the Kleinman faq for more details. Sorry, evolution occurs (whether you want to call it macro or micro).
You dim bulbs of evolutionism can try to hide behind semantics and gifs. If you think that multiple selection pressures accelerates evolution then post your evidence. We will all wait a long time for that evidence since none exists. You evolutionarians better stick with making up stories about fossils. You have lost the debate when the mathematics of mutation and selection is presented and the numerous real examples of this mathematics.
Multiple selection pressures interfere with each other and slows then ultimately stops evolution.This sentence has no meaning.
Of course this sentence has no meaning to you, you are ignorant of the mathematics of mutation and selection and do not understand the fitness landscape concept. If you did, you would understand that multiple selection conditions make the random mutation/natural selection process slow down profoundly. This is why a three drug combinations will profoundly slow the evolution of HIV despite its short genome, rapid reproduction rates, huge population and high mutation rate. None of these features exist in complex creatures yet you make mathematically baseless extrapolations that reptiles evolve to birds. What can you expect from an alchemical engineer who believes there is any reasonable scientific explanation for abiogenesis?
That is what ev shows, that is what the Wikipedia reference to fitness landscape shows and that is what reality shows.This sentence refers to the sentence that holds no meaning. therefore, this sentence also holds no meaning.
Why clown fish, you have run ev, you know what the model shows. You know what Wikipedia shows about the fitness landscape. You have chosen the evolutionarian time honored strategy of denial in addressing the mathematical facts that these mathematical explanations show. Some day you may understand the mathematics of mutation and selection.
Your answer may convince devout and brainwashed evolutionarians but it will not convince others.This sentence holds only ad homs and has no connection with reality. Not suprising, considering it follows two sentences of yours which were devoid of meaning.
You, an evolutionarian who has irrational speculations about abiogenesis and mathematically impossible speculations about reptiles evolving into birds obviously has no problem abandoning reality. Find an example where multiple selection pressures accelerate evolution, which should bring you back to reality. This debate is all about the mathematics of random mutation and natural selection. The mathematics and empirical evidence shows that multiple selection pressures slow and ultimately stop evolution. Show us one real example where multiple selection pressures accelerate evolution. Make this debate a challenge. So far, I have posted about 50 citations which show the multiple selection pressures slow evolution. Give us one example where multiple selection pressures accelerate evolution. I’ll give you a worm clown fish.
Until you can show an example where multiple selection pressures accelerate evolution your theory is without a mathematical or empirical basis, unless you are convinced by cheese wiz’s silly gif.Definition of false diachotomy.
You can’t even spell dichotomy and you can’t recognize that multiple selection pressures slow and ultimately stop the evolutionary process. Cheese wiz has plainly said that multiple selection pressures accelerate evolution. Here is what he has said:
Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
Can’t any of you evolutionarians give us a real example of this deluded thinking?
As it stands now, the only empirical evidence of how mutation and selection behaves is that it slows down and ultimately stops the greater the number of selection pressures.Nope, this has not been what you have shown.
All evidence you have shown points to the existence of evolution.
Not the evidence from ev, not the evidence from Wikipedia reference to the fitness landscape and not the evidence from the 50 or so real examples of how mutation and selection works. You dim bulbs of evolutionism are having a hard time understanding this mathematics of mutation and selection but I’ll continue to post real examples of how mutation and selection works. You can stamp your foot (flop you tail) and whine “wrong” but you won’t be able to post a real example of where multiple selection pressures accelerates evolution..
That is a mathematical and empirical fact silly clown fish.nope.
And you can flop your tail and whine “nope”.
You and the other dim bulbs of evolutionism have to come to grips with this fact. That is why the theory of evolution is mathematically impossible.nope.
And you can flop your tail twice and whine “nope” twice.
some more papers that prove evolution occurs and is mathematically possible…
Notice how clown fish is unable to quote from his references to support his arguments.
And this last one I found particularly juicy, considering your distain toward my cooperative chemistry speculation:

Justin A. Bradford and Ken A. Dill, "Stochastic innovation as a mechanism by which catalysts might self-assemble into chemical reaction networks" PNAS 2007 104: 10098-10103We develop a computer model for how two different chemical catalysts in solution, A and B, could be driven to form AB complexes, based on the concentration gradients of a substrate or product that they share in common. If A's product is B's substrate, B will be attracted to A, mediated by a common resource that is not otherwise plentiful in the environment. By this simple physicochemical mechanism, chemical reactions could spontaneously associate to become chained together in solution. According to the model, such catalyst self-association processes may resemble other processes of "stochastic innovation," such as Darwinian evolution in biology, that involve a search among options, a selection among those options, and then a lock-in of that selection. Like Darwinian processes, this simple chemical process exhibits cooperation, competition, innovation, and a preference for consistency. This model may be useful for understanding organizational processes in prebiotic chemistry and for developing new kinds of self-organization in chemically reacting systems.
Why that’s profound clown fish. Inorganic chemical reaction occurs therefore life arose spontaneously in the prebiotic soup. The field of alchemy for turning lead into gold hasn’t disappeared, it has simply moved in the silly speculation of abiogenesis. There is simply no end to the fish stories you tell clown fish. I do find them amusing.
see that bolded text there? hmm, which one of our theories has a basis in reality, your's or mine?
I'll give you a hint, It's not your's.
Isn’t cooperative chemistry wonderful? How could anyone doubt such logic? When you get a break from this ridiculous speculation, why don’t you post an example of multiple selection pressures accelerating evolution?

Dr Adequate

25th June 2007, 01:12 PM

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

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

You have no real examples of your model oh great PhD of gifematics.

I don’t have to, Dr Schneider has already done it and his model is peer reviewed and published dim bulb of evolutionism.

I’m fondue the word since the dead theory of evolution smells like limburger.

Now folks, if cheese wiz’s gif was correct, we need to contact all the infectious disease experts treating HIV and TB and tell them that combination therapy accelerates the evolution of resistance and we need to contact parasitologists and warn them that combination therapy will accelerate the evolution of resistant malaria and we need to warn agricultural experts that combination herbicides will accelerate the evolution of resistant weeds and pesticide experts and oncologists and ecologists and…

Cheese wiz’s silly gif and his silly conclusion he draws from it has no mathematical or empirical scientific basis. He is completely ignorant of the mathematics of mutation and selection and the mathematics of fitness landscape. However, he is a gifmeister.

Now what are you whining about Paul? Do you want to tell us what ev represents again on the evolutionary landscape?

Certainly I understand cheese wiz’s claims. He is claiming that multiple selection pressures evolve more quickly than single selection pressures. I am overwhelmed by the empirical evidence of his silly gif. He doubled the number of citations of real examples of his gif this weekend. His number of citations of real examples of his gif is now up to zero. You evolutionarians really know how to make your scientific skills shine.

I yes, Delphi’s secret code of evolutionism, his Rosetta stone is only understood by high priests of the evolutionarian faith and clown fish.

