Annoying creationists

[Dr Adequate]

The only thing you have been right about in this discussion is when you said you had no idea how ribose could form nonenzymatically. Of course that’s your idea of how to prove abiogenesis is true.

You think that the theory of evolution is mathematically possible. You have no idea how it occurs. You have no mathematical model to substantiate your view. You have no real examples of how it occurs. On the other hand, I have a peer reviewed and published mathematical model of mutation and selection to substantiate my argument. What the model shows is that multiple selection pressures profoundly slow evolution. I have posted about 15 references which demonstrate in reality what the mathematical model shows and why the theory of evolution is mathematically impossible. You don’t even have intellectual dishonesty; you only have ignorance and denial.

You are lying to us, about us. Whom do you hope to deceive?

I’ll continue to post more references to how multiple selection pressures slow evolution profoundly ....

Continue? You fatuous liar, you have not given one case where selection pressures per se slow evolution --- and yet you claim it as a general rule.

You don't tell us how you would get from this imaginary rule to "mathematically impossible", and I predict that you never will.

 

[Dr Adequate]

Let’s let the real world do the test. These references which show that multiple selection pressures slow evolution are not limited to random point mutations. These are real living creatures which when they reproduce can have any mutation you can imagine.

Here is another example from the prime case of combination therapy for the slowing of the evolution of resistant strains of HIV http://gateway.nlm.nih.gov/MeetingAbstracts/102225407.html


Here is an example of the use of combination antibacterial agents to delay the evolution of resistant e coli. http://www.nature.com/nature/journal/v446/n7136/abs/nature05685.html


Here is another reference to HIV and combination vs monotherapy http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8595505&dopt=Abstract


Here is another example of combination fungicides to delay the evolution of resistance. http://www.apsnet.org/education/advancedplantpath/topics/Resistan/Resistan_Lesson_5.html


This one is for Taffer who complained that a previous reference on this particular topic was not from a peer reviewed journal. Note how in the laboratory, by reducing the number of selection pressures, resistant strains of the mosquito larvae can be evolved when they don’t appear in nature. This is a clear example how single selection pressures applied sequentially will much more rapidly evolve resistance than when the selection pressures are applied simultaneously.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219


I’ll keep my eyes open looking for more of these informative links which show that selection pressures in combination slow evolution. I will also watch for examples of where combination selection pressures accelerate evolution but so far, none have appeared. I wonder how many of these references I will have to post before you evolutionists figure out that multiple selection pressures slow evolution. In case you evolutionists haven’t figured it out, I’m patient and the google search I used to find the above references (combination selection evolution resistance) gave over a million hits and the ones above were from the first page. This is going to be fun. We’ll continue on with this next week.

You are producing cases in which humans imposing artificial demographic pressures on a population slow evolution as though this could serve as evidence that as a general rule multiple selection pressures slow evolution.

This is like showing us photographs of a pig in a helicopter as evidence that all pigs fly round the sky on delicate silvery wings.

You are not going to fool anyone with this garbage, because we all recognise the nature of the deceit.

You say that you are going to "continue on" with posting similarly irrelevant articles. I have no doubt of it. I have never known anyone to persevere as you do in pointless, worthless, fatuous actions. But I might as well let you know in advance that you will deceive no-one.

 

[Dr Adequate]

Certainly evolution by mutation and selection exists. Ev models this quite nicely and explains how it works mathematically. Mutation and selection is a profoundly slow process. You need large populations with large reproduction rates and small genome lengths to accomplish anything. HIV fits these parameters perfectly. Even with these conditions, combination therapy (multiple selection pressures) slows the evolution process profoundly. The real nonsense in this discussion is you believe that reptiles evolved into birds. You have much smaller populations with much lower reproduction rates and much, much larger genomes than in the case of HIV. In addition, you need large numbers of selection pressures (none of which you can describe and mathematically has been shown would interfere with each other) to transform the huge number of genes necessary to morph a reptile genome into a bird genome. That is the nonsense in this discussion and that is what you claim has happened. It is mathematically impossible; the evolution process can not work quickly enough in the time available and you don’t have the selection processes necessary to accomplish the type of transformations you evolutionists allege. If you understood the mathematics of mutation and selection you would understand why the theory of evolution is impossible. You are both ignorant and in denial of these mathematical facts.

