Belz...
Fiend God
Let’s remind the readers of what you said:
And then Adequate goes on to say this:
Kleinman, I suggest you learn the english language before continuing to post in this thread.
Let’s remind the readers of what you said:
And then Adequate goes on to say this:
Only a creationist would be arrogant enough to believe that he is the only person alive who knows how mutation and selection actually works.kleinman said:Only an evolutionist would think it is arrogant to show how mutation and selection works in reality.
Logic, and that's all I need!kleinman said:I’ve never said that selection intensity does not affect the evolutionary process. In fact I have said the exact opposite and posted citations which show this. If you want to accelerate evolution such as done in the laboratory to identify the mutations that appear in a population from a particular drug, you use a sub-lethal concentration of the drug and increase the concentration until you obtain a resistant population. But nothing affects the evolutionary process as does the number of selection conditions. That is the dominant parameter in the mathematics of mutation and selection. Reality reflects this fact as well. So, barrister, you don’t have the science, mathematical or empirical data to support your claim. What do you have left to argue with?
If you haven't read this paper, you may find that it gives you some sort of insight into what it's like to be kleinman.
That's a very interesting link that concludes pretty much what I've said for some time: ignorance breeds confidence.
No, I'm confident that we know all there is to know about it.....oh crud.I dunno, seems like it may be a horse & cart/chicken & egg situation. I mean, are they overconfident becauase of their ignorance? Or, are they ignorant because they are prone to overconfidence, and assume they don't need to learn?
Or perhaps it's more like a snake eating it's own tail: they're overconfident so don't learn, which increase their ignorance, which makes them more confident, which convinces them they don't need to learn...
I think this study needs to be extended a bit![]()
To quote Huxley's remark on Darwinism: "How extraordinarily stupid of me not to have thought of that."
But can you explain it to kleinman?
So in other words once kleinman stops trying to "get one over" the "evolutionists" he'll be able to learn why he's wrong.
But until he learns why he's wrong he's not going to stop doing that.
Yep. It's a vicious circle alright.
I don't know how precise I can be, since Kleinman's mathematical proof of the impossibility of evolution by point mutation and natural selection is somewhat lacking in actual math.Mr. Scott said:Can you describe precisely how Kleinman is misusing Ev that leads him to believe it disproves macro evolution? Even though this is probably covered somewhere in the 6608 postings here, it's become too difficult to search out. A summary would especially help newcomers to the thread.
Most creationists only feel the need to be wrong about biology, maybe a little geology and astronomy ... kleinman finds that he can only defend his fantasies by incomprehension of simple English and by failing grade-school math --- and he's willing to go the extra mile.So in other words once kleinman stops trying to "get one over" the "evolutionists" he'll be able to learn why he's wrong.
But until he learns why he's wrong he's not going to stop doing that.
Yep. It's a vicious circle alright.
Oh the stupid... it hertz me braying.
http://www.christcenteredforums.com/forum/showthread.php/whats-wrong-evolution-3344/index.html
Adequate said:Are you listening carefully?
[/SIZE]Adequate said:
(1) With simultaneous selection pressures the [size=+4]rate of evolution (fixations/generation) increases with the number of selection pressures. [/SIZE]
(2) More optimisation takes more [size=+4]time. This is what my model shows. This is what ev shows. This is what reality shows. This is freakin' obvious.
Oh, I’m not the only one, check out the citations below.Kleinman said:Only an evolutionist would think it is arrogant to show how mutation and selection works in reality.kjkent1 said:Only a creationist would be arrogant enough to believe that he is the only person alive who knows how mutation and selection actually works.
Mr Scott said:A question for Paul:
Mr Scott said:
Can you describe precisely how Kleinman is misusing Ev that leads him to believe it disproves macro evolution? Even though this is probably covered somewhere in the 6608 postings here, it's become too difficult to search out. A summary would especially help newcomers to the thread.
Paul, I’m using the data from your own computer model. Is their some lack of math in your model? Dr Schneider said that it includes the essentials.Paul said:I don't know how precise I can be, since Kleinman's mathematical proof of the impossibility of evolution by point mutation and natural selection is somewhat lacking in actual math.
