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Old 16th October 2007, 02:28 PM   #6001
rocketdodger
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Originally Posted by kleinman View Post
What studies have you posted?
See post #5993 on the previous page of the thread.

We all know you are being purposefully ignorant, so I will make it so simple even you can't deny understanding what I say.
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Old 16th October 2007, 02:38 PM   #6002
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Originally Posted by kleinman View Post
Answer the question rocketdodger; that if someone with HIV who could not mount a humoral immune response against the virus was given therapy, would the virus evolve more slowly against that therapy than a person who could mount a humoral immune response against the given the same therapy?
No. As the studies you cite show, certain combinations of selection pressures profoundly slow the evolution of populations they affect. WTF does this have to do with my question about the validity of the studies I cited?

Originally Posted by kleinman View Post
And while you are thinking about the question, here is another example of how mutation and selection actually works.
Right back at you genius:

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

Why would antimalarial drug resistance be a problem, Kleinman, if the evolution of it happened too slow to matter?
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Old 16th October 2007, 02:40 PM   #6003
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Originally Posted by kleinman View Post
You are the whiney coward. Why donít you post under your real name so we can google search on your name and find out all about you? Of course we know plenty about you already. You are a greedy ambulance chaser who is totally ignorant of the mathematics of mutation and selection.
You said "intellectual" coward. If you want me to stop referring to you in that fashion, then stop refusing to directly address contrary evidence.

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

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

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

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

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

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

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

ROFLMAO!
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Old 16th October 2007, 03:06 PM   #6004
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You are such a dodo rocketdodger.
Originally Posted by rocketdodger
Two examples, right out of your own citations, that evolution occurs rapidly in the natural world. Care to argue with that? Many, many, many more (judging by how many of your citations I can crawl through and use against you) on the way...

http://www.omafra.gov.on.ca/english/...5/vg1105a4.htm
Originally Posted by rocketdodger quoting from the above citation
Resistance to pesticides can develop very quickly.

The quote that rocketdodger ignores from the citation.
Originally Posted by Pest Resistance to Insecticides and Miticides
Resistance to pesticides can develop very quickly. Do not use the same chemical repeatedly unless used in rotation with a different chemical or in combination with other chemicals having a different mode of action. Compounds within a chemical group usually share a common target site within the pest and mode of action. When a pest develops resistance to a chemical due to a mutation, there is a risk that the resistance will also result in cross-resistance to all the other compounds in the same sub-group. A pest population may develop cross resistance to closely related chemicals if a common detoxification mechanism exists, even in the absence of a selection pressure against individual compounds. Multiple resistance occurs through selective pressure on separate detoxification mechanisms for unrelated pesticides. In some species-specific cases, resistance develops due to an increased ability to metabolize toxins. Where these metabolic resistance mechanisms are not linked to a specific site of action, resistance to several different chemical families or mode of action can occur. Both metabolic and multiple resistant create serious challenges to the success of integrated resistance management strategies.

And
http://www.lshtm.ac.uk/people/roper.cally
Originally Posted by rocketdodger quoting from the above citation
and I am working on the problem of antimalarial drug resistance in Africa. The emergence and spread of drug resistance is a major threat to effective malaria treatment

and the part of the citation which rocketdodger ignores:
Originally Posted by Cally Roper BSc hons PhD
In my research group, Cally Roper Lab, we investigate the molecular genetic basis of drug resistance using population genetic approaches. We aim to determine which factors are most important in determining the rate of emergence and rate of spread of resistance. Our work includes the evaluation of combination therapy and its potential for slowing resistance evolution, and evaluating the selective pressure applied by intermittent preventive treatment. We are mapping the dispersal of resistance mutations in Africa.

Sure resistance can occur quickly, when you have single selection pressures, both these citations explicitly say that combination selection pressures slow the evolution of resistance. Now why donít you go through the hundreds of citations I have posted and see if you can make a single point because so far you have no point.
Originally Posted by Kleinman
Answer the question rocketdodger; that if someone with HIV who could not mount a humoral immune response against the virus was given therapy, would the virus evolve more slowly against that therapy than a person who could mount a humoral immune response against the given the same therapy?
Originally Posted by rocketdodger
No. As the studies you cite show, certain combinations of selection pressures profoundly slow the evolution of populations they affect. WTF does this have to do with my question about the validity of the studies I cited?

Because the studies you cited show that evolution occurs much more quickly with single selection pressures (single drug therapy) than with combination therapy. So answer the question, if someone with HIV who could not mount a humoral immune response against the virus was given therapy, would the virus evolve more slowly against that therapy than a person who could mount a humoral immune response against the given same therapy?
Originally Posted by Kleinman
And while you are thinking about the question, here is another example of how mutation and selection actually works.
Originally Posted by rocketdodger
Right back at you genius:
Originally Posted by rocketdodger blindly quoting from the citation
Resistance emerges as a result of selection and then disemination of spontaneous mutant parasites with reduced drug susceptibility. Combination therapy is considered as the main strategy to control antimalarial drug resistance."

I donít even have to repost the quote, you ignore that combination therapy is the strategy from slowing or stopping the evolution of resistance. If you want rapid evolution of resistance, use monotherapy. So answer the question, if someone with HIV who could not mount a humoral immune response against the virus was given therapy, would the virus evolve more slowly against that therapy than a person who could mount a humoral immune response against the given same therapy?
Originally Posted by rocketdodger
Why would antimalarial drug resistance be a problem, Kleinman, if the evolution of it happened too slow to matter?