I observe that your stupid lies about "mathematics" are unleavened by any actual math.

 

[Ichneumonwasp]

Joobz, you are still one of the favorites to win the horserace as the last evolutionist on this thread to understand the mathematics of mutation and selection.

You can't possibly be so vain as to think that others will no longer debate you because they believe a word you are saying. How far does your vanity reach, Kleinman? We are embarrassed by your ignorance and obvious mistakes.

 

[Ducky]

http://www.youtube.com/watch?v=wOe7EuHclyo


Even a comedian could pwn kleinman.







(Though I can't get the yt tags to work.)

 

[kjkent1]

http://www.youtube.com/watch?v=wOe7EuHclyo

Even a comedian could pwn kleinman.

(Though I can't get the yt tags to work.)

Lewis Black is hilarious. Thanks!

 

[kleinman]

Annoying Creationists

Let’s let the real world do the test. These references which show that multiple selection pressures slow evolution are not limited to random point mutations. These are real living creatures which when they reproduce can have any mutation you can imagine.

Yes, let's see if I, the unscientific lawyer, can pick out the flaws in your various assertions.

All you have to know is how to count to understand that the theory of evolution is mathematically impossible. Lawyers do know how to count, don’t they little gator?

Here is another example from the prime case of combination therapy for the slowing of the evolution of resistant strains of HIV http://gateway.nlm.nih.gov/MeetingAb...102225407.html

OK, the error here is pretty obvious: the combination therapy is expressly designed to inhibit replication. And, where there is no replication there is no evolution -- rather there is extinction. So, the therapy attacks not the ability of the organism to evolve, but rather its ability to reproduce.

All selection pressures inhibit replication. That is by definition what a selection pressure is, it is a stress on life forms that reduce its fitness to reproduce. If that stress is sufficient, it causes extinction.

Also, something not so obvious: the "biosphere" for an HIV-1 colony is a human being. Ultimately, the therapy is intended to reduce replication of the virus as a means of lengthening the existence of the "biosphere." But, if we were to place the virus in a biosphere with a lifetime of billions of years, rather than ~100, would the therapy slow evolution, over the long run? Doubtful, because as soon as the virus did evolve any resistance, it would then start replicating wildly as before, and return to a more natural evolutionary process.

The biosphere or environment is what it is. If small pox were not kept in the laboratory, it would be extinct.

You are unreasonably extrapolating a limited therapeutic effect and applying to nature. In nature, no set of precisely targeted selective mechanisms is working in combination to inhibit the growth of the HIV virus. Instead, the selective mechanisms are randomly applied via a relatively stable environment, and the result is an HIV organism ready to take over an unsuspecting host.

The example of combination therapy of HIV slowing the evolution of the virus is only one of many examples of how multiple selection pressures slow and ultimately stops evolution as show by the example below.

I will not bother to analyze your other citations, because they will all necessarily suffer from the one inescapable error: that the natural landscape, until the emergence of homo sapiens, did not have intelligent selection mechanisms precisely targeting organisms in the environment with the purpose of limiting their reproduction. No amount of naturally hostile conditions could possibly amount to the sort of environmental stress as is being artificially applied in all of your examples of medical intervention.

You don’t need to do the analysis; I’ll do it for you. Somehow you think that man made selection pressures behave in a different mathematical manner than natural selection pressures. Do you care to give us an example of this? Do any of you evolutionist care to give us an example of multiple natural selection pressures accelerating evolution?

Kleinman, I see you have ignored my posts, and did not read the cited paper. I explained to you why it does not say what you think it does. Remember: many people on this forum actually understand biology, genetics, and evolutionary theory. You, clearly, do not. You are a waste of time.

Taffer, I appreciate your complaint about my citing a link from a non-peer reviewed article about bacteria being used to suppress the evolution of resistant mosquito larvae. Below is an example from a peer reviewed journal of how multiple selection pressures stops evolution of mosquito larvae. All mechanisms of mutation and recombination are available to the mosquito larvae yet resistance only occurs when the number of selection pressures are reduced.

Joobz, you are still one of the favorites to win the horserace as the last evolutionist on this thread to understand the mathematics of mutation and selection.

You can't possibly be so vain as to think that others will no longer debate you because they believe a word you are saying. How far does your vanity reach, Kleinman? We are embarrassed by your ignorance and obvious mistakes.