That’s hundreds of experiments I have run and posted the results from ev and longer genomes taking longer to evolve to a “perfect creature” than do smaller ones is a bit of an understatement, in fact it is a huge understatement. The evolution of the same binding sites on Dr Schneider’s single published case of G=256 which takes less than 1,000 generations takes hundreds of millions of generations on a G=100k by your own estimate. Dr Schneider had no problem estimating the evolution of a human from his model let alone leopards, flagella or any other complex biological system.Paul said:At first, Kleinman ran some experiments with Evj that demonstrate that larger genomes take longer to evolve a "perfect creature" than do smaller ones. A perfect creature is defined as one with zero mistakes, when all the mistake points (New dialog, Advanced) are equal. For some reason, he decided that when we extrapolate to the real world, there hasn't been enough time to evolve humans, or leopards, or flagella, or something. This in spite of the fact that he has no idea which biological features evolved when, on what size genomes, with what size populations, or under the influence of what sorts of mutations.
I didn’t discover the “mistakes points feature” in ev. Kjkent1 pointed it out for me, thank you kjkent1. What I was looking for was the parameter which was causing ev to evolve so slowly for all but the tiniest genomes. It was the “mistake point feature” which reveals why the sorting process becomes so profoundly slow with all but the tiniest genomes. Set two of the three selection conditions to zero and the remaining selection condition sorts very rapidly, even with small populations. This extremely simple mutation and selection sorting/optimization algorithm demonstrates exactly how the mutation and selection process works. It is the number of selection conditions which dominates the mathematical and empirical behavior of the mutation and selection sorting/optimization process. Hundreds of empirical examples of mutation and selection verifies what Dr Schneider’s computer model shows.Paul said:After awhile, Kleinman discovered the mistake points feature, which I had added at the behest of another Creationist. That's when he got into the whole "multiple selection pressures" thing. No amount of repetition can convince him that different functions are being evolved when one or two mistake points are set to zero, and so comparing the times to evolve a perfect creature are problematical. In particular, the concept of a perfect creature doesn't even make sense unless all mistake points are nonzero.
If you mean that I am decorating the hypothesis that combination selection pressures profoundly slow the evolutionary process with hundreds of real examples of mutation and selection then your use of the word “baroque” is appropriate. Since you evolutionists have yet to produce a single example of n+1 selection pressures evolving more rapidly than n selection pressures, how would you describe your architecture, plain, how about nonexistent?Paul said:Since then, the multiple selection pressures thing has evolved from a simple "three pressures stop evolution" to the extraordinarily baroque concept that you see today.
That’s a fitting “backstory” for the theory of evolution since ev converges to a local optimum, it just doesn’t happen to be a “perfect creature” local optimum for longer genomes. Those are the routes that Adequate’s space zeppelin takes when he makes his excursion from Skeptiwikiland to the James Randi Educational Forum.Paul said:Finally, we have had an ongoing backstory discussion about Rcapacity.
http://jvi.asm.org/cgi/content/abstract/71/2/1089Patients with plasma viral RNA >50,000 copies/mL, despite a protease-inhibitor regimen, received abacavir, amprenavir, and efavirenz to assess efavirenz-amprenavir drug interactions and to evaluate safety and antiviral response. Patients first received amprenavir with abacavir and other nucleoside analogs. Amprenavir levels were measured before and after adding efavirenz. Patients then received a second protease inhibitor. There was evidence of genotypic and phenotypic resistance at study entry. No patient had study drugs discontinued because of toxicity. Efavirenz decreased the steady-state area under the curve, maximum plasma concentration, and minimum plasma concentration of amprenavir by 24%, 33%, and 43%, respectively. Three of 10 patients had >1.5 log10 viral response to abacavir and amprenavir. All 8 patients who added efavirenz had >0.5 log10 decline in viral load, and this response lasted >24 weeks for 3 of the patients. A combination regimen that included abacavir, amprenavir, and efavirenz was well tolerated and had sustained activity in some patients. Concomitant efavirenz therapy decreases amprenavir concentrations.