The point is rocketwhomissesthetarget is that the use of monotherapy has led to rapid evolution of resistance of these drugs. Thatís why combination therapy is now the considered the standard of care in order to avoid selection of resistant parasites. Now are you going to answer the question, if someone with HIV who could not mount a humoral immune response against the virus was given therapy, would the virus evolve more slowly against that therapy than a person who could mount a humoral immune response against the given same therapy?
Originally Posted by Kleinman
You are the whiney coward. Why donít you post under your real name so we can google search on your name and find out all about you? Of course we know plenty about you already. You are a greedy ambulance chaser who is totally ignorant of the mathematics of mutation and selection.
Originally Posted by kjkent1
You said "intellectual" coward. If you want me to stop referring to you in that fashion, then stop refusing to directly address contrary evidence.

I would never mistake you as an ďintellectualĒ. You seem to think you understand how strong and weak selection pressures work, post your data and explain to us how they work. While you are not posting your data or giving us your explanation, here is another real example of how mutation and selection actually works.
http://www.anopheles.org/showabstract.php?pmid=2571247
Originally Posted by Delay in emergence of mefloquine resistance in Plasmodium berghei by use of drug combinations.
Blood induced Plasmodium berghei infection in Swiss mice was exposed during successive passages to mefloquine alone or mefloquine in combination with dapsone or primaquine or erythromycin, and the level of resistance to mefloquine in four sub-lines was compared at ED90 level. Treatment with mefloquine alone resulted in a 201.14 fold increase in resistance after 21 passages. Use of drug combination (mefloquine + dapsone) delayed the acquisition of resistance as shown by a marginal increase of ED90 by 5.76 fold after 34 passages. Similarly, there was a 17.84 fold increase of resistance after 32 passages involving exposure to mefloquine-primaquine and a 112.28 fold increase after exposure to melfoquine-erythromycin combination for 31 passages. The study emphasizes that rational drug combinations should be developed to protect the melfoquine against the emergence of resistance in P. falciparum cases.
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Old 16th October 2007, 03:18 PM   #6005
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yawn.
Horribly wrong assumptions in the Kleinman theory:
1.) Mutation rate remains constant
2.) Mutation rate is known

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


/prediction: Kleinman will pretend that these assumptions aren't relavent to his theory, but all his references clearly indicate otherwise.
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Old 16th October 2007, 03:23 PM   #6006
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Originally Posted by kleinman View Post
The point is rocketwhomissesthetarget is that the use of monotherapy has led to rapid evolution of resistance of these drugs.
So you agree that rapid evolution exists in nature (where by "nature" I mean "not in a controlled environment"). Thank you. Why has it taken 150 pages of rubbish for you to reach this conclusion?

Originally Posted by kleinman View Post
Now are you going to answer the question, if someone with HIV who could not mount a humoral immune response against the virus was given therapy, would the virus evolve more slowly against that therapy than a person who could mount a humoral immune response against the given same therapy?
I did answer, in the first paragraph of my very last post. Read what I wrote if you are interested (but I know you are not).

Originally Posted by kleinman View Post
While you are not posting your data or giving us your explanation, here is another real example of how mutation and selection actually works.
That study confirms that evolution can occur rapidly in nature. Why do you keep posting studies that are PREDICATED on the fact that evolution can occur rapidly? Every single study you cite, Kleinman, only solidifies the fact that evolution is fast enough to get results.
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Old 16th October 2007, 03:38 PM   #6007
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Originally Posted by joobz
/prediction: Kleinman will pretend that these assumptions aren't relavent to his theory, but all his references clearly indicate otherwise.

First, joobz doesnít make predictions, he makes speculations, second, joobz doesnít read his own citations let alone citations posted by others. Joobz thinks just if a citation has the word ďenvironmentĒ in it, they are talking about the weather. Hereís another citation for you not to read joobz.
http://www.anopheles.org/showabstract.php?pmid=15667718
Originally Posted by Variations in the insecticide-resistance spectrum of Anopheles stephensi after selection with deltamethrin or a deltamethrin-piperonyl-butoxide combination.
When the larvae of Anopheles stephensi, a malaria vector, were selected with deltamethrin for 40 successive generations, there was a 60-fold increase in larval resistance to deltamethrin but no increase in the resistance of the adult mosquitoes. This result, and the observation that deltamethrin selection of adults for 40 generations resulted in only a six-fold increase in adult resistance to deltamethrin, indicated some stage specificity. When F(24) deltamethrin-resistant larvae were selected with 1:5 deltamethrin-piperonyl butoxide (deltamethrin-PBO), instead of deltamethrin alone, for 16 generations, the level of resistance to deltamethrin in the F(40) larvae was reduced by 6%-21%. Similarly, selection with deltamethrin-PBO of adults of the parental strain for 20 generations reduced the speed of the development of resistance to deltamethrin, compared with that seen using selection with deltamethrin alone. Deltamethrin selection appears to select initially a monooxygenase-based mechanism. When the monooxygenase-based mechanism is blocked, by treatment with PBO, selection of a kdr-type mechanism is accelerated, as is evident from increased cross-resistance to 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT) in the adults selected with deltamethrin-PBO. The implications of these results are discussed in terms of the management of the larval and adult stages of An. stephensi .