Sure I’ll start the explanation for you clown fish. Let’s start with what we know now. We know now that multiple selection pressures slow and ultimately stop evolution silly Dodo. However, long ago in a place far away, multiple selection pressures accelerated evolution and inorganic chemicals cooperated to make life, those were the good ole days.

No worm for you yet clown fish, you have to give us examples where multiple selection pressures accelerate evolution.

So what? Combination herbicides still slows the evolution of resistant weeds, perhaps you want to give us an example where illegitimate recombination overcomes the effect of multiple selection pressures, then you can get your worm.

Again, so what? Multiple selection pressures still slows the evolution of the HIV virus. Just because people are having difficulty developing a vaccine for HIV (and for the influenza virus and many other infectious agents) doesn’t change the mathematical and empirical facts that multiple selection pressures slow and ultimately stop evolution.

So what^3? None of these citations address the mathematical and empirical facts that multiple selection pressures slow and ultimately stop evolution.

Well that explains why we see new species every 250 generations. However clown fish, that is not enough to get your worm.

Now cyborg, I would never dodge your cruft theory of evolution, in fact I embrace it with open arms. I consider it a mozzarella ball of a theory. (That one’s for you cheese wiz.)

Oh no, not the strawman argument, anything but that, help me, help me, I’ve been strawmanned. Sure I’m interested in learning things. You (and Wikipedia) taught me about the fitness landscape. Now are you evolutionarians ready to learn anything about the mathematics of mutation and selection?

Too bad that mutation and selection can’t accomplish any of these things. Mutation and selection does not work this way. Mutation and selection is far too slow a process to do any of what you allege here. It is mathematically impossible. The books don’t balance. Ev shows this, your reference to the fitness landscape shows this and the empirical data shows this. Multiple selection pressures confound the evolutionary process. This is why it takes hundreds of millions and billions of generations to evolve only a 100 loci on a bacterial size genome. The mathematics only gets worse on the huge genomes of complex life forms. Your theory is mathematically impossible.

Gould proposed the concept of punctuated equilibrium to account for the lack of transitional forms in the fossil record. The evolutionarian version of a Rorschach test for the interpretation of fossils as transitional form does not overcome the mathematical fact the multiple selection pressures slow and ultimately stop evolution. This is what ev shows, this is what the fitness landscape shows and this is what the empirical data shows. Delphi, your theory is mathematically impossible.

Since you dim bulbs of evolutionism are having difficulty understanding the mathematics of mutation and selection, I now post more empirical examples that demonstrate that multiple selection pressures slow and ultimately stop evolution.

http://www.malariaconsortium.org/data/files/pages/act_6.pdf (http://www.malariaconsortium.org/data/files/pages/act_6.pdf)

http://jama.ama-assn.org/cgi/content/abstract/286/2/196 (http://jama.ama-assn.org/cgi/content/abstract/286/2/196)

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

Now, I feel like I’m being a bit unfair, ganging up on you poor helpless evolutionarians so I’ve decided to help you find citations which support your belief system that multiple selection pressures accelerate evolution. You may use the search engine of your choice.

For Paul, your key words for your search are, “crapola”, “goalposts”, “evolutionary landscape” and “Zing! Sproing! Fwoop!”.

For cheese wiz, “red line”, “blue line”, “gif”. “jpeg”, “cheese”, “FAQ”.

For clown fish, “cooperative chemistry”, “speculation”, “anything is possible”, “fish story”.

For Delphi, “skateboard”, “stop action photography”, “sock drawer”, “job.com”

For evolutionarians in general, “denial”, “speculation”, “extrapolation”, “any web site that engages in mushy soft mathematically deficient science”

So you evolutionarians don’t whine that I haven’t tried to help you find citations which show that multiple selection pressures accelerate evolution.

Clown fish, you will never get your worm this way. Of course evolution happens, microevolution. The reason why macroevolution can not happen is that it is mathematically impossible. Multiple selection pressures interfere with each other and slows then ultimately stops evolution. That is what ev shows, that is what the Wikipedia reference to fitness landscape shows and that is what reality shows.

Your answer may convince devout and brainwashed evolutionarians but it will not convince others. Until you can show an example where multiple selection pressures accelerate evolution your theory is without a mathematical or empirical basis, unless you are convinced by cheese wiz’s silly gif.
http://forums.randi.org/images/smilies/doglaugh.gif
As it stands now, the only empirical evidence of how mutation and selection behaves is that it slows down and ultimately stops the greater the number of selection pressures. That is a mathematical and empirical fact silly clown fish. You and the other dim bulbs of evolutionism have to come to grips with this fact. That is why the theory of evolution is mathematically impossible. I don't think there are any new lies here. But there's a lot more magic words.

I suppose I should be flattered that a man who lies so much about science should also feel the need to lie about me personally. I am in good company.

Dr Adequate

25th June 2007, 01:28 PM

You have no real examples of your model oh great PhD of gifematics. And you have produced no cases where my model has been tested and found wrong. Perhaps you could find one?

If not, then it appears all the data we have to go on is the model.

I don’t have to, Dr Schneider has already done it and his model is peer reviewed and published dim bulb of evolutionism. Actually, this is a new lie, isn't it? Dr Schneider's model has nothing to do with the simulataneous/sequential question, and you know that perfectly well, you halfwitted liar.

I’m fondue the word since the dead theory of evolution smells like limburger. I suppose that answers my question about your mental health.

Now folks, if cheese wiz’s gif was correct, we need to contact all the infectious disease experts treating HIV and TB and tell them that combination therapy accelerates the evolution of resistance and we need to contact parasitologists and warn them that combination therapy will accelerate the evolution of resistant malaria and we need to warn agricultural experts that combination herbicides will accelerate the evolution of resistant weeds and pesticide experts and oncologists and ecologists and… It's odd that you have absolutely no idea what my model shows, since I said what it shows, and you've repeatedly quoted me saying what it shows.

Wait ... it's not odd at all --- it's you doing it.

Read my explanation again until you understand what my model shows.

Cheese wiz’s silly gif and his silly conclusion he draws from it has no mathematical or empirical scientific basis. This is of course a lie. Its basis is a simulation of mutation and selection.

He is completely ignorant of the mathematics of mutation and selection and the mathematics of fitness landscape. This is of course a lie, and everyone reading this thread knows it.

Why do you tell lies when you know you're going to get caught?

Moreover, we've all seen you make enough stupid blunders in basic math for your lie to seem even more ridiculous and disgusting coming from you than it would by its intrinsic falsehood alone.

joobz

25th June 2007, 01:34 PM

..the mythical evolutionary ..evolutionarians ...
You dim bulbs of evolutionism ..You evolutionarians ..you are ignorant of the mathematics ..alchemical engineer ..clown fish, ..the evolutionarian ..You, an evolutionarian ..irrational ..a worm clown fish.....Cheese wiz ..You dim bulbs of evolutionism..You can stamp your foot (flop you tail) and whine ..And you can flop ...
And you can flop ...clown fish...clown fish. ..alchemy ...fish stories ...clown fish.
you make such a convincing argument.:rolleyes:
I see you haven't refuted the references I gave.
I see you are still holding to your false dichotomy.

kleinman

25th June 2007, 02:24 PM

You have no real examples of your model oh great PhD of gifematics.And you have produced no cases where my model has been tested and found wrong. Perhaps you could find one?