Ichneumonwasp joins the competition to be the last evolutionist to understand the mathematics of mutation and selection. Perhaps if he realizes there is no way that multiple selection pressures accelerates evolution he may avoid the winner’s circle of ignorance and denial of the mathematics of mutation and selection.

NOTE that word, delay. Hoy was talking about delaying the resistance development against pesticides. But Hoy doesn't say, Halt, stop, prevent, abolish, never will happen,.... Hoy says delay. We can only ever delay things, we can't stop evolution.

Joobz thinks that evolution can not be stopped. If he reads this article carefully http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219 he will find that if evolution is not stopped, it delayed for a long period of time. Here is how evolution is stopped.

Insecticides based on Bacillus thuringiensis subsp. israelensis have been used for mosquito and blackfly control for more than 20 years, yet no resistance to this bacterium has been reported.

What hasn’t resistance evolved?

The mosquitocidal bacterium Bacillus thuringiensis subsp. israelensis is highly effective as a larvicide against a wide range of mosquito (Diptera: Culicidae) and blackfly species (Diptera: Simuliidae) and has been used routinely in many pest and vector control programs for more than 20 years (1, 10, 12, 30). The principal insecticidal component of B. thuringiensis subsp. israelensis is a spherical parasporal body produced during sporulation and composed of four major endotoxin proteins, Cyt1Aa, Cry4Aa, Cry4Ba, and Cry11Aa (6, 11).

There are four agents acting on the larva. How can the larvas evolve resistance to these toxins?

Although no resistance to B. thuringiensis subsp. israelensis has been reported under field conditions, studies in the laboratory have shown that high levels of resistance can be developed when larval populations are selected against recombinant bacilli that produce only one, two, or three of this bacterium's mosquitocidal Cry proteins.

Reduce down the number of selection pressures and the evolutionary process can proceed. Multiple selection conditions slow the evolutionary process and in this case four selection conditions stop the evolutionary process in a real situation. This is exactly analogous with what ev shows. The question is, how many real examples of the mathematical behavior of mutation and selection which ev shows before evolutionists finally understand this fact? Just how wide and deep is this river of ignorance and denial of the mathematics of mutation and selection that flows out of the theory of evolution?

 

[kjkent1]

You don’t need to do the analysis; I’ll do it for you. Somehow you think that man made selection pressures behave in a different mathematical manner than natural selection pressures. Do you care to give us an example of this?

Hmmm, I must have missed your analysis. I wonder if that's because you forgot to do it, between telling me that I don't need to do any and where you ask me to give you an example to refute your non-existent analysis.

Do you tell your patients when you're practicing faith healing in favor of medicine?

Do any of you evolutionist care to give us an example of multiple natural selection pressures accelerating evolution?

I already did that, twice in this thread -- using ev, and I posted the data. Of course, you immediately disregarded both examples -- but, that's not my problem.

Seek professional help, Alan.

 

[Taffer]

Kleinman, when you post a citation which actually states what you think it does, then we can have a discussion. But your refusal to realise that what every single citation is saying is not what you think it is leads this discussion to a dead end. You have not provided a single paper which shows that the rate of evolution slows as a result of multiple selection pressures. All you have shown is that the rate of emergence of a trait can be slowed, which is blindingly obvious. Yet again, emergence is not evolution. Emergence is that chance of a specific trait actually appearing in a population, and it is governed by such things as population size, the effect of the drug, and so-on. What you still fail to realise is that the rate of evolution is increased by heavy selection pressures. Our models show this. Reality shows this. Stop confusing emergence with the rate of evolution. All you have shown is that using many drugs makes the emergence of a multi-resistant individual less likely. Of course it does, because the number of allelic variations in the population is reduce. But evolution is the change in allele frequency over time. It doesn't matter how those alleles arose, once they exist evolution acts the same. More selection pressures do not slow this process. What is lowered is the amount of available variation to 'work with', so to speak.

 

[Dr Adequate]

All you have to know is how to count to understand that the theory of evolution is mathematically impossible. Lawyers do know how to count, don’t they little gator?

All selection pressures inhibit replication. That is by definition what a selection pressure is, it is a stress on life forms that reduce its fitness to reproduce. If that stress is sufficient, it causes extinction.

The biosphere or environment is what it is. If small pox were not kept in the laboratory, it would be extinct.

