Dr Adequate
Banned
- Joined
- Aug 31, 2004
- Messages
- 17,766
I think kleinman's just pressing the buttons on his Lying Machine at random now.
It's hard to imagine that somebody could be more dull and boring than Adequate but now we have found someone who is trying to imitate him. So which one of you two is OMG?joobz said:Until then, here's a new image.![]()
Kleinman said:Ah yes, the gap theory of evolution, is there anyplace you don’t have a gap in your theory?
Ev does not evolve binding sites de novo according to Paul.
HIV evolves resistance much more quickly if monotherapy is used.
The use of combination therapy for HIV is a good analogy to what ev shows.
Of course I have, and if you had read this thread, you would know what I have to say about it.
Yes, he's taking into account the distances from valuation to threshold for all positions.Kleinman said:Here are the changes Unnamed made to ev:
That would be Unnamed's job.Why don’t you post a version of ev with these changes online so everyone can study the behavior of these changes?
He must have meant that only variations that support the theory of evolution should be investigated. Paul, I love it when you squirm.
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Paul, Dr Schneider was quite clear what he intended ev to be used for when he said the following:
That statement suggests to you that he only wants the program to be used to investigate things that support evolution? All righty then.Schneider said:Variations of the program could be used to investigate how population size, genome length, number of sites, size of recognition regions, mutation rate, selective pressure, overlapping sites and other factors affect the evolution.
I would be happy to address this claim if you could first define what you mean by "evolving binding sites de novo."Kleinman said:Ev does not evolve binding sites de novo according to Paul.
Who is claiming that a program disproves intelligent design? Certainly no one in this thread.T'ai said:Has anyone worked out how an intelligently designed program can possibly disprove the concept of intelligent design yet?
Has anyone worked out how an intelligently designed program can possibly disprove the concept of intelligent design yet?
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Has anyone worked out how an intelligently designed program can possibly disprove the concept of intelligent design yet?
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No, but many people have explained to you how an intelligently designed program can prove the concept of evolution.Has anyone worked out how an intelligently designed program can possibly disprove the concept of intelligent design yet?
Now?I think kleinman's just pressing the buttons on his Lying Machine at random now.
littleman, if you find string theory silly, take it up with Dr. Susskind.Let’s see if I can help you with the word serious. Try the word “earnest” instead of “serious”. Dr Schneider has made an earnest application of the mathematics of mutation and selection while you have made earnestly silly application of the string cheese theory to mutation and selection.
littleman, no one cares what you believe. We are waiting for you to prove your theory. Until you do, you are the supreme whiner in this thread.When considering other mutation mechanisms, the question is whether these other mutation mechanisms will significantly alter the behavior of the mathematics of mutation and selection process. I don’t believe it will for several reasons. Point mutations are the least destructive of mutations as well as the most common type of mutation. They don’t cause frame shifts which alter large numbers of codons. If you think that other mutation mechanism will somehow accelerate the mutation selection process, feel free to prove this. With respects to Dr Schneider’s selection scheme, it is very forgiving. What I mean by this is that you don’t have the possibility of extinction. The weight factors are not tied to survival of a creature. There are many examples of single mutations which cause the death of the creature with that mutation, yet ev does not have this effect. Including these types of features in the model would only slow evolution more so. In addition, how would you formulate the selection process that would evolve a gene de novo? There is no such selection process.
Same ****, different words. We are waiting for you to prove your case. Schneider has already proved his.That’s an easy one. Introduce whatever feature you want in the model and see whether you can speed up evolution sufficiently and prove your case. Since ev is already showing that it is the multiple selection conditions which slow the evolution process, the changes you advocate will not alter the fundamental mathematics already revealed.
You're drawing your conclusions based on a version of the program which does not model anything close to the reality of variations in the evolutionary process. So, your conclusions are pure conjecture.Everybody has biases. The question is whether I am drawing my conclusion based on these biases or am I drawing my conclusions based on the results from ev and the numerous real examples which show that multiple selection pressures slow evolution.
You will need to accurately model all of the known real evolutionary processes. Until then, all you've proved is that random point mutation, by itself is prettyt slow. Don't think anyone would argue with that conclusion.I have demonstrated why Dr Schneider improperly extrapolated the evolution of a human genome. You evolutionists refuse to acknowledge this. Instead, you look for ways to parse words to justify this type of unscientific approach. That said, Dr Schneider’s underlying simulation has properly captured the mathematics of mutation and selection. In particular, the effect of multiple selection pressures is properly revealed.