If not, then it appears all the data we have to go on is the model.
Certainly I have gifmeister, I have posted more than 50 real cases of mutation and selection, all of which show that multiple selection pressures slow and ultimately stop the evolutionary process. This is direct contradiction to your gif in which you propose that multiple selection pressures accelerate evolution. However, I must admit that your choice of red and blue lines in you gif make for an awesome argument for your mathematically irrational viewpoint.
I don’t have to, Dr Schneider has already done it and his model is peer reviewed and published dim bulb of evolutionism.Actually, this is a new lie, isn't it? Dr Schneider's model has nothing to do with the simulataneous/sequential question, and you know that perfectly well, you halfwitted liar.
Well cheese wiz (+ clown fish=1/2 wit), if you had read Dr Schneider’s publication you would have seen the following line:
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.
I highlighted the text so even an evolutionarian can see it, great PhD of mathematics without reality.
I’m fondue the word since the dead theory of evolution smells like limburger.I suppose that answers my question about your mental health.
Hey, you are the one who believes in a gif that has no basis in reality. We’ll rescue you from your brainwashed delusions. I’ll continue to post examples of how mutation and selection actually works and then you will come to understand that multiple selection pressures slow and ultimately and ultimately stop evolution. We’ll help to brighten your light dim bulb of evolutionism.
Now folks, if cheese wiz’s gif was correct, we need to contact all the infectious disease experts treating HIV and TB and tell them that combination therapy accelerates the evolution of resistance and we need to contact parasitologists and warn them that combination therapy will accelerate the evolution of resistant malaria and we need to warn agricultural experts that combination herbicides will accelerate the evolution of resistant weeds and pesticide experts and oncologists and ecologists and…It's odd that you have absolutely no idea what my model shows, since I said what it shows, and you've repeatedly quoted me saying what it shows.
Post a real example of what your model shows oh great wiz of cheese.
Cheese wiz’s silly gif and his silly conclusion he draws from it has no mathematical or empirical scientific basis.This is of course a lie. Its basis is a simulation of mutation and selection.
Your gif has no real examples so it simulates nothing. You and clown fish make a good team. He has an irrational explanation for a biogenesis and you have and irrational explanation of mutation and selection. Maybe you should call your model cooperative mutation and selection in the world of survival of the fittest. Your gif is the dumbest thing posted on this thread. It is totally contradicted by reality. Cyborg’s cruft theory of evolution makes more sense and his theory is complete nonsense.
He is completely ignorant of the mathematics of mutation and selection and the mathematics of fitness landscape.This is of course a lie, and everyone reading this thread knows it.
Clown fish has an excuse, he has a PhD in alchemical engineering, you cheese wiz have no excuse, you have a PhD in amathematics yet you still propose that multiple selection pressures accelerate evolution in your nonsensical gif. Ev shows you wrong, the fitness landscape shows you wrong and more than 50 real examples of how mutation and selection works shows you wrong. I will continue to post real examples of how mutation and selection actually works. When are you going to post a real example of your gif, clone of clown fish? Wait, clown fish has a new avatar, has he evolved?
http://forums.randi.org/images/smilies/doglaugh.gif

joobz

25th June 2007, 03:35 PM

It is moments like this I still read this thread...I don’t have to, Dr Schneider has already done it and his model is peer reviewed and published dim bulb of evolutionism.
Actually, this is a new lie, isn't it? Dr Schneider's model has nothing to do with the simulataneous/sequential question, and you know that perfectly well, you halfwitted liar.
Well cheese wiz (+ clown fish=1/2 wit), if you had read Dr Schneider’s publication you would have seen the following line:
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.
I highlighted the text so even an evolutionarian can see it, great PhD of mathematics without reality.
:D :D :D
Please explain how the phrase "selective pressure" is remotely the same thing as multiple simultaneous/sequential selection pressure?

This ranks up there with Lie #5 and "thermodyanmics is kinetics" as the dumbest things on this forum. Both of which, we have you to thank. Keep them coming, I'm sure you have more dumb in you.

Dr Adequate

25th June 2007, 03:57 PM

Certainly I have gifmeister, I have posted more than 50 real cases of mutation and selection, all of which show that multiple selection pressures slow and ultimately stop the evolutionary process. No you haven't. We all know you're lying, remember? None of your citations has shown anything of the sort, have they? You cannot find one single paper which backs up your halfwitted delusions and lies, can you?

Well cheese wiz (+ clown fish=1/2 wit), if you had read Dr Schneider’s publication you would have seen the following line:

I highlighted the text so even an evolutionarian can see it, great PhD of mathematics without reality. And we can all see that you are lying when you say that Schneider supports your lies about multiple selection pressures. He says nothing of the sort.

Why do you lie when you know you're going to be caught?

Are you retarded? Insane? Driven by helpless hatred of the truth?

Why do you lie when you know you're going to be caught?

Hey, you are the one who believes in a gif that has no basis in reality. We’ll rescue you from your brainwashed delusions. I’ll continue to post examples of how mutation and selection actually works and then you will come to understand that multiple selection pressures slow and ultimately and ultimately stop evolution. We’ll help to brighten your light dim bulb of evolutionism. If reciting crazy stuff like this magically made you right, you'd have been right long ago.

Post a real example of what your model shows oh great wiz of cheese. Post one real counterexample.

Your gif has no real examples so it simulates nothing. But of course this is a lie. It simulates mutation and selection. If you are unable to find an example of an experiment that tests it, that is your problem.

Clown fish has an excuse, he has a PhD in alchemical engineering, you cheese wiz have no excuse, you have a PhD in amathematics yet you still propose that multiple selection pressures accelerate evolution in your nonsensical gif. Ev shows you wrong, the fitness landscape shows you wrong and more than 50 real examples of how mutation and selection works shows you wrong. We all know you're lying, you do know that, don't you?