http://www.pnas.org/cgi/content/abstract/93/4/1648Impaired fitness of human immunodeficiency virus type 1 variants with high-level resistance to protease inhibitors said:One hope to maintain the benefits of antiviral therapy against the human immunodeficiency virus type 1 (HIV-1), despite the development of resistance, is the possibility that resistant variants will show decreased viral fitness. To study this possibility, HIV-1 variants showing high-level resistance (up to 1,500-fold) to the substrate analog protease inhibitors BILA 1906 BS and BILA 2185 BS have been characterized. Active-site mutations V32I and I84V/A were consistently observed in the protease of highly resistant viruses, along with up to six other mutations. In vitro studies with recombinant mutant proteases demonstrated that these mutations resulted in up to 10(4)-fold increases in the Ki values toward BILA 1906 BS and BILA 2185 BS and a concomitant 2,200-fold decrease in catalytic efficiency of the enzymes toward a synthetic substrate. When introduced into viral molecular clones, the protease mutations impaired polyprotein processing, consistent with a decrease in enzyme activity in virions. Despite these observations, however, most mutations had little effect on viral replication except when the active-site mutations V32I and I84V/A were coexpressed in the protease. The latter combinations not only conferred a significant growth reduction of viral clones on peripheral blood mononuclear cells but also caused the complete disappearance of mutated clones when cocultured with wild-type virus on T-cell lines. Furthermore, the double nucleotide mutation I84A rapidly reverted to I84V upon drug removal, confirming its impact on viral fitness. Therefore, high-level resistance to protease inhibitors can be associated with impaired viral fitness, suggesting that antiviral therapies with such inhibitors may maintain some clinical benefits.
http://aac.asm.org/cgi/content/full/44/3/794?ck=nckHuman immunodeficiency virus type 1 viral background plays a major role in development of resistance to protease inhibitors said:The observed in vitro and in vivo benefit of combination treatment with anti-human immunodeficiency virus (HIV) agents prompted us to examine the potential of resistance development when two protease inhibitors are used concurrently. Recombinant HIV-1 (NL4-3) proteases containing combined resistance mutations associated with BMS-186318 and A-77003 (or saquinavir) were either inactive or had impaired enzyme activity. Subsequent construction of HIV-1 (NL4-3) proviral clones containing the same mutations yielded viruses that were severely impaired in growth or nonviable, confirming that combination therapy may be advantageous. However, passage of BMS-186318-resistant HIV-1 (RF) in the presence of either saquinavir or SC52151, which represented sequential drug treatment, produced viable viruses resistant to both BMS-186318 and the second compound. The predominant breakthrough virus contained the G48V/A71T/V82A protease mutations. The clone-purified RF (G48V/A71T/V82A) virus, unlike the corresponding defective NL4-3 triple mutant, grew well and displayed cross-resistance to four distinct protease inhibitors. Chimeric virus and in vitro mutagenesis studies indicated that the RF-specific protease sequence, specifically the Ile at residue 10, enabled the NL4-3 strain with the triple mutant to grow. Our results clearly indicate that viral genetic background will play a key role in determining whether cross-resistance variants will arise.
AndDelavirdine Susceptibilities and Associated Reverse Transcriptase Mutations in Human Immunodeficiency Virus Type 1 Isolates from Patients in a Phase I/II Trial of Delavirdine Monotherapy (ACTG 260) said:The development of human immunodeficiency virus type 1 resistance to delavirdine (DLV) was studied in subjects receiving DLV monotherapy. Phenotypic resistance developed in 28 of 30 subjects within 8 weeks. K103N and Y181C, which confer nonnucleoside reverse transcriptase inhibitor (NNRTI) cross-resistance, were the predominant reverse transcriptase mutations. P236L, which confers DLV resistance but hypersensitivity to other NNRTIs, developed in <10% of isolates.