The example of combination therapy of HIV slowing the evolution of the virus is only one of many examples of how multiple selection pressures slow and ultimately stops evolution as show by the example below.

You don’t need to do the analysis; I’ll do it for you. Somehow you think that man made selection pressures behave in a different mathematical manner than natural selection pressures. Do you care to give us an example of this? Do any of you evolutionist care to give us an example of multiple natural selection pressures accelerating evolution?

Taffer, I appreciate your complaint about my citing a link from a non-peer reviewed article about bacteria being used to suppress the evolution of resistant mosquito larvae. Below is an example from a peer reviewed journal of how multiple selection pressures stops evolution of mosquito larvae. All mechanisms of mutation and recombination are available to the mosquito larvae yet resistance only occurs when the number of selection pressures are reduced.

Ichneumonwasp joins the competition to be the last evolutionist to understand the mathematics of mutation and selection. Perhaps if he realizes there is no way that multiple selection pressures accelerates evolution he may avoid the winner’s circle of ignorance and denial of the mathematics of mutation and selection.

Joobz thinks that evolution can not be stopped. If he reads this article carefully http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219 he will find that if evolution is not stopped, it delayed for a long period of time. Here is how evolution is stopped.

What hasn’t resistance evolved?

There are four agents acting on the larva. How can the larvas evolve resistance to these toxins?

Reduce down the number of selection pressures and the evolutionary process can proceed. Multiple selection conditions slow the evolutionary process and in this case four selection conditions stop the evolutionary process in a real situation. This is exactly analogous with what ev shows. The question is, how many real examples of the mathematical behavior of mutation and selection which ev shows before evolutionists finally understand this fact? Just how wide and deep is this river of ignorance and denial of the mathematics of mutation and selection that flows out of the theory of evolution?

No new lies, no math, but at least "all you have to know is how to count" is quite funny.

 

[Paul C. Anagnostopoulos]

All selection pressures inhibit replication. That is by definition what a selection pressure is, it is a stress on life forms that reduce its fitness to reproduce. If that stress is sufficient, it causes extinction.

Selection pressure is defined as the intensity of the selection acting on a population of (presumably variable) organisms. It makes no sense to say that all selection pressures inhibit replication.

~~ Paul

 

[Dr Richard]

Selection pressure is defined as the intensity of the selection acting on a population of (presumably variable) organisms. It makes no sense to say that all selection pressures inhibit replication.

~~ Paul

Since when did anything kleinman said make sense?

I asked him for a defintion of selection pressure over a week ago; seems he still can't get it right. Guess there is no chance of him answering the other questions put to him...

 

[Mr. Scott]

Annoying Questions for Kleinman

Since when did anything kleinman said make sense?

I asked him for a defintion of selection pressure over a week ago; seems he still can't get it right. Guess there is no chance of him answering the other questions put to him...

Dr. Kleinman will answer an uncomfortable question, or state some kind of reason why he won't (e.g. "it's none of your business") if your question is the only part of a posting. He is likely to ignore uncomfortable questions if they are within a post that has another comment or question.

A question I'd like to ask him is, "What transpired in your latest communication with Jesus about your efforts to undermine evolution?"

 

[kleinman]

Annoying Creationists

You don’t need to do the analysis; I’ll do it for you. Somehow you think that man made selection pressures behave in a different mathematical manner than natural selection pressures. Do you care to give us an example of this?

Hmmm, I must have missed your analysis. I wonder if that's because you forgot to do it, between telling me that I don't need to do any and where you ask me to give you an example to refute your non-existent analysis.

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

Do you tell your patients when you're practicing faith healing in favor of medicine?

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

Do any of you evolutionist care to give us an example of multiple natural selection pressures accelerating evolution?

I already did that, twice in this thread -- using ev, and I posted the data. Of course, you immediately disregarded both examples -- but, that's not my problem.

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

Seek professional help, Alan.