---

I see that "gifmeister" has joined your collection of magic words. Let's check if it's magically made me wrong ... oh look, it hasn't!

kleinman

25th June 2007, 05:32 PM

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.I highlighted the text so even an evolutionarian can see it, great PhD of mathematics without reality.Please explain how the phrase "selective pressure" is remotely the same thing as multiple simultaneous/sequential selection pressure?
There you go again can’t brain, trying to parse words in order to extract you dead theory of evolution from the mathematical vise that Dr Schneider’s computer simulation has place it in. The difference between selection pressure and selection pressures is simply a matter of number. One is singular and the other is plural. This is how these concepts are remotely related. Here is an example of the difference between singular and plural. Can’t brain believes in the theory of evolution, that is a singular dumb idea, can’t brain believes in the theory of evolution and abiogenesis, these are plural dumb ideas.
This ranks up there with Lie #5 and "thermodyanmics is kinetics" as the dumbest things on this forum. Both of which, we have you to thank. Keep them coming, I'm sure you have more dumb in you.
I noticed that you recommended a thermodynamics text in another thread. Shouldn’t you have recommended an elementary school grammar text (of course you would need to read it first), or better yet, a dictionary where they teach you how to spell the word thermodynamics? By the way, I like your new avatar.
Certainly I have gifmeister, I have posted more than 50 real cases of mutation and selection, all of which show that multiple selection pressures slow and ultimately stop the evolutionary process.No you haven't. We all know you're lying, remember? None of your citations has shown anything of the sort, have they? You cannot find one single paper which backs up your halfwitted delusions and lies, can you?
Cheese wiz, your whining is pathetic. These papers I have and will continue to post are all examples of mutation and selection. You are either in complete denial of what the citations are about or completely ignorant of evolution by mutation and selection. But not to worry, I will show you the way out of your intellectual quagmire.
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.I highlighted the text so even an evolutionarian can see it, great PhD of mathematics without reality.And we can all see that you are lying when you say that Schneider supports your lies about multiple selection pressures. He says nothing of the sort.
How did you find out that I hacked into Dr Schneider’s web site and the Oxford University Press computers and put the words “selective pressure” into Dr Schneider’s paper? I think we need to call you Sherlock cheese wiz.

Now you may be correct that Dr Schneider does not support my contention about multiple selection pressures as the reason why his model converges so slowly with realistic length genomes. The last time I talked with Dr Schneider about the reason his model converged so slowly, he had no idea why it was doing this. He was looking to embrace Paul’s Rcapacity concept but thought it need more study. It has since been shown that Paul’s Rcapacity concept disappears when you reduce the number of selection conditions to one in the model.
Why do you lie when you know you're going to be caught?
I’m not lying you whining little crybaby. It will be interesting to watch how you try to squirm out of the corner that you’ve put yourself in with your silly gif. Everyone has seen this and everyone knows that your claiming it shows that multiple selection pressures accelerate evolution. Here, let’s post what you’ve said again and watch you squirm.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
The red line shows generations to achieve fixation of n alleles acted on by n selection pressures, the n+1th selection pressure being introduced only after the nth allele is fixed.

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

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

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
I added the highlighting because I think what you’ve said here is so profound. We would all be very interested in you posting a real example of your gif.
:dl:
Hey, you are the one who believes in a gif that has no basis in reality. We’ll rescue you from your brainwashed delusions. I’ll continue to post examples of how mutation and selection actually works and then you will come to understand that multiple selection pressures slow and ultimately and ultimately stop evolution. We’ll help to brighten your light dim bulb of evolutionism.If reciting crazy stuff like this magically made you right, you'd have been right long ago.
Cheese wiz, the truth has a way of making itself known.
Post a real example of what your model shows oh great wiz of cheese.Post one real counterexample.
Another one, I’ve already posted more than 50 counterexamples, ok, for you I’ll post another counterexample, see below.
Your gif has no real examples so it simulates nothing.But of course this is a lie. It simulates mutation and selection. If you are unable to find an example of an experiment that tests it, that is your problem.
Ah, the squirming begins. I wonder if you squirm as well as Paul does. Do you want to borrow Paul’s bicycle, it has 6 reverse gears and no forward gears and the seat is mounted backwards.
Clown fish has an excuse, he has a PhD in alchemical engineering, you cheese wiz have no excuse, you have a PhD in amathematics yet you still propose that multiple selection pressures accelerate evolution in your nonsensical gif. Ev shows you wrong, the fitness landscape shows you wrong and more than 50 real examples of how mutation and selection works shows you wrong.We all know you're lying, you do know that, don't you?
I enjoy posting real examples of multiple selection pressures slowing and ultimately stopping evolution. Cheese wiz, you should try it sometime with your gif, if you could.

http://www.ann-clinmicrob.com/content/5/1/25 (http://www.ann-clinmicrob.com/content/5/1/25)
Abstract: combinations of drugs has been proposed as an alternative for oxacillin-resistant staphylococci infections, however, limited information about in vitro combinations are available for multi-resistant strains. The objective of this study was to describe the interaction of beta-lactams in combination with vancomycin or amikacin against 26 oxacillin and amikacin-resistant nosocomial Staphylococcus spp. isolates.
and
Conclusion: The best synergistic combination was cephalothin or dicloxacillin plus amikacin. The vancomycin combination with cephalothin or imipenem showed additivity. Vancomycin and amikacin had and indifferent effect. In vivo synergy and clinical efficacy cannot be predicted, but information of in vitro assays with resistant strains, could be useful to propose clinical studies to validate this information, most of all, in developing countries with a limited formulary.
Cheese wiz, you need to contact these authors and tell them that multiple selection pressures accelerate evolution before they make the biggest mistake of their research careers. I think they would be very thankful for your cheese wizardly advice and would immediately turn back to monotherapy.

Dr Adequate

25th June 2007, 06:40 PM

There you go again can’t brain, trying to parse words in order to extract you dead theory of evolution from the mathematical vise that Dr Schneider’s computer simulation has place it in. The difference between selection pressure and selection pressures is simply a matter of number. One is singular and the other is plural. This is how these concepts are remotely related. Here is an example of the difference between singular and plural. Can’t brain believes in the theory of evolution, that is a singular dumb idea, can’t brain believes in the theory of evolution and abiogenesis, these are plural dumb ideas. So, you're still trying to lie about what Dr Schneider wrote?

We all know you're lying.

Why are you lying?

We all know that he was talking about the effect of the strength of selection pressure on evolution. He was not talking about the number of simultaneous selection pressures. Even if a stupid stinking liar should twist his words so as to pretend he's talking about the number of simultaneous selection pressures, it would still require a further drooling drivelling lie to pretend that he's agreeing with your halfwitted fantasies about them, since he does not say that "selection pressure" retards evolution, does he, you halfwitted liar?

Cheese wiz, your whining is pathetic. These papers I have and will continue to post are all examples of mutation and selection. You are either in complete denial of what the citations are about or completely ignorant of evolution by mutation and selection. Or I actually know what they show, unlike you.

Given the fact that you make a stupid childish mess of everything, doesn't it seem likely that once again I'm right and you're wrong, even if you're too revoltingly stupid to understand why?

How did you find out that I hacked into Dr Schneider’s web site and the Oxford University Press computers and put the words “selective pressure” into Dr Schneider’s paper? I think we need to call you Sherlock cheese wiz. This raving nonsense is not a reply to anything I posted, is it, halfwit? It may relate in some way to your delusional fantasy world, but no-one else happens to live in it. What are you drooling about, nutjob?