Sorry the title of this article doesnít have the word ďenvironmentĒ in it joobz, but it does have the word ďspectrumĒ, you probably thing they are talking about colors.
Originally Posted by Kleinman
The point is rocketwhomissesthetarget is that the use of monotherapy has led to rapid evolution of resistance of these drugs.
Originally Posted by rocketdodger
So you agree that rapid evolution exists in nature (where by "nature" I mean "not in a controlled environment"). Thank you. Why has it taken 150 pages of rubbish for you to reach this conclusion?

How would you know what is written in the 150 pages of this thread? The only way you can get rapid evolution of any gene is with a single selection pressure, of course, feel free to post a citation which says otherwise. And now are you going to answer the question, if someone with HIV who could not mount a humoral immune response against the virus was given therapy, would the virus evolve more slowly against that therapy than a person who could mount a humoral immune response against the given same therapy?
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Old 16th October 2007, 04:04 PM   #6008
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Originally Posted by kleinman View Post
The only way you can get rapid evolution of any gene is with a single selection pressure, of course, feel free to post a citation which says otherwise.
IT IS IMPOSSIBLE TO EXERT ONLY A SINGLE SELECTION PRESSURE ON A POPULATION.



Originally Posted by kleinman View Post
And now are you going to answer the question, if someone with HIV who could not mount a humoral immune response against the virus was given therapy, would the virus evolve more slowly against that therapy than a person who could mount a humoral immune response against the given same therapy?
In post #6006 I told you that I answered that question already in post #6002, which means this is the second time I have told you I already answered it. Because you are not smart enough to navigate this thread accordingly, I will paste it here to make it simple for you:

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

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

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

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

A 60-fold increase in only 40 generations, Kleinman? That seems to be pretty rapid to me.
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Old 16th October 2007, 04:11 PM   #6009
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Originally Posted by kleinman View Post
First, joobz doesnít make predictions, [snip repeated nonsense]
Excellent. I predicted correctly!

Do I win anything?
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Old 16th October 2007, 05:31 PM   #6010
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Originally Posted by Kleinman
The only way you can get rapid evolution of any gene is with a single selection pressure, of course, feel free to post a citation which says otherwise.
Originally Posted by rocketdodger
IT IS IMPOSSIBLE TO EXERT ONLY A SINGLE SELECTION PRESSURE ON A POPULATION.

You are correct rocketdodger! That is why the theory of evolution is mathematically impossible.
Originally Posted by Kleinman
And now are you going to answer the question, if someone with HIV who could not mount a humoral immune response against the virus was given therapy, would the virus evolve more slowly against that therapy than a person who could mount a humoral immune response against the given same therapy?
Originally Posted by rocketdodger
In post #6006 I told you that I answered that question already in post #6002, which means this is the second time I have told you I already answered it. Because you are not smart enough to navigate this thread accordingly, I will paste it here to make it simple for you:
Originally Posted by rocketdodger quoting himself
In post #6006 I told you that I answered that question already in post #6002, which means this is the second time I have told you I already answered it. Because you are not smart enough to navigate this thread accordingly, I will paste it here to make it simple for you:
Originally Posted by Kleinman
Originally Posted by rocketdodger
Originally Posted by rocketdodger quoting himself

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

I know you are trying to squirm out of answering the question.
Originally Posted by rocketdodger
Here is what your last citation has to say about the rapidity of evolution in nature:

http://www.anopheles.org/showabstract.php?pmid=15667718
Originally Posted by rocketdodger quoting the citation
... were selected with deltamethrin for 40 successive generations, there was a 60-fold increase in larval resistance to deltamethrin . . . deltamethrin selection of adults for 40 generations resulted in only a six-fold increase in adult resistance to deltamethrin . . .
Originally Posted by rocketdodger
A 60-fold increase in only 40 generations, Kleinman? That seems to be pretty rapid to me.

Of course when you are applying a single selection pressure to a population, mutation and selection can evolve rapidly to that single selection pressure. If you had run any cases with ev you would see this exact same effect. But then you missed this part of the quote.
Originally Posted by Variations in the insecticide-resistance spectrum of Anopheles stephensi after selection with deltamethrin or a deltamethrin-piperonyl-butoxide combination.
When F(24) deltamethrin-resistant larvae were selected with 1:5 deltamethrin-piperonyl butoxide (deltamethrin-PBO), instead of deltamethrin alone, for 16 generations, the level of resistance to deltamethrin in the F(40) larvae was reduced by 6%-21%. Similarly, selection with deltamethrin-PBO of adults of the parental strain for 20 generations reduced the speed of the development of resistance to deltamethrin, compared with that seen using selection with deltamethrin alone.

The combination of deltamethrin and PBO slows the evolution of resistance when compared to deltamethrin alone, thereís a lesson here if you want to learn it rocketdodger.
Originally Posted by Kleinman
First, joobz doesnít make predictions, [snip repeated nonsense]
Originally Posted by joobz
[snip everything joobz says is nonsense especially about mutation and selection and abiogenesis]

At least youíre smart enough to admit that you donít make predictions, you only make speculations.