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

Kleinman, when you post a citation which actually states what you think it does, then we can have a discussion. But your refusal to realise that what every single citation is saying is not what you think it is leads this discussion to a dead end. You have not provided a single paper which shows that the rate of evolution slows as a result of multiple selection pressures. All you have shown is that the rate of emergence of a trait can be slowed, which is blindingly obvious. Yet again, emergence is not evolution. Emergence is that chance of a specific trait actually appearing in a population, and it is governed by such things as population size, the effect of the drug, and so-on. What you still fail to realise is that the rate of evolution is increased by heavy selection pressures. Our models show this. Reality shows this. Stop confusing emergence with the rate of evolution. All you have shown is that using many drugs makes the emergence of a multi-resistant individual less likely. Of course it does, because the number of allelic variations in the population is reduce. But evolution is the change in allele frequency over time. It doesn't matter how those alleles arose, once they exist evolution acts the same. More selection pressures do not slow this process. What is lowered is the amount of available variation to 'work with', so to speak.

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

All selection pressures inhibit replication. That is by definition what a selection pressure is, it is a stress on life forms that reduce its fitness to reproduce. If that stress is sufficient, it causes extinction.

Selection pressure is defined as the intensity of the selection acting on a population of (presumably variable) organisms. It makes no sense to say that all selection pressures inhibit replication.

Tell that to the editors of Wikipedia:

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

A process driven by evolutionary pressure is, for example, the natural selection for erythrocytes carrying the sickle cell hemoglobin gene mutation (Hb S)—causing sickle cell anaemia—in areas where malaria is a major health concern, which grants some resistance to this infectious disease. Therefore, the concept can be described as the application of Charles Darwin's principle of "survival of the fittest" (which actually should be understood as "extinction of the un-fittest") via some selection mechanism.

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

Selection pressure is defined as the intensity of the selection acting on a population of (presumably variable) organisms. It makes no sense to say that all selection pressures inhibit replication.

Since when did anything kleinman said make sense?

I asked him for a defintion of selection pressure over a week ago; seems he still can't get it right. Guess there is no chance of him answering the other questions put to him...

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

Since when did anything kleinman said make sense?

I asked him for a defintion of selection pressure over a week ago; seems he still can't get it right. Guess there is no chance of him answering the other questions put to him...

Dr. Kleinman will answer an uncomfortable question, or state some kind of reason why he won't (e.g. "it's none of your business") if your question is the only part of a posting. He is likely to ignore uncomfortable questions if they are within a post that has another comment or question.

A question I'd like to ask him is, "What transpired in your latest communication with Jesus about your efforts to undermine evolution?"

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

 

[joobz]

You have, rather than repeating it again, I’ll show you how to do it using ev...[snip]

Rather than repeating it again, You'll repeat it again?
We know your position and it has been refuted. Come up with something new to present.

 

[kleinman]

Annoying Creationists

You have, rather than repeating it again, I’ll show you how to do it using ev...[snip]

Rather than repeating it again, You'll repeat it again?

We know your position and it has been refuted. Come up with something new to present.

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

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

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

Pyrethroid-treated nets are an efficient tool for reducing malaria transmission and morbidity. The recent evolution of pyrethroid resistance in several Anopheles species represents a major threat for the future success of roll back malaria in Africa. The possible use of nonpyrethroid insecticides, such as carbamates, on nets is a promising alternative solution because these insecticides are effective against susceptible and pyrethroid-resistant populations of Anopheles and Culex mosquitoes. Unfortunately, carbamate resistance as a result of insensitive acetylcholinesterase has recently been detected in Anopheles gambiae s.s. populations from Côte d’Ivoire. Using biochemical assays on surviving Anopheles mosquitoes from an experimental hut trial, we showed evidence for selection for an insensitive acetylcholinesterase mechanism by carbamate impregnated bednets. However, no such selection has been found with nets treated with pyrethroid alone or pyrethroid/carbamate “two-in-one”-treated nets. Because pyrethroid-impregnated nets were suspected to select for the Kdr mutation in An. gambiae, we propose that use of two-in-one nets could be a promising alternative strategy for the management of insecticide resistance in malaria vectors.

I added the highlighting.

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

The elegant principles of evolution by natural selection pose a major problem throughout the world’s hospitals. Whenever an antibiotic is given to treat an infection, a small proportion of the bacteria present in the patient’s body may possess mutations, accessory genes or other genetic changes that protect them from the antibiotic. As the drug kills the susceptible bacteria, the few resistant organisms find that their competition for scarce resources in the environment of the patient’s body has greatly decreased. They proliferate more aggressively than before, resulting in the drug resistance mutation becoming more common. Therefore, the use of antibiotics commonly results in the spread of organisms resistant to them. The problem is compounded by the fact that this evolution occurs not only for the disease-causing organism, but potentially for all the bacteria present in the patient, some of which may cause disease later. In recent years, the spread of resistance has outpaced the development of new antibiotics, making many infections ever more difficult to treat. This process can be slowed to some extent by judicious use of antibiotics, but not eliminated.