If you're still trying to conflate "selective pressure" with "number of selective pressures", then be advised --- we all know you're just telling stupid lies again.

Now you may be correct that Dr Schneider does not support my contention about multiple selection pressures as the reason why his model converges so slowly with realistic length genomes. Of course he doesn't, he's not a halfwitted liar.

I’m not lying you whining little crybaby. It will be interesting to watch how you try to squirm out of the corner that you’ve put yourself in with your silly gif. Your witless fantasies about me are as degrading and pathetic as your witless fantasies about science.

Once more, I find myself in good company.

Everyone has seen this and everyone knows that your claiming it shows that multiple selection pressures accelerate evolution. Here, let’s post what you’ve said again and watch you squirm.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg What on earth has this to do with your stupid lies about Dr Schneider?

I do indeed claim that my model shows that simultaneous selection pressures drive evolution faster than the same pressures applied sequentially, because of course it does. This has nothing to do with your lies about Dr Schneider agreeing with your lies about multiple selection pressures, does it, you halfwitted liar?

So why do you start jabbering about my model as a response to my pointing out your stupid lies about Dr Schneider? Are you stupid? Insane? Or just really really desperate to change the subject?

I added the highlighting because I think what you’ve said here is so profound. We would all be very interested in you posting a real example of your gif. So, you have no criticism of my model and no counterexample.

Cheese wiz, the truth has a way of making itself known. Quite so. For example, the theory of evolution is known to scientists worldwide, whereas you are an obscure non-entity of interest only to a handful of people who enjoy laughing at buffoons.

Another one, I’ve already posted more than 50 counterexamples, ok, for you I’ll post another counterexample, see below. No. I advise you again to find out what it is I'm modelling.

Ah, the squirming begins. I wonder if you squirm as well as Paul does. Do you want to borrow Paul’s bicycle, it has 6 reverse gears and no forward gears and the seat is mounted backwards. So, you have no couterexample to my model?

I enjoy posting real examples of multiple selection pressures slowing and ultimately stopping evolution. Really? Then why don't you try it sometime?

Cheese wiz, you need to contact these authors and tell them that multiple selection pressures accelerate evolution before they make the biggest mistake of their research careers. I think they would be very thankful for your cheese wizardly advice and would immediately turn back to monotherapy. Actually, they are intelligent people, and would understand my explanation of why combination therapy is successful.

It is true that a snivelling insane retard with crap where his brains should be might conclude that my results speak in favor of monotherapy, but fortunately people like that don't get to be scientists.

joobz

25th June 2007, 06:53 PM

kleinman

25th June 2007, 07:21 PM

There you go again can’t brain, trying to parse words in order to extract you dead theory of evolution from the mathematical vise that Dr Schneider’s computer simulation has place it in. The difference between selection pressure and selection pressures is simply a matter of number. One is singular and the other is plural. This is how these concepts are remotely related. Here is an example of the difference between singular and plural. Can’t brain believes in the theory of evolution, that is a singular dumb idea, can’t brain believes in the theory of evolution and abiogenesis, these are plural dumb ideas.So, you're still trying to lie about what Dr Schneider wrote?
Cheese wiz, you must have just come from the paranormal forum.
Cheese wiz, your whining is pathetic. These papers I have and will continue to post are all examples of mutation and selection. You are either in complete denial of what the citations are about or completely ignorant of evolution by mutation and selection.Or I actually know what they show, unlike you.
Oh really, why don’t you enlighten us?
I did indeed claim that my model shows that multiple selection pressures accelerate evolution. This has nothing to question with your lies about whether Dr Schneider agrees with your lies about multiple selection pressures, does it, you halfwitted liar?
http://forums.randi.org/images/smilies/doglaugh.gif
Now this will be a big laugh if Dr Schneider agrees with you that multiple selection pressures accelerate evolution considering he works for the National Cancer Institute and oncologist now know the multiple drug therapy slows the evolution of resistant cancers.
I added the highlighting because I think what you’ve said here is so profound. We would all be very interested in you posting a real example of your gif.So, you have no criticism of my model and no counterexample.
Squirm cheese wiz, squirm.
Cheese wiz, the truth has a way of making itself known.Quite so. For example, the theory of evolution is known to scientists worldwide, whereas you are an obscure non-entity of interest only to a handful of people who enjoy laughing at buffoons.
Why cheese wiz, we see what kind of scientist embrace the theory of evolution, they are just like you. They think that multiple selection pressures accelerate evolution and ignore the mathematics of mutation and selection and the huge amount of evidence that multiple selection pressures slow evolution. Don’t worry cheese wiz, we’ll work to get you out of your intellectual quagmire.
Another one, I’ve already posted more than 50 counterexamples, ok, for you I’ll post another counterexample, see below.No. I advise you again to find out what it is I'm modelling.
Cheese wiz, you are modeling unreality, that’s why you can’t post any real example of your model, so let’s see you squirm out of this ridiculous gif that you have posted.
Ah, the squirming begins. I wonder if you squirm as well as Paul does. Do you want to borrow Paul’s bicycle, it has 6 reverse gears and no forward gears and the seat is mounted backwards.So, you have no couterexample to my model?
Correct, I have more than 50 counterexamples to your model.
I enjoy posting real examples of multiple selection pressures slowing and ultimately stopping evolution.Really? Then why don't you try it sometime?
Well ok, I’ll post another citation at the end of this post, again, just for you my favorite little annoyee.
Cheese wiz, you need to contact these authors and tell them that multiple selection pressures accelerate evolution before they make the biggest mistake of their research careers. I think they would be very thankful for your cheese wizardly advice and would immediately turn back to monotherapy.Actually, they are intelligent people, and would understand my explanation of why monotherapy is successful.
Oh, come on, tell us, I’m sure there is someone on this thread who would understand why you think monotherapy is better than combination therapy for delaying the evolution of resistance to theses selection pressures.
It is true that a snivelling insane retard with crap where his brains should be might conclude that my results speak in favor of monotherapy, but fortunately people like that don't get to be scientists.
You think you can squirm out of your ridiculous hypothesis like this? Let’s remind the readers what you said.
Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
Perhaps you can come up with some elegant experiment that proves your irrational gif, while this poor ole unscientific creationist has to post these boring old examples of how mutation and selection actually works.

http://www.actions-traitements.org/breve.php3?debut_brevesmemerubrique=200&id_breve=1324 (http://www.actions-traitements.org/breve.php3?debut_brevesmemerubrique=200&id_breve=1324)
ABSTRACT Objectives: 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
Results: K65R was selected infrequently by ABC-containing regimens in the absence of ZDV (13 of 127 patients), while L74V/I was selected more frequently (51 of 127 patients). Selection of both K65R and L74V/I was significantly reduced by co-administration of ZDV with ABC (one of 86 and two of 86 patients, respectively). Y115F was uncommon in the absence (seven of 127 patients) or presence (four of 86 patients) of ZDV. M184V was the most frequently selected mutation by ABC alone (24 of 70 patients) and by ABC plus 3TC (48 of 70 patients). Thymidine analogue mutations were associated with ZDV use. The K65R mutation conferred the broadest phenotypic cross-resistance of the mutations studied.