Hereís another citation for joobz and rocketthatmissesthetarget.
http://www.anopheles.org/showabstract.php?pmid=17092790
Originally Posted by Preventing antimalarial drug resistance through combinations.
Throughout the tropical world antimalarial drug resistance is increasing, particularly in the potentially lethal malaria parasite Plasmodium falciparum. In some parts of Southeast Asia, parasites which are resistant to chloroquine, pyrimethamine-sulfadoxine, and mefloquine are prevalent. The characteristics of a drug that make it vulnerable to the development of resistance are a long terminal elimination half-life, a shallow concentration-effect relationship, and that one or two base-pair mutations confer a marked reduction in susceptibility. The development of resistance can be delayed or prevented by drug combinations. The artemisinin derivatives are the most potent of all antimalarial drugs. They reduce the infecting parasite biomass by approximately 10 000-fold per asexual life cycle. There are good arguments for combining, de novo, an artemisinin derivative with all newly introduced antimalarial drugs.

Hey joobz, these authors seem to think they can stop the evolution of resistance. You better contact them and tell them slow doesnít mean stop.
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Old 16th October 2007, 05:40 PM   #6011
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Originally Posted by kleinman
You are correct rocketdodger! That is why the theory of evolution is mathematically impossible.
ROFLMAO! You've done it again, Alan. If it's impossible, then how do you explain the fact that every one of your quoted papers begins with a "single" pressure, and produces rapid resistance?

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

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

But, it can't be possible, says the creatonist -- evolution must be impossible -- otherwise, when I die, I may go nowhere, and I'm afraid of the dark. Mommy, save me -- the boogyman is in the closet!
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Old 16th October 2007, 06:08 PM   #6012
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Originally Posted by Kleinman
You are correct rocketdodger! That is why the theory of evolution is mathematically impossible.
Originally Posted by kjkent1
ROFLMAO! You've done it again, Alan. If it's impossible, then how do you explain the fact that every one of your quoted papers begins with a "single" pressure, and produces rapid resistance?

Because thatís the way mutation and selection works.
Originally Posted by kjkent1
That would be impossible, because as you've just said, a single selective pressure is impossible.

You are correct kjkent1, thatís why the theory of evolution is mathematically impossible.
Originally Posted by kjkent1
Of course, the answer is obvious to an open-minded person: intensity of selection pressure accounts for why evolution in nature occurs. For the closed-minded creationist, however, the answer is simply that intensity cannot have any effect, because that would make evolution by mutation and selection possible.

Now I understand how your theory of evolution works, a little weather change here, a little breeze there and reptiles evolve feathers and wings. It is all so obvious, how could I have missed this?
Originally Posted by kjkent1
But, it can't be possible, says the creatonist -- evolution must be impossible -- otherwise, when I die, I may go nowhere, and I'm afraid of the dark. Mommy, save me -- the boogyman is in the closet!

Hey kjkent1, I heard there are lots of golf courses in hell, just no clubs or balls.
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Old 16th October 2007, 06:08 PM   #6013
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Originally Posted by kleinman View Post
At least youíre smart enough to admit that you donít make predictions, you only make speculations.
Too bad I can't say the same. You haven't offered any reason for anyone to label you as smart, or even smart enough regarding anything related to evolution.

Originally Posted by kleinman View Post
Hereís another citation for joobz and rocketthatmissesthetarget.
Originally Posted by kleinman View Post
http://www.anopheles.org/showabstract.php?pmid=17092790

Hey joobz, these authors seem to think they can stop the evolution of resistance. You better contact them and tell them slow doesnít mean stop.
See what I mean.
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Old 16th October 2007, 06:18 PM   #6014
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Originally Posted by Kleinman
At least you’re smart enough to admit that you don’t make predictions, you only make speculations.
Originally Posted by joobz
Too bad I can't say the same. You haven't offered any reason for anyone to label you as smart, or even smart enough regarding anything related to evolution.

I realize this; the theory of evolution is only understandable to speculators and extrapolators. Do you think that some day you would teach me how to speculate and extrapolate? How’s the weather in your rainforest? Do you see evolution accelerating as the earth’s plates are moving?

One thing I have learned from you is that if there is enough free energy, anything is possible.
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Old 16th October 2007, 06:22 PM   #6015
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Originally Posted by kleinman View Post
One thing I have learned from you is that if there is enough free energy, anything is possible.
I see were back to this nonsense?

Dr. Alan Kleinman, Have you stopped killing your patients?
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What's the best argument for UHC? This argument against UHC.
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Old 16th October 2007, 06:25 PM   #6016
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Originally Posted by rcronk View Post
P.S. What is the goal of each side of this nearly 6000-post thread?

It's a study in abnormal psychology. Shhhh - several Ph.D.'s are being created here.
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Old 16th October 2007, 06:32 PM   #6017
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Originally Posted by Kleinman
Perhaps if you ask yourself the question, why does ev converge when Rfrequency < Rcapacity? Then perhaps you would understand that the fitness landscape is finally getting small enough with isoclines that allow for convergence to perfect creature local optima. Another way to get an easier to traverse fitness landscape is to reduce down the selection pressures to one and then the Rcapacity issue disappears. That is a real phenomenon.
The Rcapacity issue disappears because Rcapacity is irrelevant when you're not trying to evolve a creature that distinguishes binding sites from other positions on the genome.

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

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

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

~~ Paul
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Old 16th October 2007, 06:44 PM   #6018
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Originally Posted by kjkent1
ROFLMAO! You've done it again, Alan. If it's impossible, then how do you explain the fact that every one of your quoted papers begins with a "single" pressure, and produces rapid resistance?
Originally Posted by Kleinman
Because thatís the way mutation and selection works.
Originally Posted by kjkent1
That would be impossible, because as you've just said, a single selective pressure is impossible.
Originally Posted by Kleinman
You are correct kjkent1, thatís why the theory of evolution is mathematically impossible.
Is it just me, or ?