Using only point mutation and an extremely simple selective process. Since neither is a complete model of evolution, your numbers are pure conjecture.That’s a bit of an understatement. Simply using a realistic mutation rate of 10^-6 instead of 1 mutation per 256 bases per generation in Dr Schneider’s published case makes his estimate of 1 billion years for the evolution of a human genome go to 4 trillion years. And what real living thing has a genome length of 256?
I'm not parsing away anything. Given more sophisticated algorithms, ev's basic premise could be extended to show a more complete explanation of evolution. Without more sophisticated algorithms, ev proves information gain, which is what the paper sought to prove.Kjkent1, you can’t parse away this statement from the NAR paper...
Let's see you do some of the work to prove your theory. As it stands, Schneider's proven info gain, and you've proven random point mutation is slow. Your miles from proof that evolution is impossible.Only evolutionist cultists would end the discussion here. I have no objection to adding any feature to ev. Let’s see if it changes any of my conclusions.
Your "real examples" are all based on random point mutations and a simplistic selection algorithm. So, your examples are not real, therefore all of your conclusions are unsubstantiated.My conclusions are unsubstantiated except for the results from ev and numerous real examples of these results.
Absolutely, littleman. You can have all you can digest. Personally, I think you need a "Reglan," because you just can't seem to digest reality.Would you pass the red herring, string cheese and whine please.
If you are "bored" by requests that you should tell a new lie, then the solution is very much in your own hands. All you have to do is tell a new lie.
It's hard to imagine that somebody could be more dull and boring than Adequate but now we have found someone who is trying to imitate him. So which one of you two is OMG?
Has anyone worked out how an intelligently designed program can possibly disprove the concept of intelligent design yet?
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Do you suppose Dr. Kleinman is happy he's joined in this debate by such a brilliant mind?Has anyone worked out how an intelligently designed program can possibly disprove the concept of intelligent design yet?
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What you describe is the fundamental purpose of ev: to show that information gain can arise from a randomly ordered system using the process of random mutation and natural selection.Has anyone worked out how an intelligently designed program can possibly disprove the concept of intelligent design yet?
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You do realise of course that software engineering shows us that the most, THE MOST, used design technique is:
"Try it, if it works keep it, if not throw it away."
Which just blows friggin' great chunks in your nonsense.
Well, a good programmer is supposed to adhere to top-down design principles that, if followed religiously, should result in error-free development.
The biggest non-sequitor in this thread is the one evolutionist make. That non-sequitor is mutation and selection leads to the evolution of birds from reptiles. This is mathematically impossible.Kleinman said:Ah yes, the gap theory of evolution, is there anyplace you don’t have a gap in your theory?Ichneumonwasp said:Is there a word for a non-sequitor following a non-sequitor following a non-sequitor? To what in the friggin' world are you responding? It has no relation, whatever, to anything that I wrote.
I thought you read Dr Schneider’s Ev Evolution of Biological Information and this thread. Here’s what Dr Schneider says that ev does:Kleinman said:Ev does not evolve binding sites de novo according to Paul.Ichneumonwasp said:What is it that ev does?
Dr Schneider said:A small population (n=64) of `organisms' was created, each of which consisted of G= 256 bases of nucleotide sequence chosen randomly, with equal probabilities, from an alphabet of 4 characters (a, c, g, t, Fig. 1). At any particular time in the history of a natural population, the size of a genome, G, and the number of required genetic control element binding sites, γ, are determined by previous history and current physiology respectively, so as a parameter for this simulation we chose γ=16 and the program arbitrarily chose the site locations, which are fixed for the duration of the run. The information required to locate γ sites in a genome of size G is Rfrequency = -log2(γ/G) = 4 bits per site, where γ/G is the frequency of sites [4,14].