Conclusions: The resistance pathway selected upon virological failure of ABC-containing regimens is significantly altered by concurrent ZDV use, but not by concurrent 3TC use. These data may have important implications for the efficacy of subsequent lines of NRTI therapies.

kleinman

25th June 2007, 07:34 PM

joobz

25th June 2007, 07:45 PM

Dr Adequate

25th June 2007, 07:54 PM

Cheese wiz, you must have just come from the paranormal forum. No. I notice that this garbage has nothing to do with your stupid lies about Dr Schneider, and is not in fact a reply to my observations on this subject.

Oh really, why don’t you enlighten us? The usual reason: because of the problems with your brain. I have of course explained the results several times, as you would know if you were not stupid --- but enlightening you? I am but mortal.

Now this will be a big laugh if Dr Schneider agrees with you that multiple selection pressures accelerate evolution considering he works for the National Cancer Institute and oncologist now know the multiple drug therapy slows the evolution of resistant cancers. I presume that Dr Schneider understands evolution as well as I do; if not, a couple of minutes with the math would suffice to show him why the model works.

Squirm cheese wiz, squirm. Why, you stupid snivelling little halfwit, why?

Why cheese wiz, we see what kind of scientist embrace the theory of evolution, they are just like you. They think that multiple selection pressures accelerate evolution and ignore the mathematics of mutation and selection and the huge amount of evidence that multiple selection pressures slow evolution. Don’t worry cheese wiz, we’ll work to get you out of your intellectual quagmire. Remember what I told you about reciting gibberish not changing reality?

Cheese wiz, you are modeling unreality, that’s why you can’t post any real example of your model, so let’s see you squirm out of this ridiculous gif that you have posted.
Your pretense that I wish to "squirm out of" a model which I stand by is a new lie, and a spectacularly stupid one, since everyone who reads this thread can see that you're lying.

Correct, I have more than 50 counterexamples to your model. You have none, and your previous ravings suggest that you don't even know wwhat it is that I've modeled. Though it's hard to tell on this issue whether it's the liar or the halfwit side of your character that's predominant. Perhaps you do understand the model but are pretending that you don't. It's hard to telll with lying halfwits.

Oh, come on, tell us, I’m sure there is someone on this thread who would understand why you think monotherapy is better than combination therapy for delaying the evolution of resistance to theses selection pressures. Everyone reading this thread understands that I think no such thing, and that when you pretend that I do you are drivelling out a halfwitted lie.

You think you can squirm out of your ridiculous hypothesis like this? Let’s remind the readers what you said. Again, your ridiculous pretense that I wish to "squirm out of" the implications of my model.

Everyone reading this thread can see that I do not, and that when you pretend I do you are a stupid snivelling liar.

Dr Adequate

25th June 2007, 08:01 PM

kleinman

25th June 2007, 08:42 PM

You can try to make that argument but the selection pressures in ev are mathematically separable which Paul has done. And when you set any two of the three selection pressures to zero, the model evolves the remaining selection pressure very rapidly, even when the model will not converge with all three selection pressures. The model behaves exactly as described in the Wikipedia reference to fitness landscape and behaves exactly like the numerous real examples of mutation and selection. And with three selection pressures and a genome that is too long, the model stops evolving or didn’t you get to those cases.don't get too exact here. this is fast, this is slow, this is stop, this is go.
You have much more in common with nursery rhymes than with reality.
You haven’t run very many cases with ev have you can’t brain. If you had, you would realize that it doesn’t take a very long genome for it to take billions of generations to evolve the binding sites. Even for rapidly reproducing life forms like viruses and bacteria that takes a long, long time. Then if you lengthen the genome more, the program stops converging all together.
Why have you not presented any of these results? We'd be happy to review your findings. In the mean time, why have you not tried to critique the model Dr. A has created? I'm sure he'd be happy to present you with the code upon request.
The data has been posted. Don’t be so lazy can’t brain, either read the threads (this one and the thread on the evolutionisdead forum or run the cases yourself. Cheese wiz can post whatever he wants. We would be interested in him posting a real example of his gif which shows multiple selection pressures accelerating evolution. That would give us all a big laugh.
Cheese wiz, you must have just come from the paranormal forum.No. I notice that this garbage has nothing to do with your stupid lies about Dr Schneider, and is not in fact a reply to my observations on this subject.
My goodness cheese wiz, you are such a whining crybaby, why don’t you just post a real example of multiple selection pressures accelerating evolution. We all know you have made this claim so stop whining and prove it.
Oh really, why don’t you enlighten us?The usual reason: because of the problems with your brain. I have of course explained the results several times, as you would know if you were not stupid --- but enlightening you? I am but mortal.
Your squirming convinces nobody. You have no real examples of your silly gif. Your model simulates nothing in reality. Dr Schneider’s model on the other hand gives a good simulation of what happens with multiple selection pressures. It slows and ultimately stops evolution.
Now this will be a big laugh if Dr Schneider agrees with you that multiple selection pressures accelerate evolution considering he works for the National Cancer Institute and oncologist now know the multiple drug therapy slows the evolution of resistant cancers.I presume that Dr Schneider understands evolution as well as I do; if not, a couple of minutes with the math would suffice to show him why the model works.
Why don’t you ask Dr Schneider to publicly support your model? He hardly advertises his own model anymore; let’s see if he’ll support your model.
Squirm cheese wiz, squirm.Why, you stupid snivelling little halfwit, why?
Because everyone knows that you made an irrational statement about a nonsensical gif stating multiple selection pressures accelerate evolution. We are all waiting for a realistic example of this nonsense you claim.
Why cheese wiz, we see what kind of scientist embrace the theory of evolution, they are just like you. They think that multiple selection pressures accelerate evolution and ignore the mathematics of mutation and selection and the huge amount of evidence that multiple selection pressures slow evolution. Don’t worry cheese wiz, we’ll work to get you out of your intellectual quagmire.Remember what I told you about reciting gibberish not changing reality?
And the reality is that multiple selection pressures slow and ultimately stop evolution, that is what the mathematics of ev shows, that is what the Wikipedia reference to the fitness landscape shows and that is what more than 50 real examples of mutation and selection shows. Now let’s see you show a single real example of your nonsensical postulate that multiple selection pressures accelerate evolution.
Cheese wiz, you are modeling unreality, that’s why you can’t post any real example of your model, so let’s see you squirm out of this ridiculous gif that you have posted.Your pretense that I wish to "squirm out of" a model which I stand by is a new lie, and a spectacularly stupid one, since everyone who reads this thread can see that you're lying.
Stand by your model, squirm by your model, just show us a real example of what you propose, that is that multiple selection pressures accelerate evolution. Otherwise, not only are you my favorite annoyee on this thread, you are the biggest blow hard as well.
Correct, I have more than 50 counterexamples to your model.You have none, and your previous ravings suggest that you don't even know wwhat it is that I've modeled. Though it's hard to tell on this issue whether it's the liar or the halfwit side of your character that's predominant. Perhaps you do understand the model but are pretending that you don't. It's hard to telll with lying halfwits.
Your whining is useless, your gif is useless, and your proposal that multiple selection pressures accelerate evolution is nonsense. You have no elegant example that supports your unrealistic view of reality. Mutation and selection does not work the way you propose. It works the way the 50+ examples which I have posted, that is multiple selection pressures slow and ultimately stops evolution.
Oh, come on, tell us, I’m sure there is someone on this thread who would understand why you think monotherapy is better than combination therapy for delaying the evolution of resistance to theses selection pressures.Everyone reading this thread understands that I think no such thing, and that when you pretend that I do you are drivelling out a halfwitted lie.
What everybody realizes is that you have made an irrational proposal that multiple selection pressures accelerate evolution and you have no real examples of this.
You think you can squirm out of your ridiculous hypothesis like this? Let’s remind the readers what you said. Again, your ridiculous pretense that I wish to "squirm out of" the implications of my model.
Fine cheese wiz, don’t squirm out of you model, post a real example of multiple selection pressures accelerating evolution.