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Old 16th October 2007, 06:50 PM   #6019
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Originally Posted by Kleinman
One thing I have learned from you is that if there is enough free energy, anything is possible.
Originally Posted by joobz
I see were back to this nonsense?

This is one of my favorite of your quotes.
Originally Posted by joobz
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.


Originally Posted by joobz
Dr. Alan Kleinman, Have you stopped killing your patients?

Come on into the office and find out but you had better make an appointment, we are very busy.

Originally Posted by rcronk
P.S. What is the goal of each side of this nearly 6000-post thread?
Originally Posted by balrog666
It's a study in abnormal psychology. Shhhh - several Ph.D.'s are being created here.

Now that’s a good one, someone running around calling himself balrog666 is going to tell us what is normal and abnormal.
Originally Posted by Kleinman
Perhaps if you ask yourself the question, why does ev converge when Rfrequency < Rcapacity? Then perhaps you would understand that the fitness landscape is finally getting small enough with isoclines that allow for convergence to perfect creature local optima. Another way to get an easier to traverse fitness landscape is to reduce down the selection pressures to one and then the Rcapacity issue disappears. That is a real phenomenon.
Originally Posted by Paul
The Rcapacity issue disappears because Rcapacity is irrelevant when you're not trying to evolve a creature that distinguishes binding sites from other positions on the genome.

You really like clinging to this issue. When are you going to learn that optimization problems have domains of convergence?
Originally Posted by Kleinman
Every example of convergence with ev is easy to explain. A local optimum is found by the model. You are hung up on the fact that ev stops converging to perfect creature local optima when Rcapacity > Rfrequency. Why you would think that ev should behave in a linear manner shows your lack of experience with non-linear mathematics.
Originally Posted by Paul
Say what? I don't think Ev should behave in a linear manner. I think it should be prevented from converging when Rcapacity > Rfrequency.

Paul, it’s all about the shape of the fitness landscape and the starting point for the search for a local optimum. Map out the fitness landscape and you will know exactly why ev stops converging. You only have to computer 4^G points.
Originally Posted by Kleinman
The rationale for this was that benzyl benzoate and 5% tea tree oil were consistently the topical scabicides that killed scabies mites the quickest in our earlier in vitro studies [7].
Originally Posted by Paul
What does this have to do with evolution?

Aren’t they killing scabies with selection pressures? Isn’t that what ev does? For that matter, they are using combination selection pressures.
Originally Posted by Kleinman
Are you claiming that benzyl benzoate alone and 5% tea tree oil alone are both fatal to scabies? If so, why would these authors subject their patient to the distressing effects of the combination?
Originally Posted by Paul
No, I'm asking what killing mites has to do with evolution.

They are trying to evolve perfect scabies.
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Old 16th October 2007, 06:53 PM   #6020
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Originally Posted by Paul
Is it just me, or ?

It’s just you Paul.
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Old 16th October 2007, 07:20 PM   #6021
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Originally Posted by kleinman View Post
This is one of my favorite of your quotes.
I'm sure you love it. It's completely correct in regards to what it was refering to.



Originally Posted by kleinman View Post
Come on into the office and find out but you had better make an appointment, we are very busy.

Not sure what this means. or how it relates to your half-brained theory.

But continue to dance for us. It's funny watching you derail your own foolish thread.
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Old 16th October 2007, 08:33 PM   #6022
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Originally Posted by kleinman View Post
It’s just you Paul.
No, Alan it's just "you." You make a jackass out of yourself over and over by not recognizing the substantial flaws in your logic.

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

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

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

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

Not ONE person on planet Earth agrees with your theory.

If I were arguing a legal theory, and I couldn't find a single human being who would agree with me, I damn certain wouldn't bring that theory into a courtroom, because that would be a loooooooooser.
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Old 16th October 2007, 09:40 PM   #6023
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Originally Posted by kleinman View Post
You are correct rocketdodger! That is why the theory of evolution is mathematically impossible.
Then how do pathogens/rodents/weeds evolve resistance to drugs/poisons/herbicides?

Originally Posted by kleinman View Post
I know you are trying to squirm out of answering the question.
You quoted my answer immediately above this statement in your post, you human paraquat.

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

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

Originally Posted by kleinman View Post
Here’s another citation for joobz and rocketthatmissesthetarget.
http://www.anopheles.org/showabstract.php?pmid=17092790
Here is the first half of the first sentence in the abstract: "Throughout the tropical world antimalarial drug resistance is increasing"

Contrast this with Kleinman's latest absurdity:
Originally Posted by kleinman View Post
"You are correct rocketdodger! That is why the theory of evolution is mathematically impossible."
...which, of course, is totally the opposite of his earlier statement:
Originally Posted by kleinman View Post
The point is rocketwhomissesthetarget is that the use of monotherapy has led to rapid evolution of resistance of these drugs.
Does anybody have info on this Kleinman tool? I would like to put a face with the stupidity I am seeing here.