Against this background, a welcome study appearing in the April 5 issue of Nature suggests that some carefully chosen combinations of antibiotics might actually reverse the problem of resistance, selecting for antibiotic-sensitive organisms over resistant ones. Antibiotic combinations can have a range of effects. If two drugs are synergistic, each is more effective at any given dose when they are used in combination. This is often used as a rationale for combining antibiotics in clinical practice. However, it is also possible for antibiotics to partially antagonize each other’s effects, so that higher concentrations are needed than if the drugs were used separately. In the most extreme case, adding a second drug (antibiotic B) can actually cause the bacteria to survive and grow better than they did under treatment with a single antibiotic A. This effect is called suppression, and is, of course, generally avoided in clinical practice.

This link is particularly interesting since it appears that the evolution of drug resistance can be reversed.

 

[joobz]

Joobz, not only have you failed to refute my hypothesis, I have given you a real case where multiple selection pressures stops evolution.

Really??? Hmm, I seem to remember things a bit differently. And look, the thread remembers it differently too.

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.

This won't go away becuase you wish it to. Your argument is without basis.

This link is particularly interesting since it appears that the evolution of drug resistance can be reversed.

Please explain what reverse evolution is and how it is different from plain ol' regular evolution?

 

[kleinman]

Annoying Creationists

Joobz, not only have you failed to refute my hypothesis, I have given you a real case where multiple selection pressures stops evolution.

Really??? Hmm, I seem to remember things a bit differently. And look, the thread remembers it differently too.

Of course your brainwashed and prejudiced evolutionist’s mind remembers things differently. Now if you can only recall your mathematical training that was required of you in order to obtain your degree in alchemical engineering, we can free you from your unscientific bias.

This link is particularly interesting since it appears that the evolution of drug resistance can be reversed.

Please explain what reverse evolution is and how it is different from plain ol' regular evolution?

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

The elegant principles of evolution by natural selection pose a major problem throughout the world’s hospitals. Whenever an antibiotic is given to treat an infection, a small proportion of the bacteria present in the patient’s body may possess mutations, accessory genes or other genetic changes that protect them from the antibiotic. As the drug kills the susceptible bacteria, the few resistant organisms find that their competition for scarce resources in the environment of the patient’s body has greatly decreased. They proliferate more aggressively than before, resulting in the drug resistance mutation becoming more common. Therefore, the use of antibiotics commonly results in the spread of organisms resistant to them. The problem is compounded by the fact that this evolution occurs not only for the disease-causing organism, but potentially for all the bacteria present in the patient, some of which may cause disease later. In recent years, the spread of resistance has outpaced the development of new antibiotics, making many infections ever more difficult to treat. This process can be slowed to some extent by judicious use of antibiotics, but not eliminated.

Against this background, a welcome study appearing in the April 5 issue of Nature suggests that some carefully chosen combinations of antibiotics might actually reverse the problem of resistance, selecting for antibiotic-sensitive organisms over resistant ones. Antibiotic combinations can have a range of effects. If two drugs are synergistic, each is more effective at any given dose when they are used in combination. This is often used as a rationale for combining antibiotics in clinical practice. However, it is also possible for antibiotics to partially antagonize each other’s effects, so that higher concentrations are needed than if the drugs were used separately. In the most extreme case, adding a second drug (antibiotic B) can actually cause the bacteria to survive and grow better than they did under treatment with a single antibiotic A. This effect is called suppression, and is, of course, generally avoided in clinical practice.

I added the highlighting.

Researchers from Harvard Medical School reasoned that suppressive antibiotic combinations might create an opportunity for favoring the growth of drug-sensitive organisms over drug-resistant ones. Suppose that two antibiotics, A and B, interact in a suppressive manner as described above. According to the definition of suppression, organisms that are sensitive to the effects of drug B will experience increased survival and growth when drug B is added to drug A, compared to when drug A is used alone. Organisms that are resistant to drug B will not be affected by its presence, and will be inhibited by drug A just as effectively as before. Therefore, the addition of drug B will select for B-sensitive organisms over B-resistant ones. At the end of treatment, the surviving bacterial population (if any) will have evolved to be more sensitive to drug B, reversing the problem of evolution of drug resistance.