Dr Schneider said:A section of the genome is set aside by the program to encode the gene for a sequence recognizing `protein', represented by a weight matrix [15,7] consisting of a two-dimensional array of 4 by L = 6 integers. These integers are stored in the genome in twos complement notation, which allows for both negative and positive values. (In this notation, the negative of an integer is formed by taking the complement of all bits and adding 1.) By encoding A=00, C=01, G=10, and T=11 in a space of 5 bases, integers from -512 to +511 are stored in the genome. Generation of the weight matrix integers from the nucleotide sequence gene corresponds to translation and protein folding in natural systems. The weight matrix can evaluate any L base long sequence. Each base of the sequence selects the corresponding weight from the matrix and these weights are summed. If the sum is larger than a tolerance, also encoded in the genome, the sequence is `recognized' and this corresponds to a protein binding to DNA (Fig. 1). As mentioned above, the exact form of the recognition mechanism is immaterial because of the generality of information theory.
The weight matrix gene for an organism is translated and then every position of that organism's genome is evaluated by the matrix. The organism can make two kinds of `mistakes'. The first is for one of the γ binding locations to be missed (representing absence of genetic control) and the second is for one of the G - γ non-binding sites to be incorrectly recognized (representing wasteful binding of the recognizer). For simplicity these mistakes are counted as equivalent, since other schemes should give similar final results. The validity of this black/white model of binding sites comes from Shannon's channel capacity theorem, which allows for recognition with as few errors as necessary for survival [1,16,7].
The organisms are subjected to rounds of selection and mutation. First, the number of mistakes made by each organism in the population is determined. Then the half of the population making the least mistakes is allowed to replicate by having their genomes replace (`kill') the ones making more mistakes. (To preserve diversity, no replacement takes place if they are equal.) At every generation, each organism is subjected to one random point mutation in which the original base is obtained 1/4 of the time. For comparison, HIV-1 reverse transcriptase makes about one error every 2000-5000 bases incorporated, only 10 fold lower than this simulation [17].
When the program starts, the genomes all contain random sequence, and the information content of the binding sites, Rsequence, is close to zero. Remarkably, the cyclic mutation and selection process leads to an organism that makes no mistakes in only 704 generations (Fig. 2a). Although the sites can contain a maximum of 2L = 12 bits, the information content of the binding sites rises during this time until it oscillates around the predicted information content, Rfrequency = 4 bits, with Rsequence, = 3.983 ± 0.399 bits during the 1000 to 2000 generation interval (Fig. 2b). The expected standard deviation from small sample effects [4] is 0.297 bits, so about 55% of the variance ( 0.32/0.42) comes from the digital nature of the sequences. Sequence logos [5] of the binding sites show that distinct patterns appear during selection, and that these then drift (Fig. 3). When selective pressure is removed, the observed pattern atrophies (not shown, but Fig. 1 shows the organism with the fewest mistakes at generation 2000, after atrophy) and the information content drops back to zero (Fig. 2b). The information decays with a half-life of 61 generations.
The evolutionary steps can be understood by considering an intermediate situation, for example when all organisms are making 8 mistakes. Random mutations in a genome that lead to more mistakes will immediately cause the selective elimination of that organism. On the other hand, if one organism randomly `discovers' how to make 7 mistakes, it is guaranteed (in this simplistic model) to reproduce every generation, and therefore it exponentially overtakes the population. This roughly-sigmoidal rapid transition corresponds to (and the program was inspired by) the proposal that evolution proceeds by punctuated equilibrium [18,19], with noisy `active stasis' clearly visible from generation 705 to 2000 (Fig. 2b, Fig. 3).
I repeat this because it is a perfect example of how single selection pressures evolve much more quickly than multiple selection pressures, this is what the mathematics of ev shows and this is how mutation and selection works.Kleinman said:HIV evolves resistance much more quickly if monotherapy is used.Ichneumonwasp said:The point being what? Once again, now for, I think, the fifth time, I haven't argued against this idea so I haven't the slighest idea why you repeat it. It has nothing whatever to do with the conversation.
It's also not always true.
Why don’t you tell us how many people survive HIV for any length of time when the three selection pressures from antiretroviral medicines are not applied?Kleinman said:The use of combination therapy for HIV is a good analogy to what ev shows.Ichneumonwasp said:No, it's not. As repeatedly emphasized --HIV triple therapy involves, by its definition more than three selection pressures since it must also include patient selection pressures including the rapid death of T cells and the potential death of the patient and the immune response.