Last edited by rocketdodger; 16th October 2007 at 09:50 PM.
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Old 16th October 2007, 09:47 PM   #6024
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Originally Posted by kleinman View Post
Itís just you Paul.
Well... actually... no, Kleinman, Paul is not the only person who thinks you are clueless.
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Old 17th October 2007, 01:08 AM   #6025
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Originally Posted by kleinman View Post
The theory of evolution is mathematically impossible.
Once upon a time people thought it was mathematically impossible for bumble bees to fly.
Their theories were wrong, just like yours.
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Old 17th October 2007, 04:32 AM   #6026
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Originally Posted by kleinman View Post
All the more reason not to separate the posts, you need to learn how mutation and selection actually works.
I STILL skip to the answers to my posts, Klein. It's just more work for no reason.

Quote:
This discussion is not about your faith system
You're the creationist and you call MY opinion faith-based ?



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

Quote:
Itís easy to understand Belz; all you have to do is read what he means, not what he writes.
Perhaps, but don't do it like Kleinman does, because he is obviously incapable of doing that.

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

Quote:
The goal in this thread is the same as it was in the beginning of this discussion; to show that ev demonstrates that the theory of evolution is mathematically impossible and that real empirical examples of mutation and selection demonstrates what ev shows. Here are some more citations which show that combination selection pressures profoundly slow the evolutionary process.
Fine. Get a real scientist in here -- you know, those you say agree with you -- because it's obvious you are incapable of making your case.
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Old 17th October 2007, 04:33 AM   #6027
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Originally Posted by rocketdodger View Post
Kleinman's goal is to show that evolution happens too slow to actually work in the natural world, using, get this, data from experiments designed to find ways of slowing the rapid evolution that can occur in the natural world.
That's the best summary of a thread I've ever seen.
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Old 17th October 2007, 04:34 AM   #6028
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http://http://www.internationalskept...postcount=5981

Still waiting, Klein.
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Old 17th October 2007, 04:45 AM   #6029
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Woah, woah. Wait a minute...

You say:

Originally Posted by kleinman View Post
The point is rocketwhomissesthetarget is that the use of monotherapy has led to rapid evolution of resistance of these drugs.
Bolding mine. So, rapid evolution IS possible, since it happened.

But then,

Quote:
The only way you can get rapid evolution of any gene is with a single selection pressure, of course, feel free to post a citation which says otherwise.
Okay... so there ARE instances of a single selection pressure, since rapid evolution DID happen, by your admission.

And lastly...

Quote:
Originally Posted by Rocket
IT IS IMPOSSIBLE TO EXERT ONLY A SINGLE SELECTION PRESSURE ON A POPULATION.
You are correct rocketdodger! That is why the theory of evolution is mathematically impossible.
Huh ? How is it impossible if YOU ADMIT IT HAPPENS ?

You have seriously shot yourself in the foot now, Kleinman.
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Old 17th October 2007, 04:50 AM   #6030
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Originally Posted by kleinman View Post
Because thatís the way mutation and selection works.
You are a walking paradox, Klein.

Quote:
Now I understand how your theory of evolution works, a little weather change here, a little breeze there and reptiles evolve feathers and wings. It is all so obvious, how could I have missed this?
Don't forget the planet-busting meteors...

Quote:
Now thatís a good one, someone running around calling himself balrog666 is going to tell us what is normal and abnormal.
Ad hominem.

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

Good luck.
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Old 17th October 2007, 05:26 AM   #6031
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Originally Posted by Kleinman
You really like clinging to this issue. When are you going to learn that optimization problems have domains of convergence?
As soon as you learn that there are reasons why there are domains of convergence. In the case we are talking about, the reason is Rcapacity.

Do you treat everything in life as an amorphous mystery?

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

Quote:
They are trying to evolve perfect scabies.
They are?

~~ Paul
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Old 17th October 2007, 05:44 AM   #6032
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Mod WarningTone it down, folks.

Quote:
ďAttack the argument, not the arguer." Having your opinion, claim or argument challenged, doubted or dismissed is not attacking the arguer.
Posted By:LibraryLady
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Old 17th October 2007, 08:07 AM   #6033
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Annoying Creationists

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

Itís so correct, letís read it again.
Originally Posted by joobz
I acknowledge this is complete speculation, but well within the range of chemical possibility. As long as there was enough free energy for these reaction to occur.

Joobz, you are correct, it is complete speculation.
Originally Posted by kjkent1
Apparently you don't want anyone to take you seriously. If you did, then you would take your opponent's seriously.

Oh, I take you seriously; I think your string cheese theory of evolution is seriously funny. How many alternative universes are there kjkent1, 10^500? How many of these alternative universes have you visited? Next time you visit one of your alternative universes, send us a postcard, post mark the Twilight Zone.
Originally Posted by Kleinman
You are correct rocketdodger! That is why the theory of evolution is mathematically impossible.
Originally Posted by rocketdodger
Then how do pathogens/rodents/weeds evolve resistance to drugs/poisons/herbicides?

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

Pathogens/rodents/weeds evolve resistance to drugs/poisons/herbicides in the same way that HIV evolves resistance in the presence of a weak humoral immune response. The greater the number of selection pressures, the more difficult for these populations to adapt to these selection pressures.
Originally Posted by Kleinman
Itís just you Paul.
Originally Posted by rocketdodger
Well... actually... no, Kleinman, Paul is not the only person who thinks you are clueless.

Oh no questiondodger, I have plenty of clues, both mathematical and empirical, check below, Iíll post more clues for you.
Originally Posted by Kleinman
The theory of evolution is mathematically impossible.
Originally Posted by Deetee
Once upon a time people thought it was mathematically impossible for bumble bees to fly. Their theories were wrong, just like yours.