joobz

25th June 2007, 09:18 PM

delphi_ote

25th June 2007, 09:25 PM

Now are you evolutionarians ready to learn anything about the mathematics of mutation and selection?
We've been ready the entire time you've been here, so shut the **** up with all your nonsense and show us already. No more anecdotes. No more blanket generalizations. If it's mathematically impossible, I expect some equations. How about you take the time to learn some LaTex instead of running your mouth all day?
“job.com”
With as much time as you spend posting nonsense in this thread, I have a feeling you probably need that link a lot more than I do.

Dr Adequate

25th June 2007, 09:42 PM

Dr Adequate

25th June 2007, 09:48 PM

Why don’t you ask Dr Schneider to publicly support your model? He hardly advertises his own model anymore ... Actually, is this a new lie? You've whined out so many stupid lies about Dr Schneider, I've lost track.

joobz

25th June 2007, 09:55 PM

Actually, is this a new lie? You've whined out so many stupid lies about Dr Schneider, I've lost track.
Yes, his multiples simultaneous directional lies has helped rapidly evolve my ability to tune most of them out.

kleinman

26th June 2007, 04:41 PM

You haven’t run very many cases with ev have you can’t brain. If you had, you would realize that it doesn’t take a very long genome for it to take billions of generations to evolve the binding sites. Even for rapidly reproducing life forms like viruses and bacteria that takes a long, long time. Then if you lengthen the genome more, the program stops converging all together.So, you can make ev go really fast to just fast? Impressive. that sure does prove evolution doesn't happen.
Not the massive evolutionary changes that exist only in your imagination. Mutation and selection is a profoundly slow process. Put two or more selective pressures on any population and it slows down the evolutionary process.
The data has been posted. Don’t be so lazy can’t brain, either read the threads (this one and the thread on the evolutionisdead forum or run the cases yourself.
Um, it's not my job to go out and find more of your insanity. You've posted enough lies, gibberish, foolish meanderings, completely dumba$$ statements and quotes that have no bearing on your point in this thread. Why would I want to subject myself to other places where you act like a moronic fool?

Post your results here. Or are you afraid you'd just expose yourself more the imbecile?
Ok lazy can’t brain; I’ll repost some of the data so you can get an idea how many generations it take to accumulate information. The following series is for a population of 64, mutation rate=1/G, gamma=16, site width=6, weight width=5
Genome length\generations to Rs>=Rf
256 \ 675
512 \ 2,925
1024 \ 10,108
2048 \ 35,486
4096 \ 162,892
8192 \ 710,152
16384 \ 6,894,433 (Perfect Creature)
Can’t brain, why don’t you run the G=32k for this series?
Your squirming convinces nobody. ...Fine cheese wiz, don’t squirm out of you modelUm, nobody here believes Dr.A. is squirming. Writing it doesn't make it real. It simply exposes your own weaknesses.
Sure cheese wiz is squirming. He has taken a mathematically ridiculous position that has no basis in reality. He has no real examples of his gif and his view is contradicted by ev, the Wikipedia reference to the fitness landscape and numerous real examples of how mutation and selection works. If you think cheese wiz’s silly gif is true, why don’t you post a real example of his nonsense?
Also, you realize your use of avatars as insults makes you look even more the idiot. Afterall, all of those "clever" comments become sad and missplaced once an avatar changes. Keep using this strategy, though, it is indeed more effective than your attempts to wish evolution away.
So not only do you not understand the mathematics of mutation and selection, you don’t understand what an avatar is. Here’s what Wikipedia has to say about avatars.
http://en.wikipedia.org/wiki/Avatar_(virtual_reality) (http://en.wikipedia.org/wiki/Avatar_(virtual_reality))
An avatar (abbreviations include AV, ava, avie, avy, avi, avvie, and avvy) is an Internet user's representation of himself or herself, whether in the form of a three-dimensional model used in computer games, [1] a two-dimensional icon (picture) used on Internet forums and other communities, [2][3] or a text construct found on early systems such as MUDs. The term "avatar" can also refer to the personality connected with the screen name, or handle, of an Internet user.[4]
Any problem with that definition can’t brain?
Now are you evolutionarians ready to learn anything about the mathematics of mutation and selection?We've been ready the entire time you've been here, so shut the **** up with all your nonsense and show us already. No more anecdotes. No more blanket generalizations. If it's mathematically impossible, I expect some equations. How about you take the time to learn some LaTex instead of running your mouth all day?
Oh dear, have I annoyed an evolutionarian. Delphi, study Dr Schneider’s ev model and associated publications a bit. He has nicely documented his model. If you will do a parametric study with his model, you will get some understanding of the mutation/selection process. What you will find is that the rate of information acquisition by the mutation/selection process strongly dependent on the genome length, the model is less dependent on mutation rate and population but is strongly dominated by the number of selection conditions. In fact, the number of selection conditions in ev can prevent ev from evolving at all.

Hey, tell me, how long did it take you to make the skateboarding video?
“job.com”With as much time as you spend posting nonsense in this thread, I have a feeling you probably need that link a lot more than I do.
Delphi, your feelings aren’t serving you well and mathematics is not serving your theory of evolution well either.
To summarise:
No real examples of your ridiculous proposal that multiple selection pressures accelerate evolution?
Why don’t you ask Dr Schneider to publicly support your model? He hardly advertises his own model anymore ... Actually, is this a new lie? You've whined out so many stupid lies about Dr Schneider, I've lost track.
http://img514.imageshack.us/img514/3974/genegraphhx4.jpg
The red line shows generations to achieve fixation of n alleles acted on by n selection pressures, the n+1th selection pressure being introduced only after the nth allele is fixed.