Why don’t you tell us how many loci must evolve for HIV to have resistance to three drugs?Ichneumonwasp said:1. HIV triple therapy attacks one, or at most, two sites. For the most part we are talking about two different types of reverse transcriptase inhibitors and/or a protease inhibitor. There are not 16 different "binding sites" that must "find" the correct base. Instead, all that HIV must "do" is develop the correct strain that is not inhibited by the reverse transcriptase inhibitor and/or protease inhibitor by producing so many copies that one of them will have the proper mutation in it. For the most part we are talking about one, two, or possibly three point mutations that are selected (depends a bit on what triple therapy protocol is used). That is not what ev does. Most of the ev models that I have seen have required something on the order of 96 point mutations for convergence.
This is one of the stranger arguments you evolutionary cultists have come up with. You contradict yourselves with this argument. The set goal in the theory of evolution is survival of the fittest. That is what natural selection does. You then turn around and say there is no goal in nature. Which is it? No set goal or survival of the fittest?Ichneumonwasp said:2. Ev models the development of information that is already pre-determined. Nature does not pre-determine what will or will not work in any particular situation (outside of determinism itself). There is no set goal in nature. If HIV arrives at a solution, then it arrives at a solution to the problem plaguing it -- triple therapy. If it doesn't, then it doesn't.
The only set goal is satisfying the three selection conditions and this goes profoundly slow when realistic genome lengths and mutation rates are used.Dr Schneider said:An advantage of the ev model over previous evolutionary models, such as biomorphs [20], Avida [21], and Tierra [22], is that it starts with a completely random genome, and no further intervention is required.
If you mean “first” when you use the word “prime” then HIV is my “prime” example of how multiple selection pressures slows evolution. However there are numerous other examples which are just as valid as this case. These examples include multiple drug therapy for the treatment of TB in order to prevent the emergence of resistant strains of this bacteria, the rapid emergence of resistance in HIV and TB when monotherapy is used, combination pesticides to prevent evolution of resistant strains, combination herbicides to prevent the evolution of resistant strains, combination rodenticides to prevent the evolution of resistant strains and combination cancer therapy to prevent the evolution of resistant strains. Each of these is real examples of what ev shows with its three selection pressures. That is multiple selection pressures slow the evolutionary process. This is a mathematical and demonstrated real fact. Now perhaps you would tell us what that selection pressure is that would evolve reptiles into birds? Pretty please?Ichneumonwasp said:3. You specifically stated when I joined this thread that HIV triple therapy was the prime example of how three selection pressures in ev work; and that this proved that evolution was so slow that it could never happen. Yet you have been confronted with the actual evidence that resistance forms to triple therapy in short order. This would seem to prove that evolution is not stopped by three selection pressures but continues along quite nicely, thank you very much. You have tried to squirm out of this fact in various ways -- initially by pretending that I was the one pushing HIV triple therapy, then by pretending that ev predicted that triple therapy could not stop HIV from producing resistant strains (even though your original argument was that HIV could never produce resistant strains in short time periods).
You can believe it because I have the data from a peer reviewed and published mathematical model of random point mutation and natural selection and numerous real examples of this mathematics.Ichneumonwasp said:I see no reason why I, or anyone else, should believe a word typed by your fingers.
You didn’t read far enough back in the threads but let’s see if you can reason this out by asking you a question. What changes in the ev model when you lengthen the genome while keeping all other parameters constant?Kleinman said:Of course I have, and if you had read this thread, you would know what I have to say about it.Ichneumonwasp said:The only explanation I can find is that you think three selection pressures somehow, and magically, interferes with the process in the presence of longer genomes. Do you have a more formal explanation?
What relationship to reality does this have?Kleinman said:Here are the changes Unnamed made to ev:Paul said:Yes, he's taking into account the distances from valuation to threshold for all positions.
It seems Unnamed has abandoned the discussion after this last exchange:Kleinman said:Why don’t you post a version of ev with these changes online so everyone can study the behavior of these changes?Paul said:That would be Unnamed's job.
Kleinman said:In addition, there is no selection process for a partially completed gene.Unnamed said:I don't think that's true, but if it were, then my change would be meaningless.