You got it wrong Deetee, itís Dr Schneiderís model which shows this, not my model and surprise, surprise, what his model shows is backed up by empirical evidence.

Now Deetee, once upon a time people thought that life arose from a primordial soup and evolved into everything we see today, your theory are wrong, the mathematics and empirical evidence of how mutation and selection works proves this.
Originally Posted by Kleinman
All the more reason not to separate the posts, you need to learn how mutation and selection actually works.
Originally Posted by BelzÖ
I STILL skip to the answers to my posts, Klein. It's just more work for no reason.

No wonder you have no idea how mutation and selection works. You are still trying to figure out the difference between atheist and agnostic. Have you figured out the difference between evolve and beggaminases?
Originally Posted by Kleinman
You really like clinging to this issue. When are you going to learn that optimization problems have domains of convergence?
Originally Posted by Paul
As soon as you learn that there are reasons why there are domains of convergence. In the case we are talking about, the reason is Rcapacity.

Do you treat everything in life as an amorphous mystery?

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

Paul itís not Rcapacity or beggaminases. Ev will always converge to a local optima, even when Rfrequency > Rcapacity.
Originally Posted by Kleinman
Arenít they killing scabies with selection pressures? Isnít that what ev does? For that matter, they are using combination selection pressures.
Originally Posted by Paul
No, they are killing scabies with poisons. Killing them. Like dead. With weapons. Like you might stomp on a spider.

Selection pressures do that to populations.
Originally Posted by Kleinman
They are trying to evolve perfect scabies.
Originally Posted by Paul
They are?

Isnít that what evolution is supposed to do?

Chillzero and Librarylady are both moderators.
http://www.internationalskeptics.com/forums/showpost.php?p=3044651&postcount=5894
And
http://www.internationalskeptics.com/forums/showpost.php?p=3065762&postcount=6032
Seems some of the moderators on this site are suffering from some despotism. Letís see if they can come up with a coherent counterargument to the hypothesis that combination selection pressures profoundly slow the evolutionary process. Here are some clues for the moderators and questiondodgers to ponder.
http://www.anopheles.org/showabstract.php?pmid=10212909
Originally Posted by Qinghaosu in combinations.
Antimalarial combinations make therapeutic sense. As we have few antimalarial drugs and even fewer in development, and as the malaria parasite shows a remarkable ability to develop resistance, all possible measures should be taken to protect those drugs that we do have available. Although in experimental animals combinations have been shown unequivocally to delay the onset of resistance, this has not yet been proved formally in human malaria. Yet formal proof is extremely difficult to obtain. However, there is sufficient circumstantial evidence to suggest that resistance can be delayed. As there are no counter arguments and the stakes are high, it seems reasonable that an artemisinin derivative should be combined with all slow acting antimalarial drugs. Those drugs with a particularly vulnerable profile, in which a single or double point mutation confers high level resistance, should not be deployed alone and should always be combined with an artemisinin derivative.

http://www.anopheles.org/showabstract.php?pmid=12803854
Originally Posted by The chemotherapy of rodent malaria. LXI. Drug combinations to impede the selection of drug resistance, part 4: the potential role of 8-aminoquinolines.
The influence of combinations containing the blood schizontocides chloroquine (CQ) or mefloquine (MEF), together with the 8-aminoquinolines (8AQ) primaquine (PQ) or the new, long-acting compound, tafenoquine (TAF), on the rate of selection of resistance to the individual compounds was examined using the asexual, intra-erythrocytic stages in rodent malaria models. The two main procedures used were a 'serial technique' (ST) and the '2%- relapse technique' (2%RT). The ST provided evidence for the contention that a combination with PQ slowed the selection of resistance to CQ or MEF; it has been shown previously that synergism exists between CQ and either PQ or TAF in rodent malaria. Data obtained with the 2%RT, and three parasite lines derived from Plasmodium berghei N (the 238B line), P. chabaudi ASS (the 238C line) or P. yoelii ssp. NS (the 238Y line), indicated that resistance to TAF used alone is acquired rapidly under drug pressure and that this resistance is stable when selection pressure is removed. In the 2%RT, resistance to CQ developed when another line of P. chabaudi (AS15) was exposed to that compound alone, although more slowly than the development of resistance to TAF in the 238C line. However, treatment of a TC line of P. chabaudi, developed in a 2%RT using a combination of CQ with TAF, led to little resistance to either compound. A totally unforeseen phenomenon was the appearance of a high level of resistance to CQ in the 238C line of P. chabaudi that had been exposed only to TAF; this was not observed with the 238B or 238Y lines. Attention has been refocused recently on the use of 8AQ for prophylaxis in man. It remains to be determined if resistance in the asexual intra-erythrocytic forms is carried over to the other stages of the malarial life-cycle, especially the hepatic, pre-erythrocytic schizonts. The implications of the present results for the possible clinical deployment of 8AQ in the future are discussed. It is concluded that, whereas use of an 8AQ alone carries a high risk of selecting resistance, combinations containing 8AQ may have a place in the protection of blood schizontocides that are to be deployed in endemic areas. Furthermore, the inherent gametocytocidal action of the 8AQ should promote the reduction of transmission.