The researchers tested this hypothesis using two strains of the common pathogen Escherichia coli that were tagged with fluorescent proteins of different colors, permitting their survival and growth to be measured separately. One strain was resistant to the antibiotic doxycycline, while the other was sensitive to this drug, which acted as “drug B” in the above scenario. The experiment was run with two different candidates for “drug A.” One, erythromycin, interacts synergistically with doxycycline. In this case, combination drug treatment always selected for doxycycline-resistant bacteria. The other “drug A,” ciprofloxacin, has a suppressive interaction with doxycycline. In this case, certain concentrations of ciprofloxacin and doxycycline resulted in selection for doxycycline-sensitive bacteria, as predicted.

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

Understand rubberband?

 

[joobz]

Of course your brainwashed and prejudiced evolutionist’s mind remembers things differently. Now if you can only recall your mathematical training that was required of you in order to obtain your degree in alchemical engineering, we can free you from your unscientific bias.

Ad hom, ad hom, ad hom..., but look, No refutation of your intellectual dishonesty. Hmm, I wonder why that is?

Po’ old joobz can’t understand the link so I have to spell it out for him.
[URL="http://www.ucsf.edu/synapse/content/51007/bacteria.html[/quote"]http://www.ucsf.edu/synapse/content/51007/bacteria.html[/URL]

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

Really, and evolution was "reversed"? Do you also believe in reverse-racism?

Understand rubberband?

Actually, no. I can't understand the gibberish you speak.

Let me play your highlight game

The elegant principles of evolution by natural selection pose a major problem throughout the world’s hospitals. Whenever an antibiotic is given to treat an infection, a small proportion of the bacteria present in the patient’s body may possess mutations, accessory genes or other genetic changes that protect them from the antibiotic. As the drug kills the susceptible bacteria, the few resistant organisms find that their competition for scarce resources in the environment of the patient’s body has greatly decreased. They proliferate more aggressively than before, resulting in the drug resistance mutation becoming more common. Therefore, the use of antibiotics commonly results in the spread of organisms resistant to them. The problem is compounded by the fact that this evolution occurs not only for the disease-causing organism, but potentially for all the bacteria present in the patient, some of which may cause disease later. In recent years, the spread of resistance has outpaced the development of new antibiotics, making many infections ever more difficult to treat. This process can be slowed to some extent by judicious use of antibiotics, but not eliminated.

Look at that. slowed but not stopped, and that's in our short little life time.

 

[kleinman]

Annoying Creationists

Of course your brainwashed and prejudiced evolutionist’s mind remembers things differently. Now if you can only recall your mathematical training that was required of you in order to obtain your degree in alchemical engineering, we can free you from your unscientific bias.

Ad hom, ad hom, ad hom..., but look, No refutation of your intellectual dishonesty. Hmm, I wonder why that is?

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

Po’ old joobz can’t understand the link so I have to spell it out for him.

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

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

Really, and evolution was "reversed"? Do you also believe in reverse-racism?

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

Understand rubberband?

Actually, no. I can't understand the gibberish you speak.

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

Let me play your highlight game

The elegant principles of evolution by natural selection pose a major problem throughout the world’s hospitals. Whenever an antibiotic is given to treat an infection, a small proportion of the bacteria present in the patient’s body may possess mutations, accessory genes or other genetic changes that protect them from the antibiotic. As the drug kills the susceptible bacteria, the few resistant organisms find that their competition for scarce resources in the environment of the patient’s body has greatly decreased. They proliferate more aggressively than before, resulting in the drug resistance mutation becoming more common. Therefore, the use of antibiotics commonly results in the spread of organisms resistant to them. The problem is compounded by the fact that this evolution occurs not only for the disease-causing organism, but potentially for all the bacteria present in the patient, some of which may cause disease later. In recent years, the spread of resistance has outpaced the development of new antibiotics, making many infections ever more difficult to treat. This process can be slowed to some extent by judicious use of antibiotics, but not eliminated.

Look at that. slowed but not stopped, and that's in our short little life time.

This author has yet to learn that extinction does occur. Perhaps you and he need to read this link http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=544219 where multiple selection pressures can and do stop the evolution of resistance.