I don’t think that at all. kjkent1, Ichneumonwasp and numerous other evolutionists attempt to suggest that Dr Schneider’s only purpose for ev was to show how information gain occurs by mutation and selection and nothing more than that. It is clear by the above statement, which was not Dr Schneider’s intention.Kleinman said:He must have meant that only variations that support the theory of evolution should be investigated. Paul, I love it when you squirm.
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Paul, Dr Schneider was quite clear what he intended ev to be used for when he said the following:Dr Schneider said:Variations of the program could be used to investigate how population size, genome length, number of sites, size of recognition regions, mutation rate, selective pressure, overlapping sites and other factors affect the evolution.Paul said:That statement suggests to you that he only wants the program to be used to investigate things that support evolution? All righty then.
De novo = from the beginning. I’ve started using this terminology again since Mr Scott used a reference from Nature that includes this.Kleinman said:Ev does not evolve binding sites de novo according to Paul.Paul said:I would be happy to address this claim if you could first define what you mean by "evolving binding sites de novo."
Now Paul, don’t get into a tizzy. Just because ev shows that the theory of evolution is mathematically impossible doesn’t mean that you shouldn’t try to prove intelligent design mathematically impossible. Why don’t you prove that it is mathematically impossible for intelligent scientists to do recombinant DNA?T’ai said:Has anyone worked out how an intelligently designed program can possibly disprove the concept of intelligent design yet?Paul said:Who is claiming that a program disproves intelligent design? Certainly no one in this thread.
Articulett, I must have missed your description of the selection pressure that would evolve a gene de novo. Could you repeat it again for us?T’ai said:Has anyone worked out how an intelligently designed program can possibly disprove the concept of intelligent design yet?articulett said:Oddly enough...unintelligent naturally selected DNA does just that.
You posted the concept on this thread. So why not defend what you post?Kleinman said:Let’s see if I can help you with the word serious. Try the word “earnest” instead of “serious”. Dr Schneider has made an earnest application of the mathematics of mutation and selection while you have made earnestly silly application of the string cheese theory to mutation and selection.kjkent1 said:littleman, if you find string theory silly, take it up with Dr. Susskind.
The proof is out there. Multiple selection pressures slow evolution, ev shows this, numerous real examples shows this. I’ll keep whining this until it gets through your prejudiced and biased mind.Kleinman said:When considering other mutation mechanisms, the question is whether these other mutation mechanisms will significantly alter the behavior of the mathematics of mutation and selection process. I don’t believe it will for several reasons. Point mutations are the least destructive of mutations as well as the most common type of mutation. They don’t cause frame shifts which alter large numbers of codons. If you think that other mutation mechanism will somehow accelerate the mutation selection process, feel free to prove this. With respects to Dr Schneider’s selection scheme, it is very forgiving. What I mean by this is that you don’t have the possibility of extinction. The weight factors are not tied to survival of a creature. There are many examples of single mutations which cause the death of the creature with that mutation, yet ev does not have this effect. Including these types of features in the model would only slow evolution more so. In addition, how would you formulate the selection process that would evolve a gene de novo? There is no such selection process.kjkent1 said:littleman, no one cares what you believe. We are waiting for you to prove your theory. Until you do, you are the supreme whiner in this thread.
Are you talking about Dr Schneider’s extrapolation that a human genome could evolve in a billion years based on the rate of information acquisition on a 256 base genome and a mutation rate of 1 mutation per 256 bases per generation. Which one of the 10^500 alternative universes did this happen in?Kleinman said:That’s an easy one. Introduce whatever feature you want in the model and see whether you can speed up evolution sufficiently and prove your case. Since ev is already showing that it is the multiple selection conditions which slow the evolution process, the changes you advocate will not alter the fundamental mathematics already revealed.kjkent1 said:Same ****, different words. We are waiting for you to prove your case. Schneider has already proved his.
If you don’t think the model is anything close to reality then why don’t you correct it to prove your point? I have already shown how ev’s three selection conditions parallels what happens in reality with numerous different real examples, and you, well you have shown us string cheese.Kleinman said:Everybody has biases. The question is whether I am drawing my conclusion based on these biases or am I drawing my conclusions based on the results from ev and the numerous real examples which show that multiple selection pressures slow evolution.kjkent1 said:You're drawing your conclusions based on a version of the program which does not model anything close to the reality of variations in the evolutionary process. So, your conclusions are pure conjecture.