http://www.anopheles.org/showabstract.php?pmid=10697872
Originally Posted by Delaying antimalarial drug resistance with combination chemotherapy.
Resistance to antimalarial drugs arises when spontaneously occurring mutants with gene mutations or amplifications which confer reduced drug susceptibility are selected, and are then transmitted. Simultaneous use of two or more antimalarials with different modes of action and which therefore do not share the same resistance mechanisms will reduce the chance of selection, because the chance of a resistant mutant surviving is the product of the parasite mutation rates for the individual drugs, multiplied by the number of parasites in an infection that are exposed to the drugs. The artemisinin derivatives are very active antimalarials, which produce large reductions in parasite biomass per asexual cycle, and reduce malaria transmissibility. To date no resistance to these drugs has been reported. These drugs therefore make particularly effective combination partners. This suggests that antimalarial drugs should not be used alone in treatment, but always in combination, as in the treatment of tuberculosis or HIV, and that the combination should include artemisinin or one of its derivatives.

http://www.anopheles.org/showabstract.php?pmid=12641911
Originally Posted by The de novo selection of drug-resistant malaria parasites.
Antimalarial drug resistance emerges de novo predominantly in areas of low malaria transmission. Because of the logarithmic distribution of parasite numbers in human malaria infections, inadequately treated high biomass infections are a major source of de novo antimalarial resistance, whereas use of antimalarial prophylaxis provides a low resistance selection risk. Slowly eliminated antimalarials encourage resistance largely by providing a selective filter for resistant parasites acquired from others, and not by selecting resistance de novo. The de novo emergence of resistance can be prevented by use of antimalarial combinations. Artemisinin derivative combinations are particularly effective. Ensuring adequate treatment of the relatively few heavily infected patients would slow the emergence of resistance.

Joobz, here are some other authors who donít seem to understand slow does not equal stop. You better contact them and give them your speculations.

Now I hate to disappoint you evolutionists (my goal is to annoy you with the facts of how mutation and selection actually works) but I have something else which I must attend to and will not be back until next week. Iím sure you will find something interesting to discuss about the mathematics of mutation and selection and the empirical evidence which supports this mathematics. Until then, may all your selection pressures be weak selection pressures.
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Old 17th October 2007, 09:03 AM   #6034
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Originally Posted by kleinman View Post
Why should I answer your questions? You donít answer my questions. I think we should call you questiondodger instead of rocketdodger. Just to show you that I am not a questiondodger, Iíll answer your question.
I did answer your question, the same question, three times -- in posts #6002, #6006, and #6023. Yet, you insist I have not, trying to rally any idiots who browse this forum to your case. Guess what, Kleinman -- it isn't happening. People who come here (well, not all of them, obviously) can read. They see what is going on. If you were vomiting this nonsense at your local church, and had tough guys to throw out people like me when we called your hand, maybe your misinformation tactics would work. But not here.

Originally Posted by kleinman View Post
Pathogens/rodents/weeds evolve resistance to drugs/poisons/herbicides in the same way that HIV evolves resistance in the presence of a weak humoral immune response. The greater the number of selection pressures, the more difficult for these populations to adapt to these selection pressures.
So evolution is possible again?

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

Originally Posted by kleinman View Post
Oh no questiondodger, I have plenty of clues, both mathematical and empirical, check below, Iíll post more clues for you.
Thank you for posting more evidence that shows evolution occurs rapidly in nature. Here are the relevant statements from the abstracts:

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

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

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

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

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

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

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

"Antimalarial drug resistance emerges de novo predominantly in areas of low malaria transmission."
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Old 17th October 2007, 09:04 AM   #6035
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Originally Posted by Klein
No wonder you have no idea how mutation and selection works. You are still trying to figure out the difference between atheist and agnostic. Have you figured out the difference between evolve and beggaminases?
There's so much vitriol there it's hard to know where to start.

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

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

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

Please learn to read.
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Old 17th October 2007, 09:06 AM   #6036
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Originally Posted by Rocketdodger
The only way I can account for your series of posts, Kleinman, is that you are in fact a group of bible-study children experimenting with the wonders of the internet, and you all are taking turns making posts. Otherwise, one would notice at least a little consistency between them.
Ouch.
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Old 17th October 2007, 09:08 AM   #6037
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Another day, another post from kleinman clearly showing that his proofs prove how evolution works (assuming that we concede that this is all there is to it, which I, for one, do not). To wit:

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


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

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

Thanks!!!

ROFLMAO!
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Old 17th October 2007, 09:11 AM   #6038
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Originally Posted by kleinman View Post
Now I hate to disappoint you evolutionists (my goal is to annoy you with the facts of how mutation and selection actually works) but I have something else which I must attend to and will not be back until next week. Iím sure you will find something interesting to discuss about the mathematics of mutation and selection and the empirical evidence which supports this mathematics. Until then, may all your selection pressures be weak selection pressures.[/size][/font]
We all agree with each other, so if we discuss anything, it will be how badly you just got whipped in the last few pages of this thread.

If you ever come back, you will just get whipped again. I have half a mind to do the same over in those stupid "evolution is dead" forums, but luckally for you the large backlog of games I need to play and porn I need to dl is where I would rather spend my time.
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Old 17th October 2007, 09:35 AM   #6039
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Originally Posted by Klein
my goal is to annoy you with the facts of how mutation and selection actually works
Oh, you annoy us, allright. But not with facts.
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Old 17th October 2007, 09:36 AM   #6040
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Originally Posted by rocketdodger View Post
We all agree with each other, so if we discuss anything, it will be how badly you just got whipped in the last few pages of this thread.

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