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

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

Note how with simultaneous selection pressures the rate of evolution (fixations/generation) increases with the number of selection pressures.
http://forums.randi.org/images/smilies/doglaugh.gif
Hey Dr Schneider, cheese wiz has something to tell the oncologists at the National Cancer Institute. Care to sign on?

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

http://asmcourse.ivic.ve/articulos/Hastings-2004.pdf (http://asmcourse.ivic.ve/articulos/Hastings-2004.pdf)
The main consequence is that anti-malarial drug policy must be considered on an inter-national, rather than a national, basis. A sophisticated and expensive national policy designed to suppress the emergence and spread of resistance can be easily negated by mutations originating and spreading from neighbouring countries. This does not necessarily mean that all countries in a region should have the same policy, simply that their policies should not undermine each other. For example, suppose a country deploys drug A and drug B as a CT. A neighbouring country deploying drug C as a monotherapy would not undermine this policy (providing the mechanism of resistance to C is independent to that of A or B), but a neighbouring country deploying either drug A or B as a monotherapy is likely to pose a significant threat.
See how simple it is cheese wiz? Make a postulate that multiple selection pressures slows evolution, prove it mathematically with a peer reviewed and published mathematical model of mutation and selection and then post a real example of this postulate (or is that greater than 50 real examples of the postulate).

delphi_ote

26th June 2007, 07:19 PM

joobz

26th June 2007, 07:50 PM

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

Ok lazy can’t brain; I’ll repost some of the data so you can get an idea how many generations it take to accumulate information. The following series is for a population of 64, mutation rate=1/G, gamma=16, site width=6, weight width=5
Genome length\generations to Rs>=Rf
256 \ 675
512 \ 2,925
1024 \ 10,108
2048 \ 35,486
4096 \ 162,892
8192 \ 710,152
16384 \ 6,894,433 (Perfect Creature)
Can’t brain, why don’t you run the G=32k for this series?
um? isn't this series again showing that as the genome length increases, the number of generations to perfect creature? that's nice. completely not related to your claim at all and completely not what I was asking about.

While your busy doing this, make sure to include, recombination in your model. These people find it highly relavent to HIV's rapid resistence capacity.
Carvajal-Rodríguez A, Crandall KA, Posada D. "Recombination favors the evolution of drug resistance in HIV-1 during antiretroviral therapy" Infect Genet Evol. 2007 Jul;7(4):476-83

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

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

Any problem with that definition can’t brain?
Yawn... You sure are clever.:rolleyes: Maybe, I'll change my avatar to a carrot and you'll chase after that as well?

kleinman

28th June 2007, 08:36 AM

If you will do a parametric study with his model, you will get some understanding of the mutation/selection process. What you will find is that the rate of information acquisition by the mutation/selection process strongly dependent on the genome length, the model is less dependent on mutation rate and population but is strongly dominated by the number of selection conditions. In fact, the number of selection conditions in ev can prevent ev from evolving at all.I will not do ****, because this is your claim. Put up or shut up. You've repeatedly stated evolution is "mathematically impossible." That doesn't mean, "If you take this model with these parameters, it won't work if you extrapolate it through all of history." That means "a+a=3a".
Delphi, I have done the parametric studies with ev and it shows how the mathematics of mutation and selection works. I have reposted a series for clown fish can’t brain which demonstrates how mutation and selection works as you lengthen the genome in ev. What you see is that as you lengthen the genome, the number of generations required for the acquisition of the same amount of information increases at an exponential rate. That is a starting for you to understand the mathematics of mutation and selection.
Either show us in direct equation form why it is impossible or stop making this claim. I'm not interested in any of the rest of your ********. This entire thread has dragged on for pages because you've made a sensational claim you refuse to substantiate. You're either a coward or a liar. Whichever it is, we've all had quite enough.
Don’t be silly Delphi. Mutation and selection can not be written as a direct algebraic equation. It is a complex relationship of multiple parameters. That is what the ev computer model does. These variables only have functional relationships that can not be expressed in closed form algebraic format. That doesn’t mean that you can’t map these variables, which is what a parametric study of Dr Schneider’s model does. If you want a direct equation form for the mathematics of mutation and selection it would look as follows.
f(G,γ,sw,nsc,n,mr,…) = 0
where,
G=genome length
γ =number of binding sites
sw=site width
nsc=number of selection conditions
n=population
mr=mutation rate
… and so on
Delphi, you know well that the above functional equation can be mapped and described. That is what the fitness landscape is all about. When you map the above functional equation, you will find out which variables dominate the mathematics of this system. Dr Schneider’s model describes very well how mutation and selection works. In particular, the number of selection conditions dominates the model and this is seen in reality as shown in the numerous citations I have posted and will continue to post. I wonder how many of these citations I can find? This thread may go on for hundreds of more pages.

Delphi, must you use so many asterisks? There are so many sensitive evolutionarians reading this thread that may be offended by such blatant keystrokes.
Not the massive evolutionary changes that exist only in your imagination. Mutation and selection is a profoundly slow process. Put two or more selective pressures on any population and it slows down the evolutionary process.

Ok lazy can’t brain; I’ll repost some of the data so you can get an idea how many generations it take to accumulate information. The following series is for a population of 64, mutation rate=1/G, gamma=16, site width=6, weight width=5
Genome length\generations to Rs>=Rf
256 \ 675
512 \ 2,925
1024 \ 10,108
2048 \ 35,486
4096 \ 162,892
8192 \ 710,152
16384 \ 6,894,433 (Perfect Creature)
Can’t brain, why don’t you run the G=32k for this series?um? isn't this series again showing that as the genome length increases, the number of generations to perfect creature? that's nice. completely not related to your claim at all and completely not what I was asking about.
Now can’t brain, can’t see.
While your busy doing this, make sure to include, recombination in your model. These people find it highly relavent to HIV's rapid resistence capacity.
Now I do appreciate your reference to HIV recombination because it shows that multiple selection pressures slow the evolution of resistance despite HIV does recombination, huge populations, high reproductive rate, high mutation rate and short genome length. Every possible beneficial condition for evolution of this virus is still slowed by multiple selection conditions. Hmm, I wonder what variable dominates the mathematics of mutation and selection (and recombination)?
Sure cheese wiz is squirming. He has taken a mathematically ridiculous position that has no basis in reality. He has no real examples of his gif and his view is contradicted by ev, the Wikipedia reference to the fitness landscape and numerous real examples of how mutation and selection works. If you think cheese wiz’s silly gif is true, why don’t you post a real example of his nonsense?So, you can't critique it? I figured as much.
I have critiqued cheese wiz’s gif, don’t you recall?
http://forums.randi.org/images/smilies/doglaugh.gif
Now I will give you and cheese wiz a hint on how to search for a real example of his gif, use the following search terms “+selection”, “-mutation”, “+recombination”.
So not only do you not understand the mathematics of mutation and selection,