It is not the random point mutations that make the theory of evolution slow, it is the multiple selection pressures which slow the process, of course, that is just in the alternative universe that we live in. Do you think that the real example of combination therapy slowing the evolution of resistant strains of HIV is limited to point mutations? How about combination therapy of TB in order to slow the evolution of resistant strains of this bacterium? Is this case limited to random point mutations? How about combination pesticides, combination herbicides, combination rodenticides and combination cancer therapy, are these cases limited to random point mutations? It isn’t the type of mutation which slows the evolution process, it is multiple selection pressures which slow this process.Kleinman said:I have demonstrated why Dr Schneider improperly extrapolated the evolution of a human genome. You evolutionists refuse to acknowledge this. Instead, you look for ways to parse words to justify this type of unscientific approach. That said, Dr Schneider’s underlying simulation has properly captured the mathematics of mutation and selection. In particular, the effect of multiple selection pressures is properly revealed.kjkent1 said:You will need to accurately model all of the known real evolutionary processes. Until then, all you've proved is that random point mutation, by itself is prettyt slow. Don't think anyone would argue with that conclusion.
The numerous real examples of how multiple selection pressures work is not conjecture; they are nails in the coffin for the theory of evolution. It is just handy to have a mathematical model of mutation and selection to drive those nails in.Kleinman said:That’s a bit of an understatement. Simply using a realistic mutation rate of 10^-6 instead of 1 mutation per 256 bases per generation in Dr Schneider’s published case makes his estimate of 1 billion years for the evolution of a human genome go to 4 trillion years. And what real living thing has a genome length of 256?kjkent1 said:Using only point mutation and an extremely simple selective process. Since neither is a complete model of evolution, your numbers are pure conjecture.
It could but it won’t. The effect of multiple selection pressures will not disappear no matter how sophisticated you make your algorithm. Ev shows the important mathematical principle that crushes the theory of evolution. That is that multiple selection pressures slow the mutation and selection process profoundly. Add that to the fact you don’t have a selection pressure to evolve a gene de novo and you don’t have a selection pressure that would evolve a reptile into a bird makes the theory of evolution the biggest fraud to hit the scientific community since the flat earth theory.Kleinman said:Kjkent1, you can’t parse away this statement from the NAR paper...kjkent1 said:I'm not parsing away anything. Given more sophisticated algorithms, ev's basic premise could be extended to show a more complete explanation of evolution. Without more sophisticated algorithms, ev proves information gain, which is what the paper sought to prove.
I have done some work; I did what Dr Schneider suggested to do in his paper. I studied what happens to his model of mutation and selection when you vary the parameters. What it shows is that the theory of evolution is mathematically impossible. Of course there are numerous real examples which demonstrate what ev shows and why the theory of evolution is mathematically impossible.Kleinman said:Only evolutionist cultists would end the discussion here. I have no objection to adding any feature to ev. Let’s see if it changes any of my conclusions.kjkent1 said:Let's see you do some of the work to prove your theory. As it stands, Schneider's proven info gain, and you've proven random point mutation is slow. Your miles from proof that evolution is impossible.
Really, what limits the numerous real examples to random point mutations?Kleinman said:My conclusions are unsubstantiated except for the results from ev and numerous real examples of these results.kjkent1 said:Your "real examples" are all based on random point mutations and a simplistic selection algorithm. So, your examples are not real, therefore all of your conclusions are unsubstantiated.
Would you like to have an Irish wake for the theory of evolution?Kleinman said:Would you pass the red herring, string cheese and whine please.kjkent1 said:Absolutely, littleman. You can have all you can digest. Personally, I think you need a "Reglan," because you just can't seem to digest reality.
Mr Scott, I don’t mind if a pussycat joins this debate.Mr Scott said:Do you suppose Dr. Kleinman is happy he's joined in this debate by such a brilliant mind?
What a minute, isn’t this the cruft theory of evolution?Cyborg said:You do realise of course that software engineering shows us that the most, THE MOST, used design technique is:
"Try it, if it works keep it, if not throw it away."
Which just blows friggin' great chunks in your nonsense.
Now don’t forget the other fundamental purpose of ev: that is to annoy evolutionists.kjkent1 said:What you describe is the fundamental purpose of ev: to show that information gain can arise from a randomly ordered system using the process of random mutation and natural selection.