That’s the story of how mutation and selection works. Combination selection pressures profoundly slow a population’s ability to do the sort of beneficial and detrimental mutations. You have too many routes on the fitness landscape that lead to no where. Single selection conditions which target a single gene give relatively rapid sorting of beneficial and detrimental mutations but as soon as you have multiple selection conditions targeting multiple different genes, the sorting process is interfered with by the multiple different selection conditions. That is what ev shows and that is what the hundreds of real examples of mutation and selection demonstrates. Now you evolutionists could overwhelm me with a single empirical example of n+1 selection pressures evolving more rapidly than n selection pressures, alas I suspect we are in for a long wait for that. The failure of you evolutionists to understand this simple principle has and will continue to contribute to the premature death of millions of people with HIV, cancer and other infectious diseases subject to the principles of mutation and selection.Delavirdine Susceptibilities and Associated Reverse Transcriptase Mutations in Human Immunodeficiency Virus Type 1 Isolates from Patients in a Phase I/II Trial of Delavirdine Monotherapy (ACTG 260) said:In vitro passage of HIV-1 in the presence of DLV leads to the emergence of a unique RT mutation, P236L (5). In contrast to Y181C and K103N, P236L confers an increase in HIV-1 susceptibility to other NNRTIs. This observation suggested that cross-resistance to other NNRTIs might not be an inevitable consequence of bis(heteroaryl)piperazine resistance. However, P236L was only rarely detected in patients given DLV in combination with didanosine, and the majority of isolates in these patients had a Y181C and/or K103N mutation (3).
That’s the story of how mutation and selection works. Combination selection pressures profoundly slow a population’s ability to do the sort of beneficial and detrimental mutations. You have too many routes on the fitness landscape that lead to no where. Single selection conditions which target a single gene give relatively rapid sorting of beneficial and detrimental mutations but as soon as you have multiple selection conditions targeting multiple different genes, the sorting process is interfered with by the multiple different selection conditions. That is what ev shows and that is what the hundreds of real examples of mutation and selection demonstrates.
You're welcome, however you continue to misunderstand the effect of setting a mistake count to zero.kleinman said:I didn’t discover the “mistakes points feature” in ev. Kjkent1 pointed it out for me, thank you kjkent1. What I was looking for was the parameter which was causing ev to evolve so slowly for all but the tiniest genomes. It was the “mistake point feature” which reveals why the sorting process becomes so profoundly slow with all but the tiniest genomes. Set two of the three selection conditions to zero and the remaining selection condition sorts very rapidly, even with small populations.
And then you wonder why people think that you're insane.Ladies and Gentlemen: We interrupt our regularly schedule discussion for this important announcement. An evolutionator and his clones have time traveled from Skeptiwikiland to the here and now James Randi Educational Forum. It is their goal to evolutionate the annoying creationist. The evolutionator has accomplished this time travel by increasing the number of routes he can take, even though most of his routes lead to no where. He has accomplished this by increasing the speed of his space zeppelin to 40 furlongs per fortnight from its normal travel speed of 20 furlongs per fortnight. Not only has the evolutionator been able to increase his speed by increasing the number of routes, he has been reduce his fuel consumption by 1.3 gallons per furlong. Beware of the evolutionator! Now back to our regularly scheduled discussion, the funeral for the theory of evolution.
I'm guessing that it's the same obscure Internet message board that I keep pointing out to you is an obscure Internet message board.Sure Adequate, I’m listening carefully. I love your quote above. And your use of font size and color are strikingly convincing. Hey Adequate, I was listening to CNN this weekend and they mentioned “an obscure Internet message board”. I wonder if you can guess which “obscure Internet message board” was mentioned?
We know that you're talking bollocks, and if you could ever get your head round grade-school-level math, so would you.That’s the story of how mutation and selection works. Combination selection pressures profoundly slow a population’s ability to do the sort of beneficial and detrimental mutations. You have too many routes on the fitness landscape that lead to no where. Single selection conditions which target a single gene give relatively rapid sorting of beneficial and detrimental mutations but as soon as you have multiple selection conditions targeting multiple different genes, the sorting process is interfered with by the multiple different selection conditions. That is what ev shows and that is what the hundreds of real examples of mutation and selection demonstrates. Now you evolutionists could overwhelm me with a single empirical example of n+1 selection pressures evolving more rapidly than n selection pressures, alas I suspect we are in for a long wait for that. The failure of you evolutionists to understand this simple principle has and will continue to contribute to the premature death of millions of people with HIV, cancer and other infectious diseases subject to the principles of mutation